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ICU & Fluids – Electrolytes – Nutrition

ICU & Fluids – Electrolytes – Nutrition:

Edited by Andy S. Binder, MD, Pulmonologist, Critical Care.  Contents:  Electrolytes:  Fluids:  Dehydration:  Shock:  Nutrition & Vitamins:  Common Conversions: Therapeutic Levels:  Hypoxemia: Hypoxia:  Pulse Oximetry: Hypercapnea:  Intubation:  Mechanical Ventilation: Sedation: Vascular Access: PA Cath Patterns:  Acid-Base Physiology:  Preamble & Abbrev & Labs:    9-08-01.

Serum Electrolytes:

Links:  Sodium (Na):   Magnesium (Mg):   Potassium (K):   Calcium (Ca):   Phosphate (P):   Always repeat to r/o artifact (laboma).

Chloride (Cl):  closely related to Na metabolism.  Requirements:  adult –> 90-120 mEq/d.  Child–> 5-7 mEq/kg/d.  Bicarbonate: Major extracellular anion with Cl.

Sodium (Na) Metabolism:

Links:  FENa:   Hyponatremia:   SIADH:   Hypernatremia:

Major determinant of body tonicity, primarily an extracellular cation.  Serum Na reflects body water.

Na requirements:  3 mEq/L ECF = 0.6 X wt in kg X 3.    Adults need ~75-150 mEq/d.  Child needs 3-5 mEq/kg/d.   1 teaspoon table salt = 100 mEq of Na.   1g salt = 17  1 mEq of Na.   1g Na = 43.5 mEq of Na.

FENa: [UrNa X SCr/ SNa X UCr] X 100–> <1 = pre-renal.  > 1= renal (ATN).  FENa is the fraction of Na in the urine filtered by the glomerulus and not reabsorbed. Corrected Na = (0.016 X BS) – 100 + Na (measured). As Na falsely decreases 1.6 mEq/L for each 100mg/dL inc glucose over 100mg/dL.

Hyponatremia:

Links:  Etiology:  S/s:  W/u:  Spot Ur Na:  Ur Osm:  Tx:  Hypotonic (Hyposmotic hyponatremia):  SIADH: Isotonic (Isosmotic hyponatremia): Hypertonic (Hyperosmotic hyponatremia):

Too much extracellular water relative to Na.   Na <136 mEq/L (mmol/L) (normal = 136-145).  Na+ deficit: 0.6 X (wt in kg) X (140- Na).  The tonicity (osmolality) is usually low (hypotonic), but may be normal or high.

Causes:  ACEi. Renal Na loss–> diuretic, adrenal insufficiency, RTA, salt losing nephritis.  Nonrenal Na loss–> emesis, diarrhea, pancreatitis, rhabdo, burns.  Water excess–> SIADH, secondary adrenal insuf.  Hypovolemic –> Saline excess with dec ECV–>  CHF, cirrhosis, nephrotic syndrome.   Saline Excess w/o dec ECV–>  ARF, CRF.

S/s: muscle twitching, inc DTR, sz, HTN (20 to inc ICP), salivation, lacrimation, watery diarrhea.    Na <120 w/o sx, then gradual depletion.

W/u: get initial wt, daily wts, check serum osmolality, Ur Osm, Chem 7, Alb, Ca, Mg, FENa, spot urine Na/ K/ Cl/ Cr.  Step #1: Assess serum osmolality:   A. Normal (280-295) = isoosmotic hyponatremia (pseudohyponatremia) and is due to either 1. Hyperproteinemia or 2. Hyperlipidemia.     B. Elevated (>295) = hypertonic hyponatremia and is due to either 1. Hyperglycemia (no osmolar gap) or 2. Hypertonic infusions (mannitol, glycine).   C. Low (<280) = hypotonic hyponatremia. —->  Step #2: Assess volume status and Ur-Na.  A. Hypovolemic = total body depletion of Na disproportionately to water losses, due to 1. Urine Na >20-renal loss (osmotic diuresis, salt-losing nephropathy, diuretic, proximal RTA, adrenal insufficiency, vomiting with bicarbonaturia and obligate Na loss).  2. Urine Na <20 = extrarenal loss (vomiting, diarrhea, third-spacing).  Or B. Hypervolemic = retention of free water. 1. Urine Na >20 = renal failure.  2. Urine Na <20 = nephrotic syndrome, CHF, cirrhosis.  Or C. Euvolemic = a mixed bag.   1. Urine Na >20 = renal failure, SIADH, hypothyroidism, pain/emotional stress, various drugs (amitriptyline, carbamazepine, clofibrate, Cytoxan, morphine, vincristine), selective glucocorticoid deficiency.   2. Urine Na <20 = water intoxication.

Calculating the Na (mEq) deficit:  Not very accurate as it assumes a closed system (kidneys clamped), in real life the kidneys assist in correcting the deficit much quicker.   Na deficit = 0.6 x (wt kg) x (desired [Na] – actual [Na]).  Ex: if wt is 64kg and serum Na is 113–>  0.6 (113)  X 140-113 = 38.4 X 27 = ~1040.  If have 154 mEq Na in NS, then 1040 / 154 = ~6.7 L NS needed to correct.   To estimate the effect of 1L of infusate on serum Na:    Change in Na = [(infusate Na +K) — serum Na] / (total body water —1).

Spot Ur NA in Hyponatremia:  Interpret based on estimated volume status. Ur Na reflects aldo effect.  1. Inc Extracellular Volume (Hypervolemic): <10-20 mEq/L –> CHF, Cirrhosis, Nephrotic, hypo-albumen.   >20-40 mEq/L –> Renal Failure (acute or chronic).

2. Dec Extracellular Volume (Hypovolemic): <10-20 mEq/L –> Emesis, diarrhea, pancreatitis, lung/ skin loss (burns).   >20-40 mEq/L –> Renal Loss: Na-wasting nephropathy, osmotic diuretics, obstruction, RTA, adrenal insufficiency.

3. Isovolumic (Euvolemic):  <10-20 mEq/L –> Water intoxication.   >20-40 mEq/L –> Renal failure, hypothyroid, pain, SIADH, emotion, adrenal insufficiency, post-op states.  Variable Urine-Na concentration with decreased solute intake, psychogenic polydipsia and resetting of osmostat (pregnancy, psychiatric disorders).

Urine Osmolality:  reflects ADH effect.   Normal is >700-1400 mOsm/kg.  If 600-700 then minimal impairment in renal concentrating ability.  If 400-600 moderate impairment.  If <400 mOsm/kg then severe impairment.   In complete diabetes insipidus (DI) Ur Osm 50-200.  In partial DI 250-500.  In Nephrogenic DI 100-200.  In primary (psychogenic) polydipsia Ur Osm are 700-1200 mOsm/kg.  In high-set osmoreceptor DI it is 700-1400.

Tx:  Correct underlying d/o with volume and correct the cause.  Water restricting to <800-1000 ml/d will ameliorate all forms of hyponatremia, but it is not considered the optimal therapy as uncomfortable to the pt (only ice chips if IV at “keep vein open”) and slow (1mEq/d).  Loop diuretics with hourly K and Na replacement in hypervolemic forms.

If symptomatic–>  Hypertonic saline (3-5%) @ 2ml/kg/hr, to inc Na by a max 1-2 mEq/h, up to serum Na of 125-130.    The initial rate of correction can be 1-2 mmol/L/hr in patients with severe sx’s, but the maximum rate of correction should not exceed 8 mmol/L on any day of treatment.   Max rate of infusion of 100ml of 5% saline/h to avoid central pontine myelinolysis (demyelination, think hypo – pons, hyper = edema- cerebral).   Rule of thumb:  1ml/kg 3%NS raises serum Na by 1mEq/L.  Correct slowly over 48hr.  To raise the sodium 1mEq/hr infuse at rate of–>  (wt in kg X 0.6) / (0.513 mEq/L X 1hr). Or take the amount of NS calculated from the deficit and divide by 24hr.  The pt usually correct faster as the calculations are based on the kidneys being clamped, so re-check in 4-6hr to make sure not correcting too quick as you may need to add free water (½NS or D5W).

1.  Hypotonic (Hyposmotic hyponatremia):  Plasma Osm <280 mOsm/kg (normal = 280-295). Check Uosm –> if <150, then psychogenic polydipsia as appropriate dilution.  If Uosm >150–>  assess renal function to r/o primary renal dz.  If normal renal function, assess extracellular volume status.

W/u:   Check urine Osm, if <150 mOsm/kg then psychogenic polydipsia.  If >150 mOsm/kg assess renal function.  If inc BUN or Cr, then primary renal dz.  If normal renal function, assess extracellular fluid volume, check UrNa.  Consider the Cosyntropin Stimulation Test for adrenal insufficiency.

Etiology of Hypotonic Hyponatremia:   1. Excessive water intake:  primary polydipsia, accidental intake of water (swimming lessons), dilute infant formula, Na-free irrigant solutions during surgery, multiple tap-water enemas.

2.  Impaired capacity of renal water excretion:     A.  Decreased Volume of Extracellular Fluids (Hypovolemic):   Loss of isotonic fluids or replacement with inadequate volume of excessively hypotonic fluid. GI loss (vomit, diarrhea), skin, lungs, kidneys (diuretics, RTA, diuretic phase of ATN, adrenal insufficiency, hypo-aldo), third spacing.    Tx: 3% NS.

B.  Increased Volume of ECF (Hypervolemic):  Due to fluid retaining states such as CHF, nephrotic syndrome, hepatic failure (cirrhosis), malnutrition, acute/ chronic renal failure, pregnancy.    Tx: water restrict, consider diuresis.

C.  Normal ECF Volume (Isovolumic): Iatrogenic free water overloading, SIADH (unable to dilute urine in response to a water load), renal insufficiency, dec K (sensitizes kidney to ADH), thiazides, hypothyroid, adrenal insufficiency.   Tx: restrict water, consider hypertonic saline if sx’s.

Other:   Oxytocin: Used to induce labor, has an ADH effect, mimics SIADH.   Avoid giving Oxytocin with hypotonic fluids.  Tx:  D/c Oxytocin.

Cyclophosphamide: has antidiuretic effect and pt’s encouraged to drink fluid to avoid chemical cystitis.  Tx:  3% NS and Furosemide.

Psychotic Self Induce Water Intoxication:  Polydipsia (>1L/hr).

Tx: monitor diurnal wt for early detection.  Avoid antidiuretic meds, water restrict.  R/o SIADH.

Marathon runner:  especially if uses NSAIDs before race and female.  Pain and stress + ECF depletion due to salt loss (minimal contributor as if lose 9L sweat, only lose 1/17 of total body sodium), sugar water consumed during race + volume expansion from lots of fluid (excess hydration with plain water) –>  promotes ADH (vasopressin) release–>  hyponatremia and risk of cerebral edema and sz.  Whenever an athlete collapses, the first step is to place in Trendelenburg, then check a rectal temperature (if >39C, treat as heat illness).

Tx:  3% NS if sz’s.  Isotonic saline and water restriction if milder sx’s.  If post race Na >130, then observe pt.   If 126-130 give NS IV by estimating ECFV.    If <126 give 100ml of 3%NS IV qh until Na >130 (takes 3-5h).

Syndrome of Inappropriate Antidiuretic Hormone (SIADH):

Criteria:  1.  Hypotonic Hyponatremia (Na <125 mEq/L) and hypo-osmolarity (<270-280 mOsm/kg).   2.  Urine osmolality greater than appropriate (>75-100 mOsm/kg = 75-100 mmol/kg, usually >400 mOsm/kg, but less than maximally dilute) for the degree of systemic hypotonicity.    3.  Urinary Na excretion is high, usually >20-40 mEq/d. May go to 154 if pt treated with NS.     4. Absence of volume contraction (no extracellular fluid depletion). Euvolemic appearing (really volume expanded as have low uric acid level). Uric acid is low in SIADH (<2.5) (Hypouricemia in SIADH. NEJM 301:528, 1979).   5. R/o other causes:  normal renal, adrenal, thyroid, cardiac, hepatic function.

Etiology of SIADH:  Cancer –> lung (small cell) >pancreas> duodenum> bladder> prostate> lymphoma/ leukemia> thymoma> mesothelioma> Ewings.   Any pulmonary lesion–>  TB, CF, any type of pneumonia, abscess, asthma, positive pressure mechanical ventilation, acute respiratory failure.    Endocrine–>  hypothyroid, glucocorticoid def (hypopituitarism).   Neurologic d/o–>  psychosis, any CNS lesions (neoplasia, vascular, trauma), stroke, Guillan-Barre’s, infection (meningitis, abscess), hydrocephalus, MS.  Drugs–>  chlorpropamide (Diabinese), tolbutamide, clofibrate, antineoplastic (vincristine, cyclophosphamide, vinblastine), antidiuretic hormones (oxytocin, DDAVP, Vasopressin), tricyclics, Haldol, nicotine, phenothiazines, carbamezapine (Tegretol), opiates, bromocriptine, NSAIDs, SSRI’s.  Other–>  Idiopathic, surgical (post-op)/ emotional stress, pain, nausea, porphyria, delirium tremens, AIDS, decreased intake of solutes (beer potomania, tea-and-toast diet).  Postoperative–>  vasopressin secreted in response to surgical stress, free water from hypotonic IV fluids.

Tx: 3% saline and Furosemide (Lasix makes the kidneys excrete ½NS as get dec Na in the urine).   Avoid hypotonic fluids (D5W, 0.45% saline) and excessive volumes of isotonic (LR, NS).  The osmostat often resets to the lower serum Na level.  Demeclocycline: 150-300mg PO BID-QID, indefinitely.

2.  Isotonic (Isosmotic hyponatremia):  (250-280 mOsm/L)  “Pseudohyponatremia”, see in presence of inc Trig (serum Na decreases by 1mmol/L for each inc serum lipids of 4.6g/L), inc protein. Or isotonic infusions of glucose, mannitol, glycine, glycerol, sorbitol, ethanol, methanol.   Due to lab artifact as plasma water as smaller fraction than normal leading to an underestimation of true Na concentration.   Suspect when the serum is milky appearing.  Need to compare measured plasma osmolarity with calculated or measure plasma Na with a direct-reading Na electrode.

3.  Hypertonic (Hyperosmotic hyponatremia): Posm >285.

Due to a non-Na hyperosmotic infusion of a substance that has an intracellular water osmotic redistribution (glucose, mannitol, glycine, isopropyl, ethylene glycol, sorbitol).  For each 100mg/dL greater than 100, serum Na decreases by 3 mEq/L.  Hyperglycemia–>  anticipate 3 mEq/L inc Na for every 200mg/dL reduction in BS.  IV Mannitol–>  water shift from ICF to ECF as with hyperglycemia.  Should be rapidly excreted if normal renal function. IVIG–> maltose in the solution acts like mannitol.    Irrigant absorption–> seen in prostatectomy and intrauterine surgery.  The solute (glycine, mannitol or sorbitol) is initially confined to ECF causes dec Na with little change in plasma osmolarity.   Glycine is a neurotoxin and causes blindness, it is metabolized to ammonia and may cause encephalopathy.

**Ref:(Hyponatremia. N Eng J Med 2000;342:21) (Ann IM 1990;113:417-19) (J IM 1994;235:497) (Hyponatremia: age-related risk factors and therapy decisions.  Geriatrics. 1998;53:32-8) (Beer potomania: two cases and review of the literature.  Clin Nephrol. 1996;45:61-4) (Severe hyponatremia in the polydipsia-hyponatremia syndrome.  J Clin Psychiatry. 1994;55:355-61) (Acute hyponatremia in ultra-endurance athletes.  Am J Emerg Med. 1994;12:441-4) (Management of symptomatic hyponatremia: dependence on the duration of development. J Intern Med. 1994;235:497-501) (Hyponatremia: epidemiology, pathophysiology, and therapy.  Curr Opin Nephrol Hypertens. 1993;2:636-52)

Hypernatremia:

Links:  Etiology:  S/s:  Labs:  W/u & Tx:

Na >145-150 mEq/L (mmol/L).  Free water deficit or water loss (>Na loss) or a Na gain with free water restriction.  Always associated with a hyperosmolar state (hypertonic hyperosmolality) leading to at least a transient state of cellular dehydration.

Etiology:  1. Net Water Loss:  neurogenic/ nephrogenic diabetes insipidus, renal diuresis (osmotic, Loop diuretics), postobstructive diuresis, polyuric phase of ATN, intrinsic renal dz, GI or cutaneous losses.  Poor fluid intake–> mental or physical disability, limited access to fluids, inadequate thirst response.     Free Water loss–> osmotic diuresis (DM, DI), diuretic use, febrile illness (unreplaced insensible losses).      2.  Hypertonic Sodium Gain:  Salt poisoning–> inappropriate administration of hypertonic salt solution (hemodialysis pt).  Hypertonic NaHCO3 infusion, hypertonic feeding preparations, ingestion of salt or seawater, hypertonic saline enemas, primary hyperaldosteronism, Cushings syndrome.

S/s: restlessness, sz, coma, delirium, mania, sticky mucous membranes, dec salivation/lacrimation, inc temp, red/swollen tongue, thirst, weakness.  In infants it causes hyperpnea, weakness, high-pitched cry, insomnia, lethargy and coma.   In elderly there may be few sx’s until Na >160. Brain shrinkage may cause vascular rupture leading to a cerebral bleed or a SAH.

Lab: Elev Na (>145 mEq/L), inc serum Osm, inc Ur Osm (if extrarenal losses), inc Ur Na (if renal losses), dec GFR.  Check ADH (vasopressin) level on admission labs (low in central DI, high in nephrogenic DI). Step #1:  assess volume status. This helps to determine underlying cause. A. Hypovolemia–> usually from Na (and hence H2O) losses with H2O losses predominating.   Urine Na >20 meq/L reflects renal losses from diuretics, glycosuria, mannitol, renal failure, etc. Urine volume also tends to be high with high osmolality.    Urine Na <10 meq/L reflects extrarenal losses (sweat, GI, insensible). Urine volume is low with high osmolality.    B. Isovolemia–> reflects loss of free water.  R/o diabetes insipidus (DI), consider extrarenal losses-skin & respiratory insensible losses.   C. Hypervolemia–> usually from net Na gain, can be iatrogenic-IVF with hypertonic saline or NaHCO3, NaCl tablets, hypertonic IVF (e.g. cryoprecipitate with Nacitrate anticoagulant), dialysis with hypertonic solutions or from mineralocorticoid excess-primary hyperaldosteronism, Cushing’s disease, congenital adrenal hyperplasia

Tx:   Links:  Step #1: FWD:  Step #2: Volume Status: Hypovolemic:  Isovolumic: Hypervolemic:

Basics:  correct free water deficit slowly with ½ the calculated amount over 8hr, then reassess and give remaining ½ over 16-24hr.  If too rapid correction, cerebral edema may result.  Hypotonic fluids such as D5W, dextrose are metabolized in the liver to leave electrolyte free water.  May need to stop GI losses, control pyrexia, hyperglycemia and treat the possible associated inc Ca and dec K.  Isotonic fluids if there is significant depletion of extracellular fluid as to cause hemodynamic compromise.

Step #1: Free (body) Water Deficit (FWD) in Liters:   FWD in Hypernatremia:  FWD = [Serum Na (measured) – serum Na (normal) x 0.6 Wt in kg/ normal serum Na].     Also written as, FWD = [(Na-140)/140] baseline wt X F. (F = fraction of wt that is water, 0.6 for male, 0.5 for females).  Also written as, FWD = FWD  = 0.6 X wt in kg X (1- 140/Na).   Kg is estimated wt when fully hydrated.  Generally, about half of deficit can be replaced in the first 24 hours; rest over 1-2 days.  Avoid correcting the serum Na concentration >1mEq/L/hr.

Step #2: Determine patients specific etiology & volume status: Hypovolemic:  Electrolyte-free water loss.  If UrNa >20–> renal loss (diuretic, glycosuria, RF, diabetes insipidus, excess urea excretion).

If <10–> extrarenal loss (GI, sweating, repiratory loss, fever). Labs seen with low volume status: dec Ur Na, Ur Osm >400mOsm/kg.   Diuretic use:  Ur Na >20, Ur Osm +300 mOsm/kg (isotonic), serum Osm is variable depending on free water loss.   If pt awake & alert, nl BP, no sx’s–> free water, PO 300 ml q2hr during waking hours for a total daily intake of 2.4-2.7 L.  Replace ½ the deficit and decrease the serum Na by 3/d.  If pt obtunded or comatose–> 5% dextrose in water IV at no more than 12 mEq/d for 72hr.  Monitor serum Na q8-12hr, switch to PO when tolerated.  If pt severely dehydrated, postural hypotension, tachycardia and high BUN/Cr ratio. –> Rapidly administer NS until tissue perfusion adequate, then immediately exchange to 5% Dextrose as for obtunded pt.   If pt has DM–> add small amounts of regular insulin to IV solution PRN.  If pt has Central DI, inc Ur Na, Ur Osm <150, inc serum Osm, Vasopressin level low after 8hr water deprivation test–> Vasopressin 5 U SC q 24-72hr or Desmopressin 5-10 ug intranasal or 0.1-0.4 mg PO BID.  If pt has Nephrogenic DI, same labs as central but normal vasopressin level –> Hydrochlorothiazide 25mg PO BID, low Na diet.

Isovolumic:  Loss of water or inadequate intake.  Hypotonic losses.   If UrNa >20–> renal loss (Diabetes insipidus, glycosuria, mannitol, glycerol, diuretics).  If <10–> insensible skin (sweat), repiratory, upper GI, osmotic cathartics loss.  Variable Urine-Na with renal loss and hypothalamic disorders.

Tx: water replacement, D5W + vasopressin for central DI.

Hypervolemic:  gain water +Na. Salt poisoning.   If UrNa >20–> Iatrogenic (NaCl tablets, hypertonic solutions such as 3-5% saline, hypertonic NaHCO3), Mineralocorticoid (adrenal, Cushings, primary hyperaldosterone), hemodialysis with hypertonic dialysate.

Tx: diuretics + dialysis.

**Ref:(Hypernatremia. N Engl J Med 2000;342:20) (Ann IM 1996;124:197) (Hypernatremia.  Semin Nephrol. 1998;18:20-30) (Hyponatremia and hypernatremia.  Med Clin North Am. 1997;81:585-609) (Hypernatremia in hospitalized patients.  Ann Intern Med 1996;124:197-203)

Magnesium (Mg) Metabolism:

Links:  Hypomagnesemia:  Hypermagnesemia:

Mg is the 2nd most abundant intracellular cation.  It plays a crucial role in enzymatic reactions utilized in storing and using energy.  The average dietary intake is 25mEq/d, which only marginally meets the requirements. 54% is in bone and teeth (~14g), 46% in cells (~12g) and 1% extracellular.  Normal serum level is ~1.6-2.6 mg/dL

Hypomagnesemia:

Links:  Ddx:  S/s:  Dx:  Tx:

Distribution is similar to K, effects similar to Ca.   Require 20 mmol/d.  Rarely sx’s unless <1mg/dL.  Often due to dec Alb as it is protein bound like calcium.

Ddx:  Malnutrition (ETOHism, prolonged fasting, TPN w/o replacement, short gut syndrome, malabsorption, fistulas), ETOH (causes renal loss), burns, pancreatitis, chronic diarrhea and fistulas, SIADH, vigorous diuresis, primary hyperaldosteronism, post- parathyroidectomy, Meds (AmphoB, Cisplatin, Aminoglycosides, Dig, Foscarnet, Cyclosporin, Pentamidine, Diuretics), s/p ATN, NG drainage, DKA.

Bartter Syndrome: a familial hypokalemic, hypochloremic metabolic alkalosis.  Due to ion channel abnormalities in of renal tubular cells.

S/s:  HTN is not present, despite high renin and angiotensin II levels. Delayed growth, mild cognitive developmental deficits, polyuria and polydipsia, rare tetany.  Hypomagnesemia in ~20%.  Normal to high urine calcium (nephrocalcinosis variable), high urine prostaglandins.  Renin, aldosterone & angiotensin II markedly elevated.  Tx:  correcting sx’s and electrolyte anomalies.  Indomethacin to inhibit prostaglandin secretion is variably effective.  Gitelman Syndrome:  a variant of Barrter syndrome, presents in childhood or adolescence.  S/s: pt has normal growth and cognitive development, polyuria and polydipsia may be present.  Prominant neuromuscular irritability with positive Chvostek and Trousseau signs (with normal serum calcium levels), tremor, fasciculations and tetany is common.  Hypomagnesemia in ~100%.  Chondrocalcinosis occurs as dec Mg blunts release and function of parathyroid hormone, this can lead to hypocalcemia.   They have a low urine calcium, normal urine prostaglandins.  Renin & angiotensin II are elevated, aldosterone is normal to high.  Tx: Correct electrolyte anomalies

S/s: Weakness, muscle fasciculation’s/ tremor/ tetany, apathy, MS changes, sz, hyperreflexia, cardiac dysrhythmia, inc QT, dec K, dec Ca, N/V, ileus.

Dx: Serum Mg may not reflect intracellular, if the serum Mg is equivocal consider measuring a 24hr Urine Mg and Cr (to ensure adequate collection).   If the Ur-Mg is 10 mg–> then poor intake, GI malabsorption, small bowel dz, redistribution or normo- magnesemic Mg depletion.   If >20mg–> then due to primary renal tubular defect, inc Ca, saline infusion, diuretics, Cisplatin toxicity, aminoglycoside toxicity or Barters syndrome.   Or can do a Mg load study by giving 60mEq in 500ml D5W over 12hr, if > ½ is excreted in 24hr then depletion.

Tx:  IV:  PO:   Most cases need no supplements unless <1.0, sx’s or causing dec K or arrhythmia.  Correct slowly over days by giving 50-60 mEq/d X 5-6 days, caution if pt has chronic renal failure (reduce dose by ~50%). Consider adding a K-sparing diuretic if already taking a thiazide or loop diuretic.

IV: 1-2g MgSO4 (22mg or 4ml of 50% MgSO4) in 100ml D5W as 10% solution over 15 min. Can give 4g/hr, if acute situation (i.e. Torsades) give 1-2g over 1min IVP. Follow with a continuos infusion over the next 6hr of 5g diluted in NS or D5W.   Monitor closely if oliguric.  Follow replacement with dec patellar reflexes, serial serum and sx’s resolution.  Check EKG if large doses.  MgSO4 for IV comes in amps, 1 amp = 1 gram (8 mEq). You may write a sliding scale in the units. Serum Mg–> gm of MgSO4 to give IV. If 1.8-1.9–> 2. 1.6-1.7–> 3. 1.4-1.5–> 4. 1.2-1.3–> 5. <1.2–> 6 & call HO.

PO Forms: ~500mg PO qd-BID.  Mg Oxide: 400 mg (20mEq = 70% of RDA/tab) or 420 mg (240 mg elemental Mg) at a max of 4-6X/d.  A laxative, the sulfate or gluconate forms may cause less diarrhea.  Beelith: 600mg Mg-oxide = 362 mg of elemental Mg (30mEq = 90% RDA).

Slow Mag (Mg-Cl): 64mg of Mg (5.3 mEq or 16% of RDA) + 110mg Ca carbonate per tab.    Mag-Tab (Mg-lactate): 84mg of Mg per tab (=7 mEq or 21% of RDA).  Give 2 tabs TID-QID if severe or 2 tabs qd-BID if mild asymptomatic dz.    Mag complex: 300 mg elemental Mg @ 1-2 tab qd.   Mag gluconate: 500 mg (27 mg elemental Mg) @ 1-2 tab qd.

Hypermagnesium:

Ddx: Renal insufficiency, antacid abuse, rhabdo, tumor lysis, burns, tissue trauma, hypothyroid, adrenal insufficiency, excessive intake (tx of eclampsia), cathartic abuse.

Sx: N/V, weakness, MS changes lethargy, coma, hyporeflexia, respiratory depression, dec BP, arrhythmia, inc QT, AVB.

Tx: Stop external sources (antacids, cathartics), IV CaGluconate: 10ml of 10% solution IVP.  Or CaCl (10%) @ o.2-0.3 ml/kg (max 5ml) IV.   Volume expansion with NS, IV Lasix if good renal function, dialysis in renal failure.

**Ref: (Hypomagnesemic hypocalcemia in chronic renal failure.  Am J Kidney Dis. 1993;21:167-71) (Cecil Textbook of Medicine 2000, 21st ed, Saunders, pp1137-39) (Magnesium: physiology and pharmacology. Br J Anaesth 1999;83:302-20)

Potassium:

Links:  TTKG:  Foods:  Hypokalemia:   Hyperkalemia:

90% K is intracellular. A major cation along with Mg.   Normal value is 3.6-5.2 mmol/L.   Serum level does not reflect intracellular level; 1 mEq/L ECF = 200 mEq/L ICF.  Level is influenced by the kidneys, intestines, endocrine, acid-base status.  Both high and low may lead to arrhythmia’s.  Important in glucose transport, intracellular protein depolarization, and myoneural conduction.  Requirements:  2 mEq/l ICF : 0.4 X wt in kg X 2.   Or  ~50-100 mEq/d adult, and 2-3 mEq/kg/d as child.

Transtubular Potassium Gradient (TTKG):

Normal = 4-14, varies with diet.  = (UrK / PlasmaK) / (Uosm / Posm).

If Dec K: <2, GI loss.  >4, renal loss or excess aldo.

If Inc K: Helps to determine if the hyperkalemia is of renal or extrarenal origin.   If TTKG is <6, suggests a renal cause (dec aldo or lack of response). If the renin is normal it suggests hypoaldosteronism. If serum aldo is low and the renin is also low, it suggests hyporeninemic hypoaldosteronism. If the serum aldo is normal it suggests a renal tubular deficit.  If >6-10 suggests non renal, normal aldo effect. Such as increased K intake in diet, hemolysis or rhabdo.

Foods with High Potassium (K):

Highest (>10mg/g) –> dried figs, molasses, seaweed.

Very High (>5mg/g) –> dried dates/ prunes, nuts, avocados, bran cereals, wheat germ, lima beans.   High (>2.5 mg/g) –> vegetables such as spinach, tomatoes, broccoli, squash, beets, carrots, cauliflower, potatoes.   Fruits such as banana, cantaloupe, kiwi, oranges, mango.    Meats such as beef, pork, veal, lamb.

Hypokalemia:

Links:  Ddx:  S/s:  Tx:

K <3.6 mmol/L.  The most common electrolyte abnormality in clinical practice as it occurs in 25% of pt’s treated with thiazide diuretics.

Ddx: dec intake, Lab error, hyperthyroidism (thyrotoxicosis related dec K), decreased Mg (must repleat this 1st as there are Mg dependent ATPases in the renal tubules).   Hypokalemic periodic paralysis (Mostly seen in Asians with thyrotoxicosis, have severe weakness that spares the CN’s and diaphragm, no precipitants, lasts 2-3d, replete K).  Inc GI loss–> gastric/ diarrhea/ laxative abuse (very low Ur sodium)/ bile/ fistula/ vomiting/ geophagia (very low UrCl, low serum Cl & Na).    Inc Renal Loss–> diuretic abuse (high UrCl and UrNa./ dec Mg / RTA/ steroid excess (Cushings/ Conn’s/ Hyperaldosterone/ CAH/ Adenoma/ renovascular HTN/ vasculitis).    Bartters Syndrome–> (Hypokalemia + metabolic alkalosis + hyper-reninimeic hyperaldosteronism.  HypoMg common.  3 gene defects cause, renal K loss.  Presents in childhood with growth failure and weakness.).  Liddle’s Syndrome–> an inherited tubular d/o with dec K, metabolic alkalosis, HTN and subnormal aldo secretion.   Inc Skin loss–> sweat,/ burns.   Redistribution (cellular shifts) –> Metabolic Alkalosis (hyperventilation/ resp or metabolic–> cells remove the inc H+, K is drawn into cell), OD of insulin/ Verapamil/ Chloroquine, B12, beta2-Agonist, periodic paralysis (familial or thyroid dz), tocolytic such as Ritodrine, theophylline, caffeine (even 1-2 cups).  Type I RTA (metabolic acidosis).  Drugs–> barium, mineralocorticoid effects (licorice, Fludrocortisone), amphotericin, diuretics, phenolphthalein, Na-polystyrene, high dose Abx (PCN, Nafcillin, Ampicillin, Carbenicillin), Mg depletion (aminoglycosides, Cisplatin, Foscarnet, Ampho-B), toluene, Verapamil OD, thyroid hormone, theophylline OD, Chloroquine.

Thyrotoxic Periodic Paralysis:  acquired, sporadic disease associated with underlying thyrotoxicosis and resolves with tx of thyrotoxicosis.  Always associated with hypokalemia.  About 95% of cases occur in men, more common in Asians.  Suspect dx pt who developes periodic paralysis after age 30yo as typical signs and symptoms of thyrotoxicosis are often completely lacking.  Dx:  Low TSH with increased radioiodine uptake by thyroid.   Tx:  aimed at thyroid dysfunction, beta-adrenergic blockers can be of some benefit prior to definitive therapy.

Hypokalemic Periodic Paralysis:  attacks of weakness occur during periods of hypokalemia.  About 2/3 of patients have a FHx of the dz, remainder likely due to spontaneous mutations.  Onset of sx’s usually before age 20, but as early as age 3-4, always begin before age 30.  S/s:  severe weakness of the limbs occurs spontaneously, paralysis occurs without pain or changes in level of consciousness.  The limbs are primarily affected (facial and respiratory muscles usually spared), pt’s may become temporarily quadriplegic.  Attacks typically last for 3-4 hours, but may persist up to 24 hours, worse in males than females.  Attacks usually follow exercise (at rest), or during sleep.   Serum K+ level usually low, but may be low normal, during an attack, reducing K+ levels will precipitate an attack.  Weakness improves with gentle exercise.  Common to have eyelid myotonia is often present even between attacks.   A d/o of voltage-gated calcium (Ca2+) channel gene, CACNL1A3, chromosome 1q, the physiologic basis remains unclear.   Tx:  Oral potassium loading during attacks will shorten duration, IV K+ should be avoided (dextrose solutions will reduce serum K+ levels).  Attacks are prevented by acetazolamide, yet may worsen some pt’s (Triampterene or spironolactone will usually be effective).  Low carbohydrate, low Na+ diet recommended.

S/s Dec K:  Mild depletion: (3-3.5 mmol/L) usually have no sx’s.   Moderate depletion (2.5-3 mmol/L) get nonspecific sx’s such as weakness, lassitude and constipation, thirst, HTN.  Risk of cardiac arrhythmia if have underlying CHF, ischemia or LVH.  Inc Digitalis SE’s.  Severe depletion: (2-2.5) get myonecrosis, paresthesias, hyporeflexia, confusion, ileus.   Very severe: (<2 mmol/L) get an ascending paralysis and impaired respirations, coma.  Limb and trunk paralysis with “hypokalemic periodic paralysis”, due to acute dec K associated with high carb meal.  ECG changes:  Flat T’s on EKG, PVC’s, U wave, dec ST segment, wide QRS.  Does not correlate well with serum levels.  Check Chem 7.

if dec HCO2–> then likely due to metabolic acidosis (renal failure, Addisons, DKA).  If dec HCO2 & inc Cl- –> Resp Alk or diarrhea.

if Inc CO2 & dec Cl–> diuretics, vomit, laxative, licorice, Aldo.

Tx: Ensure proper renal function first:  Deficit usually greater than serum value indicated because of depleted body stores.  Check Mg level or give empirically as K gets lost via Mg-dependent ATPase.  Consider ABG to r/o acidosis or LDH to r/o hemolysis of the specimen sent.  Check Urine K, if low (<20) then non renal loss.   KCl @ 7.5-10 mEq IV in 50-100ml D5W over 1hr with peripheral IV.  Up to 20mEq/hr if central line.  Kphos if dec phosphate too.    Enteral: PO K-Dur @20-40mEq doses.    10mEq needed for each 0.1 mmol serum depletion.    A “K” of 3.0 needs ~350 mEq and a K of 2.5 needs eventually needs 500-600.    Serum K–> mEq KCl to give PO/IV:   3.8-3.9–> 20.  3.6-3.7–> 40.  3.4-3.5–> 60. 3.2-3.3–> 80. 3.0-3.1–> 100. <3.0–> 120 & call HO.

Total body potassium deficit (mEq/L)= (4 — K) X 350.  At a normal pH, a deficit of 350mEq/L occurs for each 1 mEq/L drop in the serum K below 4 mEq/L.  A low Na diet will stop renal K wasting.

Tabs–> 6.7mEq (Kaon-Cl), 8 mEq (Klor-Con, Slow-K, Micro-K) 10 mEq (K-tab, K-Dur, Ten-K, Micro-K, Kaon-Cl, Kor-Con, Klotrix).   20mEq (K-Dur).      Liquids–> 20 mEq/15ml (Cena-K, Kaochlor, Kay Ciel, Klorvess, Kaon).   40 mEq/L (Cena-K, Kaon-Cl).

Powder–> 15, 20, 25 mEq/pack.  Acetazolamide is useful for the prevention of periodic paralysis.

Hyperkalemia:

Links:  Etiology:  S/s:  Tx:

Even slightest hemolysis raises K.  Levels increase aa change from supine to upright position.   Inc 0.6 mEq/L per 0.1 dec pH or 10 mOsm inc.  Inc 0.15 per 100 X10-9th platelets/L increase.

Etiology: acidosis, tissue necrosis (rhabdo, infarct), hemolysis, blood transfusion, GI bleed, RF (acute/ chronic), DKA, pseudohyperkalemia (leuko/ thrombocytosis), lab error, dec mineralocorticoid activity (Addison’s, Hyperaldo).  Hyperkalemic periodic paralysis (diurese and give Kayexolate). Meds –> High dose PCN, succinylcholine, ACEi & ARB’s, NSAIDs, K-sparing diuretic (spironolactone >Triamterene >Amiloride), TMP-SMX , Pentamidine, Heparin (aldo suppression), Digitalis, beta-blocker, stored PRBC’s, salt substitutes (K-Cl), Cyclophosphamide and Tacrolimus.

S/s: Usually asymptomatic, weakness, paresthesias, paralysis, confusion, arrhythmia, resp alk (diaphragm paralysis).   EKG –> peaked T@ 5-6 mEq/L, inc PR interval and QT @6-6.5, dec ST, small P waves @ 6.5-7.   Inc intraventricular conduction @ 7-7.5.   Wide QRS, ST and T’s merge @ 7.5-8.    Sine wave @ >10.    Brady, cardiac arrest.  Absence of ECG changes means nothing as can go from normal to VF in seconds.

Tx: EKG monitor, correct acidosis or hypovolemia (hydration & forced diuresis).    #1: CaGluconate: 1 or 2 ampules (10ml of 10% solution) IVP q1hr as needed for K>6 or EKG changes. Or give 10% (100mg/ml) @ 20mg/kg IV over 5min. Avoid if pt is on Digoxin as worsens any Dig toxicity.  Onset immediate, lasts 30-60min to counteract the electrophysiologic effects of inc K, stop infusion if heart rate <100.     #2: Sodium Bicarb: 7.5% (1mEq/ml) @ 1-2 mEq/kg (Or 1-2 amps) IV over 10-20min.  Causes K to move into cells.  Do not give simultaneously with Ca-Gluconate or will precipitate. Onset 20 min, lasts 2hrs.   #3: Insulin with Glucose: 1amp D50 (1-2g/kg) with 10-15 U (0.3 U/g glucose) regular Insulin IVP q2-3hrs as needed.  Onset in 20min, lasts 3-6hr.   #4: Na-Polystyrene (Kayexalate):  20-50g (1g/kg PO) in 100-200ml 20-70% Sorbitol PO q3-6hr.  Often comes in 15g jars mixed with sorbitol.  Removes K from body.  Will remove 1 mEq of K/g of resin.  1g of resin = 4.1 mEq Na (Watch for volume overload), takes 4-6hr.  Retention Enema: 50g Kayexalate in 200cc water with 50g Sorbitol or 200ml of 20% Dextrose solution q1hr.     #5: Albuterol (beta-agonist): 10-20 mg nebulized or 0.5mg IV, causes redistribution.  #6: Dialysis.

**Ref: (Drug-induced hyperkalemia.  Am J Med 2000;109) (Hypokalemia. N Engl J Med 1998;339:7) (Bartter’s syndrome: the unsolved puzzle.  Am J Kidney Dis. 1995;25:813-23) (Potassium homeostasis in the elderly.  QJM. 1997;90:487-92) (Hypokalemia and hyperkalemia. Med Clin North Am 1997;81:611-39) (Hypokalemia–consequences, causes, and correction. J Am Soc Nephrol. 1997;8:1179-88)

Calcium Metabolism:

Links:   Labs:  Ca & P:  W/u:    Hypercalcemia:   Hypocalcemia:

99% of the bodies Ca is in bone (~1300g), 0.1% in extracellular and 1% is intracellular.  Ca has 3 forms ionized (“free”, active form), Protein bound (40%), anion bound (15%, bicarb, phosphate, citrate), need to correct for albumen level.   Levels regulated by PTH (low Ca and high P –> inc PTH –> increase resorption bone and Ca in DCT, inc V-D hydroxylation in PCT–> inc gut/bone Ca absorption).   Important in neuromuscular and enzyme physiology.  Body stores 1-1.2 kg.   Require 1-3g/d PO or 7-10 mmol/d IV.

Labs:   Ionized Ca is usefull if hypo/hypercalcemia, borderline serum Ca or altered serum proteins.  50% of Ca is ionized, 40% is bound to albumin and 10% is bound to other anions.  The ionized fraction is the only fractioon that is physiologically active.  Always check serum pH as acidosis increases it and alkalosis decreases it.   The normal level is 1.15-1.35 in adults.

Corrected Ca:   Correct for Low albumin –> adjust serum Ca by 0.8mg/dl for each 1g that Albumin is above or below 4g/dl. = (normal alb – Pt’s alb) X 0.8) + Pt’s Ca. =   (3.5- pt’s Alb) X 0.8 + pt’s Ca.      0.8 is the amount of Ca bound to albumen.  Ca: dec 0.8mg% per g% dec alb.  Dec 0.16mg% per g% inc globulins.  Dec 0.12mg% per 0.1 dec pH or per 10 inc mOsm.

Calcium and Phosphate Control:

PTH–> Causes inc serum Ca and dec P.  inc bone resorption of Ca & P.  Inc renal tubular Ca reabsorption.  Dec renal Ca reabsorption.  Inc renal production of 1,25(OH)2D.   1,25-Dihydroxyvitamin D–> Causes inc serum Ca & P.  inc renal reabsorption of Ca & P.  Inc bone resorption of Ca & P.  Inc gut absorption of Ca & P.  Dec parathyroid production of PTH.  Dec renal production of 1,25(OH)2D.    Calcitonin–> Causes dec serum Ca & P.   Dec bone, gut and renal absorption.   Calcium–> dec PTH, dec 1,25(OH)2D, dec P and dec Calcitonin.  Phosphate–> inc PTH, dec1,25(OH)2D, dec Ca.

W/u: CBC, Alb, total protein, Ca, P, ALT, AST, AP, Cr, TSH, UA with micro, CXR.   Check “intact” PTH, if very high–> likely PHPT (get FHx to r/o MEN syndromes.    If marginally high or nl Ca–> may still be PHTP, consider FHPC if young and asymptomatic–> if 24hr Ca <100, only thiazides or FHCP).   Low PTH –> check PTH-RP(RP=related peptide), which will be elevated in carcinoma.  Check 1,25(OH)2D will be inc in granulomatous and V-D intox.  Check 25-(OH)D: nl in granulomatous, high in V-D intox.   Check Urinary cAMP: if dec and have dec PTH likely an osteolytic process of V-D intox.   Other Labs:  SPEP, UPEP, V-A level, best-carotene, ACE, 24hr Ur Ca & Cr, bone scan, renal U/S, CT abd, mammogram, ACTH stim, PPD.

Primary –> Hyperparathyroidism –> Intact PTH: Inc. PTHrP: Dec. 1,25(OH)2D: Inc. Ca:  Inc.  PTHrP malignancy –> Intact PTH: Dec.  PTHrP: Inc. 1,25(OH)2D: Dec. Ca:  Inc.  Non-PTHrP malignancy –> Intact PTH: Dec. PTHrP: Dec. 1,25(OH)2D: Dec. Ca:  Inc.

Hypercalcemia:

Links:  Ddx:  S/s:  Tx:   Milk Alkali:  Hyperparathyroidism:  Malignancy: Familial Hypocalciuric Hypercalcemia:

Total Ca >10.5 mg/dL or ionized Ca >2.7 mEq/L (1.3 mmol/L). Hypercalcemic Crisis:  (>12)  (critical 16-20mg/dl)

Ddx:  “SHAMPOO DIRT” –> Sarcoid.  Hyperparathyroidism/ hyperthyroid.  Addisons dz, AIDS.  Metastases/ myeloma, milk-alkali syndrome.   Pagets dz, parenteral nutrition, pheo, parathyroid dz.   Osteogenesis imperfecta, Osteoporosis.    D-vitamin toxicity.  Immobility, inflammatory d/o. RTA, rhabdomyolysis. Thiazides and other drugs (Li), thyrotoxicosis.

Ddx by Mechanism:   Inc Bone resorption–> hyperparathyroid, mets, thyrotoxicosis, pheo, V-A intake >50,000 IU/d, immobilization, humeral hypercalcemia of malignancy.  Increased renal reabsorption or dec excretion–> rhabdo, thiazides, Milk-alkali syndrome, renal failure, familial hypocalciuric hypercalcemia.  Increases gut absorption–> candidiasis, coccidiomycosis, histoplasmosis, sarcoidosis, eosinophilic granuloma, berylliosis, V-D intake > 50,000 IU/wk, TB, inflammatory d/o. AIDS, lymphoma.  Unknown Etiology–> VIPoma, theophylline, Li, Addisons, parenteral nutrition, estrogen and antiestrogens.  Drugs: thiazides, Li, V-A or D intoxication.

Sx’s: Stones, bones, abdominal groans, and psychic overtones. N/V/C, dry mouth, confusion, weakness, sz, H-A, hyporeflexia, HTN, dec QT interval, brady, AVB, polyuria, polydipsia, pruritis.  If chronic: osteoporosis/ bone pain, stones, pancreatitis.   Inc Ionized Ca & inc P & inc PTH–> CRF, lithium therapy.

Labs: total and ionized Ca+, Mg+, P, lytes, AP, creatinine.   Consider PTH,TSH.  With hyperparathyroidism also have dec HCO3, inc Cl, inc AP.

Serum Phos –> PTH-mediated: Dec. Non-PTH mediated: Inc/dec or normal.  Serum Cl –> PTH-mediated: Inc.  Non-PTH mediated: Often <100 mEq/dL.  Met Acidosis –> PTH-mediated: Mild. Non-PTH mediated: None.  Serum Cl / PO4 –> PTH-mediated: >33. Non-PTH mediated: <33.  PTH –> PTH-mediated: Inc.  Non-PTH mediated: Dec.

Tx:  0.9NS hydration 1-2 L over 2-3hr, then 150-350ml/hr (2.5-4L in 24 hr, some need 10L) to promote calciuresis and correct hypovolemia, then once volume is repleated, use forced diuresis with Lasix @20-60mg IVP (often need 80-100mg IV q2hr), maintain UO @ 100-200ml/hr. Replace urine losses iv 0.45 NS + 20 mEq KCl/L with careful monitoring of CVP and Ca q4-6hrs.  Dialysis for renal failure.  Replete Mg.

Calcitonin-Salmon (Calcimar, Miacalcin): Adult @ 200 units/ml inj.  For hypercalcemia give 4 units/kg SC or IM q12 hr.  Will work in a few hours, but max drop in serum Ca of only 0.5 mmol/L.  Can increase the dose to 8 U/kg SC/IM q12hr in 1-2 days if not responding then 8 units/kg q6hr in 2 more days if still unresponsive.   Also use in Paget’s dz and osteoporosis.  Can add Prednisone 40-60mg/d PO.   SE: N/V, dermatologic reaction, nocturia, eye pain, feverish sensation.   Action: Inhibits bone resorption, decreases serum Ca, and increases excretion of P, Ca, and Na by decreasing tubular reabsorption.

Bisphosphanates (Didronel, Aredia): (inhibit osteoclast activity, slow onset (days) but safe @90mg in a single IV 24hr infusion and lasts weeks, can retreat in 7 days.  Etidronate: 7.5mg/kg with 3L NS over 24hr, repeat qd X 3d.    Mithramycin: inhib RNA synthesis in osteoclasts, if malignancy or unresponsive to other tx @ 15-25mg/kg IV over 4-6hr, takes 120, peaks in 36hr , lasts 4days, BM depression a SE.  Steroids if MM, lymphoma, V-d intox @ 100mg hydrocortisone BID IV Treat underlying disorder.  Can also use Gallium Nitrate, IV Phosphate, Dialysis, EDTA.

Other (long term): d/c thiazide diuretics, drink lots of fluids and avoid Ca+ in diet, mobilization, oral phosphates (K-phos 3 tabs TID).

Milk Alkali Syndrome:    Secondary to ingestion of excess Ca (milk) and Alkali (antacids), often in attempt to self tx PUD or GERD.

S/s: anorexia, constipation, dehydration, dizzy, H-A, irritable, abnormal taste, MS changes, myalgias, polyuria/polydipsia, N/V, weakness.

Lab: inc Ca, inc HCO3, normocalcuria, dec urine P, inc BUN/Cr, normal Alk phosphatase (AP).

Tx: Stop milk/antacids, tx inc Ca PRN with Lasix and NS, monitor kidney function, urine electrolytes, urine output.

Primary hyperparathyroidism (PHPT): (oversecreter PTH)   Dx: inc “intact” PTH. Vs.     See Endocrine Section.

Secondary HPT: Inc PTH secretion in response to: dec Ca, inc P, low calcitriol (all 3 conditions seen in CRF, most common cause). Vs.

Tertiary HPT: spontaneous change from dec Ca–> inc Ca.  PTH usually 10-20X nl.

Malignancy:  (Mets–> breast/ MM/ lymphoma/ prostate/ lung/ thyroid) or Humoral Hypercalcemia of malignancy (HHM) seen in SC Ca producing PTH related peptide.     3. Granulomatous dz: (TB, sarcoid, disseminated fungal, berylliosis, lymphoma, from V-D via macrophages)

Familial Hypocalciuric Hypercalcemia (FHHC or FHH):  Seen in young pt’s with FHx (AD) kidney reabsorbs too much Ca, check 24hr UR Ca (should be <100) with nl PTH. These pt’s are not at risk of making stones as they do not have an elevated urinary Ca.  Their disorder is thought to be a defect in the parathyroid calcium receptor.  Can mimic primary hyperparathyroidism.  Due to a defective Ca sensor on the membranes of the parathyroid and renal tubular cells.  Leads to dec renal clearance of Ca (low Ur Ca), a normal-high level of PTH, mild inc Mg, nl-dec P and FECa <1%.

**Ref: (N Engl J Med 1992;326:1196-1203) (End Clin NA 1993;22:343-62) (Hypercalcemia.  Endocrinol Metab Clin North Am. 1989;18:601-832) (Clinical manifestations of cancer-related hypercalcemia.  Semin Oncol. 1990;17(2 Suppl 5):16-25) (Hypercalcemia of malignancy.  Am J Med. 1997;103:134-45) (Hypercalcemia: mechanisms, differential diagnosis, and remedies. Postgrad Med 1996;100:119-26)

Hypocalcemia:

Links:  S/s:  Lab:  Tx:  Ddx:

Total Ca <8.5, or ionized <2 mEq/L (1 mmol/L).   Asymptomatic until serum <8mEq/dl.

S/s: numb/ tingling extremities, circumoral paresthesias, muscle/ abd cramps, tetany, inc DTR’s, sz, laryngospasm.   Chvosteks sign: twitching facial muscles after percussion of masseter muscle just anterior to the ear below the zygomatic bone. (normal in 15-25% of pop, also seen with diptheria, whopping cough, measles, scarlet fever and myxedema).    Trousseau’s sign: More specific than Chvosteks, carpopedal spasm induced by inflation of BP cuff above SBP for 3 min. Also seen with dec Mg. EKG: inc QT without U waves if <6.

Lab: check serum Mg (parathyroid needs Mg to work), dec K, inc P. Total Ca <8.5, or ionized <2 mEq/L (1 mmol/L). Ca & P:

Tx: If sx’s mix as bolus in 100ml of NS over 10min of 200mg (max 15mg/kg) elemental Ca (8ml of 10% CaCl or 22ml of CaGluconate), then follow with a continuous infusion of 1-2mg elemental Ca/kg/hr for 6-12hr.

CaCl: (max of 0.2-0.3ml/kg = 5-10ml) IVP 10ml of 10% solution = 6.5mmole (27mg (1.36mEq)/ml elemental Ca).  Risk of possible tissue necrosis if infiltrated. 1g = 13.6 mEq Ca.  Give 1-2g in 50ml over 1hr or slow IVP up to 16mEq/min.  Comes in 10ml vials = 100mg/ml.

CaGluconate (max 0.5-1ml/kg = 5-10ml) 10% soln 10ml IVP =2.2mmole of Ca (9mg (0.46mEq)/ml of elemental Ca). Less irritating if using peripheral vein. 1g = 4.5 mEq. Also used to tx inc K.

PO: Tums: 1 tab= 0.5 g CaC03 = 200mg Ca, OsCal, 1 tab= 1.25g CaC03= 500mg Ca. CaGluconate syrup: 5ml gives 115mg Ca.  1/3 of Ca is absorbed.   Phosphate binding antacids improve GI absorption of Ca.

V-D (Calciferol) -begin once phosphate is nl.  Start @50,000U/d, increase up to 200,000U as needed.  Ca may potentiate digoxin.

Ddx: hypoalbuminemia with nl ionized fraction.  May have nl serum Ca, but low ionized in acute alkalosis.  If albumen is nl–> check PTH (low PTH: hypo PTHism, dec Mg)  (high PTH: pancreatitis, inc P, dec V-D, citrated blood transfusion, renal insufficiency (CRF).  If inc PTH–> check P, Cr, LFT’s, AP, total protein, Mg, see above.  Other–> soft tissue infection, rhabdo, tumor lysis syndrome.  Drugs–> Cimetidine, Cisplatin, Dilantin, phenabarititol, glucagon, protamine, theophylline, NE, nitroprusside, heparin, loop diuretics gentamicin.

**Ref:(Hypocalcemia.  Semin Nephrol. 1992;12:146-58) (Hypocalcemic crisis.  Crit Care Clin. 1991;7:191-200) (Hypocalcemic emergencies.  Endocrinol Metab Clin North Am. 1993;22:363-75)

Phosphate Metabolism:

Links: Hypophosphatemia:   Hyperphosphatemia:

Phosphorus is the form of phosphate it the principle intracellular anion.  It has a central role in the cytoplasm as a buffer, energy carrier (ATP) and molecular switching (phosphorylation).  In the blood it is principally unbound like Mg. 86% of phosphate is in the bone (600g), 14% in cells (100g) and 0.03% in the extracellular fluid.

Calcium and Phosphate Control:

PTH–> Causes inc serum Ca and dec P.  inc bone resorption of Ca & P.  Inc renal tubular Ca reabsorption.  Dec renal Ca reabsorption.  Inc renal production of 1,25(OH)2D.   1,25-Dihydroxyvitamin D–> Causes inc serum Ca & P.  Inc renal reabsorption of Ca & P.  Inc bone resorption of Ca & P.  Inc gut absorption of Ca & P.  Dec parathyroid production of PTH.  Dec renal production of 1,25(OH)2D.    Calcitonin–> Causes dec serum Ca & P.   Dec bone, gut and renal absorption.   Calcium–> dec PTH, dec 1,25(OH)2D, dec P and dec Calcitonin.  Phosphate–> inc PTH, dec1,25(OH)2D, dec Ca. W/u:

Hypophosphatemia:

Links:  Etiology: S/s:  Tx:

Phosphorous:  important mediator of cellular energy, metabolism is related to Ca.  The most abundant intracellular anion (as is protein), require 30mmole/d.  700g in the body, 80% in bone, 9% in skeletal muscle, <1% in the plasma.  Very hard not to get enough in ones diet.

Etiology: dec Phosphate absorption–> malabsorption, PO4 binding in gut (antacids), steatorrhea, V-D Defic, hyperalimentation, inadequate intake.  Inc Renal excretion–> alcoholism, alkaluria, diuretics, Fanconi syndrome, inc Ca, hyperparathyroidism, metabolic acidosis, renal tubular defect (ATN), glucocorticoid/ mineralocorticoid therapy, PTH-related protein, renal transplantation, volume expansion. Other–> dec Mg, dec K, hemodialysis, thyrotoxicosis, pancreatitis, extensive burns.   Intracellular shift–> carbohydrate infusion, Calcitonin, catecholamines, glucagon, insulin, respiratory alkalosis (gout, sepsis, panic attack, heat stroke, salicylate OD), EPO therapy, leukemic blast crisis. Refeeding Syndrome:

S/s Hypophosphatemia: Usually no sx’s unless <1, severe if <0.5.  Neurologic – areflexic paralysis, confusion, Guillain-Barre syndrome, weakness to ascending paralysis, paresthesias, CNS dysfunction (irritability, confusion, sz, coma). Cardiac – decreased myocardial function, cardiac arrest, arrhythmias, myocardial depression (CHF from low ATP).  Hematologic – altered RBC morphology, hemolytic anemia, platelet/ granulocyte dysfunction, shift in oxyhemoglobin (from dec 2,3 DPG). Hepatic – liver dysfunction (especially in cirrhotics).  Muscular – rhabdomyolysis, weakness.  Respiratory – acute ventilatory failure.  Skeletal – bone pain, osteomalacia (long term hypophosphatemia).  GI – nausea, vomiting, poor GI motility, anorexia.

Tx:  PO:   IV:    PO Phosphate repletion: Achieved over 7-10 days, give 60 mmol in 3-4 divided doses.  Give 15mg/kg = 1g PO4 = 30 mmol, = 1 qt of milk, this raises the serum P by 1.  Use Na-P if renal failure or inc K.

Neutra-Phos (NaP): @ 2caps BID-TID with water. Has 250mg/ packet of P + 7.1 mEq Na + 7.1 mEq K.  Phospho-Soda: 5ml BID-TID. Has 150 mg/ml P + 4.8 mEq/ml Na.   Skim Cows Milk: 1g/L P + 28 mEq/L Na + 38 mEq/L K.  Neutra-Phos K: 250mg/cap P + 14.25 mEq/cap K.  K-Phos Original: 150 mg/cap P + 3.65 mEq/cap K.  K-Phos Neutral: 250 mg/tab + 13 mEq/tab Na + 1.1 mEq/tab K.

IV Phosphate repletion:  If unable to take PO or severely symptomatic (levels <1mg/dL).  It is with Na or K.    Give ~2.5mg/kg body wt over 6h if no overt clinical manifestation.   Give 5mg/kg over 6h if an emergency.

Na-Phos or K-phos (has 93mg =3mmol/ml + 4mEq Na or K) @15-30 mmol in 100ml over 4hr, max 100mm/d. Typically give ~”15-30 mmoles over 6 hours”.  If very low can write “NS with 10 ml of K-Phos/L @ 125ml/h”.    NaPhos–> 3 mmoles Phos + 4 mEq Na (so 21 of Phos with 28 of Na).    Kphos–> 3 mmoles Phos + 4.4 mEq K (so 21 of Phos with 30.8 of K).

If having adverse effects and PO4<2mg/dL–> 0.9mg (0.03mmol)/ kg/hr, slower if renal dysfunction, monitor serum P q6hr.

If recent onset–> 0.08-0.20mM/kg over 6hr,  If Prolonged–> 0.16-0.24mM/ kg over 6hr.

Can also give Neutral NK-PO3 with 0.09 mmol/ml P + 0.02 mEq/ml K + 0.2 mEq/ml Na.  Or Neutral Na-P which has 1.1 mmol P + 0.2 mEq/ ml Na.

Hyperphosphatemia:

Laxative abuse, PO4 salts for inc Ca Rx, renal insufficiency, hypoparathyroid, catabolism, V-D metabolites, sepsis, rhabdo, tumor lysis, hypo/ hyperthermia, inc GH.

Sx: same as dec Ca, may produce ectopic calcifications.

Tx: restrict diet/ external sources, P-binding antacid (Amphojel, Alternagel).  Volume expansion if normal renal function.  Al-Hydroxide @ 30cc PO q2-4hr, Acetazolamide if sx’s @ 15mg/kg IVSS q4hr, Dialysis.

**Ref:(Severe hypophosphatemia presentation and treatment.  Medicine 2000;79:1) (Tumor lysis syndrome.  Semin Nephrol. 1993;13:273-80) (Endocrine crises. Hypophosphatemia and hyperphosphatemia.  Crit Care Clin. 1991;7:201-14)

Body Fluids:

Links:  Compartments:  Free Water:  Normal Losses:  Maintenance: Other: Hypervolemia: Hypovolemia:  Dehydration:  Oral Rehydration:   IV Solutions:

Tips on correcting FEN abnormalities:   R/o Laboma–> lab error, re-check lab 1st.  Correlate to the pt’s condition.  Correct ½ the deficit, reassess the labs, then correct the remaining.  If multiple problems correct 1st Volume >pH > K/Ca/Mg > Na/Cl (osmolarity).

Serum Uric Acid:  level is a rough correlate with intravascular volume, but a need baseline to compare too.

Total Body Water (TBW): ~60% Ideal Body Weight. Increased with inc muscle mass (600ml/kg in male, 500ml in female), dec with age (highest in newborn, @ ~77%).    TBW = 0.6 in child or non-elderly male.  TBW = 0.5 in an elderly male or a non-elderly female.  0.45 in elderly females. Normally the intracellular + extracellular fluid = 40-60% of the TBW.

Desired TBW: (Measured Na X current TBW)/ normal serum Na.

Body Water Deficit:  Desired TBW- current TBW.

Intracellular Fluid (ICF): 40% of body wt or 66% of TBW, ~28 L, primarily in muscle, 160ml/kg.

Extracellular Fluid (ECF): 33% of TBW.  Interstitial is 15-20% TBW (~8 L).  Intravascular (Plasma) is 5% TBW, ~3-4 L (plasma volume is 38ml/kg, blood volume is 70ml/kg).

Free Water:  water in the body that can be removed by ultrafiltration and in which substances can be dissolved.

Free (body) Water Deficit (FWD) in Liters:   FWD in Hypernatremia:  FWD = [Serum Na (measured) – serum Na (normal) x 0.6 Wt in kg/ normal serum Na].     Also written as, FWD = [(Na-140)/140] baseline wt X F. (F = fraction of wt that is water, 0.6 for male, 0.5 for females).  Also written as, FWD = FWD  = 0.6 X wt in kg X (1- 140/Na).   Kg is estimated wt when fully hydrated.      FWD in Hyperglycemia:  Use corrected Na if necessary, particularly if hyperglycemia is present–> FWD = ( baseline wt in kg — 0.45) — [(290/Eosm) X current wt X 0.45]. Effective osm = 2 X (Na+K) + (glucose/18) = TBW in kg X 0.6 (1- normal Osm/observed Osm). Generally, about half of deficit can be replaced in the first 24 hours; rest over 1-2 days.  Avoid correcting the serum Na concentration >1mEq/L/hr.

Free Water Clearance (FWC): Used to asses a solute Vs water diuresis when have polyuria (>3L/d).  FWC = Ur volume in 1 day – Osmolar clearance.  Osmolar Clearance = (Ur Osm X Ur volume)/ plasma Osm.  No FWC if Ur Osm >300 mOsm/kg H2O.  Excess FWC if Ur Osm <150 mOsm/kg H2O.

Normal Losses of Fluid:  Insensible = stool + skin = ~500ml/d.  Stool–> ~300ml/d.  Renal excretion–> 1-1.5L/d.   Insensible Loss–> 400ml/m2/d (~750ml/d for adults = 10ml/kg/d, 60% as free water vapor from lungs, 40% perspiration). Increased Loss of Fluid:  fever–> Inc 15% =~150ml insensible loss/ 1 deg C above 37.  (or 100ml/deg F >98.6), tachypnea.  Inc 50% for each doubling of RR, evaporation (perspiration, ventilator, open wounds), GI (fistula, emesis, diarrhea, NGT), third space, operative loss (~800ml/hr for major abd surgery).

Maintenance Fluid:   If wt>20kg, simplify 4:2:1 rule by   adding 40  to pts weight  in kilograms = ml/hr.   Maintenance:  D5-1/4NS (= D5-.2NS) with 25 mEq K.    If >20kg.   Maintenance = 110 + wt in kg.   Daily Fluid Volume:  100ml/kg/d  (4cc/hr) for 1st 10kg + 50ml/kg/d (2cc/hr) for 2nd 10kg + 20ml/kg/d (1cc/hr) any kg >20.   Average adult needs:  30-35ml/kg/d water (1500ml/m2/d).  35 kcal/kg/d.  Need ~1g Na/ 160 kcals.    70kg Male–> D5 ½NS +20mEq KCL/L  @125ml/hr = ~3L free water.  Goal:  maintain urine output of 1-1.5L/d.

Other Info: Body Surface Area (BSA) = square root of (Ht in cm X wt in kg)/ 3600.   BSA (m2)= 0.007184 X wt- 0.425th X Ht- 0.725th.  (Use wt in kg, ht in cm).

Banana Bag: MVI 1 amp + 100mg Thiamine + 1mg Folate + 2g MgSO4 @ 100-125 ml/hr X 3d.

Urine Volume: should be 0.5-1 ml/kg/hr if adequate intravascular volume, renal function, cardiac output.

Anion Gap: Na – (Cl + HCO3).  Normal 8-16 mEq/L.

Osmol Gap: Measured Osm – Calculated Osm–> if 0-10= normal, if >10 abnormal, if <0 lab/ calculation error.

Serum Osmolality: tonicity of body fluids.    Calculated Osmolality (mOsm/L): 2(Na) + Glucose/18 + BUN/2.8.   For “effective osmols”, need to add in mannitol (mOsm) + Sorbitol + Glycerol as these solutes do not easily cross into muscle cells.

Fractional Excretion of Sodium (FENa %):   (UNa X PlCr)/ (PlNa X UCr) X 100.  (<1=prerenal, >1=renal).

Hypervolemia:

Usually secondary to parenteral overhydration, fluid retaining states (CHF, Acute RF), or mobilization of previously sequestered fluid.

S/s:  wt gain, pedal/sacral edema, rales/wheezing, JVD, inc CVP and PCWP.

Lab: dec HCT, dec albumen, inc/ dec Na.

Tx: water restrict to 1500ml/d, diuretics, Na restrict to 0.5g/d, anasarca may respond to combined colloid (albumen) infusion with parenteral loop diuretics.

Hypovolemia:

Seen in trauma (crush injury, burn), GI loss (vomit, NGT, diarrhea), third spacing (ascites, effusions, bowel obstruction), inc insensible losses.

Mild–> 4% of Total Body Water (TBW), 15% blood volume.    Mod–> 6% TBW, 15-30% blood volume.   Severe–> 8% TBW, 30-40% blood volume.  Shock–> >8% TBW, >40% blood volume.

S/s: sleepy, apathy, coma, OH, tachycardia, dec pulse pressure, dec CVP and PCWP, dec skin turgor, hypothermia, pale extremities, dry tongue, dec fontanelle in infant, ileus, oliguria, weakness.

Lab: BUN:Cr is >20:1, inc Hct (3% for each Liter deficit), FENa <1%, inc Ur sg.

Tx:  Bolus therapy with NS or LR.  Replace free water loss with D5W or D5W ¼ NS.

Dehydration:

Links:  S/s:  ORT:  Other: IV Solutions: Pediatric:

Dehydration:  loss of intracellular water that ultimately causes cellular dessication and inc’s the plasma Na and osmolality. Seen mostly in the elderly with infections and poor access to water.   No circulatory instability, should get 5% Dextrose slowly.  Yet most also have volume depletion and need NS (Hypovolemia refers to both conditions).

Volume Depletion: loss of Na from the extracellular space (intravascular, interstitial fluid) after GI hemorrhage, vomiting, diarrhea, diuresis.  Have circulatory instability and need NS rapidly.

Adults–> check bicarb & BUN/Cr ratio (>25 suggests dehydration or renovascular dz).    Stool specimens on need if bloody stool  or signs of invasive bacteria (abrupt onset, diarrhea precedes vomiting).  Screen with FWBC test (inc in bacterial).  Elderly: susceptible as dec thirst sensation & kidney ability, debilitating illness, meds.

S/s: Everything must be interpreted in context.    Dry axilla & dry MM’s are both unrealiable. Tongue furrows can be seen, but mouth breathing can cause this.  Cap refill and skin turgor are not good signs in the elderly.   Normal elderly may have sunken eyes, tenting (lose elastin fibers with age), tachycardia, concentrated urine and orthostatics.  Look for tongue furrows & dryness, upper body weakness, speech difficulties, confusion.  Other signs include >5% wt loss in 30d, dizziness, failure to eat, febrile illness, problems with hand dexterity, uncontrolled DM, UTI.

Labs:  Check lytes for inc Na & BUN.  Yet BUN not reliable as both starvation & liver dysfunction prevent its rising commensurate with volume loss. Measure serum Osm & urine Na.  A Ur s.g. >1.020 is dehydrated.  Urine output <2ml/kg/hr is oligouria.  Each kg BW loss is ~1L deficit.

Oral Rehydration Therapy (ORT):

Diarrhea is #1 cause.  Best if used with any diarrhea to prevent dehydration.   Advantages: less $ than IV, less complications than IV, can be used at home. Contra: severe dehydration, shock, intractable vomiting, lack of personnel to administer ORT.  Need 75-90mEq/L of Na. 2-2.5g/dL glucose (High glucose content in soda & juices –> inc osmolality–> osmotic diarrhea.), 300-330 mOsm/L.

Dietary Adjustments: inc salt with boiled starches, boiled vegetables, soups, yogurt, bananas, avoid Lactose until formed stools developed.

Rehydralyte or WHO Oral Rehydration Solution (ORS) formula and :

Home ORS Formulas:

May be given by bottle, cup, spoon, syringe, or NGT.  Give frequent small amounts, ~10ml q 10min, can inc rate by 5ml q min at tolerated.

¾-1 level tsp (3.5g) salt + ½-1 tsp baking soda + 8oz water (or OJ) + 4 level tbsp sugar + 4 tsp Cream of Tartar (KCl, K bitartrate).  Can replace the sugar with 50-60g of cereal flour or 200g mashed potatoes to make a food-based formula.

Or 1 qt water + ¾ tsp salt substitute (KCl) + ½ tsp Baking soda + 3 Tbs Karo Syrup (White Corn Syrup) + 1 packet unsweetened powdered drink mix (Kool-Aid) or fruit juice concentrate.

Or   8oz fruit beverage (OJ, apple)+ 8 oz water + ½ tsp honey/ corn syrup + pinch NaCl + ¼ tsp baking soda.     Carb-Na ratio of <2:1.

Or  (8:1 sugar:salt): 2 tsp sugar + ¼ tsp salt + squeeze lime in 8oz water.

Comparison of the Composition of Solutions:

Solution –> Na (mEq/L)\ K (mEq/L)\ Cl (mEq/L)\ Bicarb (mEq/L)\ Glucose (g/dL):    ECF –>142\4\103\27.1.  LR –> 130\109\28.  0.9% NaCl ( NS) –> 154\154.  Chicken Broth –> 250\5-8\-\-\-.  WHO-ORS –> 90\20\80\-\2.  Pedialyte –> 45\20\35\30\2.5.  Gatorade –> 28\2\-\-\2.1.  Ginger Ale –> 4.2\-\-\9.  Coke/Pepsi –> 2.5.5\9\10\10.5.  Apple Juice –> 3\17\-\-\12.  Grape Juice –> 3\25\-\-\15.  Jell-O –> 24\1.5\-\-\16.

Alternative Hydration Methods:

Hypodermoclysis:  use #21-25g butterfly needle inserted into SC skin at anterior chest, abd wall infraclavicular or scapular regions.  Can run at 80-250ml/hr (0.5-3L/d)

Proctoclysis:  rectal hydration using a #22F NGT inserted 40cm into rectum.  Use NS or tap water starting at 100ml/hr, increase to 400ml/hr if tolerated.  Can also be used to raise the core body temp.

Osteoclysis:  interosseous infusion of fluids.  Need a bone injection gun.

IV Solutions:

Links: Crystalloid:  Colloid:  Compositions:

Crystalloid Solutions:  Includes: Dextrose, NaCl, plasmalyte A, ringers.    Only 25-33% stays in the intravascular compartment.  A person who has lost 2 units of blood (1000ml) would need 3-4L of crystalloid for volume resuscitation.  ½NS provides only ½ of what LR or NS provides/L.  D5W is the worst for trying to give intravascular volume (gives 80ml/L, the rest to the cells and interstitium).   Replace 3rd space losses with isotonic crystalloids–> LR or NS.

Lactated Ringer (LR) –> 130 Na mEq/L, 4 K, 109 Cl, 28 Lactate, 3 Ca, 9 kcal/L, 272 osmol, 100ml free water, pH = 6.5).  Contra: renal failure (potassium), citrated blood to same line (Ca).  More physiological level of electrolytes, better for trauma.

0.9% NaCl (NS = normal saline) –> 154 Na mEq/L,154 Cl, 208 osmol, no free water, pH = 5.    Contra: prolonged/fast infusion may cause hyperchloremic metabolic acidosis and hypokalemia (as normal serum has Cl of only 100mEq/L).  Better for pt with protracted vomiting.

½NS–> 450ml free water.

Plasmalyte A: 140 Na mEq/L, 98 Cl, 5 K, 294 Osm, pH = 7.4.  5% Dextrose (D5W) –> 1000ml free water, 5,000mg/dL dextrose, 170 kcal/L, 250 mOsm/L.  10% Dextrose (D10W) –> 1000ml free water, 340 kcal/L, 500 mOsm/L.   D5 ½NS–> 800ml free water.      1L of D50 = 1700 kcal.

**Ref: (Critical Care Clinics 1992;8;2) (Critical Care Clinics 1993;9:2) (Dehydration: evaluation and management in older adults. JAMA 1995;274:1552-6)

Composition of Common Fluids (mEq/L):

Fluid –> Na/ K/ Cl/ HCO3/ Vol/24hr/ mOsm/L:  Extracellular –> 40\4.5\108\-\- \290. Saliva –> 20-60\15\15-30\40\1-2L\-.  Stomach –> 40-99\5-15\15-20\~2L\-.  Pancreas –> 135\4-6\40-75\95\1-2L\-.  Sweat –> 40-50\5-10\40-60\-\-.  Diarrhea –> 50-60/ 45/ 35-45/ 55/-/-.

Na/ K/ Cl/ HCO3/ Glucose/ mOsm/L / Kcal:  D5W –> 0\50 g\252\170.  D10W –> 0\100\505\340. ½NS (0.45%) –> 77\77\154. NS (0.9%) –> 154\1540\308. 3% NS –> 513\513\1026. D5 1/4NS (0.2%) –> 38\38\50\329\170.  D5 ½NS –> 77\77\50\404\170. LR –> 130\4\110\27\272\10.  D5 LR –> 130\4\110\27\50\524\180.  Albumin –> 145\145\-\-.

Colloid Solutions:  Used because crystalloids would be required in such great amount that have risk of fluid overload.  Plasma volume expanders. Albumin, Hetastarch (Hextend) (6%), Pentastarch (10%), Dextran (40, 70), Gelatins, Blood products (whole blood used if >25% of total volume is lost), plasma protein fractions and synthetic blood substitutes.

Albumin:  Typical order: 25g of 25% IV q6-12hr X 4-6 doses.  It is the major protein produced by the liver (50%), 8% turnover each day.  584 amino acids.  Accounts for 80% of plasma colloid oncotic pressure.  40% is distributed intravascular, 60% interstitial.   Each gram holds 18ml of fluid in the intravascular space.Human serum albumin is available as 5 or 25% solution, from human plasma donors.  T-½ is 18d, colloid oncotic pressure is 19mmHg. 25% Albumin Dilution:   Avoid hypotonic plasma/ hemolysis if use 0.9% NaCl instead of H2O in 1:4 dilution to make 5% albumin.  The oncotic effect of 100ml of 25% = 500ml of plasma.

Hydroxyethyl Starch (Hetastarch, HES):  synthetic molecule similar to glycogen.  In a 6% solution in NS.  Has an oncotic pressure of 30mmHg with Osm of 310.  Effects last 3-24h.   Less expensive than albumin.  May decrease platelet count and inc PTT with large volumes.

Pentastarch: 10% solution, more predictable excretion compared to hetastarch.  Volume expanding effects last 12h.

Dextran:  a mixture of glucose polymers produced by the bacteria Leuconostoc mesenteroides when grown in sucrose.  Dextran 70 has a slower excretion rate than Dextran 40.  1L of Dextran 70 will increase the plasma volume 790ml.  T½ ~7h.  Has been uses as DVT prophylaxis.  Complications:  ARF, anaphylaxis, bleeding diathesis.

Shock:

Links: Septic: Cardiogenic:  Hypovolemic:  Labs:  Tx:  Vasopressors:  Pulmonary & Cardiac Parameters:

Failure of the circulatory system to maintain adequate cellular perfusion and function.  Due to impaired blood flow to vital organs and tissues.

Ddx:  “SHOCK”: Sepsis, Hypovolemia, Other (Addisons, drugs), CNS(spinal shock), “K” cardiogenic (MI).  Anaphylaxis –> DOC is Epi.  Massive PE or TCA OD –> drug of choice (DOC) is NE.

Obstructive Shock:   Vascular etiology.  Consider aortic stenosis, PE or tamponade from tension pneumo–> inc HR, dec heart sounds, distended neck veins, +pulsus paradoxus (dec SBP >10 during insp), Kussmauls sign (inc venous pressure with insp).

Neurogenic Shock:  (dec symp tone) –> dec BP but normal HR and pulse pressure, no vasoconstriction.  Doapmine is the drug of choice.

Distributive Shock (Septic):  50% due to G-, 25% G+, from endotoxemia that leads to vascular collapse and multiple organ failure.  Hypotension from vasodilators (lipopolysaccharide, TNF, C3a, C5a).  Positive blood Cx in <50%.   Hypotension, mildly inc HR, warm, pink, wide pulse pressure.  Initial tx is an attempt to eradicate the infection via Abx + surgical drainiage.  If severe met acidosis (pH <7.2) consider bicarb. Use Dobutamine + epinephrine or Norepinephrine.  Phenylephrine @ 20-200 ug/min (pure alpha-1 agonist) has a theoretical advantage as it maintains a near normal gastric pH.  Dopamine is often used, but may not be as efficacious at reversing the hemodynamic abnormalities.

Cardiogenic Shock: Commonly seen with >35% loss of functioning of LV after an AMI.  Get dec CO and lactic acidosis due to tissue hypoxia.  MR occurs frequently with inferoposterior MI.  Ruptured LV wall may occur.   During Tx aim for a LV filling pressure of 15-18 mmHg and CI of >2.2 L/min/M2.  Start vasopressors and inotropic agents if SBP low despite fluids.  If SBP >80mmHg use dobutamine (unless tachy, arrhythmia or vasoconstriction) as it increases coronary blood flow.  If SBP <80 mmHg use Dopamine as need some additional vasoconstriction of peripheral vessels to maintain vital organ perfusion.  If SBP <70 or refractory hypotension use NE as it will rise MAP & SVR.   Consider adding a low-dose DA drip.  An intraaortic ballon pump (IABP) may be needed (see AMI) to dec systemic afterload and inc diastolic perfusion pressure as a bridging device to revascularization.  Give volume resuscitation if no pulmonary edema, correct electrolyte abnormalities, hold antihypertensives meds.

Hypovolemic Shock:  loss of >40% of circulating blood volume.  Hypotension, profound tachycardia.  Usually due to bleeding, severe diarrhea or emesis, burns, or redistribution of body fluids.

Pearl:  If can feel radial pulse–> BP must be at least 80-90mmHg.  Femoral–> 70mmHg.    Carotid only–> 50mmHg.   In shock BP is usually <70mmHg.

Labs:  CBC, lytes, blood sugar, ECG, CXR.  If bleeding get T&C.

Tx: Hemodynamic monitoring–> Swan-Ganz or bedside parameters such as UO, acid-base status, level of sensorium, skin temp.  Step #1 is Fluid resuscitation: NS or LR generously (~2L in adults) but cautiously to raise SBP to 90-100 mmHg.  If develops SOB, rales, distended neck veins then overhydration has occurred (consider a PA cath to guide therapy).   Aim for a mean arterial pressure of 65mmHg to maintain cerebral perfusion.    If the pressure fails to rise after 2L IVF, then start vasopressors.  Consider intra-arterial pressure monitoring.  If unresponsive to initial fluids and altered MS or UGI bleed, consider ETT and ventilator support.

Vasopressors:

Autonomic Nervous System:   Adrenergic Receptors:  alpha-1–> constricts the peripheral vascular and coronary smooth muscle.  Beta-1–> acts on myocardium to increase rate and contractility.   Beta-2–> dilates bronchial, peripheral vascular and coronary smooth muscle.  Dopamine–> dilates renal vasculature and GI smooth muscle, shown to decrease mortality.

Dopamine (DA, Intropin): 5-20 ug/kg/min.  0.5-2 ug/kg/min = Renal Dose, for oligouria despite “normal” BP as dopaminergic.  2-10 ug/kg/min is Beta-1.  10-20 ug/kg/min is Alpha-1 (high arrhythmogenic potential).    2-15 for emergency tx of hypotension of any cause.  1-10 for hypotension due to sepsis.

Dobutamine (Dobutrex): 2.0-20 ug/kg/min.  For cardiogenic shock, cardiac induced pulmonary edema (CHF), not used alone if pt is hypotensive as only increased CO, not SBP. Beta-1 and Beta-2.  Good if hypertensive or normotensive.

Norepinephrine (NE, Levophed): 0.5-30 ug/min IV.  For emergency tx of hypotension from any cause, especially sepsis. Alpha-1 & Beta-1.

Epinephrine (Levarterenol): 0.5-10 ug/min for anaphylaxis, pulseless arrest and sepsis. Alpha-1, Beta-1 and Beta-2.  High arrhythmogenic potential.

Phenylephrine (Neo-Synephrine): 0.1-0.5 mg IV, then 0.05-0.2 mg/min for neurogenic shock (usual dose is 10-200 ug/min). Pure alpha-1.

Isoproterenol (Isuprel): 1-10 ug/min for bradycardia.  Beta-1 and Beta-2.  High arrhythmogenic potential.

Metaraminol (Aramine): 0.5-5 mg IV bolus, then 5-15 ug/kg/min for neurogenic shock.

Hemodynamic Profiles:   Drug –>\SVR\CO\HR\Inotropy\VO2.  DA- low –>\dec\inc\inc\inc\Inc.  DA- high –>\3+ inc\2+ inc\2+ inc\2+ inc\2+ inc.  Dobutamine –>\dec\2+ inc\2+ inc\2+ inc\3+ inc.  Epi –>\2+ inc\2+ inc\3+ inc\2+ inc\3+ inc. NE –>\3+ inc\inc\3+ inc\2+ inc\Inc.  Isuprel –>\2+ dec\2+ inc\3+ inc\inc\3+ inc.

Phosphodiesterase Inhibitors:   Amrinone (Inocor): 0.75 mg/kg IV over 3min, then 5-15 ug/kg/min as short term inc cardiac contractility when catecholamine therapy is hazardous such as arrhythmia or ischemia.   Has no adrenergic effects.

Milrinone (Primacor): 50 ug/kg IV over 10min, then 0.5 ug/kg/min.

**Ref: (The case of dehydration versus volume depletion.  An Intern Med 1997:127:848-53) (The Medical Abacus, by D. Rifkind, Parthenon Publishing 2000, NY) (Dehydration. Evaluation and management in older adults. Council on Scientific Affairs, American Medical Association. JAMA. 1995;274:1552-6) (Colloidal and crystalloid fluid resuscitation in shock associated with increased capillary permeability. Curr Stud Hematol Blood Transfus. 1986;:86-100) (Emergency fluid management for hypovolemia.  Postgrad Med. 1996;100:243-54) (Crystalloid or colloid?  Br J Hosp Med. 1986;35:217) (Fluid resuscitation with colloid or crystalloid solutions.  BMJ. 1998;317:278) (Cardiogenic shock: therapy and prevention.  Clin Cardiol. 1998;21:72-80)  (Septic shock.  Crit Care Clin. 1997 ;13:553-74)   (Septic shock.  Lancet. 1998;351:1501-5) (Fluid-electrolyte balance during labor and exercise: concepts and misconceptions.  Int J Sport Nutr. 1999;9:1-12)  (Subcutaneous infusion or hypodermoclysis: a practical approach.  J Am Geriatr Soc. 1999;47:93-5)  (Abnormalities of water metabolism in the elderly.  Semin Nephrol. 1996;16:277-88) (Serum osmolality. N Engl J Med 1984;310:102-05) (Emergency fluid management for hypovolemia. Postgrad Med 1996;100:243-51) (Cardiogenic shock. Ann Intern Med 1999;131:47-59) (Hypouricemia in the syndrome of inappropriate secretion of antidiuretic hormone. N Engl J Med 301:528, 1979). (Managing shock: the role of vasoactive agents.  J Critical Care Med 2001;16:6 & 7)

Dehydration:

Links:  Types:  ORT:  Severity:  Composition of Solutions:

Dehydration:  loss of intracellular water that ultimately causes cellular dessication and inc’s the plasma Na and osmolality. Seen mostly in the elderly with infections and poor access to water.   No circulatory instability, should get 5% Dextrose slowly.  Yet most also have volume depletion and need NS (Hypovolemia refers to both conditions).

Volume Depletion: loss of Na from the extracellular space (intravascular, interstitial fluid) after GI hemorrhage, vomiting, diarrhea, diuresis.  Have circulatory instability and need NS rapidly.

Average child has 1-2 episodes/yr for 1st 5yrs of life.  85% of dehydration due to Viral (Rota, Norwalk, Adeno, astrovirus).   Most of deaths in age <12mo –> vulnerable as inc metabolic rate (loses water), immature immune system, reticence to PO when not feeling well.

For hypovolemic shock –> bolus with 20ml/kg isotonic fluids.

PE: eyes sunken back into skull, skin tents/ loses elasticity, lips parched, inability to produce tears when cry, recessed fontanelle.  Ur s.g. >1.020 is dehydrated.  Urine output <2ml/kg/hr is oliguria.  Each kg BW loss is ~1L deficit, can estimate deficit from current wt- birth wt if an infant.

Types of Dehydration:

Hyponatremic (Hypotonic):  Na < 130 mEq/L. Seen in 5%.  Physio: Na loss exceeds water loss.  ECF loss >> ICF loss

S/s: inc HR, dec BP, comatose, skin tenting and clammy

Tx: All with isotonic fluid X 1-2hr (NS or LR), then D5 in NS X 12hr, then D5 0.45% NS for balance of fluids. Inc Na to 120 mEq/L over 12hr, then to 130 over next 24-36hr. 3%NS if severe sx.

Isonatremic (Isotonic):  Na is normal Seen in 80%.  Physio: Equal Na and water loss, no fluid shifts, mod ECF depletion

S/s: inc HR, dec BP, somnolent, dec skin turgor, dry skin and MM’s

Tx: All with isotonic fluid X 1-2hr (NS or LR), then ORT OK if  <10% dehydration.  D5 in 0.45% NS X 12hr Then D5 in 0.225 NS. + 25 mEq/L Bicarb, then add 30mEq KCl once voided.  Replace ½ Na deficit over 12hr, then ¼ over next 12hr.

Hypernatremic (Hypertonic): Na >150, Seen in 15%. Physio: Water loss > Na loss.  ICF loss > than ECF.

S/s: Mild inc HR, dec BP, irritable, doughy skin.  Parched MM’s

Tx: All with isotonic fluid X 1-2hr (NS or LR), then D5 in 0.225% NS.  Add 40mEq/l KCl.  Dec Na slowly (< 10mEq/l/d over 36-48hr).  Avoid rapid correction.  Assume 4ml/kg free water deficit for each 1mEq/L Na >145.

Five steps:  1.  Asses Severity of dehydration:

Mild (3-5%): normal BP/ HR/ MS/ skin turgor, but slightly dry MM & dec  UO.   Most are isonatremic and no electrolyte or labs determination needed.  Need to replace 50ml/kg given in 4-6hr, add 10ml/kg stool for ongoing loss.

Moderate (6-9%): Need to replace 80-100ml/kg in 4-6hr with volume for volume stool/ emesis loss.    Have nl BP, but inc HR & dec fontanel/ MS/ UO/ skin turgor, dry MM, absent tearing, cap refill >2 sec, generally ill appearing.   Heck Electrolytes to determine baseline & guage clinical progress.   If ingesting hyperosmolar liquids (fruit juices) that cause free water to move into gut, then likely Hypernatremia (Na >150mEq/L).  Will have contraction of vascular space –> irritable, feverish, sz, delirium, coma.  Need slow rehydration.   Hyponatremia (Na<125mEq/L) –> More common, from consumption of free water or low Na intake.

IV Therapy if: Severe (10-15%): Need to replace 110-130ml/kg given via IV or interosseous infusion of NS or LR @ 20-40ml/kg/hr, repeated until signs of rehydration are evident. Replace 50% of loss in 1st 8hr, remaining 50% over next 16hr.  Begin PO fluids once consciousness has improved and condition stabilized.     Pt has nl to dec BP, inc HR, dry MM, oliguria, fontanel, MS, skin turgor.  ORT Failure: clinical deterioration, failure to rehydrate within 8hr, intractable vomiting.   Will also need IV therapy if have profuse diarrhea or are vomiting relentlessly.  Exhibit a marked change in mental status.   Suffer from a medical illness or physical disability that interferes with oral therapy.  Exhibit marked change in mental status.  Unreliable caregivers or simply refuse to drink.  Re-evaluate lytes periodically.

2. Rehydrate: Over 4 hours, reassess status every 1-2hr, when clinically rehydrated proceed to maintenance.   Mild: 50ml/kg + 10ml/kg stool + Est of emesis.     Moderate: 100ml/kg +10ml/kg stool + Est emesis.

3.  Maintain hydration: take Ad Lib with goal of maintenance + ongoing losses.  @40-60mEq/L Na content, 2-2.5g/dL glucose, 215-260 mOsm/L.

4. Early Re-feeding: –> dec stool output.  Best to continue breast feeding throughout/ resume with full strength milk (80% will do well, lactose intolerance is rare) Foods should be complex carbo’s, lean meats, fruits, vegies, yogurt, low fat (BRAT diet along with wheat noodles & potatoes). Formula fed infants should alternate feedings of ORS and formula.

5.  Non-use of pharmacologic agents: children more susceptible to toxicity, decreased motility may inc risk for bacterial invasion.  Abx only if bacterial (cholera, travelers, dysentery, protozoal).

6.   F/u: reassess via telephone.  RTC if diarrhea lingers >10-14d.

Composition of Solutions:    Solution –> Na (mEq/L)\K (mEq/L)\Cl (mEq/L)\Bicarb (mEq/L)\Glucose (g/dL).   ECF –> 142\4\103\27.1.   LR –> 130\ 109\ 28.   0.9% NaCl (NS) –> 154\154.   Chicken Broth –> 250\5-8\-\-\-.   WHO-ORS –> 90\20\80\-\2.   Lytren –> 50\25\45\30\2.   Pedialyte –> 45\20\35\30\2.5.   Rehydralyte –> 75\20\65\30\2.5.   Resol –> 50\20\50\34\2.   Ricelyte –> 50\25\45\10\3.   Infalyte –> 50\20\40\-\2.  Gatorade –> 28\2\-\-\2.1.   Ginger Ale –> 4.2\-\-\9.  Coke/Pepsi –> 2.5.5\9\10\10.5.  Apple Juice –> 3\17\-\-\12.  Grape Juice –> 3\25\-\-\15.  Jell-O –> 24\1.5\-\-\16.  Infant Caravel’s –> 81\61\20\4.65.  Child Caravel’s –> 132\3.8\109\27\4.8.

**Ref:  (Dehydration in young children.  Acta Paediatr. 1997;86:337-8) (Oral rehydration for children with diarrhea. JAMA. 1991;266:517) (Update on medications used to treat gastrointestinal disease in children. Curr Opin Pediatr. 1999;11:396-401)

Nutrition:

Links:  Essential Nutrients:  Vitamins & Nutrients:  Signs of Deficiencies:  Vitamin Toxicity:  Caffeine:  Basal Metabolic Rate:   Assessment:   Nutritional Support:  Enteral:  Oral: TPN:  PPN:   Healthy Diet:   Vegetarians: Refeeding Syndrome:

Roughly 30% of Americans use at least one vitamin or mineral supplement in a given month.   The highest use is seen in non-Hispanic whites (42.6%) (Arch Fam Med 2000;9:258-62)

Dietary Reference Intakes (DRI’s):

Quantitative estimates of nutrients intake, useful for planning and assessing diets for healthy people.  Comprises 4 different values:

1. Estimated Average Requirement (EAR): intake of a nutrient adequate to meet the requirement of ½ the healthy population.

2.  Recommended Daily Allowance (RDA): dietary intake sufficient to meet the requirements of nearly all (97-98%) healthy persons in a particular life-stage and gender group.  RDA= EAR + 2SD  or   RDA= 1.2 X EAR.

3.  Adequate intake (AI): based on observed or experimentally derived estimates of nutrient intake by a group or groups of healthy people.  It is used when scientific evidence is insufficient to determine an EAR or RDA.  It is less precise

4.  Tolerable Upper Intake Level (UL): the highest level of daily nutrient intake likely to pose no risks of adverse health effects to most of the population.  Ex: Niacin–> flushing, B6–> sensory neuropathy, Folic Acid mask anemia dx from B12 def, Choline in large doses–> fishy body odor.

Nutrients Requirements and & Assessment:

Determining factors an individuals requirements:   gender, age & stage of life cycle (fetus, pregnant, lactating, child, adult, elder), disease states (malabsorption, maldigestion), inborn errors of metabolism, lifestyle (smoker, ETOH), medications, bioavailability, quantity required to fulfill physiologic roles, the extent to which the body can recycle micronutrient, the distribution & storage.

Known Essential Nutrients:  There are 45 essential micronutrients in humans (15 vitamins, 20 minerals, 8 AA’s, 2 fatty acids) that must be obtained from food as the body cannot manufacture them.  Amino Acids (L forms) –> threonine, valine, isoleucine, lysine, tryptophan, methionine-cyteine, Phenylpthaline-tyrosine, histidine.     Fatty acid –> Linoleic acid.    Vitamins –> thiamine, niacin, riboflavin, pyridoxine, folic acid, B12, ascorbic acid, biotin, pantothenic acid, V-A, V-D, V-E, V-K.   Elements–> Na, K, Ca, Mg, Cl, P, Fe, Cu, Zn, Manganese, Selenium, molybdenum, iodine, fluoride.

Common Nutrients:……Links: Ascorbic Acid (Vit-C): Vitamin A: Thiamine (B1): Riboflavin (B2): Niacin (B3): Pyridoxine (B6): Vit B-12: Biotin: Calcium: Coenzyme Q10: Creatine: L-Carnitine: Chromium: Chloride: Cobalt: Copper: Vitamin D: Fatty Acids: Fluoride: Folic Acid: Vit E: Iodine: Iron: Vit K: Magnesium: Manganese: Molybdenum: Pantothenic Acid: Phosphorus: Potassium: Selenium:  Sodium: Sulfur:  Zinc:

Ascorbic Acid (Vit-C): 75 mg/d for women, 90mg/d in men (Max of 2g/d).  Found in citrus fruits, raw cabbage, tomatoes, strawberries, peppers, greens, potato, kiwi. Used in microsomal electron transport, tyrosine, tryptophan, DA synthesis, steroid synthesis, hydroxylation of collagen proline and lysine and folic acid metabolism.

Defic: Scurvy.   Gingival hypertrophy, bleeding gums, petechiae, perifollicular hemorrhages (often on posterior thigh), curled hair follicles (corkscrew hairs), ecchymosis, osteopenia with subperiosteal hemorrhages, poor wound healing.  Toxic effects include nephrolithiasis and diarrhea.  Normal levels: 0.5-1 mg/dL in serum, 15-30 mg/dL in WBC.

Vitamin A (V-A, Retinol, Retinoic Acid, Beta carotene):   RDA is 300-500ug in child, 900ug in male >14yo and 700ug in female, 1200ug if lactating.   ~= 4,000-5,000 IU/d (800-1000 mg RE) .  Found in green leafy vegetables, dairy, yellow fruits and vegetables, liver.  Needed for light sensitive pigments in the retina, epithelial maintenance (retinoic acid), immune function.  Normal level: 20-60 ug/dL (-.7-2 umol/L).   Defic:  Keratomalacia:  (dry conjunctiva, corneal ulcers and prolapse of the iris), Bitot’s spots (white/ yellow spots under the conjunctiva), gingivitis, dry skin with hyperkeratinization, night blindness.  Some carotenoids, most notably beta-carotene, are metabolized into compounds with vitamin A activity and are considered to be provitamin A compounds. Vitamin A is an integral component of rhodopsin and iodopsin, light-sensitive proteins in retinal rod and cone cells.   Toxicity: In adults, >500,000 IU may cause acute toxicity: intracranial hypertension, skin exfoliation, and hepatocellular necrosis. Chronic toxicity may occur with habitual daily intake of >25,000 IU: alopecia, ataxia, dermatitis, pseudotumor cerebri, hepatocellular necrosis, and hyperlipidemia. Daily ingestion of >15,000 IU during early pregnancy can be teratogenic. Excessive intake of most carotenoids causes a benign, yellowish discoloration of the skin. Large doses of canthaxanthin, a carotenoid, can induce retinopathy.

Beta-Carotene: 5-6mg/d.  Antioxidant, can be converted to V-A.  Found in carrots, sweet potatoes, yellow-green veges, mangoes, apricots, papaya.  Defic: same as V-A.

Thiamine (B1):  1-1.5mg/d.  Found in pork, enriched breads/ cereals, wheat germ, organ meats, nuts, legumes, beans and peas.  Cofactor for transketolase, pyruvate to metabolize branched chain ketoacids.  Essential for glucose and alcohol metabolism.  A water-soluble compound containing substituted pyrimidine and thiazole rings and a hydroxyethyl side chain. The coenzyme form is thiamine pyrophosphate (TPP). Serves as a coenzyme in many alpha-keto-acid decarboxylation and transketolation reactions. Defic:   Inadequate thiamine availability leads to impairment of the above reactions and consequently to inadequate ATP synthesis and abnormal carbohydrate metabolism.  Lactic acidosis, Wernicke-Korsakoff syndrome (ophthalmoplegia- CN VI loss, nystagmus, ataxia, amnesia, confusion, confabulation), Wet beriberi (high output CHF, edema, peripheral vasodilation), Dry beriberi (peripheral neuropathy, muscle wasting), hyperglycemia (impaired insulin secretion). Normal levels: 8-15 IU ETK or <10% TPP effect.   Tx of Defic: 50-100mg IV/IM qd X 7-14d, then PO.  Must be given before or concurrent with dextrose fluids as a glucose load will inc metabolic demand for thiamine. The most effective measure of B1 status is the erythrocyte transketolase activity coefficient, which measures enzyme activity before and after addition of exogenous TPP: RBCs from a deficient individual express a substantial increase in enzyme activity with addition of TPP.  Toxicity: excess intake is largely excreted in the urine although parenteral doses >400 mg/d are reported to cause lethargy, ataxia, and reduced tone of the gastrointestinal tract.

Riboflavin (B2):  1.3-1.7 mg/d.  Found in dairy foods, organ meats, enriched cereals, green leafy veges, eggs, nutritional yeast, fortified soy milks, vegetarian burger patties, ready-to-eat breakfast cereals and peanuts. If pt limits animal products in their diets, they should take supplements or eat fortified food.   Used as electron transporter in flavin metabolism. Can be synthesized from tryptophan in foods. A compound consisting of a substituted isoalloxazine ring with a ribitol side chain. Serves as a coenzyme for diverse biochemical reactions. The primary coenzymatic forms are flavin mononucleotide and flavin adenine dinucleotide. Riboflavin holoenzymes participate in oxidation-reduction reactions in myriad metabolic pathways.   Deficiency: Susually found in conjunction with deficiencies of other B vitamins. Isolated deficiency of riboflavin produces hyperemia and edema of nasopharyngeal mucosa, cheilosis, angular stomatitis, glossitis, seborrheic dermatitis, and a normochromic, normocytic anemia. Soreness and burning of the mouth from cheilosis, angular stomatitis, gingivitis, atrophic lingular papillae, hypertrophy of filiform and fungiform papillae, seborrheic dermatitis, conjunctivitis, photophobia, anemia.   Toxicity: not reported in humans.  Assessment:  the most common assessment is determining the activity coefficient of glutathione reductase in RBCs (the test is invalid for individuals with glucose-6-phosphate dehydrogenase deficiency). Measurements of blood and urine concentrations are less desirable methods.

Niacin (B3, Nicotinic Acid):  13-20 mg/d.  Found in meats, peanuts, liver, enriched grains/ breads.  Used in electron transport for NAD and NADP.   Defic:  = Pellagra:  4 D’s–> Dermatitis (hyperpigmented, weeping, edema with fissuring, common on the head & neck or sun exposed areas), Dry MM’s, Diarrhea, Dementia. Fissured tongue with atrophy of lingular papillae, scaling/ dry/ atrophic/ thickened/ hyperpigmented skin, dementia, diarrhea. Most common in alcoholics.  Often affects populations where corn is the major source of energy endemic in parts of China, Africa, and India.  Normal levels: 4-9 ug/ml. Blood levels of vitamin not reliable. Measurements of urinary excretion of the niacin metabolites N-methylnicotinamide and 2-pyridone are thought to be the most effective means of assessment at present. Refers to nicotinic acid and the corresponding amide nicotinamide. The active coenzymatic forms are composed of nicotinamide affixed to adenine dinucelotide to form NAD or NADP. Over 200 apoenzymes use these coenzymes as electron acceptors or hydrogen donors. The essential amino acid tryptophan is used as a precursor of niacin; 60 mg of dietary tryptophan yields approximately 1 mg of niacin. Dietary requirements depend partly on the tryptophan content of diet.

Toxicity:  hypolipidemic effects. Includes vasomotor phenomenon (flushing), hyperglycemia, parenchymal liver damage, and hyperuricemia.

Pyridoxine (B6):  2mg/d in men, 1.6mg/d in women.  Found in pork, glandular meats, bananas, bran/germ cereals, milk, egg yolk, oatmeal and legumes.  Cofactor for enzymes such as transaminase, phosphorlyase and oxidases for protein (AA) metabolism, heme synthesis, reduces blood homocysteine levels. Several derivatives of pyridine, including pyridoxine, pyridoxal, and pyridoxamine. The co enzymatic forms are pyridoxal-5-phosphate (PLP) and pyridoxamine-5-phosphate. As a coenzyme, B6 is involved in many transamination reactions (and thereby in gluconeogenesis), in the synthesis of niacin from tryptophan, and in the synthesis of several neurotransmitters, and delta-aminolevulinic acid (and therefore in heme synthesis).   Defic: seen in conjunction with other water-soluble vitamin deficiencies. Glossitis, peripheral neuropathy, dementia, MCHC anemia, sz, N/V, cheilosis, depression.  A normochromic, normocytic anemia has been reported in severe deficiency. Abnormal EEGs and, in infants, convulsions have been observed. Some sideroblastic anemias respond to B6 administration. Isoniazid, cycloserine, penicillamine, ethanol, and theophylline can inhibit B6 metabolism.    Normal levels: EGOT index <1.5.   Plasma or erythrocyte PLP levels are most common. Urinary excretion of xanthurenic acid after an oral tryptophan load or activity indices of RBC alanine or aspartic acid transaminases (ALT and AST, respectively) all functional measures of B6 -independent enzyme activity. Toxicity: chronic use with doses exceeding 200 mg/d (in adults) may cause peripheral neuropathies and photosensitivity.@Assessment of Status Many laboratory methods of assessment exist.

Vitamin B-12 (Cobalamin): 2-3ug/d.  Found in meats, milk, eggs, fish, cheese, poultry.  Used as a methyl donor in carboxylation reactions such as DNA synthesis (with folate), reduces blood homocysteine levels.   Strict vegetarians and elderly (>60yo have atrophic gastritis and cannot absorb) need supplements.   Defic: glossitis, optic neuritis, hyporeflexia, dementia, ataxia, anorexia, loss of proprioception and vibration sense, megaloblastic/ pernicious anemia.  7 P’s of pancytopenia, peripheral neuropathy, pyramidal tract signs, papillary atrophy, pH elevation (GI), psychosis and posterior column disease =subacute combined degeneration (stocking-glove paresthesias, clumsiness, ataxia, weakness and spasticity).  Nl level: 200-900 pg/ml.

Biotin: 50-200ug/d.  Found in most foods such as liver, egg yolk, mushrooms, fruits, peanuts, dark green veg.  Used as cofactor in carboxylation of pyruvate and acetyl CoA, works with B vitamins.  Defic: alopecia, seb derm, neuritis, dry skin, alterations in mental status, myalgias, hyperesthesias, and anorexia occur  Normal levels: 200-500 pg/ml.  Plasma and urine concentrations of biotin are diminished in the deficient state. Elevated urine concentrations of methyl citrate, 3-methylcrotonylglycine, and 3-hydroxyisovalerate are observed in deficiency

A bi-cyclic compound consisting of a uredio ring fused to a substituted tetrahydrothiophene tring. Most dietary biotin is linked to lysine, a compound called biotinyl lysine, or biocytin. The lysine must be hydrolyzed by an intestinal enzyme called biotinidase before intestinal absorption occurs. Acts primarily as a coenzyme for several carboxylases; each holoenzyme catalyzes an ATP-dependent CO2 transfer. The carboxylases are critical enzymes in carbohydrate and lipid metabolism. Toxicity:  not been reported in humans with doses as high as 60 mg/d in children.

Calcium: 800-1200mg/d. Found in milk, broccoli, sardines, clams, kale, turnip greens, mustard greens.  Body contains 600 g, 99% in bones.  Used for blood clotting, nerve and muscle function.  Defic–> osteomalacia, tetany.  Normal = 8.6-10.8 mg/dL (2.2-2.7 mmol/L) if normal serum albumen.  Need to take in 400-600 IU of V-D.

Ca Content of Food: 1 cup skim milk or 8 oz yogurt has 300mg.  1 oz of Swiss or Gruyere cheese or 10 figs has 280mg.  ½ cup of tofu or _ cup of Ca fortified cereal has 250mg.  1 oz cheddar or mozzarella or 6 oz of fortified orange juice has 200mg.  ½ cup of collards or 1 oz of American cheese has 175mg.  ½ cup of mustard greens, kale or broccoli has 50mg.

Ca intake (mg/d): Age 11-24–> 1200-1500mg/d.  Pregnancy–> 1,200.   25-50yo–> 1000mg/d.  50+–> 1500 if on ERT need 1000mg (men need same amounts).  1000mg Ca = 1qt milk (3-4 8oz glasses), 2.7# of broccoli.

Ca Carbonate (Caltrate, Os-Cal, Tums): inexpensive, but less soluble, requires gastric acid for absorption, lowers Thyroxine absorption.

Ca Citrate (Citracal): is more soluble and not affected by stomach acid.  Good for elderly pt’s and those on H2 blockers.

Ca Gluconate and Lactate: soluble, but give less Ca per tablet.

Ca Glubionate (Neo-Calglucon): comes in a syrup, good for kids.

Coenzyme Q10 (Ubiquinol): essential for mitochondria, 40% HTN and 60% CAD are deficient.  Takes 4-6 weeks to lower BP @50-150mg BID.  Insufficient evidence to recommend.  Fairly safe drug.

Creatine: an amino acid (methylguanidine acetic acid). Not routinely incorporated into proteins.  Endogenously synthesized from glycine, arginine and methionine. Taken orally, it will increase total muscle creatinine 20%, with 20% of that increase in the form of creatinine phosphate.   Increases energy substrate to muscle in order to delay fatigue.  May increase power and strength.  Increases wt due to water retention (not muscle), may cause dehydration, cramps and strains.

95% is in skeletal muscle as phosphocreatine, supports synth of ATP, may or may not help in recovery of muscle strength or improve performance, yet incr in body weight (fluid retention and/or stim Protein synthesis).  Naturally in meat, milk and some fish (½# raw meat has 1g creatine).  Gain 1-3# in first week, then 10# by 6wks.  Used for intermittent high intensity exercise (soccer, basketball)  Load dose of 5g QID for 5-7d, then 2-3g/d maintenance. (should use BW dose of 0.3g/kg load, .03g/kg maint), monitor LFT’s and BUN/Cr. The safest form is the monohydrate powder, which is usually mixed with 4-8 oz of juice.  When stopped creatine levels rapidly decrease in 4-12 days to normal levels. No known serious adverse effects. 25% of people do not respond to high muscle creatinine levels.

Lutein:  a carotenoid found in green and yellow veges.  Some studies show benefit in cataract and macular degeneration.  6mg/d.

L-Carnitine (Levocarnitine): helps metab FA’s by transporting free fatty acids into mitochondrial cytosol for oxidation.   Normally synthesized in the liver from Lysine.  S/s:  weakness, fatigue, cramps.    Essential to supplement if deficient.  However w/o the genetic d/o, there is little to no loss from skeletal m during high or low intensity exercise.  Even massive doses increase levels by only 1-2%.  Depletion is common in those on hemodialysis.  300-330-500mg PO TID.  2g IV with each dialysis.  Comes in 1g/10ml solution.  Mix with juice or liquids.

Androstenedione:  androgen derived from plants at 100-300mg/d.  In its natural form it is produced by the adrenal glands and gonads.  It may increase muscle mass and serum testosterone levels.  SE: dec HDL, behavioral changes, acne, testicular atrophy, premature closure of epiphysial plates.

Chromium: 50-200ug/d.  Found in corn oil, clams, whole grain cereals, meats, brewers yeast.  6mg in body, used as part of glucose receptor.   Defic: glucose intolerance.  Normal levels: 2-4ng/ml (35-73 nmol/L) plasma.   Element #24.  Dietary intake should be 50-200ug/d.  enhances insulin action to increase AA uptake in order to lose fat and gain muscle.   Deficiency may cause anemia, chromosomal damage, cognitive impairment and interstitial nephritis.  Usually combined with picolate to increase GI absorption.   Found in:  liver, American cheese, brewer’s yeast, wheat germ, meats, alfalfa, apples with skins, brown sugar, carrots, potatoes.    No proven benefit unless deficient. Deficiency seen with long-term TPN.  Advice to diabetics:  it is inexpensive, can try adding 300-1000 ug/d once BS is stable on traditional meds, if see no measurable improvement in diabetics parameters, then stop taking.

Chloride (Cl): 2-5g/d.  Found in table salt, seafood, milk, meats, eggs.  80g in body, main extracellular cation.  Defic: metabolic alkalosis.  Nl: 89-106 mEq/L.

Cobalt: 3ug/d.  Found in liver, kidney, shellfish, poultry, milk, and veges (depending on soil).  80ug in body, used as a cofactor in B12.  Defic: no know.  Normal levels: 2-5 ng/ml.

Copper (Cu): 2-3mg/d.  Found in liver, shellfish, whole grains, cherries, legumes, kidney, poultry, oysters, chocolate, nuts.  100mg in body, used as cofactor in lysyl oxidase for collagen synthesis and in cytochrome.  Defic: has been observed in premature and low-birthweight infants fed exclusively a cow’s milk diet and in individuals receiving long-term TPN lacking copper.  Get anemia, neutropenia, osteopenia in children, depigmentation of skin and hair, neurologic disturbances.  Normal levels: 90-130 ug/dL (14-20 umol/L). Deficiency is reliably detected by diminished serum copper and ceruloplasmin concentrations, as well as by low erythrocyte superoxide dismutase activity. Absorbed by a specific intestinal transport mechanism. It is carried to the liver, where it is bound to ceruloplasmin, which circulates systematically and delivers copper to target tissues in the body. Excretion of copper is largely through bile into feces. Toxicity:    absorption of copper salts applied to burned skin. Milder manifestations include nausea, vomiting, epigastric pain, and diarrhea; coma and hepatic necrosis may ensue in severe cases. Toxicity may be seen with doses as low as 70 mug/kg/d. Chronic toxicity is also described. Wilson disease is a rare, inherited disease associated with abnormally low ceruloplasmin levels and accumulation of copper in the liver and brain, eventually leading to damage to these two organs.

Vitamin D (V-D): 200-400 IU/d, 5-10mg/d). A group of sterol compounds whose parent structure is cholecalciferol (vitamin D3 ). Cholecalciferol is formed in the skin from 7-dehydrocholesterol by exposure to UV-B radiation. A plant sterol, ergocalciferol, can be similarly converted into vitamin D2 and has similar vitamin D activity. Maintains intracellular and extracellular concentrations of calcium and phosphate by enhancing intestinal absorption of the two ions and, in conjunction with parathormone, promoting their mobilization from bone mineral. Needed for Ca, P and Mg metabolism and absorption from the gut as well as Ca deposition in the bone.  Normal levels: 10-80 ng/ml (25-200 nmol/L). The serum concentration of the major circulating metabolite, 25-hydroxyvitamin D, indicates systemic status, except in chronic renal failure, n which the impairment in renal 1-hydroxylation results in disassociation of the monohydroxy- and dihydroxyvitamin concentrations. Measuring the serum concentration of 1,25-dihydroxyvitamin D is then necessary.     Daily V-D intake of 400-800 U/d–> 3.5oz Cod Liver Oil: 8,500 IU.   Herring (3.5oz): 900 IU.   Salmon (3.5oz) 600 IU.   Margarine (3.5oz): 320 IU.  Milk (1 cup): 100 IU.  Swill Cheese (3.5oz): 100 IU.   Egg (1 whole): 27 IU.   Defic: osteomalacia in adults, muscle weakness/ hypotonia, rickets in children. Expansion of the epiphyseal growth plates and replacement of normal bone with unmineralized bone matrix are the cardinal features.  D1 = Dihydrotachysterol (DHT): 0.6mg qd in osteoporosis.  0.1-0.6mg qd in renal osteodystrophy.   D2 = Ergocalciferol: 250 ug IM qd or 12,000-500-000 IU PO qd for osteomalacia/ rickets.  50,000-200,000 IU PO qd + 500mg Ca 6X/d for hypoparathyroidism.  10,000-80,000 IU PO qd + 1-2g Phos for familial hypophosphatemia. Dietary Sources of V-D (units of V-D):  Cod Liver Oil, 3.5 oz (8,500), Herring, 3.5oz (900), Salmon, 3.5oz (600), MVI with 100% RDA (400), Margarine, 3.5oz (320), Sardines, 3.5oz (300), Milk, 1cup (100), Swiss Cheese, 3.5oz (100), Chicken Liver, 3.5oz (67), Breakfast Cereal (40), One Whole Egg (27).  Toxicity: Excess amounts result in abnormally high serum concentrations of calcium and phosphate; metastatic calcifications, renal damage, and altered mentation may ensue.

Nutritional Rickets: Failure of calcification of osteoid in growing child, called osteomalacia in adult.  Caused by deficient V-D metabolites, rarely by deficient Ca or P.  Can be due to V-D def, resistance to V-D, GI d/o renal osteodystrophy or associated with other d/o (fibrous dysplasia, neurofibromatosis, malignancy, anticonvulsant tx).   Risk: darker skinned (blocks light penetration), breast fed and no oral supplements, inner city, kept inside. Milk sold in USA has 400 IU (10ug)/ qt.  D3 formed in skin–> hydroxylated in liver to 25-, then kidney to 1,25-= Calcitriol, this acts at 3 sites promotes Ca & P absorption in intestines, P reabsorption in kidney, acts to release bone Ca & P.   Clinical: generalized muscular hypotonia, ittitability, apathy, lethargy, failure to thrive, craniotabes, thick wrists and ankles, bowlegs (genu varum), rachitic rosary (knobby deformity of chest), frequent fx’s.

Lab: initially low Ca, then nl, always low P, AP elevated, low calcidiol, inc PTH, generalized aminoaciduria. Dec in 25(OH)-Vit-D3 and 1,23(OH)-Vit-D3.  X-ray: AP of knees show widened, frayed and cupped metaphyses, osteopenia (especially juxtra-articular), bowing of the long bones.

Tx: V-D 125-250 ug (5000-10,000 U) daily for 2-3mo until healing documented on Xray and AP normalizes or 15,000 ug (600,000 U) in single day in 4-6 PO doses (avoid suspension in propylene glycol, best to use 50,000 U capsules of ergosterol softened in water and fed blended in applesauce.  Prevent with 20 min UV light/ day or 10ug (400 U) V-D.  (Nutritional rickets. Am J Ortho 2000;3:214-18)

Essential Fatty Acids:1-2% of kcals. Omega-3 (alpha-linolenic acid) & Omega-6 (linoleic acid).    Found in vegetable oils (use olive/ canola oils).  Components of all lipid membranes, precursors of prostaglandins.    Defic: scaly dermatitis, Triene:tetraene ratio >0.7.   Normal levels = treine-letraene ratio >0.4, plasma or RBC membrane.   Fatty acids:  used either as stored fuel or as precursors for essential compounds such as prostaglandins, leukotrienes and thromboxane.  Can be classified by chain length:  Short–> 2-5 carbons.  Medium–> 6-11 carbons.  Long–> 12-26 carbons.  Also classified on presence of double bonds (unsaturated).  Saturated fats found in beer, pork shops, chicken/ turkey thighs.  Lower saturated levels in chicken breast, veal and pork tenderloin.     Poly or mono unsaturated depending on the number of double bonds.  Omega 3, 6 or 9 by location of the double bond when count carbons from the noncarboxyl end.   Humans can only synthesize double bonds at position #7, but can elongate or desaturate linoleic acide & alpha-linoleic acid to make others.  Whole milk is 3.3% fat and has 8.2 fat grams (150 cal) per 8oz compared to 2.6g (102 cal)in 1%.  Cheddar cheese 1oz has 9 fat g, Swiss has 8, Mozzarella has 6.

Omega-3 Fatty Acids: cold water fish *mackerel, lake trout, herring, sardines, albacore tuna, salmon, halibut), flax seed oil.   750-1,000mg will reduce the risk of sudden cardiac death.  Vegetarians can use flaxseed oil.    Three common types:  EPA= eicosapentaenoic acid found in fish and plankton, DHA = docosahexaenoic acid found in fish, plankton, algae, ALA = alpha-linolenic acid, found in flaxseed (linseed) oil, soybean, canola and walnuts, all metabolized to DHA.  Cardioprotective as slows heart rate, increases left ventricular diastolic filling, lowers postprandial triglyceride levels, reduces transcription of inflammatory cytokines and decreases secretion of platelet-derived growth factor to ¯ fibrinogen, BP and CAD.  One g/d is a safe target in adults, this can be obtained by consumer four 3oz servings/wk.  Most standard fish oil concentrates contain 300mg EPA & DHA / 1g capsule (30%).  Thus would need 10-12 cap/d.  One can get concentrates that are 50 or 80%. Olive Oil has highest content of monounsaturated fat (72%) than other sources, Canola has 62% mono, Peanut 49%, Palm 39%, Corn 26%, Soybean 24%, Sunflower 20%, Cottonseed 19%, Safflower 12%. (Heart Dz 1999;1) (JAMA 1998;279) (Mayo Clin Proc 2000;75:607-14)

Fluoride:  1.5-4mg/d.  Too much while teeth still forming beneath gum line–> fluorosis, use pea sized amount of toothpaste.  May need supplement if low intake and risk factors for dental caries (clean mouth, FHx of parents/ siblings with cavities).  2.2mg Sodium Fluoride contains 1mg Fluoride. Only 5% of bottled water contains the recommended amount of fluoride, compared to nearly 100% found in tap water.

Daily Fluoride Supplementation by Age per water content:

Age –> <0.3 ppm\ 0.3-0.6 ppm\ >0.6ppm:   ½-3yo –> 0.25 mg/d.  3-6yo –> 0.5.5.  >6yo –> 1.5.

Folic Acid (Folate):    200 ug/d (400ug if childbearing age).  Found in liver, meats, kidney/ lima beans, green leafy vegetables, wheat, lentils, eggs.  Used as a cofactor for purine and pyrimidine synthesis, need for metabolism of serine, histidine, homocystine. Reduces blood levels of homocysteine.  Defic: megaloblastic anemia due to defects in RBC’s and mucous membranes, birth defects.  Normal levels: 3-9 ng/ml serum, 150-600 ng/nl RBC. High doses may give nausea/ anorexia/ flatulence/ lower sz threshold in epileptics.  Toxicity:  a dose >400 mug/d may partially correct the anemia of B12 deficiency and mask (and perhaps exacerbate) the associated neuropathy. Doses >400 mug are also reported to lower the seizure threshold in individuals prone to seizures. Rarely, parenteral administration is reported to cause allergic phenomena,

Vitamin E (V-E, Tocopherol):  RDA for male or female is 15 mg/d (22 IU) of alpha-TE in adults, which is equivalent to 2 IU of “Natural” V-E (d-alpha-tocopherol, the RRR isomer of alpha-tocopherol, provides 0.67 mg/IU) or 33 IU of “Synthetic” V-E (d-l-alpha-tocopherol, has 8 different isomers, provides 0.45mg/IU).  The synthetic form has inactive isomers.  A group of at least 8 naturally occurring compounds that share a spectrum of biologic activities.  The natural form is what is found naturally in food and is the only type the body used.  Found in wheat germ, vegetables, milk, fat, egg yolk.  Prevents peroxidation of polyunsaturated lipids, may protect against atherosclerosis.   1200 IU/d decreases CRP levels in diabetics.  Defic: rare in developed countries, usually affects premature infants, get a hemolytic anemia of newborns, dystrophic changes in retinal and posterior column nuclei.      Etiology of Defic:  CF, chronic cholestatic hepatobiliary dz, chronic intestinal mucosal absorption defects (short bowel syndrome, celiac sprue, hypobetalipoproteinemia, other malabsorption), liver dz (Wilsons, hepatitis), chronic pancreatitis, lymphatic obstruction (Whipples dz, intestinal lymphangiectasia), Familia isolated V-E Defic.

Neurological findings:  early–> hyporeflexia, dec proprioception/vibratory sense, distal muscle weakness, night blindness (nyctalopia).   Middle–> truncal/limb ataxia, limited upward gaze, nystagmus, diffuse muscle weakness.   Late findings–> areflexia, loss of proprioception/ vibratory sense, dysphagia, dysarthria, arrhythmia, ophthalmoplegia, blindness, dementia.  Normal levels = 0.02-0.03 mmol/L (0.8-1.2 mg/dL), 10% hemolysis.  Max of 1500 IU/d of “d” form or 1100 if “di” form) Plasma or serum concentration of alpha-tocopherol is most commonly used. Additional accuracy is obtained by expressing this value per mg of total plasma lipid. The RBC peroxide hemolysis test is not entirely specific, but is a useful functional measure of antioxidant potential of cell membranes.   Toxic effects:   include headaches and V-K antagonism via depressed levels of vitamin K-dependent procoagulants and potentiation of oral anticoagulants have been reported, as has impaired leukocyte function. Doses of 50 IU/d may slightly increase the incidence of hemorrhagic stroke.

Iodine: 150 ug/d.  Found in iodized table salt, seafood, water and vegetables in non mountainous regions.  30mg in body.  Defic: cretinism’s, hypothyroidism, obesity, mental retardation.  T4 for levels.

Iron (Fe): RDA of 18 mg/d for women age 19-50.  27mg/d if pregnant.  8mg/d if male.  Found in liver, meats, egg yolk, legumes, whole/ enriched grains, dark green veges, dark molasses, seafood.  4g in body used as heme compounds, cytochrome enzymes and storage.  Defic: MCHC anemia, immunocompetence.  10% of women of childbearing age are deficient, 3.5% have anemia compared to 1% of males.

Vitamin K (Phytonadione):  40-80 mg/d.  Found in green leafy veges, wheat bran, cheese, egg yolk, liver (K1) and intestinal bacteria (K2).  Synthesis of clotting F (2), 7, 9, 10 and possibly 5 as wll a protein C & S.  Menaquinone (K2) is the form produced by bacteria.   Defic:  uncommon except in (1) breast-fed newborns, in whom it may cause “hemorrhagic disease of the newborn”; (2) adults with fat malabsorption or who are taking drugs that interfere with vitamin K metabolism (coumarin, phenytoin, broad-spectrum antibiotics); and (3) individuals taking large doses of vitamin E and anticoagulant drugs. Excessive hemorrhage is the usual manifestation. Occurs in the skin or GI, epistaxis, ecchymosis.  Normal: PT <1sec over control.  Abnormal if >2sec.  Dietary Sources of V-K (ug/100g):  Green tea (712), Turnip greens (650), Avocado (634), Brussel Sprouts (317), Chickpeas (220), Broccoli (200), Cauliflower (192), Lettuce (129), Cabbage/ Kale (125), Spinach (92), Asparagus/ Watercress (57), Green Beans (14), Potatoes (3).   Toxicity:  rapid intravenous infusion of K1 has been associated with dyspnea, flushing, and cardiovascular collapse, probably related to dispersing agents in the solution. Can be given PO, SC, IV, IM. Given PO (2.5mg) will lower the INR in 12-48hr.  Takes 4 days if just stop Warfarin intake.   Give 1-2.5mg PO if INR 5-10 w/o bleeding, give 3-5mg PO if INR >9.   Onset of IV is faster (2-3hr to dec INR, max effect in 27hrs) than PO, however it has higher risks (2%) such as anaphylaxis and allergic reactions.  Reserved for high risk patients, infuse at rate <1mg/min, get return of therapeutic INR in 4.1 days (Mayo Clin Proc 2001;76:260). (Arch Intern Med 1998; 158)

Magnesium (Mg): 300-400 mg/d (toward the higher range as age.  Found in whole grains, cereals, nuts, meat, milk, green veges, legumes.  25g in body, a cofactor for enzymes (phosphorylase, V-D hydroxylase).

Defic: tetany, weakness due to dec K & Ca.  Nl: 1.3-2.5 mg/dL.

Manganese: 2-5mg/d.  Found in blueberries, whole grains, nuts, fruit, legumes, tea, beans.  20mg in body.  A component of several metalloenzymes used as a cofactor in lipid, cholesterol, mucopolysaccharide synthesis.  Defic: hypocholesterolemia, weight loss, hair and nail changes, dermatitis, and impaired synthesis of vitamin K-dependent proteins. Abnormal clotting, not corrected by V-K, abnormal blood glucose.  Normal levels: 6-10 ng/ml.  Toxicity:  unknown in humans. Toxic inhalation causes hallucinations, other alterations in mentation, and extrapyramidal movement disorders.

Molybdenum: 0.15-0.5 mg/d.  Found in legumes, cereals, dark green leafy vegetables, organ meats.  5mg in body, used as cofactor in Xanthine oxidase and sulfite oxidase.  Defic: delirium due to inc methionine.  Normal levels: 0.5-2 ng/ml.   Toxicity:   may interfere with copper metabolism at high doses.

Pantothenic Acid: 4-10 mg/d.  Found in most foods, especially eggs, salmon, yeast and organ meats.  Converted to coenzyme A, hormone production.    Defic:  Usually seen in conjunction with other water-soluble vitamin, may see irritability, paresthesias, cramps, muscle wasting.    Normal levels: 150-400 ng/ml. Whole blood and urine concentrations of pantothenate are indicators of status; serum levels are not accurate.    Consists of pantoic acid linked to beta-alanine through an amide bond. Pantothenate serves as an essential precursor of CoA. CoA is essential for the synthesis and beta-oxidation of fatty acids and the synthesis of cholesterol, steroid hormones, vitamins A and D, and other isoprenoid derivatives. CoA is also involved in the synthesis of several amino acids and delta-aminolevulinic acid, a precursor for the corrin ring of vitamin B12 and the porphyrin ring of heme and the cytochromes. CoA is also necessary for the acetylation and fatty acid acylation of a variety of proteins.Toxicity: doses exceeding 10 g/d may induce diarrhea.

Phosphorus: 800-1200mg/d.  600g in body, 85% in bone, used for high energy phosphate bonds, chief intracellular anion.  Defic: osteomalacia, hemolytic anemia, dec HbO2 dissociation, dec phagocytosis.  Normal levels: 2.5-4.5 mg/dL (0.8-1.5 mmol/L).

Potassium (K): 2-5g/d.  Found in fruits/ vegetables (apricots, OJ, potatoes, carrots, cantaloupe, melons, mushrooms, dried beans & peas, artichokes, tomatoes), meats, milk, cereals, legumes, salt substitutes.  165g in body, the main intracellular cation.  Defic: rare in North America except in individuals receiving long-term TPN lacking selenium. Such individuals have myalgias and/or cardiomyopathies.  Weakness, arrhythmia, metabolic alkalosis.  Normal level: 3.5-5 mEq/L.

Selenium:  55 ug/d for men and women.  Found in whole grains, onions, meats (seafood, liver, chicken), milk and veges (depending on soil).  Used as cofactor in glutathione peroxidase, antioxidant similar to V-E.  This enzyme appears to prevent oxidative and free radical damage to various cell structures. Evidence suggests that the antioxidant protection conveyed by selenium operates in conjunction with vitamin E because deficiency of one seems to enhance damage induced by a deficiency of the other. Selenium also participates in the enzymatic conversion of thyroxine to its more active metabolite triiodothyronine.   Defic: weakness, hemolytic anemia, cardiac problems. Normal levels: 0.02ng/ml.   Erythrocyte glutathione peroxidase activity and plasma, or whole blood, selenium concentrations are moderately accurate indicators of status.   Toxicity:  If take >400 ug/d, nausea, diarrhea, alterations in mental status, peripheral neuropathy, and loss of hair and nails.

Sodium (Na): 1-3g/d.  Found in table salt, seafoods, animal products, milk, eggs, cheese, dried fruits, MSG, mustard, pickles, ketchup, olives, preserved meats, soy sauce, snack foods, salad dressing, bouillon, canned foods, packaged foods, most foods except fruit.  100g in body, a main extracellular cation.  Defic: low circulating blood volume, BP and urine output.  Normal levels: 135-145 mEq/L.

Sulfur:  Found in meats, milk, egg, cheese, legumes, nuts.  180g in body, found in methionine, cyteine, thiamine, insulin, chondroitin sulfate.

Zinc (Zn):  RDA of 2-3mg/d for 0-1yo, 3mg 1-3yo, 5mg 4-8yo, 8mg 9-13yo, 11mg males >14yo.  8mg for females >9yo.  12mg/d if pregnant or lactating.   Found in milk, liver, shellfish, herring, wheat bran.  1-2g in body, functions as an enzyme activator and cofactor.  Absorbed via ligand binding.  Defic: dec Intake–> poor appetite, diet high in fiber, P, Fe, Cu, tannates, oxalates, Ca.   Low protein (histidine, cysteine). Dec absorption–> lack of zinc binding ligand (acrodermatitis enterhaepatica), malabsorption syndromes.   Inc Gut losses–> prolonged NGT, high fistulas, exudative enteropathy.  Inc Urinary loss–> alcoholism, cirrhosis, nephrotic syndrome, CRF.     S/s:  4 D’s–> diarrhea, dermatitis, depression, dementia.   Alopecia, night blindness, tremor, loss of taste, poor wound healing.   Tx: zinc sulfate 3-6g/d.

Clinical Signs of Possible Nutrient Deficiency:

Hair:   Transverse depigmentation–> Protein, copper.  Easily pluckable–> Protein. Sparse and thin–> Protein, zinc, biotin.

Skin:    Dry, scaling–> Zinc, V-A, essential fatty acids.  Flaky paint dermatitis–> Protein, niacin, riboflavin.  Follicular hyperkeratosis–> V-A and C.  Perifollicular petechiae–> V-C.  Petechiae, purpura–> V-C and K.  Pigmentation, desquamation–> Niacin. Nasolabial seborrhea–> Niacin, riboflavin, pyridoxine. Pallor–> Iron, folate, V-B12, copper.  Scrotal/vulvar dermatoses–> Riboflavin.  Subcutaneous fat loss–> Calorie.

Nails:  Spooning–> Iron. Transverse lines, ridging–> Protein-calorie.

Head:  Temporal muscle wasting–> Protein-calorie.  Parotid enlargement–> Protein.

Eyes:  Night blindness–> V-A, zinc. Corneal vascularization–> Riboflavin.  Xerosis, Bitot spots–> V-A.  Keratomalacia, Conjunctival inflammation–> Riboflavin.

Mouth:  Glossitis (scarlet, raw) –> Niacin, pyridoxine, riboflavin, V-B12, folate.   Bleeding gums–> V-C, riboflavin.   Cheilosis–> Riboflavin.  Angular stomatitis–> Riboflavin, iron.  Atrophic lingual papillae–> Niacin, iron, riboflavin, folate, V-B12.  Hypogeusia –> Zinc, V-A.   Tongue fissuring–> Niacin

Neck:  Goiter–> iodine.      Chest:  Thoracic rosary–> V-D.

Heart:  High-output failure–> Thiamin.   Dec output–>Protein-calorie.

Abdomen:  Hepatosplenomegaly –> Protein-calorie.  Distention –> Protein-calorie.  Diarrhea –> Niacin, folate, V-B12.

Extremities:  Muscle tenderness, pain –> Thiamin, V-C.  Muscle wasting –> Protein-calorie. Edema –> Protein, thiamine.  Bone tenderness –> V-D, V-C, Ca, P.

Neurologic:  Hyporeflexia –> Thiamin.  Decreased position and vibratory –> V-B12, thiamine. Paresthesias –> V-B12, thiamine, niacin.   Confabulation, disorientation –> Thiamin. Dementia –> Niacin.  Ophthalmoplegia –> Thiamin, phosphorus. Tetany –> Ca, Mg.

Other:  Delayed wound healing –> Zinc, protein-calorie, V-C. Protein Calorie Deficiency –> brittle, fine, dry hair, enlargement of parotid gland edema, muscle wasting, weakness, loss of SC fat, hepatomegaly, diarrhea.

Vitamin Toxicity:

V-A:   Acute: >1mil IU for adult, >80,000 IU for child –> inc ICP with H-A, irritability, lethargy, ophthalmoplegia, papilledema.  Later get thinning hair, peeling skin and hepatomegaly.   Chronic: >30,000 IU/d in adult, >18,000 in child –> inc ICP, pseudotumor cerebri.  Dry, peeling skin, hair loss, brittle nails, cheilitis, stomatitis, gingivitis, hepatomegaly, N/V, + inc LFT.   Later get hepatic fibrosis, ascites, cirrhosis, esophageal varices, bone pain, cortical hyperostosis, premature epiphyseal closure. Teratogenic: >10,000 IU/d will cause facial, CNS and cardiac anomalies, but less than isotretinoin.

V-D: >60,000 IU/d adult, >1800 child. –> inc Ca, hypercalciuria, nephrolithiasis, metastatic calcifications of heart and vessels.

V- E:   >800-3000 IU/d –> contact dermatitis, H-A, weakness, nausea, cramps, diarrhea, inc effects of anticoagulants.

Niacin (B3): >3-4.5g/d. –> alopecia, pruritis, flushing, thrombocytopenia, A fib, gout, myopathy.

B6 (pyridoxine): >120-500mg/d. –> peripheral sensory neuropathy, porphyria cutanea tarda.

V-K: therapeutic IV dose. –> cutaneous hypersensitivity, anaphylactoid reaction.

erythematous plaques, localized urticaria, pseudo-scleroderma,

V-C: >4g/d. –> nausea, cramping, diarrhea, nephrolithiasis, hemolysis (if G6PD Defic).

Others with toxic doses:  zinc (500mg), selenium (1mg), P (12g), Mg (6g), Fe (100mg), I (2mg), Cu (100mg), Ca (12g), biotin (50mg), Folate (400mg), pantothenic acid (1g), riboflavin (1g).

Caffeine Content in mg:

180ml cup.   Brewed coffee = 80-140 mg.  Instant = 60-100.  Decaf = 1-6.  Leaf tea = 30-80.  Tea bags = 25-75.  Instant tea = 30-60.  Cocoa = 10-50.  Cola drink = 15-50.  1oz chocolate = 20.  Excedrine = 60mg.  Cafergot = 100mg.

**Ref:  (Arch Fam Med 1999;8:386-90) (Nutritional aspects of exercise. Clin Sport Med 1999;18:3) (Vitamin supplements. The Med Letter 1998;40:75) (Vitamin supplementation therapy in the elderly.  Drugs Aging. 1997;11:433-49) (Adult scurvy.  J Am Acad Dermatol. 1999;41:895-906) (Aging and the immune system: the role of micronutrient nutrition.  Nutrition. 1999;15:593-5)  (Vitamin supplementation in the elderly: a critical evaluation. Gastroenterologist. 1996;4:262-75) (Chromium.  Hosp Practice 2000;2:15) (Chromium.  Diabetes 1997;46:1786) (Creatine use in sports. Am J Med Sports 2000;2)

Estimating Nutritional Requirements:

Step #1:  Calculate Resting energy expenditure for caloric requirements.

“Small” calorie = 4.184 J and “large” Calorie = 1 kilocalorie (kcal), but when specifying energy content of foods, 1 calorie (cal) = 1 kcal.

Basal Energy Expenditure/ Requirements:

(Harris Benedict Equation):  W = IBW in kg, A = age in yrs, H = ht in cm.

BMR for Male: 66 + (13.7 X W) + (5XH) – (6.8 X A)= kcal/d.

BMR for Female: 655 + (9.6 X W) + (1.8XH) – (4.7 X A).

Multiply X activity level / stress level:   Well nourished and unstressed = 1.  Confined to bed or minor surgery = 1.2.   Out of bed =  1.3.   Mild starvation = 0.85-1.  Bone trauma = 1.35.  Major sepsis = 1.6.  Severe burn = 2.1.        Or use 25 X IBW wt in Kg.

Basal Metabolic Rate (BMR) –> 50 kg male = 1485 kcal/d, female = 1399.  60 kg male = ~1630 kcal/d, female = 1544.  70kg male = 1750, female = 1680.   78 kg male = 1900, female = 1781.

Resting Metabolic Rate:

Age in Years –> Male (kcal)\Female (kcal):   3-10 yo –> W X 22.7 + 505\W X 20.3 + 486.  10-18 –> W X 17.7 + 659\W X 13.4 + 693.  18-30 –> W X 15.1 + 693\W X 14.8 + 487.  30-60 –> W X 11.5 + 1113\W X 8.1 + 846. >60 yo –> W X 11.7 + 588\W X 9.1 + 659.

Daily energy required for maintenance = BMR X stress factor X 1.25 (an additional 25% for hospital activity, not added if paralyzed on a ventilator or heavily sedated.

Daily energy requirements for wt gain = maintenance + 750 kcal.

Step #2: Calculate protein requirements: Normal: 0.8-1 g/kg/d protein (up to 60-70g/d).   Moderate depletion/ stress: 1-1.5 g/kg/d.  Severe: 1.5-2.  Non protein (Carbs + Lipids): 25-30 kcal/kg/d.  Protein is 16% Nitrogen.   Calculate grams of nitrogen = grams of protein/ d/ 6.25.  Nitrogen-to-calorie ratio is usually 1gN to every 150 kcal (1:150).  Need less protein with renal failure before dialysis and hepatic encephalopathy.

Multiple trauma/ burn/ sepsis –> 30-50 non protein and 1.5-3 protein.

Metabolic Requirements During Stress:   Stress Level –> Non-protein\ BMR\ Nonprotein Calorie:nitrogen\ Amino Acids g/kg/d:   Starvation –> 25\1\150:1\1.  Low –> 25\1.25\100:1\1.25.  Moderate –> 30\1.25\100:1\1.5.  High –> 35\2\80:1\1.5-2.

Fat Requirements:  >40% calories as fat may decrease the immune response.   Fat calories help decrease the risk of carb overload and keep total fluid down.  Need a minimum of 4% of total calories as essential fatty acids (Linoleic).

Vitamins, minerals and trace elements:  Use RDA’s.  Can get catabolism and loss of lean body mass if low in K, Mg, Zn, P, sulfur.

Calorie Value of Macronutrients (kcal/g):

Fat –> 9.  Ethanol –> 7.  Protein –> 4.   Carbohydrates –> 4.  IV Dextrose –> 3.4 . 1ml of 10% fat emulsion –> 1.1.    0.8X (Proof of beverage / 2) X dL drank = kcal = g of alcohol X7.

Nutritional Assessment (Protein Energy Malnutrition):

Hx:  Dietary changes relative to usual intake, duration of changes and type of diet (hypocaloric, starvation, suboptimal solid), supplements taken.  GI sx’s that have persisted >2 wks (N/V/D/ pain).  Functional capacity (bedridden, ambulatory, working suboptimally).  Medical dz and its relation to nutritional requirements (no stress, moderate stress, high stress such as burns/ trauma/ sepsis).  Physical status (wasting, ascites, edema, mucosal lesions, cutaneous changes, loss of SC fat).

1.  Albumin:  T-½ = 3wks.  3-3.5g/dL mild, 2-3 mod, <2.5 severe malnutrition.  Can be deceptive, as pre-albumen both may be normal in starvation, or be markedly low in an acute illness or increase with dehydration.  Must use in combo with other clinical assessments.Level does not change with aging.

Pre-albumen: T-½ = 2-3 days.  Best lab to use.  Transferrin has T-½ =  8d. False elevation with renal dysfunction.   All three will decrease with microvascular permeability and stress.

2.  Nitrogen (Protein) Balance: = Nin – Nout = (protein intake(g)/6.25) – (UN ( 24hr UUN collection) + 4).  The “4” is added to represent the insensible nitrogen lost other than UUN, >2/3 of nitrogen derived from protein breakdown is excreted in the urine.   Since protein is 16% nitrogen, each gram of urinary nitrogen (UN) = 6.25mg of degraded protein.    The goal of nitrogen balance is to maintain a positive balance of 4g.     85% of the nitrogen in the urine is contained in urea, the remainder in ammonia and creatinine.   UUN can underestimate the urinary nitrogen losses in ICU pts (may need to add the urinary ammonia excretion).    Normal metabolism you want 0.8-1g/kg protein intake, if hypercatabolism, you need 1.2-1.6g/kg.  Growing children need 2g/kg/d.  The healthy 70kg adult excretes (urea, feces, skin) 30g of protein/d = 0.4g/kg, not all dietary protein is digestible, thus the RDA calls for 0.8g/kg/d.

3.  Total Lymphocyte Count: <1000-1200 /uL =mod to severe malnutrition.

4.  Serum Transferrin: < 100-200 = mod to severe malnutrition.

5.  % Weight loss: compare current to usual  outpatient/ preinjury wt (not IBW):   %Wt change = (usual wt / actual wt) /usual wt X100.

Significant wt loss –> 2% @1wk, 5% @1mo, 7.5% @3mo, 10% @6mo.  Severe wt loss if higher.  % Ideal Body Weight = actual wt/ IBW X 100.

6. Total Cholesterol:  <160 mg/dL in the frail elderly is associated with poor nutritional intake as well as increased mortality.  Other –> thyroid binding globulin, retinol binding protein, delayed cutaneous hypersensitivity (anergy), Triceps skinfold (Men should have 8-23mm, women 10-30mm).

Nutritional Support:

Links: Enteral:  Oral: TPN:   PPN:  Healthy Diet:

Refeeding Syndrome:  hungry bone syndrome (the opposite of tumor lysis syndrome).  Occurs with refeeding of pt’s with severe wt loss, anorexia (main cause in USA), cancer, chronic infections (including HIV), starvation conditions (kwashiorkor and classic marasmus), chronic underfeeding, chronic alcoholism, morbid obesity with massive weight loss, prolonged fasting or underfeeding (>7-10 days).   S/s:   Hypokalemia, hypomagnesemia, severe hypophosphatemia, vitamin deficiency (thiamine deficit) and fluid shifts (edema).  Refeeding adds carbohydrates to blood, increased insulin secretion, carbs cause inc uptake of electrolytes (phosphorus, K+, Mg2+) into cells with depletion of phosphorylated intermediates (ATP, 2,3 DPG).   If there is concern for development of refeeding syndrome, check a full panel electrolytes including phosphate, Ca2+, Mg2+ qd x 1 week, begin low calorie feeding with gradual increase, administer vitamins routinely including thiamin >100mg/day and follow urinary electrolytes including phosphate.

Enteral Nutrition Support:

Links:  Common Supplements: Feeding Tubes:  PEG:  PEGJ:  DPEJ:

By tube or by mouth.  Medicare covers 80% of cost if needed >3mo and pt requires >20 cal/kg/d because of an anatomic defect (poor appetite and anorexia nervosa not covered).

Requirements:  hemodynamically stable, no massive GI bleeds, intestinal obstruction, Abx induced/ severe idiopathic diarrhea, high-output enteric fistula or abd distention.

Assess GI function:  GI output should be <600ml/d via NGT, ostomy or rectal tube.   Check bowel sounds (does not correlate with peristalsis), passage of flatus or stool is better marker.

Start infusion –> @ 10-20ml/hr. of isotonic solution (300mOsm/kg) for 1st 24h. Day #1 at up to 30ml/h, 60ml on day #2, 90ml on day #3.  If intragastric can go up to 480 mOsm/kg (max of 300 if intrajejunal).

All pt’s have inc risk of aspiration, place pt in semi-recumbant position with HOB elevated to 30-40 deg.   Monitor for tube migration into the stomach.

Residual volumes: Check q6hr –> Before each feeding, delay feeding if >200ml.  Make sure tube is distal to the ligament of Treitz and HOB is elevated. If inc aspiration risk, get tube into jejunum by 1st placing tube in stomach (confirm by pH of aspirate), then placing pt on their R side for 2h and 1-2X in next 24h, then check X-ray.   If still not passed, give 10mg Reglan IV.  Can add 3-5ml of contrast into tube to verify position.  May need endoscopy.  Consider a prokinetics or avoiding narcotics to prevent gut stasis. Consider using a low fat formula.   Flush tube with 100 ml of water after each bolus. Check BS <200 as hyperglycemia causes gastroparesis.  IV dopamine may cause gut dysfunction.

Hyperglycemia is the most common metabolic abnormality seen. Try to use a formula with 30-50% of calories as fat.  May need insulin SC @ 5 U q4-6h for glucose 200-250mg/dL, 7.5 U if 250-300, 10 U if 300-350.  When the next days solution is ordered give half the SC quantity of insulin added to the bag. If need >100 U/d give a separate insulin drip/ infusion.   If severe glucose intolerance, limit the rate of administered glucose to 5mg/kg/min (~500mg/d) and give extra calories as a fat emulsion.  Need to monitor serum triglycerides and hold emulsion temporarily if it exceeds 500 mg/dL.

Indications of Intolerance: May need parenteral nutrition if –> vomiting, severe cramps, residual volume >50% of administered volume in past 4h, increasing distention, worsening diarrhea.

Complications:  Large bore NGT causing pharyngeal irritation, otitis media, sinusitis.  Obstruction of tube lumen, gastric aspiration, tube displacement.

Aspiration –> add food coloring or methylene blue to liquid, see if detect in pharyngeal or tracheal secretions.  Risks: depressed sensorium, inc GERD, h/o aspiration, meds such as theophylline, CCB, anticholinergics, beta adrenergic agonist, alpha antagonist.

Symptomatic Medications:

If get N/V, cramping, bloating –> reduce rate or concentration, use lactose free formula, bring formula to room temp before use.

If get diarrhea –> (=stool wt >300g/d or volume >30ml) –> inc rate or concentration, use continuous infusion, mix formula better, r/o Abx induced.  Use a lactose free or elemental diet, clean equipment.  Can add an antidiarrheal such as Kaolin-pectin 30ml or in J-tube q3-6h followed by 25ml NS irrigation.  If not improved in 48h add Paregoric (opiate) @1ml/100ml formula. Check C. diff assay and fecal fat content.  Avoid H2 blockers as may lead to bacterial overgrowth, if need them, titrate to gastric pH of 4.5-6.5).  Or Loperamide (Imodium) 24 mg PO or in J-tube q6h, max 16 mg/d prn OR Diphenoxylate/atropine (Lomotil) 5-10 mL (2.5 mg/5 mL) PO or in J-tube q4-6h, max 12 tabs/d.

Constipation –> increase free water intake, stool softener, fiber containing formula, prune juice, increase physical activity.

Tube clogging –> add routine irrigation with 20-25ml of NS or water after each feeding.

Special Medications:  Metoclopramide (Reglan) 10-20 mg PO, IM, IV, or in J tube q6h.  Cimetidine (Tagamet) 300 mg PO tid-qid or 37.5-100 mg/h IV or 300 mg IV q6-8h OR  Ranitidine (Zantac) 50 mg IV q6-8h or 150 mg in J-tube bid.

Specific Oral Nutritional Support:

Links: Common Supplements:

Nutrient intake is increased due to the increased nutrient density of the supplements.  Intermittent bolus feeding via 8-10F NGT.  Avoid aspiration by elevating the HOB and checking for residuals.  If need long-term feeding such as in dementia, neurological impairment a gastrostomy tube may be placed.  Caloric density: of most is 1 kcal/ml.

Modified diets: elemental diet.  Hepatic, stress and renal diets.

Thickened Feeding:  for those with dysphagia.  Start with intro Stage I: puree diet of pureed foods (mashed potatoes, yogurt, pudding, veges, meats).  Stage II is textured puree such as egg salad, cottage cheese, finely chopped & drained fruits.   Stage III is gound diet such as ground meats with gravy.  Stage IV is chopped foods such as finger sandwich, bread, scambled eggs, chopped pancakes.   Always avoid foods that melt (ice cream, ice chips, gelatin).   Liquids: can either purchase nectar consistency liquids such as Kerns fruit nectar, V-8, Ensure Plus, Nepro, Creamed soups, carrot juice with pulp, egg nog or take thinner liquids and “thicken” them with tapioca or a commercial thickener (Thick-it, Nutra-Thick, Thicken Up).   Super thick liquids are a honey consistence, can be purchased as “Resource” brand.

Hepatic formula: if in failure or hypercatabolic or encephalopathic.  Have increased amounts of branched-chain AA’s (BCAA’s) as they undergo little metabolism by the liver (also beneficial if septic or critically ill).  Also have dec aromatic AA’s (phenylthaline, tyrosine, tryptophan) and sulfur containing (methionine).  For impaired liver function use Hepatic-aid II, Nutrihep or Travasorb Hepatic.

Renal Formula: all essential AA’s, but no nonessential.  Indicated if renal failure and do not need dialysis and not on broad-spectrum Abx.

Most give 2cal/ml.  Deliver 2.0, Magnacal Renal, Nepro, Novasource renal, Suplena or Renalcal.

GI dysfunction:  use medium chain triglycerides (MCT’s) as more easily absorbed and metabolized than long-chain (LCT’s).

Diarrhea –> Isotonic, lactose free 1cal/cc formulas such as Isosource standard, Isosource HN, Isocal, Isocal HN, Osmolite, Osmolite HN, Promote or Nutren 1.0.

Impaired Fat absorption –> use MCT’s.  Lipisorb, Subdue, Peptamen, Sandosource peptide, Reabilan or Travasorb MCT.

Constipation/ Diarrhea –> use high fiber formula.  Ensure/f, Boost/f, Nuren/f, Relpete/f, Nubasics/f, Sustacal/f, Fibersource, Fibersource HN, Jevity 1.5, Jevity Plus, Poralance or Ultracal.

Fluid Restriction –> use 2 cal/cc products.  Deliver 2.0, Twocal HN, Nutren 2.0 or Novasource 2.0.

Diabetes/ hyperglycemia –> use formula with high fat and low carbs.  Choice DM, DiabetiSOurce, Glucerna, Glyctol, Resource Diabetic.

Stress –> use peptides or free AA’s as protein source.  Criticare HN, Tolerex, Petamen, Vital HN, Sanosource peptide, Vivonex Plus or TEN.

High stress and hypermetabolic –> use peptides/ free AA’s.  Alitraq, Crucial, Peptamin VHP or 1.5, Perative, Reabilan HN or Replete.

HIV Infection –> use omega-3 fatty acids.  Advera, Impact or Impact 1.5

Glutamine: the most abundant AA in the body.  Acts as the main fuel source and as a biosynthetic precursor in the gut and immune system.  Forms glutathione for antioxidants, used in acid base metabolism to release ammonia in the kidney.

Arginine: required for growth and secretion of GH, insulin, glucagon, prolactin, and somatostatin.

Enteral Feeding Formulations:

Type –> Carb g per L\ Prot g per L\ Fat g per L\ Kcal per ml\ Water ml per L:    Ensure –> 145\37\37\1.06\845.  For maintenance cals & protein, low residue.  Ensure Plus –>   200\55\53\1.5\769. High cal for maintenance proteine, low residue.  Jevity –> 152\44\36\1.06\835. High protein and fiber, 20% of fat as MCT.  For Tube feed, not PO.   Glucerna –> 94\42\56\1\870. High fat, low carb for those with abnormal glucose tolerance. Promote with fiber –> 139/62/28/1/830 Incr protein, maintenance cals with fiber in a low nutrient base for nonambulatory pt’s.   Nepro –> 215\70\95\2\700.  High cal, mod protein, low electolytes, low fluid for acute/chronic renal failure.   Nutrihep –> 290\40\20\1.5\760. High branched chain AA, low aromatic, low ammonia to support lean body mass during liver failure or stress.  Vital HN –> 185\42\11\1\860. With peptides, free AA’s and MCT oil to enhance nitrogen uptake in malabsorption states or impaired GI function.  Optimental –> 138\51\28\1\830. For malabsorption states.   Perative –>177/67/37/1.3/790  For metabolically stressed, for tube feed only, has arginine, beta-carotene, carnitine, trace minerals.  Isocal –> 135\34\44\1.06\840.  Isosource –> 170\43\41\1.2\819.  Sustacal –> 140\61\23\1.01\850.  Ultracal –> 123\44\45\1.06\850.  Osmolite –> 145\37\38\1.06\841.  Preattain –> 60\20\20.5\930.  Promote –> 130\63\26\1.0\840.  Replete –> 113\62\34\1.0\844.  Resource –> 140\37\37\1.06\842.  Nutren 1.0 –> 127\40\38\1.0\852.  Deliver –> 200\75\102\2.0\710.  Magnacal –> 250\70\80\2.0\700.  TwoCal –> 217\84\91\2.0\712.  Pediasure with fiber  –>109/30/490/1/840.  Maintenance cals.  Peptamen Junior–>   137/30/360/1/850.  Pediatric tube feeds, 60% fats as MCT for malabsorption or imparied GI function.

Additonal Additives:  Protein–> Promod powder with 3g protein/tbsp.    Carbs –> polycose liquid with 60 cal/30ml.  Fat –> MCT oil at 230 cal/30ml.

Common Oral Supplements:

Type –> Kcal per 8oz\ Gm protein per 8oz\ Other Features:   Ensure –> 254\8.9\Low residue. Ensure Plus –> 360\13.3\High cal/ protein, low residue. Pudding –> 250\6.8\Low residue.  Sustacal –> 242\14.6\High protein, low residue.  Sustacal Plus –> 365\14.6\High cal/ protein, low residue.  Pudding –> 240\6.8\Low residue. Citricource –> 180\8.8\Clear, low residue.   Other:  Boost, Mighty Shakes (milk-based, tastes better).

Dry Powder Product –> Cal per mL\ Protein g per L (%)\ Carbs g per L (%)\ Fat g per L (%):   Carnation Instant Breakfast Liquid –> 0.73\10 g/8 oz (25%)\25/8 oz. (62.5%)\2.4/ 8oz. (13.5%).   Carnation Instant Breakfast Powder –> 1\63.3\149.6 \34.6.  Carnation Instant Breakfast No Sugar Added Powder –> 0.7\62.5 \86.3 \20.8.   Forta Shake Powder (reconst with 1 cup whole milk) –> 140 / 1.4 oz mix\9/ 1.4 oz mix\26/ 1.4 oz mix\< 1/ 1.4 oz mix.  Meritene Powder –> 1.06\69 (26%)\120 (45%)\34 (29%).  Sustacal Powder (reconst with skim milk) –> 1.09\79 (29%)\180 (66%)\5.6 (5%).  Other:  Boost.

Medicare’s Enteral Product Categories:

Standard (I) –> $0.61/ 100cal, Fibersource, Isocal, Jevity, Osmolite, Promote, Resource, Ultracal.

Natural Standard (II) –> $1.71/ 100cal, Compleat Modifies.

Calorie Dense (IIb) –> $0.51, Comply, Deliver, Magnacal Renal, Nutren 1.5, Two Cal NH.

Hydrolyzed (III) –> $1.74, Criticare HN, Reabilan, Vital HN.

Disease Specific (IV) –> $1.12, Advera, Alitraq, Choice DM, Glucerna, Diabetasource, Hepatic Aid, Impact, Pulmocare, Vivonex.

Modular (V) –> $0.87, MTC oil, Microlipid, Promod.

Specialized Nutrients (VI) –> $1.24/ 100cal, Tolerex, Travasorb STD.

Total Parenteral Nutrition (TPN):

Links:  Indications:  Method: The Calculation:  Infusion:  Monitoring:  Risk:  Composition:  Standard Solutions:  Special Formulations: PPN:

Indications: Pt unable to eat or absorb nutrients for an indefinite period (permanent neurologic impairment, prematurity in infant, oropharyngeal dysfunction, short gut syndrome), severely malnourished and undergoing major surgery, major trauma, BM transplant undergoing chemo.

Unproven indications:  CA pt not tolerating PO >7-10d, AIDS pt, liver/renal failure, critically ill and NPO >7d, GI tract dysfunction (Crohns).

(N Engl J Med 1997;336:1)

Method:  Centrally administered into vena cava at a constant rate.  Reserve for pt that has nonfunctional GI tract –> Acute GI bleed, +ileus, small bowel obstruction (SBO), ischemic bowel, chylothorax.  Lines:  Tip of catheter should be in the innominate vein or SVC (avoid R atrium and subclavian vein).  Can be from a peripherally inserted central catheter (PICC).   Long term catheters (Hickman or Portacath) avoid catheter clotting.  If in groin, need to replace q2-3d due to infection risk.

Calculation:   Step #1: Determine pt’s weight.  Use actual body wt on admission unless >20% from IBW, in which case use adjusted body wt.

Step #2: Determine calorie requirements with Harris-Benedict equation and multiply by any stress factors. At rest BMR is 25 kcal/kg/d, up to 35 with increasing metabolic stress. This drops to 20 kcal/kg/d in the critically ill as stress metabolism already leads to high levels of serum glucose and triglycerides.  Kg needs to be adjusted to IBW.

Step #3: Determine Protein Requirements (g/kg/d):  Renal dysfunction @ 0.5-0.8.  Dialysis @ 1.  Maintenance (rest) @ 0.8-1.  Mod depletion/ stress @ 1-1.5.  Severe depletion/ stress @ 1.5-2 g/kg/d.

Step #4: Decide how Fat content supplied:  If 10% = 550 kcal in 500ml.  If 20% = 1000 kcal in 500ml.  Fats given a minimum of 2X/wk and should never exceed 50% of total daily calories.  High dose lipids may be immunosuppresive in critically ill pt’s, thus no more than 1g/kg/d of IV lipids should be given.

Step #5: Daily requirement — cal supplied by fat = calories supplied by TPN.

Step #6:  Calculate Flow rate:  Based on fluid requirements.  Central –> (TPN cal needed X 1000)/ 1020 kcal/L X 24h = ml/h.  Peripheral –> (TPN cal needed X 1000)/ 510 kcal/L X 24h = ml/h.  Max recommended peripheral rate is 125ml/h.

Step #7:  Additives such as lytes vitamins and trace elements as needed.

Infusion:  start @ 40-50ml/h (except renal @ 30ml/h as inc glucose, advance 10ml/d), inc at increments of 20-25ml/hr q 8hr (if controlled blood sugar or else add insulin) until caloric needs are matched.

Monitoring: VS q6hr X6 sets, then per routine.  I&O q8hr, wt QOD, finger glucose q6h, twice weekly lytes, CBC, PT, PTT, LFT, Ca, P, pre-alb.

Risks:  PTX (<3%), thrombosis of subclavian vein (tx with local heat, removal, heparin), catheter sepsis, hyperglycemia (SC insulin, inc insulin/L of solution), inc infectious, metabolic and fluid complications (cholestatic liver dz, CHF, inc Trig’s), all known nutrients not provided.  Cost 4X enteral.  Refeeding Syndrome:  a starved pt get a drop in K and P due to fluid shifts.  Avoid by starting low and going slow.

Composition:  Carbs (dextrose) concentration 15-47%,

Amino Acids (balanced or dz specific such as renal (dec AA, inc glucose)/ hepatic/ stress).

Lipid emulsions (10 or 20% solutions at 1 or 2 kcal/ml.  Can provide 20-60% of calories as lipids, only need 100ml of 10% solution/wk to prevent essential fatty acid Defic.), minor components ( V-K 5mg qMonday).  Intralipid 20% 500 mL/d IVPB infused in parallel with standard solution at 1 mL/min x 15 min. If no adverse reactions, increase to 20-50 mL/hr. Serum triglyceride level should be checked 6h after end of infusion (maintain <250 mg/dL).

Electrolytes (mEq/L) –> Na 20-80 (0-150 range).  Potassium (K): 13-40 (0-80). Magnesium –> 8.0 mEq  Chloride (Cl) 10-80 (0-150) since Cl losses are increased with NGT suction, most salts should be administered as Cl.    Phosphate (P) in mMol 14 (45-220).  Usually given as potassium salt, NaP is used if K is contraindicated.   Ca 4.7 (0-10), Mg 8 (0-15), Acetate 45-81mEq (45-220).

Other:  Regular Insulin 0-25 U/L.  1 unit per 10-15g of glucose. Bicarb is incompatible with nutrient solutions.

Standard Solution per Liter:  850kcal/L.  Amino acid solution (Aminosyn) –> 7-10% 500 mL or 5% AA (50g/L).  Trace elements (to 1st bottle each day) –> Zn 3mg (inc risk of zinc Defic in alcoholic, pancreatic insufficiency with malabsorption, renal failure with dialysis and nephrotic syndrome), Cu 1.2mg (inc risk of copper def with short bowel syndrome, jejunoileal bypass, malabsorption), Cr 12ug, Mg 0.3mg, Se 60mg, MVI 1amp. Vitamin B 12 –> 1000 mcg/week. V-K (phytonadione): 10mg is given 1X/wk unless pt is receiving Warfarin.

General Patient –> 25% Dextrose and AA 4-5% with a high carb to fat ration.  500ml D50 + 500ml 8.5% AA + multivitamin at rate (ml/hr) = [calories required — 500] / 20.

Special Formulations:  Hepatic Dysfunction –> add folate, Thiamine, V-K and reduce protein and aromatic AA.  500ml D70 + 500ml AA 7-8% hepatic formula + multivitamin at rate (ml/hr) = [calories required —500] / 29.

Fluid restriction –> increase the concentration of glucose and lipid calories.  500ml D70 + 500ml AA 10-15% + multivitamin at rate = [cal required — 500] / 29.

Pulmonary Dysfunction –> reduce carbs and increase lipids to decrease the CO2 production from excess carbs.  500ml D30 + 500ml 8.5-15% AA + multivitamin at rate of [cal req — 1000] / 12.

Head Trauma –> may need increased protein and lipids with decreased fluids and carbs.  500ml D30 + 500 ml 10-15% AA plus multivitamin at rate of [cal req — 1000] / 12.

Renal Dysfunction –> Pt need increased folate with decreased V-K, P, Mg along with close electrolyte adjustments.  500ml D70 + 500ml 8.5% AA [;us multivitamin a rate of [calories required — 500] / 20.

Cyclic Total Parenteral Nutrition: 12-hour night schedule; taper continuous infusion in morning by reducing rate to half original rate for 1 hour. Further reduce rate by half for an additional hour, then discontinue. Restart TPN in evening. Taper at beginning and end of cycle. Final rate should be 185 mL/hr for 9-10h with 2 hours of taper at each end, for total of 2000 mL.

Peripheral parenteral nutrition (PPN):

For calculations see:  TPN:

Standard solution contains:  3% AA (ProCalamine) (30g/L) (or 4.25% has 510 kcal/L) in 10% Dextrose (D10, 100g/L) @ 350kcal/L.  Osm 600-900 mOsm/kg.  If fat emulsion infused via piggyback give during an 8-12h period ending at 3 AM so the hypertriglyceridemia will not interfere with blood sampling. Max flow rate: 125ml/h = 3L/d = 1530 kcal/d.

Indicated in: malnourished, minimally stressed patients for 3-5d of support when PO intake is inadequate and have inc risk of complications of malnutrition.    Can combine 500 mL amino acid solution 7% or 10% (Aminosyn) and 500 mL 20% dextrose and electrolyte additive and infuse at up to 100 cc/hr in parallel with: Intralipid 10% or 20% at 1 mL/min for 15 min (test dose), if no adverse reactions, infuse 500 mL/d at 20 mL/hr.

**Ref: (J Parenteral Enteral Nutrition 1997;21:133) (Parenteral nutrition. Clin Perspect Gastroen 2000;12) (Sci America 1999;8:1-16) (Nutritional support in hospitalized patients. Dis Mon 1997;43:6) (Home artificial nutrition.  Curr Opin Clin Nutr Metab Care. 1999;2:387-93) (Parenteral iron supplementation.  Nutr Clin Pract. 1996;11:139-46) (Current uses and abuses of total parenteral nutrition.  Adv Surg. 1996;29:165-89) (Enteral feeding in critical care, gastrointestinal diseases, and cancer.  Gastrointest Endosc Clin N Am. 1998;8:623-43) (Nutrition in the elderly. J Clin Gastro 2000;30:4)

Healthy Diets:

Low fat diets are out as ave American has reduced their fat intake from 41 –> 32% over the last 20 years, yet has gained 8 more lbs.

Bad = saturated and partially hydrogenated fats.

Good = polyunsaturated (Eskimo diet, marine omega-3 FA’s) & monounsaturated (Mediterranean diet) fats as have cardioprotective effects.  Eat lots of the good fats found in fruits, vegies, whole grains and beans (except coconut, palm oils), and nuts.  Reduce your intake of bad fats found in chicken, meats, whole milk dairy products, eggs, solid margarine, prepared foods, bakery goods and cereals made with trans fats.  Eat no more than two 4oz servings of red meat/wk.   <30% of calories should come from fat, 60% from carbs, 12% from protein.   Eat more fresh and homemade foods (not processed foods).   Eat lots of whole grains, vegetables, beans and fruits, these have the correct types of  fat and are full of complex carbo’s, and phytochemicals that help protect from dz.   Deep sea fish have omega-3 oils that prevent clotting if taken twice a week, aim for 4oz.

Weight loss: see obesity in Endocrine section.  Avoid untested food supplements, including megavitamins, Herb’s, food extracts and amino acids.   If want to lower cholesterol, lower intake of calories and fat, eat no more than 1 egg yolk/d (including those in baking and cooking).

Fiber Content: need at least 25-30g/d.  Fiber is found only in plants, most is in the bran of whole grains and in the stems & leaves of vegetables, fruits, nuts and seeds.  Soluble fiber –> Gums (oat, beans, legumes, guar), pectin (apples, citrus fruit, carrots, potatoes, green beans), mucilage (psyllium).  Metabolized by bacteria, add little to fecal bulk.

Insoluble fiber –> Hemicellulose (barley, wheat bran, whole grains, brussel sprouts), Lignin (strawberries, peaches, pears, radish, green beans), Cellulose (broccoli, apples, corn, peas, root vegetables, beans, peppers).  Not metabolized by human or bacteria.  Increases the water content and bulk of the stool to shorten the intestinal transit time.

Weight Watchers Diet:  Attend weekly meetings, can only eat a certain number of food points from each category.  A healthy diet low in calories.

Jenny Craig Diet:  carbs are 60%, concentrating on complex ones.  Low fat foods.  A healthy diet low in calories.

Dean Ornish Diet:  avoid fat.  Eat healthy natural food like fruits and vegetables, oatmeal, soy.  Very healthy, but hard to maintain.

Zone diet: (40/30/30 diet), 40% complex carbs, 30% Protein/fat, with each meal in proper ration to avoid carbo craving from insulin bumps. Low carbs, but balance it with amount of fat and protein.  Lean meats with high protein.   Fairly healthy diet.

Body For Life:   by Bill Phillips of EAS Company.  A practical book that gives a healthy diet and exercise program that patients can follow.

Low Carbohydrate Diet’s: Best just to advise pt’s who are interested in low carb diets to limit potaties, reduce intake of white bread, white pasta and white rice.  They should select up to 4 servings of whole grains and at least 5 servings of nonstarchy fruits & vegetables (such as berries or cruciferous).  Cut back on simple sugar and hydrogenated vegetable fats. Substitute chicken, legumes, nuts and fish for red meat.  Eggs or high fiber cereals can be eaten for breakfast.  Lunch can be a salad, lean protein, nuts, cheese stick and vegetables.  For snacks eat yogurt, fruit, vegetables, for dinner can be flexible with soup with a clear broth base, a salad & vegetable eaten fist, then a protein and a starch.   Need to limit potatoes, carrots, squash and parsnips.  Atkins Diet high Protein low carbs (<20g/d)  Can eat bacon, eggs, cheeseburger, shrimp, fish, steak, cheese, sugarless foods.   Similar to Sugar Busters Diet and Carb Addict’s Diet and Schwarzbein Diet.  Have risk of loss of V-B, Ca and P due to low carbs.  Induces a ketosis that leads to water loss and anorexia.  SE of fatigue, constipation, orthostatic hypotension and renal calculi.

Suzanne Summers Diet:  No fats with carbs and if eat fruit need to wait at least 20 min before eat more carbs.

Sucralose (Splenda): artificial sweetener, no calories, no tooth decay, no effect on serum BS.

Other Common “FAD” Diets:  Zen Macrobiotic Diet: a 10 stage diet where food are eliminated progressively and replaced with grain products.  Can be hazardous to growing children.

Anti-allergenic diet:  attempt to avoid the “nightshade food” such as potatoes, tomatoes, eggplant and pepper.

Anti-Arthritis Diet:  no red meat, fruits, dairy, herb, spices, preservatives, additives or alcohol.

Vegetarian Diets:

All consume predominately plant foods: fruits, grains, legumes, nuts, seeds, vegetables.  May include eggs and dairy products.   Choose to omit animal products for religious, health, environmental, humanitarian, ethical, economic, political reasons.   Vegetarian is often used loosely as many may occasionally consume beef, fish, poultry and still consider themselves vegetarian.

Vegan:  (no meat/ poultry/ fish/ eggs/ milk)  The strictest vegetarian, as no animal products at all. Some will not eat honey or yeast products nor will they wear or use animal products such as leather, silk or wool.   Need fortified cereals/ soy drinks or supplements.

Ovovegetarian:  (no meat/ poultry/ fish/ milk) A vegan who consumes eggs.

Lactovegetarian:  (no meat/ poultry/ fish/ eggs) A vegan who consumes milk.

Lacto-ovovegetarian:  (no meat/ poultry/ fish) A vegan who eats milk and eggs, most vegetarians fall into this category.

Pescetarian: a vegetarian who eats fish.   V-D –> if Vegan need supplements or fortified foods.   Ca –> spinach, kale, broccoli, legumes, soy/ tofu.   Zinc –> need supplement or alternative source from grains, nuts, legumes. Protein –> lots in whole grains, legumes, vegetables, seeds, nuts.   Fe –> dried beans, spinach, enriched products, yeast, dried fruit.   V-B12 –> only from animal sources.

**Ref: (Diet and the prevention of cancer. BMHJ 1998;317:1636) (Mediterranean diet and the rate of cardiovascular complications. Circulation 1999;99:779) (Development of a vegetarian food guide.  Am J Clin Nutr. 1994;59:1248S-1254S) (Nutrition therapy for the cancer patient.  Hematol Oncol Clin North Am. 1996;10:221-34)

Common Conversions:

Link:  Pound to Kg:  Temp:  American to SI:  Fluids:  Milligrams: Solutions:  Drips:

Apothecary doses with metric equivalents:  1oz = 30g = 30ml.   1 grain = 60mg.  30 grains = 2000mg = 2g.  1/60 grain = 1mg = 0.001g.

Pounds to Kilograms:   Pt’s Wt in Kg = (lb/2)- 1/10 (Ex: 160= 80-8=72kg).   1 # (lb) = 0.454kg.   1 kg = 2.2# .

# = Kg –> 4 = 1.8, 6 = 2.7, 8 = 3.6, 10 = 4.5, 15 = 6.8, 20 = 9.1, 25 = 11.4, 30 = 13.6, 35 = 15.9, 40 = 18.2, 45 = 20.2, 50 = 22.7, 55 = 25, 60 = 27.3, 65 = 29.5, 70 = 31.8, 80 = 36.3, 90 = 40.9, 100 = 45.4, 125 = 56.7, 150 = 68.2, 175 = 79.5, 200 = 91.

Temperature:  F –> C: 5/9(F-32).    C –> F: (2C- 1/10) +32.

C = F –> 40.5 = 105, 40 = 104, 39.9 = 103.8, 39.7 = 103.5, 39.5 = 103.1, 39.2 = 102.6, 39.1 = 102.4, 39 = 102.2, 38.9 = 102, 38.6 = 101.5, 38.5 = 101.3, 38.4 = 101.1, 38 = 100.4, 37.9 = 100.2, 37.5 = 99.5, 37 = 98.6, 36 = 96.8.

American (Traditional) –> SI units:

SI unit = Traditional Unit / (relative or molecular atomic mass X Factor).  There are 7 fundamental (base) SI units, meter, kg, sec, ampere, kelvin, mol, candela (luminous intensity).

Common SI prefixes:  10-11st = deci, 10–2nd = centi, 10–3rd = mili, 10–6th = micro, 10–9th = nano (billionth), 1011st = deca, 10-2nd = hecto, 10-3rd = kilo, 10-6th = mega, 10-9th = giga, 10-12th = tera.

Traditional Unit –> SI Unit:    “–“ = minus.

nmol/L –> Umol/l –> Mmol/L –> mol/L:   pg/ml –> 1 –> 10-3 rd –> 10-6 th –> 10-9 th.   pg/dL –> 10-2nd –> 10-5 th –> 10-8 th –> 10-11 th.  pg/L –> 10-3rd –> 10-6 th –> 10-9 th –> 10-12 th. ng/ml –> 10–3rd –> 1 –> 10-3 rd –> 10-6 th.  ng/dL –> 10–1st –> 10-2 nd –> 10-5 th –> 10-8 th.  ng/L –> 1 –> 10-3 rd –> 10-6 th –> 10-9 th.  ug/ml –> 10–6th –> 10–3 rd –> 1 –> 10-3 rd.  ug/dL –> 10–4 th –> 10–1 –> 10-2 nd 10-5 th.  ug/L –> 10–3rd –> 1 –> 10-3 rd –> 10-6 th.  mg/ml –> 10–9 th –> 10–6 th –> 10–3 rd –> 1.  mg/dL –> 10–7 th –> 10–4 th –> 10–1 st 10-2nd.  mg/L –> 10–6 th –> 10–3 rd –> 1 –> 10-3 rd. g/ml –> 10–12 th –> 10–9 th –> 10–6 th –> 10–3 rd.  g/dl –> 10–10 th –> 10–7 th –> 10–4 th –> 10–1st.  g/L –> 10–9 th –> 10–6 th –> 10–3 rd –> 1.

Fluids:  1 tsp = 5ml.  1tbl = 15ml.  15 drops (gtt) = 1 ml or 1 cc.  1 tsp = 5 tbs.  1 tbs = 15ml.  1oz = 30ml = 0.0625 liquid pints = 0.03125 qt = 0.0296 L = 1.805 in2.    1dram = 4ml. 1L = 1000ml.  1 glass = 8oz = 240 ml.  1 pint = 16 oz = 480 ml.  1 quart = 32 oz = 960 ml.  1 gallon = 128 oz = 4 quarts = 8 pints = 3840 ml = 3.8L.

Milligram (mg) = 0.001g = 1000ug = 0.015grain.  Microgram (ug) = 0.001mg.  1ug/ml = 0.1mg% = 0.1mg/dL = 1mg/L. Nanogram (ng) = 0.001ug.  1ng/ml = 0.001ug/ml = 0.1ug = 0.1ug/dL.

Percent Solution: 1% solution = 1g/100ml = 10mg/ml = 10mg/L.   1mg% = mg/100ml = 10ug/ml = 1mg/dL = 10mg/L.  Deciliter (dl) = 100ml.  1mg/dL = 1mg/100ml = 1mg% = 10ug/ml.  1ppm = 1mg/L = 0.1mg% = 1ug/ml. 1 mole = mol wt in mg/dL. 1 millimole = MW in gm/L.

Drug Infusion Rates:    ug/kg/min = 16.7 X drug conc in mg/ml X rate in ml/hr // wt in kg.   ml/hr = Desired ug/kg/min X wt in kg X 60 // drug conc in ug/ml.

Other:  1km = 0.6 mi.  1 meter = 39.4 in.  1cm = 0.4 in.

Commonly Used Drug Therapeutic Range (Levels):

Acetaminophen–> 10-20 mg/L, toxic @ >150 mg/L 5 hr after ingestion. Alcohol–> 0, toxic @ 150-300 mg/dl: confusion, 300-450: stupor, >400: coma/ death.  Amikacin –>     Peak 25-30, trough <10 ug/mL.  Amiodarone –>   1-3.0 ug/mL.  Amitriptyline  –> 100-250 ng/mL.  Amobarbital–> 7-15 µg/ml. Bromide–> 20-120 mg/dl, toxic @ >150 mg/dl. Carbamazepine –>   4-10 ug/mL.  Chloramphenicol –>   Peaks 10-15, trough <5 ug/mL. Clonazepam–> 0.02-0.10 µg/ml.  Cyclosporine –> 100-300 ng/ml (50-150 renal transplant, 150-250 heart or liver).  Desipramine –>   150-300 ng/mL.  Digoxin –>   0.8-2.0 ng/mL.  Digitoxin–> 5-40 ng/ml. Diphenylhydantoin–> 10-20 µg/ml.  Disopyramide –>   2-5 ug/mL.  Doxepin –>   75-200 ng/mL. Ethosuximide–> 40-100 µg/ml. Flecainide –>   0.2-1.0 ug/mL.  Gentamicin –>   Peaks 6-8.0, trough <2.0 ug/mL. Glutethimide–> 1-7 µg/ml.  Imipramine –>   150-300 ng/mL.  Lidocaine –>   2-5 ug/mL.  Lithium –>   0.5-1.4 mEq/L, toxic @ 2.0 mEq/L.  Meprobamate–> 10-20 µg/ml, toxic @ 30-70 µg/ml: coma.  Mexiletine –> 1-2 ug/ml.  Nortriptyline –>   50-150 ng/mL. Pentobarbital–> 4-6 µg/ml.  Phenobarbital –>   10-30 mEq/mL (µg/ml), toxic @ >40 µg/ml. Phenytoin –> 8-20 ug/mL, 4-10 if azotemia or dec alb. Primidone–> 4-12 µg/ml.  Prograf –>    5-10 ng/ml.  Procainamide –>  4-8.0 ug/mL. Propranolol–> 50-100 ng/ml. Quinidine –>   2.5-5.0 ug/mL, toxic @ >8 µg/ml. Salicylate –> 15-25 mg/dL, toxic @ 300 mg/L.  Secobarbital–>  3-5 µg/ml.  Streptomycin –> Peak 10-20, trough <5 ug/ml.  Theophylline –>    8-20 ug/mL.  Tocainide –> 4-10 ug/ml.  Valproic acid –>    50-100 ug/mL.  Vancomycin –>   Peaks 30-40, trough <10 ug/mL.   ***All levels may vary depending on the reference lab.

Hypoxemia (Dec PaO2):

Links:  5 Mechanisms:  Labs:  Hypoxia: Cyanosis:  Pulse Oximetry:  Methemoglobin:

Decrease O2 in the tissue.  Subnormal oxygenation of arterial blood (dec delivery from the atm to the blood).  Low PO2 in arterial/ capillary or venous blood.  Short of anoxia.    Normal PAO2 = 80-100mmHg. To determine PaO2: subtract 1mmHg for each decade of age.  (or 100- 1/3Age) Subtract 3mmHg for every 1000 ft of altitude.   Usually accompanied by an acidosis (pH <7.2), base deficit >5mEq with bicarb <20.  AG >8 mEq/L, blood lactate >2mEq/L.  Ventilatory control is 3 main components:  chemosensors (carotid body senses PaO2 & H+.  Medullary senses PaCO2 & H+), the central controller (respiratory center in brainstem) and the effectors (respiratory muscles such as the diaphragm, intercostals and abd muscles).

5 Main Mechanisms of Hypoxemia:

1.  Ventilation-Perfusion (V/Q) mismatch:  airway secretions, pulmonary embolism, bronchospasm (asthma, COPD), pneumonia, CHF, ARDS, tumor-filled alveoli.   Causes >95% of hypoxemia.  Ventilation to a region of the lung is decreased in comparison to perfusion.  Have normal / dec/ inc PaCO2, inc A-aDO2, good response to inc FiO2.

2.  Shunt (R to L):  V/Q ~ = 0.  Atelectasis, pneumonia, pulmonary edema, ARDS, intracardiac shunt. This occurs when systemic venous blood enters the L heart w/o prior oxygenation.  Ventilation =0, but perfusion continues.   Shunts will not significantly correct with 100% O2 (unlike V/Q mismatch and diffusion defects).  Has normal/ dec PaCO2, inc A-aDO2, minimal response to inc FiO2.

3.  Low Inspired PO2:  high altitude.  Has normal or dec PaCO2, normal A-aDO2, good response to inc FiO2.  Normal A-a gradient.

4.  Alveolar Hypoventilation:  COPD, low respiratory drive from sedation (overdose narcotics) or hypothyroid or idiopathic alveolar hypoventilation or central (brain stem) dz, mechanical breathing problem (GBS, polio, MG, kyphoscoliosis, Pickwickian syndrome, myopathy, chest wall abnormality, crushed thoracic cage).  Has inc PaCO2, normal A-aDO2, with good response to inc FiO2. Normal A-a gradient.

S/s: H-A, somnolence, dec cognitive ability, constriced pupils, asterixis, coma, diaphoresis, tachycardia, arrythmia, cor pulmonale (late), polycythemia.

5.  Diffusion Defect: interstitial lung dz, PCP pneumonia. Has normal – dec PaCO2, inc A-aDO2, good response to inc FiO2.

Labs:  Abnormality –> PO2\ PCO2\ Room air O2/ Aa Gradient\ 100% O2 PaO2:   Hypoventilation –> dec\ inc\ Nl\ improves. V/Q Mismatch –> dec\ Inc-Dec\ inc\ improves.   Fixed Shunt –> dec\ dec or nl\ inc\ minimal Inc.  Diffusion Barrier –> dec\ nl\ inc\ Nl.  Dx of Hypoxemia:   PaO2 <60mmHg or SaO2<90%.

Hypoxia:

Usually due to the dec delivery of O2 to the tissue (shock, anemia).  Hypoxemia can occur independently, but hypoxia is often the result of severe hypoxemia.

Types of Hypoxia:   Hypoxemic Hypoxia –> a lower than normal PaO2 (hypoxemia).    Anemic Hypoxia –> dec RBC count, carboxy-Hgb, hemoglobinopathy. Circulatory Hypoxia –> dec cardiac output, dec local perfusion.   Affinity Hypoxia –> dec release of O2 from Hgb to tissues.  Histotoxic Hypoxia –> cyanide poisoning.

Respiratory Failure –> NM blockage (aminoglycosides, succinylcholine, Gallamine, Dimethyltubocurare, CCB, Mg sulfate, Nicotine, macrolides, Penicillamine, Polymyxin B).  CNS depression (sedatives, narcotics, hypnotics, ETOH, TCA’s, O2).  Inhibition of transmission at neuromuscular junction (Captopril, Cytosine-arabinoside, Danazol, Gold, Phenytoin, Vincristine), respiratory muscle myopathy (beta agonists like fenoterol, corticosteroids, Clofibrate, diuretics, narcotics, Pancuronium, Procainamide).

S/s of Hypoxia:  acute hepatic necrosis, ATN, agitation, altered MS, angina, anxiety, arrythmias, claudication, coma, confusion, cyanosis, diaphoresis, dizziness, gangrene, HTN, hypotension, lactic acidosis, sz, somnolence, syncope, tachycardia, tachypnea.

Cyanosis:

Becomes clinically apparent when there is >5g/dL of unsaturated Hgb, which corresponds to a pAO2 of <50 torr (50% of Hgb w/o O2) or SaO2 <85%.  It may not be apparent in pt has a coexisting anemia.

Central: seen in the nailbeds and mucous membranes (tongue, conjunctiva) under natural light.  Occurs in warm and cold areas.  If fingers are pink but the toes are cyanotic, consider a persistent ductus arteriosus with a reversible R-L shunt seen in pulmonary HTN (Eisenmengers syndrome).

Peripheral: seen in cool exposed areas such as fingers, earlobes, tip of nose, cheeks, outer surface of the lips.  It is due to increased capillary O2 extraction secondary to poor perfusion, and may be obliterated by warming or massaging the area.

Ddx:  Shock, arterial insufficiency, asthma, COPD, hypoventilation, methemoglobinemia, Patent ductus arteriosis, SVC obstruction, tricuspid insufficiency, tracheal obstruction, intrapulmonary shunting, polycythemia vera, R-to-L cardiac shunt, pulmonary embolism, arterial insufficiency, upper airway obstruction, respiratory failure.

Harlequin cyanosis:  one arm only, seen in aortic dissection, patent ductus arteriosis with pulmonary HTN and with embolic arterial occlusion.

Pseudo-cyanosis:  seen with Amiodarone deposits in the skin.  Silver rubbed into skin gives a blue discoloration when exposed to sun.

**Ref: (Neurologic manifestations of pulmonary disease. Neurol Clin. 1989;7:605-16) (Cecil’s Textbook of Medicine, 21st ed, 2000, Saunders, pp379-83) (Consultation with the specialist: nonrespiratory cyanosis. Pediatr Rev. 1999;20:350-2) (Pleuropulmonary manifestations of systemic lupus erythematosus. Thorax. 2000;55:159-66)

Pulse Oximetry:

The absorption characteristics of oxyhemoglobin and deoxy-hemoglobin (reduced) are at different wavelengths (660nm, red and 940, infrared).  The oximeter uses the light to estimate the ratio (assuming that the pulsatile portion represents arterial and the nonpulsatile is a mixture) to give an estimate of the SaO2.   The pulse ox is calibrated to a blood cooximeter (a spectrophotometer) that measures reduced Hgb, oxy-Hgb, Met-Hgb, carboxy-Hgb.   There is excellent correlation between 75-100% saturation, otherwise it is a nonlinear relationship.   O2 Sats (normal is 80-100%):  50% –> ~27mmHg.   60% –> ~30. 75% –> ~40.  85% –> 55mmHg. 90% –> 60.  95% –> 80.  97% –> 100mmHg.

Beer’s Law:  the concentration of an unknown solute dissolved in a solvent can be determined by light absorption.

May fail if:  pt with hypotension/ hypothermia/ shock (low perfusion states) or perfusion of vasoconstrictors, as vasoconstriction leads to underestimation of O2 sat.  Not calibrated for extremely low saturation levels (<70%).  Motion artifacts.  Erroneous reading when Hgb <5g/dL, conditions with inc venous pulsations (TR, R heart failure, a tourniquet or BP cuff above the probe), excessive light (surgical lamp, direct sunlight), dyes & pigments (methylene blue, indigo carmine, indocyanine green, nail polish), met-Hgb interferes with reading (local anesthetics, nitrates, Metoclopramide, sulfa drugs, Ca-EDTA).  Darkly pigmented skin and anemia also affect the accuracy.

**Ref: (Pulse oximetry.  Respir Care Clin N Am. 1995;1:77-105) (Methemoglobinemia: etiology, pharmacology, and clinical management. Ann Emerg Med 1999;34:646-56)

Hypercapnia = Hypercarbia (Inc PaCO2):

Links:  Causes: Tx:

Abnormally increased arterial carbon dioxide tension.   PaCO2  >45 mmHg (Torr).  The opposite of hyperventilation (PaCO2 <35 = hypocapnia).  Tends to be more tolerated than hypoxia or acidosis.  Usually the result of hypoventilation and should be suspected in a patient with:  Opioid OD, airway obstruction, brain/ spinal cord damage, bilateral phrenic nerve damage.  Inc Temp 1 deg C –> 13% inc production.

Causes of CO2 retention:   1. Inc CO2 production wit no ventilatory response.   2. dec minute ventilation.  3.  Inc dead space ventilation.

Inc CO2 production –> hyperthermia, sepsis (most common), hypertonic dextrose, trauma, burns, excess carbohydrates, post-op state, organic acidosis, increased work of breathing.  Normal lungs –> Depression of central controller by drugs (narcotics, sedatives), metabolic alkalosis, CNS dz (medullary infarct/ tumor).  Dec minute ventilation see with –> CNS depression, cervical spinal cord injury, MG, GBS, diaphragm fatigue, obstructed hypopharynx.   Abnormal N-M function –> spinal cord injury >C3 level), anterior horn cell dz (polio, ALS), peripheral neuropathy (GBS), other (MG, MD, myopathy).   Structural change in Chest Wall –> kyphoscoliosis, obesity.  Acute Ventilatory Failure –> Primary Resp. Acidosis –> inc PaCO2, dec pH, normal HCO3.     Chronic Ventilatory Failure –> Compensated Respiratory Acidosis –> inc PaCO2, normal/ dec pH, inc HCO3.  Seen in COPD, end stage ILD.  Iatrogenic–> narcotics, sedatives, paralytics.  Metabolic derangements –> myxedema, Met. Alkalosis, dec K/ P/ Mg.   Abnormal Ventilatory Control  –> primary/ central alveolar hypoventilation, morbid obesity, severe OSA.  Inc V/Q ratio –> inc dead space ventilation.  Dec CO2 elimination –> PE, asthma, bronchiolitis, shock. Other –>Cardiogenic (LV CHF), acute lung injury (overwhelming pneumonia), respiratory muscle failure, chest wall injury.

Tx: inc pulmonary blood flow with inc vascular volume, Inotropes, remove obstructive cause, bronchodilators.

**Ref: (The causes and evaluation of chronic hypercapnea.  Chest 1987;91:755-9) (Hypercapnia.  N Engl J Med. 1989;321:1223-31) (Irwin and Rippe’s Intensive Care Medicine, 4th ed, 1999, Lippincott-Raven)

Intubation:

Links: Indications:  Equipment:  Equipment by Age:  Airway Assessment:  Special Conditions: Difficult Pediatric:  Adult Rapid Sequence: After Intubation: Pediatric: Drugs Used:  Emergency Airways: Laryngeal Mask: Mechanical Ventilation: Sedation:

Indications:  Provide patent airway, prevent aspiration, facilitate positive pressure ventilation, when airway maintenance using a mask is difficult, need for prolonged mechanical ventilation.   Apnea –> RR <4.  Acute hypoxemia –> PO2 <55mmHg.    Upper airway obstruction –> Fb aspiration, edema due to anaphylaxis, trauma, inhalational injury or bleeding.   Acute Respiratory Insufficiency –> PCO2 >50 mmHg.  Acute reduction in pH.  RR >35.  Chest wall trauma (flail chest), to prevent unnecessary chest wall movement.    Airway protection –> CNS d/o, deep coma, prevention of aspiration pneumonia.  Inc ICP to hyperventilate.  General anesthesia.  Hypothermia (core rewarming).

Equipment: 2 wall suction devices with Yankauer tips, laryngoscope (check lights), appropriate size ET tube with backup 0.5-1 size smaller, + stylet, check integrity of inflatable cuff (no cuff if age <8yo).  Adult Female –> 7.5-8.5 ETT, ~21cm in length. Adult Male –> 8-9.0 ETT, ~23cm length.   A size #9 is 2X normal airway resistance, 4X the work of breathing if use size #7.

Estimate of ETT size: Internal Diameter (mm) =  (age in yr/4) + 4. May also may use size of patient’s fifth digit.

Depth of Insertion (cm): (Age in yr/2) +12 Or Internal Diameter (mm) X3.

Age 12-18yo (32-40kg) –> (Green) 6.0 ETT, size 3 laryngoscope (Miller or Macintosh), 12F suction cath, 14F stylet, 18F NG tube, 16F urine cath, 32-40F chest tube, 3 laryngeal mask. 700-800ml boluses of NS to resuscitate.

Age 8-10yo (25-32kg) –> (Orange) 5.5 ETT, size 2-3 laryngoscope, 10F suction cath, 14F stylet, 14-18F NTG, 12-14F urine cath, 28-32F chest tube. 550cc NS boluses.

Age 5-8yo (18-24kg) –> (Blue) 5.5 uncuffed ETT, 16cm long, 14F stylet, 10F suction catheter, 18-20 IV cath, 12-14F NGT, 24-32F chest tube.

Age 3-5yo (14-18kg) –> (White) 4.5 ETT, size laryngoscope, 10F suction cath, 6F stylet, 10-12F NGT, 10-12F urine cath, 20-24F chest tube.  300-450 ml boluses of NS for resuscitation.

Age 1-2yo (11-14kg) –> (Yellow) 3.5-4.5 ETT, 1-2 Miller blade, 8-10F suction cath, 6F stylet, 8-10F NGT, 8-10F urine cath, 16-24F CT. 160-280 ml NS.

Age <1yo (8-11kg) –> (Purple) 4.0 ETT, 11-12cm length, 1 Miller, 8F suction cath, 6F stylet, 5-8F NGT/ urine cath, 16-20F chest tube, 100-140ml boluses.

Neonate/ Premature –> (Red) 2.5 premature, 3-3.5 (term) ETT, 10-11cm length.6F stylet, 8F suction, 22-24 IV cath, 5-8F NGT, Infant paddle until 1yo, 10-12F chest tube.

Pediatric laryngoscope size: Use straight blade until age 4.  Newborn 0, 6mos-2yrs 1, 3-5 years 2, 6-12 years 2-3, 12-16 years 3-4.

Airway Assessment: examine/ asses mobility of neck, mandible.  Size of tongue and mandible.  Dental condition and configuration.

Difficult Adult Airway:  <40cm from chin to hyoid cartilage (<3 finger breadths),  <40cm from upper to lower incisors.  Large tongue or inability to see uvula & tonsillar pillars with mouth opened.   Limited hinge movement of TMJ joint.   If pt is unable to flex chin to chest, expect a difficult intubation.

Mallampati Class:

Rated Class I-IV for Difficulty to Intubation by anatomy of airway by visualizing 3 structures, the uvula, soft palate and palatoglossal/ palatopharyngeal pillars.   Class I:  minimal difficulty, has visible soft palate, tonsillar pillars and uvula.    Class II: uvula is masked and only the pillars and soft palate are visible.  Class III:  only the soft palate is visible, severe difficulty with intubation.   Class IV: has visible hard palate only. (Can Anesth Soc 1985;32)

Neck Trauma:

Use “over the wire” retrograde intubation or insert a “lighted stylet” blindly until see light area at larynx, then ok to pass ETT over the top.  Or use fiberoptic bronchoscopy.

Head Injury patient:  Use Thiopental: Adults @3-5mg/kg IVP over 1-2 min.  Peds @3-4mg/kg IVP over 2-3 min.  Infants @5-8mg/kg IVP over 3-5 min.  Can use +Fentanyl: 2-3mcg/kg IV and Versed: 0.15mg/kg IV over 1 min.   Avoid Ketamine.

Asthma or Hypotension:  Use Ketamine: Adults or peds @1-2mg/kg IV over 1 min.  Avoid Thiopental.   Can use Versed: IV 0.15mg/kg over 1min.  Succinylcholine: Adult @0.6-1.5mg/kg IV, Peds @2mg/kg if < 10yo.  Then Vecuronium: Adult & Peds @0.1mg/kg IV.

Difficult Pediatric Airway:

Inability to visualize tonsillar pillars/ uvula/ soft palate on oropharyngeal exam.   Extension <35 deg at atlanto-occipital joint.  Thyromental distance: with neck in neutral position should be >2 adult fingerwidths (3cm) from mandibular ramus –> thyroid cartilage.  If infant >1 fingerwidth (1.5cm).   TMJ with limited hinge movement (JRA, scoliosis, fx, trismus from infection).  Congenital airway abnormality (cleft palate, micrognathia, macroglossia, glossoptosis).  Maxillary abnormality (protruding maxillary incisors or trauma).  Upper airway swelling/ obstruction (bleeding, infection, burn, inhalational injury).

Adult Rapid Sequence Intubation:

Patient preparation –>  1.  Adjust bed to comfortable height (pt’s nose at intubators xiphoid).  Establish IV, EKG monitor, pulse oximetry, have suction set up.

2. Prepare alternate airway plan: transtracheal jet intubation, cricothyrotomy (if age >8), tracheostomy. Give Lidocaine 1.5mg/kg if pt has a head injury (to attenuate rise in ICP and blunt the CV responses).

3.  Estimate pts wt. (Breslow tape).  4.  Confirm working pulse Ox & cardiac monitor.

5.  Specify personnel for cricoid pressure, neck immobilization if trauma, handling of ETT, watching O2 sats & cardiac monitor, medications.

6.  Pre-oxygenate with 100% O2 X 3-4min via BVM (if time permits).   7.  Draw up all drugs into syringes & secure IV access.  Premedicate if appropriate with Fentanyl 2-3 ug/kg IV over 3-5min or Thiopental 2-5mg/kg rapid IV push.  Lidocaine 1.5-2 mg/kg IV over 45sec.

8.  Position head to sniffing position if no trauma.   9.  Optional:  Defasciculating med (Pancuronium/ Vecuronium @ 0.01mg/kg IV).

10.  Paralyze after sedation:  Succinylcholine 1.5mg/kg IVP.  Asses for apnea, jaw relaxation, dec resistance to bag-mask.

11.  Perform Sellick maneuver (cricoid pressure) as consciousness is lost.

Intubate:  Lift upward (do not rotate the laryngoscope) to visualize vocal cords.  Straight blade (Miller) goes in front of the epiglottis, thus will see cords only.  The curved blade (Macintosh) goes under epiglottis, need to lift epiglottis to visualize the cords)  Advance tube through the vocal cords. Inflate cuff with 5-10cc air.  Ventilate with ambu bag.

After Intubation:   1. Check tube placement (5-point auscultation:  breath sounds at bilateral chest & axilla, no low pitched gurgling sounds in the stomach, check with end-tidal CO2 detector). See symmetric chest wall movement, no bulging in epigastrium with ventilation. If unilateral BS only are heard, tube may in a mainstem bronchus, withdraw slightly and re-check    If “breath sounds” are heard in stomach and not in lungs the tube may be in the esophagus.   2.  Inflate cuff, then release cricoid pressure, stabilize tube with tape or commercial holder.

3.  Measure & record tube depth (Distance in cm from mid-trachea to incisors/ gum line = 3(ETT internal D in mm) or = 12+age in yrs)/2 or = (ht in cm)/10 +5.  Or Mid-trachea to nares = 12 + (age)/2.

4. Reassess pt’s clinical status. Pulse Ox should improve.   5. Check CXR to verify correct placement depth.   Tip of tube should be 3-5cm above the carina (T4-5 interspace, at the level of aortic arch) and 3 cm below the vocal cords.  Vocal cords are at C4-5 interspace as is inferior border of mandible when in neutral position.  Head flexed –> tube descends 2cm, head extended –> tube ascends 2cm (follows the chin).    6.  Consider longer-acting sedative & paralytic.

Pediatric Rapid Sequence Intubation:

1.  Atropine 0.01-.02 mg/kg IV (minimum dose of 0.1mg, max 0.5mg) if <5yo to block vagal reflex and thus prevent bradycardia.

2. defasciculating –> Pancuronium @ 0.01mg/kg IV, not needed if <4yo.

3.  Pre-oxygenate.    4.  Sedation –> Thiopental @ 4-6mg/kg or Ketamine 1-2mg/kg.   5.  Paralyzing –> Succinylcholine 1-2mg.kg or Pancuronium 0.04-0.1mg/kg.  See above for post-intubation checks.

Drugs for Rapid Sequence Intubation:

Links:  Defasciculating:  Reversing NM Block:  Paralyzing (NM Block):

Defasciculating drugs:

Always use defasciculating dose if pt has ruptured globe:

Pancuronium 0.01mg/kg IV, onset 3min, (SE: histamine release, tachy).

Rocuronium 0.06mg/kg IV, onset 2-3min

Vecuronium 0.01mg/kg, 3min, SE: mild tachycardia. No refrig needed.

Succinylcholine 0.1mg/kg IV, onset 3min, (SE: fasciculations, inc BP/ ICP/ IOP, GI, MH.  Contra: inc K, burns, trauma, NMD, eye injury). Keep refrigerated.   All may occasionally cause paralysis, if need to

Reverse the neuromuscular blockage:

Anticholinesterase drug. –> Always use with Glycopyrrolate (Robinol): 0.01mg/kg or Atropine 0.02mg/kg to block the muscarinic SE’s (salivation, bronchospasm, bradycardia, urination) as only want nicotinic effects.  Or Scopolamine.

Neostigmine (Prostigmine):   0.07mg/kg, onset 7-10min, may take 40min. Or    Pyridostigmine (Mestinon): 0.1mg/kg IV.  Onset 12-15min.   Or

Edrophonium (Tensilon): 0.75-1mg/kg IV, onset 3-5min.

Paralyzing Drugs (Neuromuscular Blockers):

Links: TOF:  Indications:  Depolarizing = Succinylcholine:  Non-Depolarizing: Duration of Action:

Muscle Relaxants. Degree of neuromuscular blockage is assessed by electrical stimulation of peripheral motor nerves –>

Train-of-four (TOF): ulnar nerve is given 4 twitches at 2Hz over 2 sec, observe the # of twitches in the thumb.  If have 2 twitches =75% of receptors blocked to decrease the twitch responses.   Goal is 1 twitch, =90-95% to block neuromuscular transmission but prevents over paralysis. Check q1h.

Troubleshooting:  proper electrode placement over nerve, more power, weak battery, dry electrodes (change qd), disease states.   Can also monitor facial nerve at orbicularis oculi, the posterior tibial nerve with plantar flexion of great toe or peroneal nerve with dorsiflexion of great toe.

Indications for paralysis: Short term –> intubation (prevent laryngospasm and relax airway structures), transport stability, immobility during procedures, suppression of shivering in hypothermia (O2 requirements inc 40%), status epilepticus and status asthmaticus as adjuncts.    Long term –> optimize ventilation (prevent bucking after use of narcotics and sedatives, dec airway pressure, minimize barotrauma, inc chest wall compliance, use of controlled ventilation), control ICP, tetanus, dec energy expenditure (burn patients).

Extra ICU Care with NMB: occular lubricant, frequent turning to avoid pressure ulcer, ETT suctioning as cannot swallow, DVT prophylaxis, physical therapy. Talk to the patient, explain to the family, adequate sedation.

Sequence of paralysis:  Occular muscles –> digits –> abdomen –> intercostals –> diaphragm.

Depolarizing agent: mimics the action of acetylcholine.  1st cause a contraction, then relaxation.

Succinylcholine  (Anectine): 1-2mg/kg IV, onset ~45sec, lasts 5-15min, (use 2mg/kg if <10kg & 1.5 mg/kg if defasciculating agent used)

Precautions with inc K, renal failure, severe trauma, disuse atrophy, extensive burns, open eye injury (inc IOP), spinal cord or peripheral nerve injury, malignant hyperthermia, intra-abdominal infections, preexisting N-M dz.   Mimics the action of acetylcholine by depolarizing the postsynaptic membrane at the neuromuscular junction, it is metabolized by pseudocholinesterase.   SE: Cardiac –> Sinus bradycardia, junctional rhythm, sinus arrest. Ganglionic stimulation may increase heart rate and blood pressure in adults.   High K –> muscle releases potassium to raise serum potassium by 0.5 mEq/L.   Massive release with thermal injuries, massive trauma, severe intra-abdominal infection, neurologic disorders (spinal cord injury, encephalitis, stroke, Guillain-Barre syndrome, severe Parkinson’s disease), ruptured cerebral aneurysm, polyneuropathy, myopathy (eg, Duchennes dystrophy) and tetanus. Other –> inc ICP and IOP, myalgia, myoglobinuria, fasciculations (prevented by pretreatment with a nondepolarizing relaxant), trismus, malignant hyperthermia.    Drug that potentiate the NM block such as antibiotics (streptomycin’s, colistin, polymyxin, tetracycline, lincomycin, clindamycin), antidysrhythmic (quinidine, lidocaine, calcium channel blockers), antihypertensives (trimethaphan), cholinesterase inhibitors, furosemide, inhalational anesthetics, local anesthetics, lithium, and magnesium.

Non-depolarizing agents: compete for cholinergic receptors (competitive antagonists of acetylcholine) on the post-synaptic membrane.

Dosing:  can give intermittent injections (if healthy use Pancuronium, if multi-organ system failure use Pancuronium or Doxacurium) or can give continuous infusion (if healthy use Atracurium or Vecuronium, if MOSF use Atracurium).

Pancuronium (Pavulon): 0.04-0.1mg/kg IV onset 1-5min, DUO: 60min. (SE: tachy & HTN as vagolytic, prolonged action)

Rocuronium (Zemuron): 0.6-1.2mg/kg, onset in 30-90sec, lasts only 25-60min.

Vecuronium (Norcuron): 0.1-0.2mg/kg, onset in 1-4min, lasts 30min. (SE: prolonged action).

Atracurium (Tracrium): 0.3-5mg/kg.  Onset 2-3min, lasts 30min.  Less histamine release than others.

Pipecuronium: 0.07-0.085mg/kg, onset 2-3min, DOA is 60-100min.

Doxacurium: 0.025-0.08mg/kg, onset in 4-5 min, DOA 55-160 min., Mivacurium.

Duration of action:   Ultrashort (5-8min) –> Succinylcholine.  Short (15-20min) –> Mivacurium.    Intermediate (20-30min) –> Atracurium, Rocuronium, Vecuronium.    Long (45-60min) –> Doxacurium, Pancuronium, Pipecuronium.

Post Paralysis Syndrome:  all agents with prolonged exposure, diffuse proximal & distal muscle weakness.  Myopathic process on EMG with preserved nerve conduction and sensory function.  Slow clinical recovery.

**Ref:  (New neuromuscular blocking drugs. N Engl J Med 1995;332:1691-99)  (Am Rev Resp Dis 1993;147:234-36) (Intubation. Mayo Clin 1992; 67:569-576)  (EM Clinic of NA 1988;6)

Emergency Airway Options:

Links:  Needle Crico:  Surgical Crico:  Tracheostomy:

1.  Awake Intubation (no sedation): used for difficult airway (congenital anomaly, trauma, burns), hemodynamically unstable pt (hypotensive), unconscious pt, newborns.

2.  Rapid Sequence Intubation (Crash): Use pharmacological paralysis/ sedation/ cricoid pressure.  For bowel obstruction, peritonitis, pregnancy (>2nd tri), inc ICP, undocumented fasting (or documented of <8hr fast of solid food), multiple trauma, pain.

3.  General anesthesia: need OR, anesthesiologist, for airway obstruction (acute epiglottitis), Fb aspiration.

4.  Sedation & Paralysis: elective intubation (prior to gastric lavage, radiographic procedure, cardioversion), emergent intubation in hemodynamically stable pt.

Needle Cricothyroidotomy:

Similar to percutaneous tracheostomy kits.   Using “Transtracheal Jet Ventilation”:   Buys time until definitive airway provided.  Poor CO2 elimination, thus useful for only 30-45min.

Equipment: alcohol or provodine-iodine pads, #11 scalpel, small syringe, 25g needle, lidocaine, 4″ hemostat, 5-6mm ETT or a tracheostomy tube.  Step #1:  Place pt supine, extend neck.   Betadine X3 neck. Inject 2% lidocaine with epinephrine if the patient is awake.

Step #2:  Cricothyroid Membrane identified between cricoid and thyroid cartilages.  Stabilize thyroid cartilage with opposite hand.  Make a 3-4cm vertical skin incision then a 1-2cm horizontal cricothyroid membrane incision.

Step #3:  Place 12-14g IV cannula “catheter-over-needle” (Angiocath or Jelco) attached to 3-5ml syringe through cricothyroid membrane.  Puncture vertically at midline.   Aspirate as advance needle syringe until air is  aspirated.    Advance cannula 45 deg caudally (inferiorly) and tape in place.    Can adapt Ambu bag onto this.

Step #4:  Remove needle, confirm catheter placement by aspirating air.  Attach 3mm ETT adapter (on any ped tube) to IV catheter or a 3ml locking syringe (w/o plunger).  Attach to 14g angiocath and bag pt.

Step #5:  Attach high flow oxygen source @10-50 psi 100% via O2 tubing @15L/min via a Y connector or with a hole cut into the side of the tubing.   The open end of the Y is occluded for 1sec (“on”) out of every 5s (4 sec “off”) to allow O2 to enter the pt, deliver O2 at 20 bursts/min.  On release of the hole, passive exhalation occurs.   Age <5 –> initial psi of 5, 100ml tidal volume.   Age 5-8yo –> 5-10psi, 240-340 ml TV.    Age 8-12 –> 10-25 initial psi, 340-625 TV.      Age >12yo –> 30-50 psi, 700-1000ml TV.  Eventually end up getting hypercarbia in 30-45min.

Surgical Cricothyroidotomy:

Indications: Excessive ENT hemorrhage, massive regurgitation, airway obstruction such that ETT intubation is unsuccessful.  C-spine fx and nasotracheal intubation unsuccessful.   Contra: fx or serious injury to larynx or cricoid cartilage (needs tracheostomy).

Equipment: #11 blade, Scalpel, Trousseau dilator, Tracheostomy tube (Silex or Portex), (Or a standard #5-8 size ETT that has been cut), small curved hemostats, prep solution, 4X4 gauze, scissors, 10ml syringe, tracheal suction catheter, tracheal hook, Lido with epi (if pt awake and have time)

Step #1:  Aseptically infiltrate with local anesthetic.   Step #2:  Hold larynx between thumb and middlefinger, hold membrane with index finger.  Make a transverse stab incision of 2-3cm through the skin and then the cricothyroid membrane, avoiding the large vessels that are located laterally.

Step #3:  Keep scalpel in place and insert tracheal hook into hold and retract upward before removing the blade.   (To avoid losing the tract from the skin to the trachea). Can dilate if necessary with a hemostat or by rotating the scalpel handle 90 deg to open the membrane perpendicular to the incision.

Step #4:   Insert tube of appropriate size under direct visualization.  Inflate cuff and secure.   Asses ventilation by listening for breath sounds. Should be replaced with a formal tracheostomy within a few hours.

Other:  Tracheostomy or pass wire through a catheter out the mouth then pass ETT over and into the trachea.  “Over the wire”

X-ray findings:  The tracheostomy tube is located halfway between the stoma and the carina, it should be parallel to the long axis of the trachea and be approximately 2/3 of width of the trachea.  The cuff should not cause bulging of the trachea walls. Check for subcutaneous air in the neck tissue and for mediastinal widening secondary to air leakage. Stabilization:  trach ties should be secure enough to prevent movement, but loosse enough to allow one finger width of play to decrease risk of skin necrosis.    Decannulation:  accidental removal of the reach tube.  Can occur with a strong cough, pt movement if not well-secured and with routine trach care.  Stoma Care: suction as needed.  Remove old dressing & ties (one side at a time) with constant stabelization.  Always have a spare tube nearby in case of decannulation.   Clean site with 4X4 moistened with H2O2 with single pass for each pad.  Look for swelling, redness or pulsations at site.  Next use cotton tipped applicator moistened with H2O2 to clean around the stoma & flanges of trach tube.  Rinse with sterile water and pat dry.  Never apply non-water soluble ointment. Use only dressings designed for trach or drains.  Never cut a gauze pad to fit the site as small cotton filaments get absorbed into the stoma and lead to microabcesses.

Laryngeal Mask Airway (LMA):

Intermediate between an ETT and facemask.  It is inserted blindly into the pharynx where it lies in the hypopharynx to form a low-pressure seal around the laryngeal inlet.    Technique:  get appropriate size base on wt.  Lubricate with K-Y jelly.  Sedate pt.   Place pt in sniffing position and preoxyginate.  Hold it “like a pen” with the opening facing forward and the black line of the air tube facing toward the upper lip in an anterior position.  Use your index finger to guide it in over the tongue as press the distal tip against the hard palate.  Advance until feel the “typical” resistance and inflate the cuff to around 60 cm H2O (4-40ml depending on size).  Connect to anesthesia circuit and check for proper breath sounds.  Insert bite block.  There are alternative methods of insertion.  After procedure remove when pt able to cough and swallow.   Advantages:  avoids most of the complications seen with ETT.  Disadvantage:  unable to protect airway from aspiration (2-3%).  Not effective if poor lung complinat or inc airway resistance such as in COPD or pulmonary edema.

Mask Size –>  Pt’s wt (kg) @ Internal Diameter (mm)@  Cuff Volume (ml):  1 –> <6.5kg@ 5.25@ 2-5.   2 –>  6.2-20@. 7@ 7-10.   2.5 –> 20-30@ 8.4@ 14.   3 –> 30-70@ 10@ 15-20. 4 –> 70-90@ 12@ 25-30.    5 –> >90@ 11.5@ 30-40.

**Ref:  (Retrograde intubation of the pharynx: an unusual complication of emergency cricothyrotomy.  Ann Emerg Med. 1992;21:220-2) (Emergency cricothyroidotomy.  J Laryngol Otol. 1992;106:479-80) (Emergency cricothyroidotomy.  Am Surg. 1997;63:346-9)

Initiating Mechanical Ventilation:

Links:  Criteria:  Types of Ventilators:  Ventilatory Modes:   Non-invasive Ventilation:  Initial Settings:  Monitoring:   Respiratory Physiology:  Complications of Ventilators:  Other Ventilator Considerations:   Trouble Shooting:  Weaning:  Sedation:  Intubation:

Criteria Parameters:

RR >35/min.  PaCO2 >50mmHg & pH < 7.30.   VC < 10-15 ml/kg.   VD/VT = dead space/ tidal volume >0.60.   FEV1 <10 ml/kg.   Resting Minute Ventilation >20 or ❤ L/min.   Max Insp Press < -20 cm H2O.   A-a gradient >450 mmHg.  PaO2 with O2 supplement <55-60 mm Hg.

Other Indications:   To improve pulmonary gas exchange in resp. failure of pulmonary or extrapulmonary (chest bellow, central resp. drive) etiology, to inc PAO2 and dec PaCO2.   To relieve respiratory distress, dec O2 cost of breathing. To reverse respiratory muscle fatigue.  To alter pressure-volume relationships, prevent and reverse atelectasis, improve lung compliance.  Reduced CNS resp. drive (intoxication, brainstem CVA).  To treat inc ICP by hyperventilating to reduce cerebral blood flow.  Prophylactic –> sepsis, shock, upper GI bleed with aspiration risk (varices), obtundation with loss of protective airway reflexes.

Tips:  Always consider individual pt’s characteristics, e.g. PCO2 of 55 in a young asthmatic indicates impending resp. failure, whereas in an elderly COPD’er it may be their baseline.   Consider alternative methods of non-invasive ventilation with BiPAP.

Types of ventilators:   Vent Modes:

Negative Pressure Ventilator:  Non-invasive negative pressure ventilation (NINPV). The iron lung used during polio epidemic in 1950’s.   Positive Pressure Ventilator:  Raise airway pressure to create inspiratory flow that inflates the lungs, used with cuffed ET tubes.    Divided into 4 categories:

1.  Time Cycle –> Timed delivery of gas flow.  TV = Flow rate X insp time.  Delivers a relatively constant TV to allow for precise control and variability in waveform of delivered gas.

2. Volume-cycled –> most common, reliably delivers set volume of gas at a pre-set flow regardless of pressure.  TV (tidal volume) is constant despite fluctuations in respiratory mechanics. TV will not vary with changes in pressure (compliance), unless pressure limit is reached.

3.  Pressure-cycled –> Triggered by pt’s inspiratory effort to deliver air at until a preset airway pressure is reached.  Inspiration stops when preset pressure reached.  TV = Flow rate X Time until pressure reached.  Will have variable volume if circuit pressure varies (compliance).

4.  High Frequency Ventilators:  jet ventilation, oscillation, percussive ventilation.  Have low mean airway pressure, but volume increases.  Used for closed head injuries, large pulmonary air leaks/ flail chest and refractory respiratory failure.

Ventilatory modes:

Links:  AC:  IPPC/CMV:  PCV:  PC-IRV:  IMV:  SIMV:  PSV:  PEEP:  Non-Invasive: Initial Settings:  Monitoring: Complications: Extubation Criteria:

Paralysis, sedation, controlled ventilation all lead to respiratory muscle atrophy.

Assist Control (AC) (Assisted Mandatory Ventilation = AMV or ACV) –> A combined mode of ventilation.  Pt makes a respiratory effort, vent is triggered to deliver a positive pressure breath at a preset TV. Ventilator assists if pt breaths on own.  Usually combine with minimal CMV (back-up rate) so that if pt doesn’t initiate a breath for a given period of time (e.g. 6 sec. if the RR is set at 10/min), the vent delivers a “backup” breath at the preset TV. Used for sick pt’s with CHF, sepsis or ARDS.  Risk of hypocapnia from low CO2 as even a small breath can trigger a full TV.

Intermittent Positive Pressure (Controlled Mechanical) Ventilation (IPPC/CMV) –> A mandatory mode with preset ventilatory patterns.  Either volume or pressure controlled.   Pt unable to interact with the machine, requires sedation or paralysis.  Has variable peak airway pressure.

Pressure Controlled Ventilation (PCV): where a specific pressure is set and the machine delivers a preset flow until that pressure is reached at which point inspiration ends and exhalation begins.   Uncomfortable as does not allow for spontaneous breathing.  Insufficient TV’s if pt fights the breath, low lung compliance or increased airway resistance causing inspiration to end prematurely.  Appropriate for initial control of pt with little ventilatory drive, severe lung injury (ARDS), gas trapping or circulatory instability.  PCV often combined with inverse ration ventilation (IRV) to get PCIRV in pt’s with ARDS to avoid barotrauma.

Pressure Control Inverse Ratio Ventilation (PC-IRV) –> A salvage mode.  It is contrary to the normal state, inspiration phase lasts longer (50-75% of the respiratory cycle) than the expiratory phase.  We set the vent to deliver a set amount of pressure above the PEEP level and lengthen the inspiratory phase so that I:E = 1:1 or 2:1 or 3:1.  The inversion holds the lungs at peak inflation pressure for a longer period of time to increase the mean airway pressure w/o inc PIP to improve oxygenation.  The pt must be sedated and paralyzed as uncomfortable.  Can lead to auto-PEEP, worsening hypercapnea or barotrauma.

Intermittent Mandatory Ventilation (IMV) –> Vent delivers breaths at set volume and rate at predetermined time intervals.  Pt may take additional breaths but they’re not assisted, so they entail more work than pt initiated breaths in AC mode-provides “workout” of resp. muscles, especially if RR is set below pt’s spontaneous RR.  Better than AC for pts with auto-PEEP or with high spont. RR, e.g. anxiety (b/c may get severe resp. alkalosis with AC).   May get patient-vent dyssynchrony so use SIMV.

Synchronized Intermittent Mandatory Ventilation (SIMV) –> delivers a mandatory set number of mechanically imposed breaths of predetermined TV and therfore achieves a predetermined minimum mandatory minute volume (MMV).   Allows for spontaneous pressure supported breathing with minimal bucking of the ventilator as will not deliver a breath during a spontaneous breath.  Helps to add pressure support (PSV) of ~5ml to overcome tube resistance.   Useful for a pt with minimal sedation, drug overdoses and when weaning. Easy to wean, just dec the rate.

Pressure Support Ventilation (PSV) –> Inspiratory effort by the pt triggers the vent to supply a preset level of positive pressure until inspiration ceases (flow varies to meet pressure).  TV remains dependent on pt’s effort.   Pt controls the RR, inspiratory time and flow.  Helps decrease the work of breathing.  An ETT size 8 adds 5cm, size 7 requires 10-12 PSV to overcome the tube resistance, thus always add back when weaning.  No breaths are delivered in the absence of spontaneous inspirations  If have secretions or a sudden drop in compliance will not get aeration, thus only for clear airways.  Used with SIMV and for weaning and for pts who have been intubated purely for airway protection.  Can use in combination with IMV, giving some (but not full) assistance with pt-initiated breaths.   Use 5-20 cm H2O, 25= full support.

Positive End-Expiratory Pressure (PEEP) –> Positive airway pressure applied throughout the respiratory cycle during mandatory invasive ventilation. No affect on ventilation, but improves oxygenation by splinting (recruiting) open collapsed alveoli (to inc FRC) and dec V/Q mismatching to drive fluid into interstitium, allowing for reduction of FiO2. Physiologic PEEP is 3cm.  SE:  May dec CO, risk of barotrauma (PTX, lung cyst, pneumomediastinum).

Noninvasive Ventilation:  Alternative to an ET tube:

(Bi PAP) ventilator or continuous positive airway pressure (CPAP) device. Uses a silicone mask or a mouthpiece. Can use oronasal or nasal masks.  Head straps must be used, pt must keep their mouth closed.   Can use either volume or pressure cycled ventilator.

Noninvasive Positive-Pressure Ventilation (NIPPV) –> Delivers a set pressure with each breath. Delivered via a bilevel positive airway pressure (insp Vs exp).   Has fewer complications and shorter ICU stay compared to conventional ventilation.

BIPAP:  Bilevel PAP allows independent control of inspiratory and expiratory pressures, when pt initiates breath a sensor initiates a predetermined amount of inspiratory pressure.  Can be administered in either a spontaneous or timed setting or both. Can use a nasal or face mask.  Typical start level is with an IPAP (inspiritory, like pressure support) @ 10 (8-15 cm H2O) and an EPAP (expiratory, like CPAP) @ 3-8.  Short-term Indications:  acute respiratory failure due to COPD, particularly if symptomatic with inc PaCO2.  Acute hypoxic respiratory failure, status asthmaticus, cardiogenic pulmonary edema.  Long-term indications:  chronic respiratory failure due to NM dz, thoracic deformity or idiopathic hypoventilation, severe stable COPD.  Benefits:  Delivery of assisted ventilation w/o ETT.  Dec the length of ICU stay, reduced mortality, fewer nosocomial infections, less sedation needed.  Succes rates: 93% with acute cardiogenic pulmonary edema, 88% with status asthmaticus, 81% with acute-on-chronic resp failures, 66% with acute hypoxemia or mixed resp failure.  Key:  exclude pt’s with hemodynamic instability and those with little improvement in 2-3 days.  Will likely fail if agitation, ARDS, severe acidemia/ encephalopathy.   Allow pt to accomidate to mask (may need to change types).  Contra: respiratory arrest, acute cardiac ischemia, AMI, inadequate airway protective reflexes, impaired mental status, inability to wear mask due to claustrophobia or facial abnormality.  Disadvantages:  tidal volume is variable, no alarms, no monitors.

Problems:  patient-ventilator asynchrony (PVA) –> avoid by starting at a PEEP of 2-3 cm H2O and slowly titrate to 4-8.  Avoid mask leakage wich leads the vent to fail in detecting end-inspiration (adjust size, remove NGT, consider chin strap, change type, dec PSV).  Portable units –> most unable to deliver high FiO2, most lack waveform displays, have the potential for rebreathing exhaled gas.  Other: discourages coughing and clearance of bronchial secretions.  The can be uncomfortable and claustrophobic.  Can cause eye irritation, nasal abrasions and sinus congestion.

Continuous Positive Airway Pressure (CPAP) –> same objective as PEEP in a spontaneous breathing pt, it is applied to a pt breathing via ETT or nasal/ face mask. A flow generator entrains air to the desires FiO2 & pressure.  Positive pressure is typically set at 5-10cm H2O (dec risk of barotrauma).Good for pt’s with low FRC. Use carefully in pts with bronchospasm or risk of air trapping.  Used during weaning trials with PSV (=PSSV).

**Ref:  (N Engl J Med 1998; 339:429) (Mayo Clin 1999; 74:817-820) (N Engl J Med 1994; 330:1056) (Keys to effective noninvasive ventilation.  J Crit Illness 2001;16:2&3) (Advances in mechanical ventilation.  N Engl J Med 2001;344:26)

Initial Post-intubation Settings for Adults: Links: Monitoring: Vent Modes: Weaning:

Mode: Assist control (AC) and IMV are commonly used.   Use control if pt cannot breath on own, paralyzed or heavy sedation.

Tidal Volume (TV): start with 7-10ml/kg as sick pt’s tend to have stiffer lungs.  10-15ml/kg if routine surgery in healthy. (7-10 if inc peak airway pressures like in asthma, less if have ARDS). >20 causes barotrauma. Actual TV delivered may vary from setting due to pulmonary compliance, thus always measure exhaled volume.  In ARDS use 6ml/kg (based on IBW) tidal volume (~400-500ml) to avoid over-stretching the lungs which decreases shunting, hypoxemia and alveolar capillary damage.  Let the pH and CO2 be secondary concerns, if pH <7.15 give bicarb.

Respiratory Rate (RR):  12-20/min for adult and 14-25 for child.  >20 should be avoided as ventilatory efficiency will drop off.  If using ACV set at 4/min unless not breathing spontaneous and need to set at 10.  No rate is set in PSV.

FiO2: start with 100%, wean downward to <50% (to avoid O2 toxicity) ASAP keeping sats >90%.  0.6 is the threshold for toxic concentration.

PEEP: none or @ 5cm H20 if PaO2 <60 or FiO2  >50%, avoid going higher.   Increase in increments of 2-3cm until pulmonary shunt <15-20% or PaO2/FiO2 ratio exceeds 250.  May also help to reduce auto-PEEP.

Inspiratory / Expiratory (I:E) Time:  1:2 (reverse ration of >2:1 if ARDS or pulmonary edema).  Regulates respiratory rate.  Usually 0.5-3.  Increased inspiratory time leads to improved oxygenation.

Insp flow Rate: During ACV or SIMV.  50-60 L/min (if too slow, leaves inadequate time for exhalation).  In COPD often set at 100.  Higher flow rates deliver a tidal volume in a shorter period of time, leaving more time for exhalation, which favors complete emptying of the lung. But have inc peak pressures and in VQ mismatch.  Inc rate –> inc PIP.

COPD on Vent:  keep peak flow <50 as air trap can increase expiration by decreasing the rate or decrease the TV or decrease the I/E ratio.

Commonly set the TV 0.5L,  FIO2 @ 0.5, CMV 12, 5 PEEP, and write “check for auto-PEEP q12, if >5 call MD”.  If chronically acidotic (pH 7.38 and CO2 56), avoid overventilation or will get post hypercapnea metabolic alkalosis.  Thus aim to normalize their acute change in pH, not their CO2.  Predicted range of normal CO2  = (HCO3 X 1.5) +8 +2.  Insp pause:  none (leads to uneven ventilation and air trapping).

Peak Inspiratory Pressure (PIP):  start @20-30cm if pressure cycled ventilator. Keep <45 to minimize barotrauma.  Influenced by TV, inspiratory flow rate and inspiratory wave pattern.  May prevent premature collapse of airway).   Sensitivity:  to trigger an assisted breath in ACV or PSV, pt need to lower airway pressure to open a “demand valve”.  Usually set at —1 to —3 cm H2O.  Aim for plateau pressure of <30 = the elastic recoil of the lungs, a pressure measured after inspiration using a 1sec breathhold.

Neonates & Infant –> ventilator pressure limited if <10kg, rate of 30-40/min, Insp/expiratory (I:E) ratio of 1:2, settings: begin peak inspiratory pressure at 16mmHg and inc by 2mmHg until good excursion.  Start PEEP at 3-4cm H2O.  FiO2 at 5-10% above preintubation FiO2.

Older Child –> use volume limited ventilator, normal respiratory rate for age, I:E ratio of 1:2, tidal volume 10-12ml/kg, 3-4cm H2O PEEP, adjust FiO2 to O2 SATs.

Adjusting the settings:   Frequent reassessment (2-3X/24h) is the key to good results.  Two key categories, those that change the minute ventilation (=RR X TV) to change the pt’s pCO2 and pH and those that change oxygenation (FiO2, PEEP, I:E ratio).   Oxygenation:  Sats > 90% don’t significantly inc tissue oxygenation.   Sat is mostly a function of FiO2 rather than TV or RR.  If you need FiO2 >60% consider second-line approach to improving oxygenation –> Ventilation:   getting rid of CO2.   A function of alveolar minute ventilation = RR x TV.

Permissive Hypercapnea Technique:  low TV often lead to dec ventilation and inc PaCO2.  Must focus on the pH rather than PaCO2 to determine pt’s status.  Can give IV bicarb if pH is <7.15   A controlled hypoventilation by limiting TV to 5-7ml/kg.  Accept some hypercapnia in exchange for lower PIP and lower risk of barotrauma.  May exacerbate pulm HTN and cause an inc ICP (avoid if head injury).

Monitoring:

ABG: 30-60 min post any changes in vent settings, then periodically.  CXR: daily to monitor ETT position ans r/o PTX, SC emphysema, pneumomediastinum or subpleural air cysts. Lung infiltrates or atelectasis may diminish or disappear after initiation of mechanical ventilation because of increased aeration of the affected lung lobe.  O2 sat: at all times except in stable long-term vent pts.   RR: is pt overbreathing the vent? Check daily.   PIP: should be < 30mm H2O.

Auto-PEEP (Intrinsic PEEP):  Develops due to incomplete emptying of local lung units and air trapping.  Can be due to a ventilatory delivery prior to complete expiration of previous breath.  Seen in pt’s with inc minute ventilation (ARDS) and those with airflow limitations such as chronic pulmonary dz (COPD & asthma) where dynamic airway compression is present or in a rapid RR or large VT when expiratory time is inadequate.  Most vents can measure, need the application of an end-inspiratory hold.  Causes same complications as PEEP and more work to trigger the vent.

Tx of Auto-PEEP: bronchodilator, dec rate (to 8-10 to allow exhalation), sedate, paralyze, fluids for hypotension, chest PT, larger size ETT, inc exp time (dec rate or tidal volume), dec Insp time (inc peak flow, use low compressible volume circuit), allow PCO2 to rise above 60mmHg (dec rate or tidal volume), normalize pH(bicarb if met acidosis, purposeful hyperventilation), add PEEP or CPAP to decrease the work of breathing.

Tracheal cuff pressures: should allow a little leak, <15mm Hg.

Hemodynamic parameters: BP, UO, CO and PCWP in selected cases. PA Catheter indicated if PEEP >15cm H2O, cardiac dz, intracranial injury or questionable fluid status.

Fluids & Electrolytes:  mech. ventilation can cause Na and fluid retention.

Pearls:   Prophylactic H2-blockers (better at preventing ulcer than sucralfate, may have slight inc risk of infection (N Engl J Med 1998; 338:791). Carafate 1g in 5-10ml sterile H2O via NGT q6h (avoid 2h from dig, Coumadin, theo, Quinolone). DVT prophylaxis with pneumatics or Lovenox 40mg SC qd.   Check back side QOD for decubiti.  HOB at >30 deg if possible, to reduce risk of aspiration.   Adequate nutritional support.  Sedation PRN.

Respiratory Physiology:

Respiratory Exchange Ratio (RER): ~ = Respiratory Quotient. =VCO2/ VO2 = 0.8-0.85.  If eat pure carbos, will be 1.0.

Compliance = Change in volume / change in pressure.

Static Compliance (C-stat): change in vol / change in pressure. At a no flow state.  For most lungs = 50-100ml/cmH2O.  = VT / (Plateau pressure — PEEP) = 50-85 ml/cm H2O.  Reflects pulmonary parenchymal changes.  Abnormal in pneumonia, pulmonary edema, ARDS, atelectasis, intubation, PTX.  Plateau pressure is measured during the no flow state.   C-stat determines plateau pressure at end-inspiration for given TV.

Dynamic compliance (Cdyn):   Due to airways compliance resistance.  Can get high peak proximal airway pressure if this is low, e.g. in asthma. = Vt / (peak insp press – PEEP).  Inc flow or inc resistance or dec compliance all inc PIP.

Complications of Mechanical Ventilation: Other Ventilator Considerations:   Trouble Shooting:  ….Common complications include respiratory muscle deconditioning, psychological trauma.  Dec CO (need to dec PEEP, VT, PIP and bolus with fluids to inc CVP), barotrauma (PTX, SC emphysema, pneumomediastinum, interstitial emphysema, pneumoperitoneum).  Avoid PEEP >15, PIP >45 and FiO2 >50%), V/Q mismatch (need to inc PEEP and VT).  Nosocomial infection.

If Inc PIP’s (peak inspiratory pressure): inc risk of barotrauma.  Limiting PIP’s may or may not change outcomes, e.g. mortality or incidence of pneumothorax (N Engl J Med 1998; 338:355 and 335:341).   Etiology: High airways resistance (severe asthma), low lung compliance (pulmonary edema), relatively short expiratory time, use of PEEP, auto-PEEP, “Fighting the vent”.

Tx:  Sedation if fighting the vent, inc expiratory time by either dec TV, dec RR or inc inspiratory flow rate.  Change from AC to IMV so some breaths are unassisted.  Give fluid if BP is low from high PIP.

Hypotension: due to dec systemic venous return and thus dec preload, with compensatory Na and H2O retention.

Other:  Barotrauma (pneumothorax, pneumomediastinum, sub-Q emphysema).     O2 toxicity (occurs with FiO2 > 60% for > 72h, avoid by using lowest FiO2 that will give sat >90).  Auto-Peep, gas-trapping in alveoli (due to airways disease).  Get persistent positive alveolar pressure at end of exhalation (in nl people, end-expiratory alv. pressure = atmospheric pressure)   Makes it harder for pt to trigger the vent b/c pt has to generate more negative pressure (has to generate neg. pressure equivalent to the amount of Auto-PEEP plus the amount required to trigger vent), which inc effective dead space (due to inc vent and dec perfusion).  Tx:  Add extrinsic PEEP, which can make it easier to trigger vent.

Ventilator-Associated Pneumonia:  mortality rate of 30%.   Can reduce incidence by adequate handwashing, semirecumbent positioning to avoid aspiration, good nutritional support, avoid gastric distention, early removal of ETT and NGT, continuous subglottic suctioning, using Sucralfate instead of H2 blockers for stress ulcer prophylaxis, chlorhexidine oral rinses.

Other Ventilator Considerations:

Agitation:  r/o drug/ substance withdrawal, hypoxemia, meds, pneumonia.  Consider decreasing the PEEP or changing to pressure support.

Increased PaCO2:  R/o obstruction, cuff leak, PTX, right mainstem intubation.  Consider decreasing sedation, increasing rate, increasing TV, initiating NGT suction (to lower any distention and acid load), if pt has COPD consider increasing the peak flow. R/o overfeeding.

Hypotension:  r/o occult bleeding, AMI, steroid withdrawal, PTX, auto-PEEP.  Consider Narcan, giving PRBC and fluids or decreasing the PEEP.

Metabolic Alkalosis:  consider decreasing the NGT suction, adding Diamox or decreasing diuretics. Diamox 250mg IVP q12h x3 with 20 mEq KCl via NGT.

Decreased PaCO2:  Check for pain or sepsis.  Consider decreasing the rate, TV or adding sedation.  Measure Ve, consider changing to IMV or add a dead space of 6 inches every day up to 24 inches.

Decreased PaO2: r/o atelectasis, mucous plug, PTX, R mainstem intubation, cuff leak, pneumonia, fluid overload, CHF, dec CO, PE.   Sedate the pt if severe agitation.  Can try increasing the TV, rate, FIO2 or PEEP.  Can consider diuresing the pt or suctioning or using bronchodilator.

Increased Airway Pressure:  R/o mucous plugging of ETT, bronchospasm, auto-PEEP, ARDS, R mainstem intubation, PTX.  Consider sedating the patient adding bronchodilation or bronchoscopy.

Troubleshooting Respiratory Distress in the Ventilated Patient:

The rapidity of onset of the problem is a key clue.  If deterioration occurs over several hours, it is likely progression of the underlying dz.

Abrupt onset:  Examine pt and all circuits. Check CXR (infiltrate, PTX, tube).

Consider swan readings if suspect progression of dz.

High Pressure Alarm: high peak pressure from airway resistance.  Check the ETT, r/o bronchospasm.

Low Pressure Alarm: is the pt disconnected, is there inadequate flow rate.

Hypoxemia: Make dx.  Can increase PEEP incrementally up to 18cm H2O or titrate up the inspired O2.  Consider the prone position, increasing cardiac output.

Hypotension: is there volume depletion (consider fluid bolus), sedation, increased intrathoracic pressure.  May need to reduce PEEP or minute volume.  R/o PTX or auto-PEEP.

Hypercapnea: May need bicarb if acidotic.  Ok to accept mild hypercapnea in the 50-80 m Hg range.

Artificial airway problems:Malposition of the tube (should be 2-5cm above carina as flex neck tip moves 3cm down, extend and it moves 5cm up).   Inspissated secretions (need frequent suction, saline instillation and nebs), Cuff or ETT failure (cuff pressure should be <25cm or tamponade local tissue causing tracheomalacia.  Pt may bite the tube.  If cuff leak will hear bubble sounds).   T-E fistula (risks: steroids, hypotension with intermittent ischemia and poor nutrition).   Pain & cough (give 3ml of 1% Lido before suction).

External Ventilator Problems: leaks or disconnects (ask resp tech to asses).  In-line nebulizer (goofs up measured VT and VE on PSV, triggering alarm).  Tube Condensate (can prevent triggering).

Ventilator Failure: rare, if in doubt bag pt with 100% O2 and see if improves.

Patient-Ventilator System Problem: Asynchronous/ dyssynchronous breathing (“Fighting”), may need to use sedation or paralyze.  Ask resp tech to match TV to flow rate of pt. Check the trigger sensitivity, Check for Auto-PEEP, barotrauma, and inspiratory flow rate.  Consider switching to synchronized IMV, PS or PC modes.

Weaning: Extubation Criteria:

Overall clinical assessment is the most important thing.   CV stable and original problem that resulted in intubation is reversed.  Asses mental status (AAO), adequacy of secretion clearance.   Ventilatory supply, respiratory muscle and pulmonary function meets demand (high O2-consumption states, such as sepsis).   Priority –> 1. dec FiO2 to <50-60% with PaO2 > 60-80 Torr.    2. dec Mechanical rate.   3.  dec PEEP in increments of 2-3cm.  4. Ventilatory capacity: self support for >30min on T-tube with acceptable gases.

Weaning trials:   Commonly give trial of spontaneous breathing with either a T-piece or pressure support for 1-2 h.    Terminate if: RR>35/min, SATs <90%, HR >140/min, SBP >200 mmHg or have agitation and diaphoresis.  If fail, consider etiology:  poor nutrition, electrolyte abnormality, cardiac disease, neuromuscular dysfunction, excessive secretions, residual sedation, unresolved primary illness.  Can re-institute daily trials of spontaneous breathing or add additional weaning protocols such as using pressure support to keep RR <30/min, lowering the pressure by 2-4cm H2O BID to <10 or using T-piece or SIMV.

T-Piece trial –> Trial of spontaneous breathing for up to 2h qd.   Pt breathes spontaneously through T-tube connected to humidified air source for a preset duration.  Start at 5 min., not to fatigue patient, gradually lengthening.   Advantages: pt doesn’t need to work to open any demand valve.   Disadvantages: no alarms, have to stay at bedside in case poops out.  Fails to provide physiologic levels of PEEP, promoting alveolar collapse.   May shorten duration on vent (4.5 vs. 6d) and lower incidence of complications (reintubation, vent x >3wks, etc.) (N Engl J Med 1996; 335:1864)

SIMV –> Ventilations are mandatory, preset tidal volume at preset rate delivered at gradually decreasing rate. Gradually decrease the number of machine-delivered breaths.  Final rate usually 0.5-1/minute, timed not to be in synch with pt’s own efforts.  Pt breathes spontaneously on his/her own between IMV breaths.  Can take several days or more.  RR > 25 indicates failure.   Once SIMV is at 0, can gradually remove pt from pressure support until get to 5-7cm H2O, then can extubate.

Pressure support –> Pt breathes spontaneously at their own pace, each of pt’s inspirations augmented by preset positive pressure from vent.  Can result in varying tidal volumes if pt’s resp. mechanics are unstable.   Advantages: more comfortable for pt avoids asynchrony, allows pt to regulate TV, RR and inspiratory flow rate/ time.    Disadvantages: can get variable tidal volumes.

CPAP trial + PSSV –> Start with IMV of 6 for 30min if tolerate –> set CPAP 3 with PSV 3 (more if small ETT) to overcome ETT resistance.  It is like pressure support, but with positive pressure during exhalation too.  Advantages: alarms, pt is monitored by vent.   Disadvantages: pt must work to open vent’s demand valve.

Extubation –> May need ETT after weaning from vent if upper airway is obstructed, full of secretions, no gag reflex, etc.  Return of swallowing function may take hours-days, don’t rush start of oral intake.

Criteria for Extubation –> Weaning Parameters:  Opposite of intubation criteria.

Category –> Parameter:   Resp Function: Neg Inspiratory Force (NIF) –> Good: < -20 cm H2O. (nl = -60 -100).  No good: > -20. Respiratory Rate –> Good: 12-26. No good:  >35.

Ventilatory demand:  Spontaneous RR –> Good: < 30/min. No good: > 35/min. Minute vent (VE) –> Good: < 10 L/min. No good: > 10 L/min  Vd/Vt (nl = 0.3) –> Good: < 0.4. No good: > 0.6.

Ventilatory ability: Vital capacity (nl = 65-75) –> Good: > 15 ml/kg . No good: < 10 ml/kg .

Oxygenation: FiO2 <40 –> Good: < 60%. No good: > 60%.

R-L shunt –> Good: < 20%. No good: > 60%.

Other: Spontaneous TV > 5ml/kg.    RR/TV over 1min of unassisted breathing >2X resting Minute vent. of <100/min.

Sedating Drugs (IV Anesthesia):

Links:   Ramsay Scale:  Indications in ICU:  Adult Meds:  Pediatric:

Guidelines:  Scheduled bolus injections or continuous infusions of morphine or lorazepam should be administered in pt’s receiving propofol for >72h.  The level of sedation should be monitored using the Ramsay Scale.   Pt’s should be awakened from sedation qd to asses respiratory and neurologic function.    Morphine for analgesia should be used in any pt with perceived agitation secondary to pain.

Ramsay Scale for Assessment of Sedation:

Level/score:  1 –> anxious and agitated.  2 –> cooperative, oriented, tranquil.  3 –> responds only to verbal commands.  4 –> asleep with brisk response to light stimulation.  5 –> Asleep with sluggish response to stimulation.  6 –> Asleep w/o response to stimulation.

Bispectral Index (BIS):  Uses EEG leads.

Indications for Sedation in ICU:  pt is danger to self/ others, anxiety is worsening the underlying pathology, initial ETT tolerance, NMB, part of program to restore day/night cycling, protection from withdrawal syndromes.    Contra: respiratory insufficiency, CV instability, specific drug intolerance, need for “barnacle therapy (unwanted meds).

Ddx of ICU Agitation:  hypoxia, hypercarbia, hypoglycemia, encephalopathy, drug/ ETOH withdrawal, CNS catastrophes, ICU psychosis, pain, anxiety or disorientation.

Ultrashort-acting Barbiturates:   Can be used as an anesthetic induction agent.

Thiopental (Pentothal): 2-5mg/kg over 30-45s.  Onset 45s, DUO 5-10min.    SE: myocardial/respiratory depression, peripheral vasodilation.  Decreases cerebral blood flow and ICP.   Use cautiously if CAD or shock.

Methohexital (Brevital): 1mg/kg.  Immediate onset, used for induction and intubation.   SE:  myocardial depression, hypotension.

Contra: porphyria.

Narcotics:  Naloxone (Narcan): to reverse –> 0.1-2mg IV, titrate to response, may repeat in 2-3min intervals to max of 10mg.

Fentanyl (Sublimize): 0.4mg/kg IV.  50-75X more potent than morphine.  Minimal myocardial effects. Duration of analgesia is ~1h.   SE:  respiratory depression, muscle rigidity, hypotension, bradycardia, truncal rigidity (“wooden chest”).   Reverse with Naloxone (0.4mg/kg IVP).   Analgesic dose @0.05-0.1mg (2-10ug/kg) (1-2ml).

Morphine Sulfate (MSO4): 2.5-15mg IV.  SE: hypotension, bradycardia, biliary tract spasms.

Meperidine (Demerol): 0.5-2mg/kg IV/IM/PO.

Benzodiazepines:   Good amnesia.

Diazepam (Valium): 10mg IM 1-2hr pre-op or 5-10mg slow IVP for sedation.  Give 5-10mg q2-4h.  Onset in 1-5 min.  with caution in elderly.  SE: respiratory depression, disorientation, unpredictable IM absorption.  Inexpensive, but long T-½.

Midazolam (Versed): 0.1-0.2 mg/kg deep IV, onset 1-3min, IM/IV 1-2hr pre-op for sedation.   Can give constant infusion of 50-100mg/100ml D5W or NS.  1-5mg/hr.Short DUO, predictable IM absorption, anterograde amnesia.  Reduce dose 50% in elderly. SE: hypotension, respiratory and CV depression.

Lorazepam (Ativan): 0.05mg/kg (max 4mg) IM 2hr pre-op.  Contra: egg allergy. 1-4mg IV push q1-6h. No active metabolites, expensive.

Other Agents:  Ketamine (Ketalar): 1.5-5mg/kg (max 13mg/kg) IM, onset 4-10min.   0.5-1mg IV (max 4.5mg/kg).  Onset 45s-7min.  Dissociative anesthetic with good analgesia.  Maintains hypoxic pulmonary vasoconstrictor reflexes.  Does not relieve visceral sensation.  Useful in burn, peds, thoracic surgery.  Has bronchodilator effect (safe is asthma).  SE:  tachycardia, HTN, inc ICP, inc CO and myocardial O2 demand.  Inc Saliva.  Respiratory depression.  Hallucinations can be avoided by pre-treatment with benzo. 20% have unpleasant dreams on waking.  Contra:  HTN, eclampsia, inc ICP, cardiovascular dz.

Propofol (Diprivan): 2-2.5mg/kg.  Start at 5 ug/kg/min infusion, titrate by 5-10 ug q5-10min to maintenance infusion of 5-50 ug/kg/min.   Hypnotic, onset in 45s.  Very short acting (may awaken in 8-15 min, Vs 60-90 min with Midazolam).  Pharmacokinetics not changed by chronic hepatic or renal failure.  Lacks analgesic and amnestic properties. SE: hypotension, may be painful to inject unless preceded by IV lidocaine (max dose of 4mg/kg). Should be used for no longer than 72h.  “Milk of Amnesia”.  Has 1.1 fat cal/ml.  Do not use for pediatric ICU sedation.

Etomidate:  0.2-0.4mg/kg IV.   Onset in 30-90sec.  For induction and intubation. Minimal BP effects.  SE:  inc/dec BP, adrenocortical suppression.

Neuroleptic Analgesia:  Combo of tranquilizer and narcotic analgesia.

Droperidol + Fentanyl (Innovar):  50:1.  A preanesthetic, causes amnesia, analgesia, somnolence w/o unconsciousness.

Haloperidol (Haldol):  a butyrophenone, DA agonist-antagonist.  Can be given IM/PO/IV.  Causes CNS depression at subcortical levels (midbrain and RAS).  Has antiemetic properties.  Onset in minutes IV @2.5-5mg, 10min IM, 2-3h PO.  Start at 2-5mg, increase by 5mg q20min until agitation subsides.  Repeat doses q4-6h around the clock.  Can rarely cause tardive dyskinesia, NMS, dystonic reactions. T-½ of 18-54h.

Scopolamine:  3-6ug/kg.  Onset in seconds, last 2-3h, hepatic metabolism.  A natural antimuscarinic from belladonna plant.  A mydriatic, antisialogogue,  bronchodilator, vagolytic, anhidrotic.  No cardiac depression.  Can be used as ICU sedation.

Conscious Sedation in Ped’s:   Included for the purpose of completion.  All conscious sedation should be done in a hospital setting under proper monitoring with anesthesiology.

Indicated for:  BM aspiration, cardiac cath, BAE potentials, CT, dental procedure, echo, endoscopy, EEG, laceration repair, liver Bx, LP, ortho manipulation, sexual abuse exam, wound debridement, VCG.

Ketamine:  6mo-8yo, 4mg/kg IM + 0.01mg/kg Atropine Sulfate (IM/IV).  Or PO 6-10mg/kg or IV 0.5-1mg/kg.   Get vitals q5min until discharge. Onset in 3 min, lasting ~80 min, gives a Dissociative, trancelike state with rare respiratory depression, usually increasing the HR and BP from catecholamine release.   SE:  Bad dreams and hallucinations rare in children (1-2%) The inc airway secretions (hypersalivation) dec by anticholinergics like atropine or glycopyrrolate.  Excellent for burn patients needing dressing changes.

Compared to IM MCP: (2mg/kg meperidine, 1mg/kg promethazine, 1mg/kg chlorpromazine with respiratory depression, dystonic reaction, lowered sz threshold) (Arch Ped & Adol 1996, 150).

For IV: use 1-2mg/kg (additional 0.5-1 prn) Ketamine and 0.05-.1mg/kg Midazolam (max 4mg) for reduced dysphoric reactions and 90% optimal sedation. (Peds 1997:99).

Chloral Hydrate: sedative/ hypnotic, onset 15-60min, DUA: 2-8hr, dose: 50-100mg/kg (max 2000mg) PO/ PR.  SE: paradoxical hyperactivity, N/V.  Most effective for children <2yo an radiological studies.  Not good for suturing or other “noxious” procedures.  Best to have pulse ox as respiratory depression at high doses.  Unpredictable GI absorption rate.

Nitrous Oxide: 50/50 mix of 02 and NO (Nitrox).  Inhalation, short term use only.   Not a good analgesic, but effective sedation.  SE:  N/V.

Fentanyl (Sublimaze): 1-2ug/kg IV (max 5uf-kg), onset in 2-3 min, DUA: 45-60min.  SE:  respiratory depression, chest wall rigidity. Lollipop: 200, 300, 400ug doses.  Great for BM bx’s.

Midazolam (Versed): 0.05-0.15mg/kg IV onset in 3-5min, DUA: 1-2 hr.  Can also add to juice @0.5-1mg/kg PO or slowly drip into nostrils @0.2-0.5mg/kg or give IM.  SE:  respiratory depression if used in combination with opiates.

Methohexital (Brevital): 1-1.5mg/kg IV lasts 5 min.  Can be given rectally via an 8F feeding tube at dose of 25mg/kg (max 500mg) 15 min before a procedure such as CT scan.  (Pediatrics 2000;105:1110-4)

Reversal:  Flumazenil (Romazicon) @0.01 mg/kg or 0.2mg IV –> Benzo’s.    Narcan (Naloxone) @ 0.1mg/kg (max 2mg) IV/ IM –> Opioids.

Demerol-Phenergan-Thorazine (DPT): IM, unpredictable.

**Ref:  (Mechanical ventilation. Hosp Med 1999;12:26-36) (Weaning from mechanical ventilation–the team approach and beyond.  Intensive Care Med. 1994;20:317-8) (Issues in ventilator weaning.  Chest. 1999;115:1215-6) (Clinical management of weaning from mechanical ventilation.  Intensive Care Med. 1998;24:999-1008) (Weaning from mechanical ventilation. N Engl J Med. 1991;324:1496-8) (Hospital Medicine, by Wachter, 2000, Lippincott, p108-112) (Sedation in the intensive care unit, a systematic review. JAMA 2000;283:11) (Prolonged sedation with midazolam or propofol.  Crit Care Med. 1997;25:556-7) (Mechanical ventilation. Hosp Med 1999;12:26-36)

Vascular Access:

Links:  Venous cutdown:   Arterial Lines:   Femoral Artery:   Central Lines:  Vascular Anatomy:  EJ:   IJ:   SC:   PA Cath:   Pulmonary & Cardiac Parameters:   PA Cath Patterns:   CVP:  Catheter Sizes:

Venous Cutdown:

Equipment: a prepackaged cutdown tray, or a minor procedure tray and instrument tray with a silk suture (3-0, 4-0) and a catheter. Sterile gloves, sterile towels/drapes, 4 x 4 gauze sponges, povidone-iodine solution, 5 ml syringe, 25 gauge needle, 1% lidocaine with epi, adhesive tape, scissors, needle holder, hemostat, scalpel and blade, suture.

Step #1: Apply a tourniquet proximal to the site, and identify the vein. Prep the skin with povidone-iodine solution and drape the area. Infiltrate the skin with 1% lidocaine, then incise the skin transversely.

Step #2: Spread the incision long-wise in the direction of the vein with a hemostat and dissect any adherent tissue from the vein. Lift the vein and pass two chromic or silk ties (3-0 or 4-0) behind the vein.

Step #3: Tie off the distal suture, using the upper tie for traction. Make a transverse nick in the vein. If necessary, use a catheter introducer to hold the lumen of the vein open.

Step #4: Make a small stab incision in the skin distal to the main skin incision, and insert a plastic catheter or IV cannula through the incision, then insert it into vein. Tie the proximal suture, and attach IV fluid, release the tourniquet.  Suture skin with silk or nylon, and apply dressing.

Arterial Line Placement:  Link:  Femoral Artery:

Indication:  continuous monitoring of arterial pressure, serial ABG/ lytes/ Hct/ glucose measuring.  Informed consent is required.

Contra: poor collateral circulation (Allen test), local infection, need for AV fistula or shunt, bleeding d/o.

Equipment:  20 g 1 ½-2″ catheter over needle assembly (Angiocath), arterial line setup (transducer, tubing and pressure bag containing heparinized saline), arm board, sterile dressing, lidocaine, 3ml syringe, 25g needle, 3-O nylon suture with curved cutting needle.

Step #1:  Use the Allen test to verify patency of the radial and ulnar arteries. Immobilize the wrist on an arm board with a gauze (Kerlix) roll behind the wrist to maintain hyperextension.   Prep the skin with povidone-iodine and drape, infiltrate with 2-3ml of 1% Lido using a 25g needle down to the periosteum on either side of the artery, aspirating before each injection.

Anatomy:  The radial artery runs deep along the lateral aspect of the volar forearm between the radial styloid and flexor carpi radialis tendon.  Max pulsation is usually 1-2cm proximal to the transverse wrist crease.  Choose site where the artery appears most superficial and distal.  Have the pressure tubing flushed with heparin and calibrate the transducer.

Step #2:  Palpate the artery with the left hand, and advance (“dart”) the catheter-over-needle assembly into the artery at a 30-45 deg angle to the skin. When a flash of blood is seen, hold the needle in place and decrease the angle to 25 deg as advance the cath into the artery. Occlude the artery with manual pressure while the pressure tubing is connected.   If no blood is seen slowly advance until hit periosteum, then slowly withdraw to just under the skin before re-aiming.   If after the artery has been entered and are unable to thread the cath or a hematoma forms, withdraw everything and hold pressure for 10min.

Step #3: Advance the guide-wire into the artery, and pass the catheter over the guide-wire. Hook up and look for the sharp arterial tracing.  Suture the catheter in place with 3-0 silk and apply dressing.

F/u: check pt q4h for perfusion, change dressing qd. Change cath q3-4d.

Femoral Artery A-line:

Equipment:  19-20 g Teflon catheter, ~16cm (6 in)long.  A flexible guidewire small enough to pass through the catheter and needle

20-gauge needle, ~5cm long.   IV fluid and tubing.

Procedure:  Step #1: Locate the femoral artery approximately 2cm below the inguinal ligament or near the inguinal fold.

Femoral Triangle –> NAVEL –> Lat to Med.  Nerve, Artery, Vein (to draw blood, stick the needle medial to the artery), Empty (femoral canal/ hernia), Lymphatics.  Shave the groin and cleanse/prepare the area with Betadine X 3, don a mask and sterile gloves, drape the area.

Step #2: Anesthetize the area of insertion with 1% lidocaine. Place your 2nd, 3rd and 4th fingers along the course of the femoral artery beyond the inguinal ligament, the index finger is held slightly apart.   Step #3: Insert the needle between your index and middle fingers using the Seldinger technique, enter the skin and artery at 45degs.  When a free flow of blood spurts from the end of the needle, insert the wire through the needle (or catheter-over-needle) well into the artery, then remove the needle (should be no resistance).  (If the artery is not entered, insert the needle deeply until it can go no further then slowly withdraw the needle until free arterial flow is obtained).

Step #4: remove the needle and insert the catheter over the wire then remove the wire and attach the connecting tubing.  Be sure to have control of the wire at all times.  Note: if the artery is not entered, withdraw the needle completely, redetermine the location of the artery and make another attempt.  If the artery is entered but the wire/catheter cannot be passed, remove the needle and hold pressure for 5-10minutes before making another attempt.  Step #5:  Connect to IV tubing then suture the catheter in place, the cover the insertion site with povidone-iodine and a sterile dressing.

Complications:  Thrombosis, particularly if pt has peripheral vascular disease or after repeated attempts or following excessive pressure to control bleeding; the larger the catheter used, the greater the incidence.   Embolism from a thrombus that formed around the Cath may embolize to the lower leg producing gangrene, thus if any loss/weakening of lower extremity pulses, remove the Cath.   Hematoma and hemorrhage can be minimized by holding pressure over the femoral artery for 10min after removing the catheter, do not obliterate the pulse since that can lead to thrombosis.  Arteriovenous fistula may occur when large catheter is used.

Central Venous Lines:  Links: Types: Complications:

A catheter placed in a major vein such a subclavian, internal jugular or femoral.  Indications:  Monitoring of central venous pressures (CVP) in shock or heart failure, management of fluid status,  insertion of a transvenous pacemaker, administration of long term TPN, administration of irritant meds (chemotherapeutic agents), hypovolemia an unable to perform peripheral Cath.    Contra:  no absolute.  Avoid preexisting site infections, anatomic anomalies, coagulopathy.

Vascular Anatomy:

Complications: vessel trauma, thrombosis, PTX, nosocomial infection (line sepsis), cardiac dysrhythmia, air embolism, hemorrhage/ hematoma formation, catheter embolism.  The line is changed every 4-7 days, sooner if sx’s of septicemia, or local infection.

Placement:  Seldinger Technique: placement of a central line by first placing a guide wire in the vein, then the catheter over the wire.  Tip should be outside the heart (except PA catheter), stopping in the SVC 3-5cm above R atrium.  Some have tips that measure a R atrial ECG such that it has a maximal P-wave amplitude at entry into the atrium, catheter is then pulled back 3cm.   External jugular or internal jugular approach is preferable in pt’s with coagulopathy or thrombocytopenia because of the ease of external compression for hemostasis. In patients with unilateral lung pathology or a chest tube already in place, the catheter should be placed on the side of predominant pathology or on the side with the chest tube if present.

X-ray:  Catheter should be located well above the right atrium, and not in a neck vein.  Ideal location is distal to the innominate or in the proximal SVC.  Cardiac tamponade or arrhythmia if tip erodes the cardiac wall.  (Can check a lead II, if in the R atrium will see huge P waves.  Rule out PTX by checking that the lung markings extend completely to the rib cages on both sides. An upright, x-ray may be helpful, examine for hydropericardium (“water bottle” sign, mediastinal widening).

Pulmonary Artery Catheter:  tips should be located centrally and posteriorly, and not more than 3-5 cm from midline.

Estimation of insertion length:  R subclavian:  (Ht in cm/ 10) — 2cm.   For R IJ, just use Ht —10cm.

Types:  Links:  EJ:   IJ:   SC:

Femoral Venous:  Associated with a higher risk of infection and throbotic complications compared to sites in the upper extremity veins.  Major femoral or retroperitoneal hematoma in up to 1.3% of cases, infectious complications in 19.8% Vs 4.5% (JAMA 2001;286:700). For anatomy see:  Femoral Artery:..For technique use the Seligner technique as with other central venous catheters.

Hickman-Broviac Catheter:  double-lumen catheter, the smaller Broviac line is often used for the administration of IV therapy; the larger Hickman line is reserved for additional venous access and blood withdrawal. This catheter is generally inserted into the cephalic, subclavian, external, or internal jugular vein with the distal tip advanced to just above the right atrium. The proximal end exits via a subcutaneous tunnel from the lower anterior chest wall. A felt cuff (Dacron) is used to anchor it in place subcutaneously . The Hickman-Broviac catheter is made of polymeric silicone rubber that is of low thrombogenic potential but extremely flexible and soft. Because of the pliability of the material, the catheter must be treated gently. Clearing an obstructed catheter with a guidewire may cause catheter perforation. Similarly, forcing fluid through the catheter by positive pressure is contraindicated because of the risk of catheter rupture or catheter embolus. For this reason, no syringe larger than 5 ml should be used for irrigation.  Routine Care and Use. This line should be irrigated with 6 ml of normal saline solution between different infusions to prevent mixing of incompatible solutions, development of precipitation, and resultant catheter occlusion. The larger Hickman line should be used to withdraw blood. This line should be irrigated with 6 ml of heparinized saline after blood withdrawal to prevent clot formation in the catheter lumen. When a clamp is used, it should be placed over a piece of tape wrapped around the line. The clamp should have a smooth surface; those with teeth or prongs may sever or abrade the line.

Cook / Vygon/ Bard: external central line tunneled under the skin with a cuff (to prevent bacterial contamination and to hold in place).  Commonly used as widespread, experienced use.  Needs regular flushing with heparin (50 u/ml) weekly.  Inexpensive, but higher risk of infection than other long-term access lines, may interfere with activities.

Subcutaneous Ports:  Portacath:  the port is buried under the skin and thus must be accessed percutaneously.  Need special needles.  Infection worse if it occurs.  Expensive but low maintenance.  Flush with heparin (100 U/ml) qmo.

Mediport: has an injection port with the catheter.

Groshong:  a single thin-walled silicone rubber catheter designed for prolonged venous cannulation that differs from the Hickman-Broviac catheter in insertion, design, and maintenance. A decreased outer diameter-to-inner diameter ratio allows insertion into a smaller vein through a smaller introducer sheath. The catheter can be inserted at the bedside under local anesthesia without fluoroscopy using the Seldinger technique and a peel-away catheter introducer sheath. After placement of the catheter in the subclavian, internal, or external jugular vein, a subcutaneous tunnel is created with a stainless steel tunneling device through which the catheter is threaded. A cuff (Dacron) stabilizes the catheter’s placement in subcutaneous tissues and reduces the chance of inadvertent removal or retrograde infection.  The Groshong catheter is constructed with a closed end and a vocal cord-type integral valve at the distal end . This pressure-sensitive two-way valve at the intravascular end minimizes back-bleeding, eliminating the need for heparin flushes or external clamping, but permits blood sampling with gentle negative pressure. Patency of the catheter is maintained with 5 ml of saline flush once a week. A 20 ml saline irrigation is necessary after any blood transfusion or if blood is observed in the catheter lumen. A 30 ml saline irrigation is performed before blood sampling after infusion of hyperalimentation solutions.  Groshong catheters offer the advantage of bedside placement, minimal back-bleeding, elimination of heparin flushes, and elimination of external clamping when changing injection caps or connecting tubing. A lower incidence of complete obstruction to flow from clots or precipitants within the catheter lumen, however, has not been proved.Groshong catheters are otherwise subject to the same complications as described for Hickman-Broviac catheters.  Less frequent need for flushing, can use saline flush qwk, less risk of bleeding or air embolism with valve.  Easier to insert percutaneously, but smaller than a Hickman.

Quinton-Mahurkar Catheter:  the method of choice in providing immediate vascular access for hemodialysis. Its advantages include bedside placement and a functional life up to 18 months.  The Quinton-Mahurkar catheter is a single flexible polyurethane cannula with two separate D-shaped channels. Each lumen is connected by a molded Y-piece to a color-coded external port. As a precaution against a disconnected cap, each limb of the Y-piece has an attached clamp. The Quinton-Mahurkar catheter is most commonly placed in the subclavian vein and less commonly in the femoral vein by the Seldinger technique.

Apheresis: Large bore, permits high blood flow rate.   Flush with heparin (100 u/ml) 2X/wk.  Uncomfortable to pt, limited line survival.

Cimino-Brescia Fistula and Prosthetic Bridge Fistula:  the preferred means of vascular access for long-term hemodialysis. The fistula is created by using a side-to-side and side-to-end anastomosis using the radial artery and the cephalic forearm vein. The high blood flow and pressure on the venous side of the fistula “arterialize” the veins, a process that takes 3 to 5 weeks.

Complications of Catheters:   Erosions: of endocardium may cause perforation in 1-7 days if tip in contact with the heart.  Presents as dyspnea, pleural effusion, tamponade.

Catheter Sepsis:  Presents with F/C, leukocytosis and glucose intolerance.  If s/s of infection in pt, check CBC and UA.  If blood Cx needed, use a peripheral vein.  If no evidence of infection at catheter site can leave intact.  If blood Cx is +, remove catheter.  If blood Cx are negative, can change catheter over a wire and culture tip (bacteria and fungal).  Wait 24h before starting a new line, obtain blood cultures X3d to r/o recurrent bacteremia or fungemia.  If marked hyperpyrexia or hypertension remove all catheters.

Approach to Catheter Occlusion: clots/ precipitants within the catheter lumen, and mechanical obstruction. Cath that painlessly accept infusions at normal rates but cannot be aspirated, consider: cath lodged against the wall of the vessel, occluding fibrin sheath around the cath tip, ball valve or mural thrombus, and central vein thrombosis.   Pt’s who have intermittent complete occlusion and withdrawal occlusion have a type of mechanical obstruction called “pinch-off syndrome.” Clots within the catheter lumen, obstructing fibrin sheaths, and ball valve/mural thrombus often respond to low-dose intracatheter urokinase; central vein thrombosis, precipitants in the catheter lumen, and mechanical obstruction do not.   Precipitants within the catheter lumen are most commonly the result of failure to clear the line with saline after total parenteral nutrition and flushing of the line with a heparin solution instead. Heparin combines with total parenteral nutrition fluid-producing precipitants. Clots within the catheter lumen most commonly result from failure to flush the line with a heparinized saline solution after blood aspiration.  A CXR to confirm catheter position and integrity, the tip should be positioned just above the right atrium.  If the catheter is lodged against the vessel wall, the pt’s changing body position, raising the arms above the head, or performing a Valsalva maneuver may relieve withdrawal occlusion. If this is unsuccessful:   try low-dose intracatheter Urokinase (5,000 U) should be injected into the catheter and left for 30 minutes before aspiration is again attempted. If it is unsuccessful, a second dose of urokinase can be injected and the procedure repeated. Contra to thrombolytic agents should be considered, although low-dose therapy for occluded catheters appears well tolerated.   Mechanical obstruction can be due to a variety of causes, including pinch-off syndrome, in which the catheter lumen is compromised as the result of mechanical forces acting on it between the clavicle and the first rib. The catheter is intermittently obstructed during both administration and withdrawal of fluids. A chest roentgenogram demonstrates narrowing of the catheter lumen as it passes between the clavicle and the first rib. This condition is most commonly detected within 3 weeks after catheter placement; the catheter must be removed because of the frequency of fragmentation or embolization if left in place.   Because engorged collateral circulation or swelling in the affected extremity is not universally present with subclavian vein thrombosis, this diagnosis should be considered in all patients who are unresponsive to declotting attempts. Catheter removal and systemic heparinization or maintenance of the catheter’s placement and treatment with high-dose thrombolytic therapy is a therapeutic option for subclavian vein thrombosis.  Mechanical occlusion is rare and requires catheter replacement with a surgical approach. Because of variations in approach by different consultants, it is recommended that the EP seek early consultation in patients who have occluded central venous catheters.

Catheter-Related Infections:   categorized as local or systemic. Local infections primarily involve the skin and subcutaneous tissues surrounding the exit site with erythema, tenderness, and no clinical or laboratory evidence of sepsis. Skin organisms are primarily responsible for local infections, especially coagulase-negative staphylococci. Studies show that local infections usually do not require catheter removal and resolve with antibacterial therapy alone.   The source of systemic infection are urinary tract, anorectal area, upper respiratory tract, and, finally, central venous catheter. The most common organisms causing catheter infection are coagulase-negative staphylococci, S. aureus, and Candida albicans. In immunocompromised pt’s, G+ have now replaced G- bacteria as most often responsible for sepsis. Accordingly, initial empiric therapy should include an antistaph drug, in addition to G- coverage.  Get Bx X2 with Bx drawn simultaneously through the cath and from a peripheral blood vessel may assist in determining whether the cath is the source of infection. Studies now indicate that infections that do not extend through the vessel wall (“pericatheter infections”) can be successfully treated without catheter removal. Catheter removal is mandatory in patients with continued positive blood culture results despite therapy and in those with vascular access infections caused by Candida species. Catheter-related septic central venous thrombosis can progress through and around the vessel wall to cause a perivascular infection or abscess.  This rare but devastating complication is associated with serious morbidity and a reported mortality as high as 83%.  Because of the lack of specific clinical findings, the most prominent diagnostic feature is continued bacteremia after catheter removal. Diagnosis is confirmed by venography or CT scan.  Removal of the catheter, IV administration of antibiotics, and anticoagulation constitute appropriate initial therapy. Surgical treatment with thrombectomy and possible abscess drainage is indicated after failure of an adequate course of antibiotics and anticoagulation. Several studies have used thrombolytic agents as an adjunct to the management of catheter-related septic venous thrombosis, but the risk-to-benefit ratio of this approach has not been established. In patients who require removal of the catheter, a quantitative culture of the number of organisms on the surface of the removed vascular catheter correlates well with a positive blood culture result for the same organism.  This technique involves rolling the catheter on a culture medium. Broth culture of catheter tips may be less reliable in determining whether the catheter is the source of infection.

External Jugular (EJ) Vein Catheter:

Advantages:  it may be utilized in pt’s with clotting abnormalities, it is part of the surface anatomy, has minimal risk of PTX.

Disadvantage: it often takes an unpredictable course into the central compartment as there is a sharp angle where it emerges from the subclavian leads to 15% entering arm or looping cephalad.

External Jugular V:  Often can visualize the vein surface.  Safer in cases of coagulopathy, less risk of PTX.  Can be difficult to get into central vein as the catheter often turns into the subclavian.

Equipment: prep solution, drapes, gloves, mask.  A short intracath 8-12 inches and suture to secure catheter.  A J-wire and a scalpel.

Step #1: The right side is best. Pt is supine in 15 deg Trendelenburg with head turned away from the side of approach (distends the vein and minimizes air embolism). Locate the EJ, it runs from the angle of the mandible infero-laterally to the clavicle, crossing the sternocleidomastoid (SCM) 5cm above the clavicle, then behind the clavicle to join the subclavian. Cleanse skin with Betadine X3. Sterile technique, inject 1% lidocaine to produce a skin weal.  Apply digital pressure with your index finger to the external jugular vein above the clavicle to distend the vein and keep it from rolling. The valsalva maneuver may help locate the vein.

Step #2: :  With a 16-gauge thin wall needle enter with a firm and quick thrust where it courses over the anterior portion of the clavicular head of the SCM above the clavicle.  Advance the needle in the axis of the vein at 200 to the frontal plane.  Expel the skin plug once through the skin.   Once see free backflow of blood advance and additional 2mm.  Insert the J-wire (soft, flexible end first) through the needle and advance.  If any resistance is met, tilt (not rotate) to the head to straighten the IEJ as it enters the subclavian vein.   Never force it.

Step #3: Remove the needle, maintaining control over the guide wire at all times.  Make a small incision with a No. 11 scalpel blade to facilitate entry of the catheter, thread the catheter over the J-wire and into place (be sure to always have control of the wire).

Step #4: Remove the guide wire after the catheter is in place. Cover the catheter hub with a finger to prevent air embolization.  Suture catheter in place with 2-0 silk suture and tape. Attach the catheter to intravenous infusion. Check CXR to r/o hemothorax or PTX. The catheter should be replaced weekly or if there is any sign of infection.

Complications:  tearing of the subclavian vein by the wire or catheter (avoidable with careful technique). Internal carotid puncture, must apply local pressure for 10min.

Internal Jugular Vein:

Relatively contraindicated in patients with carotid bruits, stenosis, or aneurysm.   The right side is better as can access ( “straight shot”) R atrium w/o encountering major angles.

Advantage: less risk of pleural puncture, easy to compress a hematoma, easy landmarks.

Disadvantages: difficult to cannulate if hypovolemic, a “blind” puncture, risk of carotid injury, restriction of the pt’s neck mobility.

Anatomy: positioned behind the sternocleidomastoid muscle lateral to the carotid artery. The catheter should be placed at a location at the upper confluence of the two bellies of the sternocleidomastoid, at the level of the cricoid cartilage.

Step #1:  Place the patient in Trendelenburgs position and turn the patient’s head to the contralateral side.  Choose a location on the right or left. If lung function is symmetrical and no chest tubes are in place, the right side is preferred because of the direct path to the superior vena cava. Prepare the skin with Betadine solution using sterile technique and a drape. Infiltrate the skin and deeper tissues with 1% lidocaine.

Step #2:   3 main approaches:   All use the same landmarks, but differ in entry site and needle angle. While aspirating, advance the 22g scout needle until the vein is located and blood flows back into the syringe.

Anterior –> Enter at the midpoint of the sternal head of the SCM, ~5cm from both the angle of the mandible and the sternum.  Palpate the carotid and enter at 40 deg angle 1cm lateral and parallel (directed caudally and toward ipsilateral nipple).  Hit IJ in 2-4cm.

Posterior –> Enter 1cm dorsal to where the EJ crosses the posterior border of the clavicular head of the SCM (~5cm cephalad of the clavicle). Direct needle caudally toward the sternal notch at 45 deg angle.  Hit IJ in 5-7cm.

Central –> Skin puncture is at the apex of the triangle formed by the two bellies of the SCM and the clavicle.  Needle enters at 40 deg angle with the frontal plane and directed toward the ipsilateral nipple.  Hit IJ in 3-5cm.

Step #3: Now can either remove the finer “scout” needle and advance a 16-gauge, thin wall catheter-over- needle (directly above it)  with an attached syringe along the same path as the scout needle. Or remove the finer needle and introduce the larger one in the same plane.  When back flow of blood is noted into the syringe, advance the catheter into the vein. Remove the needle and confirm back flow of blood through the catheter and into the syringe. Remove the syringe, and use a finger to cover the catheter hub to prevent air embolization.

Step #4: With the 16 g catheter in position, advance a spring guide wire (0.89 mm x 45 cm) through the catheter. The guidewire should advance easily without resistance. With the guidewire in position, remove the catheter and use a No. 11 scalpel blade to nick the skin.

Step #5: Place the central vein catheter over the wire, holding the wire secure at all times. Pass the catheter into the vein, remove the guidewire, and suture the catheter with 0 silk suture, tape, and connect it to an IV infusion. Obtain a CXR to rule out PTX and confirm position of the catheter.

Subclavian Vein:

Advantage: remains open even with profound circulatory collapse.  Less restricting to the pt. Good choice in emergency situation as placement will not interfere with airway management.

Disadvantage: Has increased risk of PTX in patients with emphysema or bullae as the pleural space is easily entered with the “blind” stick. Difficult to apply pressure if the artery becomes punctured.   It is located in the angle formed by the med 1/3 of the clavicle and the first rib.

Step #1: Position the patient supine with a rolled towel located between the patient’s scapulae, and turn the patient’s head towards the contralateral side. Prepare the area with Betadine X3, using sterile technique, drape the area and infiltrate 1% lidocaine into the skin and tissues.

Step #2: The needle enters at the tubercle of the clavicle, palpated on the inferior surface ~1/3 to 1/2  the length of the clavicle form the sternum.  Depress under the clavicle distal to this area with your thumb as your pointer finger rest at the angle of Louis.   Advance the 16-gauge catheter-over-needle, with syringe attached until the clavicle bone and needle come in contact.

Step #3: Slowly probe (walk) down with the needle until the needle slips under the clavicle, and advance it slowly (should feel no resistance) towards the finger resting on the sternal notch at a 25 deg angle to the thorax (parallel to the bed).  Keep bevel pointed inferomedial to encourage the guidewire to enter the innominate vein.  Advance until see a back flow of venous blood enters the syringe.  Remove the syringe, and cover the catheter hub with a finger to prevent air embolization. Ask the pt to hum or hold breath as you pull the needle out and cover it.

Step #4: With the 16-gauge catheter in position, advance a 0.89mm x 45cm spring guide wire through the catheter. The guide wire should advance easily without resistance.  With the guide wire in position, remove the catheter, and use a #11 scalpel blade to nick the skin.

Step #5: Place the central line catheter over the wire, holding the wire secure at all times. Pass the catheter into the vein, and suture the catheter with 2-0 silk suture, tape, and connect to an IV infusion. Check CXR to confirm position and rule out PTX.

Pulmonary Artery Catheterization:  PA Cath Patterns:

Contra: none are absolute.  Preexisting site infection, known or suspected anatomic abnormality, coagulopathy, LBBB, pulmonic stenosis, pacemaker wires. Step #1: Using sterile technique, cannulate a central vein using one of the above techniques.   Step #2:  Advance a guide wire through the cannula, then remove the cannula, but leave the guide wire in place. Keep the guide wire under control at all times. Nick the skin with a number #11 scalpel blade adjacent to the guide wire, and pass a number 8 French introducer over the wire into the vein. Remove the wire and connect the introducer to an IV fluid infusion, and suture with 2-0 silk.

Step #3: Pass the proximal end of the pulmonary artery catheter (Swan Ganz) to an assistant for connection to a continuous flush transducer system.    Step #4: Flush the distal and proximal ports with heparin solution, remove all bubbles, and check balloon integrity by inflating 2ml of air. Check pressure transducer by quickly moving the distal tip and watching monitor for response.

Step #5: Pass the catheter through the introducer into the vein, then inflate the balloon with 1.0ml of air one passed the introducer, and advance the catheter until the balloon is in or near the right atrium. The catheter is marked at 10cm intervals to aid in determining the depth of insertion.  Step #6: The approximate distance to the entrance of the right atrium is

determined from the site of insertion:  Right IJ vein –> 10-15 cm.  Subclavian vein –> 10 cm.  Femoral vein –> 35-45 cm.

Step #7:  Advance the inflated balloon, while monitoring pressures and wave forms as the PA catheter is advanced. Watch for ventricular ectopy during insertion. Advance the catheter through the right ventricle into the main pulmonary artery until the catheter enters a distal branch of the pulmonary artery and is stopped (as evidenced by a pulmonary wedge pressure waveform).

Other: Do not advance catheter while the balloon is deflated, and do not withdraw the catheter with the balloon inflated. After placement, obtain a chest X-ray to ensure that the tip of catheter is no farther than 3-5 cm from the mid-line, and no PTX is present.  It shouldn’t take >1ml to wedge.  Measures pulmonary venous pressure ~= L atrial pressure ~= LV end-diastolic pressure, false readings if have mitral stenosis.  Also uses a Thermaster to determine cadiac parameters via temperature dilution.  Give a bolus of fluid to R atrium (CVP port) at room temp, simultaneously measure temp in pulmonary artery (tip), there is a smaller temp change with inc cardiac output.  False readings with TR and VSD.

**Ref:(Irwin and Rippe’s Intensive Care Medicine, 4th ed, 1999, Lippincott-Raven) (Infections related to central venous catheters.  Mayo Clin Proc. 1990;65:979-86) (Intravenous and central catheter infections.  Surg Clin North Am. 1994;74:557-70) (Central venous catheter placement and complications.  Crit Care Med. 1994;22:1516-18) (Arterial cannulation: how to do it. Br J Hosp Med 1997;57:497-9) (Arterial cannulation. Anesthesia 1995;50:576)

Normal Pulmonary Artery Catheter & Cardiac Parameters:  Link: PA Cath Patterns: PA Cath:

Directly measured and most important are the CO, PAP and PCWP.

Fick Principle:  the uptake of a substance by an organ is a product of blood flow and the arteriovenous (A-V) substance difference across the organ.  For CO = 100 X O2 Consumption / (arterial O2 content – venous O2 content).  The blood O2 content (Vol %) is calculated from the saturation % X Hemoglobin (g/dL) X 1.36.  Venous blood is from the PA, arterial blood is from the periphery.

Cardiac Output (CO): HR X stroke volume.  Nl = 3.5-8 L/min. Total body perfusion.    CO l/min = 125 mL O2 /min/M 2 x 100 = 8.5 {(1.36)(Hgb)(SaO2 ) – (1.36)(Hgb)(SvO2)}. Measured by either Fick method or thermodilution (invalid with tricuspid regurge). Stroke Volume: CO / HR = 55-100 mL.  Stroke Index:  30-65 ml/beat/m2.   Cardiac Index (CI): CO/ BSA. Nl = 2-4 L/min/m2.  Double Product: (HRXSBP)/ 100. Nl 60-140, relative myocardial O2 use.

Mean arterial Press (MAP):  (SBP + 2DBP) / 3 or [(SBP — DBP)/3] + DBP.  = 85-95mmHg.  End organ perfusion.

Systemic Vascular Resistance (SVR): [ 80 X (MAP – CVP)] / CO. Nl = 700-1600 dynes/sec/cm-5.  Geometry of systemic arterioles.  Calculated value, need to take with a grain of salt.

SVR Index (SVRI): = SVR X BSA (in m2).  Normal SVRI = 2130 +450 dyn/d/cm-5/m2.

Left Ventricular Stroke Volume (LVSV): range of 70-94 ml.   LVSVI (Index): range of 30-65 mL/m2.

Total Pulmonary Vascular Resistance (PVR):  [ 80 X (MPAP — PCWP)] / CO.   = [(PA – PCW) X 80] / CO.  Normal is ~1/6 the SVR = 100-300 dyn/sec/cm-5.  Pulmonary Vascular Resistance is 20-130.  Geometry of pulmonary arterioles.  It is elevated in shunts, myocardial dz, pulmonary vasculature obstruction, hypoxemia, toxins and primary pulmonary HTN.  PVRI = 80 X (mean PAP — PAWP) / CI = 80-240 dynes-sec/cm2/m2.

Arterial O2 Content (CaCO2): (Hgb X 1.36) SaO2 + (PaO2 X 0.0031) = 16-22 ls O2/ dL blood or vol%.

Mixed Venous O2 content (CvO2): (Hgb X 1.36) SvO2 + (PvO2 X 0.0031) = 12-17 mL O2/dL blood.  A measurement of overall tissue oxygenation extraction.  Calculated using the Fick equation after measuring the mixed venous saturation.  Mixed Venous O2 sat (Pulmonary artery):  75%.

Arterial oxygen capacity =(Hg(gm)/100 mL) x 1.36 mL O2 /gm Hg.  O2 carrying capacity is mostly due to Hgb as O2 sats have little affect.

DO2: O2 delivery: CaO2 X CO X 10.   nl = 640-1400 mL/min.

VO2: O2 uptake: C(a-v)O2 X CO X 10.  Nl = 180-280 mL/min.  The best hemodynamic parameter to asses if shock is present.

Oxygen Consumption Index (VO2I): range of 113-148 ml/min X m2.  Arteriovenous O2 Difference:  30-50 ml/L.

Measured Parameters:

Central Venous Pressure (CVP = Right Atrial Pressure): 0-8mmHg. RV preload.  If >11 and in CHF give 80mg Lasix q8hr.

Pulmonary Artery Pressure (PAP) Mean: 9-20 mmHg.  Pulmonary artery SBP (PAS): PAP Systolic: 15-30 mmHg. >35 = pulmonary HTN.  Pulmonary artery DBP (PAD): PAP Diastolic: 4-15 mmHg. Should be a points above the PCWP, can be used instead of a wedge.

Pulmonary Cap Wedge Press (PCWP): 6-12 mmHg (~16 with AMI). Preload of LV, a hydrostatic gradient.  PCWP is the dampened LA pressure (indirect measure of LA pressure) which reflects LVEDP, which reflects LVEDV.   Not a valid measurement when intrathoracic pressure exceeds the distending pressure of the pulmonary capillary bed (parenchymal lung dz, severe volume depletion, pulmonary vascular dz, catheter tip malposition).  Pearls: the diastolic pressures will be = in all 4 chamber with pericardial tamponade or constrictive pericarditis.   Normally the diastolic PA pressure = PCWP (except with pulmonary HTN).   If have an inferior AMI and see a dec CO & PCWP with inc RA pressure you have a RV infarction (check R-side ECG).  If have dec CO with inc PCWP and RA pressure then have biventricular failure due to cardiogenic shock.

Right Atrial (RA) pressure: 1-7 mmHg, if elevated, then suggests RV failure, should see JVD. The mean RA pressure is a measure of both the hydrostatic pressure on the systemic veins & RV end-diastolic (filling) pressure.   RV Pressure (RVP) Systolic: 15-30 mmHg.  RVP Diastolic: 0-8 mmHg = RV end-diastoli.  LV Systolic Pressure: 100-140 mHg.  LV End-diastolic: 3-12 mmHg.  Aortic Systolic @ 100-140, diastolic @ 60-90, mean @ 70-105.

PA Catheter Patterns:

Links:  Conditions:  Swan Orders:  CVP:  Shock:  Pulmonary & Cardiac Parameters:  PA Cath Placement:

PCWP = Wedge pressure = Pulmonary artery wedge pressure (PAWP = LAP, L atrial pressure, in mm Hg, pulmonary artery diastolic pressure may be used instead). Cardiac Index (CI). Pulmonary artery pressure (PAP = MAP).  Central Venous Pressure (CVP = RAP, R atrial pressure).  Systemic Vascular Resistance (SVR):  multiply by 80 to give SI units of dynes/sec/cm-5, normal = 1000 dyn). Almost all above conditions will have inc HR, dec venous compliance (except septic shock), dec CaO2 and dec DO2.

Various Shock States –> CO / SVR/ CVP (RAP)/ PCWP/ O2 consumption:

Hemorrhagic –> dec / inc/ dec/ dec/ inc.

Cardiogenic –>  dec/ inc/ inc or dec/ inc/ inc.

Septic  –> inc/ dec/ inc or dec/ inc or dec/ inc then dec.

Neurogenic –> dec/ inc or dec/ dec/ inc or dec/ inc or dec.

Specific Conditions –> PCWP/ CI/ SVR/ Other:

Normal –> 6-12/ 3.5L/ 11-18/ PAP 14, CVP 5-10.

Hypovolemia –> dec/ dec/ Nl-inc/ Pt is dry.

LV Failure –> inc/ dec/ inc.

Primary RV Failure (RV AMI) –> Nl-dec/ dec/ Nl/ dec RA press, steep Y-descent, RV diastolic dip and plateau.

Secondary RV Failure (LV Failure) –> nl-inc/ dec/ Nl-inc/ inc PVR, inc RA.

Tamponade –> inc/ dec/ inc/ RA=wedge, dec y-descent, inc x-descent, pulsus paradoxus always present.

Constrictive Pericarditis –> inc/ nl- dec/ Nl/M or W shape JVP, steep y-descent, Kussmauls, pulsus paradoxus in 1/3.

Acute MR –> inc, peaked v-wave so/dec/inc/Post MI, tall V-waves.

Acute VSD –> inc/ dec/ inc /Post MI, O2 step up from RA to RV to PA.

Sepsis –> dec/ nl- inc/ Nl- dec/ +F/C, Blood Cx.

ARDS –> Nl-dec /inc/ dec/ Inc / dec/ Pulmonary infiltrates with progressive hypoxemia.

Massive PE –> Nl/ dec/ inc / inc PA pressure.

COPD exac. –> 4/ inc/ dec/ inc CVP, PAP, CO.

Typical Swan Ganz Parameters Orders:  You can choose the no sleep option or write:   Maintain PCWP at 14-18 mmHg.  If PCWP <12-14 give 250 NS bolus and/or increase IV NS at 75-80 ml/hr.   If PCWP 14-15 give IV NS at 40 ml/hr.  If PCWP 16-18 TKO or dec IVF.  If PCWP >18-20 give Lasix 20-40 mg IV q6-8hr, if initial dose ineffective repeat in 1-2hr or write “If PCWP 1hr after Lasix is >18, call”.  If urine output (UO) <30-40 ml/hr >2hr call (if PCWP >12-15 consider Lasix.  If <12 give fluids & albumen).

Central Venous Pressure (CVP): varies with respiration.  When lying down it is 6-8 mmHg.  The upper limit of normal for an ill person is 10mmHg.  When on mechanical ventilation with PEEP and needing volume, commonly use 20.  If exceeds 15-18, commonly need PCWP to follow in order to precisely titrate fluids.   In normal conditions the L atrial pressure is within 2-3mmHg of the R atrial pressure.  Thermodilution techniques can be used to estimate the CO.

Catheter Sizes:

French Size–>   Outside Diameter = OD (mm) X 3 = French Inches / Millimeter.  1 –> 0.1 / 0.3. 4 –> 0.05 / 1.3. 8 –> 0.1 / 2.6. 10 –> 0.13 / 3.3. 12 –> 0.16 / 4.0. 16 –> 0.21 / 5.3. 18 –> 0.23 / 6. 20 –> 0.26 / 6.6. 22 –> 0.28 / 7.3.  30 –> 0.41 / 10.6. 38 –> 0.5 / 12.6.

Guage–> Outside Diameter:  Inches / mm. 26 –> 0.018 / 0.45. 25 –> 0.02 / .05. 24 –> 0.022 / 0.56. 23 –> 0.024 / 0.61. 22 –> 0.028 / 0.71. 20 –> 0.036 / 0.91. 18 –> 0.048 / 1.22. 16 –> 0.064 / 1.62. 14 –> 0.08 / 2.03. 12 –> 0.104 / 2.64. 10 –> 0.128 / 3.25.

**Ref: (Pulmonary artery catheters in the critically ill. An overview using the methodology of evidence-based medicine. Crit Care Clin 1996;12:777-94) (Cardiovascular-pulmonary monitoring in the ICU. Chest 1984;85:537-668) (Irwin and Rippe’s Intensive Care Medicine, 4th ed, 1999, Lippincott-Raven) (Am Fam Phys 1996;54:3) (Bedside Critical Care Manual, 1998, Hanley & Belfus, pp62-69) (Cardiac complications in the intensive care unit. Clin Chest Med 1999;20:269-85)

Acid-Base Physiology:

Links:  Evaluation Step #1: Compensation:  Anion Gap (AG):  Urinary Electrolytes:   Mixed Disorders:  Respiratory Acidosis:   Metabolic Acidosis:  Metabolic Alkalosis:  Respiratory Alkasosis:  Arterial Blood Gas (ABG): Osmolarity:  Osmolar Gap:  References:

The daily diet generates CO2 (from carbo & fat metabolism) and H+ (from protein metabolism).   Ventilation allows for the excretion of CO2.  The kidneys must deal with the acid by reclaiming filtered bicarb (HCO3-) or end up gaining H=.  Most of the acid load is excreted as ammonium.  40% is excreted as titratable acids (phosphoric and sulfuric).  The carbonic acid-bicarb system is the bodies principle buffer.    Cations: Na (140), K (4).  Anions: Bicarb (25), Cl (100).  Pearls:  in pulmonary embolus there is a mild-mod respiratory alkalosis and hypoxemia that correlates with the size of the embolus.  A pO2 >90 mmHg on room air virtually excludes a lung problem.  In acute pulmonary congestion the CO2 is not increases unless the situation is grave, hypoxemia is common.   In COPD can be either pink puffer (mild hypoxemia, nl pH, nl pCO2) or blue bloater (hypoxemia, inc pCO2, if nl pH the compensation, if low pH then decompensation).  In sepsis may have an unexplained respiratory alkalosis as the earliest sign, this progresses to a metabolic acidosis, the mixed picture may have a normal pH.  With asthma see a low pCO2 (<35) due to hyperventilation, if it rises (>40 mmHG) the impending respiratory failure.  See hypoxia even with mild attack.   With neuro d/o get a high pCO2, low pH and nl HCO3, get acidosis before hypoxemia and a rising CO2 means deterioration.   With salicylate poisoning have a poor correlation of serum level and acidosis.  In adults you usually see a respiratory alkalosis, this may progress to a metabolic acidosis if severe.

Acidosis –> inc K, Ca & Mg.   Alkalosis –> dec K, Mg & Ca.

Step #1:  pH: acidosis or alkalosis.   Step #2: Is the primary process Respiratory or Metabolic or both. Use Bicarb & PCO2.

Acid-base Disturbances:

Respiratory Acidosis: Often from COPD, hypoventilation.   Uncompensated –> inc PaCO2, nl HCO3-, dec pH.  Partially Compensated –> inc PaCO2, inc HCO3-, dec pH.  Fully Compensated –> inc PaCO2, inc HCO3-, Nl pH.

Respiratory Alkalosis: Often from PE, cirrhosis, sepsis, pregnancy.  Uncompensated –> dec PaCO2, nl HCO3-, inc pH.  Partially Compensated –> dec PaCO2, dec HCO3-, inc pH.  Fully Compensated –> dec PaCO2, dec HCO3-, Nl pH.

Metabolic Acidosis: Often from hypotension, severe diarrhea, renal failure, sepsis.  Uncompensated –> Nl PaCO2, dec HCO3-, dec pH.  Partially Compensated –> dec PaCO2, dec HCO3-, dec pH.  Fully Compensated –> dec PaCO2, dec HCO3-, Nl pH.

Metabolic Alkalosis:  Often from vomiting, diuretic use cause contraction alkalosis.  Uncompensated –> Nl PaCO2, inc HCO3-, inc pH.  Partially Compensated –> inc PaCO2, inc HCO3-, inc pH.  Fully Compensated –> inc PaCO2, inc HCO3-, Nl pH.

Step #3: Degree of Compensation.  A predictable and adaptive response to acid-base d/o by the kidney and lungs.

Met Acidosis: PCO2 = 1.3 X (dec HCO3), lose CO2 from tachypnea.     Met Alkalosis: inc PCO2 = 0.6 X (inc HCO3).

Resp Acididosis: Acute –> for every PCO2 inc of 10mmHg, HCO3 will inc by 1mEq/L.   Chronic –> every PCO2 inc of 10, HCO3 will inc by 4.

Resp Alkalosis: Acute –> for every PCO2 dec of 10, HCO3 dec by 2mEq/L.  Chronic –> for every PCO2 dec of 10, HCO3 will dec by 4 mEq/L.

Step #4: Calculate Anion Gap: = Na – (HCO3 + Cl).   Links:  Abnormal AG: Normal AGMA:   Increased AG:  Osmolarity:  Osmolar Gap:  Decreased AG:   Urinary Gap:  Delta Gap:

Normal gap = 6-12 mEq/L an is due to unmeasured anions and cations. The difference between the anions (neg charge, protein, organic acids, phosphates, sulfates) and cations (+, Ca, K, Mg).    If >25, then always metabolic acidosis.  For each 100 mg/dL increase in glucose, Na decreases by 1.6 mEq/L.

Step #5:   Determine if there is a 1:1 relationship between anions in the blood.   Inc AG Met acidosis (AGMA): every 1pt inc AG, should have dec 1mEq/L in bicarb.    Normal AG Metabolic Acidosis (Hyperchloremic): every 1 mEq/L inc Cl, have 1mEq/L dec HCO3.  Usually due to: RTA, diarrhea or carbonic anhydrase inhibitor.   Traditionally, the normal anion gap has been 12 ± 4 meq/L. With the new generation of autoanalyzers, the reference range may be lower (6 ± 1 meq/L), primarily from an inc in Cl– values. Despite its usefulness, the serum anion gap can be misleading. Non-acid-base disorders that may contribute to an error in anion gap interpretation include hypoalbuminemia, antibiotic administration (carbenicillin is an unmeasured anion, polymyxin is an unmeasured cation), hypernatremia, or hyponatremia. Decreased AG:

Increased Anion Gap Acidosis (Inc Unmeasured Anions):

The hallmark of this disorder is that metabolic acidosis (thus low HCO3–) is associated with normal serum Cl–, so that the anion gap increases. Normochloremic metabolic acidosis generally results from addition to the blood of nonchloride acids such as lactate, acetoacetate, b-hydroxybutyrate, and exogenous toxins. An exception is uremia, with underexcretion of organic acids and anions.  Pseudometabolic acidosis is caused by underfilling Vacutainer tubes. If 1 mL of blood is put into a 10-mL red-top Vacutainer tube, a significant decline in HCO3– with an increase in anion gap occurs.

Abnormal anion gap (AG):   Inc (>12 mEq):  Anion gap metabolic acidosis = “MUDPILES”    = Methanol, Uremia, Diabetic ketoacidosis (ETOH or starvation ketosis), Paraldehyde, Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates.    Other:  Metabolic anion, Renal insufficiency (PO43–, SO42–), Drug or chemical anion, Salicylate intoxication, Sodium carbenicillin therapy, Methanol (formic acid), Ethylene glycol (oxalic acid), Metformin, Cyanide, Carbenicillin, Acetaminophen (ingestion >75g), Amiloride, Ascorbic acid, CO, Dapsone, Ibuprofen (ingestion >300mg/kg), Iodine, Iron, Ketamine, Ketoprofen, Niacin, Phenol, Propofol, Strychnine, Toluene, verapamil, Zinc, Phenformin (lactic acidosis), aminoglycosides (uremic agents), generalized sz (often from toxin-induced).   ***Note in metabolic alkalosis (inc number of neg charges on the albumen protein).

Lab W/u:  serum ketones (DKA, AKA, starvation), salicylate (ASA) level, measured osmolarity, serum alcohol level, lactate level (nl 1-3 mmol/L), anion gap metabolic acidosis, check osmolal gap (nl <10).  Osmolarity = 2 [Na+] + [glucose]/ 18 + [BUN]/ 2.8.     Check for calcium oxalate crystals (antifreeze) or fluorescence of urine under a Woods lamp.  Abnormal osmolal gap w/o metabolic acidosis seen with ethyl alcohol, isopropyl alcohol.   Must use corrected osmolal gap for combined ingestion:   Osmolarity = 2 [Na+] + [glucose]/ 18 + [BUN]/ 2.8 + ETOH/ 4.6.

Osmolal Gap:  Measured Osm – Calculated Osm –> if 0-10= normal, if >10 abnormal, if <0 lab/ calculation error.  If >10-15 there is an unmeasured osmole such as methanol, paraldehyde, ethylene glycol or mannitol.   Only low MW substances are osmotically active in the serum.

Drugs that cause Osmolar Gap:  “ME DIE”  Methanol, Ethanol, Diuretics (Mannitol, Sorbitol), Isopropanol (acetone), Iodine (questionable), Ethylene glycol.  Other: Glycerol, Hypermagnesemia (>9.5 mEq/L), hyperlipidemia.  If have both an osmolal gap & anion gap then likely due to either methanol or ethelyne glycol.

Decreased Anion Gap (AG):   Links:  Normal AGMA:  Narrow Gap Metabolic Acidosis:

Can occur because of a decrease in unmeasured anions or an inc in unmeasured cations.  The major unmeasured cations are calcium (5 meq/L), magnesium (2 meq/L), gamma globulins, and potassium (4 meq/L).   The major unmeasured anions are negatively charged albumin (2 meq/L per g/dL), phosphate (2 meq/L), sulfate (1 meq/L), lactate (1–2 meq/L), and other organic anions (3–4 meq/L).   Drugs causing dec AG: acidosis, Acetazolamide, Ammonium chloride, Bromide, Iodine, Lithium, Polymyxin B, Spironolactone, Sulindac, Tromethamine.

Dec AG (< 6 mEq):  Hypoalbuminemia (dec unmeasured anion, common), Plasma cell dyscrasias, Monoclonal protein (cationic paraprotein) (accompanied by chloride and bicarbonate), Bromide intoxication.

Dec Unmeasured Anions: If the sodium concentration remains normal but HCO3– and Cl– increase, the anion gap will dec. This is seen when there dec unmeasured anions, especially in hypoalbuminemia. For every 1 g/dL decline in serum albumin, a 2 meq/L dec in anion gap will occur. The new reference range for anion gap diminishes the usefulness of a low anion gap categorization except to detect an increased anion gap acidosis mimicking a normal anion gap acidosis.

Inc Unmeasured Cations: If the sodium concentration falls because of addition of unmeasured cations but HCO3– and Cl– remain unchanged, the anion gap will dec. This is seen in severe inc Ca, inc Mg, or inc K, IgG myeloma, where the immunoglobulin is cationic in 70% of cases, and Li toxicity.

Decreased (Low, Narrow) Anion Gap Metabolic Acidosis:    Renal causes –> urine pH usually >6 with RTA, Diamox, early renal failure, urinary tract obstruction, toluene inhalation, Ampho-B.   GI causes –> urine pH of around 5.  Bicarb rich diarrhea, pancreatic fluid, ureteral diversions.    “HARD-UP AC”, use the Urine AG to determine cause.   Hyperalimentation/ hyperventilation (chronic),   Aldosterone inhibitors (Spironolactone), RTA,  Diarrhea, Ureterosigmoidostomy,  Pancreatic fistula/ small bowel fistula, Addisons, Carbonic anhydrase inhibitors (Diamox = Acetazolamide).    “USED CARPS”: Ureteroenterostomy, Small bowel fistula, Extra chloride (bromism, iodide, hyperlipidemia), Diarrhea, Carbonic anhydrase inhibitors, Adrenal insufficiency, RTA, Pancreatic fistula, Saline load (chloride load causes acidosis).

Urinary Electrolytes:

Urinary Anion Gap (UAG): = urinary anions (UA) – urinary cations (UC) = UNa + UK – UCl.   Normal = -30 to –50 mEq/L.    Used to determine the cause of non-AG acidosis:  If it’s a (+)#, then RTA (renal loss).  If it’s a (-)#, then likely G.I. loss (diarrhea or pancreatic fistula).  Ammonia is the major urinary cation.  Want to see if kidney is making NH3.   If urinary acidification is deranged as in RTA, the UC is decreased, thus get an increased primary urinary AG as it becomes more positive.    In Metabolic Acidosis the kidney makes NH3, Cl enter the urine and the kidney excretes acid like it should.   A useful calculation in pt with non-AG acidosis to determine if renal or GI loss of bicarb.  If not making enough NH3:  lack mineralocorticoid or kidney not responding to it or proximal RTA.  A normal UAG is seen with hyperchloremic metabolic acidosis due to GI loss of bicarb in the presence of normal kidneys that are producing and excreting NH4.   Negative Urinary AG: Urine pH <5.5 –> normal.  Urine pH >5.5 –> diarrhea/ GI loss.  Positive Urinary AG and Urine pH>5.5 –> type 1 RTA.

Volume Depletion: Na 0-10 mEq/L –> extrarenal Na loss.  >10 –> renal salt wasting or Addisons.

Acute Oliguria:  Na 0-10 –> pre-renal azotemia.  >30 –> ATN.

Hyponatremia:  Na 0-10 –> intravascular volume depletion.  Na > 11-15 –> SIADH or Addisons.

Hypokalemia:  K 0-10 –> extrarenal K loss.  >10 –> renal K wasting.

Metabolic Acidosis: Cl 0-10 –> Cl responsive alkalosis.   Cl >10–> Cl resistant alkalosis.

Is There a Mixed Acid-Base Disorder?:

Calculate whether the secondary response is within range of that expected for the primary disturbance.  Measure the “Delta” Gap = “Change in” AG – “change in” HCO3 = (AG observed – AG ULN) – HCO3 LLN – HCO3 observed).  AG ULN = 12.  HCO3 LLN = 24.   Delta Gap = 0, then simple AGMA.   Delta Gap >0, mixed AGMA + primary metabolic alkalosis.  Or a mixed AGMA + chronic respiratory alkalosis with compensation.   Delta Gap <0, mixed AGMA + chronic respiratory alkalosis with compensatory non-AGMA.

Short Cut Method:  If the Delta AG + HCO3 normal –> AGMA only.   Delta AG + HCO3 > normal –> AGMA + met alk.   Delta AG + HCO3 < normal –> AGMA + non-AGMA.

Ddx:  Inc pCO2:   Dec pH –> resp acidosis w/ or w/o incompletely compensated met alk or coexisting met acidosis.  Nl pH–> resp acid and compensated met alk.  Inc pH –> met alk with incompletely compensated resp acid or coexisting resp acid.

Nl pCO2:  Dec pH –> metabolic acidosis.  Nl pH –> NORMAL.   Inc pH –> met alk.

Dec pCO2:  Dec pH –> met acid ww/ incompletely compensated resp alk or coexisting resp alk.  Nl pH –> resp alk and compensated met acid.  Inc pH –> resp alk w/ or w/o incompletely compensated met acid or coexisting met alk.

Respiratory Acidosis:

PH <7.4 with PCO2 >40.  Get inc HCO3 with compensation.   Acute: Inc 1 mEq/L HCO3 = 10 mmHg PaCO2.   Chronic: inc 3.5-4 mEq/L HCO3 = inc 10 mmHg PaCO2.

Ddx: acute airway obstruction (asthma, COPD), lung dz, pleural effusions, PTX, thoracic cage abnormality (flail chest, rib fx, kyphoscoliosis, scleroderma), hypoventilation (narcotics, CVA, sedatives, tranquilizers, paralysis, neuropathy), dec K, dec P, dec Mg, muscular dystrophy.

Step #1:  Calculate ratio:  (PCO2 – 40) / (HCO3 – 25).    If 10/ <1 –> acute respiratory acidosis + metabolic acidosis. Check A-a gradient.   If 10/1 –> acute respiratory acidosis.  Check A-a gradient.  10/1 – 10/3 –> acute and chronic resp acidosis.  Check A-a and consider chronic pulmonary system disorders.  10/3 – 10/3.5 –> chronic respiratory acidosis.  10/ >3.5 –> chronic respiratory acidosis + metabolic alkalosis.

Causes of Chronic Pulmonary Disease:  COPD, OSA, obesity hypoventilation, NM dz (ALS, MD), or chronic ILD.  Check PFTs, CXR, neuro exam, consider sleep study.

Arterial-alveolar (A-a) Gradient: >15 –> consider acute parenchymal lung dz such as COPD flare, severe asthma, pulmonary edema, drug OD, ARDS or pneumonia.     <15 –> acute hypoventilation from NM dz (Guillain Barre, MG), drug OD, brainstem injury or airway obstruction.  Check CXR, PFT’s, tox screen, neuro exam.  Intubate or use non-invasive ventilation if signs of fatigue, depressed mental status, rising PCO2 despite tx, PO2 <55 despite O2 or VC <10-15 ml/kg.

Metabolic Acidosis:

Links:   Lactic Acidosis:    Alcoholic Ketoacidosis:  Uremic:  Toxins:  Anion Gap:  DKA – See Endocrine.

PH <7.35, dec HCO3 (acute), dec PaCO2 to compensate 1-1.5 for change in HCO3.   Step #1:  Determine the Anion Gap.    Consider bicarb replacement:  HCO3 deficit (mEq) = 24- HCO3 (0.4) wt in kg). One amp bicarb raises the serum HCO3 1mEq.  Put 3 amps in 1L of D5W as a volume expander, also corrects the hyperkalemia.   Inc serum K inhibits production of NH3, which can cause met acidosis.   Anion Gap Acidosis is usually one of four things, lactic acidosis (most common), ketoacidosis, toxins/ drugs and uremia.

Lactic Acidosis:

One of the most common causes of AGMA.   Arterial lactate level >5 mmol/L and pH <7.35.    Lactic acid is formed from pyruvate in anaerobic glycolysis.   Most lactate is produced in tissue with high rates of glycolysis (gut- 50% of lactate production), skeletal muscle, brain, skin, and erythrocytes).    Lactate levels usually low (1 meq/L), as metabolism of lactate is principally by the liver through gluconeogenesis or oxidation via the Krebs cycle. The kidneys metabolize about 30% of lactate.  In lactic acidosis, lactate levels rise to >4–5 meq/L but often 10–30 meq/L.  Any level >4 means tissue ischemia, usually from anaerobic metabolism.   There are two basic types of lactic acidosis, both associated with increased lactate production and decreased lactate utilization fro poor perfusion or mitochondrial dz.  Up to 30% may not have a anion gap.

Type A (Hypoxic or hypoperfusion): have hypoxia or dec tissue perfusion (dec O2 content).  More common than type B.  Often resulting from poor tissue perfusion, cardiogenic, septic, or hemorrhagic shock, CO poisoning, severe anemia/ hypoxemia, pulmonary edema. These conditions not only cause lactic acid production to increase peripherally but, more importantly, hepatic metabolism of lactate to decrease as liver perfusion declines. Severe acidosis also impairs the ability of the liver to extract any perfused lactate.

Type B (Impaired O2 utilization and/or lactate metabolism) –> not due to hypoxia.  May be due to metabolic causes, such as DKA, liver disease/ failure, renal failure, infection (sepsis, Malaria), cancer, strenuous exercise, sz, pheochromocytoma, congenital enzyme defects, toxicity from biguanides therapy, Thiamine def., leukemia, or lymphoma or as a result of toxicity from ethanol, methanol, salicylates, INH, Niacin, Nitroprusside, Cocaine, Cyanide, Acetaminophen, Streptozotocin, AZT, ASA, Nalidixic Acid or phenformin, also seen in  AIDS.  Tissue oxygen utilization is impaired.   Or from congenital erros of metabolism.

Idiopathic lactic acidosis, usually in debilitated patients, has an extremely high mortality rate.

Alcoholic Ketoacidosis (AKA):

This is a common disorder of chronically malnourished patients who consume large quantities of alcohol daily. Most of these patients have mixed acid-base disorders (10% have a triple acid-base disorder). Usually have a dec HCO3-, but half the patients may have normal or alkalemic pH.

The primary ketones produced in AKA are b-hydroxybutyrate (bHB) and acetoacetate (AcAc). The ratio of bHB to AcAc depends on the ratio of NADH to NAD. Because of dehydration, the ratio of NADH to NAD in alcoholic ketoacidosis is often elevated, resulting in a higher percent of ketones as bHB.   The nitroprusside test used for ketones detects only AcAc, patients with AKA may have falsely low to negative tests for ketones. The ratio of bHB to AcAc reverses with reversal of dehydration, which can produce an apparently “worse” laboratory ketone value with clinical improvement alcoholic ketoacidosis.  AKA may present with alkalemia or a mixed acid-base disorder, secondary to contraction alkalosis form profuse vomiting  A mild lactic acidosis, secondary to ethanol use, can also compound the patient’s acid-base status.  Both Inc/dec Phos have also been noted in patients with AKA.  Serum K level may be falsely elevated.  Mild elevations in LFT’s and/or pancreatic enzymes, may be seen secondary to ethanol use.

Three types:        1. Ketoacidosis: due to b-hydroxybutyrate and acetoacetate excess.    2. Lactic acidosis: Alcohol metabolism inc NADH:NAD ratio, causing increased production and decreased utilization of lactate. Moderate to severe elevations of lactate (> 6 mmol/L) are seen with concomitant disorders such as sepsis, pancreatitis, or hypoglycemia.

3. Hyperchloremic metabolic acidosis due to bicarb loss in the urine associated with ketonuria. If lose HCO3, the kidneys retain Cl in 1:1 ratio.  Metabolic alkalosis occurs from volume contraction and vomiting. Respiratory alkalosis results from alcohol withdrawal, pain, or associated disorders such as sepsis or liver disease. Half of the patients have either hypoglycemia or hyperglycemia. When serum glucose levels are >250 mg/dL, the distinction from diabetic ketoacidosis is difficult. The diagnosis of alcoholic ketoacidosis is supported by absence of a diabetic history and by no evidence of glucose intolerance after initial therapy.  Ddx of Hyperchloremic MA: RTA –> proximal or distal.     Acid loads –> ammonium chloride, arginine or lysine hydrochloride, sulfur, hyperalimentaion, methionine sulfate, ketoacidosis with renal ketone loss.  Bicarb loss –> diarrhea, pancreatic/ biliary/ small bowel fistulas or drainage, ureterosigmoidostomy, drugs (CaCl, MgSO4, Cholestyramine), posthypocapnea).

W/u: if low or normal plasma K, check Ur pH during acidosis.  If >5.5, then distal RTA.  If <5.5, then r/o proximal RTA, measure ammonium and titratable acidity, measure urine PCO2 during bicarb infusion to look for a rate dependent defect.

Tx:  IV hydration is the mainstay of treatment for alcoholic ketoacidosis.    Crystalloid with supplemental glucose, such as D5NS, is the fluid of choice.  Thiamine 100 mg IV or IM to prevent the development of Wernicke-Korsakoff syndrome.  Multivitamins, Mg and folate supplementation.  K replacement started as soon as adequate urine output is established, as the K+ value will fall with correction of the acidosis.   Hyperphosphatemia will usually resolve with treatment of the dehydration. Phosp is indicated in patients whose level is less than 1 mEq/L.  Benzo’s may be required for the prevention of DTs.   Treatment should be continued until dehydration, acidosis and electrolyte abnormalities have been reversed, good oral intake is established (usually requires 12-24 hrs IVF).

Diabetic Ketoacidosis:   Seen Endocrine/ diabetes complications.

Uremic Acidosis:

At glomerular filtration rates below 20 mL/min, the inability to excrete H+ with retention of acid anions such as PO43– and SO42– result in an anion gap acidosis, which rarely is severe. The unmeasured anions “replace” HCO3– (which is consumed as a buffer). Hyperchloremic normal anion gap acidosis may be seen in milder cases of renal insufficiency.

Toxins:

Multiple toxins and drugs can inc AG gap by increasing endogenous acid production. Methanol (metabolized to formic acid), ethylene glycol (glycolic and oxalic acid), and salicylates (salicylic acid and lactic acid), which can cause a mixed disorder of metabolic acidosis with respiratory alkalosis.

Metabolic Alkalosis:

Alkalosis:   Often associated with low K+ and low Cl- contraction alkalosis.   Metabolic alkalosis is often precipitated by ongoing failure of kidneys to excrete HCO3, due to volume contraction and hypokalemia.  Can be due to:  Loss of acid –> vomit, NGT, gastrocolic fistula, villous adenoma, aciduria (from K depletion).  Excess base –> admin of antacids (bicarb or milk-alkali), some vegetarian diets,  admin of salts of weak acids (Na-lactate, Na or K-citrate).  Potassium depletion (causes H+ & Na to enter cells) –> GI loss with diarrhea, poor intake, diuretics, chronic alkalosis, glycogen deposition, mineralcorticoid excess (primary aldo, Cushings, steroids, licorice), K losing nephropathy.

Ddx:  Choride-responsive: volume depleted (dehydration), responds to NaCl or KCl, (urine Cl <10 mEq/L) –> Vomiting, nasogastric suction, diuretics, post-hypercapnic alkalosis, stool loss (laxative abuse, CF, villous adenoma), massive blood transfusion, exogenous alkali administration.  Serum albumen will be elevated which will expose more binding sites and can create a GAP-alkalosis.

Ddx: Chloride-resistant:  profound dec K (800-100 mEq deficit), hyperadrenocorticoid states such as Cushing’s syndrome, primary hyperaldosteronism, secondary mineralocorticoidism such as licorice, chewing tobacco (Ur Cl >20 mEq/L) –> Hypomagnesemia, hypokalemia, Bartter’s syndrome.

Unclassified Causes:  alkali administration, recovery from organic acidosis, antacids and exchange resins administered in renal failure, Milk-Alkali syndrome, large doses of carbenicillin or PCN, glucose ingestion after starvation, nonparathyroid hypercalcemia.

Tx:  Varies depending on the cause.  Cl-responsive give saline, correct accompanying hypokalemia.  Cl-resistant correct of underlying cause, correct K depletion.  Can follow urine Cl as indicator of repletion of volume status. Diamox 250mg IVP q12h x3 with 20 mEq KCl via NGT.  Short-term improvements can be seen with adding 3 amps Bicarb/ L NS.

Bartter Syndrome: a familial hypokalemic, hypochloremic metabolic alkalosis.  Due to ion channel abnormalities in of renal tubular cells.

S/s:  HTN is not present, despite high renin and angiotensin II levels. Delayed growth, mild cognitive developmental deficits, polyuria and polydipsia, rare tetany.  Hypomagnesemia in ~20%.  Normal to high urine calcium (nephrocalcinosis variable), high urine prostaglandins.  Renin, Aldosterone & Angiotensin II markedly elevated.  Tx:  correcting sx’s and electrolyte anomalies.  Indomethacin to inhibit prostaglandin secretion is variably effective.

Respiratory Alkalosis:

Sx:  perioral and peripheral paresthesias, hyperreflexia, tetany, seizures, arrhythmias

Etiology: hypoxemia (pneumonia, PE, atelectasis, high altitudes), psychogenic hyperventilation (hysteria, anxiety, pain), drugs (salicylates, xanthines, progesterone, epinephrine, thyroxine, nicotine), CNS disorders (CVA, trauma, tumor, infections), hepatic encephalopathy (inc NH3), progesterone, hypoxia, early G- sepsis, hyponatremia, sudden recovery from metabolic acidosis, assisted ventilation, pregnancy, anemia, emboli, CHF.

Tx:  underlying cause.  If psychogenic hyperventilation rebreathe to increase. PCO2 (paper bag, breathing 5% CO2 via mask).

Arterial Blood Gas (ABG) Sampling:

Links:  A-a Gradient:  Procedure: ……  Reason:  to asses if adequate gas exchange.

Abbreviations:  PB = barometric pressure (mm Hg).  FIO2 = inspired oxygen fraction (0.21 = room air).  PaCO2 = partial pressure of carbon dioxide in arterial blood (mm Hg).  PACO2 = partial pressure of carbon dioxide in alveolar gas (mm Hg).  PaO2  = partial pressure of oxygen in arterial blood (mm Hg).  PAO2  = partial pressure of oxygen in alveolar gas (mm Hg).

Normal values at sea level room air (FIO2 = 0.21):  PaO2 –> 80-95 mmHg.  The oxygenation.   PaCO2 –> 35-45 mmHg. The ventilation.  SaO2 –> 96-99%.    pH –> 7.40 +0.02.  HCO3 –> 22-28 mEq/L  Base excess or deficit: ­-3 to +3 mEq/L.

Values should not change with age except dec PaO2.    For age 40-90yo, PaO2 = 108.75 – 0.39 X age. (Or ~100-1/3 age)

Mixed venous O2 tension (PVO2): 35-50mmHg.   Mixed venous O2 concentration (CVO2): 12-15ml/dL. Or 70-75% sat.

Arterial O2 concentration (CaO2): 17-20 ml/dL.

Arteriovenous O2 difference = C(a-v)O2: 4-5ml/dL.

Alveolar-arterial O2 Gradient (A-a)     (FIO2 X 713) – 1.25(PaCO2) – PaO2. (PAO2 is calc, PaO2 is measured.)

Normal = 4 + [(age-20) x .3]   Normal is <10-20 mmHg breathing room air at sea level for any age , or 10-60 on 100% O2.  If elevated, it indicates respiratory dz that is interfering with gas exchange.  If on O2, can remove and the O2 sat will equilibrate in 5 min, as hard to interpret unless on RA or 100%.  = 148 – 1.2(PaCO2) – PaO2.    148 = 713 X FiO2.   = PAO2 – PaO2.  Short-cut estimate:  150 – (1.25 PaCO2).  P(A-a) in adolescents = <10 mm Hg, adults <40 yo = 10 mmHg, >40 yo = 10-15.

ABG Procedure:  Best to use radial > femoral or brachial artery.   Contra: +Allen test, ESRD (may need shunt or fistula site), bleeding d/o.  Equipment: 3-5ml plastic syringe X2, one with 2ml of 1% Lido.  Two 25g, ½” needles, ice, ETOH or Iodine, drape, 1ml of Heparin 10,000 U/ml, sterile gloves, 2X2’s, towel, tape.

Step #1: Check Allen Test: asses patency of collateral circulation.  Occlude both radial & ulnar arteries with firm pressure at distal forearm.  Elevate arm, pt make a few fists to drain blood.  Release pressure on ulnar side, should pink up hand in <6sec.

Step #2: Place rolled towel under hyperextended wrist, tape to back board.  Palpate radial artery as it lies between styloid process of radius & flexor carpi ulnaris tendon.  PMI should be just proximal to transverse wrist crease.

Step #3: Don sterile gloves.  Wet the syringe with Heparin and evacuate the extra (extra heparin left in syringe –> dec pH).

Prep area with Betadine or ETOH, then give local anesthetic (optional), infiltrate skin and then down to periosteum or radius on either side of the artery with 1%Lido (may dec vasospasm).

Step #4: Tell pt to expect some discomfort but to keep as still as possible. Relocate PMI with nondominant hand as face the patient.   Hold syringe like-a-dart, insert bevel up into skin at 60 deg pointing proximally.  Slowly advance until 1-2ml of pulsatile blood fills syringe passively.

If no blood advance until hit bone, then slowly pull back to skin (may have pierced the artery), once needle is just beneath skin, repalpate artery and redirect.    Step #5: withdraw needle, apply firm pressure to area for 5-10 min.  Remove all air bubbles (affects PO2) from syringe, remove needle and apply rubber stopper.  Label and place on ice or send to lab ASAP (within 20min) as WBC’s metabolically active.  Can use elastic ace wrap and gauze pad to apply pressure, best not to let pt do it, can use an assistant.

Complications:  Pain, infection, local bleeding, venous or air contamination.  Distal ischemia if over traumatize the artery (rotate sites, avoid brachial artery).  AV fistula or false aneurysm (from over sampling same site)   Re-check pt in 15-20 min to r/o wrist hematoma and adequate perfusion.   If unable to use radial artery due to +Allen, or local infection.

Brachial Artery: use 22g 1.5”.  Consult a vascular surgeon ASAP if get transient spasm, occlusion or clotting of brachial artery.  Distal embolization with blood or cholesterol emboli, ischemia or gangrene of hand or forearm.

Femoral Artery: Commonly use is hypovolemia or shock.  Can use blind sampling of the best estimated position of the femoral artery.  Postion of vascular structure:  Lat –> Med: NAVAL:  Nerve, artery, vein, empty space, lymphatics.  If no pulse palpable –> divide the distance between ASIS & Pubic tubercle in thirds.  The artery lies at a point where the inner 1/3 and middle 1/3 meets.

***Ref: (Acid base disorders, The Principles and Practice of Nephrology, 1995, Mosby)  (Anion gap, Kidney Int 1985;27:472) (Postgrad Med 2000;107:3) (Acid-base. Arch IM 1992;152:1625-29)  (Medicine 1980;59:161-187) (Acid-base disorders: classification and management strategies.  Am Fam Physician. 1995;52:584-90) (The cellular basis of metabolic alkalosis.  Kidney Int. 1996;49:906-17) (Metabolic acidosis with extreme elevation of anion gap: case report and literature review. Am J Med Sci. 1999;317:38-49) (An approach to clinical acid-base problem solving.  Compr Ther. 1998;24:553-9) (Protection of acid-base balance by pH regulation of acid production. N Engl J Med 1998;339:12) (Arch IM 1992;152;1625-29) (The urine anion gap.  Am J Med 1986;292:198-202)

Nasogastric Tubes (NGT):

Two clinical uses, for dx of upper GI bleed and for gastric decompression.  Rule of 9’s for NGT:  1 liter of gastric fluid contains 9 mEq K, 45 mEq Na, 90 mEq Cl.    Easy NGT Placement:  Step #1: estimate the distance of insertion, usually 50cm in adults, then apply a slight caudal curve to the tip.  Can stiffen a soft tube by mixing in ice.   Step #2:  Lubricate distal 15cm of the tube with KY. Numb nostril first by squirting 3-5ml 2% Lido through a 22g needle.  If available create a 50/50 mixture by injecting 4% Lido into Afrin bottle and spray/  inject into nares. For improved ease of tube placement can add atomized 4% lidocaine:  1.5ml into nasopharynx + 3ml into oropharynx.

Step #3: For easier insertion have pt suck water out of a 30cc syringe to initiate swallow reflex and lubricate.  As swallow tube and keep neck flexed to close the epiglottis and avoid tracheal intubation.  In uncooperative, attach a 20cc with water, when pt starts to gag withdraw slightly and instill a few drops of water to trigger the swallow reflex.

Step #4: Auscultate over the stomach as inject 50cc of air to confirm placement.   Aspirate the GI contents and check pH.  Tape tube to nose.  Before using a feeding tube, always check a low CXR to confirm placement.  Preferred site is the antral or fundic pool.  If becomes clogged, use a saline flush to clear it.

Complications:  nasotracheal intubation, epistaxis, esophageal/ nasal/ gastric erosion with prolonged use, otitis media, excessive gagging (encourage the pt to deep breath or pant through the mouth after the tube passes.

Feeding Tubes:  correct location is anywhere from stomach to proximal jejunum.  Only postpyloric placement helps reduce risk of reflux and aspiration pneumonia.  Before feed, must confirm enteral position with a low CXR.  No benfit in advanced dementia.  Informed consent about the benefits, burdens and alternatives is often only brushed upon.

Percutaneous Endoscopic Gastrostomy (PEG):   Placed with an endoscope in stomach a needle is percutaneously pushed into stomach, a tube is inserted using the Seldinger technique.   Usually a 18-28F, large enough for fiber enriched or blenderized enteral formulas as well as medications.  Allows for continuous or intermittent feedings.  Since pt’s usually have a severe stroke or advanced dementia the 1yr mortality rate is 50%.  Pt’s wt at 4mo is usually unchanged, 10% have improved ADL’s and 30% have inc serum albumin. (J Am Ger Soc 2000;48)   Indications:  need nutritional support > 4wks.  Consider in any pt with a functional GI tracts unable to consume sufficient calories to meet metabolic demands.  Frequent indications include impaired swallowing due to neurological or neoplastic dz, head/ facial trauma or catabolic conditions.  0.1-1% procedure mortality rate, 3-6% morbidity rate.    Contra:  prior gastric resection, high risk for aspiration.  Ascites, hepatomegaly and severe obesity may impede gastric transillumination.   Complications: 8% overall, risk intra-abdominal leakage, peritonitis, site infection, tube displacement, aspiration.  Often get excoriation at the insertion site, diarrhea, tube gets pulled out requiring restraints.    If PEG falls out:  insert a new one, can check placement by having pt swallow (if able) a dose of acetaminophen elixir, if able to aspirate a pink liquid then tube is correctly in place.  At least insert a Foley to keep the tract open and to use as a temporary tube.

Endoscopically Positioned Transgastric Jejunal Tube (PEGJ):  A tube is inserted via an existing gastrostomy and the tip is positioned distal to the ligament of Treitz.  Small (<12F), >50% have tube dysfunction in 1 yr.

Direct Percutaneous Endoscopic Jejunostomy (DPEJ):   Feeding tube inserted directly into the jejunum with endoscopic assistance.  Mores stable access to the jejunum.  Tubes are smaller (9-12F) and thus more prone to clogging.   More prone to malabsorption diarrhea if feeding intolerance.

**Ref: (Diagnosing ant treating pt’s with refractory functional GI disorder, Annu Rev Med 1998;49:175-93)  (Cecils Textbook of Medicine 2000, 21st ed, WB Saunders, pp 667-723) (Nasogastric and feeding tubes.  Postgrad Med 1996;99:5)

Methemoglobin-forming Gases:   Met-Hgb is produced when nitric oxide or nitrogen dioxide transforms the iron if heme from ferrous (Fe2+) to ferric (Fe3+). Causes anemia because can’t carry O2, also causes O2-Hgb dissoc curve to shift to L.

Sources:   Nitrites/ ates –> contaminated well water, meat preservatives, carrot juice/ spinach, silver nitrate burn tx, industrial salts, room deodorizer propellants, amyl nitrite (cyanide antidote kits, sexual enhancers), NTG meds.  Other Inducers –> laundry ink (aniline, aminophenol)), industrial solvents/ gun cleaners (nitrobenzene), mothballs (Naphthalene), local anesthetics (lidocaine, benzocaine), Pyridium, Sulfonamides, Chloroquine, Primaquine, Dapsone, phenytoin, nitroprusside, Benzocaine/Hurricaine spray, Fungicides for plants/ seeds (copper sulfate), Resorcinol (anti-seborrheic/ pruritic/ septic), Chlorates (explosives, matches, pyrotechnics), combustion products (fires).

S/s:  parallels those of CO poisoning.  Inc Met-Hgb levels –> cyanosis and chocolate-brown discoloration of venous blood –> cyanosis without abnormal dec in arterial pO2 (except with severe anemia).  Dx is on this basis & other signs of O2 delivery.    Degree of MetHb is expressed in % of total Hgb.   1-2%= normal,  >15% get sx (DOE, inc HR, HTN, H-A.  >35% also get metabolic acidosis, agitation, sz, coma, death.       Also Dx if place drop of pt’s blood on filter paper, when dry it turns deep chocolate brown or slate gray.   Pulse Ox is unreliable and tends to overestimate the O2 sats.   ABG: see normal PO2, but dec O2 sats (both must be measured, not calculated).  Levels @ 10-20% –> mild, avoid nitrates in food/ water, give 100% O2.   If 20-45% –> moderate, likely have CNS depression, H-A, dizziness fatigue, lethargy, syncope, dyspnea.    45-55% –> coma, lactic acidosis, arrhythmia, shock, convulsions.    >70% high risk of mortality.

Tx: Give IV 1% methylene blue in NS 1-2ml/kg over 5-10min (avoid if deficiency in G6PD or methemoglobin reductase), causes ferric –> ferrous.  100% O2.  Hyperbaric O2, exchange transfusions.

Preamble and List of Abbreviations Used:

Links:   Disclaimer:   Lab Values:  Abbreviations:

Written by Carl G. Weber MD, Internal Medicine.   Any feedback is appreciated:  CGWEBER@POL.NET.   Remember, paying the nominal download fee contributes to the ongoing improvement of this text and entitles you to free email upgrades for 1 year.   Purchase at PalmGear.com, look under “clinical”.  If you have any pearls, illustrations or knowledge that you wish to add send it to me.  If it is good, I will add it and send the update back to you as soon as possible and subsequently include it in further updates.   If it is a significant contribution, I will prolong your update period (possible indefinitely) and give you recognition as a contributor.  Let’s make this book our own, we can save trees and the weight of carrying books around.  Please include any citations as evidence-based medicine is our ultimate goal.

Preamble to Book:  Thank you for supporting the production of this text.   It is called shareware, not because you can “share” it freely with others, but in order to simplify the transmittal of my frequent email updates to those who purchase it.   I hope you find it useful.   This text is designed as a quick and yet extensive reference for the diagnosis and treatment of the majority of problems that may present in a primary care physician’s practice.  It is intended to aid providers in their pursuit of optimal patient care.   This book provides concise, quick information that can be used during a busy clinical day with the goal of efficient work-ups, accurate diagnosis, and effective treatment that hopefully leads to well-informed, healthy patients, healthy families and a satisfied physician.  The information in this guide (the ultimate peripheral brain) has been culled from peer-reviewed articles and manuscripts, key textbooks and review courses published within the last few years.The goal is for these texts is to have 95% of clinical info you need at your fingertips. If you have any pearls, illustrations or knowledge that you wish to add send it to me.  If it is good, I will add it and send the update back to you as soon as possible and subsequently include it in further updates.   If it is a major contribution, I can prolong your update period.  Let’s make this book our own, we can save trees and the weight of carrying books around.

Purpose of Book:   I believe this is the first electronic textbook available that adequately summarizes medical information in a concise and easy to read format.    This book is directed at practicing clinicians.  It is also useful to residents and medical students doing clinical rotations.  It includes differential diagnosis, basic pathophysiology, clinical pearls, physical diagnostic findings as well as evaluations and treatments of a multitude of medical conditions.   This book will allow primary care physicians to interface with the specialist, and assist in deciding when referral is necessary.

Book Disclaimer:   Medicine is a constantly changing science with a continuing better understanding of disease processes and newer and diagnostic and treatment modalities emerging almost every day.  The authors, editors, and publisher of this text have given their best efforts to provide accurate, up-to-date, information that is considered to be within current medical standards. The approaches to medical problems are referenced with supporting studies, and further reading is encouraged.   Human error is always possible and the authors, editors, and publisher of this text do not warrant the information as being absolutely complete, nor are they responsible for omissions or errors in the text or for the results of using this information.  This book should not take the place of your own clinical judgment or the advice of specialists. We have tried with great fervor to limit errors, misinformation, and copyright infringement in the text.   We would greatly appreciate feedback regarding any problems you discover while perusing these pages.

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Lab Values:  Links:  Hematology:  Endocrinology:

Common Laboratory Values:  Chem 7  = basic metabolic panel, 17 = comprehensive, which includes electrolytes, renal and liver function tests.  New Medicare Labs:  **Electrolyte Panel (#4): Na, K, Cl, CO2.  **BMP: #8: Chem 7 (SMA-7) with Ca.   **Renal Panel: #10 BMP + Alb & PO4.   **CMP #14: BMP + Alb, AP, AST, ALT, Tb, Dbili.   **ECMP #17: CMP +Mg, P, LDH.  **Hepatic: Alb, Tbili, Dbili, AP, Tp, ALT, AST.

Acetoacetate:  0.3-2.0 mg/dl.

Acid phosphatase:  0-0.8 U/ml (0-5.5 U/L).

Acid phosphatase, prostatic:  2.5-12.0 IU/L.

Albumin (Alb): 3.0-5.5 g/dl.

Aldolase:  1-6 IU/L.

Alkaline phosphatase (AP):  15-20 years @ 40-200 IU/L (U/L), 20-101 years @ 35-125 IU/L.

Alpha-1 antitrypsin: 200-500 mg/dl.

Aminotransferases:   AST (SGOT): 0-35 U/L (IU/L), ALT (SGPT): 0-40 U/L.

Ammonia:  11-35 µmol/L = 80-110 mcg/dL.

Amylase:  2-40 U/L.

Anion gap: 8-12 mEq/L (mmol/L).

Ascorbic acid:  0.4-1.5 mg/dl.

AST:  5-40 IU/L.

Bilirubin:  Total @ 0.2-1.2 mg/dl, Direct @ 0-0.4 mg/dl, Indirect @ 0.2-0.7 mg/dL.

Calcium:  8.7-10.6 mg/dl.

Carbon dioxide:  18-30 mEq/L (mmol/L).

Carcinoembryonic antigen, serum (CEA):  <25. µg/dl.

Carotene (carotenoids):  50-300 µg/dl.

C3 complement: 55-120 mg/dl.  C4 @ 14-51 mg/dl.

Ceruloplasmin:  15-60 mg/dl.

Chloride:  95-106 mEq/L (mmol/L).

Cholesterol Total: <200 mg/dL, 12-19 yo @ 120-230 mg/dl, 20-29 yo @ 120-240 mg/dl, 30-39 yo @ 140-270 mg/dl, 40-49 yo @150-310 mg/dl. 50-59 yo @ 160-330 mg/dl.  HDL: 30-90 mg/dL, LDL: 50-160 mg/dL.

Copper:  100-200 µg/dl.

Creatine kinase, total (CPK):  20-200 IU/L (25-145 U/L).

Creatine kinase, isoenzymes:  MM fraction @ 94%-95%, MB @ 0%-5%, BB @ 0%-2%.  Normal values in the heart @ 80% MM, 20% MB, in the brain @ 100% BB, in the skeletal muscle @ 95% MM, 2% MB.

Creatinine (Cr):  Female adult @ 0.5-1.3 mg/dl, Male adult @ 0.7-1.5 mg/dl.

Delta-aminolevulinic acid (ALA):  <200 µg/dl

Alpha-Fetoprotein, serum:  <40 µg/dl.

Ferritin: 15-200 ng/mL.

Folate: 1.9-14.0 ng/ml.

Gamma glutamyl transpeptidase (GGT or GGTP):  Male @ 12-38 IU/L, Female @ 9-31 IU/L.

Gastrin:  150 pg/ml.

Glucose, serum (fasting, blood sugar = FBS): 70-115 mg/dl.  Subtract 15-20% if a plasma value.

Glucose-6-phosphate dehydrogenase: 5-10 IU/g Hb.

G6PD screen, qualitative:  Negative.

Haptoglobin:  100-300 mg/dl.   Hemoglobin A2 @ 0%-4% of total Hb.  Hemoglobin F @ 0%-2% of total Hb.

Immunoglobulin, quantitation:  IgG @ 700-1500 mg/dl, IgA @ 70-400 mg/dl, IgM @ Male = 30-250 mg/dl, Female = 30-300 mg/dl, IgD @  0-40 mg/dl.

Insulin, fasting: 6-20 µU/ml

Iron-binding capacity:  250-400 µg/dl (250-450 mcg/dL). Iron Saturation: 20-45.

Iron, total, serum (Fe):  40-150 µg/dl (80-180 mcg/dL).

Lactic acid:  0.6-1.8 mEq/L.

LDH: 20-220 IU/L.   LDH isoenzymes: LDH1  @ 20%-34%, LDH2 @ 28%-41%, LDH3 @ 15%-25%, LDH4 @ 3%-12%, LDH5 @ 6%-15%.

Leucine aminopeptidase (LAP):  30-55 IU/L.

Lipase: 4-24 IU/dl (49-220 U/L).

Magnesium (Mg): 1.6-2.6 mg/dL.

5′-Nucleotidase:   0.3-3.2 Bodansky units.

Osmolality: 285-295 mOsm/kg serum water.

Phenylalanine:  3 mg/dl.

Phosphorus (P): 2.5-4.5 mg/dL.

Potassium, plasma:  3.1-4.3 mEq/L.

Potassium, serum:  3.5-5.2 mEq/L.

Protein:  2-55 yo @ 5.0-8.0 g/dl, 55-101 yo @ 6.0-8.3 g/dl.

Protein electrophoresis, serum (SPEP):  Albumin @ 3.2-5.2 g/dl, Alpha-1 @ 0.6-1.0 g/dl, Alpha-2 @ 0.6-1.0 g/dl, Beta @ 0.6-1.2 g/dl, Gamma                           0.7-1.5 g/dl.

Sodium (Na): 136-145 mEq/L.

Sulfate:  0.5-15 mg/dl.

T3 uptake:  25%-45%.

T4:  4-11 µg/dl.

Triglycerides (Trig): <60 mg/dL.  2-29 yo @ 10-140 mg/dl, 30-39 yo @ 20-150 mg/dl, 40-49 yo @ 20-160 mg/dl, 50-59 yo @ 20-190 mg/dl, 60-101 yo @ 20-200 mg/dl.

Urea nitrogen,  serum (BUN):  2-65 yo @ 5-22 mg/dl.

Uric acid:  10-59 yo:  Male @ 2.5-9.0 mg/dl, Female @ 2.0-8.0 mg/dl.  60-101 yo:  Male @ 2.5-9.0 mg/dl, Female @ 2.5-9.0 mg/dl.

Viscosity:  1.4-1.8 (serum compared to H2O).

Vitamin A:  0.15-0.60 µg/ml.

Vitamin B12:  200-850 pg/ml.

Hematology Labs:

Complete blood count:  Male / Female.   Hematocrit (%): 40-52 / 38-48.

Hemoglobin (g/dl):  13.5-18.0 / 12-16.

Erythrocyte count (x 10-12th cells/L): 4.6-6.2 / 4.2-5.4.

Reticulocyte count (%):  0.6-2.6 / 0.4-2.4.

MCV (fL): 82-98 / 82-98.  MCH (pg): 27-32 / 27-32.  MCHC (g/dl): 32-36 / 32-36.

WBC (x 109 cells/L): 4.5-11.0 / 4.5-11.0.  Segmented neutrophils: 1.8-7.7 / 1.8-7.7. Ave %: 40-60 / 40-60. Bands (cells):  0-0.3 / 0-0.3. Ave (%): 0-3 / 0-3.  Eosinophils (cells x 10-9th/L): 0-0.5 / 0-0.5. Ave %:  0-5 / 0-5.  Basophils (cells x 10-9th/L):  0-0.2 / 0-0.2. Ave %:  0-1 / 0-1. Lymphocytes (cells x 109/L):  1.0-4.8 / 1.0-4.8.  Ave %: 20-45 / 20-45. Monocytes (cells x 10-9th/L): 0-0.8 /  0-0.8. Ave %:  2-6 / 2-6.

Platelet count (cells x 10-9th/L): 150-350 / 150-350.

Coagulation Normal Values:  Template bleeding time: 3.5-7.5 min.   Clot retraction, qualitative:  Apparent in 30-60 min; complete in 24 hr, usually in 6 hr.  Coagulation time (Lee-White), in glass tubes: 5-15 min, in siliconized tubes:  20-60 min.  Euglobulin lysis time: 120-240 min.

Factors II, V, VII, VIII, IX, X, XI, or XII: 100% or 1.0 unit/ml.

Fibrin degradation products:  <10 µg/ml or titer  1.4.

Fibrinogen:  200-400 mg/ml.

Partial thromboplastin time, activated (aPTT): 20-40 sec.

Prothrombin time (PT): 11-14 sec.

Thrombin time: 10-15 sec.

Whole blood clot lysis time:  >24 hr.

Acid hemolysis test (Ham): No hemolysis.

Carboxyhemoglobin: Nonsmoker @ <1%, Smoker @ 2.1%-4.2%.

Cold hemolysis test: No hemolysis

Erythrocyte life span: Normal @120 days, 51Cr-labeled half-life @ 28 days.

Erythropoietin by radioimmunassay:  9-33 mU/dl.

Ferritin (serum): Male @ 15-200 µg/L, Female @ 12-15O µg/L.

Folate, RBC: 120-670 ng/ml.

Fragility, osmotic:  Hemolysis begins @ 0.45%-0.38g% NaCl, completed @ 0.33%-0.30% NaCl.

Haptoglobin: 100-300 mg/dl.

Hemoglobin:  Hemoglobin A1C @ 0%-5% of total, A2 by column @ 2%-3% of total, fetal @ <1% of total, plasma @ 0%-5% of total, serum @ 2-3 mg/ml.

Iron:  Male @ 75-175 µg/dl, Female @ 65-165 µg/dl.

Iron-binding capacity, tota (TIBC): 250-450 µg/dl.

Iron turnover rate (plasma):  20-42 mg/24 hr.

Leukocyte alkaline phosphatase (LAP) score: 30-150.  Elevated in polycythemia vera, myeloid metaplasia and some inflammatory diseases.  Dec in CML, PNH, Wilson’s dz and occasionally in Hodgkins.

Methemoglobin:  <1.8%.

Schilling test: urinary excretion of radiolabeled vitamin B12 after “flushing” IM injection of B12 @ 6%-30% of oral dose within 24 hr.

Sedimentation rate:  Male / Female.  Wintrobe:  0-5 mm/hr / 0-15 mm/hr.   Westergren: 0-15 mm/hr / 0-20 mm/hr.

Transferrin saturation, serum: 20%-50%.

Volume:  Male / Female.  Blood:  52-83 ml/kg / 50-75 ml/kg.  Plasma: 25-43 ml/kg / 28-45 ml/kg.  Red cell: 20-36 ml/kg /19-31 ml/kg.

Differential cell count of bone marrow:   Myeloid cells:  Neutrophilic series:  Myeloblasts: 0.3%-5.0%, Promyelocytes:  1%-8%, Myelocytes:  5%-19%, Metamyelocytes:  9%-24%, Bands:  9%-15%, Segmented cells:  7%-30%, Eosinophil precursors:  0.5%-3.0%, Eosinophils:  0.5%-4.0%, Basophilic series:  0.2%-0.7%.

Erythroid cells:  Pronormoblasts:  1%-8%, Polychromatophilic normoblasts    7%-32%, Megakaryocytes: 0.1%.

Lymphoreticular cells:   Lymphocytes:  3%-17%, Plasma cells:  0%-2%, Reticulum cells:  0.1%-2.0%, Monocytes:  0.5%-5.0%, Myeloid/erythroid ratio:  0.6-2.7.

Endocrine Labs:

Adrenocorticotropin (ACTH):  15-100 pg/ml

Calcitonin:  Basal @ 0.15-0.35 ng/ml, stimulated @ <0.6 ng/ml.

Catecholamines, free urinary:  <110 µg/24 hr

Chorionic gonadotropin (hCG):   Pregnancy 1st mo @ 10-10,000 mIU/ml, 2nd-3rd @ 10,000-100,000 mIU/ml.  2nd trimester @ 10,000-30,000 mIU/ml, 3rd trimester @ 5000-15,000 mIU/ml.  Nonpregnant @ ❤ mIU/ml.

Cortisol:  8 AM @ 5-25 µg/dl, 8 PM @<10 µg/dl.   Cosyntropin stimulation @ >10 µg/dl rise over baseline (30-90 min after 0.25 mg cosyntropin IM/IV).  Overnight suppression (8 AM  after 1 mg dexamethasone PO at 11 PM) @ 5 µg/dl.   Urine @ 20-70 µg/24 hr.

C-peptide:  0.28-0.63 pmol/ml.

11-Deoxycortisol:  Basal @ 0-1.4 µg/dl.  Metyrapone stimulation (30 mg/kg PO 8 hr prior to level) @ >7.5 µg/dl.

Epinephrine, plasma:  <35 pg/ml.

Estradiol:  Male @ 20-50 pg/ml.  Female @ 25-200 pg/ml.

Estrogens, urine:  inc during pregnancy, dec after menopause.  Male / Female.   Total @ 4-25 µg/24 hr / 5-100 µg/24 hr.  Estriol @ 1-11 µg/24 hr / 0-65 µg/24 hr. Estradiol @ 0-6 µg/24 hr / 0-l4 µg/24 hr.  Estrone @ 3-8 µg/24 hr / 4-31 µg/24 hr.

Etiocholanolone, serum: <1.2 µg/dl.

Follicle-stimulating hormone (FSH):  Male @ 2-18 mIU/ml.  Female Follicular phase @ 5-20 mIU/ml.  Peak midcycle @ 30-50 mIU/ml.  Luteal phase @ 5-15 mIU/ml.  Postmenopausal  @ >50 mIU/ml.

Free thyroxine index: 1-4 ng/dl.

Gastrin, serum (fasting): 30-200 pg/ml.

Growth hormone:   Adult, fasting @ <5 ng/ml.  Glucose load (100 g orally) @ <5 ng/ml.

Levodopa stimulation test: serum growth hormone after 0.5 g (500mg) levodopa PO while fasting @ >5 ng/ml rise over baseline within 2hr.

17-Hydroxycorticosteroids, urine:  Male @ 2-12 mg/24 hr.  Female @ 2-8 mg/24 hr.

5′-Hydroxyindoleacetic acid (5′-HIAA), urine: 2-9 mg/24 hr.

Insulin, plasma:  Fasting @ 6-20 µU/ml.  Hypoglycemia (serum glucose <50 mg/dl) @ <5 µU/ml.

17-Ketosteroids, urine:  <8 yo @ 0-2 mg/24 hr.  Adolescent @ 0-18 mg/24 hr.  Adult Male @ 8-18 mg/24 hr.  Female @ 5-15 mg/24 hr.

Luteinizing hormone (LH):  Male adult @ 2-18 mIU/ml.   Female adult Basal @ 5-22 mIU/ml, Ovulation @ 30-250 mIU/ml, Postmenopausal @ >30 mIU/ml.

Metanephrines, urine:  <1.3 mg/24 hr.

Norepinephrine:  Plasma @ 150-450 pg/ml.  Urine @ <100 µg/24 hr.

Parathyroid hormone:  C-terminal @ 150-350 pg/ml.  N-terminal @ 230-630 pg/ml.

Pregnanediol, urine:  Female Follicular phase @ <1.5 mg/24 hr, Luteal phase @ 2.0-4.2 mg/24 hr,  Postmenopausal @ 0.2-1.0 mg/24 hr.  Male @<1.5 mg/24 hr.

Progesterone:  Female Follicular phase @ 0.02-0.9 ng/ml, Luteal phase @ 6-30 ng/ml.  Male @ <2 ng/ml.

Prolactin:  Nonpregnant day @ 5-25 ng/ml, night @ 20-40 ng/ml.   Pregnant @ 150-200 ng/ml.

Radioactive iodine (131I) uptake (RAIU): 5%-25% at 24 hr (varies with iodine intake).

Testosterone, total plasma:  Bound in adolescent male @ <100 ng/dl.  Adult male @ 300-1100 ng/dl.  Female @ 25-90 ng/dl.  Unbound adult male @ 3-24 ng/dl. Female @ 0.09-1.30 ng/dl.

Thyroid-stimulating hormone:  <10 µU/ml.

Thyroxine (T4):  Total @ 4-11 µg/dl,  Free @ 0.8-2.4 ng/dl.

Thyroxine-binding globulin capacity: 15-25 µg T4/dl.

Thyroxine index, free:  1-4 ng/dl.

Tri-iodothyronine (T3):  70-190 ng/dl.

T3 resin uptake:  25%-45%.

Vanillylmandelic acid (VMA), urine:  1-8 mg/24 hr.

Glucocorticoid suppression:  overnight dexamethasone suppression test (8 AM serum cortisol after 1 mg dexamethasone orally at 11 PM) @ 5 µg/dl.

Glucocorticoid stimulation: cosyntropin stimulation test (serum cortisol 30-90 min after 0.25 mg cosyntropin IM or IV) @ >10 µg/ml more than baseline serum cortisol.

Metyrapone test:  8 AM serum deoxycortisol after 30 mg/kg metyrapone PO at midnight)@ >7.5 µg/dl.

Aldosterone suppression: sodium depletion test (urine aldosterone collected on day 3 of 200 mEq day/sodium diet) @ <20 µg/24 hr.

Glucose tolerance test:  serum glucose after 100 g glucose PO.  60 min after ingestion @ <180 mg/dl.  90 min @ <160 mg/dl.  120 min @ <125 mg/dl.  Add 10 mg/dl for each decade over 50 years of age.

Growth hormone suppression: glucose tolerance test (serum growth hormone after 100g glucose orally after 8 hr fast) @ <5 ng/ml within 2 hr.

Luteinizing hormone (LH) stimulation: gonadotropin releasing hormone (GnRH) test (serum LH after 100 µg GnRH IM/IV) @ 4- to 6-fold rise over baseline.

Thyroid-stimulating hormone (TSH) stimulation: thyrotropin-releasing hormone (TRH) stimulation test (serum TSH after 400 µg TRH IV) @ >2-fold rise over baseline within 2hr.

Radioactive iodine uptake (RAIU): suppression test (RAIU on day 7 after 25 µg tri-iodothyronine PO 4 times daily) @ <10% to <50% baseline.

Commonly Used Abbreviations:   Links:  E:   J:  N:  S:

1/2 NS = 0.45% saline solution

5-HIAA = 5-hydroxyindoleacetic acid

5-HT = serotonin

17-OHCS = 17-hydroxcorticosteroids

AAA = apply to affected area, abd aortic aneurysm

ac = ante cibum (before meals)

ABG = arterial blood gas

Ab = antibody

ABI = ankle brachial index (in PVD)

Abx = antibiotics

ac = before meals

ACD = anemia of chronic dz

ACT = activated clotting time

ACTH = adrenocorticotropic hormone

Ad = R ear (aurio dextra)

ad lib = as needed or desired

AD = autosomal dominant

ADH = antidiuretic hormone

ADL = activities of daily living

AF = atrial fibrillation

AFB = acid fast bacillus

AK = actinic keratosis

AP = alkaline phosphatase

AR – autosomal recessive

ALL = acute lymphocytic leukemia

ALT = alanine amino-transferase

am = morning

AMA = against medical advice

AMI = acute myocardial infarction

AML = acute myelogenous leukemia

amp = ampule

AMV = assisted mandatory (mode) ventilation

ANA = antinuclear antibody

ante = before

AP = anteroposterior, alk phos

AR = autosomal recessive

ARB = angiotensin receptor blocker

ARDS = adult respiratory distress syndrome

ARF = acute renal failure

ASA = acetylsalicylic acid, aspirin

ASO = antistreptolysin

AST = aspartate amino-transferase

AVB = atriovenous block

AVM = atrial venous malformation

AVN = avascular necrosis

BAL = blood alcohol level

BBB = bundle branch block

BCC = basal cell carcinoma

BID = bis in die (twice a day)

B12 = vitamin B-12

BM = bowel movement, bone marrow

BMD = bone mineral density

BMR = basal metabolic rate

BMT = bone marrow transplant

BP = blood pressure

BPH = benign prostatic hypertrophy

BS = bowel sounds

BUN = blood urea nitrogen

BSA = body surface area

Bx = biopsy

CA = cancer

Cal = calorie (kilocalorie)

c/o = complaint of

c cum (with)

C/ S or C & S = culture and sensitivity

C = centigrade

Ca = calcium

CAD = coronary artery disease

cap = capsule

CBC = complete blood count

CBZ = carbamezapine

cc = cubic centimeter, creatinine clearance

CCB = calcium channel blocker

CCU = coronary care unit

CF = cystic fibrosis

CFU = colony forming units

Chem 7  = basic metabolic panel, 17 = comprehensive, which includes electrolytes, renal and liver function tests.  New Medicare Labs:  **Electrolyte Panel (#4): Na, K, Cl, CO2.  **BMP: #8: Chem 7 with Ca.   **Renal Panel: #10 BMP + Alb & PO4.   **CMP #14: BMP + Alb, AP, AST, ALT, Tb, Dbili.   **ECMP #17: CMP +Mg, P, LDH.  **Hepatic: Alb, Tbili, Dbili, AP, Tp, ALT, AST.

cm = centimeter

CMV = cytomegalovirus

CNS = central nervous system

CO2 = carbon dioxide

COPD = chronic obstr pulm dz

CP = chest pain

CPK-MB = myocardial-specific CPK

Cr = creatinine

CrCl = creatinine clearance

CRF = chronic renal failure

CSF = cerebrospinal fluid

CT = computerized tomography

CTA = cotton tip applicator

CTD = connective tissue disease

CTX = contraction

CV = cardiovascular

CVA = cerebrovascular accident, costovertebral angle

CVD = cardiovascular disease

CVP = central venous pressure

Cx = culture

CXR = chest x-ray

DA = dopamine

d/c = discharge or discontinue

D5W = 5% dextrose water solution

DBP = diastolic blood pressure

DIC = dissemin. Intravasc Coagulation

Diff = differential cell count

DHP = dihydropteridine

DJD = degenerative joint disease

DKA = diabetic ketoacidosis

dL = deciliter

DM = diabetes mellitus

DNR = do not resuscitate

DOC = drug of choice

DOE = dyspnea on exertion

DOT = directly observed therapy

Doxy = doxycycline

DT’s = delirium tremens

DTR = deep tendon reflex

DVT = deep vein thrombosis

Dx = diagnosis

Ddx = differential diagnosis

DUB = dysfunctional uterine bleeding

Dz = disease

EBV = Epstein Barr virus

ECG = electrocardiogram = EKG

ECT = electroconvulsive therapy

EDC = estimated date of confinement (due date)

EE = ethinyl estradiol

EEG = electroencephalogram

EGA = estimated gestational age

ELISA = enzyme-linked immunoabsorbant assay

EM = erythema multiforme

EMB = endometrial biopsy

Emyc = erythromycin

EPO = erythropoietin

EPS = extra pyramidal symptoms

ERCP = endoscopic retrograde cholangiopancreatography

ERT = estrogen replacement therapy

ESR = erythrocyte sedimentation rate

ET = endotracheal tube

ETD = eustachian tube dysfunction

ETOH = alcohol

Fb = foreign body

FBS = fasting blood sugar

F/C = fever and chills

FEV1 = forced expiratory volume (1 sec)

FHT/ FHR = fetal heart tones/ rate

FiO2 = fractional inspired oxygen

FOB = fecal occult blood

FSP = fibrin split product

FVC = functional vital capacity

Fx = fracture

G = gram(s)

GC = gonococcal; gonococcus

GBS = GBBHS = Group B Beta Hem Strep

GFR = glomerular filtration rate

GH = growth hormone

GI = gastrointestinal

gm = gram

GN = glomerular nephritis

gt = drop

gtt = drops

GU = genitourinary

h or hr = hour

H20 = water

HA = headache

Hb = hemoglobin concentration

HCO3 = bicarbonate

HCG = human chorionic gonadotropin

HCT hematocrit

HCTZ = hydrochlorothiazide or hydrocortisone

HCW = Health Care Worker

HDL = high-density lipoprotein

HF = heart failure

Hg = mercury

HI = homicidal ideation

HIV = human immunodeficiency virus

hr = hour

HOCM = HCM = hypertrophic cardiomyopathy

HR = heart rate

HRT = hormone replacement therapy

HS = hora somni (bedtime)

HSM = hepato-splenomegaly

HSP = Henoch-Schonlein purpura

HTN = hypertension

HUS = hemolytic uremic syndrome

Hx = history

ICP = intracranial pressure

IBD = inflammatory bowel disease

IBS = irritable bowel syndrome

ICP = intracranial pressure

IDA = iron deficiency anemia

ILD = interstitial lung disease

IM = intramuscular

I & D = incision and drainage

I & O =intake and output

IOP = intraocular pressure

IU = international units

ICU = intensive care unit

IgM = immunoglobulin M

IMV = intermittent mandatory ventilation

INH = isoniazid

INI = if not improved, RTC.

INR = International normalized ratio

IV = intravenous or intravenously

IVD = intravenous drug

IVF = intravenous fluids, in-vitro fertilization

IVP = intravenous pyelogram, intravenous piggyback

JRA = juvenile rheumatoid arthritis

K = potassium

kcal = kilocalorie

KCL = potassium chloride

KOH = potassium hydroxide

KUB = x-ray of abdomen

L = liter

LBBB = left bundle branch block

LPB = lower back pain

LDH = lactate dehydrogenase

LDL = low-density lipoprotein

LE = lower extremity

LFT = liver function tests

liq = liquid

LLSB = left lower sternal border

LLQ = left lower quadrant

LMN = lower motor neuron

LMP = last menstrual period

LN2 = liquid nitrogen

LOC = loss of consciosness

LP = lumbar puncture,

LR = lactated Ringer’s

LV = left ventricle

LVH = left ventricular hypertrophy

mEq = milliequivalent

MD = muscular dystrophy

Mg = magnesium, milligram, myasthenia gravis

MgSO4 = Magnesium Sulfate

MI = myocardial infarction

MIC = minimum inhibitory concentration

mL = milliliter

mm = millimeter, multiple myeloma

MOM = Milk of Magnesia

MR = mitral regurg

MRI = magnetic resonance imaging

MS = mitral stenosis, multiple sclerosis, mental status, morphine sulfate

MSE = mental status exam

MTX = methotrexate

MVP mitral valve prolapse

Na = sodium

NaHCO3 = sodium bicarbonate

NE = norepinephrine

Neuro = neurologic

NCV = nerve conduction velocity

NGT = nasogastric tube

NKA = no known allergies

NM(J) = neuro muscular (junction)

NMT = no more than (maximum dose)

NLT = no less than (minimum age to use drug)

NPH = neutral protamine, normal pressure hydrocephalus

NPO = nulla per os (nothing by mouth)

NS = normal saline solution (0.9%)

NSAIDs = nonsteroidal anti-inflammatory drugs

NTG = nitroglycerine

N/V/D = nausea, vomiting, diarrhea

NWB = non-weight bearing.

OCD = obsessive compulsive disorder

OCP = oral contraceptive pill

OD = right eye, overdose, optometrist

oint = ointment

OS = left eye (oculus sinister)

Osm = osmolality

OT = occupational therapy

OTC = over the counter

OU = each eye

oz = ounce

p = post after, Phosphate

pc = post cibum (after meals)

PA = posteroanterior, pulmonary artery

PAC = premature atrial contraction

PaO2 = arterial oxygen pressure

pAO2 = partial pressure of oxygen

pc = after meals

PCA = patient controlled anesthesia

PCN = penicillin

pCO2 = partial pressure of carbon dioxide

PE = pulmonary embolism, physical exam

PEEP positive end-expiratory pressure

per = by

PFS = patella-femoral syndrome

PFT = pulmonary function test

PG or PGE = prostaglandin

pH = hydrogen ion concentration (H+)

PID = pelvic inflammatory disease

pm = afternoon

PND = paroxysmal nocturnal dyspnea

PO = orally, per os

pO2 = partial pressure of oxygen

Post cib = after meals (post cibos)

polys = polymorphonuclear leukocytes

PP = pathophysiology

PPD = purified protein derivative

PPI = proton pump inhibitor

PR = per rectum

prn = pro re nata (as needed)

PT = physical therapy, pro-thrombin time

PTCA = percutaneous transluminal coronary angioplasty

PTT = partial thromboplastin time

PV or Px = prevention

PUD = peptic ulcer disease

PVC = premature ventricular contraction

PVD = peripheral vascular disease

q = (every) q6h, q2h every 6 hours, every 2h

QID = quarter in die (four times a day)

qAM = every morning

qd = quaque die (every day)

qh = every hour

qHS = every night before bedtime

QID = 4 times a day

Ql = as much as desired (quantum libet)

QOD = every other day

qs = quantity sufficient

qt = quart

R = right

RAD = right axis deviation

RAE = right atrial enlargement

R/O = rule out

RA = rheumatoid arthritis, room air, right atrial

RAST = radioallergosorbent test

RF = rheumatic fever

RMSF = rocky mountain spotted fever

RPR = syphilis test

RR = Respiratory rate

ROM = range of motion

RSD = reflex sympathetic dystrophy

RTA = renal tubular acidosis

RTC = return to clinic (pt to come back)

RV = right ventricle, residual volume

s = sine (without)

s/p = status post

sat = saturated

SBE: subacute bacterial endocarditis

SBP = systolic blood pressure

SC = subcutaneously

SE = side effect

SED = SE discussed (chart if start a new med), ESR

SES = socioeconomic status

SI = suicidal ideation

SIADH = syndrome of inappropriate antidiuretic hormone

SJS = Stevens Johnson syndrome

SK = seborrheic keratosis

SL = sublingually under tongue

SLE = systemic lupus erythematosus, slit lamp exam

SMA-7, 10, 17 = sequential multiple analysis

SMX = sulfamethoxazole

SOB = shortness of breath = DOE

sol = solution

SPEP = serum protein electrophoresis

SQ = under the skin

SR = sustained release

S(S)RI = selective serotonin reuptake inhibitor

S/s = signs and symptoms of disease

SSC = squamous cell carcinoma

STAT = statim (immediately)

STD = sexually transmitted disease

susp = suspension

T-½ = half life (of a drug)

TCN = tetracycline

TID = ter in die (three times a day)

T4 = Thyroxine level

tab = tablet

TB = tuberculosis

Tbsp = tablespoon

TCA = tricyclic antidepressant

Temp = temperature

TIA = transient ischemic attack

TKO = to keep open, an infusion rate (~500 mL/24h) just enough to keep the IV from clotting, not the same as saline lock or Heplock.

TL = toxic level

TMJ = temporomandibular joint

TMP = trimethoprim

TMP-SMX = trimethoprim-sulfa-methoxazole

TPA = tissue plasminogen activator

TS/ TR = tricuspid stenosis/ regurge

TSH thyroid-stimulating hormone

tsp = teaspoon

TPN = total parenteral nutrition

TSS = toxic shock syndrome

TT = thrombin time

TTP = tender to palpation

Tx = treatment

U = units

UA = uric acid

U/A or Ua = urinalysis

UC = ulcerative colitis

UD = as directed

UDS = urine drug screen (tox)

ug = microgram

UFH = unfractionated heparin

ULN = upper limits of normal

um = micrometer

UO = urine output

URI = upper respiratory infection

UPEP = urine protein electrophoresis

U/S = ultrasound

UTI = urinary tract infection

UV = ultraviolet light

V = vitamin, V-C, V-E, V-B6 etc

VAC vincristine, adriamycin, and cyclophosphamide

vag = vaginal

VC = vital capacity

VDRL = Venereal Disease Research Laboratory

V fib = ventricular fibrillation

VGE = viral gastroenteritis

VLDL = very low-density lipoprotein

Vol = volume

VS = vital signs

VSD = ventricular septal defect

VT = ventricular tachycardia

WBC = white blood count

X = times

Zn = zinc

 

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