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30 SHOCK

30 SHOCK
Harrison’s Manual of Medicine

30

SHOCK

Definition
Clinical Manifestations
Physical Examination
Laboratory
Bibliography

Definition
Condition of severe impairment of tissue perfusion. Rapid recognition and treatment are essential to prevent irreversible organ damage. Common causes are listed in table 30-1.

Table 30-1 Common Forms of Shock

Clinical Manifestations
Hypotension (systolic bp <90), tachycardia, tachypnea, pallor, restlessness, and altered sensorium; signs of intense peripheral vasoconstriction; weak pulses; cold clammy extremities [note: in distributive (e.g., septic) shock, vasodilatation predominates and extremities are warm]. Oliguria (<20 mL/h) and metabolic acidosis common.

Approach to the Patient

Tissue perfusion must be restored immediately (see below); also obtain history for underlying cause, including

Known cardiac disease (coronary disease, CHF, pericarditis)

Recent fever or infection (leading to sepsis)

Drugs, i.e., excess diuretics or antihypertensives

Predisposing conditions for pulmonary embolism (Chap. 132)

Possible bleeding from any site, particularly GI tract.

Physical Examination

Jugular veins are flat in oligemic or distributive shock; jugular venous distention (JVD) suggests cardiogenic shock; JVD in presence of paradoxical pulse (Chap. 112) may reflect cardiac tamponade (Chap. 120).

Look for evidence of CHF (Chap. 116), murmurs of aortic stenosis, acute regurgitation (mitral or aortic), ventricular septal defect.

Check for asymmetry of pulses (aortic dissection).

Tenderness or rebound in abdomen may indicate peritonitis or pancreatitis; high-pitched bowel sounds suggest intestinal obstruction. Perform stool guaiac to rule out GI bleeding.

Fever and chills usually accompany septic shock. Sepsis may not cause fever in elderly, uremic, or alcoholic patients.

Skin lesion may suggest specific pathogens in septic shock: petechiae or purpura (Neisseria meningitidis), ecythyma gangrenosum (Pseudomonas aeruginosa), generalized erythroderma (toxic shock due to Staphylococcus aureus or Streptococcus pyogenes).
Laboratory
Obtain hematocrit, WBC, electrolytes. If actively bleeding, check platelet count, PT, PTT, DIC screen. Arterial blood gas usually shows metabolic acidosis (in septic shock, respiratory alkalosis precedes metabolic acidosis). If sepsis suspected, draw blood cultures, perform urinalysis, and obtain Gram stain and cultures of sputum, urine, and other suspected sites.
Obtain ECG (myocardial ischemia or acute arrhythmia), chest x-ray (CHF, tension pneumothorax, aortic dissection, pneumonia). Echocardiogram may be helpful (cardiac tamponade, CHF). Central venous pressure or pulmonary capillary wedge (PCW) pressure measurements may be necessary to distinguish between the different categories of shock (Table 30-2): Mean PCW < 6 mmHg suggests oligemic or distributive shock; PCW > 20 mmHg suggests left ventricular failure. Cardiac output is decreased in pts with cardiogenic and oligemic shock, and usually increased initially in septic shock.

Table 30-2 Hemodynamic Profiles in Shock States

TREATMENT
Aimed at rapid improvement of tissue hypoperfusion and respiratory impairment:

1.
Serial measurements of bp (intraarterial line preferred), heart rate, continuous ECG monitor, urine output, pulse oximetry, blood studies: Hct, electrolytes, creatinine, BUN, ABGs, calcium, phosphate, lactate, urine Na concentration (<20 mmol/L suggests volume depletion). Continuous monitoring of CVP and/or pulmonary artery pressure, with serial PCW pressures.

2.
Augment systolic bp to >100 mmHg: (a) place in reverse Trendelenburg position; (b) IV volume infusion (500–1000 mL bolus), unless cardiogenic shock suspected (begin with normal saline, then whole blood, dextran, or packed RBCs, if anemic); continue, volume replacement as needed to restore vascular volume; (c) vasoactive drugs are added after intravascular volume is optimized; administer vasopressors (Table 30-3) if systemic vascular resistance (SVR) is decreased (begin with norepinephrine or dopamine; for persistent hypotension add phenylephrine or vasopressin); (d) if CHF present, add inotropic agents (usually dobutamine) (Chap. 116; Table 116-2); aim to maintain cardiac index >2.2 (L/m2)/min [>4.0 (L/m2)/min in septic shock].

Table 30-3 Vasopressors Used in Shock States a

3.
Administer 100% O2; intubate with mechanical ventilation if PO2 <70 mmHg.

4.
If severe metabolic acidosis present (pH < 7.15), administer NaHCO3 (44.6–89.2 mmol).

5.
Identify and treat underlying cause of shock. Cardiogenic shock in acute MI is discussed in Chap. 121. Emergent coronary revascularization may be lifesaving if persistent ischemia is present.
Septic shock can rapidly result in the acute respiratory distress syndrome, acute renal failure, DIC, multiple organ failure, or death. Successful management relies on immediate hemodynamic and respiratory support and eliminating the infecting organism. A Gram stain of the primary site of infection, if known, helps to direct antimicrobial therapy. In overwhelming sepsis (e.g., pneumococcal bacteremia in a splenectomized patient), the organism may sometimes be identified on buffy coat smear of peripheral blood. If no source of infection is identified, initiate empirical antibiotic therapy after cultures of potentially infected tissues are obtained (e.g., blood urine, sputum, pleural effusion, CSF).
It is essential to drain foci of septic material. Potentially infected intravenous or urinary catheters should be removed and cultured. Look for occult sites of infection, e.g., sinusitis, perianal abscess, dental abscess, infected decubitus ulcer. In suspected urosepsis, a renal or perinephric abscess can be evaluated by ultrasound, CT, or MRI.
Hemodynamic support must be provided as in other causes of shock to maintain tissue perfusion. Large volumes of intravascular fluid are often necessary and should be gauged by the PCW pressure (desired range 12–15 mmHg) or CVP (desired range 10–12 cmH2O) and urinary output (aim for £30 mL/h). Maintain systolic bp £90 mmHg by repleting intravascular volume and, if necessary, by vasopressors (Table 30-3): dopamine 5–10 (µg/ kg)/min, or norepinephrine 2–8 (µg/kg)/min. In refractory shock, vasopressin or phenylephrine may be added.
Consider the possible complication of adrenal insufficiency if patient has septic shock with fulminant N. meningitidis infection, refractory hypotension, recent glucocorticoid use, disseminated tuberculosis, or AIDS. Administer hydrocortisone 50 mg IV q6h while evaluating this possibility (Chap. 172).

Bibliography

For a more detailed discussion, see Maier RV: Shock, Chap. 38, 222; and Munford RS: Sepsis and Septic Shock, Chap. 124, p. 799, in HPIM-15.

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2 comments on “30 SHOCK

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