1 Comment

40 DIABETIC KETOACIDOSIS AND HYPEROSMOLAR COMA

40 DIABETIC KETOACIDOSIS AND HYPEROSMOLAR COMA
Harrison’s Manual of Medicine

40

DIABETIC KETOACIDOSIS AND HYPEROSMOLAR COMA

Diabetic Ketoacidosis
Nonketotic Hyperosmolar State
Bibliography

Diabetic ketoacidosis (DKA) and nonketotic hyperosmolar state (NKHS) are acute complications of diabetes mellitus (DM). DKA is seen primarily in individuals with type 1 DM and NKHS in individuals with type 2 DM. Both disorders are associated with absolute or relative insulin deficiency, volume depletion, and altered mental status. The metabolic similarities and differences in DKA and NKHS are summarized in Table 40-1.

Table 40-1 Laboratory Values in Diabetic Ketoacidosis (DKA) and Nonketotic Hyperosmolar States (NKHS) (Representative Ranges at Presentation)

DIABETIC KETOACIDOSIS
ETIOLOGY   DKA results from insulin deficiency with a relative or absolute increase in glucagon and may be caused by inadequate insulin administration, infection (pneumonia, UTI, gastroenteritis, sepsis), infarction (cerebral, coronary, mesenteric, peripheral), surgery, or drugs (cocaine).
CLINICAL FEATURES   The initial symptoms of DKA include anorexia, nausea, vomiting, polyuria, and thirst. Abdominal pain, altered mental function, or frank coma may ensue. Classic signs of DKA include Kussmaul respirations and an acetone odor on the pt’s breath. Volume depletion can lead to dry mucous membranes, tachycardia, and hypotension. Fever and abdominal tenderness may also be present. Laboratory evaluation reveals hyperglycemia, ketosis (b-hydroxybutyrate>acetoacetate), and metabolic acidosis (arterial pH 6.8–7.3) with an increased anion gap (Table 40-1). The fluid deficit is often 3–5L. Despite a total body potassium deficit, the serum potassium at presentation may be normal or mildly high as a result of acidosis. Leukocytosis, hypertriglyceridemia, and hyperlipoproteinemia are commonly found as well. Hyperamylasemia is usually of salivary origin but may suggest a diagnosis of pancreatitis. The measured serum sodium is reduced as a consequence of hyperglycemia (1.6 meq reduction for each 100=mg/dL rise in the serum glucose).

TREATMENT
The management of DKA is outlined in Table 40-2.

Table 40-2 Management of Diabetic Ketoacidosis

NONKETOTIC HYPEROSMOLAR State
ETIOLOGY   Insulin deficiency and inadequate fluid intake are the underlying causes of NKHS. Hyperglycemia induces an osmotic diuresis that leads to profound intravascular volume depletion. NKHS is often precipitated by a serious, concurrent illness such as myocardial infarction or sepsis, and compounded by conditions that impede access to water. Thiazide diuretics, glucocorticoids, and phenytoin have also been associated with the development of NKHS.
CLINICAL FEATURES   Presenting symptoms include polyuria, thirst, and altered mental state, ranging from lethargy to coma. Notably absent are symptoms of nausea, vomiting, and abdominal pain and the Kussmaul respirations characteristic of DKA. The prototypical pt is a mildly diabetic, elderly individual with a several week history of polyuria, weight loss, and diminished oral intake. The laboratory features are summarized in Table 40-1. In contrast to DKA, acidosis and ketonemia are usually not found; however, a small anion gap may be due to lactic acidosis, and moderate ketonuria may occur from starvation. Though the measured serum sodium may be normal or slightly low, the corrected serum sodium is usually increased (add 1.6 meq to measured sodium for each 100=mg/dL rise in the serum glucose).

TREATMENT
The precipitating problem should be sought and treated. Sufficient IV fluids (2–3 L of 0.9% normal saline over the first 1–3 h) must be given to support circulation and urine flow. The calculated free water deficit (usually 8–10 L) should be reversed over the next 1–2 days, using 0.45% saline initially then 5% dextrose in water. Potassium repletion is usually necessary. The plasma glucose may drop precipitously with hydration alone, though insulin therapy with an intravenous bolus of 5–10 units followed by a constant infusion rate (3–7 units/h) is usually required. Glucose should be added to intravenous fluid when the plasma glucose falls to 250 mg/dL. The insulin infusion should be continued until the patient has resumed eating and can be transferred to a subcutaneous insulin regimen. The mortality rate approaches 50%.

Bibliography

For a more detailed discussion, see Powers AC: Diabetes Mellitus, Chap 333, p. 2109; in HPIM-15.

Advertisements

One comment on “40 DIABETIC KETOACIDOSIS AND HYPEROSMOLAR COMA

  1. interesting and informative post thanks a lot for posting it.http://www.kvforum.net

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s

%d bloggers like this: