Page 1406 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 101: Hyperglycemic Crisis and Hypoglycemia 979

Further information can be derived from the response of plasma glu-
TABLE 101-5 Causes of Hypoglycemia
cose, insulin, C peptide, proinsulin, and ketones 1 hour after treatment
Anorexia with 1 mg IV glucagon.
Drugs Hormone deficiency The presence of circulating insulin while hypoglycemic suggests
• Alcohol • ACTH inappropriate endogenous production (insulin secretagogue use or an
• Chloroquine • Cortisol insulin producing tumor) or exogenous insulin use. The majority of
• Cibenzoline • Catecholamine secretagogues can be detected through urinalysis. Exogenous insulin
85
• Gatifloxacin • Glucagon would result in detectable insulin but absent C peptide and proinsulin,
• Glucagon (during endoscopy) Endogenous hyperinsulinemia as these components are not present in commercially available insulins.
• Insulin • Insulinoma Often symptomatic hypoglycemia is treated quickly in the hospital
• Indomethacin • Nesidioblastosis setting without performing investigations to elucidate a cause. Ideally
• Meglitinides • Noninsulinoma pancreatogenous hypoglycemia patients suspected of excess endogenous insulin production would have
• Pentamidine • Postgastric bypass hypoglycemia the above investigations done during a witnessed event. Alternatively, a
• Propranolol • Secretagogue use prolonged fast may be needed to reproduce symptomatic hypoglycemia.
• Quinine Insulin autoimmune hypoglycemia
• Salicylates Non islet cell tumor ■ TREATMENT
• Sulfonamides IGF-1 or IGF-2 secreting retroperitoneal tumors 82 Patients with DM should be concerned of the risk of hypoglycemia when
• Sulfonylureas Factitious/accidental
Critical illness their capillary blood glucose is <72 mg/dL (<4.0 mmol/L). Early treat-
ment with ingestion of fast-acting carbohydrates is preferred whenever
• Sepsis
• Burns possible. Parenteral use of glucagon or glucose can be used in the fasting
or unconscious patient. Frequent mild hypoglycemia or any episode
• Renal failure
• Hepatic failure of hypoglycemia requiring parenteral therapy should prompt a review of
the current therapy regimens.
• Cardiac failure
■ EVALUATION
The cause is frequently obvious in patients with DM or those who are KEY REFERENCES
critically ill. • Chua HR, Schneider A, Bellomo R. Bicarbonate in diabetic keto-
The Endocrine Society has issued evidenced-based guidelines on the acidosis—a systematic review. Ann Intensive Care. 2011;1(1):23.
investigation of hypoglycemic disorders in adults. A brief summary of • Committee on Fetus and Newborn, Adamkin DH. Postnatal
85
these guidelines is outlined. glucose homeostasis in late-preterm and term infants. Pediatrics.
Confirmation of a significant hypoglycemic event is aided by ensur- 2011;127(3):575-579.
ing patients without diabetes satisfy Whipple triad (see above). A clinical
evaluation should assess for evidence of likely causes such as drugs, critical • Cryer PE, Axelrod L, Grossman AB, et al. Evaluation and
illnesses, hormone deficiencies, and nonislet cell tumors. In the absence of management of adult hypoglycemic disorders: an Endocrine
these causes, the differential diagnosis should include the use of nonpre- Society Clinical Practice Guideline. J Clin Endocrinol Metab.
scribed exogenous insulin or an insulin secretagogue and excess endog- 2009;94(3):709-728.
enous insulin production. During a symptomatic hypoglycemic episode, a • Hamblin PS, Topliss DJ, Chosich N, Lording DW, Stockigt JR.
number of investigations can be performed (sometimes termed a “critical Deaths associated with diabetic ketoacidosis and hyperosmolar
sample”) to identify excess endogenous insulin production. coma. 1973-1988. Med J Aust. 1989;151(8):439, 441-442, 444.
• Plasma glucose • Kamat P, Vats A, Gross M, Checchia PA. Use of hypertonic saline
for the treatment of altered mental status associated with diabetic
• Insulin ketoacidosis. Pediatr Crit Care Med. 2003;4(2):239-242.
• C peptide • Kitabchi AE, Umpierrez GE, Murphy MB, et al. Management
• Proinsulin of hyperglycemic crises in patients with diabetes. Diabetes Care.
• β-hydroxybutyrate 2001;24(1):131-153.
• Circulating oral hypoglycemic agents • Laing SP, Swerdlow AJ, Slater SD, et al. The British Diabetic
Association Cohort Study, II: cause-specific mortality in patients with
• Insulin antibodies insulin-treated diabetes mellitus. Diabet Med. 1999;16(6):466-471.
• Marcin JP, Glaser N, Barnett P, et al. Factors associated with
adverse outcomes in children with diabetic ketoacidosis-related
TABLE 101-6 Physiological Response to Hypoglycemia cerebral edema. J Pediatr. 2002;141(6):793-797.
Arterial Plasma Glucose mg/dL (mmol/L) Response • Polonsky WH, Anderson BJ, Lohrer PA, Aponte JE, Jacobson AM,
Cole CF. Insulin omission in women with IDDM. Diabetes Care.
83 (4.6) Insulin secretion inhibited 1994;17(10):1178-1185.
68 (3.8) Glucagon secretion • Wolfsdorf J, Glaser N, Sperling MA; American Diabetes
Epinephrine secretion Association. Diabetic ketoacidosis in infants, children, and ado-
67 (3.7) Growth hormone secretion lescents: a consensus statement from the American Diabetes
Association. 2006;29:1150-1159.
Glucose transport into the brain reduced
58 (3.2) Cortisol secretion
Autonomic symptoms
51 (2.8) Neuroglycopenic symptoms REFERENCES
49 (2.7) Cognitive dysfunction Complete references available online at www.mhprofessional.com/hall

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