Hepatic Failure/GI/Endocrine Emergencies
Hypoglycemia can be caused by excessive insulin administration, reduced intake of glucose (rarely
the cause of severe hypoglycemia in the absence of insulin administration), decreased insulin
resistance (weight loss, adrenal or pituitary insufficiency), decreased clearance of insulin (renal or
hepatic insufficiency), or other drugs (commonly sulfonylureas, meglitinides, and ethanol; possibly
pentamidine, quinine, quinolones, insulin-like growth factor 1, Ξ²-blockers, or ACE inhibitors).
In a retrospective cohort study of mixed ICU patients, independent predictors of hypoglycemia
(BG less than 45 mg/dL) included continuous venovenous hemofiltration with bicarbonate-based
replacement solution (OR 14; 95% CI, 1.8β106), a decrease of nutrition without adjustment for
insulin infusion (OR 6.6; 95% CI, 1.9β23), diabetes (OR 2.6; 95% CI, 1.5β4.7), insulin use (OR 5.3;
95% CI, 2.8β11), sepsis (OR 2.2; 95% CI, 1.2β4.1), and inotropic support (OR 1.8; 95% CI, 1.1β2.9).
Other studies of critically ill patients have identified renal insufficiency, diabetes, mechanical
ventilation, female sex, greater severity of illness, longer ICU stay, liver disease, immunocompromised
state, and medical or nonelective admission as risk factors for hypoglycemia.
| d. | Renal insufficiency in the setting of insulin administration should be particularly noted because |
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patients with renal failure have decreased clearance of insulin, which may prolong the duration of
hypoglycemia.
Management
For conscious patients without severe symptoms, oral glucose should be ingested (juice, soda, or
dextrose tablets).
The typical initial glucose dose is 15 g, which should be repeated in 15β20 minutes if symptoms
have not improved or if BG remains low.
ii.
Because the response to this βrescue glucoseβ is transient (less than 2 hours), it should be
followed by more substantial glucose intake as a snack or meal.
Parenteral therapy is necessary for patients unable to take glucose orally or hospitalized patients
with moderate or severe hypoglycemia.
Glucagon 1 mg promotes hepatic glucogenesis and glycogenolysis. It is a useful therapy for
patients with type 1 diabetes (often outside a health care setting) and those without diabetes,
but it is less useful in patients with type 2 diabetes because it stimulates insulin secretion and
glycogenolysis. Nausea/vomiting is a common adverse effect of glucagon.
ii.
Hospitalized patients with severe hypoglycemia (either severe symptoms or BG less than 40
mg/dL) or those receiving an insulin infusion with BG less than 70 mg/dL (less than 100 mg/
dL in neurologic injured patients) should be treated with intravenous dextrose.
| (a) | Insulin infusion should be discontinued, as appropriate. |
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| (b) | Administer 10β20 g of 50% dextrose solution (20β40 mL of 50% dextrose in water). |
| (c) | The BG measurement should be repeated in 15 minutes, with additional dextrose doses |
administered to achieve a BG greater than 70 mg/dL.
| (d) | Care should be taken to avoid excessive dextrose administration in order to avoid |
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iatrogenic hyperglycemia and because glucose variability has been associated with
adverse outcomes.
| (e) | To prevent hypoglycemia, the insulin regimen should be reassessed if BG is less than 100 |
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mg/dL.
Clinical presentation
Thyroid crisis is characterized by severe manifestations of hyperthyroidism.
Diagnosis can be established on the basis of clinical presentation in a patient with laboratory
evidence of hyperthyroidism.