Hepatic Failure/GI/Endocrine Emergencies
iii.
A second multicenter study was terminated early because of several protocol violations.
Intensive insulin therapy was not associated with a benefit in ICU mortality (17.2% vs. 15.3%,
p=0.41), but patients allocated to intensive insulin therapy more commonly developed severe
hypoglycemia (BG of 40 mg/dL or less; 8.7% vs. 2.7%, p<0.0001).
iv.
The NICE-SUGAR study, evaluated intensive insulin therapy (target BG 81–108 mg/dL) or
conventional glucose control (BG of 180 mg/dL or less) in more than 3000 patients.
| (a) | At 90 days, intensive insulin therapy was associated with increased mortality (27.5% vs. |
|---|
24.9%, p=0.02).
| (b) | Severe hypoglycemia (BG of 40 mg/dL or less) was more common in patients allocated to |
|---|
intensive insulin therapy (6.8% vs. 0.5%, p<0.0001).
| (c) | Intensive insulin therapy was not associated with a benefit in ICU or hospital length of |
|---|
stay, days of mechanical ventilation, or need for renal replacement therapy.
A 2023 randomized study of 9230 medical and surgical ICU patients compared liberal glucose
control (insulin initiated when BG greater than 215 mg/dL) to intensive insulin control (BG
goal 80–110 mg/dL).
| (a) | Median absolute difference in daily BG between groups was about 28 mg/dL. |
|---|---|
| (b) | There were no differences between groups for ICU length of stay, 90-day mortality, or |
severe hypoglycemia between groups.
A meta-analysis that included seven randomized controlled trials and 11,425 patients found that
intensive insulin therapy was not associated with a difference in 28-day mortality (OR 1.04; 95%
CI, 0.93–1.17) but was associated with a significant increase in the incidence of hypoglycemia (OR
7.7; 95% CI, 6.0–9.9).
Children and Adults consider it good practice to maintain blood glucose less than 180 mg/dL
through evaluation of glucose intake, additional monitoring, and insulin therapy.
Guidelines suggest against titrating insulin infusion to goal BG of 80–139 mg/dL and favor a
target of 140–200 mg/dL to reduce risk of hypoglycemia.
Clinical presentation
Glucose is an obligate molecule for brain function. The brain cannot produce glucose, efficiently
use alternative fuels, or store substantial amounts of glycogen, so maintenance of brain function
requires a continuous supply of glucose from the circulation.
Multiple mechanisms exist to maintain blood glucose within physiologic range. These complex
pathways are multifaceted and include pancreatic (decreased insulin and increased glucagon),
central nervous system (CNS) (increased norepinephrine and acetylcholine), adrenal medulla
(increased epinephrine), and liver (increased glycogenolysis and gluconeogenesis) involvement.
In the early stages of hypoglycemia, symptoms such as sweating, anxiety, hunger, palpitations,
tremor, and arousal are present. As hypoglycemia persists and worsens, confusion, dizziness, and
difficulty speaking develop. Severe hypoglycemia leads to seizures and hypoglycemic coma.
| d. | Typically, complete recovery of symptoms occurs with glucose administration, but permanent |
|---|
brain damage may occur in patients with severe prolonged hypoglycemia.
Hypoglycemia, a reversible cause of cardiac arrest, should be considered for patients with an
unclear reason for cardiac arrest.
Neurologic symptoms of hypoglycemia may be masked by sedation, and the counterregulatory
response may be impaired or masked (e.g., in circulatory shock).