A 68-year-old woman presents to the emergency department after being found at home with confusion and lethargy. Her medical history includes GERD, obesity, non–insulin dependent type 2 diabetes, and depression with prior suicide attempts. Empty bottles of omeprazole, glyburide, and sertraline were found in her home. She is intubated for airway protection. Her admission laboratory test results are notable for a blood glucose of 33 mg/dL, and she is treated with an IV bolus of dextrose 50. Repeat laboratory tests an hour later show blood glucose 52 mg/dL.
Which of the following is most appropriate to treat her hypoglycemia?
Correct Answer: B
Critically ill patients can be hypoglycemic for numerous reasons, including the effects of medications, ethanol, sepsis, hepatic failure, renal failure, and the cessation of TPN. This patient’s hypoglycemia most likely results from an overdose of glyburide, a sulfonylurea oral hypoglycemic medication. Sulfonylureas act by increasing insulin release from pancreatic beta cells. The initial treatment for all hypoglycemic episodes should be a bolus of glucose, typically 0.5 to 1 g/kg of D50W. If a patient does not have intravenous access for emergent D50 administration, then IM glucagon is an effective alternative—raising blood glucose by promoting glycogenolysis and gluconeogenesis. After administering an initial glucose bolus, a dextrose infusion is typically required until the underlying cause of hypoglycemia has resolved. However, after sulfonylurea overdose a continuous glucose infusion can stimulate endogenous insulin production, leading to further hypoglycemia. If not recognized this can lead to a cycle of repeated glucose boluses and hypoglycemia episodes. Thus, after sulfonylurea overdose and an initial glucose bolus, octreotide is the preferred treatment. Octreotide is a long-acting somatostatin analog that binds to pancreatic beta cells and blocks insulin secretion. Octreotide can be administered either as an intravenous bolus followed by infusion, or subcutaneously. This patient failed to maintain normoglycemia after an initial D50 bolus, and starting a glucose infusion would likely contribute to further insulin release and repeated hypoglycemia. This patient has a functioning IV and does not require glucagon IM.
A 22-year-old man with type 1 diabetes since age 11 presents with fever, drowsiness, and abdominal pain. These symptoms started 2 days ago, and he has been unable to tolerate food or water. Vital signs are T 38.2 HR 122 and BP 105/70 mm Hg. Laboratory tests are notable for:
An ABG shows:
erum and urine ketones are positive. He undergoes fluid resuscitation with normal saline and receives an IV insulin bolus followed by a continuous insulin infusion. After 3 hours of treatment, his blood glucose is 250 mg/dL.
What is the most appropriate IV fluid management at this time?
Correct Answer: C
This patient presents in diabetic ketoacidosis. The immediate treatment is fluid resuscitation with normal saline to restore intravascular volume and an insulin IV bolus of 0.1 to 0.2 U/kg, followed by a continuous IV infusion at 0.10 U/kg/h. Serum glucose should be assessed hourly with the goal of lowering it by 50 mg/dL/h. The insulin infusion should be titrated downward as glucose levels are reduced. Serum electrolytes should be assessed every 2 to 4 hours. When the serum glucose is in the 200 range, glucose is added to the intravenous fluids. Starting glucose avoids hypoglycemia, while allowing continued administration of IV insulin to reverse ketogenesis. Once intravascular volume is restored, intravenous fluids should be changed to hypotonic saline to treat the ongoing freewater deficit and avoid hyperchloremic acidosis that can result from administration of large volumes of normal saline. Despite initial presence of hyperkalemia, with the administration of insulin and correction of acidosis hypokalemia will develop and should be treated with IV potassium.
A 58-year-old man is admitted to the ICU with pneumonia and sepsis. His medical history is notable for coronary artery disease and COPD. He is intubated and receiving a norepinephrine infusion to support blood pressure. On his serum, glucose has ranged from 191 to 283 mg/dL over the last 12 hours.
What is the most appropriate treatment at this time for his blood glucose?
Correct Answer: D
This patient is critically ill with sustained hyperglycemia, blood glucose >180 mg/dL. Sustained hyperglycemia has been associated with increased morbidity and mortality across various patient population. Thus, although hyperglycemia should be avoided, there may additional morbidity associated with hypoglycemia resulting from targeting lower blood glucose levels. Although single center studies showed an apparent benefit to such “intensive insulin therapy,” large randomized multicenter trials have shown the opposite—that intensive insulin therapy (blood glucose 81- 108 mg/dL) is associated with a higher morbidity and mortality than a conventional regimen (blood glucose <180 mg/dL).
Given the repeated blood glucose measurements >180 mg/dL, this patient should be started on insulin therapy. As explained above there is no role for a lower target of 150 mg/dL instead of 180 mg/dL as attempts at tighter control are associated with worse outcomes. Administering long acting insulin to a critically ill patient with blood glucose variability may increase the risk of hypoglycemia. Starting sliding scale insulin that can be adjusted to the specific glucose level is an appropriate starting point for this patient.
A 60-year-old man with bipolar disorder on chronic lithium therapy undergoes an uncomplicated appendectomy. In the PACU he becomes delirious and agitated. His vital signs are within normal limits. He weighs 75 kg. Laboratory values are notable for sodium 148 mEq/L. He is maintained overnight on dextrose in half-normal saline at 125 mL/h. Urine output is approximately 300 mL/h overnight. In the morning serum sodium has increased to 155 mEq/L. His urine osmolality is 120 mOsm/kg, and urine sodium is 22 mEq/L. Arginine vasopressin is administered without a change in urine output.
What is the most appropriate change in IV fluids for treatment of his hypernatremia?
Based on the medical history and laboratory results this patient likely has nephrogenic diabetes insipidus (DI) from long-term lithium therapy. Nephrogenic DI can be caused by several drugs, including lithium, demeclocycline, amphotericin B, and antiretroviral drugs such as tenofovir and indinavir. He developed severe hypernatremia from ongoing free water loss when he was unable to maintain oral intake. The goal of treatment is to correct his free water deficit by half over the 24 hours and then fully correct the sodium level within 3 days.
To determine the appropriate amount of fluid to administer, we must calculate the free water deficit. Assuming a total body water (TBW) of 60% lean body mass (this may be an overestimation in women or the elderly), this patient’s normal TBW is approximately 45 L (0.6 × 75 kg). Assuming normal sodium of 140 mEq/L, his current TBW = normal TBW × (normal sodium/current sodium) = 45 × (140/155) = 45 × 0.9 = 40.5 L. Thus, his free water deficit = 45 − 40 = 5 L. We would aim to replace half of this in 24 hours, or about 2.5 L. We also must account for urinary free water loss resulting from the elevated urine output 300 mL/h × 24 h = 7.2 L. Thus the total free water repletion for 24 hour should be 2.5 + 7.2 = 9.7 L. Averaged per hour, this is approximately 400 mL/h.
Thus, changing to D5 Water at 400 mL/h should appropriately correct his free water deficit. D5 half-normal saline at 300 mL/h would provide approximately one-fourth of the needed free water. And D5W at 200 mL/h is only half that required. Administering D5W at 300 mL/h would only provide three quarters of the needed free water. In addition he did not respond to arginine vasopressin, so response to the synthetic vasopressin analogue desmopressin would be unlikely.
A 22-year-old, 70-kg man sustained unrecoverable traumatic brain injury and is undergoing evaluation for donation of his heart, liver, and lungs. During transplant evaluation and preparation, he becomes progressively hypotensive, with increased urine output, and laboratory evaluation is notable for a sodium of 148 mEq/L (from initial of 139 mEq/L). Administration of which of the following medications is most appropriate to increase the chances of successful organ recovery?
Patients with severe brain injury and subsequent brain death before organ donation often develop multiple endocrine abnormalities. The HPA axis is particularly susceptible to ischemic injury from elevated intracranial pressure. Up to 80% of patients with brain death develop DI from reduced antidiuretic hormone (vasopressin). Hypothyroidism and hypocortisolism are also reported, albeit at lower rates. Numerous animal and clinical studies suggest that hormone replacement promotes hemodynamic stability, improves organ function, and increases the number or organs retrieved.
Several studies show that together, thyroid hormone, vasopressin, and methylprednisolone significantly increase successful organ recovery and may be associated with better cardiac recipient survival.
If DI develops and there is significant polyuria (>3 mL/kg/h), hypernatremia (sodium >145-150) and desmopressin may be administered (1-4 µg initially) and then titrated every 6 hours to urine output and osmolality, and serum sodium. If there is associated hypotension, vasopressin infusion 0.01 to 0.04 U/min may adequately treat the hypotension as well as the treat DI. Both a vasopressin infusion and desmopressin may also be administered together if one is not sufficient.
High-dose corticosteroids (methylprednisolone 1000 mg IV) reduce the inflammatory effects of brain death on organ function and may improve graft function after transplantation.
There is some controversy regarding the benefit of thyroid hormone supplementation, as not all studies have shown benefit. It seems to have the most benefit in hemodynamically unstable donors under consideration for cardiac donation. In this patient it would be warranted given his hypotension and potential cardiac donation, with little potential for harm.
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