Management of endocrine disorders in the surgical intensive care unit

Diabetes insipidus

Diabetes insipidus can be categorized as central (lack of hormone) or nephrogenic (lack of response to hormone). Central DI is caused by depletion or absence of arginine vasopressin (antidiuretic hormone (ADH)), which results in polyuria. If thirst is impaired, this may result in water diuresis of more than 3 L/day, dehydration, and hypernatremia. In the neurosurgical patient population the incidence of DI is 3.7% with a mortality rate up to 70%. DI commonly occurs in association with severe brain injury and herniation, and the diagnosis is suspected when urine output exceeds 200 mL/hr for 2 consecutive hours. A dramatic rise in serum sodium occurs in the ICU) patient population unless fluids are aggressively replaced. The urine is dilute with urine osmolality of less than 300 mOsm/kg and urine specific gravity less than 1.005 g/mL. Conversely, urine osmolality greater than 800 mOsm/kg excludes DI. Fluid and vasopressin replacement are the mainstays of treatment. Typical doses of DDAVP (1-deamino-8- d -arginine vasopressin) include 2 to 4 μg intravenously (IV) or 10 to 60 μg intranasally. Vasopressin infusion is also an acceptable treatment modality. Frequent monitoring of electrolytes and volume status is mandatory. Repeat doses of treatment medications may be needed until the DI abates. The water deficit is calculated and slowly replaced. Caution is used when severe hypernatremia is present with only half of the water deficit replaced in 24 hours to avoid demyelination ( Table 2 ). The astute clinician must be aware of the described triphasic response where the patient may exhibit DI followed by SIADH (see later), then followed by more permanent DI.

SIADH and cerebral salt wasting

Patients with hyponatremia must be evaluated for SIADH and cerebral salt wasting (CSW). The diagnosis is made in the hyponatremic patient that is found to be hypotonic with a urine osmolality >100 mOsm/kg. The diagnosis is further solidified if the urine sodium > 40 mmol/L. SIADH and CSW can be difficult to distinguish and are most different in that SIADH patients are often euvolemic whereas CSW patients are hypovolemic. Differentiating the two entities is critical due to their opposing treatments ( Table 1 ). The cause of SIADH is excessive release of ADH that leads to water retention and an increase in extracellular fluid volume. Volume expansion increases renal sodium excretion, producing hyponatremia. Cerebral salt wasting, also known as renal salt wasting, results from a natriuretic peptide, which results in sodium and volume depletion. Volume depletion results in ADH activation, which, in turn, contributes to the development of hyponatremia.

In both syndromes, the diagnosis begins with serum sodium less than 135 mmol/L, serum osmolality less than 280 mOsm/kg, and urine osmolality greater than 100 mOsm/kg. As stated previously, the differentiating factor is the patient’s volume status, which is normal in SIADH and depleted in cerebral salt wasting. Low effective blood volume normally causes orthostatic hypotension, tachycardia, low CVP, low urine sodium, low chloride, and fractional excretion of sodium with high blood urea nitrogen (BUN). Both disease states have low serum uric acid levels. With correction of the salt deficit, uric acid levels normalize in SIADH but not in cerebral salt wasting. Fractional excretion of urate (FE _urate ) may help distinguish these two entities. Correction of hyponatremia in SIADH will normalized the FE _urate (4%–11%).

Treatment of SIADH is fluid restriction (800–1000 mL/day) and occasionally hypertonic saline. Hypertonic saline is typically reserved for patients that have severe hyponatremia resulting in symptoms. Fluids administered must exceed the urine osmolality or else the hyponatremia will worsen. Hence, the use of normal saline is discouraged. Demeclocycline, phenytoin, lithium, and vaptans are used for treatment of chronic SIADH, but not in the acute setting. The treatment for cerebral salt wasting is normal saline fluid replacement to expand the extracellular fluid compartment (see Table 1 ). Misdiagnosing or confusing these two entities will result in ineffective treatment and exacerbation of hyponatremia.