Central Diabetes Insipidus is often an overlooked complication of cardiopulmonary arrest and anoxic brain injury. We report a case of transient Central Diabetes Insipidus (CDI) following cardiopulmonary arrest. It developed 4 days after the arrest resulting in polyuria and marked hypernatremia of 199 mM. The latter was exacerbated by replacing the hypotonic urine by isotonic saline.
Central Diabetes Insipidus (CDI) is characterized by the lack of antidiuretic hormone (ADH) causing loss of urinary concentrating ability, polyuria, thirst, and hypernatremia. ADH is an octapeptide synthesized in the supraoptic nuclei of the hypothalamus and then stored and released from the posterior pituitary gland. It maintains normal serum osmolality by promoting free water reabsorption in the collecting ducts of the nephron. The known causes of CDI include germinoma/craniopharyngioma; Langerhans cell histiocytosis; local inflammatory, autoimmune, or vascular diseases; trauma resulting from surgery or an accident; sarcoidosis; metastases; and midline cerebral and cranial malformations [
A 43-year-old woman with advanced amyotrophic lateral sclerosis, maintained on home ventilator, was transferred to our institution after being resuscitated following an out-of-hospital cardiorespiratory arrest. She had initially sustained a respiratory arrest secondary to pneumonia and mucus plugging which ultimately resulted in pulseless electrical activity. She was unresponsive for 30 minutes before she received resuscitation. Elapsed time before return of spontaneous circulation was 30 minutes. Upon arrival to our institution, she was unresponsive with fixed dilated pupils and no spontaneous respiratory effort. She was also in septic shock secondary to pneumonia. She received intravenous hydration with 0.9% saline, norepinephrine infusion, and broad spectrum antibiotics (piperacillin-tazobactam and vancomycin). Upon presentation, her laboratory values showed marked leucocytosis of 37,600/cm3 with a neutrophilic shift. Her serum creatinine was 0.2 mg/dl, blood urea nitrogen 13 mg/dl, sodium 137 mM, potassium 3.6 mM, chloride 98 mM, bicarbonate 19 mM, and lactate 5 mM. Her PCO2 on arterial blood gases was 48 mmHg. Her serum aspartate transaminase and alanine transaminase were 307 and 177 IU/L, respectively. Her brain computed tomography was consistent with hypoxic ischemic brain injury.
Her hemodynamic condition stabilized over the next 72 hours of hospitalization. However, on hospital day 5, the nephrology team was consulted for a significant elevation in serum sodium level from 136 to 199 mM within 24 hours. This was repeated twice with similar results and a measured plasma osmolality was 403 mOsm/kg. Her concomitant serum potassium was 2.3 mM, chloride 171 mM, and bicarbonate 15 mM. She had been polyuric for the previous 36 hours with an hourly urine output of 300–600 ml, and this has been replaced by approximately 10 liters of 0.9% NaCl (a total of 1500 mmoles of sodium) at a rate of 0.25–1 L per hour. Spot urine sodium concentration was 38 mM and urine osmolality was 112 mOsm/kg, suggestive of predominantly free water diuresis. Hence, a diagnosis of Diabetes Insipidus was made. The patient was given 1 L of 5% dextrose in water over 1 hour followed by an infusion at 225 ml/hour, together with 1 mcg of desmopressin parenterally. Following desmopressin administration, urine output dropped significantly to 50 ml/hour; urine osmolality increased to 243 mOsm/kg (in 12 hours) and to 364 (in 24 hours) (Figure
Changes in plasma sodium, plasma and urine osmolality, and urine output before and after desmopressin.
On hospital day 7, the patient developed oliguric ischemic acute kidney injury (AKI) secondary to intravascular volume depletion and hypotension. Her serum creatinine increased and then plateaued at 1.1 mg/dl for 14 days and was down to 0.6 mg/dl by hospital day 30. Her sodium came down to 158 mM on day 7, 151 on day 15, and 145 on day 39. That change in sodium has been achieved by free water only. Her CDI was transient and she did not require any further doses of desmopressin. She did, however, develop central hypothyroidism and central adrenal insufficiency for which she was receiving thyroxine replacement and hydrocortisone, respectively. The patient was transferred to another hospital on day 45 of hospitalization.
The incidence of CDI among cardiopulmonary arrest survivors varies between 12 and 21% [
Though the brain consumes 1/5 of the body’s oxygen requirements, the hypothalamus is relatively resistant to hypoxic injury given its extensive collateral blood supply [
The transient nature of CDI in our patient might reflect edema or injury rather than complete destruction of the hypothalamic/hypophyseal tissue. Though the patient had hypokalemia, which can cause nephrogenic DI, her significant response to desmopressin suggests a major component of ADH deficiency and CDI. The replacement of hypotonic urine with isotonic saline further exacerbated her hypernatremia.
The development of CDI is usually an ominous prognostic sign. In a retrospective study by Chae et al. [
Our case highlights the importance of monitoring for CDI following cardiac arrest. Front line physicians including emergency medicine physicians and intensivists should be aware of such complication which can be fatal if not discovered and treated early. They should watch for polyuria following cardiac arrest which can be the early sign for DI. Early treatment with desmopressin may reduce hypernatremia and perhaps secondary brain injury [
millimolar.
The authors declare that they have no conflicts of interest.