Severe hyponatremia is associated with a mortality rate of more than 50%, primarily from cerebral edema and central nervous system dysfunction (1). Water intoxication is an unusual but potentially lethal cause of perioperative hyponatremia. We report a patient with severe postoperative hyponatremia resulting from excessive perioperative water consumption.
A previously healthy 40-yr-old woman presented to the emergency department with symptoms of severe anxiety, diaphoresis, tremulousness, nausea, and confusion. Twelve hours earlier, the patient had undergone an uncomplicated rhinoplasty under general anesthesia at an outside facility, after which she was discharged home. Five hours after discharge, the patient experienced anxiety, which was temporarily relieved by a 0.5-mg oral dose of alprazolam. Shortly thereafter, the patient’s anxiety returned with increased severity and was unrelieved by a second dose of oral alprazolam. After she developed tremors, nausea, diaphoresis, and subjective fever, her husband brought her to the emergency department for evaluation and treatment. Her medical and surgical histories were notable only for generalized anxiety disorder. During the evaluation, the patient was confused and forgetful, often repeating herself and forgetting to answer simple questions. The patient’s vital signs were arterial blood pressure 111/63 mm Hg, heart rate 90 bpm, respirations 18 breaths/min, and temperature 36.1°C. Physical examination was unremarkable except for a flushed appearance, diaphoresis, generalized tremors, and bilateral ankle clonus.
The anesthesiology service was consulted to exclude perioperative causes of her symptoms. The evaluating anesthesiologist solicited a history of perioperative fluid intake which revealed that the patient had consumed 4 L of water before surgery and 6 L of water during the first few hours after surgery to prevent dehydration from surgery on the advice of a naturopathic physician. Laboratory evaluation was notable for a serum sodium of 120 mEq/L (reference range, 136–145 mEq/L), serum osmolality of 246 mOsm/kg (reference range, 280–300 mOsm/kg), and urine osmolality of 53 mOsm/kg (reference range, 100–1000 mOsm/kg). The urine toxicology screen was positive for benzodiazepines. Computed tomography of the head was normal and did not demonstrate any brain swelling. A diagnosis of symptomatic hyponatremia due to water intoxication was made.
The patient was admitted to the hospital by the neurology service and was treated with fluid restriction along with an infusion of IV 0.9% saline solution at 125 mL/h. A Foley catheter was placed, and the urine output over the next 10 h was 3700 mL (6 mL · kg-1 · h-1). Serial serum electrolyte measurements were made, and the serum sodium reached 140 mEq/L; urine osmolality reached 227 mOsm/kg by the following morning, coincident with complete resolution of her neurological signs and symptoms. She was subsequently discharged home without any sequelae.
Clinical conditions that result in water intoxication include psychogenic polydipsia (self-induced), pregnancy, alcoholism, tumors (altered physiologic states), and transurethral resection of the prostate syndrome (iatrogenic). Patients are also considered to be water intolerant and prone to developing hyponatremia during the immediate postoperative period (2). Our patient developed symptomatic hyponatremia after an uncomplicated outpatient procedure with general anesthesia after ingesting a large volume of water over a relatively short period of time.
During the perioperative period, subclinical volume depletion, pain, nausea, and stress act as nonosmotic stimuli for the release of antidiuretic hormone (ADH). Cases of perioperative water intoxication after IV administration of relatively large amounts of 5% dextrose in water have been reported in adults (3) and in children during surgery (4). Cases of acute symptomatic hyponatremia after voluntary intake of excessive amounts of water have also been reported in ultra-marathon runners (5,6). This is the first case of hyponatremia from perioperative voluntary excessive water consumption.
Hyponatremia is the most common electrolyte disorder in hospitalized patients, with an incidence of approximately 1%–4% (7–10). The mortality rate of hyponatremia in hospitalized patients is reported to be 7- to 60-fold more frequent compared with nor-monatremic controls (9,10). There are no data regarding the incidence of hyponatremia among surgical outpatients.
It is important to differentiate the two broad categories of causes of hyponatremia. In general, perioperative hyponatremia results either from effective depletion of circulating volume and total body sodium content with resultant secretion of ADH and impairment of the kidney’s ability to excrete free water or, less often, from excess free water in the presence of normal total body sodium (e.g., water intoxication). In response to hypovolemia or inadequate circulating volume, the kidneys secrete ADH. As free water is retained, hyponatremia develops. Hyponatremia in the presence of normal total body sodium content and excess total body free water may be secondary to water intoxication and is an uncommon entity. Hyponatremia from water intoxication can be differentiated from other causes of hyponatremia by the presence of excess free water in the setting of normal total body sodium content and normal renal function (8). Water intoxication results in plasma hyposmolality, normal excretion of free water by the kidneys, and a urine osmolality of <100 mOsm/kg. The clinical approach to making the diagnosis of water intoxication depends on specific criteria, such as the presence of hypotonic hyponatremia with a serum osmolality <280 mOsm/L, urine osmolality <100 mOsm/kg, and the absence of extracellular volume depletion in the presence of normal renal, cardiac, liver, and endocrine function (8).
In the presence of normal renal function, the capacity of the kidneys to excrete free water exceeds normal water intake. Normally, the kidneys are able to excrete in excess of 20 L/d of electrolyte-free water (7,11). In water intoxication, dilutional and hypotonic hyponatremia ensues from a rapid intake of a large volume of parenteral or oral electrolyte-free fluid in excess of renal excretion over a short period of time. However, hyponatremia may also result after ingestion of smaller volumes of free water during the perioperative period because of an effect of general anesthesia; this results in impairment of the renal diluting capacity and in secretion of inappropriate ADH (7,11).
Complications from excess total body water in the presence of a small serum sodium concentration can result in an increase of extracellular water, cerebral edema, and potential brain herniation. Patients with serum sodium levels <135 mEq/L often remain asymptomatic. However, symptoms usually manifest when severe hyponatremia (serum sodium levels <120 mEq/L) occurs. The greatest concern involving severe hyponatremia is cerebral edema, which can manifest as nausea, headache, confusion, lethargy, convulsions, seizures, or coma. Radiological diagnosis of cerebral edema is difficult, if not impossible. Other signs and symptoms may include hemiparesis, ataxia, nystagmus, tremor, rigidity, aphasia, muscle cramps, and fasciculations (12). Severe hyponatremia is also associated with cardiopulmonary dysfunction, including arrhythmias, hypotension, hypoxemia, and pulmonary edema (13), although these were absent in our patient.
The treatment of hyponatremia from water intoxication depends on the severity of the illness, and correction of hyponatremia must be tailored to the improvement of the patient’s symptoms (10). Patients with mild hyponatremia may remain asymptomatic and require only fluid restriction. Severe hyponatremia requires immediate intervention (12). Therapy typically includes fluid restriction, judicious administration of isotonic or hypertonic saline solutions, and, on certain occasions, oral or IV urea, loop diuretics, or vasopressin receptor antagonists (14). Current recommendations suggest correction of plasma sodium levels at a rate slower than 25 mmol in 24 hours, as well as avoidance of overcorrection of plasma sodium levels to avoid the risk of central pontine myelinolysis (7–9,10,15).
The current practice guidelines for preoperative fasting developed by the American Society of Anesthesiology Task Force on Preoperative Fasting and the Use of Pharmacologic Agents to Reduce the Risk of Pulmonary Aspiration recommend fasting for two or more hours after clear liquids before general or regional anesthesia (16). Allowing patients unlimited access to oral water in the time up until two hours preoperatively has been shown to have no effect on plasma osmolality (17). The increasing use of low-sodium diets and intake of water for perceived health benefits carries the theoretical possibility of predisposition to perioperative hyponatremia. Unfortunately, the incidence of perioperative hyponatremia in outpatients is unknown. Additionally, neither the benefits of defining the quantity of optimal perioperative fluid intake nor the utility of perioperative hydration guidelines as part of preanesthetic counseling has been described. Nevertheless, routine questioning and cautioning of presurgical patients about the type and amount of perioperative liquid intake might be needed, particularly because outpatients are at greater risk of loss of postoperative follow-up and because outpatients constitute approximately 63% of surgical patients (18).
In conclusion, anesthesiologists should be alert to the possibility of hyponatremia from water intoxication in all patients with neurologic symptoms during the perioperative period, particularly in patients with psychiatric or psychological illness. Routine preoperative instructions regarding maximum perioperative water intake may help to avoid this preventable complication.
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