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Severe Hypernatremia After Hypertonic Saline Irrigation of Hydatid Cysts

2002; Lippincott Williams & Wilkins; Volume: 95; Issue: 6 Linguagem: Inglês

10.1097/00000539-200212000-00062

1526-7598

Aline Albi, François Baudin, M. Matmar, Denis Archambeau, Yves Ozier,

Endometriosis Research and Treatment

When a serum sodium concentration ([Na]) increases to ≥145 mmol/L in <48 h, acute hypernatremia, caused by a net water fluid loss and/or hypertonic sodium gain, has occurred (1,2). Intravenous infusion of hypertonic saline, excessive salt ingestion, gastric lavage, topical application of salt on burned areas, and bicarbonate administration during cardiac arrest are all possible causes. Acute intraoperative development of severe hypernatremia is rare. Patients with hypernatremia are exposed to major neurological complications or death (2). Among patients with [Na] ≥160 mmol/L, the reported mortality rate is 70%, with children having better survival than adults (3). Few patients survived extreme hypernatremia ([Na] ≥200 mmol/L), and most of them were children (3). We report a case of an adult patient who survived an extreme iatrogenic acute hypernatremia (200 mmol/L) resulting from a hypertonic saline irrigation of multiple intraabdominal hydatid cysts. This is a unique report of an intraoperatively developed serum sodium increase without subsequent neurological damage. Case Report A 33-yr-old woman was admitted to the hospital because of unusual abdominal pain with palpable masses. Abdominal computed tomographic and ultrasound scans disclosed multiple peritoneal and intrahepatic cystic lesions suggestive of hydatid disease. Increasing abdominal pains prompted surgical intervention. A laparotomy was performed that showed many intraabdominal hydatid cysts, two of them located in the liver, one measuring 12 cm in diameter, and more than 50 peritoneal cysts. Ninety percent of the cysts were either excised or drained after sterilization with a 30% sodium chloride solution. The duration of the surgery was 8 h. Up to 3000 mL of hypertonic saline was used during the surgical management of the numerous cysts. The immediate postoperative course was marked by a major motor seizure followed by confusion and agitation that initially prevented extubation. Her seizure activity was successfully controlled by IV diazepam 10 mg. A continuous infusion of fentanyl and midazolam was begun with mechanical ventilation, and she was transferred to the surgical intensive care unit (ICU). On arrival, no focal motor disturbances were detected, but generalized hyperreflexia was present on examination. Arterial blood pressure was 145/85 mm Hg, with a heart rate of 150 bpm, and an external ear temperature of 39°C. Cardiac and pulmonary findings were unremarkable except for tachycardia. Whereas the preoperative serum electrolyte panel was in the normal range, the initial postoperative laboratory tests showed a marked hypernatremia (Table 1). The calculated serum osmolarity ([Na+ × 2] + glycemia + urea) was 415 mOsm/L. The amount of osmoles in relative excess was 4824 mOsm, as estimated by the formula: 0.6 × lean body weight (kg) × (current osmolarity − 280). The relative water deficit (i.e., the amount of positive water balance required to return the serum sodium concentration to 140 mmol/L) was 10.8 L, as estimated by the formula: 0.6 × lean body weight (kg) × ([current {Na}/140]−1).Table 1: Preoperative and Immediate Postoperative Serum Laboratory FindingsThe patient was treated with 2.5% dextrose IV solution at a rate of 200 mL/h for the first 24 h and a rate of 100 mL/h for the next 48 h. Hyperglycemia (12.3 mmol/L) was treated with continuous IV regular human insulin. The total volume of dextrose solution infused was 10,000 mL during the first 72 h after admission in the ICU. This rate of infusion was estimated according to the patient's relative water deficit. Twelve hours after admission in the ICU, a continuous infusion of a loop diuretic was begun (bumetanide 2 mg/d). Serum sodium concentration decreased to normal over 48 h through both a positive water balance and a negative sodium balance (Fig. 1). When [Na] returned to normal on postoperative Day 2, body weight was in excess of 3 kg. Twenty-four hours after the event, the patient was fully oriented without motor function impairment and could be tracheally extubated (serum [Na] was 154 mmol/L). Six weeks after the intraoperative hydatid cysts irrigation, the neurological clinical examination was fully normal without any apparent cognitive deficits. However, an intracranial magnetic resonance imaging was performed that did not disclose any abnormal findings.Figure 1: Postoperative evolution of serum sodium concentration with sodium and fluid balances. Bars indicate the cumulative sodium and fluid balances at the end of each time period considered (initial 12 h, and then every 24 h).Discussion This case is unusual because this adult patient survived severe hypernatremia without any neurologic deficits. In contrast to a previous case report in a 74-year-old woman (202 mmol/L), the onset of hypernatremia in the present case occurred acutely over the course of a six-hour operation (4). Hydatid disease is caused by Echinococcus granulosus that generates cysts, most often in the liver, the lung, and, occasionally, in other sites. Surgery is indicated for the complications of hydatid disease for symptomatic patients and for asymptomatic patients in whom attempts at medical treatment have failed (5). Surgical removal of the intact cyst is the preferred form of therapy. If this is impossible, conservative approaches include sterilization of the cyst contents with various scolicidal drugs. Formalin, hydrogen peroxide, silver nitrate, cetrimide, absolute alcohol, povidone iodine, and hypertonic saline may be effective, but most can have unacceptable side effects limiting their use. A few cases have indicated that sterilizing hydatid cysts using hypertonic sodium chloride carries a risk of resorption with acute hypernatremia (6–8). Regular and frequent monitoring of [Na] during such operations is of prime necessity. In our case, hypernatremia may have resulted from absorption of hypertonic saline through cysts walls and from exchange of both salt and water through the peritoneal membrane. Moreover, an inadvertent injection of hypertonic saline into a blood vessel cannot be excluded. Intraperitoneal injection of hypertonic NaCl is an established experimental model of acute hypernatremia in the rat (1). The mechanism of hypernatremia after a hypertonic saline injection involves both a total body sodium gain and a free water loss (9). Salt gain was a prevailing mechanism in our patient, as evidenced by an increased postoperative body weight. The exact cause of the frequent mortality and severe central nervous system damage in severely hypernatremic patients has not been fully elucidated. Several neurological complications may occur. Acute hypernatremia leads to a rapid decrease in brain water content (1). Dehydration of cerebral cells with brain shrinkage may result in intracranial vascular damage and subdural hematomas (10). Brain demyelinating lesions (central pontine and/or extrapontine myelinolysis) are a well-known complication of rapid correction of preexisting hyponatremia (8,11–14). In response to hypernatremia, the brain undergoes adaptive responses to minimize osmotic shrinkage. Intracellular accumulation of osmoles tends to counteract brain water loss (1,15,16). However, this protective change exposes the patient to cerebral edema that may arise from failure of the osmoles to dissipate at the same rate as hypernatremia during treatment (1,13). Optimal correction rates of acute hypernatremia in adults are not known. Based on experimental data on cerebral volume regulation, decreasing [Na] by 1 mmol · L−1 · h−1 is appropriate for hypernatremia of rapid onset, as in the present case (2). Peritoneal dialysis or hemodialysis may be used, although they have not been shown to improve survival (3). Such methods should be considered if a sufficient natriuresis cannot be obtained with diuretics. Because exogenous sodium excess was thought to be the cause, active urinary sodium depletion combined with hypotonic fluid therapy were used to restore [Na] to normal in <48 hours. Early detection and rapid correction of hypernatremia, together with the young age of our patient, were probably the determinant in the prognosis. In summary, the present case underscores the dangerous osmotic stress that may be generated by the irrigation of hydatid lesions using hypertonic saline solutions. Frequent and regular monitoring of intraoperative [Na] should be mandatory. Even after an intraoperative upward [Na] shift of 60 mmol/L, a prompt correction of hypernatremia may be associated with a survival free of neurologic sequelae.