Article, Gastroenterology

Severe hypernatremia and gastric dilation from chronic eating disorder and intentional salt ingestion

a b s t r a c t

We report the case of a 21-year-old female presenting with severe hypernatremia and a Gastric outlet obstruction due to chronic purging behavior with salt water flushes. She presented obtunded following emesis and a witnessed seizure. She was found to have a corrected sodium level of 177 mmol/L. Following initial intubation and resuscitation, her CT imaging showed massive gastric dilation with high-density material in the gastric lumen. After orogastric flushing was unsuccessful and the patient’s Abdominal distention worsened, she was managed surgically and found to have a salt bezoar leading to Bowel ischemia and perforation. This case details the complications and management of acute hypernatremia and gastric outlet obstruction in an otherwise healthy, young female. In a society where eating disorders are pervasive, Emergency Medicine physicians should be familiar with dangerous dietary behaviors as well as the management of their rare, but potentially life- threatening, complications.

(C) 2020


Eating disorders span a spectrum of restrictive, binging, and purging dietary behavior. Decreased gastric motility is a common gastrointesti- nal manifestation with both chronic anorexia and bulimia [1]. Rare manifestations of delayed gastric emptying include gastric bezoars and acute Gastric dilatation. Recently, salt water flushes have gained popularity as a means to induce osmotic diarrhea or emesis [2,3]. The use of salt water flushes can cause hypernatremia, defined as a serum sodium greater than 145 mmol/L. [4] In this case we discuss a young fe- male presenting to the Emergency Department (ED) with severe hypernatremia and acute gastric dilatation due to the chronic use of saltwater flushes to facilitate emesis.


This is the case of a 21-year-old female who was brought in by EMS to the ED obtunded. She had a vague history of an unspecified eating disorder from chart review dated several years prior, but was reported to be otherwise healthy. Prior to arrival she had been vomiting and

* Corresponding author at: 170 Manning Dr. CB #7594, Chapel Hill, NC 27599, United States of America.

E-mail address: [email protected] (C. Shenvi).

was found unresponsive by roommates on her bathroom floor. She had a seizure with EMS and received midazolam. On arrival to the ED she was unresponsive to noxious stimuli, but had an intact cough and gag reflex and equal and responsive pupils. She was hypothermic (T 35C), tachycardic (HR 157), normotensive (BP 127/80), hypoxic (O2 sat 89%) requiring Bag valve mask ventilation. With a BMI of 17, thin neck and atrophic extremities, she appeared emaciated but with a tense and distended abdomen. Following rapid sequence intubation, she was sedated with propofol and received 2 g of levetiracetam for sei- zure prevention. Initial bloodwork was remarkable for a severe meta- bolic acidosis (VBG pH 6.91/pO2 76 mmHg/pCO2 27.0 mm Hg/HCO3 15.2 mEq/L), elevated lactic acid (3.3 mmol/L), hypernatremia and hy- perglycemia (Na 172 mmol/L, K 3.6 mmol/L, Cl 150 mmol/L, CO2 16 mmol/L, BUN 5 mg/dL, Cr 0.94 mg/dL, Glucose 405 mg/dL). Urine pregnancy was negative and the remainder of the Laboratory workup including toxicity screen, acetaminophen, and Salicylate levels were within normal limits. A CT abdomen and pelvis was obtained due to the tense abdominal distention and revealed a massively dilated stom- ach filled with high-density gastric debris, but no signs of perforation (Fig. 1).

An infusion of D5W at 125 mL/h was initiated and her acidosis was corrected with hydration and mechanical respiratory compensation. Orogastric decompression was attempted using an orogastric tube, but only minimal clear liquid output was obtainable. The bulk of the gastric contents could not be suctioned or flushed through the tube. Surgery and gastroenterology were consulted and recommended admission to

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Fig. 1. CT scan of the abdomen and pelvis in coronal and sagittal planes showing severe gastric dilation, high-density material in the stomach lumen, and overall cachexia.

the medical intensive care unit with an attempt at chemical dissolution of a suspected bezoar with Coca-cola flush and continued orogastric de- compression. Shortly following admission, her abdomen became more distended and there was concern for gastric perforation. She was taken emergently for Exploratory laparotomy and found to have a gas- tric perforation and ischemic segments of small bowel. She underwent gastric decompression, repair of the gastric perforation, and small bowel resection. Unfortunately, she remained unstable following sur- gery and developed refractory shock. She was taken back to the OR and found to have extensive bowel ischemia. She passed away with her family at the bedside two days after her initial presentation.


Acute hypernatremia is typically seen in water deficient states, but can also be present after administration of hypertonic saline or, more rarely, after salt ingestion [5]. Salt water flushes have been described in some yoga literature as a way to cleanse one’s colon [16]. Most pop- ular health websites recommend the rapid ingestion of 1-2 teaspoons of salt dissolved in 1 L of warm water in order to stimulate emesis or di- arrhea. The laxative effect stems from the creation of an osmotic gradi- ent, which draws fluid into the bowel. A surprisingly small amount of salt can cause severe hypernatremia, and a lethal dose of table salt is es- timated to be less than 25 g (4 Tbs) for adults [6]. There are few cases detailing the presentation of severe acute hypernatremia from salt in- gestion alone [7]. However, there is one fatal account of a female pre- senting with a serum sodium of 187 mmol/L, after ingesting a large quantity of soy sauce, leading to cerebral damage and pulmonary edema [5]. For our case, the patient’s measured sodium was 172 mml/ L, but her corrected level accounting for the hyperglycemia, was 177 mmol/L. Her acute hypernatremia is believed to be the underlying cause of her seizure and altered mental status.

Patients suffering from chronic eating disorders often develop de- creased gastric motility, placing them at risk of acute gastric dilatation and, rarely, gastric bezoars [8-11]. Acute gastric dilation can lead to bowel ischemia, perforation, and necrosis and is associated with a mor- tality rate of roughly 80% [12]. First-line management consists of orogastric decompression, fluid resuscitation, endoscopy for evaluation

of a bezoar or necrosis [8,15]. If gastric decompression is unsuccessful and a gastric phytobezoar is suspected, chemical dissolution with 500-3000 mL of Coca-cola can be effective [14]. Once gastric necrosis or perforation is suspected, Surgical decompression or gastrectomy is often indicated [13].

This case portrays a rare presentation of severe hypernatremia due to ingestion of table salt. The patient’s seizure, coma, and resultant re- spiratory failure were sequelae of acute hypernatremia from intentional eating disorder-related ingestion. She also had severe gastric dilation from repetitive binge purging behavior and gastric outlet obstruction likely due to a salt bezoar and chronically reduced gastric motility.



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