Case Presentation: A 47-year-old male with history of hypertension presented to urgent care with one day of vomiting and bloody diarrhea. Onset of symptoms occurred 30 minutes after consuming raw juice he made at home from a lauki bottle gourd. At urgent care he was pale, ill-appearing, and hypotensive with a blood pressure of 80/36 mmHg. He was given 1 liter of intravenous fluids (IVF) and sent to the Emergency Department. Vital signs were notable for temperature of 35.2 degrees Celsius, heart rate 118 bpm, blood pressure 100/70 mmHg, respiration rate 31 breaths per minute, SpO2 95% on room air. He had altered mental status and a soft but diffusely tender abdominal exam. Laboratory results were significant for a white blood cell count of 15 x 10*9/L and lactate of 12.4 mmol/L. Venous pH was < 6.93, anion gap 20 mmol/L, potassium 6.2 mmol/L, magnesium 0.7 mg/dL, and serum creatinine was 2.1 mg/dL (baseline 0.9). Liver transaminases were elevated with ALT 1032 U/L, AST 848 U/L, and normal total bilirubin and alkaline phosphatase. Computed tomography of the abdomen/pelvis showed thickened small bowel with hyperemic small bowel mucosa and a decompressed inferior vena cava. There was enhancement around the gallbladder and small bowel without evidence of biliary obstruction. The patient received 2 liters IVF, vancomycin, and piperacillin/tazobactam. He was transferred to the intensive care unit. General surgery determined that the presentation was inconsistent with cholecystitis or cholangitis. Blood, urine, and stool cultures were negative, as were acute hepatitis and influenza testing. The patient improved with supportive care, and he was transferred to the medicine service. He achieved normalization of his vital signs, electrolyte levels, and liver enzymes. He had no further symptoms and was discharged home.
Discussion: The medicine service took additional history leading to the discovery that he likely suffered from distributive shock due to poisoning caused by the ingestion of an unintentionally hybridized lauki bottle gourd, colloquially referred to as “toxic squash syndrome”. This wild-type squash was high in the chemical compound cucurbitacin D which is associated with increased capillary permeability and drop in blood pressure in mice. Gourds in the cucurbit family (i.e. squash, zucchini, pumpkin) have been carefully cultivated to remove this toxin from edible plants, however unintentional hybridization can lead to a toxic fruit .Although toxic squash syndrome is rare, several clues point to the diagnosis including the ingestion of a cucurbit with an extremely bitter taste, immediate reaction after ingestion, and no other infectious source identified. The patient’s impressive presentation likely correlates with the consumption of the squash’s raw juice, leading to ingestion of a concentrated amount cucurbit toxin. There lacks a test of the cucurbit toxin. Diagnosis is made clinically by careful history, exclusion of alternative causes, and rapid response to early supportive interventions .
Conclusions: Obtaining a thorough history remains an essential step to accurate diagnosis and can lead to diagnostic closure for both patient and care team. Moreover, hospitalists should be aware of the potency of the cucurbit toxin and potential presentation of hypotension or distributive shock. Cultural awareness and inquiry into less common foods consumed may have revealed the diagnosis earlier, saving time and resources.