CASE PRESENTATION
A 15-year-old female was admitted to hospital with a 6-day history of intermittent nausea, recurrent vomiting without hematemesis, ‘squeezing’ abdominal pain and a 10 kg weight loss over 6 months. There were no symptoms of infection. She felt dizzy and had no appetite. Her last bowel movement was 5 days prior to presentation.
She reported three similar 1- to 2-week episodes within the previous 6 months. She was asymptomatic between episodes and the vomiting and pain subsided unaided each time. This current presentation was different in that her vomiting was continuous, her emesis was bilious and she was unable to eat or drink without vomiting.
The patient revealed smoking cannabis every second day for 2 years and recently increased her consumption to one to three times daily (~2 to 4 g/day). She denied any alcohol or other drug use, apart from a single use of amphetamine. She had no desire to lose weight and had no body image concerns. The patient was being treated for ADHD, anxiety and depression but otherwise had no significant past medical conditions. Family history revealed alcohol use disorder, depression and migraines maternally and GERD paternally.
On examination, her weight was 37.5 kg (<3rd percentile) and body mass index was 17.8. Heart rate, blood pressure, respiratory rate, temperature and oxygen saturation were 98 bpm, 96/57, 19, 37.1°C (axillary) and 99% in room air, respectively. Abdominal examination revealed a scaphoid abdomen, faint bowel sounds and diffuse tenderness upon palpation in all quadrants without rebound tenderness. Diagnostic tests were performed.
DIAGNOSIS: SMA SYNDROME AND CHS
The patient was hospitalized due to significant weight loss. An upper gastrointestinal (GI) series demonstrated a blockage of the distal duodenum. Computerized tomography (CT) scan revealed focal narrowing of the duodenum between the aorta and superior mesenteric artery (SMA) (measured at 6 degrees) in keeping with SMA syndrome. SMA syndrome is a rare gastrointestinal condition characterized by intermittent postprandial abdominal pain, nausea and bilious vomiting (1). Weight loss is considered a risk factor for SMA syndrome as the depletion in retroperitoneal fat leaves a gap between the superior mesenteric artery and the duodenum resulting in compression of the latter (1). Treatment for SMA syndrome is primarily conservative involving positional changes such as knee to chest or side-lying positions postmeal, decompression of the duodenum and stomach with a nasogastric tube and nutritional rehabilitation. Both intravenous and enteral tube feeding which may require jejunal tube placement have been utilized. Surgical intervention has been reported in intractable cases (1).
In our case, the patient’s weight loss was attributed to cannabinoid hyperemesis syndrome (CHS), which resulted in her subsequent SMA syndrome. CHS is a relatively unknown and under-recognized clinical syndrome. CHS should be considered with a presentation of cyclic vomiting associated with a history of regular, heavy cannabis use (2). CHS frequently presents as intractable nausea and vomiting, occurring in a cyclic pattern over months and may be associated with consequent significant weight loss. Additional findings include brief relief of symptoms with compulsive hot baths and showers, no relief with antinausea medications and resolution of symptoms after weeks of cessation of cannabis (2–4).
Although the pathophysiology of CHS is currently unclear, animal and in vitro studies suggest a dysregulation of the endocannabinoid system, involving endogenous cannabinoid receptors CB-1 and CB-2 located in the brain, gastrointestinal tract, peripheral nervous system and immune system (2). The direct interaction of cannabinoids with CB-1 is thought to decrease gastrointestinal motility and gastric emptying, countering the antiemetic regulation of the brainstem and leading to symptoms of nausea, vomiting, inflammation and abdominal pain. A genetic variability has been suggested to explain the discrepancy in cannabis user symptomatology, although limited evidence exists to support this theory (2).
The differential diagnosis of CHS includes bowel perforation, cholangitis, pancreatitis and ruptured aortic aneurysm, medical conditions that must be excluded before CHS is considered (2). Additionally, SMA syndrome and cyclic vomiting syndrome present many similarities to CHS.
She was treated with nasogastric tube (NGT) decompression, total parenteral nutrition, followed by slowly increasing nasogastric tube feeds as tolerated. Her weight increased by 7.5 kg over 7 weeks and she was counselled regarding cannabinoid use cessation. By the end of her hospitalization, her abdominal symptoms had subsided; she was eating and drinking well with no abdominal pain, nausea or vomiting. A repeat upper GI series done as an outpatient 2 months later after she had gained another 5 kg (weight and body mass index at 50th percentile), showed resolution of the SMA syndrome.
CLINICAL PEARLS
• Cannabinoid hyperemesis syndrome should be considered in youth who present with abdominal pain, cyclic vomiting and weight loss.
• Proper intervention for substance use reduction and cessation should be the mainstay of treatment for cannabinoid hyperemesis syndrome.
• Treatment for SMA syndrome is mainly supportive and focused on nutritional rehabilitation while addressing the underlying causes of weight loss if present
References
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