CHS has been reported more frequently in people that use cannabis daily (47.9% of people with CHS) and greater than daily (23.7% of people with CHS), compared to once weekly users (19.4% of people with CHS) and less frequent users (2.4% of people with CHS). A significant increase in the incidence of CHS (and other cannabis-related visits to the emergency department) has been noted in U.S. states that have legalized cannabis, with the incidence of cyclic vomiting prominently doubling in the US state of Colorado after legalization. As the use of cannabis continues to be legalized at the state level, the prevalence of CHS is expected to increase in the US. History
Cannabinoid hyperemesis was first reported in the Adelaide Hills of South Australia in 2004.The name "cannabinoid hyperemesis syndrome" was also coined at this time. The report focused on nine patients who were chronic cannabis users who presented with cyclical vomiting illness. One woman in the study reported that warm baths provided the only relief from the nausea, severe vomiting, and stomach pain, and reportedly burned herself in a hot water bath three times trying to get relief. Society and culture
CHS is not very well known. In lieu of a correct diagnosis, the average patient in the US may be charged $100,000 or more in medical bills through emergency department visits. An emergency department physician in 2018 commented that the condition wasnt on their "radar" in the five years prior, though the condition was being diagnosed more often now.
The vomited material does not contain bile because the pyloric obstruction prevents entry of duodenal contents (containing bile) into the stomach. The chloride loss results in a low blood chloride level which impairs the kidneys ability to excrete bicarbonate. This is the factor that prevents correction of the alkalosis leading to metabolic alkalosis.A secondary hyperaldosteronism develops due to the decreased blood volume. The high aldosterone levels causes the kidneys to avidly retain Na+ (to correct the intravascular volume depletion), and excrete increased amounts of K+ into the urine (resulting in a low blood level of potassium).The bodys compensatory response to the metabolic alkalosis is hypoventilation resulting in an elevated arterial pCO2. Diagnosis
Diagnosis is via a careful history and physical examination, often supplemented by radiographic imaging studies. Pyloric stenosis should be suspected in any young infant with severe vomiting. On physical exam, palpation of the abdomen may reveal a mass in the epigastrium. This mass, which consists of the enlarged pylorus, is referred to as the olive, and is sometimes evident after the infant is given formula to drink. Rarely, there are peristaltic waves that may be felt or seen (video on NEJM) due to the stomach trying to force its contents past the narrowed pyloric outlet.Most cases of pyloric stenosis are diagnosed/confirmed with ultrasound, if available, showing the thickened pylorus and non-passage of gastric contents into the proximal duodenum. Muscle wall thickness 3 millimeters (mm) or greater and pyloric channel length of 15 mm or greater are considered abnormal in infants younger than 30 days.