Case Presentation: A 30-year-old male presented to the ED with sudden onset flaccid paralysis involving the entire body except the head and neck. He reported heavy marijuana use 2 days prior during which he consumed excessive amounts of carbohydrates, including large bags of gummy bears and candy bars. One day after binge eating episode he noticed increased fatigue and lower extremity weakness that slowly progressed to the upper extremities throughout the day. The next morning, he woke up unable to move his body.
In the ED, he presented with bradycardia but otherwise stable vitals, and showed no signs of respiratory distress. Strength testing demonstrated upper and lower extremity weakness more profound in the lower extremities, with hypoactive deep tendon reflexes. His cranial nerve exam and sensory testing were unremarkable. Serum testing revealed severe hypokalemia (1.5mmol/L) and hypophosphatemia (0.7mg/dL). His electrocardiogram showed bradycardia, flattened T-waves, and U waves.

He was diagnosed with hypokalemic periodic paralysis and was immediately started on potassium replacement. He received a total of 180mEq of potassium supplementation over a 10 hour period. His potassium levels slowly increased from 1.5mmol/L on admission to 4.1 mmol/L in 12 hours and leveled off around 4.7 by 24 hours. As his serum potassium levels increased he started to regain motor function starting with the distal upper extremities and eventually regained full strength in his bilateral upper and lower extremities by 9 hours after starting potassium replacement.

Discussion: HPP is a rare genetic disorder (1: 100,000) that presents with sudden onset flaccid paralysis. Gene mutations affect sodium and potassium channels which cause an exaggerated response to insulin or thyroid hormone. This results in a large influx of potassium into cells leading to severe hypokalemia.

HPP can be triggered by prolonged rest after vigorous exercise, carbohydrate loading, and excessive stress. Patients present with acute onset flaccid paralysis while sensation, respiration and facial muscles remain unaffected. Diagnosis can be made via genetic testing or based on clinical presentation alone.

It is important to remember that the hypokalemia is due to transcellular potassium shifts rather than a decrease in total potassium stores. Treatment should begin with slow potassium replacement along with close monitoring for cardiac complications and rebound hyperkalemia.

Conclusions: There has been an increase in the number of marijuana related healthcare visits over the past decade as more US states join in legalizing its use for medical and recreational purposes. Shifting attitudes have led to normalization of marijuana use as many consider it to be a low risk recreational drug. However, we have yet to fully understand all the potentially hazardous health consequences associated with direct or indirect use of marijuana.

In this case study, we believe that the trigger was excessive carbohydrate intake during a marijuana binge episode. Marijuana use has been known to stimulate hunger, causing what is commonly known as “marijuana munchies”. As was the case with our patient, obtaining a through social history was key in identifying the cause of HPP, facilitating the provision of appropriate counseling surrounding prevention of further episodes. It is critical to counsel patients who are heavy marijuana users to seek immediate medical attention if they start to notice muscle weakness to prevent further complications.