Abstract: SA-PO993
Hypokalemic Periodic Paralysis Possibly Precipitated by Amphetamine Abuse
Session Information
- Fellows/Residents Case Reports: Fluid, Electrolytes, Acid Base
November 04, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Nephrology Education
- 1302 Fellows and Residents Case Reports
Authors
- Shetty, Rashna, ST. JOSEPH''S HOSPITAL AND MEDICAL CENTER, PHOENIX, Arkansas, United States
- Wang, Liang, Barrow Neurological Institute, Phoenix, Arizona, United States
- Hoskin, Justin, Barrow Neurological Society, Phoenix, Arizona, United States
- Boddupalli, Saisridhar, Dignity Health, Scottsdale, Arizona, United States
- Qaqish, Ibrahim, Mayo Clinic, Scottsdale, Arizona, United States
Background
We describe a rare case of acute hypokalemic paralysis associated with the abuse of methamphetamine.
Methods
A 28-year year old Caucasian male with a history of polysubstance abuse presented to the emergency department with a chief complaint of painless bilateral lower extremity paralysis that developed over several hours. He denies vomiting, diarrhea, diuretic use or previous similar episodes. He denied any trauma to the back or heavy carbohydrate diet preceding this event. Physical exam revealed normal vital signs and bilateral lower extremity muscle weakness; proximal greater than distal with hyporeflexia. Cranial nerves were intact. Initial serum potassium was 2.4mmol/L. Urine drug screen was positive for amphetamine and random urine potassium was 14 mmol/L. Serum magnesium and TSH were within normal limits. Electrocardiogram revealed no QT interval changes or U wave.
Patient was started on careful supplementation with 30mEq of intravenous and 40 mEq of oral potassium chloride that increased the level to 4.9 mmol/L. This lead to slow but complete resolution of the paralysis causing the patient to be able to walk after six hours.
Conclusion
Hypokalemic periodic paralysis (HPP) is neuromuscular disorder characterized by episodes of painless muscle weakness. Most cases are hereditary from calcium channel mutations but acquired cases have been described. Usually there is an increased release of epinephrine or insulin causing potassium to shift into cells. Methamphetamine is an indirect sympathomimetic amine, although it lacks direct adrenergic stimulation, it inhibits presynaptic epinephrine and dopamine reuptake mediated adenosine triphosphate dependent (ATP) channels resulting and surge of both alpha and beta adrenergic effects. The main steps in the management include exclusion of other causes of hypokalemia, potassium replacement, close monitoring of the cardiac rhythm and serum potassium levels. While the mechanism of action of amphetamine explains the physiology of HPP, no cases have ever been reported of amphetamine induced HPP in literature.