Rationale: Hypokalemia is a common finding. Typically asymptomatic presentations of neuromuscular weakness emerge at levels below 2.5 mmol/L. Causes include gastrointestinal losses, renal losses, or intracellular shift, with gastrointestinal losses and diuretics accounting for the majority. Although the cause is often apparent on clinical assessment, a systematic approach incorporating urine biochemistry can aid in narrowing the differential in obscure cases.
Presentation: We describe a case of a previously healthy 27-year-old man who presented with acute ascending paralysis, with an associated severe hypokalemia and metabolic acidosis. There were no apparent causes on clinical assessment.
Diagnosis: Based on analysis of urine biochemistry, we concluded that a pathologic kaluresis was present, and given his acidemia and transient pathology, we diagnosed the patient with hypokalemic paralysis secondary to toluene toxicity.
Interventions: We provided supportive care and electrolyte repletion for our patient; no specific therapies for toluene were required. Our patient was counseled regarding appropriate protective measures when handling toluene.
Outcomes: Complete neurologic recovery and biochemical normalization occurred within 48 hours of presentation with supportive care. He continued to use proper precautions when handling toluene, and experienced no symptom relapse, or further abnormalities on both blood and urine chemistry.
Lessons Learned: Using this case, we review an algorithmic approach incorporating urine biochemistries to aid in the workup of hypokalemia. We review toluene as a toxicologic entity and highlight its role as a cause of hypokalemia.
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http://dx.doi.org/10.1177/2054358119871594 | DOI Listing |
Muscle Nerve
December 2024
Copenhagen Neuromuscular Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Introduction/aims: Primary hypokalemic periodic paralysis (HypoPP) can present with periodic paralysis and/or permanent muscle weakness. Permanent weakness is accompanied by fat replacement of the muscle. It is unknown whether the permanent muscle weakness is solely due to fat replacement or if other factors affect the ability of the remaining muscle fibers to contract.
View Article and Find Full Text PDFIntroduction: Thyrotoxic hypokalemic periodic paralysis (THPP) is a rare but severe complication of hyperthyroidism characterized by acute muscle weakness. This study reports the first case of THPP in an adolescent with type 1 diabetes mellitus (T1DM) and Graves' disease, triggered by high-dose insulin, high carbohydrate intake, and strenuous exercise. It highlights the clinical presentation, management, and implications of THPP in this context.
View Article and Find Full Text PDFCureus
November 2024
Emergency Medicine, Mayo Clinic Arizona, Phoenix, USA.
Thyrotoxic periodic paralysis (TPP) is a rare but significant complication of hyperthyroidism, characterized by episodes of muscle weakness or paralysis and associated hypokalemia. This case report details a 30-year-old Latin American male with a history of Graves' disease, presenting with acute muscle weakness and hypokalemia. The patient reported transient episodes of weakness over recent weeks, culminating in a severe episode prompting emergency evaluation.
View Article and Find Full Text PDFCureus
November 2024
Emergency Medicine, Amrita Institute of Medical Sciences, Kochi, IND.
One type of hypokalemic periodic paralysis that is associated with hyperthyroidism is called thyrotoxic periodic paralysis (TPP). TPP can be linked to any cause of hyperthyroidism, although Graves' disease is the most common cause. This sporadic variant of hypokalaemic periodic paralysis, thyrotoxic periodic paralysis, is characterized by rapid onset weakness in the proximal muscles.
View Article and Find Full Text PDFNeurol Genet
December 2024
From the Copenhagen Neuromuscular Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Denmark.
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