Rhabdomyolysis is caused by the disintegration of skeletal muscle fibres, leading to the release of toxic intracellular components into the systemic circulation resulting from direct or indirect injury to skeletal muscle, and has potential life-threatening complications such as acute renal failure. Drug-induced rhabdomyolysis, a significant subset of this syndrome, is often idiosyncratic in nature, making it challenging to study and predict. Our report explores a case of severe rhabdomyolysis following uncomplicated general anaesthesia for parathyroidectomy in a patient who was on statin therapy perioperatively for 14 years and had relatively no side effects arising from it.
View Article and Find Full Text PDFThyrotoxicosis is a hypermetabolic condition defined by elevated levels of triiodothyronine (T3) and/or thyroxine (T4) in the serum. While irregular heart rhythms like atrial fibrillation are commonly linked to this condition, other types such as supraventricular tachycardia (SVT) characterized by sudden onset, narrow QRS complexes, and regular RR intervals in the absence of structural heart disease are much less frequently reported and often overlooked. We present a compelling case of Graves' thyrotoxicosis in a middle-aged male patient, whose only presenting symptom was SVT, in the absence of typical systemic signs of hyperthyroidism or structural cardiac abnormalities.
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March 2025
Background: Hypomagnesaemia is a common electrolyte disturbance that can lead to severe complications, including cardiac dysrhythmias and neuromuscular instability. Despite established guidelines by the York and Scarborough Teaching Hospitals NHS Foundation Trust, there is concern that these protocols are not consistently followed, potentially compromising patient outcomes. Objective: This audit aimed to evaluate the management of hypomagnesaemia at Scarborough General Hospital, focusing on adherence to trust guidelines and identifying areas for improvement in clinical practice.
View Article and Find Full Text PDFIsovaleric acidemia is a rare autosomal recessive inborn error of metabolism that affects the breakdown of the essential amino acid leucine. Acute metabolic decompensation is often triggered by stressors such as surgery, concurrent illness, excessive protein intake, or dehydration. This can lead to a catabolic state with increased endogenous protein turnover, posing a risk of potentially life-threatening crises due to the accumulation of toxic metabolites from incomplete leucine breakdown.
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