The interesting article by Vikrant and colleaguesCitation1 prompts us to contribute our recent experience. Herein we report a case in which profound hypothyroidism was the trigger for severe rhabdomyolysis. The patient's late presentation resulted in uremic encephalopathy, necessitating intensive care.
A 35-year-old man was admitted to our hospital because of oliguria, back and leg pain and generalized languor. On examination, he was somnolent but afebrile. Blood pressure was 155/70 mmHg with a heart rate of 90 beats/min. Blood glucose was 86 mg/dL. ECG revealed loss of P-waves and tented T-waves. Blood gas analysis showed profound metabolic acidosis with a pH 7.1 and a bicarbonate level of 6.2 mmol/L. pO2 and lactate were within the normal range. The patient was transferred to the intensive care unit (ICU) immediately. Laboratory results revealed severe renal failure with a serum creatinine of 32.9 mg/dL (normal: 0.7–1.2 mg/dL); blood urea nitrogen (BUN) 202 mg/dL (normal: 7–23 mg/dL). Other results were as follows: serum potassium 8.9 mmol/L, serum phosphate 5.43 mmol/L, serum calcium 1.78 mmol/L; lactate dehydrogenase (LDH), 877 U/L (normal: <250 U/L); aspartate transaminase (AST), 139 U/L (normal: <40 U/L); and creatinine phosphokinase (CPK), 14771 U/L (normal: <170 U/L). The urinary sediment suggested hematuria but no red cells were detected on microscopic examination, in keeping with myoglobinuria. During insertion of a central line, a generalized tonic-clonic seizure occurred, which was terminated by clonazepam. The patient breathed spontaneously and did not require inotropic support. No structural abnormalities were detected by renal ultrasound. Continuous veno-venous hemodiafiltration (CVVHDF) was commenced. The following day, when another generalized seizure developed, treatment with levetiracetam was started. A computed tomography (CT) scan of the brain without contrast was normal. As he was admitted over the weekend, no electroencephalography (EEG) service was available.
The patient's medical record included obesity with a body mass index (BMI) of 43 kg/m2, hypertension and hypothyroidism following total thyroidectomy for multinodular goiter in 2003. On his last appointment in our thyroid clinic eight months earlier, poor compliance was commented on.
Thyroid function was checked and severe hypothyroidism was apparent: TSH 136 mcU/mL (normal: 0.3–4 mcU/mL); free T4 1.5 pg/mL (normal 9–17 pg/mL). Parenteral thyroxin substitution was commenced. The patient's vigilance improved subsequently. CVVHDF was discontinued on ICU day 4 and he was transferred to a normal ward the following day. The history was completed: about three weeks earlier, the patient had noted myalgias, which he ascribed to his manual work as a garden assistant. Fatigue ensued and the color of his urine darkened, before he became oliguric four days prior to admission. Twitching of extremities was reported by his parents, likely representing myoclonus. He was bedbound two days before presentation to our hospital. There was no history of trauma, infection, alcohol excess or use of illicit drugs. Up to this episode there were no symptoms suggestive of an underlying myopathy and the family history was unremarkable. His only medication was lisinopril 10 mg o.d. However, he had discontinued taking thyroxine some 10 months ago (“because a friend of his mother didn't need it anymore either”). We diagnosed hypothyroidism-induced rhabdomyolysis, with late presentation culminating in uremic encephalopathy. The patient was discharged after two weeks with a serum creatinine of 2 mg/dL and normal AST, LDH and CPK. Follow up has been arranged and, when last seen in August 2013, he continued to do well with a serum creatinine of 1.4 mg/dL, corresponding to an estimated GFR of 57 mL/min. He now takes his tablets diligently.
The symptoms of hypothyroidism are myriad and hypothyroidism features frequently, albeit not prominently in the lists of causes of rhabdomyolysis.Citation2,Citation3 However, since the initial report of a patient in whom hypothyroidism caused rhabdomyolysis leading to acute kidney injury some 30 years ago, only a handful of cases of dialysis-dependent renal-failure have emerged in this setting.Citation4–7 The comparatively moderate CPK elevation in our case was thought to reflect a marker already in decline, given the patient's exceedingly high creatinine at presentation, in keeping with a protracted clinical course. Indeed, CPK peaks within one to three days after muscle injury and subsequently declines at a rate of 40% of the previous day's value.Citation8 We are not aware of any reports in which hypothyroidism culminated in uremic encephalopathy. This case adds to the spectrum of presentation for this common endocrine disorder.
Declaration of interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
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