Case Presentation: 26 year old male with no history of substance use, only history of hypothyroidism status post radioactive Iodine treatment three years ago for Graves’ disease presented with three days of lower limbs pain, numbness and edema which impaired ambulation. He reported he had been doing a lot of walking at a convention when all the symptoms started but denies any trauma or any form of strenuous muscle exercise. He was noncompliant with medications until a month ago when restarted on levothyroxine 150mcg. He reported dark urine but denied dysuria, urinary frequency changes. He noted fifteen pound weight gain in six months, generalized swelling, predominantly lower extremities and fatigue. He denied any constipation or cold intolerance. Examination revealed normal vital signs, limbs muscle were mildly swollen predominantly bilateral lower extremity. Neurological exam noted bilateral foot drop with decreased sensation over the dorsum of both feet. Relaxation of deep tendon reflexes was grossly delayed. Pulses were presents bilaterally in dorsalis pedis and tibialis posterior.
Laboratory data shown hemoglobin 12.5g/dl, total leukocyte count 13.5×10 9/l with 85 % neutrophilic predominance, Na+131mEq/dL, ,K+3.7mEq/l, urea17mg/dl, creatinine 1.34mg/dl, random blood glucose 154mg/dl, AST 1003IU/L, ALT178IU/L,creatinine phosphokinase elevation 54,740IU/l. TSH 63uIU/mL, free T4 0.49ng/dl. Urine toxicology was negative. Immunology panel was negative for ANA, anti-smooth muscle antibody, and liver/kidney microsomes antibody. Urine revealed 3+heme, 3+protein, and rare non-dysmorphic RBCs, no casts.He was given aggressive intravenous fluid and IV levothyroxine 175 mcg. Renal function and rhabdomyolysis improved. He underwent MRI due to non-resolving foot drop revealed abnormal appearance of the muscles of the anterior and lateral compartments in the proximal leg with abnormal enhancement and mass effect on common peroneal nerve. Electromyogram was consistent with severe bilateral fibular neuropathies with trace myositis and slightly decreased sural nerve action potentials.He was continued on levothyroxine with improvement of sensation deficit but had persistent foot drop.
Discussion: Rhabdomyolysis is a rapid breakdown of skeletal muscle tissue leading to release of its contents into systemic circulation. It is a life-threatening condition, may occur due to physical factors including severe exercise, trauma, convulsions, as well as to statin or chemical drugs and on rare occasions to hormonal causes. Hypothyroidism presents with different spectrum of myopathy from delayed deep tendon reflexes to myopathy and rhabdomyolisis which may progress to compartment syndrome with neurological consequences of muscle paralysis. Bilateral foot drop in this patient was from fibular neuropathy due to pressure of glycosaminoglycan deposition in the perineural sheath and possible muscle destruction and inflammation. Treatment of underlying hypothyroidism leads to improvement of rhabdomyolisis and of myopathy.
Conclusions: Hypothyroidism can manifest with different degree of muscle involvement and severe myopathy with rhabdomyolysis is a rare presentation of primary hypothyroidism which can be complicated with neuropathy and muscle paralyses. Hormone replacement is the mainstay therapy. Clinician awareness and prompt recognition of this condition is necessary to avoid irreversible neurologic damage and disease progression.