A 26-year-old man with a history of hypothyroidism and end stage renal disease presented with a three week history of severe body aches, inability to ambulate, and transient visual obscurations. Clinical examination and laboratory findings revealed myxoedema as the cause of the papilloedema.A 26-year-old man presented with severe body aches and inability to ambulate over three weeks. This was associated with transient visual obscurations (TVO) in his left eye (OS). He reported that his visual acuity was always clear, but the peripheral field OS would "turn black" for about 15 seconds, three times per day for the past three weeks. The patient denied having headaches or eye pain.Medical history included end stage renal disease (on dialysis) secondary to IgA nephropathy, hypertension, and thyroid cancer (treated surgically followed by radiotherapy) with resultant hypothyroidism. His medications included clonidine, L-thyroxine, phosphate binder, diazepam, oxycodone, and an oral multivitamin tablet.Clinical examination revealed a blood pressure of 162/108 mm Hg and a pulse of 78 beats/minute. He was noted to be lethargic and he had myxoedematous features including facial oedema, deep tendon reflexes with a slow relaxation phase, and decreased motor strength. Ophthalmological examination demonstrated a visual acuity of 20/20 in both eyes (OU) and pupils measured 4 mm OU with normal reactivity and no relative afferent pupillary defect (RAPD). His perReceived formance on Ishihara colour plates and confrontation visual field testing were normal OU. Anterior segment exam was normal and intraocular pressures were 27 mm Hg OD and 23 mm Hg OS. Dilated examination of the fundus showed optic disc oedema and peripapillary hemorrhages bilaterally (left greater than right).Blood tests revealed a markedly elevated TSH level of 381 mIU/L (0.3-3.0 mIU/L) and a low free T4 at 0.68 mcg/dL (0.7-2.0 mcg/dL). Magnetic resonance imaging (MRI) of the brain without contrast was normal. A spinal cord MRI was attempted but the patient was unable to hold still for the scan due to severe body aches. The patient was given a loading dose of levothyroxine 1000 mcg and his free T4 increased to 1.39 mcg/dL indicating that the patient can absorb levothyroxine and his previous low level was probably due to noncompliance. A lumbar puncture (LP) showed an opening pressure of 28 cm H2O (5-20 cm H2O) and an elevated protein level of 129 mg/dL (15-50 mg/dL). A presumptive diagnosis of myxoedema associated papilloedema was made. While in the hospital, his daily L-thyroxine replacement was increased to 200 mcg daily and acetazolamide 250 mg three times daily was prescribed. He slowly became more alert and was able to ambulate prior to discharge.
DISCUSSIONPatients with clinical hypothyroidism have been known to have elevated cerebral spinal fluid (CSF) 303