June 09-41-2.indd - Kma.org.kw

164Atypical Progression of Thyrotoxic Manifestations while Awaiting Laboratory ConfirmationJune 2009fatigability was noted in his ptosis. The tensilon test atbed side and repetitive nerve stimulation confirmedthe diagnosis myasthenia gravis (MG). There was nothymic enlargement in the CT mediastinum. He wasstarted on pyridostigmine and oral prednisolone.Once again all his symptoms started improving exceptmoderate restriction of eye movements. Presently heis doing well with additional medications.DISCUSSIONHyperthyroidism was first described by RobertJ Graves in 1835 [1] . Though most of the cases can bediagnosed clinically by its familiar presentation, thereis a wide variation of clinical signs and symptomsin unusual presentation. Even among generalpopulation with a prevalence of 1-2%, roughly0.5% of thyrotoxicosis remains undiagnosed [2] .Thyrotoxicosis is more common in women (2%) thanin men (0.2%) [1] . Our patient did not exhibit any ofthe classical signs of thyrotoxicosis - thyromegaly,tremors and staring look. Thyroid enlargement isusually diffuse and symmetrical in thyrotoxicosis butoccasionally it may not be palpable [2] . Though tremoris universal in thyrotoxicosis, it was not exhibited byour patient throughout the illness. The staring lookwas evident only in later part of his illness after hedeveloped corneal ulcer.Retrospective analysis suggests that respiratoryinfection unmasked his underlying thyrotoxicosis.Without being recognized he twice went into thyroidstorm requiring intubation, diagnosed as heart failureand recovered only with symptomatic treatment.Thyroid storm is a medical emergency with anincidence of 1-2% and carries a mortality of 10-75% [3] .Possibly his first storm was precipitated by palpatingthe gland while looking for cervical adenitis and thesecond one by the drugs given.Flaccid paralysis after the storm was thoughtto be due to GBS because of the absent jerks, facialweakness and respiratory failure. In thyrotoxicosisalso there may be flaccid paraplegia with absentjerks and without bladder involvement, called“Basedow’s paraplegia”. The incidence of thispolyneuropathy is around 19% [4] . Both possibilitieswere ruled out by normal nerve conduction studies.Next hypokalemic periodic palsy was considered.If such paralyses occur in thyrotoxicosis, it is calledThyrotoxic periodic paralysis. Its incidence is 10%and is most common in Asian males (M:F = 6:1)over 20 years of age. Attacks may be localized orgeneralized and each attack can last for minutes todays. Type of paralyses also differs during each attack.Except heart and sphincters, all other muscles canbe affected [5,6] . It differs from familial hypokalemicperiodic paralysis by the absence of familyhistory, older age of onset (> 20 years), worseningor precipitation of symptoms by acetazolamideand prevention of attacks by B-blockers [5] . Theflaccid paralysis responded to the replacement ofpotassium, respiratory support and B-blockerswhich are incidentally the treatment for thyrotoxicperiodic paralysis. Another possibility is thyroidmyopathy which can precede the thyrotoxicosissymptoms. It is more common in female in fifthdecade and is characterized mainly by proximalweakness. Wasting can occur especially in elderlyand weakness may involve bulbar, esophageal andrespiratory muscles. Serum creatinine kinase is notraised as a rule but electromyography is usuallyabnormal in 80% cases [6] .Hashimoto’s encephalopathy is usually associatedwith hypo rather than hyperthyroidism. Thissubacute encephalopathy has varied presentationand commonly affects females. Two less distinctpatterns of presentation are recognized. The vasculiticpresentation is like acute stroke associated with focalneurologic signs, seizures and multifocal myoclonus.Another pattern is diffuse slowly progressiveimpairment of mental function with confusion,somnolence, and psychosis [7] . Mostly there willbe raised CSF protein with occasional pleocytosis.In our patient the neuropsychiatric manifestationoccurred abruptly along with thyroid storm anddid not have myoclonus, seizures or abnormal CSF.Reversible pyramidal signs have been reported inthyrotoxicosis [8] . This patient also exhibited all themetabolic complications of thyrotoxicosis. They arehypercalcemia, hypomagnesemia, hypokalemia andhypoalbuminemia [9] .Thyroid associated ophthalmopathy (TAO) is anauto-immune disorder, with an incidence of 5% (butsub-clinical in 90%). It may precede (20%), concur(40%) or follow (40%) treatment for thyrotoxicosisand is independent of thyroid status [10] . There arefour subtypes depending upon the site of immuneattack [11] . Ocular myopathy type results fromsensitized T-lymphocytes targeting extra ocularmuscles. Congestive ophthalmopathy is due toantibodies cross reacting with orbital connectivetissue and fat to produce typical symptoms of TAO– watering, congestion and proptosis. Combinationof both is called mixed type and it is the commonestpresentation of TAO. The fourth type, chronic eyeliddisease is responsible for lid lag and corneal ulcer [7] . Inour patient, it started as acute ocular myopathy withabsent extraocular movements which was mistakenfor cranial nerve palsy or brainstem involvement.Subsequently he evolved into mixed and chronic eyelid disease type with the development of corneal ulcerwhich was conveniently labeled as exposure keratitisdue to bilateral facial palsy. The staring look wasevident later after initiating on anti-thyroid regimen.