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Pulmonary Edema in Myasthenic Crisis

DOI: 10.1155/2013/863620

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Abstract:

We report a previously asymptomatic 50-year-old lady who came with myasthenic crisis as initial presentation of myasthenia gravis. She developed pulmonary edema following intravenous immunoglobulin administration and had ischemic changes in ECG and left ventricular dysfunction on echocardiography. She improved with diuretics, dobutamine, and fluid restriction alone. This is the first report in English-language medical literature describing the association between myasthenic crisis and likely takotsubo cardiomyopathy-related pulmonary edema following intravenous immunoglobulin administration. 1. Introduction Myasthenia gravis (MG) is an antibody-mediated neurological disorder that affects the neuromuscular junction [1]. Myasthenic crisis is characterized by respiratory failure that requires mechanical ventilation [2]. Takotsubo cardiomyopathy is defined as a profound but reversible left ventricular dysfunction in the absence of coronary artery disease [3]. We present a 50-year-old lady with myasthenic crisis (MC), who developed pulmonary oedema following intravenous immunoglobulin (IVIG) and was found to have features suggestive of takotsubo cardiomyopathy (TC). 2. Case She had had cough, rhinorrhoea, headache, myalgias, and fever for 10 days and presented to another hospital with fatigue of a week’s duration, breathlessness, slurring of speech, and nasal regurgitation of liquids for two days. She was intubated and then transferred to our institution. On admission, she was conscious and afebrile with tachycardia (110/min), tachypnoea (22/min), and normal blood pressure. Cardiovascular and respiratory system examination was otherwise normal. Neurologically, she had flaccid quadriparesis (2/5), floppy neck, and bilateral facial nerve paralysis without ocular weakness or bladder incontinence. Chest radiograph (CXR), electrocardiogram (ECG), renal and liver function tests, and haemogram were normal. An initial diagnosis of Guillain-Barre syndrome was made and intravenous immunoglobulin (IVIG) was initiated at a dose of 0.4?g/kg/day. On the second day she had asymmetrical ptosis; 1?mg neostigmine administration led to improvement in ptosis and muscle power (4-/5) and neostigmine 30?mg every 4th hour was continued thereafter. Later during the day, tachycardia, tachypnoea, hypotension (96/60?mmHg), and left-sided infra-axillary crackles were observed. Chest radiograph revealed infiltrates in the left mid-zones (Figure 1(a)); ECG showed occasional VPCs (Figure 2(a)), and her total leukocyte counts were 20 × 109/L. Respiratory alkalosis was seen on arterial blood

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