|LETTER TO EDITOR
|Year : 2016 | Volume
| Issue : 1 | Page : 118-119
Management of pituitary apoplexy
Bikram Kumar Gupta, Anil Kumar Verma, MS Saravana Babu, Gynendra Gautam, Vanita R Mhaske, Chandrasekhar Singh
Department of Anaesthesiology and Critical Care Medicine, G.S.V.M Medical College, Kanpur, Uttar Pradesh, India
|Date of Web Publication||4-Feb-2016|
Dr. Bikram Kumar Gupta
Room NO.39, New Married Hostel, L.L.R.Hospital, G.S.V.M. Medical College, Kanpur, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Gupta BK, Verma AK, Saravana Babu M S, Gautam G, Mhaske VR, Singh C. Management of pituitary apoplexy. J Anaesthesiol Clin Pharmacol 2016;32:118-9
|How to cite this URL:|
Gupta BK, Verma AK, Saravana Babu M S, Gautam G, Mhaske VR, Singh C. Management of pituitary apoplexy. J Anaesthesiol Clin Pharmacol [serial online] 2016 [cited 2019 Jul 23];32:118-9. Available from: http://www.joacp.org/text.asp?2016/32/1/118/173348
Pituitary apoplexy (PA) is a rare clinical syndrome, which presents with abrupt onset of neurological deterioration due to necrosis and hemorrhage in the pituitary adenoma.  We are presenting a case of PA in an acromegaly patient and its Intensive Care Unit (ICU) management.
A 24-year-old male was admitted in ICU with respiratory distress and unconsciousness. There was a history of sudden onset with gradual progression of headache and visual disturbances since last 5 days. History revealed untreated polydipsia, polyuria and polyphagia for 2 years. On examination, he had acromegalic built, heart rate 130/min, blood pressure 160/110 mm Hg, respiratory rate 30/min,SpO 2 92% with 6L O 2 /min. Central nervous system examination revealed Glassgow coma scale (GCS)-E 1 V 1 M 1, normal sized sluggish reactive pupils on both sides. Patient was immediately intubated, and ventilatory support was provided. Blood investigations and imaging studies done [Figure 1] and [Table 1]. Arterial blood gas revealed severe metabolic acidosis with hypoxemia. Blood sugar was 596 mg/dl. Regular insulin infusion and 0.9% normal saline were started. Electrocardiogram showed sinus tachycardia. Bedside two-dimensional echocardiogram revealed diastolic heart failure with normal ejection fraction. Injection esmolol infusion was started to decrease the heart rate and blood pressure. Blood hormonal assays were sent. Injection hydrocortisone 200 mg intravenous bolus, followed by 2-4 mg/h infusion was given. Capillary glucose was measured 4 hourly and insulin dosage was titrated to maintain the blood sugar level between 150 and 200 mg/dl. After 12h, blood gas findings were pH 7.28, PaCO 2 31.8, PaO 2 125.5, HCO3− 14.7 mmol/L, serum lactate-2.5 mmol/L on FiO 2 60%. Vitals became stable, and the urine output was adequate. Esmolol infusion was tapered gradually. His blood sugar was controlled with 50U of intermediate acting insulin in three divided doses. Based on the hormonal report [Table 1], infusion of hydrocortisone was stopped on 2 nd day, tablet thyroxine 25 μg/day for asymptomatic hypothyroidism and tablet bromocryptine 1.25 mg/day for acromegaly was started through nasogastric tube. GCS improved gradually. After fulfilment of criteria, patient gradually weaned and extubated on the 6 days. He was kept in high dependency unit for 3 days and then shifted to neuromedicine ward.
|Figure 1: Magnetic resonance imaging brain showed T2-Weighted hypointense and T1-Weightediso-intense mass lesion in sellar, para-sellar, retro-sellar and supra-sellar regions|
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In this case, a sudden surge of growth hormone (GH) and insulin like growth factor (IGF-1) resulted in the hyperglycemia precipitate diabetic like condition.  The GH/IGF-1 axis has a direct endocrine effect on the myocardium, resulting in hypertrophy, enhancement of contractile performance, and elongation of the action potential of cardiac fibers.  This remodelling is further enhanced by the hypertension and glucose intolerance. As hypertrophy becomes more prominent, diastolic dysfunction may develop, leading to the development of heart failure with preserved ejection fraction. Esmolol causes increases in left ventricular end-diastolic volume, left ventricular end-systolic volume and pulmonary artery wedge pressure, as well as a decrease in heart rate and cardiac output.  Hence, esmolol was administered to this patient with left ventricular dysfunction. We started hydrocortisone prophylactically for adrenocortical suppression and tapered when serum adrenocorticotrophic hormone found to be normal. In patients with macroadenomas, even in the presence of chiasmatic syndrome, dopamine agonists (bromocriptine) are now proposed as primary treatment.  During follow-up, patient had no complaints and his blood sugar was within normal range, and he was doing his physical activity normally. This case report will help in the medical management of PA with the use of esmolol for the anaesthesiologists working in mixed ICUs.
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