[Downloaded free from http://www.ijaweb.org on Wednesday, September 28, 2016, IP: 62.250.105.169]
Letters to Editor
report a case of sudden bilateral vision loss after endoscopic surgery for pituitary tumour, where intraoperative haemodynamic instability was possibly suggestive of a devastating postoperative complication. A 23-year-old, 70kg male presented to the neurosurgical department with a complaint of coarsening of features for past 2 years. He was a known case of diabetes mellitus. A clinical diagnosis of acromegaly was confirmed by his growth hormone (GH) assessment (GH >90). Other investigations were within normal limits. Magnetic resonance imaging (MRI) revealed a 2 × 2 × 1.8 cm suprasellar lobulated mass, suggestive of pituitary tumour. His preoperative vision was 6/6 in both eyes. The patient was scheduled for endoscopic transsphenoidal removal of pituitary macroadenoma. Anaesthesia was induced with fentanyl 2 mcg/kg, propofol 2 mg/kg and rocuronium 1 mg/kg. Standard monitoring was applied. Anaesthesia was maintained with propofol infusion and a oxygen–nitrous oxide mixture (1:2) along with intermittent boluses of fentanyl and rocuronium. At the time of tumour removal, sudden bradycardia occurred and the heart rate dropped from 86 beats per minute (bpm) to 37 bpm. The surgeon was immediately informed, who stopped further manipulation and within 15 s, the heart rate came back to the baseline value. During these episodes, the mean blood pressure remained near baseline value of 85 mmHg and did not fall significantly. The surgery was allowed to continue and there occurred three episodes of bradycardia. All these episodes occurred when surgeon was operating in close proximity to the optic chiasma. No pharmacological intervention was required during any of the episode of bradycardia. At the end of surgery, anaesthesia was discontinued and neuromuscular block reversed with neostigmine 0.5 mg/kg and glycopyrrolate 10 mcg/kg. The patient was shifted to the neurosurgical intensive care unit
(ICU). Six hours later, the patient complained of bilateral vision loss. Ophthalmic examination revealed bilateral negative perception of light. Immediately, computed tomography was performed which revealed haematoma of 10 mm × 7 mm size in the sellar region, compressing optic chiasma, along with remnants of the tumour [Figure 1]. Immediately craniotomy and evacuation of haematoma was performed. Postoperatively, his ophthalmic examination revealed a 6/6 vision in the right eye while in the left eye only finger counting was present. No further improvement in vision of the patient was observed during his hospital stay. The mechanisms involved in visual complications include direct injury or devascularisation of the optic apparatus, fracture of the orbit, postoperative haematoma, cerebral vasospasm and prolapse of the optic chiasm into an empty sella[1] and tension pneumosella.[2] During the postoperative period, our patient developed bilateral vision loss that may be due to tumour residue and optical chiasmal compression by sellar haematoma. However, intraoperative events of repeat bradycardia, possibly resulting from the oculocardiac reflex cannot be ignored. The reflex elicited may act as a warning signal and at the same time predict the surgical outcome also. Tumul Choudhury, Hemanshu Prabhakar, Gyaninder Pal Singh, Ashish Bindra Department of Neuroanesthesiology, All India Institute of Medical Sciences, New Delhi, India Address for correspondence: Dr. Hemanshu Prabhakar, Department of Neuroanaesthesiology, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi – 110 029, India. E-mail:
[email protected]
REFERENCES 1. 2.
Barrow DL, Tindal GT. Loss of vision after transsphenoidal surgery. Neurosurgery 1990;27:60-8. Yorgson JG, Arthur AS, Orlandi RR, Apfelbaum RI. Endoscopic decompression of tension pneumosella following transsphenoidal pituitary tumor resection. Pituitary 2004;7:171-7.
Unusual presentation of hypocalcaemia in a peri-operative period-cause unknown DOI: 10.4103/0019-5049.65363
Sir, Figure 1: A computed tomographic scan of the head showing a large haematoma in the sellar region (bold white arrow) 270
A 36 year old female patient, ASA class 1, weighing 50 kgs, underwent cholecystectomy under conventional Indian Journal of Anaesthesia | Vol. 54| Issue 3 | May-Jun 2010
[Downloaded free from http://www.ijaweb.org on Wednesday, September 28, 2016, IP: 62.250.105.169]
Letters to Editor
general anaesthesia- -uneventfully. Six hours later she threw convulsions in postoperative recovery ward where she received inj. diazepam 10 mg IV and loading dose of inj. phenytoin followed by infusion. The patient was haemodynamically stable and had no signs of respiratory distress; however, she was shifted to ICU for observation. Two hours later her consciousness level was found to be poor., She was deeply sedated; however, response to deep painful stimulus was present and pupils were of normal size and normally reacting. Phenytoin infusion was stopped;, patient’s vitals were closely monitored and following investigations were done: -complete haemogram, renal function tests, blood glucose, liver function tests, serum albumin, serum sodium, potassium, magnesium, phosphorus and calcium. Subsequently, quick portable chest X-ray and 12-lead-ECG were performed. Chest X-ray showed no abnormality and ECG revealed prolonged QT interval. Subsequently, patient threw convulsions again, following which she developed carpo-pedal spasm (Trousseau’s sign). Hypocalcaemia[1] was suspected and 10 ml of inj. calcium gluconate 10% was given intravenously over 10 min. Arterial blood gas and electrolyte analysis revealed normal pH and gases, serum Na+ was 129 mEq, serum K was 2.5 mEq and serum Ca++ was 0.68 mmol/L, serum magnesium and phosphorus levels were normal. Inj. calcium gluconate 10%, 10 ml, was repeated in the same manner intravenously and calcium infusion[2] and potassium correction was also started simultaneously. The infusion rate of calcium was adjusted to avoid recurrent symptomatic hypocalcaemia and to maintain total serum calcium between 8 and 9 mg%. The patient regained consciousness but was still disoriented. Her fists were tightly clenched. Calcium infusion was tapered to 1 mg/kg/hr. Subsequent investigation reports revealed all values to be normal except for serum calcium that was 7.3 mg%. At this point, she had started responding to verbal commands but she was unable to recognise her kith and kin. Following this, she developed hypotension and total serum calcium levels were found to be 6.1 mg%. Inj. calcium gluconate 10%, 10 ml, was repeated intravenously. It was followed by an infusion of inj. calcium gluconate 10% which was continued for next 12 h. Thereafter her sensorium Indian Journal of Anaesthesia | Vol. 54| Issue 3 | May-Jun 2010
cleared and ECG changes and serum calcium levels also reverted back to normal. Reports of the parathormone assay were also normal. The patient was discharged successfully on the fifth day with oral supplement of calcium 1 g/day. Causes of hypocalcaemia can be many, e.g. chronic and acute renal failure, post-thyroidectomy[3] postparathyroidectomy, primary hypoparathyroidism,[4] vitamin D deficiency, massive blood transfusion, hypoalbuminaemia, alkalosis, chemotherapy, acute pancreatitis, etc. There have been various case reports of hypocalcaemia occurring post-operatively but majority of them are following thyroid and related surgeries. In few cases, it has been reported after pre-eclampsia[5] and cardio pulmonary by pass . The anaesthesiologist must always keep the possibility of hypocalcaemia in mind whenever a patient throws convulsions in the postoperative period and check for complete serum electrolytes including serum magnesium and phosphorus levels. Hypocalcaemia may be associated with hypomagnesaemia and hyperphosphataemia and these should be corrected. The direct cause could not be determined in our case,; however, it could be respiratory alkalosis or dilutional hypocalcaemia. Perhaps the patient was chronic hypocalcaemic and minor changes in the pH made her symptomatic. Fortunately, it was diagnosed and managed successfully. Rachna Wadhwa, Seema Kalra1 Department of Anaesthesia, PGIMER and RML Hospital, 1 Department of Anaesthesiology and Critical Care, IGESI Hospital, Jhilmil, Delhi, India Address for correspondence: Rachna Wadhwa, H-45, Mansarovar Park, Shahdara, Delhi - 110 032, India. E-mail:
[email protected]
REFERENCES 1.
2.
3.
4. 5.
Lorraine A, Fitzpatrick. The hypocalcemic states: Disorders of bone and mineral metabolism. Philadelphia: Lippinkot Williams and Wilkins; 2002. p. 568-88. Available from: http:// www.endotext.org. [last cited on 2010 Apr 1]. Morgan G E, Mikhail M S, Murray M S. Management of patients with fluid and electrolyte disturbances. Clinical Anaesthesiology. 4th ed. McGraw Hill Lange; 2008. p. 684-5. Chia SH, Weisman RA, Tieu D, Kelly C, Dillmann WH, Orloff LA, et al. Prospective study of perioperative factors predicting hypocalcemia after thyroid and parathyroid surgery. Arch Otolaryngol Head Neck Surg 2006;132:41-5. Shah J. Hypocalcemic tetany in a 14 year old girl. Pediatric On Call 2005;2:5. Mishra S, Bhat R, Anita, Mahesh N, Kundra P, Hemavathy B, et al. Postpartum cardiomyopathy with severe hypocalcemia and tetany. Int J Anaesthesiol 2007;1:1. 271
