Indian Journal of Anaesthesia

: 2011  |  Volume : 55  |  Issue : 3  |  Page : 313--314

Dangerous sedation in an obese patient

Leena Rachel Koshy, Shaloo Ipe, Saramma P Abraham, Grace Maria George 
 Department of Anaesthesiology, MOSC Medical College, Kolenchery, Kerala, India

Correspondence Address:
Leena Rachel Koshy
Department of Anaesthesiology, MOSC Medical College, Kolenchery, Kerala - 682 311

How to cite this article:
Koshy LR, Ipe S, Abraham SP, George GM. Dangerous sedation in an obese patient.Indian J Anaesth 2011;55:313-314

How to cite this URL:
Koshy LR, Ipe S, Abraham SP, George GM. Dangerous sedation in an obese patient. Indian J Anaesth [serial online] 2011 [cited 2020 May 31 ];55:313-314
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Obesity is an epidemic in much of the Western world and is invading the Indian population also. A 50-year-old man, an engineer, presented for anaesthesia for Eversion Tunica Vaginalis sac. He was obese (178 cm tall, weight 125 kg, Body Mass Index - 42), hypertensive and admitted to smoking five cigarettes per day and moderate alcohol intake. Blood pressure was 140/90 mm Hg and ElectroCardioGram showed sinus tachycardia and Left Ventricular Hypertrophy. Airway examination revealed normal neck movements, dentition, mouth opening and a Malampatti score of 3. Neck circumference and thyromental distance were 47 cm (19 inches) and 6 cm respectively. Investigations including thyroid function tests were within normal limits except for SGOT and SGPT (Serum Glutamic Oxaloacetic Transaminase and Serum Glutamic Pyruvic Transaminase) which were elevated to 638 and 619 IU/L respectively (alcohol-induced). He was pre-medicated with 0.5 mg Alprazolam (half life 12 h) on the previous night. On the morning of surgery, the ward nurse reported the patient to be excessively drowsy and transferred him to the operation room, where he was found to have obstructed breathing. There was central cyanosis, pulse was 98/min, bounding, blood pressure 180/98 mm Hg. Auscultation of chest revealed normal heart sound and bilateral equal air entry. Saturation was 74% in room air. Bag, mask ventilation was carried out with 100% oxygen using closed circuit system and the saturation increased to 98%. The patient was propped up and after 20 min, the patient started responding to commands. The arterial blood gas analysis revealed severe respiratory acidosis with a PaCO 2 of 104 mmHg. Direct laryngoscopy did not reveal any intraluminal airway obstruction. Non-invasive ventilation, BiPAP mode was initiated in propped up position in the Post Anaesthesia Care Unit (PACU). Echocardiogram revealed mild Pulmonary Arterial Hypertension (PAH), mild Right Ventricular (RV) enlargement and LVH. Serial Trop - I values were negative. Pulmonary embolism was ruled out by computed tomography (CT) pulmonary angiogram. After 48 h in the PACU, when he could maintain >90% saturation in room air, he was shifted out. Pulmonary function test revealed mixed type airway disease and polysomnography revealed severe Obstructive Sleep Apnoea (OSA) with Respiratory Disturbance Index > 37/h. Patient was of ASA -III as far as OSA was concerned and OSA scoring was 4 suggestive of increased peri-operative risk. [1] The patient retrospectively revealed a history of snoring, getting up from sleep five to eight times and excessive daytime sleepiness at work and while driving. Prolonged sleep after alcohol intake was reported but not loss of consciousness. Patient was discharged on non-invasive ventilation, BiPAP mode, advised weight reduction and tablet Amlodipine 5 mg twice daily.

OSA is a common finding in obese patients and clinical features include loud snoring (95%), daytime sleepiness (90%), unrefreshing sleep (40%), morning headache, nocturnal choking, and mood changes.[2],[3] Sedation compromises arousal mechanism which protects the patient from consequence of breathing disturbance. [3] In this case altered level of consciousness was because of hypercarbia, which cleared with assisted ventilation. Alcoholic liver disease could have prolonged the action of Alprazolam.

Polysomnography is the gold standard for the diagnosis of OSA. [1],[2] Regional and local anaesthesia are relatively safe. If sedation is considered, capnography and Continuous Positive Airway Pressure (CPAP) may be needed. In anticipated difficult airway, awake fibreoptic intubation is optimal. Rapid sequence induction is advisable in emergency cases. [4] Short-acting drugs like Remifentanyl and Dexmedetomedine are preferred.[3],[5] Extubation should be in lateral or semi-upright position when fully awake, after complete recovery from neuromuscular block. Postoperatively they should be managed in the high dependency area in the above position. CPAP and oxygen is used to keep saturation above 90% during sleep. [3]

High degree of suspicion of OSA should be maintained in an obese patient as it is often missed. As Dodds remarked, the question "Do you snore?" should be asked in all preoperative assessments. [6]


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2Douglas NJ. The sleep apnoea/hypopnoea syndrome and snoring. BMJ 1993;306:1057-60.
3Loadsmam JA, Hillman DR. Anesthesia and sleep apnoea. Br J Anaesth 2001;86:254-66.
4Chung SA, Yuan H, Chung F. A systemic review of obstructive sleep apnea and its implication for anaesthesiologists. Anesth Analg 2008;107:1543-63.
5Hofer RE, Sprung J, Sarr MG, Wedel DJ. Anesthesia for patients with morbid obesity using dexmedetomidine without narcotics. Can J Anaesth 2005;52:176-80.
6Dodds C. Sleep apnoea and anaesthesia. Recent Adv Anaesth Analg 1994;179-95.