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• W1566718495 abstract "A 46-year-old, ASA-1, 70-kg female presented for laparoscopic cholecystectomy. After 50 mg ranitidine, 10 mg metoclopramide and 1 mg midazolam intravenously, anaesthesia was induced with 150 mg propofol and 100 μg fentanyl and maintained with 1.2 MAC of sevoflurane. We achieved neuromuscular blockade with 75 mg suxamethonium followed by 50 mg rocuronium. We gave a total of 250 μg fentanyl, with the last bolus 60 min before the end of the 100-min surgical procedure, and also 1 g paracetamol and 40 mg parecoxib. We confirmed four twitches and no fade in the train-of-four testing following reversal of neuromuscular blockade with 2.5 mg neostigmine and 1 mg atropine. Following emergence from anaesthesia, she complained of severe pain, and received 100 mg intravenous tramadol. In the recovery unit, she was initially alert, with an arterial oxygen saturation of 98%. However, 15 min later, her level of consciousness steadily decreased, and she became apnoeic and unresponsive to pain, with dilated pupils. We re-intubated her trachea without administering any further drugs. Following 10 min of mechanical ventilation, we administered a total of 2 mg naloxone. Within one minute, she started breathing spontaneously and gradually regained consciousness, and we were able to extubate her trachea. The mydriasis subsided within one hour. Tramadol is a centrally acting analgesic with affinity for opioid receptors that rarely causes respiratory depression [1]. It also provides analgesia through inhibition of serotonin and noradrenaline reuptake. Respiratory depression could theoretically occur in the presence of liver or renal dysfunction, where tramadol’s metabolism and excretion are respectively compromised [2, 3], but our patient had no evidence of such dysfunction. However, the combination of tramadol and metoclopramide may increase sedation compared with tramadol alone [4], and it is possible that the synergistic sedative effect of tramadol and metoclopramide contributed to our patient’s respiratory depression. In a similar case, apnoea was attributed to an excess of the (+) enantiomer of the administered tramadol, which has a greater affinity for the μ-receptor than the (-) enantiomer [5]. Moreover, a delayed secondary peak concentration of fentanyl, combined with its synergistic effect with tramadol, may have also contributed to our case. Tramadol can cause mydriasis through stimulation of adrenergic receptors, or miosis through stimulation of opioid receptors, and previous reports concerning the net effect on pupillary size are conflicting [6]. Miosis is more likely to occur in extensive tramadol metabolisers, while mydriasis might develop in intermediate and poor metabolisers because of a delay in conversion of tramadol (which causes pupillary dilatation) to the active metabolite, O-desmethyltramadol (which causes pupillary constriction). Our patient may have been an intermediate metaboliser. One other possible diagnosis would be central anticholinergic syndrome. Athough tramadol is a relatively safe opioid, we believe it should be administered cautiously in the immediate postoperative period." @default.
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• W1566718495 date "2011-12-12" @default.
• W1566718495 modified "2023-09-30" @default.
• W1566718495 title "Apnea and mydriasis after postoperative tramadol administration: an unusual complication and possible underlying mechanisms" @default.
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• W1566718495 doi "https://doi.org/10.1111/j.1365-2044.2011.06969.x" @default.
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