Carotid artery rupture is fortunately an uncommon complication of head and neck cancer treatment. Eleven episodes of carotid artery rupture following irradiation and major head and neck resection were identified over a 6-year period. We review our experience and discuss the predisposing factors that can cause this complication, important aspects of management and outcome. During this 6-year period, 11 episodes of carotid artery rupture were treated in our unit. All patients had received prior irradiation (more than 60 Gy) and undergone a major surgical resection or resections. The average age was 59 years; all patients had a salivary fistula, local infection and a manifest 'herald bleed' just before their major carotid artery rupture. These patients were resuscitated, taken to theatre and the neck explored, with control of the vessel and debridement of necrotic tissue. Soft tissue coverage was in the form of a flap. Many of the factors predisposing to carotid artery rupture can be ameliorated or treated early in order to avoid this complication. Early and aggressive nutritional support together with correction of haematological abnormalities promote wound healing and prevent tissue breakdown. The detection and treatment of infection also reduces fistula formation and wound compromise. We present our protocol for the early, aggressive management of these patients with carotid artery rupture.

SummaryThe aim of this study was to investigate the performance of awake fibreoptic intubation using remifentanil sedation with topical anaesthesia limited only to the nasal mucosa. Twenty-four patients presenting for elective head and neck surgery were sedated using remifentanil titrated to effect and local anaesthetic was applied to the nasal mucosa. Vital signs were recorded throughout the procedure and both the anaesthetist and an observer rated the ease of the procedure. Intubation was successful in all patients and the procedure was rated as easy in 15 (63%) of patients. Mean arterial pressure remained within 8% of baseline in all cases and respiratory rate remained > 8 breaths.min )1 in all but three patients. Although 56% of patients interviewed postoperatively said they recalled the procedure, all but one would undertake the same procedure again if necessary. This technique appears reliable in providing adequate sedation whilst maintaining cardiovascular and respiratory stability.

case reports/case series 521 CAN J ANESTH 55: 8 www.cja-jca.org August, 2008 Purpose: To report a case of serotonin toxicity, presenting in the postoperative period, caused by an interaction between paroxetine (a selective serotonin reuptake inhibitor, SSRI) and fentanyl (a phenylpiperidine opioid). Serotonin toxicity precipitated by fentanyl is unusual and has not previously been described in combination with SSRIs in the perioperative setting. Clinical features:A 60-yr-old woman, established on paroxetine for depression, underwent excision of a chest wall myxofibrosarcoma and chest wall reconstruction. Fentanyl was administered for intraoperative and postoperative analgesia (1 mg intraoperatively, and 2.5 mg by infusion in the first 36 hr, postoperatively). She developed a vague affectation, intermittent agitation, bilateral hyper-reflexia, inducible clonus, and a period of hypertension, suggestive of serotonin toxicity. There was complete resolution after cessation of fentanyl and paroxetine. Conclusion:The co-administration of SSRIs and fentanyl may precipitate serotonin toxicity. There must be consideration of this unusual interaction when administering fentanyl to patients established on SSRIs. Physicians should be vigilant of the features of serotonin toxicity developing in such patients. SEroToNiN (5-hydroxytryptamine, 5-HT) is a neurotransmitter concentrated in the raphe nuclei of the brainstem reticular formation of the central nervous system (CNS). it is involved in regulating the sleep-wakefulness cycle, mood, appetite, emotion, temperature, and the motor system. 1 The serotonin syndrome, or serotonin toxicity, is a well-documented series of clinical features resulting from drug-induced serotonergic hyperstimulation in the CNS.

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