Recurrent opioid toxicity after pre-hospital care of presumed heroin overdose patients.

BACKGROUND: In patients with presumed heroin overdose, the recommended time of observation after reversing heroin toxicity with naloxone varies widely. The aims of this study were to examine the incidence of recurrent opioid toxicity and the time interval in which it occurs after pre-hospital treatment in presumed heroin overdose patients. METHODS: We undertook a retrospective study in Helsinki (population, 560,000). Records were reviewed from 1 January 1995 to 31 December 2000. Patients included were treated by the emergency medical service (EMS) for a presumed heroin overdose. Patients with known polydrug/alcohol use or the use of opioids other than heroin were excluded. The EMS records were compared with the cardiac arrest database and the medical examiners' records. RESULTS: One hundred and forty-five patients were included. The median dose of pre-hospital administered naloxone was 0.4 mg. After pre-hospital care, 84 patients refused further care and were not transported to an emergency department (ED). Seventy-one received pre-hospital naloxone, and no life-threatening events were recorded during a 12-h follow-up period in these patients. After pre-hospital care, 61 patients were transported to an ED. Twelve patients received naloxone in the ED for respiratory depression. All had signs of heroin use-related adverse events within 1 h after receiving pre-hospital naloxone. CONCLUSIONS: Allowing presumed heroin overdose patients to sign out after pre-hospital care with naloxone is safe. If transported to an ED, a 1-h observation period after naloxone administration seems to be adequate for recurrent heroin toxicity.

Cardiovascular changes after naloxone administration in propofol-sedated piglets during opioid overdose.

BACKGROUND: Naloxone is an opioid receptor antagonist. Even when used in modest doses, it has been associated with serious cardiopulmonary side-effects. In this experimental porcine study, we examined the cardiac effects of naloxone during an opioid overdose. METHODS: Cardiac parameters, changes in the left ventricular compliance and the magnitude of catecholamine release were evaluated in eight spontaneously breathing piglets under propofol sedation. Cardiac parameters were recorded every 30 s and transthoracic echocardiography was used for the continuous assessment of cardiac performance. Respiratory arrest was induced by morphine (8 mg/kg). Ten minutes after morphine administration, naloxone (80 microg/kg) was injected intravenously. Every 5 min, arterial blood gases were measured and, every 10 min, a sample for the analysis of plasma catecholamines was drawn. RESULTS: There were no statistically significant changes in left ventricular ejection fraction and no signs of pulmonary hypertension. There was a statistically significant increase in the mean arterial pressure immediately after naloxone administration and in norepinephrine concentration before naloxone administration. After naloxone administration, the plasma catecholamine levels decreased in all but one animal. Two animals developed cardiac arrest (pulseless electrical activity and ventricular fibrillation) shortly after receiving naloxone. Although they were both administered naloxone prematurely due to hypoxic bradycardia, naloxone could have contributed to the development of ventricular fibrillation. CONCLUSION: Naloxone did not cause changes in ejection fraction or mean pulmonary artery pressure in hypoxic and hypercarbic conditions. After naloxone administration, the plasma catecholamine levels returned to baseline in all but one animal, and two animals developed cardiac arrest.

Outcome after heroin overdose and cardiopulmonary resuscitation.

BACKGROUND: The survival of heroin overdose patients resuscitated from cardiac arrest is reported to be poor. The aim of our study was to investigate the outcome and characteristics of survivors after cardiac arrest caused by heroin overdose. METHODS: This was a retrospective study in a medium-sized city (population, 560,000). Between 1 January 1997 and 31 December 2000, there were 94 combined cardiac arrests caused by acute drug poisonings. The main outcome measure was survival to discharge. RESULTS: Cardiopulmonary resuscitation was attempted in 19 heroin overdose patients (group A) and in 53 patients with cardiac arrest caused by other poisonings (group B). Three (16%) vs. six (11%) patients were discharged alive (group A vs. B, respectively). The survivors in group A had an Emergency Medical Service (EMS)-witnessed cardiac arrest or the Emergency Dispatching Centre was called before the arrest occurred. There was no statistically significant difference between the two groups in terms of survival. Survivors in both groups suffered from acute renal failure (two), hypoglycaemia (four) and hypothermia (three). CONCLUSION: Survival after cardiac arrest caused by heroin overdose is possible if the arrest is EMS witnessed or the Emergency Dispatching Centre is called before the cardiac arrest occurs. In comparison with cardiac arrests caused by other poisonings, there was no difference in survival. The incidence and mechanism of hypoglycaemia should be examined in further studies.

Dexmedetomidine as an anaesthetic adjuvant in patients undergoing intracranial tumour surgery: a double-blind, randomized and placebo-controlled study.

BACKGROUND: Dexmedetomidine (DEX) has been shown to provide good perioperative haemodynamic stability with decreased intraoperative opioid requirements. It may have neural protective effects, and thus may be a suitable anaesthetic adjuvant to neurosurgical anaesthesia. METHODS: Fifty-four patients scheduled for elective surgery of supratentorial brain tumour were randomized to receive in a double-blind manner a continuous DEX infusion (plasma target concentration 0.2 or 0.4 ng ml(-1)) or placebo, beginning 20 min before anaesthesia and continuing until the start of skin closure. The DEX groups received fentanyl 2 microg kg(-1) at the induction of anaesthesia and before the start of operation, the placebo group 4 microg kg(-1), respectively. Anaesthesia was maintained with nitrous oxide in oxygen and isoflurane. RESULTS: The median times from the termination of N2O to extubation were 6 (3-27), 3 (0-20) and 4 (0-13) min in placebo, DEX-0.2 and DEX-0.4 groups, respectively (P<0.05 anova all-over effect). The median percentage of time points when systolic blood pressure was within more or less than 20% of the intraoperative mean was 72, 77 and 85, respectively (P<0.01), DEX-0.4 group differed significantly from the other groups. DEX blunted the tachycardic response to intubation (P<0.01) and the hypertensive response to extubation (P<0.01). DEX-0.4 group differed in the heart rate variability from placebo (93 vs 82%, P<0.01). CONCLUSIONS: DEX increased perioperative haemodynamic stability in patients undergoing brain tumour surgery. Compared with fentanyl, the trachea was extubated [corrected] faster without respiratory depression.

Medical and legal considerations of brain death.

Brain death was first defined in 1968, and since then laws on determining death have been implemented in all countries with active organ transplantation programs. As a prerequisite, the aetiology of brain death has to be known, and all reversible causes of coma have to be excluded. The regulations for the diagnosis of brain death are most commonly given by the national medical associations, and they vary between countries. Thus, the guidelines given in the medical textbooks are not universally applicable. The diagnosis is based on clinical examination, but confirmatory tests, such as angiography or EEG, are allowed on most occasions. Brain death is followed by cardiovascular and hormonal changes, which have implications in the management of a potential organ donor. Spinal reflexes are preserved, and motor and haemodynamic responses are frequently observed in brain dead patients.

QT interval and QT dispersion during the induction of anaesthesia in patients with subarachnoid haemorrhage: a comparison of thiopental and propofol.

BACKGROUND AND OBJECTIVE: Thiopental prolongs the QT interval more than propofol, and the two induction agents were compared in patients with subarachnoid haemorrhage predisposed to electrocardiographic abnormalities and cardiac dysrhythmias. METHODS: Twenty-nine patients were studied randomly. Anaesthesia was induced with either thiopental or propofol and fentanyl; vecuronium was used as a neuromuscular blocking agent. The electrocardiogram and arterial blood pressure were monitored from before the induction of anaesthesia to 2 min after endotracheal intubation. RESULTS: The median QT interval was at baseline 423 ms in the thiopental group and at 432 ms in the propofol group, and it increased in the thiopental group to 446 ms and decreased in the propofol group to 425 ms (P < 0.01 between groups). After induction and endotracheal intubation, the number of patients with increased QT dispersion was greater in the propofol group (P < 0.05). The incidence of cardiac dysrhythmias was similar in the study groups. CONCLUSIONS: Thiopental and propofol are equally suitable for the induction of anaesthesia in patients with subarachnoid haemorrhage.

Prolonged analgesia after epidural injection of a poorly soluble salt of fentanyl.

Epidurally administered fentanyl is commonly used in postoperative pain management. The onset of action is rapid, but the duration of analgesia is short. In this study we examined the hypothesis that a poorly soluble salt of fentanyl (fentanyl pamoate) would create a depot of the drug in the epidural space and thus provide prolonged analgesia. The dose-response relationship and duration of analgesic action of epidural fentanyl citrate (FC) and fentanyl pamoate (FP) were studied in white male Sprague-Dawley rats. Somatic and visceral nociceptive stimulation (tail flick and colorectal distension, respectively) were used to test the analgesic effects of the drugs. The calculated dose producing 100% of the maximum possible effect (100% MPE) for FP was 31 micrograms toward somatic and 33 micrograms toward visceral noxious stimulation, and for FC it was 3 micrograms toward both stimulations. The antinociceptive effects were similar, with 31 micrograms of FP and 3 micrograms of FC. The areas under the time-response curves (AUC) were significantly higher with FP than with FC when high doses (5 micrograms of FC or 50 micrograms of FP) were used, but with doses expected to produce 100% MPE, differences between the study drugs were not observed in the duration of analgesia. We conclude that the duration of antinociceptive effect of fentanyl can be prolonged when administered as a poorly soluble salt.

Prophylactic minitracheostomy after thoracotomy: a prospective, random control, clinical trial.

The effect of prophylactic minitracheostomy on the incidence of postoperative atelectasis and pulmonary gas exchange was evaluated in a prospective, random control study of 29 patients undergoing thoracotomy. Fourteen were randomly allocated to have a minitracheostomy, which was done in the recovery room immediately after operation, and the remainder acted as controls. Increased radiodensity and atelectasis were seen more often on the chest radiographs of the control patients on the first (p less than 0.05) and on the seventh postoperative days (p less than 0.01), irrespective of the extent of the pulmonary operation. Bronchial lavage under general anaesthesia or sedation was required by 6 of the 15 control patients, but by none of those who had had a minitracheostomy (p less than 0.05). These results support the hypothesis that minitracheostomy is a useful adjunct to postoperative care after thoracotomy.