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C. Perruchoud, M. Chollet-Rivier, Cardiac arrest during induction of anaesthesia in a child on long-term amphetamine therapy, BJA: British Journal of Anaesthesia, Volume 100, Issue 3, March 2008, Pages 421–422, https://doi.org/10.1093/bja/aen012
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Editor—The number of children on chronic amphetamine treatment for attention deficit hyperactivity disorder (ADHD) has dramatically increased during the last decade. Although several previous case reports1 have described serious adverse reactions during general anaesthesia in adult patients on chronic amphetamine, very little is known about perioperative problems with paediatric patients. We report a case in which a 10-yr-old child on long-term methyphenidate (MPH) therapy presented a cardiac arrest during induction of general anaesthesia.
A 10-yr-old male child was undergoing an ambulatory laser therapy of a haemangioma on the face. The patient had been taking MPH daily for 4 yr because of ADHD. Anaesthesia was induced by mask with sevoflurane. Arterial pressure and heart rate remained stable and oxygen saturation was 100%. After i.v. access was established, propofol 2 mg kg−1 and alfentanil 10 µg kg−1 were administered. Immediately after, the child developed a severe bradycardia followed by asystole. I.V. atropine 0.5 mg was given twice and external chest massage was performed. Normal cardiac rhythm with correct haemodynamic measures was restored 30 s after the start of the cardiopulmonary resuscitation. The planned operation was continued. Operation and emergence were uneventful. The patient was taken to the post-anaesthesia care unit where his heart rate remained stable at 90 beats min−1. He was discharged home on the same day.
Amphetamines are indirect sympathetic amines with powerful central nervous system stimulation activity and peripheral α and β actions. Chronic administration can result in depletion of norepinephrine and dopamine storage. This decreased reserve of endogenous catecholamine can contribute to a blunted sympathetic response which can lead to bradycardia and refractory hypotension during anaesthesia. In our case, the patient did not take his medication on the morning of surgery, but it has been shown that intraneuronal catecholamine levels may not return to normal for days to weeks after cessation of amphetamine use.2
Perioperative cardiac arrest in children has multiple causations.3 Propofol has been associated with bradycardia and asystole4 and the decrease in heart rate is more pronounced when propofol is combined with alfentanil.5
We found in the patient's medical files several previous uneventful general anaesthetics for the same procedure, before the patient was on amphetamine therapy. However, a severe bradycardia responding to atropine was noted during induction of a general anaesthesia several months earlier when the child was on amphetamine treatment. We believe that a blunted sympathetic response due to a chronic amphetamine exposition associated to the cardiac effects of propofol and alfentanil may have transformed a trivial bradycardia in a life-threatening asystole.
Therefore, the management of children on chronic amphetamine therapy should include avoidance or careful titration of cardiac depressor anaesthetic drugs. Direct acting vasopressors such as epinephrine or phenylephrine are preferable because of possible cross-tolerance to other indirect vasopressors such as ephedrine.6 Premedication or pre-treatment with atropine may also be useful.
In conclusion, we have observed a severe cardiovascular complication during induction of anaesthesia, possibly in relation to chronic amphetamine treatment. In view of the increasing number of children on such treatment, further studies on the anaesthetic implications of this are required to determine if a specialized anaesthetic approach is appropriate in this group.
Comments
We congratulate Perruchoud et al for enumerating perioperative implications of chronic amphetamine usage 1. We present a case of case of young woman who developed severe left ventricular failure(LVF) associated with chronic amphetamine use in the form of illicit weight loss drugs. Severe LVF associated with dilated cardiomyopathy is another effect of chronic amphetamine usage. Pregnancy, viral myocarditis and excessive alcohol consumption are some of the common causes for dilated cardiomyopathy in young woman of childbearing age. However recreational drugs are also now included .
A 35-year-old female presented to our emergency department with worsening shortness of breath and right upper quadrant abdominal pain for 1 week. On examination she was conscious but with increased respiratory rate ( 40 breaths / minute) and chest examination revealed wide spread crepitations and wheeze ,oxygen saturation with fractional inspired oxygen (FiO2) 60% was 92%. She was haemodynamically stable at this time. The patient was admitted to High dependency care for further monitoring and management. Arterial blood gas with 15 l oxygen by face mask showed PaO2 8.15 kPa, PaCO2 3.25 kPa and pH 7.393, full blood count was normal, chest x-ray revealed frank pulmonary oedema . A transthoracic echocardiogram showed a grossly dilated left ventricle and severely impaired global left ventricular function. Measured Left Ventricluar Ejection Function by apical Simpson’s biplane was 21%. Other abnormal findings were dilated left atrium, thickened mitral valve, severe mitral regurgitation; other valves were normal, with a normal right heart. Her worsening left ventricular failure was treated with Non invasive ventilation, intravenous frusemide boluses, dobutamine and glyceryl trinitrate infusions. Over next 24 h her haemodynamics improved and both intravenous infusions were stopped. Respiratory gas exchange also improved dramatically with significant decrease in FiO2 requirement. A toxicology screen revealed significant amount of Amphetamines in the urine, and on further questioning the patient revealed she was on illicit weight reducing drugs containing amphetamines. She was started on oral digoxin and an angiotensin converting enzyme (ACE) inhibitor and was discharged to the cardiac unit where she made further significant improvement. A repeat echocardiogram showed an improvement of LVEF to 28%. The patient was discharged subsequently with significant improvement in her symptoms and on oral digoxin, perindopril, carvedilol, aspirin and frusemide.
Amphetamines can cause cardiomyopathy either after chronic consumption or acute overdose; the mechanism of amphetamine-induced damage is uncertain. Proposed mechanism are due to high catecholamine state through stimulated release of catecholamine, dopamine,and serotonin from the adrenal medulla and the sympathetic nerve terminals, resulting in activation of central and peripheral alpha and beta-adrenergic autonomic receptors. Catecholamine excess can conceivably result in cardiomyopathy through recurrent coronary vasospasm, tachycardia, hypertension, accelerated atherosclerosis and/or direct myocardial toxicity 2. Some observations suggest that myocardial pathology may be reversible with early cessation of exposure to amphetamines. In addition to blunting the sympathetic responses as authors suggested 1, chronic administration can lead to a state high Catecholamine state resulting in severe left ventricular failure .
1.Perruchoud C et al. Br J Anaesth 2008;100:421-2. 2.Yeo et al. Am J Med 2007;120:165-71.
Conflict of Interest:
None declared