Correspondence
1009
Patient-controlled analgesia in burn patients Drs Choiniere, Grenier and Paquette demonstrate the benefits of patient-controlled analgesia in burns (Anaesthesia 1992; 47: 467-472) They conclude ‘that PCA is a safe, effective and improved method of controlling burn pain’. Whilst they demonstrate adequately the latter two points, there is no evidence for the former from their study
based on 12 patients. I share the same opinion with them that PCA is safe, but much larger studies will be necessary to demonstrate this conclusively. James Paget Hospital, Great Yarmouth NR31 6 L A
W.G. NOTCUTT
Fatal theophylline poisoning with rhabdomyolysis In their report of a patient with severe theophylline intoxication, Drs Parr and Willatts (Anaesthesia 1991; 4 6 557-9) draw attention to important aspects of the management of such cases. Nevertheless, questions should be raised about this particular case which are not discussed by the authors. It was evident within a short time of initial presentation that the patient had ingested a substantial overdose of a drug well known to cause life-threatening complications [l, 21. Despite this, the patient was transferred from the Accident and Emergency Department to the Coronary Care Unit (CCU) and only gained admission to the Intensive Therapy Unit (ITU) several hours later after suffering a cardiorespiratory arrest. The convulsions and cardiac arrhythmias which preceded the final transfer were probably predictable, given the magnitude of the overdose and the dangerously high theophylline level. Cardiorespiratory collapse may have been avoided, and its complications prevented, if the patient had been admitted directly to the ITU. After admission to ITU, the treatment received by the patient appears to have been thorough and appropriate; however, there are indications that the management in the CCU was illogical and may have contributed to the patient’s deterioration. For instance, supplementary oxygen therapy was apparently not given and, consequently, the initial blood gas analysis showed significant hypoxaemia. Potassium was administered in an inadequate dosage considering the admission serum potassium concentration of 2.4 mmol.l-’. Furthermore, following unsuccessful therapy with a single small dose of amiodarone, disopyramide was used. Theophylline acts by inhibiting phosphodiesterases and therefore increases cyclic A M P levels [3], the arrhythmias and hypotension seen in theophylline overdose are attributable to this effect. Treatment of theophyllineinduced arrhythmias is probably best undertaken using a beta-adrenoceptor antagonist such as propanolol [4, 51 which prevents the conversion of ATP to cyclic AMP, rather than a drug such as disopyramide which has strong anticholinergic effects and is probably inappropriate in circumstances of increased adrenergic activity. Given this mode of action, the rapid development of ventricular fibrillation following the administration of disopyramide might have been predicted. This sequence of events raises the question of whether the CCU is ever an appropriate place to monitor and manage patients who have taken potentially dangerous overdoses. Although survival has been reported after higher blood theophylline levels [6, 71 recovery could not be guaranteed in the case described. However, it is essential that prompt recognition and treatment of a deteriorating clinical state occurs if the chances of survival are to be enhanced. This requires continuous monitoring and prompt intervention by an immediately available and suitably experienced doctor at all times. For this reason, patients who are
known to be significantly intoxicated with potentially dangerous drugs should be directly admitted to the ITU for observation. This case history highlights the need for improved training of junior medical staff and greater consultant involvement in the acute specialities. Queen Alexandra Hospital, Porsmouth PO6 3 L Y
B.L. TAYLOR G.B. SMITH P.J. MCQUILLAN
References [I] PALOUCEK FP, RODVOLDKA. Evoluation of theophylline overdoses’ and toxicities. Annals of Emergency Medicine 1988; 17: 13544. [2] KELLYWJW, PARKIN WG. Charcoal hemoperfusion treatment of severe theophylline toxicity. Ausfralian and New Zealand Journal of Medicine 1985; 15: 75-77. [3] TORPHYTJ, UNDEMBJ. Phosphodiesterase inhibitors: new opportunities for the treatment of asthma. Thorax 1991; 46: 5 12-23. [4] AMIN DJ, HENRY JA. Propanolol administration in theophylline overdose. Lancer 1985; 1: 520-1. [5] KEARNEYTE, MANOGUERRAAS, CURTIS GP e t a l . Theophylline toxicity and the beta-adrenergic system. Annals of Infernal Medicine 1985; 102 7669. [6] DEANLS, BROWN JW. Massive theophylline overdose. Survival without hemoperfusion. Journal of American Medical Association 1982; 248: 1742. JJ. Survival after massive aminophylline [7] WELLSDH, FERLAUTO overdose in a premature infant. Paediafrics 1979; 64:252-3.
A reply Thank you for the opportunity to comment o n the letter from Drs Taylor, Smith and McQuillan which discusses our case report on fatal theophylline intoxication. We agree whole-heartedly with their views. The most important consideration, however, is how can such a sequence of events be avoided in the future? Training in intensive therapy should be available to all medical students and doctors training in acute medical specialties. The purpose of this is to enable them to recognise acute illness or deterioration in their patient’s condition at a time when rapid admission or transfer to an Intensive Therapy Unit can benefit the patient. It is with great pleasure that we can confirm the initiative of the Royal Colleges of Anaesthetists, Physicians and Surgeons which outlines a common core of training in intensive therapy suitable for trainees from all specialties. In due course this will overcome such problems as misplaced admission to a Coronary Care Unit, as in this case, and will result in better patient care. Intensive Therapy Unit, Bristol Royal Infirmary, Bristol BS2 8H W
S.M. WILLATTS M.J.A. PARR
1009
Patient-controlled analgesia in burn patients Drs Choiniere, Grenier and Paquette demonstrate the benefits of patient-controlled analgesia in burns (Anaesthesia 1992; 47: 467-472) They conclude ‘that PCA is a safe, effective and improved method of controlling burn pain’. Whilst they demonstrate adequately the latter two points, there is no evidence for the former from their study
based on 12 patients. I share the same opinion with them that PCA is safe, but much larger studies will be necessary to demonstrate this conclusively. James Paget Hospital, Great Yarmouth NR31 6 L A
W.G. NOTCUTT
Fatal theophylline poisoning with rhabdomyolysis In their report of a patient with severe theophylline intoxication, Drs Parr and Willatts (Anaesthesia 1991; 4 6 557-9) draw attention to important aspects of the management of such cases. Nevertheless, questions should be raised about this particular case which are not discussed by the authors. It was evident within a short time of initial presentation that the patient had ingested a substantial overdose of a drug well known to cause life-threatening complications [l, 21. Despite this, the patient was transferred from the Accident and Emergency Department to the Coronary Care Unit (CCU) and only gained admission to the Intensive Therapy Unit (ITU) several hours later after suffering a cardiorespiratory arrest. The convulsions and cardiac arrhythmias which preceded the final transfer were probably predictable, given the magnitude of the overdose and the dangerously high theophylline level. Cardiorespiratory collapse may have been avoided, and its complications prevented, if the patient had been admitted directly to the ITU. After admission to ITU, the treatment received by the patient appears to have been thorough and appropriate; however, there are indications that the management in the CCU was illogical and may have contributed to the patient’s deterioration. For instance, supplementary oxygen therapy was apparently not given and, consequently, the initial blood gas analysis showed significant hypoxaemia. Potassium was administered in an inadequate dosage considering the admission serum potassium concentration of 2.4 mmol.l-’. Furthermore, following unsuccessful therapy with a single small dose of amiodarone, disopyramide was used. Theophylline acts by inhibiting phosphodiesterases and therefore increases cyclic A M P levels [3], the arrhythmias and hypotension seen in theophylline overdose are attributable to this effect. Treatment of theophyllineinduced arrhythmias is probably best undertaken using a beta-adrenoceptor antagonist such as propanolol [4, 51 which prevents the conversion of ATP to cyclic AMP, rather than a drug such as disopyramide which has strong anticholinergic effects and is probably inappropriate in circumstances of increased adrenergic activity. Given this mode of action, the rapid development of ventricular fibrillation following the administration of disopyramide might have been predicted. This sequence of events raises the question of whether the CCU is ever an appropriate place to monitor and manage patients who have taken potentially dangerous overdoses. Although survival has been reported after higher blood theophylline levels [6, 71 recovery could not be guaranteed in the case described. However, it is essential that prompt recognition and treatment of a deteriorating clinical state occurs if the chances of survival are to be enhanced. This requires continuous monitoring and prompt intervention by an immediately available and suitably experienced doctor at all times. For this reason, patients who are
known to be significantly intoxicated with potentially dangerous drugs should be directly admitted to the ITU for observation. This case history highlights the need for improved training of junior medical staff and greater consultant involvement in the acute specialities. Queen Alexandra Hospital, Porsmouth PO6 3 L Y
B.L. TAYLOR G.B. SMITH P.J. MCQUILLAN
References [I] PALOUCEK FP, RODVOLDKA. Evoluation of theophylline overdoses’ and toxicities. Annals of Emergency Medicine 1988; 17: 13544. [2] KELLYWJW, PARKIN WG. Charcoal hemoperfusion treatment of severe theophylline toxicity. Ausfralian and New Zealand Journal of Medicine 1985; 15: 75-77. [3] TORPHYTJ, UNDEMBJ. Phosphodiesterase inhibitors: new opportunities for the treatment of asthma. Thorax 1991; 46: 5 12-23. [4] AMIN DJ, HENRY JA. Propanolol administration in theophylline overdose. Lancer 1985; 1: 520-1. [5] KEARNEYTE, MANOGUERRAAS, CURTIS GP e t a l . Theophylline toxicity and the beta-adrenergic system. Annals of Infernal Medicine 1985; 102 7669. [6] DEANLS, BROWN JW. Massive theophylline overdose. Survival without hemoperfusion. Journal of American Medical Association 1982; 248: 1742. JJ. Survival after massive aminophylline [7] WELLSDH, FERLAUTO overdose in a premature infant. Paediafrics 1979; 64:252-3.
A reply Thank you for the opportunity to comment o n the letter from Drs Taylor, Smith and McQuillan which discusses our case report on fatal theophylline intoxication. We agree whole-heartedly with their views. The most important consideration, however, is how can such a sequence of events be avoided in the future? Training in intensive therapy should be available to all medical students and doctors training in acute medical specialties. The purpose of this is to enable them to recognise acute illness or deterioration in their patient’s condition at a time when rapid admission or transfer to an Intensive Therapy Unit can benefit the patient. It is with great pleasure that we can confirm the initiative of the Royal Colleges of Anaesthetists, Physicians and Surgeons which outlines a common core of training in intensive therapy suitable for trainees from all specialties. In due course this will overcome such problems as misplaced admission to a Coronary Care Unit, as in this case, and will result in better patient care. Intensive Therapy Unit, Bristol Royal Infirmary, Bristol BS2 8H W
S.M. WILLATTS M.J.A. PARR
