497
Unreeognised chloralose poisoning Dear Sir, Self-poisoning with aipha-chloralose could be overlooked for a long time if myoclonic jerks or generalized convulsions occur without known psychiatric disorder. A 50-year-old man was admitted to our intensive care unit because of widespread clonic contractions. He had a history of alcoholism. He had been hospitalized ten times for two years because of partial myoclonic fits or myoclonic status epilepticus. During the first hospitalization, no toxic or metabolic abnormality was found (but testing for chloralose was not requested). Lumbar puncture, cerebral CT scan and cerebral magnetic resonance imaging were normal. Between attacks, the patient was prescribed various antiepileptic drugs without any effect on seizure recurrence. At each hospitalization, antiepileptic drug blood level was good. On the last admission to hospital, the patient was unconscious. There was no neurologic deficiency. Widespread clonic contractions occurred, increased by stimuli such as touch or noise. The patient was intubated and he received clonazepam and phenytoin without any effect. EEG showed slowed down basic activity and slow abnormalities with delta rhythm of monomorphic appearance at one cycle/second in frontal derivations. At that point, poisoning with alpha-chloralose was suspected and was proved by positive gastric and urine samples (FujiwaraRoss colorimetric reaction). The patient was sedated with diazepam. Gastric lavage was performed. The clinical course was good with disappearance of myoclonic jerks and complete awakening ten hours after admission. Questioning of his wife and a psychiatric examination revealed a paranoid personality with depressive state and suicidal tendancies. An empty bag of Canadian Rat Poison was found at home. A CSF sample from the first hospitalization was then tested for chloralose and was found to be positive. The diagnosis of alpha-chloralose self-poisoning was quite certain, although the patient denied the intoxication. Alpha-chloraiose was first used as a hypnotic, but its clinical use was stopped because of its side-effects. It is on sale as a rodenticide in France. In the context of self-poisoning, the diagnosis is usually easy. Myoclonic jerks, which can be spontaneous or the result of minimal stimuli, and hypersecretion of saliva, are typical [1-3]. Convulsions also can occur. The EEG shows slowed down basic activity and high amplitude delta rhythm at 2 - 3 cycles/s, predominantly in frontal derivations, mixed with bursts of spikes [4, 5]. Gastric and urine samples can be tested using the Fujiwara reaction, proving the intoxication [1], even it is not a specific reaction. The treatment involves gastric lavage, use of diazepam for myoclonic jerks and convulsions, mechanical ventilation and other support of vital functions in comatose patients. The case we describe is typical, but the diagnosis was late. It is important to suspect this poisoning when confronted by non-explained epilepsy, or partial myoclonic status unresponsive to treatment. This persistant misdiagnosis could have jeopardized the outcome with lifethreatening complications, especially as the patient had to be intubated and ventilated. All antiepileptic drugs, used alone or in association, also have some side-effects. It is necessary to seek psychiatric disturbance which may not have been known before, the self-poisoning revealing a psychiatric disorder. Yours faithfully, V. Dardaine, A. Legras, R. Lanotte, N. Brasset and Y. Furet
References 1. Tempe JD, Kurtz D (1972) Intoxication aigi~e par le chloralose. CM 94:801-813 2. Thomas HM, Simpson D, Prescott LF (1988) The toxic effects of alpha-chioralose. Hum Toxicol 7:285-287 3. Richelme C, Duval G, Gerard J, Corbin JC, Chuet C (1985) Intoxication volontaire par le chloralose. Cah d'Anesth 33:589-592
4. Boudouresque J, Roger J, Naquet R, Bille J, Guin P, Vigouroux R, Gosset A (1966) Intoxication aig0e par le chloralose. Etat de mal myoclonique. Evolution 61ectroenc6phalographique. Rev Neurol 114:312-317 5. Kurtz D, Tempe JD, Weber JM, Feuerstein I, Reeb M, Mantz JM (1967) Aspects 61ectrocliniques de l'intoxication aigOe au chloralose. Rev Neurol 117:498- 506 Dr. V. Dardaine, Service de R6animation M6dicale, CHU Bretonneau, F-37044 Tours, France
Concerning the definition of ARDS Dear Sir, I wish to point out that the expanded definition of ARDS [1] which allows a broad definition covering all conditions that might cause "low pressure permeability oedema" (Murray et al. [1] pt3 of Table 3) leads to confusion when patients are being treated in the ICU. It seems that some people are confusing pneumonia or gastric aspiration with ARDS [2], when in fact careful appraisal of each situation will usually enable the correct diagnosis to be made. This situation is serious when it comes to obtaining valid statistical analyses of possible therapies for ARDS. One cannot pretend that any treatment for gastric aspiration could be similar to that for septic ARDS. Those who work in experimental pathology know well that ARDS is reproduced exactly by an intravenous injection or infusion of endotoxin [3, 4]. At least three recent papers have described endotoxinaemia in patients developing ARDS as a result of trauma and/or sepsis [5 -7]. Thus I would define ARDS as low pressure permeability oedema of the lungs in the context of shock, sepsis, major trauma, burns or pancreatitis that is accompanied by a positive chromogenic substrate Limulus assay for endotoxin. I think this definition is expedient because ways of combating endotoxaemia are now to hand, and those who are interested in preventing ARDS should look to their application. Yours faithfully, E. Nigel Wardle
References 1. Murray JF, Matthay MA, Luce JM, Flick MR (1988) An expanded definition of the ARDS Am Rev Respir Dis 138:720-723 2. Te OH (1992) Defining adult respiratory distress syndrome. Br J Hosp Med 47:350-353 3. Wardie EN (1984) Shock lungs; the post-traumatic respiratory distress syndrome. Q J Med 53:317-329 4. Brigham KL, Meyrick B (1986) Endotoxin and lung injury. Am Rev Respir Dis 133:913-927 5. Parsons PE,'Worthen GS, Moore EE et al (1989) The association of circulating endotoxin with the development of ARDS. Am Rev Respir Dis 140:294-301 6. Vijaykumar E, Raziuddin S, Wardie EN (1991) Plasma endotoxin in patients with trauma, sepsis or severe haemorrhage. Clin Intensive Care 2 : 4 - 9 7. Danner RL, Elin R J, Hosseini JM, Wesley RA, Reilly JM, Parillo JE (1991) Endotoxemia in human septic shock. Chest 99:169-175 D.E.N. Wardle. MD, 21 Common Road, North Leigh, Nr Oxford OX8 6RD, UK
Unreeognised chloralose poisoning Dear Sir, Self-poisoning with aipha-chloralose could be overlooked for a long time if myoclonic jerks or generalized convulsions occur without known psychiatric disorder. A 50-year-old man was admitted to our intensive care unit because of widespread clonic contractions. He had a history of alcoholism. He had been hospitalized ten times for two years because of partial myoclonic fits or myoclonic status epilepticus. During the first hospitalization, no toxic or metabolic abnormality was found (but testing for chloralose was not requested). Lumbar puncture, cerebral CT scan and cerebral magnetic resonance imaging were normal. Between attacks, the patient was prescribed various antiepileptic drugs without any effect on seizure recurrence. At each hospitalization, antiepileptic drug blood level was good. On the last admission to hospital, the patient was unconscious. There was no neurologic deficiency. Widespread clonic contractions occurred, increased by stimuli such as touch or noise. The patient was intubated and he received clonazepam and phenytoin without any effect. EEG showed slowed down basic activity and slow abnormalities with delta rhythm of monomorphic appearance at one cycle/second in frontal derivations. At that point, poisoning with alpha-chloralose was suspected and was proved by positive gastric and urine samples (FujiwaraRoss colorimetric reaction). The patient was sedated with diazepam. Gastric lavage was performed. The clinical course was good with disappearance of myoclonic jerks and complete awakening ten hours after admission. Questioning of his wife and a psychiatric examination revealed a paranoid personality with depressive state and suicidal tendancies. An empty bag of Canadian Rat Poison was found at home. A CSF sample from the first hospitalization was then tested for chloralose and was found to be positive. The diagnosis of alpha-chloralose self-poisoning was quite certain, although the patient denied the intoxication. Alpha-chloraiose was first used as a hypnotic, but its clinical use was stopped because of its side-effects. It is on sale as a rodenticide in France. In the context of self-poisoning, the diagnosis is usually easy. Myoclonic jerks, which can be spontaneous or the result of minimal stimuli, and hypersecretion of saliva, are typical [1-3]. Convulsions also can occur. The EEG shows slowed down basic activity and high amplitude delta rhythm at 2 - 3 cycles/s, predominantly in frontal derivations, mixed with bursts of spikes [4, 5]. Gastric and urine samples can be tested using the Fujiwara reaction, proving the intoxication [1], even it is not a specific reaction. The treatment involves gastric lavage, use of diazepam for myoclonic jerks and convulsions, mechanical ventilation and other support of vital functions in comatose patients. The case we describe is typical, but the diagnosis was late. It is important to suspect this poisoning when confronted by non-explained epilepsy, or partial myoclonic status unresponsive to treatment. This persistant misdiagnosis could have jeopardized the outcome with lifethreatening complications, especially as the patient had to be intubated and ventilated. All antiepileptic drugs, used alone or in association, also have some side-effects. It is necessary to seek psychiatric disturbance which may not have been known before, the self-poisoning revealing a psychiatric disorder. Yours faithfully, V. Dardaine, A. Legras, R. Lanotte, N. Brasset and Y. Furet
References 1. Tempe JD, Kurtz D (1972) Intoxication aigi~e par le chloralose. CM 94:801-813 2. Thomas HM, Simpson D, Prescott LF (1988) The toxic effects of alpha-chioralose. Hum Toxicol 7:285-287 3. Richelme C, Duval G, Gerard J, Corbin JC, Chuet C (1985) Intoxication volontaire par le chloralose. Cah d'Anesth 33:589-592
4. Boudouresque J, Roger J, Naquet R, Bille J, Guin P, Vigouroux R, Gosset A (1966) Intoxication aig0e par le chloralose. Etat de mal myoclonique. Evolution 61ectroenc6phalographique. Rev Neurol 114:312-317 5. Kurtz D, Tempe JD, Weber JM, Feuerstein I, Reeb M, Mantz JM (1967) Aspects 61ectrocliniques de l'intoxication aigOe au chloralose. Rev Neurol 117:498- 506 Dr. V. Dardaine, Service de R6animation M6dicale, CHU Bretonneau, F-37044 Tours, France
Concerning the definition of ARDS Dear Sir, I wish to point out that the expanded definition of ARDS [1] which allows a broad definition covering all conditions that might cause "low pressure permeability oedema" (Murray et al. [1] pt3 of Table 3) leads to confusion when patients are being treated in the ICU. It seems that some people are confusing pneumonia or gastric aspiration with ARDS [2], when in fact careful appraisal of each situation will usually enable the correct diagnosis to be made. This situation is serious when it comes to obtaining valid statistical analyses of possible therapies for ARDS. One cannot pretend that any treatment for gastric aspiration could be similar to that for septic ARDS. Those who work in experimental pathology know well that ARDS is reproduced exactly by an intravenous injection or infusion of endotoxin [3, 4]. At least three recent papers have described endotoxinaemia in patients developing ARDS as a result of trauma and/or sepsis [5 -7]. Thus I would define ARDS as low pressure permeability oedema of the lungs in the context of shock, sepsis, major trauma, burns or pancreatitis that is accompanied by a positive chromogenic substrate Limulus assay for endotoxin. I think this definition is expedient because ways of combating endotoxaemia are now to hand, and those who are interested in preventing ARDS should look to their application. Yours faithfully, E. Nigel Wardle
References 1. Murray JF, Matthay MA, Luce JM, Flick MR (1988) An expanded definition of the ARDS Am Rev Respir Dis 138:720-723 2. Te OH (1992) Defining adult respiratory distress syndrome. Br J Hosp Med 47:350-353 3. Wardie EN (1984) Shock lungs; the post-traumatic respiratory distress syndrome. Q J Med 53:317-329 4. Brigham KL, Meyrick B (1986) Endotoxin and lung injury. Am Rev Respir Dis 133:913-927 5. Parsons PE,'Worthen GS, Moore EE et al (1989) The association of circulating endotoxin with the development of ARDS. Am Rev Respir Dis 140:294-301 6. Vijaykumar E, Raziuddin S, Wardie EN (1991) Plasma endotoxin in patients with trauma, sepsis or severe haemorrhage. Clin Intensive Care 2 : 4 - 9 7. Danner RL, Elin R J, Hosseini JM, Wesley RA, Reilly JM, Parillo JE (1991) Endotoxemia in human septic shock. Chest 99:169-175 D.E.N. Wardle. MD, 21 Common Road, North Leigh, Nr Oxford OX8 6RD, UK
