Hepatorenal problems presented in an urban high dependancy unit in a user of ecstasy and cocaine

Hepatorenal problems presented in an urban high dependancy unit in a user of ecstasy and cocaine

Medicine Hepatorenal problems presented in an urban high dependancy unit in a user of ecstasy and cocaine C. Jones, K. Little A case is presented of ...

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Medicine

Hepatorenal problems presented in an urban high dependancy unit in a user of ecstasy and cocaine C. Jones, K. Little A case is presented of a young man aged 25 years who had an episode of jaundice and renal failure after using a small amount of ecstasy and cocaine. There is a discussion of the issues raised by the case as well as some points of interest for research and health education. © 2000 Harcourt Publishers Ltd

Introduction

Chris Jones MSc, BA, RGN, RNT, ENB 100, Accident and Emergency Department, Kerry Little RGN, Dip HE, ENB 125, Accident and Emergency Department, Aintree Complex, Aintree Hospital, Longmoor Lane, Liverpool, UK. Correspondence to CJ. Manuscript accepted: 16 October 1999

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In June 1999 a 25-year-old man was brought by ambulance to an accident and emergency (A&E) unit in Liverpool. He had a 3 day history of abdominal pain, nausea and vomiting and had an increasingly jaundiced aspect. He had initially attempted to manage his own symptoms with paracetomol, but denied over use. His general practitioner (GP) had been called to see him before the jaundice had become evident and had prescribed Losec for his gastro intestinal symptoms. On admission, he was he was considered ill enough to be taken to the high dependency unit (HDU) where a central line was inserted and therapy started. Initial blood results revealed an alarming degree of liver dysfunction, but he admitted to only 20 units of alcohol per week. He also denied any recent foreign travel, any homosexual activity or any blood transfusion. On the other hand he volunteered to having taken one and a half tablets of ecstasy the night before he became ill. Further investigation revealed that the type of tablet he had taken was a ‘Mitsubishi’. This bears the characteristic mark of the Japanese manufacturing company. These are said to be commonly available in Liverpool and across the UK. He also volunteered that he had taken 1 g of cocaine. When asked about the effect of the tablet he was convinced

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that it had ‘worked’, revealing that he was not ecstasy naïve and that the tablet contained an amount of Methylenedioxymethamphetamine (MDMA) or its analogue Methylenedioxyethylamphetamine (MDEA).

The nature of ecstasy Although many substances are sold as ecstasy, purchasers are usually intending to buy MDMA. This is an amphetamine-like compound that gives users a sense of empathy with fellow users. It is frequently referred to as an empathogen. Its use is most commonly associated with the ‘rave scene’ and its use has seen an enormous increase in the last decade with around 500 000 people said to be using it per weekend. There have been numerous well-publicized cases of ecstasy-related fatalities, and one celebrated case of liver failure which led to protracted litigation (Dyer 1997). The course of these fatalities has been described elsewhere (Wake 1995; Chadwick et al. 1991) but by and large they include a process involving hyperpyrexia, collapse, disseminated intravascular coagulation (DIC) and hepatorenal problems. Theories for these relatively uncommon collapses have included idiosyncratic response, tablet adulteration and heat stroke. It seems to be the heat stroke theory that has gained

© 2000 Harcourt Publishers Ltd

Hepatorenal problems presented in an urban HDU

Day

1

2

2

2

2

3

Time

23:50

04:00

08:15

20:00

24:00

12:00

WBC

14.2

14.6

13.0

10.3

8.5

HB

14.8

15.2

15.6

15.3

15.1

PLATES

259

243

259

202

211

INR

3.3

3.2

3.0

2.3

2.2

2.1

APPT

1.3

1.2

1.1

1.0

1.1

1.1

NA

133

132

134

138

135

134

K

4.3

3.6

2.9

2.9

3.0

3.3

UREA

9.4

9.6

8.9

7.6

7.2

5.7

CREAT

247

205

168

141

124

110

GLUC

9.5

13.5

8.3

6.5

7.6

13

AST

3434

CK BILIRU-BIN AT Fig. 1

140 16 664

130

10 770

Serial blood results.

the most ground (Henry 1992). This postulates that the ‘raver’ overheats in a night club or party because of dancing, high ambient heat and humidity and the direct disruption of thermoregulation caused by the drug. Indeed, in most studies, the victim is admitted directly from a nightclub or party. The effect of heat production being enhanced while heat dispersal is compromised is to cause a rise in core temperature. Temperatures have gone as high as 44°C in some people. Traditionally, the aim of treatment has been seen as the control of core temperature as a way of heading off other serious metabolic problems. In the case of the young man under discussion, however, this line of logic is less easy to follow. On talking with him, it became clear that he was not admitted from a nightclub or party. He took his tablet in a pub where it was relatively quiet

© 2000 Harcourt Publishers Ltd

and cool and then went home. When asked, he said that he had had a good night’s sleep, ‘except, you know, for the Charlie (cocaine CJ)’. This potentially undermines the connection made between heat stroke and liver failure in MDMA toxicity. It points to the possibility of life threatening harm being the result of quiet activity in a calm atmosphere. Indeed, other cases of slow onset liver problems have been described elsewhere

Possible other causes of MDMA-induced liver problems not associated with heat stroke Liver problems have been associated with many of the cases of ecstasy poisoning (Henry et al. 1992; McCarthy & Wilkinson 1999), and have

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Hepatorenal problems presented in an urban HDU

been said to mimic episodes of hepatitis (Dykhuizen et al. 1995). It could be that there is a contaminant in the Mitsubishi brand that has caused the liver failure. The victim himself expressed the opinion that the quality of the tablet may have been compromised by its low price (£5 sterling) and that it may contain other substances. A recent analysis of captured tablets revealed the range of substances sold as ecstasy (Sherlock et al. 1999). Where the tablet contained MDMA, the range of dosage was quite remarkable, ranging from negligible amounts to 140 mg. This dose range is, in itself, problematic in that it could easily lead to inadvertent overdose. Even purchasing the same brand of tablet might produce varying dosages. Where the tablet contains no MDMA there is a bewildering variety of substances including amphetamine, caffeine, ephedrine and ketamine. Notably there is also paracetomol. In the present case, however, it is hard to imagine that the young man was overdosed. Assuming that he was truthful about his intake it is hard to imagine that 1.5 tablets would have overdosed him. Another possible explanation for his jaundice has nothing to do with his MDMA use. Perhaps the drug that damaged his liver was the cocaine rather than the MDMA.

Hepatotoxicity of cocaine Cocaine has the propensity to damage liver function without any connection to environmental factors. The method by which cocaine achieves this effect has been the subject of some debate. Theories include: 1. Directly hepatotoxic metabolites of cocaine 2. Cocaine-induced production of oxygen free radicals. In one study of four patients with cocaineinduced liver failure, damage was said to be ‘identical with acetominophen (paracetomol CJ) toxicity’ (Wanless et al. 1990). Although he may have taken 1 g of something, it is less clear that this was going to be entirely cocaine. Cocaine can be adulterated with other substances much easier than can tablets. One final possibility is that the interaction between low dose cocaine and (relatively) low dose MDMA is to produce serious liver damage.

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Perhaps there is a synergistic effect between MDMA and cocaine and this produced a near fatal outcome.

Course and outcome The patient’s condition improved over the following 3 days with conservative management. He was discharged from the HDU after 3 days. Liver function tests continued to improve and he appeared to make a full recovery.

Discussion This case might suggest that the heat stroke theory of MDMA-related harm may need some revision; it is a rare situation where the victim is admitted from a quiet environment. His case might suggest that there is another route to hepatotoxicity other than via heat stroke. This type of conclusion is supported by other, rarer cases of jaundice and underlines the conclusions of the National Poisons Information Service (NPIS) that unexplainable and acute jaundice in fit young people ought to have MDMA poisoning as part of the differential diagnosis (Henry et al. 1992). Implications for practice for nursing staff might include advice that MDMA carries risks which are present whether or not the user is at a nightclub. Where people have already been poisoned, an open and friendly attitude should be taken – the better to elicit the following information: • What were the circumstances in which the drugs were taken? • Was it hot, humid? • Did the victim dance a lot/at all? • What was the brand of the tablet? • Did it have a logo on the front? What was it called? • Did the tablet ‘work’ normally? • Did it have any unusual effects? This information is not frequently asked for, possibly because staff think that ecstasy is ecstasy. However, one brand might quickly be recognized as causing more problems than another. The A&E nurse who can gather this type of information is in a unique position to warn about a developing health problem.

© 2000 Harcourt Publishers Ltd

Hepatorenal problems presented in an urban HDU

References Chadwick IS, Curry PD, Linsley A, Freemont AJ, Doran B 1991 Ecstasy, 3,4, Methylenedioxymethamphetamine (MDMA) a fatality associated with coagulopathy and hyperthermia. Journal of the Royal Society of Medicine 84(6): 371 Dyer C 1997 Doctors accused of refusing transplant on moral grounds. BMJ 134: 1365 Dykhuizen RS, Brunt PW, Atkinson P, Simpson JG, Smith CC 1995 Ecstasy induced hepatitis mimicking viral hepatitis. Gut 36: 939–941 Henry J 1992 Ecstasy and the dance of death. BMJ 305: 4–5 Henry J, Jeffreys KJ, Dawling S 1992 Toxicity and deaths from 3,4, methylenedioxymethamphetamine. The Lancet 340: 384–387

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McCarthy M, Wilkinson ML 1999 Recent advances in hepatology. BMJ 318: 1256–1259 Sherlock K, Wolff K, Hay AWM, Conner M 1999 Analysis of illicit ecstasy tablets: implications for clinical management in the accident and emergency department. Journal of Accident and Emergency Medicine 16: 194–197 Wake D 1995 Ecstasy overdose: a case study. Intensive and Critical Care Nursing 11(1): 6–9 Wanless IR, Dore S, Gopinath N et al. 1990 Histopathology of cocaine hepatoxicity. Report of four patients. Gastroenterology 98: 497–501

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