132

Sedick Isaacs PhD, MBCS

Department of Medical Informatics

Groote Schuur Hospital

South Africa

Alicia Evans DMLT (Chem Path)

Department of Pharmacology University of Cape Town and Groote Schuur Hospital

South Africa

Correspondence

been described in the literature; myocardial injury with elevated troponin I secondary to amphetamine abuse has not been described [1-5]. We report the case of a young man who presented to our ED with a chief complaint of abdominal pain and general malaise. The patient was found to have an anterolateral ST-elevation myocardial infarction and a TnI of 362, with a urinalysis positive for amphetamines.

A 23-year-old man was brought to our ED with abdominal pain and general malaise for the last 12 hours. The patient denied any chest pain or shortness of breath

doi:10.1016/j.ajem.2005.08.004

References

1. Rosenberg J, Benowitz L, Pound SM. Pharmacokinetics of drug overdose. Clin Pharmacokinet 1981;6:161 - 92.
2. Adams BK, Mann MD, Aboo A, Isaacs S, Evans A. Prolonged gastric emptying half-time and gastric hypomotility after drug overdose. Am J Emerg Med 2004;22:548 - 54.
3. Bond GR. The role of activated charcoal and gastric emptying in gastrointestinal decontamination. Ann Emerg Med 2002;39: 273 - 86.
4. American Academy of Clinical Toxicology and European Association of Poisons Centres and Clinical Toxicologists. Position paper: cathartics. J Toxicol Clin Toxicol 2004;42:343 - 53.
5. Keller RE, Schwab RA, Krenzelhok EP. Contribution of sorbitol combined with activated charcoal in prevention of salicylate absorption. Ann Emerg Med 1990;19:654 - 6.
6. Goldberg MJ, Spector R, Park GD, Johnson GF, Roberts P. The effect of sorbitol and activated charcoal on serum theophylline concen- trations after slow-release theophylline. Clin Pharmacol Ther 1987; 41:108 - 11.
7. McNamara RM, Aaron CK, Gemborys M, Davidheiser S. Sorbitol catharsis does not enhance the efficacy of charcoal in a simulated acetaminophen overdose. Ann Emerg Med 1988;17:243 - 6.
8. Neuvonen PJ, Olkkola KT. Effect of purgatives on antidotal efficacy of oral activated charcoal. Hum Toxicol 1986;5:255 - 63.
9. Nakamura T, Oida Y, Matsumoto K, Kawasaki N, Tanada S. Inhibitory effect of sorbitol on acetaminophen adsorption by activated carbon. Environ Sci Health A Tox Subst Environ Eng 2002;37:905 - 12.
10. Farley TA. Severe hypernatremic dehydration after use of activated charcoal-sorbitol suspension. J Pediatr 1986;109:719 - 22.
11. Hirtz J. The gastrointestinal absorption of drugs in man: a review of current concepts and methods of investigation. Br J Clin Pharmacol 1985;19(Suppl 2):77S- 83S

Methamphetamine-induced myocardial infarction with elevated troponin I^B

Acute myocardial infarction (AMI) has been a reported complication of methamphetamine/amphetamine abuse. Acute myocardial infarction with associated increased creatine kinase (CK) and MB fractions has

^B No funding, sponsorship, or support was provided for this article.

on ED presentation. He described his abdominal pain as midepigastric and involving both upper quadrants radiat- ing into his chest. On further questioning, he was having difficulty taking full breaths because of pain in his chest. At presentation, blood pressure was 77/40 mm Hg, heart rate was 41 beats per minute, respirations were 20 respira- tions per minute, and temperature was 35.48C with an oxygen saturation of 100% on room air. Past medical history was insignificant. He denied drug, alcohol, or Tobacco use. Cardiovascular examination was significant for bradycardia. His lungs were clear, and his Abdominal examination was benign. An electrocardiogram (ECG) (Fig. 1) showed ST elevation in the precordial leads V₁ through V₄, a complete heart block, and an underlying junctional rhythm. Cardiac markers were significant for a TnI of 362.1 ng/mL. Cardiology took the patient to the catheterization laboratory, followed by admission to the intensive care unit. A urine drug screen was positive for amphetamines. The patient later admitted to methamphetamine inhalation less than

24 hours before presentation.

Catheterization of the left side of the heart revealed Normal coronary arteries and severe systolic left ventricular dysfunction with an ejection fraction of 15% to 20%. A transesophageal echocardiogram showed generalized left ventricular asynergy. The patient required placement of a dual-chambered pacemaker. A follow-up echocardiogram performed 7 days later demonstrated an ejection fraction of 35% to 40%. A corresponding ECG (Fig. 2) shows resolution of ST elevations. The patient was discharged 9 days after admission.

Amphetamines are increasingly abused in regions such as the western United States and Europe [1,2]. Synthetic amphetamine compounds are commonly produced in clandestine laboratories varying in purity and potency. Routes of amphetamine administration may be oral, inhalation, or injection (IV). Oral use has an approximate 1-hour delay before onset of symptoms, whereas inhaled and IV methods yield effects within a few minutes. Peak plasma concentrations occur in 5 minutes with IV use and 2 to 3 hours postingestion. Metabolism is highly variable, and up to 30% of the parent compound can be excreted unchanged in the urine. Plasma half-life varies from 5 to 30 hours depending on urine flow and pH.

Several Cardiovascular complications have been associat- ed to amphetamines [4-8]. The most common short-term

Correspondence 133

Fig. 1 ST elevation in the precordial leads V₁ through V₄, a Complete heart block, and an underlying junctional rhythm.

effects are tachycardia and hypertension. In addition, vascular spasm, myocardial infarction, cor pulmonale, cardiac dysrhythmias, cardiomyopathy, myocarditis, and necrotizing vasculitis have also been reported [6,7]. Although hypertension is common in methamphetamine abuse, severe hypotension related to paradoxical central sympathetic depression and ventricular impairment can occur.

On cardiac catheterization, the coronary arteries of our patient were free of obstructive lesions. Therefore, we conclude that the Myocardial insult he had was likely the result of coronary artery vasospasm [9]. This is based on ECG changes indicative of acute myocardial injury and results from his cardiac catheterization. A study by Turnipseed and colleagues [1] found 33 people who presented to their ED with chest pain and methamphet- amine abuse; an acute coronary syndrome (ACS) was

diagnosed in 25%. One criterion they used to define ACS was an elevation of CK-MB greater than twice normal. cardiac troponins were not used to define ACS in their study; and our literature search failed to find documenta- tion of elevated troponins associated with amphetamine- induced ACS.

Troponins are regulatory proteins found in skeletal and cardiac muscle. Studies on release kinetics of cardiac troponins indicate that they are early markers of Myocardial necrosis. They appear in serum within 4 to 8 hours after symptom onset. The cardiac isoform of TnI is not found in skeletal muscle and therefore is associated only with myocardial necrosis. This explains the cardiospecificity of TnI. Troponin I has a higher specificity for myocardial necrosis than CK-MB in selected subsets of patients, such as those presenting late in the course of AMI, those with

Fig. 2 Resolution of ST elevations.

134 Correspondence

skeletal muscle disease, and therefore potentially those with skeletal Muscle breakdown from the hyperactivity of amphetamine abuse [2]. Current recommendations of the National Academy of Clinical Biochemistry call for replacement of the CK-MB standard with cardiac troponin as the diagnostic biochemical marker of choice for myocardial injury.

Our patient had no known cardiac risk factors besides his use of methamphetamine; and his coronary arteries were normal based on cardiac catheterization. His myocardial infarction diagnosed with ECG findings and a significantly elevated TnI occurred within hours after admitted metham- phetamine use by inhalation. This represents a strong association between methamphetamine use and secondary coronary artery vasospasm-induced AMI that is unlikely to be coincidental.

David J. Watts MD Emergency Medicine/Medical Toxicology St Luke’s Hospital Bethlehem

PA 18015, USA

E-mail address: [email protected]

Laughlin McCollester MD

Emergency Medicine, Mariciopa Medical Center

Phoenix, AZ, USA

doi:10.1016/j.ajem.2005.08.005

References

1. Turnipseed SD, Richards JR, Kirk JD. Frequency of acute coronary syndrome in patients presenting to the emergency department with chest pain after methamphetamine use. J Emerg Med 200324(4): 369 - 73.
2. Richards JR, Johnson EB, Stark RW, Derlet RW. Methamphetamine abuse and rhabdomyolysis in the ED: a 5-year study. Am J Emerg Med 1999;17(7):681 - 5.
3. He SY, Matoba R, Fujitani N et al. Cardiac muscle lesions associated with chronic administration of methamphetamine in rats. Am J Forensic Med Pathol 1996;17(2):155 - 62.
4. Davis GG, Swalwell CI. Acute aortic dissections and ruptured berry aneurysms associated with methamphetamine abuse. J Forensic Sci 1994;39(6):1481 - 5.
5. Wijetunga M, Seto T, Lindsay J, Schatz I. Crystal methamphetamine- associated cardiomyopathy: tip of the iceberg? J Toxicol 2003;41(7): 981 - 6.
6. Bashour TT. Acute myocardial infarction resulting from amphetamine abuse: a spasm-thrombus interplay? Am Heart J 1994;128(6 Pt 1): 1237 - 9.
7. Waksman J, Taylor RN, Bodor GS. Acute myocardial infarction associated with amphetamine use. Mayo Clin Proc 2001;76:323 - 6.
8. Carson C, Oldroyd K, Phadke K. Myocardial infarction due to am- phetamine. BMJ 1987;294.
9. Manini AF. Acute myocardial infarction after over-the-counter use of pseudoephedrine. Ann Emerg Med 2005;45(2):213 - 6.

nonsurgical management of symptomatic posttraumatic thoracic epidural hematoma

To the Editor,

Posttraumatic Spinal epidural hematomas (SEHs) occur infrequently in neurosurgical practice. They present as an acute Spinal cord compression, and usually, emergent surgical treatment is recommended for most patients to decompress the Spinal canal [1]. We report the case of a healthy 22-year-old man who developed a symptomatic thoracic epidural hematoma after a severe Thoracic trauma. He was treated with nonsurgical management, and the hematoma resolved spontaneously. The patient remained asymptomatic over a year of follow-up.

A healthy, previously asymptomatic 22-year-old man was admitted to the Emergency Department after a traffic accident. There was no loss of consciousness at the scene, and on arrival, the patient had a Glasgow coma score of 15. Initial physical examination revealed a severe chest trauma with multiple rib fractures and dorsal back pain. Neurologic examination did not identify any focal signs. He was admitted to our Trauma Intensive Care Unit (ICU). On arrival at the ICU, he was taken for helicoidal computed tomography of the neck (normal) and thorax that confirmed the presence of the rib fractures and showed a bilateral lung contusion and T8 vertebral compression fracture with minimal invasion of the spinal canal (less than 10%).

Eight hours after the trauma, he developed neurologic symptoms of posterior cord compression which consisted in paraesthesiae in the lower limbs, with 5 strength (of a possible 5) in both lower extremities and symmetrical, normal reflexes. Neurosurgery was immediately consulted and emergent magnetic resonance imaging (MRI) of the spine was scheduled. The MRI revealed a posterior SEH (Fig. 1). Methylprednisolone 30 mg/kg was administered intrave-

Fig. 1 Sagittal and axial T2 fast spin echocardiography of T spine show a predominantly hypointense posterior intrarachidial- extradural collection that contacts with the spinal cord, and a wedged fracture of the T8 vertebral body.