Article, Cardiology

MDMA-induced acute pulmonary edema in a patient without other organ dysfunction

anti-U1RNP antibody, anti-double-stranded DNA antibody, SSA and SSB antibody, anti-SCL 70 antibody, anti-centromere antibody, anti-smith antibody, and Factor V Leiden protein were all negative. In conclusion, the patient’s only known risk factor for SCAD was an elevated homocysteine level.

Elevated fasting homocysteine levels have been associ- ated with both spontaneous cervical artery dissection [6] as well as with coronary artery dissection [7]. The proposed mechanism by which homocysteine leads to Endothelial damage lies in its ability to spontaneously (eg, nonenzymati-

doi:10.1016/j.ajem.2006.01.021

References

Gurjaipal Kang MD Department of Cardiology Hamot Medical Center Erie, PA 16550, USA

cally) react with a host of proteins, growth factors, and endothelial vasoactives [8]. Homocysteine can disrupt critical disulfide bridges in fibrillin and other connective tissue molecules, impeding the formation of microfibrils [8]. Homocysteine can also modify the release and activity of nitric oxide [8]. Furthermore, free homocysteine in vitro irreversibly destroys the biologic activity of protein C and has been implicated in the loss of function of proteins involved in anticoagulation (Protein S, antithrombin III, acute pulmonary edema in a “>plasminogen activator, among others) [8]. The result is Premature atherosclerosis and thrombophilia.

Our patient underwent intervention with a drug-eluting stent, and medical therapy with angiotensin-converting enzyme inhibitor, ASA, h-blocker, cyancobalamina folic acid, and pyridoxine. At 1-month follow up, she had an echocardiogram demonstrating an ejection fraction of 55%, with normal wall motion and no other abnormalities. At 8- month follow up, an adenosine stress test was preformed, revealing no EKG changes with exercise and normal myocardial perfusion scan, visually estimated ejection fraction of 65%. The above would suggest hibernating myocardium in the presence of acute coronary syndrome.

In conclusion, SCAD is a rare but life-threatening event, occurring in young patients without Traditional risk factors for coronary artery disease. Hypervigilance in the ED setting, in conjunction with serial monitoring of cardiac biomarkers is therefore the preferred approach for the young patient with significant chest pain.

Acknowledgment

The authors would like to acknowledge Phyllis J. Kuhn, Lake Erie Research Institute, Girard, PA, for helpful review and commentary.

Jessica Shepherd DO Brian Risavi DO

Department of Emergency Medicine

Hamot Medical Center Erie, PA 16550, USA

E-mail address: [email protected]

Matthew Zaccheo DO

Department of Internal Medicine

Hamot Medical Center Erie, PA 16550, USA

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MDMA-induced acute pulmonary edema in a patient without other organ dysfunction

Acute Noncardiogenic pulmonary edema (NCPE) caused by the use of 3,4-methylenedioxymethamphet- amine (MDMA, ecstasy) is a rare entity. MDMA-induced NCPE was noted in 5 previously reported patients [1-5], in whom Multiorgan dysfunction was demonstrated with the development of acute NCPE. Herein we present a patient with MDMA-induced NCPE without other organ failure. The patient recovered quickly and did not have significant sequelae.

A 30-year-old man visited our ED because of acute onset of dyspnea, agitation, palpitation, nausea, and vomiting. According to his statement, he took one ecstasy pill in a dance club 5 hours before his admission. He did not have a history of hypertension, diabetes, heart disease, or chronic lung disease. His family history was unremarkable.

On physical examination, he looked agitated, but no obvious orthopnea was observed. His consciousness was clear and oriented. The body temperature was 378C, with a pulse rate of 124 beats/min, blood pressure of 113/63 mm Hg, and a respiratory rate of 29 breaths/min. The pulse oximetry showed an Arterial oxygen saturation of 84%; the arterial

Fig. 1 The initial chest radiograph of this patient presented to our ED showed increased infiltrations of both lung fields without central distribution and cardiomegaly.

blood gas analysis confirmed hypoxemia and showed pH 7.39, Paco2 43 mm Hg, Pao2 84.4 mm Hg, and bicarbonate

25.7 mEq/L under supplemental oxygen via nonrebreathing face mask. He was diaphoretic, but no distended jugular vein or limb edema was noted. Diffuse crackles and rhonchi were heard over bilateral lungs, but there was no audible cardiac murmur or gallop.

The laboratory data showed blood urea nitrogen of

13.5 mg/dL, creatinine 1.0 mg/dL, sodium 126 mmol/L, potassium 3.3 mmol/L, and serum glutamic transaminase 59 IU/L. The initial creatine kinase level was 641 IU/L, and it peaked 4 hours later to a level of 1053.0 IU/L. The initial CKMB isoform was 51.1 IU/L, and the cardiac troponin I

0.18 ng/mL, and the enzymes did not elevate 4 hours later (CKMB 48 IU/L; troponin I 0.15 ng/mL), indicating the absence of myocardial injury. The 12-lead electrocardio- gram showed sinus tachycardia without significant ST-T change or signs suggesting left ventricular hypertrophy. Other laboratory results were unremarkable. A basic urine drug screen showed positive reaction for MDMA and MDA. Screenings for opiate, cocaine, and ketamine were negative in his Urine sample. The serum MDMA concentration was 245 ng/mL, documented 12 hours after ingestion by gas chromatography-mass spectrometry.

The chest radiography showed bilateral perihilar and peripheral infiltration without cardiomegaly (Fig. 1), com- patible with the classic picture of acute NCPE. He was admitted to the medical ward with supportive care. Empirical antibiotic was given because he developed fever on the second day of hospitalization. There was no need for

diuretics, morphine, or nitroglycerin. The serial followed up chest film showed gradual resolution of the pulmonary edema 4 days later (Fig. 2), and the oxygen demand was titrated to nasal prong. He was discharged 6 days later, and the chest film showed complete resolution of the infiltrates during follow-up at the outpatient clinic 2 weeks later.

During the past 2 decades, the acute toxic effects of MDMA have been widely investigated because there was an emerging trend toward its abuse in occasions such as rave parties [6]. Both observational studies in humans and direct Animal experiments had demonstrated typical acute toxic syndromes, including hyperthermia, hyponatremia, myocardial ischemia, intracerebral hemorrhage, acute he- patic failure, and acute hallucinogenic psychosis [6-9]. Severe adverse effects that may lead to death include extreme hyperthermia, cardiac arrhythmia, rhabdomyolysis, acute renal failure, decompensated Liver failure, and hyponatremia with resultant cerebral edema [9].

Although rarely encountered, acute NCPE happened in certain reported cases following the ingestion of MDMA. There were 5 previously reported patients in whom MDMA- associated acute NCPE was documented [1-5]. Among these

5 cases, 2 developed severe multiorgan failure, acute respiratory distress syndrome, and eventually died [1,2]. The other 3 patients suffered from central nervous system syndromes including cerebral edema, Generalized seizure, and coma with resultant NCPE; one of them died because of Autonomic dysfunction and profound shock [3]. The other 2 survived after ventilator support [4,5]. Our patient provided an experience of uncomplicated NCPE that resolved under supportive care without significant sequelae. Although the

Fig. 2 The chest radiograph of this patient 4 days later showed normal pulmonary hilar shadow and clearing of the pulmonary edema.

pulmonary toxicity of several illicit drugs, such as cocaine and amphetamines, had been widely studied, limited work has been done concerning the pulmonary toxic effects of MDMA [6-11]. The mechanism causing NCPE due to abuse of amphetamine, a structurally similar material with MDMA, is still not clear but may be due to direct cellular toxicity suggested by animal studies [11]. The survival rate of experimental animals with cocaine-induced pulmonary edema was reported to improve using h- adrenergic blockade [12], implying the possible role of catecholamine in the pathogenesis of stimulant-associated pulmonary edema.

It has been shown in several animal studies that the clinical toxicity of MDMA did not correlate well with the serum concentration of MDMA [9]. On the other hand, the commonly available ecstasy pills may have a wide variety of ingredients and contents, implying that the clinical toxicity could hardly be anticipated. A typical ecstasy pill contains 50 to 150 mg of MDMA, but according to previous surveys, it may vary up to 70-fold [10]. The poor correlation between clinical effects and serum concentra- tion and the unpredictability of the ingredients of ecstasy pills make the toxic effects difficult to predict. One study examining the pharmacokinetics of MDMA in humans noted that the serum concentration 12 hours after ingestion of 125 mg of MDMA is about 100 ng/mL [13]. Our patient had a higher concentration (245 ng/mL) than predicted, implying greater dosage ingested.

In conclusion, it is important for the ED physicians to bear in mind the various Toxic presentations of the popular club drug MDMA.

Shih-Heng Chang MD

Ting-I Lai MD Wen-Jone Chen MD, PhD Cheng-Chung Fang MD

Department of Emergency Medicine National Taiwan University Hospital

Taipei 100, Taiwan E-mail address: [email protected]

doi:10.1016/j.ajem.2006.01.019

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Spontaneous spinal epidural hematomas of cervical spine: report of 4 cases and literature review

Spontaneous spinal epidural hematoma (SSEH) is a Rare condition with unknown etiology that is an infrequent cause of back pain among ED patients [1]. Therapeutic outcome depends on the delay between symptom onset and accurate diagnosis and between diagnosis and surgical decompres- sion; thus, management remains a challenge for physicians [2]. We report on 4 cases of SSEHs (Table 1) and review the relevant literature.

A 54 -year-old man with a history of type II diabetes mellitus complained of sudden onset of neck pain followed by rapidly progressive right hemiparesis 4 hours before admission. Clinical examination revealed marked hypesthesia in the right hand and foot with severely limited movement (muscle power scored as 1/5 in right upper and lower limbs). Deep tendon reflexes were decreased, and a right flexor plantar response was present. Routine laboratory tests were unremarkable. Magnetic resonance imaging (MRI) of the cervical spine demon- strated an epidural mass extending from C3 through C5, causing Spinal cord compression (Fig. 1A and B). The mass had an isointense signal on T1-weighted images (T1WIs) and a hyperintense signal on T2-weighted images (T2WIs). After intravenous gadolinium was administered, no apparent enhancement was seen within the mass. Epidural hematoma was highly suspected. Two hours after admission, the patient underwent an emergent laminec- tomy with evacuation of hematoma. Histologic examina- tion revealed hemorrhage without evidence of neoplasm or vessel malformation. The postoperative course was un- eventful, with progressive Complete recovery from all of the profound deficits.

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