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 epidural hematomas of”>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

References

1. Simpson DL, Rumack BH. Methylenedioxyamphetamine: clinical description of overdose, death, and review of pharmacology. Arch Intern Med 1981;141:1507 - 9.
2. Walubo A, Seger D. Fatal multi-organ failure after suicidal overdose with MDMA, decstasyT: case report and review of the literature. Hum Exp Toxicol 1999;18:119 - 25.
3. Engebresten KM, Harris CR. Severe hyponatremia with resultant Noncardiogenic pulmonary edema and cerebral edema secondary to ecstasy intoxication. J Toxicol Clin Toxicol 2001;39:290 - 1.
4. Ron BA, Oded S, Valery R, et al. dEcstasyT intoxication: life- threatening manifestations and resuscitative measures in the intensive care setting. Eur J Emerg Med 2003;10:309 - 13.
5. Brown CR, McKinney H, Osterloch JD. Severe adverse reaction to 3,4-methylenedioxymethamphetamine (MDMA). Vet Hum Toxicol 1986;28:490.
6. Christian JT, Sally KG. A comprehensive review of MDMA and GHB: two common club drugs. Pharmacotherapy 2001;21:1486 - 513.
7. Kimberlie AG. New drugs of abuse. Emerg Med Clin North Am 2000;

18:625 - 36.

1. Una DM, Shiyoko OS, George AR. Adverse reactions with 3,4- methylenedioxymethamphetamine (MDMA, becstasyQ). drug safety 1996;15:107 - 15.
2. Thomas DS, Una DM, George AR. 3,4-Methylenedioxymethamphet- amine (MDMA, becstasyQ): pharmacology and toxicology in animals and humans. Addiction 1994;89:539 - 51.
3. Kalant H. The pharmacology and toxicology of decstasyT (MDMA) and related drugs. CMAJ 2001;165:917 - 28.
4. Timothy EA, William FW, Robert WD. Stimulant-induced pulmonary toxicity. Chest 1995;108:1140 - 9.
5. Robin E, Wong R, Pfashne K. Increased lung water and ascites after massive cocaine overdosage in mice and improved survival related to beta-adrenergic blockage. Ann Intern Med 1989;110:202 - 7.
6. Mas M, Farre M, de la Torre R, et al. Cardiovascular and neuroendocrine effects and pharmacokinetics of 3,4-methylene- dioxymethamphetamine in humans. J Pharmacol Exp 1999;290: 136 - 45.

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.

Hyper-

M indicates male; F, female.

^a The time interval between onset of symptoms and surgical intervention.

^b Complete recovery after 3-month follow-up.

posterolateral intense

of C3 through C5

Conservative Partial

treatment recovery (1 mo later)

M/20

15

Right

posterolateral of C5 through C7

Isointense Hyperintense No

Laminectomy Partial

enhancement with evacuation recovery^b of hematoma

F/75

5

Right

posterolateral of C2 through C5

Isointense Hyperintense

Laminectomy

Complete

with evacuation recovery

of hematoma

T2WI

signal

Table 1 Summary of SSEHs in our 4 patients

Sex/Age Clinical picture

(y)

Duration^a (h)

Location

CT MRI

Treatment

Result

density T1WI

signal

enhancement with evacuation recovery

of hematomas

F/62

Contrast

M/54

Sudden onset of

neck pain followed by progressive right hemiparesis Sudden onset of neck pain, right hemiparesis, and hypesthesia after neck extension Sudden onset of bilateral shoulder pain followed by paraparesis to paraplegia

Sudden onset of neck pain followed by hypesthesia, tetraparesis, and acute urine retention

6

Right

posterolateral of C3 through C5 Right

Isointense Hyperintense No

Laminectomy Complete

A 62-year-old woman with a history of headache for 2 months complained of sudden onset of neck pain after neck extension several hours before admission followed by development of weakness and numbness in the right limbs. On examination, she had hypesthesia and hemi- paresis in both right lower limbs (muscle power scored as 4/5). Right flexor plantar response was present. Biochem- ical tests showed no significant abnormal finding. Com- puted tomographic (CT) scan of the cervical spine demonstrated an epidural mass extending from C3 through

C5, causing spinal cord compression (Fig. 2A and B). Based on the clinical picture and radiographic findings, epidural hematoma was highly suspected. Because the patient refused surgical intervention, conservative treat- ment was adopted. Two weeks later, the epidural hematomas had disappeared via MRI. One month later, the remaining neurologic deficit was weakness in the right foot (muscle power scored as 3/5).

A 20-year-old man with a negative medical history complained of sudden-onset bilateral shoulder pain after he

Fig. 1 Magnetic resonance images of the cervical spine. Sagittal (A) and axial (B) T2WIs show a predominantly hyperintense posterior extradural mass that compressed the spinal cord.

Fig. 2 Computed tomographic scan of the cervical spine. Sagittal (A) and axial (B) images show an epidural mass that compressed the spinal cord.

had sat for 4 hours using his computer. Four hours after the onset of pain, progressive weakness developed bilaterally over the limbs, followed by paraplegia. Clinical examination confirmed paraplegia; bilateral flexor plantar responses were present and deep tendon reflexes were decreased. Labora- tory tests were unremarkable. Magnetic resonance imaging of the cervical spine demonstrated an epidural mass extending from C5 through C7, causing spinal cord compression (Fig. 3A and B). The mass had an isointense signal on T1WIs and a hyperintense signal on T2WIs. After intravenous gadolinium was administered, no apparent enhancement was seen within the mass. Epidural hematoma was highly suspected. He underwent emergent laminectomy with evacuation of hematoma. histologic examination revealed hemorrhage without evidence of neoplasm or vessel malformation. At discharge, the patient overall had good recovery in the lower limbs but sustained from

neurologic bladder. At 3-month follow-up, the patient was asymptomatic and had returned to normal activities.

A 75-year-old woman with a 20-year history of hypertension complained of sudden-onset neck pain fol- lowed by progressive weakness and numbness in all 4 limbs and acute Urinary retention several hours before admission. Neurologically, she had tetraparesis (muscle power scored as 3/5 in right limbs and 4/5 in left limbs). On physical examination, bilateral flexor plantar responses were present and deep tendon reflexes were decreased. Biochemical test findings were normal. Magnetic resonance imaging of the cervical spine demonstrated an epidural mass extending from C2 through C5, causing spinal cord compression (Fig. 4A and B). The mass had an isointense signal on T1WIs and a hyperintense signal on T2WIs. Epidural hematoma was highly suspected. She underwent emergent laminectomy of the cervical spine with evacuation of

Fig. 3 Magnetic resonance images of the cervical spine. Sagittal (A) and axial (B) T2WIs show a predominantly hyperintense posterior extradural mass that compressed the spinal cord.

Fig. 4 Magnetic resonance images of the cervical spine. Sagittal (A) and axial (B) T2WIs show a predominantly hyperintense posterior extradural mass that compressed the spinal cord.

hematoma. Pathologic examination revealed hemorrhage without evidence of neoplasm or vessel malformation. The postoperative course was uneventful, with progressive complete recovery of the profound deficits.

Spontaneous spinal epidural hematoma is a rare cause of spinal cord compression, with a frequency of less than 1% of spinal space-occupying lesions [2]. The annual incidence has been estimated at 0.1 per 100 000, but it may be increasing because of better diagnostics with sensitive imaging techni- ques such as CT and MRI [3]. The male/female ratio is 1.5:1, and most cases occur between the ages of 50 and 80 years [4]. Although the etiology is unknown, Predisposing factors such as hypertension, anticoagulant therapy, increased venous pressure (straining, sneezing, lifting, or whooping cough), pregnancy or labor, and vascular malformation have been described [5,6]. The causative hematomas most frequently occur at the lower cervical and thoracolumbar spinal levels in adults; they commonly affect C5 to T1 spinal levels in children [7]. However, the exact pathogenesis of the condition remains obscure. Based on the predominance of posterolateral hematomas with segmental distribution, the posterior epidural venous plexus seems to be the most likely source [3]. After exercise or other maneuvers that would cause fluctuations in intrathoracic and intraabdominal pres- sures, reversal of blood flow may induce rupture of a delicate vein in the valveless epidural plexus [7]. Because venous epidural pressure is less than intrathecal pressure, other researchers have considered an arterial rupture as the origin of the bleed [1].

The classic clinical picture usually begins with the sudden onset of severe Back or neck pain around the in- volved vertebrae with radiating pain around the cor- responding dermatomes [5]. Within minutes to days, symptoms and signs of spinal cord compression such as ascending numbness, radicular paresthesia, and progressive paraparesis appear [2]. The typically short course from pain to paralysis is common in thoracic and cervical cases

because the epidural space is narrowest between T3 and T9 [4,8]. Children commonly have long durations of symptoms before neurologic deficits appear [7]. If left untreated, progressive spinal cord compromise can lead to complete permanent neurologic deficits or even death [1].

Because of improvements in radiology and the need to avoid unnecessary prolongation of the therapy process, CT myelography has been replaced by MRI as the most suitable diagnostic method [1,5,9]. T1 and T2 signals associated with SSEH vary based on clot characteristics, age, size, and oxygenation [9]. Usually, the hematoma appears as an isointense signal on T1-weighted imaging and a hyperintense signal on T2-weighted imaging done within the first 24 hours after onset of symptoms [5]. Peripheral enhancement of the lesion is mostly found with post-gadolinium-DTPA MRI [9]. These findings may help distinguish SSEH from other diseases in the differential diagnosis, such as spinal abscess, neoplasm, ischemia, transverse myelitis, and acute vertebral disk disease [2].

Although several cases of SSEHs with minimal neuro- logic deficits have been successfully treated by nonsurgical management, early surgical intervention such as decom- pressive laminectomy with evacuation of hematoma remains the treatment of choice for most patients with symptomatic spinal epidural hematomas [3]. In a study on 22 patients with spontaneous or traumatic spinal epidural hematomas, Torres et al [10] recommended early surgical evacuation for patients who presented with severe neurologic deficits and conservative management for those with minimal neurolog- ic involvement. In a review of 330 patients, Groen and van Alphen [8] reported that surgical evacuation of hematomas within 36 hours of symptomatic onset in cases involving complete spinal dysfunction resulted in favorable outcomes, as did evacuation within 48 hours for cases involving incomplete deficits [5]. In the study by Liao et al [11], better neurologic and functional recovery was positively correlated with the shortened time interval between initial ictus and

surgical intervention, within 48 hours or even 12 hours. postoperative recovery predominantly depends on time interval between onset of symptoms and surgical decom- pression, and this interval appears to be related to the severity of the preoperative neurologic condition [2,8].

In our 4 cases, patients presented with sudden-onset neck or shoulder pain followed by development of weakness in the limbs. radiologic studies revealed that all hematomas were in the right posterolateral side of the cervical spine. Three patients underwent Surgical decompression and evacuation of hematomas, with only partial recovery in one patient (case patient 3). Conservative treatment in one patient (case patient 2) resulted in some remaining neuro- logic deficits. In our opinion, early diagnosis and surgery with decompression are essential for symptomatic patients. Because SSEH appears to be an increasingly common emergent neurologic diagnosis, physicians should keep it in mind, especially when a patient presents with sudden-onset back or neck pain followed by symptoms or signs of spinal cord compression. Urgent spinal MRI is essential for suspected cases. Early recognition, diagnosis, and appropriate treatment

may result in decreased morbidity and improved prognosis.

Cheng-Ta Hsieh MD Cheng-Fu Chang PhD En-Yuan Lin MD Tung-Han Tsai MD

Yung-Hsiao Chiang PhD

Da-Tong Ju MD Department of Neurological Surgery Tri-Service General Hospital National Defense Medical Center

Taipei 114, Taiwan, Republic of China E-mail address: [email protected]

doi:10.1016/j.ajem.2006.01.025

References

1. Dinsmore AJ, Leonard RB, Manthey D. Spontaneous spinal epidural hematoma: a case report. J Emerg Med 2005;28:423 - 6.
2. Alexiadou-Rudolf C, Ernestus RI, Nanassis K, et al. Acute non- traumatic spinal epidural hematomas. An important differential diagnosis in spinal emergencies. Spine 1998;23:1810 - 3.
3. Groen RJ. Non-Operative treatment of spontaneous spinal epidural hematomas: a review of the literature and a comparison with operative cases. Acta Neurochir (Wien) 2004;146:103 - 10.
4. Foo D, Rossier AB. Preoperative neurological status in predicting surgical outcome of spinal epidural hematomas. Surg Neurol 1981; 15:389 - 401.
5. Liao CC, Lee ST, Hsu WC, et al. Experience in the surgical management of spontaneous spinal epidural hematoma. J Neurosurg 2004;100:38 - 45.
6. Chen CJ, Hsu WC. Imaging findings of spontaneous spinal epidural hematoma. J Formos Med Assoc 1997;96:283 - 7.
7. Patel H, Boaz JC, Phillips JP, et al. Spontaneous spinal epidural hematoma in children. Pediatr Neurol 1998;19:302 - 7.
8. Groen RJ, van Alphen HA. Operative treatment of spontaneous spinal epidural hematomas: a study of the factors determining postoperative outcome. Neurosurgery 1996;39:494 - 508.
9. Jamjoom ZA. Acute spontaneous spinal epidural hematoma: the influence of magnetic resonance imaging on diagnosis and treatment. Surg Neurol 1996;46:345 - 9.
10. Torres A, Acebes JJ, Caiol J, Gabarros A, Lopez L, Plans G, et al. Spinal epidural hematomas. Prognostic factors in a series of 22 cases and a proposal for management. Neurocirugia 2004;15:353 - 9.
11. Liao CC, Lee ST, Hsu WC, Chen LR, Lui TN, Lee SC. Experience in the surgical management of spontaneous spinal epidural hematoma. J Neurosurg 2004;100:38 - 45.

A potentially fatal mystery in acute abdomen: Abdominal apoplexy

Idiopathic spontaneous hemoperitoneum is a rare but often fatal event [1]. It is usually heralded by severe abdominal pain. Other associated symptoms include ab- dominal distension, decreased hematocrit, and occasionally hypovolemic shock [2]. We report an 18-year-old male who initially presented with the symptoms of acute gastroenter- itis but finally was diagnosed as having idiopathic sponta- neous hemoperitoneum.

An 18-year-old male presented to the ED with watery diarrhea, vomiting, and abdominal cramping pain for several hours. There was no significant medical history or trauma. Vital signs were a temperature of 35.28C (95.48F), pulse rate of 93 beats/min, respiratory rate of 16 breaths/min, and blood pressure of 106/53 mm Hg. Physical examination was remarkable except for abdominal distension and localized midabdomen tenderness, without rebound or muscle rigid- ity. Bowel sounds were hyperactive. Laboratory tests showed a hemoglobin level of 11.9 g/dL and white cell count of 16,800/AL. His biochemical profiles, coagulation function, and platelet count were within normal limits. There were no remarkable findings on chest radiography or abdominal plain film. The Clinical impression was acute gastroenteritis with dehydration, and he was observed in the ED and treated with intravenous hydration.

Four hours later, the patient felt better but fainted when he was rising from his bed. His blood pressure dropped to 71/37 mm Hg with a pulse rate of 98/min. His abdomen was soft, but mild rebounding tenderness was now noted over the right lower quadrant. A rapid bedside abdominal sonography demonstrated free intraperitoneal fluid. After stabilization of his vital signs, a contrast-enhanced abdom- inal computed tomography was obtained, which showed the presence of massive ascites without other abnormalities. Internal bleeding was confirmed by peritoneocentesis, which yielded bloody fluid, and the patient underwent emergent celiotomy. Intraoperative findings revealed the presence of 2300 mL of bloody ascites and 500 mL of clotted blood. No bleeding source could be identified despite diligent repeated exploration of visceral organs, mesentery, and major abdominal vessels. Clotted blood was evacuated, but still no bleeding source was identified. Eight