be aware that the potential of spontaneous hemoperitoneum in the nontraumatic patients has a high index of suspicion and seek early operative intervention.

Table 1 Etiologies of spontaneous hemoperitoneum (nontraumatic)

Disorder Condition

Liver Benign hepatic mass rupture Malignant hepatic mass rupture

Spleen Splenic infections Splenic hamartoma Congenital cysts

Gynecologic disorders Ruptured ovarian cyst

Ectopic pregnancy Ovary carcinoma Ruptured gravid uterus Intercourse

Vascular disorders Ruptured aortic Abdominal aneurysm

Ruptured visceral aneurysm Polyarteris nodosa

Ruptured varices (liver cirrhosis with portal hypertension)

Hematologic disorders Hemophilia

myeloproliferative disorders inflammatory disorders Hemorrhagic pancreatitis

Tuberculous peritonitis

Coagulopathy Cryptogenic

Shih-Wen Hung MD Hon-Ping Ma MD

Aming Chor-Ming Lin MD Chien-Chih Chen MD Emergency Department

Shin-Kong Wu Ho-Su Memorial Hospital

Taipei 111, Taiwan (R.O.C.) E-mail address: [email protected]

units of Packed red blood cells was transfused during the operation. The abdomen was subsequently closed. The postoperation course was uncomplicated, and he was discharged on day 7 after admission.

The etiologies of spontaneous hemoperitoneum may be grouped into hepatic, splenic, gynecological, vascular, hematologic, inflammatory disorders, coagulopathy, and cyptogenic [2,3] (Table 1). The etiology of spontaneous hemoperitoneum differs in young and elderly patients [4]. Rupture of a visceral artery, due either to an aneurysm resulting from a developmental defect of the artery or to the necrosis of the media of the arterioles in Polyarteritis nodosa, is common in young patients. bAbdominal apoplexyQ [1], idiopathic spontaneous hemoperitoneum that defies explanation, was first described in 1909 by Barber [5], and only 110 new cases were reported between 1909 and 1998 [6]. A male/female ratio is 3:2. Most cases occur between 55 and 64 years. Abdominal pain is the most frequent manifestation [7,8], followed by dyspnea, chest pain, collapse, and vomiting. Diarrhea has not been mentioned in the previously reported articles. Management is focused highly on suspicion and early surgical intervention. A nontherapeutic exploration has a high mortality of 40%.

Our patient’s initially modest presentation reminds us that blood is only a minor peritoneal irritant, and the intensity of abdominal pain is usually related to the rapidity and the volume of extravasation [9]. His vomiting and diarrhea may be related to bowel irritation by the intra- abdominal blood. The source of bleeding was not identified in our patient. In conclusion, emergency physicians should

Tzong-Luen Wang MD, PhD

Emergency Department Shin-Kong Wu Ho-Su Memorial Hospital

Taipei 111, Taiwan (R.O.C.) Department of Medicine Taipei Medical University Taipei 110, Taiwan (R.O.C.)

Chee-Fah Chong MS, MD

Emergency Department Shin-Kong Wu Ho-Su Memorial Hospital

Taipei 111, Taiwan (R.O.C.)

School of Medicine Fu Jen Catholic University Taipei 242, Taiwan (R.O.C.)

doi:10.1016/j.ajem.2006.01.029

References

1. Carr SR, Dinsmore RC, Wilkinson NW. Idiopathic spontaneous Intraperitoneal hemorrhage: a clinical update on abdominal apoplexy in the year 2001. Am Surg 2001;67:374 - 6.
2. Lucey BC, Varghese JC, Soto JA. Spontaneous hemoperitoneum: causes and significance. Curr Probl Diagn Radiol 2005;34:182 - 95.
3. Tan YM, Tan BK, Chow PK. Abdominal apoplexy: a potentially fatal enigma. ANZ J Surg 2003;73:461 - 2.
4. Kleinsasser LJ. Abdominal apoplexy. Br J Surg 1970;120:623 - 8.
5. Barber MC. Intra-abdominal haemorrhage associated labour. Br Med J 1909;2:203.
6. Carmeci C, Munfakh N, Brooks JW. Abdominal apoplexy. South Med J

1998;91:273 - 4.

1. Suber Jr WJ, Cunningham PL, Bloch RS. Massive spontaneous hemoperitoneum of unknown etiology: a case report. Am Surg 1998; 64:1177 - 8.
2. Lucha Jr PA. Spontaneous hemoperitoneum. J Am Osteopath Assoc 1996;96:364 - 5.
3. Akriviadis EA. Hemoperitoneum in patients with ascites. Am J Gastroenterol 1997;92:567 - 75.

Lunesta overdose: ST-elevation Coronary vasospasm, troponemia, and ventricular fibrillation arrest

This is a report of a 52-year-old white man who pre- sented complaining of a headache after ingesting 20 tablets

of Lunesta (eszopiclone; Sepracor Inc, Marlborough, Mass), during a 10-hour period, the night before present- ing to the ED. The patient was processed and observed in the ED, then found in ventricular fibrillation arrest. He had an episode of coronary vasospasm resulting in a ST-elevation myocardial infarction. The current knowledge of Lunesta pathophysiology and clinical applications will be presented.

A 52-year-old man was admitted to the ED because of a headache after feeling depressed and unable to sleep. He admitted to ingesting 15 to 20 tablets (3 mg per tablet) of Lunesta for insomnia the previous night. The patient had been in his usual state of health until he developed a throbbing, Frontal headache 3 hours before arrival in the ED. On review of systems, the patient complained of nausea and vomiting in addition to insomnia and depression. He denied abdominal pain, chest pain, shortness of breath, sick contacts, urinary complaints, significant rashes, lateralizing weakness, numbness, visual changes, hallucinations, suicid-

al ideations, or homicidal thoughts.

The patients’ medical history included hypertension, depression, and posttraumatic stress disorder. His social history included alcohol abuse and a 1 pack per day smoking

use for more than 30 years. He has an allergy to compazine, and his medication list included Benicar, Wellbutrin 450 mg/d, Zoloft 200 mg/d, Lunesta 3 mg before sleep, Vytorin, and Norvasc. Family history was not obtained.

On physical examination, vital signs were blood pressure of 121/82 mm Hg, pulse rate of 102 beats per minute, respiratory rate of 18 breaths per minute, and temperature of 36.08C. He was a well-developed, healthy, intoxicated- appearing white man speaking in clear sentences with a flat tone. The initial electrocardiogram (ECG) (Fig. 1) at this time was unremarkable.

On physical examination, his conjunctiva was injected and the remainder of his head and neck were unremarkable. He demonstrated no signs of cardiovascular compromise. heart sounds were mildly tachycardic without murmur, gallop, or rub. Lungs were clear bilaterally, his abdomen was benign, and his extremities were without cyanosis or edema. He did not have any concerning skin lesions. His overall physical examination was unremarkable.

On neurologic examination, his pupils were equally round and reactive to light, with ocular movements intact in all directions and conjugated vision was normal. He did not have nystagmus. Sensation and strength were normal as

Fig. 1 Initial ECG of 52-year-old man presenting to the ED complaining of a headache revealing normal sinus rhythm.

well as deep tendon reflexes and cerebellar function. The patient was not tremulous and did not have asterixis.

Initial laboratory studies demonstrated a white blood cell count of 8.48 x 10³/lL, hemoglobin level of 14.8 g/dL, hematocrit of 43.2%, and platelet count of 198 x 10³/lL. The following were his chemistry values: sodium 129 mmol/L, potassium 5.9 mmol/L, chloride 98 mmol/L, bicarbonate 20 mmol/L, serum urea nitrogen 37 mg/dL, creatinine 1.6 mg/dL, glucose 80 mg/dL, calcium

8.1 mg/dL, phosphorus 2.6 mg/dL and magnesium

1.5 mg/dL. Liver function tests included c-glutamyl trans- peptidase level of 848 U/L, aspartate aminotransferase level of 420 U/L, alanine aminotransferase of 135 U/L, alkaline phosphatase level of 130 U/L, total bilirubin of 1.1 mg/dL, direct bilirubin of 0.3 mg/dL, total protein of 6.9 g/dL, and an Albumin level of 4.2 g/dL. Salicylate level was less than

2.5 mg/dL and acetaminophen level was less than 1 lg/mL. urine drug screen was only significant for the presence of benzodiazepines.

The patient’s headache improved after receiving 30 mg of toradol IV and a 1-L normal saline bolus. Residual pain

was treated with 800 mg PO of ibuprofen. Twelve hours after the patient’s initial presentation, he began feeling tremulous and received 2 mg IV of Ativan. Laboratory studies were redrawn at that time. The ECG (Fig. 2) was repeated at this time revealing sinus tachycardia.

Fourteen hours after initial presentation, the patient became rigid and cyanotic. He was found to be in ventricular fibrillation cardiac arrest and was resuscitated with epineph- rine, atropine, and defibrillated twice with restoration of sinus rhythm. A repeat ECG revealed ST-elevation in leads III, aVF, and precordial leads V₃ to V₆ (Fig. 3).

The catheterization laboratory was notified and the patient was taken immediately from the ED for cardiac catheterization. The patient had 100% occlusion of the proximal right coronary artery by vasospasm. The remain- ing coronary vasculature was normal. There was no significant coronary artery disease. The vasospasm was relieved by administration of intracoronary nitroglycerin and the ST elevations resolved. serum troponin I peaked at

6.5 ng/mL before cardiac catheterization. A transthoracic echocardiogram was performed on hospital day 2 demon-

Fig. 2 ECG of 52-year-old man complaining of bfeeling tremulous.Q Sinus tachycardia.

Fig. 3 ECG of 52-year-old man during resuscitation from ventricular fibrillation.

strating normal cardiac wall motion and normal left and right ventricular function. The remainder of the patient’s hospital stay was uneventful. An implanted cardioverter/ defibrillator was placed before discharge on hospital day 12. The ECGs from the following day postcatheterization demonstrated inverted t waves in leads II, III, aVF, and V₄, V₅, V₆ (Fig. 4).

Lunesta (eszopiclone) is a nonbenzodiazepine hypnotic agent approved by the Food and Drug Administration for oral treatment of insomnia in adults. It is the S-isomer of zopiclone, a cyclopyrrolone, which has been available in other countries for almost 20 years. It was developed to overcome some of the disadvantages of benzodiazepines, for example, next-day sedation, dependence, and withdraw- al. It is licensed for the short-term treatment of insomnia in situations where the insomnia is debilitating or is causing severe distress for the patient. Long-term continuous use is not recommended. However, Lunesta is not being restricted in its labeling to short-term use. The usual dosage of eszopiclone is 3 mg before sleep [1]. The mechanism of action of eszopiclone is not completely understood. It interacts with the c-aminobutyric acid receptor complex. It

is rapidly absorbed after oral administration, and peak concentration is achieved within 1 hour [2]. The drug is minimally bound to plasma proteins and, therefore, absorption and distribution are minimally affected by other drugs competing for protein-binding sites. Clinical trials demonstrated the effect of food on the absorption of eszopiclone noticeably when taken concomitantly with a high-fat meal; maximum absorption was delayed by approximately 1 hour [2], although the half-life remained unchanged. Eszopiclone is metabolized by oxidation and demethylation, primarily by plasma metabolites, although some metabolism occurs in the liver via CYP 3A4 and CYP 2E1 enzymes. drug metabolism in patients with severe hepatic impairment was decreased and resulted in an increased drug exposure in patients with this condition. The half-life of eszopiclone is approximately 6 hours and the metabolites are primarily eliminated through urinary excretion. Less than 10% of the orally administered drug is excreted unchanged [2].

Cases since 1966 to 2005 have reported on the misuse or dependence of this medication. The resultant symptoms of zopiclone withdrawal include anxiety, tachycardia, tremor,

Fig. 4 ECG of 52-year-old man 1-day after MI.

sweating, rebound insomnia flushes and palpitations to derealization, convulsion, and delirium. Most of the cases reported involved patients between 16 and 60 years old with 1 report of a patient who was 71 years old [3]. Eszopiclone was studied in 6 placebo-Controlled clinical trials with 2100 subjects experiencing both chronic and transient insomnia. Adverse events reported during the clinical trials in at least 2% of the study population were generally mild and resulted in minimal study subjects who discontinued treatment. The most commonly reported adverse reaction was unpleasant taste. Other reported adverse reactions included viral infection, dry mouth, dizziness, hallucina- tions, infection, and rash [2]. During the 6-month clinical trials, no tolerance or serious withdrawal syndrome to eszopiclone was observed.

Recent literature has suggested concern for the carcinogenicity and mutagenesis associated with use of eszopiclone [4], specifically to those patients with HIV/ AIDS [5].

This case that we reported is unique. The impaired Hepatic function of our patient reflected in the laboratory data may have played a role in the coronary vasospasm reported

in our patient. Perhaps our patient not only ingested a Large dose of eszopiclone, up to 60 mg, but also other potent inhibitors of CYP 3A4 (eg, ketoconazole, clarithromycin) that the providers were unaware of. It is in these patients with hepatic impairment that practitioners prescribing eszopiclone are cautioned to be particularly careful in the dosage prescribed.

Adam H. Miller MD, MSc Amanda R. Bruggman MD Division of Emergency Medicine Department of Surgery

University of Texas Southwestern Medical Center

Dallas, TX 75390-8579, USA

Parkland Health and Hospital System

Dallas, TX, USA Department of Pediatrics Dallas, TX 75235, USA

University of Texas Southwestern Medical Center

Dallas, TX 75390-8579, USA

Children’s Medical Center at Dallas E-mail address: [email protected]

Margarita M. Miller MD

Department of Pediatrics University of Texas Southwestern Medical Center

Dallas, TX 75390-8579, USA

Children’s Medical Center at Dallas

Dallas, TX 75235, USA

doi:10.1016/j.ajem.2006.02.001

References

1. Wong CP, Chiu PKC, Chu LW. Zopiclone withdrawal: an unusual cause of delirium in the elderly. Age Ageing 2005;34:526 - 7.
2. Sepracor Inc. Lunesta tablets [drug insert] 2005. http:// www.lunesta.com.
3. Hajak G, Muller WE, Wittchen HU, Pittrow D, Kirch W. Abuse and dependence potential for the non-benzodiazepine hypnotics zolpidem and zopiclone: a review of case reports and epidemiological data. Addiction 2003;98:1371 - 8.
4. www.sepracor.com: Label for eszopiclone (Lunesta). Sepracor, Marl- borough, MA.
5. Stebbing J, Bower M. What can oncologists learn from HIV? Lancet Oncol 2003;4:438 - 45.

false-negative cerebral infarction on diffusion magnetic resonance imaging

A 31-year-old male patient presented to our center with vertigo, diplopia, and right facial sensory disturbance 12 hours after onset. He had experienced these symptoms immediately after ingestion of scallops and oysters with some amount of alcohol. He had no history of illness except atopic dermatitis. There were no conventional risk factors for stroke such as hypertension, diabetes mellitus, or heart disease except current cigarette smoking.

Before magnetic resonance imaging (MRI) was per- formed, the patient underwent an emergency clinical evaluation by a stroke neurosurgeon. neurologic findings revealed anisocoric pupils (right b left), right facial sensory disturbance, and pain sensory disturbance in the left upper and lower extremities.

Initial magnetic resonance examinations were performed 12 hours after onset on a 1.5-T magnetic resonance unit. Initial diffusion-weighted imaging (DWI) was considered negative for the diagnosis of recent arterial stroke because remarkable hyperintensity areas with reduced apparent diffusion coefficient (ADC) values were not observed; however, a questionable relatively high-intensity area was observed retrospectively in clinically relevant brain regions (Fig. 1A and B). A second MRI was performed 3 hours after the first MRI that showed a marked high-intensity area on both DWI and T2-weighted images (Fig. 1C and D). On the second day after admission, 3-dimensional computed tomography angiography was performed; right vertebral artery dissection immediately distal to the posterior inferior cerebellar artery was observed (Fig. 1E and F). Intravenous

saline and Antiplatelet therapy had been administered simultaneously since admission.

This patient was almost incorrectly diagnosed with shellfish poisoning because initial DWI and fluid-attenuated inversion recovery images showed no remarkable high- intensity area in the brain 12 hours after onset. The patient exhibited symptoms of Wallenberg syndrome; however, the signs and symptoms of the syndrome may vary from patient to patient. Therefore, we initially believed that these neuro- logic findings were caused by the shellfish toxin because the onset of the symptoms was observed immediately after ingestion of scallops.

Although it has been documented that DWI is highly sensitive for the diagnosis of acute ischemic stroke, there is increasing evidence that it may fail to detect acute stroke lesions. Three large-scale studies reported false-negative DWI findings in the acute phase of ischemic stroke lesions [1-3]. The rate of negative DWI studies in patients with acute ischemic stroke is highly variable, ranging from 0%

[4] to 21% [1,5]. The sensitivity of DWI for detecting acute ischemic stroke may not be as high as was initially believed. The lesion could be too small for the resolution of the DWI echoplanar sequence. On the other hand, the symptoms may not have been caused by infarction, but by ischemia of the brain at that time.

Yukinori Akiyama

Department of Traumatology and Critical Care Medicine

Sapporo Medical University Sapporo 003-0804, Japan Department of neurosurgery Sapporo Medical University Sapporo 003-0804, Japan

E-mail address: [email protected]

Yasufumi Asai

Department of Traumatology and Critical Care Medicine

Sapporo Medical University Sapporo 003-0804, Japan

Kiyohiro Houkin Department of Neurosurgery Sapporo Medical University Sapporo 003-0804, Japan

doi:10.1016/j.ajem.2006.02.010

References

1. Ay H, Furie KL, Yamada K, et al. diffusion-weighted MRI character- izes the ischemic lesion in Transient global amnesia. Neurology 1998; 51:901 - 3.
2. Lovblad KO, Laubach HJ, Baird AE, et al. Clinical experience with diffusion-weighted MR in patients with acute stroke. AJNR Am J Neuroradiol 1998;19:1061 - 6.