A 26-year-old female took one package of over-the-counter antitussive containing chlorphenylamine malate 45mg, dihydrocodeine chloride 180mg and lysozyme chloride 180mg, with 70g of alcohol in a suicide attempt. She was found 6 hours after taking the drug and then developed a tonic convulsion. When she was admitted to our emergency department, she was drowsy and febrile with a body temperature of 39.5°C. She became alert on the 2nd hospital day, however, she then developed myoclonus in the upper limbs and the trunk. The myoclonus gradually decreased in frequency but lasted until the 5th hospital day. Computed tomography of the brain on admission and on the 5th hospital day did not show any abnormal findings. Laboratory examinations showed an elevated level of serum creatine kinase and creatinine on admission, which rapidly decreased to the normal level in a few days. She was discharged on the 7th hospital day without any sequelae. The drug analysis revealed an initial blood concentration of 1, 200ng/ml of chlorphenylamine malate, which was higher than fatal concentrations previously reported. Chlorphenylamine, a first generation H1-antihistamine, especially when taken with alcohol, may cause acute intoxications with a variety of symptoms in the central nervous system even with small doses.

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Stenting for stenosis of the intacranial cerebral artery has often been reported, and the effectiveness has been confirmed. However, the pitfalls of this treatment for acute cerebral truncal arterial occlusion have not been discussed. We encountered two cases of basilar occlusion treated by stenting. Case 1: A sixty-nine-year-old male complained of dizziness and developed consciousness disturbance. Emergency angiography and thrombolysis therapy with percutaneous transluminal angioplasty (PTA) was performed. Recanalization was obtained but stenosis remained. Anticoagulant and antiplatelet agents were continnously administered until the stenting was performed 14 days later. The patient was discharged uneventlfully. Case 2: A sixty-nine-year-old male was admitted with consciousness disturbance. Emergency angiography and thrombolysis therapy were performed. Recanalization was obtained but stenosis persisted. Anticoagulant and antiplatelet agents were administered until stenting was performed 4 weeks later, and good recanalization was obtained. We chose two-stage treatment; that is, intra-arterial thrombolysis with/without PTA in the first stage, followed by stenting in the second stage. The reason we chose two-stage treatment is that during the acute stage of occlusion, the shape of the artery can not be accurately demonstrated. We considered that staged stenting for acute cerebral truncal arterial occlusion using sufficient anti-coagulation and anti-platelet agents is an optimal strategy. More cases are needed to clarify the most stable stenting for acute cerebral truncal artery occlusion.

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We report a case of acute compartment syndrome of the leg caused by primary pyomyositis. A 37-year-old male with a history of untreated diabetes mellitus presented to the emergency room complaining of a swollen and painful right leg for 7 days. He denied any trauma and intravenous drug use. The diagnosis was established by elevated tissue pressure of the anterior and lateral tibial compartments of the lower extremity and enlargement of the muscles on computed tomographic (CT) scan. The patient underwent an immediate four compartment fasciotomy and surgical drainage. Culture of wound pus grew methicillin-sensitive Staphylococcus aureus. Blood cultures were negative. Appropriate antimicrobial therapy and surgical drainage resulted in resolution of the infection with good residual muscle function. To the best of our knowledge, this is the first reported case of primary pyomyositis causing compartment syndrome in Japan.

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We herein report a case of Sweet's syndrome presenting clinical conditions closely similar to severe sepsis. A 32-year old woman delivered a male infant with perineal incision. Since the next day, she revealed high fever with elevated WBC and CRP. Suspected of incisional infection, administration of antibiotics was initiated. Several days later, painful erythematous plaques were observed at the injection sites on her right shoulder and left forearm. Since continued administration of antibiotics failed to prevent respiratory and hemodynamic deterioration, she was admitted to the ICU on suspicion of severe sepsis. Though we performed repeated bacterial cultures of various specimens, all cultures were sterile. Since the patient did not respond to various antibiotics at all and showed negative cultivation test results, we suspected a disease other than microbial infection, and consulted a dermatologist concerning her painful erythematous plaques on her skin. As a result of this consultation, she was diagnosed with Sweet's syndrome, and her clinical condition similar to severe sepsis was ascribed to Sweet's syndrome. Her general condition and cutaneous lesions improved rapidly by systemic corticosteroid therapy against Sweet's syndrome. Sweet's syndrome is a relatively rare skin disease of unknown etiology, characterized by clinical manifestations suggestive of inflammation such as fever and leukocytosis as well as painful erythematous plaques. In a literature search, we identified only two documented cases of Sweet's syndrome with conditions closely resembling severe sepsis as in the present one. Although the etiology of this disease is unknown, its major pathologic features suggest possible contribution of cytokines, e.g., granulocyte colony-stimulating factor (G-CSF). Cases suspected of infection, but unresponsive to antibiotics and with negative bacterial cultures, may be due to Sweet's syndrome.

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