Bupivacaine crystal deposits after long-term epidural infusion.

The case of a 45-year-old male patient (body weight 52 kg, height 1.61 m) with a locally invasive gastric carcinoma infiltrating into the retroperitoneal space is reported. Because of severe cancer pain a tunnelled thoracic epidural catheter (EC) was placed at thoracic spinal level 7/8 and a local anesthetic (LA) mixture of bupivacaine 0.25 % and morphine 0.005 % was infused continuously at 6 ml h(-1). To optimize pain therapy the concentration was doubled (bupivacaine 0.5 %, morphine 0.01 %) 3 months later but the infusion rate was reduced to 3 ml h(-1) thus the total daily dose did not change. The patient died 6 months after initiation of the epidural analgesia from the underlying disease. The total amount of bupivacaine infused was 69 g and of morphine 1.37 g. The patient never reported any neurological complications. The autopsy revealed large white crystalline deposits in the thoracic epidural space which were identified as bupivacaine base by infrared spectrometry. Morphine could not be detected. A histological examination showed unreactive fatty tissue necrosis within the crystalline deposits but nerve tissue could not be identified. It is concluded that the bupivacaine crystalline deposits arose due to precipitation but the clinical significance with regard to sensory level and neuraxial tissue toxicity is unknown.

Non-HIV-associated Kaposi's sarcoma of the tongue. Case report and review of the literature.

Kaposi's sarcoma is a frequently seen AIDS-related malignant neoplasm in the head and neck region, especially in the oral cavity, but is rarely described in the HIV-negative and non-immunosuppressed individual. The case of a 76-year-old HIV-negative, non-immunocompromised woman with a solitary Kaposi's sarcoma of the tongue is reported. The tumour was locally excised with subsequent local radiotherapy. Diagnosis and therapy are discussed and compared with a review of the contemporary literature.

Fatal hepatoxicity secondary to nimesulide.

This report describes a 57-year-old female patient with chronic lumbago, who died from the sequelae of acute liver failure induced by nimesulide medication. Nimesulide is a non-steroidal anti-inflammatory drug (NSAID) which preferentially inhibits cyclo-oxygenase 2 and has been associated with a total of 13 reported cases of severe liver injury including our case. On the basis of the literature reports, the following features of nimesulide-associated hepatotoxicity were identified: female sex (84% of cases), age (mean age 62 years), jaundice as a primary manifestation (90%) and the absence of peripheral blood eosinophilia. The average duration of therapy of the published cases was 62 days (range 7-180 days). Based on spontaneous reports to the World Health Organization, nimesulide induces a high proportion of severe adverse hepatic reactions compared with other NSAIDs registered in Switzerland. Hepatotoxicity thus represents an important risk factor of nimesulide usage.

Histological findings after long-term infusion of intrathecal ketamine for chronic pain: a case report.

Ketamine, a selective, noncompetitive N-methyl-D-aspartate (NMDA)-receptor antagonist, is able to alter pain perception at the spinal level. Little clinical data exist on the intrathecal and epidural use of ketamine in chronic pain. Histopathologic findings after intrathecal injection of ketamine with and without preservatives are rarely reported. This outcome was evaluated in a 72-year-old woman with abdominal pain due to cancer who was treated with the intrathecal application of bupivacaine, clonidine, and morphine. We reached satisfactory pain relief with the addition of ketamine to the mixture for 7 days. On postmortem, focal lymphocytic vasculitis close to the catheter injection site was found. This finding has not been described previously after long-term application of ketamine intrathecally. The intrathecal infusion of ketamine with preservative, or the mixture of ketamine, clonidine, morphine, and bupivacaine resulted in isolated lymphocytic vasculitis of the spinal cord and leptomeninges without any clinical signs of neurological deficit.