A 61-year-old man developed a pyrescia accompanied by a massive intravascular hemolysis after abdominal surgery (Whipple's operation) of a pancreatic adenocarcinoma. Abdominal ultrasound and the abdominal CT-scan showed marked aerobilia and multiple liver abscesses. Laboratory tests demonstrated the presence of the Thomsen-Friedenreich cryptantigen (TCA) on the membranes of the patient's erythrocytes. The enzymatic cleavage of N-acetyl-neuraminic acid usually covering the TCA may lead to a life threatening intravascular hemolysis. Since Clostridial bacteriae typically synthesize neuraminidase, the presumptive diagnosis of Clostridial sepsis complicated by massive hemolysis was made. Immediate antibiotic therapy including penicillin G and metronidazole stopped hemolysis within a few hours and the patient servived. On the following day, microbiological examination identified Clostridium perfringens in the patient's blood cultures. Clostrial sepsis should be suspected in patients with underlying infections and/or malignant diseases, particularly of the gastrointestinal or genitourinary tract, who present with septic shock and acute intravascular hemolysis. Whereas microbiological specification of the organism is time consuming, the relatively simple agglutination test with anti-TCA peanut lectin can provide a rapid presumptive diagnosis. The immediate onset of an appropriate antimicrobial therapy is of central importance and might be life-saving.

Although whole-body hyperthermia combined with specific genotoxic chemotherapy can be shown to enhance neoplastic cell killing without a concomitant rise in bone marrow toxicity, nephrotoxicity can become treatment-limiting. This study compares the kidney toxicity to the kidney of ifosfamide, carboplatin and etoposide (ICE) chemotherapy alone, and ICE chemotherapy combined with either extracorporeal (e-WBH) or radiant-heat-induced hyperthermia (r-WBH) in 43 patients with refractory sarcoma. Within 3 days of ICE chemotherapy treatment there was a significant increase in urinary protein excretion and a reduction of the glomerular filtration rate. These effects were more pronounced if WBH was added. The use of immunoluminometric assays revealed a predominance of low-molecular-mass proteins. This increase in protein excretion persisted in the e-WBH-treated group, whereas it vanished within 3 weeks in both the group treated with ICE alone and that treated with r-WBH. Our findings suggest that ICE chemotherapy causes transient tubular and glomerular damage, which is enhanced by WBH. In terms of long-term nephrotoxicity e-WBH was more nephrotoxic than r-WBH. This finding is consistent with our clinical observations.

With suicidal intent a 72-year-old man swallowed 5.8 g aminophylline in a non-retard solution. The theophylline plasma level on admission was 120 mg/l. He had to be intubated when respiratory arrest occurred. Within the first hour he developed cerebral seizures, polymorphous ventricular premature systoles, atrial fibrillation with an irregular ventricular rate and, finally, recurrent episodes of ventricular fibrillation with prolonged circulatory shock (heart rate 120-140/min with a systolic blood pressure of 60 mm Hg for 3 hours) and severe metabolic acidosis (potassium 2.28 mmol/l, phosphate 0.21 mmol/l, pH 7.03, base excess -20.8 mmol/l). He was treated with massive fluid replacement (6.2 l in the first 12 hours), electrolyte substitution to counteract the marked hypokalaemia and hypophosphataemia, repeated defibrillation and antiarrhythmic drugs (lidocaine 240 mg/h and metoprolol twice 5 mg), as well as anticonvulsive treatment (diazepam, 10 mg twice, followed by midazolam 5 mg/h). Detoxication measures consisted initially of gastric lavage followed by high-dosage enteric administration of charcoal (210 g over 36 h), as well as haemoperfusion for 4 h. Full recovery was achieved and the patient was discharged in good health after 3 weeks.