[Neurologic complications following total endoprothesis implantation of the hip under peridural catheter anesthesia]. / Neurologische Komplikation nach Totalendoprothesen-implantation der Hüfte in Katheterperiduralanästhesie.

This case report describes paralysis of the plantar flexors and extensors after a total hip replacement in a 33-year-old woman performed under epidural anaesthesia (PDA). Six years previously, the patient had undergone a bone marrow transplantation for chronic myeloid leukaemia. She had developed a deep vein thrombosis, a pulmonary embolus, and a severe graft-versus-host reaction of the skin, leading to markedly reduced mouth opening. The hip operation was performed using PDA following antithrombotic prophylaxis with low-molecular-weight heparin. Blood could initially be aspirated after advancing the PDA catheter, and a second puncture of the epidural space 1 segment higher enabled correct placement of the catheter. The patient received 500 ml Dextran 60 perioperatively and the operation was completed without any further problems. The PDA catheter was removed 2 h after the operation following the return of movement of both thighs. Fourteen hours after the completion of surgery it was noticed that the dressing over the epidural puncture site was bloodstained, the patient was incontinent, and complete loss of movement of the operated leg was present. An epidural haematoma was the suspected cause, but could not be definitely confirmed by a CT scan. Nevertheless, a laminectomy was undertaken to evacuate the suspected haematoma. As expected, tracheal intubation was only possible bronchoscopically. Intraoperatively, some low-grade epidural oozing at the level of the initial puncture site was observed, and a hemilaminectomy of 5 was performed. For the first time postoperatively, the bleeding time was measured and was markedly prolonged to 20 min (as described by Mielke, normal value up to 8 min). A coagulopathy was suggested, with the differential diagnosis of impaired platelet function. The paralysis of the plantar flexors and extensors and some sensory loss were still present 6 months after the operation. It remains uncertain whether the PDA in a patient receiving low-molecular-weight heparin resulting in a the suspected epidural haematoma was the cause of the neurological sequelae and in agreement with the consultant neurologist, we believe that a direct traumatic lesion of the L5/S1 segment or damage to the sciatic nerve are also likely causes of the symptoms. Undoubtedly, the lack of adequate postoperative neurological monitoring and the intraoperative administration of dextran despite the known epidural vascular lesion deserve criticism. This case report demonstrates the often complex development of neurological complications after nerve blocks, where a definite cause can frequently not be determined.

[Thromboembolism prevention with low dose heparin and spinal anesthesia--a risky combination?]. / Thromboembolieprophylaxe mit niedrig dosiertem Heparin und rückenmarknahe Anästhesie--eine riskante Kombination?

UNLABELLED: Spinal or intracranial haematoma is a rare but severe complication of spinal/epidural anaesthesia with an incidence of less than 1:100,000. Coagulation defects, traumatic puncture, and anticoagulant drugs are assumed to be risk factors for the development of this kind of haematoma. Whether the risk of bleeding after spinal/epidural anaesthesia is increased by the administration of low-dose heparin (unfractionated or fractionated) for thromboprophylaxis is currently under discussion. METHODS AND RESULTS: A randomised, prospective trial answering this question is not feasible because of the rarity of the complication. As an alternative, we identified all case reports described in the literature to date and analysed them for possible risk factors. In conjunction with spinal/epidural anaesthesia, we found 4 cases of spinal and 2 cases of intracranial haematoma following treatment with unfractionated heparin and 6 cases of spinal haematoma following treatment with different low-molecular-weight (LMW) heparins. In none of these cases could thromboprophylaxis with heparin be identified as the only risk factor for bleeding: in 11 of the 12 cases a difficult or traumatic puncture was described. Eleven patients showed three or more possible risk factors, e.g., coagulation defects, concomitant therapy with other anticoagulant drugs, or anatomic abnormalities. CONCLUSION: We suggest that the development of spinal or intracranial haematoma after spinal/epidural anaesthesia is a multifactorial event. An influence of low-dose heparin prophylaxis as a cofactor cannot wholly be excluded because of the difficulty of studying the problem in a prospective way. The few case reports have to be seen in the context of millions of patients who have received either unfractionated or LMW heparin and lumbar or thoracic regional anaesthesia without any complication. We conclude that low-dose heparin prophylaxis (fractionated or unfractionated) is not a definite contraindication to spinal/epidural anaesthesia. High-risk (ASA III/IV) patients in particular benefit from effective postoperative analgesia achieved by local anaesthetics in combination with effective heparin thromboprophylaxis. Nevertheless, the absolute contraindications for regional anaesthesia must be respected and an individual risk/benefit analysis should be performed for every patient. An adequate time interval between application of heparin and regional anaesthesia or removal of a spinal/epidural catheter, atraumatic puncture technique, and careful neurologic monitoring during the post-operative period can minimise the risk of complications.

A triazolodiazepine platelet activating factor receptor antagonist (WEB 2086) reduces pulmonary dysfunction during endotoxin shock in swine.

We wanted to determine the effects of WEB 2086, a platelet activating factor (PAF) antagonist, in lipopolysaccharide (LPS) shock in anesthetized pigs. In a randomized study, LPS from S. abortus equi, 2 micrograms/kg/h was given IV for six hours. Thirteen animals received LPS and WEB 2086, 10 mg/kg/h IV for 6.5 hours, beginning 30 minutes before LPS. Eleven septic controls received saline and LPS, three nonseptic controls received saline and WEB 2086, and three nonseptic controls received saline only. In six animals we investigated the effect of synthetic PAF in doses between 50 and 10,000 ng on arterial (AP) and pulmonary arterial (PAP) pressure before and during infusion of WEB 2086. The LPS-induced rise in PAP was reduced by WEB 2086 (p = 0.01) but not the decrease in AP. The LPS-induced leukopenia, hypoxia, increase in airway pressure, and release of plasminogen activator inhibitor were reduced by WEB 2086. Platelet activating factor produced an increase in PAP and a biphasic response in AP. All PAF dose response curves were shifted to the right by WEB 2086. Platelet activating factor was a pulmonary hypertensive agent and contributed to the LPS-induced respiratory alterations.