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Background: Ethics consultations in a clinical setting can be challenging, specifically with respect to limiting therapeutic interventions in terminally ill patients. Some decisions will even be controversial., Objective: Can a clinical autopsy be used to confirm the recommendations given by the ethics committee, i. e. limitation of therapy to palliative care?, Material and Methods: We report an exemplary case of a patient with endocarditis and subsequent septic cerebral infarction. During treatment in the intensive care unit (ICU) two ethics consultations were held. Both times the patient' s clinical condition and prognosis were controversially discussed. The patient died after a recommendation had been given for supportive care. The subsequent autopsy, which is described in detail, confirmed a fatal set of symptoms with extensive destruction of the heart and disseminated brain infarcts., Conclusion: Clinical autopsies are crucial for an objective description of diseases and can corroborate the decision to limit therapeutic intervention in end of life care. It is a valuable tool in evaluating the quality of decision making in ethics counseling.

Neuropathological studies may contribute to the discovery of central nervous system complications after heart surgery and thus help to reduce the incidence of postoperative neurological or cognitive disturbances. We examined the brains of 262 such patients operated for coronary bypass, valve replacement, or heart transplantation. Circulatory disturbances (macro- and microhemorrhages, infarcts, subarachnoid hemorrhages, and hypoxemic brain damage) were present in 128 cases (49%), as the cause of death in 33 cases (12.6%). The infarcts were caused by local arteriosclerosis of brain arteries, arterial emboli originating from the operative sites or myocardial infarctions, or by fat emboli, foreign body emboli or megakaryocytic capillary emboli in rare cases. Inflammatory disturbances were present in 17 cases and consisted of fungal or bacterial septicopyemic changes (12) or of glial nodules (5) as the substrate of a viral or autoimmunencephalitis (Bickerstaff). An incidental finding was Alzheimer's disease in 37 cases (14% of the material) of elderly patients, often associated with cerebral amyloid angiopathy but not as cause of death or cause of macroscopic brain hemorrhage. Since we have conducted an autopsy study, there is a limitation to transfer the documented changes to the total group of post-cardiac surgery patients with neurologic and cognitive deficits. Contrary to some previous reports, histologically overt microembolic phenomena do not seem to play a major role in our material. On the other hand, careful scrutiny revealed non-fatal white matter microhemorrhages of varying frequency in the different groups, especially after valve operations. These as well as the occasional glial nodules, after resorption and microscarring, could well be the cause of slight neurologic and cognitive impairments.

We report on a 68-year-old patient who was admitted with hemiparesis and disorientation. Computed tomography showed several old, mostly lacunar infarcts. One week after admission, the patient became comatose. A repeat computed tomography revealed several new hypodense lesions in both hemispheres compatible with acute cerebral infarctions. Autopsy confirmed the diagnosis of numerous acute encephalomalacias of the same age which were found in different territories of the anterior cerebral circulation. Histologic examination showed the extraordinary result of multiple cholesterol emboli with a maximum in the peripheral leptomeningeal vessels. The source of the emboli was severe atherosclerosis with an ulcerated and thrombotic surface of the aorta and both carotid arteries. This case is remarkable because of its severe and synchronous emboli of cholesterol in several different cerebral territories. One has to suspect a so far unknown physical or metabolic factor responsible for the shower of emboli.

There is no information whether the BSE agent is introduced into the human food chain through contamination of the lungs of cattle with central nervous system tissue (CNS). Studies in the United Kingdom and in the USA showed that CNS tissue could contaminate the lungs after using pneumatic powered air injection stunners (e.g. "The Knocker") or after pithing. Thus, pithing was forbidden in the European Union since January 2001. In German abattoirs conventional cartridge-fired stunners (e.g. model by Schermer) are usually applied. Pithing was used up to December 2000 in approx. 75% of the German abattoirs. In the present study 323 lungs of cattle were analysed for CNS. The lungs were derived from cattle exclusive stunned by use of the knocker from Schermer. 60% of the lungs contained emboli which were tested with immuno chemistry as well as immuno histochemistry to detect CNS. Two of 108 pooled samples showed a faint immuno reaction in the anti-NSE and anti-GFAP immunoblot. Further two particles showed a faint reaction for NSE and GFAP in immuno histochemistry, thus suggesting the presence of CNS. Even though CNS tissue could not be shown in the histological investigation, we used our findings to estimate the worst case scenario for human BSE exposure risk (HER) by lung contaminated by CNS emboli. The content of CNS in the samples was estimated to be about 0.11% when the respective immuno reactions were calibrated against standards containing known brain concentrations. Under the assumption that only one lung in the pooled samples was contaminated with BSE-infected central nervous tissue, the HER was calculated to reach a maximum of 2.2 x 10(-5) CoID50/consumer after consumption of a sausage with a portion of 10% lung. The results of our study suggest that the contamination of the lung with CNS after using a conventional cartridge-fired stunner cannot be excluded, however, the incidence appears to be very low. In addition, presumed CNS emboli, if at all, are microscopically small. Furthermore the incidence of BSE in Germany is very low and lungs of cattle are usually not consumed. Thus we can judge the potential for human oral exposure after consumption of lungs of cattle which were stunned in Germany to be extremely low. A final assessment, however, is impossible as there is no knowledge about the minimum infectious dose for humans.

Background: The antiphospholipid (Huges) syndrome is a complication of connective tissue diseases characterized by thromboembolic occlusions of arterial and venous blood vessels., Case Report: At the age of 13, the patient developed connective tissue disease with arthritis and myositis. The course of her disease was characterized by frequent relapses despite immunosuppressive treatment. She developed deep venous thrombosis of her right leg as a manifestation of secondary antiphospholipid antibody syndrome at the age of 15 and was subsequently started on oral anticoagulation therapy. Approximately 10 months later, however, she decided to try alternative medicine and stopped both anticoagulation and immunosuppressive therapy. Only after 4 weeks she developed seizures followed by respiratory arrest with the need for cardiopulmonary resuscitation. Despite intensive care she died 2 days later with the signs of severe cerebral edema causing herniation of the brainstem. Autopsy confirmed the diagnosis of severe edema of the brain as a result of extensive thrombosis of all sinus veins., Conclusion: A complete sinus vein thrombosis is a rare manifestation of antiphospholipid antibody syndrome. The lethal thrombosis in this case occurred during a period of reactive hypercoagulability after termination of immunosuppressive and/or anticoagulation therapy. This case report underlines the need for long-term anticoagulation in patients with the antiphospholipid syndrome.

Arterioarterial thromboembolism from extracranial internal carotid artery (ICA) stenosis is an important pathogenic mechanism of ischemic stroke. However, even a high-grade ICA stenosis carries a greatly variable annual risk of stroke, as high as 13% following a recent occurrence of transient or minor cerebral ischemia or as low as 1-2% in clinically asymptomatic patients. There is increasing evidence that inflammatory processes play a central role in atherosclerosis and particularly in plaque destabilization converting chronic atherosclerosis into an acute neurological disorder. In thromboendarterectomy specimens from patients with high-grade ICA stenoses, the extent of inflammatory infiltration and the expression of matrixmetalloproteinase-9 correlated to clinical and ultrasonic features of plaque destabilization such as cerebral microembolism. Inflammation might become a new therapeutic target in symptomatic carotid artery disease.

The hematogenous spread of bacteria, fungi and protozoa may also reach the brain vessels, which happens mostly through septic emboli. From such an embolus a metastatic focal encephalitis and later a septic-embolic brain abscess may arise. The most frequently underlying infections that may cause septic emboli are bacterial endocarditis as well as bacterial infections of artificial heart valve prostheses. Congenital heart malformations with a right-to-left shunt also play here a certain role. Basically, however, all septic conditions and bacteriemias may cause septic-embolic brain abscesses. They occur frequently as multiple lesions. MRI is superior to CT in depicting the different stages of evolution from focal encephalitis, through the hardly encapsulated early abscess, to the formation of a membrane and later a dense fibrous capsule. The medical treatment of a brain abscess requires properly performed CT or MRI follow-up examinations in order to realize early enough a possible growing of such a lesion.