Diagnostic approaches to acute transfusion reactions.

The erroneous transfusion of ABO-incompatible red cells may lead to life-threatening hemolysis and complement-induced shock, resulting in death in less than 10% of cases (acute hemolytic transfusion reaction, AHTR). Identification of the cause of an erroneous transfusion is accomplished in nearly all incidents merely by checking the identity of the patient, blood sample and blood bag. The erroneous transfusion is confirmed by serological and--in the case of a fatality- immunohistochemical methods. The differential diagnosis should rule out transfusion-related acute lung injury (TRALI), other immunologically triggered causes such as febrile nonhemolytic transfusion reaction (FNHTR) or allergic reactions, but also nonimmunological causes such as bacterial contamination of the blood components, transfusion-associated circulatory overload (TACO) and other rare events such as citrate overload or embolism (by air or debris). In the case of a fatality, evaluation of a patient's medical records, serological and microbiological analyses, autopsy and histology, taken together, clarify questions of causality.

Macrophage subsets in mechanical brain injury (MBI)--a contribution to timing of MBI based on immunohistochemical methods: a pilot study.

Cortical hemorrhages as a consequence of closed mechanical brain injury (MBI) trigger an inflammatory response including a distinct increase of macrophages. According to published data this reactive macrophage population is heterogenous as to their immunological properties. The expression of certain immunohistochemically detectable epitopes of macrophages, however, may correlate with the posttraumatic interval (PTI). In a pilot study, 50 selected cases of cortical hemorrhages with 1 min to 1.5 years PTI were examined by light microscopy and macrophages were labeled with CD68-, HLA-D-, HAM-56-, LN-5-, and 25F9-antibodies, while hemosiderin was detected by a Prussian-blue reaction. Qualitative and semiquantitative investigations were performed. The semiquantitative study included 5 different classes. The results of the study revealed a distinct timetable of the appearance of macrophages labeled with certain antibodies. While HLA-D immunoreactivity was detected after a PTI of 6h in the cortex and white matter bordering the traumatic hemorrhage, CD68 immunopositive macrophages were present after 12h, LN-5 and HAM-56 after 48h, and 25F9 within 10d. Hemosiderin-containing macrophages were detectable within 100h in the same region. Within the hemorrhage itself a certain immunoreactivity of macrophages starts several hours before: CD68 after 3h, LN-5 after 24h, HAM-56 after 31h, hemosiderin after 76h, and 25F9 after 4d. For forensic purposes these observations are of crucial importance because the time course of the appearance of certain immunopositive macrophages labeled with different antibodies allows a differentiated timing of contusional injuries; however, the cause of this different immunopositive reaction remains unexplained. The observed time dependency of different macrophage antigen expressions in cortical hemorrhages after closed head injury is a suitable method to estimate the PTI and will allow a forensic reliable estimation if future investigations are extended on higher numbers of cases and/or additional markers.

Medicolegal assessment of blood transfusion errors--an interdisciplinary challenge.

Given a current total incidence of erroneously administered blood transfusions of 1:12,000-1:36,000 (AB0 incompatible 1:38,000), the percentage of lethal outcomes ranges between 2 and 5%; i.e. the sole fact of an erroneous transfusion does not mandatorily result in a causal connection with lethal outcome, which can give rise to problems in the medicolegal assessment. We report on the conception and results of a novel interdisciplinary approach to assess the lethal significance of blood transfusion errors. Besides autopsy, histological investigation and immunohistochemical detection of AB0 incompatible foreign red blood cells in autopsy specimens, transfusion medicine investigations offer the opportunity to assess several immunohaematologic features. We assessed the immunohaematologic gel card ("microcolumn") technique for suitability in the forensic assessment of an AB0 incompatible transfusion incident in a septic patient, who had had no history of previous blood transfusions, with lethal outcome. After such an erroneous transfusion had been simulated in vitro, pre-transfusion and cadaver patient blood samples (p.m. interval: 3 days) were analysed. Amongst other things, IgG-loaded erythrocytes were detected in pre- and post-transfusion samples; the presence of irregular antibodies directed against blood group antigens and anti-A or anti-B isoagglutinins, respectively, especially in the pre-transfusion sample was ruled out. Besides the demonstration of AB0 incompatible red blood cells in the cadaver blood sample, blood group incompatibilities other than AB0 were excluded. With regard to the cause of death, in synopsis with autopsy findings and clinical symptoms, the results did not allow for a final discrimination between the impact of the pre-existing septic inflammatory response syndrome and sepsis, respectively, and potential lethal effects of a (haemolytic) transfusion reaction. Besides pre- and post-transfusion compatibility testing in clinical transfusion medicine as required by German National Guidelines, the reported immunohaematologic investigations offer an important supportive tool for the forensic assessment of lethal erroneous transfusions and investigation of blood samples of survivors of transfusion incidents as well. Besides established morphological techniques, they allow for a certain evaluation of the pathophysiological impact of transfusion incidents as well as a diversified assessment of immunohaematologic features beyond the AB0 system.

[Diagnosis of acute transfusion reactions]. / Diagnose akuter Transfusionsreaktionen.

The erroneous transfusion of AB0-incompatible red cells may result in hemolysis and complement-mediated shock (acute hemolytic transfusion reaction, AHTR), leading to death in less than 10%. The mistake will be detected by re-checking the patient's and the blood product's identity. Evidence of the incompatible transfusion is supplied by serology and, in cases of a fatal outcome, by immunohistochemistry. Differential diagnoses to be distinguished from AHTR are other immunologically mediated events like the most important transfusion-related acute lung injury (TRALI), febrile non-hemolytic transfusion reaction (FNHTR), allergic transfusion reactions, along with a variety of nonimmunologic incidents like transfusion-transmitted bacterial infections, hypervolemia, and other rare events such as citrate reaction, air embolism, and foreign body embolism. If the outcome is lethal, the question of causality has to be answered by a comprehensive evaluation including the clinical data as well as serological, microbiological, autoptic, and histological findings.

Increase in nerve fibers and loss of mast cells in polycystic and postmenopausal ovaries.

OBJECTIVE: To quantify nerve fibers and mast cells in human ovaries at different functional stages. DESIGN: Retrospective study. SETTING: Research laboratory of the university. SPECIMEN(S): 8 human ovaries in the follicular (cyclic) phase, 7 polycystic ovaries, and postmenopausal ovaries with (n=5) or without (n=7) hyperthecosis. MAIN OUTCOME MEASURE(S): Single- and double immunohistology for the S100 antigen in glial cells of autonomic nerve fibers, for chymase and tryptase in mast cells, and for the common leukocyte antigen on leukocytes. Histometric evaluation was also performed. INTERVENTION(S): None. RESULT(S): Polycystic ovaries contained significantly more S100-positive nerve fibers in the corticomedullary region than did cyclic ovaries (mean +/- SD per 2-mm(2) area, 476 +/- 136 and 224 +/- 133; P<.01). Postmenopausal ovaries with or without hyperthecosis had the highest density of nerve fibers. In cyclic and polycystic ovaries, more tryptase-positive mast cells than chymase-positive mast cells were found in the interstitial cortex and the medulla. In cyclic ovaries, areas with a moderate density of nerve fibers contained many mast cells. Hence, with increasing nerve fiber density in polycystic ovaries, the number of mast cells decreased strikingly compared with cyclic ovaries (p<.001). Almost no mast cells were seen in postmenopausal ovaries with and without hyperthecosis. The number of leukocyte antigen-positive leukocytes was similar in all groups. CONCLUSION(S): The high density of nerve fibers in polycystic and postmenopausal ovaries, together with a conspicuous decrease in mast cells, indicates altered neuroimmune communication.

Lesion-associated accumulation of uPAR/CD87- expressing infiltrating granulocytes, activated microglial cells/macrophages and upregulation by endothelial cells following TBI and FCI in humans.

Urokinase-type plasminogen activator receptor (uPAR/CD87) together with its ligand, urokinase-type plasminogen activator (uPA), constitutes a proteolytic system associated with tissue remodelling and leucocyte infiltration. uPAR is a member of the glycosyl phosphatidyl inositol (GPI) anchored protein family. The functional role of uPAR comprises fibrinolysis by conversion of plasminogen to plasmin. In addition, uPAR promotes cell adhesion, migration, proliferation, re-organization of the actin cytoskeleton, and angiogenesis. Furthermore, uPAR is involved in prevention of scar formation and is chemoattractant to macrophages and leucocytes. In order to investigate the pathophysiological role of uPAR following human CNS injury we examined necrotic brain lesions resulting from traumatic brain injury (TBI; n = 28) and focal cerebral infarctions (FCI; n = 17) by immunohistochemistry. Numbers of uPAR+ cells and uPAR+ blood vessels were counted. Following brain damage, uPAR+ cells increased significantly within 12 h, reached a maximum after 3-4 days and remained elevated until later stages. uPAR was expressed by infiltrating granulocytes, activated microglia/macrophages and endothelial cells. Numbers of uPAR+ vessels increased in parallel subsiding earlier following FCI than post TBI. The restricted, lesion-associated accumulation of uPAR+ cells in the brain parenchyma and upregulated expression by endothelial cells suggests a crucial role for the influx of inflammatory cells and blood-brain barrier (BBB) disturbance. Through a failure in BBB function, uPAR participates in formation of brain oedema and thus contributes to secondary brain damage. In conclusion, the study defines the localization, kinetic course and cellular source of uPAR as a potential pharmacological target following human TBI and FCI.

[Distribution of morphine and morphine glucuronides in body tissue and fluids--postmortem findings in brief survival]. / Verteilung von Morphin und Morphinglucuroniden in Körpergeweben und -flüssigkeiten--Postmortale Befunde bei kurzer Uberlebenszeit.

An intoxication following administration of morphine, tramadol and atracurium in a suicide case is reported. The route of administration and the amount of the particular drug were known from the investigation of the death scene and the findings of the postmortem examination. Tramadol was present in the gastric contents as well as in blood, liver, kidney and brain samples, whereas the drug could not be detected in muscle. All body fluids and tissues investigated contained morphine as well as its 3- and 6-glucuronides with the exception of muscle tissue. The concentrations of morphine and its glucuronide metabolites were determined by LC/MS following solid phase extraction. Interestingly, the concentration of M6G in brain, liver and kidney were close to the concentration of M3G in the particular tissue. This phenomenon might be explained by a preferential hydrolysis of M3G or by a preferential formation of M6G postmortem. Measurement of morphine and M6G in femoral blood and cerebrospinal fluid may be a useful indicator in rapid deaths.

Long-term expression of heme oxygenase-1 (HO-1, HSP-32) following focal cerebral infarctions and traumatic brain injury in humans.

Extracellular heme derived from hemoglobin following hemorrhage or released from dying cells induces the expression of heme oxygenase-1 (HO-1, HSP-32) which metabolizes heme to the gaseous mediator carbon monoxide (CO), iron (Fe) and biliverdin. Biliverdin and its product bilirubin are powerful antioxidants. Thus, expression of HO-1 is considered to be a protective mechanism against oxidative stress and has been described in microglia, astrocytes and neurons following distinct experimental models of pathological alterations to the brain such as subarachnoidal hemorrhage, ischemia and traumatic brain injury (TBI) and in human neurodegenerative diseases. We have now analyzed the expression of HO-1 in human brains following TBI (n = 28; survival times: few minutes up to 6 months) and focal cerebral infarctions (FCI; n = 17; survival time: < 1 day up to months) by immunohistochemistry. Follwing TBI, accumulation of HO-1+ microglia/macrophages at the hemorrhagic lesion was detected as early as 6 h post trauma and was still pronounced after 6 months. In contrast, after FCI HO-1+ microglia/macrophages accumulated within focal hemorrhages only and were absent in non-hemorrhagic regions. Further, HO-1 was weakly expressed in astrocytes in the perifocal penumbra. In contrast to experimental data derived from rat focal ischemia, these results indicate a prolonged HO-1 expression in humans after brain injury.

[Fatal child neglect in West Germany 1 January 1985 to 2 October 1990. Results of a multicenter study]. / Tödliche Kindesvernachlässigung in der Bundesrepublik Deutschland im Zeitraum 1.1.1985 bis 2.10.1990. Ergebnisse einer multizentrischen Studie.

UNLABELLED: Up to now reliable data were available on cases of lethal child neglect in the area of the Federal Republic of Germany prior to reunification (the former West Germany). In a multicenter study we therefore examined the police and court records for such cases occurring in the period from 1 January 1985 to 2 October 1990 in nearly the entire area of Federal Republic of Germany. RESULTS: The study center received information on 19 cases of lethal child neglect. Extrapolated to all institutes of legal medicine, this corresponds to 20 cases and thus 3.5 cases a year in the whole of West Germany in the period studied. There is to be added a dark-field which cannot be limited more precisely. However, the cases of fatal child neglect might have occurred much more seldom than fatal child abuse caused by use of physical violence. Slightly more than half the victims were younger than 1 year, the oldest one was 7 10/12 years old. Most frequently the children died of starvation and thirst. Mostly the mothers/nursing mothers killed the child alone or together with the victim's father/stepfather. In the majority of the cases there was not a close affection between parents and child. Nearly 30% female/male perpetrators suffered from chronic alcohol abuse. Only 15 (= 56%) of 27 female/male perpetrators were sentenced to imprisonment (period between 7 months on probation and 10 years). Mitigation circumstances existed for nearly half the persons sentenced to imprisonment. It is true that child neglect is a rarer crime, but the experts of legal medicine always have to indicate errors made during the external inspection of the corpse (among others failures to see indications of neglect).

Pontine axonal injury after brain trauma and nontraumatic hypoxic-ischemic brain damage.

Experimental studies have shown that diffuse axonal injury is usually induced by positive or negative acceleration mechanisms. In order to determine the reliability of axonal injury (AI) as a marker of this type of traumatic insult, we compared cases of trauma-induced focal cortical hemorrhage without dural involvement (n = 67) with cases of trauma-induced subdural bleeding without cortical hemorrhage (n = 26). Both groups exhibited a wide range of post-traumatic survival times. The injuries in the first group were caused mainly by direct impact to the head, those in the second by acceleration/deceleration mechanisms. The investigations were based primarily on immunohistochemical demonstration of antibodies targeted to beta-amyloid precursor protein (beta-APP) in the pons as a marker of AI and the results were assessed semiquantitatively. No significant differences were found between the two groups. In both groups AI was detected in 80-100% of cases with survival times of more than 3 h and two thirds of all positive cases showed pronounced positivity. Additional comparison of cases of brain death due to mechanical trauma (n = 14) with cases of brain death due to non-mechanical trauma (n = 18) also disclosed no significant intergroup differences. Finally, investigations of the pons in cases of non-traumatic death due to cerebral hypoxia/ischemia (n = 51) demonstrated AI with the same frequency as in the other groups, although the expression tended to be less pronounced. Our results confirm that beta-APP expression in the pons is a reliable indicator of AI but does not discriminate between injuries caused by traumatic strain or shearing mechanisms and secondary damage due to cerebral hypoxia/ischemia or edema. In the large majority of cases with prolonged post-traumatic survival, it can therefore be assumed that AI in the pons is the consequence of primary and/or secondary events or a combination of both, as is common in non-missile head injury survived for more than 90-120 min. Therefore, positive differentiation of the type of biomechanical event based on this criterion alone is not possible.

[Fatal child abuse (caused by physical violence) in Germany during 1 January 1985 to 2 October 1990. Results of a multicenter study]. / Tödliche Kindesmisshandlung (durch physische Gewalteinwirkung) in der Bundesrepublik Deutschland im Zeitraum 1.1.1985 bis 2.10.1990. Ergebnisse einer multizentrischen Studie.

UNLABELLED: No reliable data are available on cases of lethal child abuse (by active force) in the area of Federal Republic of Germany prior to reunification (the former West Germany). In a multicenter study we therefore examined the police and court records for such cases occurring in the period 1 January 1985 to 2 October 1990 in nearly the entire area of Federal Republic of Germany. RESULTS: The study center received information on 58 cases of lethal child abuse. Extrapolated to all institutes of legal medicine, this corresponds to 62 cases in all of West Germany in the period studied. An approximately equal number of unreported cases should be added to this figure. Including unreported cases, at least 20 cases of lethal child abuse occurred per year; thus only one in every two cases ever came to light. Almost two thirds of the victims were younger than one year old. At autopsy 59% exhibited signs of repeated abuse at autopsy. By far the most common cause of death was direct impact from a blunt object, usually to the head. Mostly, the male person to whom the victim relates most closely (father, stepfather, partner of the mother) has killed the child. Twenty-one of the 74 persons charged saw the charges against them dropped or were acquitted due to lack of evidence; 51 received sentences ranging from one year probation to life. In the remaining two cases the outcome of the trial was unknown. Signs of abuse were readily apparent at autopsy in almost all cases. The high number of unreported cases underscores the need to educate medical students and practicing physicians to be on the look-out for signs of abuse and argues for an increase in the rate of autopsy.

[Fatal incidences during arrest of highly agitated persons]. / Tödliche Zwischenfälle bei der Festnahme höchstgradig erregter Personen.

We report on four cases of sudden circulatory arrest during the physical restraint of extremely excited and repugnant men by the police. Three persons died, and one became apallic. The excited states resulted from acute schizophrenic disorder in one case, from intoxications (ethanol and drugs including cocaine respectively) in two others, and from encephalitis in the fourth case. In only one case one of the police officers was condemned for involuntary mansloughter, responsability was excluded in the remainder. Similar lethal events in "excited delirium" are given in the American literature, the main etiologic factors being acute psychosis and cocaine intoxication. Most of these events occurred, differing from ours, under "hogtying" which is a technique of physical restraint in a prone position with the wrists and ankles bound behind the back. These events are thought to be cardiac in origin and to result from oxygen-consuming motor hyperactivity, excessive catecholamine release, and impaired breathing. Police officers are recommended to restrict all measures of restraint to a mininum in extremely excited persons, and to avoid any compression of the trunk or neck. A continuous monitoring for vital signs is postulated in order to recognize a medical incident as quick as possible.

Axonal injury--a diagnostic tool in forensic neuropathology? A review.

We used beta-amyloid precursor protein (beta-APP) to investigate our own forensic neuropathological case material (n = 252) in light of the current literature on the phenomenon "axonal injury" (AI) to determine the incidence, specificity and biomechanical significance of AI and its significance for determining vitality and survival time. The case material consisted of cases of fatal nonmissile closed-head injury (n = 119), gunshot injury (n = 30), fatal cerebral ischemia/hypoxia (n = 51), brain death caused by mechanical trauma (n = 14) or nonmechanical injury (n = 18), and acute hemorrhagic shock (n = 20). AI was observed in 65% to 100% of cases of closed-head injury, fatal cerebral ischemia/hypoxia, and brain death with a survival time of more than 3 h; AI could not be detected in the cases of acute hemorrhagic shock. A statistically significant difference between traumatically and nontraumatically induced (nondisruptive) AI was not found. There was no statistical evidence of a correlation between AI and the different types of external force, since AI could be demonstrated after both acceleration/deceleration injuries and traumatic impact. Therefore, biomechanical inferences for reconstruction purposes are not possible. On the other hand, beta-APP was found to be a definite marker of vitality. In our material, cases with a posttraumatic interval of under 180 min did not express beta-APP. Moreover, the literature shows that the posttraumatic interval can be determined by other methods for demonstration of AI such as by ubiquitin immunostaining (360 min), silver staining (15-18 h), hematoxylin and eosin staining (about 24 h), or by demonstration of a microglial reaction (about 4 to 10 days) or of a few remaining isolated bulbs, without accompanying fibers, which can be detected after a survival time of up to 17 months.

Insulin injection sites: morphology and immunohistochemistry.

In a case of insulin suicide in a nondiabetic woman, insulin was detected in routinely formalin fixed and paraffin embedded subcutaneous injection marks, in spite of a post-morterm interval of 24 days. Around birefringent crystalline material, probably zinc phosphate, immunohistochemistry revealed granular insulin depots as well as an insulin staining along the lipocyte membranes. A cellular reaction of granulocytic character was present, with an uptake of insulin by inflammatory cells.

[Cadaver lipid: various origins add to the difficulty of assessing postmortem time]. / Leichenlipid: Unterschiedliche Entstehungsarten erschweren zusätzlich die Abschätzung der Leichenliegezeit.

Establishing the length of time since death is particularly difficult in corpses showing advanced putrefaction. One particular sign of advanced decay is the formation of adipocere, as observed mainly in drowned bodies or following a long period of storage under airtight conditions. During storage in an open, damp environment (e.g. water) the formation of adiopocere becomes visible after approximately 3-6 months and can be found in more extensive form after approximately one year. In this state bodies show evidence of a partly waxlike and partly pasty condition. Continued storage ultimately results, among other things, in further decomposition due to the action of microorganisms from the surrounding area-even if this is chronologically delayed. An exception is provided by the formation of adipocere under air-tight conditions (e.g. wrapped in plastic material or in mass graves). Initially autolysis and heterolysis also occur, involving the release of fatty acids from the lipids produced naturally in the body. As a result of the subsequent hydrogenation of the fats by the action of bacterial enzymes, the unsaturated fatty acids are partially converted into saturated fatty acids. As the fatty acids released in large quantities during adipocere formation clearly have a bactericidal effect, further bacterial decomposition is stopped at this early adipocere stage. Additional microorganisms from outside can no longer infiltrate when this hermetic seal is in place. In addition, the lack of calcium (e.g. from water or moist earth) can be a reason for the fact that further adipocere development, leading to wax-like hardening of the fat, is arrested. The soft parts of the body retain a soft, viscous consistency. Thus the condition of the body can remain constantly preserved over many years and no longer allows a reliable estimate to be made of the period of time since death.

[Sudden fatalities in mechanically restrained patients]. / Plötzliche Todesfälle mechanisch fixierter Patienten.

We report on 7 nursing home or hospital patients who died suddenly and unexpectedly during physical restraint. Four of the patients were found dead hanging beside their beds, with their waist restraints displaced to the thorax. In spite of a variety of preexisting diseases, asphyxia by thorax compression was the most probable cause of death. Three other patients, when falling out of their beds, were strangulated by the head opening of a nursing bedcover fixed to the bed. In all instances the fatal accidents resulted from improper handling of the restraint devices, namely from the omission of bed rails as well as of the obligatory waist belt lateral fixations. The bedcover type involved in three fatalities is destined for care purposes but not licensed as a restraint device. Physical restraint fatalities can be avoided to a large extent if the producers' instructions are strictly observed, and only especially trained and supervised personnel is admitted to this field of duties.

[Fatal sodium azide poisoning in a hospital: a preventable accident]. / Tödliche Natriumazid-Vergiftung im Krankenhaus: ein vermeidbarer Zwischenfall.

A case of fatal sodium azide poisoning is reported. From the hospital staff, a 57 year old patient had obtained 1 g of sodium azide in order to put it as a preservative, in his 24 hour urinal. Probably due to an error, he swallowed the total dose. A cardiovascular collapse was cause of the death after five hours of intensive treatment and reanimation. Azide anions were found in blood (traces, less than 0.5 mg/L), vitreous (10 mg/L) and cerebrospinal fluid (20 mg/L). The use of sodium azide for disinfection of urine samples should be regarded as obsolete. Less toxic substances for disinfection are available. To avoid chemical disinfection, urine samples can be kept at 4-8 degrees C prior to rapid analysis.

[Catecholamines, myofibrillary degeneration of the heart muscle and cardiac troponin T in various types of agony]. / Katecholamine, Myofibrilläre Degeneration des Herzmuskels und Kardiales Troponin T bei verschiedenen Agonietypen.

The stress of agony (the death struggle) induces a rise in serum catecholamines. High doses of catecholamines cause myofibrillar degeneration (MFD), a form of cardiac injury. Severely damaged cardiac myocytes release troponin T (TnT), a myofibrillar cardiac protein, into the circulation. We studied serum catecholamine levels, MFD and TnT in 119 medico-legal autopsy cases. Catecholamine levels increased with the duration of agony: In the instantaneous death cases, the levels were similar to levels in humans at rest, whereas the levels in prolonged agony were comparable to concentrations found in humans in acute maximal stress. Still, it was not possible to infer the duration of agony from the catecholamine level in an individual case. The exceptionally high dopamine levels found in the group 'resuscitation and/or intensive care before death 'were most likely caused by antemortal treatment with dopamine. Slight MFD was diagnosed in nearly all hearts; its severity was neither related to catecholamine levels nor to duration of agony. TnT, not found in blood of healthy people, was present in nearly all postmortem samples, indicating autolytic effects. Heart blood contained more TnT than femoral blood. We could not detect a relationship between the serum cardiac troponin T level and MFD; but cardiac deaths had significantly higher levels of TnT in heart blood than deaths from other causes. The postulated interrelation between catecholamines, MFD and TnT was not evident from the results.

[Errors in treatment of soft tissue phlegmon : expert assessment and forensic evaluation]. / Fehler bei der Behandlung von Weichteilphlegmonen: Begutachtung und rechtliche Würdigung.

In ten cases of soft part phlegmons resulting in death (8) and amputation (2) respectively, various types of medical malpractice were evident. The diagnosis was missed, or the disease was correctly diagnosed but underestimated. Typical therapeutic mistakes were the omission of bacteriological investigations and of the proper antibiotical therapy, a delayed hospital admission, or a delayed or insufficient surgical intervention. These errors however could never be proved to have caused the unfavorable outcome in view of the doubtful prognosis of soft part phlegmons even under proper treatment. Thus, evident malpractice never resulted in a condemnation for bodily injury or involuntary manslaughter.

ABH and Lewis immunohistochemistry of the human eye.

ABH and Lewis antigens are detected by immunohistochemistry exclusively in the anterior cornea epithelium and in the conjunctiva bulbi, but not in the ciliary body, in the retina, or in the vitreous body of the eye. The ABH antigens found in the vitreous humor by the absorption elution technique (Rordorf et al., Forensic Sci. Int. 41, 1989, 111-116) are probably glycosphingolipids, which are not detected by immunohistochemistry. They may come from the plasma of uveal blood vessels, or be produced by local cells.