Criteria for the diagnosis of heat-related deaths: National Association of Medical Examiners. Position paper. National Association of Medical Examiners Ad Hoc Committee on the Definition of Heat-Related Fatalities.

The National Association of Medical Examiners Ad Hoc Committee on the Definition of Heat-Related Fatalities recommends the following definition of "heat-related death": a death in which exposure to high ambient temperature either caused the death or significantly contributed to it. The committee also recommends that the diagnosis of heat-related death be based on a history of exposure to high ambient temperature and the reasonable exclusion of other causes of hyperthermia. The diagnosis may be established from the circumstances surrounding the death, investigative reports concerning environmental temperature, and/or measured antemortem body temperature at the time of collapse. In cases where the measured antemortem body temperature at the time of collapse was > or = 105 degrees F (> or = 40.6 degrees C), the cause of death should be certified as heat stroke or hyperthermia. Deaths may also be certified as heat stroke or hyperthermia with lower body temperatures when cooling has been attempted prior to arrival at the hospital and/or when there is a clinical history of mental status changes and elevated liver and muscle enzymes. In cases where the antemortem body temperature cannot be established but the environmental temperature at the time of collapse was high, an appropriate heat-related diagnosis should be listed as the cause of death or as a significant contributing condition.

Heat-related deaths in Philadelphia--1993.

A study of heat-related deaths associated with the 1993 heat wave in Philadelphia, Pennsylvania, was conducted. Most of these deaths were in the susceptible elderly with preexisting natural diseases who lived alone without air conditioning in upstairs bedrooms with windows shut, thus creating an even hotter environment. These excessive deaths under such conditions did not meet the standard clinical criteria for hyperthermia because of varying postmortem intervals. Therefore, the authors stress the utility of a postmortem definition of heat-related death to better define the magnitude of health risk posed by hot weather and warn public health and other agencies to take preventative measures.

Involvement of mast cells in sudden infant death syndrome.

The pathogenesis of sudden infant death syndrome (SIDS) is elusive and probably multifactorial. The occurrence of mast cell activation in SIDS was assessed in this study by measuring concentrations of tryptase, a neutral protease produced mainly by mast cells, in postmortem sera from term infants with SIDS and from age-matched control infants who died unexpectedly at home from a known cause. Tryptase levels were significantly higher in the 50 infants with SIDS than in the 15 control infants (p = 0.0004). Forty percent of the infants with SIDS and none of the control infants had a tryptase level greater than 10 ng/ml, the threshold chosen to indicate premortem mast cell activation. An infant with SIDS had a 20-fold higher chance of having an elevated tryptase level compared with a control infant. The postmortem interval did not influence these results. Thus mast cell-mediated anaphylaxis is likely to be the pathogenetic mechanism involved in some but not all SIDS cases. Recognition of this pathway as operative in SIDS should facilitate a more precise identification of the allergens involved, the processes leading to mast cell activation, and procedures to identify those infants at risk for anaphylaxis, and should, in time, lead to better therapeutic interventions aimed at preventing this specific cause of SIDS.

Cocaine-induced agitated delirium, forceful struggle, and minor head injury. A further definition of sudden death during restraint.

Four cases from the Philadelphia Medical Examiner's Office are presented and the literature is reviewed to define further the syndrome of sudden death occurring during cocaine-induced agitated delirium and struggle during restraint in individuals who also sustain minor head injury. The mechanism of death involves a terminal arrhythmia, most likely due to sympathetic sensitization of the myocardium by cocaine and the stress of struggle sometimes juxtaposed upon the stratum of minimal natural disease. In the cases described, the head injury in itself was insufficient to be a cause of death. Recognition of the role of the pharmacologic effect of cocaine and the lethal effects of its use in this setting is crucial.

Ocular and optic nerve hemorrhages in abused infants with intracranial injuries.

PURPOSE: To ascertain whether the pathology of the eye and optic nerve might be useful in determining the manner of death in infants who died after sustaining apparent nonaccidental intracranial injury. METHODS: Complete autopsies were performed on 13 infants who died of acute intracranial injuries after nonaccidental trauma. The infants were divided into two groups: nine with physical evidence of blunt trauma to the head, and four without detectable scalp or skull injury whose intracranial injuries were attributed to violent shaking (shaken baby syndrome). Six infants with no intracranial injuries who died suddenly from unidentifiable causes (the so-called sudden infant death syndrome) served as controls. RESULTS: Optic nerve sheath hemorrhage, most prominent in the subdural space, was present in all 13 infants with nonaccidental intracranial injury. Multilayered retinal hemorrhage was present in at least one eye of 11 of these 13 infants. The location and quantity of the intraocular and optic nerve sheath hemorrhages did not differ in those with external head trauma and those without scalp or skull lesions. A single control infant had a few erythrocytes in the nerve fiber layer of the anterior optic nerve of one eye. The remainder of the control infants did not have evidence of hemorrhage in the eye or optic nerve sheath. CONCLUSION: Histopathologic analysis of optic nerve sheath and intraocular hemorrhages may be helpful in distinguishing traumatic from non-traumatic causes of death in infants.

Cocaine in decomposed human remains.

From March 1988 through March 1990, at the Philadelphia Medical Examiner's Office toxicology laboratory, samples from 77 decomposed human bodies were tested for the presence of cocaine, employing gas chromatography/mass spectrometry (GC-MS). The material analyzed included decomposed soft tissue, bloody decomposition fluid, mummified tissue, maggots, and beetle feces. Twenty-two cases (28.6%) were positive for cocaine, many of these cases in states of advanced decomposition. These findings indicate the usefulness of testing decomposed tissue for cocaine in all cases where its presence is suspected. This is contrary to what might be expected, since cocaine is generally labile and rapidly broken down by both enzymatic and nonenzymatic mechanisms.

Passive inhalation of free-base cocaine ('crack') smoke by infants.

Cocaine is one of the most widely abused substances in the United States, in part due to the availability of its inexpensive alkaloidal free-base form, "crack". A variety of medical complications, including sudden death, are known to occur in the adult-user population, regardless of the route of cocaine administration. We report 16 cases of infant death registered by the Philadelphia (Pa) Medical Examiner's Office over a 2-year period (1987 through 1989), where toxicologic analyses revealed the presence of cocaine and/or its metabolite, benzoylecgonine. Scene investigation documented that these infants, shortly before death, had been exposed to environments that contained the smoke from crack. We conclude that the route of cocaine administration in this infant population was the passive inhalation of crack smoke. It is possible that the cocaine may have contributed to the death of these infants. Thus, in addition to the adult users, infants and children exposed to environments where crack is smoked may inhale cocaine and potentially suffer from its adverse effects.

Atherosclerotic cardiovascular disease and sudden deaths among young adults in Wayne County.

Based on postmortem records at the Wayne County Medical Examiners' Office from 1982 to 1986, autopsy results indicated that the deaths of 129 persons aged 20-34 resulted from heart disease: 51 of these deaths were attributed to atherosclerotic cardiovascular disease (ASCVD), 29 to hypertensive cardiovascular disease, 28 to cardiomyopathy, and 21 to other cardiac causes. The majority of the deaths due to ASCVD occurred among men, both black and white, followed by black women, and the incidence increased with age. All of these deaths due to ASCVD were sudden and accounted for all deaths due to ischemic heart disease in this age group among Wayne County residents. Diabetes mellitus, left ventricular hypertrophy, a history of seizures, and the recent ingestion of alcohol were all found to be associated with sudden death from ASCVD in this group. Obesity did not seem to be a significant factor. These data suggest that ASCVD is not rare as a cause of death in young adults and some of the risk factors identified in older subjects also operate in this age group.

Suicide by captopril overdose.

We report a case of a 75 year-old male who committed suicide by taking an overdose of captopril. He took approximately ninety 12.5 mg captopril tablets. The postmortem plasma concentration of captopril was 60.4 mg/L. A review of the medical literature revealed five cases of captopril overdose all from unsuccessful suicide attempts. To our knowledge, this is the first case report of fatal captopril overdose with the measurement of plasma concentration of the drug.

Microsurgical anatomy of the venous drainage into the superior sagittal sinus.

Ten unfixed human brains were examined under an operating microscope to evaluate the feasibility of reimplanting the parasagittal veins into the superior sagittal sinus. On average, there were 6.5 veins draining the surface of each hemisphere in the anterior frontal region, 3 veins draining each posterior frontal region, 4 veins draining each parietal region, and 1 vein draining each occipital region. The veins were most frequently 0.1 to 1.0 mm in diameter, but were as large as 3.0 mm in the anterior frontal and occipital regions, 3.5 mm in the parietal region, and 5.0 mm in the posterior frontal region. The mean vein length between the superior sagittal sinus and the first lateral attachment was 3.0 to 7.4 mm; individual veins were as long as 30.0 mm. The 20 hemispheres contained a total of 5 veins in the anterior frontal region, 7 veins in the posterior frontal region, and 8 veins in the parietal region that appeared to have an adequate diameter and length for microsurgical reimplantation into the superior sagittal sinus. The superior sagittal sinus had a mean width of 4.3 mm and depth of 3.6 mm in the midanterior frontal region and enlarged to a mean width of 9.9 mm and depth of 6.8 mm in the midoccipital region. In all sites, the sinus appeared to be structurally compatible with vein reimplantation. In 3 cases, veins 2.8 to 4.6 mm in diameter were reimplanted microsurgically into the sinus; in each case, the anastomosis was technically satisfactory and patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Anomalies and variations of the middle cerebral artery: a microanatomical study.

The microvascular anatomy of the main trunk and divisions of the middle cerebral artery was studied in 104 unfixed brain hemispheres injected with polyester resin and dissected under the operating microscope. The following anomalies and variations of the middle cerebral artery were found: fenestration (1 case; 1%), located on the first 4 mm of the main trunk of the middle cerebral artery; duplication (1 case; 1%), with vessels arising from the internal carotid artery; accessory middle cerebral artery (2 cases; 2%), originating on the A1 segment of the anterior cerebral artery; single-trunk type of middle cerebral artery (4 cases; 4%), with no division of its main trunk; quadrifurcation (4 cases; 4%), in which the main trunk of the middle cerebral artery divided into four secondary trunks. The clinical implications of these anatomical findings are discussed, and photographs of representative specimens illustrate the anomalies.

Hypernatremia due to amniotic fluid embolism during a saline-induced abortion.

A case of fatal amniotic fluid embolism leading to hypernatremia during a hypertonic saline-induced abortion is reported. This sequence of events has not, to our knowledge, been previously reported. Hypernatremia as a diagnostic aid for amniotic fluid embolism is discussed.

PIP: A case of fatal amniotic fluid embolism leading to hypernatremia following instillation of hypertonic saline is reported. This complication of saline-induced abortion has not been reported previously in the literature. The patient was an obese 16-year-old black female, gravida 1, para 0, whose gestational age at time of abortion was 21.5 weeks. 26 hours after the procedure, which was well tolerated by the patient, she complained of severe abdominal cramps with projectile expulsion of amniotic fluid. Generalized convulsions and shaking followed and the patient went into shock. Death occurred within 2 hours. At autopsy, microscopic examination of lungs revealed pulmonary edema with marked vascular congestion, focal areas of atelectasis, and intra-alveolar hemorrhages. Positive test results for mucin in a few pulmonary vessels and intra-alveolar capillaries confirmed a diagnosis of amniotic fluid embolism. There was marked congestion of the blood vessels of the kidneys, liver, brain, and spleen. Amniotic fluid embolism represents about 10% of the maternal mortality in the US; however, this complication generally occurs during labor, delivery, and the immediate postpartum period. Moreover, most such cases occur in older, multiparous women in the 3rd trimester of pregnancy. It is possible that hypernatremia following amniotic fluid embolism occurs more frequently than reported. Routine examination of blood during pregnancy and of the vitreous humor in cases of pregnancy-related mortality could be useful in establishing a diagnosis of amniotic fluid embolism.

Microanatomy of the posterior communicating artery.

Fifty unfixed cerebral hemispheres were injected with polyester resin and dissected under the operating microscope to show the anatomy of the posterior communicating artery (PCoA). There was a single PCoA in every hemisphere. Eleven (22%) were of fetal origin, and 17 (34%) were hypoplastic. Infundibular dilatations were found in 5 (10%) of the arteries. The outer diameter (OD) of the PCoA at its origin was 1.5 +/- 0.8 mm on the right and 1.6 +/- 0.6 mm on the left. At the junction of the PCoA with the P1 segment of the posterior cerebral artery, the PCoA had an OD of 1.4 +/- 0.7 mm on the right side and 1.6 +/- 0.6 mm on the left. The total length of the PCoA was 12.7 +/- 3.2 mm on the right and 12.5 +/- 1.7 mm on the left side. PCoA branches originated from the superior (36%) or lateral (64%) surface of the PCoA and coursed superiorly, posteriorly, or laterally. These vessels supplied the paramedian perforated substance (21%), the tuber cinereum (16.8%), the sulcus between the optic tract and the tuber cinereum (14.4%), the circuminfundibular anastomosis (11.5%), the mamillary bodies (8.4%), the sulcus between the optic tract and the cerebral peduncles (7.6%), and the cerebral peduncles (5.7%). The largest and most constant branch of the PCoA was the premamillary artery. The number and size of the branches from the PCoA were independent of the size of the parent artery.

Surgical anatomy of the arteries of the posterior fossa.

The development of revascularization for vertebrobasilar ischemic events has created a need to identify the best sites at which to perform bypass procedures. Since the occlusive process may selectively affect various levels of the vertebrobasilar tree, sites in different vessels must be used to reestablish flow distal to the area of occlusion. Twenty-seven unfixed human brains were obtained 4 to 8 hours post mortem, and the vertebrobasilar system was injected with polyester resin. Under a surgical microscope the outer diameter, length, and site of origin of major branches were recorded for the following arteries: vertebral, basilar, posterior inferior cerebellar (PICA), anterior inferior cerebellar (AICA), superior cerebellar (SCA), and posterior cerebral (PCA). The ideal sites for an anastomosis were identified as the pretonsillar segment of the PICA, the second portion of the AICA, the perimesencephalic segment of the SCA, and the perimesencephalic part of the PCA. Based on the anatomical observations reported here, these were the best sites because of their outer diameter, degree of mobility, least number of branches, and frequency of occurrence. Use of two of these arteries, however, may pose potential problems: although the PCA has an ideal outer diameter, it also has numerous branches to the brain stem in its most accessible site in the perimesencephalic area; and the PICA is not consistently present, being found in only 75% of the 27 specimens studied.

Microanatomy of the anterior cerebral artery.

The microanatomic features of the anterior cerebral artery were studied in 30 unfixed human brains which were injected with tinted polyester resin via cannulation of the internal carotid arteries under microscopic dissection. The outer diameter, length, and number of perforating branches were measured for each of the following vessels: anterior cerebral artery (proximal A1 segment, distal A2 segment), anterior communicating artery, and recurrent artery of Heubner. The perforating branches of the proximal segment of the anterior cerebral artery penetrated the brain at the anterior perforated substance, lateral chiasm, and optic tracts. The perforating branches of the anterior communicating artery penetrated the brain at the lamina terminalis, anterior perforated substance, and medial chiasm. The first 5 mm of the distal anterior cerebral artery (A2) had perforating branches penetrating the brain at the gyrus rectus and olfactory sulcus. The recurrent artery of Heubner originated from the A2 segment of the anterior cerebral artery in 57% of the cases, from the anterior cerebral artery-anterior communicating artery junction in 35%, and from the A1 segment in 8%. The depth of the interhemispheric fissure at the genu was 36.0 +/- 0.5 mm and at the midbody of the corpus callosum, 35.0 +/- 0.5 mm. Extension of the dissection to approach the anterior communicating artery from the genu of the corpus callosum using the anterior interhemispheric route was an additional 31.7 +/- 0.7 mm. The callosal arterial supply from the anterior cerebral artery showed short callosal branches in all brain specimens and long callosal vessels in 10% of the specimens.

Anterior cerebral artery reconstruction.

Anterior cerebral artery end-to-end, end-to-side, and side-to-side anastomoses and grafting procedures including bypass and interposition using segments of the posterior cerebral artery harvested from the same specimen were performed. The reconstruction procedures were accomplished experimentally with the A1 and A2 segments of the anterior cerebral artery, the recurrent artery of Heubner (RAH), and the orbitofrontal and frontopolar arteries in end-to-end or end-to-side anastomosis to the A1 segment. Side-to-side anastomoses between both A2 or A3 segments were completed without difficulty. We utilized the anatomical and experimental reconstruction data in the performance of three surgical procedures for aneurysms in this area. An A1 to A2 end-to-end anastomosis, an A2 to A2 end-to-side anastomosis, and an end-to-end anastomosis of the RAh were performed with no technical difficulties or complications. This study shows the feasibility of these microvascular reconstruction procedures in the anterobasal part of the interhemisphere, where cerebral aneurysms frequently develop.

Microvascular anatomy of the interpeduncular fossa.

An understanding of the microvascular anatomy of the midbrain and posterior diencephalon is essential in the surgical management of lesions in that region. A description of the arterial pattern of blood supply to these areas is the purpose of this study. Perforating branches originating from the last 5 mm of the basilar artery, from the initial 7 mm of both superior cerebellar arteries (SCA's), and from the initial segment (P1 segment) of the posterior cerebral artery were studied in 56 unfixed human cadaver brain hemispheres. The brains were injected with polyester resin. The perforating branches penetrated through a small space in the upper part of the interpeduncular fossa. The anterior two-thirds of this space was occupied by the posterior perforated substance (PPS), and the posterior one-third was the site of penetration of the branches that supply the inferior mesencephalon. The PPS was divided into anterior and posterior halves. The anterior half was perforated by the paramedian thalamic arteries (diameter 0.57 +/- 0.11 mm) while the superior paramedian mesencephalic arteries (diameter 0.20 +/- 0.06 mm) perforated the posterior half. The perforating arteries originated from a trunk exclusive to the anterior half in 30%, from a trunk supplying both halves in 57%, and from a trunk exclusive to the posterior half in 13% of specimens. There were 26 naturally occurring anastomoses between the perforating branches. The paramedian inferior mesencephalic arteries penetrating the posterior one-third of the upper part of the interpeduncular fossa arose from the P1 segment in 32% of the brains studied, from the proximal 7 mm of the SCA in 45%, and from the last 5 mm of the basilar artery in 23%.

Scald burns complicated by isopropyl alcohol intoxication. A case of fatal child abuse.

Scald burns are the most common type of thermal injury in child abuse. Death associated with nonaccidental burns, however, is uncommon. We recently investigated the case of a 4-year-old child who died from extensive body burns due to scalding. A contributory cause of death was isopropyl alcohol intoxication resulting from application of this chemical to the burns.

Spontaneous rupture of the spleen due to acquired immunodeficiency syndrome in an intravenous drug abuser.

A case of spontaneous rupture of the spleen is described in a 25-year-old woman with a history of intravenous drug abuse. At autopsy the spleen and the lymph nodes were soft, slightly enlarged, and markedly congested. They showed reactive follicular hyperplasia with increased cellularity and prominent vascularity of the red pulp and the interfollicular tissue. The postmortem serum was positive for antibodies to human T-cell lymphotropic virus type III. Other serologic tests were negative, including heterophile antibody test, test for antibodies to Epstein-Barr virus, and toxoplasmosis.

The perforating branches of the middle cerebral artery. A microanatomical study.

The perforating branches (PFB's) of the middle cerebral artery (MCA) were studied in 34 unfixed brain hemispheres which were injected with a polyester resin and dissected under the operating microscope. Five hundred and eight vessels were identified and their site of origin, branching pattern, outer diameter (OD), and length recorded. Four hundred and two PFB's (79%) originated from the main trunk of the MCA before its division; the remaining 106 vessels (21%) had their origin from branches of the MCA as follows: superior trunk, 43 vessels (8.5%); inferior trunk, 30 vessels (6%); middle trunk, four vessels (0.8%); early temporal branch, 27 vessels (5.3%); and early frontal branch, two vessels (0.4%). The number of PFB's in each hemisphere varied from five to 29 (mean 14.9 +/- 0.7 vessels). The great majority of PFB's (96%) originated along the proximal 17 mm of the MCA. The PFB's arising in the first 10 mm had a mean OD of 0.35 +/- 0.01 mm and a mean length of 9.25 +/- 0.19 mm, and those arising from the second 10 mm had a mean OD of 0.47 +/- 0.02 mm and a mean length of 16.67 +/- 1.4 mm. A clear distinction between a medial and lateral group of PFB's was present in only 14 hemispheres (41%). In nine hemispheres (26%), perforating vessels from the anterior cerebral artery (A1 segment) and from the recurrent artery of Heubner replaced the medial group of PFB's of the MCA. In one case this group originated in an accessory MCA. In three hemispheres (9%) a small anastomosis (OD 0.2 mm) was seen between a PFB of the recurrent artery of Heubner and one of the MCA. From a total of 508 PFB's, 255 vessels (50%) originated as single vessels, while 253 vessels (50%) originated as branches of common stems. The OD of the single vessels ranged from 0.1 mm to 1.1 mm (mean 0.39 +/- 0.02 mm), and the length from 3 to 20 mm (mean 10.8 +/- 0.2 mm). The common stems ranged in OD from 0.6 to 1.8 mm (mean 0.87 +/- 0.04 mm), and in length from 1 to 15 mm (mean 4.1 +/- 0.4 mm). The clinical application of these anatomical data to the management of aneurysms and arteriovenous malformations of the MCA, and in the field of interventional neuroradiology is described. The most frequent pathological entities involving the perforating vessels are also discussed.