A study on house fire victims: age, carboxyhemoglobin, hydrogen cyanide and hemolysis.

Correlation among age, concentrations of carboxyhemoglobin and hydrogen cyanide, oxygen density and hemolysis were studied in 120 house fire victims. Victims aged over 60 years comprised approximately 50% of the pooled subjects. Blood samples were mainly collected from the left ventricle, but sometimes from both the right and left ventricles. The concentration of carboxyhemoglobin ranged from 1-95%, of which 71 persons (59.7%) died with carboxyhemoglobin concentrations below 60%. Carboxyhemoglobin concentrations below 10% were found in 9 persons (7.5%). Most of these cases involved the elderly persons. In this paper, we report on the death of elderly victims as a result of low carboxyhemoglobin concentrations. A significant correlation of blood carboxyhemoglobin concentrations existed between the right and left ventricles. The concentration of carboxyhemoglobin in the left ventricle was significantly higher than that in the right. Two out of 31 victims whose hydrogen cyanide concentrations were determined, succumbed to hydrogen cyanide poisoning, having a high concentration of hydrogen cyanide and a low concentration of carboxyhemoglobin. On analysis, oxygen density was found to be low in 13 persons. A negative correlation was shown between carboxyhemoglobin concentration and hemolysis. Inasmuch as hemolysis may indicate the extent of heat dissociation, hemolysis should provide an index of carbon monoxide dissociation from carboxyhemoglobin. In the present study of victims, possible causes of death i.e., carbon monoxide gas poisoning, hydrogen cyanide poisoning, oxygen deprivation, burning, shock due to burns and others were estimated. The survival time for elderly victims was considered to be short.     

The role of hydrogen cyanide and carbon monoxide in fire casualties: a prospective study

Determinations of blood cyanide and carboxyhemoglobin concentrations were performed in 18 victims found dead in buildings after fires during a 2-year period. The results indicated that 50% of the victims had been exposed to toxic levels of hydrogen cyanide and 90% to toxic levels of carbon monoxide. Lethal concentrations of carbon monoxide were found in 83% of the victims. In one case a lethal blood cyanide but a non-toxic blood carboxyhemoglobin value was found. It is concluded that carbon monoxide appears to be more important than hydrogen cyanide as a toxic agent in the fire atmosphere, but cyanide poisoning without carbon monoxide poisoning may, under certain circumstances, be the cause of death in fire victims.     

The application of NIST's Fire Dynamics Simulator to the investigation of carbon monoxide exposure in the deaths of three Pittsburgh fire fighters

A case is reported in which computer fire modeling was used to reevaluate a fire that killed three fire fighters. NIST's Fire Dynamics Simulator (FDS) was employed to model the fire in order to estimate the concentration of carbon monoxide present in the dwelling, which was the immediate cause of death of two of the fire fighters, who appear to have removed their face pieces in order to share available air. This estimate, along with an assumed respiration volume and known blood carboxyhemoglobin, was plugged into a standard equation to estimate the time of exposure. The model indicated that 27 min into the fire, the carbon monoxide concentration had already reached approximately 3600 ppm. At this concentration, and a respiration of 70 L/min, an estimated 3 to 8 min of exposure would have been required to accumulate the concentrations of carboxyhemoglobin (49, 44, and 10%) measured on the fire fighters at autopsy.     

The causes of death in fire victims

In 169 consecutive cases of autopsied fire victims about 50% had lethal levels of carboxyhemoglobin. Soot in the respiratory tract was found in about 90% of the cases. The age distribution of the fire victims showed significantly less persons in the 15-35-year group than should be expected according to the age distribution of the population, presumably due to greater agility of younger people. More than half of the fire victims had alcohol in the blood exceeding 0.05%, and alcohol intoxication should be considered accessary to many deaths in fire. The characteristic biphasic distribution of carboxyhemoglobin in fire victims together with other observations suggest that the principal causes of death are carbon monoxide followed by carbon dioxide poisoning and/or oxygen deficiency, while the influence of heat is considered to be of minor importance.     

Deaths caused by carbon monoxide poisoning in an open environment (outdoors)

Three deaths as a result of inhalation of carbon monoxide from the exhaust fumes of automobiles are reported. All deaths occurred outside and not in a structure. The individuals were white males, ages 24 to 26 years. Blood carboxyhemoglobin concentrations ranged from 58 (in a decomposing body) to 81%. The three cases illustrate the fact that even in the outdoors death from carbon monoxide inhalation can occur if an individual is in close proximity to a rich source of carbon monoxide.     

甲醛对一氧化碳中毒血检验干扰的研究

目的探讨甲醛对一氧化碳中毒血的检测是否产生干扰,提高一氧化碳中毒鉴定的可靠性。方法采用常用的血中一氧化碳或碳氧血红蛋白饱和度的检测方法对未加甲醛和加甲醛的血样分别进行实验研究。结果甲醛对加热法、氢氧化钠法、氯化钯法、分光光度法等检测方法均可产生不同程度的干扰。结论经福尔马林灌注或固定的检材不宜用于一氧化碳中毒血检测,否则可能导致错误的鉴定结论。     

Asphyxial deaths caused by automobile exhaust inhalation not attributable to carbon monoxide toxicity: study of 2 cases

The authors report two suicides that resulted from the intentional inhalation of automobile exhaust gases in which death occurred without the formation of physiologically significant amounts of carboxyhemoglobin. These circumstances are correlated with measurements of the involved vehicles' exhaust gases, which showed reduced concentrations of carbon monoxide present, reflecting improvements in automobile engine technology. In the absence of carbon monoxide toxicity, the authors attribute death in these cases to asphyxia caused by carbon dioxide intoxication and diminished atmospheric oxygen concentrations.     

An unusual case of suicidal carbon monoxide poisoning

A 35 years old student with prior suicidal tendencies was found dead laying enclosed in a plastic-bag together with four plastic-bags of minor capacity. Three bags were opened by cuts and empty, one bag contained 73 1 of 83.2 Vol.% carbon monoxide. Postmortem carboxyhemoglobin concentrations in blood of five different regions of the corpse ranged from 80.3% to 93.4%. From the circumstances--chemicals and apparatus--it could be reconstructed that carbon monoxide was produced by the reactions of formic acid and sulfuric acid.     

Experimental study on postmortem formation of carbon monoxide

Rats were drowned and kept immersed for 1 month in either boiled city water, or boiled or unboiled fresh water collected from a river. A small amount of carbon monoxide (CO) formed after death and a low carboxyhemoglobin (HbCO) saturation was found in blood and thoracic cavity fluid of the animals immersed in boiled city water and in boiled fresh water. A considerable amount of CO and a high HbCO saturation was observed in blood and thoracic cavity fluid in two out of three rats immersed in unboiled fresh water at 4-6 degrees C, and in one out of three at 6-16 degrees C. It is suggested that microorganisms in the water, in which the rats were drowned and kept immersed, and low temperatures of around 5 degrees C during storage, played an important role in the postmortem formation of carbon monoxide.     

Postmortem formation of carbon monoxide

Since carbon monoxide (CO) production after death was suggested in a drowned body, CO and carboxyhemoglobin (HbCO) levels in blood and body cavity fluids of cadavers which were not exposed to fire and CO have been analyzed. CO released from the tissues was determined by gas chromatography and gas chromatography-mass spectrometry, and the total concentration of hemoglobin (Hb) was measured as cyanmethemoglobin (CNmHb). The HbCO level was calculated by the ratio of CO content and CO-binding capacity. CO levels (ml/100 g at STP) of the seven cases in which blood and body cavity fluids could be collected ranged from 0.13 to 0.87 in blood and 0.02 to 0.80 in body cavity fluids. HbCO levels in blood and body cavity fluids were from 0.3 to 6.0% and from 2.3 to 44.1%, respectively. In a typical case showing postmortem formation of CO, the CO levels in body cavity fluids were higher than that in blood. It is suggested that CO in a putrefied body is due to CO in blood prior to death and the CO formed by the decomposition of Hb, myoglobin and other substances during putrefaction. The significance of HbCO levels in body cavity fluids of cases with marked postmortem decomposition seems difficult to interpret without the value of HbCO in blood.     

Suicide by inhalation of carbon monoxide in a residential fire

Fire deaths are usually accidental, but atypical cases of homicide or suicide have been described. In suicide by fire, the only method reported by several authors consists of self-immolation. We present here the unusual case of an adult female who committed suicide by waiting in the living room after setting fire to her bedroom. The autopsy revealed smoke inhalation and the toxicological analysis revealed carboxyhemoglobin levels of 67%. Very few cases of suicide by fire not of the self-immolation type have been reported, and all have been anecdotal. A review of the literature is presented and a new term, "suicide by inhalation of carbon monoxide in a fire," is proposed for such cases.     

Analysis of carboxyhemoglobin and cyanide in blood from victims of the Dupont Plaza Hotel fire in Puerto Rico

Ninety-seven people died from a fire that occurred in the Dupont Plaza Hotel in Puerto Rico on 31 Dec. 1986. All, except four who died later in the hospital, were found dead at the scene. All of the fatalities at the hotel (except for eight) were burned beyond recognition. Blood from seventy-eight of the victims was screened for carboxyhemoglobin at the Institute for Forensic Sciences in Puerto Rico and was then sent to the National Institute of Standards and Technology, Gaithersburg, Maryland, for analysis of carboxyhemoglobin and cyanide concentrations. The blood data indicated that carbon monoxide and hydrogen cyanide, singly or combined, were probably not responsible for the majority of the deaths that occurred in the badly burned victims. On the other hand, the significantly higher carboxyhemoglobin in the nonburned victims indicated that carbon monoxide alone or combined with hydrogen cyanide probably played a major role in the cause of their deaths.     

Fetal death following maternal trauma: two case reports and a survey of the literature.

When a fetus dies after its mother has suffered trauma, questions often arise about whether the fetal death was linked to the maternal injury. Many state statutes make it a criminal act to cause the death of a fetus by injuring the mother. The authors present two cases in which fetal death resulted from maternal trauma. In addition, we review the pertinent literature on this subject and offer guidelines that may help forensic pathologists evaluate these difficult and often emotionally charged cases.     

Infant Death Following Home Birth: A Case Report of Fatal Neonatal Hypoglycemia

Infants born to diabetic mothers are at increased risk for symptomatic hypoglycemia and death after birth. A 36-year-old G4P3 mother with a history of gestational diabetes and newly diagnosed type II insulin-dependent diabetes gave birth at home, in the care of a midwife, to a macrosomic infant girl (10 lbs.). Several hours after birth, the infant became lethargic and was found to be hypoglycemic (blood sugar: 28 mg/dL). Glucose and sugar water were administered by the midwife; however, the infant continued to decompensate. Emergency medical services were called, and the infant was transported to the hospital where, despite resuscitative efforts, she died. An autopsy and review of the literature was performed. At autopsy, characteristic features of maternal–fetal glucose dysregulation were identified, including fetal macrosomia, cardiomegaly, hepatomegaly, and severe pancreatic islet cell hypertrophy/hyperplasia. Developmental abnormalities and other potential causes of death were not identified. Although deaths due to hypoglycemia cannot be reliably diagnosed postmortem using vitreous glucose levels, a clinical history of maternal glucose dysregulation in combination with certain gross and histologic findings should prompt a pathologist to consider maternal–fetal glucose dysregulation as a diagnosis of exclusion and cause of death.     

Pediatric toxicologic deaths: a 10-year retrospective study

A 10-year retrospective study of pediatric toxicologic deaths was performed at the Medical University of South Carolina (Charleston, SC) from January 1989 to December 1998. During this time, 709 pediatric forensic autopsies were performed on children younger than 18 years of age. Eleven deaths were determined to be secondary to toxic exposures (excluding carbon monoxide poisonings secondary to fires). The remaining deaths were reviewed for the presence of alcohol or illicit drugs. The 11 toxicologic deaths were analyzed for age, sex, race, type of toxic exposure, cause and manner of death, location of incident, witness, and, in the younger age group, the primary caregiver at the time of exposure. The deaths had a bimodal age distribution (6 deaths in victims ages 15 to 17 and 5 deaths in victims ages 4 or younger), involving a wide range of toxins. The teenage group was composed of five males and one female, all white. The preschool group had three females and three males, all black. The manner of death ranged from accidental to suicidal to homicidal. In addition, in eight neonatal and fetal deaths, the victims tested positive for maternal cocaine use, and five of these victims tested positive for cocaine or benzoylecgonine. However, the cause of death was not stated to be cocaine in any of these neonatal and fetal cases.     

Interaction between carbon monoxide and ethanol in fire fatalities.

Impairment due to ethanol is clearly a risk factor in deaths due to fire. However, it is less clear whether there is a physiological interaction between ethanol and carbon monoxide (CO) that would alter the carboxyhemoglobin saturation level (COHb sat.) that accounts for death. In an attempt to explore this issue further, 196 fire fatalities investigated by the Office of the Chief Medical Examiner, State of Maryland over a 3-year period were examined. COHb sat. and blood ethanol concentrations (BAC) were tabulated. Twelve cases positive for therapeutic or abused drugs other than lidocaine or atropine were excluded; 184 cases were included. The data indicate that ethanol does not affect the COHb sat. that accounts for death, since the percentage of cases positive for ethanol at a given COHb range shows no trends. Therefore, we conclude that although ethanol remains a risk factor in fire fatalities, the risk appears to be related to the impairment that it produces as opposed to a direct interaction with CO.     

A New Approach for the Carbon Monoxide (CO) Exposure Diagnosis: Measurement of Total CO in Human Blood Versus Carboxyhemoglobin (HbCO)

The aim of the study is to present the application of a headspace–gas chromatography–mass spectrometry (HS‐GC‐MS) method for the determination of the carbon monoxide (CO) blood concentration and to compare it with carboxyhemoglobin (HbCO) saturation. In postmortem cases, the HbCO measured by spectrophotometry frequently leads to inaccurate results due to inadequate samples or analyses. The true role of CO intoxication in the death of a person could be misclassified. The estimation of HbCO from HS‐GC‐MS CO measurements provides helpful information by determining the total CO levels (CO linked to hemoglobin (HbCO) and CO dissociated from hemoglobin). The CO concentrations were converted in HbCO saturation levels to define cutoff blood CO values. CO limits were defined as less than 1 μmol/mL for living persons, less than 1.5 μmol/mL for dead persons without CO exposure, and greater than 3 μmol/mL for dead persons with clear CO poisoning.     

Comparison of Different Analytical Methods for the Determination of Carbon Monoxide in Postmortem Blood

The determination of carbon monoxide (CO) and carboxyhemoglobin (COHb) is of utmost importance in forensic toxicology to determine the cause of death in cases of CO poisoning, fire, and explosions. To this end, reliable and updated analytical methods are required. In this paper, four different methods for the determination of carbon monoxide in postmortem blood samples were compared: (i) the spectrophotometric determination of COHb applying the method proposed by Rodkey and modified by Beutler–West, (ii) the spectrophotometric determination of CO using a micro-diffusion-based method, (iii) the determination of CO by gas chromatography coupled to a TCD detector, and (iv) the determination of COHb by blood gas analysis. Three postmortem blood samples were analyzed with all methods, and the results were comparable. The applied methodologies showed different features depending on the sensitivity, sample preparation, and volume. The HS-GC/TCD method in our hand was the most appropriate, on postmortem samples, and versatile to apply. Unfortunately, only a limited number of postmortem blood samples were available for this study due to the rarity of that kind of intoxication in our jurisdiction.     

A burning issue. The Japanese "fire basin"

This article presents two deaths due to acute carbon monoxide poisoning that occurred when charcoal-burning hibachis were used as heating sources in enclosed camping facilities. In both deaths, the levels of blood carbon monoxide saturation were at or slightly below the expected lethal level. Coronary arteriosclerosis may have contributed to one death, while oxygen depletion may have been a contributing factor in the other. These cases illustrate the danger of using such heating sources in enclosed spaces, due to their carbon monoxide-generating capability. We suggest that suitable warnings be placed on the hibachis themselves.     

The stability of several compounds in formalin fixed tissues and formalin-blood solutions

Buffered formalin solutions were added to spiked blood samples containing diazepam, phenytoin, carbon monoxide and cyanide to give formalin-whole blood solutions of 5 and 8%. Sections of liver positive for desipramine, phenobarbital and phenytoin were placed in separate 5 and 8% formalin-water solutions. The formalin-blood solutions were monitored daily for 30 days, while the fixed liver and formalin-water samples were analyzed once a week for 4 weeks. In the formalin-blood solutions losses were found for diazepam and phenytoin over the 30-day period of at least 41% and 33%, respectively. Cyanide detection was not possible immediately after the addition of formalin and the presence of carboxyhemoglobin was difficult to detect after 1 week. In the liver, losses of phenobarbital and desipramine were greater than 60% while phenytoin showed little change. This study has revealed that the drugs examined at toxic concentrations can be detected, with variable recoveries, for up to 30 days after fixation with formalin. However, quantitative analysis for cyanide and carboxyhemoglobin may be significantly impaired in the presence of formaldehyde.