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Hypothermia rs

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Presentation on forensic significance of hypothermia

Presentation on forensic significance of hypothermia

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  • IntroductionDefinition:Hypothermia is the condition of the body where the core temperature of the body drops to below 35o CIndifferent temperature:Ambient Temperature at which basal metabolic rate is sufficient to maintain normal body temperature.
  • Dimaio and Dimaio have published in their book that normal body temperature is generally considered to be 98.6° F (37° C) orally and approximately 1° F (0.6° C) higher rectally. Body temperature, however, can vary from individual to individual based on the age, time of day, extent of physical exertion, etc. Also, newborns and the elderly have temperatures averaging 1° C higher. Cyclic changes in body temperature occur with decreases of 0.5° C early in the morning (approximately between 1:00 to 2:00 a.m.) and slight elevations later in the morning and afternoon. Guyton and Hall have described that exercise can raise the rectal temperature up to 104° F. Rectal temperatures of 39–40° C are common in marathoners after a race. Recent work by Mackowiak et al. indicates that 98.2° F (36.8° C) is the mean normal oral temperature, with 99.9° F (37.7° C) the upper limit. Maximum temperatures varied with time of day with a low in the early morning. They thought that 98.9° F (37.2° C) in the morning and 99.9° F (37.7° C) overall should be regarded as the upper limits of oral temperature in adults. Thus, we see that there is no exact “normal” temperature, but rather a range.
  • EpidemiologyDeath due to hypothermia occurs not only in winters but also during spring or autumn in colder periods.Death due to hypothermia occur not only outdoors but also indoorsRisk FactorsSenile mental deterioration and immobility in elderlyLack of fuel for heatingOpen windows for fresh airIntoxication (mainly due to alcohol but also caused by other drugs like tranquilizers and opiates.)New borns (New borns and elderly are especially susceptible to hypothermia)Hazardous outdoor activities (like climbing, mountaineering, sailing, fishing etc.)Death due to hyporthermia show a peculiar paradoxical hide and die phenomenon as well as cases of paradoxial undressing.J Hirvonen in 1976, R Kinzinger et al in 1995 and MA Rothschild et al. in 2004 found that individuals dying from hypothermia are usually found partially or completely naked with presence of scratches ad hematomas over the knees, elbow and feet. They may also be found in hidden places like under the bed or inside cupboards etc. These finding should be regarded with caution by the examiner and may mislead to a conclusion of foul play.
  • Factors affecting development of hypothermia:Difference in ambient temperature and core body temperature. Greater the difference, the rate of change of core body temperature is higher.Surface area/Volume ratio Children have higher surface area to volume ratio as compared to adults therefore, children are especially susceptible to cold temperatures.Stored heatMedium of transfer of heat. Cooling is three times faster in water than in dry air
  • B. Madea et al. in 2004 described that clinically, hypothermia can be divided into 4 stages – Excitation, Exhaustion, Paralysis and Apparent death.Phase 1 is when the core body temperature is between 33 and 36o C and is called the “Excitation phase”. The signs and symptoms include shivering, tachycardia, reduced perfusion of the body surfaces, stimulation of respiratory centers causing hyperventilation. The patient is in a state of raised vigilance and confusion called “Painful Acra”. Phase 2 occurs between 33 and 30o C and is called the “Exhaustion phase”. The features are decreased muscular tone, sinus bradycardia, rise of resistance of the circulatory system due to vasoconstriction, central depression of respiration leading to hypoventilation. The patient presents as being disoriented as well as apathetic. This state is called the state of “passing off pain”Phase 3 occurs when the core body temperature reaches between 30 and 27o C and is called the Paralysis phase. This phase is characterized by a rise in muscular rigidity, bradyarrythmias, rise of resistance due to increased viscosity of blood, as well as decrease in compliance to respiration causing bradypnoea as well as appearance of apnoic pauses. The patient may lose consciousness with loss of reflexes. The examiner should note that muscular rigidity should not be mistaken for rigor mortis.The final phase is called the phase of apparent death or “Vida reducta” where vital functions further deteriorate. The patient goes into cardiocirculatory arrest or ventricular fibrillation or asystolia. There is also cessation of breathing with complete apnoea. This leads to death.
  • Mechanisms in hypothermia leading to death include Disturbances of microcirculation, Changes of rheology, Cold stress and Hypoxidosis
  • Bright red color of bloodNon-specific finding (also seen in death due to other causes at low temperatures) Mechanism:Left shifting of O2-Hb dissociation curveBlood in left ventricle appears bright redNon-specific finding (also seen in post-mortem freezing) Mechanism:Blood in the left ventricle comes from the lungs where it was cooled down
  • Skin changes in general hypothermia are different from those in local hypothermiaLocal HypothermiaJA Wilkerson et al in 1986 and H Killian described the mechanismFreezing of tissue and obstruction of blood supply to the tissueM Staemmler in 1944 and B Madea et al. in 2003MicroscopicallyDamage of endothelial cellsLeakage of serum into tissueSludging of red blood cells
  • L Kreybery in 1946 , MH Bourne et al. in 1986 and JA Wilkerson et al. in 1986Three grades of local hypothermiaDermatitis congelationis erythematosaViolaceous discoloration mainly on tips of fingers, toes or noseDermatitis congelationis bullosaBlisters filled with clear or bloody fluidDermatitis congelationis gagrenosaBluish discoloration with blister formation and tissue necrosis
  • J Hirvonen in 1976, 1977 and in 2004Frost-bite like injuriesSwelling over the nose, ears, handsRed or purple skin lesions and violet patches on knees and elbows or at outside of the hip jointFrost erythema differs from hemorrhage due to lack of erythrocytes.Keferstein in 1893, B. Madea et al in 2006Mechanism: (hypothesis)Capillary damage and leakage of plasma however, B Madea et al. disproved Keferstein’s theory that it was rewarming of a frozen area led to an extra vascular diffusion of red blood cells.
  • Gastric Mucosal changes in HypothermiaWischnewsky in 1895 described presence of Multiple hemorrhagic gastric lesions as a sign indicative of hypothermiaLesions may vary from 1 mm to 2 cm in diameterLesion may vary from a few to up to 100 in numberLesions must not be mistake for true hemorrhagic erosionsF. Buchner in 1943 described that Wischnewsky spots were characterized by necrosis of mucosa with hematin formation.
  • J Hirvonen and R Elfving in 19Preuß J, Dettmeyer R, Lignitz E, Madea B (2006) found that Wischnewsky spots were a non-specific finding and that they werealso seen in death due to drug or alcohol abuse as well as in shock or stress.The pathogenesis of Wischnewsky spots has been described to be due to hemoconcentration and is also accompanied by secretion of tissue amines histamine and serotonin.R Tidow in 1943, JR Cali et al. in 1965 and B Madea in 2003 have all described that local gastric hypothermia of 2o C - 6o C for up to 24 hours has been found to be harmless.JP Sperhake et al in 2004 and M Tsokos et al in 2006 have reported to have found Wischnewsky spots to be immunopositive for hemoglobinMechanismCircumscribed hemorrhages of the gastric glands in vivo or in agonal phaseSubsequent autolysis of RBCs release hemoglobin which is hematinized on exposure to gastric acid. This lead to blackish brown appearance of Wischnewsky spots.B. Madea et al in 2003 found that Wischnewsky spots were more frequently found in elderly but they also noted that Wischnewsky spots were also found in new borns
  • R Tidow in 1943, JC Stoddard in 1962, AK Mant in 1964, 1967, 1969, and B Madea et al. in 1989 found that hemorrhagic lesions are also found in duodenum as well as jejunum and when present in other gastro-intestinal locations, they are always present in the stomach too. Ulceration of the colon as well as hemorrhagic infarcts of the colon due to rheological and hemodynamic alterations with sludge formation of red blood cells and thrombosis of sub-mucosal veins are also seen.The picture on the left is hemorrhagic infarction of the colon in a case of fatality due to hypothermia on gross. On the left is the histology of the colonic wall with thrombosis of the veins of the submucosa and an acute inflammatory infiltrate.
  • J Hirvonen in 1976, D AE Fruehan 1960, AK Mant 1967, 1969 and V Becker in 19C Thrun (1992) have described a variety of pancreas changes in association with hypothermia: focal or diffuse pancreatitis, hemorrhagic pancreatitis, patches of fat necrosis over the organs surface, increased levels of serum amylase, hemorrhages, and focal or diffuse interstitial infiltration of leukocytes. At autopsy, hemorrhages into the pancreas parenchyma as well as under the mucosa of the pancreatic duct may be seen. In animal experiments, Fisher et al. were able to reproduce these pancreatic changes; they found a non-hemorrhagic pancreatitis with fat necrosis in 10% of their cases. A recent retrospective analysis of 143 cases of death due to hypothermia revealed that pancreatic bleedings are of no diagnostic significance in deaths due to hypothermia – they are observed only very rarely and are seen in other causes of death with the same frequency.AK Mant described presence of focal pancreatitis or hemorrhagic pancreatitis in 29 of 43 cases (67%). The high incidence might be caused by the composition of his case material – mostly older people;in such a biased autopsy population the delimitation of preexisting diseases may be difficult.Preuß et al. found in 24 out of 62 cases of fatal hypothermia (38.7%) in microscopic investigations seemingly empty vacuoles in the adenoid cells of pancreas. These vacuoles were not observed in a control group without hypothermia prior to death as well as in a control group of chronic alcoholics. Although these vacuoles seem to be diagnostically significant, their pathogenesis still remains unclear.
  • Hemorrhage into core musclesHemorrhages into muscles belonging to the core of the body, for instance the iliopsoas muscle, as a diagnostic criterion of death due to hypothermia were first described by Dirnhofer and SigristHistologically, a vacuolated degeneration of subendothelial layers of the vascular walls with a lifting of epithelial cells is seen. These changes were thought to represent hypoxic damage and the hemorrhages due to diapedesis. The hypoxic damage of vessels of core muscles is interpreted as a result of insufficient circulation due to hypothermia induced vasoconstriction. However, compared to the muscles of the surface, the oxygen requirement of the core muscles is not reduced. The misbalance of reduced perfusion and normal oxygen requirement is thought to be the cause of hypoxic damage of epithelial cells with resultant raised permeability
  • Lipid accumulationK Meixner (1932) states that fatty changes in heart, liver, and kidneys have been described repeatedly in fatalities due to hypothermia but data on their diagnostic value and the sensitivity of this finding are still missing. As fatty changes of the liver may have many causes and are frequently found, they are of no diagnostic significance for the diagnosis of death due to hypothermia. Recent investigations Preuß J, Dettmeyer R, Lignitz E and Madea B 2004 and 2006 show that lipid accumulation in epithelial cells of proximal renal tubules seem to be of high diagnostic significance, pointing towards hypothermia of the affected individual prior to death. This lipid accumulation is always seen at the base of the epithelial cells; there are no concomitant changes of cell nucleus or plasma. The fatty changes may be either a result of energy depletion after shock-induced hypoxia or caused by tubular resorption after raised mobilization of triglycerides [Preuß J, Dettmeyer R, Lignitz E, Madea B (2004), C Thrun (1992)].
  • Preuß J, Dettmeyer R, Lignitz E, Madea B (2004) described that there is a strong positive correlation between the grade of fatty change with the occurrence of macroscopic signs of hypothermia (frost erythema and Wischnewsky spots.In control cases, only slight fatty changes can be found. The degree of fatty degeneration of renal tubules can therefore be used as a very helpful marker for the diagnosis of death due to hypothermia and has an equal value of diagnostic sensitivity compared to that of Wischnewsky spots
  • Preuß J, Dettmeyer R, Lignitz E, Madea B (2004)These are slide of the cardiac muscle with different grades of fatty degeneration. Fatty degeneration of myocytes may be observed in cases of fatal hypothermia. However, this fatty degeneration is only of diagnostic significance if a lipofuscin staining is also carried out and a marked difference between lipid staining and lipofuscin staining is observed.
  • These are slides of lipofuscin stained cardiomyocytes showing different grades of fatty degeneration.Preuß J, Dettmeyer R, Lignitz E, Madea B (2004) also state that there is also a correlation between fatty degeneration of cardiac myocytes and Wischnewsky spots. However, fatty degeneration of the cardiac muscle does not have the diagnostic sensitivity of fatty degeneration of proximal renal tubules
  • Various authors [Buchner F (1943), Hirvonen J, Elfving R (1974), Hirvonen J, Huttunen P, Lapinlampi T (1987), SimonA,Muller E (1971)] have studied the changes in the endocrine glands.Since endocrine glands are responsible for the maintenance of normal body temperature, a decrease of body temperature activates the function of most of the endocrine glands, especially the thyroid and adrenalsHowever, morphological findings can be expected only in long-lasting hypothermia, not after the usual exposition to cold ambient temperatures for only a few hours [Buchner F (1943)]. In animal experiments, no morphologic changes have been detected after exposure to cold temperatures for 49 h, but an activation of the thyroid has been observed after long lasting exposure (5–9 days with temperature drops from 37.5 to 36oC; morphologic changes: depletion of colloid, raise of epithelial cells). Only after long lasting hypothermia has a lipid depletion of adrenal cortex been found in animal experiments (10 days with core temperatures of 33oC) not after short exposures of 4–7 h [Buchner F (1943)].
  • Vital morphological alterations due to exposure to cold may be scarce in hypothermia fatalities. Most of the findings are unspecific and clinically of no relevance. However, external and internal findings are of diagnostic significance, not only as the sole finding of frost erythema but especially when they are found in combination like the presence of both frost erythema and Wischnewsky spots. Although unspecific as an exclusive finding, frost erythema and Wischnewsky spots are specific for hypothermia in combination. This is also true for fatty changes of proximal renal tubules which have a strong correlation with the aforementioned macroscopic signs of hypothermia. The pathogenesis of morphologic alterations caused by hypothermia differs widely including hypoxic changes, stress and disturbances of microcirculation caused by vasoconstriction and increased hematocrit.

Hypothermia rs Hypothermia rs Presentation Transcript

  • Rijen Shrestha 20-08-2068
  • Introduction• Definition: Hypothermia is the condition of the body where the core temperature of the body is below 35o C  Indifferent temperature: Ambient Temperature at which basal metabolic rate is sufficient to maintain normal body temperature.
  • Dimaio and Dimaio 2001• Normal body temperature: 98.6° F (37° C) orally• Newborns and the elderly have temperatures averaging 1° C higher.• Cyclic changes in body temperature occur with decreases of 0.5° C early in the morning (approximately 1:00 to 2:00 a.m.) and slight elevations later in the morning and afternoon.A Guyton and JE Hall in 2000, and HB Simon in 1993• Exercise can raise the rectal temperature up to 104° F.• Rectal temperatures of 39–40° C are common in marathoners after a race.Mackowiak et al.• 98.2° F (36.8° C) is the mean normal oral temperature, with 99.9° F (37.7° C) the upper limit.• Maximum temperatures varied with time of day with a low in the early morning.
  • EpidemiologyWinters as well as during spring or autumn in colderperiods.Outdoors as well as indoors • Senile mental deterioration and immobility in elderly Risk • Lack of fuel for heating • Open windows for fresh airFactors • Intoxication • New born babies • Hazardous outdoor activities
  • Factors affecting development of hypothermia:• Difference in temperatures• Surface area/Volume ratio • Children > Adults• Stored heat• Medium of transfer
  • 4 clinical phases of hypothermia Phase 1 Phase 2 Phase 3 Phase 4 36oC – 33oC 33oC – 30oC 30oC – 27oC Below 27oCMuscular System Drop of muscular Rise of muscular Shivering tonus rigidity Either further decrease of vital Heart Tachycardia Sinus bradycardia Bradyrrhythmia functions or cardiocirculatory arrest or ventricular fibrillation or Rise of resistance due asystolia Reduced perfusion of Rise of resistance due Circulation to increased viscosity body surface to vasoconstriction of blood Stimulation of Bradypnoea, apnoic Central Depression of Cessation of Ventilation respiration; pause; Decrease of ventilation breathing. Apnoea Hyperventilation compliance Raised vigilance, Disorientation, Unconsciousness, lossNervous system Confusion; Painful apathy; Passing off of reflex acra pain “Excitation” “Exhaustion” “Paralysis” “Vita reducta” – apparent death
  • Mechanism
  • Guidelines for examinationExamination of organs which contribute to bodytemperature• Thyroid• AdrenalBio-chemical changes due to counter-regulatorymechanism• Loss of glycogen in various organs• Release of catecholamines and excretion in urine• Fatty changes in organsExamination of organs responsible for death• Myocardial damage
  • Guidelines for examinationExamination of freezing tissue and tissue at surface-core border• Frost erythema• Muscle bleeding in core musclesOther organ damage ( Cold stress)• Hemorrhagic gastric lesions• Pancreatic changes• Hemorrhagic infarcts• Micro-infarcts
  • Morphological changesLeft shifting of O2-Hb dissociation curve • Bright red color of blood and lividity • Blood in left ventricle is bright redPost-mortem artifacts • Cutis anserina • Skull fractures due to freezing of brainHemorrhages and erythemas • Frost erythema • Hemorrhagic gastric erosions • Hemorrhagic pancreas • Hemorrhages into core muscles • Hemorrhage into synovial fluid
  • Morphological changesFatty changes • Liver • Heart • KidneysUnspecific changes • Brain oedema • Sub-endocardial hemorrhage • Pneumonia • Contraction of spleenCounter-regulation mechanisms • Vacuolization and loss of glycogen in cells of liver, pancreas, renal proximal tubules and adrenal cells • Colloid depletion and activation of thyroid
  • Blood changesBright red color of blood• Non-specific finding • Mechanism: Mechanism: • Left shifting of O2-Hb dissociation curveBlood in left ventricle appears bright red• Non-specific finding • Mechanism: Mechanism: • Blood in the left ventricle comes from the lungs where it was cooled down
  • Skin changes Skin changes in general hypothermia are different from those in local hypothermia• Local Hypothermia Mechanism: • Freezing of tissue and obstruction of blood supply to the tissue Microscopically: • Damage of endothelial cells • Leakage of serum into tissue • Sludging of red blood cells
  • Three grades of local hypothermiaDermatitis congelationis erythematosa• Violaceous discolorationDermatitis congelationis bullosa• Blisters filled with clear or bloody fluidDermatitis congelationis gangrenosa• Bluish discoloration with blister formation and tissue necrosis
  • Skin Changes in General hypothermia• Frost-bite like injuries – Swelling over the nose, ears, hands• Red or purple skin lesions and violet patches on knees and elbows or at outside of the hip joint Mechanism: • Capillary damage and leakage of plasma along with hemoglobin Frost erythema differs from hemorrhage due to lack of erythrocytes.
  • Gastric mucosal changes Wischnewsky in 1895 • Multiple hemorrhagic gastric lesions as a sign indicative of hypothermia • Lesions vary from 1 mm to 2 cm in diameter • Lesion vary from a few to up to 100 in number • Lesions must not be mistake for true hemorrhagic erosions F. Buchner in 1943 • Wischnewsky spots were characterized by necrosis of mucosa with hematin formation
  • Wischnewsky spotsJ Hirvonen and R Elfving in (1974)Preuß J, Dettmeyer R, Lignitz E, Madea B (2006)• Mechanism: • Disturbances of microcirculation (hemoconcentration) • Tissue amines – histamine and serotoninJP Sperhake et al in 2004M Tsokos et al in 2006• Wischnewsky spots are immunopositive for hemoglobin• Mechanism • Circumscribed hemorrhages of the gastric glands phase • autolysis of RBCs release hemoglobin which is hematinized on exposure to gastric acid to form blackish-brown spots.
  • Frequency of Wischnewsky spots in studies Author of study N % Wischnewsky, 1895 40/44 90.9% Krjukoff, 1914 44/61 72% Mant, 1969 37/43 86% Gillner and Waltz, 1971 22/25 88% Hirvonen, 1976 10/22 45% Thrun, 1992 21/23 91.3% Birchmeyer and Mitchell, 1989 15 60% Takada et al. 1991 17 88% Dreβler and Hauck, 1996 29 86% Kinzinger et al. 1995 30 40% Mizukami et al. 1999 23 44% Bonn and Greifswald, 117/145 80.7%
  • Other Gastro-intestinal lesions
  • Pancreatic changes in hypothermia – Focal or diffuse pancreatitis – Hemorrhagic pancreatitis – Patches of fat necrosis over organ surfaces – Increased serum amylase – Hemorrhages and focal or diffuse interstitial leucocytic infiltrationAt autopsy, – Hemorrhages into the pancreas parenchyma as well as under the mucosa of the pancreatic duct may be seen. Preuß et al. 24 out of 62 cases of fatal hypothermia (38.7%) empty vacuoles in the adenoid cells of pancreas
  • Hemorrhage into core muscles• Dirnhofer and Sigrist (1979) Hemorrhages into muscles belonging to the core of the body can be used as a diagnostic criterion of death due to hypothermia.Histology – Vacuolated degeneration of subendothelial layers of the vascular walls with a lifting of epithelial cells – Misbalance of reduced perfusion and normal oxygen requirement causes hypoxic damage of epithelial cells with resultant raised permeability
  • Lipid accumulation• Fatty changes in heart, liver, and kidneys have been described in fatalities due to hypothermia• Lipid accumulation in epithelial cells of proximal renal tubules seem to be of high diagnostic significance Base of the epithelial cells strong positive correlation between the grade of fatty change with the occurrence of macroscopic signs of hypothermia
  • Grade 0 (x200) fatty degeneration Grade +1 (x200) of renal tubulesGrade +2 (x200) Grade +3 (x200)
  • Grade 0 Fatty changes of Grade +1 cardiac myocytes in hypothermiaGrade +2 Grade +3
  • Grade 0 Lipofuscin staining Grade +1 of cardiomyocytesGrade +2 Grade +3
  • Endocrine glandsEndocrine glands are responsible for the maintenance of normalbody temperatureMorphological findings can be expected only in long-lastinghypothermiaF Buchner in 1943 • no morphologic changes detected after exposure to cold temperatures for 49 hours • activation of thyroid observed after long lasting exposure (5–9 days with temperature drops from 37.5 to 36oC)morphologic changes: • lipid depletion of adrenal cortex found after 10 days with core temperatures of 33oC) not after short exposures of 4–7 h • depletion of colloid, raise of epithelial cells).
  • ConclusionExternal and internal findings are of diagnostic significance• Not only as the sole finding• Especially when they are found in combination• Also true for fatty changes of proximal renal tubulesPathogenesis of alterations caused by hypothermia• Hypoxic changes• Stress• Disturbances of microcirculation
  • © Rijen Shrestha