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Diabetic ketoacidosis or positional asphyxia?
Legal Medicine 14 (2012) 219–220
Contents lists available at SciVerse ScienceDirect
Legal Medicine journal homepage: www.elsevier.com/locate/legalmed
Letter to the Editor Diabetic ketoacidosis or positional asphyxia?
Dear Sir, We read the article by Hayashi et al. [1] with great interest and would like to commend the authors on their good work. We were also very interested in reading that the authors had initially concluded that the direct cause of death was diabetic ketoacidosis and then changed it to positional asphyxia after having followed the suggestions of other forensic pathologists to reanalyze the features of the case. The case reported by the authors deals with a 70-year-old female found dead in a head-down position. Upon autopsy, numerous petechial hemorrhages were found on the superior palpebral conjunctivae, the upper part of the oral mucosa, in the cervical muscles and soft tissue of the upper part of the neck as well as in the left and right pectoralis major and minor muscles in a subfascial position. Histology revealed the presence of polymorphonuclear leukocytes both within and around the hemorrhages in the subcutaneous tissues of the neck skin. The most important features of this case are, in our opinion, the results of postmortem biochemical investigations, which showed increased glycated hemoglobin levels (10.8%), significantly increased 3-beta-hydroxybutyrate (11,844 lmol/l) and acetone (204.2 lg/ml, corresponding to 20 mg/dl or 3450 lmol/l) levels in the blood as well as markedly increased urine glucose levels (876.7 md/dl). As the authors have correctly emphasized, positional asphyxia is an exclusion diagnosis, which can be formulated when other possible, significant, underlying causes of death, natural or violent, had been eliminated [2]. In recent medico-legal literature, several interesting cases of positional asphyxia have been reported [2–5]. All the authors agree in indicating the criteria necessary to formulate a conclusion of positional asphyxia. These criteria include careful examination of the scene paying particular attention to the position of the body and the head; a review of the medical history, evaluating diseases which could predispose one to positional asphyxia carefully, as well as the physical ability of the victim to extricate him or herself from the position found; autopsy examination, which can confirm or exclude significant contributory and non-contributory organic diseases; toxicological analyses, which can assess potentially incapacitating concentrations of ethanol or drugs. In order to meet all the above criteria, especially the presence of significant contributory and non-contributory organic diseases as well as the existence of metabolic diseases which could potentially be responsible for incapacitation, we propose that postmortem biochemical analyses always be performed in addition to toxicology. In the case presented by Hayashi et al., it would have been interesting to dispose of the vitreous glucose level, to 1344-6223/$ - see front matter Ó 2012 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.legalmed.2012.03.001
estimate the antemortem blood glucose levels, as well as the vitreous 3-beta-hydroxybutyrate and acetone concentrations, to estimate the time of survival, because the equilibrium between blood and vitreous requires some delay to be established and rapid increases of ketones in the blood are not immediately reflected in parallel increases of ketones in the vitreous [6]. Polymorphonuclear leukocyte infiltrations around the subcutaneous hemorrhages in the neck may imply that the deceased had survived for a period of time. However, leucocytes and muscle cells are known to survive many hours after death whereas connective tissue cells, such as fibroblasts, for days. Leucocytes may be motile for more than 12 h and can aggregate around chemotactically active material, making the ‘‘vital reaction’’ a dubiously valid phenomenon in the perimortal period [7]. Thus, it is relatively difficult to give an opinion on the time of survival based exclusively on the leukocyte infiltrations. Kohlmeier et al. [8] have observed a neutrophilic infiltration in liver trauma in a case where the decedent survived approximately 51 min. Nevertheless, establishing the minimum interval of time which is necessary for neutrophils to infiltrate the tissues remains a difficult challenge. Based on our own experience in the postmortem diagnosis of diabetic ketoacidosis [9–11], the markedly increased ketone body levels which have been found in the blood in the presented case can explain death. Hence, it can be affirmed that the victim would have died from diabetic ketoacidosis even if she was in another position rather than head-down. In our opinion, the victim survived for a short interval of time in this position, which can be considered a contributing factor in the presence of diabetic ketoacidosis, which would have, nevertheless, led to death. To reach such 3-beta-hydroxybutyrate and acetone concentrations in the blood, the diabetic decompensation must have started several hours prior to death. Thus, it is more likely that ketoacidosis was very advanced when the victim fell, suggesting that she remained in this head-down position for a short interval of time before dying. It is less likely, in our opinion, that diabetic decompensation started when the victim fell, which leads to the conclusion that the positional asphyxia played a secondary role in the death. Based on the results of postmortem biochemical analyses and the medico-legal literature [12–14], we support the thesis of diabetic ketoacidosis as the main cause of death and positional asphyxia as a contributing factor or ultimate cause of death. In conclusion, we would mention that this interesting case once again emphasizes the importance of performing systematically postmortem biochemical analyses, which can provide useful information in interpreting the cause of death and investigating the process of death as well as contributing conditions and predisposing disorders.
220
Letter to the Editor / Legal Medicine 14 (2012) 219–220
References [1] Hayashi T, Ago K, Ago M, Ogata M. Positional asphyxia or diabetic ketoacidosis? A case report. Leg Med (Tokyo) 2011;13(4):196–200. [2] Byard RW, Wick R, Gilbert JD. Conditions and circumstances predisposing to death from positional asphyxia in adults. J. Forensic Leg. Med. 2008;15(7): 415–9. [3] Benomran FA. Fatal accidental asphyxia in a jack-knife position. J. Forensic Leg. Med. 2010;17(7):397–400. [4] Benomran FA, Hassan Al. An unusual accidental death from positional asphyxia. Am. J. Forensic Med. Pathol. 2011;32(1):31–4. [5] Padosch SA, Schmidt PH, Kröner LU, Madea B. Death to positional asphyxia under severe alcoholisation. Pathophysiologic and forensic considerations. Forensic Sci. Int. 2005;149(1):67–73. [6] Teresin´ski G, Buszewicz G, Ma˛dro R. The influence of ethanol on the level of ketone bodies in hypothermia. Forensic Sci. Int. 2002;127(1–2):88–96. [7] Saukko P, Knight B. Knight’s forensic pathology. 3rd ed. London: Arnold Publishers; 2004. p. 107–71. [8] Kohlmeier RE, Dimaio VJ, Sharkey F, Rouse EA, Reeves KE. The timing of histologic changes in liver lacerations. Am. J. Forensic Med. Pathol. 2008;29(3): 206–7. [9] Palmiere C, Mangin P. Postmortem chemistry update part I. Int J Legal Med. http://dx.doi.org/10.1007/s00414-011-0625-y. [10] Palmiere C, Sporkert F, Werner D, Bardy D, Augsburger M, Mangin P. Blood, urine and vitreous isopropyl alcohol as biochemical markers in forensic investigations. Leg Med (Tokyo) 2012;14(1):17–20.
[11] Palmiere C, Sporkert F, Vaucher P, Werner D, Bardy D, Rey F, Lardi C, Brunel C, Augsburger M, Mangin P. Is the formula of Traub still up to date in antemortem blood glucose level estimation? Int J Legal Med. http://dx.doi. org/10.1007/s00414-011-0659-1. [12] Iten PX. Meier M Beta-hydroxybutyric acid–an indicator for an alcoholic ketoacidosis as cause of death in deceased alcohol abusers. J. Forensic Sci. 2000;45(3):624–32. [13] Kanetake J, Kanawaku Y, Mimasaka S, Sakai J, Hashiyada M, Nata M, et al. The relationship of a high level of serum beta-hydroxybutyrate to cause of death. Leg Med (Tokyo) 2005;7(3):169–74. [14] Elliott S, Smith C, Cassidy D. The postmortem relationship between betahydroxybutyrate (BHB), acetone and ethanol in ketoacidosis. Forensic Sci. Int. 2010;198(1):53–7.
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Cristian Palmiere Patrice Mangin University Center of Legal Medicine, Lausanne-Geneva, Rue du Bugnon 21, 1011 Lausanne, Switzerland University Center of Legal Medicine, Lausanne-Geneva, Rue Michel-Servet 1, 1211 Genève 4, Switzerland * Tel.: +41 021 314 49 61; fax: +41 021 341 70 90. E-mail address: [email protected] (C. Palmiere) Available online 11 April 2012
Contents lists available at SciVerse ScienceDirect
Legal Medicine journal homepage: www.elsevier.com/locate/legalmed
Letter to the Editor Diabetic ketoacidosis or positional asphyxia?
Dear Sir, We read the article by Hayashi et al. [1] with great interest and would like to commend the authors on their good work. We were also very interested in reading that the authors had initially concluded that the direct cause of death was diabetic ketoacidosis and then changed it to positional asphyxia after having followed the suggestions of other forensic pathologists to reanalyze the features of the case. The case reported by the authors deals with a 70-year-old female found dead in a head-down position. Upon autopsy, numerous petechial hemorrhages were found on the superior palpebral conjunctivae, the upper part of the oral mucosa, in the cervical muscles and soft tissue of the upper part of the neck as well as in the left and right pectoralis major and minor muscles in a subfascial position. Histology revealed the presence of polymorphonuclear leukocytes both within and around the hemorrhages in the subcutaneous tissues of the neck skin. The most important features of this case are, in our opinion, the results of postmortem biochemical investigations, which showed increased glycated hemoglobin levels (10.8%), significantly increased 3-beta-hydroxybutyrate (11,844 lmol/l) and acetone (204.2 lg/ml, corresponding to 20 mg/dl or 3450 lmol/l) levels in the blood as well as markedly increased urine glucose levels (876.7 md/dl). As the authors have correctly emphasized, positional asphyxia is an exclusion diagnosis, which can be formulated when other possible, significant, underlying causes of death, natural or violent, had been eliminated [2]. In recent medico-legal literature, several interesting cases of positional asphyxia have been reported [2–5]. All the authors agree in indicating the criteria necessary to formulate a conclusion of positional asphyxia. These criteria include careful examination of the scene paying particular attention to the position of the body and the head; a review of the medical history, evaluating diseases which could predispose one to positional asphyxia carefully, as well as the physical ability of the victim to extricate him or herself from the position found; autopsy examination, which can confirm or exclude significant contributory and non-contributory organic diseases; toxicological analyses, which can assess potentially incapacitating concentrations of ethanol or drugs. In order to meet all the above criteria, especially the presence of significant contributory and non-contributory organic diseases as well as the existence of metabolic diseases which could potentially be responsible for incapacitation, we propose that postmortem biochemical analyses always be performed in addition to toxicology. In the case presented by Hayashi et al., it would have been interesting to dispose of the vitreous glucose level, to 1344-6223/$ - see front matter Ó 2012 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.legalmed.2012.03.001
estimate the antemortem blood glucose levels, as well as the vitreous 3-beta-hydroxybutyrate and acetone concentrations, to estimate the time of survival, because the equilibrium between blood and vitreous requires some delay to be established and rapid increases of ketones in the blood are not immediately reflected in parallel increases of ketones in the vitreous [6]. Polymorphonuclear leukocyte infiltrations around the subcutaneous hemorrhages in the neck may imply that the deceased had survived for a period of time. However, leucocytes and muscle cells are known to survive many hours after death whereas connective tissue cells, such as fibroblasts, for days. Leucocytes may be motile for more than 12 h and can aggregate around chemotactically active material, making the ‘‘vital reaction’’ a dubiously valid phenomenon in the perimortal period [7]. Thus, it is relatively difficult to give an opinion on the time of survival based exclusively on the leukocyte infiltrations. Kohlmeier et al. [8] have observed a neutrophilic infiltration in liver trauma in a case where the decedent survived approximately 51 min. Nevertheless, establishing the minimum interval of time which is necessary for neutrophils to infiltrate the tissues remains a difficult challenge. Based on our own experience in the postmortem diagnosis of diabetic ketoacidosis [9–11], the markedly increased ketone body levels which have been found in the blood in the presented case can explain death. Hence, it can be affirmed that the victim would have died from diabetic ketoacidosis even if she was in another position rather than head-down. In our opinion, the victim survived for a short interval of time in this position, which can be considered a contributing factor in the presence of diabetic ketoacidosis, which would have, nevertheless, led to death. To reach such 3-beta-hydroxybutyrate and acetone concentrations in the blood, the diabetic decompensation must have started several hours prior to death. Thus, it is more likely that ketoacidosis was very advanced when the victim fell, suggesting that she remained in this head-down position for a short interval of time before dying. It is less likely, in our opinion, that diabetic decompensation started when the victim fell, which leads to the conclusion that the positional asphyxia played a secondary role in the death. Based on the results of postmortem biochemical analyses and the medico-legal literature [12–14], we support the thesis of diabetic ketoacidosis as the main cause of death and positional asphyxia as a contributing factor or ultimate cause of death. In conclusion, we would mention that this interesting case once again emphasizes the importance of performing systematically postmortem biochemical analyses, which can provide useful information in interpreting the cause of death and investigating the process of death as well as contributing conditions and predisposing disorders.
220
Letter to the Editor / Legal Medicine 14 (2012) 219–220
References [1] Hayashi T, Ago K, Ago M, Ogata M. Positional asphyxia or diabetic ketoacidosis? A case report. Leg Med (Tokyo) 2011;13(4):196–200. [2] Byard RW, Wick R, Gilbert JD. Conditions and circumstances predisposing to death from positional asphyxia in adults. J. Forensic Leg. Med. 2008;15(7): 415–9. [3] Benomran FA. Fatal accidental asphyxia in a jack-knife position. J. Forensic Leg. Med. 2010;17(7):397–400. [4] Benomran FA, Hassan Al. An unusual accidental death from positional asphyxia. Am. J. Forensic Med. Pathol. 2011;32(1):31–4. [5] Padosch SA, Schmidt PH, Kröner LU, Madea B. Death to positional asphyxia under severe alcoholisation. Pathophysiologic and forensic considerations. Forensic Sci. Int. 2005;149(1):67–73. [6] Teresin´ski G, Buszewicz G, Ma˛dro R. The influence of ethanol on the level of ketone bodies in hypothermia. Forensic Sci. Int. 2002;127(1–2):88–96. [7] Saukko P, Knight B. Knight’s forensic pathology. 3rd ed. London: Arnold Publishers; 2004. p. 107–71. [8] Kohlmeier RE, Dimaio VJ, Sharkey F, Rouse EA, Reeves KE. The timing of histologic changes in liver lacerations. Am. J. Forensic Med. Pathol. 2008;29(3): 206–7. [9] Palmiere C, Mangin P. Postmortem chemistry update part I. Int J Legal Med. http://dx.doi.org/10.1007/s00414-011-0625-y. [10] Palmiere C, Sporkert F, Werner D, Bardy D, Augsburger M, Mangin P. Blood, urine and vitreous isopropyl alcohol as biochemical markers in forensic investigations. Leg Med (Tokyo) 2012;14(1):17–20.
[11] Palmiere C, Sporkert F, Vaucher P, Werner D, Bardy D, Rey F, Lardi C, Brunel C, Augsburger M, Mangin P. Is the formula of Traub still up to date in antemortem blood glucose level estimation? Int J Legal Med. http://dx.doi. org/10.1007/s00414-011-0659-1. [12] Iten PX. Meier M Beta-hydroxybutyric acid–an indicator for an alcoholic ketoacidosis as cause of death in deceased alcohol abusers. J. Forensic Sci. 2000;45(3):624–32. [13] Kanetake J, Kanawaku Y, Mimasaka S, Sakai J, Hashiyada M, Nata M, et al. The relationship of a high level of serum beta-hydroxybutyrate to cause of death. Leg Med (Tokyo) 2005;7(3):169–74. [14] Elliott S, Smith C, Cassidy D. The postmortem relationship between betahydroxybutyrate (BHB), acetone and ethanol in ketoacidosis. Forensic Sci. Int. 2010;198(1):53–7.
⇑
Cristian Palmiere Patrice Mangin University Center of Legal Medicine, Lausanne-Geneva, Rue du Bugnon 21, 1011 Lausanne, Switzerland University Center of Legal Medicine, Lausanne-Geneva, Rue Michel-Servet 1, 1211 Genève 4, Switzerland * Tel.: +41 021 314 49 61; fax: +41 021 341 70 90. E-mail address: [email protected] (C. Palmiere) Available online 11 April 2012