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Absence of rigor mortis
THE LANCET
ulceration in 6%, 11%, and 15·8%, respectively,3–5 of patients with chronic iron deficiency anaemia. O M P Jolobe Tameside General Hospital, Ashton-under-Lyne, Lancashire OL6 9RW, UK
1
2
3
4
5
Chua E, Garvey C, Kingsnorth AN, Rhodes JM. A 49-year-old with a duodenal ulcer and a mass in the head of her pancreas. Lancet 1997; 349: 174. Sheppard M, Holmes GKT, Cockel R. Clinical picture of peptic ulcer diagnosed endoscopically. Gut 1977; 18: 524–30. Gordon SR, Smith RE, Power GC. The role of endoscopy in the evaluation of iron deficiency anemia in patients over the age of 50. Am J Gastroenterol 1994; 89: 1963–67. Rockey DC, Cello JP. Evaluation of the gastrointestinal tract in patients with iron deficiency anemia. N Engl J Med 1993; 329: 1691–95. McIntyre AS, Long RG. Prospective survey of investigation in outpatients referred with iron deficiency anaemia. Gut 1993; 34: 1102–07.
Absence of rigor mortis SIR—Patel and Parekh (Jan 11, p 100)1 record the absence of rigor mortis in Indian children who had died from specific liver disease. Such findings are interesting but the conclusions drawn are not plausible. To check the intensity of postmortem stiffness we try manually to bend the joints or to move the limbs or the whole body, and feel a lower or higher degree of resistance which is usually interpreted as rigor mortis. I suppose the Indian authors tried this method and found an unexpected low resistance in their Indian childhood cirrhosis victims, which led them to conclude an absence of rigor. This is, however, a method that can raise uncertainties. The manually perceptible resistance is not only related to the intensity of rigor mortis but also to total muscle mass. Thus, in persons with very little musculature one gains the impression of a low degree of stiffness whereas athletic bodies show striking rigor. Such findings are easy to explain: if there are only few muscle fibres they cannot contribute to a higher degree of stiffness because their resistance is easily overcome. I have examined many dead infants, and children and found no rigor mortis in a considerable number. I judged that the less perceptible rigor there was the weaker the younger infants were, simply because babies have less muscle mass than older children. But children that died after chronic illness, who had mostly confined to bed for weeks or months, also showed frequently little or no postmortem stiffness because their musculature had faded away during that time. And this is exactly what I
810
believe Patel and Parekh have misinterpreted—the low degree of perceptible stiffness as absence of rigor mortis. Their biochemical interpretation with accumulation of glycogen in the muscles and postmortem synthesis of ATP is not convincing. The aerobic pathway of such reaction is impossible because in the dead body there is no circulation that could transport oxygen to the muscles. And the anaerobic phosphorylation after death is rapidly selflimiting because it produces lactic acid which lowers pH locally and cannot be buffered or removed for circulatory reasons. Moreover, it seems a bit strange that these workers compare childhood cirrhosis victims examined 12–30 h after death, with those who died from other causes who were examined 4–6 h after death. The start and end of the development of rigor mortis are dependent on temperature, and in tropical climates postmortem stiffness may have disappeared as early as 12 h after death. Achim Th Schäfer Institut für Rechtsmedizin, Medizinischen Fakultät der RWTH, Pauwelsstraße 30, D-52057 Aachen, Germany
1
Parekh SR, Patel BD. Epidemiologic survey of Indian childhood cirrhosis. Ind Paediatr 1972; 9: 431–38.
Author’s reply SIR—Indian childhood cirrhosis is rarely recorded in clinical practice and necropsy data. Schäfer believes that our conclusions are not plausible. However, long delay in the onset of rigor has been reported in well fed animals with increased glycogen stores in the muscles and in obese patients. With respect to documentation of absence of rigor mortis in all 32 patients, we might make the assumption that there would be one or more clinical or biochemical features in Indian childhood cirrhosis that might delay or prevent rigor. Clinically, the precirrhotic symptom complex1 with irritability, manifested by excessive crying and disturbed sleep, sticky steatorrhoeic stools, and increased appetite is a consistent feature throughout the illness. Biochemically gross steatorrhoea with consequent caloric loss, leads to increased appetite, insatiable hunger, and constant feeding, resulting in increased glycogen storage in the liver, as observed both on light and electron microscopy.2,3 We believe that these clinical and biochemical features of the disease are interrelated and culminate in the typical hepatocytes laden with glycogen. Although there is no supportive evidence for increased glycogen at other sites, we contend that this probably also takes place in skeletal muscles, which
would help in the resynthesis of ATP and thus prevent rigor mortis from setting in. We are not of course postulating that this is the only biochemical mechanism that is responsible for the absence of rigor mortis. There could well be other pathways that promote ATP resynthesis or delay its degradation in Indian childhood cirrhosis. Despite being aware of the limitations of manual assessment, in five inpatients with this disease, no perceptible resistance was detectable throughout the postmortem period of observation. The muscle mass did not show any obvious wasting. We have observed fully developed rigor mortis in marasmic patients with gross muscle wasting. No apparatus was used. Schäfer’s observation on absence of rigor mortis in a large number of infants and children does not provide details of time of assessment, duration, or underlying disease conditions. His were probably single rather than serial observations and hence would have been inconclusive for the absence of rigor mortis. We are well aware of the influence of various factors in the evolution of rigor mortis. In our five inpatients, the bodies were kept in the mortuary in which other bodies showed evidence of rigor mortis.3 Indian childhood cirrhosis arises mainly in rural areas, and although the environmental temperature changed with seasonal variation, absence of rigor mortis was recorded in all 32 patients. The bodies had not been kept in the mortuary. It is noteworthy that the social worker remarked that the absence of rigor mortis in Indian childhood cirrhosis was by contrast with its development within 4–6 h postmortem in children dying from other diseases. B D Patel, *Saroj Parekh 703-B Nilesh Apts, Haridas Nagar, Bhimpow Road, Borivili (W), Mumbai 400 092, India
1
2
3
Parekh SR, Patel BD. Epidemiologic survey of Indian childhood cirrhosis. Ind Paediatr 1972; 9: 431–38. Parekh Saroj R, Patel BD, Dempo K, Mori M, Chitale AR, Onoe T. Electromicroscopic features of Indian childhood cirrhosis. Bull Jaslok Hosp Res Centre 1981; 6: 42–49. Krompecher T, Beregerioux C, Brandt-Casadevall C, Gujer HR. Experimental evaluation of rigor mortis: VI effect of various causes of death on the evolution of rigor mortis. Forens Sci Int 1983; 22: 1–9.
DEPARTMENT OF ERROR Is death inevitable with multiresistant TB plus HIV infection?—In this commentary by Dr Drobnewski on Jan 11, p 71 (3rd paragraph), the follow-up period for the patients identified in New York City hospitals was 23 months (median), not 3–4.
Vol 349 • March 15, 1997
ulceration in 6%, 11%, and 15·8%, respectively,3–5 of patients with chronic iron deficiency anaemia. O M P Jolobe Tameside General Hospital, Ashton-under-Lyne, Lancashire OL6 9RW, UK
1
2
3
4
5
Chua E, Garvey C, Kingsnorth AN, Rhodes JM. A 49-year-old with a duodenal ulcer and a mass in the head of her pancreas. Lancet 1997; 349: 174. Sheppard M, Holmes GKT, Cockel R. Clinical picture of peptic ulcer diagnosed endoscopically. Gut 1977; 18: 524–30. Gordon SR, Smith RE, Power GC. The role of endoscopy in the evaluation of iron deficiency anemia in patients over the age of 50. Am J Gastroenterol 1994; 89: 1963–67. Rockey DC, Cello JP. Evaluation of the gastrointestinal tract in patients with iron deficiency anemia. N Engl J Med 1993; 329: 1691–95. McIntyre AS, Long RG. Prospective survey of investigation in outpatients referred with iron deficiency anaemia. Gut 1993; 34: 1102–07.
Absence of rigor mortis SIR—Patel and Parekh (Jan 11, p 100)1 record the absence of rigor mortis in Indian children who had died from specific liver disease. Such findings are interesting but the conclusions drawn are not plausible. To check the intensity of postmortem stiffness we try manually to bend the joints or to move the limbs or the whole body, and feel a lower or higher degree of resistance which is usually interpreted as rigor mortis. I suppose the Indian authors tried this method and found an unexpected low resistance in their Indian childhood cirrhosis victims, which led them to conclude an absence of rigor. This is, however, a method that can raise uncertainties. The manually perceptible resistance is not only related to the intensity of rigor mortis but also to total muscle mass. Thus, in persons with very little musculature one gains the impression of a low degree of stiffness whereas athletic bodies show striking rigor. Such findings are easy to explain: if there are only few muscle fibres they cannot contribute to a higher degree of stiffness because their resistance is easily overcome. I have examined many dead infants, and children and found no rigor mortis in a considerable number. I judged that the less perceptible rigor there was the weaker the younger infants were, simply because babies have less muscle mass than older children. But children that died after chronic illness, who had mostly confined to bed for weeks or months, also showed frequently little or no postmortem stiffness because their musculature had faded away during that time. And this is exactly what I
810
believe Patel and Parekh have misinterpreted—the low degree of perceptible stiffness as absence of rigor mortis. Their biochemical interpretation with accumulation of glycogen in the muscles and postmortem synthesis of ATP is not convincing. The aerobic pathway of such reaction is impossible because in the dead body there is no circulation that could transport oxygen to the muscles. And the anaerobic phosphorylation after death is rapidly selflimiting because it produces lactic acid which lowers pH locally and cannot be buffered or removed for circulatory reasons. Moreover, it seems a bit strange that these workers compare childhood cirrhosis victims examined 12–30 h after death, with those who died from other causes who were examined 4–6 h after death. The start and end of the development of rigor mortis are dependent on temperature, and in tropical climates postmortem stiffness may have disappeared as early as 12 h after death. Achim Th Schäfer Institut für Rechtsmedizin, Medizinischen Fakultät der RWTH, Pauwelsstraße 30, D-52057 Aachen, Germany
1
Parekh SR, Patel BD. Epidemiologic survey of Indian childhood cirrhosis. Ind Paediatr 1972; 9: 431–38.
Author’s reply SIR—Indian childhood cirrhosis is rarely recorded in clinical practice and necropsy data. Schäfer believes that our conclusions are not plausible. However, long delay in the onset of rigor has been reported in well fed animals with increased glycogen stores in the muscles and in obese patients. With respect to documentation of absence of rigor mortis in all 32 patients, we might make the assumption that there would be one or more clinical or biochemical features in Indian childhood cirrhosis that might delay or prevent rigor. Clinically, the precirrhotic symptom complex1 with irritability, manifested by excessive crying and disturbed sleep, sticky steatorrhoeic stools, and increased appetite is a consistent feature throughout the illness. Biochemically gross steatorrhoea with consequent caloric loss, leads to increased appetite, insatiable hunger, and constant feeding, resulting in increased glycogen storage in the liver, as observed both on light and electron microscopy.2,3 We believe that these clinical and biochemical features of the disease are interrelated and culminate in the typical hepatocytes laden with glycogen. Although there is no supportive evidence for increased glycogen at other sites, we contend that this probably also takes place in skeletal muscles, which
would help in the resynthesis of ATP and thus prevent rigor mortis from setting in. We are not of course postulating that this is the only biochemical mechanism that is responsible for the absence of rigor mortis. There could well be other pathways that promote ATP resynthesis or delay its degradation in Indian childhood cirrhosis. Despite being aware of the limitations of manual assessment, in five inpatients with this disease, no perceptible resistance was detectable throughout the postmortem period of observation. The muscle mass did not show any obvious wasting. We have observed fully developed rigor mortis in marasmic patients with gross muscle wasting. No apparatus was used. Schäfer’s observation on absence of rigor mortis in a large number of infants and children does not provide details of time of assessment, duration, or underlying disease conditions. His were probably single rather than serial observations and hence would have been inconclusive for the absence of rigor mortis. We are well aware of the influence of various factors in the evolution of rigor mortis. In our five inpatients, the bodies were kept in the mortuary in which other bodies showed evidence of rigor mortis.3 Indian childhood cirrhosis arises mainly in rural areas, and although the environmental temperature changed with seasonal variation, absence of rigor mortis was recorded in all 32 patients. The bodies had not been kept in the mortuary. It is noteworthy that the social worker remarked that the absence of rigor mortis in Indian childhood cirrhosis was by contrast with its development within 4–6 h postmortem in children dying from other diseases. B D Patel, *Saroj Parekh 703-B Nilesh Apts, Haridas Nagar, Bhimpow Road, Borivili (W), Mumbai 400 092, India
1
2
3
Parekh SR, Patel BD. Epidemiologic survey of Indian childhood cirrhosis. Ind Paediatr 1972; 9: 431–38. Parekh Saroj R, Patel BD, Dempo K, Mori M, Chitale AR, Onoe T. Electromicroscopic features of Indian childhood cirrhosis. Bull Jaslok Hosp Res Centre 1981; 6: 42–49. Krompecher T, Beregerioux C, Brandt-Casadevall C, Gujer HR. Experimental evaluation of rigor mortis: VI effect of various causes of death on the evolution of rigor mortis. Forens Sci Int 1983; 22: 1–9.
DEPARTMENT OF ERROR Is death inevitable with multiresistant TB plus HIV infection?—In this commentary by Dr Drobnewski on Jan 11, p 71 (3rd paragraph), the follow-up period for the patients identified in New York City hospitals was 23 months (median), not 3–4.
Vol 349 • March 15, 1997