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The crucifixion of Jesus: Review of hypothesized mechanisms of death and implications of shock and trauma-induced coagulopathy
Abstract
The crucifixion of Jesus is arguably the most well-known and controversial execution in history. Christian faithful, dating back to the time of Jesus, have believed that Jesus was executed by crucifixion and later returned physically to life again. Others have questioned whether Jesus actually died by crucifixion, at all. From review of medical literature, physicians have failed to agree on a specific mechanism of Jesus' death. A search of Medline/Pubmed was completed with respect to crucifixion, related topics, and proposed mechanisms of Jesus' death. Several hypotheses for the mechanism of Jesus' death have been presented in medical literature, including 1) Pulmonary embolism 2) Cardiac rupture 3) Suspension trauma 4) Asphyxiation 5) Fatal stab wound, and 6) Shock. Each proposed mechanism of Jesus' death will be reviewed. The events of Jesus' execution are described, as they are pertinent to development of shock. Traumatic shock complicated by trauma-induced coagulopathy is proposed as a contributing factor, and possibly the primary mechanism, of Jesus' death by crucifixion.
... 7 Based on this fact, the hypothesis has been put forward that a genetic predisposition, associated with dehydration and immobilization on the cross, could have caused a pulmonary embolism (PE) and, consequently, the sudden death of Jesus Christ while still on the cross. 11 A pertinent observation about this theory is the fact that this regional genetic profile did not necessarily occur some 2025 years ago and, therefore, this is really an assumption based on today's population profile, which is certainly much more heterogeneous than it was in the past. 1,2 In addition, the multiple and intense traumas in the ritual of the flagellum and its traumatic attachment to the cross could have activated the coagulation system through tissue damage via the tissue factor pathway (extrinsic pathway). ...
... 4 It's important to mention that in the Scriptures there are reports that at times Jesus Christ complained of thirst, which reinforces the idea that he could have been suffering from dehydration. 11 Other factors that may have contributed to dehydration and therefore led to hypovolemic shock would have been tachypnea caused by pain and physical stress and the ingestion of wine, possibly offered to relieve suffering, which would have caused an increase in alcohol-induced diuresis. 7 ...
... 4,5 If the spear hit the heart, there would be immediate death due to cardiac rupture and hemopericardium. 11 Some scholars assume that Jesus Christ was still alive at the time of the fatal blow with the spear, on the assumption that blood would not flow in a corpse and would have already clotted if he had still died on the cross. This possibility is reinforced by a passage in the New Testament which says that there was a sudden flow of blood and water after the piercing trauma caused by a Roman soldier's spear to Jesus Christ's right thorax. 1 However, from a medical point of view, we can't be sure that the piercing of his chest by the spear was the final event of his death, because there are doubts as to whether Christ had already suffered sudden death, by PE or fat embolism, for example, or whether he was in a comatose state, which would have confused the Roman soldier, inducing him to carry out the final act of execution. ...
There has been much speculation about the true cause of death of Jesus Christ, and this topic has been the subject of discussion by scholars all over the world. The aim of this text is to analyze some of the theories described by different authors about the possible causes of Jesus Christ’s death during his crucifixion, without any kind of religious bias. Among the most plausible hypotheses are: asphyxiation, venous thromboembolism and hypovolemic shock. The aim of this review was to collect relevant data from the literature on this subject, which has not yet been elucidated.
... The manner of Jesus' death remains a subject of controversy in the medical profession. 3 This article surveys a broad range of medical and scholarly views regarding Jesus' experience on the cross, concluding that asphyxiation or asphyxiation-dominant theories have emerged as the consensus position regarding the cause of Jesus' death. ...
... 6 At the time of this publication, the most common hypotheses on the manner of Jesus' death included pulmonary embolism, cardiac rupture, suspension trauma, asphyxiation, fatal stab wound, and shock. 3 Pulmonary embolism has been proposed as the mechanism of Jesus' death due to the high prevalence of hereditary thrombophilia (e.g., Factor V Leiden). 3 However, the more widely accepted medical hypotheses for Jesus' death are cardiac rupture, asphyxiation, and shock. These medical hypotheses are based on accounts from the Gospels and our modern understanding of traumatic injuries. ...
... 3 Pulmonary embolism has been proposed as the mechanism of Jesus' death due to the high prevalence of hereditary thrombophilia (e.g., Factor V Leiden). 3 However, the more widely accepted medical hypotheses for Jesus' death are cardiac rupture, asphyxiation, and shock. These medical hypotheses are based on accounts from the Gospels and our modern understanding of traumatic injuries. ...
The death of Jesus Christ remains a pivotal moment in world history and a symbol of love, mercy, and courage across the globe. Yet for centuries, the manner of Jesus’ death has remained a subject of controversy in academic and medical circles. Forensic pathologists and clinicians have argued for several hypotheses concerning Jesus’ death, including pulmonary embolism, cardiac rupture, suspension trauma, asphyxiation, fatal stab wound, and shock. This article surveys a broad range of medical and other specialist views regarding Jesus’ experience on the cross, concluding that asphyxiation or asphyxiation-dominant theories have emerged as the consensus position regarding the cause of Jesus’ death. Two features of this article are significant. First, it provides a rich resource of different medical opinions regarding the effects of Jesus’ crucifixion. Second, and more importantly, the survey results show that, perhaps less similar to crucifixion in general, there is a growing consensus regarding Jesus’ cause of death by medical professionals. A table maps these results, summarizing for those in the medical field as well as historians and theologians what medical professionals consider to be the cause of Jesus’ death.
... The story of how Jesus was crucified and (seemingly) died is told in the Bible. That story has been considered by several modern medical studies, which have attempted to determine the pathophysiological processes by which Jesus died: Barbet [1953], DePasquale & Burch [1963], Edwards et al. [1986], Holoubek & Holoubek [1994], DeBoer & Maddow [2002], Retief & Cilliers [2003], Brenner [2005], Zugibe [2005], Maslen & Mitchell [2006], Saliba [2006], Omerovic [2009], Bergeron [2012], Byard [2016], Kubala [2017], Bordes et al. [2020]. ...
... fluid around the lungs). Such an effusion could well have been caused by the prior beating/flogging; and it would comprise blood and a water-like substance [Sava, 1957;DeBoer & Maddow, 2002;Zugibe, 2005, p.140;Bergeron, 2012]. A stabbing sufficient to release some effusion would not need to have killed Jesus. ...
Some people have survived being underwater, without breathing, for tens of minutes. We draw an analogy between such near-drowning and crucifixion: because modern medical studies of crucifixion have generally concluded that the main cause of death was asphyxiation (induced by the position of the victim on the cross). The physiological mechanisms that enable some people to survive without breathing for tens of minutes are known from prior studies. We demonstrate that some of those mechanisms could also enable a person to survive crucifixion-induced asphyxiation for tens of minutes. The mechanisms are activated by certain conditions—and those conditions are described in the biblical story of the apparent resurrection of Jesus. Witnesses at the time of Jesus could reasonably have believed that Jesus had died; ergo, when Jesus was later found to be alive, they concluded that Jesus had been miraculously resurrected. The apparent resurrection of Jesus, though, has a naturalistic explanation.
... The story of how Jesus was crucified and (seemingly) died is told in the Bible. That story has been considered by several modern medical studies, which have attempted to determine the pathophysiological processes by which Jesus died: Barbet [1953], DePasquale & Burch [1963], Edwards et al. [1986], Holoubek & Holoubek [1994], DeBoer & Maddow [2002], Retief & Cilliers [2003], Brenner [2005], Zugibe [2005], Maslen & Mitchell [2006], Saliba [2006], Omerovic [2009], Bergeron [2012], Byard [2016], Kubala [2017], Bordes et al. [2020]. ...
... fluid around the lungs). Such an effusion could well have been caused by the prior beating/flogging; and it would comprise blood and a water-like substance [Sava, 1957;DeBoer & Maddow, 2002;Zugibe, 2005, p.140;Bergeron, 2012]. A stabbing sufficient to release some effusion would not need to have killed Jesus. ...
Some people have survived being underwater, without breathing, for tens of minutes. We draw an analogy between such near-drowning and crucifixion: because modern medical studies of crucifixion have generally concluded that the main cause of death was asphyxiation (induced by the position of the victim on the cross). The physiological mechanisms that enable some people to survive without breathing for tens of minutes are known from prior studies. We demonstrate that some of those mechanisms could also enable a person to survive crucifixion-induced asphyxiation for tens of minutes. The mechanisms are activated by certain conditions—and those conditions are described in the biblical story of the apparent resurrection of Jesus. Witnesses at the time of Jesus could reasonably have believed that Jesus had died; ergo, when Jesus was later found to be alive, they concluded that Jesus had been miraculously resurrected. The apparent resurrection of Jesus, though, has a naturalistic explanation.
... The story of how Jesus was crucified and (seemingly) died is told in the Bible. Several modern studies have considered that story from a medical perspective, so as to determine the pathophysiological processes by which Jesus died: Barbet [1953], DePasquale & Burch [1963], Edwards et al. [1986], Holoubek & Holoubek [1994], DeBoer & Maddow [2002], Retief & Cilliers [2003], Brenner [2005], Zugibe [2005], Maslen & Mitchell [2006], Saliba [2006], Omerovic [2009], Bergeron [2012], Byard [2016], Kubala [2017], Bordes et al. [2020], and references therein. ...
... fluid around the lungs). Such an effusion could well have been caused by the prior beating/flogging; and it would comprise blood and a water-like substance [Sava, 1957;DeBoer & Maddow, 2002;Zugibe, 2005, p.140;Bergeron, 2012]. A stabbing sufficient to release some effusion would not need to have killed Jesus. ...
The vital medical aspects of crucifixion are known to be similar to some medical aspects of drowning. And some people have been able to survive being underwater, without breathing, for tens of minutes (e.g. Bolte et al., Journal of the American Medical Association, 1988). We argue that some of the physiological mechanisms that enabled those people to survive could also account for Jesus being able to survive his crucifixion. Those mechanisms are known to be activated by certain conditions—and the conditions are demonstrated to be described in the biblical story. Thus, the apparent resurrection of Jesus has a reasonable naturalistic explanation.
... Due to several accessory muscles of respiration arising directly from the scapula and the spine, these conditions can cause muscles to restrict the chest wall in an extreme expiration or inspiration, making it difficult for an individual to respire and eventually leading to respiratory muscle fatigue and hypoxia. [22,23] Thus, as seen in case, the force at each arm from being pulled by the shaft's rotation would fixate the chest in a an expanded position, causing similar negative effect on breathing as seen in victims of crucifixion. [23] Moreover, the abnormal positioning of the neck (hyperflexion established to be the most frequent, with or without torso hyperflexion described in 11 cases) has been reported to cause partial or complete external airway obstruction, preventing normal oxygenation of the blood. ...
... [22,23] Thus, as seen in case, the force at each arm from being pulled by the shaft's rotation would fixate the chest in a an expanded position, causing similar negative effect on breathing as seen in victims of crucifixion. [23] Moreover, the abnormal positioning of the neck (hyperflexion established to be the most frequent, with or without torso hyperflexion described in 11 cases) has been reported to cause partial or complete external airway obstruction, preventing normal oxygenation of the blood. [10] This is particularly notable when the person is unconscious, as research shows that head posture has a marked effect on the collapsibility of the passive upper airway and the susceptibility for airway obstruction during sleep and sedation. ...
Rationale:
Positional asphyxia is a rare cause of sudden death and a difficult diagnosis, based mostly on the circumstances of the incident, along with particular external and internal findings, frequent in asphyxia (signs of sudden death).
Patient concerns:
In this report, we are describing one case of adult who was found positioned in a way that led to eventual asphyxiation.
Diagnoses:
The final diagnosis of positional asphyxia was determined after the autopsy.
Interventions:
In a head-down position, gravitation and mechanical forces lead to an increased pressure on the diaphragm from the weight of the abdominal organs. Abdominal breathing, and later, chest breathing were hindered by the raised diaphragm and the difference between abdominal and breathing pressures.
Outcomes:
It is known that death from positional asphyxia can emerge in several ways, such as the external breathing suppression when the victim's torso is compressed or deformed.
Lessons:
Therefore, the current criteria for positional asphyxia are based on the obstruction of normal gas exchange caused by the body position, the impossibility to move to another position, and the exclusion of other causes of death. The forensic medical examination must also be started at the scene of the incident.
... (3) Além disso, nas Escrituras há relatos de que em alguns momentos Jesus Cristo queixa-se de sede, o que reforça a ideia de que Ele poderia estar em franca desidratação. (10) Outros fatores que podem ter contribuído para a desidratação e, portanto, levado ao choque hipovolêmico, seriam a taquipneia provocada pela dor e estresse e a ingestão de vinho, eventualmente ofertado para aliviar o sofrimento, que provocaria um aumento da diurese pelo álcool. (6) ...
Este artigo se destina a analisar teorias descritas por diferentes autores sobre as prováveis causas da morte de Jesus Cristo. Diante das hipóteses mais plausíveis, destacam-se asfixia, tromboembolismo venoso e choque hipovolêmico. O objetivo desta revisão foi coletar dados relevantes da literatura que envolvem o assunto. Por se tratar de um tema ainda não elucidado pela ciência, este artigo ganha relevância ao reunir em um único trabalho as principais teorias relacionadas à causa mortis de Cristo.
... Blood loss from severe trauma causes the release of inflammatory factors and elevated capillary permeability, which can lead to ischemia and hypoxia in vital organs such as the kidneys thus causing severe damage to them, the basic mechanism leading to death in patients with fracture traumatic shock. erefore, early intervention in the diagnosis of fracture traumatic shock patients is very necessary [10,11]. KIM-1 is an immunomodulatory protein that is expressed at high levels in proximal tubular epithelial cells from acute tubular necrosis and in regenerating renal tissue after ischemia. ...
Traumatic shock is the most common cause of serious adverse outcomes in patients with severe traumatic diseases such as fractures, and some studies here have shown that the main cause of death from traumatic shock is the impairment of organ function that occurs after shock. In this study, we explored the role of serum kidney injury molecule-1 (KIM-1), neutrophil gelatin-related lipid transporter protein (NGAL), and N-acetyl-β-D-glucosidase (NAG) levels in evaluating and diagnosing the condition of patients with fracture traumatic shock based on the goal of contributing to the clinical diagnosis of the patient’s condition as soon as possible and taking measures to alleviate its progress. 96 patients with fracture traumatic shock were included in the study as the observation group and 58 healthy examiners as the control group, and the observation group was divided into 69 cases in the mild-moderate group and 27 cases in the severe group according to the Acute Physiology and Chronic Health Status Scale (APACHE-II). In this study, we detected and analyzed the differences in serum KIM-1, NGAL, and NAG levels between the observation group and the control group and the observation group with different disease levels. We found that the observation group was significantly higher than the control group, and the severe patients were higher than the mild to moderate patients, and we observed that serum KIM-1, NGAL, and NAG are significantly correlated with the condition of patients with fracture traumatic shock after further analysis using the Pearson model. In addition, the diagnostic value of receiver operating characteristic curve analysis showed that the AUC of serum KIM-1 for the diagnosis of fracture traumatic shock was 0.755, the AUC of serum NGAL was 0.750, the AUC of serum NAG was 0.772, and the AUC of the combination of the three indicators was 0.915. The results of this study thus suggest the possibility of serum KIM-1, NGAL, and NAG as clinical indicators for evaluating the condition of patients with fracture traumatic shock and the possibility of a combined test of serum KIM-1, NGAL, and NAG for diagnosing the condition.
1. Introduction
Currently, the risk of fractures from outdoor injuries is increasing due to the modern infrastructure and the development of transport and construction. In addition to the symptoms of local fracture, severe limb fractures and multiple fractures are usually accompanied by systemic reactions such as massive blood loss and severe pain resulting in traumatic shock which is the main cause of death in fracture patients [1]. Studies [2, 3] have shown that the main cause of death in patients with traumatic shock is the activation of the renin-angiotensin system (RAS) and the upregulation of related cytokine activity, leading to multiple organ damage, among which most commonly kidney damage. Therefore, the goal of improving the prognosis of patients with traumatic shock and reducing their mortality can be achieved by timely and accurate judgment of the patient’s condition and taking corresponding measures to alleviate the progress of the condition [4].
Kidney injury molecule-1 (KIM-1) is a transmembrane protein that is not expressed when the kidney is functioning normally. However, the expression of KIM-1 will be significantly upregulated when the kidney shows ischemia, drug poisoning, and other conditions [5, 6]. Neutrophil gelatin-related lipid transporter protein (NGAL) is a secretory protein expressed by neutrophils and renal tubular epithelial cells [7]. Serum N-acetyl-β-D-glucosidase (NAG) is an intracellular lysosomal enzyme with high relative molecular weight and widely distributed in various tissues, with the highest content in the proximal tubules of the kidney [7]. The imbalance of KIM-1, NGAL, and NAG levels is an important pathophysiological alteration in animal models of renal injury due to traumatic shock, but there are no reports about the role of serum KIM-1, NGAL, and NAG levels in the evaluation and diagnosis of patients with fracture traumatic shock [8].
In this study, the relevant information of serum KIM-1, NGAL, and NAG levels between fracture trauma shock patients and healthy people was collected and compared. The differences of serum KIM-1, NGAL, and NAG levels in patients with different injuries and their correlation with the disease were statistically analyzed, and the diagnostic value of the single index and combined index for fracture traumatic shock was analyzed by using the receiver operating curve. The results of the study suggest that serum KIM-1, NGAL, and NAG levels were significantly elevated in patients with fracture trauma and were closely related to the severity of the disease, and the combination of serum KIM-1, NGAL, and NAG is of great value in the diagnosis of fracture trauma patients.
2. Materials and Methods
2.1. General Materials
96 patients with fractures combined with traumatic shock admitted to our hospital during September 2016 to December 2019 were selected as the observation group. Among them, 52 males and 44 females were aged from 20 to 73 years, and the average age was 44.12 ± 8.26 years. Patients were grouped according to the Acute Physiology and Chronic Health Status Scale (APACHE-II) upon admission, with 69 patients scoring less than 15 in the mild-moderate group and 27 patients scoring greater than or equal to 15 in the severe group. Another 58 healthy physical examiners were selected as the control group during the same period. Among them, 32 males and 26 females were aged from 21 to 75 years, and the average age was 45.84 ± 7.63 years. Our study was approved by the hospital ethics committee, and the patients and their families were informed about the study and had signed an informed consent form.
2.2. Inclusion Criteria
The inclusion criteria were as follows: (i) patients with a history of more severe fractures and confirmed by CT, X-ray, and other imaging studies; (ii) patients exhibit signs of shock such as pale skin, cold sweats, apathy, weak pulse, and shortness of breath; (iii) the patient had systolic blood pressure < 13.3 kPa, pulse pressure < 4 kPa, urine output < 25 ml/h, central venous pressure < 5 cm H2O, and altered metabolic acidosis seen on blood gas analysis.
2.3. Exclusion Criteria
The exclusion criteria were as follows: (i) patients with severe failure of the heart, liver, spleen, and other organs; (ii) patients with malignant tumors; (iii) patients who have used hormone therapy in the past month; (iv) patients with incomplete clinical data.
2.4. Experiment Equipment
The equipment used in the experiment was as follows: serum KIM-1 ELISA kit, serum NGAL ELISA kit, serum NAG ELISA kit (Beijing Dingguo Changsheng Biotechnology Co., Ltd.), and microplate reader (Bio-Rad Company, United States; model: 450).
2.5. Methods
In the control group, 1 to 2 ml of venous blood was collected at the time of physical examination using EDTA anticoagulation tubes. Patients in the observation group were collected immediately after the diagnosis of traumatic shock. Blood specimens were naturally solidified at room temperature for 10∼20 min. After solidification, the serum was centrifuged at a speed of 2000 r/min for 20 min, and then the supernatant was collected and stored at −20°C for cryopreservation. Serum KIM-1, NGAL, and NAG were detected by the enzyme-linked immunosorbent assay, and all experimental steps were strictly performed in accordance with the instructions. The results were read at an absorbance value of 450 nm using the assay zymography, and the concentration corresponding to the sample to be measured was calculated from the standard curve.
2.6. Statistical Methods
All data were processed with SPSS 22.0 statistical software, and GraphPad Prism 8 was used to make statistical graphs. Measurement data were expressed as mean ± standard deviation (), independent sample t-test was used for comparison between groups, count data were expressed as (n (%)), and chi-square (χ²) test was performed. Pearson correlation analysis was used for correlation analysis. The diagnostic value of the ROC curve was evaluated to determine the diagnostic threshold, sensitivity, and specificity, and the area under the curve (AUC) ≥0.700 indicated a high diagnostic value. The difference is statistically significant when .
3. Results
3.1. Comparison of Serum KIM-1, NGAL, and NAG Levels between the Observation Group and Control Group
In the control group, the mean serum KIM-1, NGAL, and NAG levels were (34.32 ± 10.86) pg/ml, (76.15 ± 8.61) ng/ml, and (23.59 ± 3.15) U/g-Cr, respectively. In the observation group, the mean serum KIM-1, NGAL, and NAG levels were (53.15 ± 4.95) pg/ml, (147.68 ± 23.13) ng/ml, and (45.25 ± 6.34) U/g-Cr, respectively. Statistical analysis showed that serum KIM-1, NGAL, and NAG levels in the observation group were significantly higher than those in the control group (, Figure 1). Significant changes in serum KIM-1, NGAL, and NAG levels were seen in patients with fracture trauma shock.
(a)
... This picture is due to the correspondence among the injuries suffered by the Nazarene as described in the Holy Books and the evidence regarding the Shroud. In fact, a careful comparison highlights this perfect correspondence among Writings and vision (Barbet 1963;Bucklin 1982 andZugibe 2005;Bergeron 2012). ...
In this article, we shall study the mechanism of the Shroud body image formation with the help of both natural sciences and religion. The various possibilities can be divided into three groups of hypothesis: the first one is that of the fake, the second is the miracle and the third one of the natural event. The first hypothesis is discarded by the interdisciplinary work of the STURP (The Shroud of Turin Research Project) team. Their results do not support the hypothesis that the blood stains and the body image are due to a forger. In our opinion, even if the Miracle by God is possible, the proposed hypotheses of the supernatural event are theologically unacceptable. So, the natural one remains well supported by the “Ockham’s razor”. Obviously, this last model must be verified by experimental evidence. However, this result is not contrary to the hypothesis that the body image is the one of the Nazarene.
... Some sources mention death due to extraneous factors such as hypovolemia, cardiac arrest, and cardiac tamponade (Retief and Cilliers, 2003;Bergeron, 2012). Extreme dehydration leads to depletion of intracellular and extracellular volume, which decreases cardiac output and leads to hypovolemic shock and subsequent organ failure (Gordon and Shapiro, 1975). ...
Crucifixion was a widely used form of execution for capital crimes in antiquity. Civilizations and empires perfected the technique, leading to centuries of discussions, controversies, and questions, many of which concerned the death of Jesus Christ. To this day, much remains to be discovered in both religious and scientific realms. However, the aim of this study is to discuss such facts as are known from the medical perspectives of clinical anatomists. Nails/spikes were driven through the hands/wrists and feet of five adult cadavers, and the cadavers were then dissected to observe the anatomical structures that had been injured or placed at risk for injury. While many historical and archeological facts remain to be discovered, we hope that this cadaveric study will enhance our modern understanding of ancient practices from a medical and anatomical perspective. Clin. Anat. 32:12–21, 2019. © 2019 Wiley Periodicals, Inc.
... Although the quantity of blood present is less than might be expected in the case of a crucifixion in an orthostatic position, close observation of the frontal image of the feet also revealed blood smears and stains. According to Bergeron (2012), it must be considered that the most possible cause of death of the person wrapped in the TS was hypovolemic shock, associated with coagulopathy. This process leads to a reduced capacity for coagulation and, for this reason, a greater quantity of bleeding than normal could be expected. ...
The imprint of the feet and lower limbs, as well as the blood and rivulets, present on the Shroud of Turin were analysed with regard to anatomical and pathological characteristics. In the dorsal image of the cloth, the crucifixion position shows the left foot on top of the right one; in the frontal view, the feet are almost parallel. The nail used in the crucifixion was driven through the foot. In the frontal image, the knees, the tibiae and the ankles seem to be parallel with different varus–valgus angles; the left one is straighter than the right one, which shows a greater angle. Because of this parallelism, both ankles show a plantar flexion that is dissimilar in the dorsal images. We describe for the first time the anatomical study of the image of the Shroud through modern concepts. At the level of biomechanics and anatomy, the image on the Shroud of Turin does not comply with modern knowledge; in fact, the image fails with regard to some aspects that we cannot interpret yet.
... For religious reasons, the crucifixion of Jesus of Nazareth in 33CE has attracted the most interest from modern researchers, not least those interested in understanding how crucifixion actually caused death. At least ten distinct theories have been proposed as to the physiological reason that crucifixion victims such as Jesus of Nazareth died (Stroud, 1847;Lebec, 1925;Barbet, 1963;Davis, 1965;Wilkinson, 1972;Edwards, 1986;Lloyd-Davis and Lloyd Davis, 1991;Wijffels, 2000;Brenner, 2005;Zugibe, 2005;Bergeron, 2012). This wide-ranging opinion is at first glance quite startling. ...
The texts written by the people of past societies can provide key information that enhances our understanding of disease in the past. Written sources and art can describe cultural contexts that not only help us interpret lesions in excavated human remains, but also provide evidence for past disease events themselves. However, in recent decades many biohistorical articles have been published that claim to diagnose diseases present in past celebrities or well known individuals, often using less than scholarly methodology. This article aims to help researchers use historical written sources and artwork responsibly, thus improving our understanding of health and disease in the past. It explores a broad range of historical sources, from medical texts and histories to legal documents and tax records, and it highlights how the key to interpreting any past text is to understand who wrote it, when it was written, and why it was written. Case studies of plague epidemics, crucifixion, and the spinal deformity of King Richard III are then used to highlight how we might better integrate archaeological and historical evidence. When done well, integrating evidence from both archaeological and historical sources increases the probability of a complete and well-balanced understanding of disease in past societies.
... For religious reasons, the crucifixion of Jesus of Nazareth in 33CE has attracted the most interest from modern researchers, not least those interested in understanding how crucifixion actually caused death. At least ten distinct theories have been proposed as to the physiological reason that crucifixion victims such as Jesus of Nazareth died (Stroud, 1847;Lebec, 1925;Barbet, 1963;Davis, 1965;Wilkinson, 1972;Edwards, 1986;Lloyd-Davis and Lloyd Davis, 1991;Wijffels, 2000;Brenner, 2005;Zugibe, 2005;Bergeron, 2012). This wide-ranging opinion is at first glance quite startling. ...
The texts written by the people of past societies can provide key information that enhances our understanding of disease in the past. Written sources and art can describe cultural contexts that not only help us interpret lesions in excavated human remains, but also provide evidence for past disease events themselves. However, in recent decades many biohistorical articles have been published that claim to diagnose diseases present in past celebrities or well known individuals, often using less than scholarly methodology. This article aims to help researchers use historical written sources and artwork responsibly, thus improving our understanding of health and disease in the past. It explores a broad range of historical sources, from medical texts and histories to legal documents and tax records, and it highlights how the key to interpreting any past text is to understand who wrote it, when it was written, and why it was written. Case studies of plague epidemics, crucifixion, and the spinal deformity of King Richard III are then used to highlight how we might better integrate archaeological and historical evidence. When done well, integrating evidence from both archaeological and historical sources increases the probability of a complete and well-balanced understanding of disease in past societies.
... Similarly, as death may rarely result from extensive subcutaneous and soft tissue hemorrhage following blunt trauma [11], it is possible that bleeding into the tissues from scourging, if marked, may have exacerbated hypovolemia. Whether this may have been associated with a consumption coagulopathy is uncertain [12]. Insects and birds of prey were also known to feed off dying victims [7]. ...
... Shock promotes the initiation of early coagulation pathways in which damaged tissues release thrombuslike substances and activate anticoagulation systems; coagulopathy is closely linked to subsequent treatments for acidosis, hypothermia, and hemodilution [24]. The prompt treatment of hypothermia is needed to correct the coagulopathy, thereby avoiding the occurrence of catastrophic and fatal disseminated intravascular coagulation (DIC). ...
Cold regions are a special combat environment in which low temperatures have a great impact on human metabolism and other vital functions, including the nervous, motion, cardiovascular, circulatory, respiratory, and urinary systems; consequently, low temperatures often aggravate existing trauma, leading to high mortality rates if rapid and appropriate treatment is not provided. Hypothermia is an independent risk factor of fatality following combat trauma; therefore, proactive preventative measures are needed to reduce the rate of mortality. After summarizing the basic research on battlefield environments and progress in the prevention and treatment of trauma, this article concludes that current treatment and prevention measures for combat trauma in cold regions are inadequate. Future molecular biology studies are needed to elucidate the mechanisms and relevant cell factors underlying bodily injury caused by cold environment, a research goal will also allow further exploration of corresponding treatments.
Objectives
To investigate the changes in the coagulation function and hemodynamic parameters in patients with Hemorrhagic Traumatic Shock (HTS) after restrictive fluid resuscitation.
Methods
A total of 139 patients with HTS admitted to our hospital were enrolled, among which 69 HTS patients were divided into the control group and the remaining 70 HTS patients as the observation group. Patients in the control group underwent regular fluid resuscitation, while those in the observation group underwent restrictive fluid resuscitation.
Results
During treatment, 70 patients in the observation group had a lower bleeding amount, infusion amount, and blood transfusion volume than those in the control group (p < 0.05). After treatment, patients in the observation group had better hemodynamic parameters and blood coagulation than those in the control group (p < 0.05), and the incidence rate in the observation group was only 12.9%, which was significantly lower than 60.87% in the control group, while the cure rate in the observation group was 100%, which was significantly higher than that in the control group (p < 0.05).
Conclusions
Restrictive fluid resuscitation could remarkably increase the cure rate and reduce the bleeding amount during HTS treatment, thereby benefiting the recovery of the patient's blood coagulation.
The Turin Shroud (TS) is a Christian relic interpreted to be the burial cloth of Jesus of Nazareth. It exhibits red discolorations that have been interpreted as blood stains and that are the subjects of a highly controversial discussion. We conducted experiments to identify theoretically possible explanations for the stains attributed to the crown of thorns, the lance wound and the belt of blood. In the experiments with a focus on the stains attributed to the crown of thorns, a very similar stain pattern as on the TS could be provoked by simulating the following sequence of events: blood from antemortem scalp wounds is covering hair and face; blood is coagulating and/or drying; blood components are mobilised by postmortem washing and oiling. A stain pattern very similar to the belt of blood on the TS was successfully provoked by simulating the following sequence of events: The body is lying in a supine position, blood or bloodied water flowing from a wound at the right lateral chest wall; the body is rotated to the left side; the Shroud is tucked under the back; the body is rotated back to a supine position and laid onto the Shroud. The so-called serum ring surrounding the stain attributed to the lance wound could be reproduced by sequential application of serum and whole blood samples or of pleural effusion and whole blood samples onto cotton cloth. It is obvious that any attempt to interpret the assumed blood stain pattern on the TS has serious limitations. Nevertheless, it seems remarkable that we were able to reproduce findings that appear to be very similar to stains on the TS.
Keutamaan Yesus sebagai tokoh sejarah dan penderitaan, serta kontroversi yang terkait dengan kematianNya telah mendorong kita untuk menyelidiki, secara interdisipliner, keadaan seputar penyalibanNya. Oleh karena itu tulisan ini akan membahas penyaliban dan kematian Yesus dalam perspektif historis medis. Penelitian ini menggunakan metode pustaka dengan pendekatan kualitatif deskriptif. Penekanannya adalah pada kajian terhadap sumber-sumber pustaka dan mengurainya serta memberi penjelasan dalam sebuah kerangka uraian. Analisis sumber utama adalah literasi pustaka yang mengkaji secara luas tentang hukuman salib dan kematian Yesus dalam perspektif historis medis yang dilengkapi oleh berbagai artikel jurnal dan sumber akademik lainnya yang relevan dengan topik yang dibahas
A majority of medical and lay articles regarding crucifixion, and specifically the crucifixion of Jesus Christ, now state that suffocation was the primary cause of death from crucifixion. An in-depth analysis reveals that this theory is based on a form of torture unrelated to crucifixion and that no evidence directly linking suffocation to crucifixion has been published. Indeed, a thorough review of available ancient evidence from literature, artwork, graffiti, and modern archeology and re-enactment studies reveals no evidence in favor of suffocation and much evidence against suffocation as the cause of death in typically-portrayed crucifixions, and particularly for the crucifixion of Jesus Christ. Researchers are encouraged to look elsewhere for the most likely cause or causes of death from crucifixion. It may be time to abandon the idea that suffocation was the primary cause of death in crucifixion.
p>Due to the lack of information, the pathogenesis of the death of Jesus of Nazareth is still widely debated. A univocal pathogenesis can be detected by the close comparison between what is reported in the Holy Bible (in particular the four Gospels and the prophetic passages of the Old Testament) and what can be observed on the Turin Shroud (TS). Obviously the authenticity of the latter must be here accepted in the sense that it wrapped the corpse of Jesus of Nazareth. The criteria used to support or ignore many etiological hypotheses regarding the terminal event that caused Jesus’ death must take into account: an acute fact, the perfect lucidity and the cry of Jesus immediately before his death. We conclude that the causes of death are:
Terminal cause: myocardial infarction, heart rupture and hemopericardium.
Contributing and accelerating causes, in chronological order: 1. severe emotional stress and sweating with hematohydrosis, 2. fl uid loss without drinking, 3. beating and scourging, 4. crown of thorns, 5. blunt trauma to the neck and thorax following the fall with right shoulder dislocation, paralysis of the entire right brachial plexus, pulmonary contusion with hemothorax and cardiac contusion, 6. nailing, 7. probable left ulnar proximal paralysis from stretching during crucifi xion, 8. probable right foot dislocation from stretching during crucifi xion, 9. causalgia, 10. Hypoventilation, 11. Hemorrhagic hypovolemicpolitraumatic and suspension shock.</p
Jesus’ resurrection to bodily life after death by crucifixion is foundational to orthodox Christianity. The disciples had encounters with Jesus after his crucifixion which caused them to believe he had been bodily resurrected to life again. Psychiatric hypotheses have been proposed as naturalistic explanations for his disciples’ beliefs, which include hallucinations, conversion disorder, and bereavement experiences. Since they propose hallucinatory symptoms that suggest the presence of underlying medical pathology, clinical appraisal of these hypotheses for the disciples’ encounters with the resurrected Jesus is warranted. Psychiatric hypotheses for the disciples’ belief in Jesus’ resurrection are found to be inconsistent with current medical understanding and do not offer plausible explanations for the biblical story of Easter.
My previous theoretical research shows that the rotating circular genetic code is a viable tool to make easier to distinguish the rules of variation applied to the amino acid exchange; it presents a precise and positional bio-mathematical balance of codons, according to the amino acids they codify. Here, I demonstrate that when using the conventional or classic circular genetic code, a clearer pattern for the human codon usage per amino acid and per genome emerges. The most used human codons per amino acid were the ones ending with the three hydrogen bond nucleotides: C for 12 amino acids and G for the remaining 8, plus one codon for arginine ending in A that was used approximately with the same frequency than the one ending in G for this same amino acid (plus *). The most used codons in man fall almost all the time at the rightmost position, clockwise, ending either in C or in G within the circular genetic code. The human codon usage per genome is compared to other organisms such as fruit flies (Drosophila melanogaster), squid (Loligo pealei), and many others. The biosemiotic codon usage of each genomic population or 'Theme' is equated to a 'molecular language'. The C/U choice or difference, and the G/A difference in the third nucleotide of the most used codons per amino acid are illustrated by comparing the most used codons per genome in humans and squids. The human distribution in the third position of most used codons is a 12-8-2, C-G-A, nucleotide ending signature, while the squid distribution in the third position of most used codons was an odd, or uneven, distribution in the third position of its most used codons: 13-6-3, U-A-G, as its nucleotide ending signature. These findings may help to design computational tools to compare human genomes, to determine the exchangeability between compatible codons and amino acids, and for the early detection of incompatible changes leading to hereditary diseases.
Definitions of shock types. Hypovolaemic shock is a state of insufficient perfusion of vital organs with consecutive imbalance of oxygen supply and demand due to an intravascular volume deficiency with critically impaired cardiac preload. Subtypes are haemorrhagic shock, hypovolaemic shock in the narrow sense, traumatic-haemorrhagic shock and traumatic-hypovolaemic shock. Cardiac shock is caused by a primary critical cardiac pump failure with consecutive inadequate oxygen supply of the organism. Anaphylactic shock is an acute failure of blood volume distribution (distributive shock) and caused by IgE-dependent, type-I-allergic, classical hypersensibility, or a physically, chemically, or osmotically induced IgE-independent anaphylactoid hypersensibility. The septic shock is a sepsis-induced distribution failure of the circulating blood volume in the sense of a distributive shock. The neurogenic shock is a distributive shock induced by generalized and extensive vasodilatation with consecutive hypovolaemia due to an imbalance of sympathetic and parasympathetic regulation of vascular smooth muscles.
This review addresses the pathophysiology and treatment of hemorrhagic shock - a condition produced by rapid and significant loss of intravascular volume, which may lead sequentially to hemodynamic instability, decreases in oxygen delivery, decreased tissue perfusion, cellular hypoxia, organ damage, and death. Hemorrhagic shock can be rapidly fatal. The primary goals are to stop the bleeding and to restore circulating blood volume. Resuscitation may well depend on the estimated severity of hemorrhage. It now appears that patients with moderate hypotension from bleeding may benefit by delaying massive fluid resuscitation until they reach a definitive care facility. On the other hand, the use of intravenous fluids, crystalloids or colloids, and blood products can be life saving in those patients who are in severe hemorrhagic shock. The optimal method of resuscitation has not been clearly established. A hemoglobin level of 7-8 g/dl appears to be an appropriate threshold for transfusion in critically ill patients with no evidence of tissue hypoxia. However, maintaining a higher hemoglobin level of 10 g/dl is a reasonable goal in actively bleeding patients, the elderly, or individuals who are at risk for myocardial infarction. Moreover, hemoglobin concentration should not be the only therapeutic guide in actively bleeding patients. Instead, therapy should be aimed at restoring intravascular volume and adequate hemodynamic parameters.
Crucifixion may be defined as a method of execution by which a person is hanged, usually by their arms, from a cross or similar structure until dead. It has been used in many parts of the world and in many time periods; but is perhaps best known today as a cruel method of social control and punishment in the Roman Empire around 2000 years ago1 (pp 22-3). In modern times, the medical profession has shown considerable interest in crucifixion. The typical aim of articles by this group has been to determine how crucified individuals actually died; and they often focus on the case of Jesus of Nazareth. Since Stroud's book of 1847,2 at least 10 different theories have been proposed (Table 1), and many more articles have been published suggesting various combinations of these theories. The 10 examples referenced in Table 1 have been chosen merely as representing the wide difference of opinion in the published literature: it is not an exhaustive list of all articles published on the subject. The postulated causes of death include cardiovascular, respiratory, metabolic, and psychological pathology. Some authors have even argued that in a limited proportion of cases the victim only appeared to die, and recovered consciousness once brought down from the cross.
Table 1
A representative selection of medical hypotheses for the cause of death of Jesus, or crucifixion in general
When a large number of theories are proposed for a problem in any scientific discipline, this often demonstrates that there is no clear evidence indicating the answer. Here we investigate why there are over 10 completely different theories described in the medical literature.
Suspension trauma (also known as "harness-induced pathology" or "orthostatic shock while suspended") is the development of presyncopal symptoms and loss of consciousness if the human body is held motionless in a vertical position for a period of time. It has been described in experiments of personal fall protection, and has been implicated in causes of death in mountaineering accidents, but it seems neither to be widely known about nor to have been presented to the medical profession. This article highlights the potential existence of suspension trauma and suggests that more robust medical research using modern harnesses and healthy volunteers would be beneficial to assess whether this is purely a theoretical risk.
In Reply.—
The various comments are both informative and thought provoking and predominantly address two major issues: motives and methodology. They differ considerably from the supportive letters that have accompanied more than 100 of the 700 reprint requests received to date.Motives.—
We recognize that the nature of Jesus' death is an exceedingly sensitive and emotional issue for many groups. His death, which in early years was used as a call for love,' was transformed to justify hatred and a reprehensible history of repression. We view with utter revulsion this history and its anti-Semitic notion of collective guilt.Accordingly, the present accusations of anti-Semitism are most distressing. We categorically deny anti-Semitic intent or inference and condemn anti-Semitism loudly and passionately. Moreover, we would mourn the day that anyone would attempt to use our study to promote anti-Semitism, and we pray that the emergence of this topic may never result in
HOCK, a condition of decreased total body oxygen delivery, can be brought on by a number of mechanisms. These include failure of the heart to pump blood through the body (cardiogenic shock), loss of circulating fluid volume (hemorrhagic), decreased oxygen-carrying capacity (anemic), or loss of vascular tone (neurogenic). 1 "Traumatic shock," shock brought on by an injury in an otherwise healthy patient, is best thought of as a combination of these factors. The initial phase is usually hemorrhagic: the patient bleeds, and perfusion decreases. This may be followed by an anemic phase as the patient is resuscitated with crystalloid solutions and simultaneously mobilizes interstitial fluid into the vasculature: A cardiogenic or neurogenic component may be present initially, caused by specific injuries to the heart or central nervous system, or may be the secondary result of hypoperfusion and the release of toxic factors. It is important to recognize that the traumatic shock observed clinically in severely injured patients may be quite different from the induced shock observed in laboratory animals hemorrhaged under controlled conditions.
Hemorrhage continues to be one of the leading causes of death following trauma. Trauma patients are susceptible to the early development of coagulopathy and the most severely injured patients are coagulopathic on hospital admission. Hypothermia, acidosis, and dilution from standard resuscitation can worsen the presenting coagulopathy and perpetuate bleeding. Early identification of coagulopathy is dependent on clinical awareness and point of care laboratory values. Routinely used laboratory coagulation parameters fail to adequately describe this state. Thrombelastography is a test that can be done at the bedside and uses whole blood to provide a functional evaluation of coagulation. Rapid diagnosis of coagulopathy, followed by prevention or correction of hypothermia and acidosis should be a priority during the initial evaluation and resuscitation. Judicious use of resuscitation fluids and early replacement of coagulation factors will help prevent iatrogenic hemodilution. This review covers the pathophysiology as well as the clinical and laboratory diagnosis of coagulopathy. Prevention and treatment strategies are discussed, including early transfusion of coagulation factors during massive transfusion and the use of recombinant factor VIIa. Damage control resuscitation is briefly discussed, and it involves the combination of hypotensive resuscitation and hemostatic resuscitation. Finally, a description of the use of fresh whole blood in the military setting is included. Its use has been proven to be safe and beneficial in this setting and warrants further investigation as an adjunct to the management of civilian trauma patients.
Coagulopathy and bleeding after severe injury is a common problem. Whenever caring for critically ill patients, clinicians must anticipate, recognize and manage the coagulopathy of trauma. When left untreated, cardiovascular shock and multiorgan system failure ensue. Uncompensated hemorrhage often culminates in death, highlighting the significance of recognizing the main influences in coagulopathy of trauma.
With recent improvements in prehospital care, trauma specialists face more challenging cases than ever before. Hemostatic transfusion strategies, with early and more aggressive use of plasma, platelets, cryoprecipitate and coagulation factor isolates, decrease blood loss in trauma patients. Combined with point-of-care testing for thromboelastography, coagulation panels, lactate and local pO2, there is an opportunity for frontline trauma clinicians to directly improve patient outcomes.
Although mortality previously was thought to be summarily independent of medical interventions and resuscitations, we now know the opposite to be true; it is our expectation and indeed our obligation to recognize and manage the coagulopathy of trauma better than in past years. In as much as we continue to prevent acidosis, hypothermia and the progressive coagulopathy following injury, trauma victims the world over are benefiting and surviving longer, living proof that demonstrates the utility of managing the coagulopathy of trauma.
This article is a follow up of an original article by the author on the crucifixion of Jesus published in the March 1989 issue of the JMSMA. The pathogenesis of the death of Jesus is still widely debated with vastly divergent views as to the specific cause of His death. The author's views have been challenged in the literature. As a result, he has done spirometry studies of volunteers hanging on a cross and has a better understanding of the physiology of the terminal events. That information is presented in this update.
Bleeding is the most frequent cause of preventable death after severe injury. Coagulopathy associated with severe injury complicates the control of bleeding and is associated with increased morbidity and mortality in trauma patients. The causes and mechanisms are multiple and yet to be clearly defined.
Articles addressing the causes and consequences of trauma-associated coagulopathy were identified and reviewed. Clinical situations in which the various mechanistic causes are important were sought along with quantitative estimates of their importance.
Coagulopathy associated with traumatic injury is the result of multiple independent but interacting mechanisms. Early coagulopathy is driven by shock and requires thrombin generation from tissue injury as an initiator. Initiation of coagulation occurs with activation of anticoagulant and fibrinolytic pathways. This Acute Coagulopathy of Trauma-Shock is altered by subsequent events and medical therapies, in particular acidemia, hypothermia, and dilution. There is significant interplay between all mechanisms.
There is limited understanding of the mechanisms by which tissue trauma, shock, and inflammation initiate trauma coagulopathy. Acute Coagulopathy of Trauma-Shock should be considered distinct from disseminated intravascular coagulation as described in other conditions. Rapid diagnosis and directed interventions are important areas for future research.
In summary, I would suggest that Jesus was unable to carry his cross because of his cruel treatment and scourging. He then fell with the 100 pound crosspiece on his back and was unable to break the fall because his outstretched hands were tied to the crosspiece. This resulted in blunt chest trauma and a contused heart. On the cross the workload of the heart was greatly increased due to multiple factors, but primarily the increased effort necessary to breathe. This resulted in a rupture of the free wall of the heart, which caused Jesus to cry out in a loud voice and suddenly die. This cause of death is confirmed for us by the sword pierce to the side which resulted in the flow of blood and water. In effect, that was a brief and legitimate postmortem exam. JESUS WAS DEAD! THAT WAS FRIDAY! SUNDAY WAS COMING!
Jesus of Nazareth underwent Jewish and Roman trials, was flogged, and was sentenced to death by crucifixion. The scourging produced deep stripelike lacerations and appreciable blood loss, and it probably set the stage for hypovolemic shock, as evidenced by the fact that Jesus was too weakened to carry the crossbar (patibulum) to Golgotha. At the site of crucifixion, his wrists were nailed to the patibulum and, after the patibulum was lifted onto the upright post (stipes), his feet were nailed to the stipes. The major pathophysiologic effect of crucifixion was an interference with normal respirations. Accordingly, death resulted primarily from hypovolemic shock and exhaustion asphyxia. Jesus' death was ensured by the thrust of a soldier's spear into his side. Modern medical interpretation of the historical evidence indicates that Jesus was dead when taken down from the cross.
Crucifixion, as a method of execution was practiced in many cultures before it was outlawed in the Roman Empire by Constantine in 341 C.E., but it has been used sporadically since then. Recent archeological excavations of the remains of a crucified victim have stimulated studies of the methods used. The theories regarding the cause of death as reported in the medical literature are discussed.
In order to verify the accuracy of the commonly used statement, "I sweat blood," a survey of the literature in the subject of hematidrosis was made. Seventy-six cases were studied and classified into categories according to the causative factor. These were, component of systemic disease, vicarious menstruation, excessive exertion, psychogenic, and unknown. The psychogenic were further subdivided into those that occurred only one time, those that recurred and the stigmatics. Acute fear and intense mental contemplation were found to be the most frequent inciting causes. Hematidrosis is an extremely rare clinical phenomenon with only few instances reported to have occurred within the twentieth century.
Trauma is a serious global health problem, accounting for approximately one in 10 deaths worldwide. Uncontrollable bleeding accounts for 39% of trauma-related deaths and is the leading cause of potentially preventable death in patients with major trauma. While bleeding from vascular injury can usually be repaired surgically, coagulopathy-related bleeding is often more difficult to manage and may also mask the site of vascular injury. The causes of coagulopathy in patients with severe trauma are multifactorial, including consumption and dilution of platelets and coagulation factors, as well as dysfunction of platelets and the coagulation system. The interplay between hypothermia, acidosis and progressive coagulopathy, referred to as the 'lethal triad', often results in exsanguination. Current management of coagulopathy-related bleeding is based on blood component replacement therapy. However, there is a limit on the level of haemostasis that can be restored by replacement therapy. In addition, there is evidence that transfusion of red blood cells immediately after injury increases the incidence of post-injury infection and multiple organ failure. Strategies to prevent significant coagulopathy and to control critical bleeding effectively in the presence of coagulopathy may decrease the requirement for blood transfusion, thereby improving clinical outcome of patients with major trauma.
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