This article describes the case of a man who died after eleven days of intensive care therapy under mechanical ventilation after losing consciousness in a public sauna for unknown reasons and subsequently being exposed to extreme heat and suffering severe burns on his body. During the forensic autopsy, large amounts of almost undigested food residue were found in the stomach without any mechanical obstruction in the downstream intestinal segments. Because of the large amount of undigested food in the stomach, it could be mistakenly assumed that the man had eaten this food shortly before his death. However, since he did not regain consciousness between the sauna incident and his death, the stomach contents must have been his last meal eleven days earlier. Therefore, it can be assumed that gastric emptying was severely impaired or absent. The results of the histological examination were consistent with the autopsy findings and showed signs of multiple organ failure.
The main causes of gastroparesis are diabetes mellitus type 1 and 2 and idiopathic gastroparesis [1, 3, 4]. Metabolic, autoimmune, neuromuscular, rheumatic, or paraneoplastic diseases can also cause gastroparesis [5]. Gastroparesis is also known to occur postoperatively and due to medications (e.g. benzodiazepines and opioids) [16, 17]. The phenomenon of impaired gastric emptying has been described especially in critically ill patients in intensive care units [6, 7, 12, 18]. Ritz et al. conducted a study on 30 intensive care unit (ICU) patients and 20 healthy volunteers in which they measured the time to half gastric emptying (t50) using the 13 C-octanoic acid breath test. The time to half gastric emptying was significantly longer in critically ill patients than in healthy volunteers (t50 = 155 min vs. 133 min), with the subgroup of burn patients showing significantly slower gastric emptying (t50 = 255 min) than the other groups [12]. Nguyen et al. performed a retrospective study of 132 ICU patients in which gastric emptying was assessed using the 13 C-octanoic acid breath test. Delayed gastric emptying was defined as t50 > 140 min. 60% of the patients had delayed gastric emptying with a mean t50 of 163 ± 7 min. Patients with burns were most commonly affected (77%) followed by patients with intracerebral injury (67%). This study also found an association between gastric emptying and older age, longer ICU stay and reduced renal function. Sex, ventilation pressure, type of sedation and BMI did not influence gastric emptying [7]. Another recent retrospective multicenter study evaluated 713 critically ill patients after heat stroke for gastrointestinal symptoms such as nausea and diarrhea. 18.5% of the patients had such symptoms. An impairment of the enteric nervous system due to heat exposure was suggested as a possible cause [19].
The main question in forensic pathology regarding gastric emptying is whether it can be used to determine the time between the last meal and death, and thus the time of death. In the forensic context, one factor that appears to influence gastric emptying primarily is the effect of physical stress during the digestive process [14]. Other factors associated with delayed gastric emptying in the forensic setting include increased intracranial pressure after traumatic brain injury, emotional stress, alcohol, and various drugs [20,21,22]. Delays in gastric emptying ranging from days to a week have been described in forensic cases [13,14,15]. Because digestion and gastric emptying are subject to many individual factors, it is generally not recommended to use them to estimate time of death [21, 23].
The development of gastroparesis appears to be a multifactorial process. In a study of 43 patients with symptoms compatible with gastroparesis, Abell et al. found evidence of increased inflammation with elevated serum levels of TNF-α and IL-6, electrophysiologic abnormalities in the sense of increased cutaneous electrogastrogram frequencies, and decreased Cajal cells [24]. Other studies have also described an association with impaired gastric motor function or an increase in inflammatory cytokines in critically ill patients as a possible cause of gastric emptying disorders [25, 26].
Regarding the duration of gastric emptying disorder, studies suggest that particularly severe trauma may delay gastric emptying for up to several days [13, 15]. One author describes the case of a traffic accident victim who was in a coma for one week after a fatal head injury. The subsequent autopsy revealed large amounts of undigested stomach contents [14]. Half gastric emptying times are generally reported to be in the range of 155–163 min in critically ill patients and 255 min in burn patients [7, 12]. A recent report published the case of a man who developed severe gastroparesis during inpatient treatment of osteomyelitis after surgery for diabetic foot syndrome. The duration of gastric emptying was 748 min [11].
The man in our case had only a history of hypertension and dementia and no other known pre-existing conditions that could lead to gastroparesis. The predisposing factors for gastroparesis in this case were severe burns on the body surface, eleven days of intensive care therapy with suspected administration of drugs, such as morphine derivatives, and clinical suspicion of developing sepsis and multi-organ failure. It can be assumed that the combination of these multifactorial aspects may have favored the development of a gastric emptying disorder. The reasons for the maximum extent of the gastroparesis over the long period of eleven days remain unclear. However, to our knowledge, such a long-lasting gastric emptying disorder has not yet been described in the literature before and is therefore unusual and rare.
In conclusion, this case provides further and recent evidence that the use of gastric contents in forensic autopsies is not reliable for drawing conclusions about the possible time between last food intake and death and thus for estimating time of death. Furthermore, this case provides a starting point for further, possibly post-mortem, studies to identify possible factors and modifiers of gastrointestinal dysfunction. In this way, knowledge of the pathophysiological correlates of intestinal function can be expanded.
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