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9tory diseases - lung abscess, aspergillosis, actinomy-cosis, cavities in secondary pulmonary tuberculosis. In this case, the microscopic examination of the pathological process is of fundamental importance for making an accurate forensic diagnosis.
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HIGH-ALTITUDE SICKNESS WITH FATAL OUTCOME
Bivolarski I.
Department of General and Clinical Pathology, Medical Faculty, Medical University of Plovdiv, Bulgaria
Baltov M.
Department of Forensic Medicine and Deontology, Medical Faculty,
Medical University of Plovdiv, Bulgaria
Alakidi A.,
Department of Epidemiology and Hygiene, Faculty of Medicine, Medical University - Sofia, Bulgaria
Mihaylova V.,
Department of Physiotherapy, Faculty of Public Health, Medical University - Sofia Department of Healthcare Management, Faculty of Public Health, Medical University - Plovdiv, Bulgaria
Shilev P.
Public Health Inspector, Medical College, Medical University of Plovdiv, Bulgaria
DOI: 10.5281/zenodo.6579891
ABSTRACT
High-altitude sickness includes three conditions - acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE), which occur in mountaineer visiting high-altitude locations. Altitude sickness is due to hypobaric hypoxia and is not directly related to age or physical condition [6].
We present a case of a 32-year-old man, an alpinist who died while climbing Mont Blanc. A forensic medical autopsy was performed in Bulgaria to determine the cause of death. Autopsy and subsequent microscopic examination of the deceased's organs revealed High-altitude sickness, morphologically represented by pulmonary edema with bilateral confluent parenchymal hemorrhage (high-altitude pulmonary edema), and severe cerebral edema with hypoxic encephalopathy (high-altitude cerebral edema), as well as severe rheological disorders in the internal organs - focal subepicardial hemorrhages, small focal cortical hemorrhages in the kidneys; pronounced interstitial edema in the myocardium and renal medulla.
Keywords: high-altitude sickness, high-altitude illness, high-altitude cerebral edema, high-altitude pulmonary edema.
Introduction
About 400 million people worldwide live permanently at altitudes above 1,500 m, and more than 100 million people in the lowlands visit mountainous areas above 2,500 m per year. The interaction between low atmospheric pressure, oxygen partial pressure, climate, genetic factors of the individual, lifestyle and socio-economic status with the processes of acclimati-
zation and adaptation at high altitudes are extremely complex [7].
High-altitude sickness is due to the low amount of oxygen at high altitudes. The main risk factor is the rapid ascent to high altitudes, but the risk of developing the disease and its severity are different in each organism. Three major syndromes - acute mountain sickness (AMS), high-altitude pulmonary edema
(HAPE), and high-altitude cerebral edema (HACE), are now commonly accepted [5]. The mildest form is acute mountain sickness (AMS). Severe altitude sickness (HACE and HAPE) usually occurs at altitudes above 2,500 meters, but some people may experience symptoms at lower altitudes of 1,500 meters [1, 4]. Symptoms range from fatigue, confusion, nausea, vomiting, to a persistent dry cough, shortness of breath, dizziness and headache. Because the symptoms overlap with those of dehydration, the diagnosis of severe cases of altitude sickness sometimes requires additional medical examinations (MRI or CT scans) to rule out pulmonary and cerebral edema [3].
Preventing the development of altitude sickness requires gradual adaptation and acclimatization [2, 7]. Reaching 2500 m requires a delay in climbing (no more than 300 m above sea level per day), regular breaks, avoidance of intense physical exertion (skiing, tourism), sleeping pills (because they are respiratory depressants) and alcohol (leads to dehydration),
Progression of altitude sickness leads to pulmonary edema with bilateral confluent hemorrhage (HAPE) or cerebral edema with hypoxic encephalopa-thy. [2, 6]. High-altitude cerebral edema (HACE) is a potentially fatal metabolic encephalopathy associated with a time-dependent exposure to the hypobaric hypoxia of altitude. Symptoms commonly are headache, ataxia and confusion progressing to stupor and coma [8].
Case report
We present a case of a 32-year-old man, an alpinist who died while climbing Mont Blanc. After transporting from Italy to Bulgaria, the cadaver underwent a forensic autopsy to determine the cause of death.
Signs of visible traumatic injuries were not identified. The brain has a soft consistency and shiny pearly cut surface with punctate hemorrhages. The line between gray and white matter is not clear. The lungs are dark red-violet in color, with a diffusely compacted consistency. Bloody frothy fluid flows from their cut surface. The liver has a smooth capsule, dark red in color. A copious amount of dark blood flows from the cut surface. Dotted hemorrhages are found on the epicardium of the heart and the surface of both kidneys. The other internal organs are without visible pathological changes.
Materials and methods
The histologic specimens were made with fixative of 10% neutral formaldehyde (formaline) and embedded in paraffin. The cut sections were 4 mkm thick and stained with Hematoxylin and Eosin (HE).
Results of microscopic examination
Brain - dilated arterioles with punctate hemorrhage (Fig. 1), vascular hyperemia with hemolysis, loosening of the brain substance with initial autolytic changes, severe perivasal and pericellular edema (Fig. 2).
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Fig. 1. Brain substance with dilated arterioles and perivascular pin-point hemorrhages, magn. x 200.
Fig. 2. Brain substance with severe perivascular and pericellular edema (white vacuoles), magn. x 400.
Kidney - small focal cortical hemorrhages, autolytic changes in the epithelium of the renal tubules, severe interstitial edema in the medulla (Fig. 3).
Fig. 6., Renal medulla with severe interstitial edema (the homogeneous pink substance) and autolytic changes in
the tubules, magn. x 400.
Lungs - autolytic changes in the bronchial and lar hyperemia with hemolysis, severe pulmonary ede-alveolar epithelium, single areas with microbial colo- ma with confluent bilateral parenchymal hemorrhages nies without inflammation around them, severe vascu- and the presence of single hemosiderophages (Fig. 4),
Fig. 4. Lung with severe edema and confluent hemorrhages with single hemosiderophages with granular brown
pigment, magn. x 200.
Myocardium - small focal subepicardial hemorrhages, interstitial edema, mild lipomatosis, initial autolytic changes in cardiomyocytes (Fig. 5).
Fig. 5. Myocardium with lipomatosis (adipose tissue in the lower left corner), initial autolysis of
cardiomyocytes, magn. x 200.
Liver - sinus dilatation, vascular hyperemia, focal fatty degeneration and autolytic changes in hepatocytes (Fig. 6).
Fig. 6. Autolytic changes in hepatocytes, focal fatty degeneration (white vacuoles bottom left), magn. x 400.
Discussion
This is a case of altitude sickness, with extensive lung and brain syndrome. Hemodynamic and rheolog-ical changes in the lungs are typical of high-altitude pulmonary edema (HAPE). They are more severe, with a longer statute of limitations, as evidenced by the presence of hemosiderophages in areas with severe edema and confluent hemorrhages in the lung parenchyma. Brain damage represented by severe edema and hypoxic encephalopathy (HACE - high-altitude cerebral edema) developed at a later stage. Pathological changes in the lungs and brain are incompatible with life and are a major cause of death. High-altitude hypoxia, which plays a major role in thanatogenesis, has also led to rheological disorders in the internal organs: focal subepicardial hemorrhages, small focal cortical hemorrhages in the kidneys; pronounced interstitial edema in the myocardium and renal medulla. Autolytic changes in the parenchymal cells of the internal organs and the presence of microbial colonies in the lungs are postmortem changes, which is supported by the lack of inflammatory response. They are due to the long time between death and a forensic autopsy (12 days).
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