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10MEDICAL SCIENCES
PANCOAST-TOBIAS - LUNG CANCER OR PULMONARY ABSCESS
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.6579888
ABSTRACT
Pancoast-Tobias syndrome was first described in 1924 and 1932 by Pancoast as Superior pulmonary sulcus tumor. During this period, Tobias described the same disease as Apicocostovertebral douloureux syndrome. Various disease processes can cause the development of the syndrome - primary malignant tumors of the lung, metastatic tumors, destructive inflammatory processes with peak localization in the lung parenchyma. Clinical symptoms are initially manifested by severe pain in the shoulder, shoulder blade and chest, sometimes with attacks of tachycardia and disorders of skin pigmentation. Later is developed Claude Bernard Horner's Syndrome: miosis, enophthalmos, and eyelid ptosis [1, 4, 8].
We report a case of right-sided adenosquamous lung cancer (Pancoast-Tobias syndrome), which killed an 80-year-old man. The disease was not diagnosed in life due to lack of clinical symptoms. The malignant tumor process infiltrated the right thoracic dome, visceral and parietal pleura and the intercostal muscles. Numerous intra-organ metastases in the right lung, metastases in the hilar lymph nodes and in the right liver were also identified.
Keywords: Pancoast-Tobias Syndrome, lung cancer, pulmonary abscess, secondary tuberculosis.
Introduction
Pancoast-Tobias syndrome develops in malignant tumors located in the upper lobe of the lung, leading to destruction of the thoracic entrance and affecting the brachial plexus and cervical sympathetic nerves (ganglion). Clinical symptoms include: persistent severe pain in the shoulder area radiating to the axilla, shoulder blade and elbow. Development of atrophy of the muscles of the arms and Claude-Bernard-Horner syndrome (ptosis, miosis, enophthalmos) [1, 4, 8]. The predominant type of tumors that cause Pancoast-Tobias syndrome (80% to 85% of all cases) are Non-Small Cell Lung Cancer (NSCLC) - Squamous Cell Carcinoma (SCC) or Adenocarcinoma. Only in 3-5% of cases Small Cell Lung Carcinoma is diagnosed [1, 3, 4].
In addition to bronchogenic carcinomas, other malignancies such as primary adenoid cystic carcino-
mas, ectopic thyroid carcinomas, lymphomas, metastases, and even benign tumors with this localization can cause Pancoast-Tobias Syndrome [5, 7, 10]. Rare cases of other malignancies (paravertebral thoracic schwannoma, myxofibrosarcoma, primary hemangi-opericytoma) have been reported, as well as inflammatory processes (apical lung infections, abscesses, invasive aspergillosis, cryptococcosis) involving the chest wall and surrounding structures that may lead to Pancoast-Tobias [2, 6, 9, 11, 12].
Case report
We present a case of an 80-year-old man found dead in his home. Due to the lack of previous complaints, the patient underwent a forensic autopsy to determine the cause of death.
Signs of visible traumatic injuries were not identified. The skin on the front surface of the two lower legs was atrophic with a brown color (Fig. 1).
Fig. 1. Atrophic changes in the muscles and brown discoloration of the skin on both lower legs.
The brain weight was 1500 g, on cut section the border between gray and white brain matter was clearly visible. The folds of the brain were widened and flattened, and the furrows between them were narrowed. On the lower surface of the cerebellum, around
the cerebellar tonsils, there were impression depressions - an imprint of the large occipital foramen.
When the chest was opened, extensive pleural adhesions were found bilaterally (Fig. 2).
Fig. 2. Diffuse pleural adhesions.
Numerous enlarged lymph nodes with a whitish cut surface and a compacted consistency were found in the mediastinum.
The lungs were dark reddish in color, with a soft texture, without the presence of nodular lesions. An
incision in the upper lobe of the right lung revealed an oval cystic formation measuring 7/9 cm with a pinkish-white, unevenly thickened wall, with cartilage density (Fig. 3).
Fig. 3. Formation in the right lung with the appearance of a chronic cavity.
Among the parenchyma of the rest of the upper lobe of the right lung were found many smaller cavities with the same characteristic. The left lung had a dark red, uniform cut structure and when pressed from the parenchyma leaked a large amount of reddish foamy fluid.
The heart was enlarged with weight 420 g. When cut along the anterior wall of the left ventricle and the interventricular septum, a section measuring 3/2/1 cm, grayish-white in color and dense consistency was found. Both coronary arteries showed atherosclerotic plaques, narrowing over 75% of the vascular lumen.
The liver was enlarged, yellowish-brown in color, with weight 1500 g. Near the anterior edge of the liver a nodular area with a diameter of 2 cm, whitish color and compacted texture was found.
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The spleen was slightly enlarged, with smooth stretched capsule. The pulp was dark red-purple in color, and did not scrape off on the back of the knife.
The kidneys had the usual topic and slightly reduced size. Their decapsulation was difficult. Their surface was uneven, wrinkled by wide shallow depressions with a brownish bottom.
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 - vascular hyperemia in the meninges, perivasal and pericellular cerebral edema.
Myocardium - cardiomyocytic hypertrophy, li-pomatosis, focal myocardiosclerosis and postinfarc-tion scar area (Fig. 4).
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Fig. 4. Postinfarction scar of the myocardium, magn. x 400.
Lung - presence of adenosquamous carcinoma ceral, parietal pleura and adjacent intercostal muscles with necrosis and hemorrhage, with a pronounced (Fig. 5, 6). Multiple tumor cell emboli in various desmoplastic reaction, massive infiltration of the vis- _ blood vessels.
Fig. 5. Adenosquamous carcinoma of the lung with a pronounced desmoplastic reaction, magn. x 100.
Fig. 6. Adenosquamous carcinoma of the lung, magn. x 400. Hilar lymph node - with massive metastases of adenosquamous lung cancer (Fig. 7).
Fig. 7. Metastasis of adenosquamous carcinoma of the lung (left) in a lymph node with partially preserved
lymph tissue (right), magn. x 200.
Kidneys - tubules with thyroid-like changes, in- Liver - Metastasis of adenosquamous carcinoma
terstitial lymphocytic infiltration, pericapsular fibrosis of the lung with extensive necrotic fields, scarce
of glomeruli, cortical vascular hyperemia, medullary round-cell inflammatory infiltrates in the portal spaces
edema, hypertrophy of the media of the interlobar, (Fig. 8). arcuate and interlobular arteries.
Fig. 8. Liver metastasis from adenosquamous lung cancer, magn. x 200.
Discussion
The cause of death in this case was adenosquamous carcinoma of the lung. The advancement of the malignant tumor process has led to massive infiltration of the thoracic dome, pleural sheets and intercostal muscles. The tumor metastasized intraorgani-cally in the right lung, and also in mediastinal lymph nodes and right liver.
The malignancy developed on the background of severe generalized atherosclerosis, with two main organ manifestations - Chronic ischaemic heart disease: Postinfarction subendocardial scar on the anterior wall of the left ventricle with focal myocardiosclerosis, and
atrophic changes in the musculature of the musculo-skeletal system due to atherosclerotic changes in the branches of iliac arteries.
Chronic pyelonephritis was pathogenetically associated with left ventricular hypertrophy and dilatation, and bilateral diffuse massive pleural adhesions were the cause of chronic pulmonary heart disease, which has led to chronic venous stasis in the liver and spleen.
Conclusion:
The changes in the lung and the macroscopic appearance of the tumor formation, found during autopsy, resemble a number of acute and chronic inflamma-
tory 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.
References
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8. Munir M., Jamil S., Rehmani S., Borz-Baba C, Pancoast-Tobias Syndrome: A Unique Presentation of Lung Cancer, Cureus 2021 Feb; 13(2): e13112.
9. Mitchell D., Sorrell T.. Pancoast's syndrome due to pulmonary infection with Cryptococcus neoformans variety gattii., Clin Infect Dis. 1992 May. 14(5):1142-4.
10. Rabano A, La Sala M, Hernandez P, et al. Thyroid carcinoma presenting as Pancoast's syndrome. Thorax. 1991 Apr. 46(4):270-1
11. Simpson F., Morgan M, Cooke N., Pan-coast's syndrome associated with invasive aspergillo-sis. Thorax. 1986 Feb. 41(2):156-7.
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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
