Научная статья на тему 'VIRAL ENCEPHALITIS - CAUSE FOR A TRAFFIC ACCIDENT'

VIRAL ENCEPHALITIS - CAUSE FOR A TRAFFIC ACCIDENT Текст научной статьи по специальности «Клиническая медицина»

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VIRAL ENCEPHALITIS / PROGRESSIVE MULTIFOCAL ENCEPHALOPATHY / ROAD TRAFFIC ACCIDENT

Аннотация научной статьи по клинической медицине, автор научной работы — Yancheva S., Buchvarov E., Bivolarski I.

Slow progressing viral infections that lead to encephalitis, have a prolonged latent period and very slow development without showing the typical clinical symptoms of an infectious disease. We present a case of a 73-year old man who suffered a road traffic accident. The patient was admitted in a local thoracic surgery hospital with rib fractures and dies after spending 3 days in the hospital. According to his wife, the patient has been feeling anxious and suffered from insomnia for several weeks before the accident. The autopsy confirms the location and severity of the traumatic injuries and finds changes in the brain - ischemic parts, punctate hemorrhages and severe brain edema. The microscopic examination of the tissues finds diffuse mosaic spread of degenerative neurons with viral inclusions type Cowdry B, focal inflammatory infiltrations involving the walls of brain arterioles, ad focal lymphocytic pericarditis.

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Текст научной работы на тему «VIRAL ENCEPHALITIS - CAUSE FOR A TRAFFIC ACCIDENT»

MEDICAL SCIENCES

VIRAL ENCEPHALITIS - CAUSE FOR A TRAFFIC ACCIDENT

Yancheva S.,

Department of Forensic Medicine and Deontology, Medical Faculty,

Medical University of Plovdiv, Bulgaria Department of Forensic Medicine, St. George University Hospital,

Plovdiv, Bulgaria Buchvarov E.,

Department of Forensic Medicine, St. George University Hospital,

Plovdiv, Bulgaria Bivolarski I.

Department of General and Clinical Pathology, Medical Faculty, Medical University of Plovdiv, Bulgaria

ABSTRACT

Slow progressing viral infections that lead to encephalitis, have a prolonged latent period and very slow development without showing the typical clinical symptoms of an infectious disease. We present a case of a 73-year old man who suffered a road traffic accident. The patient was admitted in a local thoracic surgery hospital with rib fractures and dies after spending 3 days in the hospital. According to his wife, the patient has been feeling anxious and suffered from insomnia for several weeks before the accident. The autopsy confirms the location and severity of the traumatic injuries and finds changes in the brain - ischemic parts, punctate hemorrhages and severe brain edema. The microscopic examination of the tissues finds diffuse mosaic spread of degenerative neurons with viral inclusions type Cowdry B, focal inflammatory infiltrations involving the walls of brain arterioles, ad focal lym-phocytic pericarditis.

Keywords: viral encephalitis, progressive multifocal encephalopathy, road traffic accident.

Introduction

Some of the viruses which are capable of causing encephalitis include: enteroviruses - such as cox-sackievirus, poliovirus and echovirus; herpes simplex virus; varicella zoster virus; Epstein-Barr virus; cyto-megalovirus; adenovirus; rubella; measles; Murray Valley encephalitis (MVE) virus and Kunjin virus; Japanese encephalitis virus. Some of those viral brain infections present clinically with acute symptoms such as high temperature, headache, sensitivity to light (photophobia), general malaise, stiff neck and back, vomiting, seizures, coma. Others progress slower, with little or atypical symptoms - changes to personality, confusion, memory loss (amnesia), paralysis. These slow virus diseases are characterized by a long asymptomatic period, often months or years in duration, between the intraduction of the infectious agent and the appearance of clinical illness [3].

Two distinct groups cause serious degenerative diseases of the brain. The first to be identified are those caused by "unconventional agents," kuru and Creutzfeldt-Jakob disease [5]. The second category, "conventional virus diseases," include subacute sclerosing panencephalitis, progressive multifocal leukoencepha-lopathy, progressive rubella encephalitis, and HIV en-cephalopathy [4]. The common microscopic changes in different types of viral encephalitis include perivascular lymphocyte infiltrations, areas of loosening and demielinisation of white brain matter, severe degeneration and necrotic changes in neuroganglia, in some of which the viral inclusions type Cowdry A are found (eosinophilic) and type Cowdry B (basophilic) [6]. Around the dead neurons phagocyting microglial cells appear and form neurophagic clusters [2]. Unlike other

viral infections, HIV stimulates fusion of microglial cells to form multinucleated microglial cells.

Case report

On 5th of November 2020 a 73-year old man with chronic kidney disease (on hemodialysis) got involved into a road traffic accident as a driver of a car. The man was hospitalized in Thoracic surgery hospital with the following diagnoses: Polytrauma, traumatic shock, bilateral pleural effusion, effusion in the abdominal cavity, chronic kidney disease. The patient was responsive to verbal stimuli but had reduced in strength active movements of the limbs while sparing his left leg. His sensitivity was intact with his plantar reflexes missing bilaterally. Information from his attending physician during hemodialysis and his wife, the patient has been very feeling uneasy and suffered insomnia for weeks before the accident.

At the hospital, the patient was diagnosed with a fracture of the distal part of the left clavicle, fractures of four left ribs, fracture of his left iliac bone, traumatic hematoma in iliac muscle. At the CT scan of the brain fresh ischemic brain lesions were found without signs of hemorrhages in parenchyma and cerebrospinal fluid. Central and cortical cerebral atrophy was present along with degenerative perivascular transependymal resorption of the parenchyma. On the third day of the hospi-talization, the patient goes into a coma and due to which put on mechanical ventilator. Soon after the patient suffers multiple organ dysfunction. Regardless of the intensive care, his state does not improve and the patient goes into an irreversible cardiopulmonary arrest and was declared dead.

The autopsy finds smoothened brain surface with a clear distinction between gray and white matter upon

incision, mottled basal ganglia. The brain cortex was thin. In the temporooccipital lobe of the right hemisphere, a softer in consistency area was found which had unclear borders within the brain matter. On the cut surface of the brain, punctate hemorrhages were present. The cerebellar tonsils were swollen, with clear signs of cerebellar incarceration. The blood vessels of the circle of Willis and basilar artery had multiple yellowish arteriosclerotic plaques present.

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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

Cerebral cortex - small ischemic focuses with the presence of multiple "blue" neurons which had viral inclusions type Cowdry B and severe pericellular swelling (Fig. 1), early necrotic changes in other neurons can be seen - eosinophilic cytoplasm, neurons missing their nucleus, neurophagy, scarce perivascular lymphocyte infiltrates and multiple small hemorrhagic focuses in the brain matter (fig.2).

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Fig. 1. Neurons with viral inclusions type Cowdry B, ischemic changes andpericelullar swelling - magn. x 400

Fig. 2. Perivascular lymphocyte infiltrations in small fhemorrhagic focuses - magn. x 200

Heart - focal lymphocyte infiltrations in the epicardium, with severe hyperemia and significant hypertrophy

of the cardiomyocytes (fig.2), focal myocardial sclerosis.

Fig. 3. Focal lymphocyte infiltration in the epicardium - magn. X 200

Lungs - anthracosis, areas with swelling, atelecta-sis and emphysematous changes mainly under the pleura.

Kidney - focal hemorrhages with presence of si-derophages, tubules with thyroid-like appearance, interstitial lymphocyte infiltration, significant hypertrophy of the media in interlobular and arcuate arteries, pericapsular fibrosis of glomeruli, singular hypertrophic glomeruli, multiple sclerotic and 39yalinized glomerules present.

Liver - early chronic venous congestion.

Spleen - severe congestion and hemorrhages in the red pulp, atrophic lymph follicles of the white pulp.

Discussion

Based on the official data from the Ministry of Internal Affairs of Republic of Bulgaria, General Directorate National Police about the traffic traumatism incidence during 2020, the most traffic accidents occurred due to violations of traffic rules by the drivers - 5562 (97,41% of 5710). At the top of the statistic are high speed, wrong manures and taking the right of way, driving under the influence of alcohol and drugs or their analogs. There is no official statistic about proven by medical examiners health conditions of the drivers who caused traffic accidents [7, 8]. Amidst those conditions, the most common are the severe cases of Ischemic heart disease (IHD) and Cerebral small vessel disease (SVD) - myocardial infarctions, intracerebral hemorrhages and strokes, which occurred during driving. Chronic conditions with neurological symptoms could also be a cause for a traffic accident, due to different levels of cognitive impairment in the driver. Progressive multi-focal encephalopathy is part of the group of slow progressing viral infections of the brain (encephalitis).

Those conditions have long latent (asymptomatic) period and very slow progression without the typical expression of an infectious disease [4]. The viral infection in our case report, aside from the brain tissue has affected the pericardium as well in the form of focal lym-phocytic pericarditis. The brain damage in this type of infection has chronic progression, scarce, hard to notice symptoms. The patient presented with anxiety and insomnia more than a month before the accident. Degenerative changes in part of the neurons in the brain, with viral inclusions building in their nucleus is a slow process from morphological standpoint [1, 5]. This process could take months and started before the traffic accident happened. The inflammatory changes in the walls of the blood vessels caused by the encephalitis, along with already present atherosclerosis reduced the oxygen exchange in some zones of the brain. That process also has a part in the formation of the ischemic changes and pinpoint-like hemorrhages found in the brain tissue during the autopsy and microscopic examination.

Conclusion

"Slow virus" chronic / subacute encephalitis (progressive multifocal encephalopathy) is the main disease in the presented case. The immediate cause of death is severe cerebral edema unresponsive to medication, which occurred due to encephalitis with SVD as a background disease. The severe cerebral edema lead to paralysis of the vital centers in the brainstem causing respiratory and heart failure.

The progressive deterioration of the brain function due to the viral encephalitis became a cause for impaired coordination and ability to drive, which is in direct correlation to the traffic accident that occurred. The traumatic injuries were caused by blunt objects and

could occur inside of the vehicle due to a traffic accident. Those injuries are mild, without the involvement of any of the vital organs and thus have no correlation with the death of the patient.

References

1. Gadoth N., Subacute Sclerosing Panencephalitis (SSPE) - Past and Present, www.researchgate.net /publication /221920925, December 2011.

2. Henin D., Gervaz E., Seilhean D., Pathologic anatomy of cytomegalovirus encephalomyelitis and varicella-zona virus encephalomyelitis, J Neuroradiol. 1995 Sep;22(3):180-3.

3. Mocsny N., Slow virus diseases of the central nervous system, Rehabil Nurs. 1989 May-Jun;14(3):130-2.

4. Takasu T., Disease concept of the slow virus infection, Nihon Rinsho. 2007 Aug;65(8):1361-8.

5. Warecka K., "Slow virus" infections and degenerative diseases of the central nervous system, Psy-chiatr Neurol Med Psychol (Leipz). 1978 Dec;30(12):705-14.

6. www.humpath.com/spip.php?article12893, December 2007

7. www.mvr.bg/docs/librariesprovider74

8. www.strategy.bg/File-Handler.ashx?fileId=23082

CLINICAL AND HEMATOLOGICAL ASPECTS OF INDOLENT NON-HODGKIN'S LYMPHOMAS

Buruaiana S.,

The State University of Medicine and Pharmacy "Nicolae Testemitanu", Doctor of medical sciences, associate professor

Gutan D.

The State University of Medicine and Pharmacy "Nicolae Testemitanu",

student

ABSTRACT

In the retrospective study, were analyzed the clinical and hematological aspects of 49 patients with indolent non-Hodgkin's lymphomas (NHL). The study demonstrated an increased incidence of indolent NHL in people older than 50 years, in men, along with the finding of generalized stages, mainly stage IV. In all the investigated cases, it was revealed a primary and secondary damage, mainly, of the lymph nodes, the disease being detected in the IV clinical stages with intoxication syndrome. Hematologically, patients showed leukocytosis, lymphocytosis and anemia. The medullogram detected the damage of the bone marrow, and in the case of bone marrow biopsy, the hypercellularity with diffuse or foci damage of the bone marrow was determined.

Keywords: indolent non-Hodgkin's lymphoma, lymph nodes, onset of disease.

Problem statement

NHL are a heterogeneous group of malignant tumors of lymphatic tissue, distinctive by etiology, morphology, immunophenotypic and genetic properties, clinical features and response to treatment [8].

The highest prevalence of NHL morbidity is assessed in people aged between 50-60 years. In the Republic of Moldova, the index of morbidity of NHL is 4.1 per 100.000 [8]. Globally, following the researches of the American Cancer Society, the incidence of NHL turned out to be 5.1 per 100.000, with a mortality rate of 2.5 per 100.000. According to Cancer Research UK, between 2016-2018, there is a prevalence of NHL in the male sex than in the female sex. Indolent NHL, is characterized by a generally slow evolution, being often asymptomatic, being detected, in many cases, already at the appearance of B-symptoms or extranodal damage. These types of NHL respond well to treatment, but there is an increased risk of relapse, and the healing is rarely achieved [1, 3, 11]. Small lymphocytic lymphoma (SLL) accounts for about 6% of NHL, predominating in men aged between 60-71 years, the white race [4]. Marginal zone lymphoma (MZL) comprises about 10-15% of all non-Hodgkin's lymphomas [7]. Follicular lymphoma (FL) is one of the most common types of indolent NHL, constituting approximately 2025% of all LNH with a prevalence in women in the range of 60-65 years [9, 10].

The aim of the study is the learning of the clinical and hematological aspects of indolent non-Hodgkin's lymphomas for the assessment of their peculiarities.

The objectives of the study: studying the clinical aspects of indolent NHL types, depending on age, gender, living environment; assessment of the onset of disease; stage; B-symptoms depending on the indolent NHL type; interpretation of hematological indices in peripheral blood and bone marrow depending on the type of indolent NHL.

Methodology and research methods

During the research carried out, have been studied the clinical and hematological aspects of 49 patients diagnosed with indolent NHL, aged between 27 years and 79 years, who were registered in the Diagnostic Advisory Center of the IMSP Oncological Institute in 2020. 63 outpatient cards of patients with confirmed morphological and immunohistochemical diagnosis have been examined. In the study were directly included 49 patients eligible for inclusion criteria. Sociodemographic, clinical and laboratory data of the patients were extracted from the outpatient cards.

Results of the research

Following the preparation of the patients research sheets, 3 types of indolent non-Hodgkin lymphomas were identified: SLL, FL and MZL. According to the results of our study, it was found a predominance of patients with SLL (40 patients-81.6%), compared to MZL

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