Received: Jan 25, 2025; 

Revised: manuscript received; May 22, 2025

Accepted: June 18, 2025

Published: June 18, 2025

Ref: Mukesh R, Toi PC , Chaudhari VA, Pandiyan KS, Kumaran M. Death due to Clinically Undiagnosed Hematolymphoid Malignancy: An Autopsy Case Report and Review.  Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology [serial online], 2025 ; Vol. 26, No. 2 (July - December 2025): [about 16 p].

DOI: 10.5281/zenodo.15708004

Available from: https://www.anilaggrawal.com/ij/vol-026-no-002/papers/paper002

​

Email: mukeshfmt22@gmail.com

( All photos can be enlarged on this webpage by clicking on them )

Death due to Clinically Undiagnosed Hematolymphoid Malignancy: An Autopsy Case Report and Review

Abstract

B-cell lymphomas, a type of hematolymphoid malignancy, constitute 90% of all lymphomas. We report an autopsy of a 33-year-old male with a clinical history of hypothyroidism and anemia brought unresponsive to casualty. The body exhibited no external injuries. Sparse and fine hairs were present in the face, chest, axilla and pubic region, with reduced right testicular size and scrotal volume. The thyroid gland was grossly not palpable and internally untraceable. The spleen was enlarged and softened with a wedge-shaped infarct in the cortical region and a hilar abscess. Under microscopy, the liver showed periportal chronic inflammation, bridging fibrosis and focal interface hepatitis. Acute tubular necrosis with thyroidization of tubules and focal tubular atrophy was reported in the kidney. Lymphoid infiltrates were found in the testis, brain parenchyma, pituitary, and liver, positive for markers like Tdt (Terminal deoxynucleotidyl transferase), CD34, and CD79a. The cause of death was opined as acute tubular necrosis due to septicemia secondary to B-cell lymphoma. After tissue or organ infiltrations, B-cell lymphomas are frequently linked with immunosuppression and multiorgan dysfunction, leading to death. Postmortem immunohistochemistry has helped in finding the key diagnosis in this case. In cases of unexplained anemia or endocrinological abnormalities, autopsy surgeons should rule out hematolymphoid malignancy. Clinicians must include the workup for hematolymphoid diseases in cases with atypical presentation.

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Keywords-

B cell lymphoma; Splenic infarction; Thyroidization; Immunohistochemistry in lymphoma; Hypothyroidism; Thyroid Dysgenesis; life threatening anemia

Glossary

Bcl: B-cell lymphoma, a general term for lymphomas affecting B cells.

● CD: Cluster of Differentiation, a system used to classify different types of white blood cells. It was suggested in 1982.

● CD34 – CD 34 is a cell surface protein that is commonly used as a marker to identify hematopoietic stem cells (the cells that give rise to all other blood cells) and endothelial cells.

● Clone QBEnd/10 -A specific monoclonal antibody that targets the CD34 protein. Q is a designation given by the laboratory or company that developed the antibody.

BEnd: indicate the target [end part refers to endothelial cells]. CD34 is commonly used to identify endothelial cells. 10 represents a sequential identifier, indicating that this is the 10 th clone developed in a series.

● DIC - Disseminated Intravascular Coagulation

● DLBCL: Diffuse Large B-cell Lymphoma, a common type of Non-Hodgkin Lymphoma.

● ECG: Electrocardiogram

● HLM: Hematolymphoid Malignancy

● IVBCL: Intermediate-grade B-cell Lymphoma, another type of Non-Hodgkin Lymphoma.

● Ki: Ki-67, a protein marker used to assess cell proliferation.

● MUM-1: Multiple Myeloma 1. It plays a role in the differentiation of B-cells into plasma cells. It is often used as a marker in immunohistochemistry to identify certain types of lymphomas and myelomas

● NHL: Non-Hodgkin Lymphoma, a type of cancer affecting the lymphatic system.

● PAX: PAX genes - a family of genes involved in the development

● RBC- Red Blood Cells

● Tdt: Terminal deoxynucleotidyl transferase, an enzyme involved in DNA synthesis. It is a specialized DNA polymerase. TdT is primarily expressed in immature, pre-B, and pre-T lymphoid cells, as well as in acute lymphoblastic leukemia/lymphoma cells

● Thyroidization - Thyroid like appearance in renal tissue

Introduction

Natural deaths due to disease and senility may be unexplained, where the cause of death is not known or unclear to the treating physician[1,2]. "Sudden unexplained death" refers to an unexpected and sudden death in an individual older than 1 year [3]. Unexplained sudden death (Intrinsic Factor(s) Identified) is a type of cause of death statement when the causality of death can be determined. However, intrinsic natural abnormalities like known intrinsic risk factors for sudden death or those of unknown significance are present. Trauma and other unnatural etiologies are properly excluded in such cases [4,5]. In a study, about 6-12% of cases subjected to medicolegal autopsies were determined to have died of natural causes [6]. About 35% of brought dead cases were reported to have a natural cause of death at autopsy [7]. About 8% of adult cases revealed clinically undiagnosed malignancy in autopsy [8]. About 20% of the clinically unsuspected malignancy was detected at the time of autopsy, while 16% presented with metastasis. Among the autopsy-diagnosed cancers, the primary cause of death was malignancy in 16% of such cases, which also includes hematolymphoid malignancies [9].

Hematolymphoid malignancies (HLM) are primary cancers affecting blood, bone marrow, and lymphoid organs, originating from either myeloid or lymphoid cell lines. Lymphomas, lymphocytic leukemia, myelomas and other plasma cell dyscrasias arise from lymphoid cell lines. In contrast, acute myeloid leukemia (AML), chronic myeloid leukemia (CML), myelodysplastic syndromes (MDS) and other myeloproliferative disorders (MPD) are myeloid in origin. Immunohistochemical markers like CD1a(Cluster of Differentiation 1a), CD3 (Cluster of Differentiation - 3), CD7 (Cluster of Differentiation 7), CD8(Cluster of Differentiation 8), CD20 Cluster of Differentiation 20), CD30 (Cluster of Differentiation 30), CD 34 (Cluster of Differentiation - 34), CD 79a (Cluster of Differentiation -79a), TdT (Terminal deoxynucleotidyl transferase), MIB (Cell Proliferation Marker), LCA (Leucocyte Common Antigen), etc. are used in the biopsy diagnosis of various types of HLMs with their expressivity in staining. Organ infiltration from leukemia, lymphoma, myeloma, and related conditions is less likely to be symptomatic than from carcinoma. Patients with HLM are at risk of complications from the neoplasm and treatment [10]. We present an autopsy case report with a postmortem diagnosis of lymphoma in the deceased, who was brought dead to casualty in our hospital after a brief period of hospitalization in another health care center.​

Case Report

We conducted an autopsy of a moderately built 33-year-old man. The deceased allegedly had anemia and hypothyroidism and was suffering epigastric pain along with reduced urine output for 3 days prior to death. As per the clinical records, prior to death, he was admitted to a hospital for management for 13 days. The lab values during the admission period were as follows: Hb-4.5g%, WBC- 12800/mm3, Neutrophils - 67%, Lymphocytes - 29%, Eosinophils - 4%. T3- 46.96 ng/dl (Normal- 70-204 ng/dl)), T4- 2.6 microgram/dl (Normal- 4.6-10.5 microgram/dl), TSH - 1.76 microIU/ml (normal - 0.4 - 4.2 microIU/ml), Blood urea - 40 mg/dl, Serum Creatinine- 1.2 mg/dl, Blood sugar - 87 mg%. ECG showed T wave inversion in V1-V3. The treatment included diuretics, iron supplementation, packed RBC transfusion, antibiotic prophylaxis, and thyroxine supplementation.

On external general examination, the body had no injuries, measuring 165 cm in length and 55 kg in weight. The conjunctiva was pale, while fingernails and toenails had nail paint. Natural orifices were free without any discharges. Sparse and fine hairs were present in the face, chest, axilla and pubic region (Figure 1A, 1B, 1C). The volume of the scrotum appeared relatively reduced (Figure 1C).

On internal exploration, the thyroid was not traceable in the anatomical or reported ectopic locations. In front of the arch of the aorta above the tracheal bifurcation, there was a solid grey-white mass measuring 1.5cm X 0.8cm X 0.8cm situated in the superior mediastinum. The adjacent muscle tissue was flabby and more softened. The spleen was soft with an intact capsule measuring 18cm X 11cm in frontal view and 750 g in weight. The cortex showed a coalesced pale infarct involving the entire organ and a wedge-shaped advanced infarct (Figure 2A). A splenic abscess measuring 3cm X3 cm had developed in the hilar region. Liver was congested with intact capsule. Lungs were congested and edematous (Figure 2B). Most segments were firm in consistency. There were multiple petechial hemorrhages in the right atrium and at the base of great vessels, and coronaries were patent. Examination of the kidneys revealed fatty infiltration with renal pelvis hemorrhage (Figure 2C). The right testis was smaller, measuring 4cm X 2cm X 2cm. Left testis appeared grossly normal. The thoracic cavity contained straw-brown colored fluid estimated to be about 750ml (Figure 2D).

In Figure-2

2A Infected pleural fluid in thoracic cavity (Arrows)

2B Frothy edematous fluid in lungs & trachea (Arrow Heads)

2C Infarcts in spleen (asterisk - advanced)

2D Infarcts (Asterisk) & hemorrhagic extravasation with necrosis (arrow head) in kidney

Under microscopy, the lungs showed dilated alveoli with interstitial congestion, chronic inflammatory cells with bacterial clumps, and hemosiderin macrophages. The liver showed chronic inflammation, fibrosis, and sinusoidal dilatation with lymphoid cells. The testes showed atrophy of seminiferous tubules and immature lymphoid cells in the interstitium with thickened tunica (Figure 3A). The thymus showed hyperplasia and thick-walled vessels (Figure 3B). Kidney tubules showed acute tubular necrosis, thyroidization, and atrophy with tubular hyaline casts (Figure 3C). Tonsil showed increased lymphoid cells, while lymph nodes showed reactive changes (Figure 3D). The brain showed dilated vessels filled with lymphocytes and parenchymal lymphocytic infiltrates (Figure 3E). The pituitary showed diffuse infiltration of immature lymphoid cells, highlighted with CD79a. The left ventricle showed pericardial fat with chronic inflammation, interstitial oedema, and lymphoid aggregates. The right ventricle of the heart showed thick- walled vessels and lymphoid aggregates. The aorta shows atherosclerotic changes along with lymphoid aggregates (Figure 3F). The unidentified thick mediastinal mass from the thorax showed interstitial spaces and lymphoid aggregates in the background of skeletal muscle cells. The suitable tissues were subjected to immunohistochemistry.

Fig 3. Microscopic examination (Hematoxylin & Eosin) showing lymphoid infiltrates in various oegans:

A- Testis (10x)

B- Thymus (40x)

C- Kidney (10x)

D- Tonsil (4x)

E- Brain (40x)

F- Aortic wall (4x)

Immunohistochemical staining with primary and secondary antibodies (PathnSitu Biotechnologies) was performed using Ventana platform for CD3 (clone Polyclonal), CD20 (clone L26), CD34 (clone QBEnd/10), CD79a (clone HM47) and TdT (Polyclonal Rabbit Anti-Human TdT Antibody (Abcam, Cat# ab19515)) in a dilution of 1:200 with standard operating protocol. The moderate intensity of DAB chromogen in the slide image was considered positive expressivity. On immunohistochemistry, Tdt, CD34, and CD79a highlighted the immature (probably blast) cells in the pituitary, liver and testis. CD3 and CD20 were negative in the immature B cells. Hence, the possibility of B cell leukemia or lymphoma was reported from histopathological impressions. Blood and sterile fluid culture showed the growth of Escherichia coli. Toxicological examination did not detect any poison or drugs in this case. The cause of death was opined as acute tubular necrosis due to septicemia as a complication of B cell lymphoma.

Discussion

More than 30% of HLM cases diagnosed in autopsy, were earlier clinically undiagnosed [10,11]. Diffuse Large B cell lymphoma is the most common type of NHL (Non-Hodgkin Lymphoma), frequently observed in adults, and so is indolent lymphoma [12]. The mean age range of autopsy confirmation of HLM is about 36-46 years [10,11,13], whereas the age of the deceased was 33 years in the present case.

Lymphoma may be localized, and it may later tend to be rapidly progressive. Diffuse Large B Cell Lymphoma (DLBCL) involves nodal or extranodal sites, including the Waldeyer ring, lung, bone marrow, spleen, liver, and gut, manifesting as a rapidly growing mass [14,15]. Intravascular B Cell Lymphoma (IVBCL), a rare type of non-Hodgkin lymphoma, primarily invades blood vessels and presents with neurological or hemophagocytic symptoms depending on the variant [16]. The spectrum of clinical features in lymphoma includes low- grade intermittent fever, nausea, oliguria, anorexia, abdominal pain, weight loss, oedema, pallor, progressive dyspnea, cognitive decline, painless lymphadenopathy, splenomegaly and lactic acidosis [17-24]. Lymphoid malignancy may be further clinically associated with anemia, hypertension, hypothyroidism, paraplegia and multiorgan failure [25,26]. The present case had an antemortem diagnosis of anemia and hypothyroidism. T wave inversion in lead V1-V3 ECG is a normal variant in children but indicates cardiac pathology in adults [27], which does not exclude secondaries or lymphoid infiltration in the present case. In aggressive cases of lymphoma, autopsy may reveal septic and disseminated intravascular coagulation- like picture bone marrow hyperplasia and hepatosplenomegaly [18,19]. The correlation of gross autopsy features with histopathological findings remains crucial for diagnosis, especially in cases with atypical presentations of HLMs [17,18,29].

Generally, painless lymphadenopathy is found in most HLMs [17]. Enlargement of peripancreatic, mesenteric, hilar, paratracheal, paraaortic and mediastinal lymph nodes have been reported [10]. In cases of NHL, diffuse infiltration by tumor cells causes complete architectural effacement. In our case, lymph nodes showed reactive changes, which could be attributed to infection. Tonsils, in HLM, may show monomorphic proliferation of large lymphoid cells, distinct plasmacytoid features, eccentrically placed nuclei, thick nuclear membranes, variably prominent nucleoli, clumped chromatin, and copious pyroninophilic cytoplasm [36]. In the present case, diffuse infiltration of immature lymphoid cells was found in the tonsils.

Diffuse infiltration with angiotropic features, CD20 positivity and decreased ACTH immunoreactivity in the pituitary with associated hypogonadotropic hypogonadism has been reported [37,38]. Diffuse infiltration of lymphoblast cells is found in the pituitary gland with associated hypogonadotropic hypogonadism. Hatem reported diffuse lymphoid infiltration of skeletal muscle in multiple cores with pseudo-glandular structures and sheets observable in low-power microscopy [39]. Skeletal muscle exhibited immature lymphoblast infiltration, with features like large cells, irregular nuclear contours, vesicular chromatin, prominent nucleoli, and moderate cytoplasm in high-power microscopy.​

The thymus showed hyperplasia with a preponderance of immature B cells in our case. Lymphoma may cause thymus enlargement either by primary involvement or secondary infiltration following the invasion of adjacent lymph nodes. Medullary B-cell lymphoma in the thymus is found in 2% of cases with NHL [47]. Malignant lymphoma in the thymus can resemble hyperplastic thymus. Histologically proven invasion in the thymus was not revealed even in advanced imaging methods like FDG or chemical shift MRIs.[48].

Petechial hemorrhages in the ventricular subendocardial region and cardiac hypertrophy were reported in the literature [10, 49]. The tumor cell infiltrates are reported in the myocardium, epicardium, conduction pathway [49,50], cardiac septum and valves [10]. In the present case, the heart displayed petechiae, inflammation with interstitial oedema, lymphoid aggregates, thick aortic and vessel walls, myxoid changes, and enhanced fibrosis.

Pulmonary nodules, mostly calcified and peripheral lung oedema, have been reported [18,19]. Doran reported extensive neoplastic infiltration, generally filling vessels and spilling out into the alveoli while associated with thrombo-embolism and infection (pneumococcus, aspergillus) in the lungs [51]. Microscopic examination of the edematous lung, in our case, revealed dilated alveoli with interstitial congestion with chronic inflammatory cells with bacterial clumps and hemosiderin macrophages.

Reported findings of lymphoma in the liver include neoplastic infiltration, fibrosis, cancerous nodules, necrotic areas, Reed–Sternberg cells, hypocellular regions, diffuse organ filtration by leukemic cells, profound infiltration of CD30 (Ki-1) positive lymphoma cells [11,52,53]. Enlarged hemorrhagic lymph nodes at porta hepatis were also reported by Waghmare TP et al. [10]. Infiltrates in sinusoidal and periportal regions with nodular aggregates were recorded. Liver, in the present case, periportal chronic inflammation with bridging fibrosis, focal interface hepatitis, sinusoidal dilatation with large lymphoid cells, despite normal hepatic architecture.

Hemorrhagic splenic infarcts involve vascular congestion, hemorrhage, and necrosis, while septic infarcts involve acute or chronic inflammatory infiltrates. Lymphoma-induced splenic infarctions result from blood flow interruption and hence bland infarcts are pale, wedge-shaped, and subcapsular. Septic infarcts have suppurative necrosis and large depressed scars during healing. Splenic abscesses show chronic inflammatory infiltrates and necrotic cells [54]. In our case, the spleen was enlarged with massive pale infarcts, implying the possibility of splenic vessel thrombosis. About 10% of splenic infarcts progress to bacterial abscesses in immunocompromised individuals [55,56]. In the present case, there was a progression into a splenic abscess in the hilar region.

Renal enlargement and deposits are reported in HLM [10], while renal pelvic hemorrhage was found in our case. The microscopic findings include acute tubular necrosis, thyroidisation of tubules and focal tubular atrophy with hyaline casts. Tubular atrophy involving broader areas and delineated interstitial fibrosis along the medullary rays forming a striped scarring pattern suggest chronic ischemia. The thyroidization pattern is often seen in urinary reflux or chronic pyelonephritis [57].

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Testicular infiltration in leukemia cases is typically bilateral but asymmetric in severity, starting in one testis before affecting both. Specific size measurements of affected testis were hardly found in autopsy-based literature. Its severity is similar to other sites but can be second only to marrow, lymph nodes, and spleen involvement. Microscopic infiltration is most common in acute leukemia, less common in chronic leukemia, and less frequent in lymphoma [58]. Atrophy of the seminiferous tubules with immature lymphoid cells with thickened tunica was observed in our case. Abnormally small testes, smaller than the 50th percentile for age, can be caused by congenital or acquired factors.[59].

Waghmare & Moller reported leukemic infiltrates in the brain parenchyma, meningeal and Virchow robin space [10,60]. Thirunavukkarasu reported patchy myelin pallor in subcortical areas without over-demyelination due to lymphoma cell infiltration [61]. In our case, cerebral vessels were dilated, along with increased vascular and parenchymal lymphocytic infiltrates.

Immunohistochemical studies help to type the tumor cells infiltrating various organs like the lungs, liver, spleen, pituitary gland, ovaries, uterus, and bone marrow. Diffuse large cell B-cell lymphoma (DLBCL) tests positive for CD20, CD79a, bcl-2, and MUM1 but negative for CD3, CD5, CD10, CD 56, bcl-6, and cyclin D1 [20, 26]. Reportedly, diffuse CD20 positivity is found in lymphoid cells in sinusoidal and interstitial sites with a Ki-67 index of about 80% to 90% [26]. The CD20 negative subtype of DLBCL is rare and aggressive, with lesser survival rates [62]. B cell lymphoblastic leukemia also tests positive for TdT, CD34, CD79a or PAX5 [63]. IVLBCL exhibits strong intravascular CD20 and CD45 positivity [21]. In the present case, immature B cells in the pituitary, liver and testis tested positive for Tdt, CD34, and CD79a and negative for CD3 and CD20, suggesting B cell lymphoma or leukemia as a final impression on immunohistochemical confirmation. Following flow cytometry, fluorescence in situ hybridization (FISH) analysis is the method of choice for confirmatory diagnosis [64]. CD34 is a transmembrane phosphoglycoprotein found on cell surfaces in humans and animals, used to identify and isolate cancer stem cells (CSC). It is positive in leukemia, breast and lung cancer, and other types of tumors [65]. Terminal Deoxynucleotidyl Transferase (Tdt) is a DNA polymerase found in high levels in the thymus, low levels in normal bone marrow, and absent in normal peripheral blood leukocytes. In adult leukemias, the Tdt level is elevated primarily in lymphoblastic leukemia and low in myeloblastic leukemia [66]. CD79, pan B-cell marker, is a dimeric, transmembrane protein, which, along with surface immunoglobulin, is expressed from the pre-B stage to the plasma cell stage of differentiation. It is found in B-cell lymphomas, B-cell lines, most acute leukemias of precursor B-cell type, megakaryocytic lesions and certain myelomas [67].

Hematological malignancies exhibit a dynamic spectrum of infections among the affected patients [68]. Most of the infections were either systemic or pulmonary [69]. Klebsiella pneumoniae, Escherichia coli and Pseudomonas aeruginosa were the most frequent organisms isolated, resulting in mortality rates up to 48% in diagnosed cases of HLMs [70]. Escherichia Coli is isolated from blood and fluid culture in the present case, forming the primary foci for septicemia like in other cases [70-73].

The specific subtype of B-cell lymphoma may also influence the primary cause of death [10,74]. The progression and transformation into aggressive subtypes, such as diffuse large B-cell lymphoma, has an unfavourable prognosis and increased mortality rates [20]. Complications from the disease, treatment-related side effects and comorbidities contribute to mortality [28, 75-77]. Death was commonly caused by Disseminated malignancy followed by fatal respiratory illness or complications [10,71]. Any infiltrative diseases involving the spleen can also lead to spleen rupture, causing intraperitoneal bleeding, shock, and death [78- 80]. Other causes of death include infection, hemorrhagic shock, hemoperitoneum, thromboembolism, increased intracranial tension with cerebral oedema and conduction abnormalities and associated congenital heart disease [10,20]. Significant autopsy findings in cases of septicemia include pulmonary oedema, diffuse alveolar damage with micro- thrombosis, inflammation & ischemic necrosis of cardiac tissues, acute tubular necrosis, cholestatic jaundice, liver necrosis with sinusoidal aggregates, partial liquefaction of spleen, hemorrhagic adrenal gland, cerebral petechiae, sub-serosal or submucosal hemorrhages in the gastrointestinal tract and features of disseminated intravascular coagulation [81]. In the present case, death is attributed to septicemia secondary to B cell lymphoma in its advanced stage involving multiple organs. Multiple conditions, including syndromic abnormalities like hypogonadism and Kallmann syndrome, were in consideration before concluding the autopsy cause of death in this case. However, the findings from ancillary investigations of the tissues and fluids, in corroboration with the gross features of the case, directed the focus of causality towards B cell lymphoma.

Conclusion

​The unexpected discovery of B-cell lymphoma in this 33-year-old man with a history of anemia and hypothyroidism demonstrates th e potential for these conditions to remain undetected until postmortem investigation. The gross findings, extensive lymphoid infiltration observed across multiple organs on microscopy, and immunohistochemical findings provided crucial evidence for diagnosing B-cell lymphoma. Septicemia, the common fatal complication of B-cell lymphoma as in any HLM, had caused death in this case. The case report highlights the importance of comprehensive autopsy examinations in identifying clinically undiagnosed malignancies, particularly HLMs.

Limitations

The spleen and bone marrow were not subjected to microscopic studies using cytomorphology, histomorphology, and immunohistochemistry, thereby posing difficulty in locating the lymphoma's primary origin.

Suggestions

For Autopsy Surgeons: The case highlights the importance of autopsy in medical education, quality assurance, and disease understanding. Postmortem diagnosis of B-cell lymphomas can be challenging due to heterogeneity and limited tissue samples. Understanding gross autopsy findings in HLM is crucial for prompt recognition and management. In unexplained anemia or endocrinological abnormalities, an autopsy should also rule out HLM.

For Clinicians: The case report emphasizes the importance of clinicians detecting underlying malignancies in cases with atypical presentations or unexplained deterioration. Advancements in diagnostic techniques like noncoding RNAs, Next-Generation Sequencing, and radiomics provide new insights into disease pathogenesis and development, while tissue proteomics and digital pathology can enhance early detection [82-86].

Conflicts of interest

The authors have declared no conflict of interest in the submitted work. 

Funding/services

All authors have declared that no financial support or service was received from any organization for the submitted work.

Ethical Approval & Informed Consent

This article does not contain any studies with animals. This is a retrospective case report of a medicolegal autopsy. The case data has been completely anonymized with proper de- identification of contents in this report.

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*Corresponding author and requests for clarifications and further details:

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Dr Mukesh R,

Assistant Professor, Department of Forensic Medicine & Toxicology,JIPMER, Pondicherry.

Mail at: mukeshfmt22@gmail.com