Book Review Journal Aims & Objectives This journal has been started by Dr Anil Aggrawal, Professor of Forensic Medicine at the Maulana Azad Medical College, New Delhi - 110002. Dr. Aggrawal is quite keen to interact with people who are interested in books. Dr. Aggrawal adores books and literally thrives on them. Though being a medical doctor specializing in forensic medicine, he loves books on all subjects encompassing such diverse ranges from astronomy and zoology to paleontology, history, occult science, philosophy, mathematics, and classical literature, et al. His penchant for books was conceived quite early in life. Even as a three year old he always pined for books instead of toys-as his siblings did. There is a legend about the Greek mathematician and engineer Archimedes (ca. 287 B.C. - ca. 212 B.C.). When Roman armies sacked Syracuse in 212 B.C. he was busy studying a geometrical figure made in sand. When a Roman soldier commanded him to come along, he motioned to him imperiously, "Don't disturb my circles". The soldier felt so insulted that he killed Archimedes on the spot! In a similar situation Dr. Aggrawal would probably say, "Don't disturb my books!" Writers and thinkers have always been his idols. Some of the people who have inspired him are (i)Lord Buddha (he remains first on his list) (ii)Albert Einstein (iii)Robert James Fischer (The only American who has been an official World Chess Champion) and (iv)Isaac Asimov (he wrote close to 500 books, and is reputed to be the only author to have published books in all ten categories of the Dewey Decimal System! Oh, well, we all know it's not true, but he has really written so widely, it seems cruel to challenge this statement.) Aggrawal is no Asimov, but like him, he loves writing books. He has written nine books so far (till 2006 end). Four of them are quiz books, which reflect his morbid passion for quizzes. The books, in order they were published are (i) 1000 Crime Quiz (published 30 March 1992) (ii)1000 Love & Sex Quiz (published 13 August 1992) (iii) Some Common Ailments (Published 27 January 1993)(iv)The Book of Medicine (Published 5 February 1994) (v)Narcotic Drugs (Published on 2 May 1995) (vi) 1000 Biology Quiz (Published on 29 August 1995) (vii)Modern Diagnostics (Published on 8 March 2001) (viii) Health Quiz Book (Published on 5 August 2002) (ix) Self Assessment and review of Forensic Medicine and Toxicology (the first book related to his profession). And since we all love statistics, here is a detailed statistics of these books. Here they are: S. no. Book Started on Completed on Published Publisher Publisher Cost 1. 1000 Crime Quiz 1.2.91 31.5.91 31.5.91 March 1992 Rupa 30 2. 1000 Love & Sex Quiz 1.6.91 7.1.92 7.1.92 August 1992 Rupa 30 3. Some Common Ailments 1.6.91 28.11.91 28.11.91 January 1993 NBT 25 4. The Book of Medicine Nov 92 15.1.93 15.1.93 February 1994 Rupa 30 5. Narcotic Drugs 1.1.93 9.5.94 9.5.94 May 1995 NBT 46 6. 1000 Biology Quiz 6.1.92 17.3.93 19.3.93 August 1995 Rupa 80 7. Modern Diagnostics 1995 1996 1996 March 2001 NBT 80 8. Health Quiz book Feb 2002 July 2002 July 2002 August 2002 Ocean Books 200 9. Self Assessment and review of Forensic Medicine and Toxicology 2005 April 2006 April 2006 May 2006 PeePee 295 (Books published till 2007 end) N.B. 1. NBT stands for National Book Trust, India. 2. Dates mentioned are in this format: day/month/year. 3. The cost is in Indian Rupees. 4. Some Common Ailments has been translated in Assamiya, Bangla, Hindi, Kannada, Konkani, Marathi, Nepalese, Oriya, Punjabi, Telugu and Urdu (Total 12 languages). 5. Narcotic Drugs has been translated in Assamiya, Bangla, Hindi, Punjabi and Urdu (Total 6 languages). 6. Health Quiz Book has been translated in Hindi (Total 2 languages). Why is Dr. Aggrawal interested in writing book reviews? Whenever he reads a book he tries to discover its strong points. There is a subconscious effort on his part perhaps, to incorporate those points in his own writings. He then wants to share his findings with everyone. In the year 2000, he started an Internet Journal of Forensic Medicine and Toxicology , and out of his sheer interest in books, he included a book review section to it. The unprecedented popularity of the review section took him by complete surprise. He received books from authors and publishers in thousands. And they belonged to all subjects-not only forensic medicine and toxicology, which he had intended at the inception of the above journal. With time he and his group realized that they must conjure another journal devoted solely to Book Reviews for books of all genre. In this all-new journal they would accommodate all kinds of books, and hence the present Anil Aggrawal's Internet Journal of Book Reviews . Dr. Aggrawal fondly cites the examples of many regular journals (not devoted to book reviews), which have come out with issues especially devoted to book reviews. One pertinent example is Archives of Sexual Behavior , which came out with an issue (Volume 28, Number 5 / October, 1999, pages 377-467) especially devoted to book reviews in 1999. Readers can access this issue by clicking here .

Main Page > Vol-26 No.- 2 > Paper 2 (you are here) LinkedIn X (Twitter) Facebook Copy link Share Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Volume 26 Number 2 (July - December 2025) 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. 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). Fig 1. Immature & sparse hairs: Face (A), Axillary region (B) and Pubic region (C) hairs. Reduced testicular size (Arrow mark in C) 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). Fig 2. Significant internal findings 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. Thyroid dysgenesis, which includes thyroid agenesis, hypoplasia and ectopic thyroid, amounts to 80-85% of congenital hypothyroidism [40,41]. Acute leukemia is linked to autoimmune thyroid diseases like Graves' and Hashimoto's thyroiditis, with hypothyroidism being a common outcome of thyroid lymphoma [42]. Also, secondary hypothyroidism is most commonly associated with pituitary disorders/abnormalities [43, 44]. A case study by Foresti showed a cause-effect relationship between leukemic infiltration of the thyroid gland and hypothyroidism, with progressive reduction in thyroid hormones and increases in TSH levels [45]. In our case, there was no trace of thyroid in the neck or mediastinum. Clinically, the thyroid profile has shown decreased secretion of thyroid hormone levels, suggesting the possibility of ectopic thyroid. However, no glandular tissue was identifiable or appreciable in the usual reported areas of ectopic thyroid during the autopsy [46]. A mediastinal unidentified tissue excised in an autopsy suspected of ectopic thyroid also did not show any histological components of thyroid tissue; only lymphoid aggregates were found in the background of skeletal muscle cells. This is similar to a study by Waghmare TP et al. where 18% of the NHL cases had soft fleshy yellow-white mass [10]. 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]. 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. References Hanzlick R, Hunsaker JC, Davis GJ. Guidelines for Manner of Death Classification. Atlanta. GA. National Association of Medical Examiners. 1st ed. 2002. Available online from: Link Our role in investigating deaths [Internet]. Scotland. Crown Office and Procurator Fiscal Service. 2023 June 9 [Updated on 2024 July 16. Cited on 14 September 2024]. 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Main Page > Vol-26 No.- 2 > Paper 3 (you are here) LinkedIn X (Twitter) Facebook Copy link Share Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Volume 26 Number 2 (July - December 2025) Received : April 28, 2025 Accepted : June 18, 2025 Published : June 18, 2025 Ref: Kumar J, Khan IA, Reyazuddin M, Haroon A, Khan FA. Proposing a Single centre as a Drug and Toxicology Unit for Complete Care of Substance Abuse and Poisoning Patients at Tertiary Care Centers. Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology [serial online], 2025 ; Vol. 26, No. 2 (July - December 2025): [about 17 p]. Available from: https://www.anilaggrawal.com /ij/vol-026-no-002/papers/paper003 DOI: 10.5281/zenodo.15708358 Email: dr.jitendrak2@gmail.com ( All photos can be enlarged on this webpage by clicking on them ) Proposing a Single centre as a Drug and Toxicology Unit for Complete Care of Substance Abuse and Poisoning Patients at Tertiary Care Centers Abstract A Registered medical practitioner is qualified to manage all the cases of poisoning and substance abuse after passing their graduate medical education. The qualification of managing poisoning cases comes from Toxicology taught to them under the subject "Forensic Medicine and Toxicology". At tertiary care centres, the post-graduates in Internal Medicine manage poisoning and substance abuse cases under emergency care based on the knowledge they received during their undergraduate studies. However, the Teacher who taught the subject is practically not involved in managing such patients, i.e. preaching without practice. This results in a gross deficiency in the quality of care for poisoning cases. To overcome this, we propose one centre as a Toxicology unit at every tertiary care centre, corroborating Medicine, Forensic Medicine, Pharmacology, Psychiatry and various other disciplines dealing with all the aspects of Substance abuse and Poisons. With the help of this unit, we can run a single centre catering to the management of poisoning and substance abuse patients, their mental health, diagnostic centres for drugs and poisons, drugs and poison information centre (DPC) including drugs de-addiction and treatment centre (DDAC), an integrated rehabilitation centre for addicts (IRCA), Outreach and Drop-in centres (ODIC), De-addiction drug pharmacy and various training courses to the health care professionals. Keywords: Toxicology, Poisoning, Substance abuse, Mental health, Suicide Introduction Suicide is one of the preventable forms of death. Suicide is not only a personal tragedy that takes the life of an individual prematurely, but it has a continuing ripple effect, affecting the lives of families, friends and communities. The global burden of death due to suicide is more than seven lakhs per year (1). Suicide is among the top 20 leading causes of death in the world (WHO) and among the top 10 leading causes of death in India (NCRB data) (2). Although we don't have actual data on the suicide attempters, as per WHO, for each suicide, there are likely more than 20 suicide attempts (3). In that way, if we consider suicide as a preventable disease, then this will become the most prevalent disease in the world, and 2nd commonest will be far behind. Sadly, 77% of global suicide occurs in middle- and low-income countries. Suicidal behaviour is a complex phenomenon that demands a holistic approach of care and support by multiple agencies. Mental Health Care Act, 2017 and India Under Indian Penal Code (IPC) section 309, the attempt to commit suicide is a criminal offence and is punishable with one-year imprisonment with or without a fine. With the implementation of the Mental Health Care Act 2017 (4), Section 309 of IPC was decriminalized, and it was stated that "Any person who attempts to commit suicide shall be presumed, unless proved otherwise, to have severe stress. And the appropriate government shall have a duty to provide care, treatment and rehabilitation to a person having severe stress and who attempted to commit suicide to reduce the risk of recurrence of attempt to commit suicide”. This has changed the approach of every stakeholder towards suicide patients. Although suicidal behaviour was seen as a mental illness, treatment for the same is provided by the Psychiatry department of the hospital for a long apart from their regular treatment (5-9). But with this commendatory step taken under the Mental Health Care Act, every attempt of suicide shall now be seen as a disease rather than an offence for which the appropriate government and healthcare provider will provide proper care, treatment and rehabilitation as per the standard guidelines. Poisoning and Mental Health It has been observed that most of those patients who survive suicide and get admitted to the hospital, the majority of them are with poisoning incidences, and poisoning is the most typical method practised. Also, it has been reported that most of the poisoning cases are suicidal (More than 75%), followed by accidental (10, 11). In view of this, the majority of cases of poisoning need care of their mental health. Substance Abuse, Mental Illness and Toxicology Substance abuse, i.e., the harmful or hazardous use of psychoactive substances, including alcohol and illicit drugs, is a form of toxicity itself and is an essential part of pharmacology and toxicology. They are taught to undergraduates under the drug dependence chapter of Forensic Medicine and Toxicology. The emergency care of such patients is done at casualty by post-graduates in Internal Medicine and further care in the Psychiatry department. At present, we don't have substance abuse testing labs in hospitals. Essential care of such patients in a routine manner is avoided due to medico-legal reasons. Substance abuse is a shared Medicine, Pharmacology, Forensic Medicine and Psychiatry domain. So, a multi-disciplinary approach is essential for proper care of such patients. Pharmaceutical Drugs, Environmental Poisons and Toxicology lab Indiscriminate use of drugs without proper prescription is rampant in the society. This results in toxicity, resistance, chronic renal diseases and various other pathologies. We don't have toxicology labs even at the tertiary care centre for the testing of chronic drug toxicity. Similarly, air pollution, water pollution, household poisons, and other factors resulting in chronic diseases and ill health are totally ignored areas of toxicology management. We need toxicology labs and research in this part to provide proper care for such cases. Present practice in the care of Poisoning cases and Forensic Medicine and Toxicology Understanding of the management of poisoning cases is developed among Indian medical graduates through their teaching of the Subject "Forensic Medicine and Toxicology" during their second or third professional. However, Forensic Medicine and Toxicology faculties are not practically involved in the care of poisoning patients. They develop their training only theoretically. Poisoning cases at tertiary care centres are dealt mainly as emergency cases. Post-graduates in Internal Medicine provide emergency symptomatic care to the patients along with other routine emergency patients. At our hospital, ACMO (Assistant Casualty Medical Officer, mostly Post-graduate students of different disciplines posted temporarily in the casualty) sees all patients coming to casualty first, including poisoning cases. In poisoning cases, ACMO takes the patient's history, notes vitals, and categorizes the patient as stable or unstable. In case of an unstable poisoning patient, he gives a distress call to Anesthesia. The Anesthesia team does resuscitative measures and accordingly takes to a ventilator or stabilizes the patient. Once the patient is stable, Gastric lavage is done, and the patient is referred to the Medicine unit in case of an adult. Most antidotes for poisoning are unavailable. Routinely, Normal saline and sometimes charcoal are used. In the Medicine unit, routine blood testing for non-critical poisoning cases includes CBC, LFT, KFT, ABG and ECG (sometimes) are done. If nothing abnormal in the above parameters, only symptomatic supportive treatment is given, and the patient is observed for up to 24 hours and then discharged. In case of any abnormal parameters, the patient is managed in the ICU or CCU ward. In most cases, no MLC is prepared, and neither gastric lavage is preserved for MLC purposes. Also important to note is that all the care related to poisoning is done along with other emergency or ward cases. Poisoning cases in government or private are medico-legal cases, whether accidental, suicidal or homicidal. This becomes another reason for the cold approach in the care of such patients. Proper Medico-legal formalities are not done, and cases are usually sent to the home after recovery without proper medico-legal formalities. Also, the doctors of Internal Medicine don't get any separate training for poisoning cases, but they manage patients like other routine emergency cases based on the knowledge of Forensic Medicine and Toxicology taught long back. So, overall, poisoning management is developed more theoretically than practically, i.e. preaching without practice. This results in a gross deficiency in the quality of care for poisoning cases. Most tertiary centres face the unavailability of toxicology management related medicines like activated charcoal, various antidotes, etc., as well as the availability of other resources and space constraints. To overcome this, Faculties and Residents of Forensic Medicine and Toxicology need to be involved in managing poisoning patients and dedicated centres for the care of Toxicology patients are the need of the hour, particularly at the tertiary care centres. Since toxicology care is multi-disciplinary, we propose a Drug and Toxicology unit. Drug and Toxicology Unit We are proposing one single centre as a Drug and Toxicology unit at every tertiary care centre, corroborating Internal Medicine, Forensic Medicine and Toxicology, Pharmacology, Psychiatry and various other disciplines dealing with all the aspects of Substance abuse, Drugs and Poisons for better care and compliance with such patients. It shall be established near the hospital's emergency department for better patient care and to admit patients of the above categories after their emergency care. The unit shall have The Drug and Toxicology Division and the Substance Abuse and Mental Health Division. The following parts shall be attached to each division, as shown in Fig. 1. Figure 1: Different centres under the Drug and Toxicology Division and Substance Abuse and Mental Health Division Drug And Toxicology Division Substance Abuse And Mental Health Division Drug and Toxicology out-patient department Drug and Poison Information Centre (DPC) Diagnostic lab (Drug level estimation) Diagnostic lab (Poison level estimation) Drug and toxicology ward (Min. 20 bed) Antidote Bank Substance abuse out-patient department Drug de-addiction centre and treatment (DDAC) Outreach and drop-in centres (ODIC) De-addiction drug pharmacy Integrated rehabilitation centre for addicts (IRCA) Objectives A single centre dealing in all aspects of Drugs, Poisonous Substances, Substance abuse and mental health for the convenience of the patients and administration. Human resource and workforce development by training medical undergraduates, post-graduates, research scholars, and other staff in all aspects of drugs and toxicology for better running of such centers. Benefits The facility will support the hospital and the public in better diagnosis and management of drug-related events, poisoning cases and substance abuse cases. It will have a Drug and Poison information centre that will provide knowledge about all the aspects of Drugs, Poisonous substances and Substance abuse to the public and health care providers, which will save the lives of many. All the drug and toxicology-related investigations shall be available in the Drug and toxicology unit. The earliest diagnosis of the Poison can help save the lives of many and support the investigating agencies in regulating the availability of such poisons. Unit shall estimate the drug levels through therapeutic drug monitoring (TDM) in case of life-threatening events and low therapeutic index drugs. De-addiction and treatment centre (DDAC), an integrated rehabilitation centre for addicts (IRCA), and Outreach and Drop-in centres (ODIC) will be beneficial in the prevention and management of Substance abuse cases. A de-addiction pharmacy and antidote bank will provide de-addiction drugs and poison antidotes that will be very helpful in patient care and compliance. De-addiction drug pharmacies will be very supportive of patient of substance abuse to avail their prescribed drugs at ease with following norms as per the NDPS Act, 1985. Teaching and training medical undergraduates and post-graduates in clinical pharmacology and toxicology can be imparted. Various courses like DM (Pharmacology), DM (Toxicology), DM (Psycho-pharmacology), DM (Addiction Psychiatry) along with PhD programs, MSc, DMLT and other related courses in clinical pharmacology, toxicology and Substance abuse may be undertaken. New Research avenues may be inculcated through this unit. We can collaborate with institutes of high eminence for further enhancement. We can also generate good revenue from various sources, as mentioned in Table 1. For substance abuse management and care, the Department of Social Justice and Empowerment provides massive funding to such centres. Table 1: Revenue for the above unit can be generated from the below sources Drug And Toxicology Division Substance Abuse And Mental Health Division Ward admission charges OPD charges Drug and poison estimation charges Therapeutic Drug Monitoring charges Different academic and training courses Antidote bank charges Ward admission charges De-addiction pharmacy EEG Bio-feedback MBT (Aversive Therapy) Motivational enhancement therapy Social skill Training Funding by department of Social justice and empowerment. Our Proposal under HEFA Higher Education Financing Agency (HEFA) is a joint venture of the Ministry of Education, Government of India and Canara Bank to finance the creation of capital assets in premier educational institutions in India. This idea of the Drug and Toxicology unit evolved from inter-departmental activity that started while preparing such proposals that will be a revenue-generating model. HEFA provides funds for infrastructure and equipment, with the condition that they return 10% of the amount in 10 years. In brief, we have proposed an infrastructure with the Ground and first floors having the Drug and Toxicology division and the Second and third floors having the Substance abuse and Psychiatry division (as shown below in Fig. 2-5). Figure 2 : Layout plan for ground floor Figure 3 : Layout plan for first floor Figure 4 : Layout plan for second floor Figure 5 : Layout plan for third floor Tentative Cost And Revenue Generation We estimated the cost of infrastructure and equipment separately as per government norms for both divisions, along with tentative revenue generation as shown in Table 2. Table 2: Tentative cost and revenue generation for the Drug and Toxicology unit as calculated forour proposal under HEFA Drug and Toxicology Division Substance abuse and Mental health division Tentative cost Building (Ground + First floor) = 6.07 crores Instruments/Lab=20.30 crores Total cost= 26.37 crores Building (Second + Third floor) = About 6 crores Instruments/ Lab= 6.35 crore Total cost= 12.42 crores Tentative revenue About 3150 patients were considered per month as per the current hospital load. Ward admission + OPD Charges + Lab investigations (Drug and Poison analysis + TDM) may generate a revenue of about 28.23 lakhs per month and approximately four crores per year. About 750 patients were considered per month as per the current hospital load. Ward admission + OPD charges + De- addiction drug pharmacy + EEG + Biofeedback + MBT + Motivational enhancement therapy + Social skill training = 7,47,500 per month and 89.7 lakh per year further funding by the Ministry of Social Justice and Empowerment approximated to be about 1.46 crore per year for DDAC's, IRCA's, ODIC and Nasha Mukti Abhiyan. Total revenue generation = About 2.5 crore Similar Successful Projects As per our information, we could not find any such unit that incorporates drugs, toxicology and Substance abuser care under one centre all over India. However, many centres run separately for each division, with limited facilities. Drug and Toxicology Division All India Institute of Medical Sciences, Raipur, has started caring for poisoning patients under the Forensic Medicine Department and is also running a DM course in toxicology with two intakes per year. They are taking patients with poisoning cases after the emergency stabilization. The Poison Information Centre is being run at various centres, mainly under the Pharmacology department like AIIMS, New Delhi, which runs the National Poison Information Centre with toll-free (1800 116 117). Amrita School of Medicine, Cochin, runs the Poison Control Centre and Clinical Forensic Medicine with an Analytical toxicology laboratory attached and accredited by the NABL under the Forensic Medicine department. They are not directly involved in the treatment of patients. Substance Abuse and Mental Health Division National Drug Treatment Centre, Ghaziabad (NDDTC), under AIIMS, Delhi, has been established as the apex centre for the management of drugs and substance abuse disorders in India. The centre provides clinical care to patients through community-based OPD and In-patient care, speciality clinics, wards, etc. Health education & preventive measures for substance abusers are done on a community basis. The centre works as a nodal centre for evaluating the prevalence of addiction in society. The centre is involved in staff training and human resources development to cater to such services nationwide, apart from testing, documentation and research in substance abuse disorders. PhD Programme and DM in the area of Addiction Psychiatry running under this centre. Also, they are designated as a WHO Collaborating Centre on Substance Abuse (12). Further, 90 DDAC, 95 ODIC, and 375 IRCA are running under the Ministry of Social Justice and Empowerment all over the country at present (13). Conclusion Healthcare management is interdisciplinary and involves teamwork rather than individual activity. Both the poisoning patients and patients of substance abuse need the care of their mental health. All the poisoning cases and substance abuse cases are medico-legal cases and need the support of Forensic Medicine and Toxicology for Management and other formalities. Hence, the proposed Drug and Toxicological unit at tertiary care centres, with the collaboration of the Departments of Internal Medicine, Pharmacology, Forensic Medicine & Toxicology and Psychiatry for effectively managing substance abuse and poisoning patients, can be paramount. Also, their support in estimating the drug and poison level will help adequately plan healthcare management. Such centres can be nodal centres for the training and research on all aspects of substance abuse and toxicology, including general, pharmaceutical, occupational, environmental, household and others. 1. What is already known on the topic? Answer: Poison information centre is a known concept where the diagnostic facility is also provided at many centres run under Pharmacology and Forensic Medicine. Various centres for the care and management of Substance abuse are also running under the various social initiatives by the WHO and the Government of India. 2. What this study adds? Answer: The paper puts forward a concept of a single centre for the care and management of poisoning cases, substance abuse cases and accessibility of all the aspects of toxicology under a single umbrella, like a One-stop center in case of sexual assault cases. This will improve the quality of care of poisoning and substance abuse case. Also, this paper highlights the need of involvement of Forensic Medicine and Toxicology Department in the management of poisoning cases. 3. Suggestions for further development. Answer: Such a Toxicology unit may be proposed under the different health schemes and government policies to be established at tertiary care centres for streamlined management of poisoning and substance abuse cases. References World Health Organization: WHO. Suicide. Who.int . Published July 8, 2019. [ Link ] . Sharma S. The top 10 causes of death in India. https://www.hindustantimes.com/ . Published September 30, 2017. Accessed April 10, 2019. [ Link ] World Health Organization. “Suicide.” World Health Organization, World Health Organization: WHO, 28 Aug. 2023, [ Link ] The Mental Healthcare Act, 2017|Legislative Department | Ministry of Law and Justice | GoI. [ Link ] . Carrigan CG, Lynch DJ. Managing Suicide Attempts: Guidelines for the Primary Care Physician. Prim Care Companion J Clin Psychiatry. 2003 Aug;5(4):169-174. doi: 10.4088/pcc.v05n0405. PMID: 15213779; PMCID: PMC419387. Sarkhel S, Vijayakumar V, Vijayakumar L. Clinical Practice Guidelines for Management of Suicidal Behaviour. Indian J Psychiatry. 2023 Feb;65(2):124-130. doi: 10.4103/indianjpsychiatry.indianjpsychiatry_497_22. Epub 2023 Jan 30. PMID: 37063624; PMCID: PMC10096207. Wasserman, D., Rihmer, Z., Rujescu, D., Sarchiapone, M., Sokolowski, M., Titelman, D., . . . Carli, V. (2012). The European Psychiatric Association (EPA) guidance on suicide treatment and prevention. European Psychiatry, 27(2), 129-141. doi:10.1016/j.eurpsy.2011.06.003 Hill, N.T.M., Shand, F., Torok, M. et al. Development of best practice guidelines for suicide-related crisis response and aftercare in the emergency department or other acute settings: a Delphi expert consensus study. BMC Psychiatry 19, 6 (2019). [ Link ] Jacobs DG, Baldessarini RJ, Conwell Y, et al. Assessment and Treatment of Patients with Suicidal Behaviors WORK GROUP on SUICIDAL BEHAVIORS.; 2006. [ Link ] Das A, Datta A, Nath A, Bhowmik A. Profile of poisoning cases treated in a teaching hospital of Northeast India with special reference to Poison severity score: A cross-sectional study. J Family Med Prim Care. 2022 Nov;11(11):7072-7076. doi: 10.4103/jfmpc.jfmpc_1076_22. Patel NS, Choudhary N, Choudhary N, Yadav V, Dabar D, Singh M. A hospital-based cross-sectional study on suicidal poisoning in Western Uttar Pradesh. J Family Med Prim Care. 2020 Jun 30;9(6):3010-3014. doi: 10.4103/jfmpc.jfmpc_306_20. “National Drug Dependence Treatment Centre.” AIIMS NEW, [ Link ] . Accessed 31 Oct. 2023. Department of Social Justice and Empowerment National Action Plan for Drug Demand Reduction (NAPDDR) Nasha Mukt Bharat Abhiyaan (NMBA): Annual Action Plan (2021-22) for 272 Most Affected Districts. [ Link ] *Corresponding author and requests for clarifications and further details: Dr. Jitendra Kumar Assistant Professor, Department of Forensic Medicine, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, UP Email- dr.jitendrak2@gmail.com

< Back To Main Page. LinkedIn X (Twitter) Facebook Copy link Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Volume 27 Number 1 ( January - June 2026) Contents Papers Posttraumatic Ischemic Brain Stroke After Sharp Neck Injury: A Case Report Based on Autopsy Ivan Tsranchev Pavel Timonov Stela Yancheva Kristina Hadzhieva Teodora Gudelova Mirena Sotirova Antoaneta Fasova Elizabet Dzhambazova Petar Uchikov 1. Medical University of Plovdiv, Republic of Bulgaria, Europe DOI: 10.5281/zenodo.15743623 Read Can Lip Prints Change Overnight?: A Study of Lip Print Stability Across Day and Night as a Forensic Identification Tool Noor Hazfalinda Hamzah Khairul Osman Naakshectra Nadarajan Tham Jia Ci Nurhanis Khairuddin Muhammad Izhan Sabri Atikah Mohd Nasir Nur Mahiza Md Isa ¹⁻⁷ Forensic Science Program, Centre Diagnostic, Therapeutic and Investigative Studies (CODTIS), Faculty of Health Sciences, Universiti Kebangsaan Malaysia Bangi, Selangor D.E. , Malaysia ⁸ Department of Veterinary Pathology & Microbiology, Faculty of Medical Veterinary, Universiti Putra Malaysia, Serdang, Selangor D.E. , Malaysia DOI: 10.5281/zenodo.15743496 Read

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< Back To Main Page. LinkedIn X (Twitter) Facebook Copy link Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Volume 27 Number 2 ( July - December 2026) Contents Papers Domestic Violence Leading to Pediatric Burns: A Clinical Forensic Case From East Java, Indonesia Ibnu Chaldun ¹ , Ahmad Yudianto ² , Putu Bagus Dharma Permana ³ Forensic Medicine and Medicolegal Specialist Program, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia Postgraduate Forensic Science Study Program, Faculty of Medicine, Universitas Airlangga, Surabaya Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia DOI: 10.5281/zenodo.15743408 Read

Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE MAY 2000 ISSUE THE POISON SLEUTHS DEATH BY HYDROGEN FLUORIDE -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young man today. He is showing some burns on his body, especially on his fingers. What happened to him? Please tell me.” “Good morning Tarun. The name of this person is Shamlal, and he worked in a sweetshop in a Delhi based shop as a sweetmaker. He had migrated from Bihar sometime back, and was living alone in his house. For some days he was having some conflict with a person named Sunder, who worked as a lab attendant in a chemistry lab in a local school. On this Holi (Holi is a traditional festival enjoyed by the Hindus about the month of March every year. Typically this festival is celebrated by throwing water and colors over the friends), Sunder reportedly came to Shamlal, and asked him to forget all past differences. You would surely agree with me that for Hindus, Holi is a festival when everyone tends to forget past enmities. Shamlal also wanted to bury the hatchet, and invited him inside and offered him sweets. After applying some color on the face of Shamlal, Sunder threw some watery liquid over Shamlal, as a gesture to play Holi. Shamlal immediately felt pain all over his body, but instead of helping him, Sunder immediately left the house. On hearing Shamlal’s hue and cries, the neighbors took him to a nearby hospital and admitted him there. He died in the hospital a day later.” “Oh, I see. But why is his body brought to you?” “Tarun, when Shamlal was admitted in the hospital, he told the police all the incidents. He also said that he started feeling pain after Sunder threw some watery liquid over him, under the pretext of playing Holi. The police strongly suspect that Sunder threw some corrosive substance over him, and they want me to tell them what substance it was.” “Oh, I see. So what was it doctor?” “Tarun, I have conducted a thorough autopsy on the dead body, and have examined his burns in detail. You can see this typical burn on his finger. I feel that Shamlal has been killed deliberately by a very deadly poison - Hydrofluoric acid.” “Hydrofluoric acid! Never heard of this acid being used as a poison. And come to think of it, how can you be so sure?” “Tarun, I made some discreet enquiries from the doctors who treated him at the hospital. I specifically asked them, how Shamlal described his burns. The doctors told me that he described his burns in a very strange fashion, especially those on his fingers. He said that he felt as if his fingers had been struck with a hammer! This is a very typical description of a Hydrofluoric acid burn by a patient.” “That is very strange indeed. I think, I should know more about hydrofluoric acid, before I could be able to understand your talks more fully. Please tell me in some detail about Hydrofluoric acid.” “Tarun, Hydrofluoric acid is also known as hydrogen fluoride and its formula is often written as HF or H2F2. It is a colorless, fuming liquid, with molecular weight 20.01. It boils at 19.40 C. It is its great solubility in water that causes it to fume strongly in moist air. HF is found extensively in industry and at home. It was first synthesized by the French chemist Edmond Frémy (1814-1894). It is one of the most important fluorine compounds, and is prepared by heating calcium fluoride in sulfuric acid. The aqueous solution of this acid, generally used commercially, is obtained by passing the anhydrous hydrogen fluoride vapors into a leaden receiver containing distilled water, thus yielding the acid in dilute form. Hydrofluoric acid is extremely corrosive and must be preserved in platic, lead or steel containers. It can not be preserved in glass bottles, as it has the property of dissolving glass (reacts with silica to form gaseous silicon tetrafluoride). In fact this property is used in a common test for the presence of a fluoride. For the same reason, hydrofluoric acid is also used extensively in various forms of glass etching, such as the marking of divisions on thermometer tubes and the etching of designs on glassware, and in other forms of ceramic etching, such as pottery decoration. It is also used for frosting and polishing glass, and for removing sand from metal castings. It is also used as a catalyst for the production of certain hydrocarbons for high-octane gasoline. Some of its other common uses are rust removal, in manufacture of dyes, plastics, germicides, tanning, solvents, fire-proofing, pottery glazing and photography. It is also used as a laboratory reagent.” “Oh, that is interesting. What are its harmful effects on humans” “Tarun, scientists have studied its harmful effects in animals systematically by exposing them to varying concentrations of Hydrofluoric acid vapors. This helps to study the effects in man too. When inhaled by rabbits and guinea pigs in a concentration of 15 mg/cu. meter, they could tolerate it for prolonged periods. A concentration of 24 mg/cu. meter was tolerated for a total of 41 hours without fatality, although the animals subsequently lost weight. In a concentration of 50 mg/cu. meter HF induced signs of mild irritation, such as coughing and sneezing, which appeared to lessen after 5 to 15 minutes. Inhaled in greater concentrations, it acted as a severe irritant: the eyes were kept closed, paroxysms of coughing and sneezing were frequent, the respirations were slowed, and there was a copious discharge from the nose and eyes. Concentrations below 100 mg/cu. meter could be tolerated by animals for 5 hours without causing death. When exposed to the concentration of 500 mg/cu. meter for 15 minutes or more, all animals showed signs of weakness and ill-health. Inhalation at a concentration of 1000 mg/cu. meter for 30 minutes didn’t kill any animal, but caused damage to tissues. When inhaled at a concentration of 1500 mg/cu. meter for 5 minutes, all animals died, indicating this to be the fatal dose. When necropsies were done on animals, who had survived repeated exposures of HF, increased fluoride was seen in bones. Lungs, livers and kidneys were found damaged.” “Doctor, you said that HF is used in several industries. Does this mean, that industrial workers are also exposed to HF?” “Yes, surely. And they can get harmful effects too. The highest concentration of HF that can be tolerated by man for 1 minute is 100 mg/cu. meter. This causes a definite smarting of skin, a definite sour taste, and some degree of eye and respiratory irritation. If the air contains 50 mg/cu. meter, the sour taste is apparent and there is irritation of the eyes and nose, but no smarting of the skin. The concentration of 26 mg/cu. meter can be tolerated for several minutes, but the sour taste becomes evident after a short time, and there is mild smarting of the nose and eyes. You may want to know that the American Conference of Governmental Industrial Hygienists has adopted 2 mg/cu. meter as the threshold limit for hydrogen fluoride. This comes to about 3 ppm (parts per million).” “Doctor, I have seen some burns on the body of Shamlal too. Obviously they were caused by Hydrofluoric acid. Could you tell me in some more details about these burns?” “Tarun, contact of the skin with the anhydrous liquid produces severe burns. This is the most frequently reported route of HF toxicity. If the solution is not promptly removed, the skin may be penetrated by the fluoride ion, leading to the later development of painful ulcers, which heal slowly. Solutions of less than 20% HF can produce pain and redness up to 24 hours after exposure; 20 to 50% HF produces pain and redness within 8 hours, and solutions of more than 50% produce immediate burning, redness and blister formation. Fatalities have been reported from dermal exposure to as little as 2.5% of body surface area (about the size of the sole of the foot). HF burns range from first-degree to third-degree. The characteristic features are severe pain. Patients often describe feeling as if they had struck their fingers with a hammer! The hallmark of HF exposure is pain that is out of proportion to the burns produced. Only a few days back, I treated a case of Hydrofluoric acid burns in a young boy, on whom too, someone had thrown HF with an idea to kill him. He got severe burns on his legs. But fortunately I could save him. See this picture of his legs after one month. As you can see, he has almost recovered. His burn wounds are looking much more healthy. He became all right after a few months.” “Doctor, how much HF can kill a person?” “Tarun, inhalational exposure to concentrated HF for as little as 5 minutes is usually fatal, producing death within 2-10 hours. When HF is thrown on the body, the person may die in variable periods of time, usually within a day or so.” “How does hydrofluoric acid kill doctor.” “Tarun, you must be knowing that all acids yield free hydrogen ions or protons in solution. The more hydrogen ions an acid produces, the stronger it is considered to be. These hydrogen ions or protons exert a deleterious effects on the body in several complicated ways. That is why all mineral acids such as HCl, H2SO4 and HNO3 are so dangerous. HF is far less strong than its mineral acid cousins. It produces approximately 1000 times less free hydrogen ions or protons than an equimolar solution of hydrochloric acid, and about 450 times less free hydrogen ions than an equimolar solution of sulfuric acid. Yet it is this poor dissociation that proves so lethal to man. A poorly dissociated acid can penetrate far deeper in the tissues as it is uncharged. In fact all uncharged molecules have the ability to penetrate cells much better than charged ions. Combined with this ability is the specific ability of the fluoride ion to complex with body calcium and magnesium, even when present in exceedingly small concentrations. The combination of these two factors gives HF its unique toxicity. Free proton produced by HF does contribute to the injury (as in the case of mineral acids), but what is more important are the two factors I mentioned earlier, i.e. its unique ability to penetrate tissues, and its ability to combine with calcium and magnesium. This causes body calcium and magnesium levels to fall down. The body if affected in several other ways. I may also tell you about a unique property of the fluoride ion, which makes it very deadly. It can hold an electron more tightly than any other ion. This strong electronegativity of the fluoride ion allows it to bind tightly to any cation. These effects have the potential of disrupting all metabolic pathways, and may result in several body disorders.” “Doctor, now I know about HF enough to follow your talks. Tell me what has happened in Shamlal’s case?” “Tarun, I have no doubt in my mind that Shamlal has been killed by Sunder by this unique poison. Sunder worked in a chemistry lab, so HF was available to him. He offloaded some HF in a container and smuggled it home, with a view to throw it over his long adversary Shamlal. He knew that Holi was approaching soon, and he could throw it over him and leave the house quickly. As this is such a rare corrosive, he thought that he police would never be able to determine which corrosive was Shamlal killed with. But his typical findings and especially his typical description of his pain before death have given away everything. I have conducted some chemical tests on the washings which I took from Shamlal’s burnt areas, and they have tested positive for Hydrofluoric acid. Following this, I asked police to raid Sunder’s house. They did so, and found a half empty bottle containing HF. We then contacted the chemistry teacher of the school, where he was working, and asked him to check his HF supplies. He was surprised, as HF was hardly used in a routine way, and they always kept it under lock and key. But on our insistence he opened the lock and key and checked the HF bottle. To his utter surprise, it was empty. All these facts have confirmed, that Sunder stole HF from his school lab to throw it over Shamlal. Come, let us tell the police that Sunder is guilty and that the police must apprehend him.” “That is very clever of you doctor. Without your clever deduction it would have been impossible to say how Shamlal died and Sunder may have gone scot-free. What are you going to tell me next time?” “Tarun, next time, I would tell you about a very interesting poison - Fluorine."

Main page > Vol-15 No-1 > Book001 LinkedIn WhatsApp X (Twitter) Facebook Copy link Anil Aggrawal's Book Review Journal Volume-1, Number-1 ( July - December ) Book Review (Technical Section) Basic Sciences as applied to Forensic Medicine and Toxicology By Anil Aggrawal A forensic masterclass in basic sciences for postgraduates. The current book by the Author is an attempt- novel and unique, in the sense that the effort is inspired by the Indian post-graduate curriculum designed by the erstwhile Medical Council of India (known as National Medical Commission now) for M.D. course in the discipline of Forensic Medicine, more specifically the Paper-I of the Theory examination. The import of the title “Basic Sciences as Applied to Forensic Medicine and Toxicology” is very wide in scope and pertains to all the relevant anatomy, biochemical and physiologic principles, etc which is the basis of understanding the morbid anatomy and application of those to better understand the core Forensic Pathology. The book is an attempt to provide a one stop solution to the postgraduates in the discipline who earlier had to scroll through voluminous texts of Anatomy, Physiology, Biochemistry, etc to derive examination oriented content for better presentation in the examinations. Although the relevant basic sciences applicable to particular topics of interest in Forensic Medicine have already been provided by the Author in his earlier books viz. Textbook of Forensic Medicine & Toxicology, Injuries- Forensic and Medico Legal Aspects and Clinical and Forensic Toxicology, the present book goes several leaps ahead to explain most commonly asked topics from the entire ream of basic sciences which are some of the emerging domains e.g. stem cells, immunohistochemistry and molecular pathology- to name a few. Yet, the book remains connected to the very soul of Forensic Medicine, Traumatology and Toxicology by referring back to prior cited texts and thus avoiding repetition and maintaining chronology stimulating the reader and allowing for both horizontal and vertical integration, which is also the essence of Competency Based Medical Education Curriculum. The text is amply studded with memory aids and some of the handmade diagrams by the Author- one of particular note is memory aid designed for remembering cranial nerves on Page No 18, which makes the anatomical orientation of the various cranial nerves with respect to each other as well as vastly simplifies the topographic anatomy. Not to suffice, the text contains numerous demonstration videos which are a rarity in the existing literature and help the reader in grasping the basic concept e.g. experimental demonstration of the law of Laplace given on page no 51, which helps in conceptual understanding of the abstract terminologies. General Pathology given in Chapter 4 is a welcome inclusion as it helps in understanding the basic pathologic principles which are the basis for understanding and interpreting Forensic Pathology. A clear differentiation between Septicemia, sepsis and septic shock, based on updated scientific criteria is heartening to see on Page no’s 96 and 97. Another exciting feature of the book is the innumerable case studies which make the topics both entertaining to read and further act as reminders how one particular development has a legal bearing or implication. Chapter 6 discusses general pharmacological principles which have importance in the field of clinical and forensic toxicology. Questionnaire towards the end of each topic are though provoking e.g. anti-neoplastic drug for homicide brings one to an old case of murder by means of Lomustine, which is a drug employed for brain tumor treatment but the aplastic anemia and multi-organ failure which are the consequence of it’s overdose resemble natural death. This is significant for even clinicians/ emergency physicians who treat a significant number of accidental drug over-dosages to be mindful of the drug history- both prescriptions as well as Over-the-counter (OTC). The chapter on “Radiology as Applied to Forensic Medicine and Toxicology” is very thoughtfully designed considering the advent of Virtual Autopsy at AIIMS in 2021 by the Government of India after the Virtopsy project under Prof Richard Dirnhofer of the Institute of Forensic Medicine, University of Bern, Switzerland. The radiographs important from the point of view of a forensic practitioner have been given along with comparative diagrammatic representation for simplification purposes. Readers shall be in a better position to interpret the basic postmortem radiographic findings if and when needed. National Board of Examinations (NBE) has been asking one question every year in Paper I of Forensic Medicine DNB Theory Examination based upon biostatistics accounting for 10 marks. The inclusion of statistics as applied to Forensic Medicine and Toxicology in Chapter 8 of the book is a welcome step to strengthen the students with the most essential and desired topics e.g. Null Hypothesis, P-value, Z score, etc. which could be asked. The next chapter on Research Methodology is educative for the thesis going and any researcher to understand the various study designs and how to calculate the sample size for a proposed research study. Types of citations and referencing systems have also been elaborated upon and the various indexing systems have been deliberated upon. This is very much needed for a novice researcher as imprecise understanding of these may create impediments in the growth and advancement of the latter. The last few chapters focus on infrastructural requirements related to setting up of a Museum and Analytical Toxicological Laboratory in the Department of Forensic Medicine and Toxicology. Basic chemistry has been given at the end to simplify the understanding of subtlety and nuances of Forensic Toxicology. Few sample questions have been provided in the appendix which could further be enhanced through the addition of previous year questions from various universities. Tentative thesis/ research topics given in the appendix give important food for thought to the examinees and the research oriented ones. Overall the book is a novel and fresh initiative in an unexplored genre/ theme which will bode well to the lot to whom it is intended to cover- postgraduates in Forensic Medicine & Toxicology and the faculty. - Dr. Varun Modgil He is currently working as Assistant Professor at Dayanand Medical College & Hospital, Ludhiana, Punjab. He was Senior Resident at Postgraduate Medical Education & Research (PGIMER), Chandigarh. He deposed as an expert witness at various courts in Punjab, Haryana and Chandigarh. He has completed his D.N.B. in Forensic Medicine and also published articles in various National & International journals and also delivered guest lectures in National Conferences on Forensic Medicine. He can be contacted at dr_varun_modgil@dmch.edu ,

Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE MARCH 2000 ISSUE THE POISON SLEUTHS DEATH BY RADON -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a middle aged man today. What happened to him? Please tell me.” “Good morning Tarun. The name of this 45 year old man is Ramlal, and he was working in a drug factory. He was living with his invalid wife and a 20 year old son, in his ancestral house for the last so many years. For some months now, he was not feeling well. His friends and relatives were constantly advising him to see some doctor, but he refused to believe he was sick. He died today morning. Normally in such cases, no police enquiry occurs, but this man was a Union leader, and there have been widespread rumors that the management somehow managed slow poisoning in his case. It has been alleged that this was particularly easy for the management to do so, as he was working in a drug factory, and all sorts of harmful drugs were available to the management. The pressure of the workers was so much, that the police had to arrest the top management people. Currently they are in police custody, and can’t meet anyone." "So what do you think doctor?" "Tarun, I have just now conducted a thorough autopsy on him, and I found that he has died because of lung cancer. Now there is no poison except one that can induce lung cancer, and that is the Radon gas." "You mean someone gave him radon gas to kill him? That sounds preposterous." "I will talk about it later. But first some investigations that I did in this case. When I found that his body was unusually radioactive, I visited his house, and was not very surprised to find a great amount of radioactivity in his house too. In fact this is what I had expected." "From where is that radioactivity coming doctor? Did someone from the management lace his house with radon gas?" "Tarun, the radioactivity in all probability is coming from the underground." "From the Underground? I really don't understand that. Now doctor, I feel I must know the radon story from the beginning. Otherwise I won't be able to follow you intelligently. Kindly tell me the radon story from the beginning." "Tarun, Let me tell you about some general facts about Radon first. It is a colorless, odorless, and tasteless gas found in Group 0 of the Periodic Table. It has a density of 9.25 g per cubic decimeter. In fact, it is the heaviest gas known. It is 7.5 times heavier than air and more than 100 times heavier than hydrogen. The gas liquefies at -61.80 C (-800 F) and freezes at -710 C (-960 F). On further cooling, solid radon glows with a soft yellow light that becomes orange-red at the temperature of liquid air (-1950 C [-3190 F]). Natural radon consists of three isotopes. They have the atomic weights of 219, 220 and 222, and thus are written as radon-219, radon-220 and radon-222 respectively. In chemistry the usual practice of writing the atomic weights is on the upper left hand side of the element symbol; thus the three isotopes are often represented as 219Rn, 220Rn and 222Rn. The half life of all three varieties is very short. But among themselves, the shortest half life is that of the variety having least atomic weight, and the longest half life is that of the variety having the maximum atomic weight. Thus the half life of 219Rn is only 3.92 seconds. Half life, as you surely know is the period, in which the original amount of a radioactive material is reduced by half. The half life of 220Rn is slightly more; 51.5 seconds. The longest lived of all is 222Rn, but even this variety has a half life of just 3.823 days. All the three varieties do not occur in nature as such, but are produced as a result of decay of other radioactive materials. 222Rn is produced by the decay of Radium; 220Rn from the decay of Thorium, and 219Rn from the decay of Actinium. In fact their parent elements give them their more popular names. 222Rn, since it is produced from radium, is known as radon. For similar reasons, 220Rn and 219Rn are known as thoron and actinon respectively. Thus when we speak of radon, we usually refer only to the isotope 222Rn. The other varieties, i.e. thoron and actinon, may be referred to as the isotopes of radon. I may tell you that the first isotope of radon to be discovered was thoron, which was discovered in 1899 by the British scientists R.B. Owens and Ernest Rutherford, who noticed that some of the radioactivity of thorium compounds could be blown away with the passage of time. Radon was discovered in 1900 by the German chemist Friedrich E. Dorn. The last isotope of radon to be discovered was actinon which was found in 1904, independently by Friedrich O. Giesel and André-Louis Debierne. Although these three are the naturally occurring isotopes of radon, now more than a dozen artificial radioactive isotopes of radon are known. I may tell you that radon and all its isotopes are rare in nature because they are all short-lived and because their sources, radium, thorium and actinium are rare. The atmosphere contains traces of radon near the ground as a result of seepage from soil and rocks, all of which contain minute quantities of radium. You may ask where the radium comes from within the soil and rocks. Actually Radium occurs as a natural decay product of uranium which is present in various types of rocks. It is now known that some tracts of land contain unusually high amounts of uranium beneath. This gives rise to more radium and more radon, which seeps up through the soil and collects in homes if they happen to be built on that land. Radon is now known to cause lung cancer in populations which are exposed to it. Indeed, radon is now thought to be the single most important cause of lung cancer among nonsmokers. By the late 1980s, naturally occurring radon gas had come to be recognized as a potentially serious health hazard. The gas, arising from soil and rocks, seeps through the foundations, basements, or piping of buildings and can accumulate in the air of houses that are poorly ventilated. Exposure to high concentrations of this radon over the course of many years can greatly increase the risk of developing lung cancer. Radon levels are highest in homes built over geological formations that contain uranium mineral deposits. I may tell you that 222Rn is itself radioactive, and it decays into 218Po, which in turn decays into 214Pb, 214Bi, 214Po. These four radionuclides are called the radon daughters. They all become attached to particles in the air and get breathed into lungs. 222Rn, 218Po, 214Po are all alpha emitters. Radiation can cause damage to biological molecules, and can induce cancers, genetic defects and accelerated aging." "Doctor, all this sounds very frightening indeed. You told me that by the late 1980s, radon had come to be recognized as a serious health hazard. Tell me how exactly scientists discovered that radon gas could be emanating from the soil and collecting in the houses." "Tarun, it is a very remarkable story indeed. It started on December 2, 1984, in Pennsylvania, USA. Before that it was known that radon occurs as a serious health hazard in mines, but its occurrence in ordinary homes was not known. During December 1984, the alarm bells in the Limerick nuclear power plant (in Pennsylvania, near Philadelphia, USA) were constantly ringing, indicating that someone had been contaminated with radioactivity. But it was not known who it was. There were concerns that the radioactivity might escape and pollute the environment. Then on the fateful day of 2 December 1984, a worker Stanley Watras was found to be unusually radioactive. When more investigations were done, it was surprisingly discovered that the radioactivity was coming from his house. Some people believed that he was stealing some radioactive material from the work place and taking it home, but none was found. Still more investigations showed that unusual amounts of radon were leaking in his house from the underground. The house of Watras was so radioactive that the health risk of living there was the same as smoking hundreds of cigarettes a day! On detailed investigations it was found, that his house straddled a vein of uranium ore. The authorities decided to investigate the levels of radon in other nearby houses and the results were worrying. By the end of 1986, about 20,000 houses had been checked in Pennsylvania, and one in eight were found to be overloaded with radon! Well, here in the table you can find some important dates in radon research in America. (N.B. The table is quite complex and is very difficult to put over the net. Readers desirous of having the table may want to get in touch with the webmaster.) "Oh, that is quite informative." "Gradually, the public became so concerned about radon, that the government found it imperative to decide upon a safe level of radon, which could be allowed in the homes and at workplaces. These levels were called Action Levels. Levels above these Action Levels were considered unsafe and legislations were passed, which could prosecute managements if they allowed radon levels to rise above these prescribed limits. Action Levels for homes were 200 Becquerels per cubic meters (200 Bq m-3), while those for work places were 400 Becquerels per cubic meters (400 Bq m-3).” “Sorry to interrupt you doctor, but I don’t quite understand the concept of Becquerels. Could you please explain me that?” “Sure. Antoine Henri Becquerel, as you surely know was a French physicist who discovered radioactivity through his investigations of uranium and other substances. In 1903 he shared the Nobel Prize for Physics with Pierre and Marie Curie. In his honor, scientists have named the unit of radioactivity. A sample of radioactive substance would be said to have a radioactivity of one Becquerel if in that sample one atom disintegrates per second. So if I say that the level of Radon in a particular home is 200 Becquerels per cubic meters, it means that there is so much Radon in that house that in every cubic meter of that house, 200 atoms of Radon are disintegrating per second. This is a very small Unit. A bigger Unit is Curie, which is equivalent to 3.7 X 1010 Becquerels. You might be surprised at this odd figure. Actually one Curie is the amount of radioactivity given off by one gram of radium. And it is seen that in one gram of radium, about 3.7 X 1010 atoms disintegrate per second. Hence this figure. You might think that the unit Curie is named after Marie Curie, the joint winner of Nobel Prize with Becquerel, but it is actually named after her husband Pierre Curie, who too shared the Prize with them. This is a little known interesting fact. Most people wrongly think that this unit is named after Marie Curie. While I am on the subject, I may tell you something more about the safe levels of Radon in houses. It was found that houses with levels of 2000 Bq m-3 and more were very dangerous places to live in. The house of Stanley Watras had fifty time more radioactivity than this - a radioactivity of 100,000 Bq m-3!” "Doctor, now I know enough about Radon and its dangers. Do you seriously think, someone from the management arranged for the radon gas to be accumulated in Ramlal's house so he could die of lung cancer?" "Tarun, theoretically speaking it is possible, but practically such a possibility is exceedingly low. Radon is not an easy gas to prepare. Concentrated samples of radon are prepared synthetically for medical and research purposes only and that too in highly specialized labs. Typically a supply of radium is kept in a glass vessel in aqueous solution or in the form of a porous solid from which the radon can readily flow. At intervals of a few days, the accumulated radon is pumped off, purified, and compressed into a small tube, which is then sealed and removed. The tube of gas is a source of penetrating gamma radiation, which comes mainly from one of radon's decay products, bismuth-214 (214Bi). Such tubes of radon have been used for radiotherapy and radiography. My initial thought was that Ramlal's house is built on a tract of land which is rich in Uranium, but I had to get the opinion of a geologist before I could finally say anything. I have got that opinion now, and the report says that my guess was correct. Ramlal’s house indeed is constructed over a land rich in Uranium. Come let us tell the police that those management people are innocent, and it was Radon, which took the life of Ramlal. "Unbelievable! This was a most interesting discussion doctor. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison - Hydrogen Peroxide."

Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE JANUARY 1999 ISSUE THE POISON SLEUTHS DEATH BY SODIUM NITRITE -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young woman today. Her whole body seems to have a chocolate brown color. I remember last time too, I had seen a dead body with chocolate brown color. Did this woman also die of the same poison? Please tell me." "Good morning Tarun. The name of this young woman is Radhika, and she is about 25 years old. She died in her flat at about 9 am today morning. She was a junior executive in a private firm here in Delhi, and was living alone in this flat. Her family members are living in Jaipur. She was living here solely for the purpose of this job. Her parents were looking out for a match for her marriage." "Oh, I see." "Yesterday night she was fine. In fact, she met one of her neighbors Shyamala -also a 25 year old girl- at about 9pm, and she tells us that she was perfectly in good spirits. That rules out suicide...." "Wait a minute doctor. If a person is in good spirits and cheerful a day before his or her death, does it rule out suicide? Is it not possible that she was trying to mislead the neighbors by being cheerful so that nobody gets to know her intentions?" "There are other indications too. There is no suicide note. Generally a person who commits a suicide, leaves a suicide note." "Oh, I see" "Well, the police interrogated Shyamala more about her as she was the only one, who knew Radhika very well. She told the police that she (Radhika) was in love with Chaman, a 26 year old colleague in her office. Recently she had become pregnant by him, and she was pressing him for marriage. However Chaman had lost interest in her, and was trying to avoid her. Only 2 days back she had threatened him to go to his parents if he did not agree for the marriage. Chaman's parents are very religious and God-fearing, and he knew if she approached them, they would force him to marry her. To settle matters he came yesterday to Radhika's flat at about 7 pm. Shyamala knows because when he came, Radhika called her as a mediator. Shyamala tells the police that Chaman was looking very tense and jittery. She thought it was because he had such a difficult matter to resolve. Anyway she just sat there for about an hour. When she saw that the matter is going to take more time, she left the house making an excuse. When she left, Radhika was just preparing to go inside the kitchen to make tea for everyone. She offered Shyamala to go after having tea, but she just left. She however saw Chaman leaving Radhika's house only about 15-20 minutes later. She was sitting idly at her window when she saw him. He looked to be in great hurry." "Oh, I see. So did you find anything in the post-mortem that corroborates what Shyamala is saying?" "Yes, I found a 4 month old male baby inside Radhika's uterus, which definitely tells us that she was pregnant. I have kept the tissues of this fetus for his DNA profiling, which will tell us definitely if Chaman was his father or not. More about that later. What interested me was the color of her body. I told you last time (See SR December 1998 issue) that there are certain poisons which can cause methemoglobin to form inside the body. It is this compound which imparts such color to the body. Well one of such poisons is sodium nitrite. I got a hint that she might have died of sodium nitrite poisoning when I went to her flat and saw that she had unfinished breakfast on her table. She was in the habit of having a full meal in the morning itself. She had prepared Dal and Roti and must be eating it. And it was lying there unfinished. Nearby I could see some dried vomitus on the floor. Obviously when she was eating the food, she must have got sick and must have vomited. I saw a salt cellar on her table which was open. I got quite curious, when I glanced underneath the dining table and found lot of white salt like powder spilled over there. As a poison sleuth, I don't want to take chances and intuition told me there was something either in the salt cellar or in the powder spilled over the floor that we were looking for. So I quietly kept the salt cellar in my pocket and also some of the powder spilled over the floor underneath the dining table. I examined both these substances in my lab. And do you know what I found?" "What? Please tell me doctor. I am getting curious." "Tarun, I had the most extraordinary finding in the salt cellar. It had a substance looking like salt but it was not sodium chloride. It was sodium nitrite. And the salt like powder which was spilled underneath the table was nothing but sodium chloride. Do you get the picture now?" "Well, not really. I don't understand how such a curious thing happened." "To me it is clear like glass. Obviously someone replaced the salt in the cellar with sodium nitrite. And before doing this he spilled the salt underneath the table to empty the cellar so he could fill it with the poison he had brought with him. The only commonly available poison which looks and tastes like salt is sodium nitrite" "Really? Doctor I am getting curious. Please tell me more about sodium nitrite." "Tarun, as I told you earlier, sodium nitrite causes methaemoglobinaemia; even small doses of sodium nitrite can kill within a few minutes. Even the nitrates can be dangerous. Organic nitrates in fact are reduced to nitrites in the intestine. Inorganic nitrates, bismuth subnitrate excepted, are not normally reduced to nitrites in the body, but this may occur when the upper digestive tract (stomach and upper part of small intestines) is infected with nitrate-reducing bacteria, e.g. Escherichia coli. Inorganic nitrates are irritants of the stomach and, in large doses, potassium nitrate is a diuretic. A diuretic is a chemical which increases the production of urine. Poisoning by nitrites is actually not very common. It can result from mistaking this salt for common salt or Epsom salts." "Doctor, under what circumstances can sodium nitrite poisoning occur?" "Tarun, poisoning can be homicidal, accidental or suicidal. With sodium nitrite, accidental poisoning is probably most common, although homicidal poisoning is also possible as we have seen in the case of Radhika. One of the earliest reports of sodium nitrite poisoning came from Middlesborough, UK in 1936. Two adults and their daughter aged five were suddenly taken ill after the midday meal. The adults died before a doctor could reach them and their daughter died shortly after her admission to hospital. It appears they had complained to neighbors of acute abdominal pain and vomiting. Their faces went blue. Investigation showed very similar results to what I found in Radhika's case. A basin of cooking salt and a salt cellar contained sodium nitrite; the upper layer in the latter was of 98% sodium nitrite and the lower layer 98.2% common salt. Unconsumed food contained sodium nitrite, e.g. cabbage 6.5% and Yorkshire pudding 4.5%. The gastric contents of the man contained 4.275 g and those of the woman contained 1.284g of sodium nitrite. Over a gram of the poison was present in the child's vomit. The vomit of the adults was not available for analysis, but presumably they had ingested considerably more than remained in their stomachs. The source of the poison was not determined, but the man had had access to sodium nitrite in the course of his employment. Nobody knows how the mix up happened. Probably someone filled up a half empty salt cellar either intentionally or mistakenly with sodium nitrite." "Oh, that is most extraordinary and bears an eerie resemblance to the case we have on our hands." "Yeah sure. Accidental deaths due to the ingestion of sodium nitrite used in error for common salt in the preparation of soup have also occurred. Several such accidental deaths have been reported. Death in these cases occurred within a few minutes following symptoms which included nausea, headache, vertigo, urgent vomiting, profuse diarrhoea and cyanosis (bluing of the skin). Stomach contents in most of these cases contained sodium nitrite ranging from 1.74 to 84.0 mg/kg of the gastric contents. There was a more consistent concentration in the organs, e.g. in the liver, where the concentration was between 3.0 and 4.35 mg/kg. A quarter of a litre of the soup in most of these cases contained l.5 g of sodium nitrite. I must tell you that the fatal dose of sodium nitrite is from 1 to 2 g. I have already explained you the concept of fatal dose (see "Poisoning by Thallium" SR, October 1997)." "Yes doctor, I do remember you having mentioned it." "In another case, eleven men were poisoned after eating oatmeal seasoned with sodium nitrite in mistake for common salt. The men added more salt from salt shakers later shown to contain sodium nitrite. Immediately after the meal they felt sick and vomited. There was dizziness and abdominal cramps. They went blue and five lost consciousness. Methaemoglobin was later demonstrated in their blood. One of these men, aged 82, died the next morning; his organs had a diffuse brown colour. The source of the poison was nitrite used to cure meat. Only eleven of 125 persons who ate of the oatmeal were affected and these eleven had used contaminated salt shakers of which one contained 0.137% of nitrite. It was estimated they had taken at least 163 mg. In yet another case, a boy aged two months suddenly went blue, 'almost black', after his 7.0 am feed. Sodium citrate had been prescribed for the relief of indigestion and two tablets had been added to the feed. When seen in hospital, about five hours later, the appearance of the child simulated those of congenital heart disease; he was neither distressed nor febrile. A diagnosis of toxic methaemoglobinaemia was made and the remaining tablets, fortunately available, were subjected to analysis. They proved to contain 65 mg of sodium nitrite each. The infant, therefore, had ingested 130mg, the maximum dose for an adult. There are a host of other such cases of which I am aware." "Doctor please tell me a few interesting ones out of these." "In one case, two children aged two and three months respectively took feeds to which from 35 to 40g of sodium nitrite had been added in error for sodium citrate. The elder infant died. Cyanosis and blackening of the mouth were outstanding features. In another case, a boy aged two years vomited while playing with his elder brother aged nine. After a second vomit he was given a glass of water to drink. Vomiting continued and he was taken to hospital. He was deeply cyanosed, collapsed and crying with spasms of pain. Poison was taken out from the stomach with the help of a tube and oxygen was administered, but the child died at about three hours after being poisoned. Sodium nitrite was detected by analysis of his stomach contents. There was methaemoglobin in the blood. It is probable that the boy had ingested and absorbed appreciably more of the poison. The source of the poison in this case was a bottle of sodium nitrite, now nearly empty, which the elder boy had brought for the purposes of a chemical experiment. The dead child had licked the bottle. I must tell you that sodium nitrite is highly soluble in water and its taste resembles that of common salt and that is what makes it such an attractive homicidal poison. Interestingly sodium nitrite is used in machine oil also as a corrosion inhibitor, and deaths have occurred when someone accidentally drank machine oil. There is a case of a girl on record who died in this way. She was eleven years old, and drank a mouthful of machine oil accidentally, some of which she immediately spat out...." "Just a minute doctor. I think sodium nitrite is an oxidizing agent, and if I remember my chemistry alright, corrosion is an oxidative process. Then how can nitrite be used as a corrosion inhibitor?" "Tarun, sometimes oxidizers are also reducing agents. Such is the case of nitrite, which can be further oxidized to nitrate. I must tell you that the tendency of nitrite to act as an oxidizer is increased in an acid environment such as that found in the stomach. At higher pH levels its oxidizing potential is greatly decreased. Corrosion can be inhibited by using a sacrificial reducing agent such as nitrite. Sodium nitrite is also commonly put into packaged foods like meat to keep oxidation from happening. So I was telling you about that little girl. Within an hour she was unconscious and deeply cyanosed. Fortunately she recovered after proper treatment. Analysis showed that the oil contained 36.5% sodium nitrite, 7.5% of an emulsifying agent and 56.0% water. Her stomach washings contained 7-8mg/ 100 ml of sodium nitrite." "Oh, that is certainly most extraordinary!" "Tarun, sodium nitrite poisoning has happened in other ways too. Poisoning by well water drawn from badly constructed wells near farmyards may contain an appreciable amount of nitrate which makes it unfit for drinking and a source of poisoning newborn infants. This illness is however rarely fatal. About 30 cases are on record and only one, it appears, was fatal. It is apparent that the risk is only to infants of under 90 days old, who live in rural communities..." "Doctor, can boiling the water make such water safe? I have heard that boiling the water makes it cleaner." "Yes boiling the water does make it free of infective micro-organisms, because they get killed by boiling, but when the water is contaminated with a chemical substance, it gives no protection whatsoever. On the contrary, it concentrates the nitrates, which can get concentrated upto 3 times on boiling the water! Older children are unaffected, probably because they can tolerate the amount of nitrate likely to be present in their normal fluid intake. It does appear that poisoning in these circumstances is not dependent only upon the amount of nitrate ingested· It has been suggested that poisoning by nitrate will only occur in those whose gastric juice exceeds pH 4.0 and when nitrate-reducing bacteria are present in the upper digestive tract." "Doctor, this is a most extraordinary fact that you have told me. Can you tell me what is the concentration of nitrites in such contaminated water coming from wells?" "The contaminated water, usually drawn from shallow wells, of not over 75 feet deep, usually contains over 20 ppm (parts per million) of NaN03. Methaemoglobinaemia (the existence of too much methemoglobin in the blood) does not normally occur unless the water contains 30 ppm. The upper limit of nitrate should not exceed 10 ppm because as I told you earlier, if boiled the water could be concentrated threefold and thus to a dangerous concentration. Even cows which feed on beet tops rich in nitrates develop methaemoglobinaemia. This is known as the condition of 'purple' cows and is well recognized. Purple is the color the cows get when there is lot of methemoglobin in their blood." "Oh, this is most extraordinary." "There are more interesting facts Tarun. Nitrite poisoning from spinach has also occurred. During 1959-65 in Germany there were 15 cases of nitrite poisoning in infants, aged two to ten months, who had eaten spinach. Nitrite and the remains of spinach were found in the stomach contents of one of the infants. Two factors were responsible. First, the excessive use of nitrate fertilizer, which should not, but often did, exceed 80 kg/hectare. Second, bacterial activity converted the nitrate in spinach into nitrite. Samples of spinach, fresh, frozen and tinned, showed a nitrate contamination of from 40 to 2100 mg/kg. The risk arose when the feed was prepared in advance and stored overlong at room temperature. Even after cooking, a sufficient number of bacteria remained to produce nitrite. The maximum nitrate content of spinach should not exceed 200mg/kg. It has even been recommended that during the first three months infants should not be given spinach." "Doctor, such an interesting poison must have caught the fancy of suicides also. Have there been cases of suicidal poisoning too with sodium nitrite?" "Yes, sure. Suicidal poisoning with sodium nitrite has also occurred. A medical practitioner, aged 51, committed suicide in 1942 by ingesting sodium nitrite. He had been mentally ill for some time. On the night of his death he awoke his son, a medical student, and told him that his mother had suddenly been taken ill during the night. A doctor was summoned and while he was attending to the woman a bump was heard in the passage. The deceased was then found lying on the floor; he died within five minutes of his fall. Poisoning was suspected, but a search revealed only a glass of brandy and another which appeared to contain water. Toxicological analysis demonstrated 2g of sodium nitrite in the gastric contents. The blood was 'dark'. Unfortunately no analysis was made of the brandy or water, otherwise I am sure they would have found nitrite in the brandy. The deceased had given his wife some of the brandy during the night and this may have been the vehicle of poison responsible both for her illness and his death. I feel he first gave brandy laced with nitrite to his wife and then consumed the poison himself, but of course it is only a guess. But sure enough, it is possible to kill someone by lacing his or her drink with as little as 2 grams of sodium nitrite. It was believed that the poison was taken within an hour prior to his death. It was suggested by the relatives that he had died of a heart attack, but the doctor said that he had died of nitrite poisoning." "Oh, doctor. We could go on and on with such interesting stories. Tell me how you can prove Radhika died of nitrite poisoning?" "Tarun, I told you I examined both the contents of the salt cellar as well as the powder spilled over the floor. Now I will tell you what happened. Chaman came to Radhika's house not for reconciliation, but for killing her. He was sure, killing her was his only way out. He got sodium nitrite from a chemistry lab. We have still to find out, how he got hold of it, and who gave it to him. He came fully armed with this poison in a packet. When Shyamala left and Radhika went inside the kitchen to make a cup of tea, he quickly picked up the salt cellar, spilled the salt in it on the floor underneath the table and refilled it with the powder that he had brought. He knew that sometime she would consume the contents of the salt cellar thinking it was salt and she would die. It was no doubt a very clever plan, but thankfully we could catch it. The color of Radhika's body at once told me we were looking for a poison which produces methemoglobinemia, and that was Chaman's undoing. I have found an appreciable quantity of Sodium nitrite from Radhika's stomach contents, and to top it all, the police has found some left over sodium nitrite from Chaman's house too. Initially he denied having any hand in Radhika's death, but when he was told of all the medical and circumstantial evidence against him, he broke down and admitted his guilt." "Very clever doctor. This was a most interesting discussion doctor. Without your masterly deduction, Chaman could never have been caught. People might have thought, it was an accidental death. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison. You may not have even thought that it was a poison. I will tell you about death by Potassium Permanganate."

| Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Call For Reviewers Become a reviewer for Interacting with Anil Aggrawal’s Internet Journal of Forensic Medicine and Toxicology . * This journal receives a large number of manuscripts and other material for publication as original papers/review papers/high resolution pictures for poster presentation/UG material/PG material and contributions for a number of other sections. * To be able to deal with large amount of unprocessed material, we are currently diversifying our reviewer pool. Younger scientists are encouraged specially, so they can be involved in paper publication process. * Interested in reviewing or have questions? Email the editorial office by clicking here . What is peer review ? Peer review is not only the foundation, but a very strong pillar of scientific publishing. It is an honest assessment of a piece of writing by a “peer”, a person who understands and practices the same science. When you are asked to review a manuscript that has been submitted for publication, you are helping the journal to “weed out” unsuitable material, and select what should be included in a well-respected journal. Not only this, simultaneously, your expertise is being acknowledged and your opinion is being valued. Our reviewers – by accepting only high quality original papers – help us to publish only the highest quality research and reviews. Who can become a reviewer? If you are active in the field of forensics/criminology/law and related sciences and can objectively evaluate the quality and rigor of research, we want you! Send us your latest CV attached with your high resolution photograph. We are looking for peer reviewers with following qualities: • Should have sound academic credentials • Should be active in the field of forensics; new research paradigm: interaction process and methodology • Should provide constructive criticism to authors. Benefits of reviewing for this journal Becoming involved in the peer review process for this journal can be a highly rewarding experience for the following reasons: • Reviewers are recognized on an annual basis in the journal; Please Click here to see how reviewers are acknowledged. • If you are interested in joining the editorial board , you would be able to do so, after you have completed 100 peer reviews. • You can get academic credit for your peer review by signing in your Web of Science/Clarivate/ORCID Academic profile. Please click here to sign in or register • You get complimentary access to academic material [papers/books etc needed to consult for reviewing etc.]. You need to send us PMID of the paper required. • You get a reviewers’ certificate after completing 25 reviews. Click here for an example. The peer review process Remember that authors are our friends. Our aim is to improve their manuscripts. If grammar/spellings etc. are wrong, they may be advised to get it corrected through someone who is a native English speaker, or better still with a teacher of English language. The manuscripts are checked especially for originality. We have a zero tolerance for plagiarism. Thus all manuscripts must be checked through an authentic antiplagiarism software [e.g., iThenticate ]. References must always be checked, ensuring specially that they are all in uniform style [Vancouver style]. Manuscripts are always sent to two [in rare cases more also] independent reviewers. Based on the feedback from these reviewers and the editors' judgment, a decision is given on the manuscript.

| Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Contributing Partners Gyan Fernando Gyan Fernando, MB, BS, MD, FRCPath, DMJHome Office Pathologist Devon & Cornwall UK E-mail Dr. Fernando Dr. Gyan Fernando was born in Colombo, Sri Lanka (then Ceylon) in 1949. His early education was in a Catholic school and in 1968 he entered the Faculty of Medicine, University of Ceylon, Colombo. Extra curricular activities, notably editing the student "rag" was more important to him than studies. This led to failing Anatomy and Biochemistry. He never failed another examination. However, he considers the five years spent in medical school to have been the best years of his life. In 1973, to the relief of his parents, he qualified as a doctor. Soon afterwards he got married to Ranji, a fellow medical student. He is still married to her. Because of living well away from their parents, the marriage survived the first few crucial years and a son was born in 1976. After a short spell in general medical and obstetric jobs he opted for Forensic Medicine purely because no one wanted the forensic job in a remote but beautiful part of the country where he wanted to live. In 1978 he moved to Britain where he soon discovered that training in Forensic Medicine did not exist. Wisely he decided on Histopathology and in 1984 obtained Membership of the Royal College of Pathologist by examination. (Later, "having furthered the interests of the College" without getting into trouble, he was made a Fellow.) In 1985 he obtained the Diploma in Medical Jurisprudence and was appointed the Senior Forensic Pathologist to the University of Dundee and very soon took over as caretaker head of department. In 1989 he was appointed Senior Lecturer in Forensic Medicine, University of Edinburgh. At present he is the Home Office appointed Consultant Forensic Pathologist for Devon and Cornwall in which post he has been in since 1993. As a firm believer that "autopsy" means "seeing for oneself" and not gathering knowledge from books, he has always been a hands-on pathologist and has very little respect for academics. Another of his pet dislikes is bureaucracy. Over the years he has surrounded himself with books mostly of humorous and satirical writing, favourite authors being P.G.Woodhouse and James Thurber. He also has a fondness for cartoons. Since his school days he has been interested in railways and combines holiday travel with study of railways. Ramesh Kaul Ramesh Kaul, MD., MS., FCCP USA E-mail Dr. Kaul Dr. Ramesh Kaul was born and brought up in India, where he qualified in medicine and surgery from the prestigious All India Institute of Medical Sciences. Later he obtained his post-doctoral qualification in otorhinolaryngology from the same institute. A man of many interests and tastes, he is widely known among his peers as the modern Leonardo da Vinci. He is Board Certified in Pulmonary Medicine, and is currently working as a pulmonologist in the US. His several fields of interest include investigations into metabotropic receptors. He runs his own sites on lung cancer. Among his best known and widely respected sites are www.thorax.us and www.lungcancercare.com and www.rameshkaul.com . He lives in Pittsburgh and New Castle.