Post mortem finding of acute and chronic arsenic poisoning
post mortem findings acute chronic arsenic poisoning forensic pathology
arsenic poisoning post mortem gastric mucosa red velvet appearance

This clinical photograph shows a gross pathological specimen of the human stomach mucosa, likely taken during a post-mortem or surgical examination. The gastric lining exhibits intense, diffuse hyperemia and congestion, characterized by a deep red coloration. There are visible areas of intramural hemorrhage and petechial spots across the mucosal surface. The tissue has a shiny, edematous appearance with prominent rugae. A focal area of greenish-yellow mucoid substance is present, suggesting potential chemical irritation or altered gastric contents. This image serves as an educational example of severe gastrointestinal mucosal injury, often associated with acute gastritis or toxic ingestion, such as aluminium phosphide poisoning. The specimen is being handled by a person wearing white latex gloves in a clinical or forensic setting.

This clinical gross specimen photograph displays the internal surface of a human stomach during an autopsy. The gastric mucosa shows clear signs of pathology characterized by light, focal haemorrhage. The mucosal surface exhibits an uneven, mottled appearance with scattered petechiae and larger areas of ecchymosis, particularly prominent in the region indicated by the black arrow. These haemorrhagic foci appear as dark red to purple discolorations interspersed with the paler, tan-pink tissue of the normal gastric folds (rugae). The irregular distribution of these spots suggests acute mucosal injury or congestion. Such findings in a forensic or clinical pathology context can be associated with various systemic stressors, including acute alcohol poisoning or severe physiological shock. The image serves as a teaching tool for identifying macroscopic signs of gastric mucosal haemorrhage and inflammation during post-mortem examination.

This forensic clinical photograph displays gross autopsy findings from the respiratory system of a deceased individual. Image A shows a longitudinal section of the larynx and trachea, held open with surgical forceps. The mucosa exhibits a characteristic cherry-red coloration, which is a classic post-mortem indicator of carboxyhemoglobinemia associated with carbon monoxide poisoning. Significant deposits of black, granular soot are visible lining the interior of the lower trachea. Image B shows a cross-section of pulmonary tissue, demonstrating intense congestion and a similar cherry-red hue. The primary bronchi and smaller airways contain prominent black carbonaceous material (soot). These findings collectively illustrate the pathological hallmarks of smoke inhalation and carbon monoxide toxicity, typically encountered in fire-related fatalities or enclosed-space combustion. The image serves as a teaching tool for forensic pathology, particularly in identifying indicators of vital reaction (breathing during a fire) versus post-mortem exposure.

This gastroscopic image displays a view of the gastric mucosa, likely within the antrum, showing a relatively healthy appearance following the resolution of prior pathology. The mucosa is characterized by a uniform pinkish-red color with a smooth, glistening surface and normal vascular patterns. There is a distinct absence of the diffuse erythema, edematous thickening, or wall rigidity often associated with scirrhous gastric cancer or ectopic pancreas-related inflammation. The gastric folds appear supple and undistended. In the center, the gastric lumen and the pyloric orifice are visible and patent, with no evidence of stenosis, mass effect, or significant mucosal irregularities. This image serves as a clinical reference for the interval regression of gastric wall thickening in a patient being monitored for recurrent epigastric symptoms.
| Feature | Details |
|---|---|
| General appearance | Body is shrunken due to severe dehydration |
| Rigor mortis | Lasts longer than usual |
| Eyeballs | Sunken/shrunken |
| Skin | Cold, clammy; cyanosis of hands and feet |
| Jaundice | May be present |


| Organ | Findings |
|---|---|
| Stomach | Normal or chronic gastritis; patchy inflammatory redness of rugae; patchy haemorrhagic gastritis with acute and chronic erosions |
| Small intestine | Dilated, reddened, with thickened mucosa |
| Liver | Fatty change, severe necrosis, cirrhosis, hepatomegaly, jaundice (portal hypertension with ascites reported from therapeutic arsenic use) |
| Kidneys | Tubular necrosis, chronic nephritis |
| Lungs | Congestion; haemoptysis-related changes; increased risk of lung cancer |
| Heart | Cardiac failure-related changes; myocardial degeneration |
| Bone marrow | Hypoplasia; normochromic normocytic anaemia; thrombocytopenia; leukopenia; karyorrhexis (bizarre nuclear forms on marrow exam); megaloblastic picture from folate interference |
| Peripheral nerves | Symmetrical sensorimotor polyneuropathy; disintegration of axis cylinder (axonal neuropathy); fragmentation and resorption of myelin - "glove and stocking" distribution |
| Brain | Encephalopathy; cortical changes |
| Skin histology | Bowen's disease (intraepidermal squamous cell carcinoma) as a long-term complication |
| Spleen | In arsine gas exposure: evidence of RBC destruction with deposition of blood pigment throughout |
| Feature | Significance |
|---|---|
| Red velvet stomach mucosa | Classic gross finding in acute poisoning |
| Subendocardial petechial haemorrhages (left ventricle) | Characteristic of arsenic; also seen in phosphorus, barium, mercury poisoning |
| Mees' lines on nails | Hallmark of chronic/subacute exposure |
| Raindrop pigmentation | Chronic arsenic skin finding |
| Arsenic detected in hair/nails/bones | Persists years after death; useful in exhumation cases |
| Delayed putrefaction | Arsenic is a preservative; useful forensic indicator |
| X-ray of GI tract | May show radiopaque arsenic particles |
| Fulminating cases | May show NO GI inflammation despite high blood arsenic levels |
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| Feature | Details |
|---|---|
| General appearance | Body shrunken due to severe dehydration |
| Rigor mortis | Lasts longer than usual |
| Eyeballs | Sunken/shrunken |
| Skin | Cold, clammy; cyanosis of hands and feet |
| Jaundice | May be present |

Toxicological threshold: Arsenic values in liver and blood in excess of 1 mg% are typically present in deaths from acute poisoning.
Putrefaction note: If putrefaction has occurred, yellow streaks appear in the subperitoneal layer of the stomach/intestines (absorbed arsenic converted to arsenic sulphide). Arsenic delays putrefaction and remains detectable in decomposed and charred bodies.
| Feature | Details |
|---|---|
| Skin pigmentation | "Raindrop" type - finely mottled brown pigmentation on flexures, temples, eyelids, nipples, lower abdomen, neck |
| Palms & soles | Hyperkeratosis with irregular thickening |
| Nails | Transverse white lines (Aldrich-Mees lines) 1-2 mm wide above base of each fingernail; double lines if repeated exposures |
| Hair | Patchy or diffuse alopecia; arsenic deposits detectable by segmental hair analysis |
| Oedema | Face, periorbital region, ankles |
| Jaundice | May be present in hepatic involvement |

| Organ | Findings |
|---|---|
| Stomach | Normal or chronic gastritis; patchy inflammatory redness of rugae; haemorrhagic gastritis with acute and chronic erosions |
| Small intestine | Dilated, reddened, with thickened mucosa |
| Liver | Fatty change, severe necrosis, cirrhosis, hepatomegaly; portal hypertension with ascites |
| Kidneys | Tubular necrosis, chronic nephritis |
| Lungs | Congestion; lung cancer risk (arsenic is a carcinogen) |
| Heart | Myocardial degeneration; cardiac failure changes |
| Bone marrow | Hypoplasia; normochromic normocytic anaemia; thrombocytopenia; leukopenia; karyorrhexis (bizarre nuclear forms); megaloblastic picture from folate interference |
| Peripheral nerves | Symmetrical axonal neuropathy; disintegration of axis cylinder; fragmentation and resorption of myelin; "glove and stocking" distribution |
| Brain | Encephalopathy; cortical changes |
| Skin histology | Bowen's disease (intraepidermal carcinoma) as a long-term complication |
| Spleen | Arsine exposure: destruction of RBCs with blood pigment deposition throughout the organ |
| Feature | Type | Significance |
|---|---|---|
| Red velvet stomach mucosa | Acute | Classic gross pathology finding |
| Subendocardial petechial haemorrhages (left ventricle) | Acute | Characteristic; also seen in phosphorus, barium, mercury poisoning |
| Mees' lines on nails | Chronic/Subacute | Hallmark of repeated exposure |
| Raindrop pigmentation | Chronic | Pathognomonic skin finding |
| Fulminating cases with no GI changes | Acute | Do not miss - toxicology is essential |
| Arsenic in hair, nails, bones | Both | Persists years after death; key in exhumation cases |
| Delayed putrefaction | Both | Arsenic acts as a preservative |
| X-ray abdomen | Acute | May show radiopaque arsenic particles in GI tract |
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post mortem findings acute chronic arsenic poisoning forensic pathology autopsy
arsenic poisoning Mees lines nails chronic

Clinical photography of the nails demonstrating Muehrcke lines. Anterolateral view of several fingernails (index, middle, ring, and little fingers) on both hands. The nail plates show paired, parallel, transverse white bands crossing the lunula region and extending toward the distal edge. These lines are non-palpable and lie within the nail bed/plate interface, giving the appearance of alternating light bands against the surrounding pinkish nail bed. The bands do not accompany surface textural changes and disappear with recovery of serum albumin; they are not true leukonychia. The finding is best explained by hypoalbuminemia leading to edema of the nail bed and reduced capillary perfusion, producing transverse opacities. Associated clinical context includes liver dysfunction, nephrotic syndrome, malnutrition, inflammatory states, or protein loss; systemic edema may be present. Distinguish from Beau lines (transverse ridges within the nail plate from growth arrest) and Mees’ lines (arsenic poisoning) which are embedded in the nail plate rather than the nail bed. This image underscores the dermatologic sign’s diagnostic significance as a noninvasive clue to systemic protein deficiency. Potential clinical use cases include screening for hypoalbuminemia in hospitalized patients, monitoring nutritional status in malnourished individuals, and differential diagnosis of white nail banding in clinical dermatology in practice.

This clinical dermatologic photograph depicts chronic arsenic-related skin pigmentation. Modality: clinical photography; technique: gross macro image with standard lighting. The skin surface shows diffuse, mottled hyperpigmentation characterized by numerous small, irregular brown-to-slate macules and patches arranged in a raindrop pattern across the trunk and proximal extremities. Borders are variable, with some coalescing into larger pigmented fields; texture remains largely normal but may appear slightly rough in exposed areas. The appearance is typical of long-standing arsenic exposure from contaminated groundwater and is often accompanied by palmoplantar keratoses (not shown here). The color contrast between pigmented and adjacent normal skin is pronounced, aiding recognition. Pathophysiology involves arsenic-induced dysregulation of melanocyte activity and epidermal changes, producing “raindrop” hyperpigmentation that may herald cutaneous malignancy risk (basal cell carcinoma, squamous cell carcinoma) with chronic exposure. Clinical significance includes confirming exposure history, guiding public health intervention, and prompting systemic evaluation for arsenic-related toxicity. Differential considerations include postinflammatory hyperpigmentation, tinea versicolor, solar lentigines, and other drug- or metal-induced pigmentary disorders. Clinical correlation with urinary, hair, or nail arsenic levels is recommended, along with surveillance for Mees’ lines and hyperkeratosis. This image is valuable for education, toxicology, environmental health, and dermatology curricula. Useful for clinical training and health.

This clinical comparison photograph displays the plantar surfaces (soles) of two different individuals to illustrate skin manifestations of chronic arsenic exposure (arsenicosis). The image on the left shows an affected foot characterized by diffuse hyperpigmentation, mottled melanosis (darkened patches), and palmoplantar hyperkeratosis. Visible features include a rough, thickened skin texture with numerous small, raised, corn-like keratotic papules and irregular desquamation. In contrast, the image on the right depicts a healthy sole with a smooth, uniform skin texture, normal light pigmentation, and clearly defined dermatoglyphic lines without any evidence of lesions, nodules, or abnormal thickening. This comparison serves as an educational tool for identifying the dermatological signs of arsenic poisoning, specifically highlighting the diagnostic transition from healthy tissue to pathological keratotic and pigmentary changes characteristic of environmental or occupational toxin exposure.
Key facts: Fatal dose of arsenic trioxide = 180-300 mg | Fatal period = 12-48 hours (can occur in 2-3 hours)
| Feature | Details |
|---|---|
| General appearance | Body appears shrunken and emaciated due to profound dehydration |
| Rigor mortis | Lasts longer than usual; appears early |
| Putrefaction | Delayed - arsenic has antibacterial action and acts as a tissue preservative |
| Eyeballs | Sunken (shrunken) |
| Skin | Cold, clammy; cyanosis of hands and feet |
| Jaundice | May be present in cases of liver involvement |
| Blood-tinged vomitus | May be found on the body and clothing |
Fulminating cases (important!): The stomach and intestines may show NO signs of inflammation at all, despite lethal arsenic levels in blood. Always perform toxicology.

Note: Subendocardial petechial haemorrhages are also seen in phosphorus, barium, and mercury poisoning, and in heat stroke, acute infectious diseases (influenza), and traumatic asphyxia.
| Sample | Significant Level |
|---|---|
| Liver and blood (death) | Arsenic values > 1 mg% typically present |
| Blood | > 1.5 mg/100 mL indicates serious poisoning |
| Urine | Normal < 0.03 mg/L; thousands of mcg in acute poisoning (first 2-3 days) |
| X-ray abdomen | May show radiopaque arsenic particles in GI tract |
| Organ | Finding |
|---|---|
| Skin | Dirty yellow colour (jaundice from haemolysis) |
| Stomach & intestines | Mucous membrane is yellow and inflamed |
| Liver | Small or enlarged; shows fatty degeneration |
| Spleen | Evidence of RBC destruction; deposition of blood pigment throughout |
| Kidneys | Enlarged, congested; tubular necrosis |
| Lungs | Congested and oedematous |



| Organ/System | Post Mortem Findings |
|---|---|
| Stomach | Normal or chronic gastritis; patchy inflammatory redness of rugae; patchy haemorrhagic gastritis with acute and chronic erosions; focal ulceration |
| Small intestine | Dilated, reddened, thickened mucosa |
| Liver | Hepatomegaly; fatty degeneration or severe necrosis; non-cirrhotic portal hypertension; cirrhosis; jaundice |
| Kidneys | Tubular necrosis; chronic nephritis; urine may be red or green (haemoglobinuria) |
| Lungs | Congestion; haemoptysis-related changes; lung carcinoma (arsenic is a Group 1 carcinogen for lung cancer) |
| Heart | Myocardial degeneration; cardiac failure changes; peripheral vascular disease |
| Blood/Bone marrow | Bone marrow hypoplasia; normochromic normocytic anaemia; thrombocytopenia; leukopenia; karyorrhexis (bizarre nuclear forms on marrow); megaloblastic picture from folate interference; pancytopenia; basophilic stippling of erythrocytes |
| Peripheral nerves | Symmetrical sensorimotor polyneuropathy; disintegration of axis cylinder (axonal neuropathy); fragmentation and resorption of myelin; "glove and stocking" distribution; wrist drop, foot drop, muscular atrophy |
| Brain | Encephalopathy; cortical changes; severe headache; personality changes |
| Spleen | Congested |
| Feature | Acute | Chronic |
|---|---|---|
| Body habitus | Shrunken (dehydration) | Emaciated (wasting) |
| Putrefaction | Delayed | Delayed |
| Stomach | Red velvet; petechiae; submucosal haemorrhages; sticky mucus with arsenic | Chronic gastritis; patchy redness; erosions |
| Intestine | Flaccid; pale-violet; submucosal haemorrhages | Dilated; reddened; thickened mucosa |
| Heart | Subendocardial petechial haemorrhages (left ventricle) | Myocardial degeneration; cardiac failure |
| Liver | Enlarged; fatty degeneration; cloudy swelling | Hepatomegaly; cirrhosis; non-cirrhotic portal hypertension |
| Kidneys | Acute tubular necrosis; glomerulonephritis | Chronic nephritis; tubular necrosis |
| Lungs | Congested; oedematous; subpleural ecchymoses | Congested; carcinoma (long-term) |
| Brain | Congested; haemorrhagic encephalitis | Encephalopathy |
| Skin | Cyanosis; jaundice | Raindrop pigmentation; hyperkeratosis; Bowen's disease; alopecia |
| Nails | No nail changes (appear 5-6 weeks post-exposure) | Aldrich-Mees lines |
| Bone marrow | Pancytopenia (within 1 week) | Hypoplasia; karyorrhexis |
| Nerves | Ascending sensorimotor neuropathy (2-6 weeks delay) | Symmetrical polyneuropathy; glove-stocking |
| Feature | Arsenic Poisoning | Cholera |
|---|---|---|
| Pain in throat | Before vomiting | After vomiting |
| Purging | Follows vomiting | Precedes vomiting |
| Stools | Dark, bloody; later rice-watery | Rice-watery only; involuntary jet |
| Tenesmus | Present | Absent |
| Vomitus | Mucus, bile, and blood | Watery, no mucus/bile/blood |
| Conjunctivae | Inflamed | Not inflamed |
| Analysis | Arsenic in excreta | Cholera vibrio |