Define death due to hanging. What are the probable causes of death in hanging? What are the findings in a case of judicial…

(a)(i) Death due to hanging: definition and causes of death

Definition. Hanging is death caused by suspending the body by a ligature around the neck. The constricting force is the weight of the body, whole or partial. Hanging may be:

• complete, with the body free, or partial, with the feet, knees or buttocks touching the ground;
• typical, with the knot over the occiput, or atypical, with the knot elsewhere.

It differs from ligature strangulation, where the force is applied externally rather than by body weight.

Probable causes of death. Classical figures for occlusion are about 2 kg for the jugular veins, 5 kg for the carotids, 15 kg for the trachea and 30 kg for the vertebral arteries, so even partial suspension kills.

1. Asphyxia: the larynx and tongue base are pushed against the posterior pharyngeal wall.
2. Venous congestion: jugular compression causes cerebral congestion, cyanosis and petechiae.
3. Cerebral ischaemia (cerebral anaemia): carotid and vertebral occlusion cause rapid unconsciousness, which is why suicidal hanging is usually painless.
4. Reflex vagal inhibition: carotid sinus pressure causes sudden cardiac arrest.
5. Fracture-dislocation of C2–C3 (hangman's fracture): a long drop, as in judicial hanging, crushes the cord or brainstem.
6. Combination of the above, most often asphyxia with venous congestion, which is the commonest cause of death in hanging. Delayed deaths follow hypoxic encephalopathy, aspiration pneumonia or laryngeal oedema.

(a)(ii) Findings in judicial hanging

The condemned person is dropped a calculated distance with the knot under the angle of the jaw or chin. This produces violent hyperextension and lateral flexion of the neck, and death is almost instantaneous.

• Ligature (suspension) mark: pressed, parchment-like and running obliquely upward. It forms an inverted "V", is non-continuous at the knot, and is often abraded with bruised tissue beneath.
• Cervical spine: fracture-dislocation of C2 on C3 with bilateral C2 pedicle fracture. The upper cord or medulla is crushed or transected, and the neck may be stretched.
• Soft tissues: torn neck muscles, carotid intimal tears, and hyoid or thyroid cartilage fractures.
• Face: usually pale or only slightly congested, with few petechiae and slight cyanosis, because death is not primarily asphyxial.
• Saliva: there is no dribbling of saliva, the vital sign seen in suicidal hanging.

(b)(i) Haematemesis in a 55-year-old HBsAg-positive woman

1. Diagnosis. The most likely diagnosis is post-hepatitic (HBV) macronodular cirrhosis with portal hypertension, with bleeding oesophageal varices. Pallor reflects blood loss, and the absence of organomegaly fits a shrunken, fibrotic liver.

2. Microscopic findings

• Architecture: diffuse bridging fibrous septa link portal tracts and central veins.
• Nodules: regenerative nodules (pseudolobules) lack a central vein and are mostly more than 3 mm across (macronodular).

Signs of hepatitis B:

• ground-glass hepatocytes, with HBsAg in the smooth ER (orcein or Shikata positive);
• "sanded" nuclei containing HBcAg.
• Inflammation: portal and interface lymphocytic infiltrate with ductular reaction.
• Varices: dilated, thin-walled submucosal oesophageal veins.

3. Pathogenesis

1. Immune injury: HBV is not cytopathic; CD8⁺ T cells destroy infected hepatocytes and cause chronic necro-inflammation.
2. Stellate cell activation: Kupffer cells and injured hepatocytes release TGF-β and PDGF. These activate hepatic stellate (Ito) cells into collagen-secreting myofibroblasts.
3. Architectural distortion: sinusoids are capillarised, and bridging fibrosis with nodular regeneration distorts the architecture.
4. Portal hypertension: raised intrahepatic resistance plus splanchnic hyperdynamic inflow produce portal hypertension.
5. Varices and bleeding: left gastric–azygos collaterals form oesophageal varices. These rupture once the portal pressure gradient exceeds about 12 mmHg, causing haematemesis, and coagulopathy aggravates the bleeding.

(b)(ii) Acute lymphoblastic leukaemia

ALL is a malignancy of precursor B or T lymphoblasts and the commonest childhood cancer, peaking at 2–5 years.

Clinical features

• Onset: abrupt.

Marrow failure:

• anaemia causes pallor and fatigue;
• neutropenia causes fever and infections;
• thrombocytopenia causes petechiae and bleeding.

Infiltration:

• bone pain and sternal tenderness;
• lymphadenopathy and hepatosplenomegaly;
• a mediastinal mass in T-ALL;
• testicular swelling;
• rarely, leukaemia cutis.
• CNS disease: headache, vomiting and cranial nerve palsies.

Microscopic findings

• Peripheral smear: the leucocyte count is variable, with circulating blasts, normocytic anaemia and thrombocytopenia.
• Bone marrow: hypercellular, replaced by lymphoblasts (generally ≥20%).

Blast morphology:

• small to medium cells with a high N:C ratio;
• scant agranular basophilic cytoplasm;
• fine chromatin and inconspicuous nucleoli;
• no Auer rods.
• FAB types: L1 small uniform blasts, L2 large pleomorphic blasts, L3 vacuolated Burkitt-type blasts.
• Cytochemistry: MPO negative with block PAS positivity.
• Immunophenotype: TdT positive, plus CD10, CD19 and CD22 for B-ALL, or CD3 and CD7 for T-ALL.

(c)(i) Role of diuretics in hypertension

• First-line status: low-dose thiazide or thiazide-like diuretics (hydrochlorothiazide, chlorthalidone, indapamide) are first-line alongside ACE inhibitors or ARBs and CCBs. JNC 8 supports this, as do outcome trials such as ALLHAT and SHEP. They are cheap.
• Mechanism: early natriuresis reduces plasma volume and cardiac output. The sustained effect comes from reduced peripheral vascular resistance.
• Best suited to: the elderly, isolated systolic hypertension, salt-sensitive patients and heart failure.
• Combination use: they potentiate other drugs and are integral to triple therapy; spironolactone is added in resistant hypertension.
• Loop diuretics: used when eGFR is below 30 or there is volume overload.
• Cautions: hypokalaemia, hyponatraemia, hyperuricaemia and hyperglycaemia.

(c)(ii) Paracetamol hepatotoxicity and its management

Mechanism. Normally most paracetamol is glucuronidated or sulphated, and about 5–10% is converted by CYP2E1 to NAPQI, which glutathione neutralises. In overdose (above about 150 mg/kg), conjugation saturates, glutathione is depleted, and free NAPQI binds mitochondrial proteins. The result is oxidative stress, ATP loss and centrilobular (zone 3) necrosis. Alcoholism, enzyme inducers and starvation increase the risk.

Management

1. Initial care: resuscitation, and activated charcoal 1 g/kg within about an hour.
2. Risk assessment: plot the 4-hour paracetamol level on the Rumack–Matthew nomogram, and check LFT, INR, creatinine, glucose and pH.
3. N-acetylcysteine: this glutathione precursor is most effective within 8 hours but is still given late. The IV regimen is 150 mg/kg over 1 hour, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours.
4. Supportive care for acute liver failure.
5. Transplant referral if King's College criteria are met: pH below 7.3, or INR above 6.5 with creatinine above 3.4 mg/dL and grade III–IV encephalopathy.

(c)(iii) SGLT-2 inhibitors in diabetes mellitus

Dapagliflozin, empagliflozin and canagliflozin block SGLT-2 in the proximal tubule, which reabsorbs about 90% of filtered glucose. They cause insulin-independent glucosuria.

Advantages

• Glycaemic control: HbA1c falls by about 0.5–1% with little hypoglycaemia.
• Weight and blood pressure: both fall.
• Heart: fewer cardiovascular deaths and heart-failure hospitalisations (EMPA-REG OUTCOME, DAPA-HF).
• Kidney: renal protection (CREDENCE, DAPA-CKD) through reduced intraglomerular pressure.
• Convenience: oral, once-daily dosing.

Disadvantages

• Infection: genital mycotic infections and UTI.
• Volume depletion: hypotension and an early fall in eGFR.
• Ketoacidosis: euglycaemic DKA, so the drug is withheld before surgery.
• Rare harms: Fournier's gangrene, and amputations with canagliflozin.
• Limitations: efficacy falls with low eGFR, and cost is higher.

They are therefore preferred in diabetics with heart failure, CKD or cardiovascular disease.