(a) Define 'pre-eclampsia'. Enumerate the risk factors which may lead to this condition. What are its clinical signs and what are…

(a) Pre-eclampsia

Definition: new-onset hypertension (140/90 mmHg or more on two readings 4 hours apart) after 20 weeks of gestation with proteinuria (300 mg or more in 24 hours, or dipstick 1+), or, in the absence of proteinuria, with features of end-organ involvement (thrombocytopenia, raised liver enzymes, renal insufficiency, pulmonary oedema, cerebral or visual symptoms). It reflects abnormal placentation and maternal endothelial dysfunction.

Risk factors:

1. Primigravida, new partner, long inter-pregnancy interval.
2. Pre-eclampsia in a previous pregnancy, family history.
3. Multiple pregnancy, hydatidiform mole, hydrops.
4. Chronic hypertension, renal disease, diabetes, antiphospholipid syndrome, SLE.
5. Obesity, age over 35 or teenage pregnancy, IVF conception.

Clinical signs: raised blood pressure, oedema (non-dependent, face and hands) with rapid weight gain, proteinuria, brisk reflexes or clonus, right upper quadrant tenderness, oliguria, fetal growth restriction.

Alarming (imminent eclampsia) symptoms: severe frontal headache, blurring of vision or scotomas, epigastric or right upper quadrant pain, nausea and vomiting, oliguria, breathlessness. Severe features: BP of 160/110 mmHg or more, platelets under 1 lakh, HELLP syndrome.

Management:

• Prevention: low-dose aspirin (75-150 mg) from 12 weeks to 36 weeks in high-risk women, calcium supplementation.
• Non-severe: BP, urine protein, platelets, liver and renal function, fetal growth and Doppler monitoring, oral labetalol or nifedipine, delivery at 37 weeks.
• Severe: admit, IV labetalol or oral nifedipine to keep BP below 150/100 mmHg, magnesium sulphate (Pritchard: 4 g IV plus 10 g IM loading, 5 g IM 4-hourly, continued 24 hours after delivery). Monitor knee jerk, respiratory rate (12/min or more) and urine output (30 mL/h or more), with calcium gluconate as antidote.
• Delivery is the definitive cure: at 34 weeks in severe disease, earlier if maternal or fetal condition worsens, with antenatal corticosteroids if preterm.
• Postpartum BP monitoring for 6 weeks.

(b) Ileo-caecal tuberculosis

Clinical features: the ileo-caecal region is the commonest site of abdominal TB because of lymphoid tissue, stasis and absorption.

• Ulcerative type: diarrhoea, malabsorption, weight loss.
• Hyperplastic type: right iliac fossa mass, colicky pain, features of subacute obstruction (borborygmi, visible peristalsis).
• Constitutional: low-grade evening fever, night sweats, anorexia. Complications: obstruction, perforation, fistula, bleeding.

Diagnosis:

• Colonoscopy: transverse ulcers, nodularity, deformed and patulous ileo-caecal valve. Biopsy for caseating granulomas, AFB, culture and CBNAAT (GeneXpert, also showing rifampicin resistance).
• Barium study: pulled-up contracted caecum, Fleischner (inverted umbrella) sign, Stierlin sign, goose-neck deformity.
• CECT abdomen: asymmetric ileo-caecal thickening, necrotic mesenteric nodes, ascites.
• Supportive: chest X-ray, raised ESR, ascitic ADA, Mantoux or IGRA (not confirmatory). Differentiate from Crohn’s disease and carcinoma caecum.

Management:

• Anti-tubercular therapy under NTEP for 6 months (2HRZE plus 4HRE), extended if response is slow, with nutritional support (Ni-kshay Poshan Yojana).
• Surgery for complications: obstruction not settling, perforation, fistula, bleeding, diagnostic doubt. Options: stricturoplasty, limited ileo-caecal resection, right hemicolectomy, followed by full ATT.

(c)(i) Objectives of epidemic investigation

1. Define the magnitude of the outbreak by time, place and person.
2. Determine the conditions and factors responsible for it.
3. Identify the cause, source of infection and mode of transmission so that control measures can be applied.
4. Recommend measures to prevent recurrence.

(c)(ii) Steps of investigation

1. Verification of diagnosis: clinical examination and laboratory confirmation of a sample of cases.
2. Confirmation of the epidemic: compare current cases with the expected (past) frequency.
3. Defining the population at risk: map the area, obtain the population denominator.
4. Rapid search for all cases: case definition, house-to-house search, line list of cases.
5. Data analysis by time (epidemic curve), place (spot map) and person (age, sex, occupation), attack rates.
6. Formulation of hypotheses on source, vehicle and transmission.
7. Testing of hypotheses: case-control or cohort studies, environmental samples.
8. Evaluation of ecological factors: water, food, vectors, sanitation.
9. Further investigation of the population at risk to find missed or subclinical cases.
10. Control measures applied from the start (isolation, safe water, vaccination, vector control), and writing of the report with recommendations, shared through IDSP (now IHIP).