Define sepsis. Discuss its epidemiology, clinical presentation, diagnosis, management and prognosis in the older person

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection (Sepsis-3, 2016). Organ dysfunction = an acute rise in the SOFA score by 2 or more points.

Septic shock = sepsis with persisting hypotension requiring vasopressors to keep MAP ‡ 65 mmHg plus lactate > 2 mmol/L after adequate fluid resuscitation. The old terms severe sepsis and septicaemia are obsolete.

Roughly 49 million cases and 11–13 million sepsis-related deaths occur worldwide each year; it is a leading cause of death globally (SSC 2026).

Older adults carry most of the burden — those aged ‡ 65 years account for about 60–85% of all sepsis cases and the incidence rises roughly 100-fold from young adulthood to the ninth decade.

In India, sepsis is the commonest reason for ICU admission; reported ICU mortality from severe sepsis is 34–58%, higher than Western cohorts, driven by late presentation, multidrug-resistant gram-negative organisms and limited critical-care access.

Predisposing factors in the elderly: immunosenescence and inflammaging, diminished cell-mediated immunity, protein–energy malnutrition, multimorbidity (diabetes, heart failure, CKD, COPD, dementia), prostatic obstruction, swallowing disorders and aspiration, pressure ulcers, indwelling catheters and institutional residence.

Commonest sources: respiratory tract (pneumonia is the single largest source), urinary tract, skin and soft tissue, intra-abdominal/biliary (acute cholecystitis, cholangitis), and device-related infection. Gram-negative bacilli are more frequent at every site than in the young.

Presentation is atypical and non-specific. The febrile response is blunted or absent in up to 30–50%; hypothermia is an ominous sign, and absence of leucocytosis does not exclude bacterial infection.

Delirium or acute confusion is frequently the only presenting feature, especially in pre-existing dementia. Other geriatric presentations: falls, being ‘off legs’, new incontinence, anorexia, tachypnoea and unexplained functional decline.

A textbook axiom: acute unexplained functional deterioration should alert the physician to an acute infectious process, and one should suspect infection (including TB) whenever an older patient is inexplicably failing.

Tachypnoea (RR > 20–22/min) is the earliest and most reliable sign; hypotension is a late sign because of stiff vasculature and pre-existing hypertension — a ‘normal’ BP of 110/70 may represent shock in a chronic hypertensive.

Sepsis is a clinical diagnosis and must not be ruled in or out on a single biomarker. Screen with NEWS/NEWS2, MEWS or SIRS criteria; calculate SOFA in the ICU.

Baseline work-up: haemogram with differential, serum lactate, CRP ± procalcitonin, blood urea and creatinine (mg/dL), electrolytes, liver function, coagulation profile and D-dimer (DIC screen), arterial blood gas, blood sugar.

Two sets of blood cultures before antibiotics, plus site-directed cultures (urine, sputum, pus, CSF), chest radiograph, ultrasound abdomen/CT for source, and echocardiography if endocarditis is suspected.

Key geriatric pitfall: asymptomatic bacteriuria is very common in older people — a positive urine culture alone must never be accepted as the source, or a genuine pneumonia or intra-abdominal source will be missed.

Hour-1 bundle: measure lactate, take blood cultures, give broad-spectrum antibiotics immediately (ideally within 1 hour) in septic shock or probable sepsis, start 30 mL/kg balanced crystalloid for hypotension or lactate ‡ 4 mmol/L, and add vasopressors if hypotension persists.

Antibiotics: cover gram-negatives empirically (third-generation cephalosporin ± aminoglycoside per the textbook; locally, a beta-lactam/beta-lactamase inhibitor or carbapenem where ESBL prevalence is high). Dose-adjust for renal function — sarcopenia falsely lowers creatinine, so estimate GFR (Cockcroft–Gault) rather than trusting creatinine, and monitor aminoglycoside levels. De-escalate at 48–72 hours.

Haemodynamics: noradrenaline is first-line; add vasopressin if doses escalate, then adrenaline; add IV hydrocortisone in shock requiring ongoing vasopressors. Fluids must be given cautiously and reassessed — reduced cardiac and renal reserve makes the elderly prone to pulmonary oedema; use dynamic measures (passive leg raise, stroke-volume variation) and capillary refill rather than large fixed boluses.

Source control within 6 hours — drain abscess, remove infected catheter/line, decompress obstructed biliary or urinary tract, debride necrotic tissue.

Geriatric supportive care bundle: delirium prevention (orientation, sleep, avoid anticholinergics/benzodiazepines), LMWH thromboprophylaxis, PPI stress-ulcer prophylaxis if risk factors, early enteral nutrition within 72 h, early mobilisation and physiotherapy, oral care, pressure-ulcer prevention, glycaemic control (start insulin at glucose ‡ 180 mg/dL) and medication review with withdrawal of nephrotoxins.

Goals of care must be addressed early (within 72 hours), framed by Pathy's functional categorisation (robust / frail / moderately demented / end of life): decide ceilings of treatment, escalation to ICU, resuscitation status and time-limited trials, incorporating advance directives (in India, valid under Common Cause 2018 as modified in 2023).

Mortality rises steeply with age — roughly 1.5–2 times that of younger patients for the same severity; but frailty, baseline functional status and comorbidity predict outcome better than chronological age, so age alone must never be used to deny critical care.

Post-sepsis syndrome is the rule in survivors: new physical disability, accelerated cognitive decline, depression and anxiety, sarcopenia, high 30-day readmission and a one-year mortality of 30–40%. Institutionalisation after the illness is common.