Types of shock; aetiopathogenesis, diagnosis and treatment of septic shock

Definition of shock. Acute circulatory failure causing inadequate tissue oxygen delivery relative to demand, leading to cellular dysoxia, anaerobic metabolism, lactate accumulation and progressive organ dysfunction. Hypotension is a late sign — compensated shock with a normal blood pressure but raised lactate is common, and in a chronically hypertensive older patient a "normal" pressure may already represent profound shock. Clinically: tachycardia, tachypnoea, cool or mottled peripheries, prolonged capillary refill, oliguria and altered mentation.

The four types of shock.

Definitions of sepsis and septic shock (Sepsis-3, 2016). Sepsis = life-threatening organ dysfunction caused by a dysregulated host response to infection, operationalised as an acute rise in the SOFA score of 2 or more points. Septic shock = sepsis with persisting hypotension requiring vasopressors to maintain a MAP ≥65 mmHg AND a serum lactate >2 mmol/L despite adequate volume resuscitation — a subset with hospital mortality exceeding 40%. qSOFA (respiratory rate ≥22, altered mentation, systolic BP ≤100 mmHg) is a bedside prompt, not a diagnostic tool; NEWS2 performs better for screening.

Aetiology in the older adult. Commonest sources: respiratory (pneumonia), urinary, intra-abdominal, skin and soft tissue including pressure injury, and device-related. Kane's makes the key microbiological point that Gram-negative bacilli increase in frequency in every infection category in older adults — E. coli, Klebsiella, Proteus, Enterobacter and Pseudomonas — alongside S. pneumoniae, S. aureus, Enterococcus, Listeria and Candida. Predisposing factors: immunosenescence, malnutrition, diabetes, indwelling devices, institutionalisation, and recent hospitalisation or antibiotics (which raise the risk of multidrug-resistant organisms).

Pathogenesis — six linked mechanisms. Pathogen-associated molecular patterns bind pattern-recognition (Toll-like) receptors → NF-κB activation → a cytokine storm of TNF-α, IL-1 and IL-6, producing: (i) vasodilatation through inducible nitric oxide synthase and loss of vascular tone — the distributive component; (ii) endothelial injury with glycocalyx shedding → capillary leak, interstitial oedema and relative hypovolaemia; (iii) immunothrombosis — tissue factor expression, microvascular thrombi and, at the extreme, DIC; (iv) septic cardiomyopathy — direct cytokine-mediated myocardial depression; (v) mitochondrial dysfunction and cytopathic hypoxia, so cells cannot use the oxygen that is delivered; and (vi) a later immunoparalysis phase with lymphocyte apoptosis and monocyte deactivation, which explains secondary infection and the late deaths that are so characteristic of older survivors.

Presentation in the elderly — atypical and easily missed. Kane's: fever may be blunted or absent, and the absence of leucocytosis does not exclude bacterial infection; hypothermia in an older patient should promptly be treated as sepsis unless proven otherwise. Delirium, falls, functional decline, incontinence, anorexia and unexplained tachypnoea may be the only features. Kane's list of the signs that should raise suspicion of infection in a long-term care resident — decline in functional status, increasing confusion, incontinence, falling, deteriorating mobility, reduced food intake, or failure to cooperate with staff — is worth reproducing verbatim.

Diagnosis and investigations. At least two sets of blood cultures before antibiotics where this does not delay them, plus site-directed cultures (urine, sputum, wound, CSF, drain fluid). Serum lactate, repeated to guide resuscitation. CBC, renal and liver function, coagulation screen with fibrinogen and D-dimer, arterial blood gas, glucose, procalcitonin and CRP, ECG and troponin, chest radiograph, and focused ultrasound or CT to identify the source. Echocardiography to assess cardiac function and volume status. Calculate the SOFA score and document a Clinical Frailty Scale score.

Treatment — the first hour. Oxygen to target saturation; obtain cultures and lactate; broad-spectrum intravenous antibiotics within 1 hour for septic shock, chosen from the local antibiogram and covering Gram-negatives; fluid resuscitation with at least 30 mL/kg of balanced crystalloid over the first 3 hours; and vasopressors if hypotension persists. Critical geriatric modification: in an older patient with heart failure, valvular disease or chronic kidney disease, give fluid in 250–500 mL aliquots with reassessment after each rather than an unmonitored bolus — over-resuscitation causes pulmonary oedema and is a common iatrogenic death. Source control within 6–12 hours is non-negotiable: drain the abscess, remove the infected line or urinary catheter, debride the necrotic tissue, decompress the obstructed urinary tract.

Vasopressors and adjunctive therapy. Noradrenaline is first-line, and may be started peripherally to avoid delay while central access is obtained. Add vasopressin when the noradrenaline requirement is escalating (usually around 0.25–0.5 µg/kg/min) rather than escalating noradrenaline indefinitely; add adrenaline if the MAP remains inadequate. Use dobutamine or adrenaline for septic cardiomyopathy with persistent hypoperfusion despite adequate filling. Give intravenous hydrocortisone 200 mg/day for shock requiring ongoing vasopressors. Supportive care: lung-protective ventilation if ARDS develops, VTE prophylaxis, stress-ulcer prophylaxis, glucose target 140–180 mg/dL, early enteral nutrition, renal replacement therapy for the usual indications, and daily antibiotic review with de-escalation as cultures return.

Geriatric-specific management and outcome. Age is an independent predictor of mortality, and survivors face a "post-sepsis syndrome" of long-term functional and cognitive decline, sarcopenia, readmission and late death — so recovery, not just survival, is the outcome that matters. Therefore: renal dose-adjust every drug and monitor aminoglycoside and vancomycin levels; avoid nephrotoxins; screen for and prevent delirium; mobilise early and start rehabilitation in the ICU; prevent pressure injury; attend to nutrition; and hold an early, explicit discussion of goals of care and ceilings of treatment with the patient and family — frailty and comorbidity, not chronological age, should inform escalation decisions.

The Surviving Sepsis Campaign 2026 international guidelines confirm crystalloids as first-line fluid, balanced crystalloids in preference to 0.9% saline, at least 30 mL/kg in the first 3 hours with frequent ongoing reassessment to avoid both under- and over-resuscitation, and crystalloids alone rather than routine supplemental albumin. Noradrenaline remains first-line with vasopressin added on escalation. Two changes are directly geriatric: an initial MAP target of 60–65 mmHg rather than a higher target in adults aged 65 and over (permissive hypotension, from the 65 trial), and the suggestion to use capillary refill time as an adjunct to lactate for guiding resuscitation — a bedside measure available in any Indian hospital.

Antibiotic timing has been formally stratified rather than made universally one-hour. Current guidance recommends antimicrobials within 1 hour for definite septic shock or high-probability sepsis, but permits up to 3 hours where sepsis is only possible and there is no shock, allowing rapid assessment for a non-infectious mimic. This matters most in older adults, in whom pulmonary embolism, myocardial infarction, gastrointestinal bleeding, adrenal crisis, drug reactions and hypothermia routinely mimic sepsis. Counterbalancing this, the stewardship agenda now emphasises de-escalation and procalcitonin-guided discontinuation to shorten courses.

Vasopressor (noradrenaline) · Source control.