Infectious DiseasesTier 1Disease (DEADMAN)

Septicaemia and septic shock

Description

Sepsis = life-threatening organ dysfunction caused by a dysregulated host response to infection (Sepsis-3 definition)
Septic shock = sepsis + persisting hypotension requiring vasopressors to maintain MAP >=65mmHg + lactate >2mmol/L despite adequate fluid resuscitation

Leading cause of in-hospital death; mortality ~10% for sepsis, ~30-40% for septic shock
Incidence rising (ageing population, more immunosuppression, resistant organisms)
Every hour of delayed appropriate antibiotics in septic shock increases mortality

Mechanism

Infection -> dysregulated cytokine release (TNF-alpha, IL-1, IL-6) -> endothelial dysfunction, vasodilation, capillary leak, coagulopathy -> relative and absolute hypovolaemia + impaired tissue oxygen extraction -> multi-organ dysfunction

Common sources

Respiratory (commonest), urinary tract, intra-abdominal, skin/soft tissue, line-associated, unknown focus
Organism varies by source and setting (community vs healthcare-associated, immune status)

Screening/recognition

qSOFA (RR>=22, altered mentation, SBP<=100) - bedside screening tool for risk, not a diagnostic criterion
SOFA score increase >=2 with suspected/confirmed infection = sepsis (formal Sepsis-3 criteria, typically retrospective/ICU use)
Clinical: fever or hypothermia, tachycardia, tachypnoea, altered mental state, mottled skin, reduced urine output

Investigations - performed in parallel with treatment, not before it

Lactate - severity marker and resuscitation target; note intermediate elevation (2-4mmol/L) is clinically significant, not just >=4
Blood cultures (x2 sets) before antibiotics if it does not delay treatment
FBE, UEC, LFT, coagulation, CRP, VBG
Source-directed cultures/imaging (urine, sputum, wound, CSF, CT abdomen) guided by clinical focus

A. The hour-1 bundle - time-critical, run concurrently

Measure lactate (repeat if initial >2mmol/L to guide resuscitation)
Obtain blood cultures before antibiotics (do not delay antibiotics beyond ~45 min to achieve this)
Broad-spectrum empirical antibiotics within 1 hour of recognition - source- and setting-directed, then de-escalate on culture results
30mL/kg IV crystalloid for hypotension or lactate >=4mmol/L, given over the first 3 hours, individualised to patient factors (heart failure, renal function)
Vasopressors (noradrenaline first-line) if hypotension persists despite/during fluid resuscitation, to maintain MAP >=65mmHg

B. Ongoing/source control

Identify and control the source - drain abscess, remove infected line, relieve obstruction - as urgently as antibiotics themselves
Reassess fluid responsiveness dynamically (avoid indiscriminate large-volume fluids in the volume-overloaded or cardiac-impaired)
Escalate to ICU for refractory shock, need for vasopressors, or multi-organ dysfunction

C. Adjuncts (selected patients)

Hydrocortisone for septic shock refractory to fluids and vasopressors
Lung-protective ventilation if ARDS develops
Glucose control (avoid hypoglycaemia, target moderate range), stress ulcer/VTE prophylaxis in ICU

D. De-escalation

Narrow antibiotic therapy once culture and sensitivity results available
Define appropriate duration by source (e.g. typically 7 days for many bacteraemias, longer for endocarditis/osteomyelitis/undrained collections)

Mortality rises sharply with delayed recognition and antibiotic administration
Complications: acute kidney injury, ARDS, DIC, multi-organ failure, critical illness myopathy/neuropathy
Post-sepsis syndrome - persistent physical, cognitive and psychological impairment in survivors, often under-recognised
Recurrent sepsis risk higher with unresolved source or ongoing immunosuppression

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