3. Sepsis and Septic Shock
Sepsis and Septic Shock
Sri Lankan Surgery MD Part One / Common Selection Examination Master Note
This is a core Principles of Surgery, critical-care, trauma, physiology, pathology, pharmacology and OSCE topic. Examiners may test it through definitions, postoperative deterioration, source control, fluids, antibiotics, vasopressors, lactate interpretation, organ support and common treatment errors.
The latest international adult guidance is the 2026 Surviving Sepsis Campaign, published on March 23, 2026. Your exam may still quote elements from the 2021 guideline and the traditional “Hour-1 bundle,” so you should know both the current nuanced recommendations and the older examination shorthand. (Society of Critical Care Medicine (SCCM))
1. Essential definitions
Infection
Invasion of normally sterile tissue by pathogenic microorganisms, producing a local or systemic host response.
Sepsis — Sepsis-3 definition
Life-threatening organ dysfunction caused by a dysregulated host response to infection.
Clinically, organ dysfunction is represented by an acute increase in SOFA score of at least 2 points attributable to infection. If no pre-existing organ dysfunction is known, baseline SOFA may be assumed to be zero. (JAMA Network)
Septic shock
A subset of sepsis in which circulatory and cellular/metabolic abnormalities are sufficiently severe to substantially increase mortality.
Operational criteria are:
Sepsis is present.
Hypotension persists despite adequate fluid resuscitation.
Vasopressors are required to maintain MAP ≥65 mmHg.
Serum lactate remains >2 mmol/L.
Both vasopressor requirement and lactate >2 mmol/L must be present after adequate volume resuscitation. This phenotype carries hospital mortality exceeding approximately 40% in the original Sepsis-3 data. (JAMA Network)
Important terminology trap
“Severe sepsis”
This term is no longer used in Sepsis-3 because sepsis itself now requires organ dysfunction.
Older classification:
Infection
SIRS
Sepsis = infection plus SIRS
Severe sepsis = sepsis plus organ dysfunction
Septic shock = severe sepsis with persistent hypotension
Current classification:
Infection without organ dysfunction
Sepsis
Septic shock
“Septicaemia”
This is imprecise and should generally be avoided. Sepsis does not require demonstrable organisms in the bloodstream, and blood cultures may be negative.
2. SIRS, qSOFA and SOFA
SIRS criteria
Two or more of:
| Parameter | Abnormality |
|---|---|
| Temperature | >38°C or <36°C |
| Heart rate | >90/min |
| Respiratory rate | >20/min or PaCO₂ <32 mmHg |
| WBC | >12,000/mm³, <4,000/mm³ or >10% immature forms |
SIRS is sensitive but nonspecific. Trauma, burns, pancreatitis, surgery, haemorrhage and pulmonary embolism can all produce SIRS without infection. Conversely, some septic patients do not satisfy two SIRS criteria. (JAMA Network)
qSOFA
One point each for:
Respiratory rate ≥22/min
Altered mentation
Systolic BP ≤100 mmHg
Mnemonic: RAS
A score ≥2 identifies a patient with suspected infection at increased risk of deterioration, but:
qSOFA does not define sepsis.
qSOFA does not exclude sepsis when negative.
It should trigger investigation, escalation and assessment of organ dysfunction.
The 2026 guideline recommends NEWS/NEWS2, MEWS or SIRS rather than qSOFA as the sole hospital screening tool. (JAMA Network)
SOFA score
Six organ systems are assessed.
| System | Main variable |
|---|---|
| Respiratory | PaO₂/FiO₂ ratio and respiratory support |
| Coagulation | Platelet count |
| Liver | Bilirubin |
| Cardiovascular | MAP and vasopressor requirement |
| CNS | Glasgow Coma Scale |
| Renal | Creatinine or urine output |
High-yield SOFA thresholds
| Score | 0 | 1 | 2 | 3 | 4 |
|---|---|---|---|---|---|
| PaO₂/FiO₂ | ≥400 | <400 | <300 | <200 with support | <100 with support |
| Platelets ×10³/µL | ≥150 | <150 | <100 | <50 | <20 |
| Bilirubin mg/dL | <1.2 | 1.2–1.9 | 2–5.9 | 6–11.9 | >12 |
| Cardiovascular | MAP ≥70 | MAP <70 | Dopamine <5 or dobutamine | Dopamine 5.1–15 or noradrenaline/adrenaline ≤0.1 | Dopamine >15 or noradrenaline/adrenaline >0.1 |
| GCS | 15 | 13–14 | 10–12 | 6–9 | <6 |
| Creatinine mg/dL | <1.2 | 1.2–1.9 | 2–3.4 | 3.5–4.9 | >5 |
| Urine output | — | — | — | <500 mL/day | <200 mL/day |
A rise of ≥2 from baseline in the context of infection operationalises sepsis. (JAMA Network)
3. Pathophysiology
Sepsis is not simply “infection spreading through the blood.” It is a failure of regulated host defence.
Sequence
1. Recognition of infection and tissue injury
Microbial structures—pathogen-associated molecular patterns—and molecules released from injured cells—damage-associated molecular patterns—activate pattern-recognition receptors such as Toll-like receptors.
2. Dysregulated inflammatory response
Inflammatory mediators include:
TNF-α
IL-1
IL-6
Complement products
Prostaglandins
Leukotrienes
Platelet-activating factor
Reactive oxygen species
The inflammatory response becomes widespread rather than remaining locally protective.
3. Endothelial and glycocalyx injury
This causes:
Increased vascular permeability
Capillary leak
Interstitial oedema
Loss of vascular tone
Abnormal leukocyte-endothelial interaction
Disordered microvascular blood flow
4. Vasodilatation
Inducible nitric oxide synthase increases nitric oxide production, producing profound vasodilatation and reduced systemic vascular resistance.
5. Relative and absolute hypovolaemia
Relative hypovolaemia: vascular capacity increases because of vasodilatation.
Absolute intravascular volume loss: fluid moves into the interstitium through leaky capillaries.
Additional loss may occur from vomiting, diarrhoea, fever, poor intake, drains or third spacing.
6. Coagulation activation
Tissue-factor pathways are activated while natural anticoagulant systems such as protein C and antithrombin are impaired. Fibrinolysis is suppressed.
Consequences:
Microvascular thrombosis
Organ ischaemia
Consumption of platelets and clotting factors
Disseminated intravascular coagulation
7. Cellular and mitochondrial dysfunction
Even when global oxygen delivery appears adequate, cells may not extract or use oxygen normally. Microcirculatory shunting and mitochondrial dysfunction contribute to organ failure.
8. Myocardial dysfunction
Sepsis may produce reversible depression of:
Left ventricular systolic function
Right ventricular function
Diastolic function
Cardiac output may therefore become inadequate despite severe vasodilatation.
9. Immunosuppression
Sepsis can progress from hyperinflammation to immune exhaustion or “immunoparalysis,” with lymphocyte apoptosis and impaired antigen presentation. This contributes to secondary and opportunistic infections.
Sepsis-3 emphasises that the key abnormality is a dysregulated, non-homeostatic host response causing organ injury. (JAMA Network)
4. Haemodynamic pattern
Early “warm” septic shock
Typical findings:
Reduced systemic vascular resistance
Normal or increased cardiac output
Warm peripheries
Bounding pulse
Wide pulse pressure
Tachycardia
Rapid capillary refill may occur early
Hypotension
Later or “cold” phenotype
May result from hypovolaemia, myocardial depression or advanced shock:
Reduced cardiac output
Cold, mottled peripheries
Weak pulse
Narrow pulse pressure
Delayed capillary refill
Oliguria
Altered consciousness
Do not assume every patient with septic shock will be warm.
5. Common sources of surgical sepsis
Intra-abdominal
Perforated peptic ulcer
Perforated appendix
Anastomotic leak
Colonic perforation
Ischaemic or gangrenous bowel
Perforated diverticulitis
Intra-abdominal or pelvic abscess
Infected pancreatic necrosis
Ascending cholangitis
Acute cholecystitis with perforation/empyema
Secondary peritonitis
Tertiary peritonitis
Urinary
Infected obstructed ureter
Pyonephrosis
Complicated pyelonephritis
Catheter-associated infection
Prostatic abscess
An infected obstructed urinary system requires urgent decompression, not antibiotics alone.
Skin and soft tissue
Necrotising fasciitis
Gas gangrene
Infected diabetic foot
Deep surgical-site infection
Infected pressure ulcer
Fournier gangrene
Thoracic
Pneumonia
Aspiration pneumonia
Empyema
Lung abscess
Mediastinitis
Oesophageal perforation
Device-associated
Central venous catheter
Urinary catheter
Vascular graft
Prosthetic joint
Cardiac device
Infected drain or stent
Postoperative clues
Think particularly of:
Anastomotic leak
Missed bowel injury
Infected haematoma
Intra-abdominal collection
Bile leak
Urinary leak
Wound infection
Line infection
Pneumonia
UTI
Acalculous cholecystitis
Bowel ischaemia
Clostridioides difficile infection
6. Risk factors for severe sepsis
Extremes of age
Diabetes mellitus
Chronic kidney or liver disease
Malignancy
Immunosuppressive medication
Neutropenia
HIV/AIDS
Malnutrition
Recent surgery or trauma
Prolonged hospitalisation
Previous broad-spectrum antibiotics
Indwelling lines, drains or catheters
Mechanical ventilation
Recent colonisation or infection with resistant organisms
Poor source control
Delayed antibiotic therapy
Splenectomy or functional asplenia
7. Clinical presentation
General
Fever or hypothermia
Rigors
Malaise
Confusion
Reduced mobility
Poor oral intake
Hyperglycaemia, including in non-diabetic patients
Older, immunocompromised and severely septic patients may be hypothermic rather than febrile.
Respiratory
Tachypnoea is often an early sign
Hypoxaemia
Respiratory alkalosis early
Metabolic acidosis with respiratory compensation later
ARDS
Cardiovascular
Tachycardia
Hypotension
Warm peripheries initially
Mottling or cold extremities later
Reduced pulse pressure in low-output shock
Arrhythmias, particularly atrial fibrillation
Elevated troponin from demand injury or septic cardiomyopathy
Neurological
Anxiety or agitation
Delirium
Confusion
Reduced GCS
Coma
Renal
Oliguria: <0.5 mL/kg/hour
Rising creatinine
Acute tubular injury
Fluid overload
Electrolyte and acid-base disturbance
Gastrointestinal and hepatic
Ileus
Feed intolerance
Stress-related mucosal bleeding
Cholestasis
Rising bilirubin and transaminases
Hypoglycaemia in severe hepatic dysfunction
Haematological
Thrombocytopenia
Prolonged PT/APTT
Low fibrinogen in advanced DIC
Elevated D-dimer
Anaemia
Leukocytosis or leukopenia
Skin/perfusion
Prolonged capillary refill
Mottling
Cool extremities
Cyanosis
Peripheral oedema from capillary leak
8. Lactate: a major examination topic
Why lactate rises
Elevated lactate may result from:
Inadequate oxygen delivery
Microcirculatory failure
Accelerated aerobic glycolysis driven by catecholamines
Mitochondrial dysfunction
Reduced hepatic clearance
Reduced renal clearance
Seizures
β₂-agonists or adrenaline
Severe liver disease
Therefore:
Elevated lactate does not automatically mean anaerobic metabolism, and normal lactate does not exclude sepsis.
Interpretation
2 mmol/L: abnormal and relevant to septic-shock definition when associated with vasopressor dependence.
≥4 mmol/L: severe hyperlactataemia and traditionally used as a trigger for aggressive resuscitation.
Serial trend is more useful than a single value.
Lactate should be interpreted with:
Blood pressure
Capillary refill
Mental status
Urine output
Skin temperature and mottling
Acid-base state
Liver function
Vasopressor treatment
Current guidance supports serial lactate measurements but warns against blindly continuing fluids until lactate normalises. (Society of Critical Care Medicine (SCCM))
9. Investigations
Investigations should occur concurrently with treatment.
Immediate bedside assessment
Full A–E assessment
Continuous ECG
SpO₂
Non-invasive BP at short intervals
Temperature
Capillary refill
Mental status/GCS
Hourly urine output
Fluid balance
Blood glucose
Examine wounds, drains, lines and catheters
Blood tests
Full blood count
Urea, creatinine and electrolytes
Liver profile and bilirubin
CRP
Arterial or venous blood gas
Lactate
Glucose
PT/INR, APTT
Fibrinogen and D-dimer if DIC suspected
Calcium, magnesium and phosphate
Group and save/crossmatch
Troponin/BNP where cardiac dysfunction is suspected
Peripheral blood film where indicated
Microbiology
Obtain cultures as soon as possible and ideally before antimicrobials, provided this does not cause a clinically important delay.
Usually obtain:
Two sets of blood cultures from separate peripheral sites
Cultures from a central line if line infection is suspected
Urine culture
Sputum or tracheal aspirate
Wound or pus specimen
Drain fluid
Bile or peritoneal fluid
CSF when indicated and safe
Relevant viral testing
Sepsis remains a clinical diagnosis; no single biomarker rules it in or rules it out. (Society of Critical Care Medicine (SCCM))
Imaging
Based on likely source:
Chest radiograph
Bedside lung ultrasound
Abdominal ultrasound
CT chest/abdomen/pelvis
CT with IV contrast when required for source detection
Echocardiography
Doppler studies
MR imaging in selected spinal, neurological or deep soft-tissue infection
Do not allow nonessential imaging to delay life-saving source control.
Procalcitonin
Do not use procalcitonin alone to decide whether to start antibiotics.
It may assist, together with clinical assessment, when deciding when to stop antibiotics if duration is uncertain and source control is adequate. (Society of Critical Care Medicine (SCCM))
10. Immediate management
Initial mental framework: “Sepsis Six plus source control”
Within the first assessment period:
Give appropriate oxygen/respiratory support.
Obtain IV access and cultures.
Measure lactate and essential blood tests.
Give appropriate IV antibiotics.
Begin crystalloid resuscitation.
Monitor urine output.
Identify and control the source.
Start vasopressors early when needed.
11. A–E approach
A: Airway
Assess patency.
Look for reduced consciousness, vomitus, secretions or airway oedema.
Use airway adjuncts as necessary.
Intubate when airway protection, oxygenation, ventilation or work of breathing cannot be maintained.
Be cautious during induction: critically ill septic patients can develop profound cardiovascular collapse due to vasodilatation, hypovolaemia and myocardial depression.
B: Breathing
Give oxygen for hypoxaemia.
Obtain ABG where appropriate.
Look for pneumonia, aspiration, pulmonary oedema and ARDS.
Use high-flow nasal oxygen in appropriate acute hypoxaemic respiratory failure.
Do not delay intubation when non-invasive support is failing.
The 2026 guideline describes typical oxygen targets across studies ranging approximately from 90–93% for conservative strategies to ≥96% for liberal strategies and recommends individualisation. (Society of Critical Care Medicine (SCCM))
C: Circulation
Two large-bore IV cannulae.
Take cultures and blood samples.
Start crystalloid.
Assess response dynamically.
Begin noradrenaline early if hypotension is severe or persists.
Insert arterial line when appropriate.
Central access should be obtained but should not delay vasopressor initiation.
Insert urinary catheter for hourly output where indicated.
D: Disability
GCS
Pupils
Blood glucose
Delirium assessment
Correct hypoglycaemia
Consider meningitis, intracranial infection or metabolic encephalopathy
E: Exposure
Examine the entire patient.
Inspect operation sites, perineum, back, pressure areas, drains and lines.
Look for cellulitis, crepitus, bullae, skin necrosis and disproportionate pain.
Assess abdomen and rectum where indicated.
12. Fluid resuscitation
Initial fluid
For sepsis-induced hypoperfusion or septic shock, the 2026 guideline suggests at least 30 mL/kg of IV crystalloid during the first three hours, with frequent reassessment and individualisation.
In unstable shock, vasopressors may need to be started concurrently rather than waiting for completion of the fluid volume. (Society of Critical Care Medicine (SCCM))
Which fluid?
First line
Crystalloid
Preferred
Balanced crystalloid, such as Ringer’s lactate or Plasma-Lyte, rather than 0.9% saline for most patients.
Exception: 0.9% saline may be preferred in sepsis with traumatic brain injury. (Society of Critical Care Medicine (SCCM))
Avoid
Hydroxyethyl starch: should not be used.
Gelatin: generally discouraged.
Routine albumin supplementation: not normally needed.
Albumin may occasionally be considered after very large crystalloid volumes or in selected patients with cirrhosis, but it is not first-line resuscitation fluid. (Society of Critical Care Medicine (SCCM))
Do not give 30 mL/kg blindly
Adjust the rate and aliquot size in:
Heart failure
Severe renal impairment
Pulmonary oedema
Frailty
Cirrhosis
Right ventricular failure
Significant valvular disease
A practical method is to give 250–500 mL aliquots and reassess, although profoundly unstable patients may require faster resuscitation.
Assessing fluid responsiveness
Preferred dynamic methods:
Passive leg raise with change in stroke volume/cardiac output
Stroke-volume response to a fluid bolus
Pulse-pressure variation
Stroke-volume variation
Bedside echocardiography
Change in end-tidal CO₂ in ventilated patients in selected settings
Static measurements such as CVP alone are poor predictors of fluid responsiveness.
Targets of resuscitation
Look for combined improvement in:
MAP
Mental status
Capillary refill
Mottling
Peripheral temperature
Urine output
Lactate trend
Respiratory status
Stroke volume/cardiac output where measured
Current guidance supports dynamic assessment, serial lactate and capillary refill as an adjunct rather than repeatedly administering fluid based on a single static parameter. (Society of Critical Care Medicine (SCCM))
Signs of fluid overload
Rising oxygen requirement
New crackles/B-lines
Pulmonary oedema
Raised JVP
Worsening peripheral oedema
Increasing intra-abdominal pressure
Hepatic congestion
Failure of stroke volume to increase after bolus
After stabilisation, active deresuscitation with diuretics or ultrafiltration may be considered when fluid accumulation is harmful. (Society of Critical Care Medicine (SCCM))
13. Vasopressors
When to start
Start when:
Hypotension persists despite initial fluid resuscitation, or
Shock is so unstable that waiting for completion of fluids would be dangerous.
Peripheral initiation through a good proximal cannula is preferable to delaying treatment while waiting for a central line. Inspect the site frequently and transfer to central access when practical. (Society of Critical Care Medicine (SCCM))
MAP target
Initial target: 65 mmHg
In adults ≥65 years, the 2026 guideline suggests an initial range of 60–65 mmHg.
Individualise upward in selected chronic hypertensive patients if renal, cerebral or coronary perfusion appears inadequate. (Society of Critical Care Medicine (SCCM))
First-line: noradrenaline
Noradrenaline is preferred because it raises vascular tone effectively with less tachyarrhythmia than dopamine.
Typical starting range in practice:
Approximately 0.02–0.05 micrograms/kg/min
Titrate rapidly according to MAP and perfusion
Exact preparation and dosing must follow local ICU protocols.
Second agent: vasopressin
Add vasopressin when noradrenaline requirement is escalating.
Typical practical dose:
0.03 units/min as a fixed infusion
Usually not titrated like noradrenaline
It reduces catecholamine requirement but is not normally the initial sole vasopressor.
Third agent: adrenaline
Add adrenaline if MAP remains inadequate despite noradrenaline and vasopressin.
Important adverse effects:
Tachycardia
Arrhythmias
Hyperglycaemia
Increased lactate from β₂-mediated glycolysis
An adrenaline-associated lactate rise does not always indicate worsening tissue hypoxia.
Dopamine
Not routine.
Problems include:
Tachyarrhythmias
Increased myocardial oxygen consumption
Less predictable haemodynamic response
It may occasionally be considered in selected patients with significant bradyarrhythmia and low arrhythmia risk.
Vasopressor sequence
Noradrenaline → add vasopressin → add adrenaline
This is the main examination sequence. (Society of Critical Care Medicine (SCCM))
14. Inotropes and septic cardiomyopathy
Suspect cardiac dysfunction when there is persistent hypoperfusion despite:
Adequate intravascular volume
Adequate MAP
Noradrenaline treatment
Clues include:
Low cardiac output on echocardiography
Reduced ventricular function
Cool peripheries
Persistent oliguria
Rising lactate
Low central venous oxygen saturation in the appropriate context
Options:
Add dobutamine to noradrenaline, or
Use adrenaline as a combined vasopressor/inotrope.
Dobutamine may cause hypotension because of vasodilatation and may provoke tachyarrhythmias. Do not use an inotrope instead of the vasopressor required to maintain arterial pressure. (Society of Critical Care Medicine (SCCM))
15. Antibiotic therapy
Timing — current 2026 approach
Septic shock
Administer immediately, ideally within one hour of recognition.
Probable or definite sepsis without shock
Administer immediately, ideally within one hour.
Possible sepsis without shock
Perform a rapid, time-limited diagnostic assessment. If infection remains a concern, give antimicrobials within three hours from first suspicion.
Low likelihood of infection, no shock
Antibiotics may be deferred with close monitoring and continued investigation. (Society of Critical Care Medicine (SCCM))
Before antibiotics
Obtain blood cultures and relevant specimens ideally first.
Do not create a dangerous delay merely to obtain cultures.
Empirical selection should consider
Likely anatomical source
Community- or hospital-acquired infection
Local antibiogram
Previous culture results
Prior antibiotics
Duration of hospitalisation
Previous resistant-organism colonisation
Immunosuppression
Renal and hepatic function
Drug allergy
Presence of foreign material
Severity of illness
Typical surgical principles
Community-acquired intra-abdominal sepsis
Cover:
Enteric Gram-negative organisms
Streptococci
Anaerobes
Hospital-acquired intra-abdominal sepsis
May require broader cover for:
Resistant Enterobacterales
Pseudomonas
Enterococcus in selected patients
MRSA when risk factors exist
Candida in selected high-risk patients
Necrotising soft-tissue infection
Requires:
Broad Gram-positive, Gram-negative and anaerobic cover
MRSA cover where relevant
A toxin-suppressing agent such as clindamycin when streptococcal or clostridial disease is suspected
Immediate surgery
Specific drug choices must follow local Sri Lankan or institutional antimicrobial policy because resistance patterns differ substantially.
Double Gram-negative coverage
Do not use routinely.
Consider two active agents initially only when there is a high risk of resistant Gram-negative infection or a very high risk of death before sensitivities become available.
Empirical antifungal therapy
Not routine.
Consider it individually in patients with factors such as:
Significant immunosuppression
Prolonged broad-spectrum antibiotics
Long hospitalisation
Recurrent gastrointestinal perforation
Anastomotic leak
Necrotising pancreatitis
Multifocal Candida colonisation
Total parenteral nutrition
Intra-abdominal source with clinical deterioration
The 2026 guideline generally suggests against routine empiric antifungal treatment but recognises selected high-risk exceptions. (Society of Critical Care Medicine (SCCM))
Administration principles
Give a full loading dose.
Do not reduce the initial loading dose merely because of renal failure; adjust maintenance dosing.
Prolonged or extended infusion of β-lactams after a loading dose is recommended where operationally feasible.
Review microbiology daily.
Narrow or stop therapy when appropriate.
Use the shortest effective duration following adequate source control. (Society of Critical Care Medicine (SCCM))
16. Source control
For a surgeon, this is often the decisive treatment.
Methods
Drain an abscess
Debride necrotic or infected tissue
Resect gangrenous bowel
Repair or resect a perforated viscus
Control an anastomotic leak
Decompress an obstructed infected urinary system
Drain an empyema
Decompress an obstructed biliary system
Remove an infected line
Remove infected foreign material when required
Amputate a non-salvageable septic limb
Perform washout and drainage where indicated
Timing
Anatomical diagnoses requiring source control should be identified rapidly. Current guidance suggests early source control, ideally within six hours of diagnosing sepsis or septic shock requiring source control. (Society of Critical Care Medicine (SCCM))
Operative principle in the unstable patient
Use the least physiologically stressful procedure that reliably controls contamination.
Examples:
Damage-control laparotomy rather than prolonged definitive reconstruction
Drainage rather than major resection where appropriate
Temporary abdominal closure
Stoma rather than high-risk anastomosis
Percutaneous drainage in selected collections
Nephrostomy or ureteric stent for infected obstruction
ERCP or biliary drainage for cholangitis
Do not delay essential source control while trying to normalise every laboratory abnormality.
Necrotising fasciitis
Immediate radical debridement is required when suspected. Antibiotics and imaging must not delay theatre when the clinical diagnosis is clear.
Features include:
Pain out of proportion
Rapid progression
Skin anaesthesia
Bullae
Dusky skin
Crepitus
Systemic toxicity
Haemorrhagic blistering
“Dishwater” fluid at operation
Necrotic fascia with easy finger dissection
Repeat debridement is frequently necessary.
17. Corticosteroids
The 2026 guideline suggests IV corticosteroids for adults with septic shock. In practice, they are particularly relevant when hypotension persists and there is an ongoing vasopressor requirement despite fluids and vasopressors. (Society of Critical Care Medicine (SCCM))
Standard examination regimen
Hydrocortisone 200 mg/day IV, either:
50 mg every six hours, or
Continuous infusion
This is not the same as high-dose pulse steroid therapy. (Springer Nature Link)
Key points
Do not routinely use steroids for sepsis without shock.
Do not use very high-dose, short-course steroids for septic shock.
ACTH stimulation testing is not routinely required to decide treatment.
Benefits are mainly faster shock reversal; mortality effect is less certain.
Monitor glucose, sodium, infection risk, delirium and muscle weakness.
18. Sodium bicarbonate
Generally avoid
Do not give bicarbonate merely to correct lactic acidosis or reduce vasopressor requirement in septic shock.
Potential problems:
CO₂ generation
Intracellular acidosis
Hypernatraemia
Volume overload
Reduced ionised calcium
Left shift of the oxygen dissociation curve
Overshoot alkalosis
When it may be considered
Current guidance suggests bicarbonate in septic shock with:
Severe metabolic acidaemia, pH ≤7.2, and
Moderate-to-severe AKI, approximately AKIN stage 2 or 3.
Treat the cause—perfusion failure and infection—rather than chasing the bicarbonate value. (Society of Critical Care Medicine (SCCM))
19. Respiratory support and ARDS
Indications for intubation
Refractory hypoxaemia
Exhaustion
Severe work of breathing
Reduced consciousness
Inability to protect the airway
Severe acidosis with inadequate respiratory compensation
Haemodynamic instability where controlled ventilation is required
ARDS ventilation
Tidal volume: approximately 6 mL/kg predicted/ideal body weight
Plateau pressure: ≤30 cmH₂O
Appropriate PEEP
Prone ventilation for moderate-to-severe ARDS, generally >12 hours/day
Conservative fluid strategy after shock has stabilised
Consider venovenous ECMO for selected severe refractory cases in experienced centres
Tidal volume is based on height and sex—not actual body weight. (Society of Critical Care Medicine (SCCM))
20. Renal support
AKI management
Restore perfusion
Avoid nephrotoxins
Review antibiotic doses
Correct severe electrolyte abnormalities
Monitor fluid balance
Exclude obstruction
Avoid repeated non-beneficial fluid loading
Indications for renal replacement therapy
Remember AEIOU:
Acidosis refractory to medical management
Electrolyte abnormality, especially refractory hyperkalaemia
Intoxication with dialysable toxin
Overload refractory to diuretics
Uraemic complications
Do not start RRT solely because creatinine is elevated if no definitive indication exists. Either continuous or intermittent therapy may be used when RRT is indicated; CRRT is often easier haemodynamically in unstable shock. (Society of Critical Care Medicine (SCCM))
21. Blood products and coagulation
Red cells
Use a restrictive transfusion strategy in most patients.
A common examination threshold is:
Transfuse at Hb approximately <7 g/dL in a stable non-bleeding patient.
Do not use a rigid threshold when there is:
Active major bleeding
Myocardial ischaemia
Severe hypoxaemia
Ongoing haemodynamic instability
Inadequate oxygen delivery despite other measures
The 2026 guideline recommends restrictive rather than liberal transfusion. (Society of Critical Care Medicine (SCCM))
Platelets
Transfusion is generally based on bleeding risk, procedure and count rather than sepsis alone.
Common practical thresholds:
<10 ×10⁹/L without bleeding
<20 ×10⁹/L when significant bleeding risk exists
<50 ×10⁹/L for active bleeding or most invasive procedures
Higher thresholds for neurosurgical or selected critical-site procedures
DIC management
Treat sepsis and achieve source control.
Give platelets, FFP or cryoprecipitate primarily for bleeding or an invasive procedure.
Do not try to normalise every coagulation result in a non-bleeding patient.
Maintain adequate fibrinogen during significant bleeding.
22. Glucose, nutrition and prophylaxis
Glucose
Start insulin therapy when glucose is persistently ≥180 mg/dL or 10 mmol/L.
Avoid tight normoglycaemic control because hypoglycaemia is dangerous. (Society of Critical Care Medicine (SCCM))
Nutrition
Start enteral feeding early once haemodynamic stability permits.
The 2026 recommendation supports enteral nutrition within 72 hours.
Avoid full feeding during uncontrolled shock or escalating vasopressor requirement.
Increase progressively according to tolerance. (Society of Critical Care Medicine (SCCM))
VTE prophylaxis
Pharmacological prophylaxis unless contraindicated.
LMWH is preferred over unfractionated heparin for most patients.
Use mechanical prophylaxis when anticoagulation is contraindicated. (Society of Critical Care Medicine (SCCM))
Stress-ulcer prophylaxis
Use in patients with significant GI bleeding risk, such as:
Mechanical ventilation
Coagulopathy
Previous ulcer/GI bleeding
Severe burns
Traumatic brain injury
Multiple major risk factors
Do not prescribe automatically to every septic patient. (Society of Critical Care Medicine (SCCM))
23. Treatments not recommended routinely
Do not routinely use:
IV vitamin C
IV immunoglobulin
Vitamin D as sepsis treatment
High-volume haemofiltration for “cytokine removal”
Polymyxin-B haemoperfusion
Plasma exchange solely for ordinary sepsis
High-dose steroids
Hydroxyethyl starch
Routine dopamine
Routine empiric antifungal treatment
Routine bicarbonate for lactic acidosis
Routine antipyretics solely to improve survival
Probiotics as a sepsis treatment
β-blockers as routine septic-shock treatment
The 2026 guideline specifically advises against several unproven adjunctive therapies, including IV vitamin C, IVIG and blood purification techniques. (Society of Critical Care Medicine (SCCM))
24. Monitoring response
Continuous or frequent
Heart rate and rhythm
MAP
SpO₂
Respiratory rate
Temperature
GCS
Urine output
Peripheral perfusion
Vasopressor dose
Fluid balance
Serial
Lactate
ABG
Creatinine and electrolytes
Glucose
Platelets
Coagulation
Bilirubin/LFT
Haemoglobin
CRP or procalcitonin where clinically useful
Signs of improvement
Reduced vasopressor requirement
Improving mentation
Normalising capillary refill
Warmer peripheries
Urine output >0.5 mL/kg/hour
Falling lactate
Improved acid-base state
Improved oxygenation
Source controlled
Persistent shock: reassess the diagnosis
Consider:
Ongoing uncontrolled infection
Missed abscess or leak
Inadequate antimicrobial cover
Resistant organism
Inadequate intravascular volume
Fluid overload with cardiac dysfunction
Septic cardiomyopathy
Haemorrhage
Pulmonary embolism
Tension pneumothorax
Cardiac tamponade
Abdominal compartment syndrome
Adrenal insufficiency
Anaphylaxis
Mesenteric ischaemia
Drug-induced vasodilatation
25. Complications
ARDS
AKI
DIC
Septic cardiomyopathy
Atrial fibrillation and other arrhythmias
Acute liver dysfunction
Encephalopathy and delirium
Critical illness polyneuropathy/myopathy
Stress ulceration
Ileus
Acalculous cholecystitis
Pressure injury
Limb ischaemia from shock/vasopressors
Secondary nosocomial infection
Malnutrition
Venous thromboembolism
Post-intensive-care syndrome
Cognitive, psychological and functional impairment
26. Traditional Hour-1 bundle — know for examinations
The commonly taught SSC Hour-1 bundle is:
Measure lactate; remeasure if initially elevated.
Obtain blood cultures before antibiotics.
Give broad-spectrum antibiotics.
Give 30 mL/kg crystalloid for hypotension or severe hyperlactataemia.
Start vasopressors if hypotension persists to maintain MAP ≥65 mmHg.
For modern answers, add the nuances:
The 30 mL/kg volume is delivered during the initial three hours with individualisation and reassessment.
Antibiotic timing depends on shock and the certainty of infection.
Possible sepsis without shock permits rapid investigation, but shock requires immediate treatment.
Do not continue fluids simply until lactate normalises.
Source control is a central component, ideally within six hours where required. (Society of Critical Care Medicine (SCCM))
27. Common MCQ traps
Trap 1
“SIRS is necessary for sepsis.”
False. SIRS may be absent.
Trap 2
“qSOFA ≥2 defines sepsis.”
False. It is a risk prompt, not the diagnostic definition.
Trap 3
“Severe sepsis is the current term for sepsis with organ dysfunction.”
False. The term has been removed from Sepsis-3.
Trap 4
“Septic shock is any infection with BP <90 mmHg.”
False. Current criteria require sepsis, vasopressors to maintain MAP ≥65 and lactate >2 mmol/L after adequate resuscitation.
Trap 5
“Negative blood cultures exclude sepsis.”
False.
Trap 6
“Normal lactate excludes septic shock.”
A normal lactate means the formal Sepsis-3 septic-shock criteria are not met, but severe infection with hypotension or organ dysfunction can still be present and requires urgent treatment.
Trap 7
“All septic patients must receive exactly 30 mL/kg regardless of response.”
False. Give early crystalloid but reassess and individualise.
Trap 8
“Normal saline is always the preferred fluid.”
False. Balanced crystalloids are preferred for most patients.
Trap 9
“Albumin is first-line.”
False. Crystalloid is first-line.
Trap 10
“Dopamine is the first vasopressor.”
False. Noradrenaline is first-line.
Trap 11
“Vasopressin replaces noradrenaline.”
Usually false. It is generally added to escalating noradrenaline.
Trap 12
“Dobutamine should be used for all hypotensive patients.”
False. Use it for cardiac dysfunction with persistent hypoperfusion despite adequate volume and pressure.
Trap 13
“Procalcitonin should determine whether antibiotics are started.”
False.
Trap 14
“Bicarbonate is routinely beneficial in septic lactic acidosis.”
False.
Trap 15
“Steroids are indicated in all sepsis.”
False. Their role is septic shock with vasopressor requirement.
Trap 16
“Antibiotics alone are sufficient for an abscess or perforation.”
False. Source control is essential.
Trap 17
“A postoperative CT should always precede treatment.”
False. Resuscitation and antibiotics must not be delayed, and obvious surgical catastrophes may require immediate theatre.
28. OSCE/viva answer
Scenario
A patient on postoperative day 5 after colorectal surgery has:
Temperature 39°C
HR 132/min
BP 82/48 mmHg
RR 30/min
Confusion
Urine output 10 mL/hour
Increasing abdominal pain
High-scoring response
“This patient has suspected septic shock, most likely from an anastomotic leak or intra-abdominal collection. I would call for senior surgical, anaesthetic and critical-care help and manage using an A–E approach. I would provide oxygen and assess the need for intubation, establish large-bore IV access, obtain blood cultures, lactate, blood gas, full blood count, renal and liver profiles, coagulation and crossmatch, and start source-appropriate broad-spectrum IV antibiotics immediately. I would begin balanced-crystalloid resuscitation with repeated assessment of perfusion and fluid responsiveness. If hypotension is severe or persists, I would start noradrenaline early, initially peripherally if necessary, targeting a MAP around 65 mmHg. I would catheterise the patient and monitor hourly urine output. I would urgently evaluate the abdomen, wound and drains, arrange appropriate imaging if this does not delay treatment, and achieve source control—likely drainage, re-laparotomy or damage-control surgery—as soon as possible.”
This answer scores because it includes:
Recognition
Escalation
A–E
Cultures and lactate
Antibiotics
Balanced crystalloid
Early noradrenaline
Monitoring
Probable source
Urgent source control
29. Final memory framework
The seven pillars
R-A-F-T-S-O-M
R — Recognition
Infection plus organ dysfunction
SOFA rise ≥2
A — Antibiotics
Immediately in shock
Cultures first if no delay
F — Fluids
Balanced crystalloid
Approximately 30 mL/kg in first three hours
Reassess dynamically
T — Tone
Noradrenaline first
MAP approximately 65
S — Source control
Drain, debride, decompress, remove or resect
Ideally within six hours when required
O — Organ support
Ventilation, RRT, glucose, nutrition, blood products
M — Monitoring
Lactate trend, urine output, capillary refill, mental state, MAP and fluid balance
One-line examination answer
Sepsis is infection-associated life-threatening organ dysfunction; septic shock is sepsis requiring vasopressors to maintain MAP ≥65 mmHg with lactate >2 mmol/L despite adequate fluid resuscitation. Management is immediate recognition, cultures and lactate, source-directed antibiotics, balanced-crystalloid resuscitation, early noradrenaline, urgent source control and appropriate organ support.
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