Sepsis
Sepsis and septic shock for surgical patients, covering infection-triggered organ dysfunction, source control, investigations, antimicrobial therapy, haemodynamic resuscitation, and complications using current 2026 guidance with Hong Kong relevance.
| Exam domain | One-glance essentials |
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| Definition / diagnosis |
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| Epidemiology / risks |
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| Core mechanism |
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| Clinical picture |
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| Investigations |
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| Management |
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| Complications |
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| Prevention / follow-up |
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| Exam traps |
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References
[1] Lecture slides: Surviving Sepsis Campaign International Guidelines for Management of Sepsis and Septic Shock 2026.
Sepsis - Etiology, Pathophysiology, Classification, and Clinical Features
Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection [1].
That definition has three parts:
| Component | Meaning | Why it matters |
|---|---|---|
| Infection | A pathogen is present or strongly suspected | No infection = not sepsis, even if the patient is shocked |
| Dysregulated host response | The immune response is no longer proportionate or localised | The host response causes endothelial injury, vasodilatation, capillary leak, microthrombosis, and organ dysfunction |
| Organ dysfunction | SOFA score rises by 2 or more from baseline | This separates sepsis from uncomplicated infection |
Septic shock is the severe subset of sepsis where circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality: vasopressor requirement to maintain MAP at least 65 mmHg plus lactate > 2 mmol/L despite adequate fluid resuscitation [1].
The Key Concept
Sepsis is not "infection plus fever." It is infection plus organ dysfunction from a maladaptive host response. A patient with cellulitis and fever may not be septic. A hypothermic elderly patient with UTI, confusion, AKI, and lactate elevation is septic until proven otherwise.
Sepsis is common in emergency departments, surgical wards, and ICUs. In Hong Kong public emergency departments, sepsis has been perceived as a leading cause of in-hospital mortality and an important preventable cause of death; local practice has emphasised early IV antibiotics, microbiological workup, and adoption of international sepsis targets, although implementation has historically varied across departments [4].
Local relevance in Hong Kong:
- Ageing population with multimorbidity -> more frailty, diabetes, CKD, malignancy, and healthcare exposure
- High surgical burden -> intra-abdominal sepsis, biliary sepsis, post-operative infection, catheter-related infection
- High antimicrobial resistance pressure -> empiric therapy must account for local antibiograms and stewardship
- IMPACT and SmartASP support local antimicrobial prescribing and de-escalation [3]
- Important local resistant organisms include MRSA, ESBL-producing E. coli/Klebsiella, carbapenem-resistant Acinetobacter, emerging CPE, and VRE resurgence [3]
- Sepsis comes from Greek "sepein" = to make rotten / putrefy. Historically it described decay; clinically it now means a systemic dysregulated response to infection.
- Septicaemia means bacteria/toxins in blood in older teaching. Avoid using it as a precise modern term because patients can have sepsis without positive blood cultures.
- Shock means circulatory failure with inadequate tissue perfusion.
4. Aetiology - Where Surgical Sepsis Comes From
| Source | Examples | Pathophysiological reason it becomes severe |
|---|---|---|
| Intra-abdominal | Perforated viscus, appendicitis, diverticulitis, peritonitis, anastomotic leak | Peritoneal contamination gives large bacterial burden plus endotoxin -> intense cytokine response and third-spacing |
| Biliary | Acute cholangitis, infected obstructed CBD, gangrenous cholecystitis | Obstruction raises biliary pressure, bacteria translocate into blood -> Gram-negative bacteraemia |
| Pancreatic | Infected necrosis, infected pseudocyst | Necrotic tissue has poor perfusion -> antibiotics penetrate poorly and source control is difficult |
| Skin and soft tissue | Necrotising fasciitis, infected diabetic foot, abscess | Toxin production and fascial spread can cause shock before skin signs look dramatic |
| Urinary | Obstructed infected stone, pyelonephritis, catheter-associated UTI | Obstruction converts infection into a closed high-pressure system -> bacteraemia and AKI |
| Respiratory | Aspiration pneumonia, HAP, ventilator-associated pneumonia | Hypoxaemia plus systemic inflammation accelerates organ failure |
| Line/device | Central line infection, infected prosthesis, drain infection | Biofilm protects organisms and causes persistent bacteraemia until device removal |
| Source | Common organisms | HK-relevant caveat |
|---|---|---|
| Biliary / intra-abdominal | Enterobacterales such as E. coli and Klebsiella, anaerobes, Enterococcus | ESBL-producing Enterobacterales are important in healthcare-associated infection [3] |
| Skin/soft tissue | Staphylococcus aureus, Streptococcus pyogenes, anaerobes, Gram-negatives in diabetic foot | Consider MRSA risk and necrotising infection |
| Urinary | E. coli, Klebsiella, Proteus, Enterococcus | ESBL risk rises with prior antibiotics, healthcare exposure, recurrent UTI |
| Hospital-acquired pneumonia | Gram-negative bacilli, S. aureus, Pseudomonas | Local ICU antibiogram matters |
| Catheter-related bloodstream infection | Coagulase-negative staph, S. aureus, Candida, Gram-negatives | Remove infected devices where feasible |
| Patient factor | Why it increases sepsis risk |
|---|---|
| Extremes of age | Neonates and elderly have less physiological reserve and altered immune responses |
| Diabetes mellitus | Neutrophil dysfunction, vascular disease, neuropathy, diabetic foot ulcers |
| CKD / dialysis | Immune dysfunction, vascular access, altered antibiotic dosing |
| Cirrhosis | Complement deficiency, gut bacterial translocation, spontaneous bacterial peritonitis |
| Malignancy / chemotherapy | Neutropenia, mucosal barrier injury, central lines |
| Recent surgery | Tissue injury, drains, catheters, anastomotic leak risk |
| Indwelling devices | Biofilm infection and direct access to bloodstream |
| Prior broad-spectrum antibiotics | Selects resistant organisms such as ESBL, CPE, VRE |
| Immunosuppression | Steroids, transplant drugs, biologics blunt fever and inflammatory signs |
6. Pathophysiology - From Infection to Multi-Organ Failure
Pathogen-associated molecular patterns are recognised by innate immune receptors:
- Gram-negative endotoxin / LPS
- Gram-positive lipoteichoic acid
- Bacterial DNA
- Viral RNA
- Fungal cell wall components
These activate macrophages, neutrophils, complement, and endothelial cells.
The host releases TNF-alpha, IL-1, IL-6, nitric oxide, prostaglandins, complement fragments, and platelet-activating mediators.
This causes:
- Vasodilatation -> low SVR -> distributive shock
- Capillary leak -> plasma leaves vascular space -> oedema plus intravascular depletion
- Endothelial activation -> leukocyte adhesion and microvascular plugging
- Coagulation activation -> microthrombi, DIC, consumption of platelets and clotting factors
- Mitochondrial dysfunction -> cells cannot use oxygen efficiently even when delivery improves
Why Septic Patients Can Be Warm Then Cold
Early sepsis may be "warm shock": vasodilatation gives warm peripheries, bounding pulse, and wide pulse pressure. Late or severe sepsis becomes "cold": myocardial depression, hypovolaemia from capillary leak, microvascular failure, and vasopressor-dependent circulation cause cool mottled skin.
| Organ system | Mechanism | Clinical expression |
|---|---|---|
| Brain | Neuroinflammation, hypoperfusion, BBB dysfunction | Confusion, agitation, delirium, coma |
| Lungs | Capillary leak into alveoli, neutrophil injury | Hypoxaemia, ARDS |
| Kidneys | Hypoperfusion, microthrombi, tubular injury | Oliguria, AKI, rising creatinine |
| Liver | Hypoperfusion, cholestasis, cytokine injury | Jaundice, raised bilirubin, coagulopathy |
| Cardiovascular | Vasodilatation plus myocardial depression | Hypotension, high lactate, vasopressor need |
| Haematological | Platelet consumption, DIC | Thrombocytopenia, bleeding, microthrombi |
Lactate rises because of:
- Tissue hypoperfusion -> anaerobic glycolysis
- Beta-adrenergic stimulation -> accelerated glycolysis
- Mitochondrial dysfunction -> impaired oxygen utilisation
- Reduced hepatic clearance
This is why lactate is a severity marker and resuscitation guide, not a perfect oxygen meter.
| Term | Practical definition |
|---|---|
| Infection | Localised or systemic infection without organ dysfunction |
| Sepsis | Infection plus acute organ dysfunction, usually SOFA rise at least 2 |
| Septic shock | Sepsis with persistent hypotension requiring vasopressor to maintain MAP at least 65 mmHg and lactate > 2 mmol/L after fluids |
| SIRS | Systemic inflammatory response; sensitive but non-specific and can occur without infection |
| Bacteraemia | Bacteria in blood; may occur without sepsis and sepsis may occur without positive blood cultures |
8. Clinical Features With Mechanisms
| Symptom | Pathophysiological basis |
|---|---|
| Fever or rigors | Pyrogen cytokines reset hypothalamic set-point; rigors suggest bacteraemia |
| Hypothermia | Severe sepsis, elderly, immunosuppressed; failure of thermoregulation and poor reserve |
| Confusion | Sepsis-associated encephalopathy from inflammation and hypoperfusion |
| Dyspnoea | Pneumonia, metabolic acidosis respiratory compensation, ARDS |
| Reduced urine | Renal hypoperfusion and tubular injury |
| Severe pain at infection site | Abscess pressure, tissue necrosis, peritonitis, fascial infection |
| Diarrhoea/vomiting | GI infection, peritonitis, ileus, cytokine-mediated gut dysfunction |
| Sign | Mechanism |
|---|---|
| Tachycardia | Fever, catecholamines, reduced stroke volume, pain |
| Tachypnoea | Metabolic acidosis compensation, hypoxaemia, pneumonia |
| Hypotension | Vasodilatation, capillary leak, myocardial depression |
| Warm peripheries / bounding pulse | Early vasodilatory distributive shock |
| Cool mottled skin | Late shock, vasoconstriction, microcirculatory failure |
| Delayed capillary refill | Peripheral hypoperfusion; useful bedside perfusion marker [2] |
| Oliguria | Kidney hypoperfusion, AKI |
| Petechiae / bleeding | DIC, thrombocytopenia, meningococcaemia |
High Yield Summary
Definition: Sepsis = infection plus life-threatening organ dysfunction from dysregulated host response. Septic shock = sepsis with vasopressor requirement for MAP at least 65 mmHg plus lactate > 2 mmol/L after adequate fluids.
Pathophysiology: Pathogen recognition -> cytokines -> endothelial injury -> vasodilatation, capillary leak, microthrombi, mitochondrial dysfunction -> organ failure.
Surgical sources: Perforation, peritonitis, biliary obstruction/cholangitis, infected pancreatic necrosis, necrotising soft tissue infection, obstructed infected kidney, post-op anastomotic leak.
HK relevance: Use local antibiograms and IMPACT principles. Important resistant organisms include MRSA, ESBL-producing Enterobacterales, carbapenem-resistant Acinetobacter, emerging CPE, and VRE.
Clinical trap: Fever is not required. Elderly/immunosuppressed patients may be hypothermic, confused, and hypotensive without dramatic localising signs.
Active Recall - Sepsis Etiology and Pathophysiology
References
[1] Lecture slides: Surviving Sepsis Campaign International Guidelines for Management of Sepsis and Septic Shock 2026.
[2] Lecture slides: ESICM guidelines on circulatory shock and hemodynamic monitoring 2025.
[3] Senior notes: Hong Kong IMPACT antimicrobial guideline and CHP antimicrobial resistance materials.
[4] Senior notes: Hong Kong emergency department sepsis management study.
Differential Diagnosis of Sepsis
Sepsis is commonly overcalled and undercalled, which is why 2026 guidance emphasises clinical screening plus organ dysfunction rather than fever alone [1].
- Overcalled: fever + tachycardia from a non-infective inflammatory condition
- Undercalled: elderly, immunosuppressed, post-operative, or diabetic patient with no fever but new organ dysfunction
The key diagnostic question is:
Is there infection causing organ dysfunction, or is another inflammatory/haemodynamic process mimicking infection?
| Syndrome | Why it becomes sepsis | Surgical relevance |
|---|---|---|
| Peritonitis | Large bacterial load and peritoneal cytokine activation -> capillary leak and shock | Perforated viscus, anastomotic leak |
| Ascending cholangitis | Obstructed infected bile duct -> high-pressure bacteraemia | Needs antibiotics plus biliary drainage |
| Pyelonephritis / obstructed infected kidney | Infected hydronephrosis behaves like an abscess under pressure | Needs antibiotics plus JJ stent or nephrostomy |
| Necrotising fasciitis | Toxin-mediated tissue necrosis and shock | Needs immediate debridement |
| Pneumonia | Alveolar infection -> hypoxaemia + systemic inflammation | Common post-op and aspiration source |
| Line infection | Direct bloodstream inoculation | Remove infected line if source |
| Infected collection / abscess | Antibiotics penetrate poorly into pus | Drainage is source control |
Surgical Rule
Sepsis from an obstructed or walled-off source rarely resolves with antibiotics alone. Pus, infected bile, infected urine under pressure, necrotic bowel, and necrotising soft tissue need source control.
| Mimic | Why it looks like sepsis | Clues against infection |
|---|---|---|
| Acute pancreatitis | SIRS from enzyme injury and cytokines; fever, tachycardia, high CRP | Epigastric pain radiating to back, lipase/amylase, CT findings |
| Major trauma / burns | Tissue injury releases DAMPs -> sterile SIRS | Clear injury mechanism, cultures negative early |
| Pulmonary embolism | Tachycardia, hypoxia, hypotension, lactate | Pleuritic pain, RV strain, D-dimer/CTPA |
| Myocardial infarction | Shock, diaphoresis, lactate, pulmonary oedema | ECG/troponin, chest pain, echo |
| Haemorrhage | Tachycardia, hypotension, lactate | Falling Hb, bleeding history, FAST/CT/endoscopy |
| Anaphylaxis | Distributive shock, rash, wheeze, airway oedema | Trigger exposure, urticaria, rapid onset |
| DKA / HHS | Tachypnoea, dehydration, altered mental state, infection may coexist | Glucose, ketones, anion gap acidosis |
| Thyroid storm | Fever, tachycardia, delirium, diarrhoea | Goitre, tremor, TFTs, AF |
| Malignant hyperthermia / NMS | Hyperthermia, rigidity, acidosis, rhabdomyolysis | Anaesthetic or antipsychotic exposure, high CK |
| Drug fever / transfusion reaction | Fever, rigors, hypotension | Temporal relationship to drug/blood product |
SIRS means systemic inflammation. Sepsis means infection plus organ dysfunction.
| Feature | SIRS without infection | Sepsis |
|---|---|---|
| Trigger | Trauma, pancreatitis, burns, surgery | Bacterial, viral, fungal, parasitic infection |
| Cultures | Usually negative | May be positive, but negative cultures do not exclude sepsis |
| Source control | Treat inflammatory trigger | Drain/debride/remove infected source |
| Antibiotics | Not routine unless infection suspected | Early empiric antibiotics when probable/definite sepsis |
| Organ dysfunction | Can occur in severe sterile inflammation | Defines sepsis when due to infection |
| Timing | Think of |
|---|---|
| Immediate hours | Bleeding, anaesthetic complication, aspiration, MI, PE, transfusion reaction |
| Day 1-2 | Atelectasis is over-blamed; also look for pneumonia, aspiration, leak, UTI, line issue |
| Day 3-5 | Pneumonia, UTI, wound infection, anastomotic leak beginning |
| Day 5-7 | Anastomotic leak, intra-abdominal abscess, infected collection |
| Any time | PE, MI, drug fever, C. difficile after antibiotics |
Exam Pearl
Post-operative fever is not automatically wound infection. In a sick post-op patient, first exclude the dangerous causes: bleeding, leak, PE, MI, aspiration pneumonia, and deep collection.
High Yield Summary
Sepsis DDx principle: Do not diagnose sepsis from fever alone. Diagnose it from suspected infection plus new organ dysfunction.
Main infective surgical sources: Peritonitis, cholangitis, obstructed infected kidney, necrotising fasciitis, pneumonia, line sepsis, infected collection.
Main mimics: Pancreatitis, trauma, burns, PE, MI, haemorrhage, anaphylaxis, DKA, thyroid storm, malignant hyperthermia, drug fever.
SIRS vs sepsis: SIRS is inflammation; sepsis is infection-driven organ dysfunction.
Source control clue: If the infected focus is obstructed, necrotic, foreign-body-associated, or pus-filled, antibiotics alone are usually insufficient.
Active Recall - Sepsis DDx
References
[1] Lecture slides: Surviving Sepsis Campaign International Guidelines for Management of Sepsis and Septic Shock 2026.
Diagnosis of Sepsis and Septic Shock
Sepsis is a clinical emergency diagnosis supported by physiology and investigations. You do not wait for the culture report because organ dysfunction progresses through cytokine injury, endothelial leak, mitochondrial dysfunction, microthrombi, and maldistributed flow long before microbiology confirms the organism.
The 2026 Approach
The 2026 SSC keeps the big pillars: early recognition, lactate measurement, cultures before antibiotics where feasible, early antimicrobials when sepsis is likely, resuscitation for hypoperfusion, vasopressors for persistent shock, and source control when an anatomic source exists [1].
| Entity | Practical diagnostic meaning | Why it matters |
|---|---|---|
| Infection | Pathogen invasion causing host inflammatory response | Antibiotics/source control may be needed, but organ dysfunction may be absent |
| Sepsis | Suspected/proven infection plus life-threatening organ dysfunction | Mortality rises sharply once organs fail |
| Septic shock | Sepsis with circulatory/metabolic failure: vasopressor required to maintain MAP at least 65 mmHg and lactate > 2 mmol/L after adequate fluids | Higher mortality phenotype; needs ICU-level haemodynamic support |
The 2026 SSC recommends NEWS, NEWS2, MEWS, or SIRS over qSOFA as a single screening tool for acutely ill inpatients [1].
Why?
- qSOFA is specific but insensitive; it misses early sepsis
- NEWS2 and MEWS detect physiological deterioration earlier
- SIRS is sensitive but non-specific
| Tool | Components | Use | Limitation |
|---|---|---|---|
| NEWS2 | RR, oxygen saturation, oxygen use, temperature, SBP, HR, consciousness | Best practical ward deterioration score | Not sepsis-specific |
| MEWS | HR, SBP, RR, temperature, consciousness, urine output depending version | Simple ward screening | Thresholds vary |
| SIRS | Temperature, HR, RR/PaCO2, WBC | Sensitive infection screen | Too non-specific after surgery |
| qSOFA | RR at least 22, SBP at most 100, altered mentation | Risk enrichment; prompts escalation | Not recommended as sole screen |
| SOFA | Respiration, coagulation, liver, CVS, CNS, renal | Defines organ dysfunction | Needs labs; less immediate at bedside |
| Organ system | Bedside/lab clue | Pathophysiological basis |
|---|---|---|
| CNS | Confusion, drowsiness, agitation | Hypoperfusion, cytokines, BBB dysfunction, metabolic encephalopathy |
| CVS | Hypotension, vasopressor need, tachycardia | Vasodilatation, capillary leak, myocardial depression |
| Respiratory | Tachypnoea, hypoxaemia, ARDS | Endothelial leak and inflammatory alveolar injury |
| Renal | Oliguria, rising creatinine | Renal hypoperfusion, microvascular injury, venous congestion |
| Haematological | Thrombocytopenia, DIC | Platelet consumption, thrombin generation, endothelial injury |
| Hepatic | Rising bilirubin, coagulopathy | Cholestasis of sepsis, hypoperfusion, mitochondrial dysfunction |
| Metabolic | Elevated lactate, acidosis | Adrenergic glycolysis plus tissue hypoxia and impaired clearance |
Think septic shock when all are present:
- Suspected/proven infection
- Persistent hypotension or need for vasopressor
- Lactate > 2 mmol/L after adequate fluid resuscitation
- No better explanation such as haemorrhage, MI, PE, tamponade, or anaphylaxis
Lactate Is Not Just Anaerobic Metabolism
In sepsis, lactate reflects tissue hypoperfusion, adrenergic-driven glycolysis, mitochondrial dysfunction, impaired hepatic clearance, and sometimes beta-agonist therapy. It is a danger signal, not a pure oxygen-meter.
| Source | Diagnostic clues | Why source control matters |
|---|---|---|
| Perforated viscus | Sudden severe abdominal pain, peritonism, free air | Antibiotics cannot sterilise ongoing faecal contamination |
| Appendicitis with perforation | RIF pain, fever, abscess/phlegmon | Drain/operate depending abscess and stability |
| Cholangitis | Fever, jaundice, RUQ pain, hypotension/confusion | Biliary pressure prevents antibiotic penetration; ERCP drains source |
| Necrotising fasciitis | Pain out of proportion, shock, bullae, crepitus | Dead fascia has no blood supply; antibiotics cannot reach it |
| Infected pancreatic necrosis | Late sepsis, gas in collection, persistent organ failure | Step-up drainage/necrosectomy if infected |
| Anastomotic leak | Post-op tachycardia, ileus, fever, peritonitis, drain faeculent | Needs drainage/reoperation/diversion |
| Catheter-related bloodstream infection | Line sepsis, positive blood cultures, no other source | Remove infected line when indicated |
High Yield Summary
Sepsis = infection plus life-threatening organ dysfunction.
Septic shock = sepsis with persistent circulatory/metabolic failure: vasopressor needed for MAP at least 65 mmHg and lactate > 2 mmol/L after fluids.
2026 screening: use NEWS/NEWS2/MEWS/SIRS over qSOFA as a single tool. qSOFA is too insensitive for early screening.
Diagnosis is clinical: do not wait for cultures. Use infection suspicion + organ dysfunction + lactate + source assessment.
Surgical source control is diagnostic and therapeutic: perforation, abscess, cholangitis, necrotising infection, anastomotic leak, infected necrosis.
Active Recall - Sepsis Diagnosis
References
[1] Lecture slides: Surviving Sepsis Campaign International Guidelines for Management of Sepsis and Septic Shock 2026.
Investigations for Sepsis
Investigations in sepsis have four purposes:
- Confirm infection and identify the organism
- Quantify organ dysfunction
- Find the source requiring control
- Monitor response to resuscitation
Do not wait for all tests before treatment. Sepsis is a clinical emergency.
| Investigation | What it tells you | Why it matters |
|---|---|---|
| Continuous HR, BP, SpO2, respiratory rate | Physiological instability | Sepsis can deteriorate quickly |
| Temperature | Fever or hypothermia | Hypothermia in sepsis often means severe physiological failure |
| Strict fluid balance | Perfusion and ongoing losses | Oliguria suggests renal hypoperfusion or AKI |
| Urinary catheter | Accurate urine output | Target at least 0.5 mL/kg/hr in adults |
| Capillary refill and mottling | Microcirculatory perfusion | 2026 SSC supports capillary refill as a resuscitation endpoint [1] |
| ECG | Arrhythmia, ischaemia, baseline QT | Sepsis triggers AF, demand ischaemia, and drug-related QT issues |
| Test | Expected finding | Interpretation |
|---|---|---|
| FBC | High or low WBC, thrombocytopenia | Leukopenia and thrombocytopenia are poor prognostic signs |
| Urea, creatinine, electrolytes | AKI, Na/K derangement | Guides fluids, drug dosing, RRT need |
| LFT | Hyperbilirubinaemia, transaminitis | Cholestasis, liver hypoperfusion, biliary source |
| Coagulation profile | Prolonged PT/APTT, low fibrinogen | DIC and hepatic dysfunction |
| ABG/VBG | Acidosis, hypoxaemia, lactate | Perfusion and respiratory failure |
| CRP | Inflammation | Useful trend, non-specific |
| Procalcitonin | Bacterial signal | Can help de-escalation; not a standalone diagnostic test [1] |
| Glucose | Hyperglycaemia or hypoglycaemia | Stress response or liver failure |
2026 SSC suggests measuring lactate in adults with possible, probable, or definite sepsis or septic shock [1].
Why lactate rises:
- Tissue hypoxia -> anaerobic glycolysis
- Adrenergic stimulation -> accelerated glycolysis
- Hepatic dysfunction -> reduced clearance
- Mitochondrial dysfunction -> impaired oxygen utilisation
Interpretation:
| Lactate | Meaning |
|---|---|
| Normal | Does not exclude sepsis |
| > 2 mmol/L | Increased risk; in Sepsis-3, septic shock includes lactate > 2 despite fluids with vasopressor requirement |
| > 4 mmol/L | Severe hypoperfusion signal; historically triggers aggressive resuscitation |
| Falling lactate | Response improving, but interpret with clinical perfusion |
| Persistently high lactate | Ongoing shock, inadequate source control, hypoxaemia, seizures, liver failure, drugs |
Lactate Is Not Just Lack of Oxygen
Students often equate lactate with pure anaerobic metabolism. In sepsis, catecholamines, inflammation, mitochondrial dysfunction, and impaired hepatic clearance also contribute. That is why lactate must be interpreted alongside perfusion, blood pressure, capillary refill, urine output, and source control.
| Sample | When |
|---|---|
| Blood cultures x 2 sets | As soon as possible, ideally before antibiotics [1] |
| Urine microscopy/culture | Urinary symptoms, elderly, catheter, unclear source |
| Sputum culture | Pneumonia or ventilated patient |
| Wound/pus culture | Surgical site infection, abscess |
| Drain fluid culture | Biliary, pancreatic, intra-abdominal drain sepsis |
| CSF | Meningitis suspected, after safety assessment |
| Stool tests | Severe diarrhoea, C. difficile risk |
| Viral PCR | Influenza/COVID or respiratory viral syndrome |
HK relevance:
- Use local hospital/cluster antibiograms and IMPACT guidance where available.
- Hong Kong faces important AMR pressure from MRSA, ESBL Enterobacterales, CRE/CPE, carbapenem-resistant Acinetobacter, and VRE [3].
- Cultures are what allow de-escalation; without cultures, broad-spectrum treatment stays broad for longer.
| Suspected source | Imaging |
|---|---|
| Pneumonia | CXR; CT chest if unclear or complicated |
| Intra-abdominal sepsis | CT abdomen/pelvis with contrast if stable enough |
| Biliary sepsis | LFT + ultrasound; MRCP/CT/ERCP depending on obstruction |
| Urinary obstruction/pyonephrosis | USS KUB or CT KUB/urogram |
| Necrotising fasciitis | Clinical diagnosis; CT/MRI may help but must not delay surgery |
| Line infection | Line assessment, blood cultures from line and peripheral |
| Endocarditis | Echocardiography if bacteraemia, murmur, emboli, prosthetic valve |
Active Recall - Sepsis Investigations
References
[1] Lecture slides: Surviving Sepsis Campaign International Guidelines for Management of Sepsis and Septic Shock 2026.
[3] Senior notes: Hong Kong IMPACT antimicrobial guideline and CHP antimicrobial resistance materials.
Management of Sepsis and Septic Shock
Sepsis management has four urgent jobs:
- Recognise organ dysfunction early
- Give appropriate antimicrobials early
- Restore perfusion
- Control the source
The 2026 Surviving Sepsis Campaign frames sepsis care around early recognition, timely treatment of infection, hemodynamic resuscitation, antimicrobial stewardship, and source control [1]. In surgery, source control is the part students must never forget: antibiotics cannot sterilise pus under pressure, dead bowel, necrotic fascia, an infected prosthesis, or an obstructed infected kidney.
Ward Round Rule
In surgical sepsis, ask: Where is the source, and does it need drainage, decompression, debridement, removal, or resection? If yes, do not let fluids and antibiotics create false reassurance.
| Action | Why |
|---|---|
| ABCDE assessment | Sepsis kills through hypoxia, shock, acidosis, and organ failure |
| Oxygen if hypoxaemic | Improves arterial oxygen content while perfusion is restored |
| Two IV cannulae | Allows antimicrobials, fluids, and vasopressors if needed |
| Blood cultures ASAP | 2026 SSC recommends blood cultures as soon as possible and ideally before antibiotics [1] |
| Lactate | Identifies occult hypoperfusion and tracks response [1] |
| Empiric antimicrobials | Mortality rises with delay in true septic shock |
| Fluid if hypoperfused | Restores venous return, preload, stroke volume, and oxygen delivery |
| Source control plan | Definitive treatment for drainable or obstructed infection |
D. Antimicrobial Therapy
Practical approach:
- Septic shock or high likelihood of sepsis: give broad-spectrum IV antibiotics immediately after cultures if this does not delay treatment.
- Possible sepsis without shock: assess rapidly, obtain cultures, and avoid unnecessary broad-spectrum antibiotics if infection is uncertain.
The 2026 SSC emphasises responsible antimicrobial use, proper diagnostic strategies, and de-escalation [1].
Choose by:
- Likely source
- Community vs hospital acquisition
- Recent antibiotics
- Prior cultures
- Colonisation history
- Local resistance pattern
- Renal and hepatic function
- Allergy
Hong Kong relevance:
- The IMPACT guideline is the local reference for antimicrobial use and is designed around Hong Kong resistance epidemiology [3].
- Hong Kong AMR priorities include MRSA, ESBL-producing Enterobacterales, CRE/CPE, carbapenem-resistant Acinetobacter, and VRE resurgence [3].
- HA antimicrobial stewardship and SmartASP aim to reduce inappropriate broad-spectrum antibiotic use [3].
| Suspected surgical source | Typical empiric logic |
|---|---|
| Intra-abdominal sepsis | Gram-negative + anaerobic cover; escalate if healthcare-associated or ESBL risk |
| Biliary sepsis | Enterobacterales + anaerobes; decompress obstruction if cholangitis |
| Urosepsis | Enterobacterales cover; consider ESBL risk in HK if prior ESBL or healthcare exposure |
| Necrotising fasciitis | Broad Gram-positive, Gram-negative, anaerobic cover plus toxin suppression; urgent debridement |
| Line infection | Cover staphylococci including MRSA if risk factors |
| Post-operative sepsis | Consider leak, abscess, infected collection, pneumonia, UTI, line infection |
2026 SSC recommends prolonged infusion beta-lactams for maintenance after an initial loading dose [1].
Why?
- Beta-lactams are time-dependent antibiotics.
- Their effect depends on time above MIC.
- Septic patients have expanded volume of distribution and altered renal clearance.
- A loading dose rapidly reaches therapeutic concentration; prolonged infusion keeps levels above MIC.
De-escalate when cultures and susceptibilities are available [1].
This is not "weakening treatment"; it is precision treatment:
- Reduces resistance pressure
- Reduces C. difficile risk
- Reduces nephrotoxicity
- Preserves carbapenems and anti-MRSA agents
Hong Kong Antibiotic Stewardship Point
In Hong Kong, broad agents such as piperacillin-tazobactam and meropenem are stewardship-sensitive. Use them when the risk justifies them, then narrow promptly when culture data returns [3].
E. Fluids
For adults with sepsis-induced hypoperfusion or septic shock, 2026 SSC suggests at least 30 mL/kg IV crystalloid in the first 3 hours [1].
What counts as hypoperfusion?
- MAP < 65 mmHg
- SBP < 90 mmHg or marked relative hypotension
- Lactate elevation, especially lactate > 2 mmol/L and strongly if lactate is at least 4 mmol/L
- Oliguria
- Altered mental state
- Cool mottled skin
| Fluid | Role |
|---|---|
| Balanced crystalloid | Preferred over 0.9% saline for sepsis resuscitation [1] |
| 0.9% saline | Consider when concomitant traumatic brain injury or chloride replacement need exists [1] |
| Albumin | Not routine; may be considered after large crystalloid volumes or selected cirrhotic/hypoalbuminaemic contexts |
| Starches | Avoid; 2026 SSC recommends against starches [1] |
| Gelatin | Avoid routine use; adverse reactions and renal concerns |
Do not blindly continue fluids.
Use:
- Passive leg raise with stroke volume/cardiac output response
- Fluid challenge with objective response
- Echocardiography
- Pulse pressure variation or stroke volume variation in suitable ventilated patients
- Capillary refill time
- Lactate trend
- Urine output
The 2025 ESICM shock monitoring guideline supports dynamic variables over static preload markers and reassessing fluid responsiveness after initial resuscitation [2].
F. Vasopressors and Inotropes
Initial MAP target: 65 mmHg [1].
Why not higher for everyone?
- Higher MAP requires more catecholamine.
- More catecholamine can cause tachyarrhythmia, myocardial oxygen demand, digital ischaemia, and splanchnic vasoconstriction.
- Some chronic hypertensive patients may need higher renal perfusion pressure, but start with 65 mmHg and individualise.
| Situation | Drug |
|---|---|
| Septic shock needing vasopressor | Norepinephrine first-line [1] |
| Escalating norepinephrine requirement | Add vasopressin [1] |
| MAP inadequate despite norepinephrine + vasopressin | Add epinephrine [1] |
| Cardiac dysfunction with persistent hypoperfusion | Add dobutamine to norepinephrine or use epinephrine alone [1] |
Mechanisms:
- Norepinephrine: alpha-1 vasoconstriction restores SVR; beta-1 support is modest.
- Vasopressin: V1 receptor vasoconstriction; useful because septic shock may have relative vasopressin deficiency.
- Epinephrine: alpha and beta agonist; raises MAP and cardiac output but can increase lactate and arrhythmias.
- Dobutamine: beta-1 inotrope; improves cardiac output when myocardial depression is the limiting problem.
Peripheral norepinephrine may be started initially if central access would delay restoration of MAP, with careful site choice and monitoring [1].
2026 SSC suggests IV corticosteroids in septic shock [1].
Typical regimen:
- Hydrocortisone 200 mg/day IV, often 50 mg Q6H or continuous infusion.
Why it helps:
- Septic shock causes dysregulated inflammatory signalling and relative adrenal insufficiency.
- Cortisol increases vascular responsiveness to catecholamines.
- It can shorten shock duration and reduce vasopressor requirement.
It is not a substitute for fluids, vasopressors, antibiotics, or source control.
2026 SSC suggests early source control, ideally within 6 hours of diagnosis when source control is required [1].
Surgical source control methods:
| Source | Control |
|---|---|
| Abscess | Drainage |
| Perforated viscus | Operation or selected radiological drainage plus definitive repair |
| Anastomotic leak | Drainage, diversion, repair, resection depending on physiology |
| Necrotising fasciitis | Immediate radical debridement |
| Cholangitis | ERCP decompression |
| Obstructed infected kidney | Ureteric stent or nephrostomy |
| Infected line | Remove line |
| Infected prosthesis | Washout/removal depending on site and stability |
Source Control Is Physiology
An abscess is low pH, low oxygen tension, high bacterial load, and poor antibiotic penetration. Drainage converts an uncontrolled biological reactor into a treatable infection.
| Problem | Management |
|---|---|
| Hypoxaemia / ARDS | Lung-protective ventilation, prone positioning if severe ARDS |
| AKI | Optimise perfusion, avoid nephrotoxins, renal replacement therapy if indicated |
| Hyperglycaemia | Insulin protocol, avoid hypoglycaemia |
| Nutrition | Early enteral nutrition when feasible |
| VTE risk | Pharmacological prophylaxis unless contraindicated |
| Stress ulcer risk | Prophylaxis in high-risk ICU patients |
| Delirium and weakness | Sedation minimisation, mobilisation, rehabilitation |
| Goals of care | Early communication, time-limited trials when appropriate |
High Yield Summary
Sepsis is a medical and surgical emergency: recognise, culture, lactate, antibiotics, fluids, vasopressors, source control.
2026 SSC initial fluid: sepsis-induced hypoperfusion or septic shock -> at least 30 mL/kg IV crystalloid in first 3 hours.
Fluid choice: crystalloids first-line; balanced crystalloids preferred over NS unless specific exception such as TBI. Avoid starches.
MAP target: 65 mmHg initially.
Vasopressors: norepinephrine first-line. Add vasopressin if escalating norepinephrine. Add epinephrine if MAP inadequate despite norepinephrine + vasopressin.
Inotrope: dobutamine if cardiac dysfunction with persistent hypoperfusion despite fluids and adequate MAP.
Steroids: hydrocortisone for septic shock; helps restore catecholamine responsiveness.
Antibiotics: early empiric therapy, local HK IMPACT guidance, loading dose then prolonged beta-lactam infusion for maintenance, de-escalate with cultures.
Source control: early, ideally within 6 hours when needed.
Active Recall - Management of Sepsis
References
[1] Lecture slides: Surviving Sepsis Campaign International Guidelines for Management of Sepsis and Septic Shock 2026.
[2] Lecture slides: ESICM guidelines on circulatory shock and hemodynamic monitoring 2025.
[3] Senior notes: Hong Kong IMPACT antimicrobial guideline / Centre for Health Protection antimicrobial-resistance materials.
Complications of Sepsis
Complications of sepsis are consequences of dysregulated inflammation, endothelial injury, microvascular thrombosis, mitochondrial dysfunction, organ hypoperfusion, and treatment toxicity [1].
Sepsis causes:
- Vasodilatation
- Capillary leak
- Relative hypovolaemia
- Myocardial depression
- Microcirculatory maldistribution
Complications:
| Complication | Mechanism |
|---|---|
| Septic shock | Vasoplegia plus hypovolaemia plus cellular oxygen-utilisation failure |
| Arrhythmias | Catecholamines, hypoxia, acidosis, electrolyte disturbance |
| Myocardial dysfunction | Cytokine-mediated reversible cardiomyopathy |
| Ischaemia | Hypoperfusion plus vasopressor-related vasoconstriction in vulnerable beds |
| Complication | Pathophysiology |
|---|---|
| ARDS | Endothelial and alveolar epithelial injury -> protein-rich pulmonary oedema -> impaired gas exchange |
| Ventilator-associated pneumonia | Intubation bypasses airway defences; biofilm forms on tube |
| Atelectasis | Immobility, pain, abdominal sepsis, sedation |
ARDS is the lung version of capillary leak: the alveolus fills with inflammatory fluid, so oxygen cannot diffuse effectively even when oxygen is delivered to the airway.
| Complication | Mechanism |
|---|---|
| AKI | Hypoperfusion, inflammation, microvascular dysfunction, nephrotoxic drugs |
| Acute tubular injury | Prolonged renal ischaemia and cytokine injury |
| Need for RRT | Severe acidosis, hyperkalaemia, fluid overload, uraemia |
Do not think AKI in sepsis is only "low BP to kidney." Venous congestion from over-resuscitation can also worsen renal perfusion by reducing the arterial-to-venous pressure gradient.
| Complication | Why it happens |
|---|---|
| DIC | Tissue factor activation -> thrombin generation -> fibrin deposition -> consumption of platelets and clotting factors |
| Microvascular thrombosis | Immunothrombosis becomes pathological |
| Bleeding | Platelet/clotting factor consumption, liver dysfunction, procedures |
| Anaemia | Inflammation, phlebotomy, bleeding, haemodilution |
Sepsis turns the coagulation system into a defensive trap: clotting helps wall off infection locally, but systemic activation blocks microcirculation and consumes clotting factors.
| Complication | Mechanism |
|---|---|
| Cholestasis of sepsis | Cytokines impair bile transporters -> conjugated hyperbilirubinaemia |
| Ileus | Inflammation, opioids, electrolyte derangement, hypoperfusion |
| Stress ulcer bleeding | Mucosal ischaemia plus acid injury |
| Gut barrier failure | Hypoperfusion disrupts tight junctions -> bacterial translocation |
| Acalculous cholecystitis | Critical illness, bile stasis, gallbladder ischaemia |
| Complication | Mechanism |
|---|---|
| Sepsis-associated encephalopathy | Neuroinflammation, blood-brain barrier dysfunction, hypoperfusion, metabolic derangement |
| Delirium | Infection, drugs, sleep disruption, hypoxia, organ failure |
| Critical illness neuropathy/myopathy | Inflammation, immobilisation, hyperglycaemia, steroids, neuromuscular blockers |
| Hypoglycaemia / hyperglycaemia | Liver dysfunction, insulin resistance, nutrition changes |
| Lactic acidosis | Tissue hypoxia plus adrenergic glycolysis plus impaired clearance |
| Source | Complications |
|---|---|
| Peritonitis | Abscess, fistula, adhesions, ileus, wound infection |
| Necrotising soft tissue infection | Limb loss, renal failure from rhabdomyolysis, toxic shock |
| Biliary sepsis | Liver abscess, recurrent cholangitis, secondary biliary cirrhosis if obstruction persists |
| Urosepsis | Pyonephrosis, renal abscess, obstructive nephropathy |
| Line infection | Persistent bacteraemia, septic thrombophlebitis, endocarditis |
| Treatment | Complication | Why |
|---|---|---|
| Fluids | Pulmonary oedema, abdominal compartment syndrome | Capillary leak and positive balance |
| Vasopressors | Digital/ischaemic complications | Alpha-mediated vasoconstriction in low-flow states |
| Antibiotics | Allergy, AKI, C. difficile, resistance | Drug toxicity and microbiome disruption |
| Steroids | Hyperglycaemia, weakness, secondary infection | Glucocorticoid metabolic and immune effects |
| Central lines | Pneumothorax, arterial puncture, CLABSI | Invasive access |
| Ventilation | Barotrauma, VAP, delirium | Positive pressure and sedation |
Complication Prevention Is Management
The best way to prevent sepsis complications is early recognition, early antibiotics, early source control, careful haemodynamic resuscitation, and daily de-escalation of unnecessary invasive support.
Active Recall - Sepsis Complications
References
[1] Lecture slides: Surviving Sepsis Campaign International Guidelines for Management of Sepsis and Septic Shock 2026.
High Yield Summary
Definition: Sepsis = life-threatening organ dysfunction caused by dysregulated host response to infection. Septic shock = sepsis with vasopressor requirement to maintain MAP at least 65 mmHg and lactate > 2 mmol/L despite adequate fluids [1].
Pathophysiology: PAMPs/DAMPs trigger innate immunity -> cytokines, complement, coagulation activation, endothelial leak, vasodilatation, microthrombi, mitochondrial dysfunction -> maldistributed oxygen delivery and organ failure [1].
2026 screening: Use NEWS, NEWS2, MEWS, or SIRS over qSOFA as a single screening tool in acutely ill inpatients. qSOFA is specific but not sensitive enough as the only screen [1].
Diagnosis: Suspected infection plus acute organ dysfunction. Use SOFA conceptually; in practice recognise hypotension, hypoxaemia, AKI/oliguria, thrombocytopaenia, bilirubin rise, confusion, lactate elevation.
Initial actions: Sepsis is a medical emergency. Measure lactate, obtain cultures promptly if this does not delay antibiotics, start antimicrobials according to severity, resuscitate hypoperfusion, and look for surgical source control [1].
Antibiotics: Septic shock/high likelihood sepsis -> immediate broad-spectrum IV antibiotics. Possible sepsis without shock -> rapid assessment, then antibiotics if infection likely. De-escalate when cultures and susceptibilities return [1].
HK relevance: Use IMPACT/local HA guidance and discuss with microbiology/ID early when ESBL, MRSA, CRE, CRAB, VRE, healthcare-associated infection, or prior broad-spectrum antibiotic exposure is relevant [3].
Fluids: Sepsis-induced hypoperfusion/septic shock -> at least 30 mL/kg IV crystalloid in first 3 hours. Balanced crystalloids preferred over 0.9% saline for most; 0.9% saline is preferred if concomitant TBI [1].
Vasopressors: Target MAP 65 mmHg. Norepinephrine first line; add vasopressin on escalating norepinephrine; add epinephrine if inadequate MAP despite norepinephrine plus vasopressin [1].
Source control: Drain pus, remove infected devices, debride necrosis, relieve obstruction, operate when needed. Aim as early as medically and logistically practical; 2026 SSC suggests ideally within 6 hours when source control is required [1].
Steroids: IV corticosteroids are suggested in septic shock, especially persistent vasopressor requirement. They shorten shock duration; they are not a substitute for source control [1].
Complications: Septic shock, ARDS, AKI, DIC, myocardial dysfunction, encephalopathy, cholestasis, ileus, pressure injury, line infection, antimicrobial toxicity, ICU-acquired weakness, cognitive/psychological sequelae, and recurrent infection.
One-Page Surgical Sepsis Algorithm
Active Recall - Sepsis Summary
References
[1] Lecture slides: Surviving Sepsis Campaign International Guidelines for Management of Sepsis and Septic Shock 2026.
[3] Senior notes: Hong Kong IMPACT antimicrobial guideline and CHP antimicrobial resistance materials.
Shock
A systematic surgical approach to shock: classification, pathophysiology, differential diagnosis, diagnosis, investigations, management, complications, and high-yield summary.
Abdominal Aortic Aneurysm
Abnormal focal dilation of the abdominal aorta exceeding 3 cm in diameter, most commonly occurring infrarenally, with risk of rupture and life-threatening hemorrhage.