GC059 High Fever Low BP
A clinical scenario of high fever accompanied by low blood pressure, typically indicative of sepsis or septic shock resulting from a systemic inflammatory response to infection.
High Fever, Low Blood Pressure — Sepsis & Septic Shock
Big Idea: When a patient presents with high fever and low blood pressure, think sepsis and septic shock — a life-threatening condition where the body's dysregulated immune response to infection causes multi-organ dysfunction. This lecture, delivered by Dr. Chan Wai Ming (AICU, QMH), walks through the modern definition of sepsis (Sepsis-3), the hemodynamic profile of septic shock, the cascade of multi-organ dysfunction syndrome (MODS), and the evidence-based management principles from the Surviving Sepsis Campaign. Critically, it is a tour of landmark ICU trials — many of which were negative — that shaped current practice.
How it fits in exams: This lecture is a favorite for MCQs on shock classification, SAQs on acute management of septic shock (antibiotics, fluids, vasopressors, targets), and mini-cases where a septic patient deteriorates. Examiners love testing the "why" behind choosing noradrenaline over dopamine, crystalloids over colloids, and the evidence against tight glucose control. Past papers from 2019–2025 have repeatedly tested septic shock management, ARDS definitions, and lactate-guided resuscitation.
Learning Objectives (from slide 2):
- Definition of Sepsis (old SIRS concept → Sepsis-3)
- Multi-Organ Failure in sepsis
- Treatment of Sepsis — Surviving Sepsis Campaign Guidelines
- Targets of Resuscitation (EGDT and beyond)
- Use of Vasopressors (noradrenaline vs. dopamine, renal-dose dopamine debunked)
- Use of Fluids (crystalloid vs. colloid, balanced vs. NS, starch harm)
37.4% of ICU patients had sepsis in a European multinational study (SOAP, 2006). Hospital mortality was 24%. In China (Xie et al., CCM 2019), 33.9% of ICU sepsis was hospital-acquired with a D90 mortality of 35.5%. [1]
Why this matters: Sepsis is not a rare diagnosis — it is the leading cause of death in ICU patients. The trend over the last two decades is increasing incidence (143 → 343 per 100,000 from 2000–2007) but decreasing mortality (39.6% → 27.3%) — meaning we are seeing more sepsis but treating it better [1]. However, more patients are being discharged to long-term care facilities (27% → 35%), reflecting the morbidity burden.
2. Definitions: From SIRS to Sepsis-3
SIRS = Systemic Inflammatory Response Syndrome — the systemic activation of the innate immune response to injury regardless of cause. [1]
SIRS criteria (for historical context):
- Temperature > 38°C or < 36°C
- Heart rate > 90 bpm
- Respiratory rate > 20 or PaCO₂ < 32 mmHg
- WBC > 12,000 or < 4,000 or > 10% bands
Problem with SIRS: Too sensitive, not specific. A patient running a marathon meets SIRS criteria. By 2001, the consensus moved away from requiring SIRS as obligatory for sepsis diagnosis.
"Definition after 2001: SIRS Not Obligatory" — Sepsis is the response of the body to infection, not simply inflammation. [1]
Infection is defined as a microbial phenomenon — the invasion of pathogens into normally sterile spaces (CNS, lung, pericardium) or pathological manifestations (abscess, endocarditis). [1]
Key lecture point:
"No commonly accepted serum marker of sepsis. Procalcitonin is promising but not the gold standard." [1]
Exam Trap
Don't write that procalcitonin definitively diagnoses sepsis. The lecture explicitly states it is NOT the gold standard. Use it as a supportive marker, not a diagnostic one.
Sepsis-3 Definition: "Life-threatening organ dysfunction caused by a dysregulated host response to infection." [1]
This is a conceptual shift: it's not just having an infection + inflammation. It's infection causing organ dysfunction through a dysregulated (not just activated) immune response.
Septic Shock = subset of sepsis with circulatory AND cellular/metabolic dysfunction associated with higher risk of mortality. [1]
Clinical identification of septic shock (must know for exams):
A vasopressor requirement to maintain MAP ≥ 65 mmHg AND serum lactate > 2 mmol/L, in the absence of hypovolemia. [1]
| Concept | Definition | Key Discriminator |
|---|---|---|
| Sepsis | Life-threatening organ dysfunction from dysregulated host response to infection | Organ dysfunction is the hallmark |
| Septic Shock | Sepsis + need vasopressor for MAP ≥ 65 AND lactate > 2 mmol/L despite adequate fluids | Both hemodynamic AND metabolic criteria must be met |
High Yield
Septic shock requires both vasopressor dependence AND elevated lactate. If a patient needs noradrenaline but their lactate is 1.5 mmol/L, they technically do not meet Sepsis-3 criteria for septic shock. This is a common MCQ discriminator.
From supporting notes [2]:
- RR > 22/min
- sBP < 100 mmHg
- Altered GCS
Score ≥ 2 → mortality ≥ 10%. Used for quick bedside recognition outside the ICU. Not part of the formal Sepsis-3 definition but a screening tool.
The lecture references a complex immunological cascade (Int. J. Mol. Sci. 2021) [1]. Here's the conceptual framework:
- Pathogen invasion → Pattern recognition receptors (PRRs) on immune cells recognize pathogen-associated molecular patterns (PAMPs)
- Innate immune activation → Massive release of pro-inflammatory cytokines (TNF-α, IL-1, IL-6) and anti-inflammatory mediators simultaneously
- Dysregulation → The balance tips: excessive inflammation damages host tissues; excessive immunosuppression allows secondary infections
- Endothelial dysfunction → Vasodilation (↓SVR), capillary leak, microvascular thrombosis (DIC), impaired oxygen extraction
- Multi-organ dysfunction → The final common pathway
Why "dysregulated"? In normal infection, the immune response is proportional and self-limited. In sepsis, positive feedback loops amplify the response beyond what is needed, and regulatory mechanisms fail. This is why sepsis is a host problem, not just a pathogen problem.
Septic shock is a DISTRIBUTIVE shock — characterized by vasodilation (↓SVR), high cardiac output, and low blood pressure. [1]
| Parameter | Distributive | Cardiogenic | Hypovolemic | Obstructive |
|---|---|---|---|---|
| Blood Pressure | ↓ | ↓ | ↓ | ↓ |
| Cardiac Output | ↑ (initially) | ↓↓ | ↓ | ↓ |
| Preload | ↓ (relative) | ↑ | ↓↓ | Variable |
| SVR (Afterload) | ↓↓↓ | ↑ | ↑ | ↑ |
| Extremities | Warm, flushed | Cold, clammy | Cold, clammy | Cold, clammy |
| Pulse pressure | Wide | Narrow | Narrow | Narrow |
The manifestation of septic shock is normally stereotypic — warm peripheries, bounding pulses, wide pulse pressure, high cardiac output state. [1]
Why is CO high in septic shock? The massive drop in SVR (afterload) makes it easier for the heart to eject blood. Cardiac output rises as a compensatory mechanism. But despite high CO, tissue perfusion is impaired because:
- Blood is maldistributed (pooling in dilated splanchnic beds)
- Microvascular dysfunction prevents oxygen extraction
- Capillary leak reduces effective circulating volume
Clinical Pearl
A patient with septic shock will have warm extremities initially (distributive physiology). If they become cold and shut down, think of either late-stage septic shock with myocardial depression, or consider concomitant cardiogenic/hypovolemic shock.
5. Multi-Organ Dysfunction Syndrome (MODS)
MODS is the hallmark of severe sepsis. Each organ system has a characteristic pathology and clinical manifestation. [1]
| Organ System | Pathology | Clinical Manifestation |
|---|---|---|
| CVS | Septic Shock | High cardiac output, vasodilation |
| Respiratory | ARDS | Type I respiratory failure |
| Renal | Acute Tubular Necrosis (ATN) | Oliguric renal failure |
| Blood | DIC | ↓ Platelets, bleeding |
| GI | Multi-factorial | GI bleeding, ileus |
| Liver | Multi-factorial | Jaundice |
| CNS | Septic Encephalopathy | Encephalopathy, confusion |
| Peripheral NS | Critical Illness Polyneuropathy | Weakness, ventilator weaning failure |
ARDS = Non-cardiogenic pulmonary oedema, Type I failure, low lung compliance. [1]
Why does ARDS happen in sepsis? Inflammatory mediators damage the alveolar-capillary membrane → protein-rich fluid leaks into alveoli → impairs gas exchange → refractory hypoxemia. The lungs become stiff (low compliance) because fluid-filled alveoli resist inflation.
ARDS Berlin Definition (2012) — Know this table cold:
| Feature | Criteria |
|---|---|
| Timing | Within 1 week of known clinical insult or new respiratory symptoms |
| Chest Imaging | Bilateral opacities not fully explained by effusions, lobar/lung collapse, or nodules |
| Origin of edema | Not fully explained by cardiac failure or fluid overload; need objective assessment if no risk factor |
| Mild | 200 < PaO₂/FiO₂ ≤ 300 mmHg with PEEP or CPAP ≥ 5 cmH₂O |
| Moderate | 100 < PaO₂/FiO₂ ≤ 200 mmHg with PEEP ≥ 5 cmH₂O |
| Severe | PaO₂/FiO₂ ≤ 100 mmHg with PEEP ≥ 5 cmH₂O |
Historical vs. Current Definition
The older 1993 Euro-American definition used PAWP < 18 mmHg to exclude cardiogenic pulmonary edema and defined ALI as PaO₂/FiO₂ < 300. The Berlin 2012 definition dropped the term "ALI" and reclassified severity into mild/moderate/severe. Both are mentioned in the lecture — the Berlin definition is current practice. [1]
The lecture references the RIFLE criteria (ADQI 2004) [1] for classifying AKI:
| Stage | GFR Criteria | Urine Output |
|---|---|---|
| Risk | ↑Cr × 1.5 or ↓GFR > 25% | < 0.5 mL/kg/hr × 6 hrs |
| Injury | ↑Cr × 2 or ↓GFR > 50% | < 0.5 mL/kg/hr × 12 hrs |
| Failure | ↑Cr × 3 or ↓GFR > 75% or Cr ≥ 354 | < 0.3 mL/kg/hr × 24 hrs or anuria × 12 hrs |
| Loss | Persistent ARF > 4 weeks | — |
| ESRD | End-stage > 3 months | — |
In sepsis, the mechanism is predominantly ATN from renal hypoperfusion and inflammatory mediator–induced tubular injury. Don't forget pre-renal AKI from hypovolemia too.
6. Treatment of Sepsis — Surviving Sepsis Campaign 2021
The SSC 2021 guideline forms the backbone of sepsis management. [1]
Eradication of the infection source if possible. [1]
Examples: drain an abscess, debride necrotic tissue, remove infected device, repair perforated viscus. Without source control, no amount of antibiotics will save the patient.
Each hour of delay in antimicrobial therapy over the ensuing 6 hours was associated with an average decrease in survival of 7.6% per hour. — Kumar et al., CCM 2006 [1]
Ultra-High Yield
This is one of the most quotable statistics in critical care. Every hour without antibiotics = 7.6% drop in survival. This is why sepsis bundles emphasize antibiotics within 1 hour of recognition. Get blood cultures FIRST, then start empirical broad-spectrum antibiotics IMMEDIATELY — do not wait for culture results.
Favour crystalloids over colloids. Weak recommendation of using balanced solution. [1]
Key Trials on Fluid Choice:
| Trial | Design | Key Finding |
|---|---|---|
| SAFE Study (NEJM 2004) | 4% albumin vs. normal saline, multicentre RCT | No difference in D28 mortality: 20.9% vs. 21.1% (p=0.87) |
| CHEST (NEJM 2012) | 6% HES (Voluven) vs. NS | No survival benefit; MORE renal failure with HES (RR 1.21, p=0.04) |
| 6S Trial (NEJM 2012) | 6% HES (Tetraspan) vs. Ringer's acetate | Higher D90 mortality with HES (51% vs. 43%, p=0.03); MORE renal failure (RR 1.35, p=0.04) |
| Hammond meta-analysis (NEJM Evidence 2022) | Balanced crystalloids vs. NS, 6 trials, n=34,450 | Trend toward benefit with balanced solutions but NOT statistically significant (mortality RR 0.96, 95% CI 0.91–1.01) |
Bottom line from the lecture:
For starch-based colloids: No survival benefits, More Renal Failure. [1]
Balanced solutions have theoretical advantages (physiological electrolyte composition, pH neutral on massive infusion) but the evidence is NOT conclusive. [1]
Why is Hyperchloremia a Concern?
Normal saline has 154 mmol/L of chloride (vs. plasma 100 mmol/L). Massive NS infusion → hyperchloremic metabolic acidosis → renal vasoconstriction → AKI. This is the theoretical rationale for balanced solutions like Ringer's Lactate or Plasmalyte. However, the Hammond 2022 meta-analysis showed the difference is NOT statistically significant in hard endpoints. The SSC makes only a weak recommendation for balanced solutions. [1]
Comparison of Common IV Solutions (from lecture slide 26):
| Component | Plasma | NS (0.9% NaCl) | Ringer's Lactate | Plasmalyte | Gelofusine |
|---|---|---|---|---|---|
| Na⁺ | 140 | 154 | 130 | 140 | 154 |
| K⁺ | ~4 | 0 | 4 | 5 | 0 |
| Cl⁻ | 100 | 154 | 109 | 98 | 125 |
| Ca²⁺ | 2.2 | 0 | 1.5 | 0 | 0 |
| HCO₃⁻ | 24 | 0 | 0 | 0 | 0 |
| Lactate | 1 | 0 | 28 | 0 | 0 |
| Acetate | 0 | 0 | 0 | 27 | 0 |
6.4 Vasopressors
Preferred vasopressor: Noradrenaline [1]
| Receptor | Action | Dopamine | Dobutamine | Adrenaline | Noradrenaline |
|---|---|---|---|---|---|
| α₁ | Vasoconstriction | ++ (high dose) | 0 | +++ | ++++ |
| β₁ | ↑ Cardiac Output | + (low dose) | +++ | +++ | ++ |
Inotropes (e.g., dobutamine) increase cardiac output but cause peripheral vasodilation and may DROP blood pressure. [1]
Vasopressors (noradrenaline, high-dose dopamine, phenylephrine, vasopressin) are vasoconstrictors that increase blood pressure. [1]
Why noradrenaline is preferred:
- Potent α₁ agonist → restores SVR (the primary problem in distributive shock)
- Some β₁ activity → maintains cardiac output
- Less arrhythmogenic than dopamine
SOAP II (NEJM 2010) — Dopamine vs. Noradrenaline:
| Dopamine | Noradrenaline | P value | |
|---|---|---|---|
| N | 858 | 821 | |
| D28 Mortality | 52.5% | 48.5% | 0.10 (NS) |
| Arrhythmias | 24.1% | 12.4% | < 0.001 |
| Discontinued for arrhythmias | 6.1% | 1.6% | < 0.001 |
No difference in D28 survival. Dopamine group had MORE patients discontinued for arrhythmias. [1]
Subgroup analysis: In cardiogenic shock, dopamine was associated with HIGHER mortality (p=0.03). [1]
High Yield
Noradrenaline is the recommended first-line vasopressor for septic shock. Dopamine causes more arrhythmias and is worse in cardiogenic shock. This is a classic MCQ answer. [1]
ANZIC Trial (Lancet 2000) — "Renal-Dose" Dopamine:
Dopamine 2 μg/kg/min vs. placebo in ICU patients at risk of renal failure: NO difference in peak creatinine, need for RRT, ICU/hospital stay, or mortality. [1]
"Renal Dose" Dopamine is OUT. [1]
Exam Trap
If an MCQ asks about "low-dose dopamine for renal protection," the answer is that it does NOT work. The ANZIC trial debunked this practice. Never recommend renal-dose dopamine.
NOT NECESSARY to target supranormal cardiac output (Class 1B recommendation). [1]
Targets derived from Early Goal-Directed Therapy (EGDT): [1]
| Target | Value |
|---|---|
| Central Venous Pressure | 8–12 mmHg |
| Mean Arterial Pressure | > 65 mmHg |
| Urine Output | > 0.5 mL/kg/hr |
| Central Venous O₂ Saturation (ScvO₂) | > 70% |
| Mixed Venous O₂ Saturation (SvO₂) | > 65% (if PA catheter used) |
EGDT — Rivers (NEJM 2001):
| EGDT | Control | P | |
|---|---|---|---|
| N | 130 | 133 | |
| D28 Mortality | 33.3% | 49.2% | 0.01 |
| D60 Mortality | 44.3% | 56.9% | 0.03 |
This was the landmark study showing protocolized early resuscitation saves lives. However, subsequent multicentre trials (ProCESS, ARISE, ProMISe) did not replicate the dramatic benefit — the concept of early, aggressive resuscitation stuck, but the rigid protocol did not.
SEPSISPAM Study (NEJM 2014):
| MAP 65–70 mmHg | MAP 80–85 mmHg | ||
|---|---|---|---|
| N | 388 | 388 | |
| D28 Mortality | 34.0% | 36.6% | p=0.57 (NS) |
| New AF | 2.8% | 6.7% | p=0.02 |
| RRT in chronic HT patients | 42.2% | 31.7% | p=0.046 |
A higher blood pressure target (80–85) is NOT associated with better overall outcome. It caused more atrial fibrillation. However, in the subgroup with pre-existing chronic hypertension, a higher MAP target reduced need for RRT. [1]
Clinical Nuance
The standard MAP target is ≥ 65 mmHg. In patients with chronic hypertension, their autoregulatory curve is shifted right — their kidneys may need a higher perfusion pressure. The SEPSISPAM data supports considering a higher MAP target (80–85) specifically in this subgroup. But for the general population, aiming higher just causes harm (more arrhythmias).
Lactate clearance is associated with better prognosis in sepsis. RR of death with lactate clearance = 0.38 (95% CI 0.29–0.50). [1]
| Population | Sensitivity | Specificity |
|---|---|---|
| All patients | 0.75 (0.58–0.87) | 0.72 (0.61–0.90) |
| ICU only | 0.83 (0.67–0.92) | 0.67 (0.59–0.75) |
Why lactate matters: Lactate rises in sepsis due to:
- Tissue hypoperfusion → anaerobic metabolism
- Impaired lactate clearance by the liver
- Catecholamine-driven aerobic glycolysis
Serial lactate measurement guides resuscitation adequacy. A falling lactate = tissues are being resuscitated. A rising or persistently elevated lactate = ongoing tissue hypoxia → escalate therapy.
Aim at preventing hyperglycemia > 10 mmol/L. Do NOT target normal glucose (tight control is harmful). [1]
| Trial | Protocol | Key Finding |
|---|---|---|
| Van den Berghe (NEJM 2001) | Surgical ICU, tight glucose (4.4–6.0) vs. control (10–11) | ↓ ICU mortality with tight control (4.6% vs. 8.0%, p=0.04) |
| NICE-SUGAR (NEJM 2009) | Multicentre, tight glucose (4.5–6.0) vs. < 10 | ↑ D90 mortality with tight control (27.5% vs. 24.9%, p=0.02); severe hypoglycemia 6.8% vs. 0.5% |
"Tight Glucose Control Could Be Harmful!" [1]
The Van den Berghe study was single-centre and predominantly surgical patients. The much larger NICE-SUGAR trial (multicentre, medical + surgical) showed tight control increased mortality, primarily through severe hypoglycemia (glucose < 2.2 mmol/L). Current practice: keep glucose < 10 mmol/L but avoid tight control.
Appropriate ventilatory strategy, appropriate use of renal replacement therapy, appropriate nutritional protocol. [1]
These are broad categories. The key principles:
- Lung-protective ventilation for ARDS (low tidal volume 6 mL/kg IBW, plateau pressure < 30 cmH₂O)
- RRT for refractory AKI with metabolic derangement
- Early enteral nutrition when feasible
The lecture concludes with a powerful table [1]:
| Study | Reference | Result |
|---|---|---|
| ANZICS Renal Dose Dopamine | Lancet 2000 | Negative |
| Albumin Study (SAFE) | NEJM 2004 | Negative |
| VASST (NE vs. Vasopressin) | NEJM 2008 | Negative |
| CORTICUS (Steroids) | NEJM 2008 | Negative |
| NICE-SUGAR | NEJM 2009 | Intensive group WORSE |
| SOAP II (Dop vs. NE) | NEJM 2010 | Negative |
| PROWESS-SHOCK (Activated Protein C) | NEJM 2012 | Negative |
| 6S Study (HES vs. Ringer's) | NEJM 2012 | Starch WORSE |
"Specific drugs to modulate the process of sepsis in favour of survival is still lacking." [1]
Exam Intelligence
This table is the lecturer's summary of evidence-based ICU practice. Examiners may ask "which interventions have been shown NOT to improve outcomes in sepsis?" or "what fluid should be avoided in sepsis?" Know that starch-based colloids are harmful (more renal failure), activated protein C was withdrawn, tight glucose control is harmful, and renal-dose dopamine doesn't work.
1. Sepsis is a complicated immune process of the body in response to infection. [1]
2. Early recognition of sepsis and effective antimicrobial therapy are important. [1]
3. Treatments that work theoretically need to be validated in RCTs. [1]
4. Specific drugs to modulate the process of sepsis in favour of survival is still lacking. [1]
9. Integration with Related Material
- 2024 SAQ Q11 [3]: A 65-year-old with cough, high fever, SOB, confusion, hypotension, ABG showing mixed acidosis with lactate 4.5 → classic septic shock from pneumonia. Expected answers: identify acid-base disturbance, investigations within 1 hour (blood cultures, lactate), and 5 management steps (O₂, IV fluids, blood cultures, empirical antibiotics, vasopressors).
- 2023 Minicase Case 3 [4]: S. aureus bacteremia → deterioration with T 41°C, warm extremities, BP 85/45 → septic shock. Asked for airway management, diagnosis of hemodynamic condition (septic shock), and 5 acute management points.
- 2021 Minicase Case 2 [5]: Acute cholecystitis with BP 95/50, HR 120 → asked about causes of hemodynamic instability (sepsis + hypovolemia) and pathophysiology.
Neutropenic fever → septic shock is the most feared complication. ANC < 500 + fever = empirical broad-spectrum antibiotics within 1 hour. Same urgency as Kumar et al. data.
Post-op sepsis management follows the same SSC principles. Source control may involve returning to OT.
MCQ-style:
- A patient with septic shock has warm extremities and bounding pulses. What type of shock is this? → Distributive (high CO, low SVR)
- Which vasopressor is first-line in septic shock? → Noradrenaline
- A critically ill patient is given "renal-dose" dopamine. What does evidence show? → No benefit (ANZIC 2000)
- Which IV fluid is associated with increased renal failure in sepsis? → HES/starch-based colloids
- What is the MAP target in septic shock? → ≥ 65 mmHg
- What blood glucose target is recommended in ICU? → < 10 mmol/L (NOT tight control)
SAQ-style:
- Define septic shock according to Sepsis-3. → Subset of sepsis with vasopressor requirement to maintain MAP ≥ 65 mmHg AND lactate > 2 mmol/L despite adequate fluid resuscitation.
- List the components of the Surviving Sepsis Campaign bundle. → Source control, early antibiotics, crystalloid fluid resuscitation, noradrenaline, target MAP ≥ 65, lactate-guided resuscitation, lung-protective ventilation, RRT, nutrition, glucose < 10.
- What is ARDS? Give the Berlin definition severity criteria. → See table above.
- Describe the hemodynamic profile of septic shock. → ↓BP, ↑CO, ↓SVR, warm peripheries.
- Why is starch-based colloid avoided in sepsis? → CHEST and 6S trials showed no survival benefit and MORE renal failure requiring RRT.
Minicase-style:
- Patient with pneumonia developing shock → identify sepsis → manage with SSC bundle → patient develops ARDS → manage with lung-protective ventilation → develops AKI → consider RRT.
High Yield Summary
Sepsis-3: Life-threatening organ dysfunction from dysregulated host response to infection. Septic shock = vasopressor needed for MAP ≥ 65 + lactate > 2 after fluids. Shock type: Distributive (↑CO, ↓SVR, warm). MODS: CVS (shock), Resp (ARDS), Renal (ATN), Blood (DIC), GI (ileus/bleed), Liver (jaundice), CNS (encephalopathy), PNS (polyneuropathy). Treatment: Source control + antibiotics ASAP (7.6% mortality increase per hour delay) + crystalloid fluids (avoid starch) + noradrenaline (not dopamine — more arrhythmias) + target MAP ≥ 65 + lactate clearance monitoring + glucose < 10 (tight control harmful). Negative studies era: renal-dose dopamine, albumin vs. NS, activated protein C, tight glucose — all failed or caused harm.
Active Recall - High Fever Low BP
[1] Lecture slides: GC 059. High fever low BP.pdf (slides 1–40) [2] Senior notes: Ryan Ho Critical Care.pdf (pp. 15, 21–22) [3] Past papers: 2024 Fourth Summative SAQ.pdf (Q11, p.12) [4] Past papers: 2023 Fourth Summative Minicase.pdf (Case 3, pp.23–25) [5] Past papers: 2021 Fourth Summative Minicase.pdf (Case 2, pp.14–17) [6] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p.1329 — neutropenic fever) [7] Past papers: 2021 Fourth Summative SAQ.pdf (Q12, p.14)
GC058 High Blood Pressure
High blood pressure (hypertension) is a chronic cardiovascular condition defined by persistently elevated systemic arterial pressure, typically ≥140/90 mmHg, that increases the risk of end-organ damage to the heart, brain, kidneys, and vasculature.
GC060 High White Cell Count
Leukocytosis is an elevation of the total white blood cell count above the normal range (typically >11,000/μL), indicating infection, inflammation, stress, or hematologic malignancy.