📋 Key Information Summary
- Oncological emergencies — spinal cord compression (SCC), superior vena cava (SVC) syndrome, tumour lysis syndrome (TLS), and febrile neutropenia (FN) — require rapid recognition, early specialist involvement, and time-critical intervention to reduce morbidity and mortality.
- SCC: New back pain in a cancer patient is malignant spinal cord compression until proven otherwise. Urgent MRI spine (within 24 h ideally) and early dexamethasone 16 mg IV stat are essential. Refer urgently to radiation oncology and/or neurosurgery.
- SVC syndrome: Caused most commonly by lung cancer and lymphoma. CT chest with contrast confirms diagnosis. Stenting may relieve symptoms rapidly. Anticoagulation if indwelling catheter-related thrombus is identified.
- TLS: Prophylaxis (IV hydration + allopurinol) is indicated for all intermediate- and high-risk patients. Rasburicase (PBS Authority Required) is first-line for established high-risk TLS. Monitor urate, phosphate, potassium, calcium, creatinine at 0, 6, 12, 24 h.
- Febrile neutropenia: Fever ≥ 38.0 °C on a single reading or ≥ 38.3 °C sustained + neutrophils < 0.5 × 10⁹/L. Administer piperacillin-tazobactam (Tazocin®) IV within 60 minutes of presentation. Risk-stratify with MASCC score.
- Time-critical nature: Each emergency has a distinct window for optimal intervention — SCC ideally < 24 h to surgery/radiotherapy; TLS prophylaxis pre-chemotherapy; FN antibiotics within 60 min.
- Dexamethasone is used in both SCC (16 mg IV stat then 8 mg BD) and SVC syndrome (4–16 mg IV/PO) to reduce tumour-related oedema and inflammation.
- Multi-disciplinary coordination between oncology, emergency medicine, radiation oncology, neurosurgery, nephrology, and haematology is critical for all four emergencies.
- MASCC risk-index score ≥ 21 identifies low-risk febrile neutropenia patients potentially suitable for oral antibiotic therapy in a supervised ambulatory setting.
- TLS metabolic derangements — hyperkalaemia, hyperphosphataemia, hyperuricaemia, hypocalcaemia — can cause fatal arrhythmias and acute kidney injury if untreated.
- Aboriginal and Torres Strait Islander patients present with higher-stage malignancy at diagnosis and experience greater barriers to timely emergency oncological care — early liaison with Indigenous health workers is essential.
- Advanced care planning and goals-of-care discussions should be integrated into emergency management where prognosis permits.
Introduction & Australian Epidemiology
Oncological emergencies are acute, life-threatening conditions arising directly from a malignancy, its complications, or anti-cancer therapy. In Australia, cancer accounts for approximately 150,000 new diagnoses annually, and roughly 50,000 deaths per year — making it the leading cause of premature mortality. A significant proportion of cancer patients will present to emergency departments with an oncological crisis at some point during their disease trajectory.
The four most common oncological emergencies encountered in Australian practice are malignant spinal cord compression, superior vena cava syndrome, tumour lysis syndrome, and febrile neutropenia. Each demands rapid clinical recognition, systematic investigation, and time-sensitive therapeutic intervention. Delay in diagnosis and treatment is associated with significantly worse outcomes — including permanent neurological deficit in spinal cord compression, fatal arrhythmia in tumour lysis syndrome, and septic death in febrile neutropenia.
The Australian Institute of Health and Welfare (AIHW) reports that cancer-related emergency presentations have risen by approximately 15% over the past decade, driven by expanding treatment options, an ageing population, and increased use of myelosuppressive and immunomodulatory regimens. Aboriginal and Torres Strait Islander Australians experience a 14% higher cancer mortality rate compared to non-Indigenous Australians, with later-stage presentation and barriers to timely specialist care contributing to poorer outcomes.
This guideline provides a structured, evidence-based approach to the recognition, investigation, and management of each emergency, aligned with Australian therapeutic standards, PBS-listed medications, and contemporary multidisciplinary practice.
| Emergency | Key Mechanism | Most Common Cancer | Time to Intervention |
|---|---|---|---|
| Spinal Cord Compression | Epidural metastasis compressing the thecal sac | Lung, breast, prostate, myeloma | < 24 h for surgery/radiotherapy |
| Superior Vena Cava Syndrome | External compression or thrombosis of SVC | Lung cancer (NSCLC), lymphoma | Stenting/emergent chemo within hours–days |
| Tumour Lysis Syndrome | Massive cell lysis releasing intracellular contents | Haematological — AML, ALL, high-grade lymphoma | Prophylaxis pre-chemo; Rx within 6 h of lab derangement |
| Febrile Neutropenia | Immune compromise + infection | All — particularly post-chemotherapy haematological malignancies | Antibiotics within 60 min |
Spinal Cord Compression
Epidemiology & Aetiology
MSCC occurs in 5–10% of patients with cancer and is the presenting feature of malignancy in approximately 20% of cases. In Australia, the most common primary tumours causing MSCC are lung cancer (25–30%), breast cancer (15–20%), prostate cancer (10–15%), and multiple myeloma (10%). The thoracic spine is the most frequently affected site (60–70%), followed by lumbosacral (20–30%) and cervical regions (5–10%).
Pathophysiology
Metastatic deposits extend into the epidural space via the vertebral body (most commonly) or the pedicles. Progressive expansion leads to direct compression of the spinal cord and/or cauda equina, venous congestion, and local ischaemia. Oedema extends both rostral and caudal to the level of compression, creating a zone of potentially reversible injury surrounding a core of irreversible infarction. Dexamethasone reduces this perilesional oedema.
Clinical Presentation & Diagnostic Criteria
- Back pain — present in > 95% of cases; typically localised, worse when supine, nocturnal, and progressive over days to weeks.
- Motor weakness — ranging from difficulty walking to paraplegia/quadriplegia.
- Sensory loss — a sensory level may be identifiable on examination.
- Autonomic dysfunction — urinary retention or incontinence, faecal incontinence, constipation.
- Lhermitte sign — electric-shock sensation radiating down the spine on neck flexion.
Investigations
Immediate Management
Definitive Management
Superior Vena Cava Syndrome
Epidemiology & Aetiology
Superior vena cava (SVC) syndrome results from obstruction or compression of the SVC, impairing venous return from the head, neck, and upper extremities. Malignant causes account for approximately 85–95% of cases in adult practice. In Australia, non-small cell lung cancer (NSCLC) is the most common cause (60–75%), followed by lymphoma (10–15%) and small cell lung cancer (5–10%). Increasingly, SVC syndrome is associated with indwelling central venous catheters, pacemaker wires, and mediastinal fibrosis.
Clinical Presentation & Diagnostic Criteria
- Facial swelling and plethora — worse in the morning and with bending forward.
- Distended neck veins and superficial thoracic venous collaterals.
- Dyspnoea — may be positional; stridor in severe cases due to laryngeal oedema.
- Cough, hoarseness, dysphagia — from associated mediastinal mass effect.
- Central nervous system symptoms — headache (typically worse on waking), visual disturbance, confusion, syncope in severe obstruction.
- Upper extremity oedema.
Severity grading: Mild (facial/neck swelling only) → Moderate (dyspnoea on exertion, stridor, mild oedema) → Severe (rest dyspnoea, laryngeal oedema, cerebral oedema with obtundation).
Investigations
Management
Tumour Lysis Syndrome
Epidemiology & Risk Factors
Tumour lysis syndrome (TLS) is a metabolic emergency caused by rapid release of intracellular contents — potassium, phosphate, nucleic acids (metabolised to uric acid), and cytokines — from lysed malignant cells. It occurs spontaneously or, more commonly, within 1–5 days of initiating cytotoxic chemotherapy. TLS is most frequently associated with haematological malignancies: acute myeloid leukaemia (AML), acute lymphoblastic leukaemia (ALL), Burkitt lymphoma, and other high-grade non-Hodgkin lymphomas (NHL). Solid tumours — particularly small cell lung cancer and germ cell tumours — can also cause TLS but less commonly.
Risk Stratification
Cairo-Bishop Diagnostic Criteria
TLS is present if ≥ 2 of the following occur within 3 days before to 7 days after cytotoxic therapy:
- Uric acid ≥ 476 µmol/L (8 mg/dL) or ≥ 25% increase from baseline
- Potassium ≥ 6.0 mmol/L or ≥ 25% increase
- Phosphate ≥ 1.45 mmol/L (adults) or ≥ 2.1 mmol/L (children) or ≥ 25% increase
- Calcium ≤ 1.75 mmol/L or ≥ 25% decrease
Clinical TLS = laboratory TLS + ≥ 1 of: serum creatinine ≥ 1.5× ULN, cardiac arrhythmia, seizure, or sudden death.
Investigations — Monitoring Schedule
Prophylaxis & Treatment
Management of Specific Derangements
| Derangement | Immediate Management | Definitive Management |
|---|---|---|
| Hyperkalaemia (K⁺ > 6.0) | Calcium gluconate 10% 10 mL IV over 10 min (cardiac membrane stabiliser). Insulin 10 U + 50 mL 50% dextrose IV. Salbutamol nebuliser 10–20 mg. | Calcium resonium 15–30 g PO/PR. Haemodialysis if refractory or K⁺ > 7.0 with ECG changes. |
| Hyperphosphataemia | Phosphate binders: calcium carbonate 500 mg PO TDS with meals or sevelamer 800 mg PO TDS. | Restrict dietary phosphate. Haemodialysis if PO₄ > 3.2 mmol/L or symptomatic hypocalcaemia. |
| Hypocalcaemia | Calcium gluconate 10% 10–20 mL IV slowly if symptomatic (tetany, seizures, QT prolongation). | Treat underlying hyperphosphataemia. Do NOT give IV calcium unless symptomatic — risk of ectopic calcium phosphate deposition. |
| Acute kidney injury | Optimise hydration. Avoid nephrotoxins. Furosemide if oliguric with fluid overload. | Rasburicase if hyperuricaemia is the cause. Haemodialysis/haemofiltration if AKI is refractory (Cr rising, K⁺ uncontrolled, fluid overload). |
Febrile Neutropenia Management
Epidemiology & Definitions
Febrile neutropenia (FN) is the most common oncological emergency in Australia, accounting for approximately 30,000 hospitalisations annually. It carries an overall mortality rate of 5–10%, with mortality exceeding 30% in patients with documented bacteraemia or septic shock.
Definitions (IDSA/ACSQHC):
- Fever: Single oral temperature ≥ 38.0 °C, or ≥ 38.3 °C sustained over 1 hour.
- Neutropenia: Absolute neutrophil count (ANC) < 0.5 × 10⁹/L, or ANC < 1.0 × 10⁹/L with expected decline to < 0.5 × 10⁹/L within 48 h.
- Profound neutropenia: ANC < 0.1 × 10⁹/L — higher infection risk and broader empiric coverage may be warranted.
Risk Stratification — MASCC Score
| Variable | Weight |
|---|---|
| Burden of illness: no or mild symptoms | +5 |
| No hypotension (SBP > 90 mmHg) | +5 |
| No COPD | +4 |
| Solid tumour or no previous fungal infection | +4 |
| No dehydration requiring parenteral fluids | +3 |
| Outpatient at fever onset | +3 |
| Age < 60 years | +2 |
Score ≥ 21 = Low risk (mortality < 5%) — consider oral antibiotics or early discharge with GP follow-up.
Score < 21 = High risk (mortality 9–36%) — inpatient IV antibiotics required.
Investigations
Empirical Antibiotic Therapy
Addition of Vancomycin — Indications
Add vancomycin IV empirically (do not wait for culture results) if any of the following are present:
- Suspected catheter-related infection (erythema, tenderness over CVC insertion site)
- Known MRSA colonisation or prior MRSA infection
- Skin/soft tissue infection
- Haemodynamic instability / septic shock
- Institutional MRSA prevalence > 10%
Low-Risk Febrile Neutropenia — Oral Therapy Option
Sepsis / Septic Shock — Escalation
Monitoring & Duration of Therapy
- Daily FBC, EUC, CRP, lactate (if septic).
- Repeat blood cultures at 48–72 h if initial cultures positive or ongoing fever.
- Low risk, responding: Switch to oral antibiotics at 48 h if afebrile, clinically improving, and ANC recovering. Total minimum course 7 days or until ANC > 0.5 × 10⁹/L.
- High risk, culture-negative at 72 h: Continue empiric antibiotics. Reassess source (CT, repeat cultures, consider antifungal if prolonged neutropenia > 7 days and persistent fever).
- Add antifungal (fluconazole, voriconazole, or caspofungin) if fever persists > 4–7 days on broad-spectrum antibiotics with ongoing profound neutropenia — suspect invasive fungal infection.
Aboriginal and Torres Strait Islander Health Considerations
Special Populations
📚 References
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