oncologic emergencies

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superior vena cava syndrome

• aetiology — malignancy in ~90%; NSCLC (~50%) most common, followed by lymphoma, SCLC, germ cell tumours
• presentation — facial/arm oedema, distended neck/chest veins, dyspnoea, stridor, hoarseness
• most SVC syndrome is subacute and not an emergency — the features below define a life-threatening presentation

rapidly expanding mediastinal mass — differential

• SCLC — very aggressive, smoking-related, centrally located, can expand visibly over weeks
• lymphoma — particularly aggressive subtypes (DLBCL, Burkitt, lymphoblastic)
• germ cell tumour — primary mediastinal or testicular metastasis; check β-hCG + AFP
• all three are chemosensitive — tissue diagnosis critical to avoid wrong therapy

life-threatening vs uncomplicated

Life-threatening = any of stridor, confusion, or haemodynamic compromise → triggers urgent endovascular therapy.

management

Life-threatening (stridor, confusion, hypotension):

• ABCs with early anaesthesia/ICU involvement — airway is high-risk (distorted anatomy, mucosal oedema, bleeding-prone collaterals); plan for difficult intubation with most experienced operator
• femoral or lower-extremity IV access — upper-limb infusions pool proximal to obstruction
• elevate head of bed; supplemental O₂; consider heliox as temporising bridge for stridor
• cautious fluids for hypotension — consider concurrent pericardial tamponade, PE, or sepsis
• urgent endovascular SVC stenting (± catheter-directed thrombolysis if thrombus present) — first-line for life-threatening SVC syndrome; technical success ~97%, clinical success ~93%, symptom relief typically within 24–72 hours; does not compromise later tissue diagnosis
• contrast-enhanced CT chest as soon as safe to define level, thrombus, and airway involvement
• corticosteroids and loop diuretics are widely used but lack evidence of efficacy; steroids may be reasonable for airway oedema prophylaxis or if lymphoma suspected, but may obscure histology

Non-life-threatening:

• obtain tissue diagnosis first, then initiate directed therapy (radiation for NSCLC; chemotherapy for SCLC, lymphoma, germ cell)
• consult thoracic surgery + radiation oncology + medical oncology

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malignant spinal cord compression

• presentation — back pain (first sign in ~95%), progressive weakness, sensory level, bowel/bladder dysfunction (late — urinary retention is a classic autonomic sign)
• UMN signs (brisk reflexes, bilateral symmetric weakness) → cord compression (above conus, ~T12/L1)
• LMN signs (flaccid, often asymmetric weakness, hypo/areflexia) + saddle anaesthesia → cauda equina syndrome (below L1–L2)
• thoracic spine is the most common site

management

1. dexamethasone on clinical suspicion — 10 mg IV stat, then 4 mg IV/PO q6h; higher loading doses (16–96 mg) have been used but Cochrane found no clear efficacy benefit with more serious adverse effects
2. imaging — urgent MRI whole spine (not just the symptomatic level — 15–20% have additional non-contiguous lesions); CT myelogram if MRI contraindicated
3. supportive — urinary catheterisation for retention; opioid titration for pain; bed rest/log-roll with spinal precautions until stability assessed
4. definitive — consult spine surgery AND radiation oncology; multidisciplinary decision

surgical decision factors

• Spinal Instability Neoplastic Score (SINS) — guides need for stabilisation
• surgery ± RT preferred over RT alone when: spinal instability, single-site compression, prognosis ≥3 months, paraplegia duration <24 hours
• primary RT when: radiosensitive tumour (lymphoma, myeloma, SCLC), multilevel disease, poor surgical candidate

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brain metastases & leptomeningeal disease

• diagnosis — urgent MRI brain; if leptomeningeal disease suspected → MRI brain + whole spine ± LP (cytology, protein, glucose)
• management:
  • IV dexamethasone to reduce vasogenic oedema
  • consult neurosurgery + radiation oncology
  • seizure prophylaxis only if seizures have occurred (not routine)

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hypercalcaemia of malignancy

aetiologies

Always check PTH to exclude primary hyperparathyroidism — even in patients with known malignancy, concurrent pHPT is common enough to miss.

clinical effects beyond “stones, bones, groans, moans”

• hypertension — calcium-mediated vascular smooth muscle contraction; may require treatment with a CCB alongside correction of the hypercalcaemia
• sclerotic metastases and hypercalcaemia — osteoblastic lesions (prostate, carcinoid) store excess calcium in bone matrix; hypercalcaemia in prostate cancer is uncommon but when present typically signals very advanced disease with high tumour burden

management

1. aggressive IV hydration — isotonic saline 1–2 L bolus then 200–500 mL/hr, target urine output 100–150 mL/hr; lowers calcium ~0.25–0.375 mmol/L over first 24 hours alone; reassess for volume overload frequently
2. calcitonin 4–8 U/kg SC/IM q6–12h — onset 4–6 hours, drops calcium 0.25–0.5 mmol/L; bridge therapy only → tachyphylaxis within 48–72 hours
3. antiresorptive — same day:
   • zoledronic acid 4 mg IV — normalises calcium in 80–90% at 48–72 hours; requires dose adjustment if GFR <60 mL/min, avoid if GFR <30–35 mL/min (nephrotoxic); infuse over 30–60 min after rehydration
   • denosumab 120 mg SC — preferred in renal insufficiency (no renal dose adjustment); onset slower (3–10 days), duration longer (~104 days); FDA-approved for bisphosphonate-refractory hypercalcaemia of malignancy
4. loop diuretic — only after euvolaemia and only if volume overload risk; not routine
5. refractory/life-threatening — dialysis with low/calcium-free dialysate (especially with severe renal failure refractory to medical therapy), corticosteroids (especially 1,25-(OH)₂D-mediated / lymphoma)

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other emergencies (see dedicated notes)

• febrile neutropaenia — 60-minute antibiotic bundle, MASCC stratification, antifungal escalation
• tumour lysis syndrome — Cairo-Bishop criteria, rasburicase, electrolyte management
• immune checkpoint inhibitor toxicity — organ-specific irAEs, steroid management