Oncological Emergencies

SVCO

Definition, pathophysiology and aetiology

Superior vena cava obstruction (SVCO) is impaired venous return from the head, neck, upper limbs and upper thorax due to extrinsic compression, intraluminal tumour, thrombosis, or catheter/device-related stenosis. The SVC is a thin-walled, low-pressure vessel confined by rigid mediastinal structures; therefore even modest increases in mediastinal mass effect may substantially reduce flow. Symptoms reflect raised venous pressure above the obstruction and depend on rapidity of onset, site relative to the azygos vein, and development of collateral pathways via azygos, internal mammary, lateral thoracic, vertebral and oesophageal venous systems.

Malignancy accounts for most cases in oncology examinations. Bronchogenic carcinoma is the commonest cause, especially small-cell lung cancer (SCLC) and squamous non-small-cell lung cancer; lymphoma and metastatic mediastinal nodal disease are next most frequent. Benign causes are increasingly important: tunnelled central venous catheters, pacemaker/ICD leads, dialysis catheters and fibrosing mediastinitis. In cancer patients, thrombosis may coexist with extrinsic compression, and missing this distinction alters treatment.

Cause	Typical clues	Management implication
SCLC	Rapid onset; bulky mediastinal disease; chemosensitive	Histology before treatment if stable; chemotherapy often rapid response
NSCLC	Smoking history; hilar/mediastinal mass	Stent for severe symptoms; radiotherapy/systemic therapy according to stage/molecular profile
Lymphoma	B symptoms; high LDH; mediastinal mass	Avoid empirical steroids if possible because they may obscure histology
Catheter/device thrombosis	Indwelling line; arm swelling; no large mass	Anticoagulation ± thrombolysis/stent; line removal only if infected, non-functional or unnecessary

Clinical features and severity assessment

Classical features include facial plethora, periorbital oedema, distended neck and chest wall veins, upper limb swelling, dyspnoea, cough, hoarseness and headache worse on bending forward or lying flat. Cyanosis, stridor, syncope, confusion, visual disturbance or reduced consciousness indicate severe compromise from laryngeal/cerebral oedema or associated airway obstruction. Pemberton’s sign may be positive but is neither sensitive nor specific.

SVCO is often described as an oncological emergency, but immediate death from venous obstruction alone is uncommon; the true emergencies are airway compromise, cerebral oedema, haemodynamic instability, or rapidly progressive symptoms. The Kishi score, sometimes used to select patients for stenting, assigns points for neurological symptoms, laryngeal oedema, facial oedema, venous distension, arm oedema and dyspnoea; a score ≥4 has been used as a threshold for endovascular intervention.

Investigation

The key MRCP principle is: obtain tissue diagnosis before definitive oncological treatment unless the patient is unstable. Corticosteroids or radiotherapy can cause tumour necrosis and compromise histological diagnosis, particularly lymphoma. Baseline tests include FBC, U&E, LFT, calcium, coagulation screen, LDH, urate if high-grade lymphoma suspected, and group and save if biopsy/intervention is planned.

Contrast-enhanced CT chest extending to neck and upper abdomen is the investigation of choice: it defines the level and length of obstruction, collateralisation, thrombus, airway compression, mediastinal anatomy and biopsy target. Duplex ultrasound may identify upper limb/central venous thrombosis but is limited for intrathoracic SVC. CT venography is useful for procedural planning. Tissue may be obtained by bronchoscopy with endobronchial ultrasound-guided transbronchial needle aspiration, CT-guided biopsy, supraclavicular node biopsy, or pleural fluid cytology. Avoid blind mediastinoscopy in severe venous hypertension unless specialist-supported because bleeding risk is increased.

Immediate and definitive management

Initial measures are supportive: sit upright, administer oxygen if hypoxaemic, secure urgent oncology/respiratory/interventional radiology input, and assess airway. Intravenous access should preferably be in the lower limbs if severe obstruction, because upper limb infusions may not reach the central circulation reliably and may worsen oedema. Routine diuretics have weak physiological rationale and are not definitive; they may be considered only for coexistent fluid overload.

Intervention	Typical use	Key exam details
Endovascular SVC stenting	Severe symptoms, airway/cerebral compromise, need for rapid relief, or failure of oncological therapy	Symptom improvement usually within 24–72 h; technical success commonly >90%; patency improved by treating underlying malignancy
Dexamethasone	Suspected steroid-responsive tumour or oedema-related airway compromise	Common regimen: 8–16 mg/day PO/IV; avoid before biopsy if lymphoma suspected and patient stable
Radiotherapy	Radiosensitive tumour or palliation when stent unsuitable	Response usually days to weeks, not immediate; typical palliative schedules include 20 Gy in 5 fractions or 30 Gy in 10 fractions
Chemotherapy	SCLC, lymphoma, germ-cell tumour	Can produce rapid tumour shrinkage; requires histology and tumour lysis risk assessment
Anticoagulation	Confirmed thrombosis or post-stent according to local protocol	LMWH or DOAC if no contraindication; thrombolysis reserved for selected acute extensive thrombosis

Modern guidelines, including UK emergency oncology pathways and interventional radiology practice standards, emphasise stenting as the fastest method of symptomatic relief for life-threatening or very symptomatic malignant SVCO. Unlike radiotherapy, stenting does not preclude subsequent biopsy or systemic treatment, although venography and anticoagulation decisions require multidisciplinary discussion. Complications include stent migration, SVC rupture, pulmonary embolism, bleeding and restenosis; serious complications are uncommon but potentially fatal.

For stable patients, management should be histology-directed. SCLC and high-grade lymphoma may respond dramatically to systemic therapy, whereas NSCLC treatment depends on stage, performance status, PD-L1 expression and actionable mutations. In suspected lymphoma, empirical dexamethasone should be withheld unless airway or neurological compromise mandates it; if given, document timing and dose because even short exposure can reduce diagnostic yield.

High-yield examination points

• SVCO is most commonly malignant; lung cancer is the leading cause, but device-related thrombosis is increasingly recognised.
• CT with contrast is the pivotal diagnostic and staging investigation; tissue diagnosis should precede radiotherapy/chemotherapy if clinically safe.
• Immediate stenting is preferred for severe SVCO because it relieves symptoms within 1–3 days; radiotherapy is slower.
• Steroids are not universally indicated; they are most defensible in lymphoma, thymoma, germ-cell tumour or airway oedema, but may compromise lymphoma diagnosis.
• Use lower limb venous access in severe SVCO and actively look for coexistent thrombosis.

Spinal Cord Compression

Definition, mechanisms and anatomical patterns

Metastatic spinal cord compression (MSCC) is compression of the dural sac and spinal cord or cauda equina by direct tumour extension or metastatic disease, causing potentially irreversible neurological injury. It is an oncological emergency: neurological outcome is strongly determined by pre-treatment ambulatory status. Common primaries are breast, lung, prostate, renal cell carcinoma, myeloma and lymphoma; thoracic involvement is most frequent owing to the long thoracic segment and venous drainage via Batson’s plexus.

Mechanisms include vertebral body metastasis with posterior cortical breach and epidural extension, pathological vertebral collapse, paraspinal mass extension through neural foramina, intradural metastasis, and rarely haematoma or treatment-related instability. Injury is mediated by mechanical compression, venous congestion, vasogenic oedema, arterial compromise and demyelination; prolonged compression progresses to infarction, explaining why delayed decompression produces poor recovery.

Clinical recognition

Back pain is usually the earliest symptom and is classically severe, progressive, nocturnal, radicular or worsened by coughing/straining. Neurological features include limb weakness, sensory level, gait disturbance, hyperreflexia and extensor plantars for cord lesions; cauda equina involvement produces lower motor neurone weakness, saddle sensory change and bladder/bowel dysfunction. Sphincter disturbance and loss of ambulation are late adverse prognostic signs. A normal plain radiograph does not exclude MSCC.

Feature	Exam significance
Known cancer plus new severe spinal pain	MSCC until proven otherwise; urgent same-day specialist assessment
Motor weakness, sensory level, gait disturbance	Requires emergency MRI and corticosteroids unless contraindicated
Autonomic dysfunction	Late presentation; reduced likelihood of neurological recovery
Ambulatory at treatment	Best predictor of retaining walking ability

Investigation and classification

MRI of the whole spine with gadolinium is the investigation of choice because multifocal epidural disease occurs in approximately 20–35% of cases. NICE guidance recommends MRI within 24 hours for suspected MSCC, and urgently/immediately where neurological signs are present. MRI sensitivity and specificity for epidural compression are typically quoted above 90%. CT myelography is reserved for contraindication to MRI. CT is useful for bony anatomy and operative planning but is less sensitive for epidural soft tissue disease.

Score/classification	Components	Use
Bilsky ESCC scale	0: bone-only; 1a–c: epidural impingement without cord compression; 2: cord compression with CSF visible; 3: cord compression without CSF visible	Guides urgency and feasibility of radiotherapy versus decompression
SINS spinal instability neoplastic score	Location, pain, alignment, collapse, posterolateral involvement, lesion quality	0–6 stable; 7–12 potentially unstable; 13–18 unstable; surgical opinion if ≥7
Tokuhashi/Tomita scores	Performance status, metastases, primary tumour biology, visceral disease, neurological status	Estimate survival to select surgery versus palliative radiotherapy

Immediate management

Initial management is simultaneous rather than sequential: immobilise if mechanical instability is suspected, provide opioid analgesia, protect pressure areas, assess bladder retention, and involve oncology, neurosurgery/spinal surgery and radiology urgently. Do not wait for histology if there is established cancer and typical imaging.

Intervention	Typical regimen or threshold	Key caveats
Dexamethasone	16 mg orally/IV daily immediately, often 8 mg twice daily; continue during definitive treatment then taper over 1–2 weeks	Use PPI and glucose monitoring; avoid or discuss before steroids if lymphoma is strongly suspected and tissue diagnosis is needed, because steroids may lyse tumour and obscure histology
High-dose historical regimens	e.g. 96 mg/day dexamethasone	No clear functional superiority; higher rates of sepsis, psychosis, myopathy, hyperglycaemia and gastrointestinal bleeding
Venous thromboembolism prophylaxis	LMWH unless contraindicated	Immobility and malignancy confer high VTE risk; coordinate around surgery

Definitive treatment: surgery, radiotherapy and systemic therapy

Choice depends on neurological status, level and degree of compression, spinal stability, radiosensitivity, burden of disease, performance status and expected survival. Surgical decompression with stabilisation is favoured for single-level compression, spinal instability, vertebral collapse/retropulsion, radioresistant tumour, diagnostic uncertainty, or relapse after radiotherapy, provided expected survival is usually >3 months and operative fitness is acceptable.

The landmark Patchell randomised trial compared direct decompressive surgery plus postoperative radiotherapy with radiotherapy alone in selected patients with MSCC. Ambulation after treatment was superior with surgery plus radiotherapy (84% versus 57%), and among non-ambulant patients, recovery of walking occurred more often (62% versus 19%). The trial excluded very radiosensitive tumours and multilevel disease, so its results should not be overgeneralised.

Radiotherapy is appropriate for radiosensitive tumours, multilevel disease, poor surgical candidates, or stable spines without major bony retropulsion. Common schedules include 8 Gy single fraction, 20 Gy in 5 fractions, or 30 Gy in 10 fractions. Single-fraction treatment is convenient for limited prognosis; longer courses may improve local control in patients expected to survive longer. Lymphoma, myeloma, breast and prostate cancer are relatively radiosensitive; renal cell carcinoma, melanoma and sarcoma are more radioresistant, though stereotactic body radiotherapy may be considered in selected centres.

Systemic anticancer therapy is not the primary emergency treatment for cord compromise, but is important in chemosensitive disease such as lymphoma, germ-cell tumours and myeloma once compression is stabilised. Bisphosphonates or denosumab reduce skeletal-related events but do not acutely decompress the cord.

Prognosis and MRCP pitfalls

• Do not request plain radiographs first; urgent whole-spine MRI is the diagnostic standard.
• Steroids are immediate when neurological signs suggest MSCC, but consider withholding briefly only where lymphoma is suspected and biopsy is imminent.
• Ambulatory status at presentation is the central prognostic and exam discriminator.
• Back pain in cancer is MSCC until excluded, particularly if thoracic, nocturnal, radicular or rapidly progressive.
• Surgery is not only for “fit young patients”; instability, bony compression and radioresistant histology are key indications.

Tumour Lysis Syndrome

Tumour lysis syndrome (TLS) is a metabolic emergency caused by rapid tumour cell breakdown, releasing potassium, phosphate and nucleic acids. Purine catabolism generates hypoxanthine, xanthine and ultimately uric acid via xanthine oxidase; uric acid and calcium phosphate precipitation within renal tubules cause acute kidney injury (AKI), which further amplifies hyperkalaemia, hyperphosphataemia and hypocalcaemia. TLS is classically post-chemotherapy but may be spontaneous, particularly in high-grade haematological malignancy.

Risk factors and pathophysiology

Risk is determined by tumour biology, tumour burden and host renal reserve. Highest-risk settings are Burkitt lymphoma/leukaemia, lymphoblastic lymphoma, acute lymphoblastic leukaemia with WCC >100 × 10⁹/L, acute myeloid leukaemia with WCC >50 × 10⁹/L, bulky diffuse large B-cell lymphoma, highly chemosensitive germ-cell tumours and small-cell lung cancer. Additional risk factors include LDH >2 × upper limit of normal, bulky disease >10 cm, pre-existing CKD, dehydration, obstructive uropathy, baseline hyperuricaemia or hyperphosphataemia, and exposure to highly active agents such as venetoclax, obinutuzumab, rituximab-based regimens or intensive induction chemotherapy.

The dominant lethal complication is hyperkalaemia, causing malignant arrhythmia. Hyperphosphataemia produces secondary hypocalcaemia; calcium replacement is avoided unless symptomatic because it promotes calcium phosphate deposition. Uric acid nephropathy is favoured by acidic urine, but routine urinary alkalinisation is no longer recommended because it increases calcium phosphate precipitation and xanthine crystallisation, particularly if xanthine oxidase is inhibited.

Diagnostic classification

The Cairo–Bishop definition remains commonly examined. Laboratory TLS requires at least two biochemical abnormalities occurring from 3 days before to 7 days after cytotoxic therapy; clinical TLS requires laboratory TLS plus end-organ toxicity. Howard’s modification removed the requirement for a 25% change from baseline and emphasises simultaneous abnormalities and clinical relevance.

Criterion	Threshold used in Cairo–Bishop laboratory TLS
Uric acid	≥476 micromol/L, or ≥25% rise from baseline
Potassium	≥6.0 mmol/L, or ≥25% rise from baseline
Phosphate	≥1.45 mmol/L in adults, or ≥25% rise from baseline
Calcium	≤1.75 mmol/L, or ≥25% fall from baseline
Clinical TLS	Laboratory TLS plus creatinine ≥1.5 × upper limit of normal, seizure, cardiac dysrhythmia or sudden death

Prevention and monitoring

Management is risk-adapted and should begin before cytotoxic therapy. High-risk patients require inpatient monitoring, continuous ECG if potassium is rising, strict fluid balance and frequent biochemistry. Measure U&Es, calcium, phosphate, urate, creatinine and LDH at baseline; repeat 6–8-hourly in high-risk patients during the first 24–72 hours, and at least daily in lower-risk patients. Aim for urine output approximately 100 mL/m²/hour or >2 mL/kg/hour where feasible.

Intervention	Exam-relevant detail
Intravenous hydration	0.9% saline commonly 2–3 L/m2/day, adjusted for heart failure, renal impairment and age; avoid potassium-containing fluids.
Allopurinol	Xanthine oxidase inhibitor; prevents new uric acid formation but does not remove existing urate. Adult dose typically 300 mg/day orally in divided doses, adjusted in renal impairment; start 24–48 hours before therapy if possible. Important interactions: azathioprine/6-mercaptopurine dose reduction required; risk of severe cutaneous adverse reactions.
Rasburicase	Recombinant urate oxidase converting uric acid to allantoin, which is 5–10 times more soluble. Standard licensed dose 0.2 mg/kg IV daily for up to 5–7 days, but many protocols use single fixed doses such as 3 mg or 6 mg with repeat urate-guided dosing. Contraindicated in G6PD deficiency due to haemolysis and methaemoglobinaemia. Blood for urate after rasburicase must be transported on ice to avoid ex vivo uricolysis and falsely low results.

Rasburicase has rapid onset: plasma urate often falls within 4 hours. Trials in paediatric haematological malignancy showed markedly superior urate reduction versus allopurinol, with mean uric acid area-under-curve reduced by approximately 90% compared with around 12% for allopurinol in early comparative studies. Current UK and international guidance broadly reserves rasburicase for established TLS, high-risk disease, baseline hyperuricaemia, renal impairment, or when cytoreduction cannot be delayed.

Established TLS: emergency treatment

Established TLS is managed with senior haematology/oncology, nephrology and critical care involvement. Stop nephrotoxins, withhold further cytotoxic therapy if appropriate, maintain aggressive isotonic hydration, and give rasburicase unless contraindicated. Hyperkalaemia is treated according to standard emergency algorithms: IV calcium gluconate 10 mL of 10% solution for ECG changes, insulin–glucose, nebulised salbutamol, potassium binders and dialysis when refractory. Treat severe symptomatic hypocalcaemia with cautious IV calcium; otherwise avoid correction. Hyperphosphataemia is treated with dietary restriction, phosphate binders and renal replacement therapy if severe or associated with AKI.

Indications for urgent dialysis include refractory hyperkalaemia, severe hyperphosphataemia with symptomatic hypocalcaemia, fluid overload, uraemic complications, or worsening AKI despite optimal therapy. Continuous renal replacement therapy may be preferable in haemodynamically unstable patients and provides sustained phosphate and potassium clearance. For MRCP, remember: TLS is prevented by hydration plus urate-lowering therapy; allopurinol prevents urate formation, rasburicase removes existing urate; do not alkalinise urine routinely; and the immediate fatal abnormality is hyperkalaemia.

Neutropenic Sepsis

Definition, pathophysiology and risk stratification

Neutropenic sepsis is a time-critical oncological emergency: infection may be clinically occult because neutrophils generate much of the inflammatory phenotype. NICE defines suspected neutropenic sepsis as anticancer treatment within the previous 6 weeks plus either temperature >38°C or other features consistent with clinically significant sepsis, with neutrophils <0.5 × 10⁹/L or expected to fall below this. The absolute neutrophil count is calculated as total leucocyte count × neutrophil fraction; severe neutropenia is <0.5 × 10⁹/L and profound neutropenia is <0.1 × 10⁹/L. Risk rises sharply when neutropenia lasts >7 days.

The usual chemotherapy neutrophil nadir occurs at 7–14 days, although this varies by regimen. Mechanisms include marrow suppression, mucosal barrier injury with gut translocation, indwelling central venous catheter colonisation, corticosteroid-related immune dysfunction and altered microbiota from antibiotic exposure. Pathogens have shifted from predominantly Gram-negative bacilli to mixed epidemiology: Escherichia coli, Klebsiella and Pseudomonas aeruginosa remain critical because of rapid shock; Gram-positive infection is associated with lines, mucositis and quinolone prophylaxis; fungal infection, especially Candida and Aspergillus, is more likely with prolonged profound neutropenia.

Tool	Use	Key interpretation
MASCC index	Adult febrile neutropenia risk assessment	Maximum 26; score ≥21 suggests low risk for serious complications, but does not justify delaying antibiotics
CISNE score	Stable solid-tumour febrile neutropenia	Identifies low-, intermediate- and high-risk patients; not for unstable patients or haematological malignancy
Sepsis physiology	Immediate severity assessment	Hypotension, lactate ≥2 mmol/L, hypoxia, confusion or oliguria indicate high-risk sepsis/shock irrespective of fever

Immediate assessment and investigations

Management is simultaneous: broad-spectrum intravenous antibiotics within 1 hour of presentation is the exam-critical principle. Blood cultures should be taken first if this causes no delay: one peripheral set and one set from each central-line lumen if present. Investigations include full blood count, U&E, LFTs, CRP, coagulation, venous/arterial blood gas with lactate, urinalysis and culture, chest radiograph if respiratory symptoms, stool testing for Clostridioides difficile if diarrhoea, and targeted imaging for focal signs. Do not await neutrophil confirmation or imaging before treatment. Rectal examination and rectal temperatures are avoided because of mucosal trauma and bacteraemia risk.

Empirical antimicrobial therapy

Empirical therapy must cover Pseudomonas and other Enterobacterales. In UK practice, NICE CG151 supports piperacillin–tazobactam monotherapy as initial empiric treatment unless local resistance or allergy dictates otherwise. Beta-lactams exhibit time-dependent killing; prolonged or extended infusions may improve pharmacodynamic target attainment in septic or renally augmented patients, although local protocols govern administration.

Clinical situation	Typical regimen	Comments
Standard first-line	Piperacillin–tazobactam 4.5 g IV every 6 h	Adjust for renal impairment; covers Pseudomonas, anaerobes and many Gram-negatives
Severe sepsis, prior resistant Gram-negative, ESBL risk	Meropenem 1 g IV every 8 h	Carbapenem-sparing is desirable, but inadequate early cover increases mortality
Immediate severe beta-lactam allergy	Aztreonam 2 g IV every 8 h plus vancomycin or teicoplanin	Requires local microbiology input; aztreonam lacks Gram-positive cover
Suspected catheter infection, skin/soft tissue infection, pneumonia, haemodynamic instability, known MRSA	Add vancomycin, e.g. 15–20 mg/kg IV every 8–12 h with levels, or teicoplanin loading	Do not add glycopeptide routinely; unnecessary use promotes toxicity and resistance

Aminoglycosides are not routinely required for uncomplicated presentations, but may be added in septic shock or known resistant Gram-negative infection; gentamicin is commonly dosed at 5–7 mg/kg IV once daily with level monitoring. Renal function, prior colonisation, recent antimicrobial exposure and institutional antibiograms should drive escalation. Fluoroquinolone prophylaxis may be used in selected high-risk haematology patients, but breakthrough sepsis should be treated as potentially resistant.

Ongoing management, complications and de-escalation

Resuscitation follows sepsis principles: oxygen, crystalloid for hypoperfusion, vasopressors if shock persists, source control including line removal for tunnel infection, persistent bacteraemia, fungal infection or septic thrombosis. Persistent fever alone during the first 48–72 hours does not mandate automatic antibiotic change if the patient is stable; review cultures, drug levels, imaging and occult foci. If fever persists beyond 4–7 days with expected prolonged neutropenia, consider empirical or pre-emptive antifungal therapy, guided by CT chest, galactomannan, beta-D-glucan and haematology/microbiology advice. Options include liposomal amphotericin B 3 mg/kg IV daily, voriconazole for suspected aspergillosis, or an echinocandin for candidiasis.

Granulocyte colony-stimulating factor is not routine treatment for established uncomplicated neutropenic sepsis, but may be considered for profound neutropenia, pneumonia, invasive fungal infection, hypotension, multiorgan dysfunction or expected prolonged neutropenia. Filgrastim is commonly 5 micrograms/kg subcutaneously daily until neutrophil recovery; pegfilgrastim 6 mg once is used mainly prophylactically after chemotherapy cycles.

Mortality varies from approximately 5–20% and is highest with Gram-negative bacteraemia, shock and delayed therapy. De-escalation is individualised: low-risk, clinically stable patients may switch to oral therapy such as ciprofloxacin plus co-amoxiclav where appropriate; high-risk patients generally continue IV therapy until afebrile, cultures controlled and neutrophils are recovering, commonly >0.5 × 10⁹/L. MRCP pitfalls are delaying antibiotics for investigations, assuming absence of fever excludes sepsis, adding vancomycin routinely, and under-recognising abdominal, catheter and fungal sources.