Cancer Care - Oncological Emergencies Flashcards
Metastatic Spinal Cord Compression (MSCC)
Spinal Metastases Pathophysiology of MSCC Clinical Features Medical Management General Management
- ) Spinal Metastases - back pain
- may present with spinal metastases before MSCC
- sx: unrelenting lumbar back pain, any thoracic or cervical back pain, worse with sneezing, coughing or straining, nocturnal, spinal tenderness
- a whole spine MRI should be done within 1 week
- suspect MSCC if there are any neurological features
- Mx: analgesia, bisphosphonates, radiotherapy - ) Pathophysiology - often occurs from extradural compression due to metastases in the vertebral body
- affects up to 5% of cancer patients, more common in patients with lung, breast and prostate cancer
- 2/3 of cases occur in the thoracic spine whilst the rest is often lumbosacral
- other causes: trauma, infection, disc prolapse, epidural haematoma - ) Clinical Features
- deep and localised back pain: earliest symptom
- lower limb weakness and stabbing radicular sensory disturbance at the level of the lesion
- L1 and above: UMN sx in the legs and a sensory level
- below L1: LMN sx in the legs, signs of CES
- hyperreflexia above the level of the lesion
- hypo/areflexia below the level of the lesion
4.) Medical Management - oncological emergency
- requires an urgent whole MRI spine within 24hrs
- high-dose PO dexamethasone 16mg BD w/ PPI cover,
to help reduce pressure and swelling around the SC
- tx depends on type of cancer, area of the spine affected, and the patient’s general fitness
- radiotherapy: most common
- surgical decompression: should occur w/in 48hrs
- ) General Management
- advised to lie flat and not move your spine: will be examined by physio to assess movement, may be given a collar/brace to help support the neck of spine
- complications: may have permanent paralysis, pain, difficulty moving, bladder changes, bowel changes
- help and support at home is available and would be organised before leaving the hospital
- prognosis: life expectancy is reduced (months)
Neutropenic Sepsis
Pathophysiology
Assessment
Investigations
Management
- ) Pathophysiology - temp >38.5°C (or 2x 38°C) in a patient with a neutrophil count of less than 0.5
- temp is often the only indication of a severe infection
- mainly in patients receiving cytotoxic chemotherapy
- risk factors: neutropenia expected to last > 7 days, clinically unstable, high-intensity chemo, underlying malignancy, significant co-morbidities - ) Assessment
- history: chemo and drug hx, localised sx (e.g. SOB, RLQ pain), PMH inc recent infections and abx used, latent infections, sick contacts, blood transfusions
- examination: A-E assessment, systems-based examinations, ENT, fundoscopy, DO NOT perform DRE until antibiotics are given) - ) Investigations - sepsis 6
- bloods: cultures (2 sets), FBC, CRP, LFTs, U+Es, ABG
- monitor urine output
- identify source of infection: CXR, sputum/urine/stool sample where indicated, swabs from indwelling lines, serology and PCR for viruses - ) Management
- URGENT Abx (don’t wait for WCC): IV Tazocin 4.5g TDS (IV meropenem if allergic)
- can stop antibiotics once the patient has been apyrexial for 48 hours and is no longer neutropenic
- add meropenem +/- vancomycin if still febrile and unwell after 48hrs
- consider antifungal therapy if not responding after 4-6 days (fungal chest infections not seen on CXR and may need HR-CT)
- consider prophylactic recombinant G-CSF e.g. filgrastim in patients at high risk of neutropenia, can be symptomatic in patient’s in early stages of their chemotherapy cycle
- consider prophylactic abx in those on high dose chemo (levofloxacin, acyclovir, posaconazole, Co-trimoxazole)
- can offer prophylactic fluoroquinolones (ciprofloxacin, levofloxacin etc.
Superior Vena Cava Obstruction
Pathophysiology
Clinical Features
Management
- ) Pathophysiology - compression of the SVC
- most common cause is lung cancer
- other malignancies: lymphoma, thymoma, metastatic seminoma, Kaposi’s sarcoma, breast cancer
- other: SVC thrombosis, aortic aneurysm, goitre, mediastinal fibrosis (chronic, can be asymptomatic for years) - ) Clinical Features
- sx can develop quickly over a few days to weeks
- dyspnoea: swelling around the trachea
- facial plethora: swelling and redness of the face, can also affect the neck, arms, hands, eyes (periorbital)
- headaches: worse in mornings or leaning forwards
- visual disturbance, dizziness
- dilated/engorged veins (neck and upper chest)
- pulseless jugular venous distension
- Pemberton’s sign: raising hands over the head for >1min precipitates facial plethora and cyanosis - ) Management - oncological emergency if SOB
- sit the patient up, oxygen, analgesia, sedatives
- short-term high dose (8mg) PO dexamethasone (reduces tumour oedema and laryngeal oedema)
- imaging: CXR, ultrasound or CT
- diuretics may be given w/ corticosteroids
- emergency treatment (treat resp distress/cerebral oedema): steroids, diuretics, endovascular stenting
- conservative tx: radiotherapy, chemo, surgery
- average life expectancy is 6 months
Tumour Lysis Syndrome (TLS)
What is it?
Pathophysiology
Clinical Features
Management
- ) What is it? - severe electrolyte disturbances from the breakdown of tumour cells due to treatment
- most common w/ chemotherapy but can also occur w/ steroid treatment, hormonal therapy, radiation etc
- ↑prevalence in high-grade lymphoma and leukaemia and cancers that respond very well to treatment
- prophylactic medication can be given to prevent the potentially deadly effects of tumour cell lysis - ) Pathophysiology - breakdown of tumour cells leads to the release of their intracellular contents:
- hyperkalaemia: release of K+ from cells
- hyperuricemia: release of purine from DNA in cells
- hyperphosphataemia: release of PO4- from cells
- hypocalcemia: Ca2+ binds to increased PO4- - ) Clinical Features
- occurs within 72hrs (3d) of treatment up to 7 days
- sx: lethargy, N+V, diarrhoea, anorexia, muscle cramps, syncope, pruritus, joint pains, paraesthesia and tetany, cardiac arrhythmias, seizures
- AKI: due to formation of urate crystals in renal tubules
- lab results: K+ >6mM, uric acid >0.475mM, phosphate > 1.125mM, calcium < 1.75mM - ) Management
- high risk: IV allopurinol OR IV rasburicase 48hrs before treatment to reduce effects of hyperuricemia
- allopurinol: xanthine oxidase inhibitor
- rasburicase: recombinant urate oxidase which metabolises uric acid to allantoin
- aggressive IV hydration (3L/24hrs)
- lower risk: PO allopurinol during chemo cycles
- acute Mx: consider dialysis
Hypercalcaemia
Pathophysiology
Clinical Features
Management of Mild Hypercalcaemia
Management of Mod/Severe Hypercalcaemia
- ) Pathophysiology
- malignancy is the most common cause in patients in hospital, this may be due to a number of processes:
- bone metastases, myeloma, PTHrP in NSCLC (SCC),
- primary hyperparathyroidism is the most common cause in non-hospitalised patients
- other potential causes of hypercalcemia include:
- dehydration, thyrotoxicosis, vitamin D intoxication
- acromegaly, Addison’s disease
drugs: thiazides, calcium-containing antacids
- granulomatous: sarcoidosis, TB, lymphoma - ) Clinical Features
- mild: asymptomatic, polyuria, polydipsia, mild cognitive impairment, dyspepsia
- moderate: dehydration, fatigue, weakness, nausea, constipation
- severe: abdominal pain, vomiting, pancreatitis, cardiac dysrhythmias, coma
- moans: constipation, N+V, ↓appetite, pancreatitis
- groans: confusion, delirium, poor conc, depression
- bones: pain, weakness, fractures, osteoporosis
- stones: kidney stones, AKI (nephrocalcinosis)
- other: secondary HTN, short QT interval on ECG, corneal calcification - ) Management of Mild Hypercalcaemia - Ca2+ <3mM and asymptomatic/mild symptoms (e.g. constipation)
- it does not require immediate treatment, but advise regular hydration to prevent stones, and to avoid:
- dehydration, prolonged bed rest/inactivity
- high calcium diet, calcium/vitD supplements
- dx: thiazide diuretics, lithium - ) Management of Mod/Severe Hypercalcaemia
- asymptomatic patients with chronic moderate ↑Ca2+ (3-3.5mM) may not require immediate treatment ^^^
- acute rise to >3.5mM requires aggressive treatment:
- 1.) aggressive IV hydration: 0.9% NaCl ≈ 3L/24hrs, consider loop diuretics in renal failure or HF
- 2.) IM/SC calcitonin: along with fluids, should lower serum Ca2+ within 12-48 hours
- 3.) IV zoledronic acid 4mg/15mins: long term control as it takes 2-4 days to become effective for 2-4 weeks
- renal impairment: consider slower infusion of bisphosphonates or consider denosumab instead
- 4.) Refractory Hypercalcaemia: if it returns after treating, has very poor prognosis
- prognosis of malignant hypercalcaemia is up to 1 yr
Diagnosis of a DVT
Clinical Features
Wells Criteria x10
Differential Diagnosis
- ) Clinical Features
- unilateral localised pain when weight bearing
- calf swelling or swelling of entire leg
- tender, oedema, redness, warmth, vein distension - ) Wells Criteria - assessment for suspected DVT
- whole leg swelling, swelling (>3cm), pitting oedema,
- collateral superficial veins, localised tenderness along distribution of deep venous system
- active cancer, previous DVT, recently bedridden or major surgery, recent immobilisation of lower limbs
- alternative diagnosis as likely (score -2) - ) Differential Diagnoses
- cellulitis, ruptured Baker’s cyst, compartment syn…
- right sided HF, lymphoedema, venous insufficiency
Suspected DVT: Diagnosis and Initial Management
Suspected DVT Likely
Suspected DVT Unlikely
Ultrasound Scan Positive
Ultrasound Scan Negative
- ) Suspected DVT Likely - wells score 2 and above
- proximal leg vein ultrasound scan within 4 hours, OR:
- scan within 24hrs + D-dimer test + interim anticoagulation - ) Suspected DVT Unlikely - D-dimer test
- interim anticoagulation if results will take > 4hrs
- if D-dimer positive, treat like suspected DVT likely
- if negative, stop anticoagulation - ) Ultrasound Scan Positive - diagnostic
- diagnose DVT and offer/continue treatment - ) Ultrasound Scan Negative - depends on D-dimers
- if positive D-dimers, stop anticoagulation and repeat scan 6-8 days later
- if negative D-dimers or second USS, stop anticoagulation and think about other diagnoses
Suspected PE: Diagnosis and Initial Management
PE Wells Score Suspected PE Likely Suspected PE Unlikely CTPA Positive CTPA Negative
- ) PE Wells Score
- 3: clinical features of DVT, most likely diagnosis
- 1.5: HR >100, previous DVT/PE, immobilisation for >3days or surgery in previous 4 weeks
- 1: haemoptysis, malignancy in last 6 months - ) Suspected PE Likely - wells score of 5 and above
- immediate CTPA (anticoagulation while awaiting) - ) Suspected PE Unlikely - D-dimer test
- interim anticoagulation if results will take > 4hrs
- if D-dimer positive, treat like suspected PE likely
- if D-dimer negative, stop anticoagulation - ) CTPA Positive - diagnostic
- diagnose PE and offer/continue treatment - ) CTPA Negative
- if DVT is suspected, consider proximal leg vein USS
- if DVT not suspected, stop any anticoagulation
Anticoagulation
General Information
Normal Usage of Anticoagulants
Active Cancer
- ) General Information
- perform bloods but start anticoagulation before results are available: FBC, U+Es, LFTs, clotting
- anticoagulation is for at least 3 months (up to 6 months in active cancer) and then reviewed
- in a PE with haemodynamic instability (sysBP <90), treat w/ UFH infusion and consider thrombolytic therapy with IV alteplase
- contraindicated if platelet count is <50 - ) Normal Usage of Anticoagulants
- 1°: apixaban OR rivaroxaban
- 2°: dabigatran/edoxaban (bridging therapy w/ LMWH)
- 3°: warfarin (w/ LMWH as bridging therapy for 5 days)
- severe renal impairment (eGFR <15m/min): DOACs are contraindicated so LMWH or UFH or warfarin (with bridging therapy w/ LMWH or UFH) are used - ) Active Cancer - this is defined as any cancer that has been diagnosed in the past 6 months OR receiving antimitotic treatment OR recurrent/metastatic/inoperable
- can use any DOAC and LMWH can be used on its own:
- 1°: consider a DOAC
- 2°: LMWH
- 3°: warfarin (with LMWH as bridging therapy for 5 days)