Cancer Care - Oncological Emergencies Flashcards

1
Q

Metastatic Spinal Cord Compression (MSCC)

Spinal Metastases
Pathophysiology of MSCC
Clinical Features
Medical Management
General Management
A
  1. ) 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
  2. ) 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
  3. ) 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

  1. ) 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Neutropenic Sepsis

Pathophysiology
Assessment
Investigations
Management

A
  1. ) 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
  2. ) 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)
  3. ) 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
  4. ) 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Superior Vena Cava Obstruction

Pathophysiology
Clinical Features
Management

A
  1. ) 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)
  2. ) 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
  3. ) 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Tumour Lysis Syndrome (TLS)

What is it?
Pathophysiology
Clinical Features
Management

A
  1. ) 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
  2. ) 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-
  3. ) 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
  4. ) 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hypercalcaemia

Pathophysiology
Clinical Features
Management of Mild Hypercalcaemia
Management of Mod/Severe Hypercalcaemia

A
  1. ) 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
  2. ) 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
  3. ) 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
  4. ) 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Diagnosis of a DVT

Clinical Features
Wells Criteria x10
Differential Diagnosis

A
  1. ) Clinical Features
    - unilateral localised pain when weight bearing
    - calf swelling or swelling of entire leg
    - tender, oedema, redness, warmth, vein distension
  2. ) 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)
  3. ) Differential Diagnoses
    - cellulitis, ruptured Baker’s cyst, compartment syn…
    - right sided HF, lymphoedema, venous insufficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Suspected DVT: Diagnosis and Initial Management

Suspected DVT Likely
Suspected DVT Unlikely
Ultrasound Scan Positive
Ultrasound Scan Negative

A
  1. ) 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
  2. ) 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
  3. ) Ultrasound Scan Positive - diagnostic
    - diagnose DVT and offer/continue treatment
  4. ) 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Suspected PE: Diagnosis and Initial Management

PE Wells Score
Suspected PE Likely
Suspected PE Unlikely
CTPA Positive
CTPA Negative
A
  1. ) 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
  2. ) Suspected PE Likely - wells score of 5 and above
    - immediate CTPA (anticoagulation while awaiting)
  3. ) 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
  4. ) CTPA Positive - diagnostic
    - diagnose PE and offer/continue treatment
  5. ) CTPA Negative
    - if DVT is suspected, consider proximal leg vein USS
    - if DVT not suspected, stop any anticoagulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Anticoagulation

General Information
Normal Usage of Anticoagulants
Active Cancer

A
  1. ) 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
  2. ) 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
  3. ) 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly