Oncological emergencies Flashcards
Neutropenic sepsis.
a) Criteria for diagnosis
b) Neutropenia: risk factors and pathogens
c) Investigations and management of suspected neutropenic sepsis
d) Additional therapies that may be required
e) Who MAY be suitable for oral ABx?
f) Prophylaxis
a) 1. Neutrophils < 0.5 (at risk once count is < 1.0)
2. Fever > 38 C or signs of sepsis (hypothermia, CV collapse)
b) - Congenital: e.g. X-linked agammaglobulinaemia
- Acquired: chemotherapy, bone marrow infiltration (leukaemia, bone mets), aplastic anaemia, B12/ folate / iron deficiency, hypersplenism, immunosuppression (HIV, steroids, DMARDs, post-transplant/HSCT), Felty syndrome (RA, splenomegaly, neutropenia)
- Pathogens: G+ve cocci (staph aureus/epidermidis, strep pneumonia/pyogenes/viridans, etc.), G-ve bacilli (e.coli, klebsiella, pseudomonas), fungal (candida, aspergillus)
c) SEPSIS 6 within 1 hour: (BUFALO)
(if outside hospital, immediate 999 and alert on-call haematologist/ oncologist)
1. Oxygen to maintain SpO2 > 94% (and support airway)
2. Two large bore IV cannulae in each ACF, take 2x blood cultures and the following bloods:
- FBC, CRP, clotting (neutropenia, infection, DIC)
- UEs/creatinine and calcium (dehydration, AKI, electrolytes, tumour lysis, hypercalcaemia)
- Lactate, glucose, LFTs
3. Administer broad-spectrum IV ABx (eg. tazocin)
4. Administer fluid bolus for resuscitation (500 ml 0.9% NaCl) and maintenance fluids
5. Serial lactate measurements
6. Monitor urine output via catheter/fluid balance chart
Other investigations:
- Look for source: urine, indwelling lines/tubes, chest, skin, wounds, GI, etc.
- Bedside: urine dip (culture urine if catheterised)
- Imaging: ?CXR, ?CT
- Special tests: ?LP, ?sputum/stool/skin/line swabs
(note: signs of infection may be minimal in neutropenic patients)
d) - Macrolide in pneumonia (atypicals, eg. pseudomonas)
- IV antifungal if persistent fever with no identified cause
e) Those without a haematological cancer, who are minimally symptomatic, with no haemodynamic instability, and no infection of the lungs (pneumonia), soft tissues or indwelling catheter.
f) - Prophylactic ciprofloxacin in adults likely to have a prolonged period of neutropenia
- G-CSF to reduce duration of neutropenia (not used routinely)
Hypercalcaemia.
a) Cause: in malignancy, other
b) Symptoms - mild-moderate, severe, and chronic
c) Investigations
d) Explain corrected calcium level
e) Management
a) Malignant: osteolytic (bone mets, myeloma), ectopic PTH-related peptide production (e.g. SCC)
- Hyperparathyroidism: primary (mainly post-menopausal women; adenoma most commonly), secondary (kidney, liver, bowel disease causing low Ca2+), tertiary (CKD)
- Other: Vitamin D toxicity, thiazide diuretics, lithium, granulomatous conditions (sarcoid, TB)
b) Bones, moans, groans, stones, thrones…
- Acute (mild-mod): thirst, polyuria, confusion, constipation, fatigue, weakness
- Acute severe: acute abdomen, pancreatitis, arrhythmia, coma
- Chronic: depression, constipation, calcium deposits: nephrocalcinosis, nephrolithiasis, chondrocalcinosis (pseudogout)
c) - ECG: may have short QT (risk of arrhythmias)
- Bone profile: corrected calcium, phosphate, Alk Phos, albumin (add PTH)
- Imaging: XR affected bones (pepperpot skull in myeloma), ?CT KUB
d) - Uncorrected serum calcium measurement measures both unbound and bound calcium.
- Only unbound (ionised) calcium is physiologically active; the rest is inactive and bound to albumin.
- If albumin is low, the unbound (active) calcium will be raised; hence, corrected calcium accounts for low/raised albumin levels
e) - Asymptomatic/non-severe: consider ‘watch and wait’
- Manage AKI: fluids (0.9% NaCl) + furosemide if overload
- 1st line: IV bisphosphonates (eg. zoledronic acid)
- 2nd line: denosumab
- Treat underlying cause
Hypercalcaemia: spot diagnosis
a) Serum phosphate low, Alk Phos normal-high, PTH high
b) Serum phosphate low, Alk Phos high, PTH variable
c) Serum phosphate low, Alk Phos normal, PTH variable
d) Serum phosphate normal, Alk Phos low, PTH low
a) Hyperparathyroidism
b) Bony mets
c) Myeloma
d) Vit D toxicity
Calcium homeostasis.
a) How is it absorbed?
b) How is it excreted?
c) Low levels of calcium activate what hormone? Actions?
a) Via vitamin D in the gut
b) Via the kidneys
c) PTH:
- Increases osteolysis (Ca2+ and Pi release from bone),
- Increases renal reabsorption of Ca2+ / excretion of Pi
- Stimulates vitamin D production in the kidneys, which increases calcium uptake in the gut
Tumour lysis syndrome.
a) What is it? - characterised by what 4 metabolic findings?
b) Who is at-risk?
c) When does it typically occur?
d) Presentation
e) Investigations
f) Prevention
a) Severe metabolic disturbance caused by abrupt release of broken-down malignant cells into the blood:
- Hyperuricaemia, hyperkalaemia, hyperphosphataemia and hypocalcaemia
b) - Haematological malignancies, e.g. ALL, high-grade lymphoma (eg. Burkitt’s) - rapid turnover of cells
- Malignancies with rapid response to treatment
- Usually occurs following chemotherapy; may also occur post- radiotherapy, surgery or ablation procedures
c) - Typically, 1 - 5 days after starting chemotherapy
- Longer in solid tumours (days - weeks)
d) - The metabolic abnormalities may cause:
seizures, acute kidney injury and cardiac arrhythmias
e) - Bedside: ECG
- Bloods: FBC, biochemistry (K+, Ca2+, Pi, uric acid), urea and creatinine, lactate and LDH
- Note: high pre-treatment uric acid, LDH and lactate increase risk of developing tumour lysis syndrome)
f) PREVENTION:
- Identify at-risk patients (eg. haematological malignancy undergoing chemotherapy; high pre-treatment LDH, lactate and uric acid)
- Keep at-risk patients well-hydrated
- Intermediate risk: allopurinol (xanthine oxidase inhibitor)
- High risk: single dose of 3 mg rasburicase (recombinant urate oxidase)
g) Acute management:
- Hydration (no added K+, just NaCl 0.9%)
- Daily rasburicase infusion (+/- allopurinol)
- Calcium gluconate (if symptomatic hypocalcaemia)
- Cardiac monitoring
- Correct any metabolic abnormalities
- Dialysis if needed
Leukostasis.
a) What is it?
b) Who is at risk?
c) How might it present?
d) Management
a) - Very high WCC (usually blast cells) in the blood
- Leading to microvascular hypoperfusion, typically affecting the pulmonary and intracranial vasculature (note: similar to hyperviscosity syndrome, which is caused by a raised haematocrit/ paraproteinaemia)
b) Generally acute haematological malignancies (eg. ALL, AML)
c) - General : pyrexia, confusion
- Resp: hypoxia, SOB, pulmonary infiltrates
- Neuro: raised ICP (headache, papilloedema, reduced GCS), focal neurology, retinal haemorrhages
- Other: acute MI, acute limb ischaemia, AKI, DIC
d) - FBC: confirm very raised WCC
- Rapid cytoreduction: induction chemotherapy (preferred) or leukopheresis (if very high blast count)
- Prophylaxis of tumour lysis syndrome using hydration, allopurinol and rasburicase (and monitoring electrolytes)
Raised ICP.
a) Cancers most commonly metastasising to the brain
b) Monroe-Kellie doctrine and CPP
c) Features of raised ICP (early and late)
d) Triad of brain malignancy
e) Management
a) Lung, breast, melanoma
b) - Cranium is a fixed box (inelastic)
CPP = MAP - ICP
c) - Early: triad of headache (worse in morning, lying flat, Valsalva), vomiting (without nausea) and papilloedema
- Later signs: altered mental state, low GCS, weakness, CN palsies (III/VI most common), Cushing reflex
d) Raised ICP, new seizures, focal neurology
- Mets may bleed and cause acute presentation
e) - Urgent CT/MRI head to identify lesion
- A-E: stabilise airway (if GCS < 8, need support), oxygen and hyperventilation (aim for low CO2 to reduce ICP), HR and BP (Cushing), bloods (inc blood gas), assess GCS/ pupils/ neurology, avoid pyrexia (increases ICP)
- Raise head of bed
- Dexamethasone 8mg BD (8am and 12pm)
- Mannitol: osmotic diuresis
- Anticonvulsants if seizures present
- Further management: surgical, radiotherapy
Spinal cord compression.
a) Location (cord vs CES)
b) Causes - malignant vs. non-malignant
c) Presentation (cord vs CES)
d) Features typical of the pain in spinal mets
e) Management
a) - Above L1 (cord/ conus medullaris syndrome)
- Below L1 (cauda equina)
b) - Malignant*: bone tumours (primary, mets). myeloma, lymphoma, meningioma; also acute myelopathy caused by irradiation or paraneoplastic myelitis
* note: may be through direct extradural spread or secondary to crush fracture
- Non-malignant: trauma, herniated disc, fracture, epidural haematoma, epidural abscess, infection (HIV, TB, discitis), inflammatory causes (RA, sarcoid, late-stage AS)
c) - Cord: back pain, UMN signs* (spastic weakness, hyper-reflexia, hypertonia, Babinksi), sensory changes, Lhermitte’s sign, bladder, bowel and sexual dysfunction
- CES: back pain, LMN signs (bilateral sciatica, flaccid weakness, absent reflexes), bladder/bowel/sexual dysfunction, saddle anaesthesia, reduced anal tone
*note: acute myelopathy can cause spinal shock, presenting with initial LMN signs
d) - Location (cervical/thoracic pain rare in disc herniation)
- Pain increased when straining (coughing, crapping)
- Localised tenderness
- Nocturnal pain waking them from sleep
e) - Urgent MRI spine
- Dexamethasone 8mg BD (give PPI and monitor BMs)
- Urgent discussion with oncology and spinal surgeons
- Options: decompression/stabilisation and/or RT
- Prevention of VTE, pressure sores and infection
Superior vena cava obstruction (SVCO).
a) Causes - 85%? - other
b) Presentation
c) Management
a) 85% lung Ca; others: lymphoma, metastases
- Children: ALL, lymphoma
b) - Fullness in the face (especially on bending forward or lying down)
- Swelling of face, neck, arms, hands, and veins on chest
- Headaches, dizziness, blurred vision (and engorged conjunctiva)
- SOB, cough, CP
c) - CXR/CT to identify mass/ widened mediastinum
- Conservative: elevate head, oxygen
- Initial treatment: 8mg dexamethasone BD +/- diuretics
- Treatment of malignancy: chemotherapy/RT/surgery
- If severe (eg. stridor): stenting of SVC (intubate if required)
Syndrome of inappropriate ADH secretion (SIADH).
a) Causes (mnemonic: SIADH)
b) Criteria for diagnosis (triad)
c) Presentation
d) Should be suspected in all cancer patients presenting with…?
e) Management
a) Mainly pulmonary, CNS, malignant and drug-induced causes. SIADH:
- Small cell lung cancer/other malignancy (eg brain mets)
- Infection (pneumonia, TB, HIV)
- (sub)Arachnoid haemorrhage (and other CNS - head injury, SOL, meningitis, GBS, MS)
- Drugs: diuretics, SSRIs, ACEIs, PPIs
- Hereditary (rare)
b) - Euvolaemic hyponatraemia
- Low serum osmolality and raised urine osmolality
- Normal thyroid and adrenal function
c) - Often asymptomatic
- Hyponatraemia: anorexia, headache, cramps, nausea, vomiting, lethargy. Severe: reduced GCS, seizures
d) Hyponatraemia
e) - Investigate for cause (if unknown): CT TAP / CT head
- Treat underlying cause
- 1st line: fluid restriction
- 2nd line: demeclocycline (blocks ADH and induces partial nephrogenic diabetes insipidus)
- 3rd line: vaptans (eg, tolvaptan): vasopressin V2 receptor antagonists
Massive haemorrhage.
a) More likely with what cancers?
b) Presentation
c) Management - if treatment appropriate
d) Management - if palliative and likely terminal event
a) GI, ?lung, ?head and neck, haematological (low platelets)
b) - Overt bleeding
- Covert bleeding and shock / collapse, etc.
c) - A-E: gain access, take bloods, etc.
- Stop anticoagulation +/- vitamin K + PTC +/- TxA
- Transfuse (eg. FFP, red cells, cryo, PTC)
d) - Stop anticoagulation
- Dark towels
- Don’t leave the patient
- Midazolam 10 mg STAT
