Oncology emergencies Flashcards
What are the main oncology emergencies?
Hypercalcaemia
Superior Vena Cava Obstruction
Tumour lysis syndrome
Neutropenic sepsis
Spinal cord compression
What is meant by corrected calcium?
40% of circulating calcium is bound to albumin, but labs only measured unbound calcium
Corrected calcium is calculated based on serum albumin levels
Your patient is hypercalcaemic.
Their PTH level is also high, what could be the cause?
Hyperparathyroidism
High PTH:
- Increases bone resorption
- Increases calcium reabsorption in kidneys
- Converts inactive vit D to active vit D which increases Ca absorption in intestine
What does the body do to correct low calcium?
Stimulate parathyroid hormone release
Which increases bone resorption and renal calcium reabsorption.
Also stimulates renal conversion of inactive vit D to active vit D, which increases intestinal calcium absorption.
These mechanisms restore the serum calcium to normal
Your patient is hypercalcaemic.
Their PTH level is normal, what could be the cause?
Malignancy
Drugs: thiazide diuretics, vit D
Endocrine: thyrotoxicosis, primary adrenal insufficiency
Granulomatous conditions: sarcoidosis, TB
How does malignancy cause hypercalcaemia?
Ectopic production of PTH or PTH-related peptide by tumour cells
Osteolytic (bone mets)
Ectopic calcitriol (active vit D)
Clinical presentation of hypercalcaemia?
Bones: pain
Stones: renal stones
Abdominal groans: nausea, constipation
Psychic moans: confusion, drowsy
Also:
- prologed QT
- pancreatitis
- coma
- muscle weakness
What investigations would you do for hypercalcaemia?
Bedside:
- Obs
- BMs
- ECG (Qt interval)
Routine:
- Bloods: FBC, U+E, Ca, CRP, LFT (esp alk phos), Clotting, PTH, TFTs
- XR
- Urine Ca and P
Specialist:
- CT
- MRI
Which blood tests are particularly important for hypercalcaemia?
Albumin and urea: if raised could indicate dehydration
Alkaline Phosphatase: if raised indicates bony mets, thyrotoxicosis
Calcitonin: if raised indicates possible B cell lymphoma
Acute management of hypercalcaemia in cancer patient?
- Rehydrate: 0.9% NaCl
- Bisphosphonates: pamidronate, zolendronic acid
- Treat underlying cause
How do bisphosphonates help in hypercalcaemia?
They inhibit osteoclasts so reduce bone absorption and turnover
This reduces Ca levels
How can you manage persistent hypercalcaemia in malignancy?
Denosumab: a monoclonal antibody drug which inhibits maturation of osteoclasts
Where does the SVC connect to at either end?
What does it do?
It runs from where R and L brachiocephalic veins join to the RA
It’s the venous drainage for the head, neck, upper limbs and upper thorax
What causes SVC obstruction?
Inside the vessel:
- thrombus
Inside the vessel wall:
- direct tumour invasion
Outside the vessel:
- tumour (lung cancer, lymphoma)
Clinical features of SVC obstruction?
SYMPTOMS: Dyspnoea Chest pain at rest Cough Neck and face swelling Arm swelling Dizzy Headache Visual disturbance Syncope
SIGNS:
Dilated veins over arms, neck and chest wall
Resp distress
Cyanosis
Investigations of SVC obstruction?
Clinical diagnosis
Usual bedside and routine
Specialist:
- CXR
- CT scan
- Contrast venography
Management of SVC obstruction?
Elevation of head
Oxygen therapy
High dose steroids
Endovascular stenting
Anti-coagulation if thrombosis
Treat tumour: chemo, radiotherapy
What is tumour lysis syndrome?
What causes it?
The abrupt release of large quantities of cellular components into the bloodstream following rapid lysis of the malignant cell
Caused by treatment
Or spontaneously, this commonly occurs in haematological malignancies like ALL, Burkitt’s lymphoma
What are the risk factors for tumour lysis syndrome?
Treatment sensitive tumours
Volume depletion (bleeding, dehydration)
Renal impairment
High pre-treatment lactate, urate, LDH levels
Clinical features of tumour lysis syndrome?
Weakness
Paralytic ileus: constipation, vomiting, abdo pain
Arrhythmias: palpitations, chest pain, collapse
Seizures
AKI: reduced UO, lethargy, nausea
What investigations would you do in suspected tumour lysis syndrome?
Bedside:
- UO
- Urinalysis
Routine:
- Bloods: FBC, U+E, serum LDH, urate, phosphate, Ca
What is LDH?
Lactate dehydrogenase
An enzyme the body uses in respiration (glucose -> energy)
Found in muscles, liver, heart, pancreas, kidneys, brain, blood cells
What would you see in bloods of someone with tumour lysis syndrome?
HypERuricaemia
HypERphosphataemia
HypERkalaemia
HypOcalcaemia
AKI: so raised creatinine, urea
Why does tumour lysis syndrome cause AKI.
Tumour lysis syndrome causes release of allsorts into the blood, including uric acid and Ca phosphate crystals
Deposition of both these in the renal tubules causes AKI
How can you prevent tumour lysis syndrome?
When should you think about doing this?
Before starting chemotherapy in an at-risk patient
- IV fluids
- Rasburicase: catalyses uric acid -> allantoin which is more soluble
- Allopurinol: blocks conversion of xanthines to uric acid
Management of tumour lysis syndrome?
Vigorous hydration
Correct high potassium:
- calcium gluconate
- IV insulin + dextrose
- salbutamol
Rasburicase: uric acid -> soluble allantoin
Acetazolamide: alkalinise urine b/c uric acid more soluble at higher pH
Phosphate binders
Dialysis in severe cases
What’s the treatment for raised potassium?
Fluids
Calcium gluconate
IV insulin + dextrose
Salbutamol nebs
Where does the spinal cord terminate and the cauda equina start?
Which important nerves does the cauda equina contain?
L1
Lumbar, sacral and coccygeal nerves
Which nerve roots control these reflexes?
Knee jerk
Ankle jerk
Which nerve roots control anal sphinchter?
L3, 4 keeps foot off the floor (knee jerk)
S1 (ankle jerk)
S2,3,4 keeps poo off the floor
What things can cause spinal cord compression?
Malignancy, more commonly secondary
Trauma
Disc prolapse
Inflammatory arthritis
Spinal infection
Haematoma
Clinical features of spinal cord compression?
Depends on where the lesion is
Radicular pain
Sensory loss below level
UMN signs:
- hypertonia
- weakness
- brisk reflexes
Only LMN signs if compression on the spinal nerves, so they’re often present at the level of the lesion only
What are UMN and LMN signs?
Which are UMN and LMN?
UMN (spinal cord)
- hypertonia
- brisk reflexes
- weakness
- no wasting or fasciculations
LMN (spinal nerves, all other nerves)
- hypotonia
- weakness
- absent reflexes
- wasting
- fasciculations
Signs of cauda equina?
Lower back pain
Perineal numbness
Loss of anal sphincter tone
Urinary retention
Where are the spinal nerves?
The nerves that come out of the spinal cord at each level, C1-L1
Investigations of possible spinal cord compression?
Urgent MRI of whole spine (within 24hrs)
Bloods: FBC, U+E, LFTs (could indicate liver and bone mets)
What are the red flag signs of cord compression?
Insidious onset
Gait disturbance
Clumsy, weak hands
Loss of sexual, bladder or bowel function
UMN signs in lower limbs
LMN signs in upper limbs
Sensory changes
Lhermitte’s sign: electric shocks
Management of spinal cord compression?
Analgesia
High dose corticosteroids: dexamethasone
Surgery, radiotherapy, chemo
Bisphosphonate for bone pain caused by mets
VTE prophylaxis
Manage bladder and bowel, catheterise
Refer to spinal rehab
Which cancer causes sclerotic bone mets?
What do these look like on XR?
Prostate
They look white and bright
Which cancers commonly metastasise to bone?
BLT + KP
Breast Lung Thyroid Kidney Prostate
A patient has is 9 days into their chemotherapy for breast cancer. They present with a fever and feeling generally unwell. What do you think?
Neutropenic sepsis!
What is neutropenic sepsis?
Chemotherapy can cause myelosupression
- leukopenia
- thrombocytopenia
- low red cell count
Neutropenia is low neutrophil count
Makes patients susceptible to serious infections
On what day of chemo is neutropenia most likely to happen?
Day 7-14
At what neutrophil count does a patient become susceptible to sepsis?
Below 1x10^9/L
Patients should be treated for neutropenic sepsis if they meet criteria, what criteria?
They have a temperature over 38
OR
A temp over 37.5 for two consecutive readings for two hours
AND
A neutrophil count below 1x10^9 or expected to fall below
Clinical features of neutropenic sepsis?
Fever
Any infective signs
Can have no symptoms except fever
Suspect it in all patients with new deterioration within 6 weeks of cytotoxic chemo
What infections can patients get when they’re neutropenic?
Meningitis Encephalitis Chest: pneumonia, empyema Liver abscess Gastroenteritis Pyelonephritis UTI Skin: cellulitis etc.
LINE INFECTION
Investigations of neutropenic sepsis?
Bedside:
- BM
- Obs
- Urinalysis
- ABG, VBG
Routine:
- Bloods: FBC, LFTs, U+E, lactate, CRP, ESR, Coag
- Cultures: blood, urine, faecal, sputum, swab
- CXR
Do a full septic screen
Management of neutropenic sepsis?
ANTIBIOTICS, do not wait until confirmed
Start within an hour of arrival at hosp
Empirical abx: tazocin +/- gentamicin
Low risk patients: oral abx, observe for 24hrs as inpatient
High risk: IV abx and review daily as inpatient, can switch to oral after 24-48hrs if improvement
Monitor for complications: AKI, DIC, organ failure
Supportive tx
How long should you give abx for in neutropenic sepsis?
When neutrophils have normalised, patient has been afebrile for 24 hours and cultures are negative
If patient is still neutropenic but they’ve been asymptomatic for 5-7 days abx can be stopped
How can you prevent neutropenic sepsis?
Prophylactic abx: a fluroquinolone (like cipro)
G-CSF: stimulate bone marrow to produce WBCs
Reduce chemo if palliative setting
What is the name of the drug which stimulates bone marrow to produce WBCs?
G-CSF
Granulocyte colony-stimulating factor
