Oncological Emergencies

Question 1

Do you have to have a fever to have neutropenic sepsis?

Answer 1

Some chemo patients can’t mount a fever due to corticosteroid use so do not rule out due to apyrexial.

Question 2

What are the risk factors for neutropenic sepsis?

Answer 2

Most commonly neutropenia occurs 10-14 days post treatment
Most common in haematological malignancies
Significant co-morbidities
Systemic and progressing disease
Indwelling catheters or central lines
Mucosal disruption
Inpatient

Question 3

What organisms often cause neutropenic sepsis?

Answer 3

Majority are endogenous flora
Gram -ve cocci increasingly common especially indwelling plastic lines/catheters
Staph Aureus, Epidermidis, Enterococcus and streptococcus

Question 4

What are the clinical features of neutropenic sepsis?

Answer 4

Suspect in anyone receiving chemo (or within 6 weeks of receiving) who feels unwell
Temperature >38
Neutrophil count <0.5
Can present septic

Question 5

What investigations should be done in a patient you suspected has neutropenic sepsis?

Answer 5

FBC, Us and Es, LFTs, CRP and Lactate 
Blood culture as well as urine and sputum where appropriate 
ABG
Clinically relevant imaging 
Examine indwelling catheters 
Central and PICC lines
Skin wounds and mouth

Question 6

How is neutropenic sepsis managed?

Answer 6

Fluid resuscitation
Broad Spectrum antibiotics (Tazocin and consider Meropenem if no improvement in 48 hours) – start immediately do not wait for results
Culture and routine bloods
Oxygen
Monitor urine output
Lactate
Consider GCSF (granulocyte colony stimulating factor such as filgrastim or
perfilgrastim)
If still unwell after 4-6 days then consider fungal investigation

May need alteration to chemo in future e.g. dosage, GCSF or stop.

Question 7

What should you give prophylactically if someone is at high risk of neutropenic sepsis?

Answer 7

Consider prophylaxis with fluoroquinolone if it is likely neutrophil count will drop below 0.5

Question 8

What is metastatic spinal cord compression?

Answer 8

More commonly due to collapse of the spinal vertebrae or compression of nerves. Direct tumour invasion into the vertebral column rare. Common to have more than 1 place involved and remember it is cauda equina if below L2 and not spinal cord compression.

Question 9

What are the initial and prolonged effects of spinal cord compression?

Answer 9

Initial compression causes venous congestion, oedema and demyelination which are reversible.

Prolonged compression leads to vascular injury, cord necrosis and permanent damage.

Question 10

What are the risk factors for spinal cord compression?

Answer 10

Metastatic disease

Especially: prostate, lung, myeloma and melanoma

Question 11

What are the clinical features of metastatic cord compression?

Answer 11

Back pain (95%)
Pain with straining, straight leg raising, coughing or sneezing
Limb weakness – flaccid paralysis progressing to spasticity with increased tone, clonus and hyperreflexia. Reflexes are absent at level of the lesion. Above L1 compression = Upper motor neuron signs, below L1 compression = lower motor neuron sign
Difficulty walking
Sensory loss
Bowel/bladder dysfunction (bladder retention)

Question 12

How should suspected spinal cord compression be investigated?

Answer 12

MRI (preferred over CT) – within 24hours if symptomatic or within 1 week if just pain suggestive of spinal mets

Question 13

What is the management of spinal cord compression?

Answer 13

Dexamethasone (with PPI protection and BM monitoring) NOT IF LYMPHOMA)
Bisphosphonates - alendronic acid
Analgesics
Refer for surgical opinion (only if fit, single lesion and no other visceral metastasis). Can be actually stabilising with metal or balloon kyphoplasty.
Radiotherapy – most common due to extensive disease and poor reserve.

If reduced mobility, consider thromboprophylaxis

Question 14

What is superior vena cava obstruction?

Answer 14

Compression of SVC due to lung or lymph node involvement of cancer that causes compression or thrombosis. This results in reduced venous return to the heart.

Question 15

What are the risk factors for vena cava obstruction?

Answer 15

Central lines (venous thrombosis)
Malignancy
Lung, lymphoma, breast, thymoma and germ cell tumours

Question 16

What are the clinical features of superior vena cava obstruction?

Answer 16

SOB, orthopnoea, stridor, choking sensation and cyanosis
Venous congestion in head neck and arms
Raised JVP and engorged veins
Headache and fullness in the head

Question 17

How should vena cava obstruction be investigated?

Answer 17

CT chest

Consider heart failure differential

Question 18

How is superior vena cava obstruction managed?

Answer 18

Prop up to improve breathing
Give oxygen
Dexamethasone
Balloon venoplasty
SVC stenting
Chemotherapy or radiotherapy depending on the cancer sensitivity
(Chemo and radio for small cell, just radio for non-small cell)

Question 19

What is tumour lysis syndrome?

Answer 19

Release of electrolytes due to rapid turnover of cells that causes organ dysfunction. Primarily urate is the problem but can also get hyperkalaemia, hyperphosphataemia and hypocalcaemia.

Question 20

What are the risk factors for tumour lysis syndrome?

Answer 20

Usually after starting treatment but can be just due to steroids
Leukaemias, Lymphomas and Myelomas 
Testicular tumours  
Rarely in small cell and breast
Recent initiation of chemo treatment 
Pre-existing renal problems 
Dehydration and hypovolaemia

Question 21

What are the clinical features of tumour lysis syndrome?

Answer 21

Arrythmias and Heart failure
Kidney failure (from urate and/or calcium phosphate crystals) causing haematuria, oliguria or anuria
Diarrhoea and anorexia
Lethargy

Usually day 3-7 post chemotherapy
Can rarely be primary presentation ‘spontaneous tumour lysis’

Question 22

How is tumour lysis syndrome managed?

Answer 22

Pre-rehydration and vigorous hydration throughout treatment
Close monitoring of Us and Es
Allopurinol orally to low risk groups (xanthine oxidase inhibitor reducing urate)
Allopurinol IV or Rasburicase IV (synthetic uricase that degrades urate to allantoin which is water soluble) just before and during chemotherapy treatment prophylactically

Question 23

How do you measure calcium when suspecting hypercalcaemia?

Answer 23

Must use corrected calcium levels as it is highly protein bound and will change with albumin levels.

Question 24

What are the risk factors for hypercalcaemia?

Answer 24

Myeloma
Any cancer that spreads to bone and is osteolytic
Squamous cell carcinomas (lung, H&N, Kidney and Cervix)

Question 25

What is the most common oncological emergency?

Answer 25

Hypercalcaemia is the most common metabolic abnormality in cancer with a high mortality rate.

Question 26

What causes hypercalcaemia?

Answer 26

80% paraneoplastic phenomenon of PTH related peptide
20% osteolytic metastases
Tumour production of Calcitriol – negligible

Question 27

What are the clinical features of hypercalcaemia?

Answer 27

Weight loss 
Anorexia and nausea
Polydipsia and polyuria 
Constipation 
Abdominal pain 
Dehydration 
Weakness 
Confusion
Seizure 
Coma

Question 28

How should hypercalcaemia be managed?

Answer 28

Aggressive rehydration
Bisphosphonates e.g. zoledronic acid or pamidronate (help bone pain and increase osteoblastic activity). Given IV and Calcium should normalise over 3 days
Calcitonin – rapid but short-term effect but tolerance can develop
Loop diuretics and steroids are other options.
Long term – control underlying malignancy

Question 29

What causes raised ICP in cancer?

Answer 29

Usually as a result of brain metastases.

Question 30

What cancers most commonly metastasise to the brain causing raised ICP?

Answer 30

Most common in: Lung, breast colorectal and melanoma

Question 31

What are the clinical features of raised ICP?

Answer 31

Headache that’s worse in the morning or when bending down 
Focal neurological signs 
Ataxia 
Seizures
Nausea and vomiting 
Papilloedema

Question 32

How should suspected raised ICP be investigated?

Answer 32

CT head

Question 33

What is the management of raised ICP?

Answer 33

Dexamethasone to reduce cerebral oedema 
Stereotactic radiotherapy (will need dex still due to localise inflammation for radiation)

Discussion with neurosurgery

Question 34

What are the risk factors for bowel obstruction in cancer?

Answer 34

Bowel Cancer

Metastatic disease

Question 35

How does bowel obstruction present?

Answer 35

Abdominal Pain
Distention
Anorexia
Absolute constipation of both flatus and solids
Vomiting
Symptoms generally worsen over time
Can get overflow diarrhoea secondary to bacterial overgrowth in blocked faecal matter

Question 36

How should bowel obstruction be investigated?

Answer 36

Abdominal X-ray

3D CT reconstruction

Question 37

How is bowel obstruction managed in cancer patients?

Answer 37

NG tube for decompression and symptoms relief
Surgical resection (only if single obstruction)
Stenting if not fit for surgery (only if single obstruction)
Gastric decompression with PEG if needed (venting percutaneous gastrostomy)
If rectal may not resect due to complicated anatomy and instead form a defunctioning colostomy

Question 38

What medications can be useful to give to someone with bowel obstruction and cancer?

Answer 38

Anti-secretory medications – Octreotide (somatostatin analogue) or anticholinergics such as glycopyrronium and buscapan
Dexamethasone may have its uses
Stool softeners and anti-emetics

Question 39

What is hyper-viscosity syndrome?

Answer 39

Increase in plasma viscosity due to protein or cells in the blood. Note different cells and proteins have varying levels of stickiness so for some it takes only a small increase to cause Hyperviscosity whilst for others it takes a lot more.

Question 40

What causes hyperviscosity syndrome?

Answer 40

Polycythaemia haematocrit > 50
Leucocytosis >100
Immunoglobulins in myeloma
Drugs such as COCP, diuretics, IV IG, erythropoietin, chemo and radio-contrast media

Question 41

What are the clinical features of hyperviscosity syndrome?

Answer 41

Lethargy and confusion 
Reduced cognition and CNS disturbance 
Chest pain 
Abdominal pain 
Spontaneous GI/GU bleeding 
Faints 
Visual disturbances (like looking through watery car window)

Question 42

How is hyperviscosity syndrome managed?

Answer 42

Urgent treatment 
Fluids 
Treatment of underlying cause 
Polycythaemia – venesection 
Leucocytosis – leukapheresis usually with hydroxycarbamide 
Plasmapheresis of non-cellular component

Question 43

What scoring system is used to diagnose tumour lysis syndrome?

Answer 43

Diagnosis made by the Cairo-Bishop scoring system when 1 or more laboratory finding – raised urate, phosphate, potassium, or low calcium and 1 or more clinical finding – increased creatinine (1.5 x normal), cardiac arrhythmia or seizure.