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Cancer Care > Oncological Emergencies > Flashcards

Oncological Emergencies Flashcards

1
Q

What is neutropenic sepsis?

A

Life-threatening complication of anti-cancer treatment

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2
Q

When do you diagnose neutropenic sepsis

A

neutrophil count <0.5 and

temp >38 on 2 readings OR other signs/symptoms of sepsis

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3
Q

When does neutrophil count typically reach its lowest in sepsis?

A

5-10 days post chemo

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4
Q

What most commonly causes neutropenic sepsis?

A

Gram + cocci

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5
Q

When should you suspect a patient may have neutropenic sepsis?

A

Feeling unwell and having anti-cancer therapy

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6
Q

What questions must you ask a patient if you are worried about neutropenic sepsis?

A

Chemo regime - time since last dose
Recent blood products?
Lines in situ?

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7
Q

What do you examine on a patient with ?neutropenic sepsis?

A 
Cardio
Resp
Lymph nodes
Lines
focus on causes - GI exam
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8
Q

What investigations should you ask for if you queery sepsis?

A 
Neutrophil count
Culture from vein and any lines
Blood film
D-Dimer - DIC?
LFT U&amp;E CRP
Sputum culture
Urine analysis
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9
Q

How is neutropenic sepsis treated?

A

IV Tazocin (piperacillin with tazobactam)

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10
Q

A patient in hospital with neutropenic sepsis has been treated with IV tazocin for 2 days without change, what do you do?

A

Change antibiotic

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11
Q

A patient in hospital with neutropenic sepsis has been treated for 5 days but there is still no change, what do you do?

A

Consider fungi/parasite causes

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12
Q

How can neutropenic sepsis be prevented?

A

Prophylactic fluroquinolone
Dose reduction
Prophylactic G-CSF - not routinely offered
Stop treatment

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13
Q

When should anti-biotics be started?

A

As soon as you suspect sepsis! Don’t wait for blood results

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14
Q

What cancers commonly cause MSCC?

A

Lung
Breast
Prostate

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15
Q

How many patients tend to get MSCC?

A

10% of patients with spinal mets

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16
Q

What are the consequences of early MSCC?

A

Cord compression –> oedema –> venous congestion

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17
Q

What are the consequences of late MSCC?

A

Irreversible vascular injury –> cord necrosis

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18
Q

What signs are indicative of metastatic spinal cord compression?

A 
Back pain - worse on waking and aggravated by straining
Spinal tenderness
Limb weakness
Sensory loss
Incontinence
Generally unwell
Spasticity
Babinski +ve
Palpable bladder
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19
Q

What is the prognosis for MSCC?

A

30% live >1 year

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20
Q

How is MSCC investigated?

A

MRI within 24 hours

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21
Q

How is pain suggestive of metastases investigated?

A

MRI within week

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22
Q

How is MSCC managed?

A

Bed rest with neutral spine alignment need to be (log rolled)
Dexamethasone (unless lymphoma suspected)
Analgesia
Bisphosphonates (myeloma, breast and prostate mets only)
Definitive treatment: Decompression or radiotherapy within 24hrs
Supportive care - VTE prophylaxis, catheter, bed sore management, temperature checks

23
Q

What is the tole of radiotherapy in MSCC management?

A

Relieve compression of spine and nerves - cause cell death

Pain relief and stabilise neurological deficit

24
Q

When is SVCO seen?

A

External compression from Lung cancer but can be from lymphoma

25
Q

What signs and symptoms are indicative of SVCO?

A 
Breathlessness
Face and upper limb oedema
Headache
Choking sensation
Lethargy
Neck vein distention
Raised JVP
Increased RR
26
Q

How is SVCO investigated?

A

CXR - mass

CT contrast

27
Q

How is SVCO managed?

A

Steroids
Stent
Chemo/radio - depend on cause

28
Q

What is extravasation?

A

Leakage of IV drugs into extravascular space leading to nearby tissue damage

29
Q

Why are chemo agents susceptible to causing extravasation?

A

Poorly soluble in aqueous media and are vesicant

30
Q

How can extravasation be prevented?

A

Ensure IV fluid runs without resistance
Stop infusion if pain at injection site
Don’t leave infusion unattended if highly vesicant
Immediately stop infusion if suspicion

31
Q

How common is hypercalcaemia in cancer patients?

A

Affect upto 1/3

Esp. lung, breast, renal, myeloma and T cell lymphoma

32
Q

What is hypercalcaemia associated with?

A

Uncontrolled disease progression

33
Q

Why does hypercalcaemia occur?

A

Osteolysis
Humoral mediators
Dehydration

34
Q

Explain how cancers cause osteolysis and how this causes hypercalcaemia

A

Tumour cells of lytic bone mets produce cytokines to activate osteoclasts –> bone resoption –> increase calcium

Phosphate normally remain normal

35
Q

Explain how cancers affect humoral mediators and how this causes hypercalcaemia

A

systemic release factors which activate osteoclasts (PTHrP)

Phosphate low

36
Q

How does dehydration affect hypercalcaemia?

A

Exacerbate any underlying hypercalcaemia

37
Q

How does hypercalcaemia present?

A

Vague, non-specific symptoms

Can be acute or over long time

38
Q

What symptoms may be seen in hypercalcaemia?

A 
N&amp;V
Malaise
Drowsiness
Weakness
Depression
Anorexia
Abdo pain
Constipation
Pancreatitis
Polydipsia and dehydration
Renal colic - stones
Arrhythmias
39
Q

What investigations would be requested for hypercalcaemia?

A

Corrected serum Ca - allow for hypoalbuminaemia
Renal function
Electrolytes

40
Q

How is hypercalcaemia managed?

A

Rehydrate
Monitor
Bisphosphonates

41
Q

What electrolyte distubances are seen in tumour lysis syndrome?

A

Hyperuricaemia
Hyperphosphataemia
Hyperkalaemia
Hypocalcaemia

42
Q

When does tumour lysis syndrome occur?

A

Within hours to days of chemo

43
Q

What is tumour lysis syndrome?

A

Metabolic disturbances and renal impairment due to lysis of rapidly proliferating tumour cells

44
Q

Why do patients get hyperuricaemia in TLS? What does it cause?

A

Nucleic acids are released and metabolised

It causes crystal deposits in renal tubules –> AKI

45
Q

In TLS, what happens to phosphate and calcium and why?

A

Phosphate is released - high phoshpate

Phosphate precipitate with calcium - low calcium

46
Q

What do calcium phosphate precipitates lead to?

A

Calcium phosphate deposition in:

Renal tubules - AKI
Skin - Gangrene
Heart - Arrhythmia

47
Q

What complication can hyperkalaemia lead to?

A

Arrhythmias

48
Q

What are the main risk factors for TLS?

A

Large volume disease
Chemosensitive
Haematological malignancy
Poor renal function

49
Q

How can TLS be prevented?

A

Keep hydrated

Allopurinol or Rasburicase

50
Q

How is TLS managed?

A

Correct electrolytes
Monitor fluid balance
Assess need for haemodialysis

51
Q

What is the mechanism of action of allopurinol and rasburicase in regards to TLS

A

Allopurinol - prevents uric acid formation

Rasburicase - metabolises uric acid to allantoin which is water soluble and can be excreted by the kidneys

52
Q

How could you manage a suspected line infection?

A

Line locks - if not systemically very poorly can give high concentration abx (commonly gentamicin) through the line to sterilise it and save it from needing removal

53
Q

When would a bone scan for bony metastasis not be useful?

A

Multiple myeloma - bone scan works by picking up areas where there is increased uptake of radioactive traced indicating osteoblastic activity. Multiple myeloma produced purely lytic lesions so it is not useful.

54
Q

What should you do in a suspected line infection?

A 
Give Teicoplanin (provides gram +ve cover)
Can do line lock with high dose Gentamicin

Cancer Care (25 decks)

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