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Oncology > Oncological emergencies > Flashcards

Oncological emergencies Flashcards

Hypercalcaemia Superior Vena Cava obstruction Tumour lysis syndrome Neutropenic sepsis Spinal cord compression

1
Q

What is the formula for corrected calcium?

A

corrected [Ca] = measured [Ca] + {(40 - [albumin]) * 0.02}

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2
Q

What is classed as mild hypercalcaemia?

A

2.65–3.00mmol/L adjusted calcium

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3
Q

What is classed as moderate hypercalcaemia?

A

3.01–3.40 mmol/L adjusted calcium

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4
Q

What is classed as severe hypercalcaemia?

A

Adjusted calcium concentration is greater than 3.40 mmol/L

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5
Q

What are the causes of hypercalcaemia?

A
  1. Hyperparathyroidism (increased or normal PTH)
    If the PTH is normal or low:
  2. Malignancy
  3. Drugs - thiazides, high dose fit D, lithium
  4. Thyrotoxicosis
  5. Adrenal insufficiency
  6. Sarcoidosis or TB
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6
Q

How does hypercalcaemia typically present? Think about the different systems

A

BONES STONES MOANS and GROANS
Painful bones, renal stones, abdominal groans, psych moans
GI - abdo pain, vomiting, constipation, WL
GU - polyuria, polydipsia
NEURO - fatigue, weakness, confusion
PSYCH - depression

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7
Q

What are the tests for hypercalcaemia?

A
  • bloods, PTH
  • Mg2+, Ca2+ (+REPEAT!!)
  • ECG - shortened QT?
  • Imaging for bone mets
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8
Q

What is the acute management of hypercalcaemia

A
  1. Find cause
  2. Correct dehydration - 0.9% saline
  3. After - IV bisphosphonates (zolenronic acid, pamidronate)
  4. Rx cause
  5. Denosumab for raised Ca2+ of malignancy
  6. Furosemide
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9
Q

How does denosumab work

A

inhibits maturation of osteoclasts

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10
Q

How does furosemide work in hypercalcaemia? why does it have to be used cautiously

A

promotes renal excretion of Ca2+
BUT
can cause dehydration which worsens hypercalcaemia

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11
Q

What is the function of the SVC

A

venous drainage for head, neck upper limbs and upper thorax

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12
Q

Where does the SVC start and end

A

Starts at junction of L + R brachiocephalic veins to the R atrium

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13
Q

What structures surround the SVC

A 
sternum
trachea 
R bronchus 
aorta
pulmonary artery 
perihilar + paratracheal LNs
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14
Q

What are the causes of SVC obstruction

A
  1. Inside the vessel - thrombus, intravascular device
  2. Inside the wall - direct tumour invasion
  3. Outside the vessel (most common) - tumour: lung cancer, lymphoma, germ cell tumours, ALL. Fibrosing mediastinitis
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15
Q

What are the sx of SVC obstruction?

A 
SOB
Orthopnoea 
Chest pain
Cough, stridor 
Swelling (arm neck and face)
Feeling of fullness around their head
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16
Q

What are the signs of SVC obstruction?

A 
Dilated veins over arms, neck and anterior chest wall
Non-pulsatile elevated JVP
Oedema 
SRD
Cyanosis
Engorged conjunctiva 
Convulsions and coma
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17
Q

What test can be used to demonstrate SVC obstruction?

A

Pembertons - elevation of the arms to the side of the head causes facial plethora/cyanosis

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18
Q

How is SVC obstruction diagnoseD?

A

clinical diagnosis
CXR
CT used to describe anatomy

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19
Q

What is the management of SVC obstruction?

A
  1. Elevate head, O2 therapy, assess for hypoxia(ABG, sats)
  2. High dose dexamethasone 16mg/24h
  3. Balloon venoplasty + SVC stunting provides rapid relief of sx
  4. Treat cancer
  5. Anticoagulation
20
Q

What is tumour lysis syndrome?

A

abrupt release large quantities of cellular components into the blood after rapid lysis of malignant cells

21
Q

What are the RFs for TLS?

A
  • Hypovolaemia
  • Renal impairment
  • Rx sensitive tumours
  • High pre-rx urate lactate + LDH
22
Q

What are the causes of TLS?

A

chemotherapy for rapidly proliferating tumours (leukaemia, lymphoma, myeloma)

23
Q

How does TLS present?

A 
weakness
constipation 
vomiting + abdo pain (paralytic ileus)
palpitations 
chest pain, collapse
seizures 
AKI - reduced UO, lethargy, nausea
24
Q

What are the metabolic abnormalities found in TLS

A
  • Hyperuricaemia
  • Hyperphosphataemia
  • Hyperkalaemia
  • Hypocalcaemia
  • AKI - raised urea + creatinine
  • Renal impairment - uric acid + calcium phosphate crystals deposit in renal tubules causing AKI, exacerbated by concomitant intravascular depletion
25
Q

What are the key principles of management of TLS?

A
  1. Be aware of causes
  2. identify at risk patients
  3. Implement prophylaxis
  4. monitor during chemo
  5. start active rx when necessary
26
Q

How can TLS be prevented?

A

IV fluids
Rasburicase - recombinant urate oxidase
Allopurinol

27
Q

What is the acute treatment of TLS

A
  1. vigorous hydration
  2. Correct hyperkalaemia:
    i. IV calcium gluconate 10ml 10%
    ii. IV insulin + dextrose
    iii. Salbutamol 2.5mg nebs
    iv. calcium resonium
  3. Rasburicase (stop allopurinol)
  4. Acetazolamide - alkalinise urine as uric acid is more soluble at PH7 than pH 5
  5. Phosphate binders - treat raised phosphate
  6. Dialysis if severe
28
Q

What does TLS put pts at risk of

A

Arrhythmia and renal failure

29
Q

What is the definition of neutropenic sepsis

A

neutrophil count <1x10^9/L

30
Q

When does neutropenic sepsis require treatment?

A

temp ≥38 (oral)
OR
2 consecutive readings of ≥37.5 for 2 hrs AND neutrophil ≤1x10^9/L or expected to fall below this

31
Q

How does neutropenic sepsis present?

A
  1. infective sx or signs:
    - headache
    - vomiting
    - diarrhoea
    - flu like sx
    - productive cough
  2. Asymptomatic but febrile
  3. New clinical deterioration within 6 weeks of cytotoxic therapy
32
Q

What investigations would you do in neutropenic sepsis

A

i. FBC
ii. U+E, creatinine, LFT, CRP/ESR, coag screen
iii. blood cultures
iv. septic screen
v. +/- CXR
vi. clinically relevant swabs/cultures

33
Q

What is the management of neutropenic sepsis?

A

Use local guidelines or treat empirically with Tazocin
Aim to give w/in hr of pt getting to hospital
Assess risk of sepsis complications e.g. AKI, DIC, multiorgan failure

34
Q

How would u manage low risk and high risk neutropenic sepsis

A

LOW - oral abs, discharge after 24hr obs

HIGH - review daily, switch oral abs after 24-48hrs of IV rx if pt improving and then low risk

35
Q

How can neutropenic sepsis be prevented in a high risk pt on chemo

A

Fluoroquinolone

Granulocyte colony-stimulating factor (stimulates BM to produce white cells)

36
Q

How can neutropenic sepsis be prevented in the palliative setting

A

reduce chemo doses w subsequent cycles

37
Q

What level does the spinal cord terminate?

A

L1

38
Q

What spinal nerves are responsible for the knee jerk?

A

L3/4

39
Q

What spinal nerve is responsible for the ankle jerk?

A

S1

40
Q

what nerves make up the cauda equina?

A

L2-5, S1-5, Coccygeal nerve

41
Q

What are the causes of spinal cord compression?

A
  • malignancy - primary, secondary (most common)
  • Trauma
  • Disc prolapse
  • Inflammatory disease (esp. RA)
  • Spinal infection
  • Epidural or subdural haematoma
42
Q

How does spinal cord compression present?

A
  1. radicular pain
  2. limb weakness below level of compression
  3. difficulty walking
  4. sensory loss below level
  5. bowel/bladder dysfunction
43
Q

What tests would you do in spinal cord compression?

A
  1. FBC, U&E, LFTs (liver mets)

2. MRI WHOLE SPINE (within 24 hrs)

44
Q

What is the management of spinal cord compression?

A
  1. Analgesia
  2. High dose CS - dexamethasone 8mg BD
  3. Surgery - spinal decompression
  4. Radiotherapy (if can’t have surgery - common in palliative care)
  5. Chemo - if chemo sensitive
  6. Hormone deprivation - in newly diagnosed prostate cancer causing MSCC
  7. Bisphosphonates - metastatic bone pain
  8. VTE prophylaxis
  9. Pressure sore prevention
  10. Long term catheter
  11. Rehabilitation plan
45
Q

How determines prognosis of spinal cord compression?

A

severity of neurological deficit at time of presentation

46
Q

When is recovery expected to be uncommon in spinal cord compression?

A

if paraplegic and sphincter involvement

47
Q

Who is most likely to be affected by hypercalcaemia?

A

myeloma

those who have tumours that are likely to metastasise to the bone

Oncology (4 decks)

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