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Year 4 Cancer Care and Haem > Oncological Emergencies > Flashcards

Oncological Emergencies Flashcards

1
Q

Define Neutropenic Sepsis

A

Potentially life threatening complication of anti cancer and immunosuppressive treatment

Temperature greater than 38 degrees/any signs or symptoms of sepsis in someone with an absolute neutrophil count of <0.5x10^9

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2
Q

Define Febrile Neutropenia

A

Presence of fever in a person with Neutropenia
Two consecutive readings of more than 38 degrees for two hours

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3
Q

Give four causes of Neutropenic Sepsis

A

Chemotherapy
HSCT
Drugs (Immunosupressants, Clozapine)
Bone Marrow Failure

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4
Q

How does Neutrophil count vary with chemotherapy?

A

Neutrophil count typically lowest 5-10 days after last chemotherapy dose and recovery is normally 5-10 days later

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5
Q

What are the normal infective organisms in Neutropenic Sepsis?

A

S.Pyogenes, S.Aureus. S. Enterococcus, S.Pneumoniae

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6
Q

Other than chemotherapy, give four risk factors for Neutropenic Sepsis

A

Age (Infants and Over 60s)
Corticosteroids and Abx
Central Venous Access device
TPN (increased fungal risk)

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7
Q

How should you assess a patient with suspected Neutropenic Sepsis?

A

Temperature history (may present with hypo)
Focus on current symptoms
Cancer and Chemo History
Recent Abx/Steroid use

A to E

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8
Q

How quickly should Sepsis 6 be started in Neutropenic Sepsis?

A

Within one hour

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9
Q

What is the first line antibiotic in Neutropenic Sepsis?

A

Tazocin

Meropenem if Pen Allergic

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10
Q

Other than the Sepsis 6, what investigations can be done if Neutropenic sepsis is suspected?

A

CXR
Urine Culture
Sputum Culture
Swab any lines

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11
Q

What is Spinal Cord Compression?

A

Occurs as a result of metastatic/spinal tumour growth that either directly or indirectly causes impingement of spinal cord

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12
Q

Name 5 cancers that have the highest incidence of spinal cord compression

A

Myeloma
Prostate
Nasopharynx
Breast
Lung

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13
Q

Describe the pathophysiology of Malignant Compression

A

Primary (Primary Bone Tumours, CNS malignancy)

Secondary (Metastatic, Non Metastatic - mechanical weakness secondary to cancer, paraneoplastic)

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14
Q

Give three possible mechanisms of metastatic spread to spine

A

Haematogenous arterial seeding

Shunting of abdominal venous flow to epidural plexus by Valsalva

Extension through intervertebral foramen

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15
Q

Name three non malignant causes of Spinal Cord Compression

A

Trauma
Disc Prolapse
Haematogenous

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16
Q

Describe the common distribution of Spinal Cord Compression

A

60% Thoracic
30% Lumbar
10% Cervical

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17
Q

How can a Spinal Cord Compression above L1/2 present?

A

95% severe progressive pain
85% weakness
Upper Motor Neurone lesion picture

May have peripheral paraesthesia

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18
Q

How would a Cauda Equina compression present?

A

LMN pattern (normally unilateral)

Saddle Anaesthesia, Reduced Anal Tone, Painless Urinary Retention, Impotence, Absent Ankle Jerk

Lower back pain

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19
Q

What is the gold standard investigation for Spinal Cord Compression?

A

MRI

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20
Q

Describe the general management of Spinal Cord Compression

A

Analgesia using WHO ladder
VTE Prophylaxis
Catheter for any bladder dysfunction
High dose Dexamethasone

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21
Q

Describe the definitive management of Spinal Cord Compression

A

Surgical decompression and reconstruction ideally (if not then vertebroplasty and kyphoplasty)

+/- External Beam Radiotherapy or Stereotactic Body Radiotherapy

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22
Q

Define Malignant Hypercalcaemia

A

Serum Calcium >2.6mmol/l secondary to a malignant process

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23
Q

Describe the normal distribution of Calcium

A

99% Bone, 0.1% Extracellular, 0.9% Intracellular

Extracellular: 50% Ionised (Active), 41% Bound, 9% Complexed

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24
Q

Name three hormones involved in the balance of Calcium

A

Vitamin D
Calcitonin
PTH

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25
Q

What molecule must Calcium be corrected for and how?

A

Albumin
0.1 mmol added for every 4g/l below 40 that the albumin is

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26
Q

State the parameters of severity in Malignant Hypercalcaemia

A

Mild = 2.6 -3 mmol/l
Mod = 3-3.5 mmol/l
Severe = >3.5mmol/l

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27
Q

What four cancers is Malignant Hypercalcaemia most commonly associated with

A

Breast Cancer
Multiple Myeloma
Lymphoma
Lung Cancer (SCC)

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28
Q

What three mechanisms cause Malignant Hypercalcaemia?

A

PTHrP (Breast and Non Hodgekins)
Osteolytic Mets
Increased Activation of Vitamin D (Hodgekins Lymphoma)

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29
Q

How do Osteolytic Metastases cause Hypercalcaemia?

A

Deposition of tumour cells leads to local production of inflammatory cytokines, causing osteoclast stimulation

30
Q

Malignant Hypercalcaemia can be entirely asymptomatic. How would mild Hypercalcaemia present?

A

Polydipsia
Polyuria
Confusion

31
Q

How is Malignant Hypercalcaemia investigated?

A

Based on measurement of serum calcium and identifying underlying cancer
PTH should be low

32
Q

If Serum Calcium is >3mmol or they are symptomatic, how is Malignant Hypercalcaemia managed?

A

Admit
IV Rehydration, Calcitonin and Bisphosphonate Therapy

33
Q

If Serum Calcium is <3mmol or they are symptomatic, how is Malignant Hypercalcaemia managed?

A

Outpatient management with oral rehydration (3-4L/d) and regular review

34
Q

What is Superior Vena Cava Obstruction?

A

Obstruction of the flow of blood through the Superior Vena Cava secondary to cancer

35
Q

Describe the anatomy of the Superior Vena Cava

A

Venous drainage of upper limbs, head and neck
Valveless Structure

36
Q

Name two cancers classically causing SVCO

A

Lung Carcinoma
NHL

37
Q

Why is it of benefit to the patient if the SVCO is gradual?

A

Allows collateral vasculature to form

38
Q

State three symptoms of SVCO

A

Dyspnoea
Facial Swelling
Head Fullness

39
Q

State three signs of SVCO

A

Facial Swelling
Distended Vein
Facial Plethora

40
Q

What is Pemberton’s Sign for SVCO?

A

Patient asked to raise both arms above head for 1-2 minutes
Positive result is congestion, cyanosis, and respiratory distress

41
Q

How is SVCO investigated?

A

CXR (>80% have an abnormality)
CT is diagnostic (shows extent of obstruction, presence of collateral vessels, and staging of any lung cancer)

42
Q

What is the Emergency Management of SVCO?

A

Normally if patient is in RDS or has Cerebral Oedema

Diuretics +/- Steroids
Stent (+/- Anticoagulation)

43
Q

What is the non emergent management of SVCO?

A

Elevation of Head and Neck
Titred Oxygen
Radiotherapy
Stent
Steroids (if steroid responsive)

44
Q

What stents can be used in SVCO?

A

Balloon Expandable and Self Expanding
Percutaneously inserted

45
Q

SVCO is a poor prognostic indicator. If this is their first presentation then what is the life expectancy?

A

6 months

46
Q

What is Tumour Lysis Syndrome?

A

Metabolic disturbances caused by breakdown of malignant cells following initiation of treatment for malignancy

47
Q

What electrolyte abnormalities come from rapid cellular breakdown?

A

Hyperkalaemia
Hyperphosphataemia
Hypocalcaemia
Hyperuricaemia

Can cause AKI and arrhythmias

48
Q

Name four risk factors for Tumour Lysis Syndrome

A

Haematological Malignancy
Chemosensitivity
Large Tumour Burden
Renal Impairment

49
Q

Why is risk stratification important in Tumour Lysis Syndrome?

A

Assesses need for prophylactic therapy and monitoring

50
Q

Describe the pathophysiology of Tumour Lysis Syndrome

A

Hypocalcaemia develops secondary to hyperphosphataemia with precipitation in soft tissues

Hyperuricaemia occurs due to metabolism of nucleic acids

Leads to AKI due to precipitation of uric acid and calcium phosphate in renal tubules

51
Q

What is the onset of Tumour Lysis Syndrome?

A

Normally within 72 hours of treatment (but can occur up to seven days)

52
Q

How does Tumour Lysis Syndrome present?

A

Lethargy, Nausea and Vomiting, Diarrhoea, Anorexia, Muscle Cramps

Generally presents as the electrolyte abnormalities that are caused

53
Q

What bloods would you want to do for suspected Tumour Lysis Syndrome?

A

Renal Function
Electrolytes
Serum LDH
Serum Lactate

If high risk, repeat every 4-6 hours

54
Q

Diagnosis of Tumour Lysis Syndrome is based on the Cairo Bishop Definition which divides into lab and clinical definition. What is the lab definition?

A

Two or more abnormal serum values occurring 2 days before treatment or up to 7 days after

55
Q

Diagnosis of Tumour Lysis Syndrome is based on the Cairo Bishop Definition which divides into lab and clinical definition. What is the clinical definition?

A

One of:
Serum Creatinine >1.5 times upper limit
Cardiac Arrhythmia/Sudden Death
Seizure

The above criteria form basis of graded severity

56
Q

Describe the production of Uric Acid

A

Purines get converted to Hypoxanthines

Xanthine Oxidase converts Hypoxanthine into Xanthine and Uric Acid

57
Q

What two agents can be used against Hyperuricaemia in Tumour Lysis Syndrome?

A

Allopurinol (only useful as prophylaxis as cannot act against existing uric acid)

Rasburicase (converts uric acid into soluble allontoin)

58
Q

How would Hyperphosphataemia in Tumour Lysis Syndrome be managed?

A

Hydration and Dietary Restriction
Phosphate Binders
Severe - Haemofiltration

59
Q

How would Hypocalcaemia in Tumour Lysis Syndrome be managed?

A

Mild - Do not treat, as calcium phosphate deposits could form in kidney

Symptomatic - IV replacement

60
Q

What prophylaxis would you give a low risk patient for Tumour Lysis Syndrome?

A

Oral Hydration
Monitor

61
Q

What prophylaxis would you give an intermediate risk patient for Tumour Lysis Syndrome?

A

Saline
Allopurinol

62
Q

What prophylaxis would you give a severe risk patient for Tumour Lysis Syndrome?

A

Saline
Rasburicase

63
Q

When would you consider Haemofiltration in Tumour Lysis Syndrome?

A

Intractable fluid overload

Refractory Hyperkalaemia

Hyperphosphataemia induced symptomatic hypocalcaemia

64
Q

Describe Virchow’s Triad

A

Venous Stasis
Endothelial Dysfunction
Hypercoaguable state

65
Q

Why does Cancer predispose patients to venous stasis?

A

Prolonged immobility
Direct compression of tumour

66
Q

Why does Cancer predispose patients to Hypercoaguablity?

A

Malignant cells themselves are hypercoaguable and can induce normal cells to be hypercoaguable (by cytokine and adhesion alteration)

67
Q

What is the Khorana Risk Model?

A

Validated screening tool to assess patients VTE risk and whether they need prophylaxis.
Determines the risk of VTE at 2.5 month follow up

68
Q

What are the parameters for Khorana Risk Model?

A

Site (2 if stomach/pancreas, 1 if lung/lymphoma/gynae/GU)
Platelet > 350
Leucocyte > 11
Hb < 100
BMI > 35

69
Q

What score from the Khorana Risk Model indicates the need for prophylaxis?

A

Greater than or equal to three

70
Q

How is VTE in oncology managed?

A

DOAC (standard duration is 6 months but should be re-evaluated)

71
Q

How would Moderate Hypercalcaemia present?

A

Constipation
Fatigue
Weakness

72
Q

How would severe Hypercalcaemia present?

A

Abdominal Pain
Nausea and Vomiting
Pancreatitis
Arrhythmias (short QT, J waves)

Year 4 Cancer Care and Haem (16 decks)

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