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Cancer Care > Oncological Emergencies > Flashcards

Oncological Emergencies Flashcards

1
Q

What is neutropenic sepsis?

A

Fever > 38
Or features of sepsis

In a patient with a neutrophil count of < 0.5 x 10^9/L

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2
Q

What are the causes of neutropenic sepsis?

A

Genetic - congenital neutropenia, syndromes such as Chediak-Higashi

Cytotoxic related - therapies

Intrinsic disease of bone marrow; haematological malignancies, tumour infiltration, aplastic anaemia, ionising radiation

Immune mediated - uncommon, IBD inflammatory conditions, arthritides

Drugs stimulating formation of antibodies damaging granulocytes e.g. anti-thyroid drugs, carbimazole

Nutritional deficiencies e.g. folate and Vitamin B12

Increased neutrophil turnover - bone marrow cannot adequately replace them
Bacterial infections and hypersplenism

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3
Q

What are the causative organisms of neutropenic sepsis?

A

Most commonly bacteria
Gram neg - E Coli, Klebsiella, pseudomonas aeruginosa

Gram pos - S. epidermis, Staph aureus, strep pneumoniae

Other - c. diff

Viruses in high risk patients, usually prevented by prophylactic antiviral therapy
Otherwise herpes, varicella zoster, EBV - secondary to reactivation of latent infections

Fungi - Candida, aspergillus
Patients with haematological malignancies often require anti-fungal prophylaxis e.g. fluconazole

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4
Q

What are the clinical features of neutropenic sepsis?

A

Patients may have blunted response and subtle signs
High index of suspicion

Patients may present with signs for specific infection, or fever and non-specific symptoms

Temp >38 or hypothermia <36
Resp rate >20 breaths/min
Blood pressure systolic < 90
HR >90 BPM

Cognition - acute confusion
Urine output <0.5-1ml/kg/hr

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5
Q

What are the investigations for neutropenic sepsis?

A

Bedside
Obs, sugar, preg test

Bloods
VBG/ABG
FBC
CRP
U&Es
LFTs
Bone profile
Clotting
Fungal assays
BBV Screen
Cultures
Blood, line
Sputum, urine, stool
C diff
Viral PCR
Wound swabs

Imaging
CXR, LP, ECHO

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6
Q

What is the sepsis six bundle?

A

Three In

High flow oxygen target of 94-98 unless COPD 88-92
IV fluids, 500ml crystalloid over 15 mins
Abx empirical e.g. tazocin

Three Out
Two sets of blood cultures
Serum lactate via blood gas - arterial or venous
Urine output

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7
Q

What is the Multinational Association for Supportive Care in Cancer (MASCC) Risk Index?

A

Patients with neutropenic sepsis can be risk stratified with this

Disease Burden
5 none/mild
3 moderate
0 severe

Co-morbidities
5 No hypotension
4 No COPD
4 Solid tumour/haematological but no previous fungal infection
3 no dehydration needing IVF

If yes to any = 0

Status of onset
3 outpatient
0 inpatient

Age
2 less than 60
0 60 or older

LOW RISK > 21
HIGH RISK < 21

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8
Q

What is the treatment of neutropenic sepsis?

A

LOW RISK
Oral abx, consider outpatient care

HIGH RISK
IV abx, inpatient management

Identify source of infection
Sepsis 6

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9
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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10
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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11
Q

When should antibiotics be started for neutropenic sepsis?

A

As soon as suspected

Don’t wait for bloods

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12
Q

What is malignant cord compression?

A

Radiological evidence of indentation of the thecal sac secondary to cancer

or also cauda equina - collection of lumbar, sacral, coccygeal nerve roots descending from end of spinal cord at L1.

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13
Q

What can cause malignant compression of the spinal cord

A

Primary
Primary bone tumours
CNS malignancies

Secondary
Mets
Non-metastatic - mechanical structural weakness due to cancer
Paraneoplastic

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14
Q

What are other causes of cord compression important to recognise?

A 
Trauma
Intervertebral disc prolapse
Haematoma
Epidural abscess - secondary to osteomyelitis or discitis
Cervical spondylitic myelopathy
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15
Q

What cancers are most commonly associated with cord compression secondary to metastatic disease?

A 
Lung
Breast
Kidney
Prostate
Thyroid
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16
Q

Where do most cord compressions occur?

A

Thoracic - 60%

Lumbar 30%, cervical 10%

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17
Q

What are some of the causes of vertebral mets?

A

Arterial seeding
Shunting of blood through epidural venous plexus
Extension through intervertebral foramina

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18
Q

How many patients tend to get MSCC?

A

10% of patients with spinal mets

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19
Q

What are the consequences of early MSCC?

A

Cord compression –> oedema –> venous congestion

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20
Q

What are the consequences of late MSCC?

A

Irreversible vascular injury –> cord necrosis

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21
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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22
Q

How is MSCC investigated?

A

MRI within 24 hours

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23
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

Surgery
Decompression
Reconstruction

Vertebroplasty
Kyphoplasty
If unable to undergo full decompression and reconstruction

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24
Q

What is the role of radiotherapy in MSCC management?

A

Relieve compression of spine and nerves - cause cell death

Pain relief and stabilise neurological deficit

External beam radiotherapy as an adjuvant or definitive for those unable to undergo surgical intervention

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25
Q

What are the signs of cauda equina?

A 
Back pain
Radiculopathy
Reduced anal tone
Saddle anaesthesia
Painless retention of urine, change to urine/bowels
Paralysis
Hyporeflexia
Hypotonia
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26
Q

What is malignant hypercalcaemia?

A

Serum calcium >2.6 mmol/L

Secondary to malignant process

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27
Q

What is normal serum calcium?

A

Between 2.2-2.6 mmol/L

Mild is 2.6-3.0
Severe is >3.5

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28
Q

What are the most common malignancies associated with hypercalcaemia?

A

Breast cancer
Multiple myeloma
Lymphoma
Lung cancer e.g. squamous cell carcinoma

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29
Q

What are the three main mechanisms causing malignant hypercalcaemia?

A

Osteolytic metastasis
PTH related protein secretion
Increased 1.25-Vit D production

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30
Q

Why does PTHrP secretion cause hypercalcaemia?

A

Release of PTHrP from tumour cells e.g. breast carcinomas and non-Hodgkin’s lymphoma

Is structurally similar to PTH and leads to increased bone resorption
Distal renal tubular calcium absorption
Inhibition of proximal phosphate transport

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31
Q

How does osteolytic mets cause hypercalcaemia?

A

Commonly associated with breast cancer
Deposition of tumour cells in bone leads to local production of inflammatory cytokines and other mediators
Causes osteoclasts to be stimulated leading to bone resorption

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32
Q

In what malignancies can there be an increased production of 1.25-Vit D?

A

Increased Vit D leads to increased absorption of calcium

Hodgkin’s lymphoma

May also be seen in chronic granulomatous disease e.g. sarcoidosis

33
Q

What are the clinical features of malignant hypercalcaemia?

A

Stones, bones, groans, psychiatric moans

Mild - often asymptomatic
Polyuria, polydipsia, mild cog impairment, dyspepsia

Mod - all mild features
Constipation, weakness
Fatigue, dehydr, nausea

Severe
Abdo pain, vomiting
Cardiac dysrhythmias
Pancreatitis, coma

34
Q

What are the investigations needed for diagnosis of malignant hypercalcaemia?

A

Serum calcium level
Identification of underlying cancer

Biochemical markers can differentiate between primary hyperparathyroidism and malignant hypercalcaemia

In malignant hypercalcaemia, PTH should be suppressed

Full examination, breast exam
Investigations targeted to any potential cause
Myeloma screen - immunoglobulins, protein electrophoresis, urinary light chains

Imaging e.g. CT

35
Q

What is the management of malignant hypercalcaemia?

A

Intravenous rehydration
Calcitonin and bisphosphonates

Admission for any patient with serum calcium >3mmol/L or if symptomatic and lower
and underlying malignancy

If underlying malignancy cannot be addressed - likely to recur within 2 weeks

Additional therapies e.g. glucocorticoids, denosumab, dialysis

36
Q

What is the function of calcitonin?

A

Mod or severe hypercalcaemia

Promotes urinary calcium excretion and inhibits bone resorption

37
Q

How do bisphosphonates work?

A

Analogues of inorganic pyrophosphate
Absorbed onto the surface of the bony network
Inhibit the action of osteoclasts

Pamidronate or zoledronic acid

38
Q

What is the anatomy of the SVC?

A

Provides venous drainage for the upper limbs, head and neck

Originates posterior to lower aspect of right first costal cartilage
at union of right and left brachiocephalic veins

Descends to join the right atrium, valveless

39
Q

What are the most common causes of SVCO?

A

Lung carcinoma most commonly NSCLC

Non-Hodgkin’s

40
Q

What is the pathophysiology of SVCO?

A

Obstruction results in formation of collateral vessels

  • azygous system
  • internal mammary
  • long thoracic

therefore if slow progressing obstruction, adequate time for collaterals and so mild symptoms

41
Q

What are the clinical features of SVCO?

A 
Symptoms
Dyspnoea, facial swelling
Head 'fullness', headache
Symptoms exacerbated bending forwards/lying down
Cough, blurred vision
Dysphagia
Signs
Facial swelling
Distended neck and chest wall veins
Upper limb oedema
Facial plethora
Cyanosis
Cognitive dysfunction
Coma
42
Q

What is Pemberton’s sign?

A

Elevate both arms above head for 1-2 mins

Positive sign - causes congestion, cyanosis or resp distress

Occurs due to increased venous return from upper extremities exacerbating obstruction

43
Q

How can SVCO be diagnosed?

A

80% have abnormal CXR
Need to see underlying cause

Findings include mediastinal widening, malignant pleural effusion

CT shows extent and level of obstruction and collateral vessels

Duplex USS in those with indwelling catheters

May need biopsy for malignant cause

44
Q

What is the emergency management of SVCO?

A

Rare, to treat respiratory distress or cerebral oedema
Stridor may be present

Senior review, peri-arrest

Diuretics
Steroids
Related to thrombus - stent, not related - thrombolysis

45
Q

What is the general management of SVCO?

A

Relieve obstruction
Imaging and histology

Elevation of head and neck
Oxygen titrated to sats

Stenting
Radiotherapy - NSCLC, lymphomas
Chemo

Anticoag or thrombolysis may be used if SVCO occurs secondary to intravascular thrombosis

Glucocorticoids may help reduce swelling; dex

Stent placed percutaneously, access via internal jugular, basilic or femoral veins

46
Q

When is SVCO seen?

A

External compression from Lung cancer but can be from lymphoma

47
Q

What is extravasation?

A

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

48
Q

Why are chemo agents susceptible to causing extravasation?

A

Poorly soluble in aqueous media and are vesicant

49
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

50
Q

How does dehydration affect hypercalcaemia?

A

Exacerbate any underlying hypercalcaemia

51
Q

What is tumour lysis syndrome?

A

Results from metabolic disturbances
arising from the breakdown of malignant cells
following initiation of treatment for malignancy

52
Q

What electrolyte abnormalities are seen in TLS?

A

Hyperkalaemia
Hyperphosphataemia
Hypocalcaemia
Hyperuricaemia

Phosphate produced by tumour cells binds to calcium

53
Q

What factors are associated with increased risk of TLS?

A

High proliferation rate
Chemosensitivity
Large tumour burden

Pre-exisitng metabolic abnormalities e.g. hyperuricaemia and hyperphosphataemia
Renal impairment

54
Q

Who is at low risk of TLS?

A

<1% chance of developing TLS

AML with certain WBC, LDH criteria
CLL with WBC and tx criteria
Multiple myeloma
CML
NHL normal LDH
Other solid tumours
55
Q

Who is at an intermediate risk of TLS?

A

Certain NHLs with high LDH and absence of bulky disease
Certain early stage NHLs
ALL, AML, CLL with certain WBC, LDH, Tx criteria
Bulky tumours highly sensitive to chemo e.g. germ cell, small cell

56
Q

Who is at high risk of developing TLS?

A

Burkitt’s leukaemia
Certain Burkitt’s lymphoma

ALL with certain WBC, LDH
AML with high WBC
Certain NHLs with high LDH and bulky disease

Intermediate risk with evidence of high risk clinical factors e.g, renal dysfunction

57
Q

What is the pathophysiology of tumour lysis syndrome?

A

Cytotoxic mediated lysis of tumour cells
Release of intracellular components

Hypocalcaemia develops secondary to hyperphosphataemia with precipitation of calcium in soft tissues

Can lead to AKI

58
Q

What are the clinical features of TLS?

A

Tend to develop within the first 72 hours following tx initiation

Can occur up to 7 days post treatment

Symptoms
Lethargy, N&V, diarrhoea
Anorexia, muscle cramps, syncope, pruritus, arthritis

Signs
Fluid overload, haematuria, tetany, paraesthesia, bronchospasm

59
Q

What are the investigations for TLS?

A

Renal function, electrolytes, serum urate to diagnose and assess severity

High risk patients may need serial bloods every 4-6 hrs

Urine dip, microscopy - uric acid crystals
Serum lactate, LDH
ECG, cardiac monitoring

Serum urate levels in patients on rasburicase sent on ice to prevent falsely low levels

60
Q

What is required for a laboratory diagnosis of TLS?

A

Cairo Bishop definition - lab definition and clinical def

Presence of two or more abnormal serum values that occur three days prior to or seven days after beginning treatment

61
Q

What clinical diagnosis is needed for TLS?

A

Meets lab diagnosis
Presence of one or more features not due to therapeutic agent

Serum creatinine >1.5 upper limit normal
Cardiac arrhythmias/sudden death
Seizure

62
Q

What hypouricaemic agents are given to prevent TLS?

A

Prevent hyperuricaemia and the subsequent precipitation of uric acid in nephrons

Allopurinol - xanthine oxidase inhibitor
Does not act on pre-existing uric acid so is prophylactic

Rasburicase 
Recombinant urate oxidase
Metabolises uric acid
Works on established renal deposits
Contraindicated with G6PD deficiency
63
Q

What is involved in prophylaxis of TLS?

A

Low risk - oral hydration and monitor

Intermediate - saline, allopurinol up to 600mg OD
TLS screen

High risk - saline; aim for UO >100ml/hour, rasburicase, TLS screen

64
Q

What is involved in the management of TLS?

A

Calcium glutinate, insulin, dextrose for hyperkalaemia

Hypouricaemic agents
Phosphate binders
IV hydration

65
Q

What are some indications for haemofiltration in TLS?

A

Intractable fluid overload
Refractory hyperkalaemia
Hyperphosphataemia induced symptomatic hypocalcaemia
High calcium phosphate product

66
Q

What do calcium phosphate precipitates lead to?

A

Calcium phosphate deposition in:

Renal tubules - AKI
Skin - Gangrene
Heart - Arrhythmia

67
Q

What are the main risk factors for TLS?

A

Large volume disease
Chemosensitive
Haematological malignancy
Poor renal function

68
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

69
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.

70
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
71
Q

What are the most common causes of central line associated blood stream infections?

A

Coagulase negative staphylococci e.g. S epidermidis

Enteroccoci

72
Q

Who does the risk of neutropenic sepsis increase with?

A 
Prolonged neutropenia >7 days
Severity of neutropenia
Significant comorbidities
Aggressive cancer
Central lines
Mucosal disruption
Hospital inpatient
73
Q

What are the most common responsible pathogens for neutropenic sepsis?

A

From endogenous flora
Gram positive cocci from indwelling catheters promoting colonisation

Staph aureus, epidermidis, enterococcus, streptococcus
MRSA and vancomycin resistant enterococcus increasingly prevalent

74
Q

When do you need to give empirical IV antibiotics in neutropenic sepsis?

A

Within the hour

75
Q

Where is the most common site of MSCC?

A

Thoracic

Below L2 vertebra = caudal equina

76
Q

Who is likely to be fit for surgery for MSCC?

A 
Fit and good prognosis
Multiple myeloma, lymphoma, breast, prostate, renal cancers
Good motor function at presentation
Good performance status
Limited comorbidity
Single level spinal disease
Absence of visceral mets
Long interval from primary diagnosis
77
Q

What is the management of SVCO?

A 
Sit upright/elevate head
Oxygen
Dexamethasone 16mg plus PPI
Opioids
Benzodiazepines

Treatment
Steroids
Stent if not radio or chemo sensitive
Anticoag if thrombus

78
Q

What are other potential oncological emergencies?

A 
Toxicity with newer oncological treatments e.g. immune checkpoint inhibitors - pneumonitis, colitis
Seizures
SIADH
PE
Non-neutropenic sepsis
Massive haemorrhage
Uncontrolled pain

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