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Cancer care > Oncological Emergencies > Flashcards

Oncological Emergencies Flashcards

1
Q

What is neutropenic sepsis?

A

Neutrophil count of 0.5 x 109 per litre or lower (check guidelines), plus:

Temp > 38oC

Other signs consisent with significant sepsis

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2
Q

What are some other terms for neutropenic sepsis?

A

Febrile neutropenia

Neutropenic fever

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3
Q

How does neutropenia predispose to infection?

A

Neutrophils are key component of the innate immune system

Lack of signs / symptoms causing isolated pyrexia

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4
Q

What are some causes of neutropenia?

A

Recent chemo (within 7-10 days) due to BM suppression

Malignant bone marrow infiltration

Extensive radiotherapy

Bone marror failure secondary to non-malignant disease (e.g. aplastic anaemia)

Hypersplenism

Megaloblastic anaemia

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5
Q

What increases the risk of developing neutropenic sepsis?

A

> 60

Advanced malignancy

Previous neutropenic sepsis

Mucositis (entry for bacteria)

Poor performance status

Co-morbidities

Indwelling central venous catheters

Corticosteroids (causing immunosuppression)

Prolonged hospital admission

Severe neutropenia

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6
Q

What are some non-specific symptoms of neutropenic sepsis?

A

Fatigue

Feeling warm / cold

Rigors / shaking

Sweaty / clammy

Palpitations

Dizziness

Confusion / disorientation

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7
Q

What symptoms may reflect a specific infective source in neutropenic sepsis?

A

Chest: SoB, cough, chest pain, sore throat

Urine source: dysuria, increased frequency, urgency, LUTS

Skin: rashes, blisters, pain

GI: diarrhoea, nausea, vomiting, rectal bleeding, abdo oain, sore mouth (mucositis)

Indwelling line source: pain around the line

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8
Q

What may the clinical findings in neutropenic sepsis be?

A

Haemodynamic instability (hypotension, tachycardia, tachypnoea, hypoxia)

Fever

Reduced urine output

Mottled / ashen appearance

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9
Q

What may be the examination findings of an identifiable source in neutropenic sepsis?

A

Chest: increased work of breathing, crepitations, dullness to percuss, reduced air entry

Urine: suprapubic / flank pain, cloudy urine in catheter bag

Skin: rashes, blistering, tenderness

GI: abdo tenderness, dehydration, evidence of oral mucositis, jaundice

Indwelling line source: surrounding erythema, tenderness on palpation

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10
Q

What else may cause a fever in cancer?

A

Underlying malignancy (both solid and haematological)

Immunotherapy toxicities

Inflammatory disorders (e.g. SLE, vasculitis, RA)

Drug induced

Hypothalamic dysfunction

Thyroiditis

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11
Q

What are the common gram-negative bacilli that cause neutropenic sepsis?

A

E. Coli

Klebsiella spp.

Pseudomonas aeruginosa

Enterobacter spp.

Proteus spp.

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12
Q

What are the most common gram-positive bacilli in neutropenic sepsis?

A

Staphylococcus aureus

Corynebacterium

Staphylococcus epidermidis

Streptococcus pneumoniae

Viridans streptococci

Enterococci

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13
Q

What are some common fungal causes of neutropenic sepsis?

A

Candida spp.

Aspergillus spp.

Mucorales

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14
Q

How may an infective cause be investigated in neutropenic sepsis?

A

Bedside = Urinalysis (UTI), ECG (all acutely unwell patients), Capillary blood glucose (exclude hypoglycaemia)

Lab investigations = Blood tests (FBC, U&E, coagulation, CRP, LFTs = WCC low / raised, CRP raised), Serum lactate, G&S (for transfusion), Blood cultures (two sets from peripheral vein, plus from indwelling line), ABG (extent and severity), cultures (wounds, urine, stool, sputum line tip), Viral resp swab

Imaging = CXR (pneumonia), chest CT (fungal pneumonia suspected), abdo ultrasound (biliary / abdo infection suspected)

Other = Bronchoalverlar lavage (atypical chest source = penumocystis jirovecii)

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15
Q

What is the management of neutropenic sepsis?

A

Empirical abx within one hour of arrival at hospital

Sepsis 6

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16
Q

Give example of empirical antibiotic therapy for neutropenic sepsis?

A

First-line = IV piperacillin with tazaobactam (tazocin)

Second-line (penicillin allergy) = IV meropenem

Additional anti-microbial cover = teicoplanin for gram positive organisms (e.g. for indwelling central venous catheters)

Antifungal = if fever persists beyond 4-6 days

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17
Q

What may be used for both prophylaxis and treatment of neutropenia to reduce the risk of sepsis?

A

Granulocyte-colony stimulating factor

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18
Q

How does G-CSF work?

A

Stimulates bone marrow to produce neutrophils (may form part of specific chemo regimens) e.g. filgrastim

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19
Q

What are some complications of neutropenic sepsis?

A

Single / multi-organ failure (renal failure, heart failure, ARDS)

VTE (PE)

DIC

Delerium

Psycholigical complications (anxiety around future infections and chemo treatment)

Delays in chemo leading to worse cancer outcomes

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20
Q

What is the spinal cord?

A

Part of CNS - main communication between brain and peripheral nerves

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21
Q

What is the spinal cord surrounded by?

A

Meninges

Dura

Arachnoid

Pia mater

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22
Q

What is the thecal sac?

A

Component of the dura mater (outermost meningeal layer)

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23
Q

What is malignant cord compression defined as?

A

Radiological evidence of indentation of the thecal sac

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24
Q

What is the cauda equina? (syndrome included in cord compression)

A

Lumbar, sacral and coccygeal nerve roots that descend from the end of the spinal cord at L1

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25
Q

Where does the spinal cord originate and end?

A

Base of medulla oblongata (exiting through the skull through foramen magnum) - ending at level of L1 / L2 spinal vertebrae

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26
Q

How many segments are there of the spinal cord?

A

31 segments

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27
Q

What is the terminal end of the spinal cord called? (Beyond which is cauda equina / horses tail)

A

Conus medullaris

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28
Q

When does malignant spinal cord compression occur?

A

Secondary to metastatic deposits within the spinal column

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29
Q

Which cancers are associated with cord compression?

A

Lung

Breast

Kidney

Prostate

Thyroid

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30
Q

What are the other causes of cord compression?

A

Trauma

Intebertebral disc prolapse

Haematoma

Episural asscess (secondary to osteomyelitis or discitis)

Cervical spondylitic myelopathy

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31
Q

Where does malignant cord compression most commonly occur?

A

Thoracic spine

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32
Q

What can cause vertebral metastasis?

A

Arterial seeding

Shunting of blood through epidural venous plexus (in prostate cancer)

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33
Q

What are the features of cord compression?

A

Pain - severe, progressive, radicular character

Weakness - symmetrical, pyramidal (affects the extensors in upper extermities and flexors in lower)

UMN lesions = increased tone

Hypereflexia - below level of lesions e.g. extensor plantar reflex (positive babinski)

Sensory symptoms - less common than motor symptoms

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34
Q

What are the features of cauda equina syndrome?

A

Lower motor neurone pattern

Unilateral features

Saddle anarsthesia

Reduced anal tone

Painless urinary retention (overflow incontinence)

Impotence

Absent ankle jerk

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35
Q

What is the investigation in malignant cord compression?

A

MRI scan

Other imagine (myelography, CT, bone scan, plain radiographs)

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36
Q

What is the management of acute cord compression?

A

Surgical emergency - prompt recognition and treatment

General measures (analgesia from WHO ladder, VTE prophylaxis - TED stockings, LMWH, catheter)

Glucocorticoids (high-dose dexamethasone, reducing oedema, relieving compression)

Definitive treament (External beam RT - adjuvant or stand alone)

Stereotactic body radiotherapy - enables higher doses of radiotherapy to be targeted more directly at the tumour - useful if radioresistant e.g. sarcoma, renal cell carcinoma

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37
Q

What are the surgical management options for cord compression?

A

Surgical decompression and reconstruction

Vertebroplasty

Kyphoplasty

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38
Q

What is malignant hyperclacaemia defined as?

A

Serum calcium > 2.6 mmol/L secondary to a malignant process

39
Q

What are the most common causes of hypercalcalcaemia?

A

Primary hyperparathyroidism

Malignant hypercalcaemia

40
Q

Where is calcium stored?

A

Bone (99%)

Intracellular

Extracellular (ionised - free pool, bound to albumin and globulin, complexed with phosphate and citrate)

41
Q

How is the balance between stored calcium and extracellular calcium managed?

A

PTH (parathyroid hormone)

Vitamin D

Calcitonin

42
Q

How does the body respond to decreased extracellular calcium?

A

Detected by calcium-sensing receptor (CaSR) on parathyroid glands

Parathyroid glands release PTH (stimulating resorption of calcium from bone, activation of vitamin D and increased renal tubular reabsorption of calcium)

43
Q

How does activated vitamin D cause increases in calcium?

A

Calcium absorption from enterocytes

44
Q

What effect does a rise in extracellular calcium have?

A

Reduction in release of PTH

Stimulates the release of calcitonin

45
Q

What is the normal calcium range?

A

2.2-2.6 mmol/L

46
Q

What are the grades of hypercalcaemia?

A

Mild = 2.6-3.0

Moderate = 3.0-3.5

Severe > 3.5

47
Q

What is calcium corrected for?

A

The amount binded to albumin

48
Q

What does acidosis do to the levels of calcium?

A

Decreases level of calcium

49
Q

Which are the most common malignancies associated with hyperclaemia?

A

Breast cancer

Muliple myeloma

Lymphoma

Lung cancer

50
Q

What are the three mechanisms which cause malignant hypercalcaemia?

A

Osteolytic metastasis

PTH-related protein (PTHrP) secretion

Increased 1,25-dihydroxyvitamin D production

51
Q

What does PTHrP cause?

A

Increased bone resorption

Distal tubular calcium absorption

Inhibition of proximal phosphate transport

52
Q

What is osteolytic metastasis most linked with?

A

Breast cancer

53
Q

Why does calcium rise in osteolytic metastasis?

A

Deposition of tumour cells in bone causes local inflammatory cytokines and other mediators, stimulating osteoclasts causing bone resorption

54
Q

Which cancer causes increased expression of activated vitamin D (causing increased absorption from GI tract)?

A

Hodgkin’s lymphoma

55
Q

What are the clinical features of malignant hypercalcaemia?

A

Stones, bones, abdo groans, psychiatric moans

Stones = renal calculi

Bones = pains, fractures

Groans = abdo pain, pancreatitis

moans = mood disturbances, fatigue

thrones = polyuria, constipation

56
Q

How does milde hypercalcaemia present?

A

Often asymptomatic

Polyuria

Polydipsia

Mild cognitive impairment

Dyspepsia

Nausea

57
Q

How does severe hypercalcaemia present?

A

Abdo pain

Vomiting

Cardiac dysrhythmias

Pancreatitis

Coma

58
Q

How is malignant hypercalcaemia diagnosed?

A

Measurement of serum calcium level

Identification of underlying cancer

59
Q

How to investigations differentiate between hyperparathyroidism and malignant hypercalcaemia?

A

PTH should be suppressed

60
Q

Which investigations are usually indicated in suspected malignant hypercalcaemia?

A

Full examination (including breast)

Myeloma screen (immunoglobulins, protein electrophoresis, urinary light chains)

CT

61
Q

What form the management of malignant hypercalcaemia?

A

IV rehydration (prompts calcium diuresis - if HF loop diuretics may be required)

Calcitonin (promotes urinary calcium excretion, inhibits bone resorption)

Bisphosphonate therapy (inhibit osteoclasts e.g. pamidronate or zoledronic acid)

Admit if serum calcium > 3 mmol/L (if less then managed as outpatient with oral hydration (3-4 L / day)

62
Q

What is malignant superior vena cava obstruction (SVCO)?

A

Obstruction to the flow of blood through the superior vena cava secondary to a cancer

63
Q

What does the SVC provide drainage for?

A

Upper limbs

Head

Neck

64
Q

What unites to form SVC?

A

Brachiocephalic veins

65
Q

Which cancers commonly cause SVC obstruction?

A

Lung carcinoma (small cell)

non-Hodgkin’s lymphoma

66
Q

Which collateral systems may develop in SVC?

A

Azygous system

Internal mammary

Long thoracic

67
Q

Which lung cancer mostly causes SVCO?

A

Non-small cell lung cancer

68
Q

How does SVCO present?

A

Dyspnoea

Facial swelling

Head fullness

Cough

69
Q

Which signs may warrant urgent management in SVCO?

A

Airway obstruction (stridor)

Neurological symptoms (cerebral oedema)

70
Q

What are the signs and symptoms of SVCO?

A

Symptoms

Dyspnoea

Facial swelling

Head ‘fullness’

Symptoms exacerbated by bending forwards / lying down

Cough

Dysphagia

Signs

Facial swelling

Distended neck veins

Upper limp oedema

Facial plethora

Cyanosis

Cognitive dysfunction

Coma

71
Q

What is pemberton’s sign in SVCO?

A

Pt elevates both arms above head for 1-2 minutes

Positive if causes congestion, cyanosis and respiratory distress (increased venous return exacerbates obstruction)

72
Q

What are the investigations in SVCO?

A

Initially

Abnormal chest radiograph (FINDINGS = mediastinel widening and malignant pleural effusion & helps exclude other causes of breathlessness)

Diagnostic

Extent and level of obstruction, presence of collateral vessel formation and underlying cause (PET CT, CT abdo / pelvis / MRI to identify mets)

Duplex ultrasound may be used to diagnose SVCO (indwelling catheters, MRI and contrast venography are rarely used)

73
Q

How may a histological diagnosis be obtained?

A

Minimally invasive procedures = sputum / pleural fluid cytology, lymph node biopsy, bone marrow biopsy

Invasive = bronchoscopy, mediastinoscopy, video assisted thoracoscopy

74
Q

What is the emergency management of SVCO?

A

(treats respiratory distress / cerebral oedema)

Thrombus related = stent / thrombolysis

Not thrombus related = stent

75
Q

What is the general and definitive management of SVCO?

A

General = elevation of head and neck, titrated oxygen, glucocorticoids to reduce swelling (dex)

Definitive = stenting, RT, CT

76
Q

How to choose between RT and CT in SVCO?

A

RT = NSCLC and lymphomas

Chemo = SCLC and NHL

77
Q

What is the life expectancy of patients presenting with SVCO?

A

6 months

78
Q

What causes tumour lysis syndrome?

A

Metabolic disturbances arising from breakdown of malignant cells following initiation of treatment for malignancy

79
Q

What are the electrolyte imbalances in tumour lysis syndrome?

A

Hyperkalaemia

Hyperphosphataemia

Hypocalcaemia

Hyperuricaemia (from metabolism of nucleic acids)

80
Q

What may result from tumour lysis syndrome?

A

AKI

Arrythmias

Sudden death

81
Q

Which tumour factors are associated with increased risk of TLS?

A

High proliferation rate

Chemosensitivity

Large tumour burden

Follwogin initation of cytotoxic therapy

82
Q

Which clinical factors also increased likelihood of developing TLS?

A

Pre-existing metabolic abnormalities e.g. hyperuricaemia, hyperphosphataemia

Renal impairment

83
Q

Why does hypocalcaemia occur in TLS?

A

Secondary to hyperphosphataemia (calcium precipitates in soft tissues)

84
Q

When do features of TLS occur after initiation of chemo?

A

First 72 hours (up to 7 days post-treatment)

85
Q

What are the symptoms and signs of TLS?

A

Symptoms = lethargy, N&V diarrhoea, anorexia, muscle cramps, syncope, pruritus, arthritis

Signs = fluid overload, haematuria, tetany & paraesthesia (hypocalcaemia), bronchospasm (wheezing)

86
Q

Which investigations are essential to assess and diagnose severity of TLS?

A

Renal function

Electrolytes

Serum urate

87
Q

Which other investigations may be required for TLS?

A

Urine dip

Urine microscopy (for uric acid crystals)

Serum lactate

Lactate dehydrogenase (LDH)

ECG

Cardiac monitoring

88
Q

How is TLS diagnosed?

A

Cairo-Bishop definition

Lab diagnosis = 2 / more abnormal serum values in three days prior or seven days after treatment (uric acid, potassium, phosphate or calcium)

Clinical diagnosis = if lab diagnosis with presence of raised serum creatinine, cardiac arrhythmias, sudden death or seizure (can’t be attributed to therapeutic agent)

89
Q

What hypouricaemic agent may be used to prevent hyperuricaemia?

A

Allopurinol

Rasburicase

90
Q

What is the MOA for allopurinol?

A

Xanthine oxidase inhibitor (doesn’t act on pre-existing uric-acid)

91
Q

How does rasburicase work?

A

Metabolises uric acid to allantoin

92
Q

What are the options for prophylaxis against TLS?

A

Oral hydration

IV hydration

Allopurinol

Rasburicase

93
Q

What is the management of TLS?

A

Hyperphosphataemia = hydration, dietary restriction, haemofiltration

Hyperkalaemia = IV calcium gluconate, insulin / dextrose infusion, nebulised salbutamol

Hypocalcaemia = shouldn’t be treated, causes increased calcium phosphate deposits in kidney if treated (if arrythmias then treat)

Hyperuricaemia = hypouricaemic agents

94
Q

When is haemofiltration indicated in TLS?

A

Intractable fluid overload

Refractory hyperkalaemia

Hyperphosphataemia-induced symptomatic hypocalcaemia

High calcium-phosphate product

Cancer care (5 decks)

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