Oncological Emergencies Flashcards by Amy Fielding

Define Neutropenic Sepsis

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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Define Febrile Neutropenia

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

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Give four causes of Neutropenic Sepsis

Chemotherapy
HSCT
Drugs (Immunosupressants, Clozapine)
Bone Marrow Failure

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How does Neutrophil count vary with chemotherapy?

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

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What are the normal infective organisms in Neutropenic Sepsis?

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

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Other than chemotherapy, give four risk factors for Neutropenic Sepsis

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

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How should you assess a patient with suspected Neutropenic Sepsis?

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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How quickly should Sepsis 6 be started in Neutropenic Sepsis?

Within one hour

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What is the first line antibiotic in Neutropenic Sepsis?

Tazocin

Meropenem if Pen Allergic

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

CXR
Urine Culture
Sputum Culture
Swab any lines

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What is Spinal Cord Compression?

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

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

Myeloma
Prostate
Nasopharynx
Breast
Lung

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Describe the pathophysiology of Malignant Compression

Primary (Primary Bone Tumours, CNS malignancy)

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

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Give three possible mechanisms of metastatic spread to spine

Haematogenous arterial seeding

Shunting of abdominal venous flow to epidural plexus by Valsalva

Extension through intervertebral foramen

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Name three non malignant causes of Spinal Cord Compression

Trauma
Disc Prolapse
Haematogenous

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Describe the common distribution of Spinal Cord Compression

60% Thoracic
30% Lumbar
10% Cervical

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

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

May have peripheral paraesthesia

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How would a Cauda Equina compression present?

LMN pattern (normally unilateral)

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

Lower back pain

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What is the gold standard investigation for Spinal Cord Compression?

MRI

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Describe the general management of Spinal Cord Compression

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

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Describe the definitive management of Spinal Cord Compression

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

+/- External Beam Radiotherapy or Stereotactic Body Radiotherapy

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Define Malignant Hypercalcaemia

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

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Describe the normal distribution of Calcium

99% Bone, 0.1% Extracellular, 0.9% Intracellular

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

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Name three hormones involved in the balance of Calcium

Vitamin D
Calcitonin
PTH

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What molecule must Calcium be corrected for and how?

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

State the parameters of severity in Malignant Hypercalcaemia

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

What four cancers is Malignant Hypercalcaemia most commonly associated with

Breast Cancer Multiple Myeloma Lymphoma Lung Cancer (SCC)

What three mechanisms cause Malignant Hypercalcaemia?

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

How do Osteolytic Metastases cause Hypercalcaemia?

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

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

Polydipsia Polyuria Confusion

How is Malignant Hypercalcaemia investigated?

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

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

Admit IV Rehydration, Calcitonin and Bisphosphonate Therapy

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

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

What is Superior Vena Cava Obstruction?

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

Describe the anatomy of the Superior Vena Cava

Venous drainage of upper limbs, head and neck Valveless Structure

Name two cancers classically causing SVCO

Lung Carcinoma NHL

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

Allows collateral vasculature to form

State three symptoms of SVCO

Dyspnoea Facial Swelling Head Fullness

State three signs of SVCO

Facial Swelling Distended Vein Facial Plethora

What is Pemberton's Sign for SVCO?

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

How is SVCO investigated?

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

What is the Emergency Management of SVCO?

Normally if patient is in RDS or has Cerebral Oedema Diuretics +/- Steroids Stent (+/- Anticoagulation)

What is the non emergent management of SVCO?

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

What stents can be used in SVCO?

Balloon Expandable and Self Expanding Percutaneously inserted

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

6 months

What is Tumour Lysis Syndrome?

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

What electrolyte abnormalities come from rapid cellular breakdown?

Hyperkalaemia Hyperphosphataemia Hypocalcaemia Hyperuricaemia Can cause AKI and arrhythmias

Name four risk factors for Tumour Lysis Syndrome

Haematological Malignancy Chemosensitivity Large Tumour Burden Renal Impairment

Why is risk stratification important in Tumour Lysis Syndrome?

Assesses need for prophylactic therapy and monitoring

Describe the pathophysiology of Tumour Lysis Syndrome

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

What is the onset of Tumour Lysis Syndrome?

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

How does Tumour Lysis Syndrome present?

Lethargy, Nausea and Vomiting, Diarrhoea, Anorexia, Muscle Cramps Generally presents as the electrolyte abnormalities that are caused

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

Renal Function Electrolytes Serum LDH Serum Lactate If high risk, repeat every 4-6 hours

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

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

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

One of: Serum Creatinine >1.5 times upper limit Cardiac Arrhythmia/Sudden Death Seizure The above criteria form basis of graded severity

Describe the production of Uric Acid

Purines get converted to Hypoxanthines Xanthine Oxidase converts Hypoxanthine into Xanthine and Uric Acid

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

Allopurinol (only useful as prophylaxis as cannot act against existing uric acid) Rasburicase (converts uric acid into soluble allontoin)

How would Hyperphosphataemia in Tumour Lysis Syndrome be managed?

Hydration and Dietary Restriction Phosphate Binders Severe - Haemofiltration

How would Hypocalcaemia in Tumour Lysis Syndrome be managed?

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

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

Oral Hydration Monitor

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

Saline Allopurinol

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

Saline Rasburicase

When would you consider Haemofiltration in Tumour Lysis Syndrome?

Intractable fluid overload Refractory Hyperkalaemia Hyperphosphataemia induced symptomatic hypocalcaemia

Describe Virchow's Triad

Venous Stasis Endothelial Dysfunction Hypercoaguable state

Why does Cancer predispose patients to venous stasis?

Prolonged immobility Direct compression of tumour

Why does Cancer predispose patients to Hypercoaguablity?

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

What is the Khorana Risk Model?

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

What are the parameters for Khorana Risk Model?

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

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

Greater than or equal to three

How is VTE in oncology managed?

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

How would Moderate Hypercalcaemia present?

Constipation Fatigue Weakness

How would severe Hypercalcaemia present?

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

Oncological Emergencies Flashcards

(72 cards)