Oncological emergencies Flashcards

1
Q

How can you classify ontological side effects and emergencies? Give examples in each category

A

Treatment related:

  • (pan) Cytopenias (neutropaenic sepsis)
  • Electrolyte imbalance (hypercalcaemia)
  • Tumour lysis syndrome (rare but examinable)
  • Diarrhoea
  • Vomiting
  • Anaphylaxis
  • Extravasation
  • Colitis (from immune therapies)
  • Radiotherapy side effects

Tumour related

  • Spinal cord compression
  • SVCO
  • Upper airway obstruction
  • Brain mets, raised ICP and seizures
  • Bowel obstruction
  • VTE
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2
Q

What are the risk factors for and presentation of neutropaenic sepsis?

A

Risk factors:

  • Cytotoxic chemo
  • Poor nutritional state
  • Mucosal barrier defect
  • Central venous lines
  • Abnormal host colonisation

Presentation:

  • Infective symptoms/signs with or without fever
  • Asymptomatic yet febrile
  • Suspect in any patients presenting with a new clinical deterioration within 6wks of cytotoxic chemo (most often occurs within 7-10 days of a 3wk chemo therapy cycle)

Should be treated for if they have a temp >38c and an absolute neutrophil count of <1x10^9/L

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3
Q

How do you investigate and manage neutropaenic sepsis?

A

Standard sepsis 6/Bufalo (cultures, urine monitoring, fluids, Abx, lactate, O2)

Investigation:

  • FBC, U+E, creatinine, CRP/ESR, coag
  • Septic screen = blood + clinically relevant (swabs+) cultures, CXR

Management:

  • DO NOT AWAIT CULTURES, GIVE WITHIN 1HR
  • Initial Abx - Piperacillin + Tazobactam IV
  • Switch to oral - after 24-48hrs of IV if clinically improving
  • No improvement after 48hrs - consider adding second line Abx
  • No improvement after 5 days - consider opportunistic infections e.g. fungal/PCP

If there are central lines present, consider these as a possible source of infection - identify and remove

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4
Q

How do you prevent neutropaenic sepsis?

A

Patients having chemo + high risk of developing neutropaenia - offer prophylaxis with fluoroquinolone Abx (e.g. ciprofloxacin), anti-fungals or granulocyte colony-stimulating factor

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5
Q

How do you diagnose malignant hypercalcaemia?

A

c. 40% of calcium is bound to albumin

The unbound, ionised calcium is physiologically important - CORRECTED CALCIUM should therefore be used to diagnose

Severity:

  • Mild - 2.6-3.0 mmol/L
  • Moderate - 3.01-3.39 mmol/L
  • Severe - >3.4 mmol/L
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6
Q

What are the causes of malignant hypercalcaemia?

A

Osteolysis - from lytic bone metastases

Humoral - Parathyroid hormone-related protein (or PTHrP) is a protein member of the parathyroid hormone family, secreted by some cancer cells e.g. in squamous cell lung carcinoma, some breast cancers

Dehydration

Other tumour specific mechanisms

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7
Q

How does malignant hypercalcaemia present?

A

BONES STONES GROANS AND PSYCHIC MOANS:

  • GI - abdo pain, vomiting, constipation, anorexia, weight loss
  • GU - polyuria, polydipsia
  • Neuro - fatigue, weakness, confusion
  • Psych - depression
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8
Q

How do you investigate malignant hypercalcaemia?

A

Repeat blood sample - isolated raised values are often of little use (unless wildly high)

ECG - shortened QT interval

Imaging - for bone mets if appropriate

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9
Q

How do you manage malignant hypercalcaemia acutely?

A

1) Correct dehydration:
- 0.9% saline, 4-6L depending on clinical condition and PMH (e.g. CHF)

2) IV bisphosphonates
- Inhibits osteoclasts - reducing bone turnover and reducing Ca levels over several days
- Zolendronic acid, pamidronate = commonly used
- SEs: flu-like symptoms, bone pain, myalgia, reduced phosphate levels, N+V, headache, osteonecrosis of the jaw

If persistent/relapsing hypercalcaemia or malignancy:
- Denosumab - monoclonal Ab inhibiting RANK ligand and thus inhibiting the maturation of osteoclasts

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10
Q

What is malignant spinal cord compression?

A

Spinal cord extends from base of skull - terminating at L1

Cauda equina extends below L1 and contains lumbar, sacral and coccygeal spinal nerves

Cord compression is therefore pressure on the cord above the level of L1 (AND SO NOT THE SAME AS CAUDA EQUINA SYNDROME)

Injury from:

  • Primary malignancy
  • Secondary malignancy = more common - prostate, lung, breast, kidney, thyroid - most common
  • Crush fracture
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11
Q

How does malignant spinal cord compression present?

A

Worsening back pain

Limb weakness below the level of compression

Sensory loss (sensory level present) below the level of compression

  • Sensory level is defined as the lowest spinal cord level that still has normal pinprick and touch sensation
  • If there is a spinal cord level below which there is no voluntary motor or conscious sensory function, the person is called a “complete” spinal cord injury

Abnormal neurological examination
- LMN signs at the level of the lesion and UMN signs below that level
E.g. a spastic paralysis with brisk reflexes (unlike the flaccid paralysis and arreflexia of cauda equina syndrome - but both cause sensory and power loss)

Radicular pain

  • Radiates from your back and hip into your legs through the spine
  • The pain travels along the spinal nerve root

Bowel or bladder dysfunction = a late sign, so do not wait for this…

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12
Q

How do you investigate malignant cord compression?

A

MRI WHOLE SPINE

As patients may have multiple levels of compression that need addressing

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13
Q

How do you manage malignant cord compression?

A

High dose corticosteroids

Analgesia

VTE and pressure sore prophylaxis

Definitive treatment will depend on patient and disease factors:

  • Surgery - spinal decompression + spinal column stabilisation
  • Radiotherapy - for those unsuited to surgery; can be used for pain control
  • Chemotherapy - for very chemosensitive tumours
  • Hormone deprivation - if newly diagnosed prostate cancer
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14
Q

What is the prognosis of malignant spinal cord compression?

A

Related to severity of neurological deficit at time of presentation e.g. if paraplegia and sphincter involvement has occurred then recovery is uncommon

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15
Q

What is superior Vena Cava obstruction (SVCO)?

A

SVC provides venous drainage to the head, neck, upper limbs and thorax - if obstructed, collateral pathways form to provide an alternative route for blood to return to the right atrium

Obstructed by:

  • Intravascular - thrombus, intravascular device e.g. central line
  • Inside vessel wall - direct tumour invasion
  • Outside the vessel - tumour mass effect (lung Ca, lymphoma, germ cell tumour), fibrosing mediastinitis
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16
Q

What are the symptoms and signs of SVCO?

A

Symptoms:

  • Dyspnoea
  • Chest pain, often at rest
  • Cough
  • Neck and face swelling
  • Arm swelling
  • Dizziness
  • Headache
  • Visual disturbance
  • Syncope

Signs:

  • Dilated veins over arms, neck and anterior chest wall
  • Oedema of upper torso, arms, neck and face
  • Severe respiratory distress
  • Cyanosis
  • Engorged conjunctivae
  • Convulsions and coma
17
Q

How do you investigate SVCO?

A

May be a clinical Dx

CXR - widened mediastinum/mass on right side of heart

Chest CT

18
Q

How do you manage SVCO?

A

Elevation of head and oxygen therapy may provide symptomatic relief

High dose steroids in acute SVCO
- 8-10mg dex STAT

Endovascular stenting

Consider:

  • Chemo, radiotherapy
  • Anticoag - if central venous thrombosis
19
Q

What is chemotherapy extravasation ?

A

Leakage of chemotherapeutic agents into tissues from veins

Effects depend on the drug being given - some can be harmless, some can lead to loss of function, need grafting or amputation

Drugs are classified into:
Vesicant – blistering and necrosis
Exfoliant – inflammation and skin shedding
Irritant – sclerosis, burning, local warmth, hyper-pigmentation, discomfort, erythema or tenderness n
Inflammitant – flare, inflammatory reaction
Neutral – no inflammation or tissue damage on extravasation

Damage will depend on where the drug is being given e.g. peripherally or centrally

Protocols for management will differ depending on these factors

20
Q

What is tumour lysis syndrome?

A

When tumour cells release their contents into the blood stream in response to therapy or spontaneously

Not common, most common with lymphomas (Burkitt’s) and leukemias (ALL)

Characteristic findings: (any 2 of the following)

  • Hyperuricemia
  • Hyperkalaemia
  • Hyperphosphataemia
  • Hypocalcaemia

Also may present with:

  • Increased serum creatinine - Cardiac arrhythmia
  • Seizure activity
  • Sudden death

Managed with aggressive hydration and hypouricaemic agents (to enhance excretion of uric acid - allopurinol)