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Cancer Studies > Oncological Emergencies (know best for exams) > Flashcards

Oncological Emergencies (know best for exams) Flashcards

1
Q

List the main oncological emergencies

A
  • Spinal cord compression
  • Superior vena caca obstruction
  • Raised intracranial pressure
  • Hypercalcaemia
  • Pulmonary embolism
  • Neutropenic sepsis
  • Thrombocytopenia
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2
Q

What are the symptoms and signs of spinal cord compression?

A

Localised back pain and tenderness:
• Most common early symptom
• Exacerbated by coughing, sneezing, straining or lying flat
• Uncontrolled by analgesia
• Pain may travel along the nerve root distributing (radicular pain)
Neurological problems develop as disease advances:
• Bladder dysfunction -retention, dribbling, incontinence of urine
• Bowel dysfunction -faecal incontinence, constipation
• Weakness in arms or legs
• Hypoesthesia

Tumours below L1/2 may cause cauda equine compression:
• Sciatic pain -often bilateral
• Bladder dysfunction with retention and overflow incontinence
• Impotence
• Sacral aesthesia
• Loss of sphincter tone
• Weakness and wasting of gluteal muscles
Bilateral motor neurone signs → assumed to be SCC until proven otherwise.
• A swelling or lump may be visible over the area of SCC on the back (Gibbus: swelling due to spinal angulation caused by vertebral collapse)

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3
Q

What are the investigations of spinal cord compression?

A
  • Full neurological examination

- MRI whole spine (1st line)

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4
Q

What is the management of spinal cord compression?

A

MEDICAL EMERGENCY DO NOT DELAY!!
Immediate Actions:
• Dexamethasone 8mg PO/IV BD and proton pump inhibitor
• Analgesia
• Log roll if unstable (seek orthopaedic advice)
Surgical decompression
• treatment of choice if feasible
• Radioresistant tumours e.g. melanoma, clear cell carcinoma
Radiotherapy:
radiosensitive tumours
• 8Gy in 1# or 20Gy in 5# or 30Gy in 10#

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5
Q

What are clinical outcomes of spinal cord compression?

A
  • Outcome is strongly dependent on the level of neurological dysfunction the patient had before treatment as well as the pathology.
  • 80% of patients ambulatory before treatment will remain able to walk.
  • If the diagnosis is made late or left untreated they are at risk of irreversible paraplegia, quadriplegia and loss of bowel or bladder function. Functional recovery is poor in general
  • ~30% of patients with SCC will survive for 1 year.
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6
Q

What are the symptoms of superior vena cava obstruction (SVCO)?

A 
Gradual onset over several weeks as the tumour grows. 
• Dyspnoea
• Swelling of neck, face and arms.
• Cough
• Headache
• Visual disturbance
• Dizziness
• Syncope
• Chest pain
• Hoarseness
• Nasal congestion
• Epistaxis
• Haemoptysis
• Dysphagia
*Symptoms exacerbated by lying down or bending over (ask in history)
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7
Q

What are the signs of SVCO?

A

SVCO causes increased intravenous pressure:
• Jugular veins become engorged with absent waveforms
• Collateral veins become prominent over the neck and chest wall.
• Dusky skin
• Facial oedema and plethora
• Arm oedema
• Proptosis, stridor
• Papilloedema (late)

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8
Q

What are the causes of SVCO?

A
  • Most commonly malignancy
  • SCLC (usually right upper lobe)
  • Non-Hodgkin’s Lymphoma
  • Other mediastinal tumours
  • Metastases
  • Rarely sarcoidosis/TB
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9
Q

Recall the investigations for SVCO

A

Chest X-Ray:
• Right para-tracheal mass
• Mediastinal lymphadenopathy
• Other signs of lung cancer e.g. pleural effusion

CT Chest:
• Investigation of choice
• Define the level and degree of venous blockage
• Identify cause and help staging
• Plan biopsy (CT guided or bronchoscopy)

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10
Q

How is SVCO managed?

A
  • ABCDE
  • Sit patient upright
  • High flow O2
  • Dexamethasone 8mg BD w/ PPI
  • Get a tissue diagnosis (determine radio and chemosensitivity)
  • Stenting (interventional radiology)
  • Chemotherapy (for chemosensitive tumours e.g. SCLC/germ cell)
  • Radiotherapy
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11
Q

What is the clinical outcome of SVCO?

A

Prognosis is dependent on:
• Underlying condition causing the obstruction
• Extent to which the SVC is obstructed.
When treated with XRT the average survival is at least 30 months in:
• 45% of lymphomas patients
• 10% of lung cancer patients
Untreated or no response: survival time is 30 days

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12
Q

What are the causes of increased intracranial pressure (ICP)?

A
  • Space occupying lesions • primary brain tumour, brain metastases, abscess, haematoma
  • Hydrocephalus• CSF obstruction
  • Benign intracranial hypertension
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13
Q

Which tumours typically metastasise to the brain?

A
  • Lung cancer
  • Breast cancer
  • Melanoma
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14
Q

What are the signs and symptoms of increased intracranial pressure/brain metastases?

A
  • Headache (early symptom, worse in morning and when coughing or sneezing)
  • Nausea and vomiting (in morning)
  • Cognitive Impairment
  • Drowsiness
  • Seizures (10% of these patients, often focal)
  • Behavioural changes
  • Focal neurological changes
  • Altered gait

*Papilloedema is present in 50% of cases and is usually associated with neurological deficit.

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15
Q

Recall the appropriate investigations in increased ICP

A
  • Full clinical examination
  • FBC, U&Es, LFTs and Tumour Markers (especially if primary unknown)
  • Contrast enhanced CT
  • MRI where in doubt from CT or for further characterisation
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16
Q

How are brain metastases managed?

A

Immediate:
• Steroids (Dexamethasone 8mg PO/IV b.d. and proton pump inhibitor)
• Reduced the tumour associated oedema

Further:
• Surgery or SRS
• Possible for small numbers and volume of metastases with controlled extracranial disease
• Whole brain radiotherapy (20Gy in 5# most common)
• Tissue diagnosis may be required

*CANNOT DRIVE AND MUST BE ADVISED TO INFORM DVA

17
Q

Discuss brain metastases outcomes

A
  • Prognosis is dependent on the type of primary tumour, e.g. breast cancer brain metastases have better prognosis than those due to colorectal cancer.
  • Median survival without treatment is 1 month
  • XRT has not always shown to be of benefit over steroids and best supportive care
18
Q

What are the causes of hypercalcaemia?

A
  • Bone metastases
  • ↑ parathyroid hormone-related protein production (PTH-rp)
  • Calcitriol secretion
  • Hyperparathyroidism
  • 20% of cases in patients with cancer are due to bone resorption by osteoclasts in areas of bone invaded by malignancy.
  • 80% of cases are due to PTH-related protein production by tumour cells
19
Q

What are the symptoms of hypercalcaemia?

A 
Non specific and depend on severity (bones, stones, moans, and abdominal groans). 
• Fatigue, malaise and weakness
• Anorexia
• Polyuria and polydipsia (common in malignant aetiology)
• Nausea and vomiting
• Confusion
• Constipation
• Bone pain

*Symptoms not common when cCa <3.0mmolL-1`
*Neurological symptoms present above 3.5mmol/L:
• Confusion
• Drowsiness
• Lethargy
• Coma and eventually death

20
Q

What are the signs of hypercalcaemia?

A 
DEHYDRATION!
• Dry mucous membranes
• Reduced skin turgor
• Tachycardia
• Postural hypotension
21
Q

How is hypercalcaemia investigated?

A

•Bloods: FBC, U&Es, LFTs CRP, Glucose, PTH, Alkphos
•12-lead ECG
shortened QT interval
severe hypercalcaemia(> 3.75 mmol/L) → widened T waves, may mimic
myocardial infarction
•Chest X-ray –If underlying cause unknown

22
Q

Recall the management of hypercalcaemia

A
  1. Immediate rehydration:
    IV 0.9% NaCl to promote high volume urine output.
    4-6 L in 24 hours if not contraindicated (heart failure)
  2. IV bisphosphonate:
    - zolendronic acid 4 mg IV given after 24 hours
  3. Discontinue medications which elevate calcium e.g. thiazide diuretics, calcium or vitamin D supplements
23
Q

Discuss clinical outcomes of hypercalcaemia

A

•IV fluids and bisphosphonates can achieve normalisation of serum
calcium in 80% but can take up to 3 days
•Hypercalcaemia is an indicator of poor prognosis
•When severe it is associated with short survival weeks to a few
months

24
Q

What are the symptoms of pulmonary embolism?

A
  • Pleuritic chest pain
  • Haemoptysis
  • Dyspnoea
  • Tachypnoea
  • Cough
25
Q

What are the signs of pulmonary embolism?

A 
•Tachycardia
•Cyanosis
•Raised JVP
•Low grade fever
•Pleural friction rub on 
auscultation over infarcted area
26
Q

How is PE investigated?

A
  • FBC, Electrolyte profile
  • ABG –hypoxia, alkalosis
  • Coagulation
  • D-dimer
  • ECG S1Q3T3
  • CXR
  • CT Pulmonary Angiogram
27
Q

How is PE managed?

A

•Oxygen if hypoxic
•Analgesia
•Anticoagulate
- LMWH - Enoxaparin (If on chemotherapy) or
- DOAC –Apixaban/Rivaroxaban or related
•Thrombolysis is indicated if systolic BP <90mmHg and no contraindications

28
Q

What are the clinical outcomes of PE?

A
  • If left untreated the prognosis is poor.
  • Even if treated the patient can develop chronic thromboembolic pulmonary hypertension which can lead to right heart failure.
  • Mortality is lower in patients who are haemodynamically stable.
  • Poor prognostic factors include:
  • ↑age
  • congestive heart failure
  • COPD
  • Tachypnoea
  • Systolic arterial hypotension.
29
Q

What is neutropenic sepsis?

A

•Sepsis with an absolute neutrophil count (ANC) of <1.0 x 109L-1
•Sepsis is ≥2 SIRS criteria and a source of infection
- Temp >38oC or <36oC
- HR > 90bpm
- RR > 20
•Fever must be assumed to be due to infection until proven otherwise
•Infection can quickly become fatal due to low ANC

30
Q

What are the symptoms of neutropenic sepsis?

A
  • Confusion
  • Headache
  • Malaise
  • Lethargy
Local symptoms of infection:
• Sore throat
• Dysuria
• Cough
• Sputum
• Skin inflammation
• Abdominal tenderness
31
Q

What are the signs of neutropenic sepsis?

A 
•Crackles in chest
•Inflammation around vascular 
access sites
•Tachycardia
•Hypotension
•Confusion
32
Q

How is neutropenic sepsis investigated?

A
  • Full physical examination for source of infection and signs
  • FBC, CRP, U&E, LFTs, serum glucose, serum lactate
Infection screen:
• Blood cultures (central line and peripheral)
• Urinalysis and culture
• Chest X-Ray
• Swab lines, throat
• Atypical respiratory viral screen
• LP if meningism
• ECHO and CT if persistent sepsis and source unclear (?vegetation or collections)
33
Q

What is the immediate management of neutropenic sepsis?

A

SEPSIS SIX:

  1. Give O2 to maintain Sats >94%
  2. Take blood cultures
  3. Give IV antibiotics
  4. Give IV fluid challenge
  5. Measure lactate
  6. Measure urine output
34
Q

What is the extended management of neutropenic sepsis?

A
  • Modify antibiotics depending on results.
  • Consider second line antibiotic, if fever does not resolve after 48 hours or patient is deteriorating.
  • Consult with microbiologist, if there is failure to respond after 5 days
  • fungi or parasitic
  • abscess or endocarditis
  • Granulocyte Colony Stimulating Factor (GCSF)• can help ↑neutrophil count in prolonged neutropenia in context of severe sepsis
  • used as prophylactic for further treatment.
35
Q

What are the clinical outcomes of neutropenic sepsis?

A
  • Prognosis depends on the severity of neutropenia and how long it takes until the patient receives treatment.
  • Mortality from neutropenic sepsis has been reduced due to improvements in care and use of broad-spectrum antibiotics but remains a significant problem.
36
Q

What are the symptoms of thrombocytopaenia?

A 
•Malaise
•Fatigue
•General weakness
•Unexplained bleeding or 
brushing
37
Q

What are the signs of thrombocytopaenia?

A
  • Bruising: purpura, petechial
  • Epistaxis
  • Bleeding mucosa
  • Major life threatening bleeds
38
Q

Recall the the investigations for thrombocytopaenia

A
  • FBC, LFTs, U&Es
  • Coagulation screen
  • D-dimer
  • Vit B12 and Folic acid levels
  • Bone marrow biopsy if clinically indicated
39
Q

How is thrombocytopaenia managed?

A

•Group and crossmatch
•Arrange platelet transfusion if:
- PLT <10 x 109L-1 or
- PLT <20 x 109L-1 with active sepsis or bleeding

Cancer Studies (14 decks)

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