Oncological Emergencies Flashcards

1
Q

Spinal cord compression is an oncological emergency and affects up to 5% of cancer patients. Extradural compression accounts for the majority of cases, usually due to vertebral body metastases.

How does it present?

A

back pain: may be worse on lying down and coughing

lower limb weakness

sensory changes: sensory loss and numbness

neurological signs depend on the level of the lesion: tendon reflexes tend to be increased below the level of the lesion and absent at the level of the lesion

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2
Q

What are the different causes of malignant spinal cord compression?

A

It can result from direct pressure, vertebral collapse or instability due to metastatic or local spread of tumours.

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3
Q

Give some risk factors for developing malignant spinal cord compression

A

some cancers carry a higher risk than others

Prostate cancer (20%)
Lung cancer (20%)
Breast cancer (17%)
Renal cancer (12%)
Multiple myeloma

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4
Q

How should suspected spinal cord compression (MSCC) be investigated and managed?

A

Investigation
urgent MRI: whole MRI spine within 24 hours of presentation

Management
high-dose oral dexamethasone
urgent oncological assessment for consideration of radiotherapy or surgery

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5
Q

What bedside and lab investigations should be considered for MSCC?

A

Bladder scan: to assess for urinary retention

Baseline blood tests (FBC, U&Es, LFTs): to assess general fitness and for imaging
Clotting and group & save: if the patient is likely to require surgery

Bone profile: to assess for hypercalcaemia
LDH: higher levels are associated with poor prognosis
Myeloma screen: if the patient does not have a known cancer diagnosis

Tumour markers: may help with the assessment of cancer stage and suitability for treatment or diagnosis if MSCC is the initial presentation

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6
Q

What should be considered in the rehabilitation of patients with MSCC?

A

Weaning of dexamethasone
Pain control
Thromboprophylaxis
Breathing exercises and forced expiratory techniques to aid chest clearance
Prevention of contractures/spasticity
Prevention of pressure ulcers
Mobility aids
Continence management

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7
Q

Give some complications of MSCC

A

Pressure ulcers
DVT / PE
Falls
Urinary tract infections

Emergency:
Autonomic dysreflexia - uncontrolled htn and arrythmias due to spinal cord injury

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8
Q

Superior vena cava (SVC) obstruction is an oncological emergency caused by compression of the SVC. It is most commonly associated with lung cancer.

How does it present?

A

dyspnoea is the most common symptom
swelling of the face, neck and arms - conjunctival and periorbital oedema may be seen
headache: often worse in the mornings
visual disturbance
pulseless jugular venous distension

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9
Q

What is Pemberton’s sign?

A

The Pemberton manoeuvre may worsen the signs and symptoms of SVCO. The patient should lift both arms until they touch the side of the face. A positive Pemberton’s sign is the presence of facial congestion, cyanosis and respiratory distress after ~1 minute.

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10
Q

What can cause SVCO?

A

external pressure, malignant infiltration, or thrombus formation within the vessel

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11
Q

What are the risk factors for developing SVCO?

A

Lung cancer: particularly small-cell lung cancer
Lymphoma
Metastatic disease: particularly breast cancer, colon cancer and oesophageal cancer
Smoking: due to the increased risk of lung cancer, rather than a direct association
Central venous catheter use: may be used in cancer patients for the administration of medication
Radiation to the mediastinum

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12
Q

How can SVCO be investigated?

A

Chest X-ray: may show a widening of the superior mediastinum and right hilar prominence to indicate a mediastinal mass

CT chest with contrast: imaging modality of choice; shows the location and severity of obstruction and may help with identification/staging of underlying malignancy

Doppler ultrasound: may help to identify the presence of obstruction

Diagnosis can be made clinically or based on contrast CT

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13
Q

How can SVC obstruction be managed?

A

securing the airway : endotracheal intubation, surgical airway

endovascular stenting is often the treatment of choice to provide symptom relief

certain malignancies such as lymphoma, small cell lung cancer may benefit from radical chemotherapy or chemo-radiotherapy rather than stenting

the evidence base supporting the use of glucocorticoids is weak but they are often given

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14
Q

Symptomatic treatment for SVCO includes:

A

Elevating the head
Loosening restrictive clothing
Benzodiazepines and opioids to relieve breathlessness and agitation
Oxygen to maintain oxygen saturations if required

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15
Q

Give some complications of SVCO

A

Laryngeal oedema
Acute upper airway obstruction

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16
Q

Give some complications of endovascular stenting

A

Stent thrombosis
Stent migration
Superior vena cava dissection or perforation
Infection
Volume overload/acute decompensation of heart failure: due to the sudden increase in venous return after relief of the obstruction

17
Q

What is Tumour lysis syndrome (TLS)?

A

an oncological emergency that occurs when malignant cells rapidly break down, releasing their contents into the bloodstream. This causes significant changes to the levels of electrolytes within the blood and can be life-threatening if not recognised and treated.

It most commonly occurs in patients with lymphoproliferative malignancies after initiation of treatment (usually after 12-72 hours)

18
Q

What electrolyte abnormalities may be seen in tumour lysis syndrome?

A

Hyperkalaemia
Hyperuricaemia
Hyperphosphataemia
Hypocalcaemia (secondary to hyperphosphataemia)

19
Q

What are some of the main risk factors for developing TLS?

A

Poorly differentiated lymphomas

Leukaemia

Fast-growing solid tumours (e.g. hepatocellular carcinoma, small cell lung cancer, breast cancer)

Large tumour burden

LDH >1,500 IU

High tumour sensitivity to chemotherapy

Pre-existing renal impairment
Concurrent use of nephrotoxic agents
Dehydration

20
Q

Symptoms of TLS are vague and non-specific.

Patients will present generally unwell with symptoms related to the electrolyte disturbances found in TLS such as :

A

D + V
Reduced urine output
Confusion, Lethargy
Muscle cramps and tetany
Syncope
Chest pain
Palpitations

21
Q

What may be found on examination of a patient with TLS?

A

signs of underlying malignancy e.g. masses, organomegaly, lymphadenopathy, pallor

Peripheral oedema: due to renal failure
Trousseau’s sign: due to hypocalcaemia
Chovstek’s sign: due to hypocalcaemia
Tachycardia: due to cardiac arrhythmias

22
Q

How should TLS be investigated?

A

Bedside:
* ECG
* Urine pH: if hyperuricaemia; urine pH < 5 = increased risk of precipitation of uric acid crystals, which may cause obstruction

Laboratory investigations:
* FBC: leukocytosis correlates with tumour burden
* U&Es: to identify renal impairment and electrolyte abnormalities
* Bone profile: hyperphosphataemia and hypocalcaemia.
* Uric acid: raised uric acid is both a risk factor for and a feature of TLS
* LDH: raised LDH is a risk factor for TLS

23
Q

Preventative measures for patients at high risk of developing TLS?

A

Intravenous hydration with normal saline for two days before treatment (aim to maintain urine output 100 mL/m²/hour)

Regular monitoring of blood tests (U&Es, bone profile, uric acid, LDH), including 3-4 times daily after starting treatment

Rasburicase should be given to patients with hyperuricaemia

24
Q

How can TLS be managed?

A

Intravenous fluids: aiming to maintain urine output >100 mL/m²/hour (monitor urine output hourly)

Observations should be monitored at least 4-6 hourly, including fluid balance assessment

Daily weights

Blood tests every 6 hours after diagnosis of TLS

ECG at baseline, consider cardiac monitor if hyperkalaemia/hypocalcaemia

25
Q

How can hyperuricaemia in TLS be corrected?

A

intravenous rasburicase for 3-7 days (use maximum dose allopurinol if rasburicase contraindicated)

26
Q

How can hyperkalaemia in TLS be corrected?

A

calcium gluconate for cardiac protection, followed by a glucose/insulin infusion

27
Q

How can hypocalcaemia in TLS be corrected?

A

symptomatic hypocalcaemia should be treated with IV calcium gluconate; seizures can be managed with anticonvulsant medication according to local guidelines

28
Q

Give some complications of TLS

A

AKI: due to calcium phosphate deposition and uric acid
Cardiac arrhythmias: due to hyperkalaemia and/or hypocalcaemia
Seizures: due to hypocalcaemia and/or hyperphosphataemia
Lactic acidosis: due to chemotherapy-induced cell death and AKI

29
Q

What type of pleural effusion does malignancy more commonly cause?

A

exudative

30
Q

Typical symptoms of a pleural effusion include:

A

Breathlessness
Cough
Pleuritic chest pain

Clinical findings may include reduced chest expansion, reduced air entry and a stony dull percussion note on the affected side.

31
Q

How might malignant pleural fluid appear once aspirated?

A

bloody

32
Q

Define neutropenic sepsis

A

a neutrophil count of 0.5 × 109 per litre or lower, plus one of the following:

Temperature ≥ 38°C or
Other signs or symptoms consistent with significant sepsis

33
Q

What can cause neutropenia?

A

Recent chemotherapy (most commonly within 7 – 10 days) causes neutropenia through bone marrow suppression and is the major cause of neutropenic sepsis

Extensive radiotherapy

Malignant bone marrow infiltration

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

Hypersplenism

Megaloblastic anaemia

Drug-induced (e.g. clozapine)

34
Q

Give some risk factors for neutropenic sepsis

A

Previous neutropenic sepsis
Patients over the age of 60
Significant co-morbidities
Advanced malignancy
Prolonged hospital admission
Mucositis (chemotherapy can induce mucosal damage and allow bacterial translocation)
Indwelling central venous catheters
Corticosteroids (causes immunosuppression)

35
Q

How should neutropenic sepsis be investigated?

A

Urinalysis: to look for UTI
ECG: all acutely unwell patients
Capillary blood glucose: to exclude hypoglycaemia

  • Baseline blood tests (FBC, U&E, LFTs coagulation, CRP)
  • Serum lactate
  • Group and save
  • Blood cultures: at least two sets from a peripheral vein plus a set from an indwelling line if present to look for a causative organism
  • ABG: respiratory failure
  • Microbiological cultures: wounds, urine, stool, sputum, and line tip (if indwelling line infection suspected).
  • Viral respiratory swab
36
Q

How should neutropenic sepsis be managed?

A

Patients with suspected or confirmed neutropenic sepsis should receive empirical antibiotic therapy within one hour of arrival at hospital. Antibiotic therapy must not be delayed to wait for confirmation of neutropenia

Tazocin first line

Start sepsis 6!!!

37
Q

Give some complications of neutropenic sepsis

A

Single or multi-organ failure
VTE (e.g. pulmonary embolism)
DIC
Opportunistic or hospital-acquired infections
Delirium
Delays in chemotherapy leading to worse cancer outcomes
Psychological complications (e.g. anxiety regarding future infections and chemotherapy treatment)