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METABOLIC > ONCOLOGY - ONCOLOGICAL EMERGENCIES > Flashcards

ONCOLOGY - ONCOLOGICAL EMERGENCIES Flashcards

1
Q

What are the oncological emergencies?

A

Hypercalcaemia
Neutropenic sepsis
Tumour lysis syndrome
Leukostasis -
Hyperviscocity syndrome -
Raised ICP -
Spinal cord compression
Cauda equine syndrome -
SVC obstruction
Syndrome of inappropriate ADH secretion -

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2
Q

How common is Hypercalcaemia in patients with malignancy?

A

10-30%
(40% of myeloma)
Most common oncological emergency

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3
Q

Which cancers is hypercalcaemia usually associated with?

A

Breast cancer
Lung cancer
Non-Hodgkin lymphoma
Multiple myeloma
Renal cancer

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4
Q

What is the 3 month mortality rate of cancer patients admitted to hospital with hypercalcaemia?

A

75% - a poor prognostic indicator in malignant disease!!

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5
Q

What are some presenting features of Hypercalcaemia?

A

Stones - kidney stones (chronic), polyuria and diabetes insipidus
Thrones - constipation, lethargy
Groans - abdo pain, nausea, vomiting, peptic ulcers and pancreatitis (last 2 chronic only)
Bones - bone pain and muscular weakness
Psychotic overtones - anxiety, depression, cognitive dysfunction, coma
Cardiac - bradycardia, hypertension and arrhythmias (at very high levels)

At low calcium levels, polyuria, depression, thirst and mild cognitive impairment are most common symptoms

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6
Q

Why are calcium levels, when measured, corrected?

A

Because calcium can exist in a free ionised form or exist bound to albumin
Total calcium levels are the sum of both
If albumin levels are low then there isn’t much albumin-bound calcium which means more of the total calcium will be ionised and active
The corrected calcium equation takes into account the albumin level and adjusts the total calcium level accordingly

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7
Q

Whats normal serum corrected calcium?

A

2.2-2.7mmol/L

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8
Q

Outline calcium control in the body?

A

High calcium levels are detected by the thyroid gland. Parafollicular cells release calcitonin which can bring the calcium levels down; it encouraged calcium deposition in the bones, reduces the reabsorption of calcium by kidneys

When calcium levels are low, parathyroid glands release parathyroid hormone. This causes calcium release from bones, increases calcium reabsorption from kidneys and increases levels of calcitriol (active vitamin D) which stimulates small intestine to absorb more calcium

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9
Q

Whats the most common pathology of Hypercalcaemia of malignant disease?

A

Tumour parathyroid-related-protein production which increases serum calcium levels as can bind same receptors as parathyroid hormone (most effects on bones and kidneys but doesn’t usually increase calcitriol)
Causes 80% of cases

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10
Q

Whats the other pathology mechanisms of hypercalcaemia of malignant disease?

A

Osteolytic metastases - bone lysis directly by tumour cells e.g. myeloma cells secrete IL-1 and TNF which increase osteoclast activity

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11
Q

How do you investigate hypercalcaemia?

A

Measure adjusted calcium
PTH - as most likely cause is primary hyperparathyroidism
Calcitriol - ?vitamin D deficiency
PTHrP - ?malignancy
Bone scan

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12
Q

How do you manage hypercalcaemia?

A

Generally no active treatment unless acute onset or severe/symptomatic hypercalcaemia (>3.5mmol/L)

Aggressive rehydration with 2-4 litres of 0.9% saline IV over 24 hours
IV Bisphosphonates e.g. zoledronic acid - inhibits osteoclast activity (take 2-4 days to see effects after introduction)
Glucocorticoids (inhibit 1,25OH vitamin D production)
Check medication list for calcium or vit D supplements

In resistance cases consider giving calcitonin or denosumab. Calcitonin has a more rapid but shorter-term effect than bisphosphonates
Long term treatment is to Manage malignancy

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13
Q

Whats the most common cause of Hypercalcaemia in hospital and in the community?

A

In hospital its metastatic cancer
In the community its primary hyperparathyroidism

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14
Q

What are the side efefcts of zoledronic acid?

A

Renal impairment
Flu-like symptoms
Hypocalcaemia
Chronic use can cause osteonecrosis of the jaw and external auditory canal

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15
Q

What are the causes of hypercalcaemia?

A

CHIMPANZEES

Calcium supplements
*Hyperparathyroidism
Iatrogenic e.g. thiazides and lithium
Milk alkali syndrome
Pager disease of the bone
Acromegaly and Addison’s disease
*Neoplasia
Zolinger-Ellison syndrome (MEN type 1)
*Excessive vitamin D
Excessive vitamin A
*Sarcoidosis

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16
Q

When would you do an ECG in patients with hypercalcaemia?
What would you expect?

A

> 3.5mmol/L
Decreased QT interval

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17
Q

What PTH, PTHrP and calcitriol levels would you expect in tumour PTHrP production?

A

Low PTH

High PTHrP

Normal-low calcitriol

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18
Q

What PTH, PTHrP and calcitriol levels would you expect in osteolytic metastases?

A

Low PTH
Low or normal calcitriol levels
Low or normal PTHrP

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19
Q

What are the most common organs for cancers to metastasize to?

A

Lung
Liver
Bones

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20
Q

Which primary tumours are most likely to metastasises to bones?

A

Prostate
Breast
Lung
Kidney
Myeloma

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21
Q

How does metastatic bone cancer usually present?

A

Pain
Pathological fractures
Spinal cord compression
Hypercalcaemia
Symptoms of nerve root compression
Swelling/deformity and loss of mobility

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22
Q

What are the most common sites for bone metastases?

A

Spine, pelvis, femur, ribs and humerus

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23
Q

What is appendicular bone mets? Which primary tumours typically cause it?

A

bone metastases. located distal to the elbow and knee
Renal and lung tumours

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24
Q

What characteristics of bone pain would make you worry about bone metastases?

A

Progressive pain over time
Pain that doesnt respond to simple analgesia
Pain that disturbs sleep
Pain associated with bone tenderness
Pain associated with weight loss

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25
What is the mechanism by which bony metastases occur?
bone metastases disturb the dynamic balance between osteoclasts and osteoblasts If there is greater osteoclast activity then lytic metastases is likely If there is greater osteoblast activity then disordanised ossification is more likely
26
Does sclerotic or lytic bony metastases have. A higher risk of fracture?
Lytic
27
How do we investigate bone metastases?
FBC Bone related ALP Kidney function and liver function tests PSA to rule out prostate cancer Paraproteins and bence jones proteins in urine to rule out multiple myeloma Plain x-ray Bone scans
28
Why do we test for ALP in suspected bone metastases?
Your bones make an isoenzyme called ALP-2. Levels of this enzyme increase when your bones are growing or bone cells are active
29
Why are x-rays not as sensitive as bone scans for bone metastases?
The lesion has to be at least 1-2cm to be seen In contrast, bone scans use a radioactive tracer to detect areas of abnormal bone turnover, which can help detect bone metastases earlier and more accurately than x-rays
30
How can you manage bone pain?
Pain meds using the analgesia ladder Palliative radiotherapy Zoledronic acid IV every 3-4 weeks Surgical fixation if fractures
31
Whats a serious side effects of bisphosphonates?
Osteonecrosis of the jaw
32
Moa of denosumab?
A human monoclonal antibody specific for RANKL that inhibits the formation, activation and survival of osteoclasts which decreases bone resorption
33
What is a vertebroplasty?
an outpatient procedure for stabilizing compression fractures in the spine. Bone cement is injected into back bones (vertebrae) that have cracked or broken. The cement hardens, stabilizing the fractures and supporting your spine.
34
What are the most commonly used isotopes in treatment of painful bone metastases?
Strontium 89 and samarium 153
35
How does spinal cord compression present?
Pain in back that’s worse on lying down/worse on movement/increases with vasalva manoeuvre May cause radicular pain Tenderness Autonomic dysfunction Sensory deficits Motor weakness Hypereflexia and increased tone Bowel and bladder dysfunction
36
Whats the prevalence of MSCC?
3-5% of all cancer patients
37
What are the most common causes of Spinal cord Compression?
Tumours Trauma Osteoarthritis Herniated disc RA Spinal injury Infection Etc…
38
How do we grade spinal cord compression?
Epidural spinal cord compression scale grade 0: bone-only disease grade 1: epidural extension without cord compression 1a: epidural extension only 1b: deformation of thecal sac 1c: deformation of the thecal sac with spinal cord abutment grade 2: spinal cord compression, with CSF visible around the cord grade 3: spinal cord compression, no CSF visible around the cord
39
Why is there often a delay in diagnosis of spinal cord compression?
Slow onset progressive pain that precedes other symptoms by 7 weeks
40
At what vertebral level does the spinal cord end?
L1-L2 junction (conus medularis)
41
What region of the spinal cord is spinal cord compression most likely and why?
60% thoracic 30% lumbar and sacral 10% cervical This is roughly equivalent to the relative bone mass in each segment
42
How does Cauda equina present?
Pain Flaccid paralyses Sensory deficits Bladder retention and bowel dysfunction Sexual dysfunction Areflexia and decreased muscle tone
43
At what level can spinal cord injury cause neurogenic shock?
Above T6
44
What is neurogenic shock?
a distributive type of shock resulting in hypotension often with bradycardia caused by disruption of autonomic nervous system pathways (loss of SNS so PNS is unopposed)
45
Why can neurogenic shock only happen with spinal cord compression above T6?
loss of thoracic sympathetic outflow which results in decreased venous tone, causing pooling of the blood volume in the extremities and hypotension.
46
How can you prevent neurogenic shock?
Compression stockings
47
How do you manage spinal cord compression/Cauda equina syndrome?
Immobilisation (consider compression socks and thromboprophylaxis) Dexamethasone with a PPI Whole spine MRI urgently If MRI confirms then urgent neurosurgical referral or radiotherapy if not indicated Analgesia
48
Who should get surgery for spinal cord compression/Cauda equina syndrome?
Those who can still walk or have residual distal sensory and motor function and a good prognosis If completely paraplegic for >24 hours then only offer spinal re-alignment for pain relief
49
What makes MSCC and Cauda equina syndrome have a good prognosis?
A single lesion Responsive to steroids Limited neurological deficits Radiation sensitive e.g. multiple myeloma and small cell lung cancer Moderately sensitive e.g. breast and prostate cancers Early surgery and radiotherapy within 24 hours of developing neurological signs
50
What is superior vena cava syndrome?
SVC becomes blocked, commonly due to tumours. They either compress the vessel or invade the vessel itself. This causes reduced venous return from head, neck and upper limbs
51
Which cancers is SVC most associated with?
Lung cancers (50% cases by non-small cell cancers but this may just be because they’re more common) Lymphomas Metastatic Note 90% of cases are caused by maliganncy
52
What are non-cancer causes of SVC syndrome?
Aortic aneurysms Blood clots near a pacemaker or intravascular catheter TB (very rare)
53
What are the signs and symptoms of SVC syndrome?
SOB Facial swelling, particularly worse lying down Arm swelling Cough and chest pain Distended veins in neck and chest Distended collateral veins Pembertons test - elevation of arms to side of head causes facial cyanosis
54
Why is SVC syndrome a oncological emergency?
Itself is not life-threatening but if left untreated, tumours can go on to invade the trachea and block the airway leading to cardio-respiratory arrest There is also a risk of cerebral oedema due to excess fluid which potentially could cause ischaemia and increased ICP
55
What are symptoms of cerebral oedema?
Headaches Confusion Loss of consciousness
56
How is SVC syndrome diagnosed?
Clinical signs Abnormal chest X-ray (in 85% of cases) - most commonly mediastinal widening and pleural effusion Contrast CT to identify level of obstruction and presence of collateral veins Sputum cytology, pleural fluid cytology or biopsy of supraclavicular lymph nodes (if not possible then bronchoscope or mediastinoscopy)
57
How do you treat superior vena cava syndrome?
Sit patient up and assess for hypoxia. give oxygen if required. 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
58
Which cancers is spinal cord compression and Cauda equina syndrome most commonly associated with?
Lung Prostate Breast Myeloma Melanoma
59
How soon should you treat spinal cord compression and Cauda equina syndrome?
Within 24 hours wherever possible
60
What is neutropenic sepsis?
It may be defined as a neutrophil count <0.5 x 10 power 9/L in a patient who is having anti cancer treatment Temperature over 38 degrees or other signs/symptoms consistent with clinically significant sepsis
61
What is febrile neutropenia?
The presence of fever in a person with neutropenia
62
Who should you suspect neutropenic sepsis in?
Any patients who are unwell within 6 weeks of recieving chemotherapy
63
What are the main causes of neutropenic sepsis?
Indwelling catheters e.g. PICC or hickman lines Commonly caused by coagulase-negative, Gram-positive bacteria - particularly Staphylococcus epidermidis
64
How do you manage neutropenic sepsis?
Sepsis 6 bundle of care within the first hour following recognition of sepsis This includes empirical broad spectrum antibiotic therapy with piperacillin and tazobactam within 1 hour of arriving at hospital the addition of antifungal coverage considered in high risk patients who remain febrile 3-7 days after antibiotics given Chest X-ray
65
How long after chemo is the lowest neutrophil count?
5 to 10 days after the last dose of chemotherapy
66
How can we prevent neutropenic sepsis?
For adult patients with acute leukaemias, stem cell transplants or solid tumours in whom significant neutropenia is an anticipated consequence of chemotherapy, fluoroquinolone is offered prophylactically
67
What is tumour lysis syndrome
An oncological emergency with a severe metabolic disturbance caused by the abrupt release of large quantities of cellular components into the blood following the rapid lysis of malignant cells. It leads to a high potassium, high urate and high phosphate level in the presence of a low calcium.
68
Who should tumour lysis syndrome be suspected in?
any patient presenting with an acute kidney injury in the presence of a high phosphate and high uric acid level
69
How is laboratory tumour lysis syndrome diagnosed? (Cairo-bishop classification)
Abnormality in 2 or more of the following, occurring within 3 days before or 7 days after chemotherapy: - uric acid >8mg/dL - potassium >6mmol/L - phosphate >2.1mmol/L - Calcium <1.75mmol/L (Or 25% change in these)
70
How is clinical tumour lysis syndrome diagnosed?
Laboratory tumour lysis syndrome plus one or more of the following: - increased serum creatinine (1.5 times upper limit of normal) - i,.e. AKI - cardiac arrhythmia or sudden death -seizure
71
Outline the pathology of tumour lysis syndrome?
When cancer cells lyse, they release potassium, phosphorus, and nucleic acids, which are metabolized into hypoxanthine, then xanthine, and finally uric acid, an end product in humans Uric acid precipitates out in the DCT and collecting tubules of kidney and damage the kidneys, causing AKI Malignant cells often have 4x the phosphorous. It meets with calcium in blood stream and forms calcium phosphate. This can deposit in the kidneys causing AKI and can deposit in the heart. this causes secondary hypocalcaemia which causes prolonged QT interval and has effects on CNS causing seizures Release of high levels of K+ cause unstable myocardial cells which can cause arrhythmias and cardiac arrest
72
What are the risk factors for tumour lysis syndrome?
High proliferation rate of tumour Those recieving chemo/radiotherapy Those with haematological cancers Those with bulky disease Pre-existing hyperuricaemia Pre-existing renal disease Dehydration
73
What symptoms can tumour lysis syndrome cause?
Nausea, vomiting diarrhoea, anorexia, lethargy, muscle cramps, syncope, tetany, dark urine or reduced urine output, heart palpitations
74
How is tumour lysis syndrome treated prophylactically?
Rasburicase and IV hydration for high risk cases (uric oxidase) Allopurinol and IV hydration for intermediate risk Give these immediately prior to and during the first days of chemotherapy
75
How do we manage tumour lysis syndrome?
Monitor K+, Calcium and phosphate levels Treat any electrolyte abnormalities that occur e.g. phosphate binders, calcium replacement, Haemofiltration if AKI, fluid overload or refractory hyperkalaemia
76
What are the side effects of rasburicase
Methaemoglobinaemia Anaphylaxis Vomiting and nausea Headache Fever Diarrhoea
77
How does rasburicase work?
a recombinant version of urate oxidase, an enzyme that metabolizes uric acid to allantoin. Allantoin is much more water-soluble than uric acid and is, therefore, more easily excreted by the kidneys
78
Who is rasburicase contraindicated in
G6PD deficiency - causes haemolysis
79
What is leukostasis?
a pathologic diagnosis in which white cell plugs are seen in the microvasculature It’s associated with a very high WCC, resp failure, intercranial haemorrhage and early death
80
Which cancer is leukostasis mostly associated with?
Acute leukaemias
81
What is syndrome of inappropriate ADH secretion?
the unsuppressed release of ADH from the pituitary gland or nonpituitary sources or its continued action on vasopressin receptors. It should be considered whenever a patient with malignancy presents with hyponatraemia
82
Which cancer is most commonly associated to SIADH?
70% of cases are associated with small cell carcinoma of the lung
83
What score tool can be used to identify patients at low risk for poor outcome with febrile neutropenia?
MASCC risk index
84
What does the MASCC risk index use to calculate risk for poor outcome with febrile neutropenia?
Symptom severity Hypotension sBP<90 Active COPD Type of cancer Dehydration requiring IV fluids Inpatient or outpatient at onset of fever <60 or >60
85
What are symptoms of brain metastases?
Headache that is often worse in the morning or when coughing or bending Focal neurological signs Ataxia Fits\ Nausea vomiting Papilloedema
86
Whats the first sign of spinal cord compression?
Loss of reflexes
87
When does hypercalcaemia typically become symptomatic?
>3mmol/L
88
What could a raised ALP with normal liver function tests mean??
Malignancy - particularly bone metastasis
89
whats the most common cause of SVC syndrome in cancer patients
Non-small cell lung cancer

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