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Oncological Emergencies Flashcards

1
Q

What is neutropenic sepsis?

A

Fever > 38
Or features of sepsis

In a patient with a neutrophil count of < 0.5 x 10^9/L

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2
Q

What are the causes of neutropenic sepsis?

A

Genetic - congenital neutropenia, syndromes such as Chediak-Higashi

Cytotoxic related - therapies

Intrinsic disease of bone marrow; haematological malignancies, tumour infiltration, aplastic anaemia, ionising radiation

Immune mediated - uncommon, IBD inflammatory conditions, arthritides

Drugs stimulating formation of antibodies damaging granulocytes e.g. anti-thyroid drugs, carbimazole

Nutritional deficiencies e.g. folate and Vitamin B12

Increased neutrophil turnover - bone marrow cannot adequately replace them
Bacterial infections and hypersplenism

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3
Q

What are the causative organisms of neutropenic sepsis?

A

Most commonly bacteria
Gram neg - E Coli, Klebsiella, pseudomonas aeruginosa

Gram pos - S. epidermis, Staph aureus, strep pneumoniae

Other - c. diff

Viruses in high risk patients, usually prevented by prophylactic antiviral therapy
Otherwise herpes, varicella zoster, EBV - secondary to reactivation of latent infections

Fungi - Candida, aspergillus
Patients with haematological malignancies often require anti-fungal prophylaxis e.g. fluconazole

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4
Q

What are the clinical features of neutropenic sepsis?

A

Patients may have blunted response and subtle signs
High index of suspicion

Patients may present with signs for specific infection, or fever and non-specific symptoms

Temp >38 or hypothermia <36
Resp rate >20 breaths/min
Blood pressure systolic < 90
HR >90 BPM

Cognition - acute confusion
Urine output <0.5-1ml/kg/hr

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5
Q

What are the investigations for neutropenic sepsis?

A

Bedside
Obs, sugar, preg test

Bloods
VBG/ABG
FBC
CRP
U&Es
LFTs
Bone profile
Clotting
Fungal assays
BBV Screen
Cultures
Blood, line
Sputum, urine, stool
C diff
Viral PCR
Wound swabs

Imaging
CXR, LP, ECHO

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6
Q

What is the sepsis six bundle?

A

Three In

High flow oxygen target of 94-98 unless COPD 88-92
IV fluids, 500ml crystalloid over 15 mins
Abx empirical e.g. tazocin

Three Out
Two sets of blood cultures
Serum lactate via blood gas - arterial or venous
Urine output

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7
Q

What is the Multinational Association for Supportive Care in Cancer (MASCC) Risk Index?

A

Patients with neutropenic sepsis can be risk stratified with this

Disease Burden
5 none/mild
3 moderate
0 severe

Co-morbidities
5 No hypotension
4 No COPD
4 Solid tumour/haematological but no previous fungal infection
3 no dehydration needing IVF

If yes to any = 0

Status of onset
3 outpatient
0 inpatient

Age
2 less than 60
0 60 or older

LOW RISK > 21
HIGH RISK < 21

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8
Q

What is the treatment of neutropenic sepsis?

A

LOW RISK
Oral abx, consider outpatient care

HIGH RISK
IV abx, inpatient management

Identify source of infection
Sepsis 6

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9
Q

What do you examine on a patient with ?neutropenic sepsis?

A 
Cardio
Resp
Lymph nodes
Lines
focus on causes - GI exam
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10
Q

A patient in hospital with neutropenic sepsis has been treated for 5 days but there is still no change, what do you do?

A

Consider fungi/parasite causes

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11
Q

When should antibiotics be started for neutropenic sepsis?

A

As soon as suspected

Don’t wait for bloods

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12
Q

What is malignant cord compression?

A

Radiological evidence of indentation of the thecal sac secondary to cancer

or also cauda equina - collection of lumbar, sacral, coccygeal nerve roots descending from end of spinal cord at L1.

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13
Q

What can cause malignant compression of the spinal cord

A

Primary
Primary bone tumours
CNS malignancies

Secondary
Mets
Non-metastatic - mechanical structural weakness due to cancer
Paraneoplastic

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14
Q

What are other causes of cord compression important to recognise?

A 
Trauma
Intervertebral disc prolapse
Haematoma
Epidural abscess - secondary to osteomyelitis or discitis
Cervical spondylitic myelopathy
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15
Q

What cancers are most commonly associated with cord compression secondary to metastatic disease?

A 
Lung
Breast
Kidney
Prostate
Thyroid
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16
Q

Where do most cord compressions occur?

A

Thoracic - 60%

Lumbar 30%, cervical 10%

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17
Q

What are some of the causes of vertebral mets?

A

Arterial seeding
Shunting of blood through epidural venous plexus
Extension through intervertebral foramina

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18
Q

How many patients tend to get MSCC?

A

10% of patients with spinal mets

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19
Q

What are the consequences of early MSCC?

A

Cord compression –> oedema –> venous congestion

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20
Q

What are the consequences of late MSCC?

A

Irreversible vascular injury –> cord necrosis

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21
Q

What signs are indicative of metastatic spinal cord compression?

A 
Back pain - worse on waking and aggravated by straining
Spinal tenderness
Limb weakness
Sensory loss
Incontinence
Generally unwell
Spasticity
Babinski +ve
Palpable bladder
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22
Q

How is MSCC investigated?

A

MRI within 24 hours

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23
Q

How is MSCC managed?

A

Bed rest with neutral spine alignment need to be (log rolled)
Dexamethasone (unless lymphoma suspected)
Analgesia
Bisphosphonates (myeloma, breast and prostate mets only)
Definitive treatment: Decompression or radiotherapy within 24hrs
Supportive care - VTE prophylaxis, catheter, bed sore management, temperature checks

Surgery
Decompression
Reconstruction

Vertebroplasty
Kyphoplasty
If unable to undergo full decompression and reconstruction

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24
Q

What is the role of radiotherapy in MSCC management?

A

Relieve compression of spine and nerves - cause cell death

Pain relief and stabilise neurological deficit

External beam radiotherapy as an adjuvant or definitive for those unable to undergo surgical intervention

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25
What are the signs of cauda equina?
``` Back pain Radiculopathy Reduced anal tone Saddle anaesthesia Painless retention of urine, change to urine/bowels Paralysis Hyporeflexia Hypotonia ```
26
What is malignant hypercalcaemia?
Serum calcium >2.6 mmol/L | Secondary to malignant process
27
What is normal serum calcium?
Between 2.2-2.6 mmol/L Mild is 2.6-3.0 Severe is >3.5
28
What are the most common malignancies associated with hypercalcaemia?
Breast cancer Multiple myeloma Lymphoma Lung cancer e.g. squamous cell carcinoma
29
What are the three main mechanisms causing malignant hypercalcaemia?
Osteolytic metastasis PTH related protein secretion Increased 1.25-Vit D production
30
Why does PTHrP secretion cause hypercalcaemia?
Release of PTHrP from tumour cells e.g. breast carcinomas and non-Hodgkin's lymphoma Is structurally similar to PTH and leads to increased bone resorption Distal renal tubular calcium absorption Inhibition of proximal phosphate transport
31
How does osteolytic mets cause hypercalcaemia?
Commonly associated with breast cancer Deposition of tumour cells in bone leads to local production of inflammatory cytokines and other mediators Causes osteoclasts to be stimulated leading to bone resorption
32
In what malignancies can there be an increased production of 1.25-Vit D?
Increased Vit D leads to increased absorption of calcium Hodgkin's lymphoma May also be seen in chronic granulomatous disease e.g. sarcoidosis
33
What are the clinical features of malignant hypercalcaemia?
Stones, bones, groans, psychiatric moans Mild - often asymptomatic Polyuria, polydipsia, mild cog impairment, dyspepsia Mod - all mild features Constipation, weakness Fatigue, dehydr, nausea Severe Abdo pain, vomiting Cardiac dysrhythmias Pancreatitis, coma
34
What are the investigations needed for diagnosis of malignant hypercalcaemia?
Serum calcium level Identification of underlying cancer Biochemical markers can differentiate between primary hyperparathyroidism and malignant hypercalcaemia In malignant hypercalcaemia, PTH should be suppressed Full examination, breast exam Investigations targeted to any potential cause Myeloma screen - immunoglobulins, protein electrophoresis, urinary light chains Imaging e.g. CT
35
What is the management of malignant hypercalcaemia?
Intravenous rehydration Calcitonin and bisphosphonates Admission for any patient with serum calcium >3mmol/L or if symptomatic and lower and underlying malignancy If underlying malignancy cannot be addressed - likely to recur within 2 weeks Additional therapies e.g. glucocorticoids, denosumab, dialysis
36
What is the function of calcitonin?
Mod or severe hypercalcaemia | Promotes urinary calcium excretion and inhibits bone resorption
37
How do bisphosphonates work?
Analogues of inorganic pyrophosphate Absorbed onto the surface of the bony network Inhibit the action of osteoclasts Pamidronate or zoledronic acid
38
What is the anatomy of the SVC?
Provides venous drainage for the upper limbs, head and neck Originates posterior to lower aspect of right first costal cartilage at union of right and left brachiocephalic veins Descends to join the right atrium, valveless
39
What are the most common causes of SVCO?
Lung carcinoma most commonly NSCLC | Non-Hodgkin's
40
What is the pathophysiology of SVCO?
Obstruction results in formation of collateral vessels - azygous system - internal mammary - long thoracic therefore if slow progressing obstruction, adequate time for collaterals and so mild symptoms
41
What are the clinical features of SVCO?
``` Symptoms Dyspnoea, facial swelling Head 'fullness', headache Symptoms exacerbated bending forwards/lying down Cough, blurred vision Dysphagia ``` ``` Signs Facial swelling Distended neck and chest wall veins Upper limb oedema Facial plethora Cyanosis Cognitive dysfunction Coma ```
42
What is Pemberton's sign?
Elevate both arms above head for 1-2 mins Positive sign - causes congestion, cyanosis or resp distress Occurs due to increased venous return from upper extremities exacerbating obstruction
43
How can SVCO be diagnosed?
80% have abnormal CXR Need to see underlying cause Findings include mediastinal widening, malignant pleural effusion CT shows extent and level of obstruction and collateral vessels Duplex USS in those with indwelling catheters May need biopsy for malignant cause
44
What is the emergency management of SVCO?
Rare, to treat respiratory distress or cerebral oedema Stridor may be present Senior review, peri-arrest Diuretics Steroids Related to thrombus - stent, not related - thrombolysis
45
What is the general management of SVCO?
Relieve obstruction Imaging and histology Elevation of head and neck Oxygen titrated to sats Stenting Radiotherapy - NSCLC, lymphomas Chemo Anticoag or thrombolysis may be used if SVCO occurs secondary to intravascular thrombosis Glucocorticoids may help reduce swelling; dex Stent placed percutaneously, access via internal jugular, basilic or femoral veins
46
When is SVCO seen?
External compression from Lung cancer but can be from lymphoma
47
What is extravasation?
Leakage of IV drugs into extravascular space leading to nearby tissue damage
48
Why are chemo agents susceptible to causing extravasation?
Poorly soluble in aqueous media and are vesicant
49
How can extravasation be prevented?
Ensure IV fluid runs without resistance Stop infusion if pain at injection site Don't leave infusion unattended if highly vesicant Immediately stop infusion if suspicion
50
How does dehydration affect hypercalcaemia?
Exacerbate any underlying hypercalcaemia
51
What is tumour lysis syndrome?
Results from metabolic disturbances arising from the breakdown of malignant cells following initiation of treatment for malignancy
52
What electrolyte abnormalities are seen in TLS?
Hyperkalaemia Hyperphosphataemia Hypocalcaemia Hyperuricaemia Phosphate produced by tumour cells binds to calcium
53
What factors are associated with increased risk of TLS?
High proliferation rate Chemosensitivity Large tumour burden Pre-exisitng metabolic abnormalities e.g. hyperuricaemia and hyperphosphataemia Renal impairment
54
Who is at low risk of TLS?
<1% chance of developing TLS ``` AML with certain WBC, LDH criteria CLL with WBC and tx criteria Multiple myeloma CML NHL normal LDH Other solid tumours ```
55
Who is at an intermediate risk of TLS?
Certain NHLs with high LDH and absence of bulky disease Certain early stage NHLs ALL, AML, CLL with certain WBC, LDH, Tx criteria Bulky tumours highly sensitive to chemo e.g. germ cell, small cell
56
Who is at high risk of developing TLS?
Burkitt's leukaemia Certain Burkitt's lymphoma ALL with certain WBC, LDH AML with high WBC Certain NHLs with high LDH and bulky disease Intermediate risk with evidence of high risk clinical factors e.g, renal dysfunction
57
What is the pathophysiology of tumour lysis syndrome?
Cytotoxic mediated lysis of tumour cells Release of intracellular components Hypocalcaemia develops secondary to hyperphosphataemia with precipitation of calcium in soft tissues Can lead to AKI
58
What are the clinical features of TLS?
Tend to develop within the first 72 hours following tx initiation Can occur up to 7 days post treatment Symptoms Lethargy, N&V, diarrhoea Anorexia, muscle cramps, syncope, pruritus, arthritis Signs Fluid overload, haematuria, tetany, paraesthesia, bronchospasm
59
What are the investigations for TLS?
Renal function, electrolytes, serum urate to diagnose and assess severity High risk patients may need serial bloods every 4-6 hrs Urine dip, microscopy - uric acid crystals Serum lactate, LDH ECG, cardiac monitoring Serum urate levels in patients on rasburicase sent on ice to prevent falsely low levels
60
What is required for a laboratory diagnosis of TLS?
Cairo Bishop definition - lab definition and clinical def Presence of two or more abnormal serum values that occur three days prior to or seven days after beginning treatment
61
What clinical diagnosis is needed for TLS?
Meets lab diagnosis Presence of one or more features not due to therapeutic agent Serum creatinine >1.5 upper limit normal Cardiac arrhythmias/sudden death Seizure
62
What hypouricaemic agents are given to prevent TLS?
Prevent hyperuricaemia and the subsequent precipitation of uric acid in nephrons Allopurinol - xanthine oxidase inhibitor Does not act on pre-existing uric acid so is prophylactic ``` Rasburicase Recombinant urate oxidase Metabolises uric acid Works on established renal deposits Contraindicated with G6PD deficiency ```
63
What is involved in prophylaxis of TLS?
Low risk - oral hydration and monitor Intermediate - saline, allopurinol up to 600mg OD TLS screen High risk - saline; aim for UO >100ml/hour, rasburicase, TLS screen
64
What is involved in the management of TLS?
Calcium glutinate, insulin, dextrose for hyperkalaemia Hypouricaemic agents Phosphate binders IV hydration
65
What are some indications for haemofiltration in TLS?
Intractable fluid overload Refractory hyperkalaemia Hyperphosphataemia induced symptomatic hypocalcaemia High calcium phosphate product
66
What do calcium phosphate precipitates lead to?
Calcium phosphate deposition in: Renal tubules - AKI Skin - Gangrene Heart - Arrhythmia
67
What are the main risk factors for TLS?
Large volume disease Chemosensitive Haematological malignancy Poor renal function
68
How could you manage a suspected line infection?
Line locks - if not systemically very poorly can give high concentration abx (commonly gentamicin) through the line to sterilise it and save it from needing removal
69
When would a bone scan for bony metastasis not be useful?
Multiple myeloma - bone scan works by picking up areas where there is increased uptake of radioactive traced indicating osteoblastic activity. Multiple myeloma produced purely lytic lesions so it is not useful.
70
What should you do in a suspected line infection?
``` Give Teicoplanin (provides gram +ve cover) Can do line lock with high dose Gentamicin ```
71
What are the most common causes of central line associated blood stream infections?
Coagulase negative staphylococci e.g. S epidermidis Enteroccoci
72
Who does the risk of neutropenic sepsis increase with?
``` Prolonged neutropenia >7 days Severity of neutropenia Significant comorbidities Aggressive cancer Central lines Mucosal disruption Hospital inpatient ```
73
What are the most common responsible pathogens for neutropenic sepsis?
From endogenous flora Gram positive cocci from indwelling catheters promoting colonisation Staph aureus, epidermidis, enterococcus, streptococcus MRSA and vancomycin resistant enterococcus increasingly prevalent
74
When do you need to give empirical IV antibiotics in neutropenic sepsis?
Within the hour
75
Where is the most common site of MSCC?
Thoracic Below L2 vertebra = caudal equina
76
Who is likely to be fit for surgery for MSCC?
``` Fit and good prognosis Multiple myeloma, lymphoma, breast, prostate, renal cancers Good motor function at presentation Good performance status Limited comorbidity Single level spinal disease Absence of visceral mets Long interval from primary diagnosis ```
77
What is the management of SVCO?
``` Sit upright/elevate head Oxygen Dexamethasone 16mg plus PPI Opioids Benzodiazepines ``` Treatment Steroids Stent if not radio or chemo sensitive Anticoag if thrombus
78
What are other potential oncological emergencies?
``` Toxicity with newer oncological treatments e.g. immune checkpoint inhibitors - pneumonitis, colitis Seizures SIADH PE Non-neutropenic sepsis Massive haemorrhage Uncontrolled pain ```

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