Oncological Emergencies Flashcards
Define Neutropenic Sepsis
Potentially life threatening complication of anti cancer and immunosuppressive treatment
Temperature greater than 38 degrees/any signs or symptoms of sepsis in someone with an absolute neutrophil count of <0.5x10^9
Define Febrile Neutropenia
Presence of fever in a person with Neutropenia
Two consecutive readings of more than 38 degrees for two hours
Give four causes of Neutropenic Sepsis
Chemotherapy
HSCT
Drugs (Immunosupressants, Clozapine)
Bone Marrow Failure
How does Neutrophil count vary with chemotherapy?
Neutrophil count typically lowest 5-10 days after last chemotherapy dose and recovery is normally 5-10 days later
What are the normal infective organisms in Neutropenic Sepsis?
S.Pyogenes, S.Aureus. S. Enterococcus, S.Pneumoniae
Other than chemotherapy, give four risk factors for Neutropenic Sepsis
Age (Infants and Over 60s)
Corticosteroids and Abx
Central Venous Access device
TPN (increased fungal risk)
How should you assess a patient with suspected Neutropenic Sepsis?
Temperature history (may present with hypo)
Focus on current symptoms
Cancer and Chemo History
Recent Abx/Steroid use
A to E
How quickly should Sepsis 6 be started in Neutropenic Sepsis?
Within one hour
What is the first line antibiotic in Neutropenic Sepsis?
Tazocin
Meropenem if Pen Allergic
Other than the Sepsis 6, what investigations can be done if Neutropenic sepsis is suspected?
CXR
Urine Culture
Sputum Culture
Swab any lines
What is Spinal Cord Compression?
Occurs as a result of metastatic/spinal tumour growth that either directly or indirectly causes impingement of spinal cord
Name 5 cancers that have the highest incidence of spinal cord compression
Myeloma
Prostate
Nasopharynx
Breast
Lung
Describe the pathophysiology of Malignant Compression
Primary (Primary Bone Tumours, CNS malignancy)
Secondary (Metastatic, Non Metastatic - mechanical weakness secondary to cancer, paraneoplastic)
Give three possible mechanisms of metastatic spread to spine
Haematogenous arterial seeding
Shunting of abdominal venous flow to epidural plexus by Valsalva
Extension through intervertebral foramen
Name three non malignant causes of Spinal Cord Compression
Trauma
Disc Prolapse
Haematogenous
Describe the common distribution of Spinal Cord Compression
60% Thoracic
30% Lumbar
10% Cervical
How can a Spinal Cord Compression above L1/2 present?
95% severe progressive pain
85% weakness
Upper Motor Neurone lesion picture
May have peripheral paraesthesia
How would a Cauda Equina compression present?
LMN pattern (normally unilateral)
Saddle Anaesthesia, Reduced Anal Tone, Painless Urinary Retention, Impotence, Absent Ankle Jerk
Lower back pain
What is the gold standard investigation for Spinal Cord Compression?
MRI
Describe the general management of Spinal Cord Compression
Analgesia using WHO ladder
VTE Prophylaxis
Catheter for any bladder dysfunction
High dose Dexamethasone
Describe the definitive management of Spinal Cord Compression
Surgical decompression and reconstruction ideally (if not then vertebroplasty and kyphoplasty)
+/- External Beam Radiotherapy or Stereotactic Body Radiotherapy
Define Malignant Hypercalcaemia
Serum Calcium >2.6mmol/l secondary to a malignant process
Describe the normal distribution of Calcium
99% Bone, 0.1% Extracellular, 0.9% Intracellular
Extracellular: 50% Ionised (Active), 41% Bound, 9% Complexed
Name three hormones involved in the balance of Calcium
Vitamin D
Calcitonin
PTH
What molecule must Calcium be corrected for and how?
Albumin
0.1 mmol added for every 4g/l below 40 that the albumin is
State the parameters of severity in Malignant Hypercalcaemia
Mild = 2.6 -3 mmol/l
Mod = 3-3.5 mmol/l
Severe = >3.5mmol/l
What four cancers is Malignant Hypercalcaemia most commonly associated with
Breast Cancer
Multiple Myeloma
Lymphoma
Lung Cancer (SCC)
What three mechanisms cause Malignant Hypercalcaemia?
PTHrP (Breast and Non Hodgekins)
Osteolytic Mets
Increased Activation of Vitamin D (Hodgekins Lymphoma)
How do Osteolytic Metastases cause Hypercalcaemia?
Deposition of tumour cells leads to local production of inflammatory cytokines, causing osteoclast stimulation
Malignant Hypercalcaemia can be entirely asymptomatic. How would mild Hypercalcaemia present?
Polydipsia
Polyuria
Confusion
How is Malignant Hypercalcaemia investigated?
Based on measurement of serum calcium and identifying underlying cancer
PTH should be low
If Serum Calcium is >3mmol or they are symptomatic, how is Malignant Hypercalcaemia managed?
Admit
IV Rehydration, Calcitonin and Bisphosphonate Therapy
If Serum Calcium is <3mmol or they are symptomatic, how is Malignant Hypercalcaemia managed?
Outpatient management with oral rehydration (3-4L/d) and regular review
What is Superior Vena Cava Obstruction?
Obstruction of the flow of blood through the Superior Vena Cava secondary to cancer
Describe the anatomy of the Superior Vena Cava
Venous drainage of upper limbs, head and neck
Valveless Structure
Name two cancers classically causing SVCO
Lung Carcinoma
NHL
Why is it of benefit to the patient if the SVCO is gradual?
Allows collateral vasculature to form
State three symptoms of SVCO
Dyspnoea
Facial Swelling
Head Fullness
State three signs of SVCO
Facial Swelling
Distended Vein
Facial Plethora
What is Pemberton’s Sign for SVCO?
Patient asked to raise both arms above head for 1-2 minutes
Positive result is congestion, cyanosis, and respiratory distress
How is SVCO investigated?
CXR (>80% have an abnormality)
CT is diagnostic (shows extent of obstruction, presence of collateral vessels, and staging of any lung cancer)
What is the Emergency Management of SVCO?
Normally if patient is in RDS or has Cerebral Oedema
Diuretics +/- Steroids
Stent (+/- Anticoagulation)
What is the non emergent management of SVCO?
Elevation of Head and Neck
Titred Oxygen
Radiotherapy
Stent
Steroids (if steroid responsive)
What stents can be used in SVCO?
Balloon Expandable and Self Expanding
Percutaneously inserted
SVCO is a poor prognostic indicator. If this is their first presentation then what is the life expectancy?
6 months
What is Tumour Lysis Syndrome?
Metabolic disturbances caused by breakdown of malignant cells following initiation of treatment for malignancy
What electrolyte abnormalities come from rapid cellular breakdown?
Hyperkalaemia
Hyperphosphataemia
Hypocalcaemia
Hyperuricaemia
Can cause AKI and arrhythmias
Name four risk factors for Tumour Lysis Syndrome
Haematological Malignancy
Chemosensitivity
Large Tumour Burden
Renal Impairment
Why is risk stratification important in Tumour Lysis Syndrome?
Assesses need for prophylactic therapy and monitoring
Describe the pathophysiology of Tumour Lysis Syndrome
Hypocalcaemia develops secondary to hyperphosphataemia with precipitation in soft tissues
Hyperuricaemia occurs due to metabolism of nucleic acids
Leads to AKI due to precipitation of uric acid and calcium phosphate in renal tubules
What is the onset of Tumour Lysis Syndrome?
Normally within 72 hours of treatment (but can occur up to seven days)
How does Tumour Lysis Syndrome present?
Lethargy, Nausea and Vomiting, Diarrhoea, Anorexia, Muscle Cramps
Generally presents as the electrolyte abnormalities that are caused
What bloods would you want to do for suspected Tumour Lysis Syndrome?
Renal Function
Electrolytes
Serum LDH
Serum Lactate
If high risk, repeat every 4-6 hours
Diagnosis of Tumour Lysis Syndrome is based on the Cairo Bishop Definition which divides into lab and clinical definition. What is the lab definition?
Two or more abnormal serum values occurring 2 days before treatment or up to 7 days after
Diagnosis of Tumour Lysis Syndrome is based on the Cairo Bishop Definition which divides into lab and clinical definition. What is the clinical definition?
One of:
Serum Creatinine >1.5 times upper limit
Cardiac Arrhythmia/Sudden Death
Seizure
The above criteria form basis of graded severity
Describe the production of Uric Acid
Purines get converted to Hypoxanthines
Xanthine Oxidase converts Hypoxanthine into Xanthine and Uric Acid
What two agents can be used against Hyperuricaemia in Tumour Lysis Syndrome?
Allopurinol (only useful as prophylaxis as cannot act against existing uric acid)
Rasburicase (converts uric acid into soluble allontoin)
How would Hyperphosphataemia in Tumour Lysis Syndrome be managed?
Hydration and Dietary Restriction
Phosphate Binders
Severe - Haemofiltration
How would Hypocalcaemia in Tumour Lysis Syndrome be managed?
Mild - Do not treat, as calcium phosphate deposits could form in kidney
Symptomatic - IV replacement
What prophylaxis would you give a low risk patient for Tumour Lysis Syndrome?
Oral Hydration
Monitor
What prophylaxis would you give an intermediate risk patient for Tumour Lysis Syndrome?
Saline
Allopurinol
What prophylaxis would you give a severe risk patient for Tumour Lysis Syndrome?
Saline
Rasburicase
When would you consider Haemofiltration in Tumour Lysis Syndrome?
Intractable fluid overload
Refractory Hyperkalaemia
Hyperphosphataemia induced symptomatic hypocalcaemia
Describe Virchow’s Triad
Venous Stasis
Endothelial Dysfunction
Hypercoaguable state
Why does Cancer predispose patients to venous stasis?
Prolonged immobility
Direct compression of tumour
Why does Cancer predispose patients to Hypercoaguablity?
Malignant cells themselves are hypercoaguable and can induce normal cells to be hypercoaguable (by cytokine and adhesion alteration)
What is the Khorana Risk Model?
Validated screening tool to assess patients VTE risk and whether they need prophylaxis.
Determines the risk of VTE at 2.5 month follow up
What are the parameters for Khorana Risk Model?
Site (2 if stomach/pancreas, 1 if lung/lymphoma/gynae/GU)
Platelet > 350
Leucocyte > 11
Hb < 100
BMI > 35
What score from the Khorana Risk Model indicates the need for prophylaxis?
Greater than or equal to three
How is VTE in oncology managed?
DOAC (standard duration is 6 months but should be re-evaluated)
How would Moderate Hypercalcaemia present?
Constipation
Fatigue
Weakness
How would severe Hypercalcaemia present?
Abdominal Pain
Nausea and Vomiting
Pancreatitis
Arrhythmias (short QT, J waves)
