Transcript oncologic emergencies

Oncologic Emergencies
Dr Karenza Alexis
Spinal Cord Compression
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1-5% of patients with systemic cancer
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MUST BE TREATED IMMEDIATELY
 Can lead to irreversible paralysis or loss
of bowel and bladder function
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Tumor or collapsed fragments in the
epidural space
Spinal Cord Compression
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Most Common sites
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Thoracic spine (70%)
Lumbrosacral (20%)
Cervical (10%)
Most common malignancies
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Lung
Breast
Unknown primary
Prostate
Renal
Multiple myeloma
Lymphoma
Spinal Cord Compression
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Symptoms and Signs
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Localized pain to the spine
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Exacerbated by movement, recumbency, coughing,
sneezing, straining
May appear weeks to months before neurological symptoms
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Radicular pain
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Weakness +/- sensory loss
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Autonomic dysfunction
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Urinary retention, constipation
Spinal Cord Compression
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Evaluation- complete neurologic and
physical exam that includes:
Gentle percussion of spinal column
 Passive neck flexion
 Straight Leg raise
 Motor and sensory exam, Reflexes
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 Pinprick
testing toe to head- sensory level
Is there a “sensory level”
 RECTAL exam
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Spinal Cord Compression
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Diagnosis- image the ENTIRE spine
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Xray
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MRI
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66% will have bony abnormalities
Erosion, loss of pedicles, vertebral body collapse,
paraspinous soft tissue mass
Cannot exclude epidural mets
Does not exclude cord compression if normal
Follow-up with MRI
STANDARD!!!!!!!
CT scan
Spinal Cord Compression
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Goal of treatment:
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recovery and maintenance of normal neurological
function,
stabilization of the spine
Local tumor control
pain control
Treatment Outcome:
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Degree of neurologic impairment
Radiosensitivity of tumor
Spinal Cord Compression
Treatment:
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Steroids
 START
DEXAMETHASONE IMMEDIATELY if you
suspect cord compression
 10 mg IVP followed by 4 mg IV every 6 hours
(higher doses be used if patient presents with significant
neurological impairment)
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Radiation
 Stable
spine with radiosensitive tumors, nonsurgical candidates with spinal instability,
 Port includes area of epidural involvement plus two
vertebral bodies above and below
Spinal Cord Compression
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Surgery
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Tissue diagnosis needed
Spinal instability
Prior radiation to affected area
Progression of cord compression despite steroids and
radiation
Resection followed by radiation therapy vs radiation
alone
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ASCO proceedings 2003: combine modality patients had higher
ambulatory rate and retained ability to walk longer
Spinal Cord Compression
In addition to initial evalutaion, imaging,
steorids: multidisciplinary management
 Neurology Consult
 Oncology Consult
 Neurosurgery Consult
 Radiation oncology Consult
Superior Vena Cava Syndrome
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Malignant causes
intrathoracic malignancies (60-85%)
 Lung cancer (more common in small cell), breast
cancer, testicular cancer, thymoma
 lymphoma and other malignancies with mets to
mediastinum
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Non-malignant causes
Thrombosis (most common cause in cancer
patients)
 Substernal thyroid goiter, TB, RT, sarcoidosis
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Superior Vena Cava Syndrome
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Signs and symptoms
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Facial edema/ erythema
Dilatation of veins of upper body
Laryngeal or glossal edema
Periorbital edema
Dyspnea
Cough
Orthopnea
Arm and neck edema
Hoarseness
Dysphagia
Headaches
Dizziness
syncope
Symptoms worse with positional changes: bending forward,
stooping or lying down
Superior Vena Cava Syndrome
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Result in:
 Life-threatening
 Laryngeal
cerebral edema
edema- airway compromise
Superior Vena Cava Syndrome
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Diagnosis- determine etiology
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Thorough Physical Examination
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CXR
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May show mediastinal widening
Doppler USG of jugular or subclavian vein
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Differentiate thrombus from extrinsic compression
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CT scan or MRI
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Bronchoscopy
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thoracoscopy
Superior Vena Cava Syndrome
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Treatment
Goal: alleviate symptoms and treat underlying disease
Initial management depends on Grade of SVCS,
underlying disease, anticipated resposbse
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Determine underlying cause- especially if SVCS is presenting
symptom
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Pace of progression of symptoms
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Treatment goal- Cure vs Palliation
Superior Vena Cava Syndrome
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Treatment
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Symptom management: Elevation of head of bed, O2, bed rest
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Radiotherapy
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Cure vs Palliation
Accurate histologic diagnosis needed prior
EMERGENT RT needed if life-threatening symptoms/signs (stridor/ CNS
symptoms from cerebral edema)
If Non-small cell lung cancer
Combine with chemotherapy if limited stage small cell lung cancer and NonHodgkin’s lymphoma
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Stenting for life threatening symptoms especially in tumors not sensitive
to chemotherapy or radiation or no diagnosis of cancer
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Chemotherapy
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Lymphoma or germ cell tumor or small cell lung cancer
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Consider thrombolysis, angioplasty if thrombosis
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Diuretics- transient, may cause dehydration and reduced blood flow
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Steroids
Hypercalcemia
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Occurs in 10-20% of cancer patients- bony
mets v paraneoplastic
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Assocciated most commonly with:
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myeloma, lung cancer (squamous cell), renal
cancer, breast cancer, head and neck tumors,
leukemias, unknown primaries
Hypercalcemia
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Symptoms/ signs
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Presence may depend on speed at which hypercalcemia
develops
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General: dehydration, anorexia, pruritis, weight loss, fatigue
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CNS: weakness, hypotonia, proximal myopathy, mental status
changes, seizure, coma
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Cardiac: bradycardia, short QT interval, prolonged PR interval,
wide T wave, atrial or ventricular arrythmias
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GI: nausea/vomiting, constipation, ileus, pancreatitis, dyspepsia
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Renal: Polyuria, nephrocalcinosis
Hypercalcemia of malignancy
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Diagnosis
 Ionized
calcium, Serum immunoreactive PTH- like
substance, phosphorus, 1,25 dihydroxyvitamin D
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If calcium only mildly elevated (<12) AND NO symptoms:
encourage PO hydration, eliminate any offending agents,
follow closely
If calcium is >12 OR symptoms:
 saline
infusion (be aware of cardiac and renal
function),
 loop diuretics (once euvolemia achieved). Follow
urine output and potassium, magnesium.
 Bisphosphonates
inhibit osteoclast function e.g
pamidronate
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Onset of action 24 to 48 hours
 Calcitonin
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Inhibits bone degradation by binding directly to receptors
on the osteoclast
onset of action is 2-4h but effect of short duration. Dose
is 2-8 U/kg SC or IM every 6-12 h
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If calcium >12 or symptoms
Gallium nitrate- inhibits bone resorption
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Onset of action 24 to 48 hours
100-200 mg/m2/d IV over 24 hours for up to 5 days in volume
replete non-oliguric patients
Once calcium is normal, stop treatment but CONTINUE TO
MONITOR for its continued effect
AVOID use of nephrotoxic drugs
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Plicamycin (25 ug/kg)
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Direct osteoclast inhibitory effects, may also block Vit D and
PTH activity
Onset of action is 24-48 h
Toxicity with repeated use: renal and liver toxicity,
thrombocytopenia
Tumor Lysis Syndrome
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Metabolic triad of hyperuriciemia, hyperkalemia,
hyperphosphatemia
Can also lead to renal failure and hypocalcemia as
secondary complications
Chemotherapeutic agents cause cell lysis and cell death
with release of intracellular components into the blood
stream
Breakdown of nucleic acid, catabolism of hypoxanthine
and xanthine leads to elevated uric acid
Potassium and phosphate are present at high levels in
cytoplasm
LDH also released but not considered part of syndrome
Tumor Lysis Syndrome
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Risk Factors, Signs or Symptoms
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Increased LDH, uric acid, creatinine
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Bulky, rapidly proliferating tumors treated with chemotherapy
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Most often occurs with treatment of leukemias or high grade
lymphomas
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Cardiac arrythmias if hyperkalemia or hypocalcemia
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Tetany if hypocalcemia
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Renal failure if hyperphosphatemia and hyperuricemia
Tumor Lysis Syndrome
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Prophylaxis
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Patient at high risk: leukemia, high grade lymphma,
rapidly proliferating bulky solid tumor (e.g small cell)
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Vigorous Prehydration
Allopurinol
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Inhibits xanthine oxidase
Can cause xanthinuria
Prevents new uric acid formation
Careful Metabolic monitoring
Treatment
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Rasburicase
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(works for prevention and treatment) degrades uric acid to
more water soluble form
Contraindicated in G6PD deficiency
Can cause hemolysis
Hyperuricemia
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Hematological disorders: leukemias, high-grade
lymphomas, myeloproliferative disorders (e.g
PCV)
Aggressive tumors, extensive disease
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Treatment of malignancies
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Medications
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Renal impairment
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Hyperuricemia- treatment
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Prophylaxis
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Alkalinization of urine (urine pH >7)
 Sodium bicarbonate to IVF
 Diamox
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Allopurinol
Neutropenic Fever
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Medical Emergency
Neutropenia: ANC<1000 (multiply total wbc by
percentage neutrophils and bands)
Single temperature greater than 101.3F or
sustained temperature >100.4F for more than
one hour (for clnical purposes , single
temo>100.4F)
Remember there may still be infection in the
absence of fever: e.g elderly patients or patients
on steroids
May present with hypothermia, hypotension,
clinical deterioration
START BROAD SPECTRUM ANTIBIOTICS
ASAP!!!!
Neutropenic Fever
 Risk
factors for occult infection
Degree
of neutropenia
Rapid decline in ANC
Prolonged duration neutropenia (> 7
to 10 days)
Cancer not in remission
Comorbid illness
Peripheral lines and central venous
catheters
Use of monoclonal antibodies
Neutropenic Fever
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Infectious source identified in 30%
80% infection believed to arise from patient’s
endogenous flora
Risk for specific types of infection may be
influenced by underlying malignancy
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Abnormal antibody production in CLL, functional
asplenia: encapsulated organisms- Strep
pneum.,hemophilus influenzae, Neisseria
meningitidus, capnocytophaga canimorsus
T cell defects e.g lymphoma: intracelluar pathogensListeria monocytogenes, Salmonella, Mycobacterium,
Cryptococcus
High dose steroids: Pneumocystis carinii
ALWAYS COVER Gram negatives
Fungal and viral infections also possible
Neutropenic Fever
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Patients should be pancultured including from central line as well as CXR
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Further imaging depending on symptoms
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Generally start cefipime 2g Q8 (also take into consideration signs,
symptoms, recent antibiotic use)
GROWTH FACTOR support
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Consider vancomycin if hypotension,mucositis, skin infection, presence of
catheter, hx MRSA, recent quinolone
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Addition of antibiotics (including antifungal) depending on clinical response
and duration of neutropenia (add antifungal if anticipate or patient has
prolonged neutropenia)
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Consider catheter removal
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Oncology Consultation
Infectious disease consultation
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