Lecture 18 - Oncologic Emergencies Flashcards
Oncologic emergency
potentially morbid or life-threatening events directly or indirectly related to a patient’s tumor or its treament
can occur at any time during a malignancy, from the presenting sx to end-stage disease
Examples of oncologic emergencies
metabolic, neurologic, cardiovascular, pulmonary, infectious
Metabolic
hypercalcemia of malignancy (HCM)
tumor lysis syndrome (TLS)
Neurologic
spinal cord compression
Cardiovascular
superior vena cava syndrome (SVC)
malignant pericardial effusion
cardiac tamponade
Pulmonary
pleural effusions
Infectious
neutropenic fever
Tumor lysis syndrome (TLS)
constellation of metabolic derangements resulting from death of malignant cells - massive release of intracellular contents into bloodstream that overwhelms the body’s homeostasis
serious and life-threatening
TLS risk factors
tumor specific risk factors: high tumor burden, high tumor grade with rapid cell turnover, and treatment sensitive tumors
pt specific risk factors: age, preexisting renal impairment, concomitant use of drug known to increase uric acid (aspirin, alcohol, thiazide diuretics, caffeine)
TLS pathophysiology
hyperkalemia, exacerbated by AKI
hyperuricemia - catabolism of nucleic acids, poor solubility in urine = uric acid crystal precipitation in renal tubules –> AKI
hyperphosphatemia - excess phosphate binds to calcium and crystalize –> deposits into tissues, exacerbates AKI
hypocalcemia
Acute renal failure
48-72 hours after initiation of therapy
sx: oliguria, N/V, lethargy, fluid overload, edema, CHF, seizures
TLS: principles of management
prevention and immediate management is key
management of acute TLS: identify high risk pts - proactively institute aggressive prophylactic strategies to prevent and/or reduce the severity of TLS; monitor electrolytes; aggressive hydration - enhances urine flow, promotes uric acid and phosphate excretion; control of hyperuricemia - with uric acid lowering drugs
Low risk prophylaxis
monitoring, hydration, +/- allopurinol
Intermediate risk prophylaxis
monitoring, hydration, allopurinol
High risk prophylaxis
monitoring, hydration, rasburicase
Aggressive hydration
fluids and hydration: improves intravascular volume, renal perfusion, and glomerular filtration
decreases risk of life-threatening hyperkalemia
maintain urine output = 80-100 mL/m^2/hr
always consider cardiac function when assessing fluid rate and volume!
Hyperuricemia
uric acid + xanthine are both potentially nephrotoxic –> freely filtered at glomerulus; becomes overwhelmed = crystalizes within tubular lumen, causes direct tubular injury = AKI
humans lack a functional gene for urate oxidase –> further metabolizes uric acid to freely soluble and excretable allantoin
Allopurinol medical management
allopurinol is converted to oxypurinol which inhibits the conversion of xanthine to uric acid, decreases generation of uric acid
only prevents formation of new uric acid, does not facilitate breakdown of uric acid already produced
reduces risk of obstructive uropathy
renal adjustment for CrCl < 20
Allopurinol limitations
doesn’t reduced already formed uric acid, may take several days to lower uric acid, decreases clearance of certain chemos - 6-MP, azathioprine, high-dose methotrexate
Rasburicase
recombinant urate oxidase that catalyzes the oxidation of uric acid into soluble metabolite, allantoin
decreases uric acid levels, including already formed uric acid
Rasburicase limitations
if you have glucose-6-phosphate dehydrogenase deficiency, do not use rasburicase - risk of severe hemolysis reactions
contraindicated in women pregnant/breast-feeding
degrades uric acid within blood samples
very expensive
TLS management of electrolyte abnormalities: hyperkalemia
eliminate all IV and oral potassium supplements
mild: can give IV fluids and loop diuretic PRN or sodium polystyrene sulfonate
severe: IV calcium gluconate or dextrose and regular insulin or sodium bicarb or IV fluids and loop diuretics
TLS management of electrolyte abnormalities: hyperphosphatemia
minimize phosphate intake
oral phosphate binder for short term use
sevelamer
TLS management of electrolyte abnormalities: hypocalcemia
do NOT treat if asymptomatic
symptomatic: IV calcium gluconate
TLS monitoring
prior to initiation of certain chemo: uric acid, phosphorous, potassium, calcium, LDH, serum creatinine, urine output
Malignant spinal cord compression (MSCC)
caused by compression of dural sac, spinal cord, or cauda equina by an extradural or intradural mass
hematogenous spread with bony metastasis to vertebral spine causes collapse and compression
early diagnosis and treatment are ESSENTIAL to prevent permament damage and possible paralysis
What cancers cause MSCC?
all cancers can
most common: breast, lung, prostate
MSCC sx
pain: most common 1st sx
motor deficit: limb weakness is 2nd most comon sx; unsteady gait, rapid onset/difficulty walking, standing, transferring from bed to chair
sensory deficit: paresthesia, decreased sensation and numbness of toes/fingers
autonomic dysfunction: bladder + bowel dysfunction: urinary retention, urinary or fecal incontinence or constipation
MSCC pathophysiology
1st stage is development of compression in spinal column from tumor cells; destruction of corticol bone by tumor can compound this compression (vertebral-body collapse)
vasogenic edema because of spinal cord compression ischemia leads to white matter necrosis + gliosis –> caused by cytokines, inflammatory markers, and neurotransmitters
MSCC diagnosis
MRI of WHOLE spine
MSCC treatment
start steroids immediately! - dexamethasone: reduces edema, inhibits inflammatory responses, delays onset of neurological deficit
surgery + radiotherapy are the only treatments that leads to immediate relief of MSCC
bisphosphonates
Radiotherapy
effective in prevention of further tumor growth and neurologic damage, especially in pts with radiosensitive tumors
Surgery
indications: spinal instability, previous radiation, disease progression despite radiation, radioresistant tumor, paraplegia
laminectomy/anterior decompression
vertebroplasty
kyphoplasty
Laminectomy/anterior decompression
some or all surgical removal of pathological vertebral body and tumor mass
Vertebroplasty
bone cement injected into fractured bone
Kyphoplasty
balloon inserted and inflated to expand the compressed vertebra to its normal height before filling the space with bone cement
Bisphosphonates
should be offered in pts with vertebral involvement to reduce risk of vertebral fracture/collapse
also alters/reduces pain
Superior vena cava syndrome
SVC: major blood vessel for venous blood flow from head, neck, upper extremities to heart and lungs to the heart
disease pressing on SVC, not getting adequate blood flow; thin-walled SVC gradually compressed by tumor outside vessel –> impaired venous drainage from head, neck, and upper extremities
SVC syndrome occurs in setting of
an extrinsic compression or other occlusion of the superior vena cava
SVC syndrome s/s
facial/arm edema, distention of superficial neck and chest wall veins, hypotension, dyspnea at rest, cough, stridor, dysphagia, HA, syncope, dizziness
SVC syndrome treatment
if left untreated: hemodynamic compromise, airway compromise, increased intracranial pressure leading to cerebral edema, intracerebral bleeding
primary goal in SVC management = alleviation of sx and treatment of underlying disease
tumor-specific, stage-specific treatment plan
SVC syndrome: adjunctive therapies
elevation of head to decrease hydrostatic pressure + edema
steroids - only in pts with steroid sensitive tumor and pts undergoing radiation therapy
diuretics to decrease arterial pressure
Malignant pleural effusion (MPE)
complication of advanced malignancy
most common cancers: lung, breast, and lymphoma
pleural effusions: accumulation of fluid within pleural space (thin membranes that lines lungs and chest wall)
Effusions form when
cancer cells spread to pleural space –> increases production and decreases absorption of pleural fluid
MPE sx
no sx –> acute respiratory distress
dyspnea most common presenting sx; pleuritic chest pain
MPE diagnosis
chest x-ray
ultrasound of chest immediately pre-procedure to identify appropriate sites for drainage
MPE management
thoracentesis
pleural fluid analysis
Thoracentesis
needle aspiration of fluid from pleural effusion
risk: pneumothorax, puncture of intra-abdominal organ, re-expansion pulmonary edema, chest discomfort
Pleural fluid analysis
fluid sent for total protein, LDH, cell count, cell differential, gram stain, aerobic/anaerobic bacterial cultures
fluid examination: gram stain, acid-fast stain, total cell counts, LDH, glucose, protein, pH
classified as transudate or exudate
Thoracentesis indication
minimize acute sx temporarily
used in pts with life expectancy < 1-3 mo
risks: re-expansion pulmonary edema, pleural adhesions, infection, hypotension
Pleurodesis indication
activates inflammatory cascade leading to adhesion of pleural layers
useful for pts with life expectancy > 1-3 mo
administered through chest catheter or through video-assisted thorascopic surgery
agents: talc, doxycyline, bleomycin
risks: pleuritic chest pain, fever, systemic inflammation
Pleural catheters and pleurectomy
pleural catheter indication: indwelling pleural catheter drained frequently
risks: infection, tumor seeding of catheter
pleurectomy indication: partial or radical removal of pleura, beneficial for pts with prolonged life expectancy or pts with uncontrolled pleural effusions
