Transcript Oncologic Emergencies

Oncological
Emergencies
Dr. Gary Harding MD, FRCPC
Medical Oncology Fellow
CancerCare Manitoba
CASE 1…
Mr. SV
 ID:
65 year old male with PMHx of
CAD and emphysema
 EC: present to clinic with one week
history of increasing SOB
 HPI: 3 month history of weight loss,
decreased appetite, a change in his
chronic cough, and intermittent
hemoptysis
On Physical Examination

Inspection:
Respiratory Examination
 Stridor
 Dullness
to percussion on right lower
lung fields
 Increased
tactile fremitus to right
lower lung fields
 Decreased
fields
A/E to right lower lung
Chest X-Ray…
right pleural effusion
Thoracentesis
 Exudate
 Gram
stain
– Negative
 AFB
stain
– Negative
 Cytology
– non-small cell lung cancer
 Large
cell type
T1-weighted axial MRI demonstrating
paratracheal soft tissue mass that invades into
the SVC
Superior Vena Cava
Syndrome
Definition
 Obstruction
of blood flow in the
superior vena cava results in signs
and symptoms of SVC syndrome
Etiology
 Caused
by either invasion or external
compression of the SVC by
contiguous pathologic process
 Right
lung pathology, lymph nodes,
other mediastinal structures, or
thrombosis
Etiology
 Before
antibiotics the most common
causes were from complications of
untreated infection
– Syphilitic thoracic aneurysms
– fibrosing mediastinitis
 Malignancy
is presently the most
common cause
Symptoms and Signs
 As
the obstruction develops venous
collaterals are formed
 Symptom onset depends on speed of
SVC obstruction onset
 Malignant disease can arise in weeks
to months
– Not enough time to develop collaterals
 Fibrosing
mediastinitis can take
years to have symptoms
Symptoms and Signs
 Central
venous pressures remain
high even in collaterals
– High pressures cause the characteristic
clinical picture
 Shortness
of breath is the most
common symptom1
1. Parish, JM, Marschke, RF Jr, Dines, DE, Lee, RE. Etiologic
considerations in superior vena cava syndrome. Mayo Clin Proc 1981;
56:407.
Signs and Symptoms
 Facial
swelling or head fullness
– exacerbated by bending forward or lying
down
 Cough
 Arm
edema
 Cyanosis
Facial swelling associated with SVC
Syndrome in a patient with malignancy
Physical Findings
 Venous
distension
– neck
– chest wall
 Pemberton’s
 Facial
Sign
Edema
Patient who presented with progressively enlarging
veins over the anterior chest wall. A diagnosis of a
right-sided superior sulcus (Pancoast) tumor
compressing the SVC was made.
Etiology: Malignancy
 Lung
cancer is the most common2
 Lymphoma
 together
is second most common
represent 94% of cases
2. Escalante, CP. Causes and management of superior vena
cava syndrome. Oncology (Huntingt) 1993; 7:61.
NSCLC
 2-4%
of bronchogenic cancer
patients develop SVC syndrome3
 extrinsic
invasion
compression or direct
– primary tumor or by enlarging
mediastinal nodes
3. Armstrong, BA, Perez, CA, Simpson, JR, Hederman, MA.
Role of irradiation in the management of superior vena cava
syndrome. Int J Radiat Oncol Biol Phys 1987; 13:531.
Small Cell Lung Cancer
 Greatest
 20%
 more
risk
will develop SVC obstruction3
common because SCLC tends
to occur centrally in contrast to other
types
Lymphoma

2-4% of patients

predominantly non-Hodgkin’s lymphoma4

Hodgkin’s rarely causes SVC syndrome
4. Perez-Soler, R, McLaughlin, P, Velasquez, WS, et al. Clinical
features and results of management of superior vena cava
syndrome secondary to lymphoma. J Clin Oncol 1984; 2:260.
Lymphoma
 Extrinsic
compression caused by
enlarging lymph nodes
 subtypes of large B cell can be
intravascular and cause occlusion
(angiotropic)
 diffuse large cell and lymphoblastic
are most commonly associated with
SVC syndrome
Other cancers
 Thymoma
 primary
mediastinal germ cell
neoplasm
 solid
tumors with mediastinal
nodal metastases
– breast cancer most common type
Other causes
 Post
radiation local vascular fibrosis
can also be considered in oncology
patients
– Thoracic radiation treatment may
predate syndrome by many years
Other causes
 Thrombosis
 Indwelling
central venous catheters
 Subcutaneous tunneled catheters
have fewer thrombotic and infectious
complications
– Can also cause pulmonary embolism5
5. Sivaram, CA, Craven, P, Chandrasekaran, K. Transesophageal
echocardiography during removal of central venous catheter
associated with thrombus in superior vena cava. Am J Card
Imaging 1996; 10:266.
Diagnosis
 Timely
identification of the cause is
essential
 Radiographic studies are useful
 Up to 60% of patients with SVC
syndrome related to neoplasm do not
have a known diagnosis of cancer6
– Need a tissue biopsy for histologic
studies
6. Schraufnagel, DE, Hill, R, Leech, JA, Pare, JA. Superior vena caval
obstruction. Is it a medical emergency?. Am J Med 1981; 70:1169.
Radiographic Studies
 Most
patients have an abnormal
chest x-ray at presentation
 Most
common findings are
– Mediastinal widening
– Pleural effusion
CT Chest
 Preferred
 IV
choice
contrast
– defines the level of obstruction
– Maps out collateral pathways
– Can identify underlying cause of
obstruction
Venography
 Bilateral
upper arm venograpy
– superior to CT to define site of
obstruction
– Does not define cause unless
thrombosis is solely responsible
Helical CT
 With
bilateral upper arm IV contrast
injection
 Best
visualization of level of
obstruction and cause
MRI
 Can
be useful in patients with IV
contrast allergies
T1-weighted axial MRI demonstrating the
primary tumor and the paratracheal soft
tissue mass that invades into the SVC
Same patient’s MRI with different
technique to further define the
intramural mass
Histologic Diagnosis
 Essential
 Guides
 Aids
treatment
in defining prognosis
Histologic Diagnosis
 Sputum
cytology, pleural fluid
cytology, biopsy of enlarged
peripheral nodes
 Bone
marrow biopsy for NHL
 Bronchoscopy,
mediastinoscopy, or
thoracotomy are more invasive but
sometimes necessary
Treatment of Oncologic
Causes
Treatment
 Aimed
at underlying cause
 Evolution
of thought has occurred in
recent years
 Historically
SVC syndrome was
considered a potentially lifethreatening emergency
 Standard of care was immediate
radiotherapy
–Zap now
–Ask questions later
 The
emergent approach is not
appropriate for most patients
Newer strategies
Emergent to Urgent
 Symptomatic
obstruction is usually a
prolonged process
 Most
patients are not in immediate
danger at presentation
 Most
have time for a full diagnostic
work up
Emergent to Urgent
 Prebiopsy
diagnosis
 Current
radiation can obscure the
strategies aim at accurate
diagnosis of underlying etiology
before therapy
Exception to new rule
 Stridor
– Central airway obstruction or laryngeal
edema
 True
medical emergency
 Immediate action needed
– Possible intubation and ICU admission
– Immediate therapy to target obstruction
needed
Prognosis…
Linked to tumor histology and
stage at presentation
Treatment Sensitive Tumors
 NHLs,
germ cells, and limited-stage
small cell lung cancers usually
respond to chemotherapy and or
radiation
 Can achieve long term remission
with tumor specific directed therapy
 Symptomatic improvement usually
takes 1-2 weeks after start of
therapy
Note: Corticosteroids
 Controversial
issue with regards to
treatment benefit at presentation
Non-small cell lung cancer
 SVC
obstruction is a strong predictor
of poor prognosis
 Median survival around 5 months7
 Choice of therapy considers
likelihood of response to each
modality
7. Martins, SJ, Pereira, JR. Clinical factors and prognosis in
non-small cell lung cancer. Am J Clin Oncol 1999; 22:453.
Non-small cell lung cancer
 Goal
usually directed to palliation
rather than long term remission
 Palliative
radiation and
chemotherapy can be used
Intraluminal Stents
 Endovascular
fluoroscopy
placement under
 Patients
who have recurrent disease
in previously irradiated fields
 Tumors
 Patient
refractory chemotherapy
too ill to tolerate radiation or
chemotherapy
Intraluminal Stents
 Some
data suggests benefit from
immediate stent placement in NSCLC
at presentation8
 Tends to provide more rapid relief of
symptoms
 Issue of anticoagulation after is not
resolved
8. Rowell, NP, Gleeson, FV. Steroids, radiotherapy,
chemotherapy and stents for superior vena caval obstruction in
carcinoma of the bronchus: a systematic review. Clin Oncol (R
Coll Radiol) 2002; 14:338.
CASE 2…
Mr. EC
 ID:
56 year old man with history of
HTN and osteoarthrtis
 EC: presents to family doctor with
one month history of back pain that
is not responding to Tylenol
– Pain beginning to wake him at night
– More pain with recumbancy
– Some shooting pains down right leg
 ROS:
negative
On examination
 vitals
stable, no fever
 CVS, Respiratory, GI, GU exams
reported as normal
 Back exam
– Inspection: normal
– Palpation: some pain in L1
– ROM: normal
– Some pain in right leg with straight leg
raising
Investigation in Clinic
 Lumbar
Spine X-ray
– Some age related degeneration
Diagnosis
 Sciatica
vs. Back strain
 Treatment:
– NSAIDS
– Few days of bed rest
The story continues…
 Mr.
EC’s pain does not resolve
 More trials of various forms of pain
control fail
 One month later Mr. EC awakens in
the morning and has difficulty
supporting his weight
– Subjective leg muscle weakness
 Goes
to HSC Emergency room
In ER
 Patient
has objective leg weakness
on physical exam
 A very keen medical student does a
rectal exam and discovers a large
nodular prostate
 PSA: 45.0
 MRI Spine…..
Spinal Cord Compression
Malignant Epidural Spinal Cord
Compression (ESCC)
 Neoplastic
invasion of the space
between vertebrae and spinal cord
(epidural invasion)
– Usually from bone metastases
 Compresses
thecal sac of spinal cord
 Frequent complication of malignancy
 Can cause pain
 Can cause irreversible loss of
neurologic function
Definition
 Any
radiological indentation of the
thecal sac
 Tip
of the spinal cord lies at the L1
vertebral level
 Lumbosacral
nerve roots form the
cauda equina
Epidemiology
 Many
cases of unrecognized ESCC
 Difficult
to define incidence
 Autopsy
review studies suggest
around 5% of cancer patients die
with ESCC9
9. Barron, KD, Hirano, A, Araki, S, Terry, RD. Experiences with
metastatic neoplasms involving the spinal cord. Neurology 1959;
9:91.
Causes
 Metastatic
tumor from any primary
site
 Tumors with predilection to
metastasize to spinal column
 Prostate, breast, and lung carcinoma
– 15-20% of cases
 Renal
cell, non-Hodgkin’s lymphoma,
or myeloma
– 5-10% of cases
 Vertebral
metastases are more
common than ESCC
 Prostate cancer: 90%
 Breast Cancer: 74%
 Lung Cancer: 45%
 Lymphoma: 29%
 Renal cell: 29%
 GI: 25%
10. Posner, JB. Neurologic Complications of Cancer. FA Davis,
Philadelphia, 1995
 ESCC
can be initial presentation of a
malignancy
– Around 20% of cases
– In many cases diagnosis is made by
biopsy of the spinal lesion
Spinal Location10
 Thoracic
spine: 60%
 Lumbosacral spine: 30%
 Cervical spine: 10%
 Specific
tumor predilection is difficult
to define
Clinical Features
 Important
to recognize
 Early recognition leads to better
outcomes
 Efficacy of treatment depends most
on patient’s neurological function at
presentation
 Median time from symptoms to
diagnosis is around 2 months11
 More than half of patients who
present to hospital are nonambulatory
11. Husband, DJ. Malignant spinal cord compression:
Prospective study of delays in referral and treatment. BMJ
1998; 317:18.
RED FLAGS…..
First Red Flag: Pain
 Usually
first symptom12
– 80-90% of the time
 Usually
precedes other neurologic
symptoms by seven weeks
– Increases in intensity
 Severe
local back pain
 Aggravated by recumbency
– Distension of venous plexus
 May
become radicular
12. Bach, F, Larsen, BH, Rohde, K, et al. Metastatic spinal cord
compression. Occurrence, symptoms, clinical presentations and prognosis
in 398 patients with spinal cord compression. Acta Neurochir (Wien)
1990; 107:37.
Second Red Flag: Motor
 Weakness:
60-85%13
 At or above conus medularis
– Extensors of the upper extremities
 Above
the thoracic spine
– Weakness from corticospinal dysfunction
– Affects flexors in the lower extremities
 Patients
may be hyperreflexic below
the lesion and have extensor
plantars
13. Greenberg, HS, Kim, JH, Posner, JB. Epidural spinal cord
compression from metastatic tumor: Results with a new treatment
protocol. Ann Neurol 1980; 8:361.
 Weakness
tends to be symmetrical
 Progressive
weakness is followed by
lost of gait function then paralysis
 The
severity of weakness is greatest
with thoracic metastases
Third Red Flag: Sensory
 Less
 Still
common than motor findings
present in majority of cases
 Ascending
numbness and parathesias
Fourth Red Flag: Bladder and
Bowel Function
 Loss
is late finding
 Autonomic
neuropathy presents
usually as urinary retension
– Rarely sole finding
Radiologic Investigation
 Diagnosis
depends on ability to
demonstrate a mass compressing the
thecal sac
 Plain radiographs are not enough
 Historically this involved invasive
procedures
 Advent of MRI has allowed noninvasive diagnosis
 Clinical examination is not reliable in
determining level of lesion
 Entire
imaging of spine is ideal
– Focused CT imaging can miss clinically
unapparent lesions
 Myelography
and MRI are better than
plain X-Rays, bone scans and CT for
diagnosis
Plain Spine Radiographs
 Easiest
and cheapest
 Need
large bony destruction or
vertebral collapse to be diagnostic
 High
 Not
false negative rate
recommended to confirm
diagnosis
MRI vs. CT Myelography
 Both
image thecal sac and display
indentation and encircling
 CT
myelography involves a lumbar
puncture
– Contraindicated in brain metastases,
thrombocytopenia, or coagulopathy
– Can diagnose leptomeningeal
metastases
– Available in Winnipeg in middle of the
night
MRI
 Images
 High
whole spine
detail
 Spares
lumbar puncture
 Patients
in pain must lie still
 Roughly
equivalent in terms of
sensitivity and specificity
 Presently
no large comparative
studies b/c MRI in the US has
become so readily available
 MRI
standard of care in centers that
have access
Bone Scan
 More
sensitive than plain radiograph
 Visualizes
 Can
entire skeleton
miss neoplasms that do not
have increased blood flow
CT Scan alone
 Does
not visualize spinal cord and
epidural space clearly
Intramedullary Metastases
 Less
common
 Often
present with hemicord
symptoms
– Unilateral weakness below lesion
– Contralateral diminution of pain and
temperature sensation
– Can progress to bilateral dysfunction
Radiation Myelopathy
 Can
 MR
mimic ESCC
imaging can make distinction
MRI of epidural spinal cord compression in a
women with past history of breast cancer.
Treatment
Treatment delays…….
2
month median delay in treatment
from onset of back pain11
 14
day delay in treatment from onset
of neurological symptoms11
Why the delay?
 Patient
factors
 General
practitioner factors
 Hospital
factors
EDUCATION
Treatment Objectives
 Pain
control
 Avoidance
 Preserve
function
of complications
or improve neurological
Pain management
 Corticosteroids
– Decrease edema
 Opiates
– Needed to decrease pain for comfort
and examination purposes
Bed Rest
 No
 No
 No
 No
Anticoagulation
 Cancer
is a hypercoaguable state
 High burden of tumor in metastatic
disease
 Possible value in prophylaxis against
venous thromboembolism
 If patient not mobile subcutaneous
heparin or compression devices is
indicated
Prevention of Constipation
 Factors
– Autonomic dysfunction
– Limited mobility
– Opiate analgesic
 Risk
of perforation
– Masked by corticosteroids
 Bowel
regimen needed
Corticosteroids
 Part
of standard regimen
 Limited
effects
data on benefit vs. side
 Many
studies suggesting lower doses
can be effective
– No randomized trials
Corticosteroid Recommendations
 High
dose dexamethasone and half
dose every three days
 Pain
with minimal neurological
dysfunction can have lower dose
 Small
asymptomatic lesions can
forgo steroids
Radiation Therapy
 Definitive
 Portal
choice
8 cm wide
 Centered on spine
 Extends one to two vertebral bodies
above and below the epidural
metastasis
 Relieves
pain in most cases
 Post-neurological function usually
determines response
 Response most associated with
tumor type and radiosensitivity; eg.
lymphoma
 Dosing 20 to 40 Gy in 5 to 20
fractions
 Popular
– 30 Gy in 10 fractions
Surgery
 Changing
role
 Historically
posterior vertebral
decompression was done
– No survival benefit with or without
radiation15
15. Findlay, GF. Adverse effects of the management of malignant
spinal cord compression. J Neurol Neurosurg Psychiatry 1984;
47:761.
 Better
techniques today allow
aggressive approach
 Gross
spinal tumor resection with
vertebral reconstruction now possible
 Experienced
surgeon required
 Recent
controlled trial comparing
aggressive surgery followed by
radiation vs. radiation alone16
 Improvement in surgery+rads
– Days remained ambulatory (126 vs. 35)
– Percent that regained ambulation after
therapy (56% vs. 19%)
– Days remained continent (142 vs. 12)
– Less steroid dose, less narcotics
– Trend to increase survival
16. Patchell, R, Tibbs, PA, Regine, WF, et al. A randomized trial of
direct decompressive surgical resection in the treatment of spinal
cord compression caused by metastasis (abstract). proc Am Soc
Clin Oncol 2003; 22:1.
Chemotherapy
 Can
be successful in chemosensitive
tumors
– Hodgkin’s lymphoma
– Non-Hodgkin’s lymphoma
– Neuroblastoma
– Germ cell
– Breast cancer (hormonal manipulation)
– Prostate cancer (hormonal
manipulation)
Bisphosphonates
 Recommended
 Decrease
pathologic fractures in
bony disease
– Multiple myeloma
– Breast cancer
Prognosis
 Median
survival with ESCC is 6
months14
 Ambulatory
patients with
radiosensitive tumors have the best
prognosis
14. Sorensen, PS, Borgesen, SE, Rohde, K, et al. Metastatic epidural
spinal cord compression. Results of treatment and survival. Cancer
1990; 65:1502.
Treatment Delay
 Education
 EXPERIENCE
 Education
 EXPERIENCE
Case 3: Mrs. HC
 ID:
75 year old female living alone
with no significant past medical
history
 EC:
brought to ER by paramedics
after neighbor called b/c she was
found in her apartment unresponsive
 No
collateral history
Examination
 Fluctuating
 Vitals
level of consciousness
normal, no fever
 Dehydrated
 Coarse
 No
upper airway sounds
other pertinent findings
Investigations
 CBC
normal
 Mildly
elevated BUN and Cr
 Normal
LFTs
 Standard
electrolytes normal
 Concern
 Chest
of pneumonia
x-ray ordered……
Multiple Pulmonary Metastasis
 Calcium
– 4.5
checked
Hypercalcemia
Symptoms
 Usually
nonspecific
 Many
times patients present with
very high calcium level
 Most
research done in
hyperparathyroidism
Gastrointestinal
 Constipation
is most common15
– Exacerbated or confused with narcotic
effects
– Related to autonomic dysfunction
 Anorexia
 Vague
abdominal pain
 Rarely can lead to pancreatitis
15. Heath, H 3d. Clinical spectrum of primary
hyperparathyroidism: Evolution with changes in medical practice
and technology. J Bone Miner Res 1991; 6(Suppl 2):S63.
Renal Dysfunction
 Nephrolithiasis
– More common in hyperparathyroidism
 Nephrogenic
diabetes insipidus
– Defect in concentrating ability
– Polyuria and polydipsia
 Chronic
renal failure
– Longstanding high calcium
 Calcifcation,
tubules
degeneration, and necrosis of
Neuropsychiatirc
 Anxiety
 Depression
 Cognitive
dysfunction
– Delerium
– Psychosis
– Hallucinations
– Somnolence
– Coma
Cardiovascular
 Short
QT interval
 Supraventricualr
 Ventricular
arrhythmias
arrhythmias
Physical Findings
 Usually
not specific
 Dehydration
secondary to diuresis
caused by the hypercalcemia
 Corneal
deposition of calcium
– “band keratopathy” on slit lamp exam
Epidemiology
 Occurs
in about 10 to 20% of
patients with cancer
 Both solid tumors and leukemias
 Most common
– Breast
– Lung
– Multiple myeloma
Pathogenesis
Three mechanisms
 Osteolytic
metastases with local
cytokine release
 Tumor
secretion of parathyroid
hormone-related protein (PTHrP)
 Tumor
production of calcitriol
Osteolytic Metastases
 Breast
cancer
 Non-small cell lung cancer
 Cytokines released
– Tumor necrosis factor
– Interleukin-1
– Stimulate osteoclast precursor
differentiation into mature osteoclasts
 Leading
to more bone breakdown and
release of calcium
PTH-Related Protein
 Most
common in patients with nonmetastatic tumors
 Called humoral hypercalcemia of
malignancy
 Secretion of PTH itself is a rare event
 PTHrP binds to same receptor as PTH
and stimulates adeynylate cyclase
activity
– Increased bone resorption
– Increases kidney calcium reabsorption
and phosphate excretion
Calcitriol
 Hodgkin’s
majority)
disease (mechanism in
 Non-Hodgkin’s
 Usually
therapy
(mechanism in 1/3)
responds to glucocorticoid
Diagnosis
 Clinical
symptomology with
– History of cancer
– Risk factors for cancer
– Suppressed PTH
 Some
centers can test for PTHrP to
confirm Dx of humoral hypercalcemia
 High PTHrP may predict response to
pamidronate16
– Less of a response
16. Gurney, H, Grill, V, Martin, TJ. Parathyroid hormonerelated
protein and response to pamidronate in tumourinduced
hypercalcemia. Lancet 1993; 341:1611.
 Malignancy
must be ruled out in
patients that present with a very
high calcium and no other obvious
cause
Treatment
Aims
 Lower
serum calcium concentration
 Treat
complications if present
 Treat
underlying disease
 Large
Volume
volume of normal Saline
administration
 Expands intravascular volume
 Increases calcium excretion
– Inhibition of proximal tubule and loop
reabosrption
– Reduces passive reabsorption of calicum
 Follow
fluid status b/c of danger of
fluid overload
Inhibition of Bone Resorption
 Three
therapies
– Calcitonin
– Bisphosphonates
– Gallium nitrate
 Historical
therapy
– Antitumor antibiotic plicamycin
(mithramycin)
 Multiple
serious side effects
 No longer manufactured
Calcitonin
 Salmon
calcitonin
 Increases renal excretion of calcium
 Decreases bone reabsorption by
interfering with osteoclast
maturation
 Weak agent
 Works the fastest
Bisphosphonates
 Adsorb
to the surface of bone
hyroxyapatite
 Interfere with osteoclast activity
 Cytotoxic to osteoclasts
 Inhibit calcium release from bone
 Three commonly used
– Pamidronate
– Zoledronic acid
– Etidronate (1st generation, weaker)
Bisphosphonates
 More
potent than calcitonin
 Maxium effect occurs in 2 to 4 days
 Trend to use of IV zoledronic acid in
the acute situation
 Both are can be renal toxic
– More potent than pamidronate
– Administered over a shorter period of
time (15 minutes vs. 2 hours)
Prophylactic Bisphosphonates
 Pamidronate
use in patients with
known lytic lesions17
– Less
– Less
– Less
– Less
– Less
episodes of hypercalcemia
pathologic fractures
pain
spinal cord compression
need for radiation or surgery
17. Hortobagyi, GN, Theriault, RL, Porter, L, et al for the Protocol 19
Aredia Breast Cancer Study Group. Efficacy of pamidronate in
reducing skeletal complications in patients with breast cancer and lytic
bone metastases. N Engl J Med 1996; 335:1785.
Newly discovered side effect…
 Osteonecrosis
of the jaw
 Recent
case reports of jaw bone
necrosis in patients on pamidronate
 EDUCATION
needed
Gallium Nitrate
 Effective
 More
potential for nephrotoxicity
 Rarely
used
Dialysis
 Last
resort
 Dialysis
fluid with little or no calcium
is effective
 Useful
when patients can’t tolerate
large volume resuscitation
 If
calcium needs to be correct
emergently
Recommendations in symptomatic
situation
 Volume
expansion
 Salmon
calcitonin
 IV
zoledronic acid or pamidronate
 Close
follow up of calcium level and
symptoms
Transitions in
Treatment
Chemotherapy
 Two
roles
 Direct
treatment of cancer
 Palliation
of symptoms
Palliative Chemotherapy
 Goal
is not cure
 Goals
– Control of tumor
– Preservation of function
– Help tumor symptoms
 Pain
 Dsypnea
 Pruritis
 Poor
appetite
 Weight loss
Fine Balance
 Chemotherapy
can be very toxic
 Ratio:
benefit vs. toxicity
 Host factors and tumor factors
 Delicate
situation
 Want
balance in palliative
medications that affect tumor
but do not heavily affect host
Psychology of Cancer
 Psychological
evolution during cancer
treatment
 Many people have fought very hard
with their disease
 Chemotherapy for “relief” not “cure”
can be difficult concept for patients
 ART of medicine
Evolution
 Chemotherapeutic
protocols that
have less side effects

molecular targeted therapies
– Attack tumor specifically
– Less effect on host
 Breast
 Colon
cancer
Cancer
 Prostate
 Lung
cancer
cancer
Breast Cancer
 Aromatase
tumors
inhibitors for ER positive
– Anastrozole, Letrozole, Exemestane
 Trastuzumab
(Herceptin)
– Humanized monoclonal antibody
targeting Her-2/neu protein on breast
cancer cells
– Inhibits growth factor signal
transduction
– Tolerated quite well
Colon Cancer
 Capecitabine
(Xeloda)
 Oral
drug that is transformed into 5FU with three enzymatic reactions
– Final enzyme is at higher levels in tumor
cells
– Contributes to drug’s less toxic side
effect profile
 Less
stomatitis, less myelosupression
Targeted GI Therapies
 Bevacizumab
– Monoclonal antibody to vascular
endotheial growth factor receptor
– Some cardiac toxicity
 Cetuximab
– Monoclonal antibody to human
epidermal growth factor receptor
– Skin toxicity
Prostate Cancer
 LHRH
analogues
 Leuprolide
 Goserelin
 Stop
(Lupron)
(Zoladex)
testosterone production with
limited side effects
Lung Cancer
 In
stage IV disease patients who
receive Cisplatin based doublet
chemotherapy live longer and feel
better than best supportive care
 Hard
to balance side effects
Gefitinib (Iressa)
 Targets
epidermal growth factor
receptor (tyrosine kinase small
molecule inhibitor)
 May
have a role in the palliation of
advanced non small cell lung cancer
patients
Palliative Care Debate
 Do
not accept any patient on “active”
therapy
 This needs to be further elucidated
 Patients being palliated with
chemotherapy or targeted therapies
still have other palliative care issues
and needs
 Should a patient still on Xeloda for
breast or colon cancer not be
admitted to St. Boniface 8A?
Thank you
Any questions?