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 tactile fremitus to right lower lung fields A/E to right lower lung

 Increased

 Decreased

fields

Chest X-Ray X-

right pleural effusion

Thoracentesis
 Exudate  Gram  AFB

stain

Negative

stain

Negative
 Cytology

non-small cell lung cancer non Large

cell type

T1T1-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 lung pathology, lymph nodes, other mediastinal structures, or thrombosis

 Right

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

 Pembertons

Sign

 Facial

Edema

Patient who presented with progressively enlarging veins over the anterior chest wall. A diagnosis of a rightright-sided superior sulcus (Pancoast) tumor compressing the SVC was made.

Etiology: Malignancy
 Lung

cancer is the most common2 is second most common

 Lymphoma

 together

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 compression or direct

 extrinsic

invasion
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

risk

 20%

will develop SVC obstruction3

 more

common because SCLC tends to occur centrally in contrast to other types

Lymphoma


2-4% of patients predominantly non-Hodgkins lymphoma4 nonHodgkins rarely causes SVC syndrome

4. Perez-Soler, R, McLaughlin, P, Velasquez, WS, et al. Clinical Perezfeatures 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 tumors with mediastinal nodal metastases

breast cancer most common type

 solid

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 xcommon findings are

 Most

Mediastinal widening Pleural effusion

CT Chest
 Preferred

choice

 IV

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 visualization of level of obstruction and cause

 Best

MRI
 Can

be useful in patients with IV contrast allergies

T1T1-weighted axial MRI demonstrating the primary tumor and the paratracheal soft tissue mass that invades into the SVC

Same patients MRI with different technique to further define the intramural mass

Histologic Diagnosis
 Essential

 Guides

treatment

 Aids

in defining prognosis

Histologic Diagnosis
 Sputum

cytology, pleural fluid cytology, biopsy of enlarged peripheral nodes marrow biopsy for NHL

 Bone

 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 lifelifethreatening 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 patients are not in immediate danger at presentation have time for a full diagnostic work up

 Most

 Most

Emergent to Urgent
 Prebiopsy

radiation can obscure the

diagnosis
 Current

strategies aim at accurate diagnosis of underlying etiology before therapy

Exception to new rule

 Stridor

Central airway obstruction or laryngeal edema

medical emergency  Immediate action needed

 True

Possible intubation and ICU admission Immediate therapy to target obstruction needed

Prognosis Prognosis

Linked to tumor histology and stage at presentation

Treatment Sensitive Tumors

 NHLs,

germ cells, and limited-stage limitedsmall 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 1therapy

Note: Corticosteroids
 Controversial

issue with regards to treatment benefit at presentation

NonNon-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 nonnon-small cell lung cancer. Am J Clin Oncol 1999; 22:453.

NonNon-small cell lung cancer

 Goal

usually directed to palliation rather than long term remission radiation and chemotherapy can be used

 Palliative

Intraluminal Stents
 Endovascular

placement under

fluoroscopy
 Patients

who have recurrent disease in previously irradiated fields refractory chemotherapy

 Tumors

 Patient

too ill to tolerate radiation or chemotherapy

Intraluminal Stents
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.

 Some

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 Inspection: Palpation: some pain in L1 Palpation: ROM: normal ROM: Some pain in right leg with straight leg raising

Investigation in Clinic
 Lumbar

Spine X-ray X-

Some age related degeneration

Diagnosis
 Sciatica

vs. Back strain

 Treatment:

NSAIDS Few days of bed rest

The story continues

 Mr.

ECs 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 of the spinal cord lies at the L1 vertebral level nerve roots form the cauda equina

 Tip

 Lumbosacral

Epidemiology
 Many

cases of unrecognized ESCC to define incidence

 Difficult

 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 15 Renal

cell, non-Hodgkins lymphoma, nonor myeloma

5-10% of cases

 Vertebral

metastases are more common than ESCC  Prostate cancer: 90% cancer:  Breast Cancer: 74% Cancer:  Lung Cancer: 45% Cancer:  Lymphoma: 29% Lymphoma:  Renal cell: 29% cell:  GI: 25% GI:
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 patients neurological function at presentation  Median time from symptoms to diagnosis is around 2 months11  More than half of patients who present to hospital are nonnonambulatory
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  Usually

first symptom12

80-90% of the time 80-

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

6060-85%13  At or above conus medularis
 Weakness:

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 severity of weakness is greatest with thoracic metastases

 The

Third Red Flag: Sensory

 Less

common than motor findings present in majority of cases numbness and parathesias

 Still

 Ascending

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 nonnoninvasive 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 Xdiagnosis

Plain Spine Radiographs

 Easiest  Need

and cheapest

large bony destruction or vertebral collapse to be diagnostic false negative rate

 High  Not

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

whole spine

 High

detail lumbar puncture in pain must lie still

 Spares

 Patients

 Roughly

equivalent in terms of sensitivity and specificity no large comparative studies b/c MRI in the US has become so readily available standard of care in centers that have access

 Presently

 MRI

Bone Scan
 More

sensitive than plain radiograph entire skeleton

 Visualizes

 Can

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

mimic ESCC

 MR

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 day delay in treatment from onset of neurological symptoms11

 14

Why the delay?

 Patient

factors practitioner factors factors

 General

 Hospital

 EDUCATION

Treatment Objectives
 Pain

control of complications

 Avoidance

 Preserve

or improve neurological

function

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 data on benefit vs. side

 Limited

effects
 Many

studies suggesting lower doses can be effective

No randomized trials

Corticosteroid Recommendations
 High

dose dexamethasone and half dose every three days with minimal neurological dysfunction can have lower dose asymptomatic lesions can forgo steroids

 Pain

 Small

Radiation Therapy

 Definitive

choice

 Portal

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 Postdetermines 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 spinal tumor resection with vertebral reconstruction now possible surgeon required

 Gross

 Experienced

 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

Hodgkins lymphoma Non-Hodgkins lymphoma Non 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 collateral history

 No

Examination
 Fluctuating

level of consciousness

 Vitals

normal, no fever

 Dehydrated

 Coarse

upper airway sounds

 No

other pertinent findings

Investigations
 CBC

normal elevated BUN and Cr LFTs electrolytes normal

 Mildly

 Normal

 Standard

 Concern

of pneumonia

 Chest

xx-ray ordered

Multiple Pulmonary Metastasis

 Calcium

checked

4.5

Hypercalcemia

Symptoms
 Usually

nonspecific

 Many

times patients present with very high calcium level research done in hyperparathyroidism

 Most

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
degeneration, and necrosis of

Longstanding high calcium

 Calcifcation,

tubules

Neuropsychiatirc
 Anxiety  Depression  Cognitive

dysfunction

Delerium Psychosis Hallucinations Somnolence Coma

Cardiovascular
 Short

QT interval arrhythmias

 Supraventricualr

 Ventricular

arrhythmias

Physical Findings
 Usually

not specific

 Dehydration

secondary to diuresis caused by the hypercalcemia deposition of calcium

 Corneal

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 secretion of parathyroid hormonehormone-related protein (PTHrP) production of calcitriol

 Tumor

 Tumor

Osteolytic Metastases

 Breast

cancer  Non-small cell lung cancer Non Cytokines released

Tumor necrosis factor Interleukin-1 Interleukin Stimulate osteoclast precursor differentiation into mature osteoclasts
 Leading

to more bone breakdown and release of calcium

PTHPTH-Related Protein
 Most

common in patients with nonnonmetastatic 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
 Hodgkins

disease (mechanism in

majority)
 Non-Hodgkins Non-

(mechanism in 1/3)

 Usually

responds to glucocorticoid

therapy

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 underlying disease

 Treat

Volume
 Large

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 needed

 EDUCATION

Gallium Nitrate
 Effective

 More

potential for nephrotoxicity used

 Rarely

Dialysis
 Last

resort

 Dialysis

fluid with little or no calcium is effective when patients cant tolerate large volume resuscitation calcium needs to be correct emergently

 Useful

 If

Recommendations in symptomatic situation

 Volume

expansion calcitonin

 Salmon

 IV

zoledronic acid or pamidronate

 Close

follow up of calcium level and symptoms

Transitions in Treatment

Chemotherapy
 Two

roles treatment of cancer of symptoms

 Direct

 Palliation

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  Ratio:

can be very toxic

benefit vs. toxicity  Host factors and tumor factors

 Delicate

balance in palliative

situation
 Want

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

cancer

 Colon

Cancer cancer

 Prostate

 Lung

cancer

Breast Cancer
 Aromatase

inhibitors for ER positive

tumors
Anastrozole, Letrozole, Exemestane
 Trastuzumab

(Herceptin)

Humanized monoclonal antibody targeting Her-2/neu protein on breast Hercancer cells Inhibits growth factor signal transduction Tolerated quite well

Colon Cancer
 Capecitabine

(Xeloda)

 Oral

drug that is transformed into 55FU with three enzymatic reactions

Final enzyme is at higher levels in tumor cells Contributes to drugs 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 (Lupron)

 Leuprolide

 Goserelin

(Zoladex)

 Stop

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 to balance side effects

 Hard

Gefitinib (Iressa)
 Targets

epidermal growth factor receptor (tyrosine kinase small molecule inhibitor) have a role in the palliation of advanced non small cell lung cancer patients

 May

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?