THE ONCOLOGIC

EMERGENCIES AND
MANAGEMENT OF CANCER
COMPLICATIONS
NURSING CARE MANAGEMENT 106
 Learning Outcomes:  Integrate the concept of malignancy to the development
At the end of the of oncologic emergencies.
Explain the clinical manifestations of clients with
learning session, the 

oncologic emergencies.
students shall  Distinguish signs and symptoms indicative of oncologic
emergencies.
 Differentiate the manifestations of various oncologic
oncologic emergencies.
 Interpret diagnostic and laboratory tests results of
clients with oncologic emergencies.
 Prioritize nursing goals and evidence-based nursing
interventions.
 Relate the pathophysiology of oncologic emergencies to
the medical management.
 Evaluate the outcomes of the care of clients with
oncologic emergencies.
 ONCOLOGIC EMERGENCIES
• Acute, life-threatening oncologic complications
• Clinical situations in which the condition is
secondary to a malignancy or its treatment,
and when there are potentially immediate
catastrophic consequences in the absence of
successful intervention
 ONCOLOGIC EMERGENCIES
• Arise from the neoplastic process itself or from
the treatment
• Two key concepts:
–Identification of patients at risk
–Involvement of family and significant other
 ONCOLOGIC EMERGENCIES
• PROMPT IDENTIFICATION OF PATIENTS AT
RISK
– Depending on the specific type of cancer and
treatment modality employed
 ONCOLOGIC EMERGENCIES
• JUDICIOUS INVOLVEMENT OF THE FAMILY
AND SIGNIFICANT OTHERS
– Cancer is a familial diagnosis
– Psychological support
 ONCOLOGIC EMERGENCIES
• Oncology Nursing Society Core Curriculum for Oncology Nursing
• STRUCTURAL
• Neoplastic Cardiac Tamponade
• Increased Intracranial Pressure
• Spinal Cord Compression (SCC)
• Superior Vena Cava (SVC)
Syndome
• METABOLIC
• Disseminated Intravascular
Coagulation
• Hypercalcemia of Malignancy
• Hypersensitivity Reaction
• Sepsis
• Syndrome of Inappropriate
Antidiuretic Hormone (SIADH)
• Tumor Lysis Syndrome
  Compression of the cardiac muscle
 Pathologic fluid accumulation under pressure within the
pericardial sac.
 Compression of the myocardium interferes with the dilation of
the heart chambers
 Prevents adequate cardiac filling during diastole because of
increased intrapericardial pressure.
 Reduction of blood flow during diastole reduces stroke volume,
and ultimately cardiac output.
Tachycardia compensates for low stroke volume and increases
NEOPLASTIC


systolic emptying;

CARDIAC  While peripheral vasoconstriction maintains arterial pressure

and venous return.

TAMPONADE  Without compensation, circulatory collapse may be fatal.

 Risk Factors
• Radiation Pericarditis
• Neoplastic Pericarditis
– Primary Tumors (Sarcoma, Mesothelioma)
– Metastatic Tumors
• lung cancer, breast cancer, leukemia,
lymphoma

 Blockage of lymphatic drainage occurs

because of direct tumor extension
 Malignant lymphatic engorgement and
impairment of drainage
 Tumor implantation in and around the
pericardium with inflammation and fluid
production
Signs and Symptoms
• Asymptomatic for slowly developing tamponade
• Dyspnea
• Tachycardia
• Retrosternal chest pain
• Non- productive cough, Hoarseness, Dysphagia as
effusion impinges on bronchi, esophagus and laryngeal
nerves
• Fatigue, Weakness, Palpitations, Dizziness and
Orthopnea
Signs and
Symptoms
• Fever and Pleuritic Chest Pain for Radiation
Pericarditis
• Jugular Vein Distention
• Increased CVP, Muffled Heart Sounds, Arterial
Hypotension
• Lateral Shifting of the PMI
Signs and
Symptoms
• Pulsus Paradoxus
• Increased Hepatojugular
Reflex
 Diagnostic Tests
Chest X Ray – Enlarged Cardiac Silhouette, Water bottle heart, Absence of
normal contours between great vessel and cardiac chambers
 ECG – Electrical Alternans where amplitude and direction of P wave and

QRS complex alternate on every other beat because of change in position of

heart during depolarization
 2D Echo – Most sensitive and specific indicator of effusions in determining

presence, location and approximate quantity

 Transesophageal Echo

 Cardiac Catheterization- Measures intracardiac pressure

 CT, MRI of the Chest

 Cytologic Examination of Pericardial Fluid

 Electrolytes and ABG for differential diagnosis

 Medical Management
 Prednisone
 Furosemide or Spirinolactone and Hydrochlorthiazide
 NSAIDs and Steroids for Radiation Pericarditis
 Blood Transfusions and IVFs for expansion of blood volume
and increase ventricular filling pressures
 Isoproterenol to increase Heart Rate.
 Low-Dose Dopamine for improvement of contractility
 Oxygen Therapy
 Intervention for Fluid Removal
 Cyanosis, Dyspnea Changes in Mental Status or Signs of
Shock

 Rule of 20’s:
 Decrease in pulse pressure >20 mmHg,

 Pulsus Paradoxus >20 mmhg;

 CVP>20cm H2O
Pericardiocentesis  Percutaneous Needle pericardiotomy
with Aspiration used as emergency
treatment option for cardiac
Tamponade
 Commonly guided by Catheterization
or 2D Echo for detection of location of
the fluid
 Large bore needle is introduced in the
pericardial space through a small stab
incision by the sub-xiphoid approach,
where the needle is angled though the
left shoulder to avoid the pleural
space. Fluid is withdrawn for 10-30
minutes.
Pericardiocentesis

 Successful interventions include a palpable pop upon aspiration; and an

increase in QRS voltage.
 Acute elevation of the ST segment, PR interval, PAC’s or PVC’s indicate
contact with pericardium. Withdraw needle.
 The aspirate is judged as Malignant Effusions described as protein rich fluid
leaked from blood vessels with increased permeability caused by irritation
of the serous membrane from sloughed cancer cells or tumor implants.
Malignant Effusions are bloody with hematocrit and fibrinogen levels than
circulating blood.
 Fluid reaccumulates in 24 to 48 hours, hence a short term pericardial
catheter may be inserted which is then drained every shift.
 Surgical
Percutaneous Balloon Angioplasty
• Guide Wire inserted into the pericardium followed by a

Interventions balloon catheter, which is then inflated to create a

window to drain the fluid into the pleural space
• The adhesion of parietal and visceral pericardium
prevents reaccumulation of fluid
Subxiphoid Pericardiotomy (Pericardial
Window)
• Resection of 2 to 4 cm of pericardium followed by fluid
withdrawal.
• May be performed under local or general anesthesia
 Surgical Surgical Pericardiectomy

Interventions • For Long Term Survivors

• Thoracotomy or Median sternotomy followed by
resection of a large portion of the pericardial space to
drain into the pleural space
Total Pericardiectomy
• For Radiation Induced Effusive- Constrictive Pericardial
Disease, or Fibrosis, and also those with Pericardial
Mesothelioma
• Extensive Metastatic Disease is contraindicated
• *Complications: Dysrhythmias, Bleeding, Infection and
Hemothorax
 • Performed after pericardiocentesis to prevent fluid
reaccumulation
• When drainage has slowed, successful instillation of a

Sclerotherapy
sclerosing agent, causes irritation of the pericardial sac
causing the two linings to adhere, obliterating the
space
• Sclerosing Agents used include Bleomycin,
Tetracycline, Doxorubicin, 5 Fluorouracil,
Methotrexate, Nitrogen Mustard
• Expected Outcome: No drainage in 24 hours
• Complications: Localized pain, Fever, PVC’s, Atrial
Dysrhythmias, Pericarditis and Myelosuppression
 – Radiation
• If the cause is radiosensitive tumor (lung,
Breast, Hematopioetic)
Interventions • Assess previous radiation therapy to establish
tissue tolerance

– Chemotherapy
• Chemosensitive tumors of the Lymphoma,
Breast, or Small Cell Carcinoma
• May be administered after pericardiocentesis
 • Close monitoring of cardiovascular and
hemodynamic status
– CVP

Nursing – ST segment elevation, T wave Inversion,

– Pulsus Paradoxus, Kussmaul’s Respiration Hypoxemia

Interventions • Serum Electrolytes: Ca and K

• Be prepared for cardiac arrest and emergency
CPR
• Reduce cardiac workload
– Rest periods
– Relaxation
– Pain Relief
– Assistance in activities
 Spinal Cord
Compression
• Second most common complication of cancer after brain
metastasis. Considered a medical emergency because it
can lead to permanent neurological deficits: paralysis and
loss of bladder control
– Direct compression of the spinal cord or cauda
equine
• Extradural Tumors (displace spinal cord,
irritate nerve roots, obstruct CSF)
• Intramedullary Tumors
• Extramedullary Tumors
– Interruption of vascular supply by the tumor
– Compression caused by vertebral collapse from
pathologic fracture or dislocation that extrudes to the
cord
 • Metastatic Disease is the most

Spinal Cord
common cause.
– Lung
Compression – Breast
– Prostate
– Multiple Myeloma, Lymphoma,
Melanoma, Renal Cancer and Sarcoma
• Cancer clients with pre existing bone
disease
 • Appear weeks or months prior to neurologic deficits, though fast
Back Pain growing tumors may cause permanent paraplegia in hours or days
after appearance of neurologic deficit

• Localized or Radicular (from Nerve Root Compression from

pathologic fracture and vertebral compression),
• Distribution of pain is dependent on spinal involvement, moves
along dermatomal distribution,
• and is aggravated by movement (coughing, sneezing, straining,
straight leg raising).
• Most common is thoracic radicular pain which is most common,
radiates in a band around the chest or abdomen.
• Intense, persistent, progressive Pain
• Vertebral Tenderness on Percussion at or near level of compression
• Unilateral Pain (Cervical/Lumbosacral) Bilateral (Thoracic)
• Worsens at night because of the stretching of the periosteum; and
compression of abdominal structures
• *Requires detailed assessment for any alteration
 • Weakness before Sensory Loss

Motor • Weakness is commonly restricted to the lower

extremities but may vary dependent on tumor location

Weakness • Commonly described as stiffness, heaviness of the

affected extremity
• Unsteady gait, ataxia, Dragging of affected extremity +
Hyperreflexia, Spasticit, Positive Babinski’s sign
 • Sensory Loss
• Progress similarly with motor losses

Sensory • Deficits appear on 1-5 levels below the compression

• Numbness, Tingling, Paresthesia, Coldness in the
Dysfunction affected area
• Loss of sensation to light touch, pain, thermal
sensation
• Severe: Loss of Proprioception, Deep Pressure and
Position
 • Bladder disturbances
– Hesitancy, Retention, Overflow, Incontinence
• Bowel Disturbances
Autonomic – Lack of urge to bear down and defecate leading to

Dysfunction
constipation, obstipation and incontinence
– Loss of Sphincter Control
• Sexual Dysfunction
• Horner’s syndrome (Paraspinal Cervical or Upper
Thoracic Affectation)
• Absence of sweating below the level of compression
 • Plain X Ray

Diagnostics *Limitations include delayed

detection
• MRI
– Detects bone damage, detect location
of cause (Intramedullary,
Extramedullary, Extradural)
• Myelography
Treatment
• Preserve or Restore Neurologic Function
• Maintain Spinal Stability

Goals • Control Tumor Growth

• Pain Relief
 Steroids
- Reduce inflammation of cord and nerve root compression
– Bolus doses followed by daily doses

Medical – Tapering is done by reducing 1/3 of the dose every 3 to 4 days

after treatment is initiated

Management Radiation
– Initiated within 24 hours of diagnosis
– 3000 gy in 10 fractions, to 2500 to 4000 gy in 10-20 fractions over
2 to 4 weeks
– Reduces pain, compression and tumor size in 70 to 80% of cases
and can prevent local recurrence

– *No evidence of spinal instability/ radical spinal

compression
 • Anterior or Posterior Decompression followed by spinal
stabilization depending on the location of the tumor.

– Spinal instability

Surgical – Rapid neurologic deterioration

– No known primary malignancy

management – Prior maximum tolerance radiation at the site of

compression
– Radioresistant tumor

• Chemotherapy
• Adjuvant therapy after radiation for clients
experiencing lymphoma, myeloma, and breast,
prostate and germ cell tumors
 • Close monitoring of tumors known to have the propensity
to metastasize to the spinal cord.
• Close Monitoring of

Nursing
– Pain
– Motor Status, Gait, ROM, Coordination

Interventions – Sensory Status, Assessment of Deep Tendon Reflexes

– Bowel and Bladder Functions
• Monitor serum calcium levels in case of immobility
• Assess for venous thrombosis related to immobility
– Redness, Swelling, Warmth
– Positive Homan’s Sign
– Venous streaking, Erythema
• Implement pain management
 • Engage patient in PROM.
• Assist client in transfers and mobility
• Encourage self care as much as possible
Nursing • Encourage and assist in pulmonary hygiene, need for

Interventions
spirometry
• Assess skin integrity especially bony prominences .
Institute skin care protocol.
• Institute bowel training program as necessary.
• Insert an indwelling catheter with repeated
catheterization to relieve distention or to empty
residual
• Bladder training program
 Superior Vena
Cava Syndrome

• A constellation of physical findings due to obstruction of SVC

which impairs venous drainage and shunts blood to collateral
pathways to reach the right atrium
• Impairment in the circulation reduces blood flow to the right
atrium resulting in venous hypertension, venous stasis and
decrease in cardiac output.
• If untreated, may lead to vascular congestion to thrombosis,
cerebral edema, pulmonary complications and death.
Superior Vena Cava Syndrome
• SVC is thin walled, low venous pressure
surrounded by rigid structures of the
sternum, trachea, vertebrae, lymph nodes,
aorta, right bronchus

• Obstruction is due to:

– External Compression by an extrinsic mass,
solid tumor, or enlarged lymph node
– Intravascular obstruction by tumor or
thrombosis
– Intraluminal reaction to tumor invasion or
inflammation
 • Malignant causes

Superior
– Bronchogenic Cancer, Small Cell Lung Carcinoma
– Squamous cell Cancer of the Lung

Vena Cava – Lymphoma

– Kaposi’s sarcoma

Syndrome – Breast Cancer

– Esophageal, Colon and Testicular Cancers
• Venous Thrombosis related to Indwelling Central
Venous Catheters
• Radiation Induced Fibrosis of the SVC
Superior Vena Cava
Syndrome
• Dyspnea (65%)
• Facial swelling with fullness of the head (Plethora)
• Periorbital Edema
• Engorgement of Veins in the Upper Torso
• Cough
• Edema of neck, upper thorax, breasts and upper extremities
• Chest Pain
• Signs and symptoms are worsened by bending forward
• Increased pressure on the jugular vein
• Compensatory tachycardia
• Stokes’ sign or tightness of shirt collar
• Swelling of the fingers
 • Bronchoalveolar lavage
• Thoracostomy
• Chest X Ray reveal lung or mediastinal mass, widening
Diagnosis and Pleural Effusion
• CT and MRI further define the lesion and its location
• Contrast Venography to assess the percentage of SVC
obstruction when surgical bypass is being considered.
 • Symptom relief
• Reduction of obstructing lesion

Diagnosis • Cure of primary tumor

• Maintain an adequate airway
• Adequate cardiac output
 • Radiation Therapy
– Treatment of Choice for SVCS
– Immediate treatment in acute and life threatening
situations

Medical – High dose fractionation followed by lose dose

fractionation

Management – Subjective improvement begins in 3 days, relief in 7 days,

objective resolution in 7 to 14 days
• Chemotherapy
– Cause is SCLC, Lymphoma, Germ Cell Tumor
– Single modality or Neoadjuvant Therapy
– Most lung carcinomas are responsive to platinum
containing compounds
– Commonly administered by central catheters
 • Insertion of a wire stent except in tumor invasion of svc;
Fibrinolytics are administered before, followed by
Heparinization during the procedure and then by
anticoagulation.

Surgical • Takes 4 weeks for the stent to be incorporated to the

endothelium. (Relief in 24 to 72 hours)
Management • SVC Bypass
– One end is sutured to the right atrium and the other to the
internal jugular or innominate vein through the patient’s own
saphenous vein or a synthetic Dacron prosthesis
– Used when the tumor can be excised with the SVC,
inadequate venous return despite venous circulation, or it
results from venous thrombosis or benign cause
– Followed by anticoagulation therapy and aspirin for an
indefinite period for graft patency
 • Fibrinolytic Therapy (Streptokinase, Urokinase T-PA)
– Intraluminal Thrombosis
– Bleeding Disorders, History of Stroke, Spinal Cord

Pharmacologic Metastasis
– Appropriate when administered within 5 to 7 days of

Therapy SVCS symptoms

• Anticoagulant Therapy
– For Venous Stasis
– After 5 to 7 days have lapsed
– Inpatient Heparan followed by long- term Coumadin
– Alone or after Fibrinolytic Therapy, After removal of
central line
 • Diuretics for edema

Medical – WOF hypovolemia and decreased venous return

• Corticosteroids

Management – Active inflammation or after radiation and

chemotherapy to alleviate tissue necrosis
• Oxygen
 – Observe for respiratory distress (dyspnea, SOB,
tachypnea, air hunger, stridor, orthopnea)
• Observe ventilatory movement (use of accessory

Nursing breathing muscles, clubbing of fingernails, discoloration of

nailbeds or mucous membranes)

Interventions • Assess for tracheal deviation, asymmetrical chest

expansion.
• Auscultate breath sounds
• Provide oxygen and mechanical ventilation
• Administer respiratory medications, steroids and
analgesics as ordered.
 Nursing – Assess for changes in cardiac function

Interventions • Obstruction in venous outflow

• Monitor ECG’s
– Position patient for comfort.
– Elevate upper extremities. Do not elevate lower
extremities
– Avoid constricting clothing.
– Avoid invasive and constricting procedures in upper
extremities
– Maintain cool room temperature.
– Prevent activities that increase intrathoracic
pressure or intracerebral pressure
– Reduce anxiety
 • The systemic inflammatory response to a variety of
SYSTEMIC severe clinical insults

INFLAMMATORY • SIRS Criteria: one of the following

RESPONSE – Temperature: > 38 C or < 36 C

SYNDROME – Heart Rate: > 90 beats/minute

– Respirations: > 20 breaths/min
– WBC: > 12,000/mm3
SEPSIS
– Defined as a response to infection, evidenced by
elevated temperature, heart rate, and respiratory
rate that can progress to severe sepsis.
– Characterized by two of the abovementioned
criteria.

SEVERE • Sepsis with organ dysfunction, hypotension or

SEPSIS
hypoperfusion.
• Lactic acidosis, Oliguria, or an Acute alteration in
mental status.
 • Vasodilation
• Increased vascular permeability

RATIONALE
• Decreased arterial or venous tone
• Clot formation
Bacterial, viral or fungal invasion • CELLULAR HYPOXIA
leading to release of endotoxin and
other cell components into the • CELLULAR ISCHEMIA
bloodstream (plasma cells, neutrophils,
• Cell Death
macrophages, monocytes)
• End Organ Damage
 • Hypotension that is refractory to adequate
SEPTIC fluid resuscitation requiring vasopressor

SHOCK
therapy or both;
• Acute Circulatory Failure.
• Produces a severe maldistribution of blood
flow in the microcirculation which leads to
inadequate tissue perfusion, cellular
ischemia, cellular hypoxia, or organ or
system failure
• Septic shock can lead to multiple organ
dysfunction syndrome (MODS), which may
lead to death.
 SYSTEMIC Temperature: > 38 C or < 36 C
INFLAMMATORY Heart Rate: > 90 beats/minute

RESPONSE Respirations: > 20 breaths/min

WBC: > 12,000/mm3
SYNDROME
 Temperature: > 38 C or < 36 C
Heart Rate: > 90 beats/minute
Respirations: > 20 breaths/min
WBC: > 12,000/mm3

SEPSIS CNS – Confusion, Agitation, Chills

CV- Sinus Tachycardia, Hypotension
• Prolonged PT or Aptt
• Decreased Platelets
• Decreased fibrinogen
• Hyperglycemia
• Increased lactic acid
• Positive blood cultures
• Increased WBC in urinalysis
• Increased WBC in CBC
 CNS – Obtundation, Coma

SEPTIC CV – Tachycardia, Arrhythmias, Hypotension

SHOCK
Respiratory- SOB, Decreased Breath Sounds,
Crackles, Wheezes, Pulmonary Edema, Acute
Respiratory Distress Syndrome
Renal – Oliguria, Anuria, Acute Renal Failure
Skin – Cold, Pale, decreased perfusion,
Mottling
GI – Decreased GI Motility, Jaundice
 • Elevated Liver Function Test Results
SEPTIC • Increased levels of BUN or Creatinine

SHOCK • Decreased Hgb or Hct

• Hypoglycemia
 1. Recent antineoplastic treatment related to
neutropenia
2. Medical devices such as Central Venous
Catheter, Urinary Catheter and Drains
RISK 3. Respiratory Infection, Abdominal Infection,

FACTORS Urinary Tract infection

4. Mucositis
5. Aging > 65 years
6. Poor Nutritional Status
7. Hospitalization
8. Concurrent immunosuppressive diseases
 1. Basic Metabolic Panel
2. CBC
3. Coagulation Studies
4. Lactic Acid

Laboratory 5. Arterial Blood Gases

6. Tests to determine potential areas of infection

Review •
•
Blood Cultures
Urinalysis and Urine Culture
• Wound Culture
• Computed Tomography
• Chest Radiography
• Sputum Analysis
• Stool Analysis
• CT of abdomen, pelvis, UTZ
 • Fluid Resuscitation for hypotension and lactic

Medical
acid accumulation using crystalloid solutions
as first line therapy

Interventions • Establishing vascular access if not yet in place

• Broad Spectrum antimicrobial therapy within
45 minutes of recognition
– Cephalosporin, Aminoglycoside, Beta Lactam,
Carbapanems, Vancomycin
– Antifungal and Antiviral Agents
 • Transfer to ICU if vasopressor, arterial catheters,
MV needed.
• Vasopressor therapy need to maintain a mean
Medical arterial pressure of 65 mmHg using
Norepinephrine as first line therapy; and the
Interventions establishment of arterial catheter placed if
administering vasopressors.
• Addition of Inotropic Therapy such as dobutamine
added on the basis of ongoing signs of
hypoperfusion.
• Oxygen therapy depending on appropriate airway.
 • Supportive Therapy
– Blood Transfusion for HgB less than 7 g/dl

Medical
– Fresh frozen plasma to correct coagulopathies
– Platelet transfusion used when less than

Interventions
10,000/mm3; if with active bleeding, platelet
goal should be less than 50,000/mm3
– Glucose control whether patient have DM or not
– Renal Replacement Therapy or Intermittent
Hemodialysis
– Deep Vein Thrombosis Prophylaxis
– Nutrition
 • Monitoring for SIRS and Early Signs of Sepsis

Nursing – Laboratory Values

– Monitoring VS, Especially clients at risk of

Interventions Infection
– Assess for potential sites of infections; cultures
as ordered.
– Assess each organ system for possible signs
 • Prevention of infection in patients with neutropenia, per
institution protocol.
– Meticulous skin and mouth care.
– Lubrication to skin and mucous membranes, avoidance of
rectal trauma

Nursing – Prevent invasive procedures.

Interventions • Use of protective Isolation.

• Care for neutropenic client first. Do not care for clients
with neutropenia and those with infection.
• Wash hands consistently and thoroughly after each
patient contact.
• Patient should not be exposed to someone who has had
recent vaccination or exposure to communicable illness.
• Interventions to education patients and caregivers on
infection control
 – Administer antibiotics as ordered.
– Monitor for organ system failure

Sepsis and – Monitor signs and symptoms of fluid overload: Daily

weight and Intake and Output Monitoring

Septic Shock – Monitor for oxygen saturation; administer O2 as

needed
– Administer blood products as needed.
– Encourage mobility and frequent deep breathing.
– Provide nutritional support
– Observe for nephrotoxicity and neurotoxicity as side
effects of antibiotic therapy.
– Control fevers with antipyretics as ordered.
 • Is an alteration of the blood clotting mechanism with
Disseminated abnormal acceleration of the coagulation cascade
resulting in thrombosis. Hemorrhage occurs
Intravascular simultaneously as a result of the depletion of clotting
factors.

Coagulation • Endothelial tissue injuries occurring in malignancies

such as acute promyelocytic myelogenous leukemia
(APML) and mucin producing adenocarcinomas
(lung, colon, breast and prostate) are commonly
related with DIC’s, but the most common cause is
Sepsis.
 • Release of tissue Factor (TF), a transmembrane
glycoprotein, stimulates the coagulation cascade
which results in the formation of thrombin and

Disseminated fibrinolysin, in response to cytokines, tumor necrosis

factor and endotoxins.

Intravascular • TF is present on the surface of endothelial

cells, macrophages, and monocytes. The

Coagulation remaining portion of fibrin continues to form

clots.
• At the same time, fibrinolysin degrades some
of the fibrin into a soluble monomer form; this
initiates clot dissolution.
• The remaining portion of fibrin is an insoluble polymer
which continues to form clots. These clots may be
deposited in the extremities or in vulnerable organs.
 • Capillary clots slow the blood flow, resulting in
tissue ischemia, hypoxia and necrosis.

Disseminated • The clots trap circulating platelets in the

microvasculature, resulting in

Intravascular thrombocytopenia
• As the fibrinolysin continues to degrade fibrin,
Coagulation the by products, FDP’s are produced,
• These FDP’s disrupt the conversion of fibrin to
a polymer; coat platelets; decreasing their
adherence; and degrade factors V, VII and X
which leads to capillary hemorrhage.
 • The blast cells in APML are hypergranular and release a
procoagulant substance similar to thromboplastin that
stimulates the clotting cascade.

Disseminated
• Annexin II, a phospholipid binding protein on
endothelial cell surfaces binds to plasminogen and
increases production of plasmin, that leads to
Intravascular unopposed fibrinolysis and bleeding.

Coagulation • Solid tumors develop new blood vessels with abnormal

endothelial lining that are thought to activate the
procoagulant system.
• Necrotic tissue or tissue enzymes may also be released
into the circulation and stimulate coagulation. Many
solid tumors are associated with an increased
production of clotting factors that increase incidence of
thromboses.
 • Acute DIC can be caused by extensive disease, Tumor
Disseminated Lysis Syndrome, and Sepsis.

Intravascular • Endotoxins associated with sepsis are thought to

activate factor XII and initiate coagulation. Gram (+)

Coagulation organisms, HIV, Varicella, Hepatitis and CMV

 • Signs of Bleeding observed from any body orifice,
venipuncture sites, mucous membrane, incisions
• Oozing, frank bleeding or hemorrhage
Signs and • Occult bleeding may be manifested by mental status
changes, orthopnea and tachycardia
Symptoms • Signs of clotting: oliguria, hypoxemia, cool and mottled
extremities which may progress to severe tissue ischemia
and necrosis.
• The most risk of microvascular thrombosis include
cardiac, pulmonary, renal, hepatic and central nervous
systems
• Raynaud’s sign (generalized sweating with symmetric
mottling of the nose, the fingers, toes, and genitalia)
which can lead to gangrene
• Pulmonary signs such as severe, sudden dyspnea at rest
with tachypnea and progressive rales and rhonchi, are
similar to those observed with ARDS
• Signs of GI Insult such as an ulceration.
• Mental status changes, visual changes, and headaches
 • FDP Levels
• D Dimer, formed when plasmin digests fibrin
• Thrombocytopenia

Laboratory • Prothrombin Time measures extrinsic pathway is

prolonged ( 10 -13 seconds); decreasing levels of

Review Clotting Factors II, V, and X, and of fibrinogen

• Fibrinogen level is decreased
• Prolonged PTT (39 to 48 seconds), measures the
extrinsic pathway
• The amount of FDP’s or FSP’s are increased
• Factor Assays (V and VIII) are decreased
• Serum creatinine and liver transaminase levels are
increased with enhanced clotting
Treatment • Cure the underlying cause of DIC
– Antibiotic treatment with sepsis
– Surgery, chemotherapy and radiation therapy for the
underlying malignancy
– All- trans retinoic acid rapidly reverses DIC in patients with
APML

• Fluid Replacement for hypotension and proteinuria

• Platelet transfusion to strengthen endothelium, prevents
petechial hemorrhage, facilitates conversion of
prothrombin to thrombin; functions as a mechanical plug
by adhering to the vessel wall
• Fresh Frozen Plasma for volume expansion, containing
clotting factors V, VIII and XIII and antithrombin III
• Cryoprecipitate that contain fibrinogen, commonly used
for severe hypofibrinogenemia
 • Packed RBC’s
• Heparin therapy which interferes with
thrombin and stops the conversion of
fibrinogen to fibrin, preventing clot formation.

Treatment • Effective therapy is indicated by cessation of

clot formation, rise in platelet count and
fibrinogen levels and decrease in levels of
FDP’s;
• PTT is increased 1.5 to 2 times the normal.
• Antifibrinolytic Therapy using e- aminocaproic
acid
Integumentary system – Skin, Mucous Membranes
of Mouth, Sclera, Nose, Ears, Urethra, Vagina,
Rectum, Venipuncture Sites, Puncture Sites,
Wound Sites
Pulmonary System – Hemoptysis and Chest Pain
Cardiovascular System – Palpitations and Angina
Renal – Intake and Output Monitoring, Peripheral
Edema
GI – Abdominal Palpation for Pain, Abdominal Girth
Measurement
Neurologic – Changes in mental status
• Monitor laboratory values closely, especially
the CBC levels
• Avoid administration of aspirin and aspirin
containing products
• Discourage activities that increase ICP or
intraabdominal pressure
• Stool softener administration
Adequate hydration
Avoid constrictive clothing and devices
Use prescribed elastic support hose
Discourage leg dangling, sitting for long periods,
and crossing legs
Elevate legs at intermittent intervals to prevent
venous stasis when sitting or lying.
Perform ROM exercises for legs
Encourage deep breathing and coughing.
Administer heparin therapy as ordered using an
infusion controlling device.
Limit venipunctures
Use small gauged needles
Avoid subcutaneous and IM injections. If
necessary, apply pressure on site for 5 minutes
Avoid rectal manipulation
Use electric razors instead of straight edged
razors
Avoid use of indwelling catheters, but if necessary,
keep well lubricated and without tension.
Avoid vaginal manipulation.
Perform frequent gentle oral hygiene
Avoid mouthwashes with high alcohol content
 • Humoral Hypercalcemia of
Hypercalcemia Malignancy
• Local Osteolytic Hypercalcemia
 • Solid Tumors commonly metastasizing to the

Hypercalcemia: bone – Breast, Lung, Prostate

• Hematologic Emergencies – Multiple Myeloma,
Risk Factors Lymphoma
• Non oncologic disorders – Hyperparathyroidism
 • Serum Calcium

Hypercalcemia: • Serum albumin and prealbumin

– Readjustment (Base albumin level (mg/dl) –
Laboratory Values measured serum albumin concentration (g/dl) x 0.8
mg/dl + reported serum calcium level)
• PTH level
• Hydration with 0.9 % Normal Saline
• Loop Diuretics
• Biphosphonates administered IV
– Zoledronic Acid – 4 mg in 15 minutes
• Monoclonal Antibody
– Inhibit osteoclast production and survival
– May potentially cause severe hypocalcemia
– 120 mg SQ injection q 4 weeks
• Calcitonin
– Rapid onset of action; decreases serum calcium levels
inhibiting osteoclast in bone and increasing urinary
excretion
– May be given in conjunction with corticosteroids to
prolong effect of calcitonin
• Gallium Nitrate
– Used in quick relapse of hypercalcemia after initial use of
bisphosphonate
– Nephrotoxicity is a common complication
 Metabolic: • Risk Factors:
Tumor Lysis – Radiation
– Chemotherapy

Syndrome – Aggressive lymphomas, Leukemias, Small Cell

Lung Carcinoma
– Renal Compromise

– Release of potassium,
phosphate and nucleic acids in
the extracellular compartment.
 Metabolic: • Neurologic: altered mental status, tetany,
paresthesia, seizures

Tumor Lysis • Cardiac: elevated BP, short-ended QT

Syndrome
complexes, wide QRS, dysrhythmias
• GI: Anorexia, n/v, abdominal cramps, diarrhea
• Renal: Uric Acid Kidney Stones, Flank pain,
oliguria / anuria, renal failure
 Metabolic: • Aggressive fluid hydration 48 hours before and
after initiation of cytotoxic therapy

Tumor Lysis • Sodium bicarbonate

Syndrome
• Acetazolamide
• Allopurinol
• Kayexalate
• Hypertonic dextrose and regular insulin
• Aluminum hydroxide
• Hemodialysis
 Metabolic: • Institute essential preventive measures (fluid
hydration)

Tumor Lysis • Assess for signs of electrolyte imbalance

Syndrome