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3/6/2018 1 Oncologic Emergencies Ellen Alberts MSN, ARNP-CNS, AGCNS-BC, AOCNS PSONS Fundamentals of Oncology Spring 201 Overview The Basics Oncologic emergencies are life-threatening medical emergencies and must be treated as such! Why do they occur? Malignancy Treatment of malignancy When do they occur? Early in disease process (initial manifestation of malignancy itself) Late in disease process (manifestation of treatment of malignancy) Structural Emergencies Spinal Cord Compression Superior Vena Cava (SVC) Syndrome Increased Intracranial Pressure (ICP) Cardiac Tamponade Metabolic Emergencies Tumor Lysis Syndrome (TLS) SIRS/Sepsis/Septic Shock Disseminated Intravascular Coagulation (DIC) Thrombotic Thrombocytopenia (TTP) Hypercalcemia Inappropriate Antidiuretic Hormone Secretion (SIADH) Anaphylaxis Hypersensitivity (Maloney, 2016; Vogel 2016) The Basics

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3/6/2018

1

Oncologic Emergencies

Ellen Alberts MSN, ARNP-CNS, AGCNS-BC, AOCNS

PSONS Fundamentals of Oncology

Spring 201

Overview

The Basics Oncologic emergencies are life-threatening medical

emergencies and must be treated as such!

Why do they occur?

• Malignancy

• Treatment of malignancy

When do they occur?

• Early in disease process (initial manifestation of malignancy itself)

• Late in disease process (manifestation of treatment of malignancy)

Structural Emergencies

• Spinal Cord Compression

• Superior Vena Cava (SVC) Syndrome

• Increased Intracranial Pressure (ICP)

• Cardiac Tamponade

Metabolic Emergencies

• Tumor Lysis Syndrome (TLS)

• SIRS/Sepsis/Septic Shock

• Disseminated Intravascular Coagulation (DIC)

• Thrombotic Thrombocytopenia (TTP)

• Hypercalcemia

• Inappropriate Antidiuretic Hormone Secretion (SIADH)

• Anaphylaxis

• Hypersensitivity

(Maloney, 2016; Vogel 2016)

The Basics

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Structural Emergencies

• Spinal Cord Compression

• Superior Vena Cava (SVC) Syndrome

• Increased Intracranial Pressure (ICP)

• Cardiac Tamponade

Metabolic Emergencies

• Tumor Lysis Syndrome (TLS)

• SIRS/Sepsis/Septic Shock

• Disseminated Intravascular Coagulation (DIC)

• Thrombotic Thrombocytopenia (TTP)

• Hypercalcemia

• Inappropriate Antidiuretic Hormone Secretion (SIADH)

• Anaphylaxis

• Hypersensitivity

(Maloney, 2016; Vogel 2016)

The Basics

SIRS/Sepsis/Septic Shock

Occurs on a continuum!! Septicemia

SIRS

Sepsis

Severe Sepsis

SEPTIC SHOCK! (Maloney, 2016)

SIRS/Sepsis/Septic Shock

• Septicemia: Invasion of blood by microorganisms

• Sepsis: Systemic response to infection (vasodilation, displacement of intravascular volume)

• Septic Shock: Vascular collapse caused by vasodilation, leakage intravascular volume into interstitial space ***

What are some of the criteria used to identify where a patient may be on this

continuum?

(Maloney, 2016)

SIRS/Sepsis/Septic Shock

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Pathophysiology:

1. Infection (can be bacterial, viral, or fungal)

2. Endotoxins and other cellular components released

3. Vasodilation

4. Increased vascular permeability

5. Decreased arterial/venous tone

6. Clot formation

7. End-organ damage

8. Cell death

(Maloney, 2016)

SIRS/Sepsis/Septic Shock

• Neutropenia

• Infection

• Medical devices

• Mucositis

• Hospitalization

• Corticosteroids or other immunosuppressants

Risk Factors:

• Splenectomy

• Age

• Poor nutritional

status

• Concurrent

immunosuppressive disease

• Type of malignancy

(Maloney, 2016)

SIRS/Sepsis/Septic Shock

(Maloney, 2016)

SIRS/Sepsis/Septic Shock

Mr. J.: Seven days post-3rd cycle R-CHOP

•Wife calls outpatient clinic at 5 pm on Friday and reports husband has:

–Fever –Dry cough –Discomfort with swallowing

(Maloney, 2016)

SIRS/Sepsis/Septic Shock

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(Maloney, 2016)

SIRS/Sepsis/Septic Shock

•Stat CBC with differential, CXR, & cultures of

blood (peripheral blood and central lines),

urine, sputum, stool, CVC exit site

•Stat Electrolytes, Blood Glucose, BUN, &

Creatinine

(Maloney, 2016)

SIRS/Sepsis/Septic Shock

Sepsis

• confusion, agitation

• tachycardia, hypotension

• tachypnea, hypoxia on RA, decreased breath sounds

• decreased UO

• warm, dry, flushed skin

• nausea/vomiting

• fever

Clinical Presentation:

Septic shock

• obtunded, coma

• arrhythmias, tachycardia,

hypotensive

• SOB, decreased breath

sounds, crackles/wheezes,

ARDS, pulmonary edema

• oliguria or anuria, ARF

• cold, pale, mottled skin

• decreased GI motility,

jaundice

• fever

(Maloney, 2016)

SIRS/Sepsis/Septic Shock

Septic shock

• elevated LFTs

• increased BUN and/or creatinine

• decreased hematocrit and/or hemoglobin

• hypoglycemia

Laboratory manifestations:

Sepsis

• hyperglycemia

• leukocytosis

• long PT and aPTT

• decreased fibrinogen and

platelets

• Elevated lactate

• + blood cultures

• WBCs in urine

(Maloney, 2016)

SIRS/Sepsis/Septic Shock

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Diagnosis:

• BMP

• CBC

• Coagulation studies

• Lactate

• ABGs

• Anything else to help determine potential site of infection

(Maloney, 2016)

Like what?

SIRS/Sepsis/Septic Shock

(Maloney, 2016)

SIRS/Sepsis/Septic Shock

Mr. J clinical presentation in the ED:

• Awake, alert, anxious

• Skin warm, appears flushed

• ↓ breath sounds lower lobes bilaterally with rales in

right lung base

•Oral cavity without erythema or lesions, skin intact

• Implanted port - site without redness or drainage;

however, c/o slight tenderness to area above port

•O2 sat 88% room air

• Temp 1020F, HR irregular 96, RR 24, BP 87/45

Mr. J’s labs in ER:

Lab Value Result

WBC 1,100/m2

Absolute Neutrophil Count 450/mm3

Hemoglobin 10 g/dl

Platelets 30,000/mm3

Sodium 134 mEq/l

Potassium 3.5 mEq/l

Glucose 167mg/dl

BUN 20mg/dl

Creatinine 1.4mg/dl

Lactate 4.6 mmol/L

Sepsis Case Study

Managment:

• Fluid resuscitation (crystalloids)

• Broad spectrum antibiotics

• Oxygen therapy

• Vasopressor therapy

• Supportive therapy

Like what?

(Maloney, 2016)

SIRS/Sepsis/Septic Shock

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SIRS/Sepsis/Septic Shock

Start Immediately Complete Within 3

Hours

Complete Within 6 Hours

• Measure lactate level • Administer 30 mg/kg

crystalloid over 10-15 minutes

• Obtain blood cultures • Administer broad-

spectrum antibiotics following blood cultures

• Administer vasopressors for hypotension unrelieved by crystalloids

• Measure central venous pressure and venous oxygen saturation

• Re-measure lactate

Dellinger, RP et al (2013). Surviving sepsis campaign: International guidelines

for management of severe sepsis and septic shock, 2012. Intensive Care

Medicine, 39, 165-228.

SIRS/Sepsis/Septic Shock

Complete Within 24

Hours

Additional Supportive

Measures

• Administer low-dose corticosteroids if hypotensive despite vasopressors

• Maintain glucose between lower limit of normal and 150 mg/dl

• Maintain inspiratory plateau pressure <30 cm H2O for mechanically ventilated

• Maintain adequate nutrition

• Prevent deep vein thrombosis

• Prevent stress and pressure ulcers

• Prevent additional infection

Dellinger, RP et al (2013). Surviving sepsis campaign: International guidelines for management

of severe sepsis and septic shock, 2012. Intensive Care Medicine, 39, 165-228.

Sepsis Case Study Admission orders for Mr. J:

•Meropenem 1 gm IV stat & Q8h

•Vancomycin 1000 mg IV stat & Q12h

•Supplemental O2 to keep saturations > 92%

•Vital signs Q_ hours

•Blood glucose checks Q_ hours

•CBC, CMP Qam

• Immunocompromised diet

•Admit to medical oncology unit

•Neutropenic precautions

Sepsis Case Study Nursing Assessment of Mr. J upon inpatient admission: •Extreme restlessness & anxiety

•Shaking chills

•Skin warm, flushed

•Temp 102.40F

•HR 120 irregular, bounding

•RR 26, oxygen saturation 89% 2 lpm via nc

•BP 74/40

•No urine output since early am

•Blood glucose 61 mg/dl

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Sepsis Case Study

RRT

Transfer to higher level of care

Nursing Management:

• Prevention and early recognition!!!!

• Frequent vitals and assessments

• Maintain adequate oxygenation

• Administer fluids and antibiotics on time

• Educate!

(Maloney, 2016)

SIRS/Sepsis/Septic Shock

Test your knowledge!

You have just started your shift and received bedside report. Which patient should you go to see first?

A. The independent patient receiving EPOCH and is

starting to have frequent diarrhea

B. The patient who is receiving their second bag of

PRBCs, which they are tolerating well

C. The independent, neutropenic patient, who is

having frequent diarrhea

D. The patient with a central line and a peripheral IV,

both of which are being used

SIRS/Sepsis/Septic Shock

Test your knowledge!

You have just started your shift and received bedside report. Which patient should you go to see first?

A. The independent patient receiving EPOCH and is

starting to have frequent diarrhea

B. The patient who is receiving their second bag of

PRBCs, which they are tolerating well

C. The independent, neutropenic patient, who is

having frequent diarrhea

D. The patient with a central line and a peripheral IV,

both of which are being used

SIRS/Sepsis/Septic Shock

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Test your knowledge!

Which of the following oncologic emergencies is a potential

complication of septic shock?

A. Increased intracranial pressure

B. Disseminated intravascular coagulation

C. Tumor lysis syndrome

D. Anaphylaxis/hypersensitivity

SIRS/Sepsis/Septic Shock

Test your knowledge!

Which of the following oncologic emergencies is a potential

complication of septic shock?

A. Increased intracranial pressure

B. Disseminated intravascular coagulation

C. Tumor lysis syndrome

D. Anaphylaxis/hypersensitivity

SIRS/Sepsis/Septic Shock

Disseminated Intravascular Coagulation

(DIC)

Disseminated Intravascular Coagulation

Definition: Generalized activation of the hemostatic system, which results in widespread

intravascular deposition of fibrin in the microvasculature and the simultaneous consumption of coagulation factors and

platelets. DIC is never a primary diagnosis. It ALWAYS is

a symptom of an underlying disease.

(Maloney, 2016; Viele, 2008)

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Causes:

• Sepsis

• Severe infection

• Vascular abnormalities

• Severe allergic reactions

• Severe immunologic reactions

• Malignancy (both solid and liquid)

(Maloney, 2016; Viele, 2008)

Disseminated Intravascular Coagulation

Disseminated Intravascular Coagulation

Basic pathophysiology:

• Overactivation of coagulation cascade from certain proteins

• can be intrinsic (blood vessel damage)

• can be extrinsic (tissue damage)

• Clots begin to form and are deposited throughout the body’s vasculature

• Because of excessive clotting, clotting factors and platelets are all used up!

• This means there is no more clotting factors and platelets for normal clotting anymore, which allows for abnormal bleeding!

(Maloney, 2016; Viele, 2008)

Disseminated Intravascular Coagulation

Clinical Presentation:

• Skin: pallor, petechiae, jaundice, ecchymosis,

hematomas, acrocyanosis

• EENT: visual disturbances, scleral injection, periorbital edema, subconjunctival hemorrhage, eye and ear pain,

petechiae on nasal and/or oral mucosa, epistaxis, tender and bleeding gums

• Cardiac: tachycardia, hypotension, weak

peripheral pulses, color and temperature changes to extremities

• Respiratory: dyspnea, tachypnea, hypoxia, hemoptysis, cyanosis, SOB

(Maloney, 2016; Viele, 2008)

Disseminated Intravascular Coagulation

Clinical Presentation (continued):

• GI: tarry stools, hematemesis, abdominal pain, abdomina distension, guiac positive stools

• GU: hematuria, decreased UO

• Musculoskeletal: joint pain and stiffness

• Neuro: headache, restlessness, confusion, lethargy, altered LOC, obtundation,

seizures, coma

(Maloney, 2016; Viele, 2008)

Disseminated Intravascular Coagulation

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Diagnosis:

• clotting studies: platelet count, fribrinogen level, thrombin level

• clotting factors studies: PT, aPTT, INR

• fibrinolysis studies: fibrin degradation products, D-dimer, antithrombin

• Bilirubin

• BUN

(Maloney, 2016; Viele, 2008)

Disseminated Intravascular Coagulation

Diagnosis:

Platelet Decreased

Fibrinogen Decreased

Thrombin Time Prolonged

Prothrombin Time Prolonged

Activated Prothrombin

Time Prolonged

Fibrin Degradation Products

Increased

Antithrombin Decreased (Viele, 2008)

Disseminated Intravascular Coagulation

DIC Case Study

Mr. J: Clinical presentation at 0730 in AM after admit to floor and transfer to ICU

•Disoriented, lethargic

•Skin pale, cool, fingertips cyanotic

• ↓ breath sounds lower lobes bilaterally with diffuse

bilateral rales, hemoptysis

•RR 28 on 2 lpm via nasal cannula, O2 sat 88%

•Abdomen distended, rebound tenderness

•Still no urine output

•Oozing blood from venipuncture sites

•HR 136 irregular, weak

•BP 78/37

• Temp 103.1oF

DIC Case Study

Laboratory

Value

Labs from ED 0730 Normal

Values

Hemoglobin 10 g/dl 8.9 g/dl 14 – 18 g/dl

(male)

Platelets 30,000/mm3 12,000/mm3 150,000 –

400,000/mm3

Fibrinogen 96 mg/dl 170 – 410

mg/dl

PT 15.8 seconds 11.3 – 13.1

seconds

Fibrin

Degradation

Products

60 mcg/ml > 10 mcg/ml

Mr. J’s labs at:

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Managment:

1. Treat underlying cause!!

May include:

✴ Transfusions (platelets, FFP,

cryopreciptate)

✴ Anticoagulants

✴ Fibrinolytic agents

✴ Anticoagulant factor concentrates

(Maloney, 2016; Viele, 2008)

Disseminated Intravascular Coagulation

Nursing Management

(Vogel, 2016)

• Early recognition!

• Good assessments

• VS

• Hemodynamics

• Oxygenation

• Fluid status

• Ensure patient safety

• Manage active bleeding

• Administration of anticoag therapy,

other meds, fluids, blood products

• Assist in patient coping

Disseminated Intravascular Coagulation

DIC Case Study

Orders for Mr. J:

• IV Heparin per hospital protocol

• 2 units PRBCs

• Strict I/O

• VS Q_ hours

• Supplemental O2 titrate to O2sat >92%

Spinal Cord Compression

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Spinal Cord Compression

Definition:

A neurological

emergency where the

spinal cord or cauda

equina is compromised by direct pressure,

vertebral collapse, or

both caused by direct

extension or

metastatic spread of

malignancy.

(Schulmeister & Gatlin, 2008; Vogel, 2016)

http://www.medscape.com/viewarticle/442735

Spinal Level % Involvement Associated Cancers

Cervical 10 Lung, breast, kidney,

lymphoma, myeloma,

melanoma

Thoracic 70 Lung, breast, kidney,

lymphoma, myeloma,

prostate

Lumbosacral 20 Lung, breast, kidney,

lymphoma, myeloma,

melanoma, prostate, GI

Cancers associated with spinal cord compression:

(Schulmeister & Gatlin, 2008)

Spinal Cord Compression

Risk Factors:

• Cancers that have a natural history of spreading to the bone

• Cancers that have a natural history of spreading to the brain and spinal cord

• Primary cancers of the spinal cord

• History of vertebral compression fractures

(Vogel, 2016)

Spinal Cord Compression

Pathophysiology: • Compression of spinal cord ✴Direct tumor pressure on cord ✴Tumor invasion of the vertebral column causing collapse & pressure on cord

• Compression leads to: ✴Edema ✴Inflammation

• Resulting in: ✴Direct neural injury to cord ✴Vascular damage

(Kaplan, 2013)

Spinal Cord Compression

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Early signs:

• Neck pain

• Motor

weakness and dysfunction

• Sensory loss

Clinical Presentation:

90% of patients with SCC experience back pain as the first symptom.

Late signs:

• Loss of sensation for deep pressure, vibration, and position

• Incontinence or retention

• Impotence

• Paralysis

• Muscle atrophy

• Loss of sweating below lesion

(Vogel, 2016)

Spinal Cord Compression Spinal Cord Compression

Signs & Symptoms

•Pain

•Motor weakness or gait

changes

•Sensory Loss (numbness,

tingling, sensory changes)

•Constipation and/or bladder

retention

•Bowel and/or bladder

incontinence

•Paralysis

Time Frame

Early

Late

Back pain characteristics:

• Localized: usually occurs at level of lesion, described as dull and constant, more severe with movement, coughing, weight bearing, during a Valsalva maneuver

• Radicular: along dermatomes

• Referred: in a non-radicular pattern

May be a combination of all three!

(Schulmeister & Gatlin, 2008)

Spinal Cord Compression SCC Case Study

Mr. B is a 56-year-old male with stage IV prostate cancer, with wide-spread metastases to the bone He previously failed several cycles of chemotherapy and is being treated with hormonal therapy

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Mr. B presents to Emergency Department with:

–Bi-lateral weakness in lower extremities

•Initial onset 5 days ago

•Difficulty ambulating, reports falling this

morning

–Numbness in the lower extremities

•Began earlier in the day

–Increasing back pain

•Has been taking oxycodone every 4 hours

which controlled his pain well until 4-5 days ago

•Currently rates his pain as 7 out of 10

SCC Case Study

Diagnosis: • MRI

– Gold standard for diagnosis – Accurate, sensitive, and specific diagnostic for malignant spinal cord compression

• Other diagnostic tests – Spinal x-rays

– CT scan – Bone scan and/or PET scan

(Vogel, 2016)

Spinal Cord Compression

Nonpharmacologic:

• Radiation

• Surgery

• Surgery followed by radiation

Treatment:

Immediate and aggressive!

Pharmacologic:

• Corticosteroids

• Chemotherapy

• Analgesics

• Bone remodeling

agents

(Vogel, 2016)

Spinal Cord Compression

Nursing Management:

(Vogel, 2016)

Spinal Cord Compression

• Manage pain and increase comfort • Promote physical mobility

• Improve or maintain neurologic function • Improve or maintain skin integrity • Increase knowledge of disease process

and therapeutic interventions • Preserve self-image and role performance

• Administer treatment as ordered!

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(Vogel, 2016)

•Mr. B received a loading dose of dexamethasone

10 mg, followed by tapering doses.

•He was admitted to the inpatient oncology unit

with initial activity orders for bed rest with only

log-rolling

•Surgical & radiation therapy consults were

ordered

SCC Case Study

•Three days after initiating radiation therapy, Mr.

B. developed urinary retention

•The following day he developed paraplegia,

urinary & bowel incontinence.

•Surgical consult re-evaluated Mr. B for emergent

decompression of spinal cord

•After family conference, Mr. B and his family

decided against surgical intervention and decided

on palliative care

SCC Case Study

Spinal Cord Compression

Nursing Interventions Early recognition:

• Thorough assessment of neck & back pain in high risk patients

Neurological assessments Assess effectiveness pain control Monitor bowel & bladder function PT, OT referrals, as appropriate

• Assess need for home care referrals and supportive medical equipment

Promote physical mobility Protect and/or improve skin integrity

•Mr. B completed his course of radiation

therapy while inpatient

•A hospice consult was obtained. Mr. B was

discharged from inpatient care to a hospice

facility

•Mr. B passed away 23 days later

SCC Case Study

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Superior Vena Cava Syndrome

Superior Vena Cava Syndrome

Definition: Describes a pattern of physical findings that results from the obstruction of

blood flow through the superior vena cava, due to tumor or thrombus, compromising venous drainage from the head, neck, upper

extremities, and thorax.

(Mack & Becker, 2008; Vogel, 2016)

Risk Factors:

• Mediastinal malignancy

• Presence of a CVC and/or pacemaker

• History of radiation to the mediastinum

• Other associated conditions

• mediastinal fibrosis

• fungal infection

• aortic aneurysm

• benign mass

(Mack & Becker, 2008; Vogel, 2016)

Superior Vena Cava Syndrome

Pathophysiology:

1. Obstruction of the SVC occurs (depending on cause)

2. Venous pressure and congestion in the head, neck, thorax, upper extremities, and throat increases

3. Decreased cardiac filling and output occurs

4. Blood flow is diverted to smaller collateral vessels

(Mack & Becker, 2008; Vogel, 2016)

Superior Vena Cava Syndrome

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• Redness and edema in conjunctiva and around eyes and face

• Swelling of neck, arms, and hands

• Neck and thoracic vein distention

• Dyspnea

Early Clinical Presentation: Symptoms are more pronounced in AM or when bending over.

• Nonproductive cough

• Hoarseness, occasionally dysphagia

• Cyanosis of upper torso

• Nasal stuffiness and head fullness

• Breast swelling

(Vogel, 2016)

Superior Vena Cava Syndrome

• Symptoms of ICP

• Irritiability, altered mental status

• Stridor, signs of CHF

• Tachcardia, tachypnea, orthopnea

Late Clinical Presentation:

• Hypotension, no peripheral pulses

• Dysphagia,

hoarseness, hemoptysis

• Progressive cyanosis, facial edema

• Horner syndrome

(Vogel, 2016)

Superior Vena Cava Syndrome

SVC Case Study

• Mr. A is a 67 yo male referred to pulmonologist after a right upper lobe lung

mass was found on X-ray.

• After bronchoscopy with biopsy, he was diagnosed with stage 3 small cell lung

cancer, and sent to an oncologist.

SVC Case Study At his first oncologist visit, he c/o SOB when bending over, dizziness and head pain.

Review of systems and physical exam:

• AM neck swelling

• Hoarseness

• Purple discoloration to check and neck

• Dyspnea

• Difficulty swallowing

• Dry cough • Engorged chest veins and under tongue

• Left arm/hand edema

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Superior Vena Cava Syndrome

http://www.nejm.org/doi/full/10.1056/NEJMcp067190

Superior Vena Cava Syndrome

https://upload.wikimedia.org/wikipedia/commons/thumb/2/28/SVCcombo.JPG/300px-SVCcombo.JPG

Diagnosis:

• CXR

• MRI

• CT

• Contrast venography

• PET

(Vogel, 2016)

Superior Vena Cava Syndrome

Nonpharmacologic:

• Radiation

• Removal of CVC*

• Percutaneous intravascular stent placement

• Surgical reconstruction of SVC

• Oxygen therapy

Treatment: Goal is relief of obstruction and addressing of underlying cause. Determined by rate of onset.

Pharmacologic:

• Chemotherapy

• Chemotherapy + radiation

• Corticosteroids

• Diuretics

• Thrombolytic therapy

(Vogel, 2016)

Superior Vena Cava Syndrome

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SVC Case Study

Mr. A started chemotherapy immediately.

Additional orders included:

• VS Q_hours

• Maintain O2 saturation > __%

• Elevate head of bed

• Scheduled lasix and methylprednisolone

He responded quickly and was able to breath

easily when he was eventually discharged home.

Nursing Management:

(Vogel, 2016)

Superior Vena Cava Syndrome

• Maintain adequate gas exchange • Maintain adequate cardiac output

• Decrease anxiety • Increase knowledge of disease process and

therapeutic interventions

• Prevent injury • Administer treatment as ordered

Clinical Pearls Know your patient! Know the risk factors! Know how to complete a good physical assessment! Early recognition may save a life!

References Brashers, V. L. (2014). Alterations in Cardiovascular Function. In K. L. McCance & S. E. Huether (Authors) & V. L.

Brashers & N. S. Rote (Eds.), Pathophysiology: The Biologic Basis for Disease in Adults and Children (7th ed., pp. 1129-1193). St. Louis, MO: Elsevier.

Camp-Sorrell, D. (2008). Cardiac Tamponade. In R. A. Gates (Author) & R. M. Fink (Ed.), Oncology Nursing Secrets (3rd ed., Nursing Secrets Series, pp. 513-517). St. Louis, MO: Mosby Elsevier.

Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses. (2nd ed., pp. 433-459). Pittsburgh, PA. Oncology Nursing Society.

Jensen, G. (2008). Hypercalcemia of Malignancy (HCM). In R. A. Gates (Author) & R. M. Fink (Ed.), Oncology Nursing Secrets (3rd ed., Nursing Secrets Series, pp. 523-527). St. Louis, MO: Mosby Elsevier.

Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses. (2nd ed., pp. 337-383). Pittsburgh, PA. Oncology Nursing Society.

Mack, K. C., & Becker, C. (2008). Superior Vena Cava Syndrome. In R. A. Gates (Author) & R. M. Fink (Ed.), Oncology Nursing Secrets (3rd ed., Nursing Secrets Series, pp. 551-556). St. Louis, MO: Mosby Elsevier.

Maloney, K. W. (2016). Metabolic Emergencies (J. M. Brant, F. A. Conde, & M. G. Saria, Eds.). In J. K. Itano (Ed.), Core Curriculum for Oncology Nursing (5th ed., pp. 478-494). St. Louis, MO: Elsevier.

National Comprehensive Cancer Network (2016). Non-Hodgkin’s Lymphomas, Version 3.2016. Retrieved from https://www.nccn.org/professionals/physician_gls/pdf/nhl.pdf

Sanofi-Aventis US (2016). Elitek Package Insert. Retrieved from http://products.sanofi.us/elitek/elitek.html#section-4.1

Schulmeister, L., & Gatlin, C. G. (2008). Spinal Cord Compression. In R. A. Gates (Author) & R. M. Fink (Ed.), Oncology Nursing Secrets (3rd ed., Nursing Secrets Series, pp. 546-550). St. Louis, MO: Mosby Elsevier.

Viele, C. S. (2008). Disseminated Intravascular Coagulation (DIC). In R. A. Gates (Author) & R. M. Fink (Ed.), Oncology Nursing Secrets (3rd ed., Nursing Secrets Series, pp. 518-522). St. Louis, MO: Mosby Elsevier.

Vogel, W. H. (2016). Structural Emergencies (J. M. Brant, F. A. Conde, & M. G. Saria, Eds.). In J. K. Itano (Ed.), Core Curriculum for Oncology Nursing (5th ed., pp. 495-508). St. Louis, MO: Elsevier.

Zobec, A. (2008). Tumor Lysis Syndrome (TLS). In R. A. Gates (Author) & R. M. Fink (Ed.), Oncology Nursing Secrets (3rd ed., Nursing Secrets Series, pp. 557-560). St. Louis, MO: Mosby Elsevier.