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Oncologic Emergencies
Juanita Madison, RN, MN, AOCN
CHI Franciscan Health
Oncologic Emergencies
Life-threatening medical emergencies caused by:
Malignancy
Treatment of malignancy
When do they occur?
Initial manifestations of malignancy
or
Late in disease process
Oncologic Emergencies
Metabolic Oncologic Emergencies Tumor Lysis Syndrome (TLS)
Sepsis & Septic Shock
Disseminated Intravascular Coagulation (DIC)
Hypercalcemia
Inappropriate Antidiuretic Hormone Secretion (SIADH)
Anaphylaxis
Structural Oncologic Emergencies Spinal Cord Compression
Superior Vena Cava Syndrome
Increased Intracranial Pressure (ICP)
Cardiac Tamponade
Tumor Lysis Syndrome (TLS)
Metabolic imbalance
Caused by breakdown of malignant cells
Large number of rapidly proliferating cells killed
Cell lysis, rupture of tumor cell membranes
Intracellular components released into blood stream
Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing
oncologic emergencies: A resource for nurses .Oncology Nursing Society, Pittsburgh, PA. pp: 433-459.
2
TLS: Pathophysiology
Intracellular components Potassium
Phosphorous
Nucleic acids (DNA, RNA)
Cell killed (lysed), cell membrane ruptures
Nucleic acids released into blood stream
Potassium & Phosphorous released into blood stream
Results in: Hyperuricemia
Hyperkalemia
Hyperphosphatemia
Hypocalcemia
K+
PO4- PO4
-
Nucleic Acids
K+ K+
K+ PO4-
K+
Nucleic
Acids
Hypoxanthine
Xanthine
Uric Acid
Urine
PO4- K+ K+ PO4
- PO4-
Ca++ Ca++ Ca++ Xanthine
Oxidase
(Liver)
Tumor Lysis Syndrome: Who’s At Risk?
Most common in: Patients with large tumor burden that is highly responsive to antineoplastic therapy (resulting in rapid cell kill)
Risk Factors: Tumor-related
High-grade lymphomas
Hematologic malignancies (acute or chronic leukemia's with WBC)
Tumors with high growth fractions (anticipated to be responsive to treatment)
Patient-related Large tumor burden/bulky tumors
Elevated LDH
Pre-existing renal dysfunction
Treatment-related Chemotherapy & biologic agents
Radiation therapy
National Comprehensive Cancer Network (NCCN), 2014. NCCN Guidelines: Non-Hodgkin’s Lymphoma,
version 4.2014. Accessed on August 30, 2014 at http://www.nccn.org/professionals/physician_gls/pdf/nhl.pdf
Tumor Lysis Syndrome: Onset, Duration, Incidence
Onset:
Usually within 12-72 hrs. after initiation of antineoplastic therapy
Duration:
May persist for 5-7 days post-therapy
Incidence:
Exact incidence unknown
Occurs mostly in patients with
Hematologic malignancies with large proliferative growth fractions
Large bulky disease (acute leukemias, high-grade lymphomas)
National Comprehensive Cancer Network (NCCN), 2014. NCCN Guidelines: Non-Hodgkin’s Lymphoma,
version 4.2014. Accessed on August 30, 2014 at http://www.nccn.org/professionals/physician_gls/pdf/nhl.pdf.
Clinical Manifestations
Often asymptomatic initially
Detected initial via abnormalities in blood chemistries
Signs & symptoms patients exhibit depend on extent of metabolic abnormalities
Hyperkalemia
Hyperuricemia
Hyperphosphatemia
Hypocalcemia
Holmes Gobble, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing
oncologic emergencies: A resource for nurses .Oncology Nursing Society, Pittsburgh, PA. pp: 433-459.
3
TLS: Signs & Symptoms Hyperkalemia Serum K+ >6.5 mEq/L
Early cardiac:
• Tachycardia
• EKG Changes: Prolonged QT and ST segment, lowering and inversion of T wave
Late cardiac:
• Bradycardia
• EKG Changes: Shortened QT, elevated T wave, wide QRS
• Ventricular tachycardia, ventricular fibrillation, cardiac arrest
• Nausea/vomiting
• Diarrhea
• Increased bowel sounds
• Twitching
• Muscle cramps
• Weakness
• Paresthesias
• Lethargy
• Syncope
Hyperuricemia Serum uric acid >10 mg/dl
Severe = >20 mg/dl
• Oliguria, anuria, azotemia
• Edema, hypertension
• Acute renal failure
• Chronic renal failure
• Malaise, weakness, fatigue
• Nausea, vomiting
• Flank pain, gout
• Pruritus
Gobel, B. H. (2013). In M. Kaplan (Ed.), Understanding an managing oncologic emergencies: A resource for nurses
2nd Edition (pp. 433 - 459). Pittsburgh, PA: ONS
TLS: Signs & Symptoms Hyperphosphatemia Serum PO4 >5 mg/dl
• Anuria
• Oliguria
• Azotemia
• Edema
• Hypertension
• Acute renal failure
Secondary
Hypocalcemia Serum Ca++ < 8.7 mg/dl
Neurological/Neuromuscular
•Twitching, paresthesias
• Restlessness
• Muscle cramps & weakness
• Anxiety, depression
• Carpopedal spasms
• Seizures
• Confusion
• Hallucinations
Cardiac
• Tetany
• Ventricular arrhythmias
• Prolonged QT interval, inverted T wave
• Heart block
• Cardiac arrest
Gobel, B. H. (2013). In M. Kaplan (Ed.), Understanding an managing oncologic emergencies: A resource for nurses
2nd Edition (pp. 433 - 459). Pittsburgh, PA: ONS
TLS: Management
Prevention Strategies
Recognition of at-risk patients
Hydration
Prevention of hyperuricemia
Frequent monitoring of electrolytes
Intervention Strategies
Hydration
Control of hyperuricemia
Aggressive correction of electrolytes
Management of acute renal failure
National Comprehensive Cancer Network (NCCN), 2014. NCCN Guidelines: Non-Hodgkin’s Lymphoma,
version 4.2014. Accessed on August 30, 2014 at http://www.nccn.org/professionals/physician_gls/pdf/nhl.pdf.
TLS Prevention
Hydration IV Normal saline or 5% dextrose
Begin 24 – 48 hours prior to therapy
Ensure urine output >150 – 200 ml/hr
Diuresis Typically used if urine output not maintained by hydration alone
Loop diuretics or osmotic diuretics
Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies:
A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459; McGraw, B. (2008). CJON 12 (4); 563-565.
4
Prevention of TLS: Control of Hyperuricemia
Allopurinol (Oral or IV) Dosing:
Oral: 300 mg/m2/day (not to exceed 600 mg/day)
IV: 200 – 400 mg/m2/day
Begin 2 – 3 days prior to chemotherapy
Continue for 10-14 days
Blocks uric acid production by inhibiting xanthine oxidase (liver enzyme)
Prevents uric acid precursors from converting to uric acid, ↓ risk uric acid crystallization
Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies:
A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459; McGraw, B. (2008); NCCN, 2014.
Control of Hyperuricemia
Rasburicase (Elitek®) IV Recombinant urate-oxidase
Catalyzes the oxidation of uric acid into allantoin (which has a much greater solubility than uric acid)
Recommendations for preventative therapy (NCCN, 2014):
Patients with any high-risk features
Urgent need to initiate therapy in high-bulk patient
Situations where adequate hydration may be difficult
Acute renal failure
Sanofi-Aventis US, 2011. Elitek Package Insert. Bridgewater, NJ.; NCCN, 2014. NCCN Guidelines: Non-Hodgkin’s
Lymphoma,v4.2014. Accessed on August 30, 2014 at http://www.nccn.org/professionals/physician_gls/pdf/nhl.pdf.
Rasburicase (Elitek®)
FDA approved dosing 0.2 mg/kg IV as a 30 minute infusion daily for up to 5 days
NCCN dosing recommendations One dose frequently adequate
Doses of 3 – 6 mg IV usually effective
Uric acid levels decrease within 4 hours of injection
Sanofi-Aventis US, 2011. Elitek Package Insert. Bridgewater, NJ.; NCCN, 2014. NCCN Guidelines: Non-Hodgkin’s
Lymphoma,v4.2014. Accessed on August 30, 2014 at http://www.nccn.org/professionals/physician_gls/pdf/nhl.pdf.
Prevention TLS
Urinary Alkalinization Sodium bicarbonate added to IV fluid (50-100 meq/liter)
Goal: urine pH level > 7.0
Use is controversial Potential complications associated with alkalinization
Metabolic alkalosis
Calcium phosphate precipitation
Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies:
A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459; McGraw, B. (2008). CJON 12 (4); 563-565.
5
TLS Preventative Measures
Monitor serial lab values
Serum potassium, phosphorous, calcium, uric acid
Renal function studies – BUN & creatinine
Frequency of monitoring
Prior to initiation of therapy
Every 8 – 12 hours during the first 48 – 72 hours of treatment
Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies:
A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459; McGraw, B. (2008). CJON 12 (4); 563-565.
Mr. J.: 63 Year-Old Male
diagnosed with High-Grade NHL
Past Medical History: Noninsulin-dependent diabetes mellitus, supraventricular arrhythmia
Scheduled to receive 1st cycle CHOP-R chemotherapy in outpatient clinic
Cyclophosphamide (Cytoxan), doxorubicin (Adriamycin), vincristine (Oncovin), prednisone, + Rituximab (Rituxan)
Started on oral allopurinol 300 mg daily
IV hydration pre & post chemotherapy in clinic
Instructed to increase oral intake to 8 glasses fluid per day
Mr. J: Two Days Post 1st Chemo
Mr. J’s wife calls clinic and reports:
Weakness, muscle cramping, numbness & tingling of extremities
Nausea/vomiting
Decreased urine output
Swelling both feet
What could be the cause of Mr. J’s symptoms?
What should we advise Mrs. J. to do?
Mr. J: Two Days Post 1st Chemo
ED intake interview revealed Mr. J. had not been able to tolerate oral medications after his chemotherapy
Had not taken prescribed allopurinol
Had not taken in recommended 8 glasses fluid per day
6
Mr. J’s Labs in ER (2 Days Post CHOP-R Chemotherapy)
Baseline Pre-Chemo Labs
Hgb 11.1 g/dl
Platelets 245,000/mm3
Na++ 136
K+ 4.1
BUN 45 mg/dl
Creatinine 2.2 mg/dl
Uric acid 12.6 mg/dl
ER: 2 days post-chemo
Hgb 11.2 g/dl
Platelets 200,00/mm3
Na++137 mmol/l
K+ 6.5 mmol/l
BUN 100
Creatinine 5.1 mg/dl
Uric acid 25 mg/dl
TLS Intervention Strategies
Hydration
Control of hyperuricemia
Aggressive correction of electrolyte imbalances
Management of acute renal failure
NCCN Guidelines: Non-Hodgkin’sLymphoma,v4.2014. Accessed on August 30, 2014 at
http://www.nccn.org/professionals/physician_gls/pdf/nhl.pdf.
Treatment of TLS Hyperuricemia • Hydration, urinary alkalinization
• Oral allopurinol or IV allopurinol
• Rasburicase
• Hemodialysis for significant renal compromise
Hyperkalemia Mild (Potassium<6.5 mEq/L):
• Sodium polystyrene sulfonate orally or by retention enema
Potassium >6.5 mEq/L or cardiac changes:
• IV calcium gluconate or calcium carbonate
• IV sodium bicarbonate, hypertonic glucose & insulin accompanied by sodium polystyrene sulfonate
• Loop diuretics & aggressive hydration
Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies:
A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459.
Treatment of TLS
Hyperphosphatemia • Phosphate-binding agents
• Aluminum-containing antacids
• Hypertonic glucose plus insulin
• Aggressive hydration
Hypocalcemia • Appropriate management of hyperphosphatemia
• IV calcium gluconate or calcium chloride to treat arrhythmias
Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies:
A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459.
7
Mr. J. was treated with: 1 amp D50, 10 units regular insulin
D51/2 NS plus 100 mEq NaHCO3 at 250 cc/hr
Allopurinol 300 mg/day po
IV Lasix 40 mg
Transferred to inpatient telemetry unit with following orders:
Strict I & O Notify MD for urine output < 200 ml/hr
BID weights
Vital signs Q2 hrs
Repeat Laboratory tests in 1 hr, monitor Q4 hrs: Electrolytes, Ca++, PO4-, BUN, Creatinine, Uric Acid
TLS: Nursing Interventions
Recognize patients at risk Leukemia, lymphoma, small-cell lung cancer
Large tumors with large growth fractions or elevated LDH
Recent chemo or radiation therapy
High LDH, concurrent renal disease
Careful assessment of fluid balance
Patient teaching – strategies to reduce incidence or severity of symptoms
Maintain adequate oral fluid intake
Take Allopurinol as ordered
Signs & symptoms to report to health care team
Written instructions
Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies:
A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459.
.
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
Continuum Septic Shock:
Infection/
Septicemia SIRS Sepsis Severe Sepsis Septic Shock
Sepsis Continuum Phase Definition
Infection/ bacteremia
Presence of bacteria or fungi in blood as evidenced by positive blood culture or positive catheter culture
Systemic Inflammatory Response Syndrome (SIRS)
Indicated by presence of two or more of the following: • Oral temperature >100.40F (380C) or <96.80F (360C) • Heart rate > 90 beats/minute • RR>20/min or PaCO2 >32 mmHg • WBC >12,000 cells/mm2, <4,000 cells/mm2 , or >10% bands in
peripheral blood
Sepsis Documented infection with presence of two or more SIRS criteria
Severe Sepsis Presence of sepsis with one or more of the following: organ dysfunction, hypotension, or hypoperfusion
Septic Shock Presence of sepsis with hemodynamic instability that persists despite aggressive fluid challenge
Multiple Organ Dysfunction Syndrome
Dysfunction of more than one organ; homeostasis must be maintained with immediate intervention
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.
8
Risk Factors in Cancer
Neutropenia
Single most important risk factor
Increased duration and severity of neutropenia increases risk
Treatment-related risk factors
Chemotherapy
Biotherapy
Radiation therapy
Infiltration of bone marrow by solid tumor
Patient-related
Disruption in mucosal barriers
Splenectomy and functional asplenia
Corticosteroids or other immunosuppressant's
National Comprehensive Cancer Network (2014). NCCN Clinical Practice Guidelines in Oncology: Prevention and
treatment of cancer-related infections, v2.2014. Retrieved July 25, 2014 from http://www.nccn.org/professionals/p
hysician_gls/pdf/infections.pdf.
Incidence and Mortality
Incidence in cancer patients
Bacteremia or sepsis: 10-20% of patients with febrile neutropenia
Hematologic Malignancies have higher incidence than solid tumors
Hematologic malignancies: 66.4 per 1,000 hospitalized patients
Solid tumors: 7.6 per 1,000 hospitalized patients
Mortality in cancer patients
Approximately 28%, same mortality rates for hematologic malignancies & solid tumors
Courtney, et al (2007). Oncologist, 12, 1019-1026; Shelton, B.K. (2011), in Yarbro et al (eds), Cancer Nursing: Principles and Practice
(7th ed., pp 713-744). Jones & Bartlett.; Williams, et al (2004).Critical Care 8, 291-298.
Sepsis and Septic Shock
Incidence in cancer patients
Bacteremia or sepsis:
Occurs in 10-20% of patients with febrile neutropenia
Severe Sepsis
Hematologic Malignancies have higher incidence than solid tumors
Hematologic malignancies: 66.4 per 1,000 hospitalized patients
Solid tumors: 7.6 per 1,000 hospitalized patients
Mortality in cancer patients
Approximately 28%, same mortality rates for hematologic malignancies & solid tumors
Courtney, et al (2007). Oncologist, 12, 1019-1026; Shelton, B.K. (2011), in Yarbro et al (eds), Cancer Nursing: Principles and Practice
(7th ed., pp 713-744). Jones & Bartlett.; Williams, et al (2004).Critical Care 8, 291-298.
Septic Shock: Pathophysiology Micro-organisms in blood stream release chemical mediators & hormones
Endotoxins – released by gram negative bacteria
Exotoxins – released by gram positive bacteria
Profound systemic vasodilation Hypotension
Tachycardia
Increased vascular permeability Fluid leaks from vascular space to interstitial space
Decreases circulating blood volume
Hypoxic tissues
Metabolic acidosis
Holmes Gobel, et al (2013). Sepsis & septic shock. In Kaplan, M (Ed). Understanding and managing oncologic emergencies:
A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 287-335.
9
Causes of Sepsis Bacterial organisms (most common cause of sepsis)
Gram-negative bacteria (responsible for 50-60% cases of septic shock)
Escherichia coli Klebsiella pneumoniae Pseudomonas aeruginosa
Gram-positive bacteria (increased incidence due to use of vascular access devices)
Streptococcus pneumoniae Staphylococcus aureus Corynebavcterium
Other organisms Invasive fungal infections, viruses
Lewis, et al (2011). Oncologic emergencies: Pathophysiology, presentation, diagnosis, and treatment. CA: A Cancer Journal for
Clinicians, 61, 287-314.
.
Mr. J.: Seven days post-3rd cycle chemotherapy (CHOP-R)
Wife calls outpatient clinic at 5 pm on Friday and reports husband has:
Fever
Dry cough
Discomfort with swallowing
Mr. J & Wife arrive in ER at 7:30 pm:
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 98% room air
Temp 1020F, HR irregular 96, RR 16, BP 126/84
Sepsis Bundles
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.
10
Sepsis Bundles
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.
Diagnostic Evaluation
CBC with differential Complete metabolic panel Serum lactate Blood cultures X 2 Cultures of body fluids
Urine, stool, throat, wounds, sputum
Chest X-Ray
Holmes Gobel, et al (2013). Sepsis & septic shock. In Kaplan, M (Ed). Understanding and managing oncologic emergencies:
A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 287-335.
Treatment of Sepsis/Septic Shock
Immediate initiation IV antibiotics (within 3 hours) Fluid resuscitation
Goals: MAP: > 65 mmHg CVP: 8-12 mmHg Urine output: > 0.5 mg/kg/hr
Oxygen therapy Antipyretics
Holmes Gobel, et al (2013). Sepsis & septic shock. In Kaplan, M (Ed). Understanding and managing oncologic emergencies:
A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 287-335.
ER Orders for Mr. J.:
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
Meropenum 1 gm IV stat & Q8h
Vancomycin 1000 mg IV stat & Q12h
Admit to medical unit
Neutropenic precautions
11
Mr. J’s Labs in ER:
• WBC 1,100/mm3
• ANC 450/mm3
• Hgb 10 g/dl
• Plt 30,000/mm3
• Glucose 201 mg/dl
• Na++ 134 mEq/l
• K+ 3.3 mEq/l
• BUN 12 mg/dl
• Creatinine 0.9 mg/dl
Nursing Assessment on Admission to Inpatient Unit: 9 PM
Extreme restlessness & anxiety
Shaking chills
Skin warm, flushed
Temp 102.40F
HR 120 irregular, bounding
RR 20, oxygen saturation 96% room air
BP 128/60
No urine output since early am
Stat IV antibiotics ordered in ER not yet given
Nursing Management Sepsis
Frequent vital signs & assessments
LOC, skin color & temp, lungs
Ensure antibiotics administered within 3 hours
Maintain oxygenation
Oxygen therapy & ventilatory support
Administer IV fluids,
Expand intravascular volume (fluid resuscitation)
Monitor I & O
Antipyretics
Assess for fluid overload
Mr. J: Nursing Assessment 9:45 pm
Disoriented, lethargic
Skin pale, cool, fingertips cyanotic
↓ breath sounds lower lobes bilaterally with diffuse bilateral rales, hemoptysis
Abdomen distended, rebound tenderness
No urine output
Oozing blood from venipuncture sites
HR 136 irregular, weak
RR 28 labored, oxygen saturation 88% room air
BP 88/50
12
Nursing Interventions
Neutropenic patients with fever Must be assessed immediately
Started on broad spectrum antibiotics
Monitor for sequelae of septic shock Frequent vital signs
Assess tissue perfusion (skin color, temperature, capillary refill)
Lung assessments
I & O – report urine output < 30cc/hr
Monitor for symptoms of DIC
Monitor response to medical treatment Assess for fluid overload
Monitor lab values, especially renal function & culture reports
Infection control measures
Holmes Gobel, et al (2013). Sepsis & septic shock. In Kaplan, M (Ed). Understanding and managing oncologic emergencies:
A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 287-335.
Possible Complications of Sepsis/Septic Shock
DIC
Multiple organ dysfunction syndrome
Death
Disseminated Intravascular Coagulation (DIC)
Syndrome of:
Thrombus formation (clotting)
Simultaneous Hemorrhage
Caused by over stimulation of normal coagulation processes
Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 69 – 102.
Pathophysiology DIC
Paradox of DIC: bleeding & clotting
Triggered by: Intrinsic coagulation system activation (damage to blood vessels)
Transfusion reactions
Endotoxins/Septicemia
Sickle Cell Disease
Malignant hypothermia
Extrinsic coagulation system activation (tissue injury) Obstetrical Conditions
Extensive surgery
Crush injuries
Malignancies
Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 69 – 102.
13
DIC in the Oncology Population:
Malignancy Induced
Acute Promyelocytic Leukemia (APL)
Procoagulant material release by granules of the immature promyelocyte initiates clotting cascade
Occurs in 85% patients with APL
Solid Tumors (adenocarcinomas)
Lung, pancreas, prostate, stomach, colon, ovary, gall bladder, breast, kidney
Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 69 – 102.
Other Causes DIC (Oncology Population)
Chemotherapy May induce DIC by damaging tumor, normal cells, or endothelium causes release procoagulant material
Large tumor burden/large cell kill release granule procoagulant from dead cells into systemic circulation
Infection/sepsis Especially gram negative bacteria sepsis (release of endotoxin)
Hemolytic transfusion reactions Rupture of RBC’s platelet aggregation, release platelet factors that initiate clotting cascade
Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 69 – 102.
Types of DIC
Acute DIC
Medical emergency
Chronic DIC
Produces coagulation abnormalities, with or without clinical manifestations, that can be medically managed
Most cases of chronic DIC due to underlying malignancy
Laboratory Values in DIC Laboratory Test Result Comments or Cause
Prothrombin Time (PT) Prolonged Nonspecific in DIC
Activated Partial Thromboplastin time (APPT)
Prolonged Nonspecific in DIC
International normalized ratio (INR)
Prolonged Nonspecific in DIC
Fibrin Degradation Products Elevated Indicates breakdown of fibrin & fibrinogen
D-Dimer Elevated Indicates hyperfibrinolysis
Platelet Count Decreased Platelets consumed
Fibrinogen Decreased Fibrinolysis; decreases very slowly only in severe DIC
Antithrombin Decreased Anticoagulant activity inhibited Accelerated coagulation
Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 69 – 102.
14
DIC Clinical Presentation
Decreased tissue/organ perfusion Brain, CV, Lungs, Kidney, GI Tract, Skin
Decreased platelet count Petechiae, ecchymosis
Hemorrhage Tachycardia, hypotension
Tachypnea
Overt bleeding
Occult bleeding
Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 69 – 102.
Mr. J: Nursing Assessment 9:45 pm
Disoriented, lethargic
Skin pale, cool
↓ breath sounds lower lobes bilaterally with diffuse bilateral rales, hemoptysis
Abdomen distended, rebound tenderness
No urine output
Oozing blood from venipuncture sites
HR 136 irregular, weak
RR 28 labored, oxygen saturation 88% room air
BP 88/50
Mr. J’s Labs at 10:00 pm
Lab 7:30 pm 10:00 pm Normals
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 sec 11.3 – 13.1 sec
Fibrin Degradation Products
60 mcg/ml <10 mcg/mL
Treatment of DIC
Early recognition & treatment of underlying disorder
Chemotherapy for malignancy
Antibiotics for infection
Correct hypoxia
Oxygen to maintain saturation >95%
Correct hypovolemia, hypotension, & acidosis
NS until type & cross match completed & blood available
Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 69 – 102.
15
Treatment of DIC Stop the micro clotting to maintain perfusion & protect vital function
IV Heparin
Antithrombin III (inhibits action of thrombin)
Stop the bleeding
Pressure to active sites of bleeding
Blood products (FFP, cryoprecipitate, platelets, red blood cells)
Antifibrinolytic agents (EACA)
Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 69 – 102.
Nursing Interventions
Prevent severity of symptoms
Direct pressure sites of bleeding, pressure dressings, sand bags
Monitor for progression DIC
Worsening vital signs, hypotension, anuria, ’s LOC
Monitor response to therapy
Sites & amounts of bleeding
Changes in lab values
Assess tissue perfusion parameters – color, temperature, peripheral pulses
Patient Teaching
Avoid ASA or NSAID’s (effects on platelet aggregation)
Signs and symptoms of DIC (bleeding and/or clotting)
Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 69 – 102.
Hypercalcemia of Malignancy (HCM)
Metabolic disorder
Most commonly develops as a consequence of pathologic destruction of bone, mediated by factors released by malignant cells
One of the most common, life-threatening complications of malignancy
Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd Ed., 103-155, ONS, Pittsburgh, PA.; Makras, P & Papapoulous, SE (2009).
Medical treatment of hypercalcemia. Hormones, 8, 83-95.
HCM: Incidence
Occurs in approximately 30% of cancer patients
Most often in advanced stages of disease
50% of patients die within 30 days of diagnosis
Survival beyond 6 months is rare
Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd Ed, pp 103-155,ONS, Pittsburgh, PA.
16
Normal Regulation of Ca++ Parathyroid gland
Production of parathyroid hormone (PTH)
PTH is major hormone regulating extracellular Ca++
PTH increases Ca++ by 3 mechanisms: Direct action on bone
Stimulates activity of osteoclasts → breaks down bone (bone resorption)
Direct action on kidneys Increases renal excretion of phosphate stimulates reabsorption of Ca++
Indirect action in gut Enhances absorption of ingested Ca++ by stimulating kidney conversion of vitamin D to biologically active form
Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd Ed, pp 103-155,ONS, Pittsburgh, PA.
Normal Regulation of Ca++ Ca++ levels below normal:
Parathyroid stimulated to produce PTH
Acts on bone release of calcium (bone resorption) into circulation
Acts on kidneys increase renal secretion of phosphorous stimulates reabsorption of Ca++
Acts indirectly gut enhance absorption Ca++
Ca++ levels above normal:
Kidneys excretion of calcium
Distribution of Calcium
Bone stores: 99% of body’s calcium
Serum calcium: 1% circulates in serum, divided into fractions:
50% is free ionized calcium
Only type that is biologically active
40% is bound to protein
Mostly albumin, but also globulin & paraproteins
10% forms serum complexes with anions
Bicarbonate, phosphate, & citrate
Moe, SM (2008). Disorders involving calcium, phosphorus, and magnesium. Primary Care, 35, 215-237.
Measuring Serum Calcium Total calcium =
Ionized calcium + protein-bound calcium
Used to “infer” the fraction of ionized calcium
The result is usually accurate, EXCEPT when
serum albumin is low
If albumin < 3.5 – 5.5 g/dL, results in:
↓in the fraction of protein-bound calcium
↑ in the ionized free calcium
Ionized calcium more accurately reflects true serum calcium levels
Moe, SM (2008). Disorders involving calcium, phosphorus, and magnesium. Primary Care, 35, 215-237.
17
Corrected Serum Ca++
Corrected Total Serum Calcium =
Total serum Ca++ + (4.0 – serum albumin) X 0.8
Example: Ca++ 13.8 Albumin 2.1
= 13.8 + (4.0 – 2.1) X 0.8
= 13.8 + 1.9 X 0.8
= 13.8 + 1.52
= 15.32 (rounded to 15.3)
*Normal Total Serum Calcium: 8.5 to 10.2 mg/dL.
HCM: Etiology Tumor-induced bone breakdown releasing Ca++ into bloodstream
Tumor secretion of a parathyroid hormone-related protein (PTHrP)
Squamous cell tumors: Lung, breast, prostate, head & neck, esophagus, kidney
Non-Hodgkin lymphoma, chronic myeloid leukemia (blast phase), adult T-cell leukemia - lymphoma
Tumor production of 1,25-dihydroxyvitamin D (calcitrol)
Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 103 – 155.
Hypercalcemia: Clinical Presentation
Clinical signs & symptoms related to rapidity of onset & serum calcium level
Corrected total serum calcium (TSC) needs to be calculated if albumin is low
Corrected Total Serum Calcium (mg/dl)=
Measured serum Ca++ + (4.0 – serum albumin g/dl) X 0.8
**Normal Serum Ca++ = 8.5 – 10.5 ml/dl
HCM: Signs & Symptoms
Reflect direct depressive effects ↑ serum
Ca++ exerts on:
Excitability of nerve tissue
Contractility of cardiac, smooth, skeletal muscles
Signs & symptoms:
Lethargy, confusion
Cardiac dysrhythmias
Constipation
Muscle hypotonia
McCurdy, M. & Shanholtz, CB (2012). Oncologic emergencies. Critical Care Medicine, 40 (7): 2212-2222.
18
Signs and Symptoms of Hypercalcemia of Malignancy
System Early Late
Neurologic Drowsiness, lethargy, weakness, restlessness, irritability, confusion, cognitive dysfunction, disorientation
Seizures Stupor Coma
Renal Polyuria, polydipsia, nocturia, dehydration, kidney stones, renal insufficiency
Renal failure
GI Anorexia, nausea, vomiting, constipation, vague abdominal pain, weight loss, peptic ulcers
Atonic ileus Obstipation
Cardiovascular EKG changes (slowed conduction, Prolonged PR, wide QRS, short QT, short ST), sinus bradycardia
Heart block Cardiac arrest
Musculoskeletal Muscle weakness, fatigue, hypotonia, bone pain
Ataxia Pathologic fractures
Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 103 – 155.
HCM: Treatment
Degree Total Serum Calcium
Management
Mild 10.5 – 11.9 mg/dL
Observe & treat as outpatient
Moderate 12.0 – 13.9 mg/dL Requires specific but non-urgent treatment
Severe > 14.0 mg/dL Requires urgent treatment
Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 103 – 155.
Hypercalcemia: Treatment
Treat the cancer – tumor control or reduction is the only long-term measure for reversing hypercalcemia
Hydration & forced diuresis Oral fluids (3-4 L/day)
IV Saline
Loop diuretics (furosemide)
Mobilization
Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 103 – 155.
Agents to Inhibit Bone Resorption Agent Mechanism of Action Dosing
Bisphosphonates
• Pamidronate (Aredia) • Inhibits osteoclast activity
IV: 60-90 mg over 2 hrs May repeat after 7 days
• Zoledronate (Zometa) • Inhibits osteoclast activity
IV: 4 mg over 15 minutes May repeat after 7 days
Calcitonin • Direct inhibition of osteoclast receptors
• Increases renal calcium excretion
SC or IM: 4-8 IU/kg every 6-12 hours for 2 days
Gallium nitrate (Ganite) • Used when HCM resistant to bisphosphonates
• Inhibits osteoclast activity
IV: 200 mg/m2/day continuous for 5 days
Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 103 – 155.
19
Hypercalcemia Treatment Dietary recommendations
Maintain salt intake
Dietary calcium restrictions not necessary
Medications to avoid
Thiazide diuretics (↓ renal excretion Ca++)
NSAIDS, H2 receptor antagonists (inhibit renal blood flow)
Vitamins A & D (increase bone resorption)
Parenteral/enteral solutions with calcium
Corticosteroids
Therapy of choice multiple myeloma or lymphomas
Inhibits vitamin D conversion to calcitriol
Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 103 – 155.
Nursing Interventions
Recognize early signs & symptoms
Careful monitoring of patients taking: Thiazide diuretics (inhibits calcium excretion)
Digitalis preparations (action potentiated in hypercalcemic states)
Measures to decrease calcium removal from bone: Ambulation, weight bearing, ROM, isometric exercises
Careful assessment & monitoring Fluid balance & renal function
GI motility
Cardiac Status
Mental status
Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 103 – 155.
Mr. C: Hypercalcemia
62-year-old male diagnosed with stage IV squamous cell cancer of lung CT of spine showed metastatic disease in thoracic & lumbar spine at T1 & L3 vertebrae Based on extent of disease & poor pulmonary function, Mr. C. was not a surgical candidate. Scheduled for second course of palliative chemotherapy Also receiving concurrent radiation for the spinal metastasis
2nd Cycle Chemotherapy
Wife consults with nursing staff & reports:
Concern re: husband’s ↑ forgetfulness,
wonders if confusion is because of recent change in pain medication (oxycodone)
Husband experiencing more fatigue than usual (4-5 naps per day)
20
Mr. C’s Labs: 2nd Cycle Chemotherapy
WBC 4,500/mm3
Hgb 11.2 g/dl
Hct 35%
Platelets 119,000/mm3
Serum Ca++ 10.4
Creatinine 1.1 mg/dl
BUN 19 mg/dl
Albumin 2.3 g/dl
Corrected Serum Ca++
Mr. C’s : Ca++ 10.4 Albumin 2.3
Corrected Serum Calcium =
Measured serum Ca++ + (4.0 – serum albumin) X 0.8
= 10.4 + (4.0 – 2.3) X 0.8
= 10.4 + 1.7 X 0.8
= 10.4 + 1.36
= 11.78 (rounded up to 11.8)
Mr. C’s 3rd Cycle Chemotherapy
Wife reports confusion improved for 1st two weeks following last chemotherapy
Past week, he has been increasingly forgetful, depressed, and fatigued (stayed in bed last 2 days)
Mr. C’s Lab Trends
Lab Test 2nd Chemo Visit 3rd Chemo Visit
WBC 4,500/mm3 2,200/mm3
Hgb 11.2 d/dl 10.4 g/dl
Hct 35% 29%
Platelet count 119,000/mm3 102,000 mm/3
BUN 19 mg/dl 28 mg/dl
Creatinine 1.1 mg/dl 1.5 mg/dl
Serum calcium 10.4 mg/dl 12.8 mg/dl
Albumin 2.3 g/dl 2.1 g/dl
21
Corrected Serum Ca++
Mr. C’s : Ca++ 12.8 Albumin 2.1
Corrected Serum Calcium =
Measured serum Ca++ + (4.0 – serum albumin) X 0.8
= 12.8 + (4.0 – 2.1) X 0.8
= 12.8 + 1.9 X 0.8
= 12.8 + 1.52
= 14.32 (rounded to 14.3)
Structural Oncologic Emergencies
Spinal Cord Compression
Superior Vena Cava Syndrome (SVCS)
Increased Intracranial Pressure (ICP)
Cardiac Tamponade
Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 337 – 383.
Spinal Cord Compression Compression of spinal cord
Direct tumor pressure on cord
Tumor invasion of the vertebral column causing collapse & pressure on cord
Compression causes:
Edema
Inflammation
Mechanical compression
Leads to:
Direct neural injury to cord
Vascular Damage
Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 337 – 383.
Epidemiology
Most cases (77%) diagnosed in patients with known history of cancer
23% present with MSCC as first presentation of malignancy
Most common location in spine:
Thoracic (69%)
Lumbosacral (29%)
Cervical (10%)
L’Esperance et al, 2012; Levack, et al, 2002; Schiff et al, 1998
22
Cancers Associated with MSCC Frequency Cancer Type
Most Common
• Breast (15% - 20%) • Lung (15% - 20%) • Prostate (15% - 20%) • Multiple Myeloma (10% -
15%)
• Unknown primary (10%) • Renal cell carcinoma (5% -
10%) • Non-Hodgkin lymphoma
5% - 10%) • Hodgkin lymphoma (5%)
Less Common
• GI malignancies • Soft Tissue sarcoma
• Thyroid cancer • Neuroblastoma
Uncommon • Melanoma • Leukemia
• Uterine, cervical, bladder cancers
Rare • Head and neck cancer • Brain cancer • Pancreatic cancer • Liver cancer
• Liver cancer • Ovarian cancer • Testicular cancer • Esophageal cancer
Clinical Presentation: Back Pain
Most common presenting symptom
Occurs in 90% of patients
Precedes other signs and symptoms (e.g. neurological) by weeks to months
Median time from onset of pain to diagnosis of spinal cord compression: 2 months
Levack et al, 2002; McLinton & Hutchison, 2006; Giglio & Gilbert, 2010;
Lewis, Hendrickson, & Moynihan, 2011
Clinical Presentation: Back Pain Characteristics
Local (near site of compression)
Radicular (distributed along dermatomes)
Referred (in a non-radicular distribution)
May be a combination of all 3 types
Levack et al, 2002; McLinton & Hutchison, 2006; Giglio & Gilbert, 2010;
Lewis, Hendrickson, & Moynihan, 2011
Progression of Symptoms Time Frame
Early
Late
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
National Institute for Health and Care Excellence, 2008; Levack et al, 2002
23
Diagnostic Tests 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
Histology of primary tumor
National Institute for Health and Care Excellence, 2008; Loblaw et al, 2005
Treatment of MSCC
IMMEDIATE & aggressive
Corticosteroids – usually initial treatment
High-dose steroids to spinal cord edema & inflammation
High-dose Dexamethasone (16 mg loading, short course of 16 mg daily) followed by tapering doses over several days
Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 337 – 383.
Surgery
Primary purposes
Preserve or recover neurological function
Maintain functional independence
Achieve highest possible quality of life
May include separately or in combination:
Spinal cord decompression: avert or treat MSCC
Spinal column stabilization: treat mechanical pain or bone instability)
Resection/reconstruction of spinal column
National Institute for Health Care and Excellence, 2008
Surgical Techniques
Laminectomy (no longer typically performed)
Anterior vertebral body resection with stabilization
Vertebroplasty
Kyphoplasty
Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing
oncologic emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 337 – 383.
24
Radiation Therapy First-line treatment in asymptomatic MSCC
Dose of 30 Gy administered in 10 fractions is most widely used regimen in North America
Combined with surgery (multimodal therapy)
Radiation therapy alone
Pain relief may not be achieved for up to two weeks
Does not correct spinal instability or prevent vertebral body collapse
L’Esperance, et al, 2012; National Institute for Health and Care Excellence, 2008;
Gregory, 2008
Chemotherapy Acute management of MSCC
Response to treatment slow
In combination with radiation therapy for chemo-sensitive tumors
Hodgkin disease
Non-Hodgkin lymphoma
Neurobastoma
Germ cell tumors
Breast cancer
Sun & Nemeck, 2009
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
Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 337 – 383.
Superior Vena Cava Syndrome (SVCS)
Obstruction of blood flow through the superior vena cava (SVC) Obstruction venous return from head, neck, upper arms, upper thorax impaired
Venous pressure increases
Cardiac output decreases
May be caused by: Invasion or compression of SVC
Thrombosis within SVC
Shelton, BK, (2013). Superior vena cava syndrome. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd Ed., pp 385 - 410, ONS, Pittsburgh, PA.
25
SVCS: Etiology
Malignant Causes
Lung Cancer
Non-Hodgkin Lymphoma
Thymoma
Mesothelioma
Solid tumors with mediastinal lymph node metastasis (e.g. breast cancer)
Post-radiation fibrosis
Non-Malignant Causes
Intraluminal Thrombosis
Related to indwelling central venous catheter
Mediastinal fibrosis
Related to infection
Benign mass
Shelton, BK, (2013). Superior vena cava syndrome. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd Ed., pp 385 - 410, ONS, Pittsburgh, PA.
.
SVCS: Incidence
Occurs in 3 – 4% of oncology population
Majority of cases (70% - 95%) related to underlying malignancy
Shelton, BK, (2013). Superior vena cava syndrome. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd Ed., pp 385 - 410, ONS, Pittsburgh, PA.
Clinical Presentation
Gradual onset (rarely occurs rapidly)
Symptoms vary depending on extent of obstruction, location, collateral circulation
Shelton, B. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 385 - 410.
SVCS: Early Signs & Symptoms
Dyspnea**
Facial and neck swelling
Occurs when supine, subsides after arising
Sensation of fullness in head
Cough
Arm Swelling
Chest pain
Venous distention of neck & chest wall
Cyanosis
Shelton, BK, (2013). Superior vena cava syndrome. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd Ed., pp 385 - 410, ONS, Pittsburgh, PA.
26
SVCS: Late Signs & Symptoms
Cyanosis of face & upper torso
Decreased or absent peripheral pulses
CHF
Decreased BP
Chest pain
Mental status changes
Tachypnea
Tachycardia
Engorged conjunctivae
Visual disturbances
Syncope
Hoarseness
Stridor
Shelton, BK, (2013). Superior vena cava syndrome. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd Ed., pp 385 - 410, ONS, Pittsburgh, PA.
SVCS: Clinical Diagnosis
Based on characteristic signs & symptom of central venous obstruction
Imaging studies
Chest x-ray
Computed tomography scan (contrast enhanced)
MRI
Histologic diagnosis
Treatment SVCS Based on etiology, severity of symptoms
Relieve obstruction & control underlying disease
Radiation Therapy
Gold standard for non-small cell lung cancer
Chemotherapy Primarily treatment for chemo-sensitive malignancies
Small cell lung cancer
Non-Hodgkin lymphoma
Surgical intervention
Thrombolytic therapy
SVC caused by intraluminal thrombus Shelton, B. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 385 - 410.
SVCS: Radiotherapy
Most malignancies causing SVCS are radiation sensitive
Currently, no standard regarding dose and schedule of radiation therapy
Generally provides good to excellent relief of symptoms
70% of patients with lung cancer
90% of patients with lymphoma
Initial symptom relief within 2 weeks,
Choe, KS & Salama JK (2009). Advances in radiotherapy for tumors involving the mediastinum. Thoracic Surgery
Clinics, 19, 133 – 141.
27
SVCS: Chemotherapy
Primary treatment for chemo-sensitive tumors
Small cell lung cancer (SCLC)
Non-Hodgin lymphoma (NHL)
Germ cell tumors
Possibly breast cancer
May be used for less chemo-sensitive tumors
Non-small cell lung cancer (NSCLC)
Symptom relief within 7-14 days
Drews, RE & Rabkin, DJ. (2014, June 25). Malignancy-related superior vena cava syndrome. Retrieved from
http://www.uptodate.com/contents/malignancy-related-superior-vena-cava-syndrome.
SVCS: Interventions
Endovenous stenting
Preferred initial approach
In conjunction with thrombolytic therapy or venous angioplasty
Surgical venous bypass
Reserved for patients with severe, persistent symptoms
Rarely used
Drews, RE & Rabkin, DJ. (2014, June 25). Malignancy-related superior vena cava syndrome. Retrieved from
http://www.uptodate.com/contents/malignancy-related-superior-vena-cava-syndrome.
Nursing Interventions Assess for signs & symptoms in patients at risk
Non-small cell lung cancer, small cell lung cancer, non-Hodkgin lymphoma
Central venous access devices
Interventions to relieve symptoms
Elevate HOB, avoid supine position & elevation of lower extremities
Avoid venipuncture, BP, IV therapy upper extremities
Monitor responses to treatment Assess for progressive respiratory distress or edema
Monitor tolerance of activities
Monitor fluid status (over hydration exacerbates symptoms)
Assess CNS (LOS, mental status changes, visual changes, headache)
Shelton, B. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic
emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 385 - 410.
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