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This document discusses oncologic emergencies, focusing on tumor lysis syndrome (TLS). It provides details on: - The pathophysiology of TLS, which is caused by the breakdown of rapidly proliferating malignant cells, releasing intracellular components like potassium, phosphorus, and nucleic acids. - Risk factors for TLS including certain cancers, large tumor burdens, and chemotherapy or radiation therapy. - Clinical manifestations of TLS which are due to electrolyte abnormalities and can include arrhythmias, seizures, and renal failure. - Prevention strategies like hydration, allopurinol to control uric acid, and rasburicase. Monitoring of at-risk patients is also important.

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Oncologic Emergencies Juanita Madison, RN, MN, AOCN CHI Franciscan Health
Oncologic Emergencies Life-threatening medical emergencies causedby: 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). Understandingand managing oncologicemergencies: A resource for nurses.Oncology Nursing Society, Pittsburgh, PA.pp: 433-459.
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+ 4 4 PO - PO - Nucleic Acids K+ K+ 4 K+ PO - Nucleic Acids Hypoxanthine Xanthine UricAcid Urine K+ K+ K+ 4 4 4 PO - PO - PO - 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, version4.2014. Accessedon 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). Understandingand managing oncologicemergencies: A resource for nurses.Oncology Nursing Society, Pittsburgh, PA.pp: 433-459.
TLS: Signs & Symptoms Hyperkalemia Serum K+ >6.5mEq/L Early cardiac: • Tachycardia • Nausea/vomiting • Diarrhea • Increased bowel sounds • Twitching • Muscle cramps • Weakness • Paresthesias • Lethargy • Syncope •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 Hyperuricemia Serum uric acid >10mg/dl Severe = >20mg/dl • Oliguria, anuria, azotemia • Edema, hypertension • Acute renal failure • Malaise, weakness, fatigue • Nausea, vomiting • Flank pain, gout • Chronic renal failure • Pruritus Gobel,B. H. (2013).In M. Kaplan(Ed.), Understandingan managing oncologicemergencies: A resource for nurses 2nd Edition(pp. 433 - 459).Pittsburgh, PA:ONS
TLS: Signs & Symptoms Hyperphosphatemia Serum PO4 >5mg/dl • Anuria • Oliguria • Azotemia • Edema • Hypertension • Acute renal failure Secondary Neurological/Neuromuscular Cardiac Hypocalcemia Serum Ca++ < 8.7mg/dl • Twitching, paresthesias • Restlessness • Tetany • Ventricular arrhythmias • Muscle cramps & weakness • Anxiety, depression •Prolonged QT interval, inverted T wave • Carpopedal spasms • Heart block • Seizures • Cardiac arrest • Confusion • Hallucinations Gobel, B. H. (2013).In M. Kaplan(Ed.), Understandingan managing oncologicemergencies: 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). Understandingand managing oncologicemergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459;McGraw,B. (2008).CJON 12 (4); 563-565.
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). Understandingand managing oncologicemergencies: 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-AventisUS, 2011.ElitekPackage 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.pd f.
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-AventisUS, 2011.ElitekPackage 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). Understandingand managing oncologicemergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459;McGraw,B. (2008).CJON 12 (4); 563-565.
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). Understandingand managing oncologicemergencies: 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 mgdaily 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
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). Understandingand managing oncologicemergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459.
Treatment of TLS Hyperphosphatemia • Phosphate-binding agents • Aluminum-containingantacids • 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). Understandingand managing oncologicemergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459.
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). Understandingand managing oncologicemergencies: 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 interstitialspace 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 SevereSepsis 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 MultipleOrgan Dysfunction Syndrome Dysfunction of more than one organ; homeostasis must be maintained with immediate intervention Dellinger,RP et al (2013). Surviving sepsiscampaign: International guidelines for management of severe sepsisand septicshock, 2012. Intensive Care Medicine,39, 165-228.
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& septicshock. In Kaplan,M (Ed). Understandingand managingoncologicemergencies: A resource for nurses,2nd ED. ONS, Pittsburgh, PA. pp: 287-335.
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 7:30pm: 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 ordrainage; however, c/o slight tenderness to area above port O2 sat 98% room air Temp 1020F, HR irregular 96, RR 16, BP126/84
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 sepsiscampaign: International guidelines for management of severe sepsisand septicshock, 2012. Intensive Care Medicine,39, 165-228.
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 H2Ofor mechanically ventilated • Maintain adequate nutrition • Prevent deep vein thrombosis • Prevent stress andpressure ulcers • Prevent additional infection Dellinger,RP et al (2013).Surviving sepsiscampaign: International guidelines for management of severe sepsisand septicshock, 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& septicshock. In Kaplan,M (Ed). Understandingand managingoncologicemergencies: 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& septicshock. In Kaplan,M (Ed). Understandingand managingoncologicemergencies: 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
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 3hours 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% roomair BP 88/50
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& septicshock. In Kaplan,M (Ed). Understandingand managingoncologicemergencies: 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). Understandingand managingoncologic 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). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh,PA. pp: 69 – 102.
DIC in the Oncology Population: Malignancy Induced Acute Promyelocytic Leukemia (APL) Procoagulant material release by granules ofthe 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). Understandingand managingoncologic 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). Understandingand managingoncologic 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.
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). Understandingand managingoncologic 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 – 13.1sec Fibrin Degradation Products 60 mcg/ml <10mcg/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). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh,PA. pp: 69 – 102.
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). Understandingand managingoncologic 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 ofbleeding 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). Understandingand managingoncologic 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 resourcefor 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). Understandingand managingoncologic emergencies: A resource for nurses,2nd Ed, pp 103-155,ONS,Pittsburgh, PA.
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). Understandingand managingoncologic 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.
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). Understandingand managingoncologic 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.
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 Cardiacarrest Musculoskeletal Muscle weakness, fatigue, hypotonia, bone pain Ataxia Pathologic fractures Kaplan,M. (2013)Hypercalcemia of malignancy.In Kaplan,M (Ed). Understandingand managingoncologic 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). Understandingand managingoncologic 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). Understandingand managingoncologic 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 5days Kaplan,M. (2013)Hypercalcemia of malignancy.In Kaplan,M (Ed). Understandingand managingoncologic emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA.pp: 103 – 155.
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 orlymphomas Inhibits vitamin D conversion to calcitriol Kaplan,M. (2013)Hypercalcemia of malignancy.In Kaplan,M (Ed). Understandingand managingoncologic 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). Understandingand managingoncologic 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 CycleChemotherapy 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)
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 ChemoVisit 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
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).SpinalCord Compression. In Kaplan,M (Ed). Understandingand managingoncologic 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). SpinalCord Compression. In Kaplan,M (Ed). Understandingand managingoncologic 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
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 orgait 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
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).SpinalCord Compression. In Kaplan,M (Ed). Understandingand managingoncologic 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.
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).SpinalCord Compression. In Kaplan,M (Ed). Understandingand managingoncologic 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).Superiorvena cava syndrome. In Kaplan,M (Ed). Understandingand managing oncologic emergencies: A resource for nurses, 2nd Ed., pp 385 - 410, ONS, Pittsburgh, PA.
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).Superiorvena cava syndrome. In Kaplan,M (Ed). Understandingand 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).Superiorvena cava syndrome. In Kaplan,M (Ed). Understandingand 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).SpinalCord Compression. In Kaplan,M (Ed). Understandingand 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). Superiorvena cava syndrome. In Kaplan,M (Ed). Understandingand managing oncologic emergencies: A resource for nurses,2nd Ed., pp 385 - 410, ONS, Pittsburgh, PA.
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).Superiorvena cava syndrome. In Kaplan,M (Ed). Understandingand 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). SpinalCord Compression. In Kaplan,M (Ed). Understandingand 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 & SalamaJK (2009).Advances inradiotherapy for tumors involvingthe mediastinum.ThoracicSurgery Clinics,19, 133 – 141.
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. Retrievedfrom 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. Retrievedfrom 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 oflower 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). SpinalCord Compression. In Kaplan,M (Ed). Understandingand managing oncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh, PA.pp: 385 - 410.

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22-Oncologic-Emergencies-Madison-March-2105-Syllabus-converted.pptx

  • 1.
    Oncologic Emergencies Juanita Madison,RN, MN, AOCN CHI Franciscan Health
  • 2.
    Oncologic Emergencies Life-threatening medicalemergencies causedby: Malignancy Treatment of malignancy When do they occur? Initial manifestations of malignancy or Late in disease process
  • 3.
    Oncologic Emergencies Metabolic OncologicEmergencies 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
  • 4.
    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). Understandingand managing oncologicemergencies: A resource for nurses.Oncology Nursing Society, Pittsburgh, PA.pp: 433-459.
  • 5.
    TLS: Pathophysiology Intracellular components Potassium Phosphorous Nucleicacids (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+ 4 4 PO - PO - Nucleic Acids K+ K+ 4 K+ PO - Nucleic Acids Hypoxanthine Xanthine UricAcid Urine K+ K+ K+ 4 4 4 PO - PO - PO - Ca++ Ca++ Ca++ Xanthine Oxidase (Liver)
  • 6.
    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, version4.2014. Accessedon August 30, 2014 at http://www.nccn.org/professionals/physician_gls/pdf/nhl.pdf
  • 7.
    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.
  • 8.
    Clinical Manifestations Often asymptomaticinitially 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). Understandingand managing oncologicemergencies: A resource for nurses.Oncology Nursing Society, Pittsburgh, PA.pp: 433-459.
  • 9.
    TLS: Signs &Symptoms Hyperkalemia Serum K+ >6.5mEq/L Early cardiac: • Tachycardia • Nausea/vomiting • Diarrhea • Increased bowel sounds • Twitching • Muscle cramps • Weakness • Paresthesias • Lethargy • Syncope •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 Hyperuricemia Serum uric acid >10mg/dl Severe = >20mg/dl • Oliguria, anuria, azotemia • Edema, hypertension • Acute renal failure • Malaise, weakness, fatigue • Nausea, vomiting • Flank pain, gout • Chronic renal failure • Pruritus Gobel,B. H. (2013).In M. Kaplan(Ed.), Understandingan managing oncologicemergencies: A resource for nurses 2nd Edition(pp. 433 - 459).Pittsburgh, PA:ONS
  • 10.
    TLS: Signs &Symptoms Hyperphosphatemia Serum PO4 >5mg/dl • Anuria • Oliguria • Azotemia • Edema • Hypertension • Acute renal failure Secondary Neurological/Neuromuscular Cardiac Hypocalcemia Serum Ca++ < 8.7mg/dl • Twitching, paresthesias • Restlessness • Tetany • Ventricular arrhythmias • Muscle cramps & weakness • Anxiety, depression •Prolonged QT interval, inverted T wave • Carpopedal spasms • Heart block • Seizures • Cardiac arrest • Confusion • Hallucinations Gobel, B. H. (2013).In M. Kaplan(Ed.), Understandingan managing oncologicemergencies: A resource for nurses 2nd Edition(pp. 433 - 459).Pittsburgh, PA:ONS
  • 11.
    TLS: Management Prevention Strategies Recognitionof 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.
  • 12.
    TLS Prevention Hydration IV Normalsaline 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). Understandingand managing oncologicemergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459;McGraw,B. (2008).CJON 12 (4); 563-565.
  • 13.
    Prevention of TLS: Controlof 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). Understandingand managing oncologicemergencies: A resource for nurses,2nd ED. ONS, Pittsburgh,PA. pp: 433-459;McGraw,B. (2008);NCCN, 2014.
  • 14.
    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-AventisUS, 2011.ElitekPackage 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.pd f.
  • 15.
    Rasburicase (Elitek®) FDA approveddosing 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-AventisUS, 2011.ElitekPackage 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.
  • 16.
    Prevention TLS Urinary Alkalinization Sodiumbicarbonate 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). Understandingand managing oncologicemergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459;McGraw,B. (2008).CJON 12 (4); 563-565.
  • 17.
    TLS Preventative Measures Monitorserial 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). Understandingand managing oncologicemergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459;McGraw,B. (2008).CJON 12 (4); 563-565.
  • 18.
    Mr. J.: 63Year-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 mgdaily IV hydration pre & post chemotherapy in clinic Instructed to increase oral intake to 8 glasses fluid per day
  • 19.
    Mr. J: TwoDays 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?
  • 20.
    Mr. J: TwoDays 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
  • 21.
    Mr. J’s Labsin 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
  • 22.
    TLS Intervention Strategies Hydration Controlof 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.
  • 23.
    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). Understandingand managing oncologicemergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459.
  • 24.
    Treatment of TLS Hyperphosphatemia• Phosphate-binding agents • Aluminum-containingantacids • 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). Understandingand managing oncologicemergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459.
  • 25.
    Mr. J. wastreated 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
  • 26.
    TLS: Nursing Interventions Recognizepatients 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). Understandingand managing oncologicemergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459.
  • 27.
    Sepsis & SepticShock 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 interstitialspace Continuum Septic Shock: Infection/ Septicemia  SIRS  Sepsis  Severe Sepsis  Septic Shock
  • 28.
    Sepsis Continuum Phase Definition Infection/ bacteremia Presenceof 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 SevereSepsis 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 MultipleOrgan Dysfunction Syndrome Dysfunction of more than one organ; homeostasis must be maintained with immediate intervention Dellinger,RP et al (2013). Surviving sepsiscampaign: International guidelines for management of severe sepsisand septicshock, 2012. Intensive Care Medicine,39, 165-228.
  • 29.
    Risk Factors inCancer 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.
  • 30.
    Incidence and Mortality Incidencein 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.
  • 31.
    Sepsis and SepticShock 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.
  • 32.
    Septic Shock: Pathophysiology Micro-organismsin 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& septicshock. In Kaplan,M (Ed). Understandingand managingoncologicemergencies: A resource for nurses,2nd ED. ONS, Pittsburgh, PA. pp: 287-335.
  • 33.
    Causes of Sepsis Bacterialorganisms (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.
  • 34.
    Mr. J.: Sevendays 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
  • 35.
    Mr. J &Wife arrive in ER at 7:30pm: 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 ordrainage; however, c/o slight tenderness to area above port O2 sat 98% room air Temp 1020F, HR irregular 96, RR 16, BP126/84
  • 36.
    Sepsis Bundles Start Immediately CompleteWithin 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 sepsiscampaign: International guidelines for management of severe sepsisand septicshock, 2012. Intensive Care Medicine,39, 165-228.
  • 37.
    Sepsis Bundles Complete Within24 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 H2Ofor mechanically ventilated • Maintain adequate nutrition • Prevent deep vein thrombosis • Prevent stress andpressure ulcers • Prevent additional infection Dellinger,RP et al (2013).Surviving sepsiscampaign: International guidelines for management of severe sepsisand septicshock, 2012. Intensive Care Medicine,39, 165-228.
  • 38.
    Diagnostic Evaluation CBC withdifferential 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& septicshock. In Kaplan,M (Ed). Understandingand managingoncologicemergencies: A resource for nurses,2nd ED. ONS, Pittsburgh, PA. pp: 287-335.
  • 39.
    Treatment of Sepsis/SepticShock 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& septicshock. In Kaplan,M (Ed). Understandingand managingoncologicemergencies: A resource for nurses,2nd ED. ONS, Pittsburgh, PA. pp: 287-335.
  • 40.
    ER Orders forMr. 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
  • 41.
    Mr. J’s Labsin 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
  • 42.
    Nursing Assessment onAdmission 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
  • 43.
    Nursing Management Sepsis Frequentvital signs & assessments LOC, skin color & temp, lungs Ensure antibiotics administered within 3hours Maintain oxygenation Oxygen therapy & ventilatory support Administer IV fluids, Expand intravascular volume (fluid resuscitation) Monitor I & O Antipyretics Assess for fluid overload
  • 44.
    Mr. J: NursingAssessment 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% roomair BP 88/50
  • 45.
    Nursing Interventions Neutropenic patientswith 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& septicshock. In Kaplan,M (Ed). Understandingand managingoncologicemergencies: A resource for nurses,2nd ED. ONS, Pittsburgh, PA. pp: 287-335.
  • 46.
    Possible Complications of Sepsis/SepticShock DIC Multiple organ dysfunction syndrome Death
  • 47.
    Disseminated Intravascular Coagulation (DIC) Syndromeof: Thrombus formation (clotting) Simultaneous Hemorrhage Caused by over stimulation of normal coagulation processes Kaplan,M. (2013).Disseminated Intravascular Coagulation. In Kaplan,M (Ed). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh, PA.pp: 69 – 102.
  • 48.
    Pathophysiology DIC Paradox ofDIC: 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). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh,PA. pp: 69 – 102.
  • 49.
    DIC in theOncology Population: Malignancy Induced Acute Promyelocytic Leukemia (APL) Procoagulant material release by granules ofthe 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). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh,PA. pp: 69 – 102.
  • 50.
    Other Causes DIC (OncologyPopulation) 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). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh, PA. pp: 69 – 102.
  • 51.
    Types of DIC AcuteDIC 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
  • 52.
    Laboratory Values inDIC 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.
  • 53.
    DIC Clinical Presentation Decreasedtissue/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). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh,PA. pp: 69 – 102.
  • 54.
    Mr. J: NursingAssessment 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
  • 55.
    Mr. J’s Labsat 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 – 13.1sec Fibrin Degradation Products 60 mcg/ml <10mcg/mL
  • 56.
    Treatment of DIC Earlyrecognition & 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). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh,PA. pp: 69 – 102.
  • 57.
    Treatment of DIC Stopthe 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). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh,PA. pp: 69 – 102.
  • 58.
    Nursing Interventions Prevent severityof 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 ofbleeding 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). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh,PA. pp: 69 – 102.
  • 59.
    Hypercalcemia of Malignancy (HCM) Metabolicdisorder 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 resourcefor nurses, 2nd Ed., 103-155, ONS, Pittsburgh, PA.; Makras, P & Papapoulous, SE (2009). Medical treatment of hypercalcemia. Hormones, 8, 83-95.
  • 60.
    HCM: Incidence Occurs inapproximately 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). Understandingand managingoncologic emergencies: A resource for nurses,2nd Ed, pp 103-155,ONS,Pittsburgh, PA.
  • 61.
    Normal Regulation ofCa++ 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). Understandingand managingoncologic emergencies: A resource for nurses,2nd Ed, pp 103-155,ONS,Pittsburgh, PA.
  • 62.
    Normal Regulation ofCa++ 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
  • 63.
    Distribution of Calcium Bonestores: 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.
  • 64.
    Measuring Serum Calcium Totalcalcium = 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.
  • 65.
    Corrected Serum Ca++ CorrectedTotal 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.
  • 66.
    HCM: Etiology Tumor-induced bonebreakdown 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). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh,PA. pp: 103 – 155.
  • 67.
    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
  • 68.
    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.
  • 69.
    Signs and Symptomsof 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 Cardiacarrest Musculoskeletal Muscle weakness, fatigue, hypotonia, bone pain Ataxia Pathologic fractures Kaplan,M. (2013)Hypercalcemia of malignancy.In Kaplan,M (Ed). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh, PA.pp: 103 – 155.
  • 70.
    HCM: Treatment Degree TotalSerum 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). Understandingand managingoncologic emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA.pp: 103 – 155.
  • 71.
    Hypercalcemia: Treatment Treat thecancer – 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). Understandingand managingoncologic emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA.pp: 103 – 155.
  • 72.
    Agents to InhibitBone 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 5days Kaplan,M. (2013)Hypercalcemia of malignancy.In Kaplan,M (Ed). Understandingand managingoncologic emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA.pp: 103 – 155.
  • 73.
    Hypercalcemia Treatment Dietary recommendations Maintainsalt 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 orlymphomas Inhibits vitamin D conversion to calcitriol Kaplan,M. (2013)Hypercalcemia of malignancy.In Kaplan,M (Ed). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh, PA.pp: 103 – 155.
  • 74.
    Nursing Interventions Recognize earlysigns & 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). Understandingand managingoncologic emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA.pp: 103 – 155.
  • 75.
    Mr. C: Hypercalcemia 62-year-oldmale 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
  • 76.
    2nd CycleChemotherapy Wife consultswith 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)
  • 77.
    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
  • 78.
    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)
  • 79.
    Mr. C’s 3rdCycle 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)
  • 80.
    Mr. C’s LabTrends Lab Test 2nd ChemoVisit 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
  • 81.
    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)
  • 82.
    Structural Oncologic Emergencies Spinal CordCompression Superior Vena Cava Syndrome (SVCS) Increased Intracranial Pressure (ICP) Cardiac Tamponade Kaplan,M. (2013).SpinalCord Compression. In Kaplan,M (Ed). Understandingand managingoncologic emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA.pp: 337 – 383.
  • 83.
    Spinal Cord Compression Compressionof 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). SpinalCord Compression. In Kaplan,M (Ed). Understandingand managingoncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh,PA. pp: 337 – 383.
  • 84.
    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
  • 85.
    Cancers Associated withMSCC 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
  • 86.
    Clinical Presentation: Back Pain Mostcommon 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
  • 87.
    Clinical Presentation: Back PainCharacteristics 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
  • 88.
    Progression of Symptoms TimeFrame Early Late Signs & Symptoms Pain Motor weakness orgait 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
  • 89.
    Diagnostic Tests MRI Gold standardfor 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
  • 90.
    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).SpinalCord Compression. In Kaplan,M (Ed). Understandingand managingoncologic emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 337 – 383.
  • 91.
    Surgery Primary purposes Preserve orrecover 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
  • 92.
    Surgical Techniques Laminectomy (nolonger 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.
  • 93.
    Radiation Therapy First-line treatmentin 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
  • 94.
    Chemotherapy Acute management ofMSCC 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
  • 95.
    Nursing Interventions Early recognition: Thoroughassessment 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).SpinalCord Compression. In Kaplan,M (Ed). Understandingand managingoncologic emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh,PA. pp: 337 – 383.
  • 96.
    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).Superiorvena cava syndrome. In Kaplan,M (Ed). Understandingand managing oncologic emergencies: A resource for nurses, 2nd Ed., pp 385 - 410, ONS, Pittsburgh, PA.
  • 97.
    SVCS: Etiology Malignant Causes LungCancer 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).Superiorvena cava syndrome. In Kaplan,M (Ed). Understandingand managing oncologic emergencies: A resource for nurses, 2nd Ed., pp 385 - 410, ONS, Pittsburgh, PA.
  • 98.
    SVCS: Incidence Occurs in3 – 4% of oncology population Majority of cases (70% - 95%) related to underlying malignancy Shelton, BK, (2013).Superiorvena cava syndrome. In Kaplan,M (Ed). Understandingand managing oncologic emergencies: A resource for nurses, 2nd Ed., pp 385 - 410, ONS, Pittsburgh, PA.
  • 99.
    Clinical Presentation Gradual onset(rarely occurs rapidly) Symptoms vary depending on extent of obstruction, location, collateral circulation Shelton, B. (2013).SpinalCord Compression. In Kaplan,M (Ed). Understandingand managing oncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh, PA.pp: 385 - 410.
  • 100.
    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). Superiorvena cava syndrome. In Kaplan,M (Ed). Understandingand managing oncologic emergencies: A resource for nurses,2nd Ed., pp 385 - 410, ONS, Pittsburgh, PA.
  • 101.
    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).Superiorvena cava syndrome. In Kaplan,M (Ed). Understandingand managing oncologic emergencies: A resource for nurses, 2nd Ed., pp 385 - 410, ONS, Pittsburgh, PA.
  • 102.
    SVCS: Clinical Diagnosis Basedon characteristic signs & symptom of central venous obstruction Imaging studies Chest x-ray Computed tomography scan (contrast enhanced) MRI Histologic diagnosis
  • 103.
    Treatment SVCS Based onetiology, 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). SpinalCord Compression. In Kaplan,M (Ed). Understandingand managing oncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh, PA.pp: 385 - 410.
  • 104.
    SVCS: Radiotherapy Most malignanciescausing 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 & SalamaJK (2009).Advances inradiotherapy for tumors involvingthe mediastinum.ThoracicSurgery Clinics,19, 133 – 141.
  • 105.
    SVCS: Chemotherapy Primary treatmentfor 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. Retrievedfrom http://www.uptodate.com/contents/malignancy-related-superior-vena-cava-syndrome.
  • 106.
    SVCS: Interventions Endovenous stenting Preferredinitial 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. Retrievedfrom http://www.uptodate.com/contents/malignancy-related-superior-vena-cava-syndrome.
  • 107.
    Nursing Interventions Assess forsigns & 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 oflower 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). SpinalCord Compression. In Kaplan,M (Ed). Understandingand managing oncologic emergencies: A resource for nurses,2nd ED. ONS, Pittsburgh, PA.pp: 385 - 410.