Oncologic Emergencies

Transcription

1 Oncologic Emergencies Oncologic Emergencies Juanita Madison, RN, MN, AOCN Franciscan Health System Life-threatening medical emergencies caused by: Malignancy Treatment of malignancy When do they occur? Initial manifestations of malignancy or Late in disease process Oncologic Emergencies Metabolic Oncologic Emergencies Tumor Lysis Syndrome (TLS) Sepsis & Septic Shock Disseminated Intravascular Coagulation (DIC) Hypercalcemia Inappropriate Antidiuretic Hormone Secretion (SIADH) Anaphylaxis Structural Oncologic Emergencies Spinal Cord Compression Superior Vena Cava Syndrome Increased Intracranial Pressure (ICP) Cardiac Tamponade Tumor Lysis Syndrome (TLS) Metabolic imbalance Caused by breakdown of malignant cells (spontaneous, or induced by chemotherapy, biotherapy, or radiation therapy) Large number of rapidly proliferating cells killed Cell lysis, rupture of tumor cell membranes Intracellular components released into blood stream Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses.oncology Nursing Society, Pittsburgh, PA. pp:

2 TLS: Pathophysiology Intracellular components Potassium Phosphorous Nucleic acids (DNA, RNA) Cell killed (lysed), cell membrane ruptures Nucleic acids released into blood stream Potassium & Phosphorous released into blood stream Results in: Hyperuricemia Hyperkalemia Hyperphosphatemia Hypocalcemia K + PO 4 - PO 4 - Nucleic Acids K + K + K + PO 4 - PO - PO - PO - 4 K + K Ca ++ Ca ++ Ca ++ K + Xanthine Oxidase (Liver) Nucleic Acids Hypoxanthine Xanthine Uric Acid Urine 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 Tumor Lysis Syndrome: Onset, Duration, Incidence Onset: Usually within 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 leukemia's, high-grade lymphomas) 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 2

3 Hyperkalemia Serum K + >6.5 meq/l TLS: Signs & Symptoms Hyperuricemia Serum uric acid >10 mg/dl Severe = >20 mg/dl Early cardiac: Tachycardia EKG Changes: Prolonged QT and ST segment, lowering and inversion of T wave Late cardiac: Bradycardia EKG Changes: Shortened QT, elevated T wave, wide QRS Ventricular tachycardia, ventricular fibrillation, cardiac arrest Oliguria, anuria, azotemia Edema, hypertension Acute renal failure Chronic renal failure Nausea/vomiting Diarrhea Increased bowel sounds Twitching Muscle cramps Weakness Paresthesias Lethargy Syncope Malaise, weakness, fatigue Nausea, vomiting Flank pain, gout Pruritus TLS: Signs & Symptoms Hyperphosphatemia Serum PO 4 >5 mg/dl Secondary Hypocalcemia Serum Ca ++ < 8.7 mg/dl Anuria Oliguria Azotemia Neurological/Neuromuscular Twitching, paresthesias Restlessness Muscle cramps & weakness Anxiety, depression Carpopedal spasms Seizures Confusion Hallucinations Edema Hypertension Acute renal failure Cardiac Tetany Ventricular arrhythmias Prolonged QT interval, inverted T wave Heart block Cardiac arrest Gobel, B. H. (2013). In M. Kaplan (Ed.), Understanding an managing oncologic emergencies: A resource for nurses 2 nd Edition (pp ). Pittsburgh, PA: ONS Gobel, B. H. (2013). In M. Kaplan (Ed.), Understanding an managing oncologic emergencies: A resource for nurses 2 nd Edition (pp ). Pittsburgh, PA: ONS Prevention TLS Hydration IV Normal saline or 5% dextrose Begin hours prior to therapy Ensure urine output > ml/hr Diuresis If urine output no maintained by hydration alone Loop diuretics or osmotic diuretics Prevention TLS Allopurinol (Oral or IV) Begin 24 hour prior to therapy Blocks uric acid production by inhibiting xanthine oxidase (liver enzyme) Prevents uric acid precursors from converting to uric acid, risk uric acid crystallization Rasburicase IV Converts uric acid into allantoin very soluble compound, excreted by kidneys Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: ; McGraw, B. (2008). CJON 12 (4); Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: ; McGraw, B. (2008). CJON 12 (4);

4 Prevention TLS Urinary Alkalinization Sodium bicarbonate added to IV fluid ( meq/liter) Goal: urine ph level > 7.0 Use is controversial Potential complications associated with alkalinization Metabolic alkalosis Calcium phosphate precipitation 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 hours of treatment Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: ; McGraw, B. (2008). CJON 12 (4); Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: ; McGraw, B. (2008). CJON 12 (4); Mr. J.: 63 Year-Old Male diagnosed with High-Grade NHL Past Medical History: Noninsulin-dependent diabetes mellitus, supraventricular arrhythmia Scheduled to receive 1 st cycle CHOP-R chemotherapy in outpatient clinic Cyclophosphamide (Cytoxan), doxorubicin (Adriamycin), vincristine (Oncovin), prednisone, + Rituximab (Rituxan) Started on oral allopurinol 300 mg daily IV hydration pre & post chemotherapy in clinic Instructed to increase oral intake to 8 glasses fluid per day Mr. J: Two Days Post 1 st 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? 4

5 Treatment of TLS 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 Hyperphosphatemia Phosphate-binding agents Aluminum-containing antacids Hypertonic glucose plus insulin Aggressive hydration Hypocalcemia Appropriate management of hyperphosphatemia IV calcium gluconate or calcium chloride to treat arrhythmias Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Mr. J s Labs in ER (2 Days Post CHOP-R Chemotherapy) Baseline Pre-Chemo Labs Hgb 11.1 g/dl Platelets 245,000/mm 3 Na K BUN 45 mg/dl Creatinine 2.2 mg/dl Uric acid 12.6 mg/dl ER: 2 days postchemo Hgb 11.2 g/dl Platelets 200,00/mm 3 Na mmol/l K mmol/l BUN 100 Creatinine 5.1 mg/dl Uric acid 25 mg/dl 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 5

6 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 Mr. J. was treated with: 1 amp D 50, 10 units regular insulin D 5 1/2 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 Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Sepsis & Septic Shock Septicemia: Invasion of blood by microorganisms Sepsis: Systemic response to infection (vasodilation, displacement of intravascular volume) Septic Shock: Vascular collapse caused by vasodilation, leakage intravascular volume into interstitial space Continuum Septic Shock: Infection Septicemia Sepsis Septic Shock 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, ; Shelton, B.K. (2011), in Yarbro et al (eds), Cancer Nursing: Principles and Practice (7 th ed., pp ). Jones & Bartlett.; Williams, et al (2004).Critical Care 8,

7 Septic Shock: Pathophysiology Micro-organisms in blood stream release chemical mediators & hormones Endotoxins released by gram negative bacteria Exotoxins released by gram positive bacteria Profound systemic vasodilation Hypotension Tachycardia Increased vascular permeability Fluid leaks from vascular space to interstitial space Decreases circulating blood volume Hypoxic tissues Metabolic acidosis Holmes Gobel, et al (2013). Sepsis & septic shock. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: 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). CA: A Cancer Journal for Clinicians, 61, Clinical Presentation: Septic Shock Early Phase Normal or elevated temperature Chills Warm, flushed skin Anorexia Normal or low BP Hyperdynamic Phase (Warm) Normal or elevated temperature Chills and rigors Changes in LOC (anxiety, restlessness, confusion) Tachycardia, bounding pulses, widening pulse pressure Decreased urine output Hypodynamic Phase (Cold) Subnormal temperature Pale, cool, and clammy skin Disorientation, lethargy Tachycardia Weak, thready pulse Hypotension Anuria Mr. J.: Seven days post-3 rd cycle chemotherapy (CHOP-R) Wife calls outpatient clinic at 5 pm on Friday and reports husband has: Fever Dry cough Discomfort with swallowing Holmes Gobel, et al (2013). Sepsis & septic shock. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

8 Mr. J & Wife arrive in ER at 7:30 pm: Awake, alert, anxious Skin warm, appears flushed breath sounds lower lobes bilaterally with rales in right lung base Oral cavity without erythema or lesions, skin intact Dual-lumen Groshong central venous catheter exit site without redness or drainage; however, c/o slight tenderness to area above catheter exit site O2 sat 98% room air Temp F, HR irregular 96, RR 16, BP 126/84 Diagnostic Evaluation CBC with differential Complete metabolic panel Serum lactate Blood cultures X 2 Cultures of body fluids Urine, stool, throat, wounds, sputum Chest X-Ray Holmes Gobel, et al (2013). Sepsis & septic shock. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Treatment of Sepsis/Septic Shock: Immediate initiation IV antibiotics (within 1 hour of fever onset) Fluid resuscitation Goals: CVP: 8-12 mmhg MAP: > 65 mmhg Urine output: > 0.5 mg/kg/hr Holmes Gobel, et al (2013). Sepsis & septic shock. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Treatment of Sepsis/Septic Shock Mean arterial pressure (MAP) < 65 Vasopressor and inotropic drugs Norepinephrine, dopamine (first line) Phenylephrine, dobutamine, etc (second line) Oxygen therapy Antipyretics Holmes Gobel, et al (2013). Sepsis & septic shock. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

9 ER Orders for Mr. J.: Mr. J s Labs in ER: 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 WBC 1,100/mm 3 ANC 450/mm 3 Hgb 10 g/dl Plt 30,000/mm 3 Glucose 201 mg/dl Na meq/l K meq/l BUN 12 mg/dl Creatinine 0.9 mg/dl Nursing Assessment on Admission to Inpatient Unit: 9 PM Clinical Presentation: Septic Shock Extreme restlessness & anxiety Shaking chills Skin warm, flushed Temp F 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 Early Phase Normal or elevated temperature Chills Warm, flushed skin Anorexia Normal or low BP Hyperdynamic Phase (Warm) Normal or elevated temperature Chills and rigors Changes in LOC (anxiety, restlessness, confusion) Tachycardia, bounding pulses, widening pulse pressure Decreased urine output Hypodynamic Phase (Cold) Subnormal temperature Pale, cool, and clammy skin Disorientation, lethargy Tachycardia Weak, thready pulse Hypotension Anuria Holmes Gobel, et al (2013). Sepsis & septic shock. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

10 Nursing Management Sepsis Frequent vital signs & assessments LOC, skin color & temp, lungs 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 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 Clinical Presentation: Septic Shock Early Phase Normal or elevated temperature Chills Warm, flushed skin Anorexia Normal or low BP Hyperdynamic Phase (Warm) Normal or elevated temperature Chills and rigors Changes in LOC (anxiety, restlessness, confusion) Tachycardia, bounding pulses, widening pulse pressure Decreased urine output Hypodynamic Phase (Cold) Subnormal temperature Pale, cool, and clammy skin Disorientation, lethargy Tachycardia Weak, thready pulse Hypotension Anuria Nursing Interventions Neutropenic patients with fever Must be assessed immediately Started on broad spectrum antibiotics Monitor for sequelae of septic shock Frequent vital signs Assess tissue perfusion (skin color, temperature, capillary refill) Lung assessments I & O report urine output < 30cc/hr Monitor for symptoms of DIC Monitor response to medical treatment Assess for fluid overload Monitor lab values, especially renal function & culture reports Infection control measures Holmes Gobel, et al (2013). Sepsis & septic shock. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Holmes Gobel, et al (2013). Sepsis & septic shock. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

11 Possible Complications of Sepsis/Septic Shock DIC Multiple organ dysfunction syndrome Death Disseminated Intravascular Coagulation (DIC) Syndrome of: Thrombus formation (clotting) Simultaneous Hemorrhage Caused by over stimulation of normal coagulation processes Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: 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 DIC in the Oncology Population: Malignancy Induced Acute Promyelocytic Leukemia (APL) Procoagulant material release by granules of the immature promyelocyte initiates clotting cascade Occurs in 85% patients with APL Solid Tumors (adenocarcinomas) Lung, pancreas, prostate, stomach, colon, ovary, gall bladder, breast, kidney Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

12 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 Pathophysiology of DIC UNDERLYING DISEASE OR CONDITION STIMULATION OF COAGULATION CASCADE WIDESPREAD FIBRIN ACTIVATION OF CLOT FORMATION FIBRINOLYSIS MICROTHROMBI CONSUMPTION OF: PRODUCTION OF: DEPOSITS PLATELETS FIBRIN SPLIT THROUGHOUT FIBRINOGEN PRODUCTS MICROCIRCULATION PROTHROMBIN tpa ISCHEMIC TISSUE DAMAGE Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: SYMPTOMS OF ORGAN DYSFUNCTION BLEEDING Acute DIC Types of 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) International normalized ratio (INR) Prolonged Prolonged Nonspecific in DIC 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, 2 nd ED. ONS, Pittsburgh, PA. pp:

13 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 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 Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Mr. J s Labs at 10:00 pm Lab 7:30 pm 10:00 pm Normal Hemoglobin 10 g/dl 8.9 g/dl g/dl male Platelets 30,000/mm 3 12,000/mm 3 150, ,000/mm 3 Fibrinogen 96 mg/dl mg/dl PT 15.8 sec sec Fibrin Degradation Products 60 mcg/ml <10 mcg/ml Treatment of DIC Early recognition & treatment of underlying disorder Chemotherapy for malignancy Antibiotics for infection Correct hypoxia Oxygen to maintain saturation >95% Correct hypovolemia, hypotension, & acidosis NS until type & cross match completed & blood available Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

14 Treatment of DIC Stop the micro clotting to maintain perfusion & protect vital function IV Heparin Antithrombin III (inhibits action of thrombin) Stop the bleeding Pressure to active sites of bleeding Blood products (FFP, cryoprecipitate, platelets, red blood cells) Antifibrinolytic agents (EACA) Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Nursing Interventions Prevent severity of symptoms Direct pressure sites of bleeding, pressure dressings, sand bags Monitor for progression DIC Worsening vital signs, hypotension, anuria, s LOC Monitor response to therapy Sites & amounts of bleeding Changes in lab values Assess tissue perfusion parameters color, temperature, peripheral pulses Patient Teaching Avoid ASA or NSAID s (effects on platelet aggregation) Signs and symptoms of DIC (bleeding and/or clotting) Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Hypercalcemia of Malignancy (HCM) Metabolic disorder, in cancer patients, results from increased bone resorption Serum calcium level >12-14 mg/dl (normal serum calcium 9-11 mg/dl) Normal Physiology Normal levels Ca ++ regulated by: Parathyroid gland (production of parathyroid hormone) GI tract (absorption of Vitamin D) Kidneys (excretion) Ca ++ levels below normal: Parathyroid stimulated to produce parathyroid hormone Acts on bone release of calcium (bone resorption) into circulation Ca ++ levels above normal: Kidneys excretion of calcium Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

15 HCM: Etiology Tumor-induced bone breakdown releasing Ca ++ into bloodstream Solid tumors of squamous cell origin potential to produce parathyroid hormone-related protein that stimulates Ca ++ release from bone Lung, breast, prostate, head & neck, esophagus, kidney Decreased ability of kidneys to clear calcium from the blood Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Incidence of Hypercalcemia of Malignancy Occurs in approximately 30% of cancer patients Most often in advanced stages of disease 50% of patients die within 30 days of diagnosis Survival beyond 6 months is rare Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Incidence of Hypercalcemia of Malignancy Malignancy Incidence of Hypercalcemia Incidence of Bone Metastasis Breast cancer with metastasis 30% - 40% 65% - 75% Multiple myeloma 20% - 40% 70% - 90% Squamous cell carcinoma of lung 12.5% - 35% 30% - 40% Squamous cell carcinoma of head & neck 2.9% - 25% Uncommon Renal cell carcinoma 3% - 17% 20% - 25% Non-Hodgkin s Lymphoma 14% - 33% Rare T-Cell Lymphoma 50% Rare 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 Serum Calcium (mg/dl)= Measured serum Ca ++ + (4.0 serum albumin g/dl) X 0.8 **Normal Serum Ca++ = ml/dl Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

16 Signs and Symptoms of Hypercalcemia of Malignancy System Early Late Neurologic Renal GI Cardiovascular Musculoskeletal Drowsiness, lethargy, weakness, restlessness, irritability, confusion, cognitive dysfunction, disorientation Polyuria, polydipsia, nocturia, dehydration, kidney stones, renal insufficiency Anorexia, nausea, vomiting, constipation, vague abdominal pain, weight loss, peptic ulcers EKG changes (slowed conduction, Prolonged PR, wide QRS, short QT, short ST), sinus bradycardia Muscle weakness, fatigue, hypotonia, bone pain Seizures Stupor Coma Renal failure Atonic ileus Obstipation Heart block Cardiac arrest Ataxia Pathologic fractures Hypercalcemia: Treatment Depends on serum calcium level & patient symptoms: Ca ++ <12 ml/dl & asymptomatic observe carefully & treat as outpatient Ca ml/dl & asymptomatic requires specific but non-urgent treatment Ca ++ >15 ml/dl & symptomatic requires emergent treatment Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: 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 Initial: NS ml/hr Maintenance: 2.5 5L/day Loop diuretics (furosemide) Mobilization Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Agents to Inhibit Bone Resorption Bisphosphonates Agent Mechanism of Action Dosing Pamidronate (Aredia) Inhibits osteoclast activity IV: 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 Gallium nitrate (Ganite) Used when HCM resistant to bisphosphonates Inhibits osteoclast activity SC or IM: 4-8 IU/kg every 6-12 hours for 2 days IV: 200 mg/m2/day continuous for 5 days Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

17 Hypercalcemia Treatment Dietary recommendations Maintain salt intake Dietary calcium restrictions not necessary Medications to avoid Thiazide diuretics NSAIDS, H 2 receptor antagonists Vitamins A & D Parenteral/enteral solutions with calcium Corticosteroids Therapy of choice multiple myeloma or lymphomas Inhibits vitamin D conversion to calcitriol Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Nursing Interventions Recognize early signs & symptoms Careful monitoring of patients taking: Thiazide diuretics (inhibits calcium excretion) Digitalis preparations (action potentiated in hypercalcemic states) Measures to decrease calcium removal from bone: Ambulation, weight bearing, ROM, isometric exercises Careful assessment & monitoring Fluid balance & renal function GI motility Cardiac Status Mental status Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: 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 2 nd Cycle Chemotherapy Wife consults with nursing staff & reports: Concern re: husband s forgetfulness, wonders if confusion is because of recent change in pain medication (oxycodone) Husband experiencing more fatigue than usual (4-5 naps per day) 17

18 Mr. C s Labs: 2 nd Cycle Chemotherapy WBC 4,500/mm 3 Hgb 11.2 g/dl Hct 35% Platelets 119,000/mm 3 Serum Ca Creatinine 1.1 mg/dl BUN 19 mg/dl Albumin 2.3 g/dl Corrected Serum Ca ++ Mr. C s : Ca Albumin 2.3 Corrected Serum Calcium = Measured serum Ca ++ + (4.0 serum albumin) X 0.8 = ( ) X 0.8 = X 0.8 = = (rounded up to 11.8) Mr. C s 3 rd Cycle Chemotherapy Wife reports confusion improved for 1 st 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 2 nd Chemo Visit 3 rd Chemo Visit WBC 4,500/mm 3 2,200/mm 3 Hgb 11.2 d/dl 10.4 g/dl Hct 35% 29% Platelet count 119,000/mm 3 102,000 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 18

19 Corrected Serum Ca ++ Mr. C s : Ca Albumin 2.1 Corrected Serum Calcium = Measured serum Ca ++ + (4.0 serum albumin) X 0.8 = ( ) X 0.8 = X 0.8 = = (rounded to 14.3) The best immediate treatment to correct Mr. C s calcium & symptoms is: a. Hydration & Bisphosphonate (anti- Resorptive therapy) infusion b. Chemotherapy administration & corticosteroids c. Growth factor to improve fatigue and minimize myelosuppression d. Hydration & observation The best immediate treatment to correct Mr. C s calcium & symptoms is: a. Hydration & Bisphosphonate (anti- Resorptive therapy) infusion b. Chemotherapy administration & corticosteroids c. Growth factor to improve fatigue and minimize myelosuppression d. Hydration & observation Structural Oncologic Emergencies Spinal Cord Compression Superior Vena Cava Syndrome (SVCS) Increased Intracranial Pressure (ICP) Cardiac Tamponade Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

20 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 Incidence Occurs in approximately 5-14% of general cancer population Highest incidence in solid tumors that metastasize via hematogenous routes to bone in the spine Most common: Breast Lung Prostate Lymphoma Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Cancers Associated with Risk of Spinal Cord Compression 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 disease (5%) Less Common GI malignancies Soft Tissue sarcoma Thyroid cancer Neuroblastoma Uncommon Melanoma Uterine, cervical, bladder cancers Leukemia Rare Head and neck cancer, brain, pancreatic, liver, ovarian, testicular, 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 to pain to diagnosis of spinal cord compression: 2 months Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

21 Back Pain Associated with Spinal Cord Compression Can occur at any level of the spine Can take several forms: Local (near the site of compression) Radicular (distributed along dermatones) Referred (in a non-radicular distribution) May be a combination of all 3 types Progression of Symptoms Time Frame Early Late Pain Signs & Symptoms Motor weakness or gait changes Sensory Loss Numbness, tingling, sensory changes Autonomic Dysfunction Constipation and/or bladder retention Bowel and/or bladder incontinence Paralysis Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Diagnostic Tests MRI Gold standard for diagnosis Accurate, sensitive, and specific diagnostic tool for spinal cord compression Other Diagnostic Tests Spinal x-rays CT scan Myelography reserved for patient s who can t undergo MRI Bone Scan and/or PET Scan Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Treatment of Spinal Cord Compression IMMEDIATE & aggressive Corticosteroids initial supportive treatment High-dose steroids to spinal cord edema & inflammation High-dose loading with Dexamethasone (up to 100 mg IV loading dose) followed by tapering doses over several days Radiation therapy (radiosensitive tumors) In general, a course of radiation with a total of 30 Gy in 10 fractions Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

22 Treatment of Spinal Cord Compression Surgery Laminectomy (no longer typically used) Anterior vertebral body resection with stabilization Vertebroplasty Kyphoplasty Chemotherapy Rarely used in acute management Response to treatment slow & unpredictable Bisphosphonates Can effectively reduce pain and other skeletal complications of vertebral metastasis Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Nursing Interventions Early recognition Thorough assessment of neck & back pain in high risk patients Neurological assessments Mental status Cranial nerves Motor & sensory system Reflexes Pain Management Mobility and safety issues Skin care Bowel and Bladder function Rehabilitation & palliative care Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Superior Vena Cava Syndrome Obstruction of superior vena cava that impairs venous drainage (above the obstruction) Obstruction venous return from head, neck, upper arms, upper thorax impaired Venous pressure increases Cardiac output decreases Shelton, B. K. (2013). Superior Vena Cava Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Incidence Occurs in 3 4% of Oncology Population Malignant conditions: Majority of cases (70% - 95%) related to underlying malignancy Most common: Small cell & non-small cell lung cancers Non-Hodgkin lymphoma (high-grade) Less common: Esophageal cancer Thyroid cancer Breast cancer, thymoma, mesothelioma, leukemia Non-Malignant conditions: Intraluminal thrombus formation Mediastinal fibrosis or benign mass Shelton, B. K. (2013). Superior Vena Cava Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

23 Clinical Presentation Gradual onset (rarely occurs rapidly) Symptoms vary depending on extent of obstruction, location, collateral circulation Early/Common Physical Signs & Symptoms Dyspnea Facial and neck swelling (occurs when supine, subside after arising) Sensation of fullness in head Cough Arm Swelling Chest pain Venous distention of neck & chest wall Cyanosis Shelton, B. K. (2013). Superior Vena Cava Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Shelton, B. K. (2013). Superior Vena Cava Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Late Physical 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 Diagnostic Evaluation Chest X-ray MRI Contrast-enhanced CT Tissue diagnosis Shelton, B. K. (2013). Superior Vena Cava Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp:

24 Treatment SVCS Based on etiology, severity of symptoms Relieve obstruction & control underlying disease Radiation therapy Gold standard for non-small cell lung cancer Chemotherapy Primary treatment for chemo-sensitive malignancies Small cell lung cancer Non-Hodgkin Lymphoma Surgical Intervention Stent placement or SVC bypass Chronic or recurrent SVCS Thrombolytic therapy SVCS caused by intraluminal thrombus) Shelton, B. K. (2013). Superior Vena Cava Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Nursing Interventions Assess for signs & symptoms in patients at risk Non-small cell lung cancer, small cell lung cancer, non-hodkin lymphoma Central venous catheter access devices Interventions to relieve symptoms Elevate HOB, avoid supine position & elevation of lower extremities Avoid venipuncture, BP, IV therapy upper extremities Monitoring response to treatment Assess for progressive respiratory distress or edema Monitor tolerance of activities Monitor fluid status(over hydration exacerbates symptoms) Assess CNS (LOC, mental status change, visual changes, headache) Shelton, B. K. (2013). Superior Vena Cava Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2 nd ED. ONS, Pittsburgh, PA. pp: Sepsis is a common cause of disseminated intravascular coagulation (DIC). Which of the following conditions most accurately describes how sepsis causes DIC? a. Sepsis causes viruses to thrive, and viruses cause DIC b. Endotoxins released from bacteria activate the coagulation cascade c. Sepsis and bleeding occur simultaneously in patients who are immunosuppressed d. Antiangiogenesis factors are released during periods of sepsis, which leads to DIC Which of the these statements is not true in regards to hypercalcemia in malignancy? a. It is a rare complication b. Early manifestations of the syndrome are insidious including fatigue, muscle weakness, and depression and easily overlooked as manifestations of the disease. c. Bisphosphonates are frequently used in the treatment of malignancy induced hypercalcemia because of their ability to interfere with osteoclastic activity d. A complication of malignancy induced hypercalcemia include decreased GFR and acute kidney failure, neuropsychiatric disturbances, and cardiovascular complications. 24