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1. ONCOLOGICAL EMERGENCIES; SUBMITTED BY Nimmy Mariam John First Year MSc Nursing Govt. College Of Nursing Kottayam

2. Metabolic Oncologic Emergencies Tumor Lysis Syndrome (TLS) Sepsis & Septic Shock Disseminated Intravascular Coagulation (DIC) Hypercalcemia Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) Structural Oncologic Emergencies Spinal Cord Compression Superior Vena Cava Syndrome Cardiac Tamponade

3. 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

4. Tumor lysis syndrome (TLS) is a group of  metabolic abnormalities  that can occur as a  complication  from the treatment of  cancer , where large amounts of  tumor  cells are killed off ( lysed ) from the treatment, releasing their contents into the  bloodstream . This occurs most commonly after the treatment of  lymphomas  and  leukemias  and in particular when treating  non-Hodgkin lymphoma ,  acute myeloid leukemia , and  acute lymphoblastic leukemia .  This is a potentially fatal complication and patients at increased risk for TLS should be closely monitored while receiving  chemotherapy  and should receive preventive measures and treatments as necessary. TLS can also occur on its own (while not being treated with chemotherapy) although this is less common.

5. 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

6. Risk Factors Most common in: Patients with large tumor burden that is highly responsive to antineoplastic therapy (resulting in rapid cell death) Risk Factors Tumor-related High-grade lymphomas Risk for Hematologic malignancies (acute or chronic leukemia's with increase WBC) Risk for 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

7. pathophysiology

8. Signs and symptoms Hyperkalemia .  Potassium  is mainly an  intracellular   ion . High turnover of tumor cells leads to spill of potassium into the blood. Symptoms usually do not manifest until levels are high (> 6.5 mmol/L) [normal 3.5–5.0 mmol/L] and they include palpitations,  cardiac  conduction abnormalities, and arrhythmias (can be fatal) muscle weakness or paralysis

9. Hyperphosphatemia . Like potassium,  phosphates  are also predominantly intracellular. Hyperphosphatemia causes  acute kidney injury  in tumor lysis syndrome, because of deposition of  calcium phosphate  crystals in the kidney  parenchyma .

10. Hypocalcemia . Because of the hyperphosphatemia,  calcium  is precipitated to form calcium phosphate, leading to hypocalcemia. Symptoms of hypocalcemia include (but are not limited to): tetany paresthesias muscle cramps muscle weakness sudden changes in mental status, including emotional lability Parkinsonian ( extrapyramidal ) movement disorders papilledema

11. Hyperuricemia  and  hyperuricosuria . Massive cell death and nuclear breakdown generates large quantities of nucleic acids. Of these, the purines (adenine and guanine) are converted to uric acid via the purine degradation pathway and excreted in the urine. However, at the high concentrations of uric acid generated by tumor lysis, uric acid is apt to precipitate as  monosodium urate crystals .

12. Onset: Usually within 12-72 hrs. after initiation of antineoplastic therapy Duration: May persist for 5-7 days post-therapy

13. Condition Signs & Symptoms Treatment Hyperkalemia Serum K + >6.5 mEq /L Early cardiac: • Tachycardia • EKG Changes: Prolonged QT and ST segment, lowering and inversion of T wave Late cardiac: • Bradycardia • EKG Changes: Shortened QT, elevated T wave, wide QRS • Ventricular tachycardia, ventricular fibrillation, cardiac arrest • Nausea/vomiting • Diarrhea • Increased bowel sounds • Twitching • Muscle cramps • Weakness • Paresthesias • Lethargy • Syncope Mild (Potassium6.5 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

14. Condition Signs & Symptoms Treatment Hyperuricemia Serum uric acid >10 mg/dl Severe = >20 mg/dl • Oliguria, anuria, azotemia • Edema, hypertension • Acute renal failure • Chronic renal failure • Malaise, weakness, fatigue • Nausea, vomiting • Flank pain, gout • Pruritus • Hydration, urinary alkalinization • Oral allopurinol or IV allopurinol • Rasburicase • Hemodialysis for significant renal compromise Hyperphosphatemia Serum PO4 >5 mg/dl • Anuria • Oliguria • Azotemia • Edema • Hypertension • Acute renal failure • Phosphate-binding agents • Aluminum-containing antacids • Hypertonic glucose plus insulin • Aggressive hydration

15. Condition Signs & Symptoms Treatment Hypocalcemia Serum Ca ++ < 8.7 mg/dl Neurological/Neuromuscular Twitching, paresthesias Restlessness Muscle cramps & weakness Anxiety, depression Carpopedal spasms Seizures Confusion Hallucinations Cardiac Tetany Ventricular arrhythmias Prolonged QT interval, inverted T wave Heart block Cardiac arrest • Appropriate management of hyperphosphatemia • IV calcium gluconate or calcium chloride to treat arrhythmias

16. Management Prevention Strategies Recognition of at-risk patients Prevention of hyperuricemia Frequent monitoring of electrolytes Intervention Strategies Hydration IV Normal saline or 5% dextrose, begin 24 – 48 hours prior to therapy and ensure urine output >150 – 200 ml/ hr Control of hyperuricemia Aggressive correction of electrolytes Management of acute renal failure

17. 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

18. 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

19. Sepsis and 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 of intravascular volume into interstitial space Continuum Septic Shock:

20. 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 90 beats/minute • RR>20/min or PaCO2 >32 mmHg • WBC >12,000 cells/mm2 , 10% bands in peripheral blood Sepsis Documented infection with presence of two or more SIRS criteria Severe Sepsis Presence of sepsis with one or more of the following: organ dysfunction, hypotension, or hypoperfusion Septic Shock Presence of sepsis with hemodynamic instability that persists despite aggressive fluid challenge Multiple Organ Dysfunction Syndrome Dysfunction of more than one organ; homeostasis must be maintained with immediate intervention

21. Risk Factors in Cancer

22. 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

23. 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

24. 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

25. Diagnostic Evaluation CBC with differential Complete metabolic panel Serum lactate Blood cultures Cultures of body fluids Urine, stool, throat, wounds, sputum Chest X-Ray

26. 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

27. Nursing Management Sepsis Frequent vital signs & assessments of LOC, skin color & temp, lungs Ensure antibiotics administered within 3 hours Maintain oxygenation Oxygen therapy & ventilator support Administer IV fluids, Expand intravascular volume (fluid resuscitation) Monitor I & O Antipyretics Assess for fluid overload

28. 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

29. Disseminated Intravascular Coagulation (DIC) Disseminated intravascular coagulation (DIC) involves an abnormal activation of the clot formation and fibrin mechanisms in the blood, resulting in the consumption of coagulation factors and platelets. Patients with DIC are at high risk for thrombus formation, infarctions, and bleeding. Syndrome of: Thrombus formation (clotting) Simultaneous Hemorrhage Caused by over stimulation of normal coagulation processes

30. Pathophysiology Paradox of DIC: bleeding and 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

31. ETIOLOGY

32. Acute Promyelocytic Leukemia (APL) Procoagulant material release by granules of the immature promyelocyte leads to initiate clotting cascade Occurs in 85% patients with APL Solid Tumors (adenocarcinomas) Lung, pancreas, prostate, stomach, colon, ovary, gall bladder, breast, kidney Chemotherapy May induce DIC by damaging tumor, normal cells, or endothelium to causes release procoagulant material Large tumor burden/large cell kill may 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 and platelet aggregation, release platelet factors that initiate clotting cascade

33. 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

34. Clinical manifestation Decreased tissue/organ perfusion Brain, CV, Lungs, Kidney, GI Tract, Skin Decreased platelet count Petechiae, ecchymosis Hemorrhage Tachycardia, hypotension Tachypnea Overt bleeding Occult bleeding

35. Diagnosis Prothrombin Time (PT) Prolonged Activated Partial Thromboplastin time (APPT) Prolonged International normalized ratio (INR) Prolonged Fibrin Degradation Products Elevated D-Dimer Elevated Platelet Count Decreased Fibrinogen Decreased Antithrombin Decreased

36. Treatment Early recognition & treatment of underlying disorder Chemotherapy for malignancy Antibiotics for infection Correct hypoxia Oxygen to maintain saturation >95% Correct hypovolemia, hypotension and acidosis Fluid management Blood transfusion if needed Bleeding precautions Pain management Manage stress and anxiety

37. 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 ( tranexamic acid,botrocetin )

38. Nursing Interventions Prevent severity of symptoms Direct pressure sites of bleeding, pressure dressings, sand bags Monitor for progression DIC Worsening vital signs, hypotension, anuria and 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)

39. Hypercalcemia of Malignancy (HCM) It is a 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

40. 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

41. Ca ++ levels decrease below normal: Parathyroid stimulated to produce PTH Acts on bone and release of calcium (bone resorption ) into circulation Acts on kidneys leads increase renal secretion of phosphorous and stimulates reabsorption of Ca ++ Acts indirectly gut and enhance absorption Ca ++ Ca ++ levels increase above normal: Kidneys increase excretion of calcium

42. 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

43. 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

44. 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 )

45. Corrected total serum calcium 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

46. 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

47. 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 Dietary recommendations Maintain salt intake Dietary calcium restrictions not necessary Medications to avoid Thiazide diuretics (↓ renal excretion Ca ++) NSAIDS, H2 receptor antagonists (inhibit renal blood flow) Vitamins A & D (increase bone resorption ) Parenteral/enteral solutions with calcium Corticosteroids Therapy of choice multiple myeloma or lymphomas Inhibits vitamin D conversion to calcitriol

48. 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

49. Syndrome of inappropriate antidiuretic hormone (SIADH) Syndrome of inappropriate antidiuretic hormone (SIADH) is a paraneoplastic endocrine disorder associated with several malignancies

50. Causes Pain Stress Nausea Surgery Pulmonary disease Central nervous system disorders Physical and emotional stress Pharmacological agents Chemotherapy drugs. Syndrome of inappropriate antidiuretic hormone is caused by the ectopic production of vasopressin by malignant cells. Melanoma Gastrointestinal Gynecological Prostatic Hematological Neurological malignancies

51. Clinical manifestations Hyponatremia with a serum sodium level of 121 to 134 mEq /L Headache Nausea Weakness, Anorexia , Fatigue Muscle cramps Seizures Coma

52. Diagnosis Serum osmolality (< 275 mOsm /kg) Serum sodium (< 135 mEq /L) Urine osmolality (urine osmolality > serum osmolality) Urinary sodium (> 30 mEq/L) Decreased levels of uric acid, blood urea nitrogen Absence of edema Normal renal, adrenal, and thyroid function

53. Management Restrict fluids: (500–1000 mL/day) Review medications Discontinue potentially offending drugs Perform neurologic assessment Institute effective anticancer treatment Monitor sodium levels Demeclocycline (600–1200 mg/day) Monitor renal function with demeclocycline therapy Assess other causes Institute seizure precautions

54. Nursing interventions Admit to intensive care Hypertonic saline (3%) Limit sodium correction to 8–12 mEq /L in first 24 hours Intravenous furosemide or conivaptan Perform frequent neurologic examinations Maintain seizure precautions Monitor sodium levels every 1–3 hours

55. Structural Oncologic Emergencies Spinal Cord Compression Superior Vena Cava Syndrome (SVCS) Cardiac Tamponade

56. Spinal Cord Compression Spinal cord compression occurs when a malignant growth compress the spinal cord. Patients at risk include those with cancers that spread to the bone and spinal cord, such as lung, breast, and prostate cancer. Symptoms Pain Motor dysfunction

57. 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

58. Cancers Associated with Metastatic spinal cord compression 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%)

59. Progression of Symptoms Time Frame Early Late Signs & Symptoms Pain Motor weakness or gait changes Sensory Loss (numbness, tingling , sensory changes) Constipation and/or bladder retention Bowel and/or bladder incontinence Paralysis

60. 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

61. Treatment IMMEDIATE & AGGRESSIVE Corticosteroids – usually initial treatment High-dose steroids to decrease spinal cord edema & inflammation High-dose Dexamethasone (16 mg loading, short course of 16 mg daily) followed by tapering doses over several days

62. 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 (metastatic spinal cord compression) Spinal column stabilization: treat mechanical pain or bone instability) Resection/reconstruction of spinal column Surgical Techniques Anterior vertebral body resection with stabilization Vertebroplasty Kyphoplasty

63. 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

64. Chemotherapy Acute management of MSCC Response to treatment slow In combination with radiation therapy for chemo-sensitive tumors Hodgkin disease Non-Hodgkin lymphoma Neuroblastoma Germ cell tumors Breast cancer

65. 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 Provide a safe environment Assist with activity Monitor for changes in neurologic status as well as changes in the location or intensity of pain.

66. Superior Vena Cava Syndrome Superior vena cava syndrome (SVCS) occurs in patients with lung cancer or cancers of the mediastinum when the tumor or enlarged lymph nodes block circulation in the vena cava. This results in edema of the head, neck, and arms. Obstruction of blood flow through the superior vena cava (SVC) Obstruction leads to 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

67. 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

68. Clinical Manifestations Gradual onset (rarely occurs rapidly) Symptoms vary depending on extent of obstruction, location, collateral circulation 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 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

69. Diagnosis Based on characteristic signs & symptom of central venous obstruction Imaging studies Chest x-ray Computed tomography scan (contrast enhanced) MRI Histologic diagnosis

70. Treatment 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

71. 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,

72. 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

73. Interventions Endo venous stenting Preferred initial approach In conjunction with thrombolytic therapy or venous angioplasty Surgical venous bypass Reserved for patients with severe, persistent symptoms Rarely used

74. Nursing Interventions Assess for signs & symptoms in patients at risk Non-small cell lung cancer, small cell lung cancer, non- Hodkgin lymphoma Central venous access devices Interventions to relieve symptoms Elevate HOB, avoid supine position & elevation of lower extremities Avoid venipuncture, BP, IV therapy upper extremities Monitor responses to treatment Assess for progressive respiratory distress or edema Monitor tolerance of activities Monitor fluid status (over hydration exacerbates symptoms) Assess CNS (LOS, mental status changes, visual changes, headache)

75. Pericardial Effusion and Cardiac Tamponade Pericardial effusion is caused by direct invasion of the cancer into pericardium. The pericardial sac fills with fluid and may lead to life-threatening compression of the heart (called tamponade ). Signs and symptoms Chest Pain Dyspnea Low Blood Pressure Distant Heart Sounds

76. Etiology Patients with cancer may develop a pericardial effusion due to a variety of reasons. Secondary to metastatic disease of the pericardium Breast and lung cancers, leukemia, and lymphoma. Metastatic disease to the heart Primary heart malignancies.

77. Pathophysiology

78. Clinical manifestations Tachycardia Peripheral vasoconstriction causing cyanosis Decreased urinary output (oliguria or anuria) Narrowing pulse pressure, hypotension, increased systemic vascular resistance Pulsus paradoxus Anxiety, restlessness, confusion, mental status changes, dizziness, lightheadedness, agitation, fatigue Dyspnea, tachypnea, orthopnea, shortness of breath, air hunger Dysphagia, cough, retrosternal chest pain and heaviness, hoarseness, hiccups Dullness to percussion, weak heart sounds, chest fullness/discomfort, Nausea, vomiting, diarrhea, hepatojugular reflux, hepatomegaly, abdominal distention

79. DIAGNOSTIC TESTS 2-dimensional echocardiography, chest radiograph, computerized tomography (CT) scan, magnetic resonance imaging (MRI), pulmonary artery catheterization, electrocardiogram (ECG), and pericardiocentesis with pericardial fluid evaluation.

80. Treatment Fluid and water restriction. Stop the buildup of excess fluid in the body. Vasopressin antagonists. These medications block the action of the vasopressin. (tolvaptan, conivaptan, lixivaptan) Surgery. Severe and/or chronic SIADH may require surgical intervention wherein the surgeon removes the tumor that produces ADH.

81. Nursing Interventions Obtain a urine sample and blood samples from the patient Place the patient on fluid restriction as per the physician’s order. Start a strict input and output monitoring Administer vasopressin antagonists as prescribed Explain to the patient the relation of SIADH to nausea and vomiting and loss of appetite. Maintain I/O chart

82. References Yarbro C H, Wujcik D, Gobel B H (2010) Cancer nursing : Principles and Practice, 7th ed. Gerszten PC, Welch WC. Current surgical management of metastatic spinal disease. Oncology . 2000;14:1013–1024. Yahalom J. Oncologic emergencies: superior vena cava syndrome. In: DeVita VT, Hellman S, Rosenberg SA, eds. Cancer: Principles and Practice of Oncology . 7th ed. Philadelphia.

83. THANK YOU