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Oncological emergencies
This document discusses tumor lysis syndrome (TLS), a metabolic oncologic emergency caused by the breakdown of malignant cells following chemotherapy or radiation therapy. TLS results in the release of potassium, phosphorus, uric acid and other intracellular components into the bloodstream, potentially causing hyperkalemia, hyperphosphatemia, hyperuricemia and other electrolyte imbalances. The document outlines risk factors for TLS, signs and symptoms of specific electrolyte abnormalities, treatment approaches, and importance of monitoring patients at risk.
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Oncological emergencies
- 1. Mr. Binu Babu Asst.Professor Mrs. Jincy Ealias Asst. Professor
- 2. Metabolic Oncologic Emergencies Structural Oncologic Emergencies Tumor Lysis Syndrome (TLS) Sepsis & Septic Shock Disseminated Intravascular Coagulation (DIC) Hypercalcemia Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) Spinal Cord Compression Superior Vena Cava Syndrome Cardiac Tamponade
- 3. 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. 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
- 5. 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 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
- 6. Onset: Usuallywithin 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)
- 7. Often asymptomaticinitially Detected initial via abnormalities in blood chemistries Signs & symptoms patients exhibit depend on extent of metabolic abnormalities ◦ Hyperkalemia ◦ Hyperuricemia ◦ Hyperphosphatemia ◦ Hypocalcemia
- 8. 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
- 9. 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
- 10. 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
- 11. Prevention Strategies Recognitionof 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
- 12. Monitor seriallab 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
- 13. Recognize patientsat 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
- 14. Septicemia: Invasionof blood by microorganisms Sepsis: Systemic response to infection (vasodilation, displacement of intravascular volume) Septic Shock: Vascular collapse caused by vasodilation, leakage intravascular volume into interstitial space Continuum Septic Shock: Infection/ Septicemia SIRS Sepsis Severe Sepsis Septic Shock
- 15. Phase Definition Infection/ bacteremiaPresence 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
- 16. Neutropenia ◦ Singlemost 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
- 17. Micro-organisms inblood 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
- 18. 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
- 19. CBC withdifferential Complete metabolic panel Serum lactate Blood cultures X 2 Cultures of body fluids ◦ Urine, stool, throat, wounds, sputum Chest X-Ray
- 20. Immediate initiationIV antibiotics (within 3 hours) Fluid resuscitation Goals: ◦ MAP: > 65 mmHg ◦ CVP: 8-12 mmHg ◦ Urine output: > 0.5 mg/kg/hr Oxygen therapy Antipyretics
- 21. Frequent vitalsigns & assessments ◦ 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
- 22. 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
- 23. Disseminated intravascularcoagulation (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
- 24. Paradox ofDIC: 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
- 25. Acute PromyelocyticLeukemia (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
- 26. 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
- 27. 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
- 28. Decreased tissue/organperfusion ◦ Brain, CV, Lungs, Kidney, GI Tract, Skin Decreased platelet count ◦ Petechiae, ecchymosis Hemorrhage ◦ Tachycardia, hypotension ◦ Tachypnea ◦ Overt bleeding ◦ Occult bleeding
- 29. Early recognition& treatment of underlying disorder ◦ Chemotherapy for malignancy ◦ Antibiotics for infection Correct hypoxia ◦ Oxygen to maintain saturation >95% Correct hypovolemia, hypotension and acidosis ◦ Normal Saline ◦ Blood transfusion if needed
- 30. Stop themicro 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)
- 31. Prevent severityof 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)
- 32. It isa 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
- 33. 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
- 34. Ca++ levelsdecrease 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
- 35. 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
- 36. 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
- 37. 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)
- 38. Corrected totalserum 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
- 39. Reflect directdepressive effects ↑ serum Ca++ exerts on: ◦ Excitability of nerve tissue ◦ Contractility of cardiac, smooth, skeletal muscles Signs & symptoms: ◦ Lethargy, confusion ◦ Cardiac dysrhythmias ◦ Constipation ◦ Muscle hypotonia
- 40. 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 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
- 41. 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
- 42. Syndrome ofinappropriate antidiuretic hormone (SIADH) is a paraneoplastic endocrine disorder associated with several malignancies
- 43. 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
- 44. Hyponatremia witha serum sodium level of 121 to 134 mEq/L Headache Nausea Weakness, Anorexia, Fatigue Muscle cramps Seizures Coma
- 45. Serum osmolality(< 275 mOsm/kg) Serum sodium (< 135 mEq/L) Urine osmolality (urine osmolality > serum osmolality) Urinary sodium (> 30 mEq/L) Euvolemia Decreased levels of uric acid, blood urea nitrogen Absence of edema Normal renal, adrenal, and thyroid function
- 46. Restrict fluids: (500–1000 mL/day) Review medications Discontinue potentially offending drugs Perform neurologic assessment Institute effective anticancer treatment Monitor sodium levels Maintain admit outpatient or based on onset and activity Demeclocycline (600–1200 mg/day) Monitor renal function with demeclocycline therapy Assess other causes Institute seizure precautions
- 47. Admit tointensive 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
- 48. Spinal CordCompression Superior Vena Cava Syndrome (SVCS) Cardiac Tamponade
- 49. Spinal cord compressionoccurs 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
- 50. Compression ofspinal 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
- 51. 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%)
- 52. 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
- 53. MRI ◦ Goldstandard 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
- 54. 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
- 55. 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 Surgical Techniques ◦ Anterior vertebral body resection with stabilization ◦ Vertebroplasty ◦ Kyphoplasty
- 56. 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
- 57. Acute managementof 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
- 58. 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.
- 59. Superior vena cavasyndrome (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
- 60. 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
- 61. 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
- 62. Based oncharacteristic signs & symptom of central venous obstruction Imaging studies ◦ Chest x-ray ◦ Computed tomography scan (contrast enhanced) ◦ MRI Histologic diagnosis
- 63. 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
- 64. 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,
- 65. 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
- 66. 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
- 67. 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 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)
- 68. Pericardial effusion iscaused 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
- 69. Patients withcancer 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.
- 70. Resulting in apericardial effusion An excess amount of pericardial fluid accumulates Obstruction of venous and lymphatic drainage occurs Tumors metastasize to the pericardium or myocardium
- 71. Tachycardia Peripheralvasoconstriction 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, retrostemal chest pain and heaviness, hoarseness, hiccups Dullness to percussion, weak heart sounds, chest fullness/discomfortNausea, vomiting, diarrhea, hepatojugular reflux, hepatomegaly, abdominal distention
- 72. 2-dimensional echocardiography, chest radiograph, computerized tomography (CT) scan, magnetic resonance imaging (MRI), pulmonary artery catheterization, electrocardiogram (ECG), and pericardiocentesis with pericardial fluid evaluation.
- 73. Fluid andwater restriction. ◦ Stop the buildup of excess fluid in the body. Vasopressin antagonists. These medications block the action of the vasopressin. Surgery. ◦ Severe and/or chronic SIADH may require surgical intervention wherein the surgeon removes the tumor that produces ADH.
- 74. Obtain aurine 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
- 75. Yarbro CH, 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.
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