oncologic emergencies - boston college · • classify types of oncologic emergencies into 3...
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22nd Annual Northeast Regional Nurse Practitioner Conference – May 6-8, 2015
Oncologic EmergenciesJill Burke, NP
D I S C L O S U R E S
• There has been no commercial support or sponsorship for this program.
• The planners and presenters have declared that no conflicts of interest exist.
• The program co-sponsors do not endorse any products in conjunction with any educational activity.
A C C R E D I TAT I O N
Boston College Connell School of Nursing Continuing Education Program is accredited as a provider of continuing nursing education by the American Nurses Association Massachusetts, an accredited approver by the American Nurses Credentialing Center’s Commission on Accreditation.
22nd Annual Northeast Regional Nurse Practitioner Conference – May 6-8, 2015
S E S S I O N O B J E C T I V E S
• Define oncologic emergency.• Identify patients at risk for oncologic
emergency.• Classify types of oncologic emergencies
into 3 groups.• Describe measures to prevent oncologic
emergencies.
Oncologic Emergencies
Jill N. Burke APRN,BC Center for Multiple Myeloma Massachusetts General Hospital Cancer Center
May 8, 2015
Overview
• Definition of oncologic emergency
• Identify patients at risk
• Classification of emergencies in cancer patients, three different groups:
1. structural or obstructive emergencies caused by
space – occupying tumor.
2. due to metabolic or hormonal problems.
3. secondary to complications arising from treatment.
• Preventive measures
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Structural and obstructive oncological emergencies:
• Superior vena cava syndrome
• Cardiac tamponade
• Spinal cord compression
• Increased intracranial pressure
• Urinary obstruction
• Hemoptysis and airway obstruction
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Superior vena cava syndrome
• Results from the partial or complete obstruction of blood flow through the superior cava vein to the right atrium, causing severe reduction in venous return to the right atrium, causing severe reduction in venous return from head, neck and upper extremities.
• Obstruction may be due to compression, invasion, thombosis or fibrosis of this vessel.
• Malignant tumors, such as lung cancer, lymphoma and metastatic tumors are responsible for > 90% of all SVCS cases. Lung cancer, particularly small-cell and squamous-cell, accounts for almost 85% of all cases.
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Superior vena cava syndrome
• As a result of a venous obstruction, there is a rise in the intra-venous-pressure and collateral circulation often flows through the azygoud system.
• SVCS most often develops insidiously over several weeks, allowing some mechanisma of compensation.
• Patients often present with: facial-swelling, particularly around eyes, dyspnea, cough, head fullness and pressure sensation are common.
• Diagnosis is SVCS is mainly clinical. CT scan is the most usual radiographic study for imaging the mediastinum and for diagnosing SVC obstruction. CT may reveal the site of the obstruction and collateral flow and is also able to differentiate extrinsic compression of the vein by tumor from intravascular thrombosis.
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SVC Syndrome
Superior vena cava syndrome
• More than 50% of patients with SVCS become symptomatic before the diagnosis of cancer is made. SVCS is rarely life-threatening by itself.
• Prognosis of patients with SVCS depends very much on the prognosis of the underlying disease.
• SVCS management is diagnostic: initial measure of oxygen, diuretics, head elevation, and corticoids may be useful in relieving symptoms.
• Emergency radiation before biopsy may preclude proper interpretation of the biopsy sample in >50% of cases. The only exception to this may be those cases with impending airway obstruction or severe increase in intracranial pressure.
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Superior vena cava syndrome
• Chemotherapy is the preferred treatment of malignant lymphoma or small-cell lung cancer.
• Most patients will experience a significant response with disappearance of all clinical manifestations of SVCS within 1-2 weeks.
• Radiation is the main option for patients having SVCS due to tumors insensitive to chemotherapy, such as recurrent non-small cell lung cancer
• When SVCS is related to central venous catheters, catheter removal should be combined with anticoagulation to prevent embolization.
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Cardiac Tamponade
• Life threatening complication of cancer
• Excess accumulation of fluid in the pericardial space
• Results in decreased cardiac output and compromised cardiac function
• Pericardial cavity
– Space between the two-layered sac surrounding the heart
– Normally filled with 50 mg of fluid and allows the heart to move without friction
Cardiac Tamponade
• Risk factures
– Cancer in the chest, mediastinum, pleural effusions
– Direct tumor invasion to the pericardial sac- primary tumor or mets
– Fibrosis of the pericardial sac related to radiation therapy (more than 4000 Cgy)
• Pathophysiology
– Left ventricular filling decreases
– Ability of the heart to pump decreases
– Cardiac output decreases
– Impaired systemic perfusion occurs
Cardiac Tamponade
• Diagnosis
– Chest xray- enlarged pericardial silhouette
– CT scan- pleural effusion, masses, or pericardial thickening
– Echocardiography- (2D) Right atrium collapse at diastole
– Electrocardiography- tachycardia, premature contractions, atrial fibrillation, and electrical alternans
– Pericardiocentesis and cytology
• Bloody fluid with positive cytology
• Significant false negative
Cardiac Tamponade
• Assessment- ROS
– Retrosternal chest pain relieved by leaning forward and intensified when lying supine
– Dyspnea
– Cough
– Anxiety and agitation, altered levels of consciousness
– Hiccups
Cardiac Tamponade
• Assessment- Physical Exam
– Muffled heart sounds
– Weak or absent apical pulse
– Tachycardiac
– Tachypnea
– Decreased systolic pressure and rising diastolic pressure
– Pulsus paradoxus greater then 10 mm Hg
– Peripheral edema
– Diaphoresis
– Cyanosis
Cardiac Tamponade
• Treatment
• Pericardiocentesis- temporary removal of excess pericardial fluid
• Pericardial window- surgical opening of the pericardium to allow fluid drainage
• Total pericardectomy- removal of the pericardial sec
• Radiation- for radiosensitive tumors
Cardiac Tamponade
• Pericardial sclerosis- installation of chemicals which cause inflammation and fibrosis through a pericardial catheter
• Systemic antineoplastic therapy for chemotherapy- sensitive maligancies
• Corticosteriods- used in mild cases to reduce inflammation of contrictive pericarditis
Chest CT
Spinal Cord Compression
• Spinal cord compression remains a true oncological emergency requiring immediate intervention, the effects may be devastating if unrecognized.
• Metastatic cord compression is estimated to effect from 5-10% of all cancer patients
• Thoracic spine is the largest percentage of cases (70%). (adult- prostate, lung, breast & pedi-sarcoma, neuroblastoma)
• Spinal cord compression is seen in 2.7-5% of children with cancer at diagnosis, progression, or recurrence of disease
• Localized back pain and tenderness due to vertebral metastases are the most common and earliest symptom of spinal cord compression.
Spinal Cord Compression
Intradural: Intramedullary (leptomeningeal) &
Extramedullary, almost all metastasis to the vertebrae (85%) or epidural space (15%)
Biphosphonates reduce pathological fractures and bone pain with patients with multiple myeloma and breast cance
Spinal Cord Compression
• Primary tumors (15%) • The resulting cord dysfunction
results, regardless of the histology.
• Spinal cord compression is rarely fatal but can increase morbidity & mortality as a result of irreversible loss of function.
Spinal Compromise
Lower extremity weakness, paresthesias, reflex asymmetry, spinal pain, and loss of bladder and bowel function. Additionally, neoplasms may compromise the vascular supply, causing edema or ischemia
Spinal cord compression symptoms:
• Early: nonspecific, pain or weakness. Gradually worsening pain preceded other signs of cord compression
• Discomfort may be radicular, localized to the back, generally bilateral, worse with movement or straining.
• There is thoracic localization and percussion tenderness. • Pain from vertebral metastasis may worsen with a
recumbent position in contrast to back pain from other sources.
• Back discomfort that is unrelieved with rest or recumbency may also be a symptom of destructive lesions
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C2: Breathing, vent depend C3-4C4-6: Shoulder Flexion &Extension: Spontaneous breathing, Trapezius function
C5: Deltoid Abduction at Shoulder C6: Biceps Flexion at Forearm C6: Wrist Extension C7: Wrist Flexion, can be independent with devices C7: Elbow Extension (Triceps) C7: Finger Extension C8: Fingers Flexion middle finger
Common Motor Levels
T1: Small finger abductors
L2: Hip flexors
L3: Knee Extension (Quadriceps)
L4: Ankle dorsiflexion
L4: Anterior Tibial, Foot Inversion
L5: Long toe extension
L5: Foot dorsiflexion
L5: Weak heel walking, foot drop
S1: Ankle plantar flexors
S1: Weak toe walking
Common Motor Levels
Common Sensory Levels
C5: Deltoid, Lateral Upper Arm & Forearm
C6: Thumb (Radial Nerve)
C7: Middle Finger (Median Nerve)
C8: Ring
C8: Little Finger (Ulnar Nerve)
T4: Nipple
T8: Xiphoid
T10: Umbilicus
T12: Symphysis
Common Sensory Levels
L4: Medial Low Leg and foot
L5: Space between 1st and second toes
S1: Lateral Foot
S3: Ischial tuberosity area
S4-5: Perianal region
Spinal cord compression
• Neoplastic epidural spinal cord compression (ESCC) is a common complication of cancer that can cause pain and potentially irreversible loss of neurologic function.
Spinal cord compression
• The single most important prognostic factor for regaining ambulation after treatment of an ESCC is pretreatment neurologic status
• Management of patients with ESCC includes the immediate administration of glucocorticoids in all patients, followed by surgery, external beam radiation therapy (EBRT), or stereotactic body radiotherapy (SBRT). Systemic therapy may be beneficial in patients with chemosensitive tumors.
Treatment of Spinal Cord Tumors
• Control pain & preserve function • Immediate steroids, bolus 4-100mg decadron,
then divided doses with tapering (Flaherty, 2000)
• Radiation therapy, epidural metastasis, 2 – 4 K cGy in 5-20 fractions/ 2-4 weeks (Ratiff & Cooper, 2004)
• Surgery for decompression or stabilization, usually within 24-48 hours.
Increased intracranial pressure
• Increased intracranial pressure may be caused by brain metastases. 25 % of cancer patients will die with intra-cranial metastases
• Lung, breast and melanoma are the most common tumors to the brain
• Clinical manifestations: headache, nausea, vomiting, seizures, behavioral changes and sometimes focal neurological changes.
• The tumor mass together with its surrounding edma may produce hydrocephalus and as the mass enlarges various herniation syndromes may occur depending on the location of the tumors within the cranium.
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Emergency treatment of increased intracranial pressure • Prepare for intubation, target PCO2- 35, avoid aggressive hyperventilation
• IV access & 20-100gms of Mannitol 20% with fluid resuscitation
• Prepare for CT scan (MRI is best radiographic exam, but in emergent situation CT is quicker and easier to obtain)
• Possible steroids
• Consider decompressive craniotomy, or ventriculostomy
• Once herniation has been controlled, a decision on the treatment of the brain metastases should be made. If multiple nodules, whole - brain irradiation is considered standard.
• Single brain noduules, surgery followed by radiation. Radiosurgery may be indicated in patients having fewer than three metastases, each measuring <2cm
Urinary Obstruction
• May occur in patients with gynecological or urological tumors particularly cervical and prostatic carcinoma.
• Urinary obstruction may lead to bilateral hydronephrosis and renal failure.
• Flank pain with sudden anuria, sometimes alternating with polyuria and a progressive rise in serum creatinine may indicate urinary obstruction.
• Renal US is the easiest was to detect bilateral hydronephrosis
• CT is helpful in detecting the exact location of the obstruction, particularly if there is a retroperitoneal or pelvic mass.
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Urinary obstruction
• Urinary obstruction associated with pain, infection or renal failure requires intervention.
• Urinary stents may be placed with local anesthesia and may relieve obstruction. If not possible, percutaneous nephrostomy is an alternative approach.
• After relief, polyuria may follow, increasing the risk of dehydration and electrolyte disturbances, particularly hypokalemia. Careful replacement of fluid and electrolytes is required.
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Hemoptysis and airway obstruction
• Massive hemoptysis is defined as the expectoration of volumes ranging from one single episode of 100 ml to > 600 ml of blood during 24-48 h.
• When respiratory difficulty occurs, hemoptysis should be treated immediately.
• Airway bleeding leading to life-threatening airway obstruction, aspiration, anemia or hypovolemic shock is also considered massive hemoptysis.
• Fatal hemorrhage may present in one-third of patients with massive hemoptysis and the risk of death is directly associated with the amount of blood expectorated.
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Hemoptysis and airway obstruction
• The rate of hemoptysis, the amount of blood retained in the lungs and the underlying pulmonary reserve are risk factors.
• 20% of cases of lung cancer patient will have hemoptysis at any time during its disease course
• Endobronchial metastases from carcinoid tumors, breast, colon or kidney cancer, melanoma or sarcoma may also cause hemoptysis.
• Hemoptysis in cancer patients may also be caused by non-malignant conditions: fungal infections, thrombocytopenia or other coagulation disorders.
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Hemoptysis and airway obstruction
• Airway should be protected and intubation is recommended in patients with hemodynamic instability, severe dyspnea or hypoxia.
• Patients may require: volume supplementation, oxygen, sough suppressants and correction of any coagulation disorder.
• Site of bleeding must be identified. The lesion should generally be treated with a surgical procedure, bronchial artery embolization or radiotherapy. Radiotherapy may inhibit hemoptysis by causing vascular thrombosis and necrosis of contributing vessels.
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Airway obstruction
• Acute airway obstruction involves the upper airways and may be caused by malignant or non-malignant conditions.
• It may result from intraluminal tumor growth or from extrinsic compression of the airway.
• Tumors that obstruct the upper airway by direct extension are primary tumors of the head and neck and lung.
• Non-malignant causes of airway obstruction are food or foreign body aspiration, airway edema or hemorrhage, tracheal stenosis and infections.
• Angioedema may also cause severe and life-threatening airway obstruction.
• Primary tumors. of the lung are the most common cause of lower airway obstruction
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Airway obstruction
• Dyspnea is frequently the only early symptom of airway obstruction.
• If dyspnea occurs on exercise, the airway is decreased to 8mm, but if dyspnea occurs at rest, the airway diameter is usually < 5mm and is related to the appearance of stridor.
• Treat depends on cause, may involve tracheostomy, radiation and/ or stenting.
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Metabolic or hormonal problems
• Hypercalcemia
• SIADH
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Hypercalcemia of Malignancy
• Sometimes called Tumor-induced hypercalcemia (TIH) or Cancer-induced hypercalcemia (CIH)
• Most common metabolic oncologic emergency • Estimated to occur in 10-20% of adults with cancer • Under diagnosed and under treated
The General Skeleton
• Consists of 206 bones • Support • Protection • Movement • Serves as a storage area for
minerals (e.g. calcium and phosphorus)
Gray, Henry. Anatomy of the Human Body. Philadelphia: Lea & Febiger, 1918; Bartleby.com, 2000. www.bartleby.com/107/.
Bone Composition: Two tissue types
Compact (cortical bone) • dense, hard, and forms the
protective exterior portion of all bones
• designed to nourish and regulate bone cells and bone matrix.
Spongy (cancellous bone) • exists inside the compact bone • very porous • contains trabeculae (spaces
between are filled with bone marrow) and bone cells (osteocytes)
OC = osteocytes http://www.cytochemistry.net/microanatomy/bone/compact_bone_histology.htm
www.anatomy.dal.ca/Human%Histology/Lab6/220DL.html
Bone Cells: Osteoclasts (bone-resorbing cells)
• Large and multinucleated • Derived from
monocyte/macrophage cells
• Dissolve mineral and degrade matrix proteins
• Function regulated by hormones, growth factors, and cytokines
Osteoclasts and Howship’s Lacunae
Marcus R, Feldman D, Kelsey J (eds). Osteoporosis. San Diego, CA: Academic Press; 1996:14.
Bone Cells: Osteoblasts (Bone-forming cells)
• Derived from stem cells in bone marrow
• Produce collagen and other proteins which become mineralized to form bone in bone matrix
• Function is regulated by hormones and growth factors
• Secrete local factors that influence other bone cells
Marcus R, Feldman D, Kelsey J (eds). Osteoporosis. San Diego, CA: Academic Press; 1996:13.
Most Common Cancers with Bone Metastases
Cancer Breast
Prostate
Myeloma
Thyroid
Lung
Kidney
Frequency
65%-75%
65%-75%
70%-95%
60%
30%-40%
20%-25%
Coleman RE. Cancer Treatment Reviews. 2001;27:165-176.
Plasmacytoma, on flat plate xray
Hypercalcemia of Malignancy
Tumor Type Percentage of Patients who develop HCM
LUNG 27.3
BREAST 25.7
MULTIPLE MYELOMA 7.3
HEAD AND NECK 6.9
UNKNOWN PRIMARY 4.7
LYMPHOMA/LEUKEMIA 4.3
RENAL 4.3
GASTROINTESTINAL 4.1
1. Lang-Kummer J(1997): Hypercalcemia In Groenwald SL et al. Cancer Nursing: Principles and Practice pg684-701).
2. Pearson KE (2009). Tumor induced hypercalcemia . In Acute Care Oncology Nursing. Saunders. Pg 286.
Types of HCM
1. Humoral Hypercalcemia
– 80% of cases
– Via release of parathyroid related protein ( PTHrP) which increases osteoclast activity
– Associated with squamous cell cancer, renal, breast, ovarian, and endometrial cancer.
– PTH and phosphate levels usually low
– Should be suspected in any case of HCM in the absence of bone mets
Types of HCM cont’d
2. Osteolytic Hypercalcemia - 20% of cases - Usually due to breast cancer, myeloma, or
lymphoma in the presence of bony disease - Release of osteoclast activating factors including
lymphotoxin, IL 6, IL-1 alpha and others have been identified
- Phosphate level usually normal, PTH low
Harrison’s Manual of Oncology 2008
Pathogenesis of HCM
• Increased bone destruction
• Increased tubular reabsorption of calcium by the kidney
• Decreased urinary calcium excretion
• Decrease in bone formation
Fleisch H. In: Bisphosphonates in Bone Disease. San Diego, California: Academic Press; 2000;90-92.
Signs and Symptoms of HCM
CNS Personality change; lethargy; somnolence; coma; confusion; depression; increased sensitivity to pain
Neuromuscular Muscle weakness; hypotonia
CV Hypertension; arrhythmia
Renal Kidney stones; decreased glomerular filtration; polyuria; polydipsia, renal failure
GI Nausea; vomiting; constipation; anorexia
Skeletal Bone pain
Ralston SH. Treatment of tumor-induced hypercalcemia. In: Body JJ (ed). Tumor Bone Diseases and Osteoporosis in Cancer Patients. New York, NY: Marcel Dekker; 2000;393-407.
Mundy GR, Martin TJ. Metabolism.1982;31:1247-1277.
Serum Calcium Levels
• Confirm by measuring corrected serum calcium
• Why calculation is necessary
– Calcium binds to albumin in the blood2,3
– Hypoalbuminemia or hyperalbuminemia distorts serum calcium measurements3
– Hypoalbuminemia is common in cachectic patients (eg, cancer patients)1
1. Iqbal SJ, Giles M, Ledger S, Nanji N, Howl T. Lancet. 1988;ii:1477-1478. 2. Mundy GR, Martin TJ. Metabolism.1982;31:1247-1277. 3. Payne RB, Little AJ, Williams RB, Milner JR. BMJ. 1973;4:643.
Calculating Corrected Serum Calcium
Corrected serum calcium = serum calcium mg/dL + 0.8 (4.0 - serum albumin, g/dL)
– Example: Serum Calcium = 12.1 mg/dL Serum albumin = 2.0 g/dL Corrected Ca = 12.1 mg/dL + 0.8 x (4.0 - 2.0 g/dL) Corrected Ca = 12.1 mg/dL + 1.6 mg/dL Corrected Ca = 13.7 mg/dL
Mundy GR, Martin TJ. Metabolism.1982;31:1247-1277.
HCM: Assessment & Diagnostic Evaluation Symptoms: • Anorexia • Nausea/Vomiting • Confusion • Polydipsia • Polyuria • constipation • Weakness “Bones, Moans and
Abdominal Groans”
Labs: • Serum calcium • Ionized calcium > 5 mg/dL
(most accurate) • PTH, PTHrP • Lytes, BUN, CR • HCM may be associated
with: – Decreased phosphate – Metabolic alkalosis – Hypochloremia – Decreased serum parathyroid
hormone (PTH)
1. Mundy GR, Martin TJ. Metabolism.1982;31:1247-1277. 2. Carroll MF, Schade DS. Am Fam Physician.2003;67:1959-1966. 3. Uptodate.com, 2012
HCM Treatment -
• Aggressive saline rehydration (5-8 liters in first 24 hours): decreases calcium levels through dilution and increases excretion.
• Loop diuretics (furosemide): BEGIN DAY 2! 40-80 mg/day orally or IV: used in conjunction with hydration to increase calcium excretion.
• Bisphosphonates (pamidronate, zoledronic acid): inhibits osteoclast activity for up to one month. Need to give with fluid and renally dose.
HCM treatment cont’d
• Other antihypercalcemic agents: Calcitonin, Plicamycin, Gallium Nitrate
• Reducing underlying tumor burden (if effective treatment is available)
**If patient is in renal failure, dialysis may be only option for
treatment. Also, best supportive care can be discussed.
Bisphosphonates- Mechanism of Action
• Attach to bone mineral surface by physio-chemical properties
• During resorption, osteoclasts release bisphosphonate embedded in bone matrix
• Bisphosphonates are taken up by osteoclasts and inhibit bone resorption
Coleman RE. Cancer Treat Rev. 2001;27:165-176.
Zoledronic acid
• Potential for longer duration of response (as opposed to pamidronate) due to higher potency
• Recommended dose of Zoledronic acid is 4 mg administered as an IV infusion in 100 mL of sterile 0.9% Sodium Chloride, USP or 5% Dextrose Injection, USP over 15 minutes*
• Requires serum Cr prior to dosing, use modified CG to calculate CrCl
• Risks:
– Osteonecrosis of the Jaw (ONJ)
– Renal toxicity (dose and time dependent)
– Infusion reaction (pain, flu like symptoms)
*ZOMETA [Package Insert]. East Hanover, NJ: Novartis Pharmaceuticals Corporation; 2003.
Osteonecrosis of the Jaw (ONJ)
• Observed among cancer patients receiving intravenous bisphosphonates and denosumab
• Less frequent among patients receiving oral bisphosphonates
• Bone under the teeth is exposed, often painfully
• Swelling and loosening of teeth may be seen
Definition of SIADH
• Syndrome of inappropriate antidiuretic hormone (SIADH) is a disorder of water intoxication.
• SIADH describes the inappropriate production and secretion of ADH that causes increased water reabsorption in the renal tubules and leads to increased water retention and dilutional hyponatremia.
Pathophysiology of SIADH
• Vasopressin, is the biologically active form of ADH in humans.
• Vasopressin is synthesized in the hypothalamus.
• After synthesis, Vasopressin is transported down to the posterior pituitary gland.
Pathophysiology
• Vasopressin is stored there until appropriate reflexes signal release into the bloodstream.
• A major physiologic action of vasopressin is to regulate water reabsorption in the renal tubules.
• ADH specifically acts on the tubular segments of the collecting duct system.
• With high plasma concentrations of vasopressin, the collecting duct becomes highly permeable to water; thus, water is retained with the excretion of a small volume of concentrated urine.
To Sum It Up
• SIADH is characterized by a primary water excess that predisposes to hyponatremia and hypoosmolality.
• When renal excretion of water is decreased, due to high plasma concentration of ADH, water is reabsorbed
• Because the total body water is increased, distribution between ICF and ECF compartments is 2:1.
• Plasma sodium levels reflect dilutional hyponatremia.
• Patients with SIADH lack the ability to stop the thirst mechanism.
Signs and Symptoms
• General
– Weakness, fatigue
• Neurologic
– Altered mental status, headache, lethargy, irritability, delirium, psychosis, personality changes
• Cardiovascular
-Normotensive, regular rate, rhythm
• Gastrointestinal
– Anorexia, nausea, vomiting, diarrhea, excessive thirst, abdominal cramping.
• Renal
– Oliguria (<400 cc/24 hours), weight gain, incontinence.
Physical exam
Hypovolemia • Orthostatic
hypotension • Poor skin turgor • Dry mucous
membranes • Tachycardia
Hypervolemia • Edema • Increased jugular
distension • Changes in breath
sounds
Diagnostic Studies
• Serum sodium (norm range 135-147 mEq/l) • Plasma osmolality (decreased in SIADH)
• Urine sodium concentration is usually below 25 meq/L in hypovolemia, unless there is renal salt-wasting, due most often to diuretic therapy and infrequently to adrenal insufficiency or cerebral salt-wasting)
• . The urine sodium concentration is usually above 40 meq/L in patients with the SIADH who are normovolemic and whose rate of sodium excretion is determined by sodium intake, as it is in normal subjects
• Urine osmolality (increased in SIADH)
Diagnostics Studies
• Electrolytes, BUN, creatinine, albumin and uric acid should be checked as they can also be lower in the setting of SIADH.
• Studies to r/o cardiac, hepatic, adrenal and thyroid causes of hyponatremia should be completed.
Laboratory Values
• Serum sodium <130 mEq/L
• Serum osmolality <280 mOsm/kg
• Urine osmolality >500 mOsm/kg
• Urine sodium >20 mEq/L
Medical Management if SIADH
• Directed at treating the underlying pathology.
• Treatment with chemotherapy or radiation causes regression of tumor and usually results in resolution of SIADH.
• Treatment for mild hyponatremia (serum Na >125 mEq/l) includes fluid restriction of 800-1000 ml/day.
• Fluid restriction often increases Na within 3-10 days.
Complications arising from treatment:
• Tumor lysis syndrome
• Sepsis
• Anaphylatic reaction related to chemotherapeutic agents.
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TLS: Tumor Lysis Syndrome
• TLS is a metabolic oncologic emergency caused by rapid cell lysis.
• Intracellular components potassium, phosphorus, and uric acid are released into the vascular system.
Incidence
• Exact Incidence Unknown
• Estimated Incidence 5%-25%
Causes of Tumor Lysis
• Spontaneous • Chemotherapy • Biotherapy • Radiation Therapy • Surgery
Risk Factors • High Grade Lymphomas • Acute Leukemias • Large, Bulky, Treatment- Sensitive, Solid Tumors • Preexisting Renal Dysfunction • Volume Depletion • Elevated Lactate Dehydrogenase • Elevated Uric Acid Level
Pathophysiology
1. Malignancy is Treated 2. Malignant Cells Undergo Rapid
Death 3. Intracellular Components are
Released Into the Vascular Circulation
Clinical Assessment
Directed toward the expected signs and symptoms of
• Hyperkalemia • Hyperphosphatemia • Hypocalcemia • Hyperuricemia
Allopurinol • Prevents Hypoxanthine From Becoming
Uric Acid • Not Helpful if Uric Acid is Already Formed,
or in Renal FailureGiven PO/IV • Interaction with 6-MP • Rash is Common Side Effect • Cost/day: <$3
Rasburicase • Converts Uric Acid into Allantoin Which
Can Be Excreted By the Urine • May Cause Severe Hemolysis in
Patients with G6PD (glucose-6-phosphate dehydrogenase) Deficiency
• Given IV: recombinant product, needs close monitoring
• Cost: ~ $13,000 for an adult dose
Hyperkalemia
• Hydration with a Lasix chaser • Sodium Polystyrene Sulfonate
(Kayexelate, now used with caution) • Sodium Bicarbonate • Insulin/Dextrose 50 • Calcium Gluconate • Dialysis
Hyperphosphatemia
• Dietary Restrictions: carbonated drinks, milk, meat, chocolate, eggs, fish, nuts, bread, poultry
• Diuretics • Aluminum Hydroxide Antacids
Hypocalcemia
• Only Treat with Severe Symptoms
• Calcium May Bind with Phosphate and Result in Calcium/Phosphate Crystal Formation
Nursing Management of TLS
• Identify Patients at Risk – Type of malignancy – Tumor burden – Lab values-
• Elevated WBC • Elevated uric acid • Hyperphosphatemia • Hyperkalemia • Hypocalcemia • Elevated LDH • Elevated creatinine
Sepsis
• 10-50% of Solid Tumor and 80% of Liquid Tumor cancer patients experience fever
• Oncology patients are at HIGH RISK for sepsis
– #11 leading cause of death in US
– Severe sepsis 20% mortality
– Septic shock 50% mortality
Sepsis in Cancer
• Complex interaction between an infectious organism and a person’s immune, inflammatory, and coagulation response.
• IMMEDIATE treatment is necessary to avoid a rapid progression to death
Sepsis Defined
Septic shock is characterized by hemodynamic instability which results in alterations in cellular metabolism and abnormal coagulation
Septic shock results when the body fails to initiate an adequate immune response
Risk Factors for Sepsis
Comorbid Conditions
Diabetes
Renal disease
Hepatic disease
Cardiovascular disease
Gastrointestinal disease
Pulmonary disease
Hospital and ICU stays
Loss of skin or mucosal integrity
Asplenic: Spleen produces IgM antibodies, which is required to encapsulate pathogens.
Endogenous Flora
Sites of Origin
Endogenous flora: Pulmonary Cutaneous Renal/GU (Urosepsis) GI (translocation of GI flora)
Indwelling devices: Port, PICC, Foley, Chest Tube, Drain, Gtube
SIRS Criteria Defined
SYSTEMIC INFLAMMITORY RESPONSE
developed to describe the hemodynamic impairment seen with severe infections
Immune Defense Mechanisms
Granulocytes phagocytize and kill bacteria Cell-mediated immunity activates monocytes,
macrophages and T lymphocytes which eliminate pathogens, viruses and malignant cells
Humoral immunity activates B lymphocytes which produce antibodies to specific foreign bodies or antigens.
Normal Physiology
Inflammation includes vasodialation, increased microvascular permeability
Lymphocytes release cytokines Tumor necrosis factor Interleukins
Cytokines cause increased vascular permeability in order to assist with phagocytosis of bacteria
Septic Shock
Systemic host response to infection with SIRS plus a documented infection
End-organ dysfunction or distal hypoperfusion
Sepsis can cause blood clots to form in your organs and limbs
Hypotension, despite fluid resuscitation
Evidence of inadequate tissue perfusion
ICU level of support is needed if reversible and in line with goals of care
Bacterial Organisms
40% gram-negative bacteria: consider this if GI/GU/Pulmonary source: E-coli, Klebsiella pneumoniae, Pseudomonas
aeruginosa ESBL enzymes that mediate resistance to
extended-spectrum (third generation) cephalosporins
5%-10% gram-positive bacteria:consider if has a indwelling line or skin compromise
Staph aureas, Strep pneumoniae
Speciation of Organisms
Fungi (associated with prolonged suppression) Candida
Aspergillus
Viruses Herpes simplex (HSV)
Cytomeglovirus (CMV)
Respiratory Synctal virus (RSV)
BK virus
Adeno virus
Endogenous Flora 20%-30% of these organisms are not identified
Pathophysiology of Sepsis
Microbes enter the circulatory system and tissue and create an UNCONTROLLED inflammatory response
Exotoxins (gram positive bacteria) and Endotoxins
(gram negative bacteria) stimulate release of macrophages, monocytes, neutrophils, and plasma cells
Tumor necrosis factor and cytokines are released,
causing a cascade of inflammation
Pathophysiology of Sepsis
Widespread tissue inflammation and vasodilatation
Decreased arterial and venous tone
Activation of clotting mechanisms
Capillary leak syndrome, third-spacing
Hypoperfusion
Organ Ischemia
Coagulapathy
Anaphylactic reactions related to chemotherapeutic agents
• May create medical emergencies
• Angioedema and urticaria are the most common manifestations of anaphylaxis and make up >90% of allergic reactions.
• Other frequent manifestations: abdominal pain, chest tightness, upper airway obstruction, bronchospasm and hypotension.
• Laryngeal edema followed by hypotension is the most frequent cause of death related to allergic reactions.
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main issues in treating anaphylactic reactions:
• Removing the drug considered to be responsible • Immediate assessment of the airway and
administration of epinephrine subcutaneously, depending on the severity,
• Intravenous fluids should be given, particularly in the case of hypotension.
• Glucocorticoids and antihistamines may also be administered.
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Preventative measures:
• Have an understanding of disease extent
• What co-morbidities may contribute to risks
• Lab values
• Patient and support system education
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