10/5/2016psons.org/wp-content/uploads/2016/09/ocn-review-course-onc-eme… · 10/5/2016 1 oncologic...

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Oncologic Emergencies Ellen Alberts, BSN, RN, OCN

OCN Review Course Fall 2016

Adapted from a previous presentation on Oncologic Emergencies by Juanita Madison.

Thank you Juanita!!

Overview

2016 OCN Test Blueprint Content Areas Content Area Percentage

of 2014 Test # of Scored Questions*

Health Promotion, Screening & Early Detection

6% 9

Scientific Basis for Practice (including Research)

9% 13

Treatment Modalities 16% 23

Symptom Management 22% 32

Psychosocial Dimensions of Care 8% 12

Oncologic Emergencies 12% 17

Survivorship 8% 12

Palliative & End of Life Care 11% 16

Professional Performance 8% 12

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Oncologic Emergencies (12% of exam) Disseminated intravascular coagulation

(DIC) Hypercalcemia

Thrombotic thrombocytopenia purpura (TTP) Cardiac tamponade

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

Spinal cord compression (SCC)

Systemic inflammatory response syndrome (SIRS)

Superior vena cava (SVC) syndrome

Sepsis Increased intracranial pressure (ICP)

Septic shock Obstructions (bowel and urinary)

Tumor lysis syndrome (TLS) Pneumonitis

Hypersensitivity Extravasations

Anaphylaxis

The Basics • Oncologic emergencies are life-threatening medical emergencies and must be

treated as such!

• Why do they occur?

• Malignancy

• Treatment of malignancy

• When do they occur?

• Early in disease process (initial manifestation of malignancy itself)

• Late in disease process (manifestation of treatment of malignancy)

Tumor Lysis Syndrome

• 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 bloodstream

(Maloney, 2016; Zobec, 2008)


• 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)

Who is most at risk?

Patients with large tumor burden that is highly responsive to chemotherapy (resulting in rapid cell kill).

– Patient-related • Large tumor burden/bulky tumors • Elevated LDH • Pre-existing renal dysfunction

– Treatment-related • Chemotherapy & biologic agents • Radiation therapy

(Maloney, 2016)

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Tumor Lysis Syndrome • Onset:

–Usually within 12-72 hrs. after

initiation of antineoplastic therapy

Duration:

–May persist for 5-7 days post-

therapy

(NCCN, 2016; Holmes Gobel, 2013)


• Clinical Presentation:

• Asymptomatic or only experiencing only vague symptoms

• Detected in blood chemistries

(Maloney, 2016)

Tumor Lysis Syndrome Pathophysiology

K+ PO4- K+ PO4-

PO4- K+ Nucleic Acids Nucleic Acids

Hypoxanthine Xanthine

Uric Acid

Xanthine Oxidase (Liver)

PO4

- PO4

- PO4

- K+ K+ K+

Tumor Lysis Syndrome Pathophysiology

K+ PO4- K+ PO4- PO4- K+

Nucleic Acids

Nucleic Acids

Hypoxanthine Xanthine

Uric Acid

Xanthine Oxidase (Liver)

PO4- PO4

- PO4

- K+ K+ K+

Ca++ PO4- K+ Uric Acid

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• So……

• What are the signs and symptoms of:

• Hyperkalemia

• Hyperphosphatemia

• Hyperurecemia

• Hypocalcemia

• ???

(Maloney, 2016)

Tumor Lysis Syndrome • General management:

• Prevention Strategies –Recognition of at-risk patients –Hydration –Prevention of hyperuricemia –Frequent monitoring of

electrolytes

• Intervention Strategies –Hydration –Control of hyperuricemia –Aggressive correction of electrolytes

–Management of acute renal failure

(Maloney, 2016)

Tumor Lysis Syndrome • Prevention:

• Hydration

–IV Normal saline or 5% dextrose

–Begin 24 – 48 hours prior to therapy

–Ensure urine output >150 – 200 ml/hr

• Diuresis

–Typically used if urine output not maintained by hydration alone

–Loop diuretics or osmotic diuretics

(Holmes Gobel, 2013)

Tumor Lysis Syndrome • Prevention:

• 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


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• Prevention and/or control of hyperuricemia:

• Allopurinol

• or

• Rasburicase

(Maloney, 2016)

Tumor Lysis Syndrome • Allopurinol (Oral or IV)

–Blocks uric acid production by inhibiting xanthine oxidase (liver enzyme)

–Prevents uric acid precursors from converting to uric acid, ↓ risk uric acid crystallization

–Dosing:

• Oral: 300 mg/m2/day

• IV: 200 – 400 mg/m2/day

• Begin 2 – 3 days prior to chemotherapy

• Continue for 10-14 days


Tumor Lysis Syndrome • Rasburicase (Elitek®) IV

–Converts uric acid into allantoin (which has a much greater solubility than uric acid)

–NCCN recommendations for preventative therapy indications

–Uric acid levels usually decrease within 4 hours of injection

• FDA approved dosing

–0.2 mg/kg IV as a 30 minute infusion daily for up to 5 days

• NCCN dosing recommendations

–One dose is usually adequate

–Doses of 3 – 6 mg IV usually effective

(Sanofi-Aventis US (2016) Elitek Package Insert.; NCCN, 2016).

Tumor Lysis Syndrome Metabolic

Abnormality Management

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 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


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Metabolic Abnormality

Management

Hyperphosphatemia • Phosphate-binding agents

• Aluminum-containing antacids

• Hypertonic glucose plus insulin

• Aggressive hydration

Hypocalemia • Appropriate management of

hyperphosphatemia

• IV calcium gluconate or calcium chloride

to treat arrhythmias


TLS Case Study • Mr J. 63 year old male

• Past Medical History:

–Non-insulin dependent diabetes mellitus, supraventricular arrhythmia

• Scheduled to receive 1st cycle CHOP-R chemotherapy in outpatient clinic

–Cyclophosphamide (Cytoxan), doxorubicin (Adriamycin), vincristine (Oncovin),

prednisone, + Rituximab (Rituxan)

• Started on oral allopurinol 300 mg daily

• IV hydration pre & post chemotherapy in clinic

• Instructed to increase oral intake to 8 glasses fluid per day

TLS Case Study • Mr. J: Two Days post 1st chemo

• Mr. J’s wife calls clinic and reports:

–Weakness, muscle cramping, numbness & tingling of extremities –Nausea/vomiting –Decreased urine output – Swelling both feet

• What could be the cause of Mr. J’s symptoms?

• What should we advise Mrs. J. to do?

TLS Case Study • Mr. J: Two Days post 1st chemo

• ED intake interview revealed Mr. J. had not been able to tolerate oral medications after his chemotherapy

–Had not taken prescribed allopurinol –Had not taken in recommended 8 glasses fluid per day

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TLS Case Study • Mr. J’s Labs in ER (2 Days Post CHOP-R Chemotherapy)

• Baseline Pre-Chemo Labs

- Hgb 11.1 g/dl - Platelets 245,000/mm3

- Na++ 136 - K+ 4.1 - BUN 45 mg/dl - Creatinine 2.2 mg/dl - Uric acid 12.6 mg/dl

ER: 2 days post-chemo - Hgb 11.2 g/dl - Platelets 200,00/mm3

- Na++137 mmol/l - K+ 6.5 mmol/l - BUN 100 - Creatinine 5.1 mg/dl - Uric acid 25 mg/dl

TLS Case Study • Mr. J’s Treatment:

• In ED:

–1 amp D50, 10 units regular insulin –D51/2 NS plus 100 mEq NaHCO3 at 250 cc/hr –Allopurinol 300 mg/day po –IV Lasix 40 mg

• Transferred to inpatient telemetry unit with following orders: –Strict I & O

• Notify MD for urine output < 200 ml/hr –BID weights –Vital signs Q2 hrs –Repeat Laboratory tests in 1 hr, monitor Q4 hrs: Electrolytes, Ca++, PO4-, BUN,

Creatinine, Uric Acid

Tumor Lysis Syndrome • 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

Septic Shock • Occurs on a continuum!!

Septicemia

SIRS

Sepsis

Severe Sepsis

SEPTIC SHOCK! (Maloney, 2016)

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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 ***

What are some of the criteria used to identify where a patient may be on this continuum?

(Maloney, 2016)

Septic Shock • Risk Factors:

• Neutropenia

• Infection

• Medical devices

• Mucositis

• Hospitalization

• Corticosteroids or other immunosuppressants

• Splenectomy

• Age

• Poor nutritional status

• Concurrent immunosuppressive disease

• Type of malignancy

(Maloney, 2016)

Septic Shock

• Pathophysiology:

1. Infection (can be bacterial, viral, or fungal)

2. Endotoxins and other cellular components released

3. Vasodilation

4. Increased vascular permeability

5. Decreased arterial/venous tone

6. Clot formation

7. End-organ damage

8. Cell death

(Maloney, 2016)

Septic Shock • Clinical Presentation:

Sepsis

• confusion, agitation

• tachycardia, hypotension

• tachypnea, hypoxia on RA, decreased breath sounds

• decreased UO

• warm, dry, flushed skin

• nausea/vomiting

Septic shock

• obtunded, coma

• arrhythmias, tachycardia, hypotensive

• SOB, decreased breath sounds, crackles/wheezes, ARDS, pulmonary edema

• oliguria or anuria, ARF

• cold, pale, mottled skin

• decreased GI motility, jaundice

(Maloney, 2016)

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Septic Shock Case Study

• Mr. J.: Seven days post-3rd cycle R-CHOP

• Wife calls outpatient clinic at 5 pm on Friday and reports husband has: –Fever –Dry cough –Discomfort with swallowing


• Mr. J & Wife arrive in ER at 7:30 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

• Implanted port - site without redness or drainage; however, c/o slight tenderness

to area above port

• O2 sat 98% room air

• Temp 1020F, HR irregular 96, RR 16, BP 126/84

Sepsis Bundles

Start Immediately Complete Within 3 Hours

Complete Within 6 Hours

• Measure lactate level • Administer 30 mg/kg

crystalloid over 10-15 minutes

• Obtain blood cultures • Administer broad-

spectrum antibiotics following blood cultures

• Administer vasopressors for hypotension unrelieved by crystalloids

• Measure central venous pressure and venous oxygen saturation

• Re-measure lactate

Dellinger, RP et al (2013). Surviving sepsis campaign: International guidelines

for management of severe sepsis and septic shock, 2012. Intensive Care

Medicine, 39, 165-228.

Septis Bundles

Complete Within 24 Hours

Additional Supportive

Measures

• Administer low-dose corticosteroids if hypotensive despite vasopressors

• Maintain glucose between lower limit of normal and 150 mg/dl

• Maintain inspiratory plateau pressure <30 cm H2O for mechanically ventilated

• Maintain adequate nutrition • Prevent deep vein

thrombosis • Prevent stress and pressure

ulcers • Prevent additional infection

Dellinger, RP et al (2013). Surviving sepsis campaign: International guidelines for management

of severe sepsis and septic shock, 2012. Intensive Care Medicine, 39, 165-228.

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Septic Shock • Diagnosis:

• BMP

• CBC

• Coagulation studies

• Lactic Acid

• ABGs

• Anything else to help determine potential site of infection

Like what?

(Maloney, 2016)

Septic Shock • Laboratory manifestations:

Sepsis

• long PT and aPTT

• decreased fibrinogen and platelets

• hyperglycemia

• leukocytosis

• elevated lactic acid

• + blood cultures

• WBCs in urine

Septic shock

• elevated LFTs

• increased BUN and/or creatinine

• decreased hematocrit and/or hemoglobin

• hypoglycemia

(Maloney, 2016)

Septic Shock

• Managment:

• Fluid resuscitation (crystalloids)

• Broad spectrum antibiotics (within 45 minutes)

• Oxygen therapy

• Vasopressor therapy

• Supportive therapy

Like what?

(Maloney, 2016)


• ER orders for Mr. J:

• Stat CBC with differential, CXR, & cultures of blood (peripheral blood and

central lines), urine, sputum, stool, CVC exit site

• Stat Electrolytes, Blood Glucose, BUN, & Creatinine

• Meropenum 1 gm IV stat & Q8h

• Vancomycin 1000 mg IV stat & Q12h

• Admit to medical oncology unit

• Neutropenic precautions

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Septic Shock Case Study • Mr. J’s labs in ED:

Lab Value Result

WBC 1,100/m2

Absolute Neutrophil Count 450/mm3

Hemoglobin 10 g/dl

Platelets 30,000/mm3

Sodium 134 mEq/l

Potassium 3.5 mEq/l

BUN 12 mg/dl

Creatinine 0.9 mg/dl

Lactic Acid 4 mmol/L

Septic Shock Case Study • Nursing Assessment of Mr. J upon inpatient admission: 9 PM

• Extreme restlessness & anxiety

• Shaking chills

• Skin warm, flushed

• Temp 102.40F

• HR 120 irregular, bounding

• RR 20, oxygen saturation 96% room air

• BP 128/60

• No urine output since early am

• Stat IV antibiotics ordered in ER not yet given

Septic Shock • Nursing Management:

• Prevention and early recognition!!!!

• Administer fluids and antibiotics on time

• Frequent vitals and assessments

• Maintain adequate oxygenation

• Educate!

(Maloney, 2016)

Disseminated Intravascular Coagulation

• Definition: Generalized activation of the hemostatic system, which results in widespread intravascular deposition of fibrin in the microvasculature and the simultaneous consumption of coagulation factors and platelets.

• DIC is never a primary diagnosis. It ALWAYS is a symptom of an underlying disease.

(Maloney, 2016; Viele, 2008)

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• Causes:

• Sepsis

• Severe infection

• Vascular abnormalities

• Severe allergic reactions

• Severe immunologic reactions

• Malignancy (both solid and liquid)


Disseminated Intravascular Coagulation • Basic pathophysiology:

• Overactivation of coagulation cascade from certain proteins

• can be intrinsic (blood vessel damage)

• can be extrinsic (tissue damage)

• Clots begin to form and are deposited throughout the body’s vasculature

• Because of excessive clotting, clotting factors and platelets are all used up!

• This means there is no more clotting factors and platelets for normal clotting anymore, which allows for abnormal bleeding!


Disseminated Intravascular Coagulation • Clinical Presentation:

• Skin: pallor, petechiae, jaundice, ecchymosis, hematomas, acral cyanosis

• EENT: visual disturbances, scleral injection, periorbital edema, subconjunctival hemorrhage, eye and ear pain, petechiae on nasal and/or oral mucosa, epistaxis, tender and bleeding gums

• Cardiac: tachycardia, hypotension, weak peripheral pulses, color and temperature changes to extremities, overt or occult bleeding

• Respiratory: dyspnea, tachypnea, hypoxia, hemoptysis, cyanosis


Disseminated Intravascular Coagulation • Clinical Presentation (continued):

• GI: tarry stools, hematemesis, abdominal pain, abdominal distension, guiac positive stools

• GU: hematuria, decreased UO

• Musculoskeletal: joint pain and stiffness

• Neuro: headache, restlessness, confusion, lethargy, altered LOC, obtundation, seizures, coma


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• Diagnosis:

• clotting studies: platelet count, fribrinogen level, thrombin level

• clotting factors studies: PT, aPTT, INR

• fibrinolysis studies: fibrin degradation products, D-dimer, antithrombin

• Bilirubin

• BUN



• Diagnosis: Platelet Decreased

Fibrinogen Decreased

Thrombin Time Prolonged

Prothrombin Time Prolonged

Activated Prothrombin Time

Prolonged

Fibrin Degradation Products

Increased

Antithrombin Decreased

(Viele, 2008)

DIC Case Study • Mr. J: Nursing Assessment 9:45 pm

• Disoriented, lethargic

• Skin pale, cool, fingertips cyanotic

• ↓ breath sounds lower lobes bilaterally with diffuse bilateral rales, hemoptysis

• Abdomen distended, rebound tenderness

• No urine output

• Oozing blood from venipuncture sites

• HR 136 irregular, weak

• RR 28 labored, oxygen saturation 88% room air

• BP 88/50

• Temp 103.1oF

DIC Case Study

Laboratory Value 7:30 pm 10:00 pm Normal Values

Hemoglobin 10 g/dl 8.9 g/dl 14 – 18 g/dl (male)

Platelets 30,000/mm3 12,000/mm3 150,000 – 400,000/mm3

Fibrinogen 96 mg/dl 170 – 410 mg/dl

PT 15.8 seconds 11.3 – 13.1 seconds

Fibrin Degradation Products

60 mcg/ml < 10 mcg/ml

Mr. J’s labs:

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• Managment:

1. Treat underlying cause!!

2. Correct hypoxia

3. Correct hypovolemia, hypotension, & acidosis

4. Stop the micro clotting

5. Stop the bleeding



• Nursing Management

(Vogel, 2016)

• Early recognition!

• Good assessments

• VS

• Hemodynamics

• Oxygenation

• Fluid status

• Ensure patient safety

• Prevent severity of symptoms

• Manage active bleeding

• Administration of anticoag therapy, other meds, fluids, blood products

• Monitor response to therapy

• Assist in patient coping

Hypercalcemia • Definition: abnormally high levels of calcium (>10.5mg/dL)

• Most common oncologic emergency!

-Occurs in 10-20% of all cancer patients

• Considered an emergency because, left untreated 50% of cases progress to renal failure, dehydration, coma, and death within days to weeks.

(Maloney, 2016; Jensen, 2008)

Hypercalcemia

• Risk Factors:

• Solid tumors (lung and breast)

• Liquid tumors (multiple myeloma)

• Non-malignant conditions

• Immobility

• Use of thiazide diuretics

• Overuse of dietary supplements


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Hypercalcemia • Normal Regulation of Ca++:

• Parathyroid gland –Production of parathyroid hormone (PTH)

–PTH is major hormone regulating extracellular Ca++

• PTH increases Ca++ by 3 mechanisms: –Direct action on bone

• Stimulates activity of osteoclasts → breaks down bone (bone resorption)

–Direct action on kidneys • Increases renal excretion of phosphate stimulates reabsorption of Ca++

– Indirect action in gut • Enhances absorption of ingested Ca++ by stimulating kidney conversion of vitamin D to

biologically active form

Kaplan, M. (2013)

Hypercalcemia • Normal Regulation of Ca++

• Ca++ levels below normal:

–Parathyroid stimulated to produce PTH

–Acts on bone release of calcium (bone resorption) into circulation

–Acts on kidneys increase renal secretion of phosphorous stimulates reabsorption of Ca++

–Acts indirectly gut enhance absorption Ca++

• Ca++ levels above normal:

–Kidneys excretion of calcium

Kaplan, M. (2013)

Hypercalcemia

• Distribution of Calcium:

• Bone stores: 99% of body’s calcium

• Serum calcium: 1% circulates in serum, divided into fractions:

–50% is free ionized calcium

• Only type that is biologically active

–40% is bound to protein

• Mostly albumin, but also globulin & paraproteins

–10% forms serum complexes with anions

• Bicarbonate, phosphate, & citrate

Moe, S. (2008).

Hypercalcemia • Measuring Serum Calcium

• Total calcium =

– Ionized calcium + protein-bound calcium

–Used to “infer” the fraction of ionized calcium

–The result is usually accurate, EXCEPT when serum albumin is low

– If albumin < 3.5 – 5.5 g/dL, results in:

• ↓in the fraction of protein-bound calcium

• ↑ in the ionized free calcium

• Ionized calcium more accurately reflects true serum calcium levels

Moe, S. (2008).

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Hypercalcemia

• Corrected Serum Ca++

• Corrected Total Serum Calcium =

• Total serum Ca++ + (4.0 – serum albumin) X 0.8

• Example: Ca++ 13.8 Albumin 2.1

• = 13.8 + (4.0 – 2.1) X 0.8

• = 13.8 + 1.9 X 0.8

• = 13.8 + 1.52

• = 15.32 (rounded to 15.3) *Normal Total Serum Calcium: 8.5 to 10.2 mg/dL.

Hypercalcemia • Pathophysiology:

Humoral (80%):

• Tumor cells produce PTH-rP

• Mimics real PTH

• bone resorption of calcium

• renal resorption of calcium

• PTH-rP is NOT controlled by the negative feedback mechanism that normal PTH is

Osteolytic (20%):

• Malignant cells invade and destruct bone

• These tumor cells release a variety of cytokines that promote bone resorption of calcium

• Osteoclasts are also active at the cites of tumor cells, furthering calcium resorption

• In certain lymphomas, vitamin D is converted into its active from which promotes calcium absorption from the GI tract.


Hypercalcemia • Clinical Presentation:

Mild (10.5-11.5mg/dL)

• GI: anorexia, N/V, abd cramping, low appetite

• Neuro: restlessness, poor concentration, lethargy, confusion

• Muscular: fatigue and weakness

• Renal: frequent urination, nocturia, polydipsia

• Cardio:orthostatic hypotention

Moderate (11.5-13.5mg/dL)

• GI: constipation, bloating, abd pain

• Neuro: psychosis, drowsiness, AMS

• Muscular: continued increased weakness, hypotonia

• Renal: dehydration

• Cardio:hypertension, ECG changes (long PR interval, wide QRS, short QT, short ST), arrhythmias,

Severe (>13.5mg/dL)

• GI: ileus

• Neuro: seizures, coma

• Muscular: ataxia and pathologic fractures

• Renal: oliguric renal failure and renal insufficiency

• Cardio: ECG changes (wide T waves, heart block, ventricular arrhythmias), cardiac arrest

(Maloney, 2016)

Hypercalcemia

• Diagnosis:

• Complete metabolic panel (including serum calcium)

• BUN and Cr

• Phosphorus

• Serum albumin and prealbumin

• PTH

(Maloney, 2016)

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Hypercalcemia • Management:

• Tumor suppression is the only long term measure for reversal

• Hydration (usually 0.9% NS and 3-4L/day PO intake)

• Remove drugs that worsen hypercalcemia (thiazide diuretics)

• Diuresis (loop diuretics)

• Biphoshponates (zometa > pamidronate)

• Additional pharmacologic options

• Dietary recommendations


Hypercalcemia

• Nursing Management:

• Early recognition!

• Administer all necessary active treatment modalities

• Intervene to maintain patient safety, particularly if confused

• Intervene to maintain patient activity level

• PT/OT

• Frequent fall risk assessment

• Manage and monitor fluid and electrolyte balance


Hypercalcemia Case Study • 62-year-old male, Mr. C., 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

Hypercalcemia Case Study

• 2nd 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)

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Mr. C’s Labs: 2nd Cycle Chemotherapy

• Serum Ca++ 10.4

• Creatinine 1.1 mg/dl

• BUN 19 mg/dl

• Albumin 2.3 g/dl

• WBC 4,500/mm3

• Hgb 11.2 g/dl

• Hct 35%

• Platelets 119,000/mm3


Corrected Serum Ca++

• Mr. C’s : Ca++ 10.4 Albumin 2.3

• Corrected Serum Calcium =

• Measured serum Ca++ + (4.0 – serum albumin) X 0.8

= 10.4 + (4.0 – 2.3) X 0.8

= 10.4 + 1.7 X 0.8

= 10.4 + 1.36

= 11.78 (rounded up to 11.8)



Mr. C’s 3rd Cycle Chemotherapy:

• Wife reports confusion improved for 1st two weeks following last

chemotherapy

• Past week, he has been increasingly forgetful, depressed, and fatigued

(stayed in bed last 2 days)

Mr. C’s Lab Trends:

Laboratory Value 2nd Chemo Visit 3rd Chemo Visit

WBC 4,500/mm3 2,200/mm3

Hemoglobin 11.2 g/dl 10.4 g/dl

Hematocrit 33% 29%

Platelets 119,000/mm3 102,000/mm3

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


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Corrected Serum Ca++

• Mr. C’s : Ca++ 12.8 Albumin 2.1

• Corrected Serum Calcium =

• Measured serum Ca++ + (4.0 – serum albumin) X 0.8

= 12.8 + (4.0 – 2.1) X 0.8

= 12.8 + 1.9 X 0.8 = 12.8 + 1.52 = 14.32 (rounded to 14.3)

Hypercalcemia Case Study Anaphylaxis

• Definition: an allergic reaction that potentiates a life-threatening emergency

• Can be generalized or localized.

• The most rapid and severe hypersensitivity reaction.

(Maloney, 2016)

Anaphylaxis • Risk Factors: various antigens and routes of exposure

• Allergy testing

• Antibiotics

• Anesthetics

• Antineoplastics

• Blood products

• Insect venom

• Latex

• Contrast media for radiographic tests

• Foods

✴egg

✴fish

✴additives

✴peanuts

✴shellfish

✴milk

(Maloney, 2016)

Anaphylaxis • Pathophysiology:

• First exposure to antigen causes IgE antibody to develop

• Upon repeat exposure to antigen, IgE antibody binds to and activates mast cells and basophils

• Inflammatory mediators are then triggered to release:

✴ histamine

✴ leukotrienes

✴ prostaglandins

✴ platelet activating factor

• These substances lead to:

✴ systemic vasodilation

✴ increased capillary permeability

✴ bronchoconstriction

✴ coronary vasoconstriction

✴ increased mucous production (Maloney, 2016)

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Anaphylaxis • Clinical Presentation:

• Derm: flushing, itching, urticaria, morbilliform rash, angioedema

• Ophthalmologic: periorbital edema, infected conjunctiva, tears

• Resp: bronchospasm, chest tightness, tachypnea, throat/nasal itching, congestion, sneezing, dysphonia, horseness, dry cough, stridor, cyanosis, respiratory arrest

• GI: nausea, vomiting, diarrhea, abdominal pain

•Cardio: chest pain, tachycardia, diaphoresis, hypotension, cyanosis, dysrhythmias, palpitations, shock

• Neuro: headache, dizziness, uneasiness, lightheadedness, confusion, tunnel vision, loss of consciousness

• Other: metallic taste, feeling of impending doom

(Maloney, 2016)

Anaphylaxis • Managment:

1. Epinephrine!!!

• Additionally:

- Oxygen therapy (100% non rebreather)

- 0.9% NS given as fast as possible

- corticosteroids

- H1 receptor anatagonist

(Maloney, 2016)

Anaphylaxis

• Nursing Management

Prevent anaphylaxis

Manage Anyphylaxis

Emotional support to patients and caregivers

Interventions for potential anaphylaxis occuring in the community

(Vogel, 2016)

Spinal Cord Compression • Definition:

• A neurological emergency where the spinal cord or cauda equina is compromised by direct pressure, vertebral collapse, or both cause a direct extension or metastatic spread of malignancy.

(Schulmeister & Gatlin, 2008; Vogel, 2016)

http://www.medscape.com/viewarticle/442735



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Spinal Cord Compression • Cancers associated with spinal cord compression

Spinal Level % Involvement Associated Cancers

Cervical 10 Lung, breast, kidney, lymphoma, myeloma,

melanoma

Thoracic 70 Lung, breast, kidney, lymphoma, myeloma,

prostate

Lumbosacral 20 Lung, breast, kidney, lymphoma, myeloma,

melanoma, prostate, GI

(Schulmeister & Gatlin, 2008)

Spinal Cord Compression

• Risk Factors:

• Cancers that have a natural history of spreading to the bone

• Cancers that have a natural history of spreading to the brain and spinal cord

• Primary cancers of the spinal cord

• History of vertebral compression fractures

(Vogel, 2016)

Spinal Cord Compression • Pathophysiology: • Compression of spinal cord ✴Direct tumor pressure on cord ✴Tumor invasion of the vertebral column causing collapse & pressure

on cord

• Compression leads to: ✴Edema ✴Inflammation

• Resulting in: ✴Direct neural injury to cord ✴Vascular damage

(Kaplan, 2013)

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• Mr. B is a 56-year-old male with stage IV prostate cancer, with wide-spread metastases to the bone

• He previously failed several cycles of chemotherapy and is being treated with hormonal therapy

Spinal Cord Compression Case Study

• Mr. B presents to Emergency Department with:

–Bi-lateral weakness in lower extremities

• Initial onset 5 days ago

• Difficulty ambulating, reports falling this morning

–Numbness in the lower extremities

• Began earlier in the day

– Increasing back pain

• Has been taking oxycodone every 4 hours which controlled his pain well

until 4-5 days ago

• Currently rates his pain as 7 out of 10


Spinal Cord Compression • Clinical Presentation:

• 90% of patients with SCC experience back pain as the first symptom.

Early signs:

• Neck pain

• Motor weakness and dysfunction

• Sensory loss

Late signs:

•Loss of sensation for deep pressure, vibration, and position

•Incontinence or retention

•Impotence

•Paralysis

•Muscle atrophy

•Loss of sweating below lesion (Vogel, 2016)

Spinal Cord Compression • Back pain characteristics:

• Localized: usually occurs at level of lesion, described as dull and constant, more severe with movement, coughing, weight bearing, during a Valsalva maneuver

• Radicular: along dermatomes

• Referred: in a non-radicular pattern

• May be a combination of all three!

(Schulmeister & Gatlin, 2008)

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• 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

Time Frame

Early

Late

Spinal Cord Compression • Diagnosis: • 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

(Vogel, 2016)

Spinal Cord Compression • Treatment:

• Immediate and aggressive!

Pharmacologic:

•Corticosteroids

•Chemotherapy

•Analgesics

•Bone remodeling agents

Nonpharmacologic:

•Radiation

•Surgery

•Surgery followed by radiation

(Vogel, 2016)

• Mr. B received a loading dose of dexamethasone 10 mg, followed by

tapering doses.

• He was admitted to the inpatient oncology unit with initial activity

orders for bed rest with only log-rolling

• Surgical & radiation therapy consults were ordered


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• Three days after initiating radiation therapy, Mr. B. developed urinary

retention

• The following day he developed paraplegia, urinary & bowel

incontinence.

• Surgical consult re-evaluated Mr. B for emergent decompression of

spinal cord

• After family conference, Mr. B and his family decided against surgical

intervention and decided on palliative care


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

Promote physical mobility Protect and/or improve skin integrity


• Mr. B completed his course of radiation therapy while inpatient

• A hospice consult was obtained. Mr. B was discharged from inpatient

care to a hospice facility

• Mr. B passed away 23 days later

Spinal Cord Compression Case Study Superior Vena Cava Syndrome

• Definition: Describes a pattern of physical findings that results from the obstruction of blood flow through the superior vena cava, due to tumor or thrombus, compromising venous drainage from the head, neck, upper extremities, and thorax.

(Mack & Becker, 2008; Vogel, 2016)

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Superior Vena Cava Syndrome

• Risk Factors:

• Mediastinal malignancy

• Presence of a CVC and/or pacemaker

• History of radiation to the mediastinum

• Other associated conditions

• mediastinal fibrosis

• fungal infection

• aortic aneurysm

• benign mass (Mack & Becker, 2008; Vogel, 2016)


• Pathophysiology:

1. Obstruction of the SVC occurs (depending on cause)

2. Venous pressure and congestion in the head, neck, thorax, upper extremities, and throat increases

3. Decreased cardiac filling and output occurs

4. Blood flow is diverted to smaller collateral vessels

(Mack & Becker, 2008; Vogel, 2016)

Superior Vena Cava Syndrome • Early Clinical Presentation: Symptoms are more pronounced in AM

or when bending over.

• Redness and edema in conjunctiva and around eyes and face

• Swelling of face, neck, arms, and hands

• Neck and thoracic vein distention

• Dyspnea

• Nonproductive cough

• Hoarseness, occasionally dysphagia

• Cyanosis of upper torso

• Nasal stuffiness and head fullness

• Breast swelling

(Vogel, 2016)


• Late Clinical Presentation:

• Symptoms of ICP

• Irritiability, altered mental status

• Stridor, signs of CHF

• Tachcardia, tachypnea, orthopnea

• Hypotension, no peripheral pulses

• Dysphagia, hoarseness, hemoptysis

• Progressive cyanosis, facial edema

• Horner syndrome

(Vogel, 2016)

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• Diagnosis:

• Based on characteristic signs & symptom of central venous obstruction • Imaging Studies:

• CXR

• MRI

• CT

• Contrast venography

• PET

(Vogel, 2016)

Superior Vena Cava Syndrome • Treatment: Goal is relief of obstruction and addressing of

underlying cause. Determined by rate of onset.

Pharmacologic:

•Chemotherapy

•Chemotherapy + radiation

•Corticosteroids

•Diuretics

•Thrombolytic therapy

Nonpharmacologic:

•Radiation

•Removal of CVC*

•Percutaneous intravascular stent placement

•Surgical reconstruction of SVC

•Oxygen therapy (Vogel, 2016)

Nursing Management:

• 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


Nursing Management

• 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)


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Clinical Pearls

•

Know your patient!

Know the risk factors!

Know how to complete a good physical assessment!

Early recognition may save a life!

References • Brashers, V. L. (2014). Alterations in Cardiovascular Function. In K. L. McCance & S. E. Huether (Authors) & V. L. Brashers & N. S. Rote (Eds.), Pathophysiology: The Biologic Basis for Disease in Adults

and Children (7th ed., pp. 1129-1193). St. Louis, MO: Elsevier.

• Camp-Sorrell, D. (2008). Cardiac Tamponade. In R. A. Gates (Author) & R. M. Fink (Ed.), Oncology Nursing Secrets (3rd ed., Nursing Secrets Series, pp. 513-517). St. Louis, MO: Mosby Elsevier. • Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses. (2nd ed., pp. 433-459). Pittsburgh, PA. Oncology

Nursing Society.

• Jensen, G. (2008). Hypercalcemia of Malignancy (HCM). In R. A. Gates (Author) & R. M. Fink (Ed.), Oncology Nursing Secrets (3rd ed., Nursing Secrets Series, pp. 523-527). St. Louis, MO: Mosby Elsevier.

• Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 103 – 155. • Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic emergencies: A resource for nurses. (2nd ed., pp. 337-383). Pittsburgh, PA. Oncology Nursing

Society. • Mack, K. C., & Becker, C. (2008). Superior Vena Cava Syndrome. In R. A. Gates (Author) & R. M. Fink (Ed.), Oncology Nursing Secrets (3rd ed., Nursing Secrets Series, pp. 551-556). St. Louis, MO:

Mosby Elsevier.

• Maloney, K. W. (2016). Metabolic Emergencies (J. M. Brant, F. A. Conde, & M. G. Saria, Eds.). In J. K. Itano (Ed.), Core Curr iculum for Oncology Nursing (5th ed., pp. 478-494). St. Louis, MO: Elsevier.

• Moe, SM (2008). Disorders involving calcium, phosphorus, and magnesium. Primary Care, 35, 215-237.

• National Comprehensive Cancer Network (2016). Non-Hodgkin’s Lymphomas, Version 3.2016. Retrieved from https://www.nccn.org/professionals/physician_gls/pdf/nhl.pdf

• Sanofi-Aventis US (2016). Elitek Package Insert. Retrieved from http://products.sanofi.us/elitek/elitek.html#section-4.1

• Schulmeister, L., & Gatlin, C. G. (2008). Spinal Cord Compression. In R. A. Gates (Author) & R. M. Fink (Ed.), Oncology Nursing Secrets (3rd ed., Nursing Secrets Series, pp. 546-550). St. Louis, MO: Mosby Elsevier.

• Viele, C. S. (2008). Disseminated Intravascular Coagulation (DIC). In R. A. Gates (Author) & R. M. Fink (Ed.), Oncology Nursing Secrets (3rd ed., Nursing Secrets Series, pp. 518-522). St. Louis, MO: Mosby Elsevier.

• Vogel, W. H. (2016). Structural Emergencies (J. M. Brant, F. A. Conde, & M. G. Saria, Eds.). In J. K. Itano (Ed.), Core Curriculum for Oncology Nursing (5th ed., pp. 495-508). St. Louis, MO: Elsevier.

• Zobec, A. (2008). Tumor Lysis Syndrome (TLS). In R. A. Gates (Author) & R. M. Fink (Ed.), Oncology Nursing Secrets (3rd ed., Nursing Secrets Series, pp. 557-560). St. Louis, MO: Mosby Elsevier.

https://www.nccn.org/professionals/physician_gls/pdf/nhl.pdf

https://www.nccn.org/professionals/physician_gls/pdf/nhl.pdf

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