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Oncologic Emergencies  

Ellen Alberts MSN, ARNP(c), AGCNS-BC, OCN

PSONS Fundamentals of Oncology Spring 2017

Overview

2017 OCN Test Blueprint Content AreasContent Area Percentage of

2017 Test# of Scored Questions*

Health Promotion, Screening & Early Detection

6% 9

Scientific Basis for Practice 9% 13Treatment Modalities 16% 23Symptom Management 22% 32Psychosocial Dimensions of Care 8% 12

Oncologic Emergencies 12% 17Survivorship 8% 12Palliative & End of Life Care 11% 16Professional Performance 8% 12

2017 OCN Test Blueprint Content Areas

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

Tumor Lysis Syndrome (TLS)

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)

Tumor Lysis Syndrome

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)

Onset:

Usually within 12-72 hours 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 SyndromePathophysiology

K+ PO4-

K+ PO4- PO4- K+ Nucleic Acids

Hypoxanthine Xanthine

Uric Acid

Xanthine Oxidase (Liver)

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

ChemoRadiation

Surgery

Immunotherapy


Pathophysiology

K+ PO4-

K+ PO4- PO4- K+ Nucleic Acids

Hypoxanthine Xanthine

Uric Acid

Xanthine Oxidase (Liver)

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

ChemoRadiation

Surgery

Immunotherapy


PO4- Ca++ K+ Uric Acid

Decreased or no urine output

Urine sediment or hematuriaSo……

What are the signs and symptoms of: Hyperkalemia

Hyperphosphatemia Hyperurecemia Hypocalcemia

???

Acute kidney

injury

Nausea, vomiting, diarrhea

Flank pain

EKG

change

s

Muscle weakness and cramping

(Maloney, 2016)

Edema and/or fluid overload

Fatigue

and

lethargy


Management:

TLS prevention and intervention includes which of the following?

A. Hydration B. Recognition of high risk patients C. Pharmacologic methods D. Frequent monitoring of electrolytes E. All of the above

Tumor Lysis SyndromeManagement:

TLS prevention and intervention includes which of the following?

A. Hydration B. Recognition of high risk patients C. Pharmacologic methods D. Frequent monitoring of electrolytes E. All of the above


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 SyndromePrevention:

• 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)


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

(Holmes Gobel, 2013)

Tumor Lysis SyndromePrevention and/or control of hyperuricemia:

Allopurinol or

Rasburicase

(Maloney, 2016)


• 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).


Metabolic Abnormality

Management

Hyperuricemia • Hydration, urinary alkalinization • Oral allopurinol or IV allopurinol • Rasburicase • Hemodialysis for significant renal compromise

Hyperkalemia 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



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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



Nursing Interventions:

Can you name a few?! • For monitoring • For managing fluid balance • For patient and family education

Tumor Lysis Syndrome Tumor Lysis Syndrome Case StudyMr 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 for his lymphoma

• Cyclophosphamide (Cytoxan), doxorubicin (Adriamycin), vincristine (Oncovin), prednisone, + Rituximab (Rituxan)

• Started on oral allopurinol 300 mg daily • IV hydration pre & post chemotherapy in clinic • Instructed to increase oral intake to 8 glasses fluid per day

Mr. J: Two Days post 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?

Tumor Lysis Syndrome 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


Mr. J’s Labs in ER (2 Days Post R-CHOP 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


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


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)

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

• Neutropenia • Infection • Medical devices • Mucositis • Hospitalization • Corticosteroids or

other immunosuppressants

Risk Factors:

• Splenectomy • Age • Poor nutritional

status • Concurrent

immunosuppressive disease

• Type of malignancy

(Maloney, 2016)

Septic ShockPathophysiology: 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

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)

Septic Shock

Septic shock • elevated LFTs • increased BUN

and/or creatinine • decreased

hematocrit and/or hemoglobin

• hypoglycemia

Laboratory manifestations:Sepsis • long PT and aPTT • decreased

fibrinogen and platelets

• hyperglycemia • leukocytosis • elevated lactic acid • + blood cultures • WBCs in urine

(Maloney, 2016)

Septic Shock

(Maloney, 2016)

Septic ShockMr. 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

(Maloney, 2016)

Septic ShockMr. 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 88% room air • Temp 1020F, HR irregular 96, RR 24, BP 87/45

Diagnosis: • BMP • CBC • Coagulation studies • Lactic Acid • ABGs • Anything else to help determine potential

site of infection

(Maloney, 2016)

Like what?

Septic Shock Septic ShockStart 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.

Septic ShockComplete Within 24

HoursAdditional 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

Septic Shock Case StudyNursing 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 22, oxygen saturation 90% 2 lpm via nc •BP 82/40 •No urine output since early am

Nursing Management:

• Prevention and early recognition!!!! • Frequent vitals and assessments • Maintain adequate oxygenation • Administer fluids and antibiotics on time • Educate!

(Maloney, 2016)

Septic Shock

Test your knowledge!

You have just started your shift and received bedside report. Which patient should you go to see first?

A. The independent patient receiving EPOCH and is starting to have frequent diarrhea

B. The patient who is receiving their second bag of PRBCs, which they are tolerating well

C. The independent, neutropenic patient, who is having frequent diarrhea

D. The patient with a central line and a peripheral IV, both of which are being used

Septic ShockTest your knowledge!

You have just started your shift and received bedside report. Which patient should you go to see first?

A. The independent patient receiving EPOCH and is starting to have frequent diarrhea

B. The patient who is receiving their second bag of PRBCs, which they are tolerating well

C. The independent, neutropenic patient, who is having frequent diarrhea

D. The patient with a central line and a peripheral IV, both of which are being used

Septic Shock

Test your knowledge!

Which of the following oncologic emergencies is a potential complication of septic shock?

A. Increased intracranial pressure B. Disseminated intravascular coagulation C. Tumor lysis syndrome D. Anaphylaxis/hypersensitivity

Septic ShockTest your knowledge!

Which of the following oncologic emergencies is a potential complication of septic shock?

A. Increased intracranial pressure B. Disseminated intravascular

coagulation C. Tumor lysis syndrome D. Anaphylaxis/hypersensitivity

Septic Shock

Disseminated Intravascular Coagulation

(DIC)


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)

Causes:

• Sepsis • Severe infection • Vascular abnormalities • Severe allergic reactions • Severe immunologic reactions • Malignancy (both solid and liquid)




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!



Clinical Presentation: • Skin: pallor, petechiae, jaundice, ecchymosis,

hematomas, acrocyanosis • 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

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



Clinical Presentation (continued): • GI: tarry stools, hematemesis, abdominal

pain, abdomina distension, guiac positive stools

• GU: hematuria, decreased UO • Musculoskeletal: joint pain and stiffness • Neuro: headache, restlessness, confusion,

lethargy, altered LOC, obtundation, seizures, coma



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 ProlongedActivated Prothrombin

Time Prolonged

Fibrin Degradation Products

Increased

Antithrombin Decreased(Viele, 2008)


DIC Case StudyMr. 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:

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

• Manage active bleeding • Administration of

anticoag therapy, other meds, fluids, blood products

• Assist in patient coping


Hypercalcemia

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)

HypercalcemiaDistribution 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).

Risk Factors: • Solid tumors (lung and breast) • Liquid tumors (multiple myeloma) • Non-malignant conditions • Immobility • Use of thiazide diuretics • Overuse of dietary supplements


Hypercalcemia

HypercalcemiaNormal 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)

HypercalcemiaNormal 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)

HypercalcemiaMeasuring 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).

HypercalcemiaCorrected 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.

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

Pathophysiology:

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


Hypercalcemia

Moderate (11.5-13.5mg/dL) • GI: constipation, bloating,

abd pain • Neuro: psychosis,

drowsiness, AMS • Muscular: continued

increased weakness • Renal: dehydration • Cardio:hypertension, ECG

changes (long PR interval, wide QRS, short QT, short ST), arrhythmias,


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

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)

Hypercalcemia Hypercalcemia Case Study62-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

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)

Hypercalcemia Case Study

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


Hypercalcemia Case StudyMr. 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)

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 3rd Cycle Chemotherapy:


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


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)


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

Anaphylaxis

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)

• Allergy testing • Antibiotics • Anesthetics • Antineoplastics • Blood products • Insect venom • Latex

Risk Factors: various antigens and routes of exposure

• Contrast media for radiographic tests

• Foods ✴ egg ✴ fish ✴ additives ✴ peanuts ✴ shellfish ✴ milk

(Maloney, 2016)

AnaphylaxisPathophysiology:

• 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)

Anaphylaxis

• 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. Epinepherine!!!

Additionally: - Oxygen therapy (100% non rebreather) - 0.9% NS given as fast as possible - Corticosteroids - H1 receptor anatagonist

(Maloney, 2016)

Anaphylaxis

Nursing Management

(Vogel, 2016)

Anaphylaxis

• Recognize risk factors • Minimize exposures (if possible) • Have emergency meds ready

• Administer treatment modalities • Patient and caregiver support • Educate!

Increased Intracranial Pressure


Definition: a potentially life-threatening neurologic event that occurs with an increase in brain tissue, blood, cerebrospinal fluid, or all of these, within the intracranial cavity, resulting in nerve cell damage, permanent neurologic defects, and/or death.

(Vogel, 2016)

Oncology specific causes:

• Tumors found within the intracranial cavity

• Leptomeningeal metastases • Blood clots • Infection • Metabolic disorders

(Vogel, 2016)


Oncology specific risk factors: • Breast, lung, kidney, melanoma • Leukemia, lymphoma, or neuroblastoma • Primary tumors to the brain or spinal cord • Thrombocytopenia, platelet dysfunction, or DIC • Infection while immunocompromised • SIADH • History of radiation • Occluded Ommaya reservoir

(Vogel, 2016)


Pathophysiology: • Volume of blood, brain tissue, or cerebrospinal fluid

increases • Compensatory mechanisms take over • Once these mechanisms fail, ICP increases and

displacement or edema of brain tissue occurs (mass effect)

• CSF outflow becomes obstructed • Cerebral perfusion decreases • Brain injury and tissue necrosis

(Vogel, 2016)


https://en.wikipedia.org/wiki/Brain_herniation#/media/

File:Brain_herniation_types-2.svg


Diagnosis: Test your knowledge!

Which of the following is diagnostic of ICP? A. MRI B. CT C. Cerebral angiography D. ICP monitoring E. All of the above

(Vogel, 2016)


Diagnosis: Test your knowledge!

Which of the following is diagnostic of ICP? A. MRI B. CT C. Cerebral angiography D. ICP monitoring E. All of the above

(Vogel, 2016)


Early: • Headaches • Visual disturbances • Lethargy, apathy,

confusion, restlessness

• Speech disturbances • Decreased LOC • Loss of appetite • Nausea and

vomiting

Clinical Presentation: Late: • Widening pulse pressure, increased BP,

bradycardia • Shallow respirations, Cheyne-Stokes

respirations • Papilledemia, poor concentration,

decreased LOC, personality changes, hemiplegia, hemiparesis, seizures, pupillary changes

• GCS < 8 • Abnormal posturing • Temperature elevations • Cushing triad

(Vogel, 2016)


Nonpharmacologic Management:

• Surgery • Hyperventilation • Radiation therapy • Patient positioning • Temperature control

(Vogel, 2016)


Pharmacologic Management:

Chemotherapy or targeted therapy Corticosteroids

Osmotherapy Anticonvulsant therapy

(Vogel, 2016)


• Monitor and manage symptoms • Prevention of ICP • Manage disturbed thought processes • Facilitate physical mobility and prevent injury • Manage acute pain • Address knowledge deficit • Manage patient/family emotional stress • Minimize environmental factors

Nursing Management

(Vogel, 2016)


Spinal Cord Compression

Spinal Cord CompressionDefinition: A neurological emergency where the spinal cord or cauda equina is compromised by direct pressure, vertebral collapse, or both caused by direct extension or metastatic spread of malignancy.

(Schulmeister & Gatlin, 2008; Vogel, 2016)http://www.medscape.com/viewarticle/442735

Spinal Level % Involvement Associated Cancers

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

melanoma

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

prostate

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

melanoma, prostate, GI

Cancers associated with spinal cord compression:

(Schulmeister & Gatlin, 2008)


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)


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)


SCC Case Study

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

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

SCC Case Study

Early signs: • Neck pain • Motor

weakness and dysfunction

• Sensory loss

Clinical Presentation: 90% of patients with SCC experience back pain as the first symptom.

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 CompressionBack 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)



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

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)


Nonpharmacologic: • Radiation • Surgery • Surgery followed

by radiation

Treatment: Immediate and aggressive!

Pharmacologic: • Corticosteroids • Chemotherapy • Analgesics • Bone remodeling agents

(Vogel, 2016)


(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

SCC Case Study

•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

SCC Case Study Spinal Cord CompressionNursing InterventionsEarly 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

SCC 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)

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)


• Redness and edema in conjunctiva and around eyes and face

• Swelling of neck, arms, and hands

• Neck and thoracic vein distention

• Dyspnea

Early Clinical Presentation: Symptoms are more pronounced in AM or when bending over.

• Nonproductive cough • Hoarseness,

occasionally dysphagia • Cyanosis of upper

torso • Nasal stuffiness and

head fullness • Breast swelling

(Vogel, 2016)


• Symptoms of ICP • Irritiability, altered

mental status • Stridor, signs of

CHF • Tachcardia,

tachypnea, orthopnea

Late Clinical Presentation:• Hypotension, no

peripheral pulses • Dysphagia,

hoarseness, hemoptysis

• Progressive cyanosis, facial edema

• Horner syndrome(Vogel, 2016)


Diagnosis:

• CXR • MRI • CT • Contrast venography • PET

(Vogel, 2016)


Nonpharmacologic: • Radiation • Removal of CVC* • Percutaneous intravascular stent placement

• Surgical reconstruction of SVC

• Oxygen therapy

Treatment: Goal is relief of obstruction and addressing of underlying cause. Determined by rate of onset.

Pharmacologic: • Chemotherapy • Chemotherapy + radiation

• Corticosteroids • Diuretics • Thrombolytic therapy

(Vogel, 2016)


Nursing Management:

(Vogel, 2016)


Assess for signs & symptoms in patients at risk –Non-small cell lung cancer, small cell lung cancer, non-Hodgkin 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:

(Vogel, 2016)


–Assess for progressive respiratory distress or edema –Monitor responses to treatment –Monitor tolerance of activities –Monitor fluid status (over hydration exacerbates symptoms) –Assess CNS (LOS, mental status changes, visual changes, headache)

Clinical Pearls Know your patient!

Know the risk factors!

Know how to complete a good physical assessment!

Early recognition may save a life!

Practice OCN Questions!A patient with lymphoma reports numbness in the feet, weakness when ambulating and dribbling urine. The nurse suspects:

A.Type 1 diabetes B.Spinal cord compression C.Peripheral neuropathy D.Hormonal disruption

Practice OCN Questions!A patient with lymphoma reports numbness in the feet, weakness when ambulating and dribbling urine. The nurse suspects:

A.Type 1 diabetes B.Spinal cord compression C.Peripheral neuropathy D.Hormonal disruption

Practice OCN Questions!Initial treatment of a patient in early septic shock includes the administration of:

A.Vasopressors B.IV antibiotics C.IV antifungals D.High-dose corticosteroids

Practice OCN Questions!Initial treatment of a patient in early septic shock includes the administration of:

A.Vasopressors B.IV antibiotics C.IV antifungals D.High-dose corticosteroids

Practice OCN Questions!A patient with acute lymphoid leukemia experiences hyperkalemia, hyperphosphatemia, and hypocalcemia within a week of initiating chemotherapy. These symptoms are most likely indicative of:

A.Disseminated intravascular coagulation B.Syndrome of inappropriate antidiuretic

hormone C.Septic shock D.Tumor lysis syndrome

Practice OCN Questions!A patient with acute lymphoid leukemia experiences hyperkalemia, hyperphosphatemia, and hypocalcemia within a week of initiating chemotherapy. These symptoms are most likely indicative of:

A.Disseminated intravascular coagulation B.Syndrome of inappropriate antidiuretic

hormone C.Septic shock D.Tumor lysis syndrome

Practice OCN Questions!A patient with small cell lung cancer has a four-pound weight gain, headache, and excessive thirst. These symptoms indicate:

A.Tumor lysis syndrome B.Hemolytic uremic syndrome C.Neoplastic cardiac tamponade D.Syndrome of inappropriate

antidiuretic hormone

Practice OCN Questions!A patient with a history of ovarian cancer reports being bloated and feeling full and vomiting after eating small amounts of food. The patient has noticed a 10-pound weight gain over the last week and states she is leaving less. The nurse instructs the patient to:

A.Come to the clinic B.Call if her ankles swell C.Eat small, frequent meals D.Report any further weight gain

Practice OCN Questions!A patient with a history of ovarian cancer reports being bloated and feeling full and vomiting after eating small amounts of food. The patient has noticed a 10-pound weight gain over the last week and states she is leaving less. The nurse instructs the patient to:

A.Come to the clinic B.Call if her ankles swell C.Eat small, frequent meals D.Report any further weight gain

Practice OCN Questions!A patient scheduled for chemotherapy complains of shortness of breath, fatigue, and facial swelling. Physical assessment reveals neck vein distention, edema of the hands, tachycardia, and cyanosis. The nurse calls the physician and instructs the patient to:

A.Sit up and anticipates and order for a chest x-ray B.Lie flat and prepares the patient for an

echocardiogram C.Lie flat and prepares the patient for a

thoracostomy D.Sit up and begins the chemotherapy infusion

Practice OCN Questions!A patient scheduled for chemotherapy complains of shortness of breath, fatigue, and facial swelling. Physical assessment reveals neck vein distention, edema of the hands, tachycardia, and cyanosis. The nurse calls the physician and instructs the patient to:

A.Sit up and anticipates and order for a chest x-ray

B.Lie flat and prepares the patient for an echocardiogram

C.Lie flat and prepares the patient for a thoracostomy

D.Sit up and begins the chemotherapy infusion

ReferencesBrashers, 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). 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 Curriculum for Oncology Nursing (5th ed., pp. 478-494). St. Louis, MO: Elsevier.

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.

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