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Oncologic Emergencies

Juanita Madison, RN, MN, AOCN

Franciscan Health System


Life-threatening medical emergencies caused by:

Malignancy

Treatment of malignancy

When do they occur?

Initial manifestations of malignancy

or

Late in disease process


Metabolic Oncologic Emergencies Tumor Lysis Syndrome (TLS)

Sepsis & Septic Shock

Disseminated Intravascular Coagulation (DIC)

Hypercalcemia

Inappropriate Antidiuretic Hormone Secretion (SIADH)

Anaphylaxis

Structural Oncologic Emergencies Spinal Cord Compression

Superior Vena Cava Syndrome

Increased Intracranial Pressure (ICP)

Cardiac Tamponade

Tumor Lysis Syndrome (TLS)

Metabolic imbalance

Caused by breakdown of malignant cells (spontaneous, or induced by chemotherapy, biotherapy, or radiation therapy)

Large number of rapidly proliferating cells killed

Cell lysis, rupture of tumor cell membranes

Intracellular components released into blood

stream

Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing

oncologic emergencies: A resource for nurses .Oncology Nursing Society, Pittsburgh, PA. pp: 433-459.

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TLS: Pathophysiology

Intracellular components Potassium

Phosphorous

Nucleic acids (DNA, RNA)

Cell killed (lysed), cell membrane ruptures

Nucleic acids released into blood stream

Potassium & Phosphorous released into blood stream

Results in: Hyperuricemia

Hyperkalemia

Hyperphosphatemia

Hypocalcemia

K+

PO4- PO4

-

Nucleic Acids

K+ K+

K+ PO4-

K+

Nucleic

Acids

Hypoxanthine

Xanthine

Uric Acid

Urine

PO4- K+ K+ PO4

- PO4-

Ca++ Ca++ Ca++ Xanthine

Oxidase

(Liver)

Tumor Lysis Syndrome: Who’s At Risk?

Most common in: Patients with large tumor burden that is highly responsive to antineoplastic therapy (resulting in rapid cell kill)

Risk Factors: Tumor-related

High-grade lymphomas

Hematologic malignancies (acute or chronic leukemia's with WBC)

Tumors with high growth fractions (anticipated to be responsive to treatment)

Patient-related Large tumor burden/bulky tumors

Elevated LDH

Pre-existing renal dysfunction

Treatment-related Chemotherapy & biologic agents

Radiation therapy

Tumor Lysis Syndrome: Onset, Duration, Incidence

Onset:

Usually within 24-48 hrs after initiation of antineoplastic therapy

Duration:

May persist for 5-7 days post-therapy

Incidence:

Exact incidence unknown

Occurs mostly in patients with

Hematologic malignancies with large proliferative growth fractions

Large bulky disease (acute leukemia's, high-grade lymphomas)

Clinical Manifestations Often asymptomatic initially

Detected initial via abnormalities in blood chemistries

Signs & symptoms patients exhibit depend on extent of metabolic abnormalities

Hyperkalemia

Hyperuricemia

Hyperphosphatemia

Hypocalcemia

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TLS: Signs & Symptoms Hyperkalemia Serum K+ >6.5 mEq/L

Early cardiac:

• Tachycardia

• EKG Changes: Prolonged QT and ST segment, lowering and inversion of T wave

Late cardiac:

• Bradycardia

• EKG Changes: Shortened QT, elevated T wave, wide QRS

• Ventricular tachycardia, ventricular fibrillation, cardiac arrest

• Nausea/vomiting

• Diarrhea

• Increased bowel sounds

• Twitching

• Muscle cramps

• Weakness

• Paresthesias

• Lethargy

• Syncope

Hyperuricemia Serum uric acid >10 mg/dl

Severe = >20 mg/dl

• Oliguria, anuria, azotemia

• Edema, hypertension

• Acute renal failure

• Chronic renal failure

• Malaise, weakness, fatigue

• Nausea, vomiting

• Flank pain, gout

• Pruritus

Gobel, B. H. (2013). In M. Kaplan (Ed.), Understanding an managing oncologic emergencies: A resource for nurses

2nd Edition (pp. 433 - 459). Pittsburgh, PA: ONS

TLS: Signs & Symptoms Hyperphosphatemia Serum PO4 >5 mg/dl

• Anuria

• Oliguria

• Azotemia

• Edema

• Hypertension

• Acute renal failure

Secondary

Hypocalcemia Serum Ca++ < 8.7 mg/dl

Neurological/Neuromuscular

•Twitching, paresthesias

• Restlessness

• Muscle cramps & weakness

• Anxiety, depression

• Carpopedal spasms

• Seizures

• Confusion

• Hallucinations

Cardiac

• Tetany

• Ventricular arrhythmias

• Prolonged QT interval, inverted T wave

• Heart block

• Cardiac arrest

Gobel, B. H. (2013). In M. Kaplan (Ed.), Understanding an managing oncologic emergencies: A resource for nurses

2nd Edition (pp. 433 - 459). Pittsburgh, PA: ONS

Prevention TLS

Hydration IV Normal saline or 5% dextrose

Begin 24 – 48 hours prior to therapy

Ensure urine output >150 – 200 ml/hr

Diuresis If urine output no maintained by hydration alone

Loop diuretics or osmotic diuretics

Holmes Gobel, B. (2013). Tumor Lysis Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic emergencies:

A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459; McGraw, B. (2008). CJON 12 (4); 563-565.

Prevention TLS

Allopurinol (Oral or IV) Begin 24 hour prior to therapy

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

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

Rasburicase IV Converts uric acid into allantoin → very soluble compound, excreted by kidneys



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Prevention TLS

Urinary Alkalinization Sodium bicarbonate added to IV fluid (50-100 meq/liter)

Goal: urine pH level > 7.0

Use is controversial Potential complications associated with alkalinization

Metabolic alkalosis

Calcium phosphate precipitation



TLS Preventative Measures

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



Mr. J.: 63 Year-Old Male

diagnosed with High-Grade NHL

Past Medical History: Noninsulin-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

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?

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Treatment of TLS 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 retention 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


A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 433-459.

Treatment of TLS

Hyperphosphatemia • Phosphate-binding agents

• Aluminum-containing antacids

• Hypertonic glucose plus insulin

• Aggressive hydration

Hypocalcemia • Appropriate management of hyperphosphatemia

• IV calcium gluconate or calcium chloride to treat arrhythmias



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


Na++137 mmol/l

K+ 6.5 mmol/l

BUN 100


Uric acid 25 mg/dl

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: 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



.

Mr. J. was treated with: 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

Sepsis & 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

Continuum Septic Shock:

Infection Septicemia Sepsis Septic Shock

Incidence and Mortality

Incidence in cancer patients

Bacteremia or sepsis: 10-20% of patients with febrile neutropenia

Hematologic Malignancies have higher incidence than solid tumors

Hematologic malignancies: 66.4 per 1,000 hospitalized patients

Solid tumors: 7.6 per 1,000 hospitalized patients

Mortality in cancer patients

Approximately 28%, same mortality rates for hematologic malignancies & solid tumors

Courtney, et al (2007). Oncologist, 12, 1019-1026; Shelton, B.K. (2011), in Yarbro et al (eds), Cancer Nursing: Principles and Practice

(7th ed., pp 713-744). Jones & Bartlett.; Williams, et al (2004).Critical Care 8, 291-298.

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Septic Shock: Pathophysiology Micro-organisms in blood stream release chemical mediators & hormones

Endotoxins – released by gram negative bacteria

Exotoxins – released by gram positive bacteria

Profound systemic vasodilation Hypotension

Tachycardia

Increased vascular permeability Fluid leaks from vascular space to interstitial space

Decreases circulating blood volume

Hypoxic tissues

Metabolic acidosis

Holmes Gobel, et al (2013). Sepsis & septic shock. In Kaplan, M (Ed). Understanding and managing oncologic emergencies:


Causes of Sepsis

Bacterial organisms (most common cause of sepsis) Gram-negative bacteria (responsible for 50-60% cases of septic shock)

Escherichia coli Klebsiella pneumoniae Pseudomonas aeruginosa

Gram-positive bacteria (increased incidence due to use of vascular access devices)

Streptococcus pneumoniae Staphylococcus aureus Corynebavcterium

Other organisms Invasive fungal infections, viruses

Lewis, et al (2011). CA: A Cancer Journal for Clinicians, 61, 287-314.

Clinical Presentation: Septic Shock

Early Phase Hyperdynamic Phase (Warm)

Hypodynamic Phase (Cold)

• Normal or elevated

temperature

• Chills

• Warm, flushed skin

• Anorexia

• Normal or low BP


temperature

• Chills and rigors

• Changes in LOC

(anxiety, restlessness,

confusion)

• Tachycardia, bounding

pulses, widening pulse

pressure

• Decreased urine output

• Subnormal temperature

• Pale, cool, and clammy

skin

• Disorientation, lethargy

• Tachycardia

• Weak, thready pulse

• Hypotension

• Anuria



Mr. J.: Seven days post-3rd cycle chemotherapy (CHOP-R)

Wife calls outpatient clinic at 5 pm on Friday and reports husband has:

Fever

Dry cough

Discomfort with swallowing

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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

Dual-lumen Groshong® central venous catheter exit site without redness or drainage; however, c/o slight tenderness to area above catheter exit site

O2 sat 98% room air

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

Diagnostic Evaluation

CBC with differential Complete metabolic panel Serum lactate Blood cultures X 2 Cultures of body fluids

Urine, stool, throat, wounds, sputum

Chest X-Ray



Treatment of Sepsis/Septic Shock:

Immediate initiation IV antibiotics (within 1 hour of fever onset) Fluid resuscitation

Goals: CVP: 8-12 mmHg MAP: > 65 mmHg Urine output: > 0.5 mg/kg/hr



Treatment of Sepsis/Septic Shock

Mean arterial pressure (MAP) < 65 Vasopressor and inotropic drugs

Norepinephrine, dopamine (first line)

Phenylephrine, dobutamine, etc (second line)

Oxygen therapy

Antipyretics



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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 unit

Neutropenic precautions

Mr. J’s Labs in ER:

• WBC 1,100/mm3

• ANC 450/mm3

• Hgb 10 g/dl

• Plt 30,000/mm3

• Glucose 201 mg/dl

• Na++ 134 mEq/l

• K+ 3.3 mEq/l

• BUN 12 mg/dl

• Creatinine 0.9 mg/dl

Nursing Assessment on Admission to Inpatient Unit: 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





temperature

• Chills


• Anorexia



temperature


• Changes in LOC


confusion)



pressure




skin


• Tachycardia


• Hypotension

• Anuria



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Nursing Management Sepsis

Frequent vital signs & assessments

LOC, skin color & temp, lungs

Maintain oxygenation

Oxygen therapy & ventilatory support

Administer IV fluids,

Expand intravascular volume (fluid resuscitation)

Monitor I & O

Antipyretics

Assess for fluid overload

Mr. J: Nursing Assessment 9:45 pm

Disoriented, lethargic

Skin pale, cool

↓ 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





temperature

• Chills


• Anorexia



temperature


• Changes in LOC


confusion)



pressure




skin


• Tachycardia


• Hypotension

• Anuria



Nursing Interventions

Neutropenic patients with fever Must be assessed immediately

Started on broad spectrum antibiotics

Monitor for sequelae of septic shock Frequent vital signs

Assess tissue perfusion (skin color, temperature, capillary refill)

Lung assessments

I & O – report urine output < 30cc/hr

Monitor for symptoms of DIC

Monitor response to medical treatment Assess for fluid overload

Monitor lab values, especially renal function & culture reports

Infection control measures



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Possible Complications of Sepsis/Septic Shock

DIC

Multiple organ dysfunction syndrome

Death

Disseminated Intravascular Coagulation (DIC)

Syndrome of:

Thrombus formation (clotting)

Simultaneous Hemorrhage

Caused by over stimulation of normal coagulation processes

Kaplan, M. (2013). Disseminated Intravascular Coagulation. In Kaplan, M (Ed). Understanding and managing oncologic

emergencies: A resource for nurses, 2nd ED. ONS, Pittsburgh, PA. pp: 69 – 102.

Pathophysiology DIC

Paradox of DIC: bleeding & clotting

Triggered by: Intrinsic coagulation system activation (damage to blood vessels)

Transfusion reactions

Endotoxins/Septicemia

Sickle Cell Disease

Malignant hypothermia

Extrinsic coagulation system activation (tissue injury) Obstetrical Conditions

Extensive surgery

Crush injuries

Malignancies



DIC in the Oncology Population:

Malignancy Induced

Acute Promyelocytic Leukemia (APL)

Procoagulant material release by granules of the immature promyelocyte initiates clotting cascade

Occurs in 85% patients with APL

Solid Tumors (adenocarcinomas)

Lung, pancreas, prostate, stomach, colon, ovary, gall bladder, breast, kidney



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Other Causes DIC (Oncology Population)

Chemotherapy May induce DIC by damaging tumor, normal cells, or endothelium causes release procoagulant material

Large tumor burden/large cell kill release granule procoagulant from dead cells into systemic circulation

Infection/sepsis Especially gram negative bacteria sepsis (release of endotoxin)

Hemolytic transfusion reactions Rupture of RBC’s platelet aggregation, release platelet factors that initiate clotting cascade



UNDERLYING

DISEASE OR

CONDITION

STIMULATION OF

COAGULATION

CASCADE

WIDESPREAD FIBRIN

CLOT FORMATION

ACTIVATION OF

FIBRINOLYSIS

MICROTHROMBI

DEPOSITS

THROUGHOUT

MICROCIRCULATION

CONSUMPTION OF:

PLATELETS

FIBRINOGEN

PROTHROMBIN

PRODUCTION OF:

FIBRIN SPLIT

PRODUCTS

tPA

ISCHEMIC TISSUE

DAMAGE

SYMPTOMS OF ORGAN

DYSFUNCTION

BLEEDING

Pathophysiology of DIC

Types of DIC

Acute DIC

Medical emergency

Chronic DIC

Produces coagulation abnormalities, with or without clinical manifestations, that can be medically managed

Most cases of chronic DIC due to underlying malignancy

Laboratory Values in DIC Laboratory Test Result Comments or Cause

Prothrombin Time (PT) Prolonged Nonspecific in DIC

Activated Partial Thromboplastin time (APPT)

Prolonged Nonspecific in DIC

International normalized ratio (INR)

Prolonged Nonspecific in DIC

Fibrin Degradation Products Elevated Indicates breakdown of fibrin & fibrinogen

D-Dimer Elevated Indicates hyperfibrinolysis

Platelet Count Decreased Platelets consumed

Fibrinogen Decreased Fibrinolysis; decreases very slowly only in severe DIC

Antithrombin Decreased Anticoagulant activity inhibited Accelerated coagulation



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DIC Clinical Presentation

Decreased tissue/organ perfusion Brain, CV, Lungs, Kidney, GI Tract, Skin

Decreased platelet count Petechiae, ecchymosis

Hemorrhage Tachycardia, hypotension

Tachypnea

Overt bleeding

Occult bleeding



Mr. J: Nursing Assessment 9:45 pm

Disoriented, lethargic

Skin pale, cool

↓ 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

Mr. J’s Labs at 10:00 pm

Lab 7:30 pm 10:00 pm Normal

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 sec 11.3 – 13.1 sec

Fibrin Degradation Products

60 mcg/ml <10 mcg/mL

Treatment of DIC

Early recognition & treatment of underlying disorder

Chemotherapy for malignancy

Antibiotics for infection

Correct hypoxia

Oxygen to maintain saturation >95%

Correct hypovolemia, hypotension, & acidosis

NS until type & cross match completed & blood available



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Treatment of DIC Stop the micro clotting to maintain perfusion & protect vital function

IV Heparin

Antithrombin III (inhibits action of thrombin)

Stop the bleeding

Pressure to active sites of bleeding

Blood products (FFP, cryoprecipitate, platelets, red blood cells)

Antifibrinolytic agents (EACA)




Prevent severity of symptoms

Direct pressure sites of bleeding, pressure dressings, sand bags

Monitor for progression DIC

Worsening vital signs, hypotension, anuria, ’s LOC

Monitor response to therapy

Sites & amounts of bleeding

Changes in lab values

Assess tissue perfusion parameters – color, temperature, peripheral pulses

Patient Teaching

Avoid ASA or NSAID’s (effects on platelet aggregation)

Signs and symptoms of DIC (bleeding and/or clotting)



Hypercalcemia of Malignancy (HCM)

Metabolic disorder, in cancer patients, results from increased bone resorption

Serum calcium level >12-14 mg/dl (normal serum calcium 9-11 mg/dl)

Kaplan, M. (2013) Hypercalcemia of malignancy. In Kaplan, M (Ed). Understanding and managing oncologic


Normal Physiology

Normal levels Ca++ regulated by: Parathyroid gland (production of parathyroid hormone)

GI tract (absorption of Vitamin D)

Kidneys (excretion)

Ca++ levels below normal: Parathyroid stimulated to produce parathyroid hormone

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

Ca++ levels above normal: Kidneys excretion of calcium



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HCM: Etiology Tumor-induced bone breakdown releasing Ca++ into bloodstream

Solid tumors of squamous cell origin – potential to produce parathyroid hormone-related protein that stimulates Ca++

release from bone Lung, breast, prostate, head & neck, esophagus, kidney

Decreased ability of kidneys to clear calcium from the blood



Incidence of Hypercalcemia of Malignancy

Occurs in approximately 30% of cancer patients

Most often in advanced stages of disease

50% of patients die within 30 days of

diagnosis

Survival beyond 6 months is rare



Incidence of Hypercalcemia of Malignancy

Malignancy Incidence of Hypercalcemia

Incidence of Bone Metastasis

Breast cancer with metastasis 30% - 40% 65% - 75%

Multiple myeloma 20% - 40% 70% - 90%

Squamous cell carcinoma of lung 12.5% - 35% 30% - 40%

Squamous cell carcinoma of head & neck

2.9% - 25% Uncommon

Renal cell carcinoma 3% - 17% 20% - 25%

Non-Hodgkin’s Lymphoma 14% - 33% Rare

T-Cell Lymphoma 50% Rare



Hypercalcemia: Clinical Presentation

Clinical signs & symptoms related to rapidity of onset & serum calcium level

Corrected total serum calcium (TSC) needs to be calculated if albumin is low

Corrected Serum Calcium (mg/dl)=

Measured serum Ca++ + (4.0 – serum albumin g/dl) X 0.8

**Normal Serum Ca++ = 8.5 – 10.5 ml/dl

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Signs and Symptoms of Hypercalcemia of Malignancy

System Early Late

Neurologic Drowsiness, lethargy, weakness, restlessness, irritability, confusion, cognitive dysfunction, disorientation

Seizures Stupor Coma

Renal Polyuria, polydipsia, nocturia, dehydration, kidney stones, renal insufficiency

Renal failure

GI Anorexia, nausea, vomiting, constipation, vague abdominal pain, weight loss, peptic ulcers

Atonic ileus Obstipation

Cardiovascular EKG changes (slowed conduction, Prolonged PR, wide QRS, short QT, short ST), sinus bradycardia

Heart block Cardiac arrest

Musculoskeletal Muscle weakness, fatigue, hypotonia, bone pain

Ataxia Pathologic fractures



Hypercalcemia: Treatment

Depends on serum calcium level & patient symptoms:

Ca++ <12 ml/dl & asymptomatic

observe carefully & treat as outpatient

Ca++ 12-15 ml/dl & asymptomatic

requires specific but non-urgent treatment

Ca++ >15 ml/dl & symptomatic

requires emergent treatment

Hypercalcemia: Treatment

Treat the cancer – tumor control or reduction is the only long-term measure for reversing hypercalcemia

Hydration & forced diuresis Oral fluids (3-4 L/day)

IV Saline Initial: NS 100-300 ml/hr

Maintenance: 2.5 – 5L/day

Loop diuretics (furosemide)

Mobilization



Agents to Inhibit Bone Resorption

Agent Mechanism of Action Dosing

Bisphosphonates

• Pamidronate (Aredia) • Inhibits osteoclast activity

IV: 60-90 mg over 2 hrs May repeat after 7 days

• Zoledronate (Zometa) • Inhibits osteoclast activity

IV: 4 mg over 15 minutes May repeat after 7 days

Calcitonin • Direct inhibition of osteoclast receptors

• Increases renal calcium excretion

SC or IM: 4-8 IU/kg every 6-12 hours for 2 days

Gallium nitrate (Ganite) • Used when HCM resistant to bisphosphonates

• Inhibits osteoclast activity

IV: 200 mg/m2/day continuous for 5 days



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Hypercalcemia Treatment Dietary recommendations

Maintain salt intake

Dietary calcium restrictions not necessary

Medications to avoid

Thiazide diuretics

NSAIDS, H2 receptor antagonists

Vitamins A & D

Parenteral/enteral solutions with calcium

Corticosteroids

Therapy of choice multiple myeloma or lymphomas

Inhibits vitamin D conversion to calcitriol




Recognize early signs & symptoms

Careful monitoring of patients taking: Thiazide diuretics (inhibits calcium excretion)

Digitalis preparations (action potentiated in hypercalcemic states)

Measures to decrease calcium removal from bone: Ambulation, weight bearing, ROM, isometric exercises

Careful assessment & monitoring Fluid balance & renal function

GI motility

Cardiac Status

Mental status



Mr. C: Hypercalcemia

62-year-old male 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)

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Mr. C’s Labs: 2nd Cycle Chemotherapy

WBC 4,500/mm3

Hgb 11.2 g/dl

Hct 35%


Serum Ca++ 10.4


BUN 19 mg/dl

Albumin 2.3 g/dl

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

Lab Test 2nd Chemo Visit 3rd Chemo Visit

WBC 4,500/mm3 2,200/mm3

Hgb 11.2 d/dl 10.4 g/dl

Hct 35% 29%

Platelet count 119,000/mm3 102,000 mm/3

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)

The best immediate treatment to correct Mr. C’s calcium & symptoms is:

a. Hydration & Bisphosphonate (anti-Resorptive therapy) infusion

b. Chemotherapy administration & corticosteroids

c. Growth factor to improve fatigue and minimize myelosuppression

d. Hydration & observation

The best immediate treatment to correct Mr. C’s calcium & symptoms is:

a. Hydration & Bisphosphonate (anti-Resorptive therapy) infusion

b. Chemotherapy administration & corticosteroids

c. Growth factor to improve fatigue and minimize myelosuppression

d. Hydration & observation

Structural Oncologic Emergencies

Spinal Cord Compression

Superior Vena Cava Syndrome (SVCS)

Increased Intracranial Pressure (ICP)

Cardiac Tamponade

Kaplan, M. (2013). Spinal Cord Compression. In Kaplan, M (Ed). Understanding and managing oncologic


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Spinal Cord Compression

Compression of spinal cord Direct tumor pressure on cord

Tumor invasion of the vertebral column causing collapse & pressure on cord

Compression causes: Edema

Inflammation

Mechanical compression

Leads to: Direct neural injury to cord

Vascular Damage



Incidence Occurs in approximately 5-14% of general cancer population

Highest incidence in solid tumors that metastasize via hematogenous routes to bone in the spine

Most common: Breast

Lung

Prostate

Lymphoma



Cancers Associated with Risk of Spinal Cord Compression Frequency Cancer Type

Most Common • Breast (15% - 20%) • Lung (15% - 20%) • Prostate (15% - 20%) • Multiple Myeloma (10% - 15%) • Unknown primary (10%) • Renal cell carcinoma (5% - 10%) • Non-Hodgkin lymphoma 5% - 10%) • Hodgkin disease (5%)

Less Common • GI malignancies • Soft Tissue sarcoma • Thyroid cancer • Neuroblastoma

Uncommon • Melanoma • Uterine, cervical, bladder cancers • Leukemia

Rare • Head and neck cancer, brain, pancreatic, liver, ovarian, testicular, esophageal cancer

Clinical Presentation: Back Pain

Most common presenting symptom

Occurs in 90% of patients

Precedes other signs and symptoms (e.g. neurological) by weeks to months

Median time from onset to pain to diagnosis of spinal cord compression: 2 months



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Back Pain Associated with Spinal Cord Compression

Can occur at any level of the spine

Can take several forms: Local (near the site of compression)

Radicular (distributed along dermatones)

Referred (in a non-radicular distribution)

May be a combination of all 3 types



Progression of Symptoms

Time Frame

Early

Late

Signs & Symptoms

• Pain

• Motor weakness or gait changes

• Sensory Loss

• Numbness, tingling, sensory changes

• Autonomic Dysfunction

• Constipation and/or bladder retention

• Bowel and/or bladder incontinence

• Paralysis



Diagnostic Tests

MRI Gold standard for diagnosis

Accurate, sensitive, and specific diagnostic tool for spinal cord compression

Other Diagnostic Tests Spinal x-rays

CT scan

Myelography – reserved for patient’s who can’t undergo MRI

Bone Scan and/or PET Scan



Treatment of Spinal Cord Compression

IMMEDIATE & aggressive

Corticosteroids – initial supportive treatment

High-dose steroids to spinal cord edema & inflammation

High-dose loading with Dexamethasone (up to 100 mg IV loading dose) followed by tapering doses over several days

Radiation therapy (radiosensitive tumors)

In general, a course of radiation with a total of 30 Gy in 10 fractions



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Treatment of Spinal Cord Compression

Surgery Laminectomy (no longer typically used)

Anterior vertebral body resection with stabilization

Vertebroplasty

Kyphoplasty

Chemotherapy Rarely used in acute management

Response to treatment slow & unpredictable

Bisphosphonates Can effectively reduce pain and other skeletal complications of vertebral metastasis




Early recognition Thorough assessment of neck & back pain in high risk patients

Neurological assessments Mental status Cranial nerves Motor & sensory system Reflexes

Pain Management Mobility and safety issues Skin care Bowel and Bladder function Rehabilitation & palliative care



Superior Vena Cava Syndrome

Obstruction of superior vena cava that impairs venous drainage (above the obstruction)

Obstruction venous return from head, neck, upper arms, upper thorax impaired

Venous pressure increases

Cardiac output decreases

Shelton, B. K. (2013). Superior Vena Cava Syndrome. In Kaplan, M (Ed). Understanding and managing oncologic


Incidence Occurs in 3 – 4% of Oncology Population

Malignant conditions: Majority of cases (70% - 95%) related to underlying malignancy

Most common: Small cell & non-small cell lung cancers

Non-Hodgkin lymphoma (high-grade)

Less common: Esophageal cancer

Thyroid cancer

Breast cancer, thymoma, mesothelioma, leukemia

Non-Malignant conditions: Intraluminal thrombus formation

Mediastinal fibrosis or benign mass



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Clinical Presentation

Gradual onset (rarely occurs rapidly)

Symptoms vary depending on extent of obstruction, location, collateral circulation



Early/Common Physical Signs & Symptoms

Dyspnea

Facial and neck swelling (occurs when supine, subside after arising)

Sensation of fullness in head

Cough

Arm Swelling

Chest pain

Venous distention of neck & chest wall

Cyanosis



Late Physical Signs & Symptoms

Cyanosis of face & upper torso

Decreased or absent peripheral pulses

CHF

Decreased BP

Chest pain

Mental status changes

Tachypnea

Tachycardia

Engorged conjunctivae

Visual disturbances

Syncope

Hoarseness

Stridor



Diagnostic Evaluation Chest X-ray

MRI

Contrast-enhanced CT

Tissue diagnosis

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Treatment SVCS

Based on etiology, severity of symptoms

Relieve obstruction & control underlying disease

Radiation therapy Gold standard for non-small cell lung cancer

Chemotherapy Primary treatment for chemo-sensitive malignancies

Small cell lung cancer

Non-Hodgkin Lymphoma

Surgical Intervention Stent placement or SVC bypass

Chronic or recurrent SVCS

Thrombolytic therapy SVCS caused by intraluminal thrombus)



Nursing Interventions Assess for signs & symptoms in patients at risk

Non-small cell lung cancer, small cell lung cancer, non-Hodkin lymphoma

Central venous catheter access devices

Interventions to relieve symptoms

Elevate HOB, avoid supine position & elevation of lower extremities

Avoid venipuncture, BP, IV therapy upper extremities

Monitoring response to treatment Assess for progressive respiratory distress or edema

Monitor tolerance of activities

Monitor fluid status(over hydration exacerbates symptoms)

Assess CNS (LOC, mental status change, visual changes, headache)



Sepsis is a common cause of disseminated intravascular coagulation (DIC). Which of the following conditions most accurately describes how sepsis causes DIC?

a. Sepsis causes viruses to thrive, and viruses cause DIC

b. Endotoxins released from bacteria activate the coagulation cascade

c. Sepsis and bleeding occur simultaneously in patients who are immunosuppressed

d. Antiangiogenesis factors are released during periods of sepsis, which leads to DIC

Which of the these statements is not true in regards to hypercalcemia in malignancy?

a. It is a rare complication

b. Early manifestations of the syndrome are insidious including fatigue, muscle weakness, and depression and easily overlooked as manifestations of the disease.

c. Bisphosphonates are frequently used in the treatment of malignancy induced hypercalcemia because of their ability to interfere with osteoclastic activity

d. A complication of malignancy induced hypercalcemia include decreased GFR and acute kidney failure, neuropsychiatric disturbances, and cardiovascular complications.

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