Oncological emergencies

1. Mr. Binu Babu
Asst. Professor
Mrs. Jincy Ealias
Asst. Professor

2. Metabolic Oncologic
Emergencies
Structural Oncologic
Emergencies
 Tumor Lysis Syndrome
(TLS)
 Sepsis & Septic Shock
 Disseminated
Intravascular Coagulation
(DIC)
 Hypercalcemia
 Syndrome of
Inappropriate Antidiuretic
Hormone Secretion
(SIADH)
 Spinal Cord Compression
 Superior Vena Cava
Syndrome
 Cardiac Tamponade

3.  Metabolic imbalance
 Caused by breakdown of malignant cells
 Large number of rapidly proliferating cells killed
 Cell lysis, rupture of tumor cell membranes
 Intracellular components released into blood stream

4.  Intracellular components
◦ Potassium
◦ Phosphorous
◦ Nucleic acids (DNA, RNA)
 Cell killed (lysed), cell membrane ruptures
◦ Nucleic acids released into blood stream
◦ Potassium & Phosphorous released into blood stream
Results in:
◦ Hyperuricemia
◦ Hyperkalemia
◦ Hyperphosphatemia
◦ Hypocalcemia

5. Most common in: Patients with large tumor burden that is highly responsive
to antineoplastic therapy (resulting in rapid cell kill)
Risk Factors
 Tumor-related
 High-grade lymphomas
 Risk for Hematologic malignancies (acute or chronic leukemia's with
increase WBC)
 Risk for Tumors with high growth fractions (anticipated to be responsive
to treatment)
Patient-related
 Large tumor burden/bulky tumors
 Elevated LDH
 Pre-existing renal dysfunction
Treatment-related
 Chemotherapy & biologic agents
 Radiation therapy

6.  Onset: Usually within 12-72 hrs. after initiation of
antineoplastic therapy
 Duration: May persist for 5-7 days post-therapy
 Incidence: Exact incidence unknown, Occurs mostly
in patients with
◦ Hematologic malignancies with large proliferative growth
fractions
◦ Large bulky disease (acute leukemias, high-grade
lymphomas)

7.  Often asymptomatic initially
 Detected initial via abnormalities in blood
chemistries
 Signs & symptoms patients exhibit depend on extent
of metabolic abnormalities
◦ Hyperkalemia
◦ Hyperuricemia
◦ Hyperphosphatemia
◦ Hypocalcemia

8. Condition Signs & Symptoms Treatment
Hyperkalemia
Serum K + >6.5
mEq/L
Early cardiac:
• Tachycardia
• EKG Changes: Prolonged QT and ST
segment, lowering and inversion of T
wave Late cardiac:
• Bradycardia
• EKG Changes: Shortened QT,
elevated T wave, wide QRS
• Ventricular tachycardia, ventricular
fibrillation, cardiac arrest
• Nausea/vomiting
• Diarrhea
• Increased bowel sounds
• Twitching
• Muscle cramps
• Weakness
• Paresthesias
• Lethargy
• Syncope
Mild (Potassium6.5
mEq/L or cardiac
changes:
• IV calcium gluconate
or calcium carbonate
• IV sodium
bicarbonate, hypertonic
glucose & insulin
accompanied by sodium
polystyrene sulfonate
• Loop diuretics &
aggressive hydration

9. Condition Signs & Symptoms Treatment
Hyperuricemia Serum
uric acid >10 mg/dl
Severe = >20 mg/dl
• Oliguria, anuria, azotemia
• Edema, hypertension
• Acute renal failure
• Chronic renal failure
• Malaise, weakness, fatigue
• Nausea, vomiting
• Flank pain, gout
• Pruritus
• Hydration, urinary
alkalinization
• Oral allopurinol or IV
allopurinol
• Rasburicase
• Hemodialysis for
significant renal
compromise
Hyperphosphatemia
Serum PO4 >5 mg/dl
• Anuria
• Oliguria
• Azotemia
• Edema
• Hypertension
• Acute renal failure
• Phosphate-binding
agents
• Aluminum-containing
antacids
• Hypertonic glucose plus
insulin
• Aggressive hydration

10. Condition Signs & Symptoms Treatment
Hypocalcemia
Serum Ca ++ < 8.7
mg/dl
Neurological/Neuromuscular
• Twitching, paresthesias
• Restlessness
• Muscle cramps & weakness
• Anxiety, depression
• Carpopedal spasms
• Seizures
• Confusion
• Hallucinations
Cardiac
• Tetany
• Ventricular arrhythmias
• Prolonged QT interval,
inverted T wave
• Heart block
• Cardiac arrest
• Appropriate
management of
hyperphosphatemia
• IV calcium gluconate
or calcium chloride to
treat arrhythmias

11. Prevention Strategies
 Recognition of at-risk patients
 Prevention of hyperuricemia
 Frequent monitoring of electrolytes
Intervention Strategies
 Hydration
◦ IV Normal saline or 5% dextrose, begin 24 – 48 hours prior to
therapy and ensure urine output >150 – 200 ml/hr
 Control of hyperuricemia
 Aggressive correction of electrolytes
 Management of acute renal failure

12.  Monitor 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

13.  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

14.  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
SIRS Sepsis
Severe
Sepsis
Septic
Shock

15. Phase Definition
Infection/ bacteremia Presence of bacteria or fungi in blood as evidenced by
positive blood culture or positive catheter culture
Systemic
Inflammatory
Response Syndrome
(SIRS)
Indicated by presence of two or more of the following:
• Oral temperature >100.40F (380C) or 90 beats/minute
• RR>20/min or PaCO2 >32 mmHg
• WBC >12,000 cells/mm2 , 10% bands in peripheral
blood
Sepsis Documented infection with presence of two or more SIRS
criteria
Severe Sepsis Presence of sepsis with one or more of the following:
organ dysfunction, hypotension, or hypoperfusion
Septic Shock Presence of sepsis with hemodynamic instability that
persists despite aggressive fluid challenge
Multiple Organ
Dysfunction
Syndrome
Dysfunction of more than one organ; homeostasis must be
maintained with immediate intervention

16.  Neutropenia
◦ Single most important risk factor
◦ Increased duration and severity of neutropenia increases risk
 Treatment-related risk factors
◦ Chemotherapy
◦ Biotherapy
◦ Radiation
◦ therapy
◦ Infiltration of bone marrow by solid tumor
 Patient-related
◦ Disruption in mucosal barriers
◦ Splenectomy and functional asplenia
◦ Corticosteroids or other immunosuppressant's

17.  Micro-organisms 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

18.  Bacterial organisms (most common cause of
sepsis)
◦ Gram-negative bacteria (responsible for 50-60% cases of
septic shock)
 Escherichia coli
 Klebsiella pneumoniae
 Pseudomonas aeruginosa
◦ Gram-positive bacteria (increased incidence due to use of
vascular access devices)
 Streptococcus pneumoniae
 Staphylococcus aureus
 Corynebavcterium
 Other organisms
◦ Invasive fungal infections, viruses

19.  CBC with differential
 Complete metabolic panel
 Serum lactate
 Blood cultures X 2
 Cultures of body fluids
◦ Urine, stool, throat, wounds, sputum
 Chest X-Ray

20.  Immediate initiation IV antibiotics (within 3 hours)
 Fluid resuscitation
 Goals:
◦ MAP: > 65 mmHg
◦ CVP: 8-12 mmHg
◦ Urine output: > 0.5 mg/kg/hr
 Oxygen therapy
 Antipyretics

21.  Frequent vital signs & assessments
◦ LOC, skin color & temp, lungs
 Ensure antibiotics administered within 3 hours
 Maintain oxygenation
◦ Oxygen therapy & ventilator support
 Administer IV fluids,
◦ Expand intravascular volume (fluid resuscitation)
 Monitor I & O
 Antipyretics
 Assess for fluid overload

22.  Neutropenic 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

23.  Disseminated intravascular coagulation (DIC)
involves an abnormal activation of the clot
formation and fibrin mechanisms in the blood,
resulting in the consumption of coagulation factors
and platelets. Patients with DIC are at high risk for
thrombus formation, infarctions, and bleeding.
 Syndrome of:
◦ Thrombus formation (clotting)
◦ Simultaneous Hemorrhage
 Caused by over stimulation of normal coagulation
processes

24.  Paradox of DIC: bleeding and clotting
 Triggered by:
 Intrinsic coagulation system activation (damage to blood
vessels)
◦ Transfusion reactions
◦ Endotoxins/Septicemia
◦ Sickle Cell Disease
◦ Malignant hypothermia
 Extrinsic coagulation system activation (tissue injury)
◦ Obstetrical Conditions
◦ Extensive surgery
◦ Crush injuries
◦ Malignancies

25.  Acute Promyelocytic Leukemia (APL)
◦ Procoagulant material release by granules of the immature
promyelocyte leads to initiate clotting cascade
◦ Occurs in 85% patients with APL
 Solid Tumors (adenocarcinomas)
◦ Lung, pancreas, prostate, stomach, colon, ovary, gall bladder, breast,
kidney
 Chemotherapy
◦ May induce DIC by damaging tumor, normal cells, or endothelium to
causes release procoagulant material
◦ Large tumor burden/large cell kill may release granule procoagulant
from dead cells into systemic circulation
 Infection/sepsis
◦ Especially gram negative bacteria sepsis (release of endotoxin)
 Hemolytic transfusion reactions
◦ Rupture of RBC’s and platelet aggregation, release platelet factors that
initiate clotting cascade

26.  Acute DIC
◦ Medical emergency
 Chronic DIC
◦ Produces coagulation abnormalities, with or without
clinical manifestations, that can be medically managed
◦ Most cases of chronic DIC due to underlying malignancy

27. Prothrombin Time (PT) Prolonged
Activated Partial Thromboplastin time
(APPT)
Prolonged
International normalized ratio (INR) Prolonged
Fibrin Degradation Products Elevated
D-Dimer Elevated
Platelet Count Decreased
Fibrinogen Decreased
Antithrombin Decreased

28.  Decreased tissue/organ perfusion
◦ Brain, CV, Lungs, Kidney, GI Tract, Skin
 Decreased platelet count
◦ Petechiae, ecchymosis
 Hemorrhage
◦ Tachycardia, hypotension
◦ Tachypnea
◦ Overt bleeding
◦ Occult bleeding

29.  Early recognition & treatment of underlying
disorder
◦ Chemotherapy for malignancy
◦ Antibiotics for infection
 Correct hypoxia
◦ Oxygen to maintain saturation >95%
 Correct hypovolemia, hypotension and
acidosis
◦ Normal Saline
◦ Blood transfusion if needed

30.  Stop 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)

31.  Prevent severity of symptoms
◦ Direct pressure sites of bleeding, pressure dressings, sand
bags
 Monitor for progression DIC
◦ Worsening vital signs, hypotension, anuria and LOC
 Monitor response to therapy
◦ Sites & amounts of bleeding
◦ Changes in lab values
◦ Assess tissue perfusion parameters – color, temperature,
peripheral pulses
 Patient Teaching
◦ Avoid ASA or NSAID’s (effects on platelet aggregation)
◦ Signs and symptoms of DIC (bleeding and/or clotting)

32.  It is a metabolic disorder, most commonly develops
as a consequence of pathologic destruction of bone,
mediated by factors released by malignant cells
 One of the most common, life-threatening
complications of malignancy

33.  Parathyroid gland
◦ Production of parathyroid hormone (PTH)
◦ PTH is major hormone regulating extracellular Ca++
 PTH increases Ca++ by 3 mechanisms:
◦ Direct action on bone
 Stimulates activity of osteoclasts → breaks down bone
(bone resorption)
◦ Direct action on kidneys
 Increases renal excretion of phosphate stimulates
reabsorption of Ca++
◦ Indirect action in gut
 Enhances absorption of ingested Ca++ by stimulating
kidney conversion of vitamin D to biologically active form

34.  Ca++ levels decrease below normal:
◦ Parathyroid stimulated to produce PTH
◦ Acts on bone and release of calcium (bone
resorption) into circulation
◦ Acts on kidneys leads increase renal secretion of
phosphorous and stimulates reabsorption of
Ca++
◦ Acts indirectly gut and enhance absorption Ca++
 Ca++ levels increase above normal:
◦ Kidneys increase excretion of calcium

35.  Bone stores: 99% of body’s calcium
 Serum calcium: 1% circulates in serum,
divided into fractions:
◦ 50% is free ionized calcium
 Only type that is biologically active
◦ 40% is bound to protein
 Mostly albumin, but also globulin &
paraproteins
◦ 10% forms serum complexes with anions
 Bicarbonate, phosphate, & citrate

36.  Total calcium =
◦ Ionized calcium + protein-bound calcium
 Used to “infer” the fraction of ionized calcium
 The result is usually accurate, EXCEPT when serum
albumin is low
 If albumin < 3.5 – 5.5 g/dL, results in:
◦ ↓in the fraction of protein-bound calcium
◦ ↑ in the ionized free calcium
 Ionized calcium more accurately reflects true serum
calcium levels

37.  Tumor-induced bone breakdown releasing Ca++
into bloodstream
 Tumor secretion of a parathyroid hormone-related
protein (PTHrP)
◦ Squamous cell tumors: Lung, breast, prostate, head & neck,
esophagus, kidney
◦ Non-Hodgkin lymphoma, chronic myeloid leukemia (blast
phase), adult T-cell leukemia - lymphoma
 Tumor production of 1,25-dihydroxyvitamin D
(calcitrol)

38.  Corrected total serum calcium (TSC) needs to be
calculated if albumin is low
 Corrected Total Serum Calcium (mg/dl) = Measured
serum Ca++ + (4.0 – serum albumin g/dl) X 0.8
 **Normal Serum Ca++ = 8.5 – 10.5 ml/dl

39.  Reflect direct depressive effects ↑ serum Ca++
exerts on:
◦ Excitability of nerve tissue
◦ Contractility of cardiac, smooth, skeletal muscles
 Signs & symptoms:
◦ Lethargy, confusion
◦ Cardiac dysrhythmias
◦ Constipation
◦ Muscle hypotonia

40.  Treat 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
◦ Loop diuretics (furosemide)
 Mobilization
 Dietary recommendations
◦ Maintain salt intake
◦ Dietary calcium restrictions
not necessary
 Medications to avoid
◦ Thiazide diuretics (↓ renal
excretion Ca ++)
◦ NSAIDS, H2 receptor antagonists
(inhibit renal blood flow)
◦ Vitamins A & D (increase bone
resorption)
◦ Parenteral/enteral solutions with
calcium
 Corticosteroids
◦ Therapy of choice multiple
myeloma or lymphomas
 Inhibits vitamin D conversion to
calcitriol

41.  Recognize 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

42.  Syndrome of inappropriate antidiuretic hormone
(SIADH) is a paraneoplastic endocrine disorder
associated with several malignancies

43.  Pain
 Stress
 Nausea
 Surgery
 Pulmonary disease
 Central nervous system
disorders
 Physical and emotional
stress
 Pharmacological agents
◦ Chemotherapy drugs.
Syndrome of inappropriate
antidiuretic hormone is
caused by the ectopic
production of vasopressin by
malignant cells.
 Melanoma
 Gastrointestinal
 Gynecological
 Prostatic
 Hematological
 Neurological malignancies

44.  Hyponatremia with a serum sodium level of 121 to
134 mEq/L
 Headache
 Nausea
 Weakness,
 Anorexia,
 Fatigue
 Muscle cramps
 Seizures
 Coma

45.  Serum osmolality (< 275 mOsm/kg)
 Serum sodium (< 135 mEq/L)
 Urine osmolality (urine osmolality > serum
osmolality)
 Urinary sodium (> 30 mEq/L)
 Euvolemia
 Decreased levels of uric acid, blood urea nitrogen
 Absence of edema
 Normal renal, adrenal, and thyroid function

46.  Restrict fluids:
 (500–1000 mL/day)
 Review medications
 Discontinue potentially
offending drugs
 Perform neurologic
assessment
 Institute effective
anticancer treatment
 Monitor sodium levels
 Maintain admit outpatient
or based on onset and
activity
 Demeclocycline
 (600–1200 mg/day)
 Monitor renal function
with demeclocycline
therapy
 Assess other causes
 Institute seizure
precautions

47.  Admit to intensive care
 Hypertonic saline (3%)
 Limit sodium correction to 8–12 mEq/L in first 24
hours
 Intravenous furosemide or conivaptan
 Perform frequent neurologic examinations
 Maintain seizure precautions
 Monitor sodium levels every 1–3 hours

48.  Spinal Cord Compression
 Superior Vena Cava Syndrome (SVCS)
 Cardiac Tamponade

49. Spinal cord compression occurs when a
malignant growth compress the spinal cord. Patients at
risk include those with cancers that spread to the bone
and spinal cord, such as lung, breast, and prostate
cancer.
Symptoms
 Pain
 Motor dysfunction

50.  Compression 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

51.  Breast (15% - 20%)
 Lung (15% - 20%)
 Prostate (15% - 20%)
 Multiple Myeloma (10% - 15%)
 Unknown primary (10%)
 Renal cell carcinoma (5% - 10%)
 Non-Hodgkin lymphoma (5% - 10%)
 Hodgkin lymphoma (5%)

52. Time Frame
Early
Late
Signs & Symptoms
 Pain
 Motor weakness or gait
 changes
 Sensory Loss (numbness,
 tingling, sensory changes)
 Constipation and/or
bladder
 retention
 Bowel and/or bladder
 incontinence
 Paralysis

53.  MRI
◦ 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
 Histology of primary tumor

54. IMMEDIATE & AGGRESSIVE
 Corticosteroids – usually initial treatment
◦ High-dose steroids to decrease spinal cord edema &
inflammation
◦ High-dose Dexamethasone (16 mg loading, short course of
16 mg daily) followed by tapering doses over several days

55.  Primary purposes
◦ Preserve or recover neurological function
◦ Maintain functional independence
◦ Achieve highest possible quality of life
 May include separately or in combination:
◦ Spinal cord decompression: avert or treat MSCC
◦ Spinal column stabilization: treat mechanical pain or
bone instability)
◦ Resection/reconstruction of spinal column
 Surgical Techniques
◦ Anterior vertebral body resection with stabilization
◦ Vertebroplasty
◦ Kyphoplasty

56.  First-line treatment in asymptomatic MSCC
◦ Dose of 30 Gy administered in 10 fractions is
most widely used regimen in North America
 Combined with surgery (multimodal
therapy)
 Radiation therapy alone
◦ Pain relief may not be achieved for up to two
weeks
◦ Does not correct spinal instability or prevent
vertebral body collapse

57.  Acute management of MSCC
◦ Response to treatment slow
 In combination with radiation therapy for
chemo-sensitive tumors
◦ Hodgkin disease
◦ Non-Hodgkin lymphoma
◦ Neurobastoma
◦ Germ cell tumors
◦ Breast cancer

58.  Early recognition:
◦ Thorough assessment of neck & back pain in high risk
patients
 Neurological assessments
 Assess effectiveness pain control
 Monitor bowel & bladder function
 PT, OT referrals, as appropriate
◦ Assess need for home care referrals and supportive
medical equipment
 Provide a safe environment
 Assist with activity
 Monitor for changes in neurologic status as well as changes
in the location or intensity of pain.

59. Superior vena cava syndrome (SVCS) occurs in patients
with lung cancer or cancers of the mediastinum when the
tumor or enlarged lymph nodes block circulation in the
vena cava. This results in edema of the head, neck, and
arms.
 Obstruction of blood flow through the superior vena
cava (SVC)
 Obstruction leads to venous return from head, neck,
upper arms, upper thorax impaired
◦ Venous pressure increases
◦ Cardiac output decreases
 May be caused by:
◦ Invasion or compression of SVC
◦ Thrombosis within SVC

60.  Malignant Causes
 Lung Cancer
 Non-Hodgkin
Lymphoma
 Thymoma
 Mesothelioma
 Solid tumors with
mediastinal lymph
node metastasis (e.g.
breast cancer)
 Post-radiation fibrosis
 Non-Malignant Causes
 Intraluminal
Thrombosis
◦ Related to indwelling
central venous catheter
 Mediastinal fibrosis
Related to infection
 Benign mass

61.  Gradual onset (rarely occurs
rapidly)
 Symptoms vary depending on
extent of obstruction, location,
collateral circulation
 Dyspnea
 Facial and neck swelling
◦ Occurs when supine, subsides
after arising
 Sensation of fullness in head
 Cough
 Arm Swelling
 Chest pain
 Venous distention of neck &
chest wall
 Cyanosis of face & upper
torso
 Decreased or absent
 peripheral pulses
 CHF
 Decreased BP
 Chest pain
 Mental status changes
 Tachypnea
 Tachycardia
 Engorged
 conjunctivae
 Visual disturbances
 Syncope
 Hoarseness
 Stridor

62.  Based on characteristic signs & symptom of central
venous obstruction
 Imaging studies
◦ Chest x-ray
◦ Computed tomography scan (contrast enhanced)
◦ MRI
 Histologic diagnosis

63.  Based on etiology, severity of symptoms
 Relieve obstruction & control underlying disease
 Radiation Therapy
◦ Gold standard for non-small cell lung cancer
 Chemotherapy
◦ Primarily treatment for chemo-sensitive malignancies
 Small cell lung cancer
 Non-Hodgkin lymphoma
 Surgical intervention
 Thrombolytic therapy
◦ SVC caused by intraluminal thrombus

64.  Most malignancies causing SVCS are radiation
sensitive
 Currently, no standard regarding dose and schedule
of radiation therapy
 Generally provides good to excellent relief of
symptoms
◦ 70% of patients with lung cancer
◦ 90% of patients with lymphoma
◦ Initial symptom relief within 2 weeks,

65.  Primary treatment for chemo-sensitive tumors
◦ Small cell lung cancer (SCLC)
◦ Non-Hodgin lymphoma (NHL)
◦ Germ cell tumors
◦ Possibly breast cancer
 May be used for less chemo-sensitive tumors
◦ Non-small cell lung cancer (NSCLC)
 Symptom relief within 7-14 days

66.  Endovenous stenting
◦ Preferred initial approach
◦ In conjunction with thrombolytic therapy or venous
angioplasty
 Surgical venous bypass
◦ Reserved for patients with severe, persistent symptoms
◦ Rarely used

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

68. Pericardial effusion is caused by direct invasion
of the cancer into pericardium. The pericardial sac
fills with fluid and may lead to life-threatening
compression of the heart (called tamponade).
Signs and symptoms
◦ Chest Pain
◦ Dyspnea
◦ Low Blood Pressure
◦ Distant Heart Sounds

69.  Patients with cancer may develop a pericardial
effusion due to a variety of reasons.
◦ Secondary to metastatic disease of the pericardium
 Breast and lung cancers, leukemia, and lymphoma.
◦ Metastatic disease to the heart
◦ Primary heart malignancies.

70. Resulting in a pericardial effusion
An excess amount of pericardial fluid accumulates
Obstruction of venous and lymphatic drainage occurs
Tumors metastasize to the pericardium or myocardium

71.  Tachycardia
 Peripheral vasoconstriction causing cyanosis
 Decreased urinary output (oliguria or anuria)
 Narrowing pulse pressure, hypotension, increased systemic
vascular resistance
 Pulsus paradoxus
 Anxiety, restlessness, confusion, mental status changes, dizziness,
lightheadedness, agitation, fatigue
 Dyspnea, tachypnea, orthopnea, shortness of breath, air hunger
 Dysphagia, cough, retrostemal chest pain and heaviness,
hoarseness, hiccups
 Dullness to percussion, weak heart sounds, chest
fullness/discomfortNausea, vomiting, diarrhea, hepatojugular
reflux, hepatomegaly, abdominal distention

72.  2-dimensional echocardiography,
 chest radiograph, computerized tomography (CT)
scan, magnetic resonance imaging (MRI), pulmonary
artery catheterization, electrocardiogram (ECG), and
pericardiocentesis with pericardial fluid evaluation.

73.  Fluid and water restriction.
◦ Stop the buildup of excess fluid in the body.
 Vasopressin antagonists. These medications block
the action of the vasopressin.
 Surgery.
◦ Severe and/or chronic SIADH may require surgical
intervention wherein the surgeon removes the tumor that
produces ADH.

74.  Obtain a urine sample and blood samples from the
patient
 Place the patient on fluid restriction as per the
physician’s order.
 Start a strict input and output monitoring
 Administer vasopressin antagonists as prescribed
 Explain to the patient the relation of SIADH to
nausea and vomiting and loss of appetite.
 Maintain I/O chart

75.  Yarbro C H, Wujcik D, Gobel B H (2010) Cancer
nursing : Principles and Practice, 7th ed.
 Gerszten PC, Welch WC. Current surgical
management of metastatic spinal disease. Oncology.
2000;14:1013–1024.
 Yahalom J. Oncologic emergencies: superior vena
cava syndrome. In: DeVita VT, Hellman S, Rosenberg
SA, eds. Cancer: Principles and Practice of Oncology.
7th ed. Philadelphia.

76. THANK YOU