Cancer Treatment Modalities: Onc Emergencies Flashcards
Disseminated Intravascular Coagulation =
A complex systemic disorder that involves activation of coagulation pathways, leading to thrombotic and hemorrhagic events
Conditions that have increased risk of developing DIC (9)
- Sepsis
- Some solid and hematologic cancers
- Trauma, (esp neurotrauma)
- Severe transfusion reaction
- Organ destruction
- Toxic reactions
- Heat stroke/hyperthermia
- Rheumatologic disorders
- Some obstetric complication
1) DIC causes ____coagulation, triggering the coagulation pathway to be initiated inappropriately.
Hyper
2) DIC cascade begins with the release of ____ ____, causing release of _____. This release then causes ______ to covert to _____, causing ______*.
tissue factor thrombin plasminogen plasmin FIBRINOLYSIS*
3) Fibrinolysis then causes excessive ______ (FDP’s), which causes ______.
The final result =
Fibrin degradation products
bleeding
Simultaneous hemorrhage and clot formation (life threatening)
Widespread activation of coagulation leads to high production of (2), which can then compromise =
Fibrinogen and FDPs
blood supply to organs
Clot formation =
Clot breakdown =
Thrombosis
Fibrinolysis
DIC imbalances
1) _____ thrombin
2) ______ anticoagulant pathways
3) _______ fibrinolysis
4) ________ response
1) Increased
2) Decreased
3) Dysfunctional
4) Inflammatory
DIC leads to the following
1) ____ deposits in vasculature
2) ______ fibrinolysis
3) _______ coagulopathy
4) Organ ____/_____
1) Fibrin
2) Dysfunctional
3) Consumptive (consumption of coagulation factors and platelets)
4) damage/hemorrhage
What is the most common underlying condition associated with acute (rapid onset) DIC?
Infection
Infx may produce a systemic inflammatory response, activating cytokine system that begins the hypercoagulation cascade
In onc, what condition is most associated with acute DIC?
Why?
Acute Promyelocytic Leukemia (APL) 85%
In APL, tissue factor released directly from promyelocyte blast cells in bloodstream
Hallmark sign of DIC
Bleeding that occurs simultaneously from at least 3 unrelated sites
Chronic DIC
1) Asctd with ____ thrombosis and _____ bleeding
2) Most often asctd with what type of Ca?
1) diffuse, minimal
2) Solid metastatic mucinous ADENOCARCINOMAs and tumors of prostate, breast, stomach, lung, and pancreas (prostate and breast most common)
DIC
Initial Sx
Bleeding
Occult/oozing to frank hemorrhage
DIC
Renal Sx
- Acidosis
- Hematuria
- Oliguria
- Uterine hemorrhage
DIC
Pulmonary Sx
- Dyspnea, hemoptysis, cough
- Tachypnea, diminished breath sounds
- Pleural friction rub
DIC
Integumentary Sx
- Jaundice
- Petachiae
- Skin necrosis of lower limbs
- Thrombosis
- Fever
DIC
Later stage Sx
Thrombus formations: organ dysfunction/failure (infarct, ischemia, necrosis)
Lab findings of DIC
Decreased results
- Platelets
- Fibrinogen
- Antithrombin III
- Plasminogen/Alpha 2 antiplasmin (degrades fibrin clots) -> hyperfibrinolysis
- Protein C
Lab findings of DIC
Elevated results
- FDPs
- D-dimer
- Thrombin
- Fibrinopeptide A level
Tx Goals of DIC
1) APL ->
2) Prostate Ca ->
3) Sepsis/infx ->
Early recognition and tx*
1) antineoplastic therapy
2) hormonal therapy
3) Antibiotics
Supportive Care of DIC
- Hospitalization for close monitoring
- Chronic DIC -> Anticoags, Blood products (antifibrinolytics)
- Care monitoring
Thrombotic Thrombocytopenic Purpura =
TTP a rare blood condition where there is excessive blood clot formation throughout the body, causing thrombocytopenia as platelets are consumed in the clotting process
2 types of TTP
Inherited
Acquired
Inherited TTP =
Primarily what age group?
What gene is faulty?
What syndrome happens typically?
- neonates and children
- ADAMTA13 gene
- Hemolytic uremic syndrome (HUS) - renal failure
Acquired TTP =
Primarily in adults bc of triggers that cause the body to produce antibodies against ADAMTS13 enzyme activity.
Development of these antibodies include some drugs/diseases gemcitabine, quinine or hormonal therapy/lupus or HIV, Bone marrow transplantation
Dx of TTP increases risk of (2)
- Hemolytic anemia
- DIC
Patho of TTP
ADAMST13 enzymes are key genes associated with blood ____
- Decreased or blocked activity of theses enzymes allows ->
- These thrombi further damage ->
Clotting
- loose strands of Von Willebrand factor (VWF) to damage platelets and rbc -> become lodged in small blood vessels
- plts exacerbating thrombocytopenia -> localize in organs such as lung, heart, brain
TTP
S/S
- Purpura
- Petechiae
- Pale skin or jaundice
- Fatigue
- Fever
- Tachycardia
- Tachypnea
- Oliguria
- Neuro changes
Lab findings in TTP
1) CBC/plts =
2) Smear =
3) Bilirubin =
4) Coombs test =
5) Lactate =
6) ADAMTS13 assay =
7) Urinalysis =
1) decreased
2) Schistocytes
3) increased
4) Negative (no antibodies)
5) increased
6) decreased activity
7) proteinuria, hematuria
Key features in dx of TTP (5)
1) hemolytic anemia w presence of shistocytes on peripheral blood smear
2) Thrombocytopenia
3) Renal dysfunction
4) Fever
5) Neuro changes
(more recent clinical consensus is that these findings are all rarely present)
Key features in dx of TTP now (2)
- Elevated LDH +
- Thrombocytopenia
these two factors alone considered highly suspicious of TTP
Tx for TTP
Inherited TTP =
Acquired TTP =
Plasma therapy
1) FFP (replaces dysfunctional or missing ADAMTS13 enzyme)
2) Plasmapheresis (removes antibodies that cause damage to ADAMTS13 enzyme and replaces it)
Tx for refractory TTP
Corticosteroids and/or Ritux to suppress immune system
Splenectomy
SIADH =
Endocrine based dysfunction causing abnormal release of ADH (arginine vasopressin) - usually released by pituitary gland in response to increased osmolality or decreased plasma volume -> causes kidneys to reabsorb water and concentrate urine to improve plasma volume
SIADH can be caused by? (4)
1) Nervous system disorders
2) Pulmonary disorders
3) Drug induced (chemo)
4) Neoplasms
Which cause of SIADH is often asctd w Cancer?
Endocrine paraneoplastic syndrome
- ADH release from tumor cells becomes unregulated by hormone negative feedback system mechanisms
Electrolyte imbalances in SIADH
Hyponatremia
Increased urine osmolality
Decreased serum osmolality
S/S of _____ SIADH
- r/t cerebral edema
- papilledema
- ataxia
- hypoactive reflexes
- seizures/psychosis
- coma
- death
- sodium levels < 120
Severe SIADH
S/S of ______ SIADH
- may be asymptomatic
- muscle cramps
- fatigue
- anorexia/n/v/ thirst
- headache
- sodium level 131-135
Mild or Chronic
S/S of ______ SIADH
- weight gain
- progressive NEURO Sx*
- Lethargy
- Abdominal cramping and diarrhea
- Oliguria/concentrated urine
- Hypoactive reflexes
- EXTRAPYRAMIDAL sx*
- Sodium 126-130
Moderate
Notably absent in SIADH are signs associated with ?
Fluid overload
- normal pulse, BP, mucous membranes, turgor, no peripheral edema
SIADH lab findings
1) Sodium
2) Potassium
3) Bicarb
4) Phosphorus
5) Serum osmolality
6) Serum BUN/Cr
7) Urinalysis
8) Renal and adrenal function
9) Thyroid function
1) decreased <130
2) normal
3) normal
4) normal or decreased
5) decreased <280mOsm/kg
6) may be decreased
7) NA >, specific gravity >, osmolality >
8) normal
9) normal
Best Tx for SIADH
Eliminate underlying cause
SIADH if unresponsive to fluid restriction consider ______
Demeclocyline
Tx for SIADH
- Fluid restriction
- treat underlying malignancy
- stabilize neuro sx
- ICU
- Hypertonic saline
- seizure precautions
- loop diuretics
- Vasopressin
Systemic Inflammatory Response Syndrome (SIRS) =
The systemic response to the presence of an infection in the blood
Includes: Sepsis, Severe Sepsis, Septic Shock
SIRS is defined as the presence of 2 or more of the following?
1) Temp =
2) HR =
3) RR =
4) WBC =
1) <36, >38 C
2) >90 bpm
3) > 20 bpm, PaCO2 <32mmHg
4) <4,000, >12,000, >10% bands
Infectious causes of SIRS
Bacterial sepsis Cellulitis Influenza Meningitis Pneumonia Toxic shock syndrome Urinary tract infections
Noninfectious causes of SIRS
Adrenal insufficiency Autoimmune conditions Burns Cirrhosis Hemorrhagic shock Hematologic malignancy Medications Myocardial infarction Seizure
Lab tests to evaluate for SIRS includes (5)
- CBC
- Urinalysis and culture
- Cardiac enzymes
- BMP
- Serum Lactate
SIRS Tx
Tx of underlying cause, early identification
Abx, glucose management, supplemental O2, consults
Sepsis =
Inflammatory response to bacteremia and manifests as at least two or more of SIRS criteria
Severe Sepsis =
Sepsis associated w hypotension, hypoperfusion of organs, organ dysfunction
Septic shock =
Severe sepsis that is unresponsive to fluid resuscitation and includes
(fever, chills, persistent hypotension, prolonged organ hypoperfusion, lactic acidosis, oliguria, tachycardia, tachypnea, mental status changes)
MODS =
(3) characteristics of MODS
Multiple Organ Dysfunction Sydrome = state in which lack of homeostasis is so severe that more than one organ system requires immediate intervention
- Metabolic acidosis
- Tissue hypoxia
- Decreased circulatory blood volume
S/S of Early Sepsis
- High cardiac output w normal or slightly elevated BP
- Capillary leak (edema)
- Subsequent hypotension
- Nausea
S/S of Severe Sepsis
- Hypotension causing hypoperfusion of organs
- Elevated temp
- Warm, flushed skin
- bounding pulse
- tachypnea, tachycardia
- decreased GI motility (n/v)
- abnormal hematologic status*
- hyperglycemia
- lactic acidosis
- oliguria
- mental status changes
S/S of Septic Shock (hypoperfusion)
- Cold, clammy skin
- lethargy, progressing to coma
- hypotension, tachycardia, weak pulse, tachypnea
- decreased breath sounds w pulmonary edema/rales
- renal failure
- persistent hematologic abnormalities
- hyperglycemia
- lactic acidosis
- hyponatremia
- hypokalemia
- hypocalcemia
- decreased albumin, magnesium, phosphate
Expected findings in CBC results during sepsis
1) WBC =
2) Hemoglobin =
3) Platelets =
1) increased or decreased
2) decreased
3) decreased
Expected findings in BMP results during sepsis
1) Glucose =
2) BUN/Cr =
3) Na =
4) K =
5) Ca =
6) Albumin =
7) Mg =
8) Phosphate =
1) increased generally, but decreased in prolonged septic shock
2) Increased
3) decreased
4) decreased
5) decreased
6) decreased
7) decreased
8) decreased
Lab findings in sepsis
1) Prothrombin =
2) lactate =
3) biochemical markers =
1) prolonged
2) elevation reflects tissue hypoperfusion
3) elevation reflects presence of sepsis
Sepsis Tx
1) _____ resuscitation
2) _____ support
3) __ __ __ prophylaxis
4) Anti____
5) Anti____
6) _____ products
7) E____ replacement
8) N____ and I____ support
9) Vaso_____ and ino___ drugs
10) Activated ______ _ replacement
1) fluid
2) respiratory
3) DVT
4) antibiotics
5) antifungals
6) Blood
7) Electrolyte
8) Nutritional, Insulin
9) pressors, inotropic
10) protein C
Severe sepsis/septic shock tax
1) admitted to ____
2) aggressive tx, ____ resususcitation, and continuous ____
3) require central venous _____ monitoring, o___ support, pulse _____
4) may require intubation and ventilation bc of ? (3)
5) > 50% will develop what syndrome? Which may develop into?
6) Supportive care: prophylaxis for (2), nutritional support, delirium, psychosocial support
1) ICU
2) fluid, monitoring
3) pressure, oxygen, oximetry
4) pulmonary edema, encephalopathy, coma
5) ARDS, lung fibrosis
6) stress ulcers, DVT
Tumor Lysis Syndrome =
Condition in which serious electrolyte imbalances occur in the body as a result of rapid cell death and necrosis of tumor tissue
TLS Patho
Tumor cells die -> intracellular components such as K phos and purine nuclei acids released in bloodstream -> high concentrations kidneys not able to eliminate quickly enough -> electrolyte and metabolic dysfunction
If TLS is not tx quickly can cause =
Neurological, GI, renal, cardiac failure -> eventual death
Usually occurs 48-72 hrs after tx
TLS is typically asctd with what types of cancer (3)?
1) Leukemia’s w high wbc
2) Non-Hodgkin lymphoma
3) Bulky, rapidly growing, tx responsive tumors
TLS risk factors (2) pre-tx
- elevated lactate
- renal dysfunction
Chemotherapies that can cause TLS
Ci Cy E P Flud H Intrathecal
Cisplatin Cytarabine Etoposide Paclitaxel Fludarabine Hydroxurea IT Methotrexate
Immunotherapies that can cause TLS
In
In
R
Tumor ____ factors
Interferons
Interleukins
Rituximab
Necrosis
What hormonal therapy drug can cause TLS
Tamoxifen
TLS can also occur from
1) Cort____
2) S_____
3) R____ therapy
1) Corticosteroids
2) Surgery
3) Radiation*
Electrolyte Imbalances in TLS (4)
Hyperuricemia
Hyperphosphataemia
Hyperkalemia
Hypocalcemia
TLS
Initial S/S
N/V Abdominal pain or dissension Dyspnea Dysrhythmias Edema Lethargy Muscle or join pain, muscle twitching
TLS
Progressive S/S
Increased GI
Sx
Oliguria, he matures, azotemia, progressing to Anuria
CHF (HTN, tachy/brady) progressin to ventricular arrhythmias
Progressive muscle weakness, parenthesis, tetany, seizures
TLS
Advanced S/S
AKI
Cardiac arrest
DIC
Death
For prevention and early detection of TLS pretx LAB Studies include (3)
Additional baseline data include (2)
Electrolytes
Renal function
Liver Function
Weight
Baseline EKG
TLS
Tx (6)
(Hint: what meds fix the electrolyte abnormalities?)
1) Hydration*
2) Allopurinol*
3) Rasburicase
4) Loop diuretics (prevents fluid overload and maintains UO)
5) Oral phosphate binding drugs -Urine alkalinization (controversial/rarely recommended bc can cause ca + pho precipitates)
6) Hemodialysis if renal failure occurs
Hypersensitivity =
Anaphylaxis =
A hypersensitivity reaction (HSR) is one in which the body mounts an immunologic response to a foreign substance or antigen resulting in local tissue injury
Anaphylaxis refers to an acute, severe inflammatory response that is sudden and systemic, caused by histamine release -> causes dyspnea, hypotension, LOC, death
What are the 4 categories of HSR?
1) Type 1: Anaphylactoid or anaphylactic
2) Type II: Cytotoxic
3) Type III: Immune-complex mediated
4) Type IV: Cell-mediated (delayed)
Characteristic of which type of HSR?
Most chemo related HSRs are of this type; also includes allergies to IV dye, hives, allergic asthma, food allergies
Occurs when there has been no previous exposure to the antigen
IgE reaction
Type 1 Anaphylactoid or anaphylactic
Characteristic of which type of HSR?
Complement fixing Ig-G mediated; result of destruction of hematopoietic cell lines
Type II Cytotoxic
Characteristic of which type of HSR?
Binding of immune complexes to endothelium
Asctd w rheumatoid arthritis, systemic lupus erythematosus
Type III: Immune complex mediated
Characteristic of which type of HSR?
Often asctd w transfusion hemolysis
Heparin induced thrombocytopenia
Type II Cytotoxic
Characteristic of which type of HSR?
Asctd with poison ivy, tuberculosis, granulomas
Type IV Cell mediated (delayed)
Uniphasic HSR =
Immediate, usually occurs as tx is being given, typically resolves within hours of administration
Biphasic HSR =
Acute and Delayed* Anaphylactic reactions. Appears at initial start of tx, responds to tx, then appears 1-72 hrs later
Biphasic responses often attributed to bee stings, food allergies, immunotherapy
Factors that influence degree of anaphylaxis (3)
1) Route
2) Rate
3) Pt degree of hypersensitivity
S/S of which Type of HSR?
Pruritis Restlessness, agitation, anxiety, feeling of impending doom Fever, flushing, chills Urticaria (hives) Maculopapular rash Edema of hands, face, feet N/V Dyspnea, wheezing, brochospasm Hypotension, cyanosis Circulatory and respiratory collapse
Type 1
PS. Risk of death bc of anaphylaxis is commonly asctd w cardiovascular collapse and asphyxiation bc of respiratory edema
S/S of which Type of HSR?
Degrees to tissue injury
Type III
S/S of which Type of HSR?
Greatest risks are hemolytic anemia, cardiovascular collapse, and death
Type II
S/S of which Type of HSR?
Pneumonitis, mucositis, contact dermatitis, granulomas, GVHD following bone or stem cell transplant
Type IV
Pretx of HSR
Prevention* (Hint: what do we do at work before administering highly reactive drugs)
- Thorough allergy hx
- Patient education to alert staff of early S/S
- Emergency meds nearby
- baseline vs
- Skin test (some drugs)
- Premeds
Tx for Localized HSR
- Evaluate urticaria, erythema
- Diphenhydramine, hydrocortisone
- close VS monitoring
- dose may be continued at same rate, decreased, or dc’d
- emotional support
Tx for Generalized HSR/Anaphylaxis
- STOP infusion, notify physician
- Fluids IV NS, adjust rate prn
- maintain airway
- Frequent VS
- Resuscitative meds (Vasoconstrictorss, antihistamines, bronchodilators, anti-inflammatories, Cardiopulmonary support, emotional support)
Hypercalcemia =
A metabolic disorder, caused by hyperparathyroidism or by malignancy in 90% of cases
Normal Ca serum level =
Hypercalcemia level =
8.5-10mg/dL
> 10.5
Primary hypercalcemia =
Also known as PTH (parathyroid hormone)- mediated hyperparathyroidism, primary hypercalcemia is the most common cause and often slow to develop and asymx
Malignant hypercalcemia =
The most common metabolic complication among patients with CA
Patho of hypercalcemia of malignancy =
Development of excessive osteoclasts activity, resulting in increased bone destruction -> release of large amounts of Ca into circulation -> overwhelms kidneys
Any disease/tx that causes dehydration worsens development of HCM
Conditions include =
- N/V
- Dysphagia
- Mucositis
- Renal dysfunction
- Thiazides diuretics
- Renal failure or dysfunction
- Immobility (rarely)
4 types of HCM
1) Local osteolytic (bone dissolving) hypercalcemia (LOH)
2) Humoral hypercalcemia of malignancy (HHM)
3) Vitamin-D mediated hypercalcemia
4) Ectopic secretion of parathyroid hormone by tumor cells
Local osteolytic hypercalcemia caused by =
Caused by direct bone destruction dt tumor or metastasis
Humoral hypercalcemia of malignancy (HHM) caused by =
Caused by stimulation of osteoclasts resorption of bone by malignant cells
Vitamin D-mediated hypercalcemia caused by =
Caused by the synthesis of active vitamin D by some tumors, the increased absorption of Ca from the GI tract, and the reabsorption of Ca from kidneys
Types of Ca that HCM occurs in and does not occur in?
Solid tumors: breast and squamous cell lung ca, multiple myeloma
Hematologist malignancies: T-cell lymphoma, Hodgkin lymphoma
Rarely occurs in malignancies that metastasize to bone: prostate, sclc, osteosarcoma
S/S of mild, moderate, or severe HCM?
- Confusion, somnolence
- Abdominal pain, constipation
- worsening weakness, bone pain
- acidosis, dehydration, development of renal calculus, thirst, poor skin turgor
- HTN, EKG changes, dysrrhythmias
Moderate HCM (12-15 mg/dL)
S/S of mild, moderate, or severe HCM
- Restlessness, lethargy, difficulty concentrating
- anorexia, N/V
- Fatigue, weakness, hyporeflexia
- Polyuria, poly dipsia, pruritus
- possible HTN, orthostatic hypotension
Mild HCM (<12mg/dL)
S/S of mild, moderate, or severe HCM?
- Obtundation* , seizures, coma, death
- worsened abdominal pain, progressing to obstipation*, ileus
- skeletal pain, weakness, pathological fractures
- Renal failure, oliguria
- Cardiac arrest
Severe HCM (>15mg/dL)
Serum ionized calcium values includes (2)
1) Free ionized calcium
2) Protein-bound calcium
Calcium bound to albumin is protein bound therefore ->
Any decline in serum albumin has correspondence _____ in percentage of free ionized ca in blood
Inactive
Increase
Why is hypercalcemia higher risk for cancer patients with declining albumin?
Tumor, cachexia, Tx side effects, poor dietary protein intake = less protein bound Ca and more Free ionized Ca in blood
Lab findings in HCM
1) Mg
2) Phosphorus
3) Chloride
4) Sodium
5) Potassium
6) Parathyroid hormone
7) Alkaline phosphate seems
8) BUN
9) Cr
10) Urine Ca
1) Normal or low
2) low (inverse relationship w ca)
3) low
4) low
5) low
6) high if primary hypercalcemia, low if HCM
7) increased in presence of bone Mets
8) High
9) High
10) Increased, often before serum Ca increases
Key to Tx of Hypercalcemia of Malignancy
Primary prevention and identification of at risk patients
Tx of HCM is based on severity of sx, paying careful attention to (2) organ functions
Cardiac
Renal
Goal of tx of HCM
1) Correct de____
2) Inhibit calcium _____ from the bone
What types of meds help to do this?
1) dehydration
2) resorption (Calcitonin, bisphosphonates, gallium nitrate, plicamycin, increase renal excretion of calcium)
Tx for Mild HCM
Hydration, mobility, observation
Tx for Moderate/Severe HCM
Hydration, bisphosphonates (bone resorption inhibitor), loop diuretics when hydration stabilized, mobility
Cardiac Tamponade =-
The physiologic event when excessive fluid that has accumulated around the heart, causing pressure on cardiac chambers -> obstruction of blood flow to ventricles -> reduced cardiac output
Pericardial effusion vs Cardiac tamponade
Pericardial effusion = accumulation of fluid in pericardial sac
Difference is that cardiac tamponade affects hemodynamic status
Cardiac tamponade = pericardial pressure >/- ____ mmHg
30
Risk factors of Cardiac tamponade
1) Malignancies to ch____
2) L____ dysfunction of chest
3) H_V
4) H____ malignancies (leuk/multiple myeloma)
5) C___ and R____
6) In____
7) Auto___ diseases, traumatic ___ to chest, Venous congestion bc of cardio___, myocardial _____
1) Chest (lung, breast, lymphoma)
2) Lymphatic
3) HIV
4) Hematologic
5) Chemo Radiation
6) Infections
7) immune, injury, myopathy, infarction
Are these early or late s/s of cardiac tamponade?
(Dyspnea, cough, fatigue, malaise, lightheaded, abdominal distress, chest pain “heaviness”, dizziness, agitation, palpitations, tachy >100, mild peripheral edema)
Early
Are there early or late s/s of cardiac tamponade?
(Dyspnea at rest, orthopedic, increased retrosternal chest pain, hypotension, oliguria to anuria, cyanosis, edema, dysphagia bc of increased venous pressure, hoarseness, coughing, anxiety, AMS)
Late
Cardiac tamponade leads to fluid ______ -> ___ cardiac output -> ____ HR -> Vaso____* -> _____ pericardial pressure -> _____ cardiac output to the point of circulatory _____.
Accumulation -> decreased -> increased -> vasoconstriction* -> increased -> decreased -> collapse
Cardiac tamponade diagnosis is based more on what than lab values?
Physical findings
Physical findings of Cardiac Tamponade
1) Absent heart _____
2) Absent lower extremity ____
3) Weak c____ pulse
4) ____ vein distension, bulging veins
5) Extremily high central ____ pressure
6) Severe peripheral e____
7) Systolic ____tension, n_____ pulse pressure
8) ____cardia, significant E__ changes, heart b____ or __systole during inspiration
9) Altered _____ status
10) Pulsus _____
11) C-xray showing grossly _____ heart
12) _____ triad
1) sounds
2) pulses
3) carotid
4) Jugular
5) venous
6) edema
7) hypotension, narrowed
8) Bradycardia, EKG, block, asystole
9) mental
10) paradoxus
11) enlarged
12) Beck’s
Beck’s Triad (3)
Distended neck veins
Hypotension
Distant heart sounds
Tx for mild cardiac tamponade
1) Cautious o_____
2) Medications (3)
3) ____ products to prevent circulatory collapse
4) O_____
5) Agressive IV ______ administration* is the key to ->
1) observation
2) Diuretics, corticosteroids, vasoconstrictors to maintain perfusion
3) blood
4) oxygen
5) fluid -> key to keep venous presssure above pericardial pressure, to improve venous return
Tx for moderate/severe cardiac tamponade
1) Percutaneous _______*
2) R____/C____ therapy
1) Pericardiocentesis
2) Radiation/Chemo
Spinal Cord Compression =
Compression of thecal sac containing the spinal cord and cauda equine bc of malignant disease extension or a pathologically collapsed vertebrae
Tumors that commonly metastasize to the spinal cord (3)
Lymphomas (3-5%)
Neuroblastomas (25%)
Seminomas (5-10%)
Tumors that are commonly associated with bone mets that can result in SCC
Breast Prostate Lung Renal Myeloma Non-Hodgkin Lymphoma Hodgkin lymphoma
Tumors that are primary spinal cord tumors (3)
Ependymoma
Gloomy
Astrocytoma
Most common sx in cord compression =
Back or neck pain
-constant or dull ache, tends to worsen with supine positioning
Parts of the spine (3)
Cervical
Thoracic
Lumbosacral
SCC S/S
Cervical: Early effects
- Occipital headache, radiating neck/shoulder pain, neck stiffness
- Neurogenic shock (hypotension, bradycardia)
- Parasthesias
- Lhermitte sign (sudden electric-like shocks extending down the spine triggered by flexing the head forward)
- Hyperactive deep tendon reflexes
SCC S/S
Cervical: Later effects
- Quadriplegia
- bladder, bowel, sexual dysfunction
- autonomic hyperreflexia
- diaphragmatic dysfunction (if lesion above C4)
SCC S/S
Thoracic: Early effects
- Pain, local or radicular, or both
- Abdominal muscle weakness, lower extremity weakness
- Parasthesias around the abdomen
- decreased sensation below site of lesion
- increased deep tendon reflexes distal to the lesion
SCC S/S
Thoracic: Later effects
- lower extremity paralysis
- bladder, bowel, sexual dysfunction
- risk of autonomic hyperreflexia
SCC S/S
Lumbosacral: Early effects
- Pain, local, or radicular, or both in groin and down legs (sciatic)
- pain while raising legs straight
- weakness in pelvic muscles, lower extremities
- ataxic gait
- paresthesias and numbness
- decreased reflexes
SCC S/S
Lumbosacral: Later effects
Autonomic effects: bladder bowel, sexual dysfunction
Gold standard test to diagnose SCC
MRI of spine
Factors for favorable prognosis for SCC
1) Early rec____ and t____
2) Ability to _____ upon presentation and slow onset of ____ness
3) Presence of radiosensitive tumor, such as (3) cancer
4) ____ gender
5) Good response to cortico____ therapy
6) ____ interval between initial diagnosis and presentation of sx of SCC
- lower or upper spine lesion?
1) recognition, treatment
2) walk, weakness
3) lymphoma, breast, prostate
4) female
5) corticosteroid
6) long
7) lower
Factors for poorer prognosis for SCC
1) Para____ before tx can begin
2) Urinary _____; Bowel _____
3) Rapidly deteriorating ____logic symptoms
1) Paraplegia (paralysis of legs and lower body)
2) Retention, dysfunction
3) Neurologic
Tx for SCC
1) Gluco____ therapy, initial tx, reduces e____
2) Local _____ for radiosensitive tumors
3) ____ for nonradiosensitive tumors if sx persist through radiation, _____ for those who cannot tolerate surgery
4) ____ectomy or ____plasty/___plasty to stabilize vertebrae
5) Bis_____
6) ___ management
1) Glucocorticoid, edema
2) radiation
3) Surgery, chemo
4) Laminectomy, kypho, vertebroplasty
5) Bisphosphonates
6) Pain
Superior Vena Cava Syndrome =
A collection of symptoms that occur when mechanical obstruction of the superior vena cava (major vein that carries blood from head and upper body to heart) occurs -> compromises venous drainage, venous hypertension -> neuro alterations caused by cerebral edema and cardiac compromise
Anatomy of Superior Vena Cava
Joins the Innominate (cephalic + subclavian vein) with brachiocephalic veins to create the SVC
Ends in right atrium
Empties head and upper body of blood for return to the heart
Intrinsic factors that could cause SVC compression =
Extrinsic factors that could cause SVC compression =
- thrombosis, intraluminal tumor
- tumor or lymph node involvement
What type of cancer causes majority of SVCS
Small cell lung cancer (65-85%)
Non small cell lung
Risk factors for SVCS
- Non Hodgkin Lymphoma, Leukemia
- Men 50-70 yrs w mediastinal disease
- Esophageal, Thyroid carcinoma
- Breast cancer w mediastinal mets, thymoma, mesothelioma, germ cell neoplasms, kaposi’s sarcoma w mediastinal involvement
- Previous radiation to mediastinum
- Central venous catheters, pacemakers
- Comorbidities, such as aortic aneurysm, TB
S/S of SVCS
- Dyspnea, Cyanosis
- Facial and neck, arm swelling
- venous distention in neck and chest wall
- full feeling in head
- nonproductive cough
- chest pain
- dysphagia
- Unilateral ptosis of eye/constricted pupil (Horner syndrome)
Severe/late sx of SVCS
- Decreased or absent peripheral pulses
- Hypotension
- Tachypnea, tachycardia
- CHF
- AMS
- Visual changes: blurred vision, diplopia
- Orbital edema
- hemoptysis
- syncope
- Vocal cord paralysis w hoarseness
- Stridor
- Cyanosis of entire face and upper body
Diagnostic tests for SVCS
- Chest X-Ray
- CT (contrast will demonstrate thrombi) spiral CT
- MRI
- Sputum specimen if SVCS is presenting sx in a suspected malignancy
Tx for SVCS
- Radiation (Gold standard particularly for small/non small cell lung CA)
- Chemo
- Thrombolysis (for SVCS resulting in thrombus formation)
- Stent
- Surgery
- Supportive care (HOB elevated, O2, analgesics, tranquilizers, loop diuretics*, emotional support, pt/fam education)
Increased intracranial pressure (ICP) =
Increase in pressure within the skull
-> causes damage to central nervous system, restriction of blood to brain, herniation of brain stem itself, death
4 ways ICP can increase
1) Increased volume* bc of tumor, hemorrhage, edema in brain
2) Increased venous failure bc of heart failure or SVCS
3) Pseudotumor cerebri
4) Obstruction of cerebral spinal flow or absorption, most often caused by brain tumors
At risk pts for increased ICP include
1) Pts with ___ tumors
2) Pts with m____ tumors
3) Previous whole brain r____
4) Disseminated __ ___
5) Herpes simplex enc_____
6) S _ _ _ _; other metabolic dysfunction
7) Hem_____
8) Central nervous system infection; enc____
1) brain
2) metastatic
3) radiation
4) DIC
5) encephalitis
6) SIADH
7) Hemorrhage
8) Encephalopathy
Early S/S of ICP
- Headache
- Blurred vision, diplopia
- Communication problems
- personality, memory changes
- changes in visual fields, acuity
- changes in LOC
- confusion, lethargy, apathy
- N/V (possible projectile)
Late S/S of ICP
- Increased temp
- abnormal posturing
- bradycardia, hypotension, widened pulse pressure
- shallow respirations, tachypnea, cheyne stokes respirations
- cushings triad (systolic hypertension, irregular respirations, bradycardia)
- personality and LOC changes, confusion, delirium, hemiplegia, hemiparesis, seizures
Diagnostic tests for ICP
Physical exam (4) Tests (3)
- Evaluation for focal neuroloic deficits, intensity of headache, papilledema, cognitive dysfunction
- CBC, chemistry
- O2 sat
- Brain MRI* (noncontrast CT is preferred in acute situations)
Goal for ICP includes immediate reduction of cerebral ____ and sx control/recognition and tx of underlying cause
Cerebral Edema
Tx for ICP
- HOB at __ degrees
- Cortico_____
- Correct ____tension (can lead to cerebral ischemia), dehy_____, m____ imbalances
- maintain normal t____
- Intracranial monitoring via ____
- Surgical de____ if ICP is associated w mass effect bc of tumor/hemorrhage
- p___ management
- s____ management
- Ma_____
- Int____ and controlled hyper_____ in critical cases (effect is not definitive)
- 30
- Corticosteroids
- hypotension, dehydration, metabolic
- temp
- catheter
- debulking
- pain
- seizure
- Mannitol
- Intubation, hyperventilation
Malignant Bowel Obstruction =
Failure of contents of intestines to move normally though the GI system
4 Types of bowel obstructions
1) Blockage in one place =
2) Blockage is in two places =
3) Involves decreased blood flow to bowel, leading to incarcerated obstructions =
4) Bowel that has lost blood flow and becomes necrotic =
1) Simple
2) Closed-Loops
3) Strangulated
4) Incarcerated
Patho of bowel obstruction
Mechanical obstruction of the bowel causes _____ of bowel above obstruction
This can lead to b____ overgrowth, increased bowel g__, systemic t_____, de____, and e____ imbalance, all contributing to bowel injury
Ultimately can lead to bowel _____
dilation
bacterial, gas, toxicity, dehydration, electrolyte
perforation
Bowel obstruction results in mal____ of nutrients and fluid and dysfunction of _____ of solid wastes.
Increased intestinal motility proximal to obstruction and stretching of intestinal wall distal to obstruction result in dis____, cramping ____, n___, v____.
malabsorption, elimination
distension, pain, nausea, vomiting
Etiology of bowel obstructions
1) highest incidence (5-40%) =
2) 4-24% =
3) 3-15% (3) =
4) 80% of bowel obstructions occur in ____ intestine
1) ovarian
2) colon
3) breast, melanoma, lung
4) small
Causes of bowel obstructions
1) ___ invasion/ of nerve ____ that controls _____
2) Div_____
3) Int_____
4) Fecal _____
5) Bowel volv____ (twisting)
6) Trauma
7) Ad_____ from surgery or radiation
8) S____ manipulation
9) H_____
10) C_____ from outside of GI tract
11) Paralytic ____
12) Em___/Th____
13) Hypo____
14) N____ disorders
15) M____ side effects
1) Tumor, plexuses, motility
2) Diverticulitis
3) Intussusception
4) Impaction
5) volvulus
7) Adhesions
8) Surgical
9) Hernias
10) Compression
11) Ileus
12) Embolus/Thrombus
13) Hypokalemia
14) Neuro (paraneoplastic syndrome, SCC)
15) Medication
S/S of Bowel Obstruction
- Abdominal pain
- Abdominal distension
- Fever or chills
- N/V
- Change in stool
- Hyperactive bowel sounds
- Abdominal tenderness
- Increased RR and depth to compensate for increased pressur on diaphragm
- Mental status changes dt electrolyte imbalances
- Orthostatic hypotension, tachycardia
Lab Findings in Bowel Obstruction
Serum
1) Potassium
2) Chloride
3) Bicarbonate
4) BUN/Cr
5) WBC
6) PH
1) decreased
2) decreased
3) decreased
4) increased ratio
5) increased (inflammation)
6) Metabolic alkalosis w high intestinal obstruction; metobolic acidosis w low intestinal obstructions
Bowel Obstruction findings on
1) Plain abdominal radiographs =
2) CT =
3) Gastrografin enema =
4) Proctosigmoidoscopy or colonoscopy =
1) Dilated bowel, no gas, or air-fluid in multiple areas
2) Dilated or air filled above obstruction, may show mass
3) If plain films are not diagnostic
4) May be used to diagnose cancer
Tx for COMPLETE bowel obstruction =
Strangulation requires immediate surgery
Tx for Partial bowel obstruction
1) ______ tube to relieve dis tension and pain
2) keep patient _ _ _
3) F____ and E_____ replacement
4) Monitor /’s (maybe needs ____)
5) Antisp_____
6) Antichol______ such as hyoscine butylbromide or scopolamine
7) Cortico______
8) O____ for pain
9) Octreo_____ subc to decrease n/v, pain
10) Monitor
11) ____ may be placed to prepare for surgery or at end of life as palliation
12) Chronic, palliative situations may need _____ tube for decompression
1) Nasogastric
2) NPO
3) Fluid, Electrolyte
4) I/O’s, foley
5) Antispasmodics
6) Anticholinergics
7) Corticosteroids
8) Opiods
9) Octreotide
11) Stent
12) Gastrostomy
Urinary obstruction in cancer pts mainly caused by=
Progressive tumor growth and obstruction of ureters
Commonly bc of GI, Gynecoloic, Genitourinary cancers
Non cancer related causes of urinary obstruction (9)
Urinary tract calculus Acute or chronic renal failure Blood clots Benign prostatic hypertrophy Neurogenic bladder Trauma Inflammatory bowel disease Stricture Abdominal surgery
S/S of Urinary Obstruction
- Pain
- Acute or chronic renal failure
- recurrent UTI
- Oliguria, Anuria
- Distended bladder
- Back, flank, or lower abdominal pain
- Straining to urinate
- Hematuria
- Fever, chills, hypotension
- Palpable mass
- Leakage
Imaging studies for urinary obstruction (5)
CT abdomen and pelvis US Helical CT without contrast MRI Cystoscoy
Laboratory testing for urinary obstruction includes (2)
BMP (serum electrolytes, Ca, Mg, Pho, BUN, CR, Uric acid, albumin)
CBC
Urinalysis
Urinary obstruction
A urinalysis will demonstrate degree of secondary renal compromise if present
1) Inadequate perfusion =
2) Acute renal failure =
3) Etiology outside of kidney =
1) Normal UA
2) Casts, red, white blood cells present
3) red, white blood cells, crystals, bacteria
With progressive urinary obstruction, urinalysis will reveal
1) _____ urine osmolality
2) _____ serum sodium
1) decreased
2) increased
Tx for urinary obstruction
1) Mechanical de_____ o bladder may be followed by severe hypotension bc of rapid changes in bladder wall tension
2) Antis___
3) IV ____; correction of electrolyte imbalances
4) Surgery; ____ placement
5) Relieve vas____ obstruction
6) A___ _ andrenoceptro antagonistin some cases
7) strict measurement of /’s
1) decompression
2) Antispasmodics
3) IV fluids
4) Stent
5) vascular
6) Alpha 1
7) I/Os
Initial goal of tax of urinary obstruction is to =
Reestablish urinary flow, followed by tx of underlying cause
Pneuomonitis =
Interstitial (between tissues) inflammation of the lungs that can occur bc of number of etiologies
Most common cause of pneumonitis in cancer patients =
Thoracic exposure to radiation therapy or a drug induced complication
Describe the acute phase of pneumonitis
Radiation to pneumocytes and endothelial cells in interstitium of lungs -> release of surfactant and exudate -> interstitial edema -> capillary obstruction/inflammation -> release of wbc, fibroblasts, collagen -> alveolar space narrows into fibrotic state
Risk factors for pneumonitis (8)
- Smoking
- Poor nutritional status
- Poor performance status
- once daily radiation fractionation dosing
- Comorbid pulmonary conditions
- Older age
- Chemoradiation
- Mammalian target of rapamycin (mTOR) inhibitors (everolimus)
S/S of Pneumonitis
Typically present from - weeks after tx
S/S (5)
2-6
- Vague chest pain
- Cough
- Dyspnea
- Fatigue
- Low grade fever
Lab findings in Pneumonitis
CBC
- ____ wbc
- ____ sedimentation rate
Chest radiograph will show =
- Increased
- Increased
infiltrates
If left untreated Pneumonitis can lead to?
Fibrosis
Typically not reversible
Tx for Pneumonitis
- Rt pneumonitis can lead to infection, requiring ____ therapy
- Cortico____ therapy
- Broncho______
- O____
- Exp_____
- _____ air
- Increased hy_____
- Bed ____
- Antibiotics
- Corticosteroids
- Bronchodilators
- Oxygen
- Expectorants
- Humidified
- hydration
- rest
Extravasation =
Leaking or escaping of fluid (either drug or solution) from the vein which it was intended to flow or from an unintentional injection into surrounding tissues
*Vesicant extravasation can cause permanent damage, nonvesicant solutions generally do not cause permanent tissue damage
What happens to cells when DNA binding vesicant extravasation occurs?
Vesicant binds to nucleic acids in DNA in healthy cells causing cell death -> releases extracellular substances that get taken up by nearby cells -> DNA binding vesicant remains and circulates -> cycle continues
DNA binding vesicant examples = _________ (3)
Anthracyclines
- Doxorubicin
- Nitrogen mustard
- Mitomycin
What happens when non-DNA binding vesicants enter the cells?
Examples (2)
Resolve more easily
Plant alkaloids
Paclitaxel
Risk factors for Extravasation
1) Use of ____ needles vs plastic cannulas
2) Use of central ____ access device
3) S___ of practitioner
4) Consistency and quality of cvc maintenance
1) metal
2) venous
3) skill
Initial S/S of extravasation (4)
Swelling
Pain
Erythema
No blood return or slowing of IV flow
Later S/S of extravasation
- If undetected/untreated, b____ of skill will occur
- Sl_____ follows 1-2 wks later
- May require _____ intervention, including skin g____
- Could progress to damage to t___ and n___ or cause functional or sensory damage or loss of l____
1) blistering
2) sloughing
3) Surgical, graft
4) tendon, nerve, limb
Tx of Extravasation
- Immediately stop
- Disconnect IV tubing from iv device but no not remove catheter
- Aspirate any residual drug that may present in 1-3 ml syringe
- remove IV device or port needle
- assess site, pt sx anxiety, pain, changes in range of motion
- notify physician
- manage guidelines per specific drug involved (ice, heat, antidote
- document
Chemos with High Potential of immediate hypersensitivity reactions (4)
1) L-asparaginase
2) Taxanes (Paclitaxel, Docetaxel)
3) Platinum compounds (Cisplatin, Carboplatin, Oxaliplatin)
4) Epipodophyllotoxins (Etoposide, Teniposide)
Chemos with Occasional potential of immediate hypersensitivity reactions (3)
1) Anthracyclines (Doxorubicin, Daunorubicin, Idarubicin, Epirubicin)
2) Mercaptopurine
3) Azathioprine
Chemos with Rare potential of immediate hypersensitivity reactions
- Bleomycin
- Chlorambucil and Melphalan
- Cyclophos and fludarabine
- Dacarbazine
- Dactinomycin
- 5FU
- Hydroxurea
- Methotrexate
- Polyethylene glycol-modified E.coli asparaginase
- Vincristine and vinblastine
