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High Acuity > Cancer and Oncological Emergencies > Flashcards

Cancer and Oncological Emergencies Flashcards

1
Q

Most Diagnosed Cancers

A
  • Lung (13%)
  • Breast (12%)
  • Prostate (11%)
  • Colorectal (10%)
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2
Q

Leading cause of mortality cancers

A
  • Lung (24%)
  • Colorectal (11%)
  • Pancreas (7%)
  • Breast (6%)
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3
Q

Intrinsic Factors influencing cancer development

A

genetic predisposition, immunity
* Heredity/genetic risk (up to 10% of cancers)
* Age: single most important risk factor for cancer
* Immunity decreases
* Time to be exposed to carcinogens increases
* Immunity

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4
Q

Extrinsic Factors influencing cancer development

A

carcinogens
* Exposure to external, ingested, and/or inhaled substances (i.e. tobacco, radiation, diet, viruses)

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5
Q

Define cellular regulation

A

Genetic/physiologic processes that control cell growth, replication, differentiation, and function.

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6
Q

Benign vs Cancer Cells

A

Benign tumor cells: normal cells but are growing in wrong place or wrong time (ex: moles, skin tags, nasal polyps, etc.).

Cancer cells: abnormal, no useful function, harmful to normal body tissues

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7
Q

4 Characteristics of Cancer Cells

A
  1. Don’t respond to normal programmed apoptosis
  2. Divide indiscriminately
  3. Lose contact inhibition
  4. Do not stick together and travel
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8
Q

Define Carcinogenesis and 3 Stages

A

The process of changing a normal cell into a cancer cell: loss of cellular regulation
1. Initiation “carcinogens” can change activity of cellular genes, so the cell becomes cancerous. Genes are altered.
2. Promotion: enhanced growth by promoters. Cell with initial insult proliferates and replicates at rate of tissue.
ii. Latency period
3. Progression: continued change of the cancer cell, making it more malignant over time
* Can develop its own blood supply
* Further mutations  less and less normal cell features
* Primary tumor vs metastasis

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9
Q

4 Steps of Metastasis

A
  1. Malignant Transformation: Cells have divided and become a clump/tumor
  2. Tumor Vascularization: Decides it needs own blood supply; secrete substance that stimulates growth of new vessels
  3. Blood Vessel Penetration: Breaking off from main tumor, enter blood supply, and travel until they get stuck
  4. Arrest and Invasion: Are stuck, decide to invade new tissue that it is near
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10
Q

4 Ways Cancer can metastasize

A
  1. Lymphatic spread – cells invade lymphatic vessels where they travel to lymph nodes
    * “regional spread”
  2. Arteriovenous spread – enter blood vessels near primary tumor and travel to the next capillary network they encounter
    * Ex: GI tumor typically spread via the hepatic portal vein to liver
  3. Serous cavity spread – Serous membranes (pleura, peritoneum) are invaded by tumors.
    * Can cause malignant pleural effusions or ascites
  4. CSF spread – cells spread through CSF
    * Ex: brain tumor metastasizes along spinal cord
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11
Q

Grading vs Staging of Cancer

A

Grading: how similar cancer cells look to parent cells

Staging: exact location of the cancer and whether metastasis has occured

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12
Q

Grading of Cancer

A

Grade 1, 2, 3, and 4
* 1: Well-differentiated - looks like normal cells
* 2: Moderately differentiated
* 3: Poorly Differentiated
* 4: Undifferentiated

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13
Q

How is the primary tumor staged

A

Tx Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ
T1, T2, T3, T4 Increasing size and/or local extent of the primary tumor

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14
Q

How are the regional lymph nodes staged

A

Nx Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1, N2, N3 Increasing involvement of regional lymph nodes

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15
Q

Haw are the distant metastasis staged

A

Mx Presence of distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis

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16
Q

“Need to knows” about a patient’s cancer

A
  1. Type (target organ and influence on patient
  2. Patient’s Age and overall health
  3. Stage
    T - tumor
    N - node involvement
    M - mets
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17
Q

Signs of Cancer

A

C
Change in bowel or bladder habits
A
A sore throat that doesn’t heal
U
Unusual bleeding or discharge
T
Thickening of a lump in breast or elsewhere
I
Indigestion or difficulty swallowing
O
Obvious change in a wart or mole
N
Nagging cough or hoarseness

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18
Q

Primary Cancer Prevention

A

strategies to prevent actual occurrence of cancer
* Genetic screening
* Avoid carcinogens/associated factors– smoking cessation, healthy eating, exercise, limit alcohol, limit sun exposure
* Remove “at risk tissue” – i.e. mole removal, breast removal, etc.
* Vaccination – HPV

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19
Q

Secondary Cancer Prevention

A

use of screening to detect cancer early
* Self-exams (breast, testicular)
* FIT test (occult blood as one of the first signs of colon cancer)/colonoscopy
* PAP tests (cervical cancer)

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20
Q

6 Things Cancer and Treatment often impact

A
  1. Immunity and clotting
    2, GI Function
  2. Peripheral Nerve Sensory Perception
  3. Motor/Sensory Function
  4. Respiratory and cardiac function
  5. Comfort and Quality of Life
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21
Q

3 Focuses of Treatment of Cancer

A
  1. Curative
  2. Control Spread
  3. Palliative
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22
Q

6 Uses of Surgery for Cancer

A
  1. Prophylaxis: removal of potentially cancerous tissues to prevent related to strong risk of development. Done only with strong disposition i.e., family history with young death
  2. Diagnosis: biopsy; removal of suspected tumor or lesion to test/rule out cancer
  3. Cure: Removes all cancerous tissue. Surgery alone can lead to cure if all microscopic tissue is removed. Usually followed up with chemo/radiation.
  4. Control: debulking of tumor when removal of entire mass is not possible due to proximity to vital organs. Alleviation of symptoms and make subsequent treatments more beneficial.
  5. Palliation: Symptom relief and quality of life.
  6. Reconstruction/restoration: Increases function, enhances appearance, or both. Typically, not done until patient is in remission. Ex) breast reconstruction or ostomy removal.
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23
Q

What is radiation therapy + symptoms

A

High-energy radiation to kill cancer cells while having minimal damaging effects on surrounding normal tissue

Radiation effects seen only in tissues in radiation field/path
* Symptoms: radiation dermatitis, hair loss, fatigue, tissue fibrosis and scaring; altered taste, bone marrow suppression

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24
Q

What is chemotherapy? Neoadjuvant vs Adjuvant?

A

Systemic therapy: antineoplastic/cytotoxic drugs used to kill cancer cells and disrupt their cellular regulation

Neoadjuvant chemo: shrink tumor before surgery or radiation
Adjuvant chemo: kill remaining cancer following surgery or radiation

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25
Q

Side Effects of Chemo

A
  1. extravasation/infiltration
  2. hematopoietic effects: anemia, neutropenia, thrombocytopenia
  3. nausea/vomiting
  4. alopecia
  5. mucositis
  6. cognitive changes
  7. chemo-induced peripheral neuropathy
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26
Q

What is immunotherapy? Side effects related to: ? 2 Types?

A

Stimulates body’s natural defenses (immune system) to attack the cancer
* “Anti-tumor” response
* Activates immune system rather than destroy all cells (as happens with cytotoxic drugs)

Side effects relate to an over amount of immunity (immune-related adverse events)
* “ITIS” of everything: exacerbation of an inflammatory response caused by immune system activation
* Mild to severe

  1. Monoclonal Antibodies: infusion of antibodies formed against targets known to be present on certain types of cancer cells
  2. Targeted Therapy: block the growth and spread of cancer by interfering with the specific cellular growth pathways/ molecules involved in cancer cells
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27
Q

Endocrine Therapy as Cancer Treatment

A

Some tumors are hormone-sensitive (grow faster/slower in the presence of certain hormones)
* Most sensitive: Breast Ca, Prostate Ca

Adds/blocks/removes hormone
* Block receptors– prevent cancer cells from receiving growth stimulation  tumor is stopped/slowed

Side effects: depend on the hormone being affected
* Fatigue, arthralgias, joint stiffness and/or bone pain, hot flashes, sexual dysfunction. Long-term side effects: osteoporosis, increased CV risks, clots

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28
Q

What is the concept of uncertainty?

A

Living with a condition in which the individual constantly questions the risk of recurrence, exacerbation, and the unknown future
* Prominent feature of the cancer experience

Influences daily activities and routines

Can negatively affect adaptation and disease outcomes

Nurses play an important role in helping patients see uncertainty as a normal event

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29
Q

Define survivorship and 3 Phases

A

A person is considered a cancer survivor from diagnosis until death; do not need to be cured to qualify as survivor

  1. Acute survival: time from diagnosis to completion of initial treatment
  2. Extended survival: beginning to return to normal life after treatment, “watchful waiting,” fear of recurrence
  3. Permanent survival: Long-term adaptation to life beyond cancer
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30
Q

Hyperleukocytosis and Leukostasis

A

Hyperleukocytosis: (WBC) count >100 x 109/L in a patient with leukemia

Leukostasis = symptomatic hyperleukocytosis Obstruction of blood flow from excessive numbers of circulating leukocytes (blasts)

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31
Q

Signs of Leukostasis

A

Impaired capillary circulation causes organ damage from increased blood viscosity and aggregation of leukemic cells.

Signs of clot and increased blood viscosity as signs and symptoms dependent on tumor area: causes resp distress, CNS abnormalities, or other organ dysfunction (heart, kidney – decreased perfusion)

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32
Q

Treatment of Leukostasis

A

1) Hydration (IV fluids)
2) Reduce uric acid (allopurinol/rasburicase)
3) Rapidly reduce number of circulating blast cells – treatment of actual cancer:
* Induction chemo, hydroxyurea (medication to reduce WBC) and leukapheresis (filtration of blood to decrease WBC)

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33
Q

Why does hypercalcemia occur as on oncological emergency?

A

Malignancies or treatment associated with bone destruction

a) Tumors which secrete parathyroid hormone related peptide (PTHrP) which stimulate bone breakdown (osteoclast activity) and then releases calcium from bone

b) Tumors which secrete bone resorbing substances (cause bones to dump calcium)

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34
Q

Symptoms of hypercalcemia as oncological emergency

A

a) Severe thirst & polyuria
b) Constipation
c) Drowsiness, confusion, hyporeflexia
d) Dry mouth, nausea, vomiting, lack of appetite
e) Fatigue, restlessness
f) Skeletal pain, kidney stones, abdominal pain
g) Altered cognition (lethargy to coma)
h) Severe muscle weakness, loss of deep tendon reflexes, paralytic ileus, dehydration, ECG changes (bradyarrhythmia; shortened QTc interval; ST elevation)
i) Cardiac arrest*

> 2.6 = hypercalcemia
3.5 hypercalcemic crisis

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35
Q

6 Points of Treatment for Hypercalcemic therapy

A
  1. Fluid Resuscitation
  2. Bisphosphonates: block calcium resorption
  3. Calcitonin + Cortico: lower serum calcium
  4. F/E monitoring
  5. Loop diuretics to promote loss (thiazide increase reabsorption
  6. dialysis
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36
Q

What is SIADH?

A

Inappropriate production & secretion of ADH. Can occur in 2 ways :
1) Ectopic ADH secreted by tumor tissue
2) Cancer stimulates the posterior pituitary to secrete ADH when not needed

Causes kidneys to excessively absorb water

Water retention dilutes blood sodium = hypotonic hyponatremia

Continues despite the decreased serum osmolality; loss of feedback mechanism

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37
Q

What does ADH do?

A

prevents diuresis leading to fluid retention
* Inappropriate = fluid overload

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38
Q

Labs Relevant to SIADH
* serum sodium
* Serum osmolality
* serum urea
* urine osmolality
* urine sodium

A
  • serum sodium (result <135 mmol/L) - low
  • Serum osmolality (<270 mmol/kg H2O) - low
  • serum urea (<3.6 mmol/L) - low
  • urine osmolality (>100mmol/kg H2O) - high
  • urine sodium (>30mmol/L) - high
39
Q

Cues of SIADH relate to:

A

hyponatremia & fluid overload

Mild: weakness, muscle cramps, loss of appetite, fatigue

Weight gain, CNS changes, personality changes, confusion, extreme muscle weakness

Severe symptoms CNS dysfunction secondary to water intoxication that leads to swelling of the brain cells

40
Q

Management of SIADH

A
  1. treat underlying cause (tumor)
  2. correct fluid overload and increase sodium
    * Restrict fluid intake
    * Hypertonic saline administration (3% NaCl) to draw fluid back into vasculature for us to pee it out  manage increased ICP
    * Monitor fluid and electrolytes closely
  3. Monitor for decreasing LOC (cerebral edema - increasing ICP)
    * GCS
    * Vital signs
    * Seizures
    * Dilantin sometimes given – for seizure prophylaxis and blocks the effect of ADH
41
Q

What is SVC syndrome?

A

a group of symptoms that occur when there is pressure on the superior vena cava, or it is partially blocked and blood can’t flow back to the heart normally.

42
Q

Treatment of SVC syndrome?

A

ABCs  secure airway!
* Fluid buildup in the top of the body, airway compromised because veins can swell.

Dexamethasone then surgery or radiation/chemotherapy
* Anti-inflammatory and effect on tumor itself

Stent, thrombolytic therapy if was caused by thrombus

43
Q

Signs/Symptoms of SVC

A
  • Face/neck/arm swelling/erythema – blood back up
  • Cough, dyspnea, orthopnea
  • Engorged blood vessels above nipple line, JVD
  • Stridor (laryngeal edema due to swelling of veins)
  • Headache/confusion (increased ICP)
  • Sudden onset can cause rapid increased pressure in SVC  increased ICP, intracranial thrombosis, bleeding, death
44
Q

What is DIC

A

Extensive, widespread abnormal clotting that uses up factors, resulting in bleeding

45
Q

What is malignant pleural effusion and what is its result?

A

Abnormal accumulation of fluid in the pleural cavity containing malignant cells

Caused by cancer cells spreading to the pleural space > causes increased production of pleural fluid and decreased absorption of the fluid

Restrict lung expansion > decreased lung volume > decreased gas exchange and oxygenation

46
Q

Cues of malignant pleural effusion

A

dyspnea, tachypnea, non-productive cough, chest pain, pleuritic rub. Presents the same as non-malignant pleural effusion, hx of cancer should suspect malignant.

47
Q

Treatment of malignant pleural effusion

A

thoracoscopy (VATS)
* Thoracentesis, chest tube, drain: If malignant, fluid will return after drain
* Pleurodesis: talcum powder inserted after thoracentesis that causes pleural and visceral layers to stick together; eliminates pleural space

48
Q

What is malignant cardiac tamponade?

A
  • Accumulation of fluid in pericardial sac, applying pressure on heart (effusion  tamponade) Heart cannot adequately fill and pump.
  • Reduces blood flow to the ventricles and stroke volume decreased CO
49
Q

Cues of malignant cardiac tamponade

A

sudden SOB, tachycardia, tachypnea, shock (cardiogenic)
* Extreme emergency*
* Main cause of cardiogenic shock

50
Q

Treatment of malignant cardiac tamponade

A

pericardial window with drain (surgical incision with drain); pericardiocentesis (drainage of pericardial sac)

51
Q

What is febrile neutropenia?

A

Deficiency of neutrophils, the first line of defence against bacteria/fungues caused by myelosuppression

52
Q

What is myelosuppression and why does it cause febrile neutropenia?

A
  • Suppression of bone marrow
  • Bone marrow produces erythrocytes, thrombocytes, and leukocytes
  • Chemotherapy attacks rapidly dividing cells
  • Drugs active against cycling AND non-cycling are more toxic to bone marrow
  • Neutrophils are constantly being produced in the bone marrow, therefore, at risk for destruction by chemotherapy
53
Q

Risk factors for myelosuppression

A
  • Current chemotherapy regimen/type of drug
  • Previous chemotherapy, especially intensive regimens
  • Bone marrow disease (e.g. myelofibrosis, cancer)
  • Older ager
  • Radiation therapy to bone marrow sites (even if that’s not what was intended to be radiated)
  • If recent treatment occurred, red flag for possibility of febrile neutropenia
54
Q

Neutrophil normal range

Short v Long Term

Nadir

A

Usual neutrophil range: 1.50-7.50 10x9/L
* Short-term neutropenia: lasts less than 10 days
* Long-term neutropenia: exceeds 10-14 days  increased risk of infection

Nadir: lowest point of WBC level following treatment
* 7-10 days for most drugs
* This is when patient is most at risk for febrile neutropenia

Recovery around 21 days post-treatment for normal patients

55
Q

At least half of neutropenia patients who become febrile have:

A

have an established or occult infection: hidden infection because first line of defense not present, inflammatory response did not occur, and thus are further along in the infection.

56
Q

What is the impact of neutropenia?

A

Reduction in neutrophil count = immunosuppression

57
Q

What happens to an infection in the body when the first line of defense is missing or compromised?

A

Neutrophils have a life-expectancy of 6-8 hours once released into circulation

Infection will spread, neutrophils responsible for inflammatory response, pus creation, etc

No pain, inflammation, redness occur; signs and symptoms missing in febrile neutropenia

Way later in infection stage because we did not identify initial infection

58
Q

Absolute Neutrophil Count

A

Defines the patient’s risk for infection
Neutropenia occurs when ANC is less than 0.5 10x9/L
- Normal low is 1.5
* Susceptibility to infection increases
* Highest risk: ANC less than 0.1 10x9/L

59
Q

Neutropenic Precautions

A

Wear a mask and observe universal precautions (HAND HYGIENE!!)

Limit visitors only to those who are feeling well or have not recently been ill

Avoid rectal suppositories and other invasive procedures if possible, especially with GI because it is common origin site

Broad spectrum oral antibiotics (prophylaxis)

Observe closely for signs and symptoms of infection

60
Q

What is important to remember when observing S+S of febrile neutropenia?

A

Redness, pain, and pus production may be delayed or absent with neutropenia because first line defense (neutrophils) are not present to start inflammatory infection
o Must look for other signs and symptoms
* Fever will often be the ONLY SIGN of infection (>38oC x 1 hour; or one-time temperature > 38.5oC)  we don’t usually wait for an hour – call doctor for septic workup!
o Will be lower fever than normal: worried around 37.3ish

61
Q

Vital sign changes with febrile neutropenia

A

Tachycardia (may also be normal)  10-20 bpm above patient baseline or normal values

Hypo- or hyperthermia (including low grade fever); septic shock can lead to hypothermia

Hypertension (early sepsis as compensation), then hypotension (septic shock);

increased work of breathing/SOB/resp rate;

normal or low SaO2

62
Q

Gold Stands for Treatment of Febrile Neutropenia

A

Start antibiotics in 1 (one) hour OR LESS after first high temperature
* We are further along in infection in febrile neutropenia at first sign and symptoms

63
Q

What happens when neutropenic patient has a suspected infection?

A
  1. Septic workup
    - many tests to find source
    - BW: lactate, cortisol, procalcitonin
    - Prophylactic AbX
    - Fluids
    - Tylenol
64
Q

Measures to Promote Neutrophil Recovery

A

Hematopoietic growth factors
o Granulocyte colony stimulating factors (G-CSF)
 Filgrastim  daily injection for a period of days
 Peg-filgrastim  long-acting G-CSF, once per cycle
* Overall stimulating neutrophil growth

Can cause a fever; can be hard to differentiate; septic workup done anyways to be safe

Side effects: Bony pains (where bone marrow is), splenic rupture, fever due to enhanced neutrophil recovery

65
Q

What is tumor lysis syndrome?

A

n oncologic emergency that is caused by massive tumor cell lysis with the release of large amounts of potassium, phosphate, and nucleic acids into the systemic circulation

May occur spontaneously in patients with high tumor burden

66
Q

Cornerstone of tumor lysis syndrome treatment>

A

HYDRATION; include assessment of fluid overload

67
Q

Pathophysiology of TLS

A

Rate of turnover (dying, regeneration) of cancer cells is very high at baseline
o Anti-neoplastic therapy/chemotherapy/radiation leads to 
o Lysis of cancer cells leads to 
o Rapid release of cell contents into bloodstream leads to
o Electrolyte shifts outside of normal range

Lysed tumor cells release DNA, proteins, and electrolytes
o DNA breaks into uric acid when broken down; eliminated by kidneys
o Chunky proteins circulating can cause damage to filtration system

68
Q

How does chemo lead to TLS?

A

causes malignant cells to die and burst (lyse). They release their contents into the blood stream. This rapid release of contents can cause a rapid electrolyte shift and lead to electrolyte values outside of normal range

69
Q

Why and how does hyperuricemia occur in TLS?

A

DNA released is broken down into uric acid

Insoluble in acidic urine (both acids)  accumulation of urate crystals in the renal tubules or collecting ducts  renal obstruction  intrarenal failure

70
Q

Complications of hyperuricemia

A

reduced urine output, renal failure, reduced renal blood flow, disrupted renal function, crystal deposits in small joints (gout)

71
Q

How and why does hyperkalemia occur in TLS? What are the complications?

A

Lysed cancer cells release large amounts of potassium (potassium intracellular; when extracellular/in the blood it is active)
* If kidneys cannot remove it fast enough
* Dangerously high levels can cause cardiac complications (usually within 6-72 hours of treatment)
* Bradycardia
* Heart block
* Ventricular fibrillation
* Asystole

72
Q

How and why does hyperphosphatemia occur in TLS? What are the complications?

A

Lysed cancer cells release large amounts of phosphorous

High levels of phosphorous binds to calcium, forming crystals  hypocalcemia  most common source of AKI in TLS

Crystals can deposit in kidneys, leading to further renal impact/failure
* Azotemia
* Anuria

73
Q

How and why does hypocalcemia occur in TLS? What are the complications?

A

Due to phosphate binding to calcium and ”removing it” from bloodstream

Complications:
* Confusion
* Muscle spasms
* Tetany
* Seizures
* Hypotension (think CCB medication), heart block, cardiac arrest

74
Q

Clinical Signs of TLS

A
  1. Electrolyte abnormalities: may be non-specific: nausea, vomiting, weakness, cardiac abnormalities, confusion
  2. stimulate coagulation cascade that leads to Disseminated Intravascular Coagulation (DIC)
  3. Decreased urine output (urine output must be greater than 100 mL/h to prevent TLS; normal 25-30ml/hr)
75
Q

Who is most at risk for TLS

A

Those with a high tumour burden (large tumor with large number of cancer cells). Acute leukemia, aggressive NHL, myeloproliferative disorders, patients with impaired renal function, splenomegaly, lymphadenopathy),

These cancers cause a high white blood cell count, have a high tumour burden or have rapidly dividing cells that respond well to treatment.

76
Q

When will TLS happen?

A

Occurs between three days prior to chemotherapy and up to 7 days after

Best way to treat it is to PREVENT it!

77
Q

Diagnosis of TLS (lab and clinical)

A

Laboratory TLS:
* Two or more electrolyte disturbances

Clinical TLS:
* Laboratory TLS plus at least one of the following:
* Acute kidney injury
* Cardiac arrhythmia
* Seizure
* Sudden death

78
Q

Focus of prevention of TLS

A

maintaining normal serum electrolyte balance and maximize renal function, prevent uric acid build up

79
Q

Prophylactic treatment of TLS

A

Prophylactic
o Hydration to maintain urinary output great than 100 mL/h
 Should begin 24-48 hours before treatment, at least 72 hours post treatment
 Diuretics may be utilized to promote urinary excretion; caution with harm – balancing game
 Allopurinol to prevent uric acid formation
* MONITOR ins and outs accurately!!!
o So, so important

80
Q

Treatment of hyperuricemia in TLS

A

Rasburicase  indicated for hyperuricemia  degrades pre-existing uric acid

81
Q

Why is sodium bicarb used in TLS treatment?

A

to alkalize urine (pH >7); monitor urine pH as ordered; promotes excretion of acidic urine due to insolubility of uric acid with acidic urine

82
Q

Treatment of hyperkalemia in TLS

A

o Kayexalate to excrete potassium through stool
o Insulin-glucose therapy to shift potassium intracellularly (50 mL dextrose 50% and 10 units of Regular insulin)
o Loop diuretics (furosemide = potassium wasting + increases renal output)
o ECG if K greater than 6.0

83
Q

Treatment of hypocalcemia and hyperphosphatemia in TLS

A
  • Hypocalcemia: calcium gluconate to replace calcium
    o ECG if calcium very low
  • Hyperphosphatemia: medications containing phosphate to be discontinued; some foods restricted
84
Q

What is SCC?

A
  • Tumor in epidural space encroaches on spinal cord or cauda equina = spinal cord compression
  • Medical emergency that requires prompt identification and treatment
  • Rarely fatal – but can cause permanent neurological defects (paralysis, loss of bowel and bladder function)
85
Q

Pathophysiology of SCC

A
  • Primary tumors arising in spinal cord are intra-medullary (rare)
  • Most SCC is caused by metastatic tumors in the epidural space
    o COMPRESSION, not invasion of tissues
    o Displace spinal cord, irritate nerve roots
    o Obstruct flow of CSF
    o Cause vertebral destruction and collapse  forces bony fragments into extradural space
86
Q

Damage to ascending nerve fibers tracts causes

A

pain or sensory deficits or both

87
Q

Damage to descending tracts causes :

A

motor deficits, bowel and bladder dysfunction, impaired sexual function

88
Q

Three major processes cause sCC

A
  1. Direction compression of spinal cord or cauda equina by tumor or destruction of bone
  2. Interruption of vascular supply to neural structure by tumor
  3. Compression caused by vertebral collapse resulting from a pathologic fracture or dislocation  bone may extrude to cause pressure on spinal cord
    o Can lead to edema and further compression
89
Q

Clinical Features of SCC

A

Symptoms directly related to location of tumor; damage below level of tumor

Fast-growing tumors can cause permanent damage with hours to days of first symptom appearing.
o Thoracic presentation –usually lung or breast
o Lumbosacral presentation usually colorectal or prostate cancer

90
Q

Clinical Signs of SCC

A

Muscle weakness
o Unsteadiness
o Footdrop
o Paralysis

Sensory impairment
o Paralysis
o Loss of bowel and bladder control and sensation to do so
o Paraplegia

91
Q

Symptoms of SCC

A
  1. PAIN
    Intense, progressive, persistent pain: (back pain in 96% of patient presentations), irritated by coughing, sneezing, straining, straight leg raises against pressure; may travel along affected dermatome
  2. SUBTLE MOTOR WEAKNESS
    usually lower extremities: stiffness, ataxia, falls, dragging, spasticity, positive Babinski’s sign
    Light touch, pain, thermal sensation
  3. SENSORY LOSS AFTER MOTOR
    numbness, tingling, feelings of coldness in affected area
  4. AUTONOMIC DYSFUNCTION
    - urinary disturbances: hesitancy, retention, overflow, incontinence
    - bowel disturbances: lack of urge to defecate, inability to bear down, incontinence; may result in loss of sphincter control if not addressed
    - sexual dysfunction: impotence
    - absence of sweating below level of compression
92
Q

Diagnosis of SCC

A

SHOULD BE IMMEDIATE TO DECREASE RX OF PERMANENT DYSFUNCTION

  • Diagnostic tool of choice: MRI - May be difficult to lie still for someone with back pain – ensure adequate pain control before test
  • tenderness with palpation at level of compression
  • XR, CT, myelography
93
Q

Treatment of SCC

A

Steroids
o High dose steroids (buys time); pain relief; usually short-term (many complications with long-term steroid use)
o Decrease inflammation associated with compression that causes pain
o Side effect of killing cancer cells, causing tumor lysis – can cause TLS

Radiation therapy – treatment of choice
o Started within 24h of diagnosis (even on weekends!); 10-20 fractions (treatments)
o Reduces pain, compression, tumor size
o Improves motor function, may reverse paralysis

Surgery
o Treatment of choice with spinal instability, bone collapse; rapid neurological deterioration; previous maximum radiation to site of compression, radioresistant tumor

Chemotherapy
o Not primary treatment because BBB doesn’t always allow penetration

Adjuvant therapy (alongside radiation and/or surgery)

94
Q

Prevention of SCC

A

Bisphosphonates: decrease skeletal complications of bony metastasis

High Acuity (20 decks)

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