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Oncology emergencies Flashcards

1
Q

Liquid/blood cancers include

A

leukemia, lymphomas, plasma cell disorders (multiple myeloma)

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2
Q

Cancer treatment options (7)

A
  1. Hormone therapy
  2. Surgery - primarily for solid cancers
  3. Bone marrow transplantation
  4. Chemotherapy
  5. Targeted therapy
  6. Radiation therapy
  7. Immunotherapy
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3
Q

Where do malignancies originate from?

A

Hemopoietic (blood producing cells) in the bone marrow –> myeloid stem cells OR lymphoid stem cells

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4
Q

What are myeloid neoplasms?

A

MDS, AA, AML, CML

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5
Q

What are lymphoid neoplasms?

A

acute lymphocytic leukemia, multiple myeloma, and lymphomas

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6
Q

What is acute leukemia?

A

Abnormal production of immature blood cells (blasts) that cannot carry out normal function so they multiply rapidly and gum up the system

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7
Q

Is acute leukemia fast?

A

Yes, it worsens quickly so it requires very aggressive and timely treatment

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8
Q

How do you diagnose acute leukemia?

A
  1. Peripheral blood tests - see blasts
  2. Bone marrow biopsy
  3. Lumbar puncture and imaging
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9
Q

S/S of acute leukemia include?

A

Systemic: Weight loss, Fever, Frequent Infection, Fatigue, Loss of appetite

Lungs: SOB

Muscles: weak - d/t anemia

Bone and joints: pain and tenderness d/t bone marrow crowded

Swollen lymph nodes

Enlargement of spleen or liver –> decrease appetite and easily full

Skin: Night sweats, easy bleeding and bruising, petechiae

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10
Q

AML s/s include

A

Fatigue, DIC, bleeding

Generally presents sicker

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11
Q

ALL s/s include:

A

hepatosplenomegaly
Lymphoid linage: B symptoms: unintentional weight loss, drenching night sweats, fever of unknown origin, painless lymphadenopathy (swollen lymph nodes)

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12
Q

How do you treat acute leukemia?

A

With chemotherapy

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13
Q

What is the induction phase of chemotherapy?

A
  1. Initial chemotherapy
  2. Meant to induce remission
  3. Response to induction can predict outcomes/responses to future treatment and prognosis
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14
Q

What is the consolidation phase of chemotherapy?

A
  1. Goal is to eradicate disease to below the level of detection
  2. Can be done with chemotherapy or stem cell transplant
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15
Q

What is the maintenance phase of chemotherapy?

A
  1. Lower doses of treatment for prolonged periods of time to improve chances of cure
  2. 5 years out from remission - kind of a cure but don’t use word often
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16
Q

What should you watch for doing induction and consolidation phase of chemo?

A

monitor s/s of anemia, thrombocytopenia, and neutropenia

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17
Q

What is chronic leukemia?

A
  1. No blasts
  2. Very high WBC count
  3. Very slow progression
  4. Patients are not usually aware that they have it
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18
Q

Chronic lymphocytic lymphoma (CLL) s/s include

A

B-symptoms, early satiety, increase risk of infection

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19
Q

Should you be worried about the very high WBC in CLL?

A

no, not really. Patient is generally fine until you see blasts which could indicate acute leukemia

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20
Q

Do patients with CLL have hyperkalemia?

A

They usually sit at the upper end of normal. The lab tests may give falsely high potassium levels because there is a lot of large WBC that are bumping into things and breaking things a part. Need a whole blood sample to determine actual potassium level

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21
Q

What is CLL treated with?

A

BTK-inhibitors (ibrutinib or acalabrutinib)
BCL-2 inhibitors (venetoclax)
** both pills that are taken on and off during life time or a low dose every day

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22
Q

Chronic myelogenous leukemia (CML) s/s include

A

weakness, fatigue, SOB, fevers, bone pain

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23
Q

How is CML treated?

A

Tyrosine Kinase Inhibitors (TKI) like ponatinib, imatinib, nilotinib
** pills taken daily

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24
Q

What is the biggest issue for keeping chronic leukemias under control?

A

medication adherence.
Nurses should make sure patents are not having severe SE that are intolerable and stopping them from taking their pills and that they have a good regimen for taking them to ensure that they are taking they. If chronic leukemias grow out of control, it can turn into acute leukemia that requires aggressive interventions

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25
Q

What are the two types of lymphomas?

A
  1. Hodgkins

2. Non-hodgkins

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26
Q

What is the difference between hodgkins and non-hodgkins?

A

Hodgkins: have reed-Sternberg cells and are considering the most treatment responsive cancers.

Non-hodgkins: huge diversity of lymphomas. B cell NHL is most common. T/NK are less common. Much more aggressive so prognosis and treatment will vary.

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27
Q

What is lymphoma?

A
  1. Type of cancer that arises in the lymphocyte (infection fighting cell)
  2. Lymphoma develops when B, T, or NK cells transform from healthy cells into malignant cells.
  3. Lymphomas can be B cell lymphomas (most common), T cell lymphoma or T/NK lymphoma (rare)
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28
Q

What is a lymphocyte? How do they circulate? What are the three types? When do they multiple?

A

WBC made in bone marrow
Circulate throughout the body in the blood and lymphatic system
B, T, and NK
Multiple in presence of bacteria or other invaders

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29
Q

S/S of B cell lymphoma include? (9)

A
  1. Enlarged lymph nodes
  2. Cough
  3. Enlarged liver and spleen
  4. Nephrotic syndrome
  5. Night sweats
  6. Itching
  7. bone marrow involvement
  8. Fever of unknown origin
  9. Early satiety –> weight loss
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30
Q

How do you diagnose lymphoma?

A
  1. Lymph node biopsy - MUST
  2. PET/CT
  3. Peripheral labs
  4. Bone marrow biopsy
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31
Q

Treatment of lymphoma includes..

A
  1. Immunotherapy
  2. Chemotherapy
  3. Radiation to specific sites
  4. Stem cell therapy
  5. CAR-T cell therapy
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32
Q

What do you see on a MRI/CT with lymphoma and multiple myeloma?

A

hot spots SPG lymphocytes

Helps stage patients later and determine if patient is responding to treatment

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33
Q

What are you looking for in peripheral labs with lymphoma?

A

Viral lab: HIV

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34
Q

When do you do a bone marrow biopsy with lymphoma

A

If not sure where patient is going to stage

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35
Q

What treatment should you do at first relapse of ALL?

A

CAR-T cell therapy

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36
Q

What is multiple myeloma?

A
  1. Cancer that forms in a plasma cell
  2. Cancerous plasma cells accumulate in the bone marrow and crowd out healthy blood cells.
  3. The plasma cells make n abnormal protein/antibody
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37
Q

What is a plasma cell?

A

Type of WBC

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38
Q

What do plasma cells do?

A

they help you fight infections by making antibodies that recognize and attack germs

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39
Q

What is the abnormal protein/antibody plasma cells in multiple myeloma called?

A

monoclonal immunoglobulin, monoclonal protein (M-protein), M-spike, or paraprotein

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40
Q

S/S of multiple myeloma?

A 
C - high calcium
R - renal problems (AKI)
A - anemia (low hemoglobin)
B - bone problems (fracture)
I -  infection
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41
Q

How do you diagnosis multiple myeloma?

A
  1. Peripheral lab for myeloma markers (Serum free light chains, immunoglobulins, M protein)
  2. Bone marrow biopsy
  3. PET/CT imaging
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42
Q

What is the treatment for multiple myeloma?

A
  1. Not curable
  2. Goal: longest and deepest remission possible
  3. Therapy including immunotherapy, radiation, chemotherapy, stem cell transplant and CAR-T cell therapy
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43
Q

What is stem cell transplant?

A

process of administering CD 34 positive cells into host after a preparatory chemo regimen

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44
Q

What is the process of stem cell transplant?

A
  1. Eradicate disease with a very high dose of chemotherapy and likely radiation at the same time
  2. Revive the patient by administering stem cells and/or initiating graft venous disease effect
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45
Q

What is the goal of stem cell transplant?

A

To have a new healthy and effective immune system and functional bone marrow that is providing anew hematopoiesis process

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46
Q

Where do the stem cells come from?

A
  1. Autologous - from self

2. Allogeneic - from others

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47
Q

What is the process of autologous stem cell transplant?

A

Take the patients own stem cells. –> store them –> give them back to the after a huge dose of chemo

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48
Q

What is the allogeneic stem cell transplant process?

A

Donor stem cells –> infused CD34 positive cells into the host –> fight the leukemia or lymphoma

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49
Q

Where can allogeneic stem cells come from?

A
  1. Match related donor (bother or sister) - Sib allo
  2. Matched unrelated done - MUD allo
  3. Cord (fetal umbilical cord blood cells) - dual cord
  4. Syngeneic (identical twin)
  5. Halo-identical (1/2 matched donor)
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50
Q

Major complications of stem cell transplant: Sinusoidal obstructive syndrome

A
  1. Gumming up of the liver

2. Given actigol or ercidial at same time decreases the risk

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51
Q

Major complications of stem cell transplant: graft vs. host disease (GVHD)

A

When donors T cells (the graft) attack and damage the patients healthy T cell because it sees them as foreign
Can be mild, moderate, or severe and life threatening

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52
Q

What is acute GVDH and how do you treat it?

A
  1. Occurs within the first 100 days
  2. Increased immunosuppressive therapy like corticosteroids (puts patient at increased risk for infection and osteoporosis)
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53
Q

What is choleric GVHD?

A

occurs more than 100 days after transplant
Can involve one organ or multiple.
Leading cause of medical problems and death after an allogeneic stem cell transplant

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54
Q

What are autologous stem cell transplant use for?

A
  1. Lymphoma​
  2. Multiple Myeloma​
  3. CLL​
  4. Amyloidosis​ (falls under multiple myeloma)
  5. Some autoimmunedisorders​
  6. Testicular
  7. Neuroblastoma
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55
Q

What are allogeneic stem cell transplants used for?

A
  1. ALL / AML / MDS​
  2. Some refractoryLymphomas​
  3. PNH​
  4. CML/CLL​** try not to**
  5. Sickle cell disease​
  6. Some autoimmunedisorders​
  7. Myelofibrosis​
  8. Aplastic Anemia
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56
Q

Where do all of the lymphoid lineage cancers start?

A

They start at the naive B cell

A lot of opportunities to differentiate and become cancerous

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57
Q

CAR-T therapy (chimeric antigen receptor T therapy)

A
  1. Autologous process
  2. Take a patients own T cells and modifies them by adding a chimeric antigen receptor which is designed to recognize and bind to the specific tumor-associated antigen on the surface of the antigen-expressing cells and then the T cell releases cytokines and injects the cancer cell leading to apoptosis
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58
Q

What is CAR-T cell therapy currently used in?

A

Multiple Myeloma
Lymphoma
Relapsed ALL (Acute Lymphocytic Leukemia)

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59
Q

Cytokine release syndrome (CRS)

A
  1. Occurs in the over activation of the immune system –> supra physiological response –> a ton of cytokines being released and IL-6 playing a central role
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60
Q

What are the symptoms of CRS?

A
  1. Mimic sepsis
  2. Fever
  3. Hypotension
  4. Hypoxia
  5. End organ dysfunction
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61
Q

How long does it take for CRS s/s to begin?

A

They can occur very rapidly and without warning within 7 weeks of CAR-T cell therapy. Usually occurs around 5-7 days after CAR-T cell therapy

62
Q

In severe form CRS can…

A

lead to life threatening complications like cardiac dysfunction, ARDS from capillary leak, renal or hepatic failure, DIC, or MAS/HLH (macrophage activation syndrome/hemophagocytic lymphohistiocytosis).

63
Q

Immune Effector cell-associated neurotoxicity (ICAN)

A
  1. Diverse process that occur in T cells
  2. IL-6 that is being filled into blood causes increased capillary permeability which will allows components of the blood to cross the BBB like cytokines and activated lymphocytes
64
Q

What are the s/s of ICAN?

A
  1. Altered mental status
  2. Aphasia** (expressive aphasia is common)
  3. Handwriting changes**
  4. Motor weakness
  5. Seizure
  6. Cerebral edema
  7. Impaired cognition
  8. Encephalopathy
  9. Non-specific: HA, tremor, myoclonus, hallucinations
65
Q

Does ICAN need to be treated promptly?

A

Yes, it can be very serious so it is very important that we recognize and intervene right away to prevent progression and improve outcomes

66
Q

What is an oncologic emergency?

A

Any acute potentially life treating event in the oncology patient that are directly or indirectly related to cancer to treatment

67
Q

When do oncologic emergencies develop?

A

At any stage of treatment including diagnosis, relapse, and progression

68
Q

Treatment for oncologic emergencies should be..

A

Immediate. Any delay in treatment could cause adverse outcomes and result in pain, suffering, and death

69
Q

What are metabolic oncologic emergencies that could occur?

A
  1. TLS
  2. Hypercalcemia
  3. SIADH
  4. Hyper/hypoglycemia
70
Q

What are structural oncologic emergencies that could occur?

A
  1. SVC obstruction
  2. Airway obstruction
  3. Cord compression
  4. Effusion
  5. Increase ICP
  6. Seizure
71
Q

What are hematologic oncologic emergencies that could occur?

A
  1. Fever
  2. Leukostatis/visocsity
  3. Bleeding
  4. Thrombosis
  5. DIC
  6. CRS/ICANS
72
Q

What are infusion oncologic emergencies that could occur?

A
  1. Extravasation
  2. Anaphylaxis
  3. Reactions
73
Q

Which metabolic emergency is this?

Blasts: high
WBC: high 
Creatinine: high
Potassium:  high 
Phosphorus: high 
Uric acid: high
A

Tumor lysis syndrome

74
Q

Tumor lysis syndrome

A
  1. Life threatening condition that occurs after cellular destruction of rapidly growing tumors
  2. Release all of their intracellular contents into the blood stream
75
Q

What happens to the blood when all the intracellular components that get released into the blood stream with tumor lysis syndrome?

A

hyperkalemia, hyperuricemia, hyperphophatemia, secondary hypocalcemia, renal failure (AKI d/t these)

76
Q

When does tumor lysis syndrome occur?

A

usually occurs during the first few days of chemo therapy but occurs spontaneously
Can also occur spontaneously before getting chemo

77
Q

As a nurse, after chemo in regards to tumor lysis syndrome you are..

A

Monitoring labs every 6 hours
Running IV fluids
Looking for s/s of electrolyte abnormalities

78
Q

What can clinical TLS progress to>

A

renal failure
seizure
cardiac dysrhythmias
death

79
Q

What does hyperkalemia look like?

A 
Muscle cramps
Paresthesias
ECG changes (tall peaked T, PR prolongation, widened QRS, loss of P)
Bradycardia
Dysrhythmias 
Cardiac arrest
80
Q

What does hyperphosphatemia look like?

A

Nausea/Vomiting/Diarrhea
Lethargy
Seizure
AKI

81
Q

What does hypocalcemia look like?

A 
Muscle cramps
Tetany
Hypotension
Dysrhythmia
AKI
Chovstek and Trousseaus
82
Q

What does hyperuricemia look like?

83
Q

Intervention for hyperkalemia

A
  1. avoid potassium supplementation
  2. NS infusion
  3. cardiac monitoring
    Stabilize heart with calcium gluconate
    Shift potassium with sodium bicarbonate, insulin/D50 and albuterol
    Remove potassium with sodium polystyrene resin (kayexalate) and dialysis
84
Q

Intervention for hyperuricemia

A
  1. allopurinol
  2. rasburicase (walk patients labs down on ice for next 48 hours)
  3. NS infusion
  4. dialysis
85
Q

Intervention for hyperphosphatemia

A
  1. avoid phos and calcium supplementation
  2. NS infusion
  3. phosphate binder (sevelamer; aluminum hydroxide, calcium acetate)
  4. dialysis
86
Q

Intervention for hypocalcemia

A
  1. if asymptomatic, no intervention

2. if symptomatic, calcium gluconate

87
Q

What is the problem with a Phosphate binder?

A

It will only work if the patient is eating so if they are not eating, nurse should advocate that it will not work to the provider

88
Q 
Tachycardic
Drowsy, lethargic and confused 
Spine pain
Weak extremities 
Decreased bowel sounds 
Distended abd and global tenderness with palpitation 
High calcium 
High creatinine 
EKG: shorted QTc
CXR: rib fractures and thoracic compression
AXR: ileus 
What does this patient have?
A

Hypercalcemia of malignancy

89
Q

What is hypercalcemia of malignancy? What cancers is it most common in?

A

Metabolic disorder that occurs in 25% of cancer patients

Most common in breast, lung squamous and myeloma

90
Q

What is the calcium level for Mild? moderate? severe?

A

Mild: 10.5-11.9
Moderate: 12-13.9
Severe: over 14

91
Q

How is calcium normally maintained and how does cancer interfere with that?

A

Calcium is normally maintained by homeostasis by bone reabsorption, intestinal absorption and renal excretion. With cancer, homeostasis interference can occur d/t renal dysfunction or hormonal dysregulation

92
Q

S/S of hypercalcemia

A

Stones (calcium stones and renal dysfunction, polyuria, polydipsia), groans (severe abdominal pain, anorexia, ulcers), bones (fractures, bone pain) and moans (drowsy, lethargy, weakness, depression, confusion delirium, decreased DTR), ECG changes

93
Q

What ECG changes will you see is hypercalcemia?

A
  1. Prolonged PR/QRS
  2. Shortened QT/ST
  3. Bradycardia
  4. Arrhythmia
  5. Complete heart block and cardiac arrest
94
Q

How to treat mild hypercalcemia?

A
  • usually sent home*
    1. Close monitoring
    2. Oral hydration
    3. Ambulation to reabsorb Ca
    4. Limit nephrotoxins
    5. Limit drugs that inc. Calcium
    6. Treat underlying malignancy

Treat as severe if symptomatic

95
Q

How do you treat moderate hypercalcemia?

A
  1. Hospitalization is usually required

Treat as severe if symptomatic

96
Q

How do you treat severe hypercalcemia?

A
  • *Everything for mild PLUS**
    1. Hospitalization required
    2. Baseline ECG and Telemetry
    3. Close electrolyte monitoring (every 6 hours)
    4. IV Fluids (200ml/hr)
    5. Diuresis (fluids + diuresis –> bathroom often)
    6. Administration of Calcitonin +/- Bisphosphonates and Steroids
    7. May need emergent Dialysis if symp. get worse

TREAT DISEASE

97
Q 
SOB and stuck in the throat
High RR and HR
Right-sided facial swelling 
Bilateral extremity edema
Mediastinal mass

What is this?

A

Superior vena cava obstruction syndrome

98
Q

What is superior vena cava obstruction syndrome?

A

Compression or invasion of the SVC by a tumor, thrombosis or infection –> obstruction of blood flow to the heart from the head, neck, arms, and supper thorax

99
Q

How common is superior vena cava obstruction syndrome?

A

Occurs in 3-4% of cancer patients but 80% of cases seen will be caused by cancer

100
Q

What are the most common cancers that cause superior vena cava syndrome?

A

Lung cancer, lymphoma, thyroid, head and neck cancer

101
Q

What are the early s/s superior vena cava obstruction syndrome?

A
  1. Edema of the face, neck, arms and thorax
  2. Dilated veins (spider veins)
  3. Facial plethora (Red, ruddy appearance to face and cheeks)
  4. Horner syndrome (due to pressure on the cervical sympathetic nerves)
102
Q

What are the late s/s superior vena cava obstruction syndrome?

A
  1. Cyanosis
  2. Chest pain/SOB/respiratory distress
  3. Hoarseness/stridor
  4. Absent peripheral pulses
  5. Mental status changes, seizure, coma
  6. CHF
  7. Decreased BP
  8. Syncope
103
Q

How do you manage superior vena cava obstruction syndrome?

A
  1. CT
  2. Tissue biopsy
  3. Radiation with or without chemotherapy
  4. Steroids
  5. Surgery/vascular stenting
  6. Thrombolysis or anticoagulation
  7. Frequent VS and tele monitoring
104
Q

Why do you give steroids first to a patient with superior vena cava obstruction syndrome?

A

first thing you do for the patient to decrease to shrink down so don’t compromise airway

105
Q 
Back pain
Bowel and bladder incontinence 
Leg weakness and tingling 
Decreased sensation in both LE
Severe point tenderness in lower spine 
Elevated calcium 
Compression fracture in lower spine on X-ray

What does this patient have?

A

Malignant spinal cord compression

106
Q

What is malignant spinal cord compression?

A

Occurs when malignant disease or pathologic fracture compresses the spinal cord or caudal equina

107
Q

How often does malignant spinal cord compression occur?

A

after 5-14% of patents with cancer

Second most common neurological complication in cancer

108
Q

What is the most common presenting symptom of malignant spinal cord compression?

A

New back pain which can be localized, radicular or referred

When this comes up asks about bowel and bladder habits, leg weakness, decrease sensation

109
Q

What are the most likely causes of malignant spinal cord compression?

A
  1. Head and neck cancer –> cervical spine
  2. Breast or lung cancer –> thoracic spine
  3. Prostate, colon, renal or bladder cancer –> lower spine
110
Q

What is the acute management of a malignant spinal cord compression?

A
  1. Aim is to alleviate pain, prevent permanent disability (if patient is in pain moving more)
  2. ROS/Physical exam (pain, neurologic impairment)
  3. Diagnostic Imaging Evaluation (MRI entire spine)
  4. Neurosurgical and Rad Onc consultation
  5. Dexamethasone (steriods)
  6. Radiation
  7. Surgery (laminectomy, vertebral resection, kypho/vertebroplasty)
  8. Chemotherapy
  9. Neuro exams*** possibly every hour
111
Q

SOB, chest pain, hypoxia
Anxiety and agitated
increase RR
Nearly absent breath sounds in right lung
Dull percussion in right mid and lower lobe
Increase lactate

What is going on with the patient?

A

Malignant pleural effusion

112
Q

What is a malignant pleural effusion?

A

Malignancy associated with collection of fluid in the pleural space

113
Q

is a malignant pleural effusion serious?

A

YES! It is life threatening that affects respiratory function by restricting lung expansion. decrease lung volume and altered gas exchange

114
Q

Is malignant pleural effusion common?

A

Yes, about 50% of cancer patients can develop this

115
Q

What is malignant pleural effusion most commonly caused by?

A

lung and breast cancer and lymphoma

Often associated with advanced disease and poor outcomes

116
Q

What are the s/s of malignant pleural effusion?

A

Subjective: dyspnea, dry cough, chest pain, orthopnea, hemopytosis, tracheal deviation, anxiety/fear or suffocation, fever, malaise, weight loss
Objective: increase RR, dull percussion, decreased or absent lung sounds, bronchial breath sounds, friction rub, cyanosis, accessory muscle use

117
Q

What do you s/s of a malignant pleural effusion depend on?

A

The speed of development (more s/s if fast), volume of expansion, and underlying lung disease

118
Q

How do you diagnose malignant pleural effusion?

A
  1. CXR-lateral and decubitus
  2. CT-detect smaller effusions; differential diagnoses
  3. US used to clarify volume of fluid and guide thoracentesis
  4. Thoracentesis
119
Q

How do you treat malignant pleural effusion?

A
  1. Treat underlying cause of effusion (Chemo, XRT, antibx, diuresis, steroids, NSAIDs)
  2. Therapeutic thoracentesis
  3. Chest tube drainage
  4. Pleurodesis/talc (gel the pleural spaces together)
  5. Pleuroperitoneal shunt
  6. Pleurex catheter
  7. Pleurectomy and pleural abrasion
120
Q

What are some nursing considerations for the treatment of malignant pleural effusion?

A
  1. Watching how how drainage is coming out
  2. Caring for any devices that have been inserted into the patient
  3. Keeping any surgical incisions clean
121
Q

What is a hypersensitivity reaction? What are two different causes?

A

A reaction that occurs in the response to chemotherapy, biotherapy or supportive care therapies

Allergic or non allergic but it doesn’t really matter because they are all treated the same

122
Q

What does grade 1 hypersensitivity reaction look like?

A
  1. Urticaria
  2. Pruritis
  3. Rash
  4. Mild upper respiratory symptoms
123
Q

What does grade 2 hypersensitivity reaction look like?

A
  1. Urticaria
  2. Pruritis
  3. Rash
  4. Mild upper respiratory symptoms
  5. Wheezing
  6. N/V
  7. SOB
124
Q

What does grade 3 hypersensitivity reaction look like?

A
  1. Urticaria
  2. Pruritis
  3. Rash
  4. Mild upper respiratory symptoms
  5. Wheezing
  6. N/V
  7. SOB
  8. Serious cardiopulmonary or neurological compromise
125
Q

Do you always need to treat a hypersensitivity reaction? Is there a range of symptoms?

A

No, the symptoms can range from mild with requires no intervention to severe anaphylactic reaction that can lead to death
If it is just a mild reaction, the best thing that you can do is just power through and give medication. In future may run the infusion slower

126
Q

How do you prevent hypersensitivity reactions?

A

Pre-medication with H1/H2 blocker, Acetaminophen, and Corticosteroids

127
Q

How do you treat a mild hypersensitivity reaction?

A
  1. slow or stop infusion
  2. H1/H2 blockers with out without corticosteroids
  3. Demerol/dilaudid for rigors
128
Q

How do you treat a anaphylactoid hypersensitivity reaction?

A
  1. STOP infusion
  2. Epinephrine
  3. Corticosteroids
  4. H1/H2 Blockers
  5. Resuscitation (O2, fluids, nebs, intubation, pressors)
129
Q

What is extravasation?

A

infiltration of a vesicant into the surrounding tissue and has the potential to cause tissue destruction, nerve and tendon damage, and function impairment

130
Q

What are the s/s of extravasation?

A
  1. No blood return from IV
  2. Anxious/uncomfortable
  3. Red around IV site
  4. Cold site
  5. Swelling
131
Q

What can extravasation lead to?

A
  1. Redness > Blisters –>Loss of surface tissues and muscle
  2. Necrosis
  3. Nerve and tissue damage
132
Q

What are the two types of vesicants?

A
  1. DNA-binding: worse

2. Non-DNA binding

133
Q

What is the best thing for extravasation?

A

First is to prevent it

If it still occurs, then emergency immediate intervention and specialty consult is required!

134
Q

What is the acute management of an extravasation?

A
  1. Stop the infusion (including chemotherapy and any other fluids)
  2. Do NOT remove the catheter/needle (disconnect IV tubing, but leave IV catheter/needle)
  3. Aspirate fluid (attempt to aspirate any fluid from the subcutaneous tissue through the IV catheter/needle)
  4. Do NOT flush the IV line/catheter
  5. If indicated, Sodium thiosulfate is the only antidote
  6. Elevate and immobilize the affected extremity (for 24-48 hrs.)
  7. Monitor the site closely (outline the extravasation area every 1-2 hours)
  8. Consultation/evaluation by plastic surgery team
135
Q

What is disseminated intravascular coagulation (DIC)?

A
  1. Widespread intravascular thrombosis causing tissue ischemia and organ dysfunction
  2. Consumption depletion of coagulant factors and platelets –> hemorrhage

lots of clotting and lots of bleeding at the same time

136
Q

Why does DIC develop in oncology patients? Is it serious? Is it common in cancer patients?

A

IT is secondary to an underlying patho condition.
Most serious thrombotic disorder that occurs in cancer
With acute leukemia, about 10-40% of patients

137
Q

What are some common causes of DIC?

A

Sepsis, trauma, obstetric conditions and malignancy

138
Q

What can DIC lead to?

A
  1. Ischemia
  2. Infarction
  3. Necrosis
  4. Organ failure
  5. Hemorrhage
  6. Death
139
Q

What are the s/s of DIC? (11)

A
  1. Thrombosis (more in solid tumors)
  2. Bleeding (more in Heme)
  3. Oozing from multiple sites
  4. Ecchymosis and petechiae
  5. Uncontrolled hemorrhage
  6. Microvascular thrombosis with hypo-perfusion, ischemia, necrosis, organ failure
  7. Mental status changes, irritability, confusion
  8. Cardiopulmonary decompensation
  9. Shock
  10. MODS
  11. Death
140
Q

What is the most common cancer that is associated with DIC?

141
Q

How do you treat DIC?

A
  1. Treat underlying cause of DIC (cancer, infection, trauma)
  2. Monitor DIC panel every 6-12hrs (cbc, dimer, fib, INR, PTT)
  3. Heparin anticoagulation if thrombosis predominates or for VTE prophylaxis if not contraindicated
  4. Blood product replacement
142
Q

When do you transfuse platelets in DIC?

A

if platelet count is below 10-20
If platelet are below 30 with a heme malignancy
If platelets are below 50 with an active bleed

143
Q

When do you transfuse FFP in DIC?

A
  1. if INR is more than 2

2. if fibrinogen is less than 100 (can also transfuse gyro for this)

144
Q

When do you transfuse PRBC in DIC?

A

if hemoglobin is less than 8

145
Q

What is immunocompromised fever a sign of? What can it lead to??

A

Sign of infection and sepsis which can lead to shock and death (progresses to shock and death very quickly)

146
Q

Is immunocompromised fever common?

A

YES
80% of patients with heme malignancy will develop fever
10-40% of solid tumor cancers with develop fever

147
Q

What is immunocompromised fever a sign of? What can it lead to??

A

Sign of infection and sepsis which can lead to shock and death (progresses to shock and death very quickly)

148
Q

What are the most common causes of immunocompromised fever?

A
  1. Gram negative bacteria (E. coli) -40-50% of septic shock and more pathogenic
  2. Gram postive bacteria (strep, staph) -5-10% of septic shock and less pathogenic
  3. Yeast/fungal (candida)
  4. Viral
149
Q

What are the diagnostics for

immunocompromised fever?

A
  1. Chest x ray
  2. CT
  3. Ultrasound
  4. Bronchoscopy
150
Q

How do you treat immunocompromised fever?

A
  1. Vital signs (Volume resuscitation and Oxygen support)
  2. Labs (CBC, CMP, PT/INR, fibrinogen, lactate)
  3. Cultures (Blood (line/peripheral), urine, sputum, wound/lesions, abscess, etc)
  4. ANTIBIOTICS
    DO NOT DELAY antibiotics for labs, diagnostic testing or any cultures OTHER THAN blood cultures (hang within 1 hour)
151
Q

Ms. N is post CAR-T infusion so in our possibilities should also be CRS because she has hypoxia, hypotension and fever. How do you treat?

A

Treat for infection AND give Tociluzumab (direct anticytokine therapy) and Steroids

152
Q

Ms. N is post CAR-T infusion so in our possibilities should also be CRS because she has hypoxia, hypotension and fever. How do you treat?

A

Treat for infection AND give Tociluzumab (direct anticytokine therapy) and Steroids

Complex Care (22 decks)

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