Oncology emergencies Flashcards
1
Q
Liquid/blood cancers include
A
leukemia, lymphomas, plasma cell disorders (multiple myeloma)
2
Q
Cancer treatment options (7)
A
- Hormone therapy
- Surgery - primarily for solid cancers
- Bone marrow transplantation
- Chemotherapy
- Targeted therapy
- Radiation therapy
- Immunotherapy
3
Q
Where do malignancies originate from?
A
Hemopoietic (blood producing cells) in the bone marrow –> myeloid stem cells OR lymphoid stem cells
4
Q
What are myeloid neoplasms?
A
MDS, AA, AML, CML
5
Q
What are lymphoid neoplasms?
A
acute lymphocytic leukemia, multiple myeloma, and lymphomas
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
7
Q
Is acute leukemia fast?
A
Yes, it worsens quickly so it requires very aggressive and timely treatment
8
Q
How do you diagnose acute leukemia?
A
- Peripheral blood tests - see blasts
- Bone marrow biopsy
- Lumbar puncture and imaging
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
10
Q
AML s/s include
A
Fatigue, DIC, bleeding
Generally presents sicker
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)
12
Q
How do you treat acute leukemia?
A
With chemotherapy
13
Q
What is the induction phase of chemotherapy?
A
- Initial chemotherapy
- Meant to induce remission
- Response to induction can predict outcomes/responses to future treatment and prognosis
14
Q
What is the consolidation phase of chemotherapy?
A
- Goal is to eradicate disease to below the level of detection
- Can be done with chemotherapy or stem cell transplant
15
Q
What is the maintenance phase of chemotherapy?
A
- Lower doses of treatment for prolonged periods of time to improve chances of cure
- 5 years out from remission - kind of a cure but don’t use word often
16
Q
What should you watch for doing induction and consolidation phase of chemo?
A
monitor s/s of anemia, thrombocytopenia, and neutropenia
17
Q
What is chronic leukemia?
A
- No blasts
- Very high WBC count
- Very slow progression
- Patients are not usually aware that they have it
18
Q
Chronic lymphocytic lymphoma (CLL) s/s include
A
B-symptoms, early satiety, increase risk of infection
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
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
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
22
Q
Chronic myelogenous leukemia (CML) s/s include
A
weakness, fatigue, SOB, fevers, bone pain
23
Q
How is CML treated?
A
Tyrosine Kinase Inhibitors (TKI) like ponatinib, imatinib, nilotinib
** pills taken daily
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
25
What are the two types of lymphomas?
1. Hodgkins
| 2. Non-hodgkins
26
What is the difference between hodgkins and non-hodgkins?
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.
27
What is lymphoma?
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)
28
What is a lymphocyte? How do they circulate? What are the three types? When do they multiple?
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
29
S/S of B cell lymphoma include? (9)
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
30
How do you diagnose lymphoma?
1. Lymph node biopsy - MUST
2. PET/CT
3. Peripheral labs
4. Bone marrow biopsy
31
Treatment of lymphoma includes..
1. Immunotherapy
2. Chemotherapy
3. Radiation to specific sites
4. Stem cell therapy
5. CAR-T cell therapy
32
What do you see on a MRI/CT with lymphoma and multiple myeloma?
hot spots SPG lymphocytes
| Helps stage patients later and determine if patient is responding to treatment
33
What are you looking for in peripheral labs with lymphoma?
Viral lab: HIV
34
When do you do a bone marrow biopsy with lymphoma
If not sure where patient is going to stage
35
What treatment should you do at first relapse of ALL?
CAR-T cell therapy
36
What is multiple myeloma?
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
37
What is a plasma cell?
Type of WBC
38
What do plasma cells do?
they help you fight infections by making antibodies that recognize and attack germs
39
What is the abnormal protein/antibody plasma cells in multiple myeloma called?
monoclonal immunoglobulin, monoclonal protein (M-protein), M-spike, or paraprotein
40
S/S of multiple myeloma?
```
C - high calcium
R - renal problems (AKI)
A - anemia (low hemoglobin)
B - bone problems (fracture)
I - infection
```
41
How do you diagnosis multiple myeloma?
1. Peripheral lab for myeloma markers (Serum free light chains, immunoglobulins, M protein)
2. Bone marrow biopsy
3. PET/CT imaging
42
What is the treatment for multiple myeloma?
1. Not curable
2. Goal: longest and deepest remission possible
3. Therapy including immunotherapy, radiation, chemotherapy, stem cell transplant and CAR-T cell therapy
43
What is stem cell transplant?
process of administering CD 34 positive cells into host after a preparatory chemo regimen
44
What is the process of stem cell transplant?
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
45
What is the goal of stem cell transplant?
To have a new healthy and effective immune system and functional bone marrow that is providing anew hematopoiesis process
46
Where do the stem cells come from?
1. Autologous - from self
| 2. Allogeneic - from others
47
What is the process of autologous stem cell transplant?
Take the patients own stem cells. --> store them --> give them back to the after a huge dose of chemo
48
What is the allogeneic stem cell transplant process?
Donor stem cells --> infused CD34 positive cells into the host --> fight the leukemia or lymphoma
49
Where can allogeneic stem cells come from?
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)
50
Major complications of stem cell transplant: Sinusoidal obstructive syndrome
1. Gumming up of the liver
| 2. Given actigol or ercidial at same time decreases the risk
51
Major complications of stem cell transplant: graft vs. host disease (GVHD)
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
52
What is acute GVDH and how do you treat it?
1. Occurs within the first 100 days
2. Increased immunosuppressive therapy like corticosteroids (puts patient at increased risk for infection and osteoporosis)
53
What is choleric GVHD?
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
54
What are autologous stem cell transplant use for?
1. Lymphoma
2. Multiple Myeloma
3. CLL
4. Amyloidosis (falls under multiple myeloma)
5. Some autoimmune disorders
6. Testicular
7. Neuroblastoma
55
What are allogeneic stem cell transplants used for?
1. ALL / AML / MDS
2. Some refractory Lymphomas
3. PNH
4. CML/CLL ** try not to**
5. Sickle cell disease
6. Some autoimmune disorders
7. Myelofibrosis
8. Aplastic Anemia
56
Where do all of the lymphoid lineage cancers start?
They start at the naive B cell
| A lot of opportunities to differentiate and become cancerous
57
CAR-T therapy (chimeric antigen receptor T therapy)
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
58
What is CAR-T cell therapy currently used in?
Multiple Myeloma
Lymphoma
Relapsed ALL (Acute Lymphocytic Leukemia)
59
Cytokine release syndrome (CRS)
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
60
What are the symptoms of CRS?
1. Mimic sepsis
2. Fever
3. Hypotension
4. Hypoxia
5. End organ dysfunction
61
How long does it take for CRS s/s to begin?
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
In severe form CRS can...
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
Immune Effector cell-associated neurotoxicity (ICAN)
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
What are the s/s of ICAN?
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
Does ICAN need to be treated promptly?
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
What is an oncologic emergency?
Any acute potentially life treating event in the oncology patient that are directly or indirectly related to cancer to treatment
67
When do oncologic emergencies develop?
At any stage of treatment including diagnosis, relapse, and progression
68
Treatment for oncologic emergencies should be..
Immediate. Any delay in treatment could cause adverse outcomes and result in pain, suffering, and death
69
What are metabolic oncologic emergencies that could occur?
1. TLS
2. Hypercalcemia
3. SIADH
4. Hyper/hypoglycemia
70
What are structural oncologic emergencies that could occur?
1. SVC obstruction
2. Airway obstruction
3. Cord compression
4. Effusion
5. Increase ICP
6. Seizure
71
What are hematologic oncologic emergencies that could occur?
1. Fever
2. Leukostatis/visocsity
3. Bleeding
4. Thrombosis
5. DIC
6. CRS/ICANS
72
What are infusion oncologic emergencies that could occur?
1. Extravasation
2. Anaphylaxis
3. Reactions
73
Which metabolic emergency is this?
```
Blasts: high
WBC: high
Creatinine: high
Potassium: high
Phosphorus: high
Uric acid: high
```
Tumor lysis syndrome
74
Tumor lysis syndrome
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
What happens to the blood when all the intracellular components that get released into the blood stream with tumor lysis syndrome?
hyperkalemia, hyperuricemia, hyperphophatemia, secondary hypocalcemia, renal failure (AKI d/t these)
76
When does tumor lysis syndrome occur?
usually occurs during the first few days of chemo therapy but occurs spontaneously
Can also occur spontaneously before getting chemo
77
As a nurse, after chemo in regards to tumor lysis syndrome you are..
Monitoring labs every 6 hours
Running IV fluids
Looking for s/s of electrolyte abnormalities
78
What can clinical TLS progress to>
renal failure
seizure
cardiac dysrhythmias
death
79
What does hyperkalemia look like?
```
Muscle cramps
Paresthesias
ECG changes (tall peaked T, PR prolongation, widened QRS, loss of P)
Bradycardia
Dysrhythmias
Cardiac arrest
```
80
What does hyperphosphatemia look like?
Nausea/Vomiting/Diarrhea
Lethargy
Seizure
AKI
81
What does hypocalcemia look like?
```
Muscle cramps
Tetany
Hypotension
Dysrhythmia
AKI
Chovstek and Trousseaus
```
82
What does hyperuricemia look like?
AKI
83
Intervention for hyperkalemia
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
Intervention for hyperuricemia
1. allopurinol
2. rasburicase (walk patients labs down on ice for next 48 hours)
3. NS infusion
4. dialysis
85
Intervention for hyperphosphatemia
1. avoid phos and calcium supplementation
2. NS infusion
3. phosphate binder (sevelamer; aluminum hydroxide, calcium acetate)
4. dialysis
86
Intervention for hypocalcemia
1. if asymptomatic, no intervention
| 2. if symptomatic, calcium gluconate
87
What is the problem with a Phosphate binder?
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
```
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?
```
Hypercalcemia of malignancy
89
What is hypercalcemia of malignancy? What cancers is it most common in?
Metabolic disorder that occurs in 25% of cancer patients
| Most common in breast, lung squamous and myeloma
90
What is the calcium level for Mild? moderate? severe?
Mild: 10.5-11.9
Moderate: 12-13.9
Severe: over 14
91
How is calcium normally maintained and how does cancer interfere with that?
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
S/S of hypercalcemia
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
What ECG changes will you see is hypercalcemia?
1. Prolonged PR/QRS
2. Shortened QT/ST
3. Bradycardia
4. Arrhythmia
5. Complete heart block and cardiac arrest
94
How to treat mild hypercalcemia?
* 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
How do you treat moderate hypercalcemia?
1. Hospitalization is usually required
Treat as severe if symptomatic
96
How do you treat severe hypercalcemia?
* *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
```
SOB and stuck in the throat
High RR and HR
Right-sided facial swelling
Bilateral extremity edema
Mediastinal mass
```
What is this?
Superior vena cava obstruction syndrome
98
What is superior vena cava obstruction syndrome?
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
How common is superior vena cava obstruction syndrome?
Occurs in 3-4% of cancer patients but 80% of cases seen will be caused by cancer
100
What are the most common cancers that cause superior vena cava syndrome?
Lung cancer, lymphoma, thyroid, head and neck cancer
101
What are the early s/s superior vena cava obstruction syndrome?
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
What are the late s/s superior vena cava obstruction syndrome?
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
How do you manage superior vena cava obstruction syndrome?
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
Why do you give steroids first to a patient with superior vena cava obstruction syndrome?
first thing you do for the patient to decrease to shrink down so don't compromise airway
105
```
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?
Malignant spinal cord compression
106
What is malignant spinal cord compression?
Occurs when malignant disease or pathologic fracture compresses the spinal cord or caudal equina
107
How often does malignant spinal cord compression occur?
after 5-14% of patents with cancer
| Second most common neurological complication in cancer
108
What is the most common presenting symptom of malignant spinal cord compression?
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
What are the most likely causes of malignant spinal cord compression?
1. Head and neck cancer --> cervical spine
2. Breast or lung cancer --> thoracic spine
3. Prostate, colon, renal or bladder cancer --> lower spine
110
What is the acute management of a malignant spinal cord compression?
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
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?
Malignant pleural effusion
112
What is a malignant pleural effusion?
Malignancy associated with collection of fluid in the pleural space
113
is a malignant pleural effusion serious?
YES! It is life threatening that affects respiratory function by restricting lung expansion. decrease lung volume and altered gas exchange
114
Is malignant pleural effusion common?
Yes, about 50% of cancer patients can develop this
115
What is malignant pleural effusion most commonly caused by?
lung and breast cancer and lymphoma
Often associated with advanced disease and poor outcomes
116
What are the s/s of malignant pleural effusion?
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
What do you s/s of a malignant pleural effusion depend on?
The speed of development (more s/s if fast), volume of expansion, and underlying lung disease
118
How do you diagnose malignant pleural effusion?
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
How do you treat malignant pleural effusion?
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
What are some nursing considerations for the treatment of malignant pleural effusion?
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
What is a hypersensitivity reaction? What are two different causes?
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
What does grade 1 hypersensitivity reaction look like?
1. Urticaria
2. Pruritis
3. Rash
4. Mild upper respiratory symptoms
123
What does grade 2 hypersensitivity reaction look like?
1. Urticaria
2. Pruritis
3. Rash
4. Mild upper respiratory symptoms
5. Wheezing
6. N/V
7. SOB
124
What does grade 3 hypersensitivity reaction look like?
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
Do you always need to treat a hypersensitivity reaction? Is there a range of symptoms?
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
How do you prevent hypersensitivity reactions?
Pre-medication with H1/H2 blocker, Acetaminophen, and Corticosteroids
127
How do you treat a mild hypersensitivity reaction?
1. slow or stop infusion
2. H1/H2 blockers with out without corticosteroids
3. Demerol/dilaudid for rigors
128
How do you treat a anaphylactoid hypersensitivity reaction?
1. STOP infusion
2. Epinephrine
3. Corticosteroids
4. H1/H2 Blockers
5. Resuscitation (O2, fluids, nebs, intubation, pressors)
129
What is extravasation?
infiltration of a vesicant into the surrounding tissue and has the potential to cause tissue destruction, nerve and tendon damage, and function impairment
130
What are the s/s of extravasation?
1. No blood return from IV
2. Anxious/uncomfortable
3. Red around IV site
4. Cold site
5. Swelling
131
What can extravasation lead to?
1. Redness > Blisters -->Loss of surface tissues and muscle
2. Necrosis
3. Nerve and tissue damage
132
What are the two types of vesicants?
1. DNA-binding: worse
| 2. Non-DNA binding
133
What is the best thing for extravasation?
First is to prevent it
| If it still occurs, then emergency immediate intervention and specialty consult is required!
134
What is the acute management of an extravasation?
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
What is disseminated intravascular coagulation (DIC)?
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
Why does DIC develop in oncology patients? Is it serious? Is it common in cancer patients?
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
What are some common causes of DIC?
Sepsis, trauma, obstetric conditions and malignancy
138
What can DIC lead to?
1. Ischemia
2. Infarction
3. Necrosis
4. Organ failure
5. Hemorrhage
6. Death
139
What are the s/s of DIC? (11)
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
What is the most common cancer that is associated with DIC?
ALL
141
How do you treat DIC?
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
When do you transfuse platelets in DIC?
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
When do you transfuse FFP in DIC?
1. if INR is more than 2
| 2. if fibrinogen is less than 100 (can also transfuse gyro for this)
144
When do you transfuse PRBC in DIC?
if hemoglobin is less than 8
145
What is immunocompromised fever a sign of? What can it lead to??
Sign of infection and sepsis which can lead to shock and death (progresses to shock and death very quickly)
146
Is immunocompromised fever common?
YES
80% of patients with heme malignancy will develop fever
10-40% of solid tumor cancers with develop fever
147
What is immunocompromised fever a sign of? What can it lead to??
Sign of infection and sepsis which can lead to shock and death (progresses to shock and death very quickly)
148
What are the most common causes of immunocompromised fever?
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
What are the diagnostics for
| immunocompromised fever?
1. Chest x ray
2. CT
3. Ultrasound
4. Bronchoscopy
150
How do you treat immunocompromised fever?
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
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?
Treat for infection AND give Tociluzumab (direct anticytokine therapy) and Steroids
152
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?
Treat for infection AND give Tociluzumab (direct anticytokine therapy) and Steroids
