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Emergency Med Exam 4 > Approach to bleeding disorders & heme emergencies > Flashcards

Approach to bleeding disorders & heme emergencies Flashcards

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1
Q

Suspect underlying ______ if easy bleeding/bruising or hemarthrosis.

A

bleeding
disorder

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2
Q

Suspect _____ anemia if there is
jaundice

A

hemolytic

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3
Q

Suspect _____ if skin ulcerations, glossitis, peripheral neuropathy, ataxia, altered mental status

A

nutritional deficiency

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4
Q

Iron metabolism is altered due to an increase in _____, which inhibits iron
absorption and recycling, leading to iron sequestration

A

hepcidin

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5
Q

RBCs w/ abnormal hemoglobin are susceptible to _____

A

hemolysis

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6
Q

Sickle Cell Disease

A

● Abnormal hemoglobin structure,
premature RBC destruction (20 days)
● 250 million people worldwide are
carriers, 2 million in the United States

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7
Q

Vaso-occlusive Crisis (sickle cell crisis)

A

● Small vessel occlusion leads to ischemia and infarct of bone, organs, and soft tissues.
● Can be triggered by cold, infection, dehydration, altitude, medications… (deoxygenated
conditions)
● Diffuse bone, muscle, and joint pain. Abdominal pain.
● Pallor, jaundice, hepatosplenomegaly, cardiomegaly

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8
Q

Acute Chest Syndrome

A

● Life-threatening complication of sickle cell anemia
● Lung injury due to microvascular occlusion (precipitated by pneumonia, rib or lung
infarct, fat embolism, opioids).
● Cough, SOB, chest pain, fever, rales

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9
Q

Thalassemia

A

● Abnormal hemoglobin production leads to microcytic, hypochromic, hemolytic
anemia.
● Defective synthesis of alpha or beta globin chains
○ Severity depends on number and type of mutations
● May see hepatosplenomegaly, jaundice, osteopenia (expansion of bone marrow
cavity in attempt to compensate for low RBC production)

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10
Q

Thalassemia treatment

A

● None required for alpha-thalassemia trait or beta-thalassemia trait (mild or
asymptomatic).
● Other forms may require RBC transfusion, iron chelation, splenectomy, stem
cell transplant.

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11
Q

_____ RBCs are susceptible to
oxidative stress

A

G6PD-deficient

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12
Q

Hereditary Spherocytosis

A

Defect in RBC membrane structural proteins, results in
microspherocytic shape of RBCs.
● Not flexible, unable to pass through the spleen, get destroyed
on the way through, resulting in hemolytic anemia.
● Anemia, jaundice, splenomegaly, spherocytes on peripheral
blood smear.
● Cause of neonatal jaundice, intermittent episodes of
hemolysis at older ages.

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13
Q

Hereditary Spherocytosis treatment

A

● RBC transfusion for severe, symptomatic anemia.
● Possible splenectomy to reverse anemia

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14
Q

Autoimmune Hemolytic Anemia

A

● Produces antibodies against own
RBCs.
● Detected with Direct Coombs Test
(direct antigen test). How does this
work again?
● May be idiopathic or triggered by
lymphoproliferative, autoimmune, or
infectious diseases.

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15
Q

Autoimmune Hemolytic Anemia treatment

A

● High dose corticosteroids, immunosuppression
● Splenectomy (what complication would this prompt us to think of in the ED
setting?

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16
Q

Thrombotic Thrombocytopenic Purpura (TTP)

A

● Microangiopathic hemolytic anemia: Deficient ADAMTS13 activity results in
long polymers of von Willebrand factor, instead of cleaving it correctly.
● Causes blood clots and also shreds red blood cells as they pass → Hemolysis
● Thrombocytopenic due to use of platelets in microthrombi (Fibrin not
involved)
● Women, 30-50, African or Hispanic descent
● Pregnancy, HIV, Influenza Vaccine, Drug-induced

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17
Q

Pentad for TTP

A

● CNS Abnormalities
● Renal Impairment
● Fever
● Microangiopathic
Hemolytic Anemia
● Thrombocytopenia

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18
Q

TTP Treatment

A

Plasma Exchange (Plasmapheresis) - Attempt to restore ADAMTS13,
gets rid of defective enzymes, von Willibrand multimers, autoantibodies

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19
Q

Hemolytic Uremic Syndrome (HUS) triad

A

Common cause of acute renal failure in childhood
1. Microangiopathic hemolytic anemia
2. Acute renal failure (Typically children)
3. Thrombocytopenia

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20
Q

Hemolytic Uremic Syndrome (HUS) treatment

A

Supportive, Transfusion, Dialysis, Long termchance of kidney injury, and neurologic injury.

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21
Q

Disseminated Intravascular Coagulation

A

DIC is an acute acquired disorder
- Simultaneous hemorrhage and thrombosis-varies by illness
⌘ - Damage to endothelial cell walls triggers intrinsic cascade
↪ Thrombin generation → Clot Formation →Ischemic changes
↪ Indirectly activates tissue plasminogen activator→ Fibrinolysis
↪ Hyperfibrinolysis causes clots to dissolve → Bleeding
↪ Also the condition consumes clotting factors→Bleeding
- Hypercoagulation - could dominate, but typically bleeding does
- Range from petechiae to diffuse hemorrhage

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22
Q

Disseminated Intravascular Coagulation PE findings

A

Petechiae, echymosis, hematuria, Mental status changes, ischemia,
renal necrosis, lung injury, May develop multi-system organ failure

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23
Q

Lab Study findings for DIC

A
  • Low Platelets
  • Prolonged PT and PTT
  • Low Fibrinogen level, <100mg/dL(severe)
  • Elevated D-Dimer
  • Low levels of coag factors
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24
Q

Disseminated Intravascular Coagulation

A

Focus on underlying illness, hemodynamic support, volume support
Otherwise, depends on if bleeding or clotting is dominant
Blood products only if bleeding is present:
- Cryoprecipitate- Hypofibrinogenemia- level goal, 100-150 mg/dL
- Platelet transfusion-<20,000 or <50,000 + bleeding
- Fresh Frozen Plasma if bleeding
- Vitamin K for prolonged PT
- LMWH when thrombotic complications dominate

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25
Primary Homeostasis
Platelet Plug
26
Secondary Homeostasis
● Coagulation Cascade ● Problems occur at various points on this cascade ● The body requires hemostatic balance
27
Common presentation for inherited bleeding disorders
● Easy bruising, Recurrent hemarthrosis, Muscle hematoma (iliopsoas common, presents w/ hip pain)- Look for compartment syndrome! ● May not be obvious at first, take patient concerns seriously ● Consult pt database of hemophilia centers, pts often have established management plan
28
Hemophilia treatment
- Replace missing factor or induce body to secrete clotting factor from intracellular stores. (Infusion of Recombinant Factor VIII or IX Concentrate) - Hemophilia A- Can give desmopressin (Increases levels of vWF, factor VIII, & tPA) - Can give fresh frozen plasma if you don’t know which factor is missing (contains all the clotting factors) - Pain control
29
When to admit for hemophillia
Hemorrhages involving head, neck, pharynx (airway compromise), retroperitoneum, compartment syndrome, uncontrolled bleeding
30
Von Willebrand Disease
● Dysfunction of primary hemostasis - cofactor of platelet adhesion, and a carrier protein for factor VIII ● Group of disorders, defect or deficiency in vWFactor (vWF) ○ Type 1- most common, decreased levels, skin and mucosal bleeding ○ Type 2- abnormal dysfunction of vWF ○ Type 3- complete factor deficiency, presents like hemophilia A
31
Von Willebrand Disease treatment
Desmopressin if mild, Factor VIII concentrate w/ vWF, sometimes platelet transfusions.
32
Von Willebrand Disease treatment
- Avoid Aspirin and NSAIDs - DDAVP (Desmopressin)- mainstay for type 1 - Factor VIII concentrate w/ vWF- type 2 and 3 - Cryoprecipitate- refractory type 1, type 2 and 3 (last resort only) - Platelet transfusion- non-responding type 3 - Oral contraceptives- menstrual bleeding/menorrhagia - E-aminocaproic acid/Tranexamic acid- dental injury/procedures
33
Immune (Idiopathic) Thrombocytopenia (ITP) treatment
Platelet Transfusion- depends on situation and numbers Corticosteroids IV Immunoglobulin Splenectomy- if refractory D/c offending medication (if drug induced
34
HELLP Syndrome
● Hemolysis-Elevated Liver enzymes, Low Platelets ● Associated with pregnancy ● Variant of pre-eclampsia, hypertension may not be present ● Gestational Thrombocytopenia ● > 20 wks till 7 days postpartum
35
Factor V Leiden Mutation
- Factor V helps convert Prothrombin to Thrombin, Inactivated by Protein C. - With the mutation → Protein C resistance, Factor V can’t be inactivated. - Long-term prophylaxis could be considered
36
Protein S and C
- Think of proteins S and C as anticoagulant proteins. Deficiency = blood clots - Protein C inactivates Factors VIII and V and protein S is a cofactor
37
Antithrombin III Deficiency
Increased action of Thrombin, overproduction of Fibrin
38
Heparin Induced Thrombocytopenia (HIT)
- Antibodies to Heparin bind to platelets and activate clotting - Leads to thrombocytopenia and hypercoagulable state - Occurs 5-7 days after Heparin - Hypercoagulable for weeks even after stopping heparin - Labs show reduced platelets in patient given Heparin
39
Treatment of HIT
● Discontinue Heparin ● Direct Thrombin Inhibitor (Pradaxa, Angiomax) ● Factor Xa Inhibitors (Xarelto) ● Hematology Consult
40
Goal of transfusion therapy
- Improve O2 delivery - Intravascular volume expansion - Replace missing or depleted clotting factors
41
Blood Transfusion treatment: what can be given
- Packed Red Blood Cells (PRBC) - Platelets - Fresh Frozen Plasma (FFP) - Cryoprecipitate - Whole blood makes sense, but hard to store. So it’s divided up.
42
Typically transfuse when Hgb is less than ____
7 gm/L
43
Packed Red Blood Cells
- Increase in oxygen carrying capacity - Usually for emergent acute blood loss - Typically transfuse when Hgb is less than 7 gm/L - Although must look at the whole clinical picture
44
Indications for PRBC
- Acute hemorrhage, > 30% loss of blood volume - Hemorrhagic shock - Surgical blood loss >2 liters - Symptomatic anemia, at risk for ischemia, sepsis - With acute blood loss, transfusions are clinically based (Not on Hgb)
45
Indications to transfuse platelets
< 10,000 and asymptomatic <20,000 minor bleeding, coag disorder, low risk procedure <50,000 and invasive procedure/surgery <100,000 cardiac/Neuro surg
46
Fresh Frozen Plasma (FFP)
separated and frozen w/in 8 hrs of collection - Contains all coagulation factors and fibrinogen - Use in bleeding patients with multiple deficiencies (Liver dz, Warfarin, DIC) - Prior to high-risk invasive procedures
47
Indications to transfuse fresh frozen plasma
- Reversal of warfarin overcoagulation (not firstline) - Bleeding w/ multiple coag defects - Correction when specific factor not available - Massive transfusion protocol - Plasma exchange thrombotic microangiopathies or neurologic disorders
48
Indications to transfuse cryoprecipitate
A. Active bleeding fibrinogen <100 mg/dL (Liver dz, DIC, etc.) B. Active bleeding in vW disease, when DDAVP not effective, factor VIII not available C. Hemophilia A, when virally inactivated VIII not available
49
Transfusion complications: acute
- Febrile nonhemolytic transfusion reaction(most common) - Acute intravascular hemolytic reaction - ABO Incompatibility - Allergic reaction and anaphylaxis - Transfusion related acute lung injury (TRALI) - More common with FFP and Plasma, not typically PRBC - Granulocyte recruitment - inflammatory reaction in lungs - Respiratory distress, pulmonary edema - Transfusion Associated Circulatory Overload (TACO)
50
Transfusion Complications: delayed
- Delayed hemolytic transfusion reaction - Transfusion associated graft vs host disease - Fatal 90% of the time - Post transfusion purpura - Infectious disease transmission
51
Bone metastases and spinal cord compression
- Solid tumors- breast, lung, prostate; pain, pathologic fracture - Symptoms- pain, weakness, bowel/bladder dysfunction - Imaging- XR, CT, MRI - Management- Pain control, dexamethasone, radiotherapy - Surgery in select cases
52
Oncologic Emergencies: airwau obstruction
Compression, bleeding, edema, infection - Symptoms- dyspnea, wheezing, stridor, tachypnea Management - Imaging CXR vs CT, Humidified O2, Intubation - Surgical airway, oncologist or surgeon consult
53
Febrile neutropenia
- Temperature above 38.3 with absolute Neutrophil count(ANC) below 1000 cells/mm3 - Counts will drop within 10-15 days after chemo, rebound 5 days later
54
Malignant pericardial effusion workup
- Asymptomatic to tamponade Symptoms - Chest heaviness, dyspnea, cough, syncope Physical Exam - Tachycardia, hypotension, distended neck veins, muffled heart sounds, pulsus paradoxus, narrowed pulse pressure Echocardiography, CXR, ECG Ultrasound-guided pericardiocentesis
55
Superior vena cava syndrome
- Compression from an external mass - Lung cancer or lymphoma/ dyspnea, chest pain, cough,
56
Superior vena cava syndrome management
- O2, elevate head/upper body (if neuro symptoms) - Dexamethasone, Methylprednisolone- ↑ICP - Consult for chemo/radiation/intravascular stenting
57
Hypercalcemia of malignancy
- Common with breast, lung, lymphoma, multiple myeloma. - Symptoms nonspecific- Polydipsia, Polyuria, weakness, anorexia, nausea, abdominal pain, AMS - Related to rate of rise, above 12 mg/dL; ECG changes-short QT
58
Management of Hypercalcemia of malignancy
- NS infusion, Bisphosphonates(prevent bone resorption) - Calcitonin SC or IM; glucocorticoids; dialysis; consult oncologist - Hormone that plays a role in reducing calcium
59
Hyponatremia due to SIADH management
- Water restriction, Furosemide, Demeclocycine, - 3% hypertonic saline- severely low sodium with seizures, coma - 25-100cc/hr titrated to a correction of 0.5-1.0 mEq/h
60
Adrenal crisis
- Exogenous steroid induced adrenal suppression - Tumor infiltration of adrenal tissue
61
Adrenal crisis management
- Hydrocortisone 100-150 mg IV IV fluids, supportive care
62
Tumor lysis syndrome
- Massive quantities of potassium, phosphate, uric acid released into the circulation. - Usually 1-3 days after chemotherapy for leukemia or lymphoma - May cause renal failure, life-threatening arrhythmias, seizures
63
Tumor lysis syndrome management
- Hyperkalemia- Insulin, glucose, bicarbonate, kayexalate, albuterol- - Hyperuricemia - Rasburicase - Hyperphosphatemia- Insulin and Glucose - Aggressive infusion of isotonic fluids - Consider hemodialysis for Potassium >6, Uric Acid >10, Phosphate >10 - Admit to ICU
64
Hyperviscosity syndrome
Impaired blood flow due to abnormal plasma contents - Dysproteinemia, acute leukemia, polycythemia - Usually hematocrits >60%, WBC counts >100,000/mm3
64
Hyperviscosity syndrome symptoms
Fatigue, abdominal pain, headache, blurry vision, AMS, Fever, dyspnea. - Thrombosis or bleeding. - Fundoscopic- Retinal hemorrhages, exudates, “sausage-linked” vessels
65
Extravasation of Chemotherapeutic Agents
- Stop infusion, attempt aspiration through line - Symptoms- pain, swelling, erythema (within hours) - Consult oncologist- use of antidotes

Emergency Med Exam 4 (5 decks)

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