Heme Flashcards

Question

What is paroxysmal nocturnal hemoglobinuria? ANesthesia management?

Answer 1

* Complement- activated RBC hemolysis * Stem cell disorder, presents during 2nd- 8th decade of life * Abnormalities or reduction in a RBC membrane protein * Life expectancy after diagnosis 10 years * Thought to be result of CO2 retention and subsequent acidosis * High risk for DVT due to complement activation * Hepatic and portal veins * Aplastic bone marrow * Anesthetic Management * Avoid respiratory depressants- *prevent CO2 retention!!!* * Avoid hypoxemia, hypo-perfusion and hypercarbia * Maintain hydration and DVT prophylaxis * If transfusion required: “washed” RBCs should be used to decrease complement activation * *if you anticipate giving blood, order washed PRBC and order the blood EARLY (at least a night in advance)* * *washed prbc take awhile...*

Answer 2

* Phosphogluconate oxidative metabolic pathway * Normally counteracts environmental oxidants and prevents globin denaturation * In deficiency of G6PD enzyme, oxidative stress causes denaturation of Hgb which precipitates on the inner surface of the RBC membrane resulting in membrane damage and hemolysis * Most common enzymatic disorder of RBCs worldwide * African Americans, Asians and Mediterranean populations * Ranges from mild/no hemolysis (Class V and IV)à chronic hemolytic anemia (Class I) * Oxidative drugs, infection, ingestion of fava beans aggravate preexisting hemolysis

Answer 3

* Tailor to severity and acuity of anemia * Class V, VI--\> little anesthetic implications * Avoid risk of hemolysis * Avoid oxidative drugs * NSAIDs, Quinolones, Sulfa drugs * Avoid drugs that depress G6PD activity * **Isoflurane, sevoflurane, diazepam, metoclopramide** * Avoid Methylene blue! * Life-threatening if administered (*hemolysis)* * Avoid drugs that cause **methemoglobinema** (*because its treated with methylene blue. also avoid NTG, SNP)* * Lidcaine, prilocaine, benzocaine, silver nitrate * Avoid and aggressively treat conditions that cause significant oxidative stress * Hypothermia, Acidosis, Hyperglycemia, infections * **_Codeine, midazolam, propofol, fentanyl and ketamine are safe_**

Answer 4

* Most common enzyme defect that results in congenital hemolytic anemia * Worldwide * Northern European descent and China * Less prevalent than G6PD deficiency but considerably greater occurrence of chronic hemolysis * **Accumulation of 2,3 DPG** * Shifts oxyhemoglobin curve to the **right** * High incidence of hemolysis in the spleen--\> **splenomegaly** * **Life-threatening, transfusion-requiring hemolytic anemia at birth** * Chronic jaundice, gallstones * **Splenectomy** improves degree of hemolysis and may eliminate need for transfusions * *increases r/f infection*

Answer 5

* Immune system induced hemolysis * Sensitization of RBCs * Disease- induced * Drug- induced * Infection induced hemolysis * Malaria * Particles released during hemolysis can result in DIC and hypersplenism

Answer 6

* ↑ risk of tissue hypoxia * If previous splenectomy may have ↑ risk of perioperative infection * Increased risk venous thrombosis due to activation of coagulation cascade * Erythropoietin is often prescribed for 3 days preoperatively * **Acute drops in Hgb below \< 8 g/dl and chronic reductions to below 6 g/ dl** should be considered for **transfusion** * Preop hydration and prophylactic administration of RBCs have been advocated * Caution **Methylene Blue administration**

Answer 7

* Inherited homozygous disorder of the hemoglobin molecule * Substitution of valine for glutamic acid on the beta globulin chain * Results in mutant hemoglobin (S)--\> 70-98% Hgb is type S * Extreme states of deoxygenation--\> Hgb aggregates forming a polymer distorting the erythrocyte’s membrane--\>sickled cell shape * Cells sickle and occlude small vessels-\> decreasing blood flow and oxygen delivery to tissues * Increased incidence of hemolysis resulting in average RBC lifespan of 10-20 days (normal 120 day lifespan) * **Oxy-hemoglobin curve shifts to the right as compensation**

Answer 8

* Begins early in life, progression highly variable * Severe hemolytic anemia--\> end- organ damage * Bone marrow, spleen, kidneys, CNS * **Splenic** infarctionà loss of splenic function within first decade of life--\> infection! * **Kidney**--\> painless hematuria and loss of concentrating ability--\>chronic renal failure in third-fourth decade of life * Pulmonary damage due to chronic persistent inflammation * Neurologic complications include both ischemic and hemorrhagic strokes * Vaso-occlusive crises * Episodic painful bone and joint pain associated with concurrent illness, stress, dehydration

Answer 9

* Life threatening * With de-oxygenation, Hgb S forms an insoluble globulin polymer * Acute episodic vaso-occlusive crisis * Ischemia / infarction of organs * Pain, stroke, renal failure, liver failure, splenic sequestration, PE * Very painful * Acute chest syndrome

Answer 10

* **Can be fatal (typically 2-3 days postop)** **S/S** * Pneumonia-like, presence of new pulmonary infiltrate involving one complete lung segment * Pulmonary vascular occlusion * Pleuritic chest pain, dyspnea, fever (\>38.5 C), acute pulmonary hypertension **Treatment:** * Transfusion or exchange transfusion to Hct of 30% * Supplemental 02, inhaled nitric oxide (reduce pulmonary hypertension) * Antibiotics * Inhaled bronchodilators * Aggressive pain management * Monitor for pain crises, stroke, and infection * *typically won't see on OR table, but may help managing pain*

Answer 11

Heterozygous carriers of sickle cell * Have one normal gene and one abnormal gene encoding hemoglobin S (genotype AS) * 40% of their Hgb is S/ 60 % is normal Hgb A * Usually do not develop anemia and or symptoms, requiring no treatment * 5% at some time have * Hematuria * Difficulty concentrating urine * Do not require pre-op transfusions * 8% African Americans have trait * *no changes in anesthetic managmeent guidelines*

Answer 12

* High incidence perioperative complications * Risk factors * Advanced age, frequent severe sickling episodes, evidence of end-organ damage **(low baseline O2 saturation, elevated creatinine, cardiac dysfunction, stroke)**, and concurrent infection * Surgical considerations * **Low risk surgeries**: extremity and minor procedures (inguinal hernia repairs) * **Moderate risk:** intraabdominal operations * **High risk:** intracranial, **_intrathoracic_** and **_hip replacement_**

Answer 13

* Look for evidence of organ damage, cardiac dysfunction, concurrent infection * May benefit from conservative transfusions with high risk surgery * **Pre-operative transfusion to increase HCT to 30% without regard to ratio of sickle Hb to normal Hb** * Major **noncardiac** surgeries may transfuse to goal of **HbS \<30%** and **cardiopulmonary bypass surgeries goal of HbS\<5%**

Answer 14

* Hypoxemia/acidosis * hypovolemia * stasis * hypothermia

Answer 15

* Supplemental O2 * Preoperative hydration for 12 hours prior to surgery * *if they were not admitted the night before, find them first thing in preop and start giving fluid!* * Pre-med * avoid respiratory depression leads to acidosis * *may want to take over ventilation and don't forget preoxygenation!* * Regional anesthesia is **advocated** for pain control * concern with hypotension, stasis of blood flow, compensatory vasoconstriction * *give fluid before regional and treat hypotension. helps to decrease crises* * Aggressive pain management, may have tolerance * Avoid infections * Avoid tourniquets (but not contraindicated) * **Keep patient WARM!** * Maintain high cardiac output * Position to prevent stasis

Answer 16

* Inability to form either ⍺ (⍺-thalassemia) or β (β-thalassemia) globin chains of hemoglobin * Severe- life-threatening anemia, often require repeated transfusions * *with repeated transfusions, neeed T&C readily available prior to OR* * *Can have lots of abs to blood and change in blood type, making itdifficult to obtain blood in individuals* * **Hallmarks: ineffective erythropoiesis, hemolytic anemia and hypochromia with microcytosis** * Chronic deficit in O2 carrying capacity**--\>** max erythropoietin release--\> increased unbalanced globin synthesis--\> aggregation and precipitate formation--\> membrane damage * Some cells destroyed in bone marrow --\>ineffective erythropoiesis * Some escape into ciulation **--\>** hemolytic anemia and hypochromia with microcytosis

Answer 17

* Extramedullary hematopoiesis--\>bone marrow hyperplasia (maxillary bone and frontal bone), stunted growth and osteoporosis, hepatomegaly * *can cause difficulty with intubation* * Hemolytic anemia--\> splenomegaly, CHF, dyspnea and orthopnea * Transfusion therapy--\> iron overload--\>cirrhosis and jaundice, right sided- heart failure, endocrinopathy--\> chelation therapy * Increased risk infection (splenectomy) * Arrhythmias and very sensitive to digitalis * Spinal cord compression * *note any paresthesias!*

Answer 18

* Pituitary- impaired growht, infertility * Thyroid- hypoparathyroidism * herat- CMP, cardiac fialure * Liver- hepatic cirrhosis * Pancreas- DM * Gonads- hypogonadism

Answer 19

* Heterozygous state (trait) for either ⍺- globin or β-globin gene mutation * Mild to moderate microcytic anemia * Normal RBC count * *no anesthesia implications* * *enough normla hgb that they're ok*

Answer 20

* CHF common with severe anemia * Cardiac arrhythmias due to heart failure * Hemodynamic compromise with induction agents if low cardiac reserve-use cardiac sparing drugs * *etomidate, high dose opioid* * Very sensitive to the effects of digitalis * Hepatosplenomegaly * Coagulopathy (? Regional Anesthesia) * *not contraindicated, need to look at plt/coags and discuss plan with surgeon* * Hypersplenism can result in thrombocytopenia and ↑ risk of infection

Answer 21

* Potential difficult airway 2º to maxillary deformities * Consider awake fiber-optic intubation * Complications of iron loading from chronic therapy * Diabetes (Blood glucose monitoring) * Adrenal insufficiency (↓ response to vasopressors) * Liver dysfunction & Coagulation abnormalities * Hypothyroidism & hypoparathyroidism * Arrhythmias (ECG) * Right-sided Heart failure (ECHO)

Answer 22

* Iron moiety in Hgb is oxidized from the ferrous (Fe2+) state to ferric (Fe3+) state * Methemoglobinemia moves the oxyhemoglobin dissociation curve markedly to the left--\> little oxygen is delivered to the tissues (left= love) * Results in polycythemia * Normal RBC maintains methemoglobin levels **\<1% through the methemoglobin reductase enzyme system** * Methemoglobin levels **\<30%= no compromise to tissue oxygenation** * Methemoglobin levels **30-50%= symptoms of oxygen deprivation** * Methemoglobin levels **\>50%= coma and death**

Answer 23

Mechanisms of development: * Globin chain mutations favor **formation of Hgb M** * **Resistant** to **reduction** by **methemoglobin reductase system** * Hgb M carry brownish blue color that does not change to red when exposed to oxygen--\> cyanotic appearance independent of PaO2 * Usually asymptomatic * Mutations impairing methemoglobin reductase system * Methemoglobinemia levels \<25%---\> cyanotic appearance independent of PaO2 * **Toxic exposure** to substances that oxidize normal Hgb iron at a rate that exceeds capacity of the normal reducing mechanisms * Infants at greater risk with oxidizing agents * **Local anesthetics (prilocaine/benzocaine), nitrates and nitric oxide**

Answer 24

* Avoid toxic levels of: **local anesthetics (prilocaine/benzocaine), nitrates, nitric oxide especially in infants, patients with Hgb M and those with G6PD deficiency** * Pulse oximetry is unreliable--\> typically reads 85% * Methemoglobin absorbs red and infrared wavelengths equally; 1:1 ratio= 85% * Falsely **underestimates** SpO2 when SaO2 is **\>85%** * Falsely **overestimates** SpO2 when SaO2 of **\<85%** * Emergency treatment of toxic methemoglobinemia * Avoid tissue hypoxia and **further left-ward shift on oxy-hemoglobin curve** * *SNP can cause methhemoglobinemia and moves oxy-hgb curve even further to the left!* * O2 therapy * **1-2 mg/kg** of intravenous methylene blue as a 1% solution in saline infused over 3-5 mins, may repeat after 30 mins * Arterial line to measure bp, methemoglobin levels and arterial blood gas * Correct acidosis * Monitor EKG for signs of ischemia

Answer 25

* Aplastic anemia refers to bone marrow failure characterized by destruction of rapidly growing cells * RBC, WBC (neutrophils) and platelets * Marrow Damage or failure from: * Genetic disorders (Fanconi Anemiaà pancytopenia and acute leukemia) * Drugs (see table 24-1 Stoelting 7th ed) (*next slide)* * Radiation * Infectious process (viral hepatitis, Epstein-Barr virus, HIV, rubella, TB) * CBC/WBC/Platelet values can be extremely low * May need pre-op transfusion * Know pre-op medications and therapies

Answer 26

* *table 24-1 Stoelting 7th ed) from previous slide* * Antibiotics (chloramphenicol, **penicillin**, **cephalosporins**, sulfonamides, amphotericin B, streptomycin * Antidepressants (**lithium**, tricyclics) * Antiepileptics (dilantin, carbamazepine, valproic acid, **phenobarbital**) * Anti-inflammatory drugs (phenylbutazone, nonsteroidals, salicylates, gold salts) * Antiarrhythmics (**lidocaine**, quinidine, **procainamide**) * Antithyroidal drugs (propylthiouracil) * Diuretics (**thiazides**, pyrimethamine, **furosemide**) * Antihypertensives (captopril) * Antiuricemics (allopurinol, colchicine) * Antimalarials (quinacrine, chloroquine) * Hypoglycemics (tolbutamide) * Platelet inhibitors (ticlopidine) * Tranquilizers (prochlorperazine, meprobamate)

Answer 27

* Patients on immunosuppressive therapy * Steroid stress dose should be considered * Reverse isolation due to thrombocytopenia and increased risk of infection * Prophylactic antibiotics due to neutropenia * Hemorrhage (GI & Intracranial) * **LV dysfunctio**n 2º high output state and fluid overload- *ECHO may be needed* * Co-existing congenital abnormalities * Fanconi anemia is the peds version * Cleft palate; cardiac defects * Dif**ficulty cross-matching blood products after multiple transfusions**

Answer 28

Preinduction/induction * Consider transfusions before induction * Airway hemorrhage possible with DVL * Avoid nasal intubation * Regional Anesthesia depends on coagulation * Labile hemodynamic response to induction (avoid decreases in CO) Maintenance * PEEP will facilitate use of ↓ FiO2 (hyperoxia depresses bone marrow) * Avoid nitrous oxide (bone marrow suppressant) * Maintain normothermia Extubation and postoperative period * Period with greatest O2 demands * Monitor coagulation status

Answer 29

* Expanded red cell mass and increased Hct * Does increase oxygen-carrying capacity but increases blood viscosityà decreased tissue perfusion * Caused by: * Reduction in plasma volume (dehydration) * Production of excess RBC (polycythemia vera) * Chronic hypoxia (pulmonary disease, extremely low CO, extreme obesity with hypoventilation, high altitudes) * Increased erythropoietin production (renal disease and EPO secreting tumors) * Increased blood viscosity * Venous / arterial thrombosis leading to CAD, pulm HTN, CNS disorders * Usually minor, until Hct \> 55% * Mild hypoxic polycythemia= no specific treatment * Phlebotomy- *if very high, (\>55%), consider canceling sx and phlebotimize*

Answer 30

**X chromosome congenital _factor VIII_ deficiency (intrinsic pathway affected)** Severe Hemophilia: * **Factor VIII levels less than 1% of normal** * Diagnosis as children due to frequent spontaneous hemorrhages in joints and muscles or organs Moderate Hemophilia: * Factor VIII levels 1% to 5% of normal * Reduced severity of the disease * Increased risk bleeding with surgery/trauma * Less problems with joints and muscles Mild Hemophilia: * Factor VIII levels as low as **6% to 30%** * often undiagnosed until adulthood * Increased bleeding risk with major surgery **Significantly prolonged PTT /normal PT**

Answer 31

Factor VIII must be brought near normal (100%) for surgery 1. Infusion of factor VIII concentrate * **initial infusion of _50 to 60 U/kg_** (3500–4000 units in a 70-kg patient). Since the half-life of factor VIII is approximately 12 hours in adults, repeated infusions of **25 to 30 U/kg every 8 to 12 hours will be needed to keep the plasma factor VIII level above 50%.** * Therapy must **be continued for up to 2 weeks** to avoid **postoperative bleeding** that disrupts wound healing 2. FFP, cryoprecipitate * *FFP has all coag factors except plt* * *cryo has VIII, XIII, vWF, fibrinogen!* * *also has smaller administration volume* 3. **Desmopressin (0.3 mcg/kg IV**) for mild Hemophilia A * Increases factor VIII threefold to fivefold

Answer 32

**Congenital factor IX deficiency** Severe disease * Factor IX levels of less than 1% * Associated with severe bleeding Moderate disease * Factor IX levels of bleeding 1% to 5% Mild disease * Factor IX levels of between 5% and 40% **Significantly prolonged PTT /normal PT**

Answer 33

* Recombinant/purified product of factor IX are used to treat mild bleeding episodes or as prophylaxis with minor procedures * *can result in increase DVT because it's an activated factor IX* * Dose of **100 U/kg** (7000 units in a 70-kg patient) needs to be administered * Half-life of 18 to 24 hours, so repeated infusions at 50% of the original dose every 12 to 24 hours are usually sufficient to keep the factor IX plasma level above 50%. * Increased risk of thromboembolic complications because these agents contain activated clotting factors * FFP * ***Cryo cannot be given because cryo does not contain factor IX (only VIII. XIII, vwf, Fibrinogen)***

Answer 34

Most common inherited disorder of PLATELET FUNCTION * Problem is either a quantity or quality issue with vWF * Type 1: Quantitative defect; Desmopressin **will work!** * Type 2: Qualitative defect; desmopressin **has varied results** * Type 3: virtual absence of vWF because endothelium lacks vWF; **desmopressin has no effect** * Mucus membrane bleeding common and results in: * Epistaxis * Easy bruising * Menorrhagia * Gingival and gastrointestinal bleeding * Type 3 will also see bleeding in muscles and joints * **_Platelet count normal_** * **Bleeding time is markedly prolonged (normal is 3-10minutes); rapid platelet function assay (RPFA)** * **May have prolonged PTT (due to low levels of factor VIII)**

Answer 35

* Avoid nasal intubations or insertion of nasal trumpets * DDAVP therapy (Desmopressin) –mild bleeding or minor surgerym (**type I and II only!)** * **IV 0.3 μg/kg diluted in 30 to 50 m**L of saline and infused over 10 to 20 minutes to minimize side effects **( tachycardia and hypotension)** * **Intranasal 300-μg dose of intranasal DDAV**P (Stimate nasal spray), administered by the application of 100 μL of a 1.5-mg/mL solution to each nostril * Short lived effect (12-24 hours); Repeated doses result in tachyphylaxis * Cryoprecipitate – more reliable for severe bleeding or surgical prophylaxis * Cryoprecipitate is a readily available and effective blood product that contains concentrated fibrinogen, vWF, and factors VIII and XIII

Answer 36

* ASA irreversible inhibition of cyclooxygenaseà inhibits thromboxane A2 (TxA2) synthesisà severely inhibits platelet aggregation * Bleeding Time is prolonged 2-3 minutes within 3 hours of ASA ingestion * Lasts the lifetime of platelet * Bleeding time returns to normal within 72 hours but aggregation may not return for normal for 7-10 days * NSAIDS--\> reversibly inhibits platelet cyclooxygenase * Antibiotics * **PCNs and cephalosporins** * Critically ill patients at greatest risk of significant bleeding * Interfere with platelet adhesion, activation and aggregation * Volume expanders * Dextran interferes with platelet aggregation * Hydroxyethyl starch in excess of 2 L

Answer 37

Platelets become very dysfunctional in setting of: * Hypothermia (\<35℃) * Acidosis (pH \<7.3) * Uremia * Liver Disease **Treatment**: * Desmopressin for **mild-moderate** dysfunction or mild risk of bleeding * Cryoprecipitate for vWF (essential in platelet adhesion) * Platelet transfusion- *if problem with plt*

Answer 38

* Low platelet count * Normal platelet count 150,000-450,000, lifespan 9-10 days * **Approximately 1/3 platelets are sequestered in the spleen** * Signs include petechial rash, bleeding from nose, GI tract, bruising * Platelet count \>**50,000** needed for major surgery to control bleeding * **20,000-30,000** appropriate for **minor** surgery * **100,000** for **neurosurgical** procedures/ **neuraxial** (regional) procedures * Each unit of apheresis platelets or **six units** of random donor platelets (six pack) should **increase** platelet count approx **50,000**

Answer 39

**Dilutional thrombocytopenia and dilution of pro-coagulants** * Blood loss replaced with crystalloid, colloid and PRBCs which dilutes platelets and factors * Massive blood transfusions 10 or more units * Surgical hemorrhage causes the release of fibrinogen from hepatic stores * Fibrinogen levels \<150mg/dl--\> coagulopathy * Must give FFP to restore pro-coagulants, and consider platelets

Answer 40

Failure in platelet production resulting from marrow damage * Radiation therapy * Chemotherapy * Exposure to toxic chemicals * Drugs such as thiazide diuretics, alcohol, and estrogen * Malignancies * Viral hepatitis * Vit B12 or folate deficiencies May require platelet transfusions

Answer 41

Disseminated Intravascular Coag * Platelet destruction disorder- *clotting all over the palce and then destroying clots all over, rapid depletion of coagulants (anti and pro)* * Associated with clinical conditions * Sepsis * Trauma * Cancer * Obstetric complications * Vascular disorders * Immunological disorders * Excessive deposit of fibrin / impaired fibrin degradation throughout the vascular tree * **Platelet consumption** * Depression of the normal coagulation mechanisms * Clinical symptoms of DIC are a consequence thrombosis and bleeding * Micro emboli accumulation in pulm system * Organ damage

Answer 42

* No single lab test can establish or rule out the diagnosis * Rapid decrease in **platelet count \< 50,000** * **Prolonged PT, PTT** * Presence of **elevated** split fibrin degradation products **(D-dimers)** * **Low** plasma concentrations of **factor VIII** * **Decreased** **fibrinogen** levels * Treatment is the management of the underlying clinical disorder that triggered the coagulation process * Transfusion of platelets, FFP, cryoprecipitate, RBCs (if indicated) * **Heparin administration** to block **thrombin** formation which **blocks consumptio**n of the other clotting factors and allows hemostasis to occur. * Hemodynamic/ respiratory support PT should not be on table unless absolutely necessary!!!

Answer 43

* Vitamin K is necessary in the liver for factors II,VII,IX,X * Deficiency occurs in the presence of * Malnutrition * GI malabsorption * Antibiotic induced elimination of intestinal flora * Liver disease/Obstructive jaundice * Prolonged PT in presence of normal PTT (because of factor VII!) * Treatment: * Vitamin K (6-24 hours for full effect) * Fresh Frozen Plasma if active bleeding is present

Answer 44

* Congenital disorders * Acquired: * Malignancies * Pregnancy * Oral contraception * Nephrotic syndrome * Systemic lupus erythematosus

Answer 45

* Anesthetic considerations: * Early ambulation * Subcutaneous heparin * Compression elastic stockings * ASA * Vena caval filter * Hydration- **KEY!!!** * Regional anesthesia beneficial, but may not be advised if on LMWH

Answer 46

Long term anti-coagulants used for : * Venous thrombo-embolisms * Hereditary hypercoagulable states * Cancer * Mechanical heart valves * Atrial fibrillation Therapy poses problem when need surgery (risk of thrombosis vs risk of surgical bleeding)

Answer 47

* Indicated for pts at risk for CVA, MI, other vascular thrombosis complications * Aspirin * NSAIDS * PDE inhibitors * ADP Receptor antagonists

Answer 48

* Competes with vit K and inhibits synthesis of vit K-dependent clotting factors * II, VII, IX, and X * Monitored with PT and INR * Reversal with vit K, 4-factor PCCs, FFP

Answer 49

Management includes: * Hold Coumadin 5 days * Measure INR one day pre-op and if **INR \>1.8 give 1mg to 2mg Vitamin K SQ** * Emergent reversal of **Coumadin _5-8 ml/kg of FFP_** If high risk without anticoagulation- * Start IV or SQ heparin **3 day**s after stopping Coumadin * Turn off heparin **6 hours** prior to surgery * Surgery can be safely performed if **INR is \<1.5**

Answer 50

* Indirectly inhibits thrombin and factor Xa by binding to AT-III * Monitor with PTT or ACT * Reversal is Protamine * Complication is HIT * (thromboembolic complications)

Answer 51

* Can develop spinal hematoma/hemorrhage * **LMWH- +/- regional (stop 24 hours)** * *****varies between providers. guidlines say 24 hours may be ok, but a lot of anesthesia providers do not feel comfortable with lovenox being administered and regional anesthesia* * **ASA/ NSAIDS-** regional may be **ok**, as long as not using other anticoagulants * **Plavix**- no regional **(stop 7 days)** * **SQ heparin**- regional may be **ok** (recommend give after regional) * **Coumadin**- stop **5 days** (INR \<1.5)

Heme Flashcards

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