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1

Overview of anticoagulation

 

 

2

What does Aspirin do and how does it work?

Introduction:

thromboxane function 

under normal conditions thromboxane is responsible for the aggregation of platelets that form blood clots

prostaglandins function prostaglandins are local hormones produced in the body and have diverse effects including

the transmission of pain information to the brain

modulation of the hypothalamic thermostat

inflammation

Mechanism of ASA inhibits the production of prostaglandins and thromboxanes through irreversible inactivation of the cyclooxygenase enzyme within platelets 

acts as an acetylating agent where an acetyl group is covalently and irreversibly attached to a serine residue in the active site of the cyclooxygenase enzyme. 

this differentiates aspirin different from other NSAIDs which are reversible inhibitors

Metabolism 

renal

3

Unfractionated Heparin (SQ)

Mechanism 

binds and enhances ability of antithrombin III to inhibit factors IIa, III, Xa  

Reversal 

protamine sulfate

Metabolism 

hepatic

Risk 

bleeding

HIT (heparin induced thrombocytopenia) 

4

EnoXAparen

Lovenox

Overview 

molecular name: enoxaparin

trade name: Lovenox, Clexane

has advantage of not requiring lab value monitoring 

Mechanism 

LMWH acts in several sites of the coagulation cascade, with its principal action being inhibition of factor Xa 

reversed by protamine sulfate

Metabolism

renal

Risk

bleeding   

5

FondaParinux

Arixtra

Overview 

trade name: Arixtra

has advantage of not requiring lab value monitoring

Mechanism 

indirect factor Xa inhibitor (acts through antithrombin III)

Metabolism 

renal

Evidence 

studies show decreased incidence of DVT when compared to enoxaparin in hip fx and TKA patients

Risk highest bleeding complications 

not to be used in conjunction with epidurals

6

Warfarin

Coumadin

Mechanism of anticoagulation  inhibits vitamin K 2,3-epoxide reductase

prevents reduction of vitamin K epoxide back to active vitamin K

vitamin K is needed for gamma-carboxylation of glutamic acid for factorsII (prothrombin), VII (first affected), IX, X protein C, protein S

Monitoring 

target level of INR (international normalized ratio) is 2-3 for orthopaedic patients

not achieved for 3 days after initiation

Reversal 

vitamin K (takes up to 3 days)

fresh frozen plasma (acts immediately)

Risk 

difficult to dose requires the frequent need for INR lab monitoring

can have adverse reaction with other drugs including 

rifampin

phenobarbital

diuretics

cholestyramine

7

RIvaroXABAN

XArelto

Overview 

others in the same class include apixaban (Eliquis) and edoxaban (Savaysa or Lixiana)

mechanism of action of these drugs can be deduced from the name. 

Rivaro(Identifier)-xa(FactorXa)-ban(inhibitor)

Mechanism

direct Xa inhibitor

Metabolism 

liver

Antidote 

no current antidote- why you have to wait with surgery

andexanet alpha being investigated

Risk 

bleeding

Half-life 

8-hours (12-hours for apixaban)

urgent surgical procedures delayed until half-life spanned from last dose

8

Diabigatran

Pradaxa

Mechanism 

reversible direct thrombin (factor IIa) inhibitor

Metabolism 

renal

Antidote 

idarucizumab (FDA approved Oct 2015)

Risk 

GI upset

bleeding

9

Transexamanic Acid 

TXA

 

synthethic lysine

Overview 

an antifibrinolytic that promotes and stabilizes clot formation

studies have shown that TXA reduce perioperative blood loss and transfusion in THA and TKA

Mechanism 

synthetic derivative of the amino acid lysine

competitively inhibits the activation of plasminogen by binding to the lysine binding site  

at high concentrations, is a non-competitive inhibitor of plasmin

has roughly 8-10 times the antifibrinolytic activity of ε-aminocaproic acid

Dosing  intravenous 

10-20 mg/kg initial bolus dose followed by repeated doses of the initial TXA dose every 3 hours for 1-4 doses

10-20mg initial bolus followed either by an infusion of 1-10 mg/kg/hr for 4-30 hours

topical application is as effective as IV

sprayed onto open wound at completion of procedure

no detectable TXA in the bloodstream after topical application

Metabolism 

<5% of the drug is metabolized

biological half-life in joint fluid is 3h, present in tissues for up to 17h

Risks

systematic review shows no increase in thromboembolic events

relatively few adverse reactions have been reported in the arthroplasty literature

 

Tranexamic acid (TXA) works through the competitive inhibition of plasminogen activation. 

TXA (Lysteda) is an antifibrinolytic that promotes and stabilizes clot formation. It competitively inhibits the activation of plasminogen by binding to the lysine binding site. TXA is effective in reducing the need for blood transfusions while not increasing the risk of VTE and renal complications. However, it is still advised that patients with cardiac stents and previous thromboembolic events including ischemic stroke not be administered TXA. 

10

Herbal supplements that affect bleeding:

Increased bleeding

gingko, ginseng, and garlic have been found to increase the rate of bleeding 

related to effect on platelets

proper history taking can avoid complications

Increased warfarin effect (increase INR)omega-3 fish oil

affects platelet aggregation and vitamin K dependent coagulation factors

Reduced warfarin effect (reduces INR)

coenzyme Q10

green tea

direct warfarin antagonist (reduces INR)

St John's wort

increases catabolism of warfarin (reduces INR)

11

where do Anticoagulants act on the clotting cascade?

12

what are the criteria vis MSIS for an infected periprosthethic joint?

13

What are the mechanism of actions for heparin, aspirin, warfarin, rivoxaban, dabigatran

 

the big Atran--

Warfarin inhibits vitamin K 2,3-epoxide reductase, thereby limiting the production of vitamin K-dependent clotting factors (II, VII, IX, X) as well as Protein C and Protein S. 


 Aspirin inhibits the production of prostaglandins and thromboxanes through irreversible inhibition of cyclooxygenase (COX, 1 and 2) and thus inhibits platelet aggregation. 


Rivaroxaban is a direct inhibitor of factor Xa. 
 

Dabigatran is a direct thrombin inhibitor.

 

14

Describe Transaminic Acid:

Factor Ia is fibrin. The enzyme that breaks down fibrin is plasmin. Tranexamic acid (TXA) is an antifibrinolytic that prevents the activation of plasmin from the inactive zymogen plasminogen. 

Tranexamic acid competitively inhibits the activation of plasminogen to plasmin by binding to specific sites on both plasminogen and plasmin. Tranexamic acid has roughly eight times the antifibrinolytic activity of an older analogue, e-aminocaproic acid. It is used during joint replacement surgery to reduce blood loss and the need for transfusion. 

Watts et al. review strategies for minimizing blood loss and transfusion. They recommend 1g of TXA prior to incision, and 1g at wound closure. They also recommend giving fluids for symptoms of anemia, rather than transfusion, as even high risk patients do well with sufficient intravascular volume even with low hemoglobin levels. 

15

what are the half-lives of anticoagulation medications as it relates to surgery?

Warfarin, which is dosed daily, can take 72 to 96 hours to reach therapeutic levels. It has a plasma half-life of 36 to 42 hours. Low-molecular heparins have a plasma half-life of 4 to 5 hours, and fondaparinux has a half-life of 17 to 21 hours. Warfarin will not affect the International Normalized Ratio (INR) until 2 to 3 days after it is given. Patients on chronic warfarin therapy should have treatment stopped 3 to 5 days before elective surgery to allow the INR to normalize.

 

Xarelto is 8-12 hours. have to hold urgent surgery for those on it. 

 

16

What herbal supplements affect platelets

Ginko

Garlic

Ginseng

 

The three G's

17

what is the clotting cascade's final product?

Thrombin--

converts soluble fibrinogen to insoluable fibrin

 

18

Review the genetic components of hypercoagulability:

19

List the risk factors for thromboembolic disease:

20

what are the recommendations on preventing VTE on arthroplasty?

21

Miller's brief review of pharmacologic treatment for SVT prophylaxis:

Pharmacologic prophylaxis:

Surgical Care Improvement Project (SCIP) quality measures require DVT prophylaxis.

 

Aspirin

Irreversibly binds and inactivates COX in platelets, thereby reducing thromboxane A2

Weakest: Use of IPCD encouraged

Low bleeding risk: Should be considered for patients at higher risk for bleeding.

Warfarin (Coumadin)

Prevents vitamin K γ-carboxylation in liver

Inhibits factors II, VII, IX, X, and proteins C and S

Vitamin K and fresh frozen plasma can reverse

Multiple reactions with drugs and diet

Must be monitored with international normalized ratio (INR; goal, 2–3)

Heparin

Activates antithrombin III (ATIII), which then inactivates factor Xa and thrombin

Protamine sulfate can reverse

Short half-life: 2 hours

High bleeding rate in arthroplasty

Binds platelets—heparin-induced thrombocytopenia

 

Low-molecular-weight heparin (LMWH)

Reversibly inhibits factor Xa through ATIII and factor II

Protamine sulfate can reverse•

No monitoring needed

Less heparin-induced thrombocytopenia

Higher risk for bleeding than with warfarin

Fondaparinux (akin to oral heparin)

Irreversibly but indirectly inhibits factor X through ATIII

Synthetic pentasaccharide

No monitoring

No antidote

Higher risk for bleeding than with LMWH

 

Rivaroxaban

Direct Xa inhibitor

Oral drug

Higher risk for bleeding than with LMWH

 

Hirudin

Direct thrombin (IIa) inhibitor

 

Intramuscular and oral (dabigatran) versions

No antidote

Inferior vena cava (IVC) filter use: controversial

Should be considered in following conditions:

Contraindication to prophylaxis

Cerebral bleed/trauma

Spine surgery

Prior complication of prophylaxis

22

How do you assess cardiac risk factors prior to surgery?

American College of Cardiology/American Heart Association (ACC/AHA) elements for assessing risk

Clinical risk factors in perioperative cardiac risk

 

 

Major predictors

 

Unstable/severe angina, recent MI (<6 weeks)

Worsening or new-onset CHF

Arrhythmias

Atrioventricular (AV) block

Symptomatic ventricular dysrhythmia: bradycardia (<30 beats/min), tachycardia (>100 beats/min)

Severe aortic stenosis or symptomatic mitral stenosis

Other

Prior ischemic heart disease

Prior CHF

Prior stroke/TIA

Diabetes

Renal insufficiency (creatine >2 mg/dL)

 

Functional exercise capacity—measured in metabolic equivalents (METs) MET: 3.5 mL O2 uptake/kg/min

Perioperative risk elevated if unable to meet 4-MET demand

 

Walk up flight of steps or hill (= 4 METs)

Heavy work around house (>4 METs)

Can patient walk four blocks or climb two flights of stairs?

23

Please quantify surgery specific risks by procedure:

Surgery-specific risk:

High risk (>5% risk of death/MI)

Aortic, major or peripheral vascular procedures

Intermediate risk (1%–5% risk of death/MI)

Orthopaedic, ENT, abdominal/thoracic or procedures

Low risk (<1% risk of death/MI)—usually do not need further clearance

Ambulatory surgery, endoscopic or superficial procedures

24

What are cardiac recommendations prior to surgery?

Twelve-lead ECG if:

CAD and intermediate-risk procedure

One clinical risk factor and intermediate-risk procedure

 

Noninvasive evaluation of left ventricular function if:

---Three or more clinical risk factors and intermediate-    risk procedure

---Dyspnea of unknown origin

---CHF with worsening dyspnea without testing in 12 months

 

 

β-Blockers and statins should be continued around the time of surgery.

Acetylsalicylic acid (ASA) should be stopped 7 days prior to surgery.

Cardiology consultation should be considered for patients taking other agents (clopidogrel, prasugrel).

 

Risk of stent thrombosis balanced with that of surgical bleed

25

What are measures of shock recovery?

Lactate—indirect marker of tissue hypoperfusion

Best measures of adequate resuscitation:

Clinical measure of organ function: urine output more than 30 mL/h

Laboratory measure: serum lactate less than 2.5 mg/dL

26

Review the types of shock and their clinical presentation:

Neurogenic shock

High spinal cord injury (also anesthetic accidents)

Loss of sympathetic tone and of vasomotor tone of peripheral arterial bed

Bradycardia, hypotension, warm extremities

Treatment: vasoconstrictors and volume

Septic shock (vasogenic)

Number one cause of ICU death

Mortality 50%

Bacterial toxins stimulate cytokine storm.

Examples: gram-negative lipopolysaccharides, toxic shock superantigen

Inflammatory mediators cause endothelial dysfunction and peripheral vasodilation

Treatment:

Identification and treatment of infections

Prompt resection of dead tissue

Appropriate antibiotics

 

 

Cardiogenic shock

Bad pump: Extensive MI, arrhythmias

 

Blocked pump (obstructive shock)

Massive “saddle” pulmonary embolism

Tension pneumothorax

Cardiac tamponade

          Beck triad: hypotension, muffled heart sounds,  

          neck vein distension

          Pulsus paradoxus

          Decreased systolic BP with inspiration

Treatment: pericardiocentesis

 

 

Hypovolemic shock:

Most common shock of trauma

Volume loss from bleeds or burns

“Third spacing” also a cause

Neuroendocrine response: save heart and brain

Peripheral vasoconstriction

BP may be normal

Pale, cold, clammy extremities

 

Percentage of blood loss key to symptoms/signs:

Class I: up to 15% blood volume loss

              Vital signs can be maintained.

               Pulse below 100 beats/min

 

Class II: 15%–30% blood volume loss

              Tachycardia (>100 beats/min), orthostatic,     

              Anxious

              Increased diastolic BP

 

Class III: 30%–40% blood volume loss

                 Decreased systolic BP

                  Oliguria

                  Confusion, mental status changes

 

Class IV: more than 40% blood volume loss

                Life threatening; patient is obtunded

                Narrowed pulse pressure

                IImmeasurable diastolic BP

 

Treatment

First, ABCs of resuscitation: then, bleeding must be stopped.

Blood products make better resuscitation fluids than saline.

27

How to address perioperative pulmonary issues around surgery:

Higher in cases that involve thorax such as scoliosis

Highest in patients with prior disease

Spinal/epidural anesthesia favored over general

Medical treatment should be maximized around surgery.

 

Symptomatic COPD: anticholinergic inhalers (ipratropium; May require corticosteroids

 

Asthma

Presence of wheezes or shortness of breath: β-agonist inhalers (albuterol)

Perioperative oral steroids safe

Systemic glucocorticoid should be considered if forced expiratory volume in 1 minute (FEV1) or peak expiratory flow rate (PEFR) is below 80% predicted values/personal best.

 

 

Postoperative atelectasis

Like the associated cough, the workup is usually nonproductive.

Deep breathing/incentive spirometry—equally effective

Postoperative pneumonia takes up to 5 days to manifest.

Productive cough, fever/chills, increased WBC count

Radiograph: pulmonary infiltrates

 

Smoking cessation improves outcomes

Patients should stop 6–8 weeks preoperatively.

Nicotine supplements do no harm to wound.

Fewer pulmonary complications

Smokers have six times more pulmonary complications.

Fewer wound healing issues and wound infections

Lower nonunion rate

Shoulder, neck, and thoracic pain in smokers

Prompts careful evaluation of lung fields

Superior sulcus tumor (Pancoast tumor)

Intrinsic atrophy of hand—C8–T1

28

Describe ARDS:

Pulmonary failure due to edema (see Fig. 1.56A)

 

Pathophysiology

       Complement pathway activated

       Increased pulmonary capillary permeability

       Intravascular fluid floods alveoli

 

Results

Hypoxia, pulmonary HTN

Right heart failure

50% mortality

 

Etiology

 

Blunt chest trauma, aspiration, pneumonia, sepsis

Shock, burns, smoke inhalation, near drowning

Orthopaedic: Long-bone trauma

 

Clinical symptoms

Tachypnea, dyspnea, hypoxia, decreased lung compliance

Pao2/fio2 ratio below 200

 

Imaging:

 

Radiographs: diffuse bilateral infiltrates, “snowstorm”

CT: ground glass appearance

 


Treatment: Aggressive supportive care

Prompt diagnosis and treatment of musculoskeletal infections:Prompt treatment of long-bone fractures

Ventilation with positive end-expiratory pressure (PEEP)

 

100% O2

29

Describe Fat Emboli Syndrome:

Petechial rash: fat to skin

Neurologic symptoms: fat to brain

Mental status changes: confusion, stupor

Rigidity, convulsions, coma

Pulmonary collapse: fat showers lung

ARDS: hypoxia, tachypnea, dyspnea

Associated with long-bone fractures

30

Characterize the common blood disoders as it relates to surgery:

Common inherited bleeding disorders:

Vonwillebrands disease AD (Vonwillebrands factor)

Hemophilia Ax-linked recessive 

Hemophilia  B. Christmas

 

Von Willebrand disease: autosomal dominant

Most common genetic coagulation disorder

 

Von Willebrand factor dysfunction

                Binds platelets to endothelium

                Carrier for factor VIII

 

Treatment: desmopressin

 

Hemophilia A (VIII): X-linked recessive

Hemophilia B (IX) Christmas disease: X-linked recessive