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Hemostasis, surgical bleeding and transfusion
1. Mae Caridad R. Martinquilla
VCMC- Surgery Department
November 2012
2. Complex process whose function is to limit
blood loss from an injured vessel
4 Major Events
Vascular Constriction
Platelet Plug Formation
Fibrin Formation
Fibrinolysis
3.
4. Initial response to vascular injury
THROMBOXANE A2 (TXA2)
ENDOTHELIN
SEROTONIN
BRADYKININ & FIBRINOPEPTIDES
Extent of vasoconstriction varies with
degree of vessel injury
5. PLATELETS : anucleate fragments of
megakaryocytes (150T – 400T/uL)
- hemostatic plug and contribute to thrombin
formation
Injury to the intimal layer exposes
subendothelial collagen platelets adhere
PLATELET ADHESION recruits other
platelets from the circulating blood to seal
the disrupted vessel PRIMARY
HEMOSTASIS
6.
7. I fibrinogen
II prothrombin
V proaccelerin, accelerator globulin, labile factor
VII proconvertin, serum prothrombin conversion accelerator,
stable factor
VIII antihemophilic factor, antihemophilic globulin
IX Christmas factor, plasma thromboplastin component
X Stuart-Prower factor
XI plasma thromboplastin antecedent
XII Hageman factor
XIII fibrinase, fibrin-stabilizing factor
8.
9.
10. PT = prothrombin time
- II,V, VII, X
- Fibrinogen
aPTT = activated partial thromboplastin time
- XII, High molecular weight kininogen,
Prekallikrein, XI, IX, VII, X, V , II and
Fibrinogen
11. Goal is to prevent further blood loss from a disrupted
vessel via direct closure of the blood vessel wall fefect
12. Digital pressure
Extremity tourniquet to occlude a major
vessel proximal to bleeding site
Pringle maneuver for liver bleeding
Simple ligature for small vessels
Direct pressure applied by packs
Harmonic scalpel: cuts & coagulates tissues
via vibration 55 kHz
13. Heat denatures CHON coagulation of large
areas of tissue
Cautery
Amplitude setting must be high enough to
produce prompt coagulation but not so high
as to set up an arc between the tissue &
cautery tip
14. Ideal topical hemostatic agent has:
Significant hemostatic action
Shows minimal tissue reactivity
Nonantigenic
Biddegrades in vivo
Provides ease of sterilization
Low cost
Tailored to specific needs
17. “O-” Blood
Emergency situations
> 4 U transfused increased risk of hemolysis
Autologous Transfusion: up to 5 U
1st
U: 40 days before; last U: 3 days before
Blood donors:
Hgb > 11 g/dL or if Hct > 34%
18.
19. Banked whole blood
- Shelf life: 6 weeks
Fresh whole blood
- blood that is administered within 24 hours of its
donation
70% of transfused RBCs remain in the
circulation for 24hrs post-BT
During storage: reduction of ADP & 2,3-DPG
alters oxygen dissociation curve
decreased oxygen transport
20. Usual product of choice
Shelf-life same as WB
Leukocyte-reduced or Washed RBCs
prepared by filtration that removes
approximately 99.9% of the white blood cells and
most of the platelets (leukocyte-reduced red
blood cells), and if necessary, by additional
saline washing (leukocyte-reduced/washed red
blood cells).
21. Prevents almost all febrile, nonhemolytic
transfusion reactions, alloimmunization to HLA
class I Ag, platelet transfusion refractoriness &
CMV transmission
For:
Chronic anemias, bone marrow & liver failure
Pre-op and post-op surgery
CHF, uremia
22. Shelf-life: 120 hrs after donation
1 U per 10kg BW (1 U = 50 mL = 5.5 x 10^10)
Apheresis = 4.4 x 10^10
For:
Massive blood loss
Nonbleeding: plt < 20T (chemo, tumor invasion)
Pre-op/invasive procedure: plt < 50T
Documented bleeding: plt < 50T
Documented abnormal plt function
23. Usual source of Vit K-dependent factors
Only source of Factor V
For:
Liver disease, Warfarin overdose
DIC, TTP
↓CF d/t large volume transfusions
24. vWF, fibronectin, fibrinogen, CF VIII & XIII
For:
vWF deficiency, Hemophilia A
↓fibrinogen, factor XIII
Bleeding related to renal failure
25. Cryo-poor plasma, cryoprecipitate depleted
Factors II, VII, IX, XI
For:
Hemophilia B
Liver disease
26. Improvement in oxygen-carrying capacity
Treatment of anemia
Hgb approaching 9 g/dL
Volume replacement
Blood loss can be evaluated by estimation in
wound, drapes, sponges, suctioned
30. Symptoms in an AWAKE patient:
Pain at site of transfusion
Facial flushing
Back & chest pain
Fever
Respiratory distress
Hypotension
tachycardia
31. Symptoms in an ANESTHETIZED patient:
Diffuse bleeding
Hypotension
Laboratory criteria:
Hemoglobinuria, hemoglobinemia
Serologic findings
Positive Coomb’s test
Jaundice
Low levels of haptoglobins
32. FEBRILE NONHEMOLYTIC REACTION
Increase in temp >1°C associated with a
transfusion (1% of transfusions)
Bacterial contamination of infused blood
Yersinia enterocolitica, Pseudomonas
Emergency!
Discontinue transfusion ASAP
Oxygen, adrenergic blocking agents, antibiotics
33. 1% of all transfusions
Mild rash, urticaria & fever within 60-90
minutes of the start of transfusion
Treatment:
Mild: Antihistamines
Severe: Steroids or epinephrine
34. Associated with transfusion-associated
circulatory overload
Occur with rapid infusion of blood, plasma
expanders, crystalloids esp in older patients
with heart disease
Rise in venous pressure, dyspnea, cough,
rales in LLF
35. TRANSFUSION-RELATED ACUTE LUNG
INJURY (TRALI)
Noncardiogenic pulmonary edema related to
transfusion
Occur with administration of any plasma-
containing blood product
Fever, rigors, bilateral pulmonary infiltrates on
CXR
Within 1-2 hrs after onset of transfiusion (before
6 hrs)
36. ACUTE HEMOLYTIC REACTION
Administration of ABO-incompatible blood
Fatal in 6% of cases
Technical or clerical errors
Administration of blood of the wrong blood type
37. IMMEDIATE HEMOLYTIC REACTION
Intravascular destruction of RBCs & consequent
hemoglobinemia & hemoglobinuria
Acute renal insufficiency d/t toxicity associated
with free Hgb in the plasma tubular necrosis &
precipitation of Hgb in tubules
38. DELAYED HEMOLYTIC REACTION
Occur 2-10 days after transfusion
Extravascular hemolysis, mild anemia,
indirect hyperbilirubinemia
Low antibody titer at time of transfusion but
titer increases after transfusion d/t
anamnestic response
40. Careful review of the patient’s history
Abnormal bleeding/bruising, drug use
Platelet count
Plt > 1M/uL Bleeding o r thrombotic
complications
Major surgical procedures: <100T/uL
Minor surgical procedures: <50T/uL
Spontaneous b;eeding: <20T/uL
41. PT aPTT INR BT
For: Vit K def;
warfarin therapy
For: heparin
therapy
Measured PT
divided by
Control PT
N: 2-3
Ivy test;
Bleeding must
stop in 7mins
VII XII
HMWK
Prekallikrein
XI
IX
VIII
X
V
II (Prothrombin)
Fibrinogen
Hinweis der Redaktion
HEMOSTASIS : limits blood loss from an injured vessel
THROMBOXANE A2 (TXA2) : produced locally at site of injury via release of arachidonic acid from platelet membranes and is a potent constrictor of smooth muscle ENDOTHELIN : synthesized by injured endothelium SEROTONIN : released during platelet aggregation BRADYKININ & FIBRINOPEPTIDES : vasoconstrictors also involved in coagulation cascade more pronounced in vessels with medial smooth muscles & dependent on local contraction of smooth muscle
NOTE about 30% of platelets are sequestered in the spleen; ave life span of 7-10 days) Platelets play an integral role in hemostasis by forming a hemostatic plug and by contributing to thrombin formation Platelets do not normally adhere to each other or to the vessel wall but can form a plug that aids in cessation of bleeding when vascular disruption occurs. Injury to the intimal layer in the vascular wall exposes subendothelial collagen to which platelets adhere. NOTE this process involves the von Willebrand factor (vWF) which binds to glycoprotein I/IX/V on the platelet membrane NOTE called as primary hemostasis; heparin does NOT interfere & thus hemostasis can occur in the heparinized patient
Coagulation Cascade Extrinsic Pathway: initiated by tissue factor Intrinsic Pathway: initiated by contact of XII & platelet with collagen vascular wall The intrinsic pathway begins with factor XII and through a cascade of enzymatic reactions activates factors XI, IX, and VII in sequence. In the intrinsic pathway all of the components leading ultimately to fibrin clot formation are intrinsic to the circulating plasma and no surface is required to initiate the process. In contrast, the extrinsic pathway requires exposure of tissue factor on the surface of the injured vessel wall to initiate the arm of the cascade beginning with factor VII. The two arms of the coagulation cascade merge to a common pathway at factor X , and activation proceeds in sequence of factors II (prothrombin) and I (fibrinogen). Clot formation occurs after proteolytic conversion of fibrinogen to fibrin . elevated activated partial thromboplastin time (aPTT) is associated with abnormal function of the intrinsic arm of the cascade, whereas an elevated prothrombin time (PT) is associated with the extrinsic arm. Vitamin K deficiency and warfarin use affect factors II, VII, IX, and X.
Fibrin clot undergoes lysis, permitting the restoration of blood flow During the wound-healing process, the fibrin clot undergoes clot lysis, which permits restoration of blood flow. The main enzyme, plasmin, degrades the fibrin mesh at various places, which leads to the production of circulating fragments that are cleared by other proteases or by the kidney and liver. Fibrinolysis is initiated at the same time as the clotting mechanism under the influence of circulating kinases, tissue activators, and kallikrein, which are present in many organs, including the vascular endothelium. Fibrin is degraded by plasmin, a serine protease derived from the proenzyme plasminogen. Plasminogen may be converted by one of several plasminogen activators, including tPA and uPA. The tPA is synthesized by endothelial cells and released by the cells on thrombin stimulation as single-chain tPA. This is then cleaved by plasmin to form two-chain tPA. Bradykinin, a potent endothelium-dependent vasodilator cleaved from high molecular weight kininogen by kallikrein, causes contraction of nonvascular smooth muscle, increases vascular permeability, and enhances release of tPA. Both tPA and plasminogen bind to fibrin as it forms, and this trimolecular complex cleaves fibrin very efficiently. After plasmin is generated it cleaves fibrin, somewhat less efficiently, and it also will degrade fibrinogen. Fully cross-linked fibrin is also a relatively poor substrate for plasmin. Plasminogen activation may be initiated by activation of factor XII, which leads to the generation of kallikrein from prekallikrein and cleavage of high molecular weight kininogen by kallikrein. Several characteristics of the enzymatic reactions ensure that fibrinolysis occurs at a controlled rate and preferentially at the site of clot formation. The tPA activates plasminogen more efficiently when it is bound to fibrin, so that plasmin is formed selectively on the clot. Plasmin is inhibited by 2 -antiplasmin, a protein that is cross-linked to fibrin by factor XIII, which helps to ensure that clot lysis does not occur too quickly. Any circulating plasmin also is inhibited by 2 -antiplasmin and circulating tPA or urokinase. Clot lysis yields fibrin degradation products, including E-nodules and D-dimers. The smaller fragments interfere with normal platelet aggregation and the larger fragments may be incorporated into the clot in lieu of normal fibrin monomers. This may result in an unstable clot. Presence of D-dimers in the circulation may be a marker of thrombosis or other conditions in which a significant activation of the fibrinolytic system is present. The final inhibitor for the fibrinolytic system is TAFI, a procarboxypeptidase that is activated by the thrombin-thrombomodulin complex. The active enzyme removes lysine residues from fibrin that are essential for binding plasminogen.
The oldest mechanical method of halting bleeding is digital pressure digital pressure over a bleeding site often is effective and has the advantage of being less traumatic than a hemostatic clamp Simple ligature- When a small vessel is transected Direct pressure applied by packs affords the best method of controlling diffuse bleeding from large areas, eg trauma The device converts electrical energy into mechanical motion. The motion of the blade causes collagen molecules within the tissue to become denatured, forming a coagulum. No significant electrical current flows through the patient. The instrument has proved advantageous in performing thyroidectomy, hemorrhoidectomy, and transsection of the short gastric veins during splenectomy, and in transecting hepatic parenchyma
- Heat achieves hemostasis by denaturation of protein that results in coagulation of large areas of tissue. - With cautery, heat is transmitted from the instrument by conduction directly to the tissue. When electrocautery is used, heating occurs by induction from an alternating current source. The amplitude setting should be high enough to produce prompt coagulation but not so high as to set up an arc between the tissue and the cautery tip. A negative grounding plate should be placed beneath the patient to avoid severe skin burns. Use of direct current also can result in hemostasis. Because the protein moieties and cellular elements of blood have a negative surface charge, they are attracted to a positive pole, where a thrombus is formed. Direct currents in the 20- to 100-mA range have successfully controlled diffuse bleeding from raw surfaces, as has argon gas.
Topical hemostatic agents play an important role in common or complex general surgical procedures classified based on their mechanism of action and include physical or mechanical, caustic, biologic, and physiologic agents Some agents induce protein coagulation and precipitation that results in occlusion of small cutaneous vessels, whereas others take advantage of later stages in the coagulation cascade, activating biologic responses to bleeding. The ideal topical hemostatic agent has significant hemostatic action, shows minimal tissue reactivity, is nonantigenic, biodegrades in vivo, provides ease of sterilization, is low in cost, and can be tailored to specific needs.
Thrombin Products: direct conversion of fibrinogen to fibrin clot formation; avoids foreign body or inflammatory rxn, wound bed is not disturbed Fibrin Sealants: from cryoprecipitate; does not promote inflammation or tissue necrosis Gelatin Agents: provides hemostasis for operative fields with diffuse small vessel oozing
0- and 0+ are equally safe for emergency transfusion risk for transfusing >4 u of blood risk for hemolysis The use of autologous transfusion is growing. Up to 5 units can be collected for subsequent use during elective procedures Patients can donate blood if their hemoglobin concentration exceeds 11 g/dL or if the hematocrit is >34%. The first procurement is performed 40 days before the planned operation and the last one is performed 3 days before the operation. Donations can be scheduled at intervals of 3 to 4 days. Administration of recombinant human erythropoietin accelerates generation of red blood cells and allows for more frequent harvesting of blood.
- Banked whole blood, once the gold standard, is rarely available.
Concentrated suspensions of red blood cells can be prepared by removing most of the supernatant plasma after centrifugation. This preparation reduces, but does not eliminate, reaction caused by plasma components. It also reduces the amount of sodium, potassium, lactic acid, and citrate administered. Leukocyte-reduced or Washed RBCs Removes 99.9% of WBCs & most of platelets Prevents almost all febrile, nonhemolytic transfusion reactions, alloimmunization to HLA class I Ag, platelet transfusion refractoriness & CMV transmission
One unit of platelet concentrate has a volume of approximately 50 mL. Platelet preparations are capable of transmitting infectious diseases and can provoke allergic reactions similar to those caused by blood transfusion C/I: ITP, TTP, Untreated DIC, thrombocytopenia with septicemia
FFP carries infectious risks similar to those of other component therapies FFP has come to the forefront with the inception of damage control resuscitation in patients with trauma-associated coagulopathy.
Is a frozen blood product prepared from plasma prepared by slowly thawing a unit of ffp at a temp above freezing centrifuged to remove majority of the plasma the precipitate is resuspended in the remaining plasma or sterile saline. - Each unit contains vWF, fibronectin, fibrinogen, CF VIII & XIII -
Refers to plasma from which cryoprecipitate has been removed Reduced levels of cf 8, vwf, 13
Volume Replacement : most common indication
Primarily related to blood-induced proinflammatory responses. Transfusion-related events occur in 10% of all transfusions, but <0.5% are serious. 16-22% : acute lung injury 12-15% : ABO hemolytic transfusion reactions 11-18% : bacterial contamination of platelets
Coombs + : indicates that the presence of transfused cells coated with patient antibody is diagnostic
NOTE preformed cytokines in donated blood & recipient antibodies reacting with donated antibodies are postulated causes Bacterial contamination sepsis & death 25%
NOTE caused by the transfusion of antibodies from hypersensitive donors or the transfusion of antigens to which the recipient is hypersensitive
NOTE related to anti-HLA or anti-human neutrophil Ag Ab in transfused blood that primes neutrophils in the pulmo circulation - Risk factor: multiparity of donor
NOTE reactions to non-ABO antigens involve Ig G-mediated clearance by reticuloendothelial system
Malaria : all blood components; incubation of 8-100 days; shaking chills, spiking fever
PT: contains thromboplastin & Ca that when added to plasma fibrin clot aPTT: phospholipid substitute + activator + Ca that when added to plasma fibrin clot Ivy Test: placing a sphyg on the upper arm inflated to 40mmHg stab 5mm incision on the flexor surface bleeding stops in 7mins