Hypovolemic Shock And Dic
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Hypovolemic Shock and Disseminated Intravascular Coagulopathy Irma A. Lee, M.D. Department of Obstetrics and Gynecology
Hypovolemic Shock
Dr. I. A. Lee
Functions of Pregnancy-Induced Hypervolemia 1. To meet the demands of the enlarged uterus with its hypertrophied vascular system 2. To protect the mother and fetus against deleterious effects of impaired venous return in the supine and erect position 3. To safeguard the mother against the adverse effects of blood loss associated with parturition Hypovolemic Shock
Dr. I. A. Lee
Causes of Hemorrhage in Pregnant Women 1. Bleeding from genital tract (antepartum hemorrhage) •
Ruptured ectopic pregnancy, Molar pregnancy, Abortion, Placenta previa, abruptio placenta, Postpartum hemorrhage
2. Intra/Postpartum •
Retained placenta, uterine atony, uterine rupture, post CS hemorrhage, lower genital tract injury
3. Others •
Subcapsular hematoma of the liver, coagulopathy (AF embolism), trauma, GI bleeding, ruptured aneurysm, burns Hypovolemic Shock Dr. I. A. Lee
Classification of Hemorrhage in Pregnancy Class
Blood Loss (ml)
% Loss
Clinical Findings
1
< 1,000
15
None
2
1,200-1,500
15-25
Orthostatic blood pressure changes, positive tilt test, pulse pressure ≤ 30 mm Hg, reduced peripheral perfusion with prolonged capillary refill time
3
1,500-2,000
25-35
Cold, clammy skin, tachycardia, tachypnea, hypotension
4
> 2,000
>35
Profound shock, nonpalpable blood pressure
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock • Circulatory collapse due to inadequate intravascular blood volume caused by hemorrhage
Hypovolemic Shock
Dr. I. A. Lee
Clinical manifestations of hypovolemic shock (symptoms) Central nervous system Respiratory system Cardiovascular system Skin Gastrointestinal system Renal system Hypovolemic Shock
Anxiety Confusion Shortness of breath Air hunger Palpitations Cold Shivers Thirst Apetite for salty food Decreased urine Dr. I. A. Lee
Clinical manifestations of hypovolemic shock (signs) Central nervous system
Delirium Restlessness Decreased level of consciousness
Respiratory system
Hyperventilation
Cardiovascular system
Tachycardia Low blood pressure
Skin
Cold Pale Clammy
Renal system
Oliguria Anuria
Pregnancy
Hypovolemic Shock
Fetal distress or death
Dr. I. A. Lee
Stages of Shock 1. Non-Progressive- compensatory phase caused by negative feedback control mechanism of the circulation • • • •
Baroreceptor reflexes eliciting sympathetic stimulation within 30 seconds after hemorrhage CNS ischemic response eliciting sympathetic stimulation occurring 10-60 minutes Absorption of large quantities of fluid from intestinal tract and interstitial spaces Conservation of water and salt by the kidney
Hypovolemic Shock
Dr. I. A. Lee
Stages of Shock 2. Progressive – shock steadily worsens 3. Irreversible- shock has progressed to state no known therapy can maintain life
Hypovolemic Shock
Dr. I. A. Lee
Maternal Compensatory Mechanism in response to volume loss
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
Complications of Hypovolemic Shock • • • •
Acute tubular necrosis ARDS DIC Hypothermia
Hypovolemic Shock
Dr. I. A. Lee
Management of Hypovolemic Shock • Pre hospital care – Prevent further injury – Transport immediately to hospital – Initiate appropriate treatment without delaying transport (adequate airway, ventilation, and circulation)
• Emergency department care – Maximize O2 delivery – Control further blood loss – Fluid resuscitation Hypovolemic Shock
Dr. I. A. Lee
Sequence of Therapeutic Diagnostic Maneuvers Priority
Mnemonic
1
V
2
I
3
P
4
P
5
S
Hypovolemic Shock
Therapy Ventilate
Purpose
Adequate pulmona CO2 and O2 exchange Infusion Blood, fluid, electrolyte balance Pump Restoration of cardiac competence Pharmacologic Use of vasoactive agents to improve perfusion Specific, Medical and surgical surgical management of primary causes Dr. I. A. Lee
Ventilate • Suspect ventilatory failure (thoracic movement feeble, decreased breath sounds) • Respiratory acidosis pH <7.35, pCO2 >46 torr, pO2 <70 torr, 93 % saturation
• Mechanical assistance of ventilation Hypovolemic Shock
Dr. I. A. Lee
Infuse • To restore adequacy of intravascular blood volume • Hgb 7-10 g/dL • CVP and PAWP- indicate relationship between volume which enter the heart and effectivity of volume ejected by heart • Initial fluid resuscitation- isotonic crystalloid 1-2 L lactated ringers or NSS • Blood component therapy- (pRBC) to improve O2 carrying capacity Hypovolemic Shock
Dr. I. A. Lee
Pump • Evaluate cardiac competence with ECG and CVP
Hypovolemic Shock
Dr. I. A. Lee
Fluid Resuscitation • Current recommendations are for aggressive fluid resuscitation with LACTATED RINGERS SOLUTION or NORMAL SALINE SOLUTION in all patients with signs and symptoms of shock regardless of underlying cause
Hypovolemic Shock
Dr. I. A. Lee
Blood Component Therapy Component Packed red cells
Indication To improve O2 carrying capacity
Notes Raise Hb 1 g/dL
Fresh-frozen plasma Reduce clotting factors PT and/or PTT >1.5 x upper normal
Start with 2 U FFP or 1520 ml/kg ideal body weight
Cryoprecipitate
Fibrinogen <75-100 ug
1U/10-kg body weight with fibrinogen<75
Platelets
Platelets<50,000
Increase platelets 500010,000/mm3 per unit
Albumin
Volume replacement, bind bilirubin in newborns albumin <1.0 g/dl (total protein<4.0)
Use 5% albumin
Hypovolemic Shock
Dr. I. A. Lee
Blood Component Therapy 1. pRBC • • •
Component of choice for anemic hypoxia For rapid transfusion, may dilute with 100 ml normal saline 1 pRBC (300 ml) → 1 g/dL Hgb or Hct 3%
2. Fresh Frozen Plasma • • • • •
Component of whole blood once platelets and cellular elements are removed Frozen at -18 to -30 °C 1u of whole blood → 200 ml ffp From plasma apheresis → 800 ml ffp Contains coagulation factors
Hypovolemic Shock
Dr. I. A. Lee
Blood Component Therapy 3. Cryoprecipitate • • •
Prepared by thawing a unit of ffp at 4°C and collecting the formed precipitate in a concentrated volume of 10-15 ml per bag A bag contains 200 to 300 mg of fibrinogen and 100 units of Factor VIII, vWF, factor XIII and 55 mg fibronectin 10 bags of cryoprecipitate from 10 units of plasma → 2 g fibrinogen raising level to 6570 mg/dL
Hypovolemic Shock
Dr. I. A. Lee
Blood Component Therapy 4. Platelets • •
Obtained from whole blood or by apheresis Indicated for thrombocytopenia or platelet disorders prior to invasive procedures to reach platelet level at 100,000/mm3
•
Platelet count of 50,000/mm3 adequate if platelets are normal Transfusion is initiated for non bleeding patients with platelets 20,000/mm3 or less
•
Hypovolemic Shock
Dr. I. A. Lee
Blood Component Therapy 5. Albumin • • •
Used for volume replacement, to bind bilirubin in hemolytic disease of the newborn Albumin replacement cannot replace feeding to improve patients’ nutritional status Low perioperative albumin levels correlate with poor prognosis
Hypovolemic Shock
Dr. I. A. Lee
Transfusion Complications • Infectious risks – Viral and bacterial
• Immunologic risks – Acute hemolytic reaction, delayed hemolytic reaction, febrile reactions, allergic reactions, transfusion related acute lung injury, post transfusion purpura
• Others – Citrate toxicity, metabolic acidosis, hyperkalemia, hypocalcemia, hypthermia, volume overload
* For every 5-7 units pRBC, give 10-20 ml of 10% calcium gluconate or 2-5 ml of 10% calcium chloride → ionized calcium level Hypovolemic Shock
Dr. I. A. Lee
Definitive Treatment As the patient is being stabilized, steps should be taken to arrest cause of bleeding
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
Summary Reliance on blood pressure and initial hematocrit level rather than signs of decreased peripheral perfusion are errors that lead to failure to recognize hypovolemic shock
Hypovolemic Shock
Dr. I. A. Lee
Hemostasis • Ingenious process that makes blood fluid and free from clots and allows formation of plugs to seal off vessel injury
Thrombosis •A pathologic process whereby there is blood clot formation within an injured vessel
Hypovolemic Shock
Dr. I. A. Lee
Maintaining Hemostatic Balance Unobstructed blood flow -------- dilutes activated coagulation factors Humoral factors --------- inactivate stable coagulation factors Reticuloendothelial system ------ removes products of coagulation and clot disintegration Prostacyclin endothelial cell -------- inhibits abnormal platelet aggregation Hypovolemic Shock
Dr. I. A. Lee
Tipping the Hemostatic Balance Extensive activation of coagulation process (various diseases)
Pre-kallikrein High molecular weight kininogen
Endothelial damage Tissue injury Platelet activation Massive thrombosis Hypercoagulability
Activation of fibrinolytic system
Secondary fibrinolysis
Fibrin deposit in micocirculation
Infarction
Hemolysis
Consumption of coagulation Factors and platelets Hypocoagulability
Massive bleeding Death
Hypovolemic Shock
Dr. I. A. Lee
MAINTENANCE OF HEMOSTASIS 1. Vascular Wall a. Endothelin – vasoconstriction b. Collagen – needed for platelet adherence c. tPa – initiates fibrinolysis d. PGI2 and NO – to limit size of thrombus
Hypovolemic Shock
Dr. I. A. Lee
2. Platelet reactions a. Adhesion and shape changes b. Secretion and release of ADP, calcium ions, serotonin and thromboxane A2 c. Platelet aggregation – stimuli for aggregation and recruitment are ADP, thromboxane A2 and thrombin
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
3. Coagulation
Process – composed of a. enzymes ( activated coagulation factor) b. substrate ( proenzyme form of coagulation factor) c. co-factor – reaction accelerator
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
The Fibrinolytic System Plasminogen Tissue activator Plasma activator Urokinase Plasmin Fibrin-Fibrinogen Fibrinolytic split products
Hypovolemic Shock
Dr. I. A. Lee
Naturally Occurring Anticoagulants 1. Anti thrombin •
Inhibits activity of thrombin and serine proteases factors IXa - XIIa
2. Protein C and S •
Inactivate cofactors Va and VIIIa
3. Plasminogen-plasmin system •
Breakdown fibrin
Hypovolemic Shock
Dr. I. A. Lee
Disseminated Intravascular Coagulopathy Acute, subacute or chronic thrombohemorrhagic disorder characterized by activation of coagulation sequence leading to formation of microthrombi throughout the microcirculation as a consequence there is consumption of platelets, fibrin and coagulation factors and activation of fibrinolytic system Hypovolemic Shock
Dr. I. A. Lee
Mechanisms that Trigger DIC 1. Release of tissue factor or thrombocytoplastic materials into the circulation 2. Widespread injury to the endothelial cells
Hypovolemic Shock
Dr. I. A. Lee
Extrinsic Pathway Tissue Injury
Abruptio placenta Amniotic Fluid Embolism
Thromboplastin
Retained Dead Fetus Saline induced abortion
VII X V PF 3 Ca++ II
Thrombin
Fibrinogen
Hypovolemic Shock
Fibrin (clot)
Dr. I. A. Lee
Intrinsic Pathway Endothelial damage
Septic abortion
Chorioamnionitis Contact activation XII XI IX VIII Platelet factor 3 Ca++ II Fibrinogen
Hypovolemic Shock
Thrombin Fibrin (clot)
Dr. I. A. Lee
Initiation of DIC by platelet activation PLATELET ACTIVATION (Platelet activation factor, diminished prostacyclin) Severe Pre-eclampsia Increased aggregation and adhesion X
V
PF3 Ca++
II
Fibrinogen
Hypovolemic Shock
Thrombin
Fibrin (clot)
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
Major Disorders Associated with DIC
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
Consequences of DIC 1. Widespread fibrin deposition → ischemia and hemolytic anemia 2. Hemorrhagic diathesis secondary to consumption of platelets and clotting factors and activation of plasminogen and fibrinolysis
Hypovolemic Shock
Dr. I. A. Lee
CLINICAL MANIFESTATIONS 1. 2. 3. 4. 5.
Microangiopathic hemolytic anemia Respiratory – dyspnea, cyanosis Neurologic – convulsions, coma Renal – oliguria, acute renal failure Circulatory failure and SHOCK
Hypovolemic Shock
Dr. I. A. Lee
Laboratory Diagnosis 1. Fibrinogen level ------ Clot observation test 5ml of blood in a 15ml test tube inverted 4-5 times * clot within 6-12 minutes or stable clot that does not lyse If clot <6mins = fibrinogen level (150mg/100ml) If clot >12mins = fibinogen level (100150mg/100ml) If no clot in 30 mins = fibinogen level (<100mg/100ml) Hypovolemic Shock
Dr. I. A. Lee
Laboratory Diagnosis 2. Platelets <4 platelets / hpf = suggest thrombocytopenia 3. Partial thromboplastin time 4, Prothrombin time 5. Fibrin degradation products- D-dimer
Hypovolemic Shock
Dr. I. A. Lee
Goals in Management 2. Good clinical judgement 3. Recognition and treatment of underlying disorder (abruptio placenta, IUFD, Amniotic fluid embolism, septic abortion, and sepsis, eclampsia) 4. Supportive measures (replacement therapy –FFP, cryoprecipitate) 4. Epsilon-Aminocaproic Acid – control fibrinolysis by inhibiting conversion of plasminogen to plasmin Hypovolemic Shock
Dr. I. A. Lee
Thank you !
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
Functions of Pregnancy-Induced Hypervolemia 1. To meet the demands of the enlarged uterus with its hypertrophied vascular system 2. To protect the mother and fetus against deleterious effects of impaired venous return in the supine and erect position 3. To safeguard the mother against the adverse effects of blood loss associated with parturition Hypovolemic Shock
Dr. I. A. Lee
Causes of Hemorrhage in Pregnant Women 1. Bleeding from genital tract (antepartum hemorrhage) •
Ruptured ectopic pregnancy, Molar pregnancy, Abortion, Placenta previa, abruptio placenta, Postpartum hemorrhage
2. Intra/Postpartum •
Retained placenta, uterine atony, uterine rupture, post CS hemorrhage, lower genital tract injury
3. Others •
Subcapsular hematoma of the liver, coagulopathy (AF embolism), trauma, GI bleeding, ruptured aneurysm, burns Hypovolemic Shock Dr. I. A. Lee
Classification of Hemorrhage in Pregnancy Class
Blood Loss (ml)
% Loss
Clinical Findings
1
< 1,000
15
None
2
1,200-1,500
15-25
Orthostatic blood pressure changes, positive tilt test, pulse pressure ≤ 30 mm Hg, reduced peripheral perfusion with prolonged capillary refill time
3
1,500-2,000
25-35
Cold, clammy skin, tachycardia, tachypnea, hypotension
4
> 2,000
>35
Profound shock, nonpalpable blood pressure
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock • Circulatory collapse due to inadequate intravascular blood volume caused by hemorrhage
Hypovolemic Shock
Dr. I. A. Lee
Clinical manifestations of hypovolemic shock (symptoms) Central nervous system Respiratory system Cardiovascular system Skin Gastrointestinal system Renal system Hypovolemic Shock
Anxiety Confusion Shortness of breath Air hunger Palpitations Cold Shivers Thirst Apetite for salty food Decreased urine Dr. I. A. Lee
Clinical manifestations of hypovolemic shock (signs) Central nervous system
Delirium Restlessness Decreased level of consciousness
Respiratory system
Hyperventilation
Cardiovascular system
Tachycardia Low blood pressure
Skin
Cold Pale Clammy
Renal system
Oliguria Anuria
Pregnancy
Hypovolemic Shock
Fetal distress or death
Dr. I. A. Lee
Stages of Shock 1. Non-Progressive- compensatory phase caused by negative feedback control mechanism of the circulation • • • •
Baroreceptor reflexes eliciting sympathetic stimulation within 30 seconds after hemorrhage CNS ischemic response eliciting sympathetic stimulation occurring 10-60 minutes Absorption of large quantities of fluid from intestinal tract and interstitial spaces Conservation of water and salt by the kidney
Hypovolemic Shock
Dr. I. A. Lee
Stages of Shock 2. Progressive – shock steadily worsens 3. Irreversible- shock has progressed to state no known therapy can maintain life
Hypovolemic Shock
Dr. I. A. Lee
Maternal Compensatory Mechanism in response to volume loss
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
Complications of Hypovolemic Shock • • • •
Acute tubular necrosis ARDS DIC Hypothermia
Hypovolemic Shock
Dr. I. A. Lee
Management of Hypovolemic Shock • Pre hospital care – Prevent further injury – Transport immediately to hospital – Initiate appropriate treatment without delaying transport (adequate airway, ventilation, and circulation)
• Emergency department care – Maximize O2 delivery – Control further blood loss – Fluid resuscitation Hypovolemic Shock
Dr. I. A. Lee
Sequence of Therapeutic Diagnostic Maneuvers Priority
Mnemonic
1
V
2
I
3
P
4
P
5
S
Hypovolemic Shock
Therapy Ventilate
Purpose
Adequate pulmona CO2 and O2 exchange Infusion Blood, fluid, electrolyte balance Pump Restoration of cardiac competence Pharmacologic Use of vasoactive agents to improve perfusion Specific, Medical and surgical surgical management of primary causes Dr. I. A. Lee
Ventilate • Suspect ventilatory failure (thoracic movement feeble, decreased breath sounds) • Respiratory acidosis pH <7.35, pCO2 >46 torr, pO2 <70 torr, 93 % saturation
• Mechanical assistance of ventilation Hypovolemic Shock
Dr. I. A. Lee
Infuse • To restore adequacy of intravascular blood volume • Hgb 7-10 g/dL • CVP and PAWP- indicate relationship between volume which enter the heart and effectivity of volume ejected by heart • Initial fluid resuscitation- isotonic crystalloid 1-2 L lactated ringers or NSS • Blood component therapy- (pRBC) to improve O2 carrying capacity Hypovolemic Shock
Dr. I. A. Lee
Pump • Evaluate cardiac competence with ECG and CVP
Hypovolemic Shock
Dr. I. A. Lee
Fluid Resuscitation • Current recommendations are for aggressive fluid resuscitation with LACTATED RINGERS SOLUTION or NORMAL SALINE SOLUTION in all patients with signs and symptoms of shock regardless of underlying cause
Hypovolemic Shock
Dr. I. A. Lee
Blood Component Therapy Component Packed red cells
Indication To improve O2 carrying capacity
Notes Raise Hb 1 g/dL
Fresh-frozen plasma Reduce clotting factors PT and/or PTT >1.5 x upper normal
Start with 2 U FFP or 1520 ml/kg ideal body weight
Cryoprecipitate
Fibrinogen <75-100 ug
1U/10-kg body weight with fibrinogen<75
Platelets
Platelets<50,000
Increase platelets 500010,000/mm3 per unit
Albumin
Volume replacement, bind bilirubin in newborns albumin <1.0 g/dl (total protein<4.0)
Use 5% albumin
Hypovolemic Shock
Dr. I. A. Lee
Blood Component Therapy 1. pRBC • • •
Component of choice for anemic hypoxia For rapid transfusion, may dilute with 100 ml normal saline 1 pRBC (300 ml) → 1 g/dL Hgb or Hct 3%
2. Fresh Frozen Plasma • • • • •
Component of whole blood once platelets and cellular elements are removed Frozen at -18 to -30 °C 1u of whole blood → 200 ml ffp From plasma apheresis → 800 ml ffp Contains coagulation factors
Hypovolemic Shock
Dr. I. A. Lee
Blood Component Therapy 3. Cryoprecipitate • • •
Prepared by thawing a unit of ffp at 4°C and collecting the formed precipitate in a concentrated volume of 10-15 ml per bag A bag contains 200 to 300 mg of fibrinogen and 100 units of Factor VIII, vWF, factor XIII and 55 mg fibronectin 10 bags of cryoprecipitate from 10 units of plasma → 2 g fibrinogen raising level to 6570 mg/dL
Hypovolemic Shock
Dr. I. A. Lee
Blood Component Therapy 4. Platelets • •
Obtained from whole blood or by apheresis Indicated for thrombocytopenia or platelet disorders prior to invasive procedures to reach platelet level at 100,000/mm3
•
Platelet count of 50,000/mm3 adequate if platelets are normal Transfusion is initiated for non bleeding patients with platelets 20,000/mm3 or less
•
Hypovolemic Shock
Dr. I. A. Lee
Blood Component Therapy 5. Albumin • • •
Used for volume replacement, to bind bilirubin in hemolytic disease of the newborn Albumin replacement cannot replace feeding to improve patients’ nutritional status Low perioperative albumin levels correlate with poor prognosis
Hypovolemic Shock
Dr. I. A. Lee
Transfusion Complications • Infectious risks – Viral and bacterial
• Immunologic risks – Acute hemolytic reaction, delayed hemolytic reaction, febrile reactions, allergic reactions, transfusion related acute lung injury, post transfusion purpura
• Others – Citrate toxicity, metabolic acidosis, hyperkalemia, hypocalcemia, hypthermia, volume overload
* For every 5-7 units pRBC, give 10-20 ml of 10% calcium gluconate or 2-5 ml of 10% calcium chloride → ionized calcium level Hypovolemic Shock
Dr. I. A. Lee
Definitive Treatment As the patient is being stabilized, steps should be taken to arrest cause of bleeding
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
Summary Reliance on blood pressure and initial hematocrit level rather than signs of decreased peripheral perfusion are errors that lead to failure to recognize hypovolemic shock
Hypovolemic Shock
Dr. I. A. Lee
Hemostasis • Ingenious process that makes blood fluid and free from clots and allows formation of plugs to seal off vessel injury
Thrombosis •A pathologic process whereby there is blood clot formation within an injured vessel
Hypovolemic Shock
Dr. I. A. Lee
Maintaining Hemostatic Balance Unobstructed blood flow -------- dilutes activated coagulation factors Humoral factors --------- inactivate stable coagulation factors Reticuloendothelial system ------ removes products of coagulation and clot disintegration Prostacyclin endothelial cell -------- inhibits abnormal platelet aggregation Hypovolemic Shock
Dr. I. A. Lee
Tipping the Hemostatic Balance Extensive activation of coagulation process (various diseases)
Pre-kallikrein High molecular weight kininogen
Endothelial damage Tissue injury Platelet activation Massive thrombosis Hypercoagulability
Activation of fibrinolytic system
Secondary fibrinolysis
Fibrin deposit in micocirculation
Infarction
Hemolysis
Consumption of coagulation Factors and platelets Hypocoagulability
Massive bleeding Death
Hypovolemic Shock
Dr. I. A. Lee
MAINTENANCE OF HEMOSTASIS 1. Vascular Wall a. Endothelin – vasoconstriction b. Collagen – needed for platelet adherence c. tPa – initiates fibrinolysis d. PGI2 and NO – to limit size of thrombus
Hypovolemic Shock
Dr. I. A. Lee
2. Platelet reactions a. Adhesion and shape changes b. Secretion and release of ADP, calcium ions, serotonin and thromboxane A2 c. Platelet aggregation – stimuli for aggregation and recruitment are ADP, thromboxane A2 and thrombin
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
3. Coagulation
Process – composed of a. enzymes ( activated coagulation factor) b. substrate ( proenzyme form of coagulation factor) c. co-factor – reaction accelerator
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
The Fibrinolytic System Plasminogen Tissue activator Plasma activator Urokinase Plasmin Fibrin-Fibrinogen Fibrinolytic split products
Hypovolemic Shock
Dr. I. A. Lee
Naturally Occurring Anticoagulants 1. Anti thrombin •
Inhibits activity of thrombin and serine proteases factors IXa - XIIa
2. Protein C and S •
Inactivate cofactors Va and VIIIa
3. Plasminogen-plasmin system •
Breakdown fibrin
Hypovolemic Shock
Dr. I. A. Lee
Disseminated Intravascular Coagulopathy Acute, subacute or chronic thrombohemorrhagic disorder characterized by activation of coagulation sequence leading to formation of microthrombi throughout the microcirculation as a consequence there is consumption of platelets, fibrin and coagulation factors and activation of fibrinolytic system Hypovolemic Shock
Dr. I. A. Lee
Mechanisms that Trigger DIC 1. Release of tissue factor or thrombocytoplastic materials into the circulation 2. Widespread injury to the endothelial cells
Hypovolemic Shock
Dr. I. A. Lee
Extrinsic Pathway Tissue Injury
Abruptio placenta Amniotic Fluid Embolism
Thromboplastin
Retained Dead Fetus Saline induced abortion
VII X V PF 3 Ca++ II
Thrombin
Fibrinogen
Hypovolemic Shock
Fibrin (clot)
Dr. I. A. Lee
Intrinsic Pathway Endothelial damage
Septic abortion
Chorioamnionitis Contact activation XII XI IX VIII Platelet factor 3 Ca++ II Fibrinogen
Hypovolemic Shock
Thrombin Fibrin (clot)
Dr. I. A. Lee
Initiation of DIC by platelet activation PLATELET ACTIVATION (Platelet activation factor, diminished prostacyclin) Severe Pre-eclampsia Increased aggregation and adhesion X
V
PF3 Ca++
II
Fibrinogen
Hypovolemic Shock
Thrombin
Fibrin (clot)
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
Major Disorders Associated with DIC
Hypovolemic Shock
Dr. I. A. Lee
Hypovolemic Shock
Dr. I. A. Lee
Consequences of DIC 1. Widespread fibrin deposition → ischemia and hemolytic anemia 2. Hemorrhagic diathesis secondary to consumption of platelets and clotting factors and activation of plasminogen and fibrinolysis
Hypovolemic Shock
Dr. I. A. Lee
CLINICAL MANIFESTATIONS 1. 2. 3. 4. 5.
Microangiopathic hemolytic anemia Respiratory – dyspnea, cyanosis Neurologic – convulsions, coma Renal – oliguria, acute renal failure Circulatory failure and SHOCK
Hypovolemic Shock
Dr. I. A. Lee
Laboratory Diagnosis 1. Fibrinogen level ------ Clot observation test 5ml of blood in a 15ml test tube inverted 4-5 times * clot within 6-12 minutes or stable clot that does not lyse If clot <6mins = fibrinogen level (150mg/100ml) If clot >12mins = fibinogen level (100150mg/100ml) If no clot in 30 mins = fibinogen level (<100mg/100ml) Hypovolemic Shock
Dr. I. A. Lee
Laboratory Diagnosis 2. Platelets <4 platelets / hpf = suggest thrombocytopenia 3. Partial thromboplastin time 4, Prothrombin time 5. Fibrin degradation products- D-dimer
Hypovolemic Shock
Dr. I. A. Lee
Goals in Management 2. Good clinical judgement 3. Recognition and treatment of underlying disorder (abruptio placenta, IUFD, Amniotic fluid embolism, septic abortion, and sepsis, eclampsia) 4. Supportive measures (replacement therapy –FFP, cryoprecipitate) 4. Epsilon-Aminocaproic Acid – control fibrinolysis by inhibiting conversion of plasminogen to plasmin Hypovolemic Shock
Dr. I. A. Lee
Thank you !
Hypovolemic Shock
Dr. I. A. Lee
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