Hypovolemic Shock and Dic

Hypovolemic Shock and

Disseminated Intravascular Coagulopathy

Hypovolemic Shock and


Irma A. Lee, M.D.Department of Obstetrics

and Gynecology

Irma A. Lee, M.D.Department of Obstetrics

and Gynecology

Hypovolemic Shock Dr. I. A. Lee Hypovolemic Shock Dr. I. A. Lee


Functions of Pregnancy-Induced Hypervolemia

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

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


Causes of Hemorrhage in Pregnant Women

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

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


Classification of Hemorrhage in Pregnancy

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 ShockHypovolemic Shock

• Circulatory collapse due to inadequate intravascular blood volume caused by hemorrhage

• Circulatory collapse due to inadequate intravascular blood volume caused by hemorrhage


Clinical manifestations of hypovolemic shock (symptoms)

Clinical manifestations of hypovolemic shock (symptoms)

Central nervous system Anxiety

Confusion

Respiratory system Shortness of breath

Air hunger

Cardiovascular system Palpitations

Skin Cold

Shivers

Gastrointestinal system Thirst

Apetite for salty food

Renal system Decreased urine


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 Fetal distress or death


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

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


Stages of ShockStages of Shock

2. Progressive – shock steadily worsens

3. Irreversible- shock has progressed to state no known therapy can maintain life

2. Progressive – shock steadily worsens

3. Irreversible- shock has progressed to state no known therapy can maintain life


Maternal Compensatory Mechanism in response to volume loss

Maternal Compensatory Mechanism in response to volume loss



Complications of Hypovolemic Shock

Complications of Hypovolemic Shock

• Acute tubular necrosis

• ARDS

• DIC

• Hypothermia

• Acute tubular necrosis

• ARDS

• DIC

• Hypothermia


Management of Hypovolemic Shock

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

• 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


Sequence of Therapeutic Diagnostic Maneuvers

Sequence of Therapeutic Diagnostic Maneuvers

Priority Mnemonic Therapy Purpose

1 V Ventilate Adequate pulmona CO2 and O2 exchange

2 I Infusion Blood, fluid, electrolyte balance

3 P Pump Restoration of cardiac competence

4 P Pharmacologic Use of vasoactive agents to improve perfusion

5 S Specific, surgical

Medical and surgical management of primary causes


VentilateVentilate

• 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

• 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


InfuseInfuse

• 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

• 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


PumpPump

• Evaluate cardiac competence with ECG and CVP

• Evaluate cardiac competence with ECG and CVP


Fluid ResuscitationFluid 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

• 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


Blood Component TherapyBlood Component Therapy

Component Indication Notes

Packed red cells To improve O2 carrying capacity 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 15-20 ml/kg ideal body weight

Cryoprecipitate Fibrinogen <75-100 ug 1U/10-kg body weight with fibrinogen<75

Platelets Platelets<50,000 Increase platelets 5000-10,000/mm3 per unit

Albumin Volume replacement, bind bilirubin in newborns albumin <1.0 g/dl (total protein<4.0)

Use 5% albumin


Blood Component TherapyBlood Component Therapy1. 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

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



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 65-70 mg/dL

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 65-70 mg/dL



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

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



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

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


Transfusion ComplicationsTransfusion 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

• 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


Definitive TreatmentDefinitive Treatment

As the patient is being stabilized, steps should be

taken to arrest cause of bleeding

As the patient is being stabilized, steps should be

taken to arrest cause of bleeding



SummarySummary

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

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


HemostasisHemostasis• Ingenious process that makes blood fluid

and free from clots and allows formation of plugs to seal off vessel injury

• Ingenious process that makes blood fluid and free from clots and allows formation of plugs to seal off vessel injury

ThrombosisThrombosis•A pathologic process whereby there is blood clot formation within an injured vessel•A pathologic process whereby there is blood clot formation within an injured vessel


Maintaining Hemostatic BalanceMaintaining 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

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


Tipping the Hemostatic BalanceTipping the Hemostatic BalanceExtensive activation of coagulation process (various diseases)

Endothelial damage

Tissue injury

Platelet activation

Massive thrombosis

Hypercoagulability

Consumption of coagulation

Factors and platelets

Hypocoagulability

Fibrin deposit in micocirculation

Infarction Hemolysis

Massive bleeding

Death

Pre-kallikrein

High molecular weight kininogen

Activation of fibrinolytic system

Secondary fibrinolysis


MAINTENANCE OF HEMOSTASISMAINTENANCE 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

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


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

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



3. Coagulation Process – composed of

a. enzymes ( activated coagulation factor)

b. substrate ( proenzyme form of coagulation factor)

c. co-factor – reaction accelerator

3. Coagulation Process – composed of

a. enzymes ( activated coagulation factor)

b. substrate ( proenzyme form of coagulation factor)

c. co-factor – reaction accelerator




The Fibrinolytic SystemThe Fibrinolytic System

Plasminogen

Tissue activator

Plasma activator

Urokinase

Plasmin

Fibrin-Fibrinogen

Fibrinolytic split products


Naturally Occurring AnticoagulantsNaturally 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

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




Acute, subacute or chronic thrombo-hemorrhagic 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

Acute, subacute or chronic thrombo-hemorrhagic 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


Mechanisms that Trigger DICMechanisms that Trigger DIC

1. Release of tissue factor or thrombocytoplastic materials into the circulation

2. Widespread injury to the endothelial cells

1. Release of tissue factor or thrombocytoplastic materials into the circulation

2. Widespread injury to the endothelial cells


Extrinsic PathwayExtrinsic Pathway

Tissue Injury

Thromboplastin

VII

X V PF 3

Ca++

II Thrombin

Fibrinogen Fibrin (clot)

Abruptio placenta

Amniotic Fluid Embolism

Retained Dead Fetus

Saline induced abortion


Intrinsic PathwayIntrinsic PathwayEndothelial damage Septic abortion

Chorioamnionitis

Contact activation

XII

XI

IX

VIII Platelet

factor 3 Ca++

II Thrombin



Initiation of DIC by platelet activationInitiation of DIC by platelet activation

PLATELET ACTIVATION

(Platelet activation factor, diminished prostacyclin)

Increased aggregation and adhesion

X V PF3

Ca++

II Thrombin


Severe Pre-eclampsia



Major Disorders Associated with DICMajor Disorders Associated with DIC



Consequences of DICConsequences 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

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


CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

1. Microangiopathic hemolytic anemia

2. Respiratory – dyspnea, cyanosis

3. Neurologic – convulsions, coma

4. Renal – oliguria, acute renal failure

5. Circulatory failure and SHOCK

1. Microangiopathic hemolytic anemia

2. Respiratory – dyspnea, cyanosis

3. Neurologic – convulsions, coma

4. Renal – oliguria, acute renal failure

5. Circulatory failure and SHOCK


Laboratory DiagnosisLaboratory Diagnosis1. 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 (100-150mg/100ml)If no clot in 30 mins = fibinogen level

(<100mg/100ml)

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 (100-150mg/100ml)If no clot in 30 mins = fibinogen level

(<100mg/100ml)


Laboratory DiagnosisLaboratory Diagnosis

2. Platelets

<4 platelets / hpf = suggest thrombocytopenia

3. Partial thromboplastin time

4, Prothrombin time

5. Fibrin degradation products- D-dimer

2. Platelets

<4 platelets / hpf = suggest thrombocytopenia

3. Partial thromboplastin time

4, Prothrombin time

5. Fibrin degradation products- D-dimer


Goals in ManagementGoals in Management

1. Good clinical judgement2. Recognition and treatment of underlying

disorder (abruptio placenta, IUFD, Amniotic fluid embolism, septic abortion, and sepsis, eclampsia)

3. Supportive measures(replacement therapy –FFP, cryoprecipitate)

4. Epsilon-Aminocaproic Acid – control fibrinolysis by inhibiting conversion of plasminogen to plasmin

1. Good clinical judgement2. Recognition and treatment of underlying

disorder (abruptio placenta, IUFD, Amniotic fluid embolism, septic abortion, and sepsis, eclampsia)

3. Supportive measures(replacement therapy –FFP, cryoprecipitate)

4. Epsilon-Aminocaproic Acid – control fibrinolysis by inhibiting conversion of plasminogen to plasmin


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Hypovolemic Shock and Dic