OB3B HYPOVOLEMIC SHOCK

DISSEMINATED INTRAVASCULAR DISEASE BLOOD VOLUME DEFICIT > 25 PERCENT

Dra. Elizabeth Ahyong-Reyes

SHOCK
CAUSE DUE TO
HYPOVOLEMIC  blood volume Hemorrhage
SHOCK Vomiting
Diarrhea
CARDIOGENIC Pump failure M.I/heart faillure
SHOCK Arrythmias
(AV) block
SEPTIC SHOCK Massive TPR Endotoxins
ANAPHYLACTIC Massive TPR Allergic reaction
SHOCK (histamine release)

HYPOVOLEMIC SHOCK
 Shock from hemorrhage evolves through several stages
 EARLY in the course of massive bleeding
mean arterial pressure
stroke volume
cardiac output
central venous pressure
pulmonary capillary wedge pressure
 Activates lymphocytes and monocytes, which interact
  arteriovenous oxygen content difference   tissue with endothelial cells
oxygen extraction BUT overall oxygen consumption falls 
 Blood flow to capillary beds - controlled by arterioles Loss of capillary membrane integrity
(partially controlled by the CNS) Additional loss of intravascular volume
 70% total blood volume are in the venules ( controlled Adverse effects mediated by peptide, leukotrienes,
by humoral factors) and cytokines
 Catecholamine release during hemorrhage causes an Improved by pharmacological antagonism activator
 in venular tone  autotransfusion from this
capacitance reservoir  HYPOVOLEMIC SHOCK

Compensatory Mechanism platelet aggregation
Release vasoactive mediators

Small vessel occlusion
Further impairment of microcirculatory perfusion

o Causes electrolyte shift and changes in

cellular transport of various ions:
 Na & water enter skeletal muscles
 K+ Loss to extracellular fluid

Survival is enhanced in acute hemorrhagic shock if blood plus

crystalloid is given compared with blood transfusion alone

ESTIMATION OF BLOOD LOSS

 Visual inspection
o Inaccurate
o half the measured loss
 In obstetrics - part or all of the hemorrhage may be
concealed

 ACUTE HEMORRHAGE
o the immediate hematocrit may not reflect
actual blood loss
o the loss of 1000 mL à hematocrit ↓ 3 vol% in
the first hour
o rapid infusion of intravenous crystalloids
causes rapid equilibration
o During an episode of acute significant
hemorrhage, the initial hematocrit is always
the highest

 URINE OUTPUT
o One of the most important "vital signs“ in
obstetrical hemorrhage
o Reflects the adequacy of renal perfusion, and
in turn the perfusion to other vital organs
o Urine flow of at least 30-60 mL per hour should
be maintained.
o In potentially serious hemorrhage, an
indwelling catheter should be inserted
promptly to measure urine flow.

 POTENT DIURETICS (FUROSEMIDE)

o invalidate the relationship between urine flow
and renal perfusion.
o Contraindicated in hypovolemic patient
o
return, ↓ ↓ ↓ cardiac output
BERNABE, Maria Katrina R. 1
Medicine 3i - 2015
RESUSCITATION AND ACUTE MANAGEMENT Blood Products Commonly Transferred in Obs. Hemorrhage
 Identify the Cause:
o uterine atony, retained placental fragments ONE UNIT VOLUME PER CONTENTS EFFECTS IN
o genital tract lacerations UNIT PER UNIT OBSTETRICAL
 One or two intravenous infusion systems of large caliber HEMORRHAGE
needle to allow rapid administration of crystalloid WHOLE BLOOD About 500ml; RBCs, plasma, Restores TBV
solutions and blood. Hct~40% 600-700mg of and
 Operating room, surgical team, and anesthesiologist fibrinogen, no fibrinogen;
should always be immediately available. platelets  Hct 3-4
 Management of specific causes volume% per
unit
Fluid Replacement PACKED RBCs About 250ml RBCs only, no Hct 3-4
(“PACKED plus additive fibrinogen, no volume% per
Crystalloid Solutions CELLS”) solutions; platelets unit
 initial volume resuscitation Hct~55~80%
 Only 20 % of crystalloid remains in the circulation of FRESH FROZEN About 250ml; Colloid plus Restores TBV
critically ill patients after 1 hour PLASMA 30-minute about 600- and
 Three times as much crystalloid for every ml of
thaw 700mg fibrinogen
estimated blood loss needed fibrinogen, no
before use platelets
Blood Replacement
CRYOPRECIPIT About 15ml, About 200mg About 3000-
ATE frozen fibrinogen 4000mg total
Hemoglobin concentration falls to about 7 g/dL(hematocrit <20
plus other is needed to
ly decrease
clotting redtore
factors, no maternal
ACUTE BLEEDING: RAPID BLOOD INFUSION IF
platelets fibrinogen to
1. hematocrit is less than 25 volume %
>150mg/dl
2. hemoglobin is less than 8 g/dL
3. imminent surgery, acute operative blood loss, acute PLATELETS About 50ml, One unit has 6-10 units
hypoxia, vascular collapse stored at 5.5 x 1010 usually
room temp platelets in transfused;
THE NUMBER OF UNITS TRANSFUSED TO REACH A TARGET 50ml plasma each
HEMATOCRIT DEPENDS ON THE BODY MASS AND ADDITIONAL increases
BLOOD LOSS platelet
5000/ul
Whole Blood and Blood Components Hct = hematocrit; RBC = red blood cells; TBV = total blood vol.
 Compatible WHOLE BLOOD is ideal for treatment of
hypovolemia from catastrophic acute hemorrhage
DILUTIONAL COAGULOPATHY
Whole Blood
 40 days shelf life
 70% of the transfused red cells function for at least 24
hours following transfusion
 1 unit raises the hematocrit by 3 to 4 vol%
 replaces many coagulation factors, especially
fibrinogen
 its plasma expands hypovolemia from hemorrhage
 IDEAL FOR HYPOVOLEMIA FROM CATASTROPHIC
HEMORRHAGE

Packed RBC
 Extracted from 1unit of whole blood have a hematocrit
of 60 to 70 vol %
 A unit raises the hematocrit by 3 to 4 vol%
 Packed red blood cell and crystalloid infusion are the
mainstays of transfusion therapy for most cases of  Thrombocytopenia
obstetrical hemorrhage.(Ratio of 2:1 or 3:1) o most frequent coagulation defect found in
women with blood loss and multiple
Platelets transfusions
 preferable if obtained by apheresis from one donor o HYPOFIBRINOGENEMIA, PROLONGED
 Cannot be stored more than 5 days PROTHROMBIN TIME AND PARTIAL
 WITH BLEEDING: THROMBOPLASTIN TIME  IMPAIRED
o platelet count should be maintained above
50,000/L with the infusion of platelet  Component replacement is rarely necessary with acute
concentrates. replacement of 5 to 10 units of packed red blood cells
 Non surgical patients -10,000 and above will not cause or less
bleeding
 One unit=5.5 x 10 10 Recombinant Activated Factor VII
 Synthetic Vit K dependent protein
Fresh Frozen Plasma  Binds to exposed tissue factor at the site of injury to
 separating generate thrombin that activate platelets and the
 Source of all stable and labile clotting factors, including coagulation cascade
fibrinogen.  Major concern-arterial/venous thrombosis
 INDICATIONS:  Will not be effective if plasma fibrinogen is less than 50
1. fibrinogen level of less than 100 mg/dL mg/dl or the platelet is less than 30,000/ul
2. prolonged prothrombin or partial thromboplastin
3. consumptive or dilutional coagulopathy AUTOTRANSFUSION

Cryoprecipitate effective
 Prepared from fresh-frozen plasma.  Recommended only for rare blood type and patients
 Each 10-15 ml unit contains 200 mg fibrinogen factor with unusual antibodies
VIII: C, factor VIII: von Willebrand factor, factor XIII and
fibronectin
 ideal source of fibrinogen if levels are dangerously low
and there is oozing from surgical incisions.

BERNABE, Maria Katrina R. 2

Medicine 3i - 2015
CELL CLEAVAGE CONSUMPTIVE COAGULOPATHY
 -
(Disseminated Intravascular Disease)
 SAFE FOR OBSTETRICAL PATIENTS WITH NO REPORTS OF
SERIOUS COMPLICATIONS
 complex disorder of the clotting mechanism, in which
COMPLICATIONS OF BLOOD TRANSFUSION coagulation factors are consumed at an accelerated
rate, with generalized fibrin deposition and thrombosis,
 Hemolytic Transfusion Reaction(Errors in matching hemorrhages and further depletion of the coagulation
leading to ABO incompatibility) factors
 Transfusion-Related Acute Lung Injury  Acute or chronic
 Bacterial Contamination  Triggered by the entry of large amounts of
 Viral Transmission thromboplastic substances in to the circulation,
resulting from any of the wide variety or severe diseases
INCOMPATIBLE BLOOD TRANSFUSION COMPLICATIONS and traumas.
 Disseminated Intravascular Coagulation
 Acute Kidney Injury PREGNANCY HYPERCOAGULABILITY
 Death  Increases in the concentrations of coagulation factors I
(fibrinogen), VII, VIII, IX, and X and plasminogen
Clinical Manifestations: together but plasminogen activator inhibitor also
 Fever
 Hypotension  plasmin activity until after delivery
 Tachycardia  Platelet count decreases by 10 %-
 Dyspnea  Increased activation of platelet, fibrinopeptide
 Chest or back pain A,thromboglobulin,platelet factor 4,fibrinogen-fibrin
 Flushing degradation products(D.Dimers)
 Severe anxiety
 Hemoglobinuria

Diagnosis:
 urine and plasma hemoglobin concentration
 antibody screen

Management:
 Stop transfusion
 Treat hypotension,hyperkalemia
 Diuretic
 Alkalinize urine

TRANSFUSION RELATED ACUTE LUNG INJURY(TRALI)

 Severe dyspnea, hypoxia, non cardiogenic pulmonary
edema
 Injury to pulmonary capillaries due to anti human
leukocyte antigen(HLA) antibodies in donor plasma 
bind to leukocytes  release of inflammatory mediators
MECHANISM OF CONSUMPTIVE COAGULOPATHY
INFECTIONS
 BACTERIAL
o Yersinia, Pseudomonas, Serratia, Acineto-
bacter, Escherichia
o Unusual because of refrigeration except for
platelets which are stored at room
temperature
 VIRUS
o HIV-most feared
o hepatitis B and C

Red-Cell Substitutes
 3 varieties of these substitutes
o Perfluorochemicals
o Liposome-encapsulated hemoglobin
o Hemoglobin-based oxygen carriers

CAUSES OF DIC
 Abruptio placenta
 Obstetric hemorrhages
 Acute fatty liver
 IUFD
 Amniotic Fluid embolism
 Septic Abortion and obstetric sepsis
 Pre eclampsia/HELLP syndrome/Eclampsia

DIAGNOSIS
 Excessive bleeding at sites of modest trauma
 Fibrinogen and degradation products - less than 150
mg/dl. Serious if less than 50 mg/dl
 Thrombocytopenia
 Prolonged prothrombin and partial thromboplastin time

BERNABE, Maria Katrina R. 3

Medicine 3i - 2015
AMNIONIC FLUID EMBOLISM Clinical Findings
 Complex disorder classically characterized by the  Hypotension
abrupt onset of hypotension, hypoxia, and  Fetal distress
consumptive coagulopathy  Pulmonary edema or ARDS
 Cardiopulmonary arrest
Predisposing Factors  Cyanosis
1. Rapid labor
2. Meconium stained amniotic fluid Management
3. Tears into uterine and other large pelvic veins  Cardiopulmonary resuscitation 
4. Older maternal age oxygenation(intubation) and support of the failing
5. Posterm pregnancy myocardium(rapid blood and component
6. Labor induction and augmentation replacement)
7. Eclampsia  Emergency CS/postmortem CS
8. Cesarean  There are no data that any type of intervention
9. 9.Forceps and vacuum improves maternal prognosis with amnionic fluid
10. 10.abruptio and previa embolism.
11. 11.hydramnios
Prognosis
UTERINE HYPERTONUS IS RATHER AN EFFECT THAN THE CAUSE OF  Profound neurological impairment is common in
AMNIOTIC FLUID EMBOLISM BECAUSE AT IF INTRAUTERINE survivors.
PRESSURE EXCEEDS 35-40 MMHG UTERINE BLOOD FLOW CEASES  Only 8 percent of women who lived despite cardiac
arrest survived neurologically intact.
 Poor fetal outcome and is related to the cardiac arrest-
to-delivery interval.
 Overall neonatal survival is 70 percent, but almost half
suffer residual neurological impairment.

SEPTICEMIA
 Endotoxin and exotoxin release
 Activation of coagulation factors
 E. Coli(pyelonephritis,puerperal infections)
 Septic abortions(Grp.A Strep.,S. Aureus,Clostridium
perfringens or sordelli)

PURPURA FULMINANS
 Severe often lethal form of consumptive coagulopathy

vasculitis
 Debridement of affected skin in a burn unit
 Seen in patients with protein c deficiency

ABORTION

1. Septic Abortion:can incite coagulation and worsen

hemorrhage
2. Induced second trimester abortions
 INITIAL PHASE: 3. IUFD
o pulmonary and systemic hypertension- 4. U oplastin release into
- maternal circulation from placenta,fetus,and decidua
injury by necrobiotic effect of hypertonic solutions
 Failure to transfer blood from right side to left side of the
heart -
cardiac output
 SECONDARY PHASE:
o lung injury and coagulopathy

POSTMORTEM Diagnosis
 Detection of squamous cells or other debris of fetal
origin in the central pulmonary circulation was believed
to be pathognomonic BUT can be found in other
conditions
 Diagnosis is generally made by identifying clinically
characteristic signs and symptoms excluding other
causes

BERNABE, Maria Katrina R. 4

Medicine 3i - 2015