ANTEPARTUM HEMORRHAGE

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ANTEPARTUM HEMORRHAGE

• Speaker Dr. Ashish
• Moderator Dr.S.Chawla

www.anaesthesia.co.in anaesthesia.co.in_at_gmail.c
om
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Obstetric hemorrhage

• Underlying cause 25 of maternal mortality
• Increasing d/t inc. rate LSCS and complication
  that ensue( placenta previa, accreta, and VBAC)
• Maternal physiology well prepared with
• increase blood volume(1-2 l)
• hypercoagulable state
• tourniquet effect of ut. contr. on blood vessels
• Resuscitation may be inadequate d/t
  underestimation of blood loss concealed or
  difficult to measure

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Obstetric hemorrhage

• Cause classified acc. timining of occurrence
• Antepartum h,age (4 of pregnancies)
• Placenta previa, Abruptio placenta ,Uterine
  rupture ,Placenta accreta, Vasa previa
• PPH- (10 of delivery) blood loss after delivery
  gt500ml , or any amount threatening hemodynamic
  stability or 10 decrease hematocrit from
  admission
• Cause PPH- 4 Ts tone, tissue, trauma, thrombin

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PLACENTA PREVIA

• Caused by placental implantation in lower uterine
  segment
• Type degree to which placenta encroaches on
  internal cervical os
• Complete totally covers int. cervical os
• Partial portion of int. cervical os covered
• Marginal placental edge at margin of cervical os
• Low lying- placenta implanted in LUS but edge
  donot impinge on cervical os
• Associated conditions multiparity, advanced
  maternal age, previous C/S, other uterine
  surgeries, and previous placenta previa

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Placenta previa

• Sign -Painless vaginal bleeding
• Bleeding stops spontaneously (usual situation)
• Sudden severe h,age can recur anytime
• B scan USG 95 sensitivity
• Definitve diagnosis direct exam. of cervical os

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Double set -up

• Vaginal examn. in o.t. prepared Em. LSCS
• Preparation
• Two 16 0R 18 G iv cannula
• Blood pump iv set
• Blood for transfusion
• Oral antacid- non particulate
• Oxygen
• Skilled assistant
• Bleeding and LSCS
• Treat hypovolemia
• Induce Ketamine(1mg/kg) and Sch (1.5 mg/kg)
• Intubate provide cricoid pressure
• Awake extubation
• 
  
  

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Obstretic mx

• Before term gestation- conservative mx.- bed rest
  
• Near term gestation- foetal maturity assesed and
  mother delivered LSCS
• If during pregnancy bleeding not stops
  spontaneously- Em. LSCS despite gestational age
  of foetus
• Expectant mgmt terminates when active labor
  begins, lungs are mature, 37 wks gestation,
  excessive bleeding, or other obstetric
  complications occur

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Placenta previa-Actively bleeding

• TC 4 units in room, type-specific if cross
  unavailable
• Two large-bore PIVs
• Volume resuscitate if possible
• GETA using ketamine (up to 1mg/kg) or etomidate
  (0.3mg/kg) and Sch(1.5mg/kg), maint with
  50O2/N2O, low dose volatile agent, 100 O2 for
  fetal distress
• 30O2/ 70 N2O with opioid and no volatile agent
  for atony problems after delivery
• Be prepared for C/Hyst as placenta accreta may
  exist
• Coagulopathy rarely occurs, usually dilutional
  thrombocytopenia is more likely

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Placenta previa-Actively bleeding

• Blood volume as assesed by B.P, CVP, U/O is
  restored to normal
• Neonate- immediate resuscitation at birth
• Neonate may be asphixated, acidotic, hypovolemic
• Intubation and ventilation with 100 O2 ,
  umblical venous catheter fluid admn., umblical
  arterial catheter B.P and blood gases
  monitoring
• Tansfer to NICU a.s.a.p

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Placenta previa Not bleeding

• If diagnosed by USG or double set-up exam.,pt.
  not bleeding currently- LSCS still required
• Careful assessment of intravascular volume
• At least one large-bore PIV, preferably two
• TC at least two units, in room at start of case
  Volume resuscitation with LR or NS
• Choice of regional or GETA

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Placenta previa and placenta accreta

• Placenta accreta- placental implantation onto
  myometrium
• Placenta increta- placental implantation into
  myometrium
• Placenta percreta- pentration through full
  thickness of myometrium- may occur into bowel,
  bladder, or other pelvic organ
• Markedly adherent placenta cannot be removed
  without tearing myometrium

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Placenta previa and placenta accreta

• Massive intraoperative blood loss common
• 2- 3 l blood loss average
• 20 pt. develop coagulopathy
• 30-70 required cesarean hysterectomy
• Placenta accreta not reliably diagnosed untill
  uterus is open
• Anaesthesist must keep this in mind and be
  prepared for sudden massive blood loss
• Regional anaesthesia not increase maternal
  morbidity

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Placenta previa and placenta accreta

• Placenta increta- chances of massive blood loss
  and caesrean hysterectomy markedly high
• Placenta percreta- if diagnosed antenatally-
  uterine incision remote from placenta , umblical
  cord clamped, baby delivered, placenta remain
  in-situ and uterus closed
• Controlled hysterectomy or abdomen closed and pt.
  followed with or without methotrexate to
  facilitate placental involution

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Placental Abruption

• Separation of the placenta from the decidua
  basalis prior to delivery (after 20 wk gestation
  before delivery)
• Incidence 0.2-2.4, maternal mortality 1.8-2.8,
  perinatal mortality as high as 50
• Bleeding occurs from exposed decidual vessels
• Fetal distress occurs due to loss of area for
  maternal-fetal gas exchange
• Associated conditions HTN, ? parity, tobacco,
  cocaine use, trauma, PROM, previous abruption
• Associated with IUGR and fetal malformations

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Placental Abruption

• Complications include hemorrhagic shock, ARF,
  coagulopathy, fetal distress, IUFD
• Most common cause of DIC in pregnancy
• Coagulopathy occurs in 10 of all cases
• Fetal RDS occurs in up to 50 of all cases
• Large retroplacental hematomas assoc with 50
  mortality, same size subchorionic assoc with 10
  mortality
• Infants have higher incidence of being SGA which
  indicates a chronic process

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Diagnosis of Placental Abruption

• Classically presents as vaginal bleeding, uterine
  tenderness, and ? uterine activity
• Amount of vaginal bleeding can lead to
  underestimation of blood loss
• gt 2500 cc of blood can be hidden by
  retroplacental hematoma

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Clotting abnormalities as/w abruptio placenta

• Theories
• Circulating plasminogen activated- enzymatically
  destroys fibrinogen(fibrinolysis)
• Thromboplastin from placenta and decidua
  activate extrinsic clotting pathway causing
  thrombin to convert fibrinogen to fibrin(DIC)
• End result -Hypofibrinogenemia, platelet
  def.,decreased factor V , VIII

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CLOT observation test

• 5ml maternal venous blood in clean glass T.T
  shaken gently, allowed to stand
• If clot does not form in 6 min or clot lysed
  within 1 hr, clotting defect probably present
• If clot fail to form within 30 min , fibrinogen
  less than 100mg/dl
• Sample also send for CBC, PT, PTT,Fibrinogen, FDP
  analysis
• TEG role in obstetric h,age is limited.

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• TEG - Measure viscoelastic property of blood

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Clotting time (CT) or reaction time( R time) The
time from the start of the curve until it reaches
1 mm wide This is the time taken to form fibrin.
Prolonged with clotting factor deficiencies,
anticoagulants and thrombocytopaenia. Clot
formation time (CFT) or K time The time taken for
the graph to widen from 1 mm to 20 mm. This is
dependent on fibrinogen and platelets . Maximum
clot firmness (MCF )or maximum amplitude This is
the width of the curve at the widest point. This
is affected by platelet function and number and
fibrinogen.  
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• Alpha angle
• This is the angle measured between the
  midline of the tracing and a line drawn from the
  1 mm point tangential to the curve.The alpha
  value and CFT indicate the rate of increase of
  elastic shear modulus in the sample i.e. how
  fast the clot structure is forming.This is
  abnormal in the presence of clotting factor
  deficiencies, platelet dysfunction,
  thrombocytopenia and hypofibrinogenaemia.
• Fibrinolysis
• This is measured as a decrease in amplitude
  from the maximum. If there is a substantial
  decrease i.e. more than 15 then this is an
  indication of fibrinolysis taking place

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Obstetric Management of Placental Abruption

• FHR monitored by scalp electrode, large-bore PIV
  placed, supplemental O2, left uterine
  displacement
• TC sent as well as CBC, coagulation profile
• Expectant management for small, stable abruptions
  in pre-term pregnancies
• Vaginal delivery is preferred when there is no
  evidence of fetal distress and a favorable cervix
  is present
• C-section is performed in other cases

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Anesthetic Management of Placental Abruption

• Epidurals may be given to parturients who are
  neither hypovolemic nor coagulopathic provided
  normal intravascular volume is maintained
• For acute fetal distress, C/S is the typical
  route of delivery
• GETA is preferred for C/S, using ketamine or
  etomidate due to potentially severe hypotension
• Volume resuscitation with crystalloid or colloid
  is critical
• Invasive monitors may be used to aid in
  determination of intravascular volume in cases of
  severe hemorrhage
• Uterine atony should be treated aggressively
• Coagulation factors replaced as necessary

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Massive transfusion is arbitrarily defined as
the replacement of a patient's total blood volume
in less than 24 hours, or as the acute
administration of more than half the patient's
estimated blood volume per hour.

• If Hb gt 10g/dl transfusion is rarely indicated.
  If Hb lt 7g/dl transfusion is usually necessary.
  With Hbs between 7 and 10 g/dl, clinical status,
  PvO2 and ER are helpful in defining transfusion
  requirements.

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Protocol for management of acute haemorrhage
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1-Every obstetric unit should have a current
protocol for major obstetric haemorrhage and
all staff should be trained to follow it.
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• 2-Initial resuscitation with replacement
• Fluids (crystalloid or colloid infusions)
• is a priority
• to restore blood volume

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DIC is a consequence of delayed or inadequate
resuscitation
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3-Obtain and send 2 blood samplesTo blood
bank for grouping and crossmatching To lab to
obtain baseline for Hb, Htc, PT, PTT ,platelet
count fibrinogen levels
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4- Inform blood bank that it is an emergency
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Give Packed Red Cell

• 5- Initial packed red cell infusion
• to restore O2 delivery to tissues - Give group
  O Rh ve cells should be available in 5 minutes
• - Give group specific uncrossmatched
  blood - Give fully matched blood

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• Combinations of stored whole blood, packed cells,
  colloids crystalloids are given to maintain
  blood volume or pressure at adequate levels and
  haemoglobin at around 7g/dl or haematocrit at 0.25

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6-Component replacement therapy according to
coagulation screen or if DIC is suspected
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Plasma fractions Blood components Blood components Blood components Blood components
Cryoprecipitate FFP Platelet Packed red cells
Clotting factor concentrates Immunoglobulin preparations Saline albumin solution Salt-poor albumin when fibrinogen level is less than 80-100mg/dl Initially a tx for VW Dz, Hemophilia Now a source of fibrinogen in obstetric emergencies when PT PTT are higher than 1.5 times control levels All clotting factors no platelets Can supplement RBCs when whole blood not available for exchange transfusion when platelet. count less than 50000/cmm or when massive blood loss or replacement has occurred -Washed RBCs Pts with allergic reactions to plasma proteins -Leuko-poor RBCs Pts with febrile, non-hemolytic reactions to plasma WBCs
Clotting disorders,HaemophiliaLiver disease 1-2 unit/ 10 kg8-10 unit 12-15ml/ kg (4-5unit (1unit/10kg) 6units
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7- Continuous lab clinical monitoring to
guide treatment. During massive transfusion
Monitoring
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• 8- The priority to Identify and treat cause of
  bleeding
• Consider surgery (definitive surgical arrest
  of haemorrhage from major vessels ) earlier
• rather than later.

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• 9- Massive transfusion of stored whole blood
• can aggravate coagulopathy due to -
  Dilutional thrombocytopenia - Coagulation
  factor depletion - Acidosis -
  Hypothermia
• thus
• 1 unit of fresh blood for every 5 10 units of
  stored blood
• IV 10 calcium gluconate 10 mls with every litre
  of transfused citrated blood
• Warming blood
• Microaggregate blood filters

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REMEMBERTHE DECISION FOR BLOOD TRANSFUSION
SHOULD ALWAYS BE A BALANCE BETWEEN
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Complications of Blood Transfusion

• Metabolic complications
• Hyperkalaemia
• Citrate toxicity hypocalcaemia
• Release of vasoactive peptides
• Release of plasticizers from PVC-phthalates
• Haemorrhagic reactions
• After massive transfusion of stored blood
• Disseminated intravascular coagulation
• Transmission of disease
• Hepatitis, CMV. EBV
• AIDS (Factor VIII)
• Syphilis
• Brucellosis
• Toxoplasmosis
• Malaria
• Trypanosomiasis
• Haemosiderosis
• After repeated transfusion in patients with
  haematological diseases

• Febrile reactions
• Bacterial contamination
• Immune reactions
• Physical complications
• Circulatory overload
• Air embolism
• Pulmonary embolism
• Thrombophlebitis
• ARDS

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Coagulopathy
Most common cause of bleeding following large
volume transfusion dilutional thrombocytopenia
At least 1.5 times blood volume must be replaced
for this to become a clinical problem
Thrombocytopenia can occur following smaller
transfusions if DIC or there is pre-existing
thrombocytopenia
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Citrate Toxicity
Citrate in the transfused blood binds to
calcium each unit of blood contains 3 grams of
citrate transfusion rates higher than one unit/5
minutes may lead to citrate toxicity
At least 1.5 times blood volume must be replaced
for this to become a clinical problem
Treatment is with intravenous calcium
administration if there is biochemical, clinical
or electrocardiographic evidence of hypocalcemia
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Hypothermia
Leads to reduction of citrate and lactate
metabolism -hypocalcemia and metabolic
acidosis Increase affinity of hemoglobin for
oxygen, Leads to platelet dysfunction, and
increase tendency for cardiac dysrhythmias
Massive transfusion is an absolute indication for
the warming of all blood to body temperature as
it is being given
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Acid/Base Disturbances
Most common abnormality is a metabolic
alkalosis -lactic acid in stored PRBC
(30-40mmol/l) -citrate and lactic acid
metabolized to bicarbonate
Final acid/base status being dependent on tissue
perfusion, rate of administration and citrate
metabolism
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Hyperkalemia
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Management of Massive Transfusion
Hypotension should be treated speedily. Do not
delay fluid administration
Initial red cell replacement is in the form of
packed red cells
Blood should be taken for group and crossmatch,
these must be properly labeled and identified in
all situations
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Management of Massive Transfusion
For extreme emergencies group O blood should be
supplied first
Type specific blood should be available in 5-10
minutes and switch promptly
Continue transfusing blood on this basis until
crossmatch blood is available
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Guidelines for red blood cell and plasma
transfusion for adults and children
 
Summary of the nature and frequency of noninfectious risks associated with red blood cell and plasma transfusion Summary of the nature and frequency of noninfectious risks associated with red blood cell and plasma transfusion Summary of the nature and frequency of noninfectious risks associated with red blood cell and plasma transfusion
Complication Usual cause Frequency
Acute hemolytic reaction121,122,123 ABO incompatibility 1 per 25 000 RBC units
Delayed hemolytic reaction122,123126 Hemolysis due to minor blood group incompatibility 1 per 25009000 RBC units
RBC alloimmunization127 Recipient antibody response to donor antigen About 8 of patients transfused with RBCs
Nonimmune hemolytic reaction122,128 Physical or chemical degradation of RBCs (freezing, heating or addition of a hemolytic drug or solution) Unknown
Febrile, nonhemolytic reaction or chills without fever122,123,129 Recipient antibody to donor WBC or platelet antigen or accumulation of cytokines in blood units during storage or both 1 per 100 RBC units
Anaphylaxis122,123,128 Complement activation 1 per 20 00050 000 units (RBC or plasma)
Urticarial reactions122,123 Antibody-mediated response to donor plasma proteins 1 per 100300 plasma transfusions (probably similar with RBC transfusions)
Transfusion-related acute lung injury122,123 Complement-mediated pulmonary edema Unknown
Graft-versus-host disease79,130,123,131,132 Engraftment of immunocompetent donor lymphocytes in host Unknown
Postransfusion purpura122,133,134 Recipient develops antibodies against donor and recipient platelets Unknown
Passive alloimmune thrombocytopenia135,136 Donor blood contains platelet-specific alloantibody that results in abrupt thrombocytopenia in the recipient Rare
Circulatory overload122,131 Excess intravascular volume 1 of transfused patients
Hypothermia, coagulopathy, acidbase disturbances, hypocalcemia, electrolyte abnormalities and citrate toxicity associated with massive transfusion88,90,94,137140 Loss, consumption or dilution of blood elements Related to volume transfused, unlikely to be seen when lt 1.5 blood volumes replaced
Iron overload Chronic RBC transfusion therapy (each unit contains 200 mg of iron) Variable, according to number of RBC units transfused begins after the transfusion of gt 20 RBC units
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Uterine Rupture

• Incidence of lt 1 in patients with a scarred
  uterus, otherwise rare
• Uterine scar dehiscence usually does not result
  in maternal or fetal distress, true uterine wall
  rupture does
• Fetal distress is most reliable sign
• Risk factors grand multiparity, malpresentation,
  administration of oxytocin/prostaglandin

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Management of Uterine Rupture

• Repair, arterial ligation, and hysterectomy
• A dehisced uterine scar bleeds less than a newly
  ruptured uterus, and blood transfusion
  requirement is less likely
• Evaluation and resuscitation by the anesthesia
  care team in preparation for surgery
• GETA is usually necessary unless prior epidural
  is in place in stable patients
• Invasive hemodynamic monitoring may be necessary

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Vasa Previa

• Fetal vessel traverse the cervical os ahead of
  the presenting fetal part Rupture may occur
  leading to fetal exsanguination
• 1 in 2,000 3,000 incidence
• 50 to 75 fetal mortality
• Associated with multiple gestations
• Shed blood can be examined for nucleated RBCs or
  HgbF

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Management of Vasa Previa

• Ruptured vasa previa needs to be delivered
  emergently by C/S
• Anesthetic management depends on urgency
• Neonatal resuscitation will usually require
  umbilical cord blood, colloid, and LR/NS

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