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ANTEPARTUM HEMORRHAGE Speaker: Dr. Ashish Moderator: Dr.S.Chawla

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Presentation on theme: "ANTEPARTUM HEMORRHAGE Speaker: Dr. Ashish Moderator: Dr.S.Chawla"— Presentation transcript:

1 ANTEPARTUM HEMORRHAGE Speaker: Dr. Ashish Moderator: Dr.S.Chawla

2 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 1. increase blood volume(1-2 l) 2. hypercoagulable state 3. tourniquet effect of ut. contr. on blood vessels Resuscitation may be inadequate d/t underestimation of blood loss – concealed or difficult to measure

3 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 >500ml, or any amount threatening hemodynamic stability or 10% decrease hematocrit from admission Cause PPH- 4 Ts: tone, tissue, trauma, thrombin

4 PLACENTA PREVIA Caused by placental implantation in lower uterine segment Type – degree to which placenta encroaches on internal cervical os 1.Complete – totally covers int. cervical os 2.Partial –portion of int. cervical os covered 3.Marginal –placental edge at margin of cervical os 4.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

5 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

6 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

7 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

8 Placenta previa-Actively bleeding T&C 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 50%O2/N2O, low dose volatile agent, 100% O2 for fetal distress 30%O2/ 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

9 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

10 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 T&C at least two units, in room at start of case Volume resuscitation with LR or NS Choice of regional or GETA

11 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

12 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

13 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

14 Placental Abruption Separation of the placenta from the decidua basalis prior to delivery (after 20 wk gestation before delivery) Incidence %, maternal mortality %, 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

15 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

16 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 > 2500 cc of blood can be hidden by retroplacental hematoma

17 Clotting abnormalities as/w abruptio placenta Theories 1.Circulating plasminogen activated- enzymatically destroys fibrinogen(fibrinolysis) 2.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

18 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.

19 TEG - Measure viscoelastic property of blood.

20 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.

21 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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23 Obstetric Management of Placental Abruption FHR monitored by scalp electrode, large-bore PIV placed, supplemental O2, left uterine displacement T&C 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

24 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

25 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 > 10g/dl transfusion is rarely indicated. If Hb < 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.

26 Protocol for management of acute haemorrhage

27 1-Every obstetric unit should have a current protocol for major obstetric haemorrhage and all staff should be trained to follow it.

28 2-Initial resuscitation with replacement Fluids (crystalloid or colloid infusions) is a priority to restore blood volume

29 DIC is a consequence of delayed or inadequate resuscitation

30 3-Obtain and send 2 blood samples: *To blood bank for grouping and crossmatching *To lab to obtain baseline for Hb, Htc, PT, PTT,platelet count & fibrinogen levels

31 4- Inform blood bank that it is an emergency

32 Give Packed Red Cell 5- Initial packed red cell infusion to restore O 2 delivery to tissues - Give group O Rh –ve cells should be available in 5 minutes - Give group specific uncrossmatched blood - Give fully matched blood

33 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

34 6-Component replacement therapy according to coagulation screen or if DIC is suspected :

35 Plasma fractions Blood components Cryoprecip itate FFPPlateletPacked red cells –Clotting factor concentrate s –Immunoglo bulin preparations –Saline albumin solution –Salt-poor albumin when fibrinogen level is less than mg/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 RBC’s when whole blood not available for exchange transfusion when platelet. count less than 50000/cm m or when massive blood loss or replacem ent has occurred -Washed RBC’s Pts with allergic reactions to plasma proteins -Leuko-poor RBC’s Pts with febrile, non-hemolytic reactions to plasma WBC’s Clotting disorders, Haemo philia Liver disease 1-2 unit/ 10 kg:8-10 unit 12-15ml/ kg (4-5unit (1unit/10 kg) 6units

36 7- Continuous lab & clinical monitoring to guide treatment. During massive transfusion Monitoring

37 8- The priority to Identify and treat cause of bleeding Consider surgery ( definitive surgical arrest of haemorrhage from major vessels ) earlier rather than later.

38 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

39 REMEMBER… THE DECISION FOR BLOOD TRANSFUSION SHOULD ALWAYS BE A BALANCE BETWEEN

40 Complications of Blood Transfusion Febrile reactions Bacterial contamination Immune reactions Physical complications –Circulatory overload –Air embolism –Pulmonary embolism –Thrombophlebitis –ARDS 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

41 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

42 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

43 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

44 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

45 Hyperkalemia

46 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

47 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

48 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 ComplicationUsual causeFrequency Acute hemolytic reaction 121,122,123 ABO incompatibility1 per RBC units Delayed hemolytic reaction 122,123­126 Hemolysis due to minor blood group incompatibility1 per 2500­9000 RBC units RBC alloimmunization 127 Recipient antibody response to donor antigenAbout 8% of patients transfused with RBCs Nonimmune hemolytic reaction 122,128 Physical or chemical degradation of RBCs (freezing, heating or addition of a hemolytic drug or solution) Unknown Febrile, nonhemolytic reaction or chills without fever 122,123,129 Recipient antibody to donor WBC or platelet antigen or accumulation of cytokines in blood units during storage or both 1 per 100 RBC units Anaphylaxis 122,123,128 Complement activation1 per ­ units (RBC or plasma) Urticarial reactions 122,123 Antibody-mediated response to donor plasma proteins 1 per 100­300 plasma transfusions (probably similar with RBC transfusions) Transfusion-related acute lung injury 122,123 Complement-mediated pulmonary edemaUnknown Graft-versus-host disease 79,130,123,131,132 Engraftment of immunocompetent donor lymphocytes in host Unknown Postransfusion purpura 122,133,134 Recipient develops antibodies against donor and recipient platelets Unknown Passive alloimmune thrombocytopenia 135,136 Donor blood contains platelet-specific alloantibody that results in abrupt thrombocytopenia in the recipient Rare Circulatory overload 122,131 Excess intravascular volume1% of transfused patients Hypothermia, coagulopathy, acid­base disturbances, hypocalcemia, electrolyte abnormalities and citrate toxicity associated with massive transfusion 88,90,94,137­140 Loss, consumption or dilution of blood elementsRelated to volume transfused, unlikely to be seen when < 1.5 blood volumes replaced Iron overloadChronic RBC transfusion therapy (each unit contains 200 mg of iron) Variable, according to number of RBC units transfused; begins after the transfusion of > 20 RBC units

49 Uterine Rupture Incidence of < 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

50 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

51 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

52 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

53 THANK YOU


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