obstetric hemorrhage (1) (2) (1).pptxxxx

Obstetric hemorrhage

1. OBSTETRIC HEMORRHAGE AND ANESTHETIC MANAGEMENT MODERATOR :Dr K MYDHILI M.D ASSOCIATE PROFESSOR SPEAKERS : DR DHAARANI DEVI DR YAMINI DR KAVYA

2. LECTURE OUTLINE INTRODUCTION ANTEPARTUM HEMORRHAGE POST PARTUM HEMORRHAGE TEAM RESPONSE TO HEMORRHAGE TRANSFUSION THERAPY

3. OBSTETRIC HEMORRAGE : World leading cause of maternal mortality WHO estimates severe hemorrhage complicates 10.5% of all live births. In India it contributes to 22.3% of all maternal deaths . Gravid uterus receive 12% of cadiac output so obstetric hemorrhage can be rapid and life threatening. Common difficulties with hemorrhage management include: inaccurate determination of blood loss, unrecognized hemorrhage risk factors, delayed intervention, improper or inadequate transfusion of blood products.

4. Obstetric hemorrhage can be classified as : ANTEPARTUM HEMORRHAGE Antepartum vaginal bleeding may occur in as many as 25% of pregnant women The majority of cases occur during the first trimester of pregnancy and bleeding occurs after 24weeks of gestation and before delivery COMMON CAUSES : PLACENTA PREVIA PLACENTAL ABRUPTION UTERINE RUPTURE VASA PREVIA POST PARTUM HEMORRHAGE Hemorrhage as blood loss ≥1000ml / blood loss accompanied by signs or symptoms of hypovolemia with in 24hrs after birth --- Primary post partum hemorrhage Secondary post partum hemorrhage occurs between 24hrs and 6 weeks COMMON CAUSES: UTERINE ATONY GENITAL TRAUMA RETAINED PLACENTA UTERINE INVERSION

5. ANTEPARTUM HEMORRHAGE

6. PLACENTA PREVIA : Placenta previa occurs when the placenta covers the cervix Incidence of placenta previa is approximately 1 in 200pregnancies Total placenta previa --completely covers the cervical os Partial placenta previa- -- covers part, but not all of the cervical os Marginal placenta previa --lies close to, but does not cover the cervical os New terms ; Any portion of the placenta overlies the os , it is referred to as a previa , any placenta near the os is termed as low-lying LOW LYING PREVIA

7. ETIOLOGY: The exact cause is unclear, but prior uterine trauma (e.g., scar from prior cesarean delivery) is a common finding Other causes; MULTIPARITY ADVANCED MATERNAL AGE SMOKING PREVIOUS CESAREAN DELIVERY PRIOR PLACENTA PREVIA

8. The classical clinical signs are painless bright red vaginal bleeding during 2 nd and 3 rd trimester The initial bleeding is rarely so profuse as to prove fatal. It usually ceases spontaneously, only to recur. Placenta previa may be associated with placenta accreta, placenta increta or percreta and placental abruption . Transvagunal ultrasonography is GOLD STANDARD for diagnosis

9. Obstetric management: Obstetric management is based on the severity of vaginal bleeding and the maturity and status of the fetus

10. ANAESTHETIC MANAGEMENT: Special consideration should be given to – airway examination Intravascular volume History of previous caesarean delivery / uterine scar Volume resuscitation should be initiated using a non–dextrose-containing balanced salt solution Availability of cross-matched blood should be ensured adequate blood reserve

11. ANAESTHETIC MANAGEMENT The choice of anesthetic technique depends on the indication and urgency for delivery, the severity of maternal hypovolemia, and the obstetric history A Randomised controlled trial comparing epidural with general anesthesia for cesarean delivery in women with placenta previa in the absence of active bleeding demonstrated that epidural anesthesia was associated with more stable blood pressure after delivery lower transfusion rates and transfusion volumes with similar hematocrit measurements the day after surgery. High risk of intra operative blood loss due to ; obstetrician may cut into the placenta during uterine incision lower uterine segment implantation site does not contract well increased risk for placenta accreta

12. Pre operative evaluation; Patient evaluation, resuscitation, and preparation for operative delivery all proceed simultaneously. Careful assessment of the parturient's airway and intravascular volume Two large-gauge intravenous catheters ,four units of PRBCS Blood administration sets ,fluid warmers ,equipment for invasive monitoring. Fasting and antacid prophylaxis : Clear liquids and solids are allowed up to 2 hours and 6 to 8 hours, respectively,surgical intervention is required, antacids such as IV (H2)-receptor antagonists or proton-pump inhibitors should be administered, if not already given, in case general anesthesia is necessary. However, these drugs take up to 30 minutes to become effective. oral administration of a nonparticulate antacid such as sodium citrate is used to increase the pH of gastric contents. A dose of sodium citrate (0.3 molar) 30 mL is effective for approximately 30 minutes and should be administered shortly before the induction of general anesthesia Metoclopramide 10MG IV promotes gastric emptying and increases lower esophageal sphincter tone

13. Rapid-sequence induction of general anesthesia is the preferred technique for bleeding patients It usually consists of preoxygenation, rapid intravenous injection of a predetermined dose of induction agent followed immediately by succinylcholine administration, application of cricoid pressure, and avoidance of positive-pressure ventilation before tracheal intubation with a cuffed endotracheal tube (ETT) The choice of intravenous induction agent depends on the degree of cardiovascular instability Ketamine [0.5-1mg/kg] and etomidate [.03mg/kg]are useful alternative induction agents for hemodynamically unstable patients.

14. MAINTENANCE : Nitrous oxide 50% and oxygen with a low concentration of a volatile halogenated agent. Concentration of nitrous oxide can be reduced (or omitted) in cases of foetal distress Oxytocin infusion[ 20IU ] immediatetly after delivery If bleeding continues, it may be best to discontinue the volatile halogenated agent completely after delivery and to substitute 70% nitrous oxide and an intravenous opioid or ketamine. These drugs, along with small doses of midazolam, can be administered without causing significant uterine relaxation or cardiovascular depression. A low-dose infusion of propofol and/or ketamine may be considered, with the caution that propofol causes decreased uterine contractility in a dose-dependent manner. If the placenta does not separate easily, placenta accreta may exist. In such cases, massive blood loss and the need for cesarean hysterectomy should be anticipated

15. PLACENTAL ABRUPTION : Placental abruption is defined as complete or partial separation of the placenta from the decidua basalis before delivery of the fetus. Placental abruption complicates 0.4%-1% of pregnancies

16. Presentation: Vaginal bleeding Uterine tenderness Increased uterine activity Abruption may manifest as idiopathic preterm labor. Patients may have a variety of nonreassuring fetal heart rate (FHR) patterns, including bradycardia, late or variable decelerations, and loss of variability. Aruption is primarily clinical , USG helps to detect abruption and placental position Complications: hemorrhagic shock, coagulopathy, DIC and fetal compromise or demise. One third of coagulopathies in pregnancy are attributable to abruption, and coagulopathy is associated with fetal demise.

17. OBSTETRIC MANAGEMENT : The definitive management is delivery of infant and placenta, Evaluate maternal stability[ vitalsigns , coagulation studies] Evaluate fetal well-being and maturity If severe fetal distress and/or maternal instability ..........urgent C/S If stable mother and fetus.....induction of labor and vaginal delivery

18. ANAESTHETIC MANAGEMENT: Preoperative preparation: Airway assessment Assessment of volume status Maternal Haemodynamic monitoring FHR monitoring Two large bore IV catheters Blood for cross matching, haematocrit, coagulation profile Maintain supplemental oxygen Left uterine displacement

19. Labour and vaginal delivery : Neuraxial labour analgesia offered in abruption provided that hypovolemia has been treated and coagulation status is normal Cesarean delivery : General anaesthesia is preferred for most of the cases Regional anaesthesia can be given for a patient with stable haemodynamics ,good intravascular volume ,minor abruption, NO foetal distress and coagulation profile is normal Ketamine and etomidate are inducing agents ofchoice Rapid sequence induction is preferred Large doses of ketamine may increase uterinetone during early gestation So dose of ketamine should be limited to singledose of 1mg/kg

20. Aggressive volume resuscitation with both crystalloids and colloids Massive Blood transfusion Central venous catheter and arterial catheter may be necessary High risk for uterine atony requiring uterotonics. Oxytocin 20U/L infused immediately after the delivery Coagulation abnormalities may require FFP , early replacement of cosgulation factors ,especially fibrinogen to minimise the risk for developing coagulopathy Most parturients recover quickly and completely after delivery Prolonged hypotension, coagulopathy, and massive blood volume/product replacement, are best monitored in a multidisciplinary intensive care unit.

21. UTERINE RUPTURE : Rupture of gravid uterus can be diasatrous for both mother and fetus Scar dehiscence : Foetal distress less common No excessive haemorrhage Rarely requires emergency section Uterine rupture : Foetal distress massive haemorrhage requires emergency caesarean section

22. Presentation: FHR abnomality is first sign of uterine rupture vaginal bleeding , maternal hypotension , cessation of labour , uterine hyperyonia , loss of fetal stations Obstetric management : Uterus repair , arterial ligation and hysterectomy { definitive treatment } Anesthetic management: Preoperative evaluation, resuscitation and preparation of OT simultaneously GA is often required RA can be given in haemodynamically stable patients, who already have a epidural catheter, absence of foetal distress Aggressive volume replacement and maintenance of urine output Invasive hemodynamic monitoring may be appropriate.

23. VASA PREVIA * Occurs rarely 1 in 2500 to 5000 deliveries. Vasa previa is associated with a velamentous insertion of the cord where foetal vessels traverse the foetal membranes ahead of the foetal presenting part. Highest foetal mortality rates 50% to 75%* No threat to the mother as it involves fetal blood loss Early diagnosis BY USG and treatment are essential to reduce the chance of foetal death Requires immediate delivery by caesarean section Neonatal resuscitation, neonatal volume replacement Choice of anaesthetic technique depends on the urgency of caesarean section

24. POSTPARTUM HEMORRHAGE

25. POSTPARTUM HEMORRHAGE T he most commonly accepted definition is blood lo ss more than 500 mL after vaginal delivery or more than 1 000 mL after cesarean delivery . (ACOG) defines hemorrhage as blood loss greater than or equal to 1000 mL, or blood lo ss accompanied by signs or symptoms of hypovolemia w ithin 24 hours of birth. Primary postpartum hemorrhage - secondary postpartum he morrhage secondary postpartum hemorrhage -occurs between 24 hours and 6 weeks after del ivery .

26. COMMON CAUSES: UTERINE ATONY GENITAL TRAUMA RETAINED PLACENTA UTERINE INVERSION

27. Uterine Atony: Uterine atony is the most common cause of severe postpartum hemorrhage, accounting for approximately 80% of cases Po stpartum hemostasis i nvolves the release of endogenous uterotonic agents—primarily oxytocin and prostaglandins—that contract the u terus and constrict uterine vessels. Uterine atony represents a failure of this process. Partur ients with obstetric hemorrhage may have uterine arteries that are relatively responsive to vasoconstrictor substances.

28. Diagnosis An atonic, poorly contractile uterus and vaginal bleeding are
the most common findings in patients with uterine atony . A bsence of vaginal bleeding - does not exclude this disorder. Unrecognized bleeding may manifest in itially as tachycardia; worsening hypovolemia eventually le ads to hypotension

29. Obstetric and Anesthetic Management Prophylaxis -The ACOG recommends active management of the third stage of labor - uterine massage -prophylactic oxytocin administration to decrease blood loss and transfusion requirements compared with expectant management

30. Endogenous oxytocin is a nine–amino acid polypeptide produced in the posterior pituitary gland . The exogenous form - of the drug (Pitocin, Syntocinon ) is a synthetic preparation with a rapid onset and short half-life. Side effects: vasodilation , tachycardia, hypotension, coronary vasoconstriction, myocardial ischemia Three classes of drugs are currently available for the treatment of uterine atony: oxytocin,
ergot alkaloids, and prostaglandins OXYTOCIN : Oxytocin is the first-line drug for prophylaxis of uterine atony after delivery of a third-trimester pregnancy.

31. High doses of oxytocin administered - large volumes of intravenous fluids, es pecially those containing free water, can lead to hyponatremia, seizures, and coma because of oxytocin’s structural similarity to vasopressin . Metabolism: rapidly metabolized by hepatic oxytocinases cleared in the urine and bile half-life of le ss than 6 minutes.

32. Er got alkaloids : natural ergot alkaloids are produced by a fungus that
commonly infests rye and other grains semisynthetic preparation : Ergonovine and
methylergonovine Availability:ampules containing 0.2 mg more effective second-line agent than carboprost .

33. stable a t room temperature for prolonged periods Route :IM route- rapid onset, and the uterotonic effect usually lasts for 2 to 4 hours Moa : Mediated by serotonergic agonism weak dopamine and alp ha-adrenergic receptor agonists. Parenteral administration of an ergot alkaloid is associated with a high incidence of nau sea and vomiting Adver se effects : vasoconstriction, hypertension, MI a nd infarction caused by coronary
vasospasm, cerebrovascular accident, seizures .

34. Relative contraindications : hypertension preeclampsia peripheral vascular disease ischemic hea rt disease. Treatment of ergot-induced vasoconstriction
and hypertension may require administration of a potent
vasodilator such as nitroglycerin or sodium nitroprusside

35. Prostaglandins Concentrations of endogenous prostaglandins
increase during labor, and levels peak at the time of placental
separation. Prostaglandins increase myometrial intracellular free calcium
concentration, ultimately leading to an increase in myosin
light-chain kinase activity. Common side effects : Fev er, chills, diarrhea,
nausea, and vomiting.

36. 15-methyl prostaglandin F2α, or carboprost recommended dose :0.25 mg (250 µg) administered intramuscularly, which may be repeated every 15 to 30 min. total dose should not exceed 2 mg S ide effects : may rarely cause bronchospasm, abnormal ventilationperfusion ratio, increased intrapulmonary shunt fraction, and
hypoxemia in susceptible patients.

37. Misoprostol prostaglandin E1 analogue Uses: cervical ripening and induction of labor. prophylactic misoprostol -reduces the incidence of postpartum hemorrhage thermostable -does not re quire intravenous access for administration. Route: 600 to 1000 µg per rectum is commonly administered oral, buccal, and sublingual routes

38. S/E: fever, chills, nausea, vomiting, and diarrhea. If hemorrhage and atony persist despite aggressive administration of multiple classes of uterotonic drugs, invasive tec hniques must be considered

39. Genital Trauma Pelvic hematomas may be divided into four types: vaginal,
vulvar, vulvovaginal, and retroperitoneal. Vaginal hematomas result from soft tissue injury during delivery, and they ma y involve bleeding from the descending branch of the
uterine artery. Vulvar hematomas involve branches of the pu dendal artery. Small vaginal or vulvar hematomas that are not
enlarging may be observed and treated conservatively with ice
packs and oral analgesics.

40. Large hematomas -incised and evacuated. Retroperitoneal hematomas A retr operitoneal hemorrhage occurs after laceration of one of
the branches of the hypogastric artery. A hematoma that originates
in the broad ligament may dissect into the retroperitoneal
space along the lateral pelvic sidewalls and may extend as far
as the kidneys.

41. Diag nosis unexpected decrease in hematocrit unexplained tachycardia and hypotension. restlessness, lower abdominal pain, a tender mass abo ve the inguinal ligament that displaces a firm uterus to the con tralateral side vaginal bleeding with hypotension out
of proportion to the external blood loss. urinary retention

42. Management: Occasionally, a retroperitoneal hematoma may be selflimiting and need no surgical intervention. Life-threatening hematomas require exploratory laparotomy and ligation of the hypogastric vessels. Anesthetic Management Choice of anesthe sia- depends on the affected area, surgical requirements, volume/hemodynamic status of the patient, and urgency of the procedure.

43. Local infi ltration and a small dose of intravenous opioid suffice
for drainage of some vulvar hematomas Rep air of e xtensive lacerations and drainage of vaginal hematomas require significant levels of analgesia or anesthesia. Exploratory laparotomy for a retroperitoneal he matoma typically requires the administration of general ane sthesia.

44. Retained Placenta Retained placenta is defined as failure to deliver the placenta
completely within 30 minutes of delivery of the infant
and occurs in approximately 3% of vaginal deliveries. Retained placenta typically results from one of three causes: (1) the placenta may be blocked behind a contracted lower
uterus/cervix (incarcerated placenta) (2) the placenta may be adh ered to the uterine wall (placenta adherens) (3) it may be i nvading the myometrium (placenta accreta)

45. Risk factors -History o f retained placenta . -Preter m delivery -Oxy tocin use during labor -Pr eclampsia -Null iparity

46. Obstetric Management Treatment of retained placenta during the early postpartum
period often involves gentle cord traction, uterine massage manual removal inspection of the placenta. If manual extr action is not successful, curettage may be required

47. Anesthetic Management Manual extraction of the placenta can be painful, requiring
analgesia Admin istration of local anesthetic through an indwelling
epidural catheter may prove helpful. In the absence of an indw elling catheter -neuraxial anesthesia may be considered in patients who are not bleeding severely and are hemodynamically stable. General anesthesia sometimes beco mes necessary, particularly in patients who are hemodynamically unstable.

48. In cases in which lower uterine or cervical contraction prevents placental passage, manual removal requires
uterine relaxation. rapid-sequence induction of general anesthesia is performed. high dose of a volatile halo genated agent to relax the uterus. Alternatively, nitroglycerin may be administered for
uterine relaxation. Nitroglycerin provides a rapid onset of reli able smooth muscle relaxation and a short plasma half-life (2 t o 3 minutes).

49. Nitroglycerin most likely prod uces uterine smooth muscle relaxation by releasing nitric oxi de, which temporarily decreases the patient’s systemic bloo d pressure. Because of nitroglycerin’s short plasma halflife, boluses rarely lead to sustained hypotension.

50. Uterine Inversion Uterine inversion is turning inside-out of all or part of the uterus It is ass ociated with severe postpartum hemorrhage, and hemodynamic instability may be worsened by concurrent vagal
reflex–mediated bradycardia. Risk factors uterine atony short umbilical cord uterine anomalies overly aggressive management of the third stage of labor

51. Diagnosis Many cases of uterine inversion are obvious because of
hemorrhage and a mass in the vagina . Inversion should be suspected in all cases
of postpartum hemorrhage. Ultrasonographic examination : characteristic findings, such as an echolucent
zone within an echogenic mass filling the uterine cavity on
transverse view.

52. Obstetric Management Immediate replacement of the uterus, even before removal
of the placenta, is the treatment goal All uterotonic drugs should be discontinued im mediately. The obstetrician should attempt to right the
inversion by applying pressure through the vagina to the
uterine fundus

53. Anesthetic Management uterine tone precludes replacement of the uterus, and
uterine relaxation is necessary for successful uterine reduction. large Iv doses (200 to 250 µg) may be required, and the
anesthesia provider typically will need to support the circulation with intravenous fluids and vasopressors. Nitr oglycerin Admin istration of general anesthesia with a volatile halogenated agent may become necessary . Once the uterus has been replaced ,Oxytocin should be infused, and additional uterotonic drugs may be needed.

54. Placenta Accreta Spectrum Placenta accreta is defined as a placenta that in whole or in
part invades the uterine wall and is inseparable from it. Placenta accreta adherence of the basal plate of the placenta
directly to uterine myometrium without an intervening
decidual layer Placenta increta Placenta percreta

55. Previous cesarean delivery or other uterine surgery
increases the risk for both placenta previa and placenta
accreta. Diagnosis In some cases of placenta accreta the condition is first suspected at vaginal delivery, when the obstetrician notes difficulty in separating the placenta from the uterine wall. Defi nitive diagnosis is then made at laparotomy.

56. Obstetric Management : Decision analysis ind icates that 34 weeks’ gestational age is the preferred time for p lanned delivery in most clinical circumstances involving pla centa previa and evidence of placenta accreta Most patients with known placenta accreta should undergo
planned preterm cesarean delivery and hysterectomy with the pl acenta left in situ because attempts to remove the placenta are likely to initiate hemorrhage.

57. Anesthetic Management Anesthetic management is similar to other cases of severe
postpartum hemorrhage and peripartum hysterectomy Preoperative suspicion for placental implantation abnormalities should alert the anesthesia provider to the potential for massive blood loss and transfusion. Invasive Treatment Options -Firs t line con servative measures may fail to control bleeding . In these case s, invasive procedures must be performed promptly once de livery has occurred to avoid severe morbidity and mortality.

58. Second-line options - Intrauterine balloon tamponade conservative method for c ontrolling postpartum hemorrhage, especially when uterin e atony or lower uterine segment bleeding is suspected Failure may also be attributed to prolapse through a partially
open cervix.

59. Uterine compression sutures (e.g., B-Lynch suture ) M ost useful in cases of refractory uterine atony but have also be en used in cases of retained placenta and accreta. The suture may slip off of the
uterine fundus and fail to provide compression. Complications include infection, uterine necrosis, and suture erosion.

60. Angiographic arterial embolization may be appropriate
if moderate blood loss continues and if the patient is stable
for transport to the interventional radiology suite. During angiography, the radiologist can identify the vessels
responsible for bleeding and embolize these vessels with
gelatin sponge pledgets

61. The patient must be observed and mo nitored carefully while undergoing the procedure. Ischemic complications of embolization therapy have been
reported,

62. Bilateral surgical ligation of the uterine arteries (O’Leary
sutures) may be used to control bleeding at laparotomy In t he case of failure to control bleeding, the surgeon may
proceed with a more complex procedure that involves ligation of the tubo-ovarian and ascending and descending
uterine arteries.

63. Internal iliac artery ligation may also be con sidered, although it is more difficult to perform Engorgement of pelvic viscera, vari ability in vascular anatomy, and the increased blood flow duri ng pregnancy contribute to the risk for complications wh en this approach is used. Ischemic complications and neu ropathy have been reported.

64. Peripartum hysterectomy D efinitive treatment for p ostpartum hemorrhage unresponsive to medical and other i nvasive therapies. The two most common indications for this pr ocedure are uterine atony and placenta accreta. Parturients with a history of previous cesarean delivery
are more than five times as likely to require a peripartum
hysterectomy as those without this history .

65. Complications: Th e uterus is enlarged, exposure may be difficult . Th e vessels are engorged, and the pregnant uterus receives a
rich collateral blood supply. patients un dergoing obstetric hysterectomy are more likely to suffer po stoperative hemorrhage & require blood transfusion. intraoperative urinary tract injury perioperative complications such as wound infection venous thr omboembolism cardiovascular and other medical
complications.

66. Anesthesia for peripartum hysterectomy Anesthesia pr oviders may elect neuraxial anesthesia in a properly prepared patient Maintenance of a T4 sensory level of anesthesia and judicious sedation may reduce the need for intraoperative conversion to general anesthesia Single-shot spinal anesthesia is unlikely to provide anesthesia of sufficient duration for an unanticipated hysterectomy. Patients who have delivered vaginally with preexisting
epidural labor analgesia may be managed successfully with
extension of epidural blockade

67. As the magnitude of blood loss increases, general anesthesia becomes the anesthetic technique of choice. However, the induction of sympatholysis during hemorrhage may compromise e nd-organ perfusion and even precipitate cardiopulmonary
arrest First, severely hy potensive patients may require tracheal intubation for ai rway protection. Second, large fluid shifts and massive tra nsfusion may adversely affect oxygenation so that contr confidence v entilation via an endotracheal tube becomes necessary two or more l arge-bore intravenous catheters should be inserted.

68. Third, these same fluid shifts increase airway edema, potentially making failed ventilation/failed tracheal intubation
more likely as the surgery proceeds Fourth, the massive tr ansfusion of blood products often results in the need for c o-administration of potent vasopressors and calcium chloride and, thus, central venous access induction in the setting of severe he morrhage may require careful use of small doses of noncardiodepressant induction agents such as ketamine or etomidate.

69. The circulation should be supported with replacement
of intravascular volume and vasopressors as needed Invasive bl ood pressure monitoring may aid in the prompt recognition of hypotension and provide access for frequent blood
draws. At least 4 units of PRBCs should be immediately available, with additional blood products, i ncluding plasma and cryoprecipitate, readily available without delay.

70. The ACOG recommends consideration of int raoperative blood salvage in cases with massive transfusion Vasoactive drugs (e.g.,
phenylephrine, epinephrine), fluid warmers, a forced-air
body warmer, and equipment for rapid infusion of fluids
and blood products should be accessible if the care team is
anticipating and managing significant blood loss.

71. General resuscitative measures include (1) additional large-bore intravenous access (2) intravenous admin istration of crystalloid and colloid solutions and vasopressors Treatment. (3) laboratory determination of hemoglobin concentration or hematocrit and assessment of coagulation status (4) blood bank preparation of blood products for trans fusion. (5) Bi manual compression and massage of the uter us and continued infusion of oxytocin may help restore uteri ne tone.

72. TEAM RESPONSE TO HEMORRHAGE

73. TEAM RESPONSE TO HEMORRHAGE Prevention of Mortality In one state-level study, 93% of hemorrhage-related deaths were found to be preventable, compared with 40% of all-cause pregnancy-related deaths Delaying in diagnosis and treatment of postpartum hemorrhage increase the severity of hemorrhage. Women who develop postpartum hemorrhage from uterine atony after vaginal birth, risk factors for progressing to severe hemorrhage (defined as a decrease in hemoglobin concentration greater than 4 g/dL) include delaying the administration of oxytocin and delaying manual exploration of the uterus.

74. Delays in care most likely result from several factors, including difficulties in accurately estimating blood loss and in diagnosing maternal hypovolemia and shock, lack of aggressive monitoring and treatment of coagulopathy, and poor coordination of team responses. Accuracy of blood loss estimation can be improved with the use of calibrated collection drapes. Separation of nonblood fluids (i.e., switching the suction canister after evacuation of amniotic fluid) and weighing pads and bedding improves assessment.

75. Obstetric patients are often mildly tachycardic, and worrisome rates of tachycardia (greater than 120 bpm) may not develop until the patient has lost 30% to 40% of her total blood volume. Similarly, hypotension and mental status changes are late signs

76. Protocols and Team Approach Because delays in care during postpartum hemorrhage result in unfavorable outcomes, efforts focus on early recognition and rapid treatment of hemorrhage. The National Partnership for Maternal Safety, sponsored by the ACOG Council on Patient Safety in Women’s Healthcare, has published a patient safety bundle a collection of evidence-based practices designed to enhance early detection of, and response to, hemorrhage and decrease hemorrhage-related morbidity and mortality It emphasizes team approaches; employment of multidisciplinary protocols, education, and drills; and review of cases of severe hemorrhage.

77. TRANSFUSION THERAPY Despite advances in the prevention, diagnosis, and treatment of the hemorrhagic complications of pregnancy, the potential for significant blood loss remains Transfusion may be indicated for treatment of severe anemia after moderate obstetric hemorrhage or to preserve life during massive hemorrhage

78. TRANSFUSION THERAPY AND STRATEGIES

79. Transfusion practices vary widely and often deviate from both national and institutional guidelines. Given current evidence, it seems reasonable that transfusion should be considered in obstetric patients with a hemoglobin concentration less than 7 g/dL and those with clinical evidence of inadequate oxygen-carrying capacity. Active hemorrhage may prompt transfusion in some patients with a hemoglobin concentration greater than 7 g/dL.

80. Treatment of Massive Blood Loss During initial resuscitation of the hemorrhaging patient, warmed non–dextrose-containing crystalloid (e.g., lactated Ringer’s, normal saline) and/or colloid (e.g., 5% albumin) solutions are acceptable choices for volume replacement. During massive hemorrhage, blood replacement therapy becomes necessary. Coagulopathy can develop rapidly in the bleeding patient because of dilution from replacement of blood with crystalloid and PRBCs, and hemostatic factor consumption. Furthermore, obstetric hemorrhage may be associated with accelerated factor consumption, especially during bleeding from the placental bed Fibrinolysis may also play a role during uterine bleeding. DIC further worsens hemorrhage

81. BLOOD PRODUCTS :Either whole blood or component products are transfused. Whole blood is an ideal choice for maintaining intravascular volume in the setting of massive hemorrhage. Whole blood is associated with lower rates of acute tubular necrosis than the two other transfusion practices PRBC : Transfusion of 1 unit of PRBCs increases the hemoglobin concentration by approximately 1 mg/dL in the absence of ongoing bleeding. PLASMA : Administration of plasma may be considered for correction of microvascular bleeding if the PT is more than 1.5 times normal, the INR is greater than 2.0, or the aPTT is more than two times normal. One unit of plasma per 20 kg of body weight is an appropriate initial dose. The prophylactic use of plasma is not effective for decreasing blood loss in patients at risk for massive blood loss. Each unit of fresh frozen plasma (FFP)/plasma contains 0.5 g of fibrinogen as well as all other coagulation proteins.

82. Cryoprecipitate (enriched in von Willebrand factor/VIII complex, factor XIII, fibronectin and most importantly, fibrinogen) administered as a supplement to plasma to increase plasma fibrinogen. Hypofibrinogenemia is not likely to contribute to bleeding until the level falls below 100 mg/dL; hence, cryoprecipitate is recommended for patients with documented decrease in fibrinogen below 100 mg/dL. It is estimated that a dose of 8–10 U of cryoprecipitate will increase the fibrinogen in a 70 kg adult by 50–70 mg/dL.

83. The rapid consumption of fibrinogen during obstetric hemorrhage calls for early monitoring and aggressive treatment of, hypofibrinogenemia. During active hemorrhage, clinicians should attempt to maintain the fibrinogen

84. Recombinant activated factor VII Factor VIIa binds not only to tissue factor, but also with low affinity to the thrombin activated platelet. This low-affinity binding to the activated platelet allows direct activation of factor X to Xa on the surface of the activated platelet, bypassing the normal need for factors VIIIa and IXa . Activation of factor X leads to a small thrombin burst. This thrombin, in turn, activates more platelets.

85. Recombinant activated factor VII ( rFVIIa ) is currently approved in the United States for the treatment and prophylaxis of bleeding in patients with hemophilia A and B with inhibitors to factors VIII and IX, acquired hemophilia, and congenital factor VII deficiency. The ASA guidelines recommend consideration of rFVIIa therapy “when tradi tional options for treating excessive bleeding due to coagulopathy have been exhausted.Importantly , maintenance of normothermia and correction of acidosis are necessary for optimal rFVIIa activity

86. Antifibrinolytic therapy. Tranexamic acid binds to plasminogen, blocking its activation, thus inhibiting fibrinolysis. Administration of tranexamic acid decreases blood loss and transfusion risk and does not increase rates of thromboembolic Practitioners are cautioned not to exceed doses of 1 g administered slowly over 10 minutes; this dose may be repeated once if bleeding continues after 30 minutes.Continuous infusion is not recommended. Aortoiliac thrombosis was reported after the concomitant use of tranexamic acid and an intra-arterial balloon catheter during urgent cesarean hysterectomy It seems plausible that tranexamic acid may benefit women who demonstrate hyperfibrinolysis on viscoelastic monitoring. The ACOG states that “tranexamic acid should be considered in the setting of obstetric hemorrhage when initial medical therapy fails.

87. MASSIVE BLOOD TRANSFUSION Definition of Massive Transfusion Replacement of a blood volume equivalent within 24hr >10 unit within 24 hr Transfusion > 4 units in 1 hr Replacement of 50% of blood volume in 3hrs A rate of loss >150ml/hr

88. Routine blood loss quantification, early uterotonic therapy, timely physician evaluation, and early fixed-ratio transfusion may reduce the transfusion requirement by ensuring treatment at an earlier stage of bleeding. Viscoelastic monitoring may accelerate the transition from fixed-ratio to goal-directed transfusion, and thereby avoid unnecessary transfusion of plasma and platelets

89. Risks Associated with Transfusion Transfusion-related acute lung injury (TRALI) is defined as a new acute lung injury (ALI) that occurs within 6 hours of transfusion in a patient without an alternative risk factor for ALI. It is usually accompanied by hypoxemia, transient leukopenia, and radiographic evidence of pulmonary edema in the absence of circulatory overload

90. Transfusion-associated circulatory overload (TACO) occurs in approximately 1% of transfused patients. It may follow the transfusion of as little as 1 unit of PRBCs, but the likelihood of TACO increases as the volume of transfused plasma increases. TACO refers to respiratory distress and pulmonary edema resulting from excess volume or circulatory overload. Unlike TRALI, TACO presents with visible neck vein distention, an S3 heart sound, and hypertension .

91. This condition also responds well to diuresis and exhibits a pulmonary artery occlusion pressure exceeding 18 mm Hg. TACO develops when there is an overly aggressive transfusion or the administration of an excessive volume within a short time frame.  Both TRALI and TACO typically occur within 6 hours of a transfusion. Patients with TRALI clinically resemble those with ARDS, presenting with a PaO 2 /FiO 2  ratio of less than 300 mm Hg but greater than 200 mm Hg, bilateral infiltrates on chest x-ray, and no signs of systolic heart failure. If symptoms occur in the 12 hours before the transfusion or more than 6 hours after a transfusion, then ARDS is the appropriate diagnosis.

92. TRANSFUSION RELATED IMMUNOMODULATION Allogeneic RBC administration also increases the risk for transfusion-related immunomodulation (TRIM). The mechanisms for development of TRIM are incompletely understood, but subsequent to RBC transfusion the host develops immune tolerance and a period of generalized immune suppression. Consequences of immune tolerance and suppression include an increased incidence of nosocomial infection, postoperative infection, and cancer recurrence.

93. JEHOVAHS WITNESS Jehovah's Witnesses believe that the Bible prohibits Christians from accepting blood transfusions. Their literature states that, "'abstaining from ... blood' means not accepting blood transfusions and not donating or storing their own blood for transfusion.“ BLOODLESS MEDICINE:Team which reduces blood loss and uses best available alternatives to allogenic transfusion therapy

94. BLOOD CONSERVATION STRATEGIES AUTOLOGOUS BLOOD TRANSFUSION: Refers to the transfusions in which the donor and recipient are the same Aims to decrease the incidence of complications associated with allogenic transfusion Intraoperative blood salvage , is a technique whereby blood shed during surgery is scavenged, processed by centrifugation, washed, and filtered before transfusion to the patient. RBCs processed in this way have an excellent survival rate. Reports of clinical experience with cell salvage in obstetric patients have accumulated over recent years; no reports of acute respiratory distress syndrome, DIC, or other complications have been described.

95. REFERENCES: CHESTNUT’S OBSTETRICS ANESTHESIA , ED 6 MILLER ‘S ANESTHESIA , ED 9

96. THANK YOU