Anesthesia Update 2017 Bibhukalyani Das
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Bleeding Obstetric Patient— How to Address the Problem?CHAPTER 1

Nibedita Pani,
Devishree Das
 
INTRODUCTION
Bleeding has always been a dreaded complication in the field of obstetrics. It is the most common cause of maternal morbidity worldwide, accounting for 25–30% of maternal death.1 World Health Organization (WHO) estimates that severe hemorrhages complicate 10.5% of live birth.2 In developing country like India, it is responsible for >60% of maternal morbidity.3
The identification of major obstetric hemo-rrhage can be challenging. Blood loss may be concealed and difficult to quantify due to dilution with amniotic fluid. In addition the physiological changes of pregnancy may mask the normal clinical signs of hypovolemia. The blood flow of placenta is approximately 700 mL/minutes at term hence bleeding can be rapid and may quickly become life-threatening.
Obstetric hemorrhage is challenging to anesthesia providers as it is usually sudden in onset, rapid and may be life-threatening.4 A multidisciplinary approach with a team consisting of obstetrician, anesthesiologist, neonatologist, and hematologist is essential for management of peripartum bleeding.
 
DEFINITION
Applying classical definition of hemorrhage to peripartum hemorrhage may be misleading as blood loss up to 1,000 mL is not uncommon during deliveries. Although no harmony exists on the definition of massive obstetric hemorrhage, presence of either of the following has been described.5
  • Sudden blood loss >1,500 mL (25% of blood volume)
  • Blood loss >3,000 mL in less than 3 hours (50% of blood volume)
  • Blood loss of 150 mL/minute in 20 minutes (>50% of blood volume)
  • Requirement of acute transfusion of >4 units of packed red blood cells.
 
ANTEPARTUM HEMORRHAGE
Antepartum hemorrhage (APH) is defined as bleeding from the vagina after 28 weeks gestation and has an estimated incidence of between 20% of all pregnancies. Causes include:
 
Placenta Previa
Placenta is implanted partially or completely over the lower uterine segment (LUS) (near internal OS) and classified according to the extent of encroachment of placenta.
 
Classification (Table 1)
  • Type I or low lying placenta
  • Type II or marginal placenta
  • Type III or partial placenta previa
  • Type IV or complete placental previa.
Placenta previa (PP) remain at risk for increased intraoperative blood loss for at least three reasons:
  1. Obstetrician may cut into the placenta during uterine incision2
  2. After delivery, the LUS implantation site does not contract as well as the normal fundus
  3. A patient with PP is at increased risk of placenta accreta, especially if there is a past history of cesarean section (CS).
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FIG. 1: Types of low lying placenta
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FLOWCHART. 1: Management of obstetric bleeding
Parturient presents with sudden onset, painless, recurrent vaginal bleeding while safest method of diagnosis is transabdominal sonography. Vaginal examination is contrain-dicated and If needed done under double set-up.
 
Double Set-Up Examination
The examination is performed in the operating room. All members of the obstetric care team, including the anesthesia provider, obstetrician, and pediatrician, make full preparation for cesarean delivery. Full preparation consists of application of maternal monitors, insertion of two large-gauge intravenous cannula, administration of a nonparticulate antacid and sterile preparation and draping of the abdomen. Two units of packed red blood cells (PRBCs) should be available in the operating room.
 
Management (Flowchart 1)
For cesarean delivery, general anesthesia (GA) is often used but consider regional anesthesia (RA) if parturient is:
  • Hemodynamically stable
  • Patient having epidural catheter
  • Absence of fetal distress
Consider aggressive volume replacement to maintain urine output and invasive hemodynamic monitoring if required.3
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FIG. 2: Varieties of placental abruption6
 
Placental Abruption
Bleeding due to premature separation of normally implanted placenta from decidua basalis that complicates 1% of pregnancies.
 
Varieties Fig 2 (A to D)
The classical presentation includes vaginal bleeding with intermittent or constant abdominal pain and fetal distress/absent fetal heart sound.
 
Management
  • Mild abruption with maternal and fetal stability vaginal delivery to be allowed after artificial rupture of membranes (ARM) with judicious use of oxytocin. Epidural analgesia can be given provided coagulation studies are normal.
  • In severe placental abruption, maternal hemorrhage or deteriorating fetal status emergent CS required and GA is technique of choice.
 
Uterine Rupture
Rupture of the gravid uterus can be disastrous to both the mother and the fetus. This refers to separation of a uterine scar that is clinically apparent and results in nonreassuring status, maternal hemorrhage requiring emergent CS or postpartum laparotomy.
Uterine scar dehiscence is a uterine wall defect that does not result in fetal heart rate (FHR) abnormalities or excessive hemorrhage and does not require emergency cesarean delivery or postpartum laparotomy whereas uterine rupture is a uterine wall defect that results in fetal compromise or maternal hemorrhage sufficient to require cesarean delivery or postpartum laparotomy.
Uterine rupture is suspected when vaginal bleeding, hypotension, cessation of labor and fetal bradycardia are present.
 
Management
  • Uterine repair and uterine artery ligation usually done but hysterectomy is the definitive treatment
  • GA often used but RA if:
    • Hemodynamically stable
    • Patient having epidural catheter
    • Absence of fetal distress
  • Aggressive volume replacement to maintain urine output and consider invasive hemody-namic monitoring if required.
 
Vasa Previa
Vasa previa is defined as the velamentous insertion of the fetal vessels over the cervical os therefore the fetal vessels are not protected by the placenta or the umbilical cord. Rupture of the membrane is accompanied by tearing of fetal vessel, which leads to exsanguination of the fetus (Fig. 3).
 
Diagnosis
Diagnosis is made when vaginal bleeding and fetal bradycardia or fetal death accompany 4rupture of membranes. Prenatal diagnosis is possible with reasonable accuracy by USG with color Doppler.
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FIG. 3: Vasa previa6
 
Management
  • Preoperative diagnosis of vasa previa → Elective LSCS under regional technique
  • Bleeding vasa previa + Alive fetus → emergency LSCS under GA
  • Bleeding previa + IUD (Conclusive) → Vaginal delivery ± epidural analgesia
Neonatal resuscitation is necessary as neonatal volume replacement with balanced salt solution and colloid.
 
Complications of Antepartum Hemorrhage
Maternal complications include APH with shock, cord prolapse, PPH, retained placenta and puerperal sepsis whereas fetal complications includes LBW, asphyxia, IUD, and congenital malformation.
 
POSTPARTUM HEMORRHAGE
Any amount of bleeding from or into genital tract following birth of baby up to the end of the puerperium which adversely affects the general health of the patient evidenced by rise in pulse rate and falling blood pressure is called Postpartum hemorrhage (PPH). PPH can be classified as primary or secondary. Primary PPH occurs during the first 24 hours while secondary PPH refers to hemorrhage occurring between 24 hours to 6 weeks after delivery. The 4 ‘T's7 pneumonic is useful to aid recall the major causes of primary PPH:
  • Tone: uterine atony
  • Tissue: retained products of conception
  • Trauma: genital tract injury
  • Thrombin: inherited or acquired coagulopathy
 
Uterine Atony
It accounts for the majority of primary PPH (80%) and complicates 5% of all deliveries.
TABLE 1   Medical management8
Agent
Dose and route
Contraindications
Side effects
Oxytocin
20–60 U/L intravenous
Infusion
None
  • Decreased systemic vascular resistance and hypotension with bolus intravenous doses
  • Free water retention
Methylergonovine
0.2 mg IM
  • Hypertension
  • Preeclampsia
  • Coronary artery disease
  • Severe nausea and vomiting
  • Arteriolar constriction
15-methyl prostaglandin
250 mg IM or IU
  • Reactive airway disease
  • Pulmonary hypertension
  • Hypoxemic patients
  • Bronchoconstriction
  • Shivering
  • Temperature elevation
  • Diarrhea
Misoprostol
800–1000 mg per
Rectum
  • None
  • Shivering
  • Temperature elevation
  • Diarrhea
  • Nausea/vomiting
5
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FLOWCHART. 2: Algorithm for management8
Medical management of uterine atony is given in table 1 and flowchart 2.
 
Retained Placenta
Secondary PPH is associated with retained products of conception. Placenta is said to be retained when it is not expelled out even 30 minutes after birth of baby.
 
Anesthetic management
Depends on:
  • Amount of placenta retained
  • Associated shock/hemorrhage
  • Previous regional block given or not.
 
Types of anesthesia
  • Intravenous (IV) analgesia with ketamine 0.5 mg/kg, benzodiazapine (BZD) and judicious use of opioids care must be taken to prevent loss of maternal reflexes
  • General anesthesia (GA) is anesthesia of choice when retained placenta presents with hemorrhage.
  • Uterine relaxation may be provided either with volatile anesthetic (1.5 MAC isoflurane) incremental doses of IV nitroglycerine 50-100 µg IV.
 
Uterine Inversion
Uterine inversion, or the turning inside-out of all or part of the uterus, is a rare but potentially disastrous event during the peripartum period. Acute peripartum inversions most likely occur in 1 in 5,000 to 1 in 10,000 pregnancies. Many cases of uterine inversion are obvious because of hemorrhage and a mass in the vagina.
 
Varieties
Varieties of uterin invessions are given in figure 4.
 
Management
Aims at quick replacement of the uterus. Atony usually resolves after placement of uterus; followed by medical treatment. It has two important components
  • Management of shock.
  • Replacement of uterus.
General anesthesia is anesthetic of choice. Uterine relaxation being produced by volatile anesthetics, nitroglycerine 50–100 µg. Recent 6reports have suggested the use of terbutaline and MgSO4 as tocolytic.
zoom view
FIG. 4: Degree of uterine prolapse. A, 1st degree; B, 2nd degree; C, 3rd degree or complete.6
 
Genital Trauma
Laceration and hematoma of perineum, vagina, cervix. Vaginal hematoma which is due to injury to descending branch of uterine artery and needs prompt evacuation. Vulval hematoma is due to injury to pudendal artery that leads to extreme pain with hypovolemia. Small hematoma can be managed with ice packs and analgesics while large hematoma requires evacuation. Retroperitoneal hematoma responsible for concealed bleeding, abrupt hypotension, unexpected decrease hematocrit, restless, lower abdominal pain due to injury to hypogastric artery. It requires exploratory laparotomy with ligation of hypogastric artery.
 
Management
  • Local infiltration and small dose opioid for drainage of small vulval hematoma
  • Pudendal nerve block not possible due to distorted anatomy
  • Low dose ketamine (10 mg) not >0.5 mg/kg used for sedation and analgesia
  • If patient hemodynamically stable then regional technique and if hemodynamically unstable general anesthesia is technique of choice.
    • Retroperitoneal bleeding: GA is the technique for exploratory laparotomy.
 
Coagulopathy
Coagulopathy can develop rapidly in the obstetric patient which may be either a dilutional coagulopathy or true Disseminated intravascular coagulatio (DIC). Dilutional coagulopathy results from replacement of blood loss with crystalloid and PRBCs, which dilutes concentrations of coagulation factors and platelets. Treatment consists of fresh frozen plasma (FFP) and platelet replacement. Sustained hemorrhagic shock may also cause DIC, resulting in worsening hemorrhage. Additional pregnancy-related causes of DIC include amniotic fluid embolism, placental abruption, uterine infection, and intrauterine fetal demise.
Platelet count, PT, aPTT, measurement of fibrinogen concentration and fibrin split products are required to diagnose coagulopathy. With coagulation factor replacement, the coagulation factor activity need only 25% of normal to achieve hemostasis. One unit of FFP increases coagulation factor levels by 8%. Cryoprecipitate is indicated in bleeding patients with fibrinogen level less than 80 to 100 mg/dL, and platelets are indicated when the platelet count is less than 50,000/mm3. Hypothermia worsens coagulopathy and increases the risk for cardiac dysrhythmias so better avoided.
 
Complication of Postpartum Hemorrhage
Includes Sheehan's syndrome, myocardial ischemia, acute respiratory failure (ARF), acute lung injury/transfusion-related acute lung injury (TRALI) and consumptive coagulopathy.
 
Assessment of Hemorrhage
 
Clinical evaluation
  • Brief history to elicit cause of hemorrhage.
  • Vital signs: Resting tachycardia and hypotension7
    • Orthostatic vital sign: Significant postural change defined as increase in pulse rate by 30 beats/min or decrease in SBP >20 mmHg or dizziness on standing.
TABLE 2   Classification8
Class I
Class II
Class III
Class IV
Blood loss (mL)
≤750
750–1500
1500–2000
>2000
% blood loss
≤15
15–30
30–40
>40
Heart rate (bpm)
<100
>100
>120
>140
SBP
N
N
Pulse pressure
N or ↑
Cap Refill
<3 sec
> 3 sec
>3 sec or absent
Absent
Respiratory rate/min
14–20
20–30
30–40
<35
Urine output (mL/h)
>30
20–30
5–15
Negligible
Mental status
Slightly anxious
Mildly anxious
Anxious and confused
Confused and lethargic
 
Investigation
Mainly by estimating hemoglobin and hematocrit but in early hours of acute hemorrhage, Hct reflects resuscitation effort and not the severity of blood loss. so use of Hct to estimate acute blood loss is unreliable and inappropriate.
 
Classification
Classification is listed in table 2.
 
Massive Obstetric Hemorrhage
Defined as blood loss >1,500 mL, Decrease in Hb >4 g/dL or acute transfusion requirements >4 units.
Transfusion in obstetric hemorrhage based on ASA guidelines and ACOG recomm-endations:9,10
  • A routine blood cross match is not necessary for normal vaginal or operative delivery.
  • Although, the physiological changes of pregnancy help to mitigate the parturient in response to hemorrhage and vital signs may not change until >1,500 mL of blood loss has occurred, patients should be transfused when there are signs of significant hypo-perfusion.
  • PRBC administration is rarely indicated when hemoglobin concentration is >10 g/dL but is almost always indicated when the hemoglobin level is ≤6 g/dL.
  • If base deficit is >15, in presence of significant and ongoing blood loss, then blood is administered.
  • O2 extraction of 50% can be used as an indication of transfusion of erythrocytes.
  • Hemoglobin should be maintained between 6–10 g/dL.
  • Platelet count maintained over 50,000/dL.
  • INR to be maintained <1.5 by using FFP @ 10–15 mL/kg body weight.
  • Cryoprecipitate should be used when fibrinogen levels fall below 100 mg/dL @ 1 U/5–10 kg body weight.
 
Intraoperative Cell Salvage
Numerous reports shows the safe use of intraoperative cell salvage in parturient and it has been recommended in women who refuse traditional blood transfusions as well as in other major hemorrhage situations.11 Consider cell salvage in both anticipated and unanticipated massive hemorrhage as this can reduce the exposure to allogeneic blood transfusion and is cost-effective. Cell salvage is started after the majority of amniotic fluid has been suctioned to lessen the risk of amniotic fluid embolism. A leukocyte depletion filter should be used prior to re-infusion of the salvaged blood to remove additional contaminants. Remember that cell salvaged blood contains only red cells with no clotting factors or platelets.
 
Additional Drugs
Recombinant factor VIIa is a controversial therapy that may be considered in obstetric 8hemorrhage. It has been used primarily as a treatment of uncontrolled hemorrhage in the trauma setting. Recombinant factor VIIa causes a thrombin burst, promoting clotting in open vessels. Its effectiveness is markedly diminished by hypothermia and acidosis and so effective resuscitation towards normal physiology is a prerequisite. The major concern is the potential for thrombotic complications. The dose is 90 μg/kg.
Antifibrinolytics are adjunct in the pharmacological management of massive transfusion and PPH. Tranexamic acid is a potentially useful drug that can decrease bleeding and reduce the need for further transfusion without many major side effects. The initial dose is a slow IV bolus of 1 g followed by 1 g 4 hours later.
Responsibilities of the anesthesiologist on arrival of an unexpected bleeding parturient:12
  • Assess vital signs like blood pressure, oxygen saturation, heart rate, capillary refill, peripheral and core temperature, and level of consciousness
  • Obtain brief history
  • Assess airway, anticipate cannot intubate cannot ventilate condition
  • Provide 100% oxygen by face mask
  • Monitor vitals like BP, HR, SPO2 at regular interval
  • Achieve proper venous access
  • Compare vital signs with estimated blood loss and communicate discrepancies to obstetric team
  • Review ongoing fluid resuscitation, pharmacotherapy and make sure that urine output is >0.5 mL/kg/h.
  • Place arterial line early if significant hemorrhage present or anticipated
  • Send initial laboratory sample (hemoglobin, coagulation status blood grouping and cross matching) if not already sent
  • Order blood and blood products as needed.
 
Preoperative Preparation
  • Patient evaluation, resuscitation and prepa-ration done simultaneously.
  • Assess airway and intravascular volume
  • Arrange 2 large-gauge IV catheters, 4 units PRBC, BT sets, fluid warmers, invasive monitors and Foley's catheter.
 
Induction
  • general anesthesia preferred technique with rapid sequence induction (RSI)
  • Acid prophylaxis: Nonparticulate antacid, metoclopramide and H2 blocker
  • Preoxygenate/denitrogenate for >3 minutes or 4 vital capacity breath for 30 seconds with 100% oxygen
  • Tell assistant to give cricoid pressure, give induction agent and muscle relaxant in rapid sequence, after 30–60 seconds intubate by direct laryngoscopy
  • Avoid propofol in hypovolemic patients
  • In bleeding patient, Ketamine (1.0 mg/kg) or etomidate (0.3 mg/kg) is preferred whereas in severe hypovolemic shock only a muscle relaxant with BZD is advised.
 
Maintenance
  • Maintain with 50% nitrous oxide with oxygen and 0.5–0.75 minimum alveolar concentration (MAC) of volatile agents
  • Maintain EtCO2 30–32 mmhg
  • N2O is avoided in fetal distress
  • Oxytocin (20 U/L) infusion started after fetal delivery
  • if bleeding continues stop uterine relaxants and after delivery of fetus stop volatile agent.
Emergence: Reversal of muscle relaxant and extubation when the patient is awake and responds to verbal commands.
 
KEY POINTS
  • The visual estimate of vaginal bleeding does not reflect the extent of intravascular volume deficit in patients with peripartum bleeding.
  • Antepartum hemorrhage represents a gre-ater threat to the fetus than to the mother.
  • Uterine atony is the most common cause of postpartum hemorrhage.
  • Prophylactic placement of internal iliac artery balloon catheters by an interventional radiologist may decrease blood loss and morbidity when patients with known placenta accreta are to undergo cesarean delivery.
  • Assessment of urine output and laboratory studies (hemoglobin measurement, arterial 9blood gas analysis) should be used to assess intravascular volume deficits and guide fluid and blood replacement therapy.
  • Recombinant activated factor VII therapy is expensive, and its safety and efficacy have not been fully evaluated in the treatment of obstetric hemorrhage.
 
CONCLUSION
The anesthesiologist plays a key role in the management of obstetric hemorrhage. As with almost all medical and surgical crises or emergencies, the principles of preparation and planning when possible, early notification when necessary, and good communication and teamwork at all times are the keys to successful outcomes.
REFERENCES
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