3 OB 3 - Obstetrical Hemorrhage.pdf
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Dr. Junio September 11, 2014
Obstetrical Hemorrhage OUTLINE I. II.
Obstetrical Hemorrhage a. Causes of Antepartum and Postpartum Hemorrhage Placenta Previa a. Classification b. Clinical Features c. Risk Factors d. Bleeding in Placenta Previa e. Ultrasound in Placenta Previa f. Management Adherent Placenta a. Placenta Previa and Accreta b. CS & Placenta Previa/Accreta c. Diagnosis of Placenta Accreta d. Management Abruptio Placenta a. Types of Abruptio Placenta i. Concealed Hemorrhage b. Cause of Bleeding c. Diagnosis d. Management e. Route of Delivery f. Route of Amniotomy g. Previa Vs. Abruptio Vasa Previa a. Risk Factors Uterine Rupture a. Classification i. Traumatic and Spontaneous Rupture b. Risk Factors c. Clinical Findings d. Pathogenesis e. Prognosis f. Management & Outcomes Postpartum Hemorrhage a. Hemostatic Mechanisms b. Causes of Post Partum Hemorrhage: 4 T’s c. Tone: Uterine Atony i. Management of Uterine Atony ii. Surgical management 1. Bimanual Uterine Compression 2. Internal Uterine Tamponade Procedures 3. Uterine Compression Sutures (B Lynch) 4. Arterial Embolization 5. Arterial Ligation iii. Active Management of Third Stage of Labor d. Tissue: Retained Secundines i. Management e. Trauma to the genital Tract i. Uterine Inversion 1. Management ii. Lacerations 1. Diagnosis 2. Management iii. Puerperal Hematoma 1. Management f. Thrombin: DIC i. Pathogenesis ii. Diagnosis iii. Management
OBSTETRICAL HEMORRHAGE BLOOD LOSS of >500 mL for NSD and >1,000 mL for CS after completion of 3rd stage of labor o However, there is no standard way to measure the post partum or intrapartum blood loss. Most of the time we underestimate and only estimate only half the amount of the actual blood loss.1 o During pregnancy, part of the normal physiologic changes is an increase in the intravascular fluid volume (IVF) by as much as 50%60% in preparation for the blood loss that is expected to happen during labor and delivery. o However, despite the increase in IVF some patients may be sensitive to blood loss of even less than 500 cc. In pre-eclamptic patients or patients with hypertension, the IVF volume increase is not as high as what is expected so that even if the actual blood loss is less than 500 cc they may become symptomatic. In the same way, in the normal pregnant patient even if the blood loss is >500cc some of them may remain asymptomatic. 1 o This just shows that this is not a hard and fast rule, that just because blood loss is 500cc ergo you have a case of hemorrhage. You also have to take into account all clinical parameters: 1 1) Is your patient stable? 2) Is your patient hypostensive? 3) Is your patient tachycardic? 4) Is your patient pale? 5) Do you need blood transfusion? 10% DECREASE IN HEMOGLOBIN AND HEMATOCRIT o If blood loss is less than the pregnancy-added volume, the hematocrit remains the same acutely and during the first several days. It then increases as nonpregnant plasma volume normalizes during the next week or so2. o Estimated Blood loss is the sum of the calculated pregnancy-added volume plus 500 mL for each 3 volume percent decrease of the hematocrit 2 NEED FOR BLOOD TRANSFUSION o Because of prevailing conservative attitudes toward blood replacement, rates cited more recently are lower than transfusion rates described in older studies2
LEARNING OBJECTIVES What is obstetric hemorrhage? What are the causes of antepartum and postpartum hemorrhage? What are their differentiating characteristics? What are the medical/surgical options in management? Figure 1.Hemorrhage (35%) is the single most important cause of maternal mortality worldwide. It still the number 1 cause of maternal death1 and is responsible for half of all postpartum deaths worldwide2. Unfortunately, this is preventable1 Group#13 | Peralta, Perez, E. Petate, Pilapil, Pineda
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CAUSES OF OBSTETRICAL HEMORRHAGE Antepartum - any pregnancy with antepartum bleeding remains at increased risk for an adverse outcome even though bleeding has stopped and placenta previa has been excluded sonographically2 o Placenta Previa o Abruptio Placenta o Vasa Previa – velamentous insertion of the umblical cord and the involved placental vessels may overlie the cervix 2 o Uterine Rupture Postpartum o Retained placental tissures o Uterine Atony – boggy soft uterus; expression of clots and hemorrhage during uterine massage o Laceration – most likely if there is persistent bleeding with well contracted uterus o Rupture o Coagulopathy Table 1. Obstetrical Hemorrhage: Causes, Predisposing Factors, and Vulnerable Patients Abnormal Placenta previa
Placentation Placental abruption Placenta accreta/increta/percreta
Ectopic pregnancy Hydatidiform mole Injuries to Episiotomy and lacerations Forceps or vacuum delivery the Birth Cesarean delivery or Canal hysterectomy Uterine rupture (Previously scarred uterus, High parity, Hyperstimulation, Obstructed labor, Intrauterine manipulation, Midforceps rotation, Breech extraction) Obstetrical Obesity
Factors Previous postpartum hemorrhage
Early preterm pregnancy Sepsis syndrome Vulnerable Preeclampsia/eclampsia – do not have normally expanded Patients blood volume, making her vulnerable to hemorrhage 2 Chronic renal insufficiency Constitutionally small size Uterine Uterine overdistention (Large fetus, Multiple fetuses, Atony Hydramnios, Retained clots) Labor induction Anesthesia or analgesia (Halogenated agents, Conduction analgesia with hypotension) Labor abnormalities (Rapid labor, Prolonged labor, Augmented labor, Chorioamnionitis) Previous uterine atony Coagulation Massive transfusions Defects – Placental abruption Intensify Sepsis syndrome Other Severe preeclampsia syndrome
Causes Acute fatty liver Anticoagulant treatment Congenital coagulopathies Amnionic-fluid embolism Prolonged retention of dead fetus Saline-induced abortion
Group#13 | Peralta, Perez, E. Petate, Pilapil, Pineda
Figure 2. Placenta Previa. Placenta is implanted over or near the internal cervical os. Normally, the placenta is very far from the cervical os. In placenta previa, the placenta covers the internal cervical os or canal. If the placenta is ahead of the baby, expect bleeding if the uterus starts to contract PLACENTA PREVIA2 Previa means “going before” – the placenta goes before the fetus into the birth canal Describes a placenta that is implanted somewhere in the lower uterine segment, either over or very near the internal cervical os Low-lying placenta is less likely to “migrate” or move away from the internal os, within a uterus with a prior cesarean hysterotomy scar2. Restriction of activity is not necessary UNLESS a previa persists beyond 28 weeks or if clinical findings such as bleeding or contractions develop before this time CASE 1 A 28-year-old G3P2 (2002) with 2 previous CS is rushed to the ER at 34 weeks because of sudden profuse vaginal bleeding of a few minutes with no associated contractions. She has stable vital signs. Fundic Height (FUH) = 27 centimeters, Fetal Heart Tone (FHT) = 155 bpm, and the hypogastrium is empty on Leopald’s III. What ancillary test is most helpful at this time? A. CBC B. Non-stress test C. Contraction stress test D. Ultrasound Impression for CASE 1: Placenta Previa Relatively young multigravid with 2 prior CS (risk factor). This is a high risk OB patient. Painless vaginal bleeding, with normal vital signs. No contractions FH=27 is quite small FHT= 155 bpm is still good Recall L3: Hypogastric Area. L3 is empty so what is the lie of the baby which may indicate the fetus is in transverse lie. It may be empty since there may be something occupying L3 that is why the baby cannot position itself. Ultrasound is most helpful at this time. Eventually, you may need to do CBC, and you may do it simultaneously with ultrasound.
CLASSIFICATION CURRENT CLASSIFICATION (Dashe, 2013) 2 1. Placenta Previa o Partially or totally covers the internal os o With both total and partial placenta previa, a certain degree of spontaneous placental separation is an inevitable consequence of lower uterine segment remodeling and cervical dilatation.
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OBSTETRICS 3.3 2. Low lying placenta o Placental edge does not reach the internal os and remains outside a 2 cm wide parameter around the os 2 o Previously called as marginal previa 2 Marginally implanted on the internal os1 Placenta that was at the edge of the internal os but did not overlie it 2 o The edge is within 2cm from the cervical canal measured through ultrasound1 Regardless, these will increase the incidence of vaginal bleeding when the mother goes into labor.1 The classification of some cases of previa will depend on cervical dilatation at the time of assessment2. For example, placenta previa that appears to be total before cervical dilatation may become partial at 4-cm dilatation because the cervical opening now extends beyond the edge of the placenta
Figure 3. Different presentations of placenta previa based on the old classification. Complete (A) and Partial (B) are now classified under placenta previa, while Marginal (C) and Low Lying (D) are under Low lying Placenta
CLINICAL FEATURES 2 PAINLESS bleeding is the most characteristic event in placenta previa, which usually does not appear until near the end of the 2nd trimester or later In 10% of women with placenta implanted near but not over the cervical os, there is no bleeding until labor onset. Bleeding may vary from slight to profuse, and may mimic placental abruption. Placenta accrete syndromes arise from abnormal placental implantation and adherence Placenta previa is rarely complicated by coagulopathy.
o Bleeding may lead to hematoma formation which may further separate the placenta away from its implantation site. With further increase and expansion of hematoma, there will be more contractions, and it goes into a vicious cycle.1 Thrombin from hemorrhage induces contractions o It acts as an irritant and because of the inability of the lower segment to contract adequately the same way as the active segment of the uterus, there may be more bleeding.1 NEVER do an Internal Examination (IE) unless placenta previa has been ruled out by ultrasound or unless done under “double set up.” o If you are encountering a patient presenting with abnormal vaginal bleeding beyond 20th week AOG, more or less you are already considering the baby to be viable. If you perform digital exam/IE you will induce more bleeding. o But if you really need to do IE, ensure a double set-up. This is done in the OR with a team consisting of an anesthesiologist, co-obstetrician who will assist you, and pediatrician. If more bleeding ensues after PE/IE, then you need to do immediate CS.1 o Applicable only in places with problems to accessibility of Ultrasound or when nobody can do the Ultrasound1 ULTRASOUND IN PLACENTA PREVIA Transabdominal ultrasound identifies placental implantation site o May be confirmatory 2 o You can actually measure the distance of the edge of the placenta to the internal os or how much of the placenta overlaps the internal os.1 Transvaginal ultrasound o Safe and more accurate in assessing distance of placental edge from the cervical os. (Level 1, Grade A) o IE is contraindicated but transvaginal ultrasound is not because the probe is not touching the cervix unlike in IE you are measuring the dilatation and effacement of the cervix.1 o If you want to measure how much of the placenta overlaps, do a transvaginal ultrasound.1 o Anteriorly implanted placenta can be easily seen in ultrasound, unlike in posteriorly implanted placenta.
RISK FACTORS 2
Increasing maternal age Multiparity Prior CS delivery Maternal cigarette smoking – carbon monoxide hypoxemia causes placental hypertrophy and more surface area High Maternal Serum Alpha-Fetoprotein BLEEDING IN PLACENTA PREVIA Partial placental separation with lower segment formation and cervical dilatation o Braxton Hicks contraction may occur in the 3rd trimester or towards the end of pregnancy. The uterus starts to contract without necessarily dilating or effacing the cervix. o There is formation of the lower uterine segment and the mother feels that the presenting part goes further down into the pelvis (“lightening”). o Partial separation of the placenta may occur during this time because the lower uterine segment is passive compared to the active segment of the uterus, the contractile ability is not as good as the active segment.
Group#13 | Peralta, Perez, E. Petate, Pilapil, Pineda
Figure 4. Total placenta previa. Transabdominal sonogram of the placenta (white arrowheads) behind the bladder covering the cervix (black arrows). Part of the placenta seems to be covering the cervical canal 1.
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Figure 5. Transvaginal sonographic image of the placenta (arrows) completely covering the cervix adjacent to the fetal head.
MANAGEMENT 2 Close observation if fetus is preterm and there is no persistent active bleeding Tocolytics, limited to 48 hours of administration or none at all Discharge if maternal bleeding stopped for about 2 days, and fetus is healthy Plans for scheduled CS delivery in women who are near term and who are not bleeding, varying from 35 to 38 weeks AOG o Low transverse hysterotomy may cause fetal bleeding if there is an anterior placenta and the placenta is cut through. Vertical uterine incision may be preferable in some instances. o When hemostasis at the placental implantation site cannot be obtained by pressure, the implantation site can be oversewn with 0chromic sutures. o Hysterectomy – if more conservative methods fail, there is brisk bleeding, or asssociated placenta accerete syndrome (likely if there is anterior implantation at the site of a prior uterine incision)
ADHERENT PLACENTA PLACENTA ACCRETE SYNDROME2 Abnormally implanted, invasive or adhered placenta Include any placental implantation with abnormally firm adherence to myometrium because of partial or total absence of decidua basalis and imperfect development of fibrinoid or Nitabuch layer Partial or total absence of decidual spongy layer may lead to absence of physiological line of cleavage, and some or all cotyledons are densely anchored Placental villi are anchored to muscle fibers rather than to decidual cells. Decidual deficiency then prevents normal placental separation after delivery. Previous uterine trauma— for example, cesarean delivery—may be partially explained by an increased vulnerability of the decidua to trophoblast invasion following incision into the decidua Increased risks for recurrence, uterine rupture, hysterectomy, and previa CASE 1 (CONTINUATION) Ultrasound revealed an anteriorly implanted placenta with the inferior edge totally covering the os. On further examination, multiple dilated blood vessels were noted extending from the placenta to the myometrium and into the posterior urinary bladder wall. What is the diagnosis? a. Placenta accreta b. Placenta increta c. Placenta percreta d. Placenta succenturiata- accesory lobe of placenta Group#13 | Peralta, Perez, E. Petate, Pilapil, Pineda
In most instances, the placenta separates spontaneously from its implantation site during the first few minutes after delivery of the infant. Infrequently, detachment is delayed because the placenta is unusually adhered to the implantation site 2
TYPES OF ADHERENT PLACENTA 1. Placenta Accreta o Superficial adherence of placental villi2 o Abnormally firm adherence to the uterine wall o Placental villi are attached to the myometrium in placenta accreta2 2. Placenta Increta o Villi invade into the myometrium 3. Placenta Percreta o Villi penetrate through the myometrium; beyond the serosal layer of the uterus o Most severe form of abnormal placental adherence.1 Villi has invaded the contiguous structures. If anteriorly implanted, may invade bladder. Bowel loops and rectum are affected if posteriorly implanted. The abnormal adherence may involve 2 o All lobules—total placenta accreta o Few to several lobules—partial placenta accreta, o All or part of a single lobule may be attached—focal placenta accreta.
Figure 6. Types of Adherent Placenta 1. Normal placenta (green arrow) shows delineating area or distinct interface between the myometrium and placenta. In Accreta (blue), there is a retroplacental hypoechoic zone. Increta (orange) shows invasion into myometrium. In Percreta (red), it has gone beyond the uterus.
PLACENTA PREVIA AND ACCRETA All women with placenta previa and previous uterine surgery should be screened for accreta. Major risk factor for accreta is a combination of previa and previous CS. Risk for previa-percreta increases proportionately with the number of CS (Level II-2, Grade B) o Placenta previa may be associated with placenta accreta or one of its more advanced forms, placenta increta or placenta percreta. Such abnormally firm attachment of the placenta might be anticipated because of poorly developed decidua in the lower uterine segment.2 o A classical hysterotomy incision has a higher risk for a subsequent accrete placenta 2
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OBSTETRICS 3.3 CS & PLACENTA PREVIA/ACCRETA Table 2. Incidence of Placenta Previa and Concurrent Placenta Acrreta No.prior CS Incidence of placenta Incidence of previa (%) concurrent accreta (%) 0 0.26 5 1 0.65 24 2 1.8 47 3 3.0 40 4 10.0 67
The more CS that you do, you increase further the incidence or risk of placenta previa as well as the risk for accreta 1 If there is anterior implantation of placenta where CS scar is located, check for placenta accreta as well1 DIAGNOSIS OF PLACENTA ACCRETA Main screening modality is Gray Scale Transvaginal Ultrasound combined with clinical risk factors o May be accompanied with bleeding in the 1st or 2nd trimester, due to coexisting placenta previa. Those who do not have associated previa may not be diagnosed until the 3rd stage labor2 Color and Power Doppler ultrasound increases accuracy of diagnosis MRI is done when ultrasound results are equivocal or when the placenta is implanted posteriorly o If the placenta is posteriorly implanted, the baby sits on the placenta and you cannot evaluate the whole retroplacental area. Ultrasound cannot show everything behind the placenta.1 o Three MR imaging findings that suggested accreta2: uterine bulging, heterogeneous signal intensity within the placenta, and dark intraplacental bands on T2-weighted imaging.
Figure 8. Color Doppler. Retroplacental vessels (white arrows) invade the myometrium and obscure the bladder-serosal interface. Abnormal intraplacental venous lakes (black arrowheads) are commonly seen in this setting.
Figure 7. (Left) Retroplacental hypoehoic zone (less echoes, appears black). There is an interface between the placenta and the rest of the myometrium. (Right) Placenta, urinary bladder, bladder wall and myometrium complex. It appears thin and there are cystic areas, if you turn on the color of the machine, there will be dilated blood vessels that has invaded into the myometrium or even up to posterior bladder wall. SWISS CHEESE appearance of the placenta indicating accreta.
MANAGEMENT OF PLACENTA ACCRETA 2 Most practitioners do not deliver these women until 36 weeks or later Intraarterial catheters to mitigate blood loss and to enhance surgical visibility. o Balloon-tipped catheters advanced into the internal iliac arteries are inflated after delivery to occlude pelvic blood flow to aid placental removal and hysterectomy Confirmation of a percreta or increta almost always mandates hysterectomy o Some abnormal placentations, especially if partial, may be amenable to placental delivery with hemostatic suture placement. o Classical hysterotomy incision is made to avoid the placenta and profuse hemorrhage before fetal delivery o With obvious percreta or increta, hysterectomy is usually the best course, and the placenta is left in situ. o Unless there is spontaneous separation with bleeding that mandates emergency hysterectomy, the operation begins after full assessment is made Leaving the placenta in situ o After the fetus has been delivered, it may be possible to trim the umbilical cord and repair the hysterotomy incision but leave the placenta in situ o Indicated for: Abnormal placentation was not suspected before cesarean delivery and uterine closure stops bleeding Strong desire for fertility o Placenta may spontaneously resorb, or subsequent hysterectomy (planned or prompted by infection or bleeding) performed once bleeding lessened ABRUPTIO PLACENTA
In Doppler Ultrasound, a normal placenta has normal arrangement of vessels. In contrast, chaotic arrangement or protrusion into the cavity of the urinary bladder, indicates invasion. Delivery of the baby may lead to further bleeding1. Suspect myometrial invasion if the distance between the uterine serosabladder wall interface and the retroplacental vessels is < 1 mm and if there are large intraplacental lacunae2 Figure 9. Types of placental abruption
Group#13 | Peralta, Perez, E. Petate, Pilapil, Pineda
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with blood and clots dissecting between membranes and decidua to the internal cervical os and then externally into the vagina.
Premature separation of a NORMALLY IMPLANTED placenta. It is away from the cervical canal. o NOTE: In Previa, there is placental separation of placenta that is implanted over or near the cervical canal1 o Internal os—that is, placenta previa.2
CASE 2 A 30 y/o G1P0, known hypertensive is admitted at 35 weeks because of vaginal bleeding associated with painful uterine contractions. PE shows a BP of 160/110, PR 102/min, FH= 27cm, FHT= 90-95/ min, and strong uterine contractions. IE shows a 5cm dilated cervix, cephalic, intact BOW and with minimal vaginal bleeding. What is the best management? a. Awaits vaginal delivery b. Do forceps delivery c. Do vacuum delivery d. Do emergency CSC In CASE 3, the patient is preterm at 35 weeks. The mother is both hypertensive and tachycardic. Her increased VS . In association with painful uterine contractions, may indicate bleeding within uterus. Increased HR may be due to pain or other existing conditions. o The fetus is small based on FH 27 cm. FHT is increased, indicating fetal distress. Uterine conditions in this case are not conducive to the fetus. o There may be bleeding, consider ABRUPTIO PLACENTA. Maternal and fetal well being are at increased risk. Fetus is also near term. It is best to consider delivery via emergency CS.
TYPES OF ABRUPTIO PLACENTA 1. External o The placenta has detached peripherally, and the membranes between the placenta and cervical canal are detached from the underlying decidua. This allows blood egress through the vagina. o The bleeding of placental abruption typically insinuates itself between the membranes and uterus, ultimately escaping through the cervix, causing external hemorrhage2. 2. Concealed o Less often, the blood does not escape externally but is retained between the detached placenta and the uterus, leading to concealed hemorrhage.2 o The periphery of the placenta and the membranes are still adhered and blood remains within the uterus o Concealed hemorrhage carries much greater maternal and fetal hazards. This is not only because of possible consumptive coagulopathy, but also because the extent of the hemorrhage is not readily appreciated, and the diagnosis typically is delayed 2 3. Partial placenta abruption - there is placental separation and external hemorrhage 4. Total separation - fetal death is expected.
Figure 11. Total placental abruption with concealed haemorrhage and fetal death. Periphery of the placenta and the membranes are still adhered and blood remains
In some cases you have profuse, moderate, or even no bleeding, but baby is dead. You’re probably dealing with this type of abruption. 1
Group#13 | Peralta, Perez, E. Petate, Pilapil, Pineda
CAUSE OF BLEEDING It is initiated by hemorrhage into the decidua basalis. The decidua then splits, leaving a thin layer adhered to the myometrium. Consequently, the process begins as a decidual hematoma and expands to cause separation and compression of the adjacent placenta2. Rupture of decidual spiral artery Bleeding into decidua basalis Formation of a retroplacental hematoma Separation, compression and destruction of adjacent villi
Figure 10. Placental Abruption. Shown at the left, is a total placental abruption with concealed hemorrhage. To the right is a partial abruption
Placental margins are still adherent Placenta may be separated but the membranes are still adherent to the deciduas. Blood remains within the uterus, pooled reptroplacentally. Blood enters the amniotic cavity after breaking through the membranes Fetal head (because already very low in the pelvis) 1 serves as a tamponade preventing egress of blood externally
As the hematoma expands there will be more separation. Thrombin will serve as uterotonic agent that induces contraction to constrict the torn vessels 3 o More bleeding → more thrombin → more contractions. May be due to: o Impaired trophoblastic invasion (Pregnancy-Induced Hypertension) o Inflammation/Infection – more common in prematurely separated placenta o Trauma (blunt or penetrating) or assault Can be caused by relatively minor trauma2 Found in some cases of external trauma like physical violence or vehicular accidents2 Significant fetal bleeding is much more likely with a traumatic abruption that results from a concomitant placental tear2. o Sudden uterine decompression When there is membrane rupture and amniotic fluid is released1 Page 6 of 15
OBSTETRICS 3.3 o o
Reason why, when doing amniotomy during labor, only small incisions/ punctures are done1 Cocaine use Vasospasm (ex. Hypertension)3 Hypertension is the most common condition associated with placental abruption2 Chronic placental separation may begin early in pregnancy. In some cases, subsequent oligohydramios may develop2 Other predisposing factors: maternal age, cigarette smoking, uterine leiomyomas if located near the mucosal surface behind the placental implantation site
DIAGNOSIS OF ABRUPTIO PLACENTA Mainly based on CLINICAL SYMPTOMATOLOGY (Level III, Grade C) o Sudden onset of abdominal pain, vaginal bleeding and uterine tenderness 2 Diagnosis is clinical and is suspected in women who present with the following o Vaginal bleeding or abdominal pain or both. Always rule out in women who present with tetanic uterine contractions and severe abdominal pain1 o History of trauma o Those who present with otherwise unexplained preterm labor Signs and symptoms can vary considerably2 Sonography infrequently confirms diagnosis of placental abruption at least acutely, because placenta and fresh clot have similar sonographic appearance 2 o Negative findings do not exclude placental abruption o Differential Diagnosis: Milder and more common forms of abruption may be difficult to recognize with certainty, and the diagnosis is often made by exclusion2 o Clinically, it has long been taught that Painful uterine bleeding is associated with Placental abruption; painless bleeding with placenta previa2 o Usually not so straightforward; wherein, at times, the cause of bleeding remains obscure even after delivery MANAGEMENT OF ABRUPTIO PLACENTA Complete abruption: Maternal outcome depends on adequate and timely replacement of blood and fluid rather than how soon delivery can be accomplished. Thrombin that forms from hemorrhage is a potent uterotonic agent, hence, may be mistaken as premature labor. Reasonable to use tocolytics with caution in stable women who have partial abruption but are remote from term. (Level II-2, Grade B) Do not rush the delivery, unless there is fetal distress. Stabilize mother first. o Check fetal heart tones, maternal vital signs, check for ongoing abruption, and if delivery can wait until fetal lung matures1
Figure 12. Immediate causes of fetal distress from placental abruption and their treatment. Fetal hemorrhage is usually only in traumatic abruption and placental tear2 Group#13 | Peralta, Perez, E. Petate, Pilapil, Pineda
ROUTE OF DELIVERY Treatment varies depending on gestational age and status of mother and fetus2 o Expectant management in pre-term pregnancy Cesarean Section indicated when there is fetal compromise, severe uterine hypertonus or life threathening vaginal bleeding. o Rapid delivery of the fetus who is alive, but in distress practically always means CS2 o Speed of response is important in neonatal outcome2 o Serious coagulation defects are troublesome: abnormal uterine incisions are prone to bleed excessively2 Expectant management an option when maternal and fetal status are reassuring or when the fetus is dead o Women with evidence of very early abruption frequently develop oligohydramnios w/ or w/o premature membrane ruptures2 o Lack of ominous decelerations, does not does not guarantee safety of intrauterine environment2 Deliver fetus if AOG is term or near term, may consider tocolysis if remote from term with stable maternal and fetal status o Some advocate tocolysis for preterm pregnancy complicated by suspected abruption, but w/ no fetal compromise Vaginal delivery o If severe placental separation where fetus has died2, but there are cases where vaginal delivery or assisted vaginal delivery is possible 1 o Stimulation of myometrium pharmacology and by uterine massage causes placental site vessels to be compressed and constricted so that serious hemorrhage is avoided even though coagulation defects present Level II-2, Grade B evidence ROLE OF AMNIOTOMY  Rationale: Decompresses the uterus to improve contraction o Compresses torn spiral vessels o Reduces entry of thromboplastin into maternal circulation. Hastens delivery Rupture of membranes ASAP has long been championed in the management of placental abruption2 o If the fetus is mature: rupture hastens delivery o If immature: intact sac may be more efficient in promoting cervical dilation than a small fetal part poorly applied to the cervix PREVIA VS. ABRUPTIO Table 3. Differetiating Placenta Previa from Abruptio Placenta CHARACTERISTICS PLACENTA PREVIA ABRUPTIO PLACENTA Vaginal bleeding Profuse Minimal to moderate w/ blood clots or none means concealed1 soaked in blood1 Uterine None to occasional Tetanic usually dx since contractions very painful1 Fetal compression Less common More common/ IUFD Seeks early consult Delayed consult since due to bleeding1 mistaken for normal labor1 DIC Unlikely (bleeding Likely w/ severy AP (due to goes out)1 concealed bleeding) Role of ultrasound Confirms location Inconclusive (retroplacental hematoma may have same appearance as placenta even in complete1 Common risk Prior uterine Hypertension factor surgery Route of Delivery Always CS CS or vaginal Anticipate Placenta accreta DIC Page 7 of 15
2nd half or 3rd trimester mothers with bleeding are usually diagnosed with a cross between previa and abruption, so very important to differentiate1
VASA PREVIA  Placenta vessels overlie the cervix Prone to compression leading to anoxia and laceration leading to fetal hemorrhage o When there’s spontaneous rupture of the membrane these vessels may rupture as well. If severe, it will lead to bleeding coming from the baby, not from the mother. Fetal death is instantaneous, hence warrants immediate CS
Figure 13. Vasa Previa RISK FACTORS OF VASA PREVIA 1. Velamentous insertion of the umbilical cord There is branching off before reaching the placenta, so are therefore exposed within the membranes In a normal placenta, the cord and the vessels go right up to the surface of the placenta before branching off Diagnosed by Color Doppler Ultrasound 3 o Blue – flow AWAY from the sonologist o Red – flow TOWARDS the sonologist o Yellow – turbulence flow
Figure 14. Velamentous insertion. Large fetal vessels extend from the cord insertion and within the membranes. From the proximity of the vessels to the site of membrane rupture, it can be seen how a vessel could easily be torn by digital manipulation or descent of the fetal head during labor 2 2. Placenta succenturiata Placenta consists of a large lobe and a smaller one connecting together by membranes.3 The umbilical cord is inserted into the large lobe and branches of its vessels cross the membranes to the small succenturiate (accessory) lobe. The accessory lobe may be retained in the uterus after delivery leading to postpartum hemorrhage 3. Placenta previa 4. In vitro fertilization
Group#13 | Peralta, Perez, E. Petate, Pilapil, Pineda
Figure 15. Uterine rupture involving fetus May develop as a result of preexisting injury, may be associated with trauma, or may complicate labor in a previously unscarred uterus2 The most common cause of uterine rupture is separation of a previous CS scar (e.g. classical incision) Caution in allowing patients to go under trial vaginal delivery Must be sure previous uterine incision was low segment (e.g. Kerr incision), not classical or low vertical CS which are prone to uterine ruptures CLASSIFICATION OF UTERINE RUPTURE May occur ante-partum or post-partum 1 Complete (all layers separated) o All layers of the uterine wall are separated o Greater morbidity and mortality rates Incomplete (intact visceral peritoneum) o When the uterine muscle is separated but the visceral peritoneum is intact o Serosal layer of the uterus is still intact1 o Commonly referred to as uterine dehiscence Primary 2 o Occurs in a previously intact or unscarred uterus Secondary 2 o Associated with a pre-existing myometrial incision, injury, or anomaly TRAUMATIC RUPTURE2 Although the uterus is surprisingly resistant to blunt trauma, pregnant women sustaining such trauma to the abdomen should be watched carefully for signs of a ruptured uterus as well as a placental abruption. Trauma accounted for a ruptured uterus in only 3 of more than 150 women2 Causes: internal podalic version and extraction, difficult forceps delivery, breech extraction, and unusual fetal enlargement such as with hydrocephaly. SPONTANEOUS RUPTURE2 Approximately 1 in 15,000 deliveries (Miller and Paul, 1996) Oxytocin stimulation of labor has been commonly associated with uterine rupture, especially in women of high parity Resulted from labor induction with prostaglandin E2 gel or E1 vaginal tablets o All uterotonic agents should be given with great caution to induce or stimulate labor in women of high parity. In women of high parity, a trial of labor with suspected cephalopelvic disproportion, high cephalic presentation, or abnormal presentation, such as a brow, must be undertaken with caution. RISK FACTORS OF UTERINE RUPTURE Previous Uterine Surgery o Most common cause Page 8 of 15
o Not only CS, also curettage – whether for abortion or gynaecologic purpose (ex. Myomectomy) Coincidental Uterine Trauma (ex. Instrumentation to induce abortion – expect to see uterine perforation) Uterine Congenital Anomaly o Occurs in abnormal and undeveloped uterus o If pregnancy developed in undeveloped uterine horn. This is not designed to accommodate a growing fetus, can only expand to a certain limit and lead to rupture Labor related o Overzealous oxytocin stimulation1 o May be external cephalic version or internal podalic version1 Delivery related o Forceps delivery, manual fundal pressure (to hasten delivery) 1 Uterine Pathology o Placenta accreta, percreta, increta1 CLINICAL FINDINGS IN UTERINE RUPTURE
Figure 16. Fetal heart rate tracing in a woman whose uterus ruptured during labor while pushing. The rupture apparently stimulated a reflex push, after which uterine tone diminished and fetal bradycardia worsened.
Non-reassuring fetal heart rate pattern with variable heart rate decelerations that may evolve into late decelerations, bradycardia and death o Most common sign of uterine rupture: do CS ASAP! Abdominal pain/tenderness o May be mistaken for labor pain o May not be obvious if mother is under anesthesia, especially epidural anesthesia Chest or shoulder pain o Due to irritation of diaphragm by intraperitoneal blood Hemodynamic instability o Important to check vital signs o Before hypovolemic shock develops, symptoms and physical findings may appear bizarre unless the possibility is kept in mind3 o Hemoperitoneum from a ruptured uterus may result in diaphragmatic irritation with pain referred to the chest, directing one to a diagnosis of pulmonary or amniotic fluid embolism instead of uterine rupture3. Loss of fetal station o The baby’s head that is previously engaged is now floating.1 First IE revealed fetal head initially at Station +1, baby then becomes bradycardic and subsequent IE reveals station -1 (floating again) o If the fetal presenting part has entered the pelvis with labor, loss of station may be detected by pelvic examination. o If the fetus is partly or totally extruded from the site of uterine rupture, abdominal palpation or vaginal examination may be helpful to identify the presenting part, which will have moved away from the pelvic inlet. A firm contracted uterus may at times be felt alongside the fetus 3
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More palpable fetal parts o If the fetus has been extruded out of uterus into the abdominal cavity3 Condition usually becomes evident because of signs of fetal distress and occasionally because of maternal hypovolemia and concealed hemorrhage2 PATHOGENESIS OF UTERINE RUPTURE  Rupture of the previously intact uterus during labor most often involves the thinned-out lower uterine segment. When the rent is in the immediate vicinity of the cervix, it frequently extends transversely or obliquely. When the rent is in the portion of the uterus adjacent to the broad ligament, the tear is usually longitudinal. Although these tears develop primarily in the lower uterine segment, it is not unusual for them to extend upward into the active segment or downward through the cervix and into the vagina. The bladder may be lacerated. If the rupture is of sufficient size, the uterine contents will usually escape into the peritoneal cavity. If the presenting fetal part is firmly engaged, only a portion of the fetus may be extruded from the uterus. Overlying peritoneum can remain intact, and this usually is accompanied by hemorrhage that extends into the broad ligament to cause a large retroperitoneal hematoma with extensive blood loss. Inherent weakness in the myometrium in which the rupture takes place (e.g., adenomyosis, onnective tissue defects such as Ehlers-Danlos syndrome). PROGNOSIS OF UTERINE RUPTURE Maternal deaths from rupture are uncommon. Fetal prognosis is largely dependent on the degree of placental separation and magnitude of maternal hemorrhage and hypovolemia. o 70% fetal mortality rate with either spontaneous or traumatic uterine rupture o 50 – 75% fetal mortality rate with rupture and expulsion of the fetus into the peritoneal cavity. o With rupture, the only chance of fetal survival is afforded by immediate delivery, most often by laparotomy. Otherwise, hypoxia from both placental separation and maternal hypovolemia is inevitable. o If rupture is followed by immediate total placental separation, then very few intact fetuses will be salvaged. Evaluate if you can save the uterus or proceed with hysterectomy.1 MANAGEMENT & OUTCOMES OF UTERINE RUPTURE Conservative o Repair the rent but with the risk of recurrent rupture Aggressive o Hysterectomy Ends reproductive potential May be necessary to control hemorrhage May be required with complete rupture during a trial of labor Increased perinatal morbidity and mortality associated with uterine rupture. o A major concern is that surviving infants develop severe neurological impairment.2 POSTPARTUM HEMORRHAGE Early – within 24 hours after delivery Late – after the first 24 hours but within 6 weeks (period of puerperium) following delivery
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HEMOSTATIC MECHANISMS Platelet aggregation and plug formation Local vasoconstriction Clot polymerization Fibrous tissue fortification of the clot Uterine contraction – primary mechanism to control bleeding. Rationale for giving oxytocin. CAUSES OF POSTPARTUM HEMORRHAGE: 4 T’S Tone (Early) o Uterine Atony Trauma (Early) o Lacerations - Persistent bleeding despite a firm, well-contracted uterus suggests that hemorrhage most likely is from lacerations.2 o Hematoma o Uterine rupture o Uterine inversion Tissue (Variable) o Concurrent placenta accreta – if there’s immediate bleeding1 o Retained placenta – the patient is already discharged doing well at home then suddenly they have profuse vaginal bleeding1 o Retained secundines Thrombin (Variable) o DIC UTERINE ATONY Identified by a boggy, soft uterus during bimanual examination and by expression of clots and hemorrhage during uterine massage.2 Most common cause of PPH (postpartum hemorrhage) o The most frequent cause of obstetrical hemorrhage is failure of the uterus to contract sufficiently after delivery and to arrest bleeding from vessels at the placental implantation site.2 RISK FACTORS: o Overdistended uterus – secondary to multifetal pregnancy, macrosomic baby, abnormalities in amniotic fluid (polyhydramnios)1 o Oxytocin induced or augmented labor – women who are subjected to long trials of labor. There has to be a limit to oxytocin administration, since it is a dangerous drug. If uterus contracting for 24 hours, it may lead to fatigue, leading to loss of contractions1 o Hypotonic uterine contractions o High parity – due to inherent weakness of the uterus, not due to overdistention o Prior postpartum hemorrhage2 is at risk for recurrence with subsequent delivery
MANAGEMENT OF UTERINE ATONY MEDICAL MANAGEMENT OF UTERINE ATONY 1. UTEROTONIC AGENTS Oxytocin o 20 units of oxytocin in 1,000 ml of crystalloid solution will often be effective given IV at 10 ml/min for a dose of 200 mU/min.2 o Should never be given as an undiluted bolus dose because serious hypotension or cardiac arrhythmias may develop.2 Carbetocin Ergot derivatives o Methylergometrine maleate o Give 0.2 mg via IM if oxytocin is not effective. Do not give intravenously as this may cause dangerous hypertension, especially in women with preeclampsia.3 Prostaglandins o Misoprostol – administered transrectally. It is not given intravaginally because the patient is bleeding. It is not given orally because the patient is on NPO1 Group#13 | Peralta, Perez, E. Petate, Pilapil, Pineda
o Carboprost – 15 methy derivative of Prostaglandin F-2-alpha; side effects include diarrhea, hypertension, vomiting, fever, flushing, and tachycardia; cannot be given in asthmatics since it causes airway constriction
SURGICAL MANAGEMENT OF UTERINE ATONY Bimanual uterine compression Internal uterine tamponade procedures Uterine compression sutures (B-Lynch) Arterial embolization Arterial ligation – uterine artery ligation (at the area of the isthmus; done bilateraly) or hypogastric artery ligation (retroperitoneal dissection); or internal iliac artery ligation Hysterectomy – done as a last resort after exhausting all means. It is easier to decide this procedure for a woman who has given birth multiple times, but for a primigravid it is imperative to exhaust all means to maintain her fertility 3 Pelvic umbrella pack - “last-ditch” attempt when exsanguination is inevitable, especially in “low-resource” areas. Preoperative Pelvic Arterial Catheter Placement BIMANUAL UTERINE COMPRESSION
Figure 17. Bimanual compression for uterine atony
Not simply a fundal massage The posterior uterine wall is massaged by one hand on the abdomen, while the other hand is made into a fist and placed into the vagina. This fist kneads the anterior uterine wall (active uterine segment1) through the anterior vaginal wall. Concurrently, the uterus is also compressed between the two hands. You do not remove your hands until the uterus is contracted. 1 Give anesthesia because this procedure is painful.3 INTERNAL UTERINE TAMPONADE PROCEDURES2
Figure 18. Intrauterine balloon/balloon tamponade
The tip of a 24F Foley catheter with a 30-ml balloon is guided into the uterine cavity and filled with 60 to 80 ml of saline. The open tip permits continuous drainage of blood from the uterus. If bleeding subsides, the catheter is typically removed after 12 to 24 hours. Page 10 of 15
Well-designed studies are needed before instituting intrauterine balloon tamponade as a second-line treatment for atony. UTERINE COMPRESSION SUTURES (B-LYNCH)
Figure 20. Uterine artery ligation. The suture goes through the lateral uterine wall anteriorly, curves around posteriorly, then re-enters anteriorly. When tied, it encompases the uterine artery.
Figure 19. Uterine compression suture or “brace”. The B-Lynch suture technique is illustrated from an anterior view of the uterus
in Figures A, B, and D and a posterior view in Figure C.
Also called braces because they give the appearance of suspenders Involves placement of a no. 2-chromic suture to compress the anterior and posterior uterine walls together.2 It’s like putting a suspender into the uterus, making the uterus contract by making use of the suture and giving the uterus a crumpled appearance .1 Uterine ischemic necrosis – complication if done with a concurrent procedure (e.g., arterial ligation)1 Steps2: 1. Beginning below the incision, the needle pierces the lower uterine segment to enter the uterine cavity. 2. The needle exits the cavity above the incision. The suture then loops up and around the fundus to the posterior uterine surface. 3. The needle pierces the posterior uterine wall to reenter the uterine cavity. The suture then traverses from left to right within the cavity. 4. The needle exits the uterine cavity through the posterior uterine wall. From the back of the uterus, the suture loops up and around the fundus to the front of the uterus. 5. The needle pierces the myometrium above the incision to reenter the uterine cavity. 6. The needle exits below the incision and the sutures at points 1 and 6 are tied below the incision. The hysterotomy incision is then closed in the usual fashion. ARTERIAL EMBOLIZATION2 Used for many causes of intractable hemorrhage when surgical access is difficult Can be used to arrest refractory postpartum hemorrhage 90% effective Less effective with placenta percreta or with concurrent coagulopathy Complications of embolization are relatively uncommon, but can be severe (e.g., uterine schemic necrosis). Fertility is not impaired
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Bilateral hypogastric artery ligation – needs retroperitoneal dissection1 Unilateral or bilateral uterine artery ligation is used primarily for lacerations at the lateral part of a hysterotomy incision Ligate at the area of the isthmus where it separates into the anterior and posterior branches1 Procedure is less helpful for hemorrhage from uterine atony2 ACTIVE MANAGEMENT OF THIRD STAGE OF LABOR Recommended to prevent postpartum hemorrhage (Level I, Grade A) Components: o Prophylactic uterotonic agent (oxytocin) given just before or immediately after delivery o Delayed cord clamping – waiting for 3 minutes or for the pulsation of the cord to stop3 o Controlled cord traction to deliver the placenta. We do not wait for signs of placental separation anymore 1.
RETAINED SECUNDINES (TISSUE) Early Post Partum Hemorrhage – associated with adherent placenta Late Post Partum Hemorrhage – associated with retained placental tissues Routine inspection of the placenta to check for missing cotyledons (maternal side) should be done
RETAINED SECCUNDINE: MANAGEMENT Inspect the placenta for missing cotyledons. The membranes would be the fetal side and the cotyledons are the maternal side. So check the maternal side, they should be complete 1. RETAINED PLACENTA (>30 mins.) o Manual delivery of placenta is done adequate analgesia and aseptic surgical technique2. o The whole hand is inserted at the uterine cavity. Feel for the edges of the placenta and try to separate it from its implantation site, grasp it and bring it out1. o Indicated if significant bleeding persists after delivery of the infant and while the placenta remains partially or totally attached RETAINED PLACENTAL FRAGMENTS o With abnormal adherence (Accreta, Increta, Percreta) o No abnormal adherence – completion curettage
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Figure 21. Manual Removal of Placenta. A. One hand grasps the fetus. The other hand is inserted into the uterine cavity, and the fingers are swept side to side as they are advanced. B. When the placenta has been detached, it is grasped and removed CASE 4 A G1P0 is admitted at term because of labor pains. She eventually delivered after 9 hours aided by FUNDAL PRESSURE because of inadequate bearing down efforts. During episiorrhaphy, sudden profuse vaginal bleeding was noted with prolapsing introital mass. a. Uterine Atony b. Uterine Inversion c. Uterine Rupture d. Vulvovaginal Hematoma
TRAUMA TO GENITAL TRACT Uterine inversion Genital Tract laceration – cervix, vaginal walls Puerperal hematomas – severe perineal pain Uterine Rupture UTERINE INVERSION “Seeing the uterus inside-out”1 Almost always a consequence of strong traction of fundally attached placenta 1 Traction-counter traction - Therefore, you should deliver the placenta with gentle traction, and you counter this with a hand pushing at the abdomen against the placenta to prevent inversion Associated with accreta, relaxed uterus with fundal pressure Uterine inversion is most often associated with immediate life threatening hemorrhage. They can be pregnant again but recurrence is high 1
RISK FACTORS2 1. Fundal placental implantation, 2. Delayed-onset or inadequate uterine contractility after delivery of the fetus, that is, uterine atony, 3. Cord traction applied before placental separation, and 4. Abnormally adhered placentation such as with the accrete
UTERINE INVERSION: MANAGEMENT Protruding introital mass with an empty hypogastrium “Last out first in” uterine repositioning simultaneous with tocolytic agent Oxytocin given once uterus is repositioned Careful evaluation of the need in many cases for transfusion of large volumes of blood, however, illustrates that blood loss is usually massive and greatly underestimated Delay in treatment increases the mortality rate appreciably. It is imperative that a number of steps be taken urgently and simultaneously2: 1. Immediate assistance from anesthesia personnel and other physicians
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2. Bring blood to the delivery suite 3. Evaluation for Emergency General Anesthesia. 4. Begin rapid crystalloid infusion to treat hypovolemia while awaiting arrival of blood for transfusion. 5. Uterus may often be replaced by pushing up on the inverted fundus with the palm of the hand and fingers in the direction of the long axis of the vagina o If the recently inverted uterus has not contracted and retracted completely and if the placenta has already separated 6. If still attached, the placenta is not removed until infusion systems are operational, fluids are being given, and a uterine-relaxing anesthetic such as a halogenated inhalation agent has been administered. 7. Intravenously administered tocolytic drug (terbutaline, magnesium sulfate, or nitroglycerin) for uterine relaxation and repositioning. o If these fail to provide sufficient relaxation, then a rapidly acting halogenated inhalational agent is administered. 8. After removing the placenta, steady pressure with the fist, palm, or fingers is applied to the inverted fundus in an attempt to push it up into and through the dilated cervix as described in Step 4. 9. Once the uterus is restored to its normal configuration, tocolysis is stopped. Oxytocin is then infused, and other uterotonics o Operator maintains the fundus in its normal anatomical position while applying bimanual compression to control further hemorrhage until the uterus is well contracted. o Operator continues to monitor the uterus transvaginally for evidence of subsequent inversion SURGICAL MANAGEMENT2 Huntington procedure – application of atraumatic clamps to each round ligament and upward traction Placing a deep traction suture in the inverted fundus or grasping it with tissue forceps If the constriction ring still prohibits repositioning, a longitudinal surgical cut—Haultain incision—is made posteriorly through the ring to expose the fundus and permit reinversion LACERATIONS CLASSIFICATION 1. Superficial lacerations o Common and may not require repair Presents as bleeding despite a well contracted uterus Usually associated with operative vaginal deliveries – vacuum and forceps 2. Deep vulvovaginal lacerations These may warrant exploratory laparotomy or uterine exploration to find possible uterine tears May extend to retroperitoneal area It is still recommended to perform a trial vaginal delivery if there are no contraindications 1 3. Injuries to Levator Ani muscles o These result from overdistension of the birth canal. Muscle fibers are separated, and diminution in their tonicity may be sufficient to interfere with pelvic diaphragm function. In such cases, pelvic relaxation may develop o If the injuries involve the pubococcygeus muscle, urinary incontinence also may result. 4. Perineal Lacerations2 o All except the most superficial perineal lacerations are accompanied by varying degrees of injury to the lower portion of the vagina. Page 12 of 15
OBSTETRICS 3.3 o May involve the anal sphincter and may extend to varying depths through the vaginal walls.
5. Vaginal Lacerations3 o Isolated lacerations involving the middle or upper third of the vagina, but unassociated with lacerations of the perineum or cervix, are encountered less commonly. o These are usually longitudinal and frequently result from injuries sustained during a forceps or vacuum delivery. However, they may even develop with spontaneous delivery. o Such lacerations frequently extend deep into the underlying tissues and may give rise to significant hemorrhage, which usually is controlled by appropriate suturing. o They may be missed unless thorough inspection of the upper vagina is performed. o Bleeding while the uterus is firmly contracted is strong evidence of genital tract laceration, retained placental fragments, or both. o Lacerations of the anterior vaginal wall in close proximity to the urethra are relatively common. o They are often superficial with little to no bleeding, and repair is usually not indicated. o If such lacerations are large enough to require extensive repair, difficulty in voiding can be anticipated, and an indwelling catheter is placed.
6. Injuries to the Cervix2 o The cervix is superficially lacerated in more than half of all vaginal deliveries. Most of these are less than 0.5 cm o Deep cervical tears may extend to the upper third of the vagina. o Rarely, the cervix may be entirely or partially avulsed from the vagina (colporrhexis). This may occur in the anterior, posterior, or lateral fornices. These may follow difficult forceps rotations or deliveries performed through an incompletely dilated cervix with the forceps blades applied over the cervix. o Rarely, cervical tears may reach to involve the lower uterine segment and uterine artery and its major branches, and even extend through the peritoneum. They may be totally unsuspected, but more often, they manifest as excessive external hemorrhage or as hematomas. o Cervical lacerations up to 2 cm must be regarded as inevitable in childbirth. Such tears heal rapidly and are rarely the source of complications.
DIAGNOSIS A deep cervical tear should always be suspected in women with profuse hemorrhage during and after third-stage labor, particularly if the uterus is firmly contracted. Extent of the injury can be fully appreciated only after adequate exposure and visual inspection of the cervix. o Visualization is best accomplished when an assistant applies firm downward pressure on the uterus while the operator exerts traction on the lips of the cervix with ring forceps. o A second assistant can provide even better exposure with right-angle vaginal wall retractors. MANAGEMENT Cervical lacerations of 1 and even 2 cm are not repaired unless they are bleeding. Suturing the cervix after bringing it into view at the vulva. o When the laceration is limited to the cervix, or even extends somewhat into the vaginal fornix o Because the hemorrhage usually comes from the upper angle of the wound, the first suture is placed proximal to the angle. o Suturing proceeds outward toward the operator.
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Associated vaginal lacerations may be tamponaded with gauze packs to retard hemorrhage while cervical lacerations are repaired. Either interrupted or running absorbable sutures are suitable. Overzealous suturing in an attempt to restore the normal cervical appearance may lead to subsequent stenosis during uterine involution. HEMATOMA PUERPERAL HEMATOMA Severe perineal pain and rapid appearance of a tender introital mass are the common presentations. Internal exams should be done before patient is wheeled out of the recovery room and before the patient is discharged Associated with laceration, episiotomy, or operative delivery. They may follow rupture of blood vessel without associated lacerations.
CLASSIFICATION Vulvar Hematomas o May involve the vestibular bulb or branches of pudendal artery (inferior rectal, perineal and clitoral arteries) o Severe perineal pain o Tense, fluctuant, and tender swelling of varying size rapidly develops o Discolored skin Paravaginal Hematomas o Involve the descending branch of uterine artery o Pelvic pressure, pain or inability to void o Round fluctuant mass encroaching on vaginal lumen Vulvovaginal Hematomas o Develop rapidly, may cause excruciating pain. This often is the first symptom noticed 2. o If bleeding stops, small to moderate-sized hematomas may be absorbed spontaneously. o The tissues overlying the hematoma may rupture as a result of pressure necrosis, and profuse hemorrhage may follow 2. Supralevator Hematomas o Can lead to hypovolemic shock and death o May extend upward in the paravaginal space and between the leaves of broad ligament DIAGNOSIS Ultrasound or CT Scan
PUERPERAL HEMATOMA: MANAGEMENT Observation Incision and drainage at point of maximal distension, evacuate blood and clots, ligation of bleeding points and suture obliteration of cavity; done in smaller vulvar hematomas2 Exploratory laparotomy if there is continued hemorrhage Blood transfusion especially with large puerperal hematomas Angiographic Embolization
DISSEMINATED INTRAVASCULAR COAGULATION (THROMBIN) PREDISPOSING FACTORS TO DIC Abruptio placenta – release of thromboplastin from retroplacental hematoma; most common cause of severe DIC in obstetrics Long dead fetus – thromboplastin released by the dead fetus and the placenta Infection – release of endotoxins from gram-negative bacteria and exotoxins from gram-positive bacteria. Amniotic fluid embolism – This causes activation of factor X by abundant mucin in fetal squames. Pre-eclampsia – Endothelial activation or injury is a hallmark of preeclampsia, eclampsia, and HELLP syndrome. In general, the clinical severity of preeclampsia is directly correlated with thrombocytopenia and fibrinogen-fibrin degradation product Page 13 of 15
PATHOGENESIS OF DIC Normal coagulation and fibrinolysis can be pathologically activated via two pathways. o Extrinsic pathway is active by thromboplastin from tissue destruction, o Intrinsic pathway is initiated by collagen and other tissue components that become exposed with loss of endothelial integrity Becomes clinically important when coagulation factors and platelets are sufficiently depleted to cause bleeding—hence, consumptive coagulopathy. DIAGNOSIS OF DIC Table 4. Algorithm for Diagnosis of Overt DIC – “DIC Score” FACTOR SCORE Presence of known underlying 0 = No disorder associated with DIC 2 = Yes Coagulation tests Platelets 0 = >100k 1 = 90 mmHg o UO = 30 ml/hour; if less than 30ml/hour, this may indicate that your intravascular fluid is in adequate and you might end up with renal failure. Normal mental status Eliminate source of bleeding ASAP Avoid overzealous volume replacement. May precipitate pulmonary edema. So monitor the input and output. Fluid Replacement2 o Treatment of serious hemorrhage demands prompt and adequate refilling of the intravascular compartment. o Crystalloid solutions typically are used for initial volume resuscitation. Such solutions rapidly equilibrate into the extravascular space and only 20 percent of crystalloid remains in the circulation of critically ill patients after 1 hour. o Because of such equilibration, initial fluid infusion should involve about three times as much crystalloid as the estimated blood loss. Blood Replacement o Red blood cells are not infused for moderate anemia in stable women.
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