case:

G1P0A0, GR 31 weeks + PLACENTA ABRUPTION

Counsellordr. Gioseffi Sp.OG

Prepared by

Christine Surbakti - 406147010Marcelly Raymando - 406147011

Melani Sugiarti Wijaya Kangmartono - 4060147014OBSTETRICS AND GYNECOLOGY CLERKSHIPTARUMANAGARA UNIVERSITYRSUD CIAWI, BOGORPeriod Desember 29th 2014 March 7th 2015Admitted to hospital on 9th February 2015Patients Identity Name

: Mrs.NH Age

: 24 years old Occupation : Housewife Education: Elementary school Race

: Sundanese Religion: Muslim Address : Kp.Sawah,Ciomas-Bogor Patients Husbands Identity Name

: Mr. I Age

: 32 years old Occupation: self-employed Education: Senior High School Race

: Sundanese Religion: Muslim Address: Kp.Sawah,Ciomas-Bogor

1. History TakingDirectly with the patient at 12.58 p.m. on February 9th 2015Main complaint: Vaginal bleeding Present Illness:

The patient came to the maternity ER with active vaginal bleeding since 12 p.m. The blood discharged was bright red. She mentioned that she had not felt the fetal movement since 7.00 a.m. She also was having uterine contractions, blurred vision, nausea and vomit. Her first day of the final menstruation was on 10th July 2014. Past Medical History: Hypertension (-) Diabetes mellitus (-) Heart Disease (-) Asthma (-) Seizures (-) Irregular menstrual cycle (-)Menstruation: Menarche

: 14 years old Menstrual cycle

: 28 days Duration

: 7 days Diaper/day

: 2-3 x/days Menstrual pain

: (-) Marriage: - Married: 1x, age 21th Contraception : noneOperation: none Antenatal Care: regular, monthly with midwife supplement: fe & folic acid (+)2. Physical ExaminationOn February 9th 2015, 12.58 pm Overall condition : moderately pain Awareness : full consciousness Vital Sign: - Blood pressure: 110/80 mmHg - Pulse: 120x/min - Respiratory rate: 25x/min

- Temperature: 36.7oc GENERAL EXAMINATION Head Eye: Anemic conjuctiva +/+, icteric sclera -/- Pupil diameter symmetrical, eyelid edema -/- Ear: tympany membrane intact +/+, earwax -/- Nose : septal deviation -/-, mucous discharge -/- Throat: T1-T1 normal, Faring hyperaemic (-) Mouth: oral hygiene (+), mucosa normal Neck: Trachea in the middle, normal lymph nodes and thyroid glandThorax Breast : normal , Inverted nipple -/- Lung : Inspection: Barrel chest(-), pectus excavatum(-), pectus carinatum(-) Palpation: tactile fremitus right=left Percussion: Resonance +/+ Auscultation: vesicular +/+, crackles -/-, wheezing -/- Heart : Inspection : Ictus cordis not visible Palpation : Ictus cordis is not palpable at ICS V MCLS

Percussion: Dull, heart margins within normal limits. Auscultation: Heart sounds I/II regular, gallop (-), murmur (-) Extremities: Oedema (-/-)

Obstetric Abdominal ExaminationInspection : striae gravidarum(+), scar (-), fetal movement (-)Palpation: Fetal parts were not palpable due to the presence of the severe abdominal pain (defans musculaire).Auscultation: FHR: absentExternal genitalia -Inspection: condition of vulva / vagina normal Bleeding (+) - In-speculo: Not done Internal Genitalia Not done Laboratory Test

Haematology

Hb

: 8,3 g/dl (12.0-15.0 g/dl) Ht

: 24% (36-46 %) Leucocyte : 29100 /ul (4000-10000/ul) Platelet count : 125000 /ul (150000-45000/ul) CT

: 1130 (6-11 minutes) BT

: 330 (1-6 minutes) Chemistry Screens

SGOT

: 32 SGPT

: 12 Ureum

: 25,5 Creatinin

: 1.27 Blood sugar

: 111

3. ResumeA 24 years old woman came to the maternity ER on 09th February 2015 because active vaginal bleeding since 12 p.m. The blood discharged was bright red. She mentioned that she had not felt the fetal movement since 7.00 a.m. She also was having uterine contractions, blurred vision, nausea and vomit. Her first day of the final menstruation was on 10th July 2014. Vital Sign: - Blood pressure: 110/80 mmHg

- Pulse : 120x/min - Respiratory rate : 25x/min

- Temperature : 36.7oc Eye : Ca +/+, SI -/-, light reflex +/+ Thorax: within normal limits Abdomen:Inspection : striae gravidarum(+), scar (-), fetal movement (-)Palpation : Leopold examination could not be done because the fetus was not palpable External genitalia Inspection : condition of vulva / vagina normal Bleeding (+) Speculum examination : not done Internal Genitalia : Not done Laboratory Test Decreased hemoglobin, hematocrite, thrombocytes Increased leucocytes

Working Diagnosis : G1P0A0, GA 31 weeks + placental abruption4. Management: Conservative treatment

IVFD RL 2000cc/ 24 hours, 20 dpm Oxygen 3-4 L Urine catheter

Observation of vital signs Kalnex 500 mg

Vit K

Gelofusin loading dose

Ceftriaxone 2gr in NaCl 100cc

SC Cito

16.00:the operation began

16.50: post op instructions:

- IVFD 2000cc/24 hrs- Ceftriaxone 1x2 gr IV

- Kaltrofen supp 3x1

- Check post op Hb

- Bed rest in supine position for 24 hrs

- Observe vital signs- Oxytocin 20 IU per 500 cc- Misoprostol 800 mg per rectal17.00: patient has been transfered to ICU23.22:Check Lab

Laboratory Test

Haematology

Hb

: 6,0 g/dl (12.0-15.0 g/dl) Ht

: 18% (36-46 %) Leucocyte

: 29200 /ul (4000-10000/ul) Platelet count

: 101000 /ul (150000-45000/ul) Chemistry Screens

Natrium

: 135 mEq/L Kalium

: 7.4 mEq/L Chlorida

: 107mg/dL Glucose tolerance test : 107 mg/dL01.00: get lasix 1Amp(IV)

02.00: get blood transfusion 3 bagsFollow Up ( 10th February 2015, at 07.00 am at ICU)S: abdominal painO: CM/moderate pain Vital Sign:BP

: 109/45 mmHg Pulse

: 78 x/mins RR : 22x/mins Temperature : 36.6oC General exam: Eye

: CA +/+ , SI -/-Thorax

: C/P within normal limitAbdomen: flat, supple, bowel sound +, fundal height: 2cm below umbilicus, uterine contraction: good,post operation wound covered verbanGen: v/v normal, bleeding(+)Extremities : Oedema (-/-)A: P1A0 mature parturition with SC for indication placental abruption(POD I)P: RL 2000 cc per 24 hrs

1 bag of blood

Ceftriaxone 1x2gr IV

Kaltrofen supp 3x1

Gradual mobilization

Feeding test07.45: infus RL 500cc + Oxytocin 1 Amp + Tramadol 1 Amp every 6 hrs

15.00: ceftriaxone

kaltrofen supp

PRC 250 cc

Follow Up ( 11th February 2015, at 07.00 am at ICU)S: pain in post operation wound

O: CM/moderate pain Vital Sign:BP

: 100/60 mmHg

Pulse

: 82 x/mins

RR

: 20x/mins

Temperature : 36.6oC General exam: Eye

: CA +/+ , SI -/-

Thorax : C/P within normal

Abdomen: flat, supple, bowel sound +, fundal height: 2cm below umbilicus, uterine contraction: good ,post operation wound covered verban

Gen

: v/v normal, bleeding(+)

Extremities: Oedema (-/-) A: P1A0 mature parturition with SC for indication placental abruption (POD II)P: RL 2000 cc per 24 hrs Cefriaxone 1 x 2gr

Asam Mefenamat 3x500 mg

Oxytocin

get blood transfusion 2 bags

Laboratory Test Haematology

Hb

: 6,9g/dl (12.0-15.0 g/dl) Ht

: 20% (36-46 %) Leucocyte : 25100 /ul (4000-10000/ul) Platelet count: 105000 /ul (150000-45000/ul) Ureum

: 84,7

Creatinin: 3,89

Follow Up ( 12th February 2015, at 07.00 am at Teratai A)S: no complaintO: CM/moderate pain Vital Sign: BP

: 110/60 mmHg Pulse

: 86 x/mins RR

: 20x/mins Temperature : 36.6oC General exam: Eye : CA -/- , SI -/- Thorax : C/P within normalAbdomen : flat, supple, bowel sound +, fundal height: 2cm below umbilicus, uterine contraction:good,post operation wound no blood,and pusGen

: v/v normal, bleeding(+) minimalExtremities: Oedema (-/-) A: P1A0 mature parturition with SC for indication placental abruption(POD III)P: Ceftriaxone 1x2 gr-12.00: Check Lab Laboratory Test Haematology

Hb

: 7,3g/dl (12.0-15.0 g/dl) Ht

: 20% (36-46 %) Leucocyte : 15500 /ul (4000-10000/ul) Platelet count: 120000 /ul (150000-45000/ul) Ureum

: 86,2

Creatinin: 2,34

Potasium: 1,29

Kalium

: 4,0

Chlorida: 106

GDS

: 76

-23.30

: patient has been transfered to Teratai A

Follow Up ( 13th February 2015, at 07.00 am at Teratai A)

S: no complaint

O: CM Vital Sign:BP

: 120/70 mmHg

Pulse

: 75 x/mins

RR

: 16x/mins

Temperature : 36.6oC General exam: Eye

: CA +/+ , SI -/-

Thorax: C/P within normal

Abdomen: flat, supple, bowel sound +, fundal height: 2cm below umbilicus , uterine contraction: good Gen

: v/v normal, bleeding(-)

Extremities: Oedema (-/-)

A: P1A0 mature parturition with SC for indication placental abruption(POD IV)

P: Cefadroxil 500 mg 2x1

Asam Mefenamat 500mg 3x1

SF 1x1

-19.30: get blood transfusion

Follow Up ( 14th February 2015, at 07.00 am at Teratai A)

S: no complaint

O: CM Vital Sign:BP

: 120/70 mmHg

Pulse

: 75 x/mins

RR

: 16x/mins

Temperature : 36.6oC General exam: Eye

: CA -/- , SI -/-

Thorax: C/P within normal

Abdomen: flat, supple, bowel sound +, fundal height: 2cm below umbilicus, uterine contraction: good Gen

: v/v normal, bleeding(-)

Extremities: Oedema (-/-)

A: P1A0 mature parturition with SC for indication placental abruption(POD V)

P: Cefadroxil 500 mg 2x1

Asam Mefenamat 500mg 3x1

SF 1x1

-09.00: Check Lab Laboratory Test Haematology

Hb

: 8,2g/dl (12.0-15.0 g/dl) Ht

: 23% (36-46 %) Leucocyte : 13300 /ul (4000-10000/ul) Platelet count: 200000 /ul (150000-45000/ul)5. Case analysis We agreed the patient has a severe placenta abruption because from sign and symptom that we found are same from references, there are :

- Vaginal bleeding

- Absence of fetal heart sounds

- Uterine tenderness

- Defans musculare

- Shock

- Trombositopenia

- Hypofibrinogenemia

We agreed the treatment in the case is caesarean delivery because in the references, the treatment of severe plancenta abruption is caesarean delivery.PLACENTAL ABRUPTIONPlacental abruption (or abruption placentae) is defined as the separation of the placenta from its site of implantation before delivery. Placental abruption complicates approximately 1 in 20 deliveries. As a significant cause of third-trimester bleeding associated with fetal and maternal morbidity and mortality, placental abruption must be considered whenever bleeding is encountered in the second half of pregnancy. Some of the bleeding of placental abruption usually insinuates itself between the membranes and uterus, and then escapes through the cervix, causing external hemorrhage. Less often, the blood does not escape externally but is retained between the detached placenta and the uterus, leading to concealed hemorrhage. Placental abruption may be total or partial. Placental abruption with concealed hemorrhage carries with it much greater maternal and fetal hazards, not only because of the possibility of consumptive coagulopathy, but also because the extent of the hemorrhage is not appreciated and the diagnosis typically is made later (Chang and co-workers, 2001).

1. Epidemiology

The frequency of abruptio placentae in the United States is approximately 1%, and a severe abruption leading to fetal death occurs in 0.12% of pregnancies (1:830).

Abruptio placentae also occurs in about 1% of all pregnancies throughout the world.

Race predilection

Placental abruption is more common in African American women than in white or Latin American women. However, whether this is the result of socioeconomic, genetic, or combined factors remains unclear.

Age predilection

An increased risk of placental abruption has been demonstrated in patients younger than 20 years and those older than 35 years

2. Etiology

The primary cause of placental abruption is usually unknown, but multiple risk factors have been identified. However, only a few events have been closely linked to this condition.

3. Risk factor

Risk factors in abruptio placentae include the following:

Maternal hypertension - Most common cause of abruption, occurring in approximately 44% of all cases

Maternal trauma (eg, motor vehicle collision [MVC], assaults, falls) - Causes 1.5-9.4% of all cases

Cigarette smoking

Alcohol consumption

Cocaine use

Short umbilical cord

Sudden decompression of the uterus (eg, premature rupture of membranes, delivery of first twin)

Retroplacental fibromyoma

Retroplacental bleeding from needle puncture (ie, postamniocentesis)

Idiopathic (probable abnormalities of uterine blood vessels and decidua)

Previous placental abruption

Chorioamnionitis

Prolonged rupture of membranes (24 h or longer)

Maternal age 35 years or older

Maternal age younger than 20 years

Male fetal sex

Low socioeconomic status

Elevated second trimester maternal serum alpha-fetoprotein (associated with up to a 10-fold increased risk of abruption)

Subchorionic hematoma

T. Boisram a,b,, N. Sanans b,c, G. Fritz b, E. Boudier b, G. Aissi a, R. Favre a, B. Langer . Placental abruption: risk factors, management and maternalfetal prognosis. Department of GynecologyObstetrics, Strasbourg University Hospitals, Centre Mdico-Chirurgical Obsttrique (CMCO), Strasbourg Cedex, France . 2014

4. Classification of placental abruptionClassification of placental abruption is based on extent of separation (ie, partial vs complete) and location of separation (ie, marginal vs central).

Clinical classification is as follows: Class 0 Asymptomatic Class 1 - Mild (represents approximately 48% of all cases) Class 2 - Moderate (represents approximately 27% of all cases) Class 3 - Severe (represents approximately 24% of all cases)

A diagnosis of class 0 is made retrospectively by finding an organized blood clot or a depressed area on a delivered placenta.Class 1 characteristics include the following:

No vaginal bleeding to mild vaginal bleeding Slightly tender uterus Normal maternal BP and heart rate No coagulopathy No fetal distress

Class 2 characteristics include the following:

No vaginal bleeding to moderate vaginal bleeding Moderate to severe uterine tenderness with possible tetanic contractions Maternal tachycardia with orthostatic changes in BP and heart rate Fetal distress Hypofibrinogenemia (ie, 50-250 mg/dL)

Class 3 characteristics include the following:

No vaginal bleeding to heavy vaginal bleeding Very painful tetanic uterus Maternal shock Hypofibrinogenemia (ie, < 150 mg/dL) Coagulopathy Fetal death5. PathologyPlacental abruption is initiated by hemorrhage into the decidua basalis. The decidua then splits, leaving a thin layer adherent to the myometrium. Consequently, the process in its earliest stages consists of the development of a decidual hematoma that leads to separation, compression, and the ultimate destruction of the placenta adjacent to it.

In its early stage, there may be no clinical symptoms. The condition is discovered only on examination of the freshly delivered organ, which has a circumscribed depression measuring a few centimeters in diameter on its maternal surface, and is covered by dark, clotted blood. Undoubtedly, it takes at least several minutes for these anatomical changes to materialize

Thus, a very recently separated placenta may appear no different from a normal placenta at delivery. According to Benirschke and Kaufmann (2000), and in our experiences, the "age" of the retroplacental clot cannot be determined exactly.

In some instances, a decidual spiral artery ruptures to cause a retroplacental hematoma, which as it expands disrupts more vessels to separate more placenta. The area of separation rapidly becomes more extensive and reaches the margin of the placenta. Because the uterus is still distended by the products of conception, it is unable to contract sufficiently to compress the torn vessels that supply the placental site. The escaping blood may dissect the membranes from the uterine wall and eventually appear externally or may be completely retained within the uterus.

CONCEALED HEMORRHAGE.

Retained or concealed hemorrhage is likely when:

1. There is an effusion of blood behind the placenta but its margins still remain adherent.

2.The placenta is completely separated yet the membranes retain their attachment to the uterine wall.

3.Blood gains access to the amnionic cavity after breaking through the membranes.

4. The fetal head is so closely applied to the lower uterine segment that the blood cannot make its way past it.

Most often, however, the membranes are gradually dissected off the uterine wall, and blood sooner or later escapes.

6.Clinical Presentation

Women presenting PA had metrorrhagia in 81.9%, uterine hypertonia in 26.1%, abdominal pains in 27.8% and abnormal fetal heart rate (aFHR) in 64.8% of cases. Overall, the classic clinical triad of metrorrhagia, uterine hypertonia and abdominalpelvic pain, was found in 24 women (9.7%). Among women who presented metrorrhagia in the second or third trimester, it was linked to PA in 13.1%: metrorrhagia was therefore the only clinical presenting sign in 60.5% of cases. Metrorrhagia plus aFHR was the most common association, found in 39.3% of PA cases.

T. Boisram a,b,, N. Sanans b,c, G. Fritz b, E. Boudier b, G. Aissi a, R. Favre a, B. Langer . Placental abruption: risk factors, management and maternalfetal prognosis. Department of GynecologyObstetrics, Strasbourg University Hospitals, Centre Mdico-Chirurgical Obsttrique (CMCO), Strasbourg Cedex, France . 2014

7. Diagnostic

PA diagnosis was made either on the basis of direct visualisation of a hematoma at the time of placental delivery or in a frank clinical setting (association of several clinical signs including: metrorrha- gia, abdominalpelvic pain, uterine hypertonia, non-reassuring fetal status, gestational hypertension, preterm premature rupture of membranes (PPROM), premature labor and IUFD). In some cases, PA was directly visualised on antenatal ultrasonography. Patho- logical examination was usually requested when PA was suspected.

8. Physical Examination

The physical examination of a patient who is bleeding must be targeted at determining the origin of the hemorrhage. Simultaneously, the patient must be stabilized quickly. With placental abruption, a relatively stable patient may rapidly progress to a state of hypovolemic shock.

Do not perform a digital examination on a pregnant patient with vaginal bleeding without first ascertaining the location of the placenta. Before a pelvic examination can be safely performed, an ultrasonographic examination should be performed to exclude placenta previa.[17] If placenta previa is present, a pelvic examination, either with a speculum or with bimanual examination, may initiate profuse bleeding.

a. Vaginal bleeding

Bleeding may be profuse and come in "waves" as the patient's uterus contracts. A fluid the color of port wine may be observed when the membranes are ruptured.b. Contractions/uterine tenderness

Uterine contractions are a common finding with placental abruption. Contractions progress as the abruption expands, and uterine hypertonus may be noted. Contractions are painful and palpable. Uterine hyperstimulation may occur with little or no break in uterine activity between contractionsc. ShockPatients may present with hypovolemic shock, with or without vaginal bleeding, because a concealed hemorrhage may be present. As with any hypovolemic condition, blood pressure drops as the pulse increases, urine output falls, and the patient progresses from an alert to an obtunded state as the condition worsens. d. Absence of fetal heart sounds

This occurs when the abruption progresses to the point of fetal deathe. Signs of possible fetal jeopardy

Signs of possible fetal jeopardy include the following:

Prolonged fetal bradycardia

Repetitive, late decelerations

Decreased short-term variability

f. High Fundal height

This may increase rapidly because of an expanding intrauterine hematoma.

9.Work Up

No laboratory studies have been shown to definitively help with the differential diagnosis of abruptio placentae; however, multiple laboratory studies may be helpful in the management of this problem. a. CBC Count

A complete blood cell (CBC) count can help to determine the patient's current hemodynamic status, but findings are not reliable for estimating acute blood loss. In an acute hemorrhage, the fall in hematocrit value lags several hours behind the bleeding and may be falsely decreased by the administration of crystalloid fluids during resuscitation.b. Fibrinogen examinationPregnancy is associated with hyperfibrinogenemia; therefore, modestly depressed fibrinogen levels may represent significant coagulopathy. A fibrinogen level of less than 200 mg/dL suggests that the patient has a severe abruption.

The goal should be to keep the fibrinogen level above 100 mg/dL, which can be accomplished via transfusion of fresh frozen plasma or cryoprecipitate, as necessary. c. Prothrombin Time/Activated Partial Thromboplastin Time

Some form of DIC is present in up to 20% of patients with severe abruptions. Because many of these patients require cesarean delivery, knowing a patient's coagulation status is imperative.

d. Blood Urea Nitrogen/Creatinine

The hypovolemic condition brought on by a significant abruption also affects renal function. The condition usually self-corrects without significant residual dysfunction, if fluid resuscitation is timely and adequate.

e. Ultrasonography

Ultrasonography is a readily available and important imaging modality for assessing bleeding in pregnancy. The quality and sensitivity of ultrasonography in detecting placental abruptions has improved significantly; however, it is not a sensitive modality for this purposefindings are positive in only 25% of cases confirmed at delivery, and the negative predictive value is low at around 50%.

In addition, there does not appear to be any clinical difference in presentation between women who have an abruption seen on ultrasonography and those who do not. Ultrasonographic studies do 1help to quickly diagnose placenta previa as the etiology of bleeding, if present.

Placental abruption shows as a retroplacental clot on an ultrasonographic image, but not all abruptions are ultrasonographically detectable. In the acute phase, a hemorrhage is generally hyperechoic, or even isoechoic, compared with the placenta; a hemorrhage does not become hypoechoic for nearly a week. Ultrasonography can help to exclude other causes of third-trimester bleeding. Possible findings consistent with an abruption include (1) retroplacental clot (ie, hyperechoic to isoechoic in the acute phase, changing to hypoechoic within a wk), (2) concealed hemorrhage, or (3) expanding hemorrhage. f. Nonstress Test

External fetal monitors often reveal fetal distress, as evidenced by late decelerations, fetal bradycardia, or decreased beat-to-beat variability. An increase in the uterine resting tone may also be noticed, along with frequent contractions that may progress to uterine hyperstimulation, as seen in the fetal tracing below.

h. Histologic Findings

After delivery of the placenta, a retroplacental clot may be noted. Another possible finding involves extravasation of blood into the myometrium, which produces a purple discoloration of the uterine serosa. This phenomenon is known as a Couvelaire uterus.

10.Differential Diagnoses

Ectopic Pregnancy Ovarian Cysts

Ovarian Torsion

Placenta Previa

Preeclampsia

Pregnancy Trauma11.Managament

In contrast to the more conservative trend that characterizes the management of placenta previa, management of abruptio placentae has for the most part become more aggressive. In the past, studies have noted the numerous deaths among viable fetuses alive at the time of admission and have urged more liberal use of cesarean section for the delivery of patients with placental abruption. However, some patients may be candidates for closely monitored ambulatory obstetric management. This includes patients who are in stable condition with a small resolving abruption, no increased uterine activity, and reassuring results of fetal surveillance.

In general, the longer the interval between diagnosis and delivery, the greater the risk for maternal complications and the poorer the outlook for fetal or neonatal salvage. If DIC occurs, its onset usually takes place within 8 hours of placental abruption. Pritchard and Brekken report that all patients in whom potentially serious hypofibrinogenemia develops have it develop within this time period.

The timing and method of delivery depend on maternal and fetal condition, gestational age, and cervical status. The premature fetus with a mild abruption and minimal bleeding may be managed expectantly with close observation, because this often is a self-limiting event. Tocolysis may be considered and has been used with caution in certain cases. It may be beneficial in the scenario of a stable mother and fetus without distress or complications, with positive sonographic signs of abruptio placentae, and who has only mild bleeding that is associated with uterine contractions. There is evidence that such pregnancies may be successfully prolonged (which would allow corticosteroid administration for fetal lung maturity enhancement) without increased jeopardy to the mother or fetus. Magnesium sulfate is the tocolytic agent of choice because betamimetic agents can have adverse hemodynamic effects on a bleeding patient by accentuating further signs of hypovolemia (hypotension and tachycardia). In the premature fetus with persistent, heavy vaginal bleeding, however, use of tocolytics would be contraindicated, and expeditious delivery is recommended. In general, any attempt at tocolysis should be weighed against the severity of abruption and likelihood of neonatal survival and morbidity.

An important aspect of the treatment is continuous, careful monitoring of mother and fetus for any signs or symptoms of deterioration. If the abruption is adversely affecting maternal or fetal condition, delivery should be performed. In cases of premature placental separation, cesarean delivery should be performed liberally for maternal or fetal reasons.

The route of delivery for patients with placental abruption and a viable fetus generally should be by rapid cesarean delivery unless vaginal delivery can be expected promptly. Many patients with placental abruption already have contractions; therefore, cesarean delivery may not be necessary. Abruption may even cause a rapid and tumultuous labor. A recent study suggests that in the absence of life-threatening hemorrhage, approximately 50% of patients with placental abruption but a normal fetal heart rate tracing could have vaginal delivery. In such cases, neonatal outcomes comparable with those obtained in infants born by cesarean delivery were reported. There is no specific time limit imposed on a trial of vaginal delivery as long as intensive maternal and fetal surveillance show no significant progression in abruption severity and labor is progressing satisfactorily. Oxytocin may be used to augment uterine contractions. Its use has been questioned and challenged in that it might enhance the escape of thromboplastin into the maternal circulation and therefore initiate or augment consumptive coagulopathy. However, there is no evidence to support this hypothesis. However, remember that the fetal condition may rapidly deteriorate. Patients may present with a live fetus, only to have that fetus die undelivered while awaiting vaginal delivery. In a recent study it was found that in cases of placental abruption, for those fetuses alive on admission, cesarean delivery was associated with a significant reduction (odds ratio: 0.10; 95% confidence interval: 0.050.20) in neonatal mortality. With an immature fetus or after intrauterine fetal death, attempts at vaginal delivery using oxytocin should be implemented if needed. However, a deteriorating clinical situation with increasing blood loss or a worsening coagulopathy may dictate operative intervention for maternal indications.

Management is most difficult and controversial in patients who have placental abruption and are admitted with clinical DIC. If bleeding is excessive, the condition must be promptly treated after evaluation of the previously mentioned hemostatic parameters. The most effective and definitive treatment is correction of the underlying process (i.e., the release of tissue thromboplastin into the circulation by the damaged placenta) by delivery of the placenta and fetus. If vaginal delivery is accomplished quickly without trauma, prompt restoration of the hemostatic mechanism usually results. Even in the most severe cases, clinically evident coagulopathy usually resolves by 12 hours after delivery. There is a decrease in the fibrin deposition products that interfere with thrombin action and platelet function and an increase in fibrinogen, factor V, and factor VIII. The platelet count returns to normal at a slower rate. This delay is caused by the time required for maturation and release of new platelets from the bone marrow. The expected order of normalization of the coagulation tests is PT followed by fibrinogen, FDP, and platelets. A clinical trial has found that the use of activated protein C intravenously in cases of placental abruption complicated by DIC resulted in rapid improvement of the DIC picture within 1 to 2 days. No adverse events related to the use of activated protein C were observed. Further study is needed to elucidate its value in DIC.

If a cesarean delivery is to be performed, the patient should be receiving fluids, oxygen, and replacement products. Coagulation factors should be given during the surgery. If given before surgery, they may provide little improvement at the time of surgery as a result of the ongoing DIC. Surgery should be performed quickly but in a meticulous manner. The surgeon should avoid unnecessary trauma to the tissues and should ligate or cauterize all bleeding points, even small bleeders that otherwise might be overlooked. The abdominal incision should be drained by a closed system. If vaginal delivery is expected, which in some cases, depending on maternal and fetal status, may be the preferred route, the obstetrician should attempt an amniotomy as soon as possible, because it may benefit labor and also allows the placement of internal monitoring if desired. If the fetus is immature, it may be best to leave the membranes intact. The intact sac may be a better dilatory wedge than a small fetal part that can be poorly applied to the cervix. After delivery, uterine blood loss can be decreased by quick infusion of oxytocin and appropriate uterine massage. The episiotomy, if needed, should be repaired meticulously and the cervix and vagina carefully examined for lacerations.

In a patient with extensive uterine involvement and uncontrollable blood loss, a hysterectomy may be indicated. A bruised Couvelaire uterus is by itself not a reason for hysterectomy. In this situation, there often is fear of uterine hemorrhage secondary to atony; however, this usually is not the rule. In most cases, the uterus will still be able to contract sufficiently, even in response to oxytocin, to prevent postpartum hemorrhage.

Treatment depends on the severity of the separation, location of the separation and the age of the pregnancy. There can be a partial separation or a complete (also called a total) separation that occurs. There can also be different degrees of each of these which will impact the type of treatment recommended.

In the case of a partial separation, bed rest and close monitoring may be prescribed if the pregnancy has not reached maturity. In some cases, transfusions and other emergency treatment may be needed as well.

In a case with a total or complete separation, delivery is often the safest course of action. If the fetus is stable, vaginal delivery may be an option. If the fetus is in distress or the mom is experiencing severe bleeding, then a cesarean delivery would be necessary.

Unfortunately, there is no treatment that can stop the placenta from detaching and there is no way to reattach it.

Any type of placental abruption can lead to premature birth and low birth weight. In cases where severe placental abruption occurs, approximately 15% will end in fetal death.12. Prognosis

If the bleeding continues, fetal and maternal distress may develop. Fetal and maternal death may occur if appropriate interventions are not undertaken. The severity of fetal distress correlates with the degree of placental separation. In near-complete or complete abruption, fetal death is inevitable unless an immediate cesarian delivery is performed.If an abruption occurs, the risk of perinatal mortality is reported as 119 per 1,000 people in the United States, but this can depend on the extent of the abruption and the gestational age of the fetus. This rate is higher in patients with a significant smoking history. Currently, placental abruption is responsible for approximately 6% of maternal deaths.The risk of recurrence of abruptio placentae is reportedly 4-12%. If the patient has abruptio placentae in 2 consecutive pregnancies, the risk of recurrence rises to 25%.If the abruption is severe and results in the death of the fetus, the risk of a recurrent abruption and fetal demise is 7%.REFERENCES

Clark SL. Placentae previa and abruptio placentae. In: Creasy RK, Resnik R, eds. Maternal Fetal Medicine. 5th ed. Philadelphia, Pa: WB Saunders; 2004:715 Cunningham GF, Gant NF, Leveno JK, Gilstrap LC, Hauth JC, Wenstrom KD. Williams Obstetrics, 23rd ed. New York: McGraw-Hill, 2010: 761-9. Lami Yeo, Cande V. Ananth and Anthony M. Vintzileos. Placental Abruption. Lippincott Williams & Wilkins.

Markhus VH, Rasmussen S, Lie SA, Irgens LM. Placental abruption and premature rupture of membranes. Acta Obstet Gynecol Scand. 2011;90:10249 Meguerdichian D. Complications in late pregnancy. Emerg Med Clin North Am. Nov 2012;30(4):919-36. Pariente G, Shoham-Vardi I, Kessous R, et al. Placental abruption as a significant risk factor for long-term cardiovascular mortality in a follow-up period of more than a decade. Paediatr Perinat Epidemiol. Jan 2014;28(1):32-8. Shad H Deering, MD Medical Director, Andersen Simulation Center, Madigan Army Medical Center . Abruptio Placentae. American College of Obstetricians and Gynecologists, Association of Professors of Gynecology and Obstetrics, and Society for Maternal-Fetal Medicine. 2014