Placental Abruption

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1 : Placental Abruption DR SAIMA HAMID Department of Obs & Gynae MH
2 : CASE HISTORY PATIENT’S PROFILE NAME: XYZ AGE: 35yrs SEX: F RESIDENCE: Rwp MF: 18yrs LMP: 9-7-11 EDD: 16-4-12 Blood grp: B+ DOA: 31-3-12
3 : PRESENTING COMPLAINTS Gestational Amenorrhea 37 wks Bleeding p/v since two hours HOPI Unplanned Spontaneous pregnancy Confirmed by UPT & USG No Folic acid Nausea, vomiting
4 : 2nd TRIMESTER Quickening at 5 months Anomaly scan not done
5 : 3RD TRIMESTER At 29 wks B.P was raised USG 29 wks ------- liquor was upper normal limit No fever, rash, pain, bleeding, urinary or bowel complaints
6 : OBSTETRIC HISTORY G10 P8 A1 L7 SVD (boy) at term-A/H SVD (boy) at term – A/H SVD(boy) at term-ENND home delivery SVD (girl) at term-A/H SVD(boy) at term-A/H 6.SVD(girl) at term-A/H SVD (Boy) at Term A/H SVD (Girl) at Term A/H (P.I.H) IUD – Hydrocephalous-TOP at 6 Months
7 : GYNAECOLOGICAL HISTORY Menarche 13 years Regular cycle 6/29 No contraception No pap smear PAST HISTORY P.I.H in her 8th pregnancy and IUD in 9th pregnancy FAMILY HISTORY Mother DM+HTN Grand mother
8 : PERSONAL HISTORY Non smoker Good nutritional status Practices clean bowel habits DRUG HISTORY Inj TT On tab aldomet 250mg T.D.S SOCIOECONOMIC STATUS Satisfactory
9 : EXAMINATION Vitals Pulse : 80/min Respiratory Rate : 18/min Temperature : 98°F Blood Pressure : 160/110 mmHg Ht : 5.2 Feet Wt : 80kgs
10 : GPE Pitting pedal Edema Cyanosis Pallor NAD Clubbing JVP ---- Not Raised No Lymphadenopathy Thyroid --- Not enlarged
11 : Systemic Examination ABDOMINAL SFH = 36 wks FHR = could not be assessed Abdomen tense VAGINAL EXAMINATION Multiparous os, cervix 2.5 cm, firm to medium consistency and posteriorly placed.
12 : Systemic Examination CVS No Murmurs CNS Conscious, oriented Respiratory Bil normal vesicular breathing
14 : BLOOD CP Hb 10.5 gm/dl Plt 164000 TLC 16 BLOOD SUGAR (R) 120 mg/dl URINE RE Albumin Present (+++) BLOOD GROUP B +
16 : USG BPD = 34wks Fetus – cephalic FCA- absent AFI = reduced Placenta upper segment retro-placental haemorrhage
18 : LSCS 31/3/12 0930 Hrs Indications: PRE ECLAMPSIA,PLACENTAL ABRUPTION Outcome,: Baby Girl Birth wt: 1.9 kg Placenta: more than One Ltr of Retro Placental Blood Clots
19 : Post OP Anti biotics Analgesia Transfusion of 2 Unit of RCC Fluids Monitoring vitals urine output intake output Discharged 1/4/12 Followup AFTER ONE WEEK
20 : Placental Abruption Definition The separation of the placenta from its site of implantation after 24 weeks of gestation or during the course of delivery. INCIDENCES 0.49%-1.8% after one episode 6-18% After two episodes 25%
21 : Etiology Uncertain (primary cause) Risk factors Increased age and parity Vascular diseases: preeclampsia, chronic hypertension, renal disease. Mechanical factors: trauma, intercourse, polyhydramnios, Chronic chorioamnionitis Smoking, cocaine use, uterine myoma Previous Abruption/ Family History Abruption Underlying Thrombophilias
22 : Pathology Main change hemorrhage into the decidua basalis ? decidua splits ? decidural hematoma ? separation, compression, destruction of the placenta adjacent to it Types revealed abruption, concealed abruption, mixed type
23 : Pathology
24 :
25 :
26 : Grades of placental abruption . 0 asmptomatic ,retroplacental clot seen after delivery . 1 vaginal bleedin,uterine tenderness,retroplacental clot after delivery. . 2 revealed bleeding may or may not be present,foetal compromise ,retroplacental clot after delivery. . 3 revealed bleeding may or may not be present,significant maternal signs,late stage fetal comromiseor fetal death.30%of these women will develop DIC.
27 : Diagnosis HISTORY AND EXAMINATION Life style Trauma Hypertension Family history of abruption Obstetrical history:c/s,pprom,prior placental abruption,multiparity,multifetal gestation,uterine fibroid,uterine malformation. Dead fetus
28 : Diagnosis SIGNS AND SYMPTOMS Abdominal pain . Uterine contractions . Abdominal tenderness . Vaginal Bleeding FETAL MONITORING LABORTORY TESTS CBC Coagulation Profile, LFTs/ RFTs Urine RE
29 : ULTRASONOGRAPHY USG is not a Good method of Diagnosis. It can be used to Confirm Fetal Viability Assess Fetal Growth Measure Liquor Volume Perform Umbilical Artery Doppler Exclude Placenta Praevia
30 : Complication MATERNAL RISKS DIC Hypovolemic shock PPH Acute renal failure FETAL RISKS Acute fetal hypoxia Fetal death
31 : Treatment Approach The treatment depends on the gestational age and on the condition of the mother and fetus. When there is fetal demise, the goal is to minimise morbidity to the mother In cases of a live fetus at term, prompt delivery is indicated. When there is evidence of fetal compromise, delivery by caesarean section is usually indicated. At gestations 34 weeks or less, conservative management may be attempted if both the mother and the fetus are stable.
32 : INITIAL MANAGEMENT Aim is to Stabilize the Patient Intravenous access with wide-bore cannulas. FBC for evidence of anaemia. Hct and Hb levels may be low. Coagulation profile looking for evidence of impaired coagulation. Low fibrinogen levels and a prolonged PT are suggestive of impaired coagulation due to DIC. Monitoring of the patient's haemodynamic status by monitoring BP, pulse, volume intake, and urine output. Continuous fetal monitoring. Anti-D immunoglobulin in Rh-negative women. Fluid, blood, or blood-product replacement, as indicated. Sonographic examination for placental location and for evidence of abruption. Placenta praevia found on sonography makes placental abruption unlikely.
33 : Live fetus: >34 weeks' gestation If the mother is in a stable condition and the fetal heart tracing is reassuring, then vaginal delivery can be attempted. If the maternal condition is worsening with severe haemorrhage, urgent caesarean delivery may be indicated (although rarely).
34 : Live fetus: =34 weeks' gestation In cases where the fetus and mother are both stable and there is no evidence of maternal coagulopathy, hypotension, or severe ongoing blood loss, conservative management with the aim of delivering a more mature fetus is the main goal of therapy In cases where the fetus or mother is not stable, delivery should take place promptly, with concurrent stabilisation of the fetus and mother. This is usually by caesarean unless delivery is imminent and can be achieved safely
35 : FETAL DEMISE The approach to management is similar to when the fetus is alive (i.e., expeditious delivery, preferably by the vaginal route). If the mother is not in active labour, she can be induced by amniotomy and oxytocin. Women who have had an abruption sufficient to cause fetal demise are highly likely to have DIC
36 : Thank You & GOD BLESS YOU


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