Proceedings of CME - EMERGENCY OBSTETRICS - SKILLS &DRILLS by Dept of Medical Informatics

PREFACE On behalf of department of Obstetrics & Gynaecology it gives us immense pleasure to bring out a booklet titled ‘Emergency Obstetrics – An update’ on the occasion of CME & workshop on ‘Obstetrics Emergencies- Skills & Drill’ on 12th and 13th October 2018. It is a well-known fact that pregnancy is a physiological process that brings happiness to a pregnant mother and everybody around her as well. Unfortunately this joyful event may turn into situation endangering the life of both mother and fetus, which is termed as obstetric emergencies. The most common emergencies are postpartum hemorrhage, fetal distress, severe pregnancy induced hypertension/ eclampsia, antepartum haemorrhage and shoulder dystocia. Other less prevalent but fatal conditions are amniotic fluid embolism, umbilical cord accident and uterine inversion. Although these emergencies occur infrequently, all the health care members need to remain vigilant always to diagnose these conditions and initiate the appropriate management, which will help to reduce maternal and perinatal mortality. Reduction of maternal and perinatal mortality is essential, as they are the key health care indicators of the society. This booklet is an effort not only to compile but also to reinforce and update the existing knowledge

Obstetric Emergencies. We express our gratitude to all the

contributors of this booklet. We hope this will be a useful source of information with recent advance for the practicing obstetrician, general physician, midwifery staff, postgraduate students in obstetrics &gynaecology and undergraduate students.

Organizing Team

CONTENTS Sl.

Title

Page No.

Cord accidents

Preterm labour / PPROM

Obstetric Coagulopathy

Eclampsia/ Hypertensive emergencies

Assessment of blood loss PPH

Uterine Inversion

Sepsis in Obstetrics and Gynaecology

Shoulder Dystocia

Non- obstetric causes of acute abdomen in pregnancy

Amniotic fluid Embolism

UMBILICAL CORD ACCIDENTS Dr Ashwini V, Prof Rani Reddi ABSTRACT Obstruction or disruption of blood flow through the umbilical vessels can lead to severe fetal compromise. Obstruction is usually mechanical in nature and is associated with compression of the umbilical cord and umbilical vessels. Disruption of umbilical or fetal vessels is usually traumatic in origin. These conditions have in common a loss of blood flow to the fetus and an association with adverse perinatal outcome. Key words: Cord accidents, cord prolapse. INTRODUCTION Umbilical cord accidents account for approximately 20% of all stillbirths worldwide. Cord accidents occur when there is diminished blood flow in the umbilical cord due to mechanical compression or circulatory compromise due to structural lesions like knots, loops, strictures, hematomas, cysts, thrombosis and vessel dilatation. The circulatory failure may be acute or chronic. Cord accidents can result in intrauterine growth restriction, intrauterine death of fetus, meconium staining of liquor, hydrops fetalis, and neurological deficits. Etiopathogenesis Umbilical cord development is different from that of the placenta. It develops from the primitive ridge of the embryo. It contains the 2 umbilical arteries and 1 umbilical vein covered by the whartonâ&#x20AC;&#x2122;s jelly and the amnion. The umbilical cord is 5060 cm in length on an average. It is usually the same length as the fetus. It grows throughout the pregnancy. There is coiling of the umbilical cord usually to the left side i.e. counterclockwise (7:1). The average coils are 0.2 coils per 1 cm of cord. The cord coiling is said to occur due to fetal activity. The cord inserts into the center of the placenta usually. Cord accidents can happen due to mechanical compression associated with abnormal length, abnormal coiling, knots, entanglements, constriction, prolapse, furcated insertion

and

velamentous

insertion.

Cord 4

disruption

can

occur

due

trauma,amniocentesis or fetal blood sampling which may lead to cord accidents. Cord disruption can also result from increased cord friability in conditions like meconium associated damage to cord, necrotizing funisitis, aneurysms, hemangiomas etc. Cord compression Abnormally long cords is defined as cord length more than 70-90 cm. Long cords can result from excessive fetal movements or because of genetic factors. Such cords are prone to entanglements and prolapse. Moreover excessively long cords require increased perfusion pressure because of greater resistance to flow. Short cords are seen in fetuses with reduced activity, uterine anomalies restricting the movements, amniotic bands and skeletal dysplasia. A cord less than 30 cm at term is short cord. Cord lengths of less than 15 cm have a strong association with fetal anomalies (abdominal wall defects, spinal and limb deformities). During labor cord rupture, premature separation of the cord from the placenta and abruption may lead to fetal hemorrhage and compromise. Cord entanglements around the body of the fetus can result in nuchal cord. They can be locked type or unlocked type. The locked type is associated with higher morbidity. They can cause cord compression when the entanglements become tighter during the fetal descent in labour after membrane rupture. There is a significant correlation between presence of tight nuchal cord at delivery and cerebral palsy. The neonates also have a low APGAR score and an increased frequency of stillbirths. True knots may be loose or tight. Loose knots may tighten during fetal movement or during descent during delivery. The incidence is 0.4-1.2%. The incidence is increased in polyhydramnios and in excessively long cords. It is also a frequent complication of monochorionic monoamniotic twin pregnancies. Cord coiling when excessive causes obstruction of blood flow by either mechanical compression or thrombosis. Also hypercoiling is associated with excessively long cords. Lack of coiling indicates fetal inactivity and is associated with fetal distress, anomalies, increased perinatal morbidity and mortality. Cord prolapse is defined as the decent of the umbilical cord through the cervix alongside (occult) or past (overt) the presenting part in the presence of ruptured 5

membranes. Cord presentation is presence of the umbilical cord between the fetal presenting part and the cervix with or without intact membranes. Incidence varies from 0.1 -0.6%. The incidence is higher in malpresentations. There is also a higher incidence in multiparity, low birth weight, preterm labour, fetal congenital anomalies, second twin, polyhydramnios, unengaged presenting part, low lying placenta, artificial rupture of membranes with high presenting part, external cephalic version, stabilizing induction in labour, insertion of intrauterine pressure transducer and large balloon catheter induction of labour. Cord prolapsed should be suspected in cases of bradycardia and variable fetal heart decelerations. The distress is due to direct compression of the vessels or due to reactive vasoconstriction caused by exposure of the cord to cold air. Velamentous insertion of the cord occurs when the cord inserts into the membranes near the placenta instead of over the placental surface. The velamentous vessels from the cord run in the membranes between the placenta and the membranous cord insertion. As there is no protection provided by the Whartonâ&#x20AC;&#x2122;s jelly these vessels are prone to compression, rupture, thrombosis and disruption particularly after membrane rupture. In furcate cord insertion the vessels separate from the cord substance before reaching the surface of the placenta. Since there is no Whartonâ&#x20AC;&#x2122;s jelly they are more prone to injury and thrombosis. When the velamentous vessels cross the cervical os it is termed as vasa previa. Severe fetal compromise can occur when the vessels are injured. It may also result in intrauterine death. Thrombosis of the velamentous vessels has been associated with neonatal thrombocytopenia, purpura and fetal death. Cord disruption Meconium present for a prolonged period can damage the umbilical cord and fetal vessels and result in disruption of the cord. This is because it contains noxious materials like bile salts, acids, enzymes and other chemical substances. The cord can also become ulcerated in rare cases. Meconium in the amniotic fluid also causes vasoconstriction of the umbilical vessels. Stricture of the umbilical cord is seen in the insertion at the fetal side. The Whartonâ&#x20AC;&#x2122;s jelly is usually absent and there is stricture of the vessels at the insertion site.

Cord hematomas can result from trauma, short cord, entanglement, amniocentesis and cordocentesis. Management Ultrasound with Doppler can be useful in detecting patients at risk for cord accidents. Antenatal ultrasonogram can be used to diagnose hypercoiling, hypocoiling, nuchal cords, velamentous insertion, vasa previa, cord presentation and sometimes true knots and entanglements. Routine ultrasound examination is not sufficiently sensitive or specific for identification of cord presentation antenatally and should not be performed to predict increased probability of cord prolapse. Selective ultrasound screening can be considered for women with breech presentation at term who are considering vaginal birth. With transverse, oblique or unstable lie, elective admission to hospital after 37+0 weeks of gestation should be discussed and women in the community should be advised to present urgently if there are signs of labour or suspicion of membrane rupture. Women with non-cephalic presentations and preterm prelabour rupture of membranes should be recommended inpatient care. Artificial membrane rupture should be avoided whenever possible if the presenting part is mobile and/or high. If it becomes necessary to rupture the membranes with a high presenting part, this should be performed with arrangements in place for immediate caesarean section. Upward pressure on the presenting part should be kept to a minimum in women during vaginal examination and other obstetric interventions in the context of ruptured membranes because of the risk of upward displacement of the presenting part and cord prolapse. Rupture of membranes should be avoided if on vaginal examination the cord is felt below the presenting part. When cord presentation is diagnosed in established labour, caesarean section is usually indicated. Cord presentation or prolapse should be excluded at every vaginal examination in labour and after spontaneous rupture of membranes if risk factors are present. In addition to the national guidance for fetal heart rate monitoring in labour, the fetal heart rate should be auscultated after every vaginal examination in labour and after spontaneous membrane rupture.

Cord prolapse should be suspected when there is an abnormal fetal heart rate pattern, especially if such changes commence soon after membrane rupture, either spontaneous or artificial. Speculum and/or digital vaginal examination should be performed when cord prolapse is suspected. When spontaneous rupture of membranes occurs, if there is normal fetal heart rate monitoring and there are no risk factors for cord prolapse, then a routine vaginal examination is not indicated. When cord prolapse is diagnosed before full dilatation, assistance should be immediately called and preparations made for immediate birth in theatre. There are insufficient data to evaluate manual replacement of the prolapsed cord above the presenting part to allow continuation of labor. This practice is not recommended. To prevent vasospasm, there should be minimal handling of loops of cord lying outside the vagina. To prevent cord compression, it is recommended that the presenting part be elevated either manually or by filling the urinary bladder. Cord compression can be further reduced by the mother adopting the kneeâ&#x20AC;&#x201C;chest or left lateral (preferably with head down and pillow under the left hip) position. Tocolysis can be considered while preparing for caesarean section if there are persistent fetal heart rate abnormalities after attempts to prevent compression mechanically, particularly when birth is likely to be delayed. During emergency ambulance transfer, the kneeâ&#x20AC;&#x201C;chest position is potentially unsafe and the exaggerated Sims position (left lateral with pillow under hip) should be used. Although the measures described above are potentially useful during preparation for birth, they must not result in unnecessary delay. Caesarean section is the recommended mode of delivery in cases of cord prolapse when vaginal birth is not imminent in order to prevent hypoxic acidosis. A category 1 caesarean section should be performed with the aim of achieving birth within 30 minutes or less if the cord prolapse is associated with a suspicious or pathological fetal heart rate pattern but without compromising maternal safety. Category 2 caesarean birth can be considered for women in whom the fetal heart rate pattern is normal, but continuous assessment of the fetal heart trace is essential. If the 8

cardiotocograph (CTG) becomes abnormal, re-categorisation to category 1 birth should immediately be considered. Discussion with the anaesthetist should take place to decide on the appropriate form of anaesthesia. Regional anaesthesia can be considered in consultation with an experienced anaesthetist. Verbal consent is satisfactory for category 1 caesarean section. Vaginal birth, in most cases operative, can be attempted at full dilatation if it is anticipated that birth would be accomplished quickly and safely, using standard techniques and taking care to avoid impingement of the cord when possible. Breech extraction is appropriate under some circumstances, for example, after internal podalic version for a second twin. A practitioner competent in the resuscitation of the newborn should attend all births that follow cord prolapse. Paired cord blood samples should be taken for pH and base excess measurement. Expectant management should be discussed for cord prolapse complicating pregnancies with a gestational age at the threshold of viability (23+0 to 24+6 weeks). Clinicians should be aware that there is no evidence to support replacement of the cord into the uterus when prolapse occurs at or before the threshold of viability. Women should be counselled on both continuation and termination of pregnancy following cord prolapse at the threshold of viability. REFERENCES 1.

Rebecca N Baergen. Cord abnormalities, structural lesions and cord accidents. Seminars in diagnostic pathology 2007;24:23-32

Umbilical cord prolapsed. Greentop guideline -50

Jason H.Collins. Umbilical cord accidents. BMC Pregnancy and Childbirth 2012;12(Suppl 1):A7

J.C.Carey, W.F. Rayburn. Nuchal cord encirclements and risk of stillbirth. International Journal of Gynecology & Obstetrics 69 (2000):173-174

Jason H.Collins. Umbilical Cord Accidents: Human Studies. Seminars in Perinatology, Vol 26, No 1 (February), 2002: pp 79-82

PRETERM LABOUR AND PPROM Dr Divya Alamelu, Prof S Habeebullah ABSTRACT Globally preterm labour is the leading cause of perinatal morbidity and mortality. It constitutes around 5-18% of all deliveries. It is characterized by onset of uterine contractions and cervical effacement and dilatation after 20 weeks and before 37 weeks of gestation. The etiology is multifactorial, influenced by infections, obstetric, demographic, dietary and psychosocial risk factors. Women with previous preterm birth are at significantly increased risk of subsequent preterm delivery. Strategies for reducing the incidence of preterm labour are focused on predicting and preventing preterm labour and early diagnosis and timely management. Methods for predicting preterm labour include fetal fibronectin, transvaginal ultrasound determination of cervical length and home uterine activity monitoring. Management of preterm labour is mainly based on the gestational age and involves antenatal corticosteroids for fetal lung maturity, tocolysis to delay delivery to facilitate in utero transfer to tertiary center and also gives time for steroids and Magnesium sulphate to act. Additionally Magnesium sulphate is given for fetal neuroprotection and antibiotics to prevent neonatal infection with Group B Streptococcus (GBS). Keywords: Preterm labour, perinatal morbidity, fibronectin, corticosteroids, tocolytics INTRODUCTION Across 184 countries, the rate of preterm birth is about 5-18%. According to WHO, globally every year about 15 million babies are born prematurely. In India, out of 27 million babies born every year, 3.5 million are preterm (2010). Almost 1 million babies die every year due to complications of preterm birth.This trend is increasing year by year. DEFINITION Preterm labour is defined as onset of labour after 20 weeks but before 37 completed weeks of gestation. Preterm labour is considered to be established ifď&#x201A;&#x2014; Uterine contractions - 4 in 20 minutes/ 8 in 60 minutes

 Cervical dilatation >1 cm  Cervical effacement >80% It may be  Late preterm - 34-36 completed weeks  Early preterm - <34 weeks Threatened preterm labour (TPL) may be diagnosed when there are documented uterine contractions but no evidence of cervical changes. Prematurity is the incomplete development of various organs at birth. It is classified according to gestational age at birth: -Near term 34-36 weeks (60-70%) -Moderate prematurity 32-33 weeks -Severe prematurity 28-31 weeks (15%) -Extreme prematurity < 28 weeks (5%) Preterm Prelabour Rupture of Membranes (PPROM) is the spontaneous rupture of the fetal membranes after 20 weeks and before 37 completed weeks before the onset of labour. RISK FACTORS OBSTETRIC RISK FACTORS:  H/O previous PTL or second trimester loss Second Birth ≤34 Weeks

Birth Outcome First birth > 35 weeks

First birth ≤34 weeks

16%

First and second birth ≤34 weeks

41%

 Prior induced/spontaneous abortion, repeated evacuation  Threatened abortion  Over distended uterus : multiple pregnancy, hydramnios 11

 APH  Medical and obstetric indication for preterm termination of pregnancy  Medical disorders- anaemia, cardiac disease, renal disease  Inter-pregnancy interval <18 months DEMOGRAPHIC FACTORS:  Age <17yrs/ >35yrs  Low socioeconomic status  Multiple sexual partners  Poor maternal weight gain  Low BMI  Overweight and obesity PSYCHOSOCIAL FACTORS:  Anxiety  Stress  Depression  Negative life events  Domestic violence  Work related stress >42hrs/wk or >6hrs/day DIETARY FACTORS:  Deficiency of iron, zinc and vitamin C  Smoking & Alcohol consumption  Illicit drug abuse CERVICAL INSUFFICIENCY:  Congenital  DES exposure in utero  Mullerian anomalies- Uterine didelphys, bicornuate and unicornuate uterus  Connective tissue disorders  Trauma- cervical tear in previous pregnancy  Cervical conisation, LEEP

 Cervical amputation  Delivery through an incompetently dilated cervix INFECTIONS (50%):  Bacterial vaginosis  Trichomonas vaginalis infection  Gonorrhoea and syphilis  Asymptomatic bacteriuria  Periodontal disease PATHOGENESIS OF PRETERM LABOUR & PPROM Chorio-decidual bleeding Thrombin Maternal/Fetal stress

Abnormal placentation

CRH

Prostaglandins

PTL Infection IL-6

& PPROM

Uterine overdistention Activation of protein kinase C

DIAGNOSIS SYMPTOMS: 

Painful or painless uterine contractions



Menstrual-like cramps



Low back ache



Pelvic pressure



Watery vaginal discharge



PPROM- Vaginal leakage of fluid either as gush or continuous stream

SIGNS: 

Regular uterine contractions with cervical dilatation and effacement 13



In PPROM- Per speculum examination- Pooling of amniotic fluid in vagina on coughing/Valsalva maneuver.

INVESTIGATIONS 

Complete blood count



Urine for routine analysis, culture and sensitivity



Cervico vaginal swab for culture and fibronectin



Ultrasonography for fetal well being and weight, cervical length and placental localization, amniotic fluid volume.



Serum electrolytes and glucose levels when tocolytic agents are to be used



For confirmation of PPROMo Nitrazine paper test o Demonstration of ferning pattern o Dye instillation tests o Nile blue sulphate tests o Immunochromatographic method (Amnisure) to detect trace amounts of placental microglobulin-1 (PAMG-1)

PREDICTION OF PRETERM LABOUR 1) Fetal fibronectin (fFN)-It is an extracellular glycoprotein secreted by the chorionic tissue at maternal-fetal interface.It acts as biological glue which binds blastocyst to endometrium. It is normally present in cervicovaginal secretions up to 20-22 wks. Around 22 wks chorion fuses completely with underlying decidua. Therefore presence of fFN between 24 to 34 wks can provide important marker of preterm labor. Swabs are taken from ectocervix or posterior vaginal fornix. A cut-off of 50ng/ml is considered positive. Presence of fibronectin indicates increased risk of preterm labor within 7 days. However ACOG (2012) does not recommend routine screening with fetal fibronectin. 2) Ultrasound measurement of cervical length-Risk of PTL is inversely proportional to the cervical length at 24 weeks. Three measurements are taken 5 minutes apart with transvaginal probe and the lowest of the three is recorded. Normal cervical length is 2.5 to 4cm. Cut off of <2.5cm at 24 weeks is a strong predictor of PTL. 14

3) Home uterine activity monitoring (HUAM)- External tocodynamometer is belted around abdomen and connected to electronic waist recorder. Results are transmitted via phone daily to the doctor. Increase in frequency of uterine activity is noted as early as 1week before onset of PTL. Ambulatory home uterine activity monitoring was introduced to identify it. Normal Baseline tone is 0 mmHg. Contraction ≥35sec or amplitude >5mmHg is considered significant. 

Until 30 wks, contraction one/hr (Primi), two/hr(Multi) – Normal



Beyond 30 wks, two/hr – Normal



>4-6 contractions/hr is predictive of PTL

PREVENTION 

Diagnosis and treatment of infections like asymptomatic bacteriuria, bacterial vaginosis and trichomonas vaginalis.



Periodontal care



Cervical cerclage



Progesterone therapy



Cessation of smoking, alcohol, drugs



Increasing inter-pregnancy interval



Nutritional supplementation According to NICE guidelines (2015), prophylactic vaginal progesterone is

offered to asymptomatic women with previous PTL and asymptomatic women with a short cervix (<25mm). CERCLAGE 1) History indicated cerclage/elective/primary/prophylactic cerclage- It is performed electively at 12-14 weeks of gestation to asymptomatic women with otherwise unexplained three or more previous preterm births and/or second trimester losses. 2) Ultrasound indicated cerclage/therapeutic/secondary cerclage-It is performed in women with history of one or more spontaneous mid-trimester losses or

preterm births with cervical length≤ 25mm diagnosed on transvaginal USG before 24 weeks of gestation. 3) Rescue cerclage- Here cerclage is done as a salvage measure in the case of premature cervical dilation with bulging fetal membranes in the vagina.

History indicated

•12-14 weeks •asymptomatic with previous ≥3 PTL/♊ trimester loss

Ultrasound indicated

Rescue

•<24 weeks •asymptomatic with previous ≥1PTL/♊ trimester loss with cervical length ≤25mm

•emergency •cervical dilation with bulging membranes in vagina

GOALS OF TREATMENT IN PRETERM LABOUR 1) Antenatal corticosteroids for fetal lung maturity 2) Tocolysis to delay delivery to facilitate in-utero transfer to tertiary centre (Level-I center) and also gives time for steroids and Magnesium sulphate to act 3) Magnesium sulphate for fetal neuroprotection to reduce incidence of cerebral palsy. 4) Antibiotics to prevent neonatal infection with Group B Streptococcus(GBS)

Tocolytics

PTL MgSO4

Steriods

& PPROM

Antibiotics

CORTICOSTEROIDSDrug

No. of doses

Dosage

Interval

Betamethasone

12mg IM (6mg each of betamethasone acetate and phosphate)

24 hours apart

Dexamethasone

6mg IM

12 hours apart

Corticosteroids promote surfactant synthesis, increase lung compliance and reduce vascular permeability. They reduce the incidence of RDS, IVH, NEC, PDA and neonatal death. ACOG recommendations are

A single course of corticosteroids is recommended for 24 to 33 6/7 weeks of gestation, including for those with multiple gestation and ruptured membranes.



Administration of betamethasone is recommended for 34 to 36 6/7 weeks of gestation at risk of preterm birth within 7 days, and who have not received a previous course of steroids.



A single repeat course of steroids should be considered in <34 weeks who have an imminent risk of preterm delivery within next 7 days, whose prior course of corticosteroid was administered more than 14 days previously. 17

TOCOLYTICS Drug

Class

Mechanism of action

Nifedipine

Calcium channel

â&#x2020;&#x201C;intramuscular free Calcium resulting in

blocker

vascular& smooth muscle relaxation

Indomethacin

COX-2 inhibitor

â&#x2020;&#x201C;Prostaglandin production

Ritodrine

Beta-2 adrenergic

Inactivates MLCK activity

agonist Terbutaline

Beta-2 adrenergic

Inactivates MLCK activity

agonist Atosiban

Oxytocin receptor Competes with oxytocin for binding to antagonist

receptors in myometrium and decidua

Magnesium sulphate

Competitive inhibitor of Ca and inhibits MLCK activity

Sulindac

COX-2 Inhibitor

Nitroglycerine

Nitric Oxide

Smooth muscle relaxation

donor

DRUG

REGIMEN

MATERNAL SIDE EFFECTS

FETAL SIDE EFFECTS

CONTRAINDIC ATIONS

Nifedipine

30 mg followed by 10-20 mg 68 hrs oral

Dizziness, flushing, headache, hypotension, suppression of cardiac contractility

Non reassuring FHR due to maternal hypotension

Hypotension, CCF, aortic stenosis

Indomethacin

Loading50-100mg followed by 25-50mg every 4-6hrs oral

Nausea, oesophageal reflux, gastritis, emesis, platelet dysfunction

Closure of ductus arteriosus, oligohydramni os if used >48hrs

Platelet dysfunction, bleeding disorder, hepatic or renal dysfunction, peptic ulcer

Ritodrine

Infusion @ 50µg/min, increase every 20 min to max of 350µg/min

Tachycardia, hypotension, tremor, dyspnea, chest pain, pulmonary oedema, myocardial ischaemia, arrhythmia,

Tachycardia

Poorly controlled DM, cardiac disease, hyperthyroidism

hypokalaemia, hyperglycaemia Terbutaline

s.c-250µg every 20-30 min 6-8 doses i.v-510µg/min, increase every 10-15 min to max 80µg/min

Tachycardia,hypo tension, tremor, dyspnoea, chest pain, pulmonary oedema, hypokalaemia, hyperglycaemia myocardial ischaemia, arrhythmia

Tachycardia

Poorly controlled DM, cardiac disease, hyperthyroidism

Atosiban

6.75mg i.v bolus followed by infusion @18mg/hr for 3 hrs and then 6mg/hr for upto 45 hrs.

Hypersensitivity, nausea, vomiting, chest pain, dyspnoea

Minimal

Hepatic and renal disorder

Magnesium sulphate

4g i.v bolus followed by 2g/hr

Flushing, diaphoresis, nausea, loss of deep Tendon reflexes, respiratory paralysis, cardiac arrest

Non reassuring FHR, decreased breathing movements, bone thinning & fracture (used >5 to 7 days)

Myasthenia gravis, heart block, renal disease, recent MI

Sulindac

200mg oral once or twice daily

Headache, dizziness, nervousness, epigastric pain, vomiting, diarrhoea

Closure of ductus arteriosus

Asthma, peptic ulcer disease

Nitroglycerine

Transdermal patch 0.4mg/hr

Dizziness, flushing, hypotension

Nil

Hypotension, aortic stenosis

Contraindications for tocolysis  Intrauterine fetal demise  Lethal fetal anomaly  Non-reassuring fetal status  Severe preeclampsia or eclampsia  Maternal bleeding with haemodynamic instability  Chorioamnionitis  PPROM  Advanced cervical dilatation Magnesium sulphate for neuroprotection It is most effective between 24 and 32 weeks. It is given at a dose of 6g IV loading dose over 20-30 minutes followed by 2g/hour infusion. Therapy is discontinued 24 hours after initiation if delivery has not occurred. Dose can be repeated if patient returns with preterm labour. It reduces the risk of cerebral palsy. ANTIBIOTICS In advanced preterm labour antibiotics are started to prevent neonatal GBS infection. Antibiotic of choice is Pencillin 5mU IV as initial dose followed by 2.5mU every 4 hrs until delivery. Alternatively Ampicillin 2g IV initial dose followed by 1g IV every 4 hrs or 2g every 6 hrs until delivery. For those who are allergic to penicillin, Clindamycin 900mg IV every 8 hrs until delivery is given. In case of PPROM, Society of Obstetrics & Gynecologists of Canada guidelines recommends 

Following PPROM ≤32 weeks – antibiotics should be administered to women who are not in labour to prolong pregnancy and to decrease maternal and neonatal morbidity.



For women with PPROM at > 32 weeks gestation, administration of antibiotics is recommended for 48 hours, if fetal lung maturity cannot be proven and/or delivery is not planned.

ď&#x201A;ˇ

Ampicillin 2g IV every 6 hours and Erythromycin 250mg IV every 6 hours for 48hours followed by Amoxicillin 250mg orally every 8 hrs and Erythromycin 333mg orally every 8 hours for 5 days.

ď&#x201A;ˇ

Erythromycin 250mg orally every 6 hours for 10 days can be given alternatively. Amoxicillin/clavulanic acid should not be used because of increased risk of NEC

in neonates exposed to this antibiotic. Amoxicillin without Clavulanic acid is safe. MANAGEMENT OF PPROM

>34 weeks

Termination of pregnancy by induction of labour

Intrapartum GBS prophylaxis

32-34 weeks

Intrapartum GBS prophylaxis

Fetal lung maturity not attained

Fetal lung maturity established

Corticosteroids

Termination of pregnancy

Termination of pregnancy after 24-48 hrs after steroids

<24 weeks

24-31 weeks

Patient counselling Corticosteroids GBS prophylaxis Tocolysis if required Expectant management/ Induction of labour

Corticosteroids, GBS prophylaxis not recommended.

Expectant Management

EXPECTANT MANAGEMENT 

Rest in bed is advised as long as there is escape of liquor with restriction of efforts later on



Temperature is recorded every 4 hours



Maternal pulse rate and fetal heart rates are checked



Observation for fever, malaise, abdominal pain, tachycardia, uterine tenderness and amount of escaped liquor on sterile vulval pads



TLC and CRP done every other day



Corticosteroid therapy



Antibiotic therapy



Monitoring of fetal growth by USG every 4 weeks



Intracervical instillation of fibrin glue, Intra-amniotic instillation of gelatin sponge / maternal platelets/cryoprecipitate and Endoscopic placement of collagen

graft over the fetal membrane defect have all been tried to seal a rent after spontaneous rupture of membranes, but the safety and efficacy of these procedures so far remain unproven. INTRAPARTUM MANAGEMENT  Fetal hypoxia and acidosis may increase the risk of IVH. Therefore, the preterm fetus should be monitored closely for signs of hypoxia during labor, preferably by continuous electronic fetal monitoring. Presence of fetal tachycardia may be an indicator of sepsis or acidaemia.  Episiotomy was traditionally thought to offer cranial protection to fragile preterm head, but there is little evidence to support this view. Similarly, prophylactic forceps to prevent ICH is unproven, and ventouse is contraindicated in preterm deliveries. The role of caesarean section to reduce ICH in a preterm infant is also not substantiated.  Delivery must be attended by an experienced neonatologist capable of dealing with complications of prematurity. CARE OF PRETERM NEONATE  The cord is to be clamped quickly. The cord length is kept long.  The air passage should be cleared of mucus promptly and gently.  Adequate oxygenation.  Maintenance of temperature to prevent hypothermia.  Timing of clamping the cord  Inj. Vitamin K 1mg IM

COMPLICATIONS OF PRETERM NEONATES Organ/system

Short-term problems

Long-term problems

Pulmonary

RDS, air leak, bronchopulmonary dysplasia, apnea of prematurity

Bronchopulmonary dysplasia, reactive airway disease, asthma

GIT

Hyperbilirubinaemia, feeding intolerance, NEC, growth failure

Failure to thrive, short bowel syndrome, cholestasis

Immunological

Hospital acquired infections, immune deficiency, perinatal infection

RSV infection, bronchiolitis

CNS

IVH, periventricular leucomalacia, hydrocephalus

CP, hydrocephalus, cerebral atrophy, neurodevelopmental delay, hearing loss

Ophthalmological

Retinopathy of prematurity

Blindness, retinal detachment, myopia, strabismus

Cvs

Hypotension, PDA, pulmonary hypertension

Pulmonary hypertension, hypertension in adults

Renal

Water & electrolyte imbalance, acid-base disturbance

Hypertension in adults

Haematological

Iatrogenic anaemia, need for frequent transfusions, anaemia of prematurity

Endocrinological

Hypoglycaemia, transiently low thyroxine levels, cortisol deficiency

Impaired glucose regulation, increased insulin resistance

CONCLUSION Preterm labour is the leading cause of perinatal mortality and morbidity. In order to reduce the rates of preterm labour, as obstetricians it is our duty not only to diagnose it as early as possible, but also to predict and prevent it antenatally.

REFERENCES 1.

WHO

2018,

Fact

Sheet-

Preterm

labour.

Retrieved

from

www.who.int/news-room/fact-

sheets/detail/pretrem-birth 2.

Liu L, Oza S, Hogan D, Chu Y, Perin J, Zhu J, et al. Global, regional, and national causes of under-5 mortality in 2000-15: an updated systematic analysis with implications for the Sustainable Development Goals. Lancet. 2016;388(10063):3027-35

Rastogi A. Preterm birth [Internet]2016.Available from: https://www.nhp.gov.in/disease/reproductivesystem/female-gynaecological-diseases-/preterm-birth

American College of Obstetricians and Gynecologists. Preterm labor. Technical Bulletin no-206. Washington DC: ACOG, 1995.

Cunningham GF, Gant NF, Lenevo KJ. Preterm birth. In Williams obstetrics.24th ed. McGraw Hill publication.USA. 2014. Chapter 42, Preterm labor; p.829-61.

Bloom SL, Yost NP, McIntire DD, et al: Recurrence of preterm birth in singleton and twin pregnancies. Obstet Gynecol 98:379,2001.

Arias F, Daftary NS, Bhide GA. Practical guide to high-risk pregnancy and delivery. 3rd ed. India: Elsevier; 2008.

American College of Obstetricians and Gynecologists: Prediction and prevention of preterm birth. Practice bulletin no.130, October 2012.

NICE guidelines. Preterm labour and birth. November 2015.

10. Simhan HN, Iams JD, Romero R. Preterm birth. In: Niebyl JR, Gabbe S. Obstetrics: Normal and Problem pregnancies.6th ed. Elsevier; 2012.Chapter 28,Pretrm birth; p.627-58. 11. American College of Obstetricians and Gynecologists: Antenatal corticosteroid therapy for fetal maturation. Committee opinion no.713, August 2017. 12. Gurunath S, Misra R. Ian Donaldâ&#x20AC;&#x2122;s practical obstetric problems. 7th ed. New Delhi: Wolters Kluwer; 2014. Chapter 21, Preterm labour; p.409-31. 13. Yudin NH, Van SJ et al. Antibiotic therapy in preterm premature rupture of the membranes. J Obstet Gynecol Can 2009 Sep; 31(9):863-7,868-74.

OBSTETRIC COAGULOPATHY Dr. Divya Rajalakshmi.S, Prof. Seetesh Ghose ABSTRACT: Obstetrics coagulation is a condition where there is abnormality in coagulation and fibrinolysis. Pregnancy is a hypercoagulable state due to increase in various natural pro-coagulants. But this effect is balanced out by proportionate increase in anticoagulation

factors.

This

delicate

balance

between

pro-coagulation

and

anticoagulation gets disturbed in certain conditions i.e. placental abruption, intrauterine fetal demise with retained dead fetus, acute fatty liver of pregnancy, amniotic fluid embolism, endotoxin induced sepsis and preeclampsia with HELLP syndrome. . Bleeding is usually the most common clinical finding which usually manifests as petechial, echymosis, mucosal oozing, bleeding from

vein puncture sites, surgical

incision sites and from various systems, especially the gastrointestinal system. The diagnosis is almost always based on clinical suspicion and supported by laboratory tests. Laboratory test includes thrombocyte count, prothrombin time (PT), activated partial thromboplastin (aPTT), estimation of fibrin degradation product and D-Dimer . Thromboelastography is a diagnostic method to analyse the hemostatic system quantitatively and qualitatively and can be performed at bedside. Correction of the underlying obstetrical cause is the corner stone of the treatment in coagulopathy besides, supportive treatment. Main stay of the treatment is judicious use of blood and blood products after consideration of clinical condition and laboratory tests results. The experience with the use recombinant Factor VIIa (rFVIIa) in massive obstetrical bleedings is increasing with its own limitation. The use of pharmacological agents inhibiting the coagulation and fibrinolytic systems in Disseminated Intravascular Coagulation is still controversial. . Fractionated heparin is especially recommended in DIC cases associated with thrombosis without stigmata of bleeding. Tranexamic acid and Ă&#x;-aminocaproic acid is in general contraindicated. Key words: Obstetrics coagulopathy, DIC, recombinant Factor VIIa INTRODUCTION: Obstetrics coagulopathy is a clinical condition arising due to abnormal coagulation and fibrinolysis as a result of some obstetrics related condition.It remains as 27

main cause of maternal mortality worldwide. So prompt identification of factors leading to hemorrhage and its management holds the corner stone of the management (1) .Disseminated Intravascular Coagulation (DIC) is the most important obstetrics related cause which leads to bleeding with high rates of mortality and morbidity. Joseph De Lee in 1901 first described this condition following placental abruption (2). The basic pathophysiology associated with DIC is systemic activation of the coagulation cascade, which lead to extensive fibrin deposition and subsequent microvascular thrombosis. Usually patients exhibit a tendency for severe bleeding as a result of consumption of platelets and coagulation factors (3,4). But DIC clinically may lead to a wide range of pictures from unnoticed intravascular thrombosis and microvascular damage to uncontrollable bleeding. The real incidence of obstetrical DIC is unknown since it represents a wide spectrum ranging from mild to severe. Various studies done showed that the incidence of DIC in all pregnancies was 0.02-0.07 % (5,6). Maternal mortality associated with DIC vary from 6 to 24% and postpartum hysterectomy, massive blood transfusions and acute tubular necrosis are listed as the main maternal morbidity indicators(6,7). Therefore, early detection of these predictors of coagulopathy and timely intervention of this lifethreatening condition is very important. Pathophysiology of the coagulation mechanisms during pregnancy The hemostasis mechanism undergoes substantial changes during pregnancy. Majority of the coagulation factors increase, whereas the level of natural anticoagulants and fibrinolytic activity. These alterations make pregnancy a state of hypercoagulability and an increased risk of thromboembolism. It has been shown that placenta has highest level of thrombotic activity due to release of thromboplastic substances. During the pregnancy fibrinogen levels doubles besides rise of D-Dimer. (8-10). All predisposing factors which lead to DIC initiate the activation of the coagulation cascade as part of the systemic inflammatory response in response to activation of cytokines(11). The pathogenesis of DIC is a complex mechanism, where the increased thrombin production in vivo, plays a central role. The other factors responsible for DIC are increased anionic phospholipid concentration Increased tissue factor production, decreased fibrinolysis and anticoagulation system dysfunction.(12)The following pictures shows the normal coagulation cascade (Fig.1) and pathophysiology of DIC(Fig.2). Coagulopathy can be of 28

two types. First one is due to dilution of the clotting factors due to massive blood transfusion and second one is due to consumption of the circulating clotting factors due to exaggerated activation of coagulation cascade. Table 1: Changes in coagulation factors in pregnancy13 Coagulation Factor

Changes in Pregnancy (At Term )

Factor II & V

No Change

Fibrinogen

Increases >100%

Factor VII

Up to 100% Increase

Factors VIII,IX,X,XII & VWF

>100% Increase

Factor XI

Variable

Factor XIII

Up to 50% Decrease

Figure 1: Normal coagulation cascade 14Figure 2: Pathophysiology of DIC14 Obstetric conditions that can lead to coagulopathy In obstetrics the following conditions are common causes of coagulopathy o Major Obstetric hemorrhage and massive transfusion o Placental Abruption o Intrauterine fetal demise with retained dead fetus o Acute Fatty Liver of Pregnancy o Amniotic fluid embolism o Endotoxin sepsis o Pre- eclampsia with HELLP syndrome. 29

Clinical findings Clinical condition varies from bleeding to thrombosis, sometimes even

fibrin

accumulation in the intravascular bed at the microvascular level result in end organ damage. Bleeding is usually the most common clinical finding which usually manifests as petechiae, echymosis, mucosal oozing, bleeding from vein puncture sites, surgical incision sites and from various systems, especially the gastrointestinal system. The overall condition of patientsâ&#x20AC;&#x2122; is often critical. Acute renal failure, altered mental status due to hypoxia and hypovolemic shock may occur as a result of blood loss(12,15).Rarely abdominal compartment syndrome may also be encountered . (16).Investigations: The diagnosis is almost always based on clinical suspicion and supported by laboratory tests. These tests include laboratory parameters indicative of procoagulant and fibrinolytic substance activation, inhibitor consumption and organ damage or failure (12, 17). Coagulopathy is a dynamic process and the test reports depict only the conditions at any given moment in time. So the tests need to be repeated to assess the hemostatic state of the patient. Thrombocyte count Prothrombin time (PT), and activated partial thromboplastin (aPTT) reflect not only the consumption but also activation of thrombocytes (18). Fibrin production is indirectly measured by the estimation of fibrin degradation product, D-Dimer (19). In pregnancy, PT and aPTT levels shorten based on the increase in coagulation factors. So, even if the consumption of coagulation factors associated with DIC leads to prolongation of PT and aPTT levels, they may still be within normal limits. Similarly, physiological thrombocytopenia associated with pregnancy should be considered while diagnosing DIC. Thromboelastography is a diagnostic method to analyse the hemostatic system quantitatively and qualitatively and can be performed at bedside. Scoring used in Disseminated Intravascular Coagulation There is no ideal single test to diagnose DIC. A scoring system was developed by the International Society of Thrombosis Hemostasis (ISTH) for the diagnosis and management of DIC (20). The flow chart of this scoring system described below (Figure 3) is only appropriate for patients with an underlying disorder. This scoring is done based on prolonged aPTT, the thrombocyte count, fibrinogen level and Fibrin degradation products. A score of 5 and higher is considered as overt DIC. This scoring can also be

used in cases with or without underlying infection (21) .The sensitivity and specificity of this scoring system as described by Bakhtiari et al was 97% and 91% respectively. (22). Table 2International Society of Thrombosis Hemostasis (ISTH) DIC Scoring System.

DIC RELATED CAUSE Yes

Order coagulation tests

Do not use this algorithm

* Prothrombin time * Platelet count * Fibrinogen level * Fibrin degradation products Prothrombin timePlatelet FibrinogenFDP < 3 sc......0

>100x109......0

> 3 - < 6 sc......1

50-100x109......1< 1 g/L......1 Growth medium......2

> 6 sc......2

>1 g/L......0

<50x109......2

Not increase......0

Significant increase......3 TOTAL SCORE

â&#x2030;Ľ5 Compatible with Overt DIC: Repeat score daily <5 suggestive of Non overt DIC: Repeat next 1-2 days

Management: Correction of the underlying obstetrical cause is the corner stone of the treatment in coagulopathy. Besides, supportive treatment should be implemented to correct the coagulation disorder (12). Main stay of the treatment is judicious use of blood and blood products after consideration of clinical condition and laboratory tests results. In general, platelet suspensions are administered to patients with platelet counts less than 50 x 109 and actively bleeding. In patients without bleeding, platelet transfusion is limited to patient's with a platelet count less than 30 x 109 (23) .Transfusion of coagulation factors and plasma is not indicated if there is no active bleeding. However, if the active bleeding occurs with prolonged PT and aPTT, then Fresh Frozen Plasma (FFP) should be administered at a dose of 10-20 ml/kg (23).Higher doses may be administered based on 31

response noted during serial follow-up testing. If FFP's are not feasible due to concerns of fluids overload, non-activated prothrombin complex concentrate (PCC) may be administered at 25-30 U/kg dose (24). So activated PCC should not be used to prevent worsen the severity of the disseminated intravascular coagulation (25). In congenital isolated fibrinogen deficiencies with levels less then 1gm/L, cryoprecipitate or fibrinogen factor concentrates should be used. Since the fibrinogen consumption may be faster, fibrinogen concentrates should be administered for values above 1gm/L in DIC. 4 gm of fibrinogen concentrates, increase serum fibrinogen levels to 1gm/L (26). Management of the Massive Bleeding: Obstetrical bleedings are the most common reason of maternal mortality. In a healthy female, vital signs alterations do not alter until loss of 10-15% of the blood volume. Tachycardia is the first sign of bleeding. Severe hypotension is noted following loss of 30% of the blood volume (27). The principle of management of bleeding is to maintain the patient normotensive, normothermic and ensure adequate replacement of clotting factors. First of all, two large bore peripheral IV lines should be placed. Initiation of crystalloid or colloid fluids remains a controversy because colloid solutions may affect coagulation (28). The modern cellular models of coagulation suggest early administration of blood components. It is now believed that early coagulopathy may occur prior to hemodilution and before consumption of clotting factors or abnormal lab values set in. 29,30,31 Pacheco et al has devised a protocol (Table.3) in attempt to improve response in massive obstetrical hemorrhage. Such a protocol is activated when the hemorrhage is massive, i.e.- >50% blood volume loss within 2 hrs-in patients with ongoing bleeding after the transfusion of 4U of packed RBCs within a short period of time .Rapid transfusion of volume expanders may lead to dilution of coagulation factors. Therefore, blood replacement should be implemented as soon as possible. O Rh negative blood transfusion must be started immediately and typed & screened, cross matched blood should be prepared within maximum 45 minutes. There are studies to suggest that dilutional coagulopathy could be inevitable with more than 5units of blood transfusion (32), use of 1:1 packed red blood cells and FFPs decrease the mortality(33,34) prophylactic administration of thrombocytes decreased the need for other blood products in massive bleedings. Therefore, the need for 1-2 adult dosing thrombocyte replacement for every 810 units of blood is emphasized (35). Literature also demonstrate administration of cyroprecipitates and fibrinogens for fibrinogen levels less than 1.5gm/L decreases 32

bleeding and need for erythrocyte and thrombocyte suspensions, FFPs (36,37). Serial measurement of whole blood count and coagulation parameters are essential in regards to whether to carry on or hold further replacement of blood products. As acidosis hinders the union of the coagulation complex and hypothermia decreases thrombocyte activation (38) care must be taken to prevent development of acidosis and hypothermia. Table 3: Massive Transfusion Protocol PRBC

FFP

Platelets

Cryoprecipitate

Round 1

10U

Round 2

20U

Recombinant activated factor VII(40Îźg/kg)

Round 3 Round 4

Round 5

10U 10U

Recombinant activated factor VII(40Îźg/kg)

Round 6

The compatibility of various blood products with group and type is summarised below (Table.4) These are very important as not all blood components of a particular blood group may be available at the time of crisis. Table.4 Summary of compatibility of various blood products Patient group

Donor Group Whole Blood

PRBC

FFP

Cryoprecipitate

Platelet

A,O

A,AB

Any Group

B,O

B,AB

Any Group

AB,O,A,B

Any Group

O, AB,A,B

Any Group

Rh positive

+/-

Any Group

+/-

Rh Negative

-ve

+/-

Any Group

-ve

The management of blood products should be done as listed below (Table.3) Table 3: Management of Massive obstetrical bleeding 22 Erythrocyte suspensions * Firstly, use O Rh (-) erythrocyte suspensions (ES) * Cross matched ABO and Rh compatible blood should be available within maximum of 45 min * Maintain circulating blood volume with ES as needed * Avoid hypothermia (use blood warmers) Fresh frozen plasma * Transfuse one unit of plasma to every one unit of ES * PT & APTT values should be less than 1.5 times normal Platelet transfusion * Transfuse one to two adult doses of platelets to every 8-10 units of ES * Platelet count should be >50x109/l Fibrinogen * Cryoprecipitate (dose = two donation pools) * Fibrinogen concentrates (4 g) * Fibrinogen level should be >1g/l

The role of activated Factor VII: The experience with the use recombinant Factor VIIa (rFVIIa) in massive obstetrical bleedings is increasing. Gabriel et al discovered that rFVIIa levels above physiological limits directly activate Factor X located on the surface of activated platelets (39). A study demonstrated that the bleeding was effectively controlled in 83% and postpartum hysterectomy could be prevented by 91 %( 83) of patients who were treated with FVIIa (40).However, yet there are questions regarding the use of rFVIIa which need to be answered. First of all, the dose to be used in massive obstetric bleedings has not been standardized, yet as doses ranging from 15 Îźg/kg to 120Îźg/kg has been used (23). Secondarily, in cases with platelet counts above 100x109 and less severe coagulopathies the response to rFVIIa is higher. This finding supports the replacement with blood products early on in the course to bring the response to rFVIIa to a more adequate level. Acidosis and low fibrinogen levels decrease the 34

optimum response to rFVIIa(41) . As a pre-hemostatic agent, rFVIIa may theoretically lead to thromboembolic complications especially, in hypercoagulable states like pregnancy. Another reason is that the cost of rFVIIa treatment is high. However, if the surgical procedures and prolonged hospital stay including admission to the ICU are considered as well, it may balance out. Pharmacological Treatment: The use of pharmacological agents inhibiting the coagulation and fibrinolytic systems in Disseminated Intravascular Coagulation is still controversial. Heparin will theoretically inhibit intravascular coagulation and subsequent fibrinolysis through inhibition of the thrombin activity. Heparin is especially recommended in DIC cases associated with thrombosis without stigmata of bleeding. In patients considered for Heparin treatment, fractionated heparin should be the treatment of choice given its short half life and reversible actions and should be administered as continuous intravenous infusion at 10 Âľ/kg/hr. In these patients, the clinical response should be taken into account rather then the use aPTT in the monitoring of the anticoagulant effect (36). The use of anti-fibrinolytic agents such as Tranexamic acid and Ă&#x;-aminocaproic acid is in general contraindicated in DIC. However, these medications may be effective in life threatening bleedings (42) . CONCLUSION: Obstetric coagulopathy is a nightmare for every obstetrician. Awareness and prompt investigations to pick up DIC in high risk cases and aggressive management is needed

prevent

morbidity

and

mortality

due

this

dramatic

condition.Multidisciplinary approach with judicious use of blood and blood product improves its outcome.Post DIC management, renal and other end organ damage has to be actively looked for. REFERENCES: 1.

Williams J, Mozurkewich E, Chilimigras J, Van De Ven C. Critical care in obstetrics: pregnancyspecific conditions. Best Pract Res ClinObstetGynaecol 2008;22(5):825-46.

DeLee JB. A case of fatal hemorrhagic diathesis, with premature detachment of the placenta. Am J Obstet Dis Women Child 1901;44:785-92.

Bick RL. Disseminated intravascular coagulation: a review of etiology, pathophysiology, diagnosis, and management: guidelines for care. ClinApplThrombHemost 2002;8(1): 1-31. 4. Bick RL. Disseminated

intravascular

coagulation

current

concepts

etiology,

pathophysiology,

diagnosis,

and

treatment.HematolOncolClin North Am 2003;17(1):149-76. 4.

Liang BL, Hong DH.Diagnosis and management of obstetric acute disseminated intravascular coagulation.Zhonghua Fu Chan KeZaZhi 1992;27(3):147-9, 188.

Kor-anantakul O, Lekhakula A. Overt disseminated intravascular coagulation in obstetric patients. J Med Assoc Thai 2007;90(5):857-64.

Rattray DD, O'Connell CM, Baskett TF. Acute disseminated intravascular coagulation in obstetrics: A tertiary centre population review (1980 to 2009). J ObstetGynaecol Can 2012;34(4):341-7.

Bremme KA. Haemostatic changes in pregnancy. Best Pract Res ClinHaematol 2003;16(2):153-68

DahlmanT, Hellgren M, Blomback M. Changes in blood coagulation and fibrinolysisin the normal puerperium. GynecolObstet Invest 1985;20(1):37-44.

O'Riordan MN, Higgins JR. Haemostasis in normal and abnormal pregnancy. Best Pract Res ClinObstetGynaecol 2003;17(3):385-96.

10. Tetik S, Ak K, Sahin Y, Isbir S, Gulsoy O, Arsan S, Yardimci T. Postoperative statin therapy attenuates the intensity of systemic inflammation and increasesfibrinolysis after coronary artery bypass grafting. ClinApplThrombHemost 2011;17(5): 526-31. 11. Levi M, Toh CH, Thachil J, Watson HG. Guidelines for the diagnosis and management of disseminated intravascular coagulation: British Committee for Standardsin Haematology. Br J Haematol 2009;145(1):24-33. 12. D. Katz, Y. Beilin; Disorders of coagulation in pregnancy, BJA: British Journal of Anaesthesia, Volume 115, Issue suppl_2, 1 December 2015, Pages ii75–ii88, https://doi.org/10.1093/bja/aev374 13. Sadik S, et al Mustafa E, Sermin T, Kadir G. Disseminated intravascular coagulation in obstetrics J Turk SocObstetGynecol 2014;11:42-51 14. Gando S, Iba T, Eguchi Y et al. A multicenter, prospective validation of disseminated intravascular coagulation diagnostic criteria for critically ill patients: comparing current criteria. Crit Care Med 2006;34(3):625-31. 15. Çakmakç› M. Abdominal kompartmansendromu. T KlinikleriCerrahiDergisi 1998;3:51-4. 16. Ak K, Isbir C, Tetik S, Atalan N, Tekeli A, Aljodi M et al. Thromboelastography based transfusion algorithm reduces blood product use after electiveCABG: A prospective randomized study. J Card Surg 2009;24(4):404-10. 17. Tetik fi, Ak K, Yard›mc› KT. The factors effecting platelet function tests. CumhuriyetT›p Der 2012;4:123-7. 18. Bick RL, Baker WF. Diagnostic efficacy of the D-dimer assay in disseminated intravascular coagulation (DIC). Thrombosis Research 1992;65(6):785-90

19. Taylor FB, Toh CH, Hoots WK, Wada H, Levi M. Towards definition, clinical and laboratory criteria, and a scoring system for disseminated intravascular coagulation. J ThrombHemost 2001;86(5):1327-30. 20. Gando S, Wada H, Asakura H, Iba T, Eguchi Y, Okamoto K. Evaluation of new Japanese diagnostic criteria for disseminated intravascular coagulation in critically ill patients. ClinApplThrombHemost 2005;11(1):71-6. 21. Bakhtiari K, Meijers JC, Levi M. Prospective validation of the international society of thrombosis and haemostasis

scoring

system

for

disseminated

intravascular

coagulation.

Crit

Care

Med

2004;32(12):2416-21. 22. Thachil J, Toh CH. Disseminated intravascular coagulation in obstetric disorders and its acute haematological management. Blood Rev 2009;23(4):167-76. 23. Josic D, Hoffer L, Buchacher A. Manufacturing of a prothrombin complex concentrate aiming at low thrombogenicity. Thromb Res 2000;100(5):433-41 24. Preston FE, Laidlaw ST, Sampson B. Rapid reversal of oral anticoagulation with warfarin by a prothrombin complex concentrate (Beriplex): efficacy and safety in 42 patients. Br J Haematol 2002;116(3):619-24. 25. Kreuz W, Meili E, Peter-Salonen K. Efficacy and tolerability of a pasteurised human fibrinogen concentrate in patients with congenital fibrinogen deficiency. TransfusApherSci 2005;32(3):247-53 26. Wise A, Clark V. Strategies to manage major obstetric haemorrhage. CurrOpinAnaesthesiol 2008;21(3):281-7. 27. Van der Linden P, Ickx BE. The effects of colloid solutions on hemostasis. Can J Anaesth 2006;53(6 Suppl):S30-9. 28. Pacheco LD, Saade GR, Costantine MM, Clark SL, Hankins GD. The role of massive transfusion protocols in obstetrics. American journal of perinatology. 2013 Jan;30(01):001-4. 29. Pacheco L.D, GeiAF , Controversies in the management of placenta accrete. ObstetGynecolClin North Am. 2011;38: 313- 322. 30. Pacheco LD ,Saade G R, Gei AF et al Cutting edge advances in the medical management of Obstetric hemorrhage. Am J Obstet Gynecol.2011;205:526-532 31. Hirshberg A, Dugas M, Banez E, Scott B, Wall M, Mattox K. Minimizing dilutional coagulopathy in exanguinating hemorrhage: a computer simulation. J Trauma 2003;54(3): 454-61. 32. Malone DL, Hess JR, Fingerhut A. Massive transfusion practices around the globe and a suggestion for a commonmassive transfusion protocol. J Trauma 2006;60(6 Suppl):S91- 6. 33. Borgman MA, Spinella PC, Perkins JG, et al. The ratio of blood products transfused affects mortality in patients receiving massive transfusions at a combat support hospital. J Trauma 2007;63(4):805-13

34. Johansson PI, Stensballe J, Rosenberg I, et al. Proactive administration of platelets and plasma for patients with aruptured abdominal aortic aneurysm: evaluating a change in transfusion practice. Transfusion 2007;47(4):593-8. 35. Fenger-Eriksen C, Lindberg-Larsen M, Christensen AQ, et al. Fibrinogen concentrate substitution therapy in patients with massive haemorrhage and low plasma fibrinogen concentrations. Br J Anaesth 2008;101(6):769-73. 36. Wikkelsoe AJ, Afshari A, Stensballe J, Langhoff-Roos J, Albrechtsen C et al. The FIB-PPH trial: fibrinogen concentrate as initial treatment for postpartum haemorrhage: study protocol for a randomised controlled trial. Trials 2012;13:110. 37. Meng ZH, Wolberg AS, Monroe 3rd DM. The effect of temperature and pH on the activity of factor VIIa: implicationsfor the efficacy of high-dose factor VIIa in hypothermic and acidotic patients. J Trauma 2003;55(5):886-91. 38. Gabriel A, Li X, Monroe DM. Recombinant human factor VIIa, (rFVIIa) can activate FX on activated platelets. J ThrombHaemost 2004;2(10):1816-22. 39. Sobieszczyk S, Breborowicz GH, Platicanov V, et al. Recombinant factor VIIa in the management of postpartumbleeds: an audit of clinical use. ActaObstetGynecolScand 2006;85(10):1239-47. 40. Haynes J, Laffan M, Plaat F. Use of recombinant activated factor VII in massive obstetric haemorrhage. Int J ObstetAnesth 2007;16(1):40-9. 41. Novikova N, Hofmeyr GJ. Tranexamic acid for preventing postpartum haemorrhage. Cochrane Database Syst Rev 2010; (7):CD007872.

ECLAMPSIA Dr Gisi Sebastian, Prof Pallavee P ABSTRACT: Eclampsia is the commonest cause of convulsions in pregnancy before epilepsy. Incidence varies from 1 in100 to 1 in 2000(1). Incidence of eclampsia accounts for 24% maternal deaths in India(2). Early prediction and diagnosis requires high index of suspicion and comprehensive training of health professionals at all levels of health care. Hypertensive emergency is a life threatening condition involving significant risk to mother and fetus. Aggressive treatment of maternal hypertensive state requires an initial consideration of effect of treatment of fetus via changes to utero placental circulation. The challenge is to correct blood pressure using appropriate safe pharmacologic agents to prevent poor maternal outcome and fetal ill effects. Key Words:- Eclampsia, Hypertensive emergency, Management of eclampsia, Management of hypertensive emergency INTRODUCTION Peripartum hypertensive disorders complicate around 10% of pregnancies worldwide and these are the main cause for maternal and prenatal morbidity and mortality(2).Among the hypertensive disorders of pregnancy eclampsia and hypertensive emergencies have most adverse outcomes in pregnancy. Eclampsia is a severe form of preeclampsia. It may occur from 20 weeksâ&#x20AC;&#x2122; gestation to 48 hours post-partum. Immediate management of the condition includes airway control, oxygen, magnesium for cessation of seizures, control of hypertension, and delivery of the baby. The incidence increases with tertiary referral centres â&#x20AC;&#x201C; multi-fetal gestation and in populations with poor prenatal care(1). Mostly eclampsia occurs as a result of delayed diagnosis of severe preeclampsia. Severe preeclampsia is defined as hypertension and proteinuria with additional symptoms of severe headache, liver tenderness , visual disturbance ,low platelet count, epigastric pain and/or vomiting ,abnormal liver enzymes (ALT or AST rising to above 70 IU/l), signs of clonus ,HELLP syndrome, papilloedema(3).Hypertensive emergencies can lead to fatal target end organ damage. It includes stroke (hemorrhagic or ischemic) pulmonary edema & myocardial ischemia. 39

The seriousness of this condition is determined by association of elevated blood pressure with new or progressive evidence of end organ damage. DEFINITION ECLAMPSIA: Convulsions or coma unrelated to other cerebral conditions occur along with signs and symptoms of preeclampsia. Depending upon timing whether before ,during , or after labor it is termed as antepartum , intrapartum & postpartum eclampsia respectively.When eclampsia occurs more than 48 hours but less than 4 weeks after delivery is called as late post partum eclampsia(2) . EPIDEMIOLOGY 91% cases of eclampsia occurs in third trimester, 7.5% cases occur between 2027weeks, and only 1.5% cases occur <20 weeks. Causes for eclampsia in early gestational age is molar pregnancy with or without coexistent twin /hypertensive encephalopathy,seizure disorder etc

(1)

. According to RCOG 2010 guidelines among all

antenatal women 5/10000 antenatal women suffer from eclampsia

(3)

.In western world

incidence ranges from 1 in 2000 to 1 in 3448 pregnancies (9) Major complications associated with eclampsia(16) 1.

Placental abruption (7-10%)

DIC (7-11%)

HELLP syndrome (10-20%)

Aspiration pneumonia (7%)

Pulmonary edema (5%)

Cardio pulmonary arrest (4-5%)

Acute renal failure (5-9%)

Pulmonary edema (3-5%)

Aspiration pneumonia (2-3%)

10.

Maternal death (1.8%)

11.

Prematurity

12.

fetal asphyxia

PATHOPHYSIOLOGY In case of eclampsia, pathophysiology is not conclusively elucidated. Autopsy studies showed that cerebral edema, cortical and sub cortical white matter micro infarcts, pericapillary and parenchymal bleeding has important role in eclampsia. Usually normal autoregulatory response to increased blood pressure is vasoconstriction but once the upper limit of auto regulation is exceeded vasodilatation 40

occurs with hyperperfusion leads to endothelial capillary damage and vasogenic edema. The cerebral perfusion pressure needed for barotraumas and seizure varies with each individual. Rupture of vascular endothelium and pericapillary hemorrhages are due to exaggerated vasoconstriction and ischemic changes cause development of foci of abnormal electrical discharges that lead to convulsions (11). DIAGNOSIS Headache

Severe hypertension +/-

Visual changes (blurred vision /photophobia)

Severe proteinuria

Right upper quadrant pain /epigastric pain

Generalized edema +/-

Altered mental status

Convulsions

Convulsions are tonic clonic (lasts for 1-2 min). Facial twitching progress to tonically rigid body with generalized muscular contractions.

Alternate contraction and relaxation of muscles of the body, these are extremely forceful. In this stage patient can fall from bed or biting their own tongue

Patient may enter into semiconscious combative state and become agitated. Coma and death rarely occurs Coma is due to cerebral edema and transtentorial herniation. Usually during seizure patient cease to respire followed by a state of hyperventilation during post ictal state due to lactic acidosis and hypercarbia. There may be evidence of decreased urine output also.

Pulmonary edema occurs secondary to aspiration of gastric content during seizure/ventricular failure (increased afterload due to overzealous intravenous fluid administration) . Retinal detachment/ occipital lobe ischemia /cerebral edema cause loss of vision which is reversible. Sudden death occurs due to massive cerebral hemorrhage. Hemiplegia and hyperthermia accompanies cerebral hemorrhage. Maternal assessment :(3) 1. Blood pressure every 15 min once until the patient is stabilized then every 30 min once in initial phase.Once the patient is stable then it can be monitored fourth hourly . 2. Complete blood count 3. Liver function test 4. Renal function test 5. BT/CT not required if paltelet >1 lakh 6. Input /output charting 7. Uric acid 8. Urine protein creatinine ratio Fetal assessment :(3) 1. Cardiotocograph-fetal well being 2. Growth scan to rule out IUGR / oligohydramnios DIFFERENTIAL DISGNOSIS 1. Hypertensive encephalopathy

2. Seizure disorder

3. Hypoglycemia

4. Hyponatremia

5. Posterior leukoencephalopathy

6. Hypoxic ischemic encephalopathy

7. Postdural puncture syndrome

8. Vasculitis/angiopathy

9. Amniotic fluid embolism

10. Cerebrovascular accidents

11.Ruptured aneurysm/malformation

12.Arterial embolism ,thrombosis

13.Venous thrombosis

MANAGEMENT: 1. Stabilizing the patient 2. Control of convulsion 3. Control of hypertension 4. Delivery of fetus 1. Stabilizing the patient Call for senior obstetrician & anesthetist

Try to prevent maternal injury during convulsion

Place the women in left lateral position in railed cot, insert oral airway without trauma to teeth and mouth

Assess airway, breathing, blood pressure and pulse

Administer oxygen @8-10L/minute

Once seizure stops secure IV line (if not present), catheterise Plan to deliver as early as possible 2. Control of convulsions : Magnesium sulfate â&#x20AC;&#x201C; anticonvulsant is the treatment of choice for eclampsia. MOA: blocks calcium receptors by inhibiting NMDA receptors in brain.

ADVANTAGES: 1. Does not produce CNS depression to mother/baby. 2. Reduce recurrent seizures 3. Reduce maternal and perinatal mortality. REGIMEN PRITCHARDS –IM

LOADING DOSE 20ml of 20%(4 g) slow iv

MAINTANENCE DOSE 10 ml of 50%(5 g) deep im

in 3-5 mins

on alternate buttock every 4

10ml 50%(5 g) deep im on

hours.

each buttock(10 g) ZUSPAN – IV

4g iv (20%) in 100ml fluid

1g /hr in 100ml fluid iv

given for 15-20 mins. DHAKA

4g as 20% solution given

2.5g as 50%solution IM on

over 15mins and 3g as 50% alternate buttock every 4 solution given im in each

hrs.

buttock. SIBAI

6 g iv over 20 mins

2g iv infusion.

Mgso4 is continued 24 hours from the time of last convulsion or delivery whichever is later

Monitor Mgso4 toxicity: Urine output at least 30 ml/hour or 100 ml in 4 hours Deep tendon reflexes should be present Respiratory rate >14/min Spo2≥96% Request mgso4 levels

Respiratory rate <16 breath/minute Urine output <25 ml /hour for 4 hours Loss of patellar reflexes Further seizure occur

Magnesium levels

Therapeutic

2.0-4.0mmol/l

Feeling of warmth , flushing , double vision Slurred speech

3.8-5.0 mmol/l

Loss of tendon reflexes

>5.0 mmol/l

Respiratory depression

>6.0 mmol/l

Respiratory arrest

6.3-7.1 mmol/l

Cardiac arrest

>12.0 mmol/l

After giving Mgso4 if seizure persist/recur

2g < 70 kg

Iv over 10 mins

4g > 70kg If still recurs phenytoin /diazepam single dose

STATUS EPILEPTICUS

Convulsion persists Inj.Thiopentone sodium 0.5g in 20 ml of 5% dextrose IV slowly

Persist ď&#x192; GA 3. Control of hypertension : Goal: Systolic - Bp 140 -160 mmhg Diastolic - Bp 90 â&#x20AC;&#x201C; 105 mmhg It prevents: 1. Congestive heart failure 2. Cerebral hemorrhage. 3. Treatment and prevention of seizures.

1 st line of drug is Labetalol -> Nifidepine Diuretics can be given post partum.

4. Delivery:

< 34 weeks

>34 weeks

Can be prolonged for 24 hrs for steroid administration.

Delivery after stabilizing (vaginal delivery to be considered if cephalic presentation)

PREVENTION: Primary prevention of eclampsia can be done by preventing development of pre eclampsia /using pharmacologic agents that prevent convulsions in women with pre eclampsia .

It includes: 1. Close monitoring 2. Use of antihypertensives, to keep maternal BP less than severe range. 3. Timely delivery. 4. Prophylactic use of MGSO4 during labour/ postpartum with pre eclampsia. SUBSEQUENT PREGNANCY OUTCOME: Approximately 20-30% of women will have preeclampsia and 2-5 % will have eclampsia in subsequent pregnancy (10).

HYPERTENSIVE EMERGENCY: When severe hypertension occurs acutely, persists for >15 min and presents in a pregnant or postpartum patient with preeclampsia or eclampsia with end organ damage

(5)

. It can cause cerebrovascular hemorrhage,

hypertensive encephalopathy and can cause eclamptic convulsions in antenatal mother with preeclampsia. EPIDEMIOLOGY Hypertensive emergencies are very rare and it accounts for only 1-2% among hypertensive disorders. Major complications include: Hypertensive after-load congestive heart failure

Placental abruption

Hypertensive encephalopathy

Hemorrhagic stroke

DIAGNOSIS (6)  Systolic blood pressure >160mmhg  Diastolic blood pressure >110 mm Hg  IUGR<fifth percentile  Severe oligohydramnios  Pulmonary edema  DIC  Placental abruption  HELLP syndrome  Reversed end diastolic flow  Progressive renal insufficiency  Severe thrombocytopenia  Neurological symptoms  Eclampsia along with end organ damage.

ď&#x192;ź 14.IUGR ď&#x192;ź 15.Oligohydramnios Maternal assessment: 1. Chest pain /cardiovascular symptoms 2. Headaches 3. Visual abnormailities 4. Consciousness 5. Difficulty in breathing 6. History (drug abuse ,current medications) 7. Physical examination for end organ damage 8. Blood investigations(Complete blood count+Differential count +Platelet count +Metabolic panel+Urinalysis ) 9. Chest xray /ECG (myocardial injury/pulmonary edema) 10. Frequent maternal pulse and blood pressure monitoring Pulmonary edema is caused by increase in hydrostatic pressure from increased effective blood volume and decreased colloid osmotic pressure

(12,

13)

. As disease advances dysfunction of glomerular apparatus in the kidney,

decreased filtration rate and renal insufficiency increases the risks. (14) Acute kidney damage is caused by acute elevation of systemic vascular resistances causes endothelial damage which activate platelets which lead to small vessel occlusion and end organ hypoperfusion (including kidney) (14) Oliguria due severe renal artery vasospasm Eclampsia, intracranial haemorrhage, stroke, subcortical edema, PRES (posterior reversible encephalopathy syndrome) are the common problems associated with hypertensive emergencies.MRI is better choice for evaluation of PRES.

MANAGEMENT: Treatment with intravenous labetalol or hydralazine or oral nifedipine.In hypertensive emergency the main goal of treatment is to lower the blood pressure to a level that decrease the risk of congestive heart failure and myocardial ischemia, renal injury,ischemic or heamorrhagic shock. Labetalol (intravenous) Sympathetic alpha 1 and beta blocker 10-20 mg iv over 2 mins/ bolus can be repeated every 20 mins max upto 80 mg per bolus with a max total iv dose of 300mg OR 1-2 mg /min infusion, titrate by increasing 1 mg per min every 10 mins.

MOA DOSE

SIDE EFFECTS

CONTRA INDICATION

Asthma, Heart disease, Congestive heart disease. C

Hydralazine Nifedipine (oral) intravenous/intramuscular) Direct vasodilator Calcium channel blocker 2.5 -5 mg iv slowly, repeat 10 mg p/o every 5-10 mg iv every 20-40 mins 20 mins. May increase to 20 mg per dose max 50 mg.

Maternal hypotension, Decreased placental perfusion, Headache, Lupus like syndrome, Renal impairment Rheumatic heart disease, Coronary artery disease, Stroke.

Headache, Dizziness, nausea, Flushing.

Aortic stenosis, Coronary artery disease, Acute Myocardial Infarction. C

PREGNANCY CATEGORY

FETAL MANAGEMENT: After fetal viability reached continuous monitoring during treatment of maternal hypertensive emergency is mandatory. 49

CONCLUSION: Eclampsia and hypertensive emergency is still a common serious complication of pregnancy. The pathophysiology and acute management has important role in reducing maternal morbidity and mortality. Management primarily involves control of blood pressure and associated complication. The collaborative eclampsia trial has shown that MGSO4 is the drug of choice for routine management of eclampsia and it has to be continued until 24 hrs postpartum or and or 24 hrs after the last convulsion REFERENCE: 1.

Sibai BM. (1996) ‘Hypertension’ in Gabbe SG, Simpson JI, (Eds.) Obstetrics : normal and problem pregnancies. Third Edition Chapter 28, pp 969-971. Churchill livingstone : New York

Joshi C, Hatwal D, Mohsin Z. Eclampsia : au enigma. Int J Reprod Contracept Obstet Gynaecol 2016;5 :878-81.

The Management of Severe Pre-eclampsia /Eclampsia. RCOG Guideline No.10(A). March 2006 Reviewed 2010.

Manning L, Robinson TG, Anderson CS.Control of blood pressure in hypertensive neurological emergencies.Curr Hypertens Rep 2014;16:436.

Aronow WS. Treatment of hypertensive emergencies. Ann Transl Med 2017;5(Suppl 1):S5. doi: 10.21037/atm.2017.03.34

Rosendorff C, Lackland DT, Allison M, et al. Treatment of Hypertension in Patients With Coronary Artery Disease: A Scientific Statement from the American Heart Association, American College of Cardiology, and American Society of Hypertension. J Am Coll Cardiol 2015;65:1998-2038.

Duley L. Maternal mortality associated with hypertensive disorders of pregnancy in Africa,Asia, Latin America and the Caribbean. Br J Obstet Gynaecol 1992;99:547–53.

Abd EI Aal DE, Shahin AY: Management of eclampsia at Assiut University Hospital, Egypt. Int J Gynaecol Cbstet 116(3):232,2012

MattarF, Sibai BM: Eclampsia VIII risk factors for maternal morbidity. Am J Obstet Gynaecol. 2000;182:307-312.

10. Sibai BM: Diagnosis, differential diagnosis, and management of eclampsia. Obstet Gynaecol. 2005;105:402-410.

11. Sibai BM. Abdella TN, Spinnato JA, et al. Eclampsia IV: the incidence of non preventable eclampsia. Am J Obstet Gynaecol. 1986;154:581-586. 12. Hankins GD, Wendel GD Jr, Cunningham FG, et al. Longitudinal evaluation of hemodynamic changes in eclampsia. Am J Obstet Gynaecol. 1984;150:506-512. 13. Phelan JP, Yurth DA. Severe preeclampsia. I. Peripartum hemodynamic observations. Am J Obstet Gynaecol. 1982;144:17-22. 14. Alexander JM, Wilson KL. Hypertensive emergencies of pregnancy. Obstet Gynaecol Clin North Am.2013;40:89-101. 15. Zeeman GG. Neurologic complications of pre-eclampsia. Semin Perinatol. 2009;33:166-172. 16. Mattar F, Sibai BM: Eclampsia VIII risk factors for maternal morbidity.

Am J Obstet

Gynecol 2000; 182:307. 17. The Eclampsia Trail Collaborative Group.Which anticonvulsant for women with eclampsia? Evidence from the Collaborative Eclampsia Trail. Lancet 1995;345:1455â&#x20AC;&#x201C;63. 18. Cipolla

MJ,

Zeeman

GG,

Cunningham

FG:

Cerebrovascular

(patho)physiology

preeclampsia/eclampsia. In Taylor RN, Roberts JM, Cunningham FG (eds): Chesleyâ&#x20AC;&#x2122;s Hypertensive Disorders in Pregnancy, 4th ed. Amsterdam,Academic Press, 2014

ASSESSMENT OF BLOOD LOSS IN PPH Dr. Madhusmita Hembram Prof. Sendhil Coumary A INTRODUCTION Postpartum haemorrhage (PPH) is an obstetric emergency which is associated with increased maternal morbidity and mortality. According to WHO there are 3 million deaths per year.1So it is always wise to prevent it.

Prophylactic routine active

management of third stage of labour is recommended by WHO to prevent postpartum haemorrhage.2 Despite active management of third stage, still postpartum haemorrhage is not completely preventable. So assessment of blood loss is very important as aggressiveness of postpartum haemorrhage increases with the amount of blood lost and the management of postpartum haemorrhage also depends on the amount of blood lost. Accuracy of amount of blood lost in PPH is vital for further plan of management. CLASSIFICATION PPH is classified as follows (3, 4, 5) Primary PPH (Within 24 hours of birth) Minor PPH (500-1000ml) Major PPH-Moderate PPH (1001-2000ml) Severe PPH (>2000ml) Secondary PPH (From 24 hours to 12 weeks) METHODS The different methods available for assessment of blood loss in PPH are as follows1) Visual estimation 2) Direct measurement 3) Gravimetric 4) Photometry 5) Clinical 6) Miscellaneous

VISUAL ESTIMATION Visual estimation of blood loss is a simple and most frequently used method of assessment of blood loss in PPH. In this method the blood loss is estimated by observing the soaked clothes and giving an approximate blood loss. Like, how much is one in-skirt, one soaked pad, swab. Total how many in-skirts soaked and how much is the final estimation. The disadvantage is that there is variation in assessment. Some authors felt there is underestimation6, 7and others8 felt there is overestimation of blood loss. Visual estimation is inaccurate when there is large volume blood loss. However visual estimation remains an important estimation method of blood loss in developing countries. Patients who deliver in areas which is remote from health care facility and when the patient is being carried to hospital at a delayed time, visual estimation remains the only available method for assessment of blood loss.

Picture 1: The above picture shows the visual method of estimation of blood loss DIRECT METHOD In direct method of estimation, blood is collected and measure in a graduated container. The different containers used are douche pan, basin, copper funnel, cholera table buttock drapes.9,10,11 The limitations of the method are that mixing of blood with other fluids like amniotic fluid, urine cannot be avoided which decreases accuracy of the

method. Second limitation is that all blood cannot be collected as soaking of the clothes with blood cannot be avoided completely.

Picture 2: The above picture shows buttock drapes used for direct estimation of blood loss GRAVIMETRIC In gravimetric method, the soaked pads, linen, swab collected are weighted and dry weight of these are deducted from it to determine the blood loss. One of the limitations of the method is that weight of the soaked clothes include weight of blood, amniotic fluid and urine which is not possible to discriminate. Second limitation is that dry weight of all the clothes should be known before using it. Third limitation is that weighing should be done as soon as possible to minimize evaporation. 12 PHOTOMETRIC METHOD In photometric method the blood pigment is converted to alkaline hematin and then blood loss is estimated. Alkaline hematin method is considered the gold standard.13Some studies found there is underestimation of blood loss7,14,15 and some studies found there is overestimation of blood loss by photometric method.16 The limitations of the method are, first specialized instrument and a formula are required to estimate the blood loss, second the blood collection, extraction of blood from the soaked clothes and conversion of haemoglobin to haematin can be erroneous and third expertise of the laboratory person is required to estimate the blood loss and fourth this is an expensive method. So, though accuracy is more than any other method, still it cannot be applied for emergency like PPH in clinical practice where every second is valuable to save the life of the woman.

CLINICAL METHOD In clinical method, clinical signs and symptoms are included to determine the volume lost. The different clinical parameters used are pulse rate, blood pressure, respiratory rate and urine output, shock index. It is practical and easier method where the estimation is quick. But one of the limitations is that there is physiological increase in amount of blood in pregnancy which decreases sensitivity of clinical method.17As body has its own compensatory mechanism, by the time signs and symptoms appear already significant amount of blood is lost. TABLE 1:- Showing clinical assessment of blood loss Compensation

Mild

Moderate

Severe

500-1000 ml

1000-1500 ml

1500-2000 ml

2000-3000 ml

10-15%

15-26%

25-35%

35-45%

Marked fall

Profound fall

(80-100mmHg)

(70-80 mmHg)

(50-70 mmHg)

Symptoms and Palpitation

Weakness

Restless

Collapse

signs

Dizziness

Sweating

Pallor

Air hunger

Tachycardia

Blood loss

Blood pressure None change

Slight fall

(Systolic pressure)

Oliguria

Anuria

MISCELLANEOUS Stafford et al. calculated blood loss by multiplying maternal blood volume with percent of blood volume lost .The limitation of the method is that the calculated blood loss is affected by the hydration status.18 There is significant decrease in diameter of inferior vena cava as measured by ultrasound when blood loss was more than 450 ml.19,20 Limitations of this method are , first before delivery diameter of the inferior vena cava is required, second ultrasound expertise is required to determine the diameter of inferior vena cava and third diameter of inferior vena cava is affected by position. So it is an impractical method to implement.

Palm estimated haemoglobin levels drawn on the last visit of antenatal care, day three of postpartum and 10 weeks of postpartum. He compared the results with the estimated blood loss during and up to four hours postpartum. But the correlation between haemoglobin on day third of postpartum and estimated blood loss was weak. There was no correlation between haemoglobin level on 10wk postpartum and estimated blood loss.21 Some authors estimated blood loss by tagging the RBC with radioactive particles.22, 23 But, the accuracy and reproducibility of the methods were poor. It is not practical to inject radioactive material to a labouring woman. Rains marked the RBC with intravenous dye and estimated the blood volume change due to the blood loss event but the results were erroneous.24 Serum specific gravity method demonstrated by Conn et al. is not a reliable method for estimation of blood loss. Most of the miscellaneous methods are not applicable for acute blood loss event. CONCLUSION There is not a single method which is idea for all PPH events irrespective of accessibility of health care facility, early detection, quick availability of the results, cost effectiveness. Being in a developing country, we have to individualize each case according to the availability of the aforementioned facility in the place of the event and management. In clinical practice more than one method can be combined to improve the accuracy. REFERENCES: 1) WHO,UNFPA,World Bank Group and United Nations Population Division. Trends in Maternal Mortality :1990 to 2015:Estimates by WHO, UNICEF,UNFPA, World Bank Group and United Nations Population Division. Switzeland : World Health Organisation ;2015 2) World Health Organization.WHO recommendations for the prevention and treatment of postpartum haemorrhage. 2012. WHO: Geneva, Switzerland. 3) Mousa HA, Blum J, Abou El Senoun G, Shakun H, Alfirevic Z. Treatment for primary postpartum haemorrhage . Cochrane Database Syst Rev 2014;(2):CD003249

4) Alexander J, Thomas PW, Sanghera J. Treatment for secondary postpartum haemorrhage . Cochrane Database Syst Rev 2002;(I):CD002867 5) Mavrides E, Allard S, Chandraharan E, Collin P, Green L, Hunt BJ, Riris S, Thomas AJ on behalf of the Royal College of Obstetric and Gynaecologists. Prevention and management of postpartum haemorrhage. BJOG 2016;124:e106-e149 6) Brant HA. Precise estimation of postpartum haemorrhage : Difficulties and importance . BMJ 1967; 1: 398-400 7) Duthie SJ, Ven D, Yung GLK, Guang DZ, Chan SYW, Ma HK. Discripancy between laboratory determination and visual estimation of blood loss during normal laboratory determination and visual estimation of blood loss during normal delivery .Eur J ObstetGynecolReprodBiol 1990;38:119-24 8) Razvi K, Chau S, Arulkumaran S, Ratham SS. A comparisionbetwwen visual estimation and laboratory determination of bllod loss during the third satge of labour. Aust N Z J ObstetGynaecol 1996;36:152-4 9) Williams W. The tolerance of freshly delivered women to excessive loss of blood. Am J Obstet 1919;80:1238-54 10) Strand RT, da Silva F, Bergostrom S. use of cholera beds in the delivery room: a simple and appropriate method for direct measurement of postpartum bleeding. Trop Doct 2003;33:215-16 11) Haswell JN. Measured blood loss at delivery. J Indiana State Med Assoc 1981;74:34-6 12) Mavis N. Schorn , CNM, Phd Disclosures . J Midwifery Womens Health. 2010 ; 55(1):20-27 13) Chua S, ho LM, Vanaja K, Nordstrom L, Roy AC, Arulkumaran S. Vallidation of a laboratory method of measuring postpartum blood loss. GynecolObstet Invest 1998;46:31-3 14) Larsson C, saltvedt S, Wilkund I, Pahlen S, Andolf E. Estimation of blood loss after caesarean section and

vaginal

delivery has low validity

with a

tendency to

exaggeration.

ActaObstetGynecolScand 2006;85:1448-52 15) Wilcox CF, Hunt AB, Owen CA. The measurement of blood lost during caesarean section. Am J ObstetGynecol 1959;77:772-9 16) Duthie SJ, Ven D, Yung GLK, Guang DZ, Chan SYW, Ma HK. Discrepancy between laboratory determination and visual estimation of blood loss during normal delivery. Eur J ObstetGynecolReprodBiol 1990;38:119-24 17) Rath WH. Postpartum haemorrhage â&#x20AC;&#x201C;update on problems of definations and diagnosis. ActaObstetGynecolScand 2011;90:421-8. 18) Stafford I, Dildy GA, Clark SL, Belfort MA. Visually estimated and calculated blood loss in vaginal and caesarean delivery. Am J ObstetGynecol 2008;199:519;e1-e7

19) Lyon M, Bhaivas M, Brannam L. Sonographic measurement of the inferior vena cava as a marker of blood loss. Am J Emerg Med 2005;23:45-50 20) Sefidbakht S, Assadsangabi R, Abbasi HR, Nabavizadeh A. Sonographic measurement of the inferior vena cava as a predictor of shock in trauma patients. EmergRadiol 2007;14:181-5 21) Palm C, Rydhstroem H. Association of blood loss during delivery to B-hemoglobin. GynecolObstet Invest 1997;44:163-8 22) Read MD, Anderson JM. Radioisotope dilution technique for measurement of blood loss associated with lower segment caesarean section. Br J ObstetGynecol 1977;84:859-61 23) Holt JM, Mayet FGM, Warner GT, Callender ST. Measurement of blood loss by means of a whole-body counter. BMJ 1967;4:86-8 24) Rains AJH. Experience in the measurement of blood- and fluid- loss at operation. Br J Surg 1955;43:191-6 25) Conn LC, Vant JR, Cantor MM. A critical analysis of blood loss in 2,000 obstetric cases. Am J ObstetGynecol 1941;42:768-85

UTERINE INVERSION Dr Kalaivani, Prof Lopamudra B John ABSTRACT Uterine inversion is a state where the endometrial surface is inverted but it is a rare obstetric emergency that can lead to hypovolemic shock or maternal death (15%). This postpartum complication has an academic importance due to its rarity and severity. The best management options for this condition are not fully known, given the worldwide scarce experience of each obstetrical team managing this type of situation. There are several therapeutic strategies described in the literature KEY WORDS Hypovolemic shock, obstetric emergencies, postpartum hemorrhage, prolapse, uterine bleeding and uterine inversion INTRODUCTION 

This is rare, but potentially life threatening complication of the third stage of labour



It occurs in approximately 1 in 20,000 Deliveries



The Obstetric Inversion is almost always an Acute One & Usually Complete

DEFINITION 

When Uterus Turns Inside Out, It Is Called Uterine Inversion



Inversion of Uterus means Uterus is Turned Inside Out Partially OR Completely



Uterine inversion is the folding of the fundus into the uterine cavity in varying degrees

CLASSIFICATION Inversion of uterus is classified in mainly 3 Types:

A. According to types 

Incomplete Inversion: When fundus of uterus has turned inside out, like toe of socks, but inverted fundus has not descended through cervix



Complete Inversion: When the inverted fundus has passed completely through cervix to lie within the vagina or lie often outside the Vaginal Wall

B. According to degrees 

First degree: o The uterus is partially turned out o Incomplete Inversion



Second degree: o The fundus has passed through the cervix but not outside the vagina o Complete inversion in the vagina



Third degree: o The fundus is prolapsed outside the vagina o Complete inversion outside the Vagina



Fourth degree: o The uterus, cervix and vagina are completely turned inside out and are visible

C. According to the Timing of Event 

Acute: It occurs within 24 hrs of delivery



Sub-acute: It presents between 24 hrs & 4 wks of delivery



Chronic: It presents beyond 4 wks of delivery or in non-pregnant stage 60

CAUSES 

Excessive cord traction (esp. with an unseparated placenta)



Excessive fundal pressure (esp. when uterus is poorly contracted Atonic)



Placenta accreta



Congenital predisposition o Fundal implantation of placenta o Either Spontaneous OR Iatrogenic causes



Spontaneous (40%) o Abnormal short umbilical cord or functionally shortened by being wrapped around the fetal body o Sudden rise in intra-abdominal pressure due to maternal coughing or vomiting o Morbid adherence of fundally implanted placenta o Connective tissue disorder such as Marfan’s syndrome



Iatrogenic (Due to mismanagement of third stage of labor) o Pulling the cord when the uterus is atonic while combined with fundal pressure o Crede’s Expression while the uterus is relaxed o Faulty technique in manual removal of placenta While separating retained placenta from the wall, a portion may remain attached and as the placenta is withdrawn, the fundus is also withdrawn

PATHOPHYSIOLOGY A portion of uterine wall prolapses through the dilated cervix or indents forward

Relaxation of part of the uterine wall Simultaneous downward traction on the fundus

Leading to inversion of the uterus

CLINICAL MANIFESTATIONS 

Haemorrhage (94%)



Severe abdominal pain in 3rd stage



Hypotension with Bradycardia: shock out of proportion to the blood loss (neurogenic due to increased vagal tone)



Uterine fundus not palpable abdominally



Mass in the vagina on vaginal examination.



Sudden cardiovascular collapse



Lump in the vagina



Abdominal tenderness



Absence of uterine fundus on abdominal palpation



Shock o Shock is initially out of proportion with the amount of blood loss. o Woman becomes sweaty with bradycardia, profound hypotension and rarely cardiac arrest o In short time there is marked haemorrhage and Hypovolemic shock

DIAGNOSIS 

The diagnosis of uterine inversion is based upon clinical findings o Bleeding, which may be severe and result in Haemorrhagic Shock o Palpation of the prolapsed uterine fundus 

Lower uterine segment - INCOMPLETE



Vagina – COMPLETE

o By Intra Uterine Manual Examination DIFFERENTIAL DIAGNOSIS 

Inversion of uterus



Uterine rupture.



Prolapse of uterine tumor (submucous fibroid)



Large endometrial polyp



Passage of succenturiate lobe of placenta

MANAGEMENT PROTOCOL Uterine inversion

Resuscitate, IV access, fluids / bolus replacement

Immediate replacement Immediate replacement

Immediate replacement UTERUS REPLACED

YES

Immediate replacement

GA / Stabilize the patient

Remove placenta Oxytocic infusion (40 units/500mls NS) Antibiotics / Observe

- Manual reduction

- O’Sullivan hydrostatic method

- Apply pressure to dependent part of uterus

- Dependent part replace into vagina

- Simultaneous pressing with other hand on other part which inverted last

-5L or more physiological solution deposited onto posterior fornix - Assistant create water tight seal



Teamwork = resuscitation + uterine repositioning simultaneously



Postpartum haemorrhage drill



The quickest way to treat neurogenic shock - to replace the uterus

TWO METHODS OF MANAGING ACUTE INVERSION 1. MANUAL – JOHNSON’S METHOD The part of the uterus which is inverted last is to be replaced first 2. REPOSITIONING OF INVERTED UTERUS MANUAL REDUCTION  Sterile procedure  Form a fist or grab the uterus and push it through the cervix of a lax uterus towards the umbilicus to its normal position  Use the other hand to support the uterus (Johnson’s maneuver) MANAGEMENT OF ACUTE INVERSION OF UTERUS 

Delay in treatment increases the mortality, so number of steps are taken immediately and simultaneously



Before shock develops, o When one is on the spot when the inversion happens TRY IMMEDIATE MANUAL REPLACEMENT, even without anaesthesia if not easily available



Principle: “The part of the uterus which has come down last, should go back first”

PROCEDURE

ď&#x201A;ˇ

If the diagnosis is made immediately after the inversion has occurred, then that same degree of relaxation of myometrium and cervix (which is required for the inversion to occur) will allow uterine replacement easily 1. The gloved hand is lubricated with suitable antiseptic cream and placed inside the vagina. 2. The uterine fundus with or without the attached placenta, is cupped in the palm of the hand. The fingers and thumb of the hand are extended to identify margins of the cervix 3. The whole uterus is lifted upwards towards and beyond umbilicus 4. Additional pressure is exerted with the fingertips systematically and sequentially to push and squeeze the uterine wall back through the cervix 5. Sustained pressure for 3-5 mins to achieve complete replacement 6. Apply counter support by the other hand placed on the abdomen 7. Once the fundus has been replaced keep the hand in the uterus while rapid infusion of oxytocin is given to contract the uterus. Initially, bimanual compression aids in control of further hemorrhage until uterine tone is recovered 8. When the uterus is felt contracting, the hand is slowly withdrawn. ď&#x201A;ˇ

If placenta is attached, it is to be removed only after the uterus becomes contracted.

ď&#x201A;ˇ

If the placenta is partially attached , it should be peeled out before replacement of uterus

BIMANUAL COMPRESSION



If uterus is relaxed - Massaging the uterus will expel any retained bits & stimulate uterine contractions

MANUAL REMOVAL OF THE PLACENTA



Starting from the edge of placenta



The placenta is separated by o Keeping the back of the hand in contact with the uterine wall o With slicing movement of the hand

O’SULLIVAN’S HYDROSTATIC METHOD



Tube passed into the posterior fornix



Assistant close vulva around operator’s wrist



Warm saline run in until pressure gradually restores position of the uterus

NEW TECHNIQUE - OGUEH / AIYDA



A modified form of O’Sullivan technique



Attach the IV tubing to silicone cup used in vacuum extraction



Place the cup in the vagina, an excellent seal is created (As against the assistant’s hand in O’Sullivan’s)



Alternatively the tubing can be attached to silastic vacuum extractor cup which is placed inside introitus and may provide better seal.



As the vaginal wall distends, there is increase in intravaginal pressure the fundus of uterus rises and inversion is corrected



Once this is achieved, fluid is allowed to escape slowly from vagina

A. Obstetric ventouse applied on the inverted uterine fundus B. Reduction of the inverted uterus after the traction with ventouse 67

Instead of allies forceps alternatively vacuum cup can be used in Huntington procedure If this technique fails, Haultain's Operation can done. 

In this following steps are taken o Exteriorize the uterus o Cervical ring may be stretched

HAULTAIN’S PROCEDURE

Incision is made posteriorly through the cervix, relieving cervical constriction to increase the size of the ring and allowing traction on the round ligament for the replacement of uterus with subsequent repair of incision from inside the abdomen VAGINAL ROUTE 

Spinellis’s method o Anterior Colpotomy is done and incision on the constricting cervical ring is given for the replacement of uterus



Kustner’s method o Posterior Colpotomy is done and incision of the cervix similar to that of spinelli’s method



Hysterectomy o Failure of conservative surgery o Family is completed o Sepsis 68

MANEUVERS TO BE AVOIDED 

Excessive traction on the umbilical cord



Excessive fundal pressure



Excessive intra-abdominal pressure



Excessively vigorous manual removal of placenta

UTERINE INVERSION 

Treatment o Fluid therapy o Restoration of uterus o Pushing the fundus with a fisted hand along the axis of vagina through cervix back into pelvis



If failed o Terbutaline o MgSO4 o General anaesthesia o Laparotomy

PREVENTION 

Do not employ any method to expel the placenta when the uterus is relaxed



Patient should not be instructed to change her position



Pulling the cord simultaneously with fundal pressure should be avoided



Manual removal of placenta should be done in proper manner

CONCLUSION Acute uterine inversion is rare but accompanied by high risk of postpartum hemorrhage. The low incidence of uterine inversion leads to sparse experience in resolving this obstetrical emergency. The best prognosis occurs in situations where the diagnosis and manoeuvres for the uterine reversal are made at an early stage. Active

management of the third stage of labour may reduce the incidence of uterine inversion which could decrease the maternal morbidity and mortality. REFERENCES 1.

Dwivedi S, Gupta N, Mishra A, Pande S, Lal P. Uterine inversion: a shocking aftermath of mismanaged third stage of labour. Int J ReprodContraceptObstet Gynecol. 2013;2(3):292â&#x20AC;&#x201C;295. doi: 10.5455/2320-1770.ijrcog20130907.

Hostetler D, Bosworth M. Uterine inversion, a life-threatening obstetric emergency. J Am Board Fam Med. 2000;13(2):120â&#x20AC;&#x201C;123. doi: 10.3122/15572625-13-2-120

Momani A, Hassan A. Treatment of puerperal uterine inversion by the hydrostatic method; reports of five cases. Eur J ObstetGynecolReprod Biol. 1989;32:281. doi: 10.1016/00282243(89)90048-8.

Antonelli E, Irion O, Tolck P, Morales M. Subacute uterine inversion: description of a novel replacement technique using the obstetric ventouse. BJOG. 2006;113:846. doi: 10.1111/j.14710528.2006.00965.

Gerber S. uterine inversion. Rev Med Suisse Romande. 1996;116:277-83.

Wendel PJ, Cox SM. Emergent Obstetric management of uterine inversion. ObstetGynecolClin North Am. 1995; 22:261-74.

Ogueh O, Ayida G. Acute uterine inversion: a new technique of hydrostatic replacement. Br J ObstelGynecol 1997; 104 (8); 951-951

Johnson AB, A new concept in the replacement of the inverted uterus and a report of the cases, AM J Obstet Gynecol. 1949 Mar;57(3):557-62.

SEPSIS IN OBSTETRICS & GYNAECOLOGY Dr Setu Rathod, Prof Satish Kumar ABSTRACT Sepsis is a complex syndrome with its wide spectrum of severity and is one of the most common causes of death in Critical Care Units. The Surviving Sepsis Campaign launched in 2004, aimed at improving diagnosis, management and survival of patients with sepsis. The common obstetric conditions leading to sepsis include puerperal sepsis, septic abortions, chorioamnionitis and pyelonephritis. Among the gynaecological causes include Toxic Shock Syndrome, PID, IUCD and gynaecological cancers. Surviving Sepsis Campaign guidelines in 2008 incorporated two sepsis care bundles. The Resuscitation bundle includes seven key interventions to be achieved in 6-hour while five interventions have to be completed within 24-hours in the management bundle. Several observational studies support the hypothesis that sepsis care bundle have crucial role in improving outcomes from sepsis and reduce mortality from sepsis. Keywords: Sepsis Care Bundle, Septic shock, obstetric & gynaecological sepsis INTRODUCTION Sepsis is a complex syndrome which can occur both in obstetric &gynaecological patients. Septic shock is a life-threatening clinical syndrome caused by decreased tissue perfusion and oxygen delivery, as a result of severe infection and sepsis. Sepsis is the systemic inflammatory response due to bacteremia. When sepsis worsen to the point where blood pressure cannot be maintained with intravenous fluid alone, then the condition is called septic shock and may be accompanied with multiple organ dysfunction (liver, kidney, heart, brain). The mortality rate remains high, range between 25 and 50%.1 Maternal sepsis is a leading cause of preventable maternal morbidity and mortality in our country. Mostly, it is due to peripartum factors and the instigating organisms are usually from the polymicrobial flora of the genitourinary tract. However, non-obstetric infections that may get aggravated due to physiological alterations in pregnancy also make a significant contribution to morbidity due to infectious etiologies in pregnancy. The majority of the cases of sepsis present within 24-48 hours of delivery, 71

abortion, or rupture of membranes.2 The expeditious recognition of maternal sepsis and meticulous and appropriate management can prevent the progression to severe sepsis and septic shock. Incidence Studies from developed countries report maternal mortality ratio from sepsis to be 1.13/100,000.3In these countries, maternal sepsis is usually the result of puerperal sepsis and urinary tract infection. Sepsis continues to account for approximately 7.6% of maternal deaths in the United States. It is estimated that puerperal sepsis causes at least 75,000 maternal deaths every year, mostly in low-income countries. Studies from highincome countries report incidence of maternal morbidity due to sepsis of 0.1-0.6 per 1000 deliveries.4 Reasons for infection and sepsis during pregnancy Physiologic changes in the lower genital tract, such as a decrease in pH and increased glycogen in the vaginal epithelium, place the pregnant woman at risk for intraamniotic

infection.

addition,

normal

pregnancy

characterized

numerous changes in the hemostatic system, creating the hypercoagulable state which increases the risk of venous thromboembolic event occurrence.5 An elevated leukocyte count, associated with a slightly increased c-reactive protein, and increased heart rate of 15- 20 bpm, may mask early signs and symptoms of infection favouring the dissemination of bacteria into the blood-stream. Table 1. Conditions that predispose women to sepsis and septic shock syndrome during pregnancy Obstetrical Intra-amniotic infections Chorioamnionitis Septic abortion Invasive procedures for prenatal diagnosis (amniocentesis, chorionic villous sampling) Cervical cerclage placement Post-partum endometritis . Wound infection Necrotizing fasciitis

Non-obstetrical Pyelonephritis Septic pelvic thrombophlebitis Abscess of the appendix Cholecystitis Pneumonia Peritonitis (colon, small bowel) Gastoduodenum, biliary tract)

Chorioamnionitis The most common route is an ascending infection from one or more of the endogenous flora of the cervix or vagina. The most frequent causative pathogens are Aerobic Bacteria (group B Î˛-hemoytic Streptoccocus, Enteroccocus, other Streptoccocus species, Escherichia coli, Hemophilus Influenzae, Pseudomonas species, Staphylococcus aureus, Klebsiella Enterobacter species, Proteus species), Anaerobic Bacteria (Peptococcus species, Peptostreptococcus species, Clostridium species, Bacteroides species, Fusobacterium species) and other (Gardnerella vaginalis, Mycoplasme Hominis, Ureaplasma Urealyticum, Chlamydia Trachomatis). It is important to note when group B Î˛-Streptococcus or Escherichia coli are the causative pathogens, the incidence of bacteremia is higher (18% and 15%, respectively).6 The key clinical findings include fever, uterine fundal tenderness, maternal tachycardia (>100/min), fetal tachycardia (>160/min), and purulent or foul amniotic fluid. Chrorioamnionitis leads to a 2 to 3-fold increased risk for caesarean delivery and to 2 to 4fold increase in endomyometritis, wound infection, pelvic abscess, bacteremia, and postpartum hemorrhage. Women with chorioamnionitis in 10% have positive blood cultures (bacteremia). Fetal exposure to infection may lead to fetal death, neonatal sepsis, and septic shock. According to data from large studies, the incidence of chorioamnionitis is 5 per 1,000 cases after CVS; 3.7 per 1,000 cases after amniocentesis; and 8.8 per 1000 cases after cordocentesis, compared with 3 per 1,000 cases in non-exposed women.7,8 Septic abortion Abortion related with infection and complicated by fever, endometritis, and parametritis, remains one of the most serious threats to the health of women throughout the world. More than 95% of the septic abortion and septic shock cases are synonymous with illegal, criminal or non-medical abortion.9 The risk of sepsis from abortion rises from the first trimester of pregnancy to the second. In the first trimester, abortion is readily performed by vacuum curettage, usually in an outpatient setting. Incomplete abortions produced by incompetent physicians represent another risk factor. Insertion of rigid foreign objects into the uterus or cervix increases the risk of perforation and infection. 73

Puerperal Sepsis WHO defines puerperal sepsis as infection of the genital tract occurring at any time between the onset of the rupture of membranes or labour and the 42nd day postpartum in which fever and one or more of the following are present: pelvic pain, abnormal vaginal discharge, abnormal odour of discharge, and delay in the rate of reduction of size of the uterus. Causes of puerperal sepsis include puerperal pyrexia, breast abscess, UTI, endomyometritis, venous thrombosis and pulmonary embolism. Pyelonephritis It is the most frequent cause of bacterial shock associated with pregnancy. Enlargement of the uterus during the 2nd and 3rd trimester of pregnancy may cause stricture and/or obstruction of the ureters, a condition that predisposes to urinary infections and pyelonephritis. Escherichia coli is responsible for most of the cases. Klebsiella pneumoniae, Proteus species, and Enterobacter-Citrobacter are less common pathogens. All pregnant women should be screened for the presence of bacteriuria at their first prenatal visit. Failure to treat bacteriuria during pregnancy may result in as many as 25% of women experiencing acute pyelonephritis.10 Acute pyelonephritis has an incidence of approximately 0.1-1% in pregnancy; most occurs at second trimester.11It is associated with multiple complications, including fetal growth restriction, preterm labour, cerebral palsy and septicemia. Sepsis in gynecologic patients In Gynecology, incidence of sepsis have been increased during the last 15 years, presumably due to an aging population, an increase in the number of invasive procedures performed, and possibly due to a resistance to the current antibiotic treatment appeaed in the infecting pathogens. Toxic shock syndrome Toxic shock syndrome (TSS) is a rare, life-threatening, multiorgan illness that is caused by toxins that circulate in the bloodstream. Menstrual TSS is more likely in women using highly absorbent tampoons, using tampoons for more days of their cycle, and keeping a single tampon in place for a longer period of time.12 In the most typical form of toxic shock syndrome, the bacteria, most commonly, group A Streptococcus, Staphylococcus aureus and Clostridium sordellii produce an

enterotoxin that transfers into the bloodstream, provoking the overstimulation of the immune system. This, in turn, causes the severe symptoms of TSS, such as: fever, rash, myalgias, diarrhea, vomiting, headache, sore throat, vaginal discharge, rigors, desquamation (typically of the palms and soles), hypotension, and multi-organ failure (involving at least 3 or more organ systems). The mortality rate of toxic shock syndrome is approximately 5-15% and recurrences have been reported in as many as 30-40% of cases.13,14 Vaginal conditions during menses and tampoon use, contribute to the proliferation of toxin-producing S.aureus. An elevated vaginal temperature and neutral pH, both of which occur during menses are enhanced by tampon use, allowing bacterial proliferation. Endometrial blood can serve as a medium for bacterial growth; persistence of this blood in the cervical and vaginal canal with tampon use has been also shown to increase the proliferation of S.aureus. Pelvic inflammatory disease (PID) Pelvic inflammatory disease (PID) refers to acute infection of the upper genital tract structures. Patients are often infected with two or more infectious agents and commonly these are Chlamydia trachomatis, Neisseria gonorrhoeae and Mycoplasma genitalium which are mainly sexually transmitted. Abdominal pain (usually lower) or tenderness, fever, nausea, vomiting, back pain, unusual or heavy vaginal discharge, abdominal uterine bleeding, painful urination, painful sexual intercourse are some of the symptoms of PID. Ascending infection occurs involving cervicitis, endometritis, salpingitis or hydro-, pyosalpinx. In tubes and ovaries, salpingo-oophoritis (acute, subacute and chronic), tuboovarian abscess generalized peritonitis or pelvic abscess can occur. Infection may be also spread through the uterine wall into broad ligaments to cause pelvic cellulitis (parametritis), a broad ligament abscess or septic thrombophlebitis of the ovarian or uterine veins, leading to septicemia with few local signs. PID may cause sepsis, septic shock and even death. Even if they survive, as many as 15% to 20% of these women experience longterm sequelae of PID, such as ectopic pregnancy, tuboovarian abscess, infertility, dyspareunia and chronic pelvic pain.15

Intrauterine devices (IUD) Intrauterine contraceptive devices (IUDs) are highly effective, long-term methods of contraception. 16 The total number of current IUD users is estimated at over 150 million women worldwide. Infection risk is a relative contraindication to fitting any woman with an IUD; it is only present for a few weeks after insertion and probably arises from an undiagnosed cervical infection at the time of insertion. Cases of vaginitis transfer of actinomyces into the uterine cavity, PID, and even toxic shock syndrome and sepsis have occasionally been reported. Conditions which represent an unacceptable health risk if an IUD is inserted are: current PID, current purulent cervicitis, chlamydial or gonorrheal infection, as well as pelvic tuberculosis, puerperal sepsis and septic abortion. Gynecologic cancer Usually after having undergone a difficult operation, followed up by several chemotherapy cycles, has reduced defenses against infection due to a) reduced antibody formation; b) deficient cell immunity c) reduced or abnormal granulocyte d) damaged mucocutaneous barriers, such as, ulceration of the oropharynx due to methotrexate toxicity e) obstruction of biliary and urinary tracts. Thus, myelosuppression may also give rise to an acute septic problem associated with neutropenia, granulocytopenia. In these patients, any infection may have an acute form leading to rapid septicemia and severe shock developing rapidly. When operations for gynecologic cancer involve the intestine there is increased possibility for sepsis. Management of Septic Shock Sepsis Care Bundles17 Sepsis and Septic shock are medical emergencies and it is recommended that treatment and resuscitation should begin immediately. As per the SSC (Surviving Sepsis Campaign) guidelines specific anatomic diagnosis of infection requiring emergent source control has to be identified or excluded as rapidly as possible in patients with sepsis or septic shock, and any required source control intervention should be implemented as soon as medically and logistically practical after the diagnosis is made. Hour 1 bundle is the latest of the good practice guidelines to be followed. 76

1. Measure lactate level (Remeasure if initial lactate>2 mmol/L) 2. Obtain blood cultures before administering antibiotics 3. Administer broad spectrum antibiotics 4. Begin to rapidly administer 30 ml/kg crystalloid for hypotension or lactate ≥4 mmol/L. 5. Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation) to maintain a MAP (mean arterial pressure) ≥65mm Hg. Norepinephrine is recommended as the first choice vasopressor. This is replacing the 3 hour bundle which includes the above 4 points and the 6 hour bundle which further includes:6. In the event of persistent hypotension after initial fluid administration(MAP<65 mm Hg) or if initial lactate was ≥4 mmol/L, reassess volume status and tissue perfusion. 7. Remeasure lactate if initial lactate elevated. If shock is not resolving quickly, further hemodynamic assessment (such as assessing cardiac function) to determine the type of shock is required. 2 broad spectrum antibiotics of 2 different classes are recommended. CONCLUSION Early intervention is the key to treatment in patient with sepsis. In Obstetrics, a prior history of peripartum infection, prolonged rupture of membranes, or genitourinary instrumentation associated with cardiovascular instability and fever should raise the possibility of septic shock. Volume expansion and correction of hypovolemia are critical. Understanding the pathways, mediators, feedback loops and interactions involved in the pathogenesis of sepsis and organ failure has advanced profoundly, giving us the opportunity to treat sepsis-related multiple organ failure, and therefore, improve both survival rate and quality of life in women patients. REFERENCES 1.

Kumar, Vinay, Abbas, Abul K; Fausto, Nelson, & Mitchell, Richard N (2007). Robbins Basic Pathology (8th ed). Saunders Elsevier, pp. 102-103 ISBN 978-1-4160-2973-1.

Ronsmans C, Graham WJ. Lancet maternal survival series steering group. Maternal mortality: who, when, where, and why. Lancet. 2006; 368:1189-200.

Cantwell R, Clutton-Brock T, Cooper G. Centre for Maternal and Child Enquiries (CMACE). Saving mothersâ&#x20AC;&#x2122; lives: reviewing maternal deaths to make motherhood safer: 2006-08. The eighth report on confidential enquiries into maternal deaths in the United Kingdom. BJOG. 2011; 118:1203.

Van Dillen J, Zwart J, Schutte J, van Roosmalen J. Maternal sepsis: epidemiology, etiology and outcome. CurrOpin Infect Dis. 2010; 23: 249-254.

Mitic G, Kovac M, Jurisic D, Djordjevic V, Ilic V, Salatic I, Spacic D, NovakovMikic A. Clinical characteristics and type of thrombophilia in women with pregnancyrelated thromboembolic disease. GynecolObstet Invest 2011; (in press).

Newton E. Chorioamnionitis and intraamniotic infection, ClinObstetGynecol 1993; 36: 79

Cederholm M, Haglund B, Axelsson O. Maternal complications following amniocentesis and chorionic villous sampling for prenatal karyotyping. BJOG 2003; 110: 392-399.

Tongsong T, Wanapirak C, Kunavikatikul C, Sirirchotiyakul S, Piyamongkol W, Chanprapaph P. Fetal loss rate associated with cordocentesis at midgestation. Am J ObstetGynecol 2001; 184: 719-72. 5-808.

Burkman RT, Atienza MF, King TM. Culture and treatment results in endometritis following elective abortion. Am J ObstetGynecol 1977; 128: 556-559.

10. Gilstrap LC 3rd, Ramin SM. Urinary tract infections during pregnancy. ObstetGynecolClin North Am 2001; 28: 581-591. 11. Cunningham FG, Gant NF, Leveno KJ, Gitstrap LC, Hauth JC, Wenstrom KD. Renal and urinary tract disorders. Williams obstetrics, New York: McGraw-Hill; 2001. p. 1251-71. 12. Shands KN, Schmid GP, Dan BB. Toxic-shock syndrome in menstruating women: association with tampon use and Staphylococcus aureus and clinical features in 52 cases. N Engl J Med 1980; 303: 1436-1442. 13. Stevens DL. Invasive group A streptococcus infections. Clin Infect Dis 1992; 14: 2-11. 14. Demers B, Simor AE, Vellend H. Severe invasive group A streptococcal infections in Ontario, Canada: 1987-1991. Clin Infect Dis 1993; 16: 792-800. 15. Dulin JD, Akers MC. Pelvic inflammatory disease and sepsis. Crit Care NursClin North Am. 2003 mar; 15(1):63-70. 16. An extremely low-cost option: IUCD Method Brief No 3. Nairobi: Kenya Ministry of Health 2003. 17. SSC Survival sepsis Campaign 2016 guidelines.

SHOULDER DYSTOCIA Dr Swathy Srinivasan, Prof. Rani Reddi ABSTRACT: Shoulder dystocia is an unpredictable and unpreventable obstetric emergency that places the pregnant women and the fetus at risk of injury. Studies have shown that pregnancy, antepartum and intrapartum risk factors have extremely poor predictive value for shoulder dystocia. Several techniques to facilitate delivery exist, and there is evidence that a systematic approach and simulation training can improve outcomes and documentation. The purpose of this document is to provide clinicians with evidence based information regarding management of pregnancies and deliveries at the risk or complicated by shoulder dystocia. Keywords: shoulder dystocia, obstetric emergencies. INTRODUCTION: Shoulder dystocia is an obstetric complication that has been recognized and discussed for atleast two centuries. It is the nightmare of obstetricians. It represents a huge risk of morbidity for both the mother and the fetus. It remains an unpreventable and unpredictable obstetric emergency. DEFINITION: Shoulder dystocia is defined when further delivery of the fetal body is prevented by impaction of the fetal shoulder behind the maternal symphysis or sacral promontory1. It is further clarified by defining as delivery with longer than 60 seconds between delivery of the fetal head and body it requires the use of ancillary obstetric maneuvers2. The incidence ranges from 0.2% to 2.1% of all vaginal deliveries3. RISK FACTORS4: Maternal- fetal (pre-labour) 1) Macrosomia 2) Diabetes 3) Maternal BMI >30KG/M2. 79

4) Short stature 5) Previous shoulder dystocia 6) Abnormal pelvic anatomy 7) Post dates pregnancy 8) Advanced maternal age 9) Male gender 10) Induction of labour INTRAPARTUM: 1) Prolonged active phase of first stage labour 2) Prolonged second stage labour 3) Assisted vaginal delivery ( forceps or vaccum) 4) Oxytocin augmentation 5) Secondary arrest 6) Epidural anesthesia DIAGNOSIS: 1) Turtle neck sign- Definite recoil of the fetal head against the perineum. 2) Fetal face becomes plethoric 3) Inadequate spontaneous restitution 4) Failure of shoulder to descend. PRINCIPLES OF MANAGEMENT: 1) Call for extra help 2) Traction over fetal head to be avoided 3) Not to apply fundal pressure 4) To give wide episotomy 5) To call the anaesthetist and the paediatrician

MANAGEMENT: When a case of shoulder dystocia is recognized, every effort should be made to prepare a rapid, in grained and well- coordinated stepwise plan. Mc Roberts maneuver: It is recommended as a initial technique for disimpaction of anterior shoulder. When combined with suprapubic pressure, it results in resolution in 58% of cases5. It involves flexion of motherâ&#x20AC;&#x2122;s legs onto her abdomen. There is rotation of pubic symphysis upward and decrease in angle of pelvic inclination. The angle created by a line bisecting the longitudinal axis of the fifth lumbar vertebra and the longitudinal axis of the upper sacrum also increased. Woodâ&#x20AC;&#x2122;s maneuver ( fetal manipulation): In this maneuver, the practioner pushes the posterior shoulder through a clockwise 180 degree arc by applying pressure on the anterior surface of posterior shoulder. This is done by inserting two fingers in the posterior vagina. Extraction of the posterior arm: The practioner hand is introduced into the vagina along the fetal posterior humerus. The arm should be swept across the fetal chest and then it is delivered by gentle traction. Zavanelli maneuver: It is done by pushing the fetus back into the uterus and delivering by caserean section. Cleidotomy: It is done by breaking the clavicles. It is done foer a dead baby or a living anencephalic baby.

Complications6: MATERNAL: 1) Post partum haemorrhage 2) 3rd or 4th drgree perineal tear 3) Symphyseal separation or diathesis 4) Recto- vaginal fistula 5) Uterine rupture FETAL: 1) Brachial plexus palsy 2) Fetal death 3) Fetal hypoxia, with or without permanent neurologic damage 4) Clavicle and humerus fracture. CONCLUSION: To conclude, despite its infrequent occurrence, all healthcare providers attending the pregnancies must be prepared with a high level of awareness and training to handle vaginal deliveries complicated by shoulder dystocia. REFERENCES: 1) Royal College of Obstetricians and Gynaecologists. RCOG Guideline No.42, Dec.2005. 2) Beall MH, Spong C,McKay J et al: Objective definition of shoulder dystocia: A prospective evaluation. Am J Obstet Gynecol 179:934,1998. 3) Lurie S, Levy R, BenArie A et al: Shoulder dystocia: could it be deducted from the labour partogram? Am J Perinatol 12:61,1995. 4) Amy G. Gottlirb, Henry L. Galan. Shoulder dystocia: an update. Obstet Gynecol Clin N Am 3492007) 501-531. 5) Gonik B, Allen R,Sorab J: Objective evaluation of the shoulder dystocia phenomenon: Effect of maternal pelvic orientation on force reduction. Obstet Gynecol 74: 44,1989. 6) Clinical Negligence Ssheme for Trusts. Maternity: Clinical Risk Management Standards. London: NHS Litigation Authority;2010.

NON-OBSTETRIC CAUSES OF ACUTE ABDOMEN IN PREGNANCY Dr. Chandana Galidevara, Prof. Seetesh Ghose ABSTRACT Abdominal pain during pregnancy presents a unique clinical and diagnostic challenge, as physiologic changes in pregnancy can alter the presentation of common pathologies and atypical presentations can occur making the diagnosis elusive. The incidence of non-obstetrical causes of pain abdomen in pregnancy is around 1 in 500 to 635. About 0.2% to 1% women would need a surgical intervention for the same. The common causes include appendicitis, cholecystitis, acute pancreatitis, pyelonephritis, ureteric colic, bowel obstruction, adnexal torsion, gastroenteritis and peptic ulcer disease. The diagnostic evaluation of these conditions is altered and constrained by pregnancy. Radiologic tests and invasive examinations raise concerns about fetal safety during pregnancy which have to be taken into consideration before subjecting the pregnant woman to them. Any decision for surgery or therapy has to take into account both the interests of the mother and the fetus. All these diagnostic uncertainties perpetuate the delay in decision making awaiting clear-cut symptoms and signs. This delay when prolonged carries a high risk to the mother and the fetus. Hence it is important to be familiar with these causes and have a high level of suspicion when obstetric causes are ruled out. Keywords: Pain abdomen, Pregnancy. INTRODUCTION Acute abdomen in pregnancy due to non-obstetric causes presents with altered symptomatology. Resemblance of early acute abdomen symptoms like nausea, vomiting, pain abdomen to those of normal pregnancy and the anatomical displacement of abdominal organs by the pregnant uterus greatly masks the clinical picture and enhances surgical delay. This delay significantly increases maternal morbidity and results in a poor fetal outcome. Those who have early surgical intervention have a better maternal and perinatal outcome. Although laparotomy is the gold standard for surgical conditions, laparoscopy can be an alternative in select cases. 83

CONDITIONS CAUSING ACUTE ABDOMEN IN PREGNANCY APPENDICITIS Appendicitis is the most common cause of acute abdomen with a frequency of 1 in 500-2000 pregnancies. It accounts for 25% of operative indications for non-obstetric surgery in pregnancy. There can be blunting of signs and symptoms and changes in location of appendix as pregnancy advances. The symptoms are right lower quadrant pain, vomiting and fever. Right iliac fossa tenderness (at McBurneys point) is a reliable sign and other signs include rebound tenderness, guarding and rigidity which are not very specific. Leucocytosis with shift to left (granulocytosis) occurs and a urine examination can help to differentiate this condition from pyelonephritis or renal calculus. Graded compression ultrasound is the imaging modality used in diagnosing appendicitis and it has better accuracy in first and second trimesters while in third trimester owing to technical difficulties and with appendiceal perforation, accuracy is decreased. Without perforation, the fetal outcome is good whereas, the fetal loss is high with perforation and peritonitis. Preterm contractions can occur due to localized peritonitis. The chance of perforation increases with delay in surgery for more than 24 hours of presentation and pregnancy should not deter a surgeon from performing appendicectomy when diagnosis is suspected. Incisions used in open appendicectomy can be a muscle splitting incision in the right iliac fossa, a right pararectal incision or a midline vertical incision. Laparoscopy can be performed using open technique (Hasson technique) in first and second trimesters. Copious irrigation and use of intraperitoneal drain in case of acute appendicitis with diffuse peritonitis is advised. Antibiotics administered are Cefuroxime, Ampicillin and Metronidazole. Overall maternal mortality is less than 1% when appendicitis is diagnosed promptly and treated. ACUTE CHOLECYSTITIS This is the second most common cause of acute abdomen in pregnancy with an incidence of 1 in 1600-10000 pregnancies. The progesterone induced smooth muscle relaxation of gallbladder promotes stasis of bile and predisposes to gallstone formation. Elevated levels of estrogen further increase the lithogenicity of bile causing cholelithiasis

and subsequently acute cholecystitis. Cholelithiasis can also lead to choledocholithiasis and biliary pancreatitis. The symptoms include colicky or stabbing right upper quadrant radiating to the back, vomiting, nausea, dyspepsia and intolerance to fatty foods. Murphyâ&#x20AC;&#x2122;s sign is less specific in pregnancy. Serum levels of direct bilirubin and transaminases may be elevated. Serum amylase may be elevated in one third of patients. Serum alkaline phosphatase levels are elevated but less helpful as estrogen causes rise in alkaline phosphatase even otherwise in pregnancy. Ultrasound is the procedure of choice due to its accuracy of 95 % in detecting gallstones. The ultrasound findings are gallbladder calculi, wall thickening, pericholecystic fluid collection, sonographic Murphyâ&#x20AC;&#x2122;s sign, dilatation of intra and extra hepatic ducts in common bile duct obstruction. Although medical management was recommended in the earlier studies , surgery is increasingly used as the primary treatment as recuurence rate is high, shorter hospital stay, minimises the development of complications like perforation, sepsis and peritonitis which can be life threatening to the mother and cause fetal loss. Non-surgical management increases the risk of gallstone pancreatitis upto 13 %. Surgical

approach

can

open

cholecystectomy

laparoscopic

cholecystectomy. It is advisable to perform laparoscopy by open technique and avoid verres needle or direct trocar entry to minimize organ injury. The procedure is safe in the first, second and early third trimester. If acute cholecystitis with symptomatic choledocholithiasis is present, then open cholecystectomy with choledochotomy and extraction of calculi is performed. The maternal mortality is low with acute cholecystitis unless complications like cholangitis or acute pancreatitis ensue leading to increase in the maternal mortality and fetal loss rate. ACUTE PANCREATITIS Incidence is 3 in 10000 pregnancies. It usually occurs in the third trimester or early postpartum. The causes for pancreatitis are cholelithiasis, abdominal surgery, blunt trauma abdomen, hypertriglyceridemia and drugs like thiazides and tetracyclines. Signs and symptoms include mid epigastric pain, left upper quadrant pain radiating to left flank, anorexia, nausea, vomiting, decreased bowel sounds and low grade fever, abdominal tenderness, muscle rigidity and hypocalcemia. 85

The main laboratory finding is increased amylase activity. Diagnostic blood tests include serum amylase, serum lipase, triglyceride levels and ionized calcium levels. Ultrasound is the first line imaging modality in pregnancy and it also identifies cholelithiasis.

Conservative

medical

management

includes

intravenous

fluids,

nasogastric suctioning, total parenteral nutrition, use of analgesics, antispasmodics, fat restriction and antibiotics. although

laparoscopic

Management of gallstone pancreatitis is controversial, cholecystectomy

and

endoscopic

retrograde

cholangiopancreatography (ERCP) are often used and may be associated with lower complication rates. Fetal shielding can be used in which a lead apron is placed over maternal abdomen. In hypertriglyceridemia-induced acute pancreatitis, lipoprotein apheresis and even therapeutic plasma exchange can be used PYELONEPHRITIS Pyelonephritis in pregnancy will generally present with urgency, frequency, dysuria (painful urination), hematuria, fever (above 100.3 Â°F), chills, flank pain, costovertebral angle tenderness, uterine contractions and preterm labour and septic shock. Treatment needs to be tailored to the individual patient. Due to the additional risk of complications in pregnancy, most women will require at least a short hospitalization Pyelonephritis is treated with antibiotics. The antibiotics the patient is given should be determined by urineculture and sensitivity analysis. We need to use the safest antibiotic in pregnancy. Common medications that are used initially include ceftriaxone, cefepime, cefotaxime, ceftazidime, cefazolin, ampicillin with gentamicin. Intravenous (IV) treatment is generally given until the patient has had no fever for at least 24 hours and symptoms have improved. Oral antibiotics should then be given until the patient has had 14 days of total treatment. Supportive treatment with antipyeretics and fluids is equally important. INTESTINAL OBSTRUCTION Intestinal obstruction in pregnancy is rare at 1 in 2500 to 1 in 16709 deliveries. Although uncommon, it carries significant maternal (6%) and fetal (26%) mortality. Often, this is due to delay in diagnosis and treatment. Furthermore, there is a reluctance to utilise radiation-based investigations.

Adhesions are the commonest cause of intestinal obstruction in pregnancy and account for more than half the causes found at laparotomy. The incidence and complication rates increase with gestational age, particularly in the third trimester. The risk increases as the uterus enlarges. Other causes include volvulus, intussusception, hernia, carcinoma, appendicitis, and idiopathic â&#x20AC;&#x153;ileusâ&#x20AC;?. The diagnosis of intestinal obstruction in pregnancy is difficult. Signs of acute abdomen may not be as prominent in the pregnant abdomen when compared to the non-pregnant one due to the stretched anterior abdominal wall being less sensitive to parietal peritoneal irritation. Signs and symptoms are generalised abdominal pain, nausea, bilious vomiting and abdominal distension, indicating an obstructive pathology. Previous history of surgery should always raise suspicion as adhesions are an important cause for intestinal obstruction. In suspected intestinal obstruction, Xray, CT or MRI are the options available. In contrast to MRI, CT involves ionizing radiation, whereas MRI requires gadolinium contrast, with an uncertain safety profile in pregnancy. However, when risks of radiation are outweighed by the maternal-fetal risks of missing the diagnosis, these imaging modalities are justified.. Management of intestinal obstruction in pregnancy is similar to nonpregnancy. Clinical suspicion is vital and joint management between surgeons and obstetricians is crucial. The basis of treatment is timely surgery, minimising delays in decision. The initial treatment consists of nasogastric aspiration with aggressive intravenous fluids to correct electrolyte disturbances. Failure of conservative treatment and demonstration of complete obstruction on CT are indications for early surgery as persistence will contribute to an increase in mortality and morbidity. Perinatal death from hypoxia secondary to maternal hypovolaemia, sepsis, and peritonitis has been reported. Maternal nutritional deficiencies can occur if the patient is kept nil per oral for a protracted period. Surgery should be performed via a midline incision to allow adequate exposure and complete exploration of abdomen with minimal manipulation of uterus. The entire bowel must be examined for other areas of obstruction and viability. Segmental resection with or without anastomosis may be necessary in the presence of gangrenous bowel. When adhesions are the cause, adhesiolysis and retrograde decompression of the bowel may be sufficient.Iffetal distress is present or if there is inadequate exposure at

laparotomy near term, delivery by caesarean section should precede the relief of obstruction. OVARIAN TORSION Ovarian torsion is a clinical entity that can involve the tube, ovary, and ovarian pedicle either separately or together. It is one of the common gynaecologic emergencies, with a reported incidence of 3% . However, the diagnosis of ovarian torsion can be difficult to make. The majority of women with torsion are seen in the emergency department with an acute onset of abdominal pain, nausea or vomiting and fever. Peritoneal signs are rare. The differential diagnosis for ovarian torsion is broad and includes many other emergency causes for abdominal pain, such as ectopic pregnancy, pelvic inflammatory disease, appendicitis, diverticulitis, ovarian cyst, and renal colic. If nonspecific severe pain is seen, torsion can be an important differential diagnosis in the evaluation of a potentially surgical abdomen. Ultrasound is the imaging modality of choice which usually shows an enlarged or cystic ovary with absent or diminished vascular flow.

Early diagnosis and

laparoscopic treatment is recommended in first and second trimester for suspected torsion, particularly to salvage the ovary and adnexa. Laparotomy is done in third trimester for detorsion or sometimes oophorectomy is performed in cases where the ovarian tissue is necrosed and cannot be salvaged. The maternal mortality is less if diagnosed and operated in 24 hours. CONCLUSION Although pregnancy blunts the clinical picture of conditions causing acute abdomen, a high index of suspicion, early diagnosis, treatment or surgical intervention results in a better perinatal outcome and decreased maternal morbidity. REFERENCES 1.Non Obstetric Causes and Presentation of Acute Abdomen among the Pregnant Women MonoarulHaque, Farah Kamal, et al. J Family Reprod Health. 2014 Sep; 8(3): 117â&#x20AC;&#x201C;122. 2. Non-obstetrical acute abdomen during pregnancy Goran Augustin *, Mate Majerovic. European Journal of Obstetrics &Gynecology and Reproductive Biology 131 (2007) 4â&#x20AC;&#x201C;12 3. Severe Acute Pancreatitis in Pregnancy .Bahiyah Abdullah, ThanikasalamKathiresan Pillai. Case Reports in Obstetrics and Gynecology, Volume 2015, Article ID 239068, 4 pages

4. Acute pancreatitis in pregnancy: A treatment paradigm based on our hospital experience. Sunil Kumar Juneja, Shweta Gupta, Satpal Sing Virk, Pooja Tandon, and VidushiBindal.Int J Appl Basic Med Res. 2013 Jul-Dec; 3(2): 122â&#x20AC;&#x201C;125 5. Acute intestinal obstruction complicating pregnancy: diagnosis and surgical management. Sanoop Koshy Zachariah, Miriam George Fenn.BMJ Case Reports 2014

AMNIOTIC FLUID EMBOLISM Dr. Rajasulochana AR., Dr.P. Pallavee ABSTRACT Amniotic fluid embolism (AFE) is one of the catastrophic complications of pregnancy in which amniotic fluid, fetal cells, hair, or other debris enters into the maternal pulmonary circulation. Etiology largely remains unknown, however there are two etiologies of AFE (i) the fetal materials create physical obstructions in the maternal microvessels in various organs, such as the lung; and (ii) the liquids cause an anaphylactoid reaction that leads to pulmonary vasospasm and activation of platelets, white blood cells and/or complements. The pathophysiology of AFE is not completely understood; possible historical reason is that any breach of the barrier between maternal blood and amniotic fluid forces the entry of amniotic fluid into the systemic circulation and results in a physical obstruction of the pulmonary circulation. The clinical findings are characterized mainly by cardiopulmonary collapse, disseminated intravascular coagulation (DIC) and atonic bleeding. Besides basic investigations, lung scan, serum tryptase levels, serum levels of C3 and C4 complements, zinc coproporphyrin, serum sialylTnare being used as serum markers of AFE. At the primary medical institution, initial treatments for shock, airway management, vascular management, fluid replacement, administration of anti-DIC therapy and administration of fresh frozen plasma should be provided. Treatment is mainly supportive, but exchange transfusion, extracorporeal membrane oxygenation are also been tried. The maternal prognosis after amniotic fluid embolism is very poor though infant survival rate is around 70%.C1 esterase inhibitor activity in AFE cases is significantly lower than those of normal pregnant women and hence may be a potential therapeutic option. Key words: amniotic fluid embolism, cardiopulmonary collapse, disseminated intravascular coagulation. INTRODUCTION Amniotic fluid embolism (AFE) is one of the most serious complications in obstetrics. It was first reported by Meyer in 1926, and the syndrome was first described by Steiner and Lushbaugh in 1941. The condition is exceedingly rare and devastating, affecting women during labour, delivery, or postpartum and the exact pathophysiology is 90

still unknown. AFE has also been described following trauma, cervical laceration, abortion, amniocentesis, and manual removal of the placenta. Despite earlier recognition and intensive critical care, the mortality of AFE remains high and has been estimated at between 5% and 15% of all maternal deaths. This review aims to summarize the current evidence surrounding the incidence, pathogenesis, diagnosis, and treatment strategies for AFE. DEFINITION The definition of AFE varies between countries throughout the world. Four criteria must be present to make the diagnosis of AFE1, 2 1. Acute hypotension or cardiac arrest. 2. Acute hypoxia. 3. Coagulopathy or severe hemorrhage in the absence of other explanations. 4. All of these occurring during labour, cesarean delivery, dilation and evacuation, or within 30 min postpartum with no other explanation of findings. Incidence and Outcome Incidence of AFE is estimated to occur between 1 in 8000and 1 in 80,000 deliveries. The true incidence is unknown because of the variability in diagnosis and reporting. Geographic differences in AFE incidence are also apparent (e.g. North America is three times higher than Europe)3. Previous studies revealed mortality rates as high as 61-86%, but recent estimates suggest a case fatality of 13-26%. This decrease in risk for maternal mortality from AFE may be the result of early diagnosis and better resuscitative care as well as changes in case inclusion criteria. Fetal outcome remains poor if AFE occurs before delivery, with a neonatal mortality rate approximately more than 10%. Etiology & Risk Factors Amniotic fluid embolism is considered an unpredictable and unpreventable event with an unknown cause. AFE may occur in healthy women during labour, during cesarean section, after abnormal vaginal delivery, during the second trimester of pregnancy or upto 48 hrs post delivery. It can also occur during abortion, after abdominal 91

trauma, during amnioinfusion and following intrauterine injection of hypertonic saline to induce abortion. Table 1.Identified risk factors4 Maternal

Fetal



Older maternal age.



Fetal distress.



Multiparity.



Fetal death.



Intense contractions during labor.



Male baby.



Abdominal trauma.



Cesarean section.



Induction of labor.



Placenta previa.



Eclampsia.



Multiple pregnancy.



Tears in the uterus or cervix.



Early separation of the placenta from the uterus wall.

Pathogenesis The pathogenesis of AFE is not completely understood but various theories have been published. There are two theories regarding the pathogenesis of AFE. The first historic idea is that a disorderly labor, abnormal placentation, surgical trauma, or any other breach of the barrier between maternal blood and amniotic fluid forces the entry of amniotic fluid into the systemic circulation and results in a physical obstruction of the pulmonary circulation6. There must be a pressure gradient that favours transfer of fluid from the uterus into the systemic circulation. The second and increasingly favoured hypothesis suggests that entry of amniotic fluid into the maternal circulation activates inflammatory mediators, causing a humoral or immunologic response7. Because of which it is named as “anaphylactoid syndrome of pregnancy.” This theory is supported by the fact that amniotic fluid contains vasoactive and procoagulant products including platelet-activating factor, cytokines, bradykinin, thromboxane, leukotrienes, and arachidonic acid.

pulmonary vessel obstruction Mechanical block pulmonary hypertension Amniotic fluid embolism

Hypoxemia

Release of inflammatory mediators

pulmonary vasospam & R heart failure

Concentrations of tissue factor and tissue factor pathway inhibitor, which trigger intravascular coagulation, are higher in amniotic fluid than in maternal serum. It is speculated that maternal plasma endothelin concentrations are increased by entry of amniotic fluid into the systemic vasculature.

Cardiopulmonary collapse. cause: emboli / anaphylactoid reaction

Atonic bleeding. cause: mainly anaphylactoid reaction

Endothelin acts as a bronchoconstrictor as well as a pulmonary and coronary vasoconstrictor, which may contribute to respiratory and cardiovascular collapse. The direct procoagulant property of amniotic fluid may explain the prevalence of disseminated intravascular clotting (DIC) in AFE .Fetal contribution toward the disease is also evident; AFE is more common in women carrying a male fetus and with rhesus iso-immunization. Severity in AFE presentation is likely because of variations in antigen exposure and individual response. Further understanding is needed to identify processes that sensitize or predispose some women to develop AFE following utero-placental breach and maternal exposure to fetal material.

Clinical Presentation The diagnosis of AFE is clinical and a diagnosis of exclusion. There is a great variability in the presentation from classical cardiopulmonary collapse with coagulopathy to minor and subclinical presentations. AFE symptomatology evolution can be divided classically into three phases. 1. The initial phase is characterized by pulmonary hypertension resulting in severe V:Q mismatch, hypoxemia, and right heart failure. 2. The second phase involves decreased left ventricular function and development of acute pulmonary edema. 3. The third phase is characterized by heart failure, worsening acute lung injury/acute respiratory distress syndrome (ARDS), and coagulopathy. Signs and symptoms Hypotension*

Chills

Hypoxia*

Headache

DIC*

Nausea

Altered mental status*

Vomiting

Bronchospasm*

Seizures

Uterine atony*

Fever

Fetal distress*

Chest pain

* - present in 80-100% of cases Signsand symptoms pertaining to systems Cardiovascular Respiratory Hypotension Respiratory arrest

Hematologic Coagulopathy

Cardiogenic shock Right heart failure Left heart failure Dysrhythmias Tachycardia Cardiac arrest

DIC

Hypoxemia

Tachypnea/dyspnea Haemorrhage Pulmonary edema / ARDS V:Q mismatch

Neurologic Altered mental status Seizures

Obstetric Fetal distress Uterine atony

Differential Diagnosis AFE

Haemorrhage

Sepsis

Anaesthetic

Pulmonary

accident

thromboembolism

Anaphylaxis

Hypotension

+++

Hypoxia

+++

+/-

+++

Coagulopathy

+++

Sudden onset

Yes

Prior fever

Yes

Recognised

Haemorrhage

Chorioamnionitis

Anaesthetic

Medication

antecedent event

administration

Atypical AFE In contrast to typical embolism, cardiopulmonary collapse does not occur in atypical embolism but the first symptom is life threatening hemorrhage due to DIC. Atypical embolism usually observed during caesarean section or immediately after it, in cases of profound rupture of uterine cervix, as well as in the course of placenta abruption and in association with induced mid trimester abortion. Biomarkers Many biomarkers have been proposed to be of benefit in the diagnosing AFE8; however, further work is needed to determine whether these markers provide adequate sensitivity and specificity for fatal and nonfatal AFE. 1. Serum tryptase levels in fatal cases of AFE have been found elevated7â&#x20AC;&#x201C;10 times greater than controls. Increased tryptase levels are also associated with anaphylaxis and should be differentiated from AFE. 2. Complement acts through either the classical pathway or indirectly by the release of anaphylactoid peptides. Complement activation products C3a and C5a bind to the high-affinity immunoglobulin E receptor expressed on mast cell membranes, which determine their activation and degranulation. Complement may potentially be a reliable diagnostic biomarker. 3. Sialyl-Tn (STN) is a component of meconium and mucin derived from amniotic fluid. The presence of STN in maternal serum in patients with suspected AFE is a direct diagnostic test confirming that amniotic derived mucin has crossed into the maternal circulation. 4. Low C3 and C4 complement levels along with high STN have been associated with complement activation. 5. C1 esterase inhibitor (C1INH) is a major inhibitor of C1 esterase, coagulation factor XII activation and kallikrein.C1INH is an important factor in the development of coagulopathy and an important future diagnostic or prognostic biomarker.

Detection of squamous cells or other debris in the pulmonary arterial bed of women is no longer considered diagnostic of AFE. Blood samples and complete autopsy supported by histological and immunehistochemical analysis are needed as soon as possible following death in cases of fatal AFE, to reduce post-mortem variations and allow for immunological marker analysis. MANAGEMENT Clinical management of AFE should focus on 

aggressive cardiovascular support



treatment of hypoxia



management of hemorrhage and coagulopathy



delivery of the fetus

In the setting of maternal cardiac arrest, basic and advanced life support should be undertaken as per American Heart Association guidelines. Key interventions in the setting of maternal cardiac arrest include 

Manual left uterine displacement (if the uterus is palpated at or above the umbilicus)



Perimortem caesarean delivery (considered if return to spontaneous circulation has not been achieved within approximately 4 min of resuscitative efforts) These interventions should be implemented to help relieve aortocaval

compression and optimize cardiopulmonary resuscitation. AFE is a diagnosis of exclusion, and all other causes of maternal collapse must be considered. Early and effective basic and advanced life support is essential to optimize maternal outcome. Following initial resuscitative measures, most patients will require continued monitoring and support in an ICU. Monitoring with ECG tracings, pulse oximetry, and noninvasive blood pressure cuffs should be immediately applied. Large bore intravenous access above the diaphragm should be obtained; interosseous or ultrasound guidance should be considered for 97

difficult vascular access. An arterial line should be sited in hemodynamically unstable women. A central line and pulmonary artery catheter may provide hemodynamic information and facilitate drug administration, but placement should not delay treatment. 1. Initial diagnostic evaluation should include continuous pulse oximetry and arterial blood gas (ABG) measurements to determine the degree of hypoxemia. 

ABG levels: Expect changes consistent with hypoxia/hypoxemia. 

Decreased pH.



Decreased PO2.



Increased PCO2 levels.



Base excess increased.

2. Serial complete blood counts and coagulation studies should be sent to follow trends and detect early coagulopathy. 

CBC with platelets. 

Hemoglobin and hematocrit levels should be within reference ranges.

 

Thrombocytopenia is rare.

Prothrombin time (PT) and activated partial thromboplastin time (aPTT). 

PT is prolonged because clotting factors are used up. Values are institution specific, but intervention is indicated when the PT is 1.5 times the control value.

 

aPTT may be within reference range or shortened.

If available, fibrinogen level should be monitored.

3. Blood type and screen in anticipation of the requirement for a transfusion. 4. Chest radiograph postero anterior and lateral findings are usually nonspecific. The chief radiographic abnormalities in AFE are diffuse bilateral heterogeneous and homogeneous areas of increased opacity, which are indistinguishable from acute pulmonary edema.

5. A 12-lead electrocardiogram may show tachycardia, ST-segment and T-wave changes, and findings consistent with right ventricle strain. 6. Lung scan may demonstrate some areas of reduced radioactivity in the lung field. 7. Increased serum tryptase, urinary histamine concentrations and significantly lower complement concentrations suggest an anaphylactoid process. Respiratory support– Oxygen (100% face mask or bag mask) should be applied to treat hypoxia and prevent further hypoxic injury. The goal should be to keep oxygen saturation greater than 90%. Intubation and advance airway support are often required. As ARDS and pulmonary edema are often present, ventilation strategies of low tidal volume, high respiratory rate, and high PEEP may be beneficial. Initial severe pulmonary vasoconstriction and ventilation to perfusion mismatch have been successfully treated with inhaled nitric oxide and aerosolized prostacyclin. Cardiovascular support – Treatment of maternal hemodynamic instability and hypotension should be goal-directed with volume resuscitation, vasopressors, and inotropic support to optimize preload, contractility, and afterload as appropriate. In the case of hypotension, epinephrine, dopamine hydrochloride or dobutamine hydrochloride (1–5 μg/kg per min) should be administrated to maintain blood pressure and urine volume. High-dose adrenocorticosteroid hormone (500–1500 mg in the form of hydrocortisone) is occasionally effective. Fluid resuscitation should be under taken with the knowledge that patients often develop significant pulmonary edema and fluid overload. Hemodynamic goals in the initial resuscitation period are systolic blood pressure more than 90mmHg, PaO2 more than 60mmHg, and urinary output more than 0.5 ml/kg/h. Coagulopathy management -Blood loss secondary to AFE can be persistent and severe, generally presenting as uncontrollable uterine hemorrhage. Massive transfusion protocol should be initiated in the setting of uncontrolled hemorrhage to ensure timely red blood cells (RBC) and blood products administration. Transfusion should be performed with O negative RBC without delay in case of massive hemorrhage. Prevention and treatment of coagulopathy requires early and ongoing administration of fresh frozen plasma (FFP), platelets, and cryoprecipitate. The target ratio between FFP and red cell concentrate should be adjusted to a level exceeding 1.5. Administration of blood products and drugs 99

in the setting of massive hemorrhage should initially be empiric, then guided by frequent laboratory coagulation profile analysis and optimized by point-of-care viscoelastic tests. Amniotic fluid can induce thrombocytopenia, and platelet transfusions should be given empirically. If the platelet count is more than 20,000/ÎźL, platelet transfusion in not needed immediately. Fibrinogen is critical for hemostasis and is the first coagulation factor to decrease in obstetric hemorrhage. Fibrinogen levels can be used as a predictor of severity of obstetric hemorrhage; low levels have been found in the setting of AFE.FFP does not contain adequate levels of fibrinogen; therefore, cryoprecipitate and/or human plasma-derived fibrinogen concentrates should be administered. The use of antifibrinolytic agents such as tranexamic acid during hemorrhage secondary to AFE has been described. Antithrombin (3000 units) should be administrated as soon as possible because severe DIC frequently develops in the early stages. Uterine atony in the setting of AFE should be treated with standard pharmacologic interventions including oxytocin, carboprost tromethamine, methylergonovine, and misoprostol, and surgical interventions including Bakri balloon tamponade, uterine artery ligation/embolization, B-Lynch suture, or hysterectomy as required. Novel Treatment Strategies In patients suffering from cardiopulmonary collapse secondary to AFE that is refractory to advance life support medications and interventions, invasive hemodynamic support may be beneficial. o Extracorporeal membrane oxygenation9,10 o Cardiopulmonarybypass11 o Intra-aortic balloon pump o Pulmonary artery thromboembolectomy o Hemofiltration12 o Plasma exchange transfusions13 High-dose corticosteroid treatment for presumed inflammatory-mediated anaphylactoid response has also been proposed. Another novel treatment described is the use of synthetic C1 esterase inhibitors (C1NH). 100

C1NHs inhibit both C1 esterase, Factor XIIa, and complement activation; low levels of C1NHmay play a role in development of AFE. Important Considerations for Preventing AFE during labour 1. Direct special attention to the pulse and shock index. Carefully consider pulse rate. A timely diagnosis of shock cannot be made if attention is directed only to blood pressure. 2. Restlessness, respiratory discomfort, severe lower abdominal pain and fetal dysfunction of unknown origin appear before AFE manifests. 3. Check for atonic bleeding and incoagulable vaginal bleeding of unknown origin. In the obstetric field, patients suffer severe bleeding characteristic of DIC after uterine atony or incoagulable vaginal bleeding resulting from consumption of coagulation factors. 4. Pay particular attention to a rupture of the membrane that can result in AFE. Carefully observe the mother and her baby for some time after the rupture of the membrane. 5. Do not rupture the membrane using a non-physiological or artificial technique. Contact of the amniotic fluid with the lumen of the cervix entails the risk for AFE. Therefore, rupture of the membrane at stations higher than station 1 and artificial rupture in a state of insufficient dilation of the uterine cervix (<5 cm) should be avoided. 6. In the event of early rupture of the membrane, induced delivery should be carefully monitored. Because amniotic fluid easily flows into maternal blood, this type of delivery should be managed as a high-risk delivery. CONCLUSION AFE remains a poorly understood condition that presents rarely but with often devastating consequences. Improvements in diagnosis by standardized case reporting coupled with development of serum biomarkers as well as histological and immunohistochemical analysis at autopsy are critical to improving our understanding of the pathogenesis and advanced treatment options of AFE. The treatment is currently 101

largely supportive with emphasis on high quality basic and advanced life support as well as haemorrhage and coagulopathy management to try to optimize patient outcome and minimize morbidity and mortality. Simulation and a multidisciplinary team-based approach to AFE management are recommended. REFERENCES 1.

Clark SL, Hankins GD, Dudley DA, Dildy GA, Porter TF. Amniotic fluid embolism: Analysis of the national registry. Am J ObstetGynecol 1995; 172:1158-67.

O’Shea A, Eappen S. Amniotic fluid embolism. IntAnesthesiolClin 2007; 45:17-28.

Conde-Agudelo A, Romero R. Amniotic fluid embolism: an evidence-based review. Am J ObstetGynecol 2009; 201:445e1–445e13.

Moore J, Baldisseri MR. Amniotic fluid embolism. Crit Care Med 2005;33:S279-85.

Toy H. Amniotic fluid embolism. Eur J Gen Med 2009;6:108-15.

Laura SD, Raford PR, Russell AH, David DH. Case scenario: Amniotic fluid embolism. Anesthesiology2012;116:186-92.

Benson MD. A hypothesis regarding complement activation and amniotic fluid embolism. Med Hypotheses 2007;68:1019-25.

Benson MD. Current concepts of immunology and diagnosis in amniotic fluid embolism. Clin Dev Immunol 2012; 2012: 946576.

SharmaNS, Wille KM, BellotSC, Diaz-Guzman E. Modern use of extracorporeal life support in pregnancy and postpartum. ASAIO J 2015; 61:110–114.

10. Hsieh YY, Chang CC, Li PC, et al. Successful application of extracorporeal membrane oxygenation and intra-aortic balloon counterpulsation as lifesaving therapy for a patient with amniotic fluid embolism. Am J ObstetGynecol 2000; 183:496–497. 11. Esposito RA, Grossi EA, Coppa G, et al. Successful treatment of postpartum shock caused by amniotic

fluid

embolism

with

cardiopulmonary

bypass

and

pulmonary

artery

thromboembolectomy. Am J ObstetGynecol 1990; 163:572–574. 12. Weksler N, Ovadia L, Stav A, et al. Continuous arteriovenous hemofiltration in the treatment of amniotic fluid embolism. Int J ObstetAnesth 1994; 3:92–96. 13. Dodgson J, Martin J, Boswell J, et al. Probable amniotic fluid embolism precipitated by amniocentesis and treated by exchange transfusion. Br Med J (Clin Res Ed) 1987; 294:1322– 1323.

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