The Journal of Postgraduate Medical Education, Training ... · Journal of Postgraduate Medical Education, Training & Research Vol. II, No. 3, May-June 2007 2 medicine ‘with conscience

The Journal of Postgraduate Medical Education,Training & Research

Available free full text at NBE website : http://www.natboard.edu.in

The Journal of Post-graduate Medical Education, Training & Research is published by National Board ofExaminations. It is basically meant to share experiences on post graduate medical education, training &research and providing a forum to DNB candidates as well as the NBE accredited hospitals/institutions topublish their research work.

All correspondence regarding submission of manuscripts, reprints, etc. must be addressed to-the Editor,The Journal of Post-graduate Medical Education, Training & Research, National Board of Examinations,Ansari Nagar, Ring Road, New Delhi-110 029.Fax : 011-26589781; Phone : 011-2658 9090; Email : journal [email protected]

Editorial Board

ChairmanProf. A. Rajaseakaran, President, National Board of Examinations

MembersProf. M.S. Ramachandran, Vice President, National Board of ExaminationsProf. K.M. Shyamprasad, Vice President, National Board of ExaminationsProf. S. Bhardwaj, Vice President, National Board of ExaminationsProf. A. Chatterjee, Vice President, National Board of ExaminationsProf. P. Khanduri, St. Stephen Hospital, DelhiProf. P.S. Shankar, Professor Emiratus, Gulbarga, KarnatakaProf. Arun Kakar, Dept. of Surgery, MAMC, New DelhiProf. Alka Ganesh, CMC, VelloreDr. Methew Verghese, St. Stephen Hospital, DelhiProf. C.S. Pandav, Dept. of Community Medicine, AIIMS, New Delhi

Editorial StaffEditor : Prof. A.K. SoodAssistant editors : Dr. Bipin Batra, Dr. Anurag Agarwal, Dr. Vishakha Kapoor, Dr Pankaj Lamba

Note : The editor or publisher assumes no responsibility for the statements and opinions of the contributors.

For restricted circulation only.

Contents

EditorialValues in health care 1P. S. ShankarCommentariesLeprosy : principles of rehabilitation 3Abhishek SrivastavaBasic principles of surgical treatment of Echinococcus Granulosusinfection (Hydatid cyst) of the liver 7Vismit P. Joshipura, Nitin R. Patel, Harshad N. Soni, Sanjiv P. HaribhaktiVertebroplasty in osteoporotic vertebral fractures 10Charanjit Singh DhillonReview ArticlesDevelopment, structure and function of placenta, umbilical cord and amniotic fluid 13Vanita Sur, Rampi SinglaAnatomy of fetus, fetal growth and development, fetal physiology, fetal circulation 20S. Batra, N. GamiManagement of breech presentation 30Poonam Goel, Parampreet KaurPost partum haemorrhage 34Minakshi Rohilla ThamiRecent advances in identification and management ofgenital tract trauma-perineal tear, episiotomy complications 40Anju Huria, Lajya DeviManagement of shock 44Neelam Aggarwal, Shelly SoniTrends in surgery of vesico-vaginal fistula 47Veena Jain, Satish Jain, Sumeet JainRole of hormones in obstetrics and Gynecology 52Rashmi BaggaDiagnostic laparoscopy 59Seema Chopra

Tip for safe laproscopic surgery 63R.P. GuptaFemale genital tuberculosis 65Umesh Nandani Jindal

CorrespondenceCase report of multicystic dysplastic kidney with pregnancy 73Pankaj SharmaUterus didelphys with unilateral hematometrocolps a case report 74A.M. Deodhar, A.P. Deshmukh, R.M. Chopade, S.J. Gulve, C.S. KaleChoroidal osteoma in a male patient-case report of a rare condition 76Ajai Kumar, J.P. Gupta, Sanjiv K. Gupta

Recent AdvancesBronchial thermoplasty 79P.S. ShankarNewer pills 82Sushma RastogiCurrent concepts in total knee replacement 84C. Lenin

Journal of Postgraduate Medical Education, Training & ResearchVol. II, No. 3, May-June 2007 1

ormer Director-Generalof World HealthOrganization (WHO), Gro

to comfort all the times’. We havevalued helping and servingothers. The sea of changes in theconcept and knowledge ofmedicine have come about dueto major advances in diagnosticand therapeutic modalities.Despite that the values and ethicshave always formed theunderlying current of medicalprofession and have guided thephysician about providing thebest and most effective care tothe patients.Medical professionMedicine is a profession. Thepersons pursuing it always put theneeds of the patients before theirown self-interests. They areneither perturbed at theunhealthy competition that hasmade the profession a business,by unscrupulous elements norlook at the financial benefits.They practice the professionfollowing the ethical principlesenunciated by Hippocrates,Charaka and Sushruta.Thesequalities of a professional man,in the words of Thomas Russel,Executive Director of AmericanCollege of Surgeons, are multi-dimensional. It consists ofcompetency and dedication toimprove the skills, becoming arole model for future generationof medical men and placementof welfare of the patient aboveeverything else. Sir William Osler,the renowned Physician oftwentieth century said, that ‘the

physician must be friend,philosopher, well-wisher andguide to the patient and thefamily under his care’. Thephysician has an obligation topractice his profession withconscience and dignity. Medicineis not only a science, but also theart of letting ourselves,individually interacting with theindividuality of the patient. OurVedas have looked the physicianas a father in illness, as a friendin convalescence and as aguardian when health is restored..According to ChristopherHufeland, the physician mustgeneralize the disease, andindividualize the patient. FrancisPeabody has stressed that thetreatment of a disease may beentirely impersonal, the care ofpatient must be completelypersonal.Ideals of medical professionFrom the times of Charaka,Sushruta and Hippocrates, themedical profession hasformulated its own code ofconduct explaining thephysician’s duties toward thepatient and his obligation to thesociety. These have beenmodified in the recent yearswithout altering the basicprinciples. The primaryobligation of the physician is hisprofessional duty. He mustwillingly ‘consecrate his life to theservice of humanity’, and mustpractice the art and science of

1Editorial

FHarlem Brundtland wrote thatWorld has entered 21st centurywith hope but also withuncertainty. The remarkable gainin health, rapid economicgrowth and unprecedentedscientific advances lead us to anew era of human progress. Butthe darker legacies fromavoidable burden of disease andmalnutrition bring uncertainty tothis vision. The scientificadvances have made enormousachievements. The things thatseem routine today would havetaxed imagination of even themost futuristic person just a fewyears ago. With scientificachievement human structureand function have reached alevel of comprehension, whichwas unknown.Health care systemLife is not merely living, but livingin health. All our efforts aredirected to maintain our healthphysically, mentally, socially,spiritually and intellectually in aproper way. The history ofmedicine is as old as the historyof mankind. The health caresystem is in a constant stage offlux. Medicine is an art andscience of promotion of health,prevention of disease, diagnosis,cure and rehabilitation. We havetaken up this profession ‘to curesometimes, to relieve often and

Values in health care

P.S. ShankarGoverning Body Member National Board of Examinations

Journal of Postgraduate Medical Education, Training & ResearchVol. II, No. 3, May-June 20072

medicine ‘with conscience anddignity’ and ‘maintain the honourand noble tradition of hisprofession’. Medical ethics is anadmirable attribute to bepossessed by the physician and itforms an integral part of thehealing art. It focuses theattention on patient care,protection of privilegedinformation and maintenance ofa special relationship betweendoctor-patient. Ever since theinception of medicine andmedical practice, there has beena special relationship between adoctor and a patient. Thiscomplex and intricate entity isunique, without any parallel inany form of human behaviour orany facet of social field. R.K.Gandhi, noted PaediatricSurgeon said, existence of asentimental bond, an emotionalattachment, an irresistible affinity,an enticing attraction, unfalteringfaith, unflinching loyalty, mutualrespect and reciprocity,compassion, and other suchfeelings and qualities have beenintricately interwoven into thisenigmatic entity.Priceless possessionDoctor-patient relationship giveslot of dividends to the patients.It has the source of doctor’senormous empathy, his sincerityof service, his anxiety for theailing, his consistent desire toallay the agony, his attention topatient’s minutest comforts etc.By doing this work diligently thedoctor lifts the medicalprofession high in the society, andbrings nobility to the profession.He is respected, adored andworshipped by the gratefulpeople. No other profession has

strived so hard to nurture such abond. This relationship, being apriceless possession, must bepreserved and protected. Apathy,indolence and inaction break thisvital relationship. ConsumerProtection Act (1986) has comedue to a steady erosion of doctor-patient relationship in the recentdecades. A physician must keepbefore him the high ideals ofprofession. While defining theideals Charaka has told that ‘onewho desires to become aphysician must previouslybecome thoroughlyknowledgeable and cultivatevirtues by working hard. Thenonly he is in a position to restorethe lost health of the patient andbring him back to normal life.Ethical values have become moreimportant in these days. Theethical considerations havehuman orientation. Thephysician, according to Charaka,must develop the qualities offriendliness, compassion for thesuffering patient and eagerness todo his best to relieve thesuffering. The advice given byCharaka to the practitioners hasall time relevance. It states, ‘hewho practices neither for moneynor for caprice, but out ofcompassion for living beings isbest among all physicians. Thephysician who set out to sell theirskill like a commodity only, losessight of the gold and acquiresheap of dust. The physician whoconsiders compassion for livingbrings as his highest religionfulfils his mission in life andobtains the highest satisfaction’.Servant of the natureRudyard Kipling classified themankind in the World into two

groups-doctors and patients.Since the times of Hippocratesand Galen, the relationshipbetween the nature andphysician has been appreciated.Hippocrates considered Naturalforces as the healers of disease;and Galen stated that thephysician is Nature’s assistant.Physician works with the aim ‘toprevent disease, to relievesuffering and to heal the sick’.Paracelsus considered physicianas the servant of the Nature, nother master, thus it behoovesmedicine to follow the will ofthe Nature. He had emphasized,that the art of healing comesfrom Nature, not fromphysician. Therefore thephysician must start fromNature, with an open mind.Thus a close co-operation existsbetween the Nature andphysician. Homer Emersonsummarized the fact as ‘Natureheals, under the auspices of themedical profession’. Voltairehumourously said, the art ofmedicine consists in amusing thepatient while nature cures thedisease. Hans Krebs has said,‘you and your family must clearlyunderstand that the great andultimate healer is always Natureitself and that the drug, thephysician, and the patient can donot more than assist Nature byproviding the very bestconditions for your body todefend and heal itself ’. AnitaHesselgesser has written that themore man follows Nature and isobedient to her laws, the longerhe will live; the further hedeviates from these, the shorterwill be his existence. Health isNature’s reward for getting intoharmony with her laws.


an innocuous appearing skinmacule or papule is hypo-pigmented and lacks sensation.This stage is often known asindeterminate leprosy, which canevolve in several ways, dependingupon the resistance of the host.The bacilli may be locallyinvasive, producing acircumscribed granuloma thatinvolves the cutaneous andsubcutaneous nerves resulting incharacteristic hypo-pigmentedpatch of superficial numbnessand sensory loss (Tuberculoidleprosy). If a large nerve in thevicinity is invaded, a sensori-motor deficit in the distributionof that nerve is added to thepatch of anaesthesia. In contrast,lack of resistance to organismleads to widespread invasion(Lepromatous leprosy) ofcutaneous nerves and producesa symmetrical pattern of pain andtemperature loss involving distalextremities- a distribution that isdetermined by relative coolnessof these parts of skin. Extensivesensory loss is followed byimpaired motor function owingto invasion of muscular nerveswhen they lie closest to the skin.There is loss of sweating in theaffected parts, otherwiseautonomic function is rarelyaffected.

Disability-When detected andtreated early, primaryimpairments may be reversible.However, 11-51% of patients donot recover. In addition, 33-56%of newly registered patientsalready have clinically detectableimpairments, often no longeramenable to drug treatment.Among new patients, 6-27%present with secondaryimpairments, such as wounds,contractures and shortening ofdigits. As the result ofimpairments, many peopleexperience limitation of activitiesof daily living. As a result of theselimitations, because of visibleimpairments, or simply becauseof the diagnosis ‘Leprosy’, manypeople are restricted in theirparticipation in society 1. Leprosyinterferes with the psychologicaland social life of the patientsleading to their ‘dehabilitation’.Therefore, it is necessary toassess the extent and direction ofdehabilitation in order to makethe treatment plancomprehensive and effective 2.Leprosy is curable now-a-days ifinitiatives are taken forprevention of disability alongwith complete and regularchemotherapy. Commondisabilities encountered inleprosy are: Claw hand, foot drop,lagophthalmos, plantar ulcers anddepressed bridge of nose Fig.(1).Objectives of prevention of

disabilities are preservation ofnerve function, preservation ofvision, to regain functional abilityand self-esteem 3.

Rehabilitation- Rehabilitationof the leprosy patient beginswhen the disease is diagnosed andcontinues through out thepatient’s lifetime. It must bestressed that the most importantaspect of the rehabilitationprogram is the prevention of theanaesthesia and paralysis. Thiscan be achieved by: (a) Earlydiagnosis, before the nerve isirreparably damaged. (b) Earlytreatment to forestall nervedamage, (c) Judicious treatment,with great vigilance of patientwith borderline leprosy, (d)Prompt recognition andtreatment of reactions involvingnerves and eyes, and (e)Convincing the patient that heneed not be disabled. Thecommon modalities employedfor patients with denervatedextremities due to leprosy are:hydrotherapy, paraffin baths, oilmassage, exercises, biofeedbacktechniques, electrical stimulation,splinting, sensory and motor re-education, foot care andspecialized foot wear, andsurgical reconstruction.

Hydrotherapy-Warm waterbaths: are used to clean andhydrate the skin. The extremityis immersed in warm water (temp

2Commentary

Leprosy is the classicexample of an infectiousneuritis. The initial lesion,

Leprosy : Principles of Rehabilitation

Abhishek SrivastavaNational Institute of Mental Health & Neuro Science, Bangalore


< 420) for 10-15 minutes, duringwhich it is gently massaged. Thissoftens the keratin and makes theskin pliable.

Paraffin bath: 9-minutes dipmethod of paraffin bath at54o which delivers less heatthan 20 minutes whirlpooltreatment at 40o is employed.It restores suppleness andflexibility of the skin and ispreferred over radiant heat/diathermy as they can causeburns.

Oil massage: Effects of oilmassage are similar toapplication of paraffin baths.Its added benefit is derivedfrom the manipulation of theskin as it is rubbed(pincement), kneaded(petrissage), and tapped(tapotement).

Exercises-Both passive andactive exercises are utilized.Exercises should be started assoon as symptoms of neuritishave subsided. Exercises arecontraindicated in the presenceof an acute infection, acuteneuritic pain or bone and jointpathology. Role of exercises arecan be divided in two phases:

Expectant phase – Whenthere is no sign of recovery.The role of therapy in thisphase is to preventcontracture and retain fullrange of movement, avoidmuscle atrophy, and toprevent overstretching of themuscles. This is achieved bypassive movements throughfull range of motion twicedaily Fig. (2).

Active phase – when there issome return of nerve con-duction. The aim is to regainas much power and range ofmovement as possible. Thisis done by carefully guidedstrengthening and practicingskilled co-ordinated move-ments.

Splinting-Splint or orthosis is anexternal device applied in orderto prevent/correct a deformity,support unstable joint, relievepain, or improve function. Theyare classified into static ordynamic splints:

Static splint: It is a rigiddevice with no moving partsand does not permitmovement Fig. (3). This typeis more commonly employedin leprosy for followingindications: (a) to allay acutepain of neuritis anddiscomfort following surgery(b) protect and supporttissues during process ofrepair (c) maintain positionand alignment during night(d) correction of deformitieseg. ulnar drift, swan neck andmallet finger (e) to arrest theprogress of contractureparticularly of claw hand and(f) immobilize the wrist in“cock up” position so thathand can function moreeffectively.

Dynamic splint: It possesboth rigid and mobilecomponents allowing freemovements. Dynamic splintis employed primarily duringthe day for the extremity thatneeds assistance and

possesses full range ofmotion Fig. (4). Indicationsfor dynamic splints are: (a) toneutralize deforming forcesresulting from muscleimbalance, eg. flexion assistor Wynn Parry splint, (b)strengthen weaker muscle,and (c) as counterforce tocorrect imbalance.

Sensory re-education- It isbased on the presumption thatduring regeneration of nerves,the patient demonstrates lessrecovery than he is capable ofachieving. This is attributed to thefact that the patient fails tointerpret the altered profile ofimpulses discharged from thedamaged nerves. The program isdesigned to help the patientinterpret the altered impulsesduring the period of recovery bydoing simple exercises. Theexercises are simple and can beeasily performed by the patient.The program is divided into twophases: early and late phase. Inthe early phase, a touch type ofstimulus is applied to the distalphalanx. This serves to promoteperception of slow adaptingnerve fibers where as moving theobject across a given areapromotes perception of quicklyadapting fibers. In the late phase,touch perception is re-establishedand the patient is taught torecognize shape by handlingvarious objects.Motor re-education-When theaction of a muscle is weak orlost, it may be initiated bycontraction of adjacent musclesthat normally participate in thesame movement. This principle


is utilized in the re-educationafter tendon transfers. Theprocess of re-education is basedon the ability of the cortical andsub-cortical centers to analyzesensory input and regulate themotor output. Re-educationinvolves two distinct processes:cortical control and automatedmovements which areindependent of cerebralcontrol4. A transition fromcortical directed movements tothe sub conscious level occurswhen motor actions are firmlyestablished by repetition,practice co-ordination and skill.

Foot care- The problems ofdenervated feet are due to lossof sensory perception and motorimpairment. Footprint presents agraphic representation of theproblem by demonstrating areasof high pressure which are atrisks for developing an ulcer.Footprint is taken on a specializedmat designed by Harris 5 Fig.(5).The denervated foot can beclassified into four categories 6:

Category I – Low risk foot:The foot is grossly normal,with diminished plantarsensation

Category II – Moderate riskfoot: The foot is grosslynormal but has scarring on itsplantar surface in addition tobeing anesthetic

Category III – High risk foot:The foot posses a flexibledeformity in addition toplantar scarring and loss ofsensation

Category IV – Disintegratedfoot: The foot is deformed

structurally, is shortened ornarrowed due to bone or jointabsorption or to amputation.

Insoles of microcellular rubber(MCR) or polyethylene foam arereasonably successful inprevention of ulcers in first threecategories of patients Fig. (6).However, they fail to distributethe weight bearing forces evenly,and hence have limited use. Evendistribution of forces can bemost efficiently be achieved byproviding rigidity to the sole asdemonstrated by the fact thatmost ulcers heal when the foot isimmobilized in a walking plastercast. Keeping in view of thesefactors, a molded plastic footwearwas made consisting of hardwearing molded plastic sole anda microcellular sponge insolewith a spring steel shank placedin between the two to givecontrolled rigidity. This foot wearis both acceptable and protectiveand is recommended for patientsin category I, II, & III. Thedeformed foot of category IVrequires custom made foot wear.The shoe must fit the contour ofthe deformed foot and this canbest be done if it is made on amodel of the foot. It must havea micro cellular sponge insole anda rigid steel shank running alongthe entire length of the shoe.These two requisites ensure thatthe weight of the body is appliedevenly on the plantar surface. Thedisintegrated foot is very difficultto manage. If there is sub-talardestruction or disarticulation ofthe ankle, it can occasionally berepaired by arthrodesis. If astable planti-grade foot

reasonably good sole can beobtained by surgery, the footconverts to category III. If not,there is no alternative toamputation.

Reconstructive surgery- Themost frequently involved parts ofman’s anatomy in leprosy are alsohis most vital tools and hiscontacts with the world abouthim, i.e. his hands, feet, and eyes.Every effort must be made tosave these parts. Reconstructivesurgical procedures can bedivided into in to functional andcosmetic. Certain precautionsmust be undertaken beforeplanning for any surgery: Patientshould be eager to co-operate,adequate time should be given fora definitive trial of conservativemanagement, clofazimine shouldbe used at the time reactions as itreduces the need for surgery, andyounger patients have betterprognosis.

Conclusions- While thedeformities of leprosy can beadequately dealt with, totalrehabilitation of the patient withleprosy is often incompletebecause it fails to treat the patientas a person. It is important todetermine whether he is capableof performing activities of dailyliving, or can he solve problemsof interpersonal relations andmost important of all, whetherhe can return to a gainfuloccupation. A multidimensionalapproach that takes care of allthese features simultaneously ismandatory for total rehabilitationof the patient.


Figure 3 - Static splint : Anklefoot orthosis (AFO)

Figure 4 - Dynamic splint Wristsplint with finger loupes

Figure 5 - Foot prints

Figure 6 - Specialized footwear

References1. Van-Brakel WH. Peripheral

neuropathy in leprosy and itsconsequences. Lepr Rev.2000; 71 Suppl: S146-53.

2. Anandaraj H. Measurementof dehabilitation in patientsof leprosy - A scale. Indian JLepr. 1995; 67(2):153-60.

3. Manglani PR. Prevention ofdisability in leprosy. J IndianMed Assoc. 2004; 102(12):680-3.

4. Sharangpani RC, KulkarniVN, Mehta JM. A newapproach in muscle trainingto rehabilitate the hand inleprosy. Indian J Lepr. 1985;57(4): 750-5.

5. Welton EA. The Harris andBeath footprint : interpreta-tion and clinical value. FootAnkle 1992; 13(8): 462-8.

6. Enna CD, Jackson RR,Trautman JR, Sturdivant M.Leprosy in the United States,1967-76. Public Health Rep.1978; 93(5): 468-73.

Figure 1 - Hand deformities

Figure 2 - Hand exercises


liver. The treatment of thisbenign disease is predominantlysurgical. There are varioussurgical options availableincluding conservative surgeries,radical surgeries and laparoscopicsurgeries. There are technicalmodifications and sub-types ineach of them. Indications andbasic principles of each surgicaloption are variable. The decision-making process should considereach option and the best suitedfor a particular patient should beapplied. Human being is anaccidental intermediate host ofEchinococcus Granulosus.Carnivorous animals (mostcommonly dog) are definitivehost while herbivorous (Sheep,goat, cow etc.) are the naturalintermediate hosts. Accidentalingestion of food contaminatedby infected dog’s faeces will leadto ingestion of eggs of the wormand they develop into larval formas a cyst, most commonly in theliver. This helminthic infestationis one of the commoninfestations in rural India andusually patients present withcomplain of dull aching pain orlump in the upper abdomen. Inmost of the cases the diagnosisis suspected clinically andconfirmed by ultrasound of theabdomen.1 CT scan of theabdomen should ideally beperformed in each case to plan

the surgery. Though variousserological tests are available theyare seldom used clinically.2

Surgery is the mainstay oftherapy for the hydatid cystthough other conservativetreatments like Drug therapies orPercutaneous Aspiration,Injection and Re-aspiration(PAIR) are described in literatureand applied clinically in selectedgroup of patients.3,4

Here, we will review certain basicprinciples and decision-makingpoints for the surgical treatmentof hydatid cyst of the liver. Thisdiscussion does not includemanagement of hydatid cyst inother organs or disease due toEchinococcus Multilocularis.

Surgical decision-making-Theentire decision making processdepends on two factors-condition of patient andcharacteristics of the cyst. Thus,the complete plan ofmanagement should be tailor-made for each individual patient.

Whether surgery is needed ornot?-Surgery is either notrequired or not advisable inconditions such as-severe cardio-respiratory instability or othersevere systemic disease, Less than4 cm sized deep parenchymalsingle cyst and completelycalcified cyst.Which surgery should beperformed-Surgery for liverhydatid can be broadly divided

into conservative surgeries orradical surgeries. Now, option oflaparoscopy is also available, Sodecision-making process shouldalso include it for the benefit ofpatient. (Figure 1)

Conservative surgery for liverhydatid - By definition,conservative surgery for hydatidcyst is a surgery in which cystcavity entered electively whileradical surgery is a surgery inwhich cyst cavity is ideally notentered. There are three basicaims of conservative surgery5;

Cyst evacuation and preventionof peritoneal implantation,management of cyst billiarycommunication, andmanagement of residual cystcavity.

Cyst evacuation andprevention of peritonealimplantation-The abdomen ismost commonly assessedthrough either sub-costal(Chevron) or sometimes midlineincision. Abdominal cavity isthoroughly explored forunidentified cyst on preoperativeimaging. The liver is bimanuallypalpated after complete carefulmobilization.Intra-operativeultrasound may identify intra-hepatic cysts that are notidentified on pre-operativeimaging. It may show relation ofthe cyst with billio-vascularstructures and hydatid debris incommon bile duct (CBD).Wound and exposed peritoneal

3Commentary

E. Granulosus or hydatidcyst of the liver is one ofthe common diseases of

Basic principles of surgical treatment of EchinococcusGranulosus infection (Hydatid cyst) of the liver

Vismit P. Joshipura, Nitin R. Patel, Harshad N. Soni, Sanjiv P. HaribhaktiDepartment of Gastrointestinal and Laparoscopic Surgery, Sterling Hospital, Ahmedabad


surfaces are protected with greenor blue coloured towels soakedin scolicidal solution to identifyany spillage of daughter cyst.Cystic fluid is evacuated by largebore needle and suction tube.The cyst is then opened aftertaking stay sutures. Daughter cyst,laminated membrane and hydatidsand are all evacuated completely.Cavity is rinsed with 5% saline.Cyst roof is excised and edges areoversewn with absorbable suturesto prevent bleeding. Exocyst anddaughter cysts in the crevices arecarefully earched and excised.Cyst cavity is packed with whitegauze to see for billiary staining.A variety of solutions areavailable as a scolicidal agent. Atpresent 20% saline, 0.5%Cetrimide, 1% Povidone iodine,10% Chlorhexidine or rarely0.5% silver nitrate are used inpractice.6 These solutions aremore or less equal in efficacy andtoxicity especially billiary injury.These solutions should not beinjected blindly into the cystcavity or if the cyst fluid is stainedwith bile.

Management of bile-ductcommunication-Preoperativelyit is difficult to suspect bile ductcommunication unless there ishistory of recurrent cholangitisor ERCP proven hydatid debrisin CBD. Intra-operatively bilestained fluid may suggestcommunication but sometimes itis difficult to identify it. Dead orcalcified cyst may have bile ductcommunication. To search forbile duct communication theeasiest way is to look meticulouslyand to pack the cavity by gauzesas described above. Othermethods include intraoperative

cholangiography, Methelyne Blueinjection etc. On detection ofsuch communication it must berepaired. The choice of repairdepends on the level of billiarychannel involvement as shown inFigure 2.

Management of residual cystcavity-There are multipleoptions available to manage theresidual cavity. Indications foreach technique can besummarized as follows:

Small, non-calcified,superficial cyst- suture closethe edges after filling thecavity with normal saline.Large, shallow, superficialsaucer like cavity- can be leftopenDeep cavity with redundantcrevices- omentoplasty.Deep cavity andomentoplasty not possible-capitonnage (imbricating thecyst wall into the depths ofcavity).

Radical surgeries for liverhydatid7 - There are five typesof radical surgeries in which cystcavity is not entered. Multipleexogenous cysts or calcifiedcyst or suspected billiarycommunication can be treated byclosed total cystopericystectomyin which a plane is developedbetween adventitia and liverparenchyma. This surgery is notpossible when major vascularstructures are abutting the cyst.If the adventitia is very thin orcyst ruptures during closedpericystectomy or a majorvascular structure is abutting thecyst wall then the cyst is opened,debrided and pericystectomy isperformed.Non-anatomicalresections are reserved for

pedunculated peripheral cysts.Formal anatomical resection isperformed only when no othersurgical options are available suchas recurrent disease, irreparablebile duct communication. Livertransplantation is very rarelyindicated in patients in whomthere is recurrent disease aftermultiple surgeries and has endstage liver failure.

Conservative surgery VsRadical surgery8,9-A generalsurgeon, in a relatively smallcenter with less specializedequipments and skills canperform conservative surgeriesfor liver hydatid cyst. Thesesurgeries are usually associatedwith less morbidity and mortalityif carefully performed withacceptable recurrence rates.Limitations of conservativesurgeries include need forentering cyst cavity and possiblespillage, use of scolicidal agentsand its potential hazards. Againstthese possible limitations ofconservative surgeries, the radicalsurgery avoids spillage and use ofscolicidal agents. Billiarycommunication can be managedwell with radical surgeries andprobably there are lesser chancesof recurrences. The mainlimitation of radical surgeries islimited availability of surgicalexpertise and infrastructureespecially in countries wherehydatid cyst is more common.Morbidity and mortality may belittle higher with radical surgeriesin less experienced hands.Laparoscopic surgery forhydatid cyst-With technologicaladvancement in laparoscopy, ithas become possible to managehydatid cyst of liver by advanced


laparoscopic techniques.10

Selection of patient for thelaparoscopic management iscrucial. The guiding criteria forsuch selection are-Primary cyst,Superficial cyst, Less than 3 innumber less than 15 cm in sizeand, No intra-billiary rupture,Proficiency of surgeon and set upfor advanced laparoscopicsurgery; At present onlyconservative surgeries can beperformed by laparoscopy. Bileduct communication is not acontraindication to surgery.Conclusion-E. Granulosusinfection of liver is a commonsurgical disease. There are varietyof surgical procedures andtechniques available. Selection ofproper technique and its properimplementation is crucial forlong-term cure. The decision tochoose a particular techniqueshould be tailor-made for anindividual patient.References1. Dziri C, Maouet K, Fingerhut

A : Treatment of hydatid cystof the liver: Where is theevidence?, World J Surg, 2004Aug;28(8):731-6.

2. Siracusano A, Bruschi F :Cystic echinococcosis :Progress and limits inepidemiology andi m m u n o d i a g n o s i s ,Parasitologia, 2006 Jun, 48(1-2):65-6.

3. Ben Amor N, Gargouri M,Gharbi NA, Golvan YJ,Ayachi K, Kchouck H : Trialtherapy for inoperableabdominal hydatid cysts bypuncture. Ann Parasitol HumComp, 1986;61(6):689-92.

4. Ettik O, Arslan H, Bay A,Sakrya ME, Harman M,Temizoz O : Abdominalhydatid disease: long termresults of percutaneoustreatment. Acta Radiol, 2004Jul; 45(4):383-9.

5. Atmatzidis KS, Pavlidis TE,Papaziogas BT, Mirelis C,Papaziogas TB : Recurrenceand long term outcome afteropen cystectomy withomentoplasty for hepatichydatid disease in an endemicarea : Acta Chir Belg, 2005Apr;105(2): 198-202.

6. Besim H, Karyalcin K,Hamamci O, Gungor C,Karkmaz A : Scolicidal agentsin hydatid cyst surgery. HPBsurgery,1998; 10(6): 347-51.

7. Gollackner B, Langle F, AuerH, Maier A, Mittlbock M,Agstner I : Radical surgicaltherapy of abdominal hydatiddisease:factors of recurrence.World J Surg, 2001 Mar;25(3): 387-9.

8. Abbas M, Nafeh AI, YoussefYF, Nasr MM, Radwan NS :Conservative versus radicalsurgery for treatment ofuncomplicated hepatichydatid cysts. J Egypt SocParasitol, 2006 Aug; 36(2):559-76.

9. Elsebaie SB, El-sebae MM,Esmat ME, Nasr MM, KamelM M : M o d i f i e dendocystectomy versuspericystectomy inechinococcus granulosus livercysts. A randomizedcontrolled study, and the roleof specific anti-hydatid IgG4in detection of early

recurrence. J Egypt SocParasitol, 2006 Dec;36(3):993-1006.

10. Palanivelu C, Jani K, MalladiV, Senthilkumar R, Rajan PS,Sendhilkumar K, ParthsarthiR, Kavalat A : Laparoscopicmanagement of hepatichydatid disease. JSLS, 2006Jan-Mar;10 (1):56-62.


4Commentary

fractures are the most commonfractures in patients withosteoporosis, along with proximalfemoral and wrist fractures.These fractures may cause acuteor chronic pain, reduce thequality of life, and shorten lifeexpectancy. Several medicationsare available that reduce the riskof fracture. Vertebroplasty mayreduce or relieve pain in carefullyselected patients. Osteoporosis is“a systemic skeletal diseasecharacterized by low bonemass and micro-architecturaldeterioration with a consequentincrease in bone fragility withsusceptibility to fracture.” Insimpler terms, it is a reduction inthe quantity and quality of bonethat leads to increasedbone fragility and fractures.Osteoporosis is a silent disease —there are no symptoms or signsof low bone mass or bone loss.Typically, years or decades ofbone loss are required before anindividual becomes at high riskfor bone fracture. Once thepatient experiences a fracture,more fractures are likely to occurin the near future. Vertebralcompression fractures are themost common fractures inpatients with osteoporosis, afterproximal femoral and wristfractures. They are identified innearly 25% of women aged

above 50 years. The incidenceincreases by about 15% with eachpassing decade. These fracturesare nearly twice as common infemales as compared with males.For reasons not clearlyunderstood, only one thirdof spinal compression fracturesare painful; most of theseare refractory to medicalmanagement. A number ofdiseases and conditionspredispose individuals toosteoporosis and secondaryvertebral compression fracture.These include - Advancedage, Asthma, Cirrhosis,Diabetes Mellitus, Emphysema,Menopause, Oophorectomy,Bilateral Renal disease,Chronic Rheumatoid Arthritis,Transplants,Tumors, Parathyroid-related peptide Vitamin Ddeficiency. In addition, certaindrugs are also associatedwith osteoporosis, such as-Anticonvulsants, Cytotoxicdrugs, Alcohol, Thyroidreplacement drugs, Steroids,HeparinPatients with compressionfractures typically present with asudden onset of intense backpain, often after a relativelybenign activity. Many patientsrefer to intractable pain after asneeze or a cough. The pain tendsto be debilitating. Patients find itdifficult to find a comfortableposition, and therefore, they havedifficulty sleeping. Many patients

refer to sleep in a seated orsemireclining position. Thoughmajority of vertebral fractureseventually heal with conservativemanagement some of them willfail to heal giving rise to chronicpain. This chronic pain is due tochanges in spinal alignment,spasm of paraspinal muscles, andstretch on posterior spinalligaments. Multiple compressionfractures lead to kyphoticdeformity (“dowager’s hump”),loss of height, crowding ofinternal organs, inactivity-induced physical deconditioning,and changes in self-image leadingto a significant impact on selfesteem and activities of dailyliving. Biomechanically with eachvertebral fracture there is forwardshift of weight bearing axis,leading to increased load onthe anterior column ofweak osteoporotic vertebraepredisposing them to furtherfractures. Relatively newprocedure, vertebroplasty havebeen introduced for themanagement of unusually severeor persistent pain fromvertebral fractures. It involvespercutaneous injection of bonecement into one or morefractured vertebra. Pain relief hasbeen reported in 60 to 100% ofcases in which this procedure wasperformed.Vertebroplasty-In 1984,vertebroplasty was firstsuccessfully performed in France

Osteoporosis is asignificant public healthproblem. Vertebral

Vertebroplasty in Osteoporotic Vertebral Fractures

Charanjit Singh DhillonDirector MIOT Center for Spine Surgery, Chennai


for the treatment of acervical vertebral hemangioma(Deramond, 1998). Since then,the application of vertebroplastyhave been expanded to includethe treatment of the intense paincaused by vertebral compressionfractures that is refractoryto conventional therapies.Vertebroplasty involves theinjection of acrylic cement underlocal anesthesia and eitherfluoroscopic guidance or, lesscommonly, CT guidance intofractured vertebra. Typically, thetechniques are performed as anoutpatient procedure and requireapproximately 40 minutes perlevel treated. Pain reduction orelimination is immediate, and therisk of complication is low.Vertebroplasty is a treatment forpain. Theoretically, 2 mechanismsmay account for the painreduction associated with theinjection of methylmethacrylate.The first mechanism may be as aresult of acrylic fusion of thefragments into a single block,preventing the painful motion ofthe individual fracture fragmentsagainst each other. The secondmechanism of pain reductionmay be related to the heatproduced by the polymerizationprocess as the acrylic hardens. Anadded benefit is that depositionof acrylic within the vertebrasignificantly strengthensosteoporotic bone, reducing thelikelihood of repeat fracture.Patient selection - A patientwith painful osteoporoticcompression fracture who hasfailed to respond to a fair andadequate trial of conservativetreatment is the ideal candidatefor vertebroplasty. Impending

vertebral fracture due to localizedosteoporosis following non-septic lesion such ashemangioma, multiple myelomamay be additional indications.Vertebroplasty may also beapplied prophylactically to an at-risk vertebra between 2 otherabnormal vertebrae. Inclusioncriteria include -Fracture lessthan 12 months old, Painlocalized to a fracture ortumor, and Pain refractory tomedical management. Theexclusion criteria include -Fracture extending to posteriorvertebral cortex , Retropulsedfragment, Cord compression,Radiculopathy, Fever and/orsepsis, Coagulopathy.

Technique-Vertebroplasty is aday-care procedure that isperformed on an outpatient basis.The procedure is not painful andrequires only mild sedation andanalgesia. Occasionally, patientsreport pain when the trocarreaches the fracture fragmentsand when the injection of acryliccement is initiated. However thiscan be tolerated by most patientswithout much discomfort. In anoccasional uncooperative patientgeneral anaesthesia may beindicated. Lumbar vertebroplastyconsists of the transpedicularplacement of an 11-gauge bonebiopsy needle into the affectedvertebra under fluoroscopicor CT guidance. Thoracicvertebroplasty is performed via13-gauge bone biopsyneedle. Once positioned,methylmethacrylate is injectedthrough the needle into theabnormal vertebral body. Theacrylic is then prepared understerile conditions for injection.

The dry, powdered polymer ismixed with a liquid monomer ofmethylmethacrylate to aconsistency similar to that oftoothpaste. The acrylic cement isthen injected with either a 1-mLLuer-Lok syringe through thetrocar. Injection is continued untilcomplete opacification of thevertebral body is achieved or thefirst sign of extension into theepidural venous plexus appears.Opacification of the paraspinousveins is common. Whenopacification occurs, the injectionof acrylic is suspended forapproximately 1 minute to allowthe cement to harden within thevein. Injection may then beresumed, and the acrylic followsa new path of lower resistance.Opacification of the vertebralbody need not be complete forsuccessful vertebroplasty. If theacrylic reaches both the superiorand inferior endplates andextends across midline,approximately 80% of the load-bearing benefit of a completelyopacified vertebral body isachieved (Belkoff et al). A smallamount of methylmethacrylate isretained on the bench as acontrol. After approximately 10minutes, the cement solidifies andbecomes harder than the nativebone. Once the control samplehas solidified, the Patient isexamined for neurological deficitbefore being transferred to apost-operative ward.Risks -The risks of theprocedure are low, but theypotentially include infection,worsening of pain, andneurological problems such asweakness or pain in the legs.Occasionally, the acrylic may


extend into the epidural orparaspinous veins. Cement in theepidural venous plexus maylead to an ascending venousthrombosis or contribute to aspinal stenosis or cord or nerveroot compression. Acrylic mayextend from the paraspinousveins into the vena cava and mayresult in a pulmonary embolus.The risk of venous embolizationincreases if the operator cannotadequately identify when thecement begins to pass into thevenous system. This risk isreduced by using angiographicequipment with the highestresolution available. The visibilityof methylmethacrylate is furtherimproved with the addition offine metallic powders such asbarium mixed with tantalum ortungsten.

Results -Approximately 85-90%of patients have rapid pain relief.This procedure is associated witha low morbidity rate. Fewer than1% of patients with havemorbidity. Morbidity may includelocal pain, rib pain, spinalstenosis, nerve root compression,and intravascular extension ofacrylic. In approximately 90% ofpatients there is completeresolution of pain. Incisional andmuscular pain may persist for thefirst few days after the procedureand it can be controlled withadequate oral anagesics. Pointtenderness that is noted beforethe procedure has not been notedin any of the patients after theprocedure. Although pain isreduced or eliminated after theprocedure, patients must exercisecaution in subsequent activities

Transpedicular placement of atrocar in the anterior third of thefractured vertebral body

Lateral radiograph of fracturedvertebra shows the initialplacement of the trocar

Injection of methylmethacrylatethrough the trocar in anteriorone third of the vertebral body.

Compression fracture aftervertebroplasty.

because other osteoporoticvertebral bodies may also beprone to fracture. Medicalmanagement of the underlyingdisorder that weakens thevertebral bodies should beinitiated. This procedure does noteliminate the need for aggressivetreatment of osteoporosis,without which other fracturesmay ensue.Conclusions-Osteoporosticvertebral fractures are commonin elderly. These fractures reducea patient’s quality of life andshorten life expectancy. Severalavailable medications have beenshown to reduce the risk offracture. In patients withunhealed compression fracturesvertebroplasty may reduce orrelieve pain in selected patients.References1. Belkoff SM, Mathis JM,

Jasper LE: The biomechanicsof vertebroplasty the effectof cement volume onmechanical behavior. Spine2001 Jul 15; 26(14): 1537-41

2. Tohmeh AG, MathisJM, Fenton DC:Biomechanical efficacyof unipedicular versusbipedicular vertebroplasty forthe management ofosteoporotic compressionfractures. Spine 1999 Sep 1;24(17): 1772-6

3. Wong W, Reiley MA,Garfin S: Vertebroplasty/kyphoplasty. J WomensImaging 2000 Aug; 2(3) :117-24.


development. The link betweenthe two is the indispensableplacenta.The two arms of fetal-maternal communication systemof human pregnancy are-Placental arm and Fetalmembranes (amnion and chorionlaeve). The placental arm of thissystem links the mother and fetussuch that at all the sites of cell tocell contact, maternal tissues arejuxtaposed to extra embryoniccells and not the embryonic orfetal cells. Before we discussabout the development ofplacenta it is important tomention about the endometrialpreparation for receiving thedeveloping embryo.The deciduaEndometrium of pregnantuterus is decidua. It is entitled sobecause it is shed off at the timeof delivery. The increasedstructural (vascularity) andsecretory activity ofthe endometrium followingimplantation is known as decidualreaction which is most marked atthe implantation site. The fibrousconnective tissue of the stromais converted to epithelia cells. Thecells are enlarged and are placedback to back with clear vesicularcytoplasm. The glands aremarkedly enlarged and becomeincreasingly tortuous. Smallinterstitial haemorrhages andleucocytic infiltration occurs,particularly at the implantationsite. Decidua differentiates into

three layers-Superficial compactlayer-compact mass of decidualcells, gland ducts and dilatedcapillaries; Intermediate spongylayer-dilated uterine glands,decidual cells and vessels. Thislayer forms the plane of cleavagewhen placental separation occurs;Basal layer-basal portion ofglands. Regeneration of mucosaoccurs from this layer.Fertilization and cleavageFertilization of the ovum occursin the fallopian tube. Afterfertilization, mature ovumbecomes zygote-a diploid cellwith 46 chromosomes. Zygoteundergoes mitotic divisionyielding blastomeres while stillinside fallopian tube and issurrounded by zona pellucida.Blastomeres continue to divideuntil solid ball of 12-16 cells(morula) is formed. Morulaenters the uterine cavity about 3days after fertilization. Zonapellucida persists even at 58- cellstage.1 Fluid graduallyaccumulates in morula leading toformation of blastocyst.Compact mass of cells at onepole of blastocyst is called innercell mass which later on formsembryo. The outer mass of cellsforms trophoblasts.ImplantationImplantation most commonlyoccurs on the upper part and theposterior wall of the uterus. Zonapellucida disappears andblastocyst touches and adheres tothe endometrial surface at 108-256 cell stage. Trophoblasts

burrow into the stroma betweenendometrial cells till theblastocyst becomes encasedwithin the endometrium. Thistype of implantation is calledinterstitial implantation. It startson 6th day and is completed by11th day. Process involvesdegradation of extracellularmatrix by urokinase typeplasminogen activator andmetalloproteinases.2Embryonic developmentAt around 7- 8 days offertilization, inner cell massdifferentiates into primitiveectoderm and underlying layer ofendoderm. The embryonicmesenchyme first appears asisolated cells within the blastocystand later completely line thecavity, forming chorionic vesicles.Its membrane is now called thechorion. Near the embryomesenchymal cells condense toform the body stalk, which servesto connect the embryo tochorion. After implantation ofblastocyst, the different parts ofdecidua become as follows:decidua basalis- in contact withbase of blastocyst, deciduacapsularis- thin superficial layercovering the blastocyst andDecidua parietalis- rest of thedecidua lining the uterine cavity.its thickness gradually increasesto 5-10mm at the end of secondmonth and then regresses to1mm by the end of 20 weeks. Asthe fetus grows, the deciduascapsularis fuses with the deciduasparietalis forming decidua vera.Deciduas capsularis is largely lost

5ReviewArticle

The fetus is entirelydependent on its maternalsupport for growth and

Development, structure and function of placenta, umbilicalcord and amniotic fluid

Vanita Sur, Rimpi SinglaDepartment of OBG, PGI, Chandigarh


by pressure and loss of bloodsupply.

TrophoblastTrophoblast is the mostimportant component of theplacenta that is involved ininvasion of blastocyst,immunological acceptance of theconceptus, nutritional support tothe conceptus and producinghormones for the maintenanceof pregnancy. Morphologicallyand functionally trophoblastdifferentiates into cellular andsynctial forms .Duringimplantation some of the innermost cytotrophoblast contiguouswith endometrium coalesce toform amorphous multinucleatemembrane, the synctium. Thisdepends on protein synthesis,calcium dependent cell adhesionmolecule E cadherin anddesmosome formation.3, 4.Functionally, cytotrophoblast isthe germinal layer and synctiumis the secretory layer.Placental developmentAfter adherence tothe endometrium thecytotrophoblast towards theembryonic pole proliferaterapidly and invade decidua. Asthe blastocyst grows, the otherpole of the mass extends towardsendometrial cavity (abembryonicpole). As the trophoblast invadeendometrium, small vacuolesappear in the syncytiotrophoblastwhich later coalesce to becomelacunae.5 These lacunae get filledwith the maternal blood from theendometrial arteries (spiralar teries) with invasion ofmaternal vessels.Cytotrophoblast invasion ofdecidual vessels -Cytotrophoblast initially invadethe superficial capillaries of the

endometrium. Subsequently, thearterioles and then the spiralarteries are invaded.Cytotrophoblast can pass severalcentimeters along the vessels andhave even been noticed in themyometrial portions of thevessels7 by around 16 weeks.Invading cytotrophoblasts forma lining within the endothelium.With invasion, degenerativechanges occur in the vessel wall,most markedly affecting thesmooth muscle cells. Graduallyconnections are establishedbetween lacunae and veinsof endometrium. The lacunaejoin each other6 to formlabyrinths around villi. This typeof placentation iscalled hemochorioendothelialplacentation.

Chorionic villi-Late in thesecond week of development,delicate columns ofcytotrophoblasts extend outbetween adjacent blood filledlacunae in thesyncytiotrophoblasts. These areknown as primary villi. Initially,villi form over the entire surfaceof chorion, later only those onthe most deeply implanted aspectof the conceptus (overlyingdeciduas basalis) persist. Thechorionic villi on the deciduascapsularis gradually atrophy frompressure and become convertedinto chorion laeve by third monththat lies between amnion anddeciduas. Cells of the extraembryonic mesoderm lining theinner aspect of the trophoblastenter the primary villi and createa core, resulting in the formationof secondary villi (16th day). Eachvillus branches and attainscomplex form at the end of thirdweek blood vessels developwithin the core of the villus and

connect to the circulatory systemof the embryo. With this formsthe tertiary villus by 21st day offertilization. Each villus hasembryonic blood flowing insideit and maternal blood bathing itsouter surface. Some of thetertiary villi extend completelysuch that cytotrophoblast incentral core make contact withdecidual cells, these are calledanchoring villi. At theundersurface of endometrium,cytotrophoblastic shell is formedas the cytotrophoblast spreadlaterally from the end of eachvillus.

Structure of a terminal villus-from outside inwards eachterminal villus has.Outer syncyciotrophoblast,Cytotrophoblast, Basementmembrane, Central stroma withfetal capillaries, mesenchymalcells and connective tissue.Placental barrierDespite close proximity there isno mixing of the maternaland fetal blood because the twoare separated by socalled placental barrier. Thiscomprises syncytiotrophoblasts,cytotrophoblasts, the basementmembrane, stromal tissue, andendothelium of the fetalcapillaries. Its thickness isapproximately 0.002 to 0.006mm.8

Placental cotyledon (Figure 2)As the placenta matures, the stemvilli branch repeatedly to formprogressively finer subdivisions.Each mainstem alongwith itsramifications form placentalcotyledon or lobe. Each of it issupplied with a branch ofchorionic artery and is drained byone vein. These cotyledons


continue to grow till term buttheir number remains the samethroughout gestation.9

Structure of placentaMature placenta is discoidshaped, measuring about 185mmin diameter and 23mm inthickness at centre, weighs about500 gms and has average volumeof 497 ml.10 Of the two surfacesof placenta, fetal surface iscovered by amnion giving itsmooth appearance, and hasumbilical cord attached at or nearcentre. The placenta is limitedinternally by the amnioticmembrane and chorionic plate,and externally by the basal plate.In between the two lie the villiand intervillus spaces.Chorionic plateIt consists of primitivemesenchyme with branches ofumbilical vessels, layer ofcytotrophoblast andsyncytiotrophoblast. It is formedby 8- 10 weeks.BASAL PLATE: from outsideinwards it consists of deciduabasalis, Nitabuch’s layer,cytotrophoblastic shell, andsyncytiotrophoblast. Branches ofumbilical vessels are visiblebeneath amnion as they radiatefrom cord insertion. On maternalsurface cotyledons appear asslightly elevated areas calledlobes, giving it rough and spongyappearance. These lobes areseparated by grooves of variabledepth occupied by decidualseptae.

Placental circulationMaternal circulation- it concernswith the circulation of maternalblood through the intervillusspace. In mature placenta volumeof blood in intervillus space is

150ml and blood flow is 500- 600ml per minute. Fetal homeostasisis dependent on an efficientmaternal placental circulation.Maternal blood enters intervillusspace via spiral arteries that enterthe space by perforating basalplate. Blood is driven high uptowards the chorionic plate by thehead of maternal arterialpressure. Then it spreads laterallyand bathes the externalmicrovillus surface of chorionicvilli. It is pushed by the pressureof continuous influx of arterialblood towards exits in the basalplate, from which it is drained byuterine veins.11 Cytotrophoblasticinvasion of vessels ultimatelystops the circulation in some ofthese vessels and thus reducingthe number of arterial openings.During uterine contractions,intervillus space distends withblood because venous outflow isreduced more than arterial inflow.Thus even at reduced rate offlow, increased volume of bloodis available for exchange12. So,uteroplacental circulation isregulated by arterial bloodpressure, intrauterine pressure,and pattern of contractions.

Hemodynamics of placentalcirculationVolume of blood in intervillusspace 150 mlUterine arterypressure 70- 80 mmHgUterine veinpressure 8 mmHgPressure in intervillus spaceDuringcontraction 30- 50 mmHgDuringrelaxation 10- 15 mmHgFetal circulationVenous blood from fetus reachesplacenta through two umbilicalarteries. After traversing throughthe umbilical cord, umbilicalvessels branch repeatedly beneaththe amnion (surface or chorionvessels) and in the villi, finallyforming capillaries. Immediatelyafter entering the chorionic plate,the two umbilical arteries arejoined by a transverse connection,the Hyrtl anastomosis. Thetruncal arteries are the perforatingbranches of the surface vesselsthat pass through the chorionplate. There is one truncal arteryfor each cotyledon. Maternal andfetal blood flow side by side butin opposite direction facilitatingmaterial exchange between the


two. The villus capillary pressurevaries between 20- 40 mmHg.Oxygenated blood returns fromplacenta to fetus through singleumbilical vein.Placental ageingAs the pregnancy advances,placenta undergoes somedegenerative changes. Ageingprocess involves both fetal andmaternal aspects of placenta. Thisphysiological process should bedifferentiated from the morbidchanges that occur in somepathological conditions.Syncytium thins out and at someplaces syncytial knots appear byaggregation of syncytium.Volume of cytotrophoblastsreduces. Vessels becomeprominent and come close to thesurfaceBasement membrane ofcapillaries thickens. Few bloodvessels are obliterated by thedeposition of fibrin. There isdecrease in stromal tissue'Hofbauer cells' and fetalmacrophages appear in thestroma. In the decidua, there isappearance of fibroid depositcalled Nitabuch's membrane inthe outer syncytiotrophoblastlayer adjacent to the decidua. Thismembrane limits the furtherinvasion of decidua by thetrophoblast.The syncytium covering the villiand extending into the intervillusspace undergoes fibroiddegeneration and form a massentangling variable number ofvilli. These are called as whiteinfarcts. Further, calcificationsmay occur on this.Placental functionApart from nidation and transferof nutrients, placenta has

indispensable metabolic,endocrine and immunologicalroles to play.Transfer of nutrients-Thetransfer function of placenta isdependent on physical propertiesof substance, integrity ofplacental membrane, rate of fetaland maternal blood flow.Transfer of oxygen acrossplacenta is blood flow limited andthat of carbon dioxide is diffusionlimited. Oxygen supply to thefetus is continuous.

Even at low pO2, fetuscompensates because of highercardiac output, higher oxygencarrying capacity of fetal bloodand more Hb level. Transfer ofCO2 is facilitated by highpermeability of chorionic villi,less affinity of fetal blood forCO2 and lower partial pressureof CO2 in maternal blood due topregnancy induced mildhyperventilation.Excretory function- Wasteproducts like urea, creatinine anduric acid are excreted to maternalblood by simple diffusion.Nutritive function-Glucosewhich is the principal source ofenergy is transferred to the fetusby facilitated diffusion via GLUT1 and GLUT 3 transportproteins14, 15. Free fatty acids crossthe placenta by simple diffusion.Amino acids are transferred byactive transport by enzymaticmechanism. Some proteins crossby the process of pinocytosis.

Dynamics of gas exchange across placenta13

Uterine artery Uterine vein Umbilical artery Umbilical vein

pO2 mmHg 95 40 20-25 mmHg 30-40 mm Hg

pCO2 mmHg 32 40 48 43

Iron is actively transported acrossplacenta, rate of transfer steadilyincreasing with gestation.16

Barrier function-Fetalmembranes act as a protectivebarrier against noxious agents inthe maternal blood. Howevercertain maternal infections anddrugs used in pregnancy can crossthe placental barrier.Enzymatic function-Numerousenzymes are elaborated in theplacenta like diamine oxidase(inactivates pressor amines),

oxyocinase (neutralizes oxytocin)and phospholipase A2(synthesizes arachidonic acid).

Endocrine function-The humanplacenta synthesizes an enormousamount of protein and peptidehormones like human placentallactogen, human chorionicgonadotrophin, ACTH,parathyroid hormone relatedprotein, calcitonin, relaxin,thyrotropin releasing hormone,somatostatin, corticotrophinreleasing hormone, inhibin,activin and atrial natriureticpeptide. Synctiotrophoblast takesup maternal plasma low densitylipoproteins (LDL) forprogesterone biosynthesis.17, 18

The de novo synthesis ofcholesterol in trophoblast isminimal. Hence it depends onmaternal plasma for progesteronebiosynthesis.19

Placenta cannot synthesizeestrogens de novo because it lacks


17 hydroxylase/17-20 desmolaseIt has high capacity toconvert C 19 steroid to estroneand estradiol 17 ß because ofplacental aromatase enzyme.20 Rich sulphatase activityof placenta allows itto convert maternaldehydroepiandrosterone sulphateto estradiol 17 ß.21

Amnion and amniotic fluidIt is the innermost avascular fetalmembrane. It provides tensilestrength to the fetal membranes.Development -On 8th day offertilization inner cell massdifferentiates into bilaminar germdisc which consists of dorsalectodermal layer and ventralendodermal layer. It is connectedwith the trophoblast bymesenchymal condensation calledconnecting stalk that later onforms umbilical cord 6. Two fluidfilled spaces appear on each sideof germ disc. The space on thedorsal aspect (between ectodermand cytotrophoblast) is calledamniotic cavity. The cavity whichappears on the ventral aspect ofbilaminar disc is known as yolksac.6 It is lined externally bymesenchyme and internally byendodermal cells migrating fromthe germ disc. The epithelial cellslining the amniotic cavity arederived from fetal ectodermalcells. A layer of fibroblast like(mesenchymal) cell derived fromembryonic mesoderm line theouter aspect of epithelial cells,thus constituting a twolayered amnion. Simultaneously,interstitial collagens I, III and Vare deposited between these twolayers of cells. The amnionic sacexpands to envelop the placentaand the chorion. Reflectedamnion is fused to the chorionleave. The epithelial cells of

amnion replicate faster thanmesenchymal cells. Also, there isprogressive reduction in thecompactness of mesenchymalcells. At term, the epithelial cellsform a continuous uninterruptedlining but mesenchymal cells arewidely dispersed.Structure of amnion22

Amnion consists of five layersInner layer of cuboidalepithelial cells derived fromectoderm of embryonic discBasement membraneAcellular layer of interstitialcollagensRow of mesenchymal cellsOutermost acellular zonaspongiosa

Functions-Amnion is not merelyan avascular layer. It ismetabolically active and isinvolved in solute and watertransport to maintain amnionicfluid homeostasis. Amnionepithelial cells are the cells that areusually referred to and studiedmost commonly in amnionicf luid. These are the site oftransfer between amnion andamnionic f luid. They aremetabolically active and are siteof synthesis of tissue inhibitor ofmetalloproteinase- 1.23Mesenchymal cells areresponsible for majority ofamnionic functions, like synthesisof interstitial collagens,24 andsynthesis of cytokines like IL-6,IL-8 and MCP-1.25 Interstitialcollagens are almost exclusivelyresponsible for the tensilestrength of amnionAmniotic fluidOrigin of amniotic fluid- theprecise origin still remainsunsolved. It is thought to be ofmixed fetal and maternalorigin26,27.During first half ofpregnancy, amniotic fluid ismainly formed by transudation

across fetal membranes and fetalskin (before keratinization). Insecond half, significantcontribution in regulating volumeand composition is from fetalurine, tracheobronchial secretionsand swallowing of amniotic fluidby fetus.Volume-It is around 200 ml at 16weeks, 1 litre at 28 weeks;thereafter it reduces such that atterm it is 800 ml, and reduces toonly 200 ml at 42 weeks.28.Composition-Amniotic fluid isslightly alkaline with low specificgravity. In early pregnancy; thecomposition is similar toextracellular fluid. Later, it isaltered by addition of fetal urinarymetabolites. Water is the mainconstituent accounting for 98-99% of composition, rest 1- 2%is solid component. The solidcomponents include proteins,glucose, urea, uric acid, creatinine,lipids and electrolytes. Varioussuspended particles includelanugo, exfoliated epithelial cells,vernix caseosa, cast off cells fromrespiratory tract etc.Functions-Amniotic fluid acts asa shock absorber duringpregnancy, maintains eventemperatureAlong with fetal membranes, ithelps in cervical dilation duringlabour. It also acts as lubricant andgives freedom of movement tothe fetus.Umbilical cordDevelopment-At first embryo isinterposed between amnion andyolk sac. The dorsal surface of theembryo grows faster than theventral surface, the embryo bulgesinto the amniotic sac and thedorsal part of the yolk sac isincorporated into the embryo toform the gut. Later yolk sacbecomes smaller. The allantoisprojects into the base of the body


stalk from the caudal part of yolksac. In third month of pregnancy,the expanding amnion obliteratesexocoelom, fuses with chorion,engulfs the embryo and covers theplacenta and body stalk. Umbilicalcord is developed from the bodystalk. Initially it is attached to thecaudal end of the embryonic discbut due to cephalocaudal foldingof the embryo29 and simultaneousenlargement of the amnioticcavity; it comes to lie on theventral aspect of the fetus. As theamniotic cavity becomes filledwith fluid, the embryo is carriedmore and more into the cavitywith simultaneous elongation ofbody stalk, the future umbilicalcord.Structure-The constituents ofumbilical cord are

Epithelium -It is single layerof amniotic epithelium.Wharton's jelly-it consists ofelongated cells in a gelatinousf luid formed by mucoiddegeneration of the extraembryonic mesodermal cells.Blood vessels- Initially thereare 4 vessels-2 arteries and 2veins. The arteries arederived from the internal iliacarteries of the foetus andcarry the venous blood fromthe foetus to the placenta. Theright umbilical vein disappearsby the 4th month. Presence ofa single umbilical artery isoften associated with foetalcongenital malformation.Remnant of the umbilicalvesicle and its vitelline duct-remnant of the yolk sac maybe found as a small yellowbody near the attachment ofthe cord to the placenta.Allantois-A blind tubularstructure present near thefetal end.Obliterated extra embryonic

coelom.Characteristics-The umbilicalcord is 50 cm long with usualvariation of 30-100 cm. Itsthickness is not uniform atpaces but present knot in itsentire length. The umbilicalarteries do not possessinternal elastic lamina buthave got well developedmuscular coat. Both thearteries and vein do notpossess vasavasorum.

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and nine days respectively.Contrib Embryol 31: 65,1945

6. Moore KL: The DevelopingHuman: Clinically OrientedEmbryology, 4th ed.Philedelphia, Saunders, 1988

7. Hamilton WJ, Boyd JD:Trophoblasts in humanutero- placental arteries.Nature 212: 906, 1966

8. Boyd JD, Hamilton WJ.Development and structureof human placenta from theend of the third month ofthe human gestation. JObstet Gynae Brit. Cwlth74:161- 226, 1967

9. Crawford JM. A study ofhuman placental growthwith observations on theplacenta in erythroblastosisfoetalis. Br J ObstetGynaecol66: 855, 1959

10. Boyd JD, Hamilton WJ: TheHuman Placenta.Cambridge, England,Heffer, 1970

11. Ramsey EM, Donner MW:Placental Vascular andCirculation. Philedelphia,Saunders, 1980

12. Blecker OP, KloostermanGJ, Mieras DJ, Oosting J,Salle HJA:Intervillus spaceduring uterine contractionsin human subjects: Anultrasonic study. Am JObstet Gynecol 123: 697,1975

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6ReviewArticle

A Gestational age in weeks at which fetal organs can bevisualized in >70% of fetuses by transabdominal andtransvaginal ultrasound 3

Fetal Structure Transabdominal TransvaginalCranium 11-13 11-12Spine 12-13 11Long Bones 12-13 10-11Feet 12 13Four-chamber Heart View 12-13 12Kidneys 12-13 11-12Bladder 12-13 13Anterior Abdominal Wall 12-13 12Face 12-13 12Stomach 13 11-12

structure of the body of thefetus. Clinical application:Knowledge of the fetal anatomyis essential for targetedultrasounds for congenitalanomalies. Transabdominaland transvaginal ultrasoundshave given us an in-depthunderstanding of normal fetalanatomy during the variousstages of development. Todayultrasound can achieve fetalanatomy assessment includingvisualization of the skull, brain,face, spine, four-chamber andthree-vessel views of the heart,stomach, abdominal wall,kidneys, bladder and extremities.Various studies have shown thatthe best time for ruling outcongenital anomalies is 10-14weeks. 1,2 This is especiallyimportant in high riskpregnancies with a previousanomaly in order to reassure themother. However, the detectionrate for structural anomalies inthe first trimester varies from 33to 64.7 % while that in the secondtrimester is between 17 to 85 %.Hence a first trimester scancannot replace an anomaly scanbetween 18 to 24 weeks in lowrisk population3.Fetal growth and developmentEstimation of gestational age-Gestational age or menstrual ageis the time elapsed since the first

natomy of fetusAnatomy of the fetusrefers to the general

day of the last menstrual period.This is usually 2 weeks beforeovulation and fertilization.Embryologists describe embryofetal development in ovulationage or the time in day or weeksfrom ovulation. Gestational agecan be calculated from the lastmenstrual period.Dating ofpregnancy is required in high risksituations for proper assessmentof growth and iatrogenictermination in maternal and fetalinterest.

Gestational dating by meansac diameter in the early first

trimester 4

Mean Sac GestationalDiameter (mm) Age (wks)2 5.03 5.14 5.25 5.46 5.57 5.68 5.79 5.910 6.0

Gestational dating by ultrasound in thefirst trimester 4

Sonographic findings Gestational Age (Weeks)Gestational sac, no yolk sac, no 5embryo or heart beatGestational sac with yolk sac, no 5.5embryo or heart beatGestational sac with heart beat 6and embryo <5 mm in lengthEmbryo/Fetus e”5 mm in length Age based on

crown-rump length

Anatomy of Fetus, Fetal Growth and Development, FetalPhysiology, Fetal Circulation

S. Batra, N. GamiDepartment OBG, Maulana Azad Medical College, Delhi


Fetal growth-Fetal growth hasbeen divided into threeconsecutive cell growth phases 5.The initial phase of hyperplasiaoccurs during the first 16 weeksand is characterized by rapidincrease in the cell number. Itcorresponds to a growth rate of5 gm per day at 15 weeks.Thesecond phase includes bothcellular hyperplasia andhypertrophy and extends up to 32weeks. The growth rate is 15- 20grams / day at 4 weeks. After 32weeks fetal growth occurs viacellular hypertrophy and growthrate is 30 to 35 gms per day at 34weeks. Most fetal fat andglycogen deposition takes placeduring this phase. In early fetallife the major determinant offetal growth is the fetal genome.Later in pregnancyenvironmental, nutritional andhormonal influences becomeincreasingly important.

Fetal Nutrition-Maternal diet istranslated into storage forms thatare made available to meet thedemands for energy , tissue repairand new growth includingmaternal needs for pregnancy.Glucose: Glucose is a majornutrient for fetal growth andenergy. Human Placentallactogen, a hormone present inabundance in the mother blocksperipheral uptake of glucosewhile promoting the mobilizationand use of free fatty acids bymaternal tissues. This ensuresglucose supply to the fetus. D-glucose is transferred across cellmembranes through carriermediated, stereo specific, nonconcentrating process offacilitated diffusion. Of theglucose transport proteins(GLUT) GLUT -1 and GLUT -3are prominent in the plasmamembrane of the microvilli ofsyncytiotrophoblast. Clinical

application: Fetal macrosomia isassociated with ahyperinsulinemic state withincreased levels of selectedgrowth factors and increasedexpression of GLUT proteins insyncytiotrophoblast. Lactate isalso transported across theplacenta by facilitated diffusion.It is co-transported withHydrogen ions as lactic acid.Most free acids are transportedcross the placenta by simplediffusion and are also synthesizedin the placenta.The Low DensityLipoprotein Particles frommaternal plasma bind to specificLDL receptors in coated pitregions of microvilli onmaternal-facing side ofsyncytiotrophoblast. It is thentaken up by a process of receptormediated endocytosis.

Amino acids : Amino acids areare concentrated insyncytiotrophoblast and thentransferred to the fetal side bydiffusion. Usually there is limitedtransfer of large proteins acrossthe placenta. Those which are,like IgG and retinol bindingprotein, are transported byreceptor mediated transport.Iodine and zinc are transferredacross the placenta by an energyrequiring , carrier mediated activeprocess. The heavy metal bindingprotein, Metallothionein – 1 isexpressed in humansyncytiotrophoblast. This bindsand sequesters a host of heavymetals , including zinc ,copper,lead and cadmium.Thus calciumand phosphorus are activelytransported across the placenta.Vitamin A is transported acrossthe syncytium bound to Retinolbinding protein. Vitamin C

Approach to gestational age assignment byultrasound on initial scan 4

State of pregnancy Basis for GA Accuracy (wks)

First trimesterEarly (5-6 wks)Mid-to-late (6-13 wks) Sonographic ±0.5

milestonesCRL ±0.5

Second trimesterIf OFD availableIf BPDc or HC ±1.2 (14-20 wks)

±1.9 (20-26 wks)OFD not BPD or FL ±1.4 (14-20 wks)measurable ± 2.1-2.5 (20-26 wks)

Third trimesterIf OFD available BPDc, HC or FL ±3.1-3.4 (26-32 wks)If OFD not FL ±3.5-3.8 (32-42 wks)measurable ±3.1 (26-32 wks

±3.5 (36-42 wks)

OFD- occipito frontal diameter, HC – Head circumference, BPD-Bipareital diameter, FL – femur length, BPDc- corrected BPD


(ascorbic acid) Is transportedacross the placenta by an energymediated carrier dependantmechanism.Fetal development - Fetaldevelopment is the process inwhich a fetus develops duringgestation, from the times ofconception until birth. Fetaldevelopment consists of 3 stages.Pre-implantationAlso known as “ all or none “period.Toxic exposures maycause fetal death but do not causedevelopmental defectsWeek 1 (3rd week after L.M.P)-Fertilization of the ovum toform a zygote which undergoesmitotic cellular division, but doesnot increase in size. A hollowcavity forms marking theblastocyst stage. The blastocystcontains only a thin rim oftrophoblast cells and a clump ofcells at one end known as the“embryonic pole” which includeembryonic stem cells. Theblastocyst hatches from itsprotein shell (zona pellucida) andimplants onto the endometriallining of the mother’s uterus bythe 11th -12th day. If the zygote isgoing to separate into identicaltwins, the outcome depends onwhen the division occurs. Ifdivision occurs within the firstthree days, the inner cell mass isyet to form and the outer layerof blastocyst has not yetcommitted to become chorion.Thus a monozygotic diamniotic,dichorionic twin pregnancydevelops.6 If division occurs between 4th

and 8th day, the inner cell masshas formed and cells destined tobecome chorion have alreadydifferentiated, but those of the

amnion have not. This gives riseto monozygotic , diamnioticmonochorionic twin pregnancy.6

Week 2 (4th week after L.M.P)- Trophoblast cells surroundingthe embryonic cells proliferateand invade deeper into theuterine lining. They willeventually form the placenta andembryonic membranes.Formation of the yolk sac. Theembryonic cells flatten into adisk, two-cells thick. If the zygoteis going to separate into twins andthe division takes place after 8days, a monozygotic ,monoamniotic monochorionictwin pregnancy results. This isbecause by then the chorion andamnion have alreadydifferentiated. If division isinitiated even later , that is afterthe embryonic disc has formed ,cleavage is incomplete andconjoined twins result.6Embryonic PeriodThis is the period from the 2nd tothe 8th week followingfertilization . It encompassesorganogenesis and is thus themost crucial period with regardto structural malformations.Toxic exposures often causemajor congenital malformationsWeek 3 (5th week after L.M.P- first missed menstrualperiod) - A notochord forms inthe center of the embryonic disk.A neural groove (future spinalcord) forms over the notochordwith a brain bulge at one end.Heart tubes begin to fuse.Week 4 (6th week after LMP)-The embryo measures 4 mm (1/8 inch) in length and begins tocurve into a C shape. Somites, thedivisions of the future vertebra,form. The heart bulges, further

develops, and begins to beat in aregular rhythm on day 21.Branchial arches, grooves whichwill form structures of the faceand neck, form. The neural tubecloses. The ears begin to form asotic pits. Arm buds and a tail arevisible.Week 5 (7th week of preg-nancy) - The embryo measures8 mm in length. Lens pits andoptic cups form the start of thedeveloping eye. A primitivemouth and nasal pits form. Thebrain divides into 5 vesicles, in-cluding the early telencephalon.Leg buds form and hands formas flat paddles on the arms.Rudimentary blood movesthrough primitive vessels con-necting to the yolk sac and chori-onic membranes.

Week 6 (8th week of preg-nancy) - The embryo measures13 mm in length. Lungs begin toform. The brain continues todevelop. Arms and legs havelengthened with foot and handareas distinguishable. The handsand feet have digits, but may stillbe webbed.Week 7 (9th week of preg-nancy) - The embryo measures22-24 mm in length. Nipplesand hair follicles begin toform.Location of the elbows andtoes are visible. Spontaneous limbmovements may be detected byultrasound. All essential organshave at least begun formation.

Week 8 (10th week ofpregnancy) - E m b r y omeasures 40 mm in length.Intestines rotate. Facial featurescontinue to develop. The eyelidsare more developed. The external


development.”Quickening” usu-ally occurs (the mother can feelthe fetus moving).The fetal heart-beat can be heard with a stetho-scope.Week 22 (24th week of preg-nancy) - The fetus reaches alength of 28 cm .The fetusweighs about 725 g .Eyebrowsand eyelashes are well formed.Allof the eye components aredeveloped.The fetus has a handand startle reflex.Footprints andfingerprints continue forming.Alveoli are forming in lungs.Weeks 23 to 26 (25th to 28thweek of pregnancy) -The fetusreaches a length of 38 cm (CRL25 cms).The fetus weighs about1.2 kg .The brain developsrapidly.The nervous systemdevelops enough to control somebody functions.The eyelids openand close. The respiratorysystem, while immature, hasdeveloped to the point where gasexchange is possible. A baby bornprematurely at this time maysurvive, but the possibilities forcomplications and death remainhigh.Weeks 27 to 31 (29th to 33rdweek of pregnancy) -The fetusreaches a length of about 38-43cm (CRL 28 cms). The fetusweighs about 2 kg. The amountof body fat rapidly increases.Rhythmic breathing movementsoccur, but lungs are not fullymature. Thalamic brainconnections, which mediatesensory input, form. Bones arefully developed, but are still softand pliable.The fetus beginsstoring iron, calcium, andphosphorus.Week 34 (36th week of preg-nancy) -The fetus reaches a

length of about 40-48 cm Thefetus weighs about 2.5 to 3 kg .Lanugo begins to disappear.Body fat increases. Fingernailsreach the end of the fingertips.A baby born at 36 weeks has ahigh chance of survival, but mayrequire medical interventions.Weeks 35 to 38 (37th to 40thweek of preganancy) - Thefetus is considered full-term atthe 37th week of pregnancy. Itmay be 48 to 53 cms inlength.The lanugo is gone excepton the upper arms and shoulders.Fingernails extend beyondfingertips. Small breast buds arepresent on both sexes.Head hairis now coarse and thickerClinical Application-For anagent to cause teratogenicity thefetus must be exposed tothe agent during a criticaldevelopment period. Majoreffects occuring from drugexposure within the first 8 weeksresult in an embryopathy, after 8weeks a fetopathy results.Fetal physiologyAmniotic f luid - In earlypregnancy , amniotic fluid is anultrafilterate of maternal plasma.By the second trimester, itconsists largely of extracellularfluid that diffuses through thefetal skin. After 20 weeks,however, the cornification offetal skin prevents this diffusion,and amniotic fluid is composedlargely of fetal urine. Pulmonaryf luid accounts for a smallproportion of the amnioticvolume, and f luid filteringthrough the placenta accounts forthe rest. The volume of amnioticfluid increases progressively andthen falls slightly at term (200 mlat 16weeks, 1000 ml at 28 weeks,

features of the ear begin to taketheir final shape.Fetal PeriodDuring the fetal period, toxicexposures often causephysiological abnormalities orminor congenital malformationWeeks 9 to 12 (11th to 14thweek of pregnancy) - Thefetus reaches a length of 6-7 cms.The head comprises nearly halfof the fetus’ size. The face is wellformed and develops ahuman appearance. Centers ofossification appear in most fetalbones. The eyelids close and willnot reopen until about the 28thweek. Tooth buds, which willform the baby teeth, appear. Thelimbs are long and thin. The fetuscan make a fist with its fingers.Genitals appear welldifferentiated. Red blood cells areproduced in the liver.Weeks 13 to 16 (15th to 18thweek of pregnancy) -The fetusreaches a length of about 15 cm( CRL – 12 cms). A fine haircalled lanugo develops onthe head.Fetal skin isalmost transparent. More muscletissue and bones have developed,and the bones becomeharder.The fetus makes activemovements.Sucking motions aremade with the mouth.Meconiumis made in the intestinal tract.Theliver and pancreas produce fluidsecretions. Gender can bedetermined by inspection of theexternal genitalia by 14 weeks.Week 18 (20th week of preg-nancy) - The fetus reaches alength of 20 cm .Lanugo coversthe entire body.Eyebrows andeyelashes appear.Nails appear onfingers and toes.The fetus is moreactive with increased muscle


900ml and 800 ml at 36 and 40weeks respectively.)Clinical applications

Abnormal amniotic fluidvolume : Diminished fluidvolume is termedoligohydramnios ( amnioticfluid index of 5 cms or less.)Increased amniotic fluid orpolyhydramnios is defined byan AFI of greater than 25cms. This condition mayresult from congenitalanomalies ( anencephaly andother open neural tubedefects, esophageal atresia),maternal diabetes mellitus,Hydrops fetalis etc.Decreased amniotic fluidvolume may be associatedwith fetal growth retardationand this requires close fetalsurveillance. If fetalcompromise is confirmed byDoppler studies, Terminationof pregnancy may beindicated. It may also beassociated with fetalChromosomal anomalies( Triploidy, Trisomy 18,Turner syndrome) orcongenital anomalies ( Fallottetrology, Septal defects,Renal agenesis or dysplasia,Urethral obstruction,Hypothyroidism etc.)Amniocentesis for geneticdiagnosis is usuallyperformed between 14 – 20weeks . It has more than 99percent diagnostic accuracyfor Down syndrome.Amniotic fluid AFP levels aremeasured if a Neural TubeDefect is suspected onultrasound and maternalserum AFP is raised.Amniotic cells can be used

for karyotyping for diagnosisof aneuploidy and otherchromosomal disorders.Early amniocentesis isperformed between 11 and14 weeks of pregnancy.

Placental Circulation-Chonionic will are first seenaround the 12th day afterfertilization. Mesenchymal cords,derived from extra embryonicmesoderm, invade the primaryvilli forming secondary villi. Afterangiogenesis these are calledtertiary villi. Maternal venoussinuses are tapped early inimplantation but maternal arterialblood enters the intervillousspace by about 14th -15th day afterfertilization. By about the 17th

day, fetal blood vessels arefunctional and the placentalcirculation is established.

Fetal circulation-The majordifferences in fetal circulation ascompared to that in an adult arethe presence of umbilical-placental circulation and theabsence of significant pulmonarycirculation.Oxygenated blood from placentacomes through the umbilical vein,which joins the left branch of theportal vein. The greater part ofthis passes directly to the InferiorVena Cava (IVC) through theductus venosus. The oxygen richblood reaching the right atriumthrough the IVC tends to coursealong the medial aspect of IVCand is directed through the valvesof the IVC towards the foramenovale. Here, it is divided into twoportions by the lower edge of theseptum secundum (cristadividens).a) Most of it passes to the left

atrium through the foramenovale

b) The rest gets mixed withdeoxygenated blood fromSuperior Vena Cava( SVC)and passes into the rightventricle.

The high venous return from theplacenta maintains the right toleft shunt through the foramenovale and delivers most of theoxygenated blood to the brainand the heart. From the rightventricle, the blood enters thepulmonary circulation. Most ofit bypasses to the systemiccirculation via the ductusarteriosus and reaches thedescending aorta. A highpulmonary vascular resistancemaintains the right to left shuntthrough the ductus arteriosus.Most of the oxygenated bloodfrom the left atrium reaches theleft ventricle and then suppliesthe brain and the upperextremities through the aorta andthe great vessels. Rest of it getsmixed with poorly oxygenatedblood from the ductus arteriosus.Much of the blood in thedescending aorta is carried by theumbilical arteries to the placenta,where it is again oxygenated andreturned to the heart.

Fetal bloodHemopoiesis-In earlyembryonic life hemopoiesis isdemonstrable first in the yolk sac.The next major site is the liver ,and finally the bone marrow.Haemoglobin content of fetalblood rises to about 12 mg/dl atmidpregnancy and at term it isabout 18 gms / dl.Erythropoiesis - This iscontrolled in the fetus by fetalerythropoietin produced mostlikely by the fetal liver. Theproduction of erythropoeitin isinfluenced by testosterone,


estrogen , prostaglandins, thyroid hormone and lipoproteins .Fetal hemoglobin - Most haemoglobin in the fetus is HbF , which has two g chains (a - 2 , g- 2 ) in placeof the adult haemoglobin HbA ( a - 2, b - 2 ) and HbA 2 (a-2 , d -2 ) . b,g and d genes lie on chromosome11. HbF is resistant to denaturation by acid and alkali. It has a higher affinity for oxygen than adult

haemoglobin. The major reason for this is that HbA binds 2,3 –diphosphoglycerate (2,3 DPG ) moreavidly than HbF , and this lowers the affinity of haemoglobin A for oxygen. 90% of fetal haemoglobin is

Modified from Moore KL, Persaud TVN: Before We Are Born: Essentials of Embryologyand Birth Defects, 5th ed. Philadelphia, W.B. Saunders, 1998). RA and LA=right and leftatria, RV and LV=right and left ventricles.


HbF between 10 and 28 weeksof gestation. From 28 to 34weeks a switch from HbF to HbAbegins. By term HbF is threefourths the total fetalhemoglobin, and by 6 monthsafter birth only 1 % of the totalhaemoglobin is HbF.Fetal Coagulation factors -with the exception of fibrinogenthe fetus star ts producingnormal, adult type , procoagulant, fibrinolytic and anticogulantproteins by about 12 weeks.However the levels are reduced.At birth factors II , VII , IX ,X,XI, XII , XIII and fibrinogen are lowin cord blood. Withoutprophylactic treatment , thevitamin K dependant coagulationfactors usually decrease evenfurther during the first five daysafter birth. This decrease isamplified in breast fed infantsand may lead to hemorrage in thenewborn. Fetal fibrinogen , whichappears as early as 5 weeks , hasthe same aminoacid compositionas adult fibrinogen but forms aless compressible clot , and thefibrin monomer has a lowerdegree of aggregation.Despite this relative reduction inprocoagulants, the fetus seemsto be well protected fromhemorrhage. Even after invasiveprocedures such as cordocentesis, excessive bleeding usually doesnot occur. Amniotic f luidthromboplastins and some factorin Wharton jelly combine tofacilitate coagulation at theumbilical cord puncture site.Fetalimmunocompetance-Inthe absence of antigenic stimulusthe fetal immunoglobulinsconsist almost entirely ofmaternal immunoglobin G (IgG)

transeferred across the placenta.Transfer of maternal IgG beginsat about 16 weeks and themaximum takes place in last 4weeks of pregnancy. Hence therelative deficiency in preterminfants. In certain situations likeisoimmunisation resulting inhemolytic disease of thenewborn, transfer of maternalIgG can be harmful to the fetus.Maternal IgM is not transportedacross the placenta to the fetus.Also, the IgM response isdominant in the fetus andremains so for weeks to monthsin the newborn. Serum IgM levelsin umbilical cord blood andidentification of specificantibodies may be useful in thediagnosis of intrauterineinfection. IgA ingested withamniotic fluid before deliveryand that ingested in colostrumafter delivery provide mucosalprotection. Newborn respondspoorly to immunization.Nervous system- The spinalcord extends along the entirelength of the vertebral columnin the embryo , but after that itgrows more slowly. By 24 weeksit extends to S1 , by birth to L3 ,and in the adult to L1.Movements of the fetus begin at7 weeks, become co-ordinatedonly by 12 weeks. Respiration isevident by 14-16 weeks. The fetuscan apparently hear sounds inutero by 24 - 26 weeks and by 28weeks the eye is sensitive tolight.Clinical application -Adefinitive negative correlationexists between fetal hypoxemiaand fetal movements. This can beassessed by the biophysicalprofile. Thoracic movements ,inappropriately called breathing

movements, disappear first ,followed by the movements offetal extremities , limb girdles ,and finally fetal trunk and spine.Gastrointestinal system -Swallowing begins at 10-12weeks. Later in pregnancy thevolume of amniotic fluid appearsto be regulated substantially byfetal swallowing, for whenswallowing is inhibited,hydramnios is common(anencephaly and esophagealatresia) Term fetuses swallowbetween 200-760 ml per day.Meconium–The fetal bowelcontents consist of varioussecretions, such asglycerophospholipids from thelungs, desquamated fetal cells,lanugo, scalp hair and vernix. Italso contains undigested debrisfrom swallowed amniotic fluid.The dark greenish – blackappearance is caused bypigments, especially biliverdin.Meconium passage can resultfrom normal bowel peristalsis inthe mature fetus or from vagalstimulation. It can also occurwhen hypoxia stimulates argininevasopressin (AVP ) release fromthe fetal pituitary . AVPstimulates the smooth muscle ofthe colon to contract, resulting inintramniotic defecation.Liver-The fetal liver has limitedcapacity to convert free bilirubinto bilirubin diglucuronoside. Thisis more so in an immature fetus.Normally unconjugated bilirubinfrom the fetal circulation isexcreted into the amniotic fluidafter 12 weeks and isthen transferred across theplacenta. This transport ishowever bidirectional. Hence


unconjugated bilirubin from amother suffering from hemolyticanaemia will readily cross theplacenta.Gall bladder -In the third monthgall bladder contains bile saltsand bile acids.Blood from umbilical cord ofnormal term infants contains anaverage 1.4 mg of bilirubin (0.2– 2.6 mg). In hemolytic diseaseof the newborn it may be upto30 – 4- mg / 100 ml.Pancreas - Insulin containinggranules can be identified in thehuman fetal pancreas by 9 – 10weeks, and insulin in fetal plasmais detectable at 12 weeks. Fetalgrowth is determined by theamounts of nutrients from themother with anabolism throughthe action of fetal insulin. Seruminsulin levels are high innewborns of diabetic mothersand in other large – for –gestational age infants, but insulinlevels are low in infants who aresmall for age.Urinary system - The fetalkidneys start producing urine at12 weeks . by 18 weeks they areproducing 7-14 ml / day and atterm this increases to 27 ml /hour or 650 ml / day.Uteroplacental insufficiency isknown to decrease fetal urineformation.Pulmonary system - In orderfor the lungs to function properlyat birth it is important that bothanatomical and morphologicaldevelopment and its capacity forsurfactant formation are present. Anatomical development of thelung cannot be hastened byantenatal or neonatal therapy.There are three essential stagesof lung development.

Pseudoglandular stage :growth of the intrasegmentalbronchial tree between the 5th

and the 17th weeks. The lunglooks like a microscopicgland.Canalicular stage : his extendsfrom the 16 to 25 weeks.During this phase thebronchial cartilage platesextend peripherally. Eachterminal bronchiole gives riseto several respiratorybronchioles, and each ofthese in turn divides intomultiple saccular ducts.Terminal sac stage : thealveoli give rise to primitivepulmonary alveoli. Anextensive capillary andlymphatic network developand type II cells begin toproduce surfactant.

Various insults can upset thisprocess . With renal agenesis, noamniotic fluid is present from thebeginning of lung growth, andmajor defects occur in all threestages. In fetuses with membranerupture and oligohydramniosbefore 20 weeks, there is normalbronchial branching butimmature alveoli. Membranerupture occurring after 24 weekshas little effect on pulmonarystructure.

Surfactant - It is a chemicalmade up of 90% lipids and 10 %proteins and is produced by typeII Pneumocytes. The principalactive component of surfactantis a specific lecithin –dipalmitoylphosphatidylcholine(DPPC) which accounts for 50 %and phosphatidylglycerine whichaccounts for 8-15% .Surfactantspreads to line the alveolus at thetime of the first breath and

prevents alveolar collapse at thetime of expiration.Role ofcorticosteroids in fetal lungmaturation: Fetal cortisol isbelieved to be the natral stimulusfor lung maturation andaugmented surfactant synthesis.Thus lung maturation is delayedand respiratory distress syndromecommon in fetuses with limitedcortisol production. These areanencephaly , adrenal hypoplasiaor congenital adrenal hyperplasia.Thus exogenously administeredcorticosteroids significantlyreduce the incidence ofrespiratory distress syndrome.Endocrine glandsPituitary glands- The pituitarydevelops from two differentsources. The adenohypophysisdevelops from the oral ectoderm– Rathke pouch and theneurohypophysis develops fromthe neuroectoderm. The fetalpituitary is responsive tohormones and is capable ofsecreting these hormones fromearly in fetal life.Adenocorticotropic hormone isfirst detected in the fetal pituitarygland by 7 weeks and Growthformone and Leutenisinghormone by 13 weeks. Theposterior pituitary gland is welldeveloped by 10- 12 weeks whenoxytocin as well as arginine andvasopressin can be found in fetalblood. Oxytocin as well as AVPprobably function at the level ofthe lung and placenta to conservewater in the fetus.AVP in fetalblood is increased during fetaldistress. There is a well developedintermediate lobe in the fetalpituitary gland which disappearsbefore term and so is absent inthe adult. The cells of this lobe


produce a melanocyte stimulatinghormone and Bendorphin.

Thyroid gland - The pituitarythyroid axis is functional by theend of the first trimester. Thethyroid gland is able to synthesizehormones by 10-12 weeks. Theplaventa actively concentratesiodide on the fetal side and from12 weeks onwards, the fetalthyroid concentrates iodide moreavidly than maternal thyroid.Hence maternal adminstration ofany form of iodides is potentiallyhazardous to the fetus. Thethyroid hormone levels increasethroughout pregnancy. The fetalpituitary is not sensitive tofeedback until very late inpregnancy. Fetal thyroidhormones have a critical role inthe development of the fetalbrain, among other tissues.Placental tissues and membranesprevent passage of maternalthyroid hormones to a largeextent by rapidly de-iodinatingmaternal T 3 and T4 to reverse T3, which is relatively inactive.Antithyroid antibodies howevercan cross the placenta.Congenital hypothyroidismresults in many neonatalproblems like neurologicalabnormalities, respiratorydifficulties, dysmorphic facies,lethargy and hypotonia. these canbe avoided with prompt thyroidreplacement after bir th.Immediately after bir th,atmospheric cooling evokessudden and marked increase inthyrotropin release which leads toa marked increase in T4 levels ,which are maximum 24 – 36hours after birth.Adrenal glands- The glands,which are much larger in the fetus

than in the adult, are made uplargely of the inner or fetal zoneof the adrenal cortex. The fetaladrenal glands also synthesizealdosterone.

Sexual differentiation of thefetusChromosomal gender: Geneticgender-XX or XY is establishedat the time of fertilization. Forthe first six weeks ofdevelopment the male and femaleembryo are morphologicallyindistinguishable. Gonadalgender: If the fetus carries a Ychromosome the indifferentgonad develops into a testis atabout six weeks after conception.Testes development is directed bya gene located on the short armof Y chromosome. This testis-determining factor (TDF) or sex-determining region (SRY) isspecific to the Y chromosomeand is expressed in the single cellzygote immediately after ovumfertilization. In addition, testisdevelopment requires a dosedependent sex reversal (DDS)region on the X chromosome, aswell as certain unidentifiedautosomal genes. Phenotypicgender: Male phenotypic sexualdifferentiation is directed by thefunction of the fetal testis. In theabsence of a testis, femaledifferentiation takes place. Thefetal testis secretes aproteinaceous substance calledmullerian inhibiting substance. Itacts as a paracrine factor to causeregression of the mullerian ductpreventing the development ofuterus, fallopian tubes and uppervagina. The fetal testes alsosecrete testosterone, whichcauses virilization of the externaland internal genitalia. In theexternal genitalia, testosterone

is converted to 5-adihydrotestosterone, whichamplifies the androgenic actionof testosterone.Genital ambiguity of thenewbornAmbiguity of the neonatalgenitalia is the result of eitherexcessive androgen action in afetus destined to be female, orinadequate androgens in onedestined to be a male. Suchabnormalities can be assigned toone of four clinically definedcategories. These are -Female pseudohermaphrodit-ism

Mullerian inhibitingsubstance is not produced,Androgen exposure of theembryo-fetus is excessive, butvariable for a fetus geneticallypredestined to be a female,The karyotype is 46 XXOvaries are present.

Male pseudohermaphroditismThere is production ofmullerian inhibitingsubstance,Incomplete but variableandrogenic representation fora fetus destined to be male,A 46,XY karyotype,The presence of testes or nogonad.

Dysgenetic gonads, includingtrue hermaphroditism

Mullerian inhibitingsubstance is not produced,Fetal androgen exposure isvariable,Karyotype is variable, mostlyabnormal,Neither normal ovaries nortestes are present.

True hermaphroditismIn addition to allcharacteristics of dysgenetic


gonads, these subjects hadboth ovarian and testiculartissues.

References1. Whitlow BJ , Economides

DL . The optimal gestationalage to examine fetal anatomyand measure nuchaltransluscency in the firsttrimester. Ultrasound inobstetrics and gynecology.Vol 11(4); April 1998:258.

2. Souka AP, Pilalis A, KavalakisY, Kosmasi Y, Antasaklis P ,Antasaklis A. Assessment offetal anatomy at the11-14 th week ultrasoundexamination. Ultrasound inobstetrics and gynecology.24(7); Dec 2004:730-734.

3. Peregrine E, Pandya P.:Structural anomalies in thefirst trimester. In RumackCM, Wilson SR, CharbonearuJ (eds) : Diagnosticultrasound 2nd edition2005,Elsevier Mosby ,London.

4. Benson CB , Doubilet PM.Fetal measurements – normaland abnormal fetal growth. InRumack CM, Wilson SR,Charbonearu J (eds) :Diagnostic ultrasound 2nd

edition 2005,Elsevier Mosby, London.

5. Lin CC, Santolayer-Forgas J:Curent conceprs of fetalgrowth restriction: Part I.Causes , classification, andpathophysiology. ObstetGynecol 92:1044,1998.

6. Multifetal Gestation. InCunningham FG,Leveno KT,Bloom SL,Hauth JC ,Gilstrap L, Wenstorm KD.(eds) Williams Obstetrics 22nd edition 2005 Mc Graw Hill, U.S.A.

Anatomical Manikins

The anatomical manikinpictured here is a rarityamong the cased sets ofsurgical instruments,amputation kits, and othermedical items that make upthe artifact collection of theUniversity Archives. Oftenthese manikins are confusedwith Chinese diagnostic dollsor “doctor’s ladies”. InChinese culture, modestyforbade a woman fromundergoing a physicalexamination or evenmentioning parts of herbody to a male physician.The circumvent thissituation, during a house callthe doctor brought along thediagnostic doll. By markingthe section giving herdiscomfort, the womancould communicate herproblems to the physician.While both anatomical anddiagnostic manikins weresomewhat similar inappearance, the craftsmenfashioned anatomicalmanikins with much moredetail. Sometimes producedin male and female pairs, itwas far more common tocreate only the female figureand always in an advancedstate of pregnancy. Medicalhistory contains littleinformation on the origin orintended use of themanikins. Since earlyanatomists had few subjects

available for dissection, mostanatomy studies focused ontwo-dimensional drawings.Historians surmise themodels provided a meansduring the 17th and 18thcenturies to study anatomywith a three-dimensionalobject or teach pelvicanatomy to midwives. K.F.Russell proposed in his 1970study that while detailed, thestructure of the manikins didnot provide enough accurateinformation for serious study.Instead the models wereprobably used to educate thelay public on the differencesbetween the sexes and thephysiology of pregnancy.Since neither the manikins ordiagnostic dolls possessdates, signatures, or anyinformation about theircreators, dating andattribution is difficult tomake. Russell studied 98manikins from severaldifferent medical libraries andhis observations allowed himto separate the manikins intoseveral different groupings.All the figures Russell studiedwere from Germany, Italy, orFrance. None were foundfrom Great Britain, the US,or other European countries.According to his grouping,the anatomical manikin in theUniversity Archives is mostlikely from Germany.


7ReviewArticle

complicates approx 4% ofdeliveries at term, thoughincidence is 7% at 32 weeks and25% of pregnancies less than 28weeks duration. Furthermore,because of the multitude ofproblems and potential problemsassociated with it, breechpresentation has become, inrecent years, the subject ofsignificant controversy. Threetypes of breech presentation arerecognized. Frank breech is mostcommon type accounting for 60-65% of breech presentations andit is more common at term.Complete breech is leastcommon type, accounting forabout 5% of breech presentation.Incomplete breech is morecommon among prematurefetuses and accounts for 25% to35% of breech presentations.The diagnosis of breechpresentation may be made byabdominal palpation and vaginalexamination and confirmed byultrasound. Prematurity, fetalmalformation, mulleriananomalies, hydramnios,oligohydramnios and polarpresentation are commonlyobserved causative factors.Congenital abnormalities of thefetus were identified in 6.3percent of breech deliveriescompared with 2.4 % of nonbreech deliveries. High rates of

breech presentation are noted incertain fetal genetic disorders,including trisomies 13, 18 and 21,Potters syndrome and myotonicdystrophy. Thus, conditions thatalter fetal muscular tone andmobility also increase thefrequency of breechpresentation. In more than 50%of cases, however, no causativefactor for breech presentationcan be identified.There is no major difficulty aboutthe mechanism of breechdelivery except that the largestand least compressible part ofthe baby (head) comes last. Theirregular outline of the breechmeans that spontaneous ruptureof the membranes may befollowed by cord prolapse. Thebreech being comparatively softis less likely than the head tocompress the cord but still acutefetal hypoxia might occur if cordgoes into spasm. Patients alsohave tardy labor because of illfitting breech especially inmultiparas. The most dreadedcomplication is entrapment ofafter coming head when body ispushed through partially dilatedcervix which causes acute fetalhypoxia when delivery has to beaffected through Duhrssensincisions. A study has shown thedanger of occipital diastasis andpossibility of intracranialhemorrhage when unmouldedfetal head descends throughpelvis.

ManagementVaginal deliveries for breechpresentation have long been atopic of debate. Cesareandelivery is commonly but notexclusively used in followingcircumstances – a large fetus (wt> 3.8 kg), any degree ofcontraction or unfavorable shapeof pelvis, a hyper extended head,when delivery is indicated in theabsence of spontaneous labor(Some clinicians used oxytocin),Uterine dysfunction (some useoxytocin augmentation),Incomplete or footling breechpresentation, An apparentlyhealthy and viable preterm fetuswith the mother in either activelabor or in whom delivery isindicated, severe fetal growthrestriction, previous perinataldeath or children suffering frombirth trauma, a request ofsterilization, lack of anexperienced operator, previouscesarean section.Cesarean sectionManagement practice variesamong different institutions andeven among different institutionsand even among differentclinicians in the same institution.The decision to perform cesareandelivery is often based onpersonal experience and fear oflitigation. Some clinicians haverecommended a policy ofcesarean section for breechpresentation at term based onresults of non-randomized

Breech Presentation themost common obstetricm a l p r e s e n t a t i o n

Management of Breech Presentation

Poonam Goel, Parampreet KaurDepartment of OBG, Government Medical College, Chandigarh


studies, anecdotal experiences,and medico legal concerns.However, these studies were notrandomized and hencepotentially biased. Otherwisealso, the clinician experience, aswell as, strict criteria for inclusionconsidered relatively safe forvaginal delivery was notcompared. A recent randomizedmultinational trial of plannedvaginal versus planned cesareandelivery for woman with a termbreech presentation wasundertaken. A total of 2083women were randomly assignedto either group. The trialpublished in 2000, confirmedthat neonatal risks associatedwith term breech births are muchhigher among planned vaginaldeliveries and implied thatcesarean deliveries should besystematically planned for allsuch women. Serious maternalcomplications are similarbetween the groups. In the laterpublication secondary analysis ofterm breech trial was done todetermine factors associated withadverse perinatal outcome and itwas concluded that the breechinfants at term are best deliveredby prelabor cesarean section. Inview of the above mentioned trialwhich demonstrated that overallrisk of perinatal death for theterm frank / complete breechfetus with planned cesareansection was reduced by 75%,RCOG in its guidelines hasrecommended that the bestmethod of delivering a termfrank or complete singletonbreech is planned cesareansection. Similarly, the ACOGCommittee opinion no. 34 hasconcluded that the persistentterm singleton breech

presentation should undergo aplanned cesarean delivery.However, the decision regardingmode of delivery should dependon the attending obstetricianunder hospital specific protocolguidelines and vaginal breechdelivery should only be plannedafter documented informedconsent from patient. Moreoverlong terms outcomes for motherand child have not been evaluatedin term breech trial. Many issueswere raised regarding the flawsand outcome of the trial insubsequently publishedcorrespondence in the Lancetand the British Medical Journal.

Various studies have shownconvincingly that cesareansection is associated withsignificant morbidity, subsequentcompromise of re-productivefunction and negative emotionaleffects. Also, numerous recentstudies that applied a relativelywide spread policy of plannedvaginal delivery in variouspractice conditions, did notobserve the excess risk as in termbreech trial. It is accordinglyessential to assess a managementpolicy in a population (like oursin India) under conditions ofevery day practice and plannedvaginal delivery remains a clinicaloption that can be offered towomen after providing them withclear, objective and completeinformation.For preterm fetuses who are atincreased risk of entrapment ofafter coming head through apartially dilated cervix, norandomized studies regardingvaginal delivery are present.Although most deaths in lowbirth weight breech group are due

to prematurity or lethalanomalies. Cesarean deliveryafter correcting perinatalmortality in the weight group ofless than 1500 grams showimproved survival comparedwith that in similar sized vertexpresentation. Also the policy forcesarean section of pretermfetuses needs to be based on thesurvival rates of neonatal centerof the hospital for that gestationand weight of the baby.

Even if a policy of liberalcesarean section for breechpresentation is followed, theattending physicians should beprepared and trained forimminent delivery in anemergency. Otherwise also, avaginal breech delivery should beallowed only in centers whereprovisions for emergencycesarean section are present,continuous fetal heartmonitoring is used, delivery isattended by trained obstetricianand pediatrician.Complicated vaginal breechdeliveries are associated withincreased maternal risks. Manualmanipulations within the birthcanal increase the risk ofinfection and subsequent postpartum hemorrhage. Delivery ofthe after coming head through anincompletely dilated cervix maycause rupture of the uterus,lacerations of cervix or both.Manipulations might also lead toextensions of the episiotomy anddeep perineal tears. Fetal injuriesinclude fracture of humerus,clavicle and femur which mayoccur in both vaginal andcesarean deliveries. Neonatalperineal tears and testicularinjuries have been reported.


Hematomas of thesternocleiodomastoid musclesoccasionally develop afterdelivery but resolvespontaneously. Brachial plexusinjury leading to paralysis of armsas well as forcible extraction offetus through a contracted pelvismight lead to spoon shapeddepressions or fractures of skull.External cephalic version(ECV)External cephalic version(ECV)is another option in a persistentbreech presentation beyond 36weeks period of gestation. Thisgestation has been chosen sincespontaneous reversion to breechdecreases at this gestation. Also,iatrogenic prematurity in case ofcomplications can be avoided.Surprisingly studies have shownthat, women potentially suitablefor ECV were not made aware ofthis option. Focus should be onincreasing the rate of offeringECV, increasing its uptake andalso its success. Reported successwith external version varies from60 to 75 percent, with a similarpercentage of this remainingvertex at the time of labor.Application of a policy ofexternal cephalic version hasbeen associated with reductionsin the caesarean delivery rate atvarious institutions. Versionshould not be attempted whenthere is a contra indication tovaginal delivery. A prior uterineincision is a relative contraindication. Success of ECV is lesswith nulliparity, anterior, lateral orcornual placenta, decreasedliquor, low birth weight, descentof breech into pelvis, obesity,posteriorly located fetal spine,extended legs and firmabdominal muscles. Attempts atexternal version should be done

in the labor and delivery suite,and a non-stress test should bereactive prior to procedure.During ECV, the fetal positionand heart rate should bemonitored with real-time ultra-sonography. A forward roll ofthe fetus is generally attemptedfirst. If unsuccessful, backwardflip is tried. Discontinuation ofattempt is done in cases ofdiscomfort, persistentlyabnormal fetal heart rate, or aftermultiple failed attempts. Thenon-stress test is repeated afterversion until a normal test resultis obtained since it is commonlyobserved that non-reactivetracings are obtained for 20-40minutes after the procedure.Temporary bradycardia and riskof placental abruption is alsopresent. Routine tocolysis (IVRitodrine, S.C. Terbutaline)appears to reduce the failure ofECV in primis but not in parouswomen. Various otherapproaches suggested forspontaneous version like kneechest position, acousticstimulation of fetus,Moxibustion, a traditionalChinese acupressure techniqueare still of uncertain value.D-immunoglobulin is given ifindicated after attempted version.References1. Collea JV: Current

Management of BreechPresentation Clin ObstetGynecol 1980, 23: 525.

2. Williams obstetrics(22nd

Edn).Mc Graw HillCompanies,Inc.2005,571

3. Braun FHT, Jones KL, SmithDW: Breech Presentation asan indicator of fetalabnormality J Pediatr 1975,86: 419.

4. Wigglesworth JS, HusemeyerRP: Intracranial birth traumain vaginal breech delivery: thecontinued importance ofinjury to the occipital bone.Br. J Obstet Gynecol 1977,84: 684.

5. Carbonne B, Goffinet F,Breart G. et al. The Debateon breech presentation:Delivery of breechpresentation, the position ofthe National College ofFrench Gynaecologists JGynecol Obstet Biol Reprod(Paris) 2001, 30: 191.

6. Cheng M, Hannah ME.Breech delivery at term: acritical review of literature.Obstet Gynecol. 1993; 82,605.

7. Gifford DS, Morton SC,Fiske M, et al. A meta-analysisof infant outcomes afterbreech delivery, ObstetGynecol 1995; 85: 1047.

8. Saunders WJ St.Controversies; the maturebreech should be delivered byelective caesarean section J.Perinat Med 1996; 24: 545.

9. Penkin P, Cheng M, HannahM. Survey of Canadianobstetricians regarding themanagement of term breechpresentation JSOGC 1996;18: 233.

10. Hannah ME, Hannah WJ,Hewson SA, et al. Plannedcaesarean section versusplanned vaginal birth forbreech presentation at term:a randomised multicentretrial. Term Breech trialCollaborative Group. Lancet2000; 356: 1375-83.

11. ACOG Committee OpinionNo. 340. Mode of termsingleton breech delivery


Obstet Gynecol. 2006; 108:235.

12. Term Breech Trial(Correspondence) Lancet2001, 357: 225.

13. Managing term breechdeliveries (Letters to Editor)BMJ 2002; 324: 50.

14. Garel M, Lelong N,Marchand A, Kaminski M.Psychological consequencesof caesarean child birth afour year follow up study.Early Hum Dev 21: 105.

15. Alarab M, Regan C,O’Connell MP, et al.Singleton vaginal breechdelivery at term: still a safeoption. Obstet Gynecol 2004;103: 407.

16. Golfier F, Vaudoyer F,Ecochard R et al. Plannedvaginal delivery versuselective caesarean section insingleton term breechpresentation, a study of 116cases. Eur J Obstet GynecolReprod Biol 2001; 98: 186.

17. Guilani A, Scholl WM, BasverA et al., Mode of delivery andoutcome of 699 termsingleton breech deliveries ata single centre. Am J ObstetGynecol 2002; 187: 1694.

18. Irion O, HirsbrunnerAlmagbaly P. Morabia A.Planned vaginal deliveryversus elective caesareansection: a study of 705singleton term breechpresentations BJOG, 1998;105, 710.

19. Kayem G, Goffinet F,Clement D, et al. Breechpresentation at term:morbidity and mortalityaccording to the type ofdelivery at Port RoyalMaternity Hospital from

1993 through 1999. Eur Jobstet Gynecol Reprod Biol2002; 102: 137.

20. Francios Goffinet, MarionCarayol, Jean. Michel Foidartet al. Is planned vaginaldelivery for breechpresentation at term still anoption? Results of anobservational prospectivesurvey in France and BelgiumACOG 2006; 104: 1002.

21. Cruikshank DP, Pilkin RM:Delivery of the prematurebreech. Obstet Gynecol 1977;50: 367.

22. Woods JR: Effects of lowbirth weight breech deliveryon neonatal mortality ObstetGynecol 1979, 53: 735.

23. Karp LE, Doney JR,McCarthy T, et al: Thepremature breech0trial oflabor or caesarean section?Obstet Gynecol 1979; 53:88.

24. Duenhoelter JH, Wells CE,Reisch JS, et al. A pairedcontrolled study of vaginaland abdominal delivery ofthe how birth weight breechfetus Obstet Gynecol 1979;54: 310.

25. Main DM, Main BK, MaurerMM. Caesarean sectionversus vaginal delivery for thebreech fetus weighing les than1500gms. Am J ObstetGynecol, 1983; 77: 498.

26. Caterini H, Langer A, SamaJC, et al. Fetal risk inhyperextension of the fetalhead in breech presentationAM J Obstet Gynecol 1975;123: 632.

27. Daw E: Hyperextension ofthe head in breechpresentation. Am J ObstetGyrecol 1974; 119: 564.

28. Awwad JT, Nahhas DE,Karam KS: Femur fracture

during caesarean breechdelivery . Int J GynecolObstet; 1993: 43; 324.

29. Vasa R, Kim MR: Fracture ofthe femur at caesareansection: case report andreview of literature AM JPerinatol 1990; 7: 46.

30. Freud E, Orvieto R, MerlobP: Neonatal labioperineal tearfrom fetal scalp electrodeinsertion, a case report JReprod Med 1993; 38: 647.

31. Tiwary CM: Testicular injuryin breech delivery Possibleimplications Urology 1989;38: 210.

32. Gentjens G, Gilbert A,Helsen K: Obstetric brachialPlexus palsy associated withbreech delivery. A differentpattern of injury. J Bone JointSung. (Br) 1996; 78: 303.

33. Zhang J, Bowes WA, FortneyJA: Efficacy of externalcephalic version: a review,Obstet Gynecol 1993; 82:306.

34. Fortunato SJ, Mercer LJ,Guzick DS: External cephalicversion with tocolysis: factorsassociated with success.Obstet Gynecol, 1988; 72: 59.

35. Hofmeyr GJ, Sadan D, MyerIG et al. External cephalicversion and spontaneousversion rates: ethnic andother determinants. Br JObstet Gynecol, 1986; 93: 13.

36. Kirkinen P, Ylostalo P.Ultrasonic examinationbefore external version ofbreech presentation. GynecolObstet Invest 1982; 13: 90.

37. Westgren M, Edvall H,Nordstrom L. SpontaneousCephalic version of breechpresentation in the lasttrimester. Br J ObstetGynaecol, 1985; 92: 19.


8ReviewArticle

morbidity and mortality in bothdeveloped and developingcountries. It is estimated thatworld wide , one women diesevery 4 minutes due to PPH withan average yearly incidence ofabout 140,000 women deaths .1PPH has been defined as anestimated blood loss in excess of500 ml following a vaginal birthor 1000 ml following a caesareanbirth. However, estimation ofblood loss at delivery is usuallyinaccurate in order to clearlydefine PPH. Similarly, decline inhaematocrit level of 10% hasoften been used to define PPHbut determination ofhemoglobin or packed cellvolume may not accuratelyreflect the current hematologicstatus in women with PPH.Features like hypotension,dizziness, pallor and oliguriaoften regarded as markers ofPPH usually do not appear untilblood loss has been substantiali.e. 10% or more of total bloodvolume.2 Etiology of PPH variesaccording to its time of onsetand may be associated with manyunderlying predisposing riskfactors. Although anticipation ofPPH in a particular clinicalsetting and consequentprevention is the most rewardingmanagement strategy but PPH

often occurs without warning inmany patients.Etiology of PPH.- Postpartumhemorrhage is convenientlydivided into primary andsecondary according to its timeof onset in relation toparturition.3, 4

Primary (within first 24 hrs ofdelivery)- Due to -Uterine atony,Retained placenta especiallyplacenta accrete, Defects incoagulation, and UterineinversionSecondary (after 24 hrs ofdelivery)- this due tosubinvolution of placental siteRetained products ofconception, Infection andInherited coagulation defectsRisk factors for PPH-Postpartum hemorrhage is oftenassociated with several riskfactors 5, recognition of whichalways helps in taking appropriateand timely preventive measuresfor PPH. These include-Prolonged labor, Augmentedlabor, Rapid labor, Past history ofPPH, Episiotomy (especiallymediolateral), Pre-eclampsia,Over distended uterus(macrosomia, multiplepregnancy, polyhydramnios),Operative delivery, Asia andHispanic ethnicity,ChorioamnionitisManagement-Management ofPPH varies in an individualpatient depending on its etiology,

availability of different treatmentoptions and patient’s desire forfuture fertility. Prevention ofPPH through anticipation in highrisk and predisposed patients ismost important part ofmanagement. However, anestablished and intractable PPHmay defy all attempts ofconservative managementthrough relatively less invasivemethod, often requiringhysterectomy for preservation oflife. At times immediate modernintervention techniques likeuterine artery embololisation maybe live saving with relativepreservation of fertility if generalcondition of the patient allowsthe same.Prevention of Post partumhemorrhage- Prevention ofPPH is one of the primeobjectives of active managementof third stage of labor which isusually implemented as a“package” including- Early cordclamping; Placenta delivery bycontrolled cord traction,Following signs of placentalseparation, Uterine massageCochrane review (2003) of activeversus expectant management of3rd stage of labor included meta-analysis of five randomizedcontrolled trials and found thatactive management of labordecreased the incidence of PPH(both 500-1000 ml and >1000ml), shortened the thirdstage of labor, decreased theneed for additional therapeutic

Postpartum hemorrhage(PPH) or excessive bloodloss after child birth is amajor cause of obstetric

Post Partum Haemorrhage

Minakshi Rohilla ThamiDepartment of OBG, PGI

Institute of Medical Science & Research, Chandigarh


uterotonics agents and need forblood transfusion for all women,including women deemed to beat low risk for post partumhemorrhage. The incidence ofPPH, 500 ml or more wasreduced in the actively managedgroup. The implementation ofactive management of labor hasbeen controversial because oflack of consensus regarding theorder of actual steps, appropriateuterotonics for low resourcecenters and which route is to beused. Despite lack of clarity thereare recommendations to offeractive management of labor to allwomen because on two grounds, i) The presence of risk factorscan not be used to predict PPHand ii) Active management hasproved to reduce the incidenceof PPH, the quantity of bloodloss and blood transfusions 6.Oxytocins with or withoutergometrine has been agent ofchoice as uterotonics for lastseveral decades; both are unstableat room temperature and need tobe given intramuscularly.However, misoprostol, a neweroral preparation of PGE-1analogue is fast becoming a primecandidate for its uterotonicproperties. Misoprostol can beused through oral, vaginal orrectal route, has a relative lowcost and is generally stable atroom temperatures 7. Review ofmisoprostol use in third stage oflabor; found that misoprostol isbetter than placebo in reducingthe need for additionaluterotonics but inferior tooxytocin in preventing PPH.8

Treatment of PPH- Treatmentof PPH involves somenonspecific measures irrespective

of the cause of PPH or tilletiology becomes obviousfollowed immediately by thespecific management of theunderlying cause of PPH.Non-specific measuresUterine massage- Uterine atonyis the single most common causeof PPH hence a bimanual pelvicexamination and emptying thebladder combined with uterinemassage can diminish bleeding,expel blood and blood clots andallow time for other measures tobe implemented.Visual assessment- If bleedingpersists, rule out traumatic PPH.Lacerations need carefulassessment and repair.Satisfactory repair may requiretransfer to a well equippedoperating room and examinationunder general anesthesia.Placental expulsion- Manualremoval or curettage by bluntinstrument may identifysuccenturiate lobe or retained bitsof the placenta as a cause ofPPH. Spontaneous expulsion ofplacenta, apparent structuralintegrity on inspection and thelack of a history of previousuterine surgery make a diagnosisof retained placental bits lesslikely.Additional uterotonics -Continous intravenous infusionof oxytocin 40 units ( maximum100 milli units / minute ) with orwithout methyl ergometrine 0.2mg intramuscular every 2-4hourly may be required to controlPPH. In absence of a desirableresponse 15 methyl PGF2á(Carboprost) 250 microgramintramuscular every 15-90 minute(8 doses maximum) or PGE-1analogue (Misoprostol) 800-1000

mg per rectally, may be given.Various studies using 800 &1000ugm of rectal misoprostol inthe treatment of PPH haveconcluded that rectal misoprostolis a relatively easy, non invasiveand potent treatment for PPH. Itcan be added to oxytocin andergometrine as a first lime agentin the therapeutic drill in the stepstaken to treat PPH9. A recentCochrane review also concludedthat 800mcg of rectalmisoprostol could be a useful‘first line’ drug for the treatmentof severe PPH10.Clotting abnormality- Abruptioplacentae, HELLP syndrome,prolonged IUD, sepsis andamniotic fluid embolism areoften associated with clottingabnormalities which may becaused or perpetuated by PPH.Baseline studies include completehaemogram, PT, APTT,fibrinogen and blood groupingand cross matching. The clottingtime provides a simple measureof fibrinogen which can beassessed using 5 ml of blood toclot within 8-10 minutes and willremain intact normally. Iffibrinogen concentration is lowthe blood will not clot or if itdoes, it will undergo partial/complete dissolution in 30-60minutes. In such cases a bloodproduct replacement may benecessary to control PPH.Uterine tamponade- Packinguterine cavity with linen gauzerolls, Foley’s catheter with a largebulb, condom catheter,Sensgstaken Blakemore tube etc.helps reducing atonic PPH.Although uterine packing isgenerally regarded as temporarymethod, the majority may not


require further surgicalintervention to control PPH.Arterial embolization- Patientswith stable vital signs andpersistent bleeding especially ifthe rate of loss is not excessiveare ideal candidates for arterialembolization. Radiographicvisualization of bleeding vesselallows embolization with gelfoam particles or coil.Embolization can be a usefulalternative to hysterectomy topreserve fertility or at times mayalso be required to manageintractable bleeding persistingafter hysterectomy.Surgical techniques -Failure ofprompt medical and other nonspecific measures warrantssurgical intervention oftendepending both upon generalcondition of the patient andtechnical expertise of theobstetrician. Various surgicaltechniques have their ownadvantages and limitations. 11

(Table 1)Blood transfusion-Bloodtransfusion in necessary,whenever extent of blood loss issignificant and ongoing,particularly it vitals signs areunstable. To avoid dilutionalcoagulopathy concurrentreplacement with coagulationfactors and platelets may benecessary. Autologoustransfusion (donation, storageand retransfusion) has beenshown to be safe in pregnancy. Itrequires anticipation of the needas well as a minimal haematocritconcentration often above thatof a normal pregnant woman 12.A good knowledge of bloodcomponent therapies (Table – 2)is of utmost importance in

instituting correct replacementof deficient component ofblood.Specific measuresPPH due to ruptured uterus-Uterine rupture during labourcan frequently occurspontaneously or at site of aprevious caesarean section scaror any other surgical procedureinvolving the uterine wall, fromintrauterine manipulation,trauma or from congenitalmalformation like rudimentaryhorn. Rarely, an abnormal labor,operative delivery, and placentaaccreta can also lead to uterinewall rupture. Surgical repair isrequired, with the specificapproach tailored to reconstructthe uterus, if possible. Caredepends on the extent and siteof rupture, the patient currentclinical condition and her desirefor future child bearing.Regardless of the patient wishesfor the avoidance ofhysterectomy, this procedure maybe necessary in a life threateningsituation.

PPH due to suspectedplacental accrete-Abnormalattachment of placenta to theinner uterine wall (placentaaccreta) can cause massivehemorrhage. Infact, placentaaccreta and uterine atony are thetwo most common reasons forpost partum hysterectomy.Several factors predisposing foroccurrence of placenta accretainclude -Placenta praevia with orwithout previous uterine surgery;Prior myomectomy; Priorcaesarean; Asherman’s syndrome;Submucosal leomyoma; Maternalage >35 years. In patients withplacenta praevia in the current

pregnancy, the risk of placentaaccreta in subsequentpregnancies has been estimatedto increase progressively to 3%,11%, 40%, 60% and 67% witheach pregnancy respectively forthose undergoing caesariandelivery 13. In the presence ofpredisposing factors like placentapraevia or a history of caesariansection, the obstetric careprovider must keep a high indexof clinical suspicion for placentaaccreta and take appropriateprecautions. Uterine conservingoptions may work in focalplacenta accreta, buthysterectomy usually is the mostdefinitive treatment of PPH dueto placenta accreta. Followingmeasures may help managing asuspected case of placentaaccrete-Ultrasonography andcolor Doppler may be helpfulalthough not diagnostic;Thepatient should be counseledabout the likelihood ofhysterectomy and bloodtransfusion; Blood product andclotting factors should beavailable; Cell saver technologyshould be considered; Deliveryshould be planned to allow accessto adequate surgical personneland equipment; A pre-operativeanaesthesia assessment should beobtained.PPH due to an inver teduterus- Uterine inversion, inwhich the uterine corpusdescends to, and some timesthrough the uterine cervix, isassociated with markedhemorrhage. On bimanualexamination, the finding of afirm mass below or near cervix,with absence of uterus onabdominal examination, suggests


inversion. Replacement ofuterine corpus involves placingthe palm of the hand against thefundus (now inverted and lowermost at or though the cervix) andexerting upward pressurecircumferentially with fingertips.Manual replacement with orwithout uterine relaxant usuallyis successful. In the unusualcircumstances abdominalprocedure may be required. TheHuntington procedure involvesprogressive upward traction onthe inverted corpus usingBabcock or Allis forceps 14. TheHaultain procedure involvesincising the cervix posteriorly,allowing for digital repositioningof the inverted uterus withsubsequent repair of theincision15.PPH due to secondary PPH-PPH occurring after first 24hours of delivery occurs in 1%of pregnancies. Uterine atonywith or without infection,retained placental tissue andbleeding diathesis 16 are thecommon causes of secondaryPPH. Ultrasonographicevaluations help in identifyingintra uterine tissue orsubinvolution of the placentalsite. Uterotonic agents,antibiotics, and dilatation and orcurettage are usually sufficient totreat secondary PPH. Patientshould be counseled about thelikely possibility of hysterectomybefore initiating any procedures.

Miscellaneous measuresTreatment of PPH in lowresource settings involvesseveral promising techniques fortreatment of PPH that arerelatively simple can be used bypersonnel with limited skills and

training in remote and /on ruralareas of less developed countries17. These include-Universal use ofactive management of labor. Useof oxytocin in the form ofprefilled sterile injection (uniject).Use of oral or rectal misoprostolfor prevention and treatment ofPPH. The non-inflatableantishock garment (NI-ASG) forstabilization and resuscitation ofhypovolemic shock secondary toPPH The Hydrostatic condomballoon catheter to controlintractable PPH secondary touterine atony.Oxytocin Uniject Device 18- Itis a sterile packet containingprefilled, non refillable, sterile,easy to use device with a fixedneedle that can be activated foruse after opening the sterilepacket. Study conducted inIndonesia over 2200 home birthscomparing the oxytocin unijectdevice with oxytocin in astandard syringe concluded thatunsafe reuse of syringes ceased,dosage accuracy increased withusage of uniject. Uniject wasfound to be less painful thanregular syringe injections.Non-inf latable antishockgarment (NI-ASG) 19, 20-Thenon-inflatable antishock garment(NI-ASG) is a neoprene garment,much like the bottom half of awet suit, designed in horizontalsegments. Using the elasticity ofthe neoprene and Velcrofasteners, the garment can apply30 to 50 mm Hg of pressure tothe lower body pressure. The NI-ASG is a refinement of thepneumatic military (or medical)antishock trousers. Both devicesprovide circumferential counterpressure to the lower body as a

means of resuscitation fromhypovolemic shock andhemostasis for bleeding in thelower body. The medicalapplications of the militaryantishock garment are describedin previous reviews. A singleprovider can place this garmentand the counter pressure ofNIASG will cause a transfer ofblood from the lower body andabdomen to the centralcirculation (Brain, heart, lungs &kidneys). It provides tamponadeto bleeding sites below the levelof diaphragm and diminishesfurther hemorrhage. Variousstudies document rapidresuscitation from hypovolemicshock and an extended period ofstabilization for patients.Contradictions to use of NI-ASG are heart failure, stenoticheart valves, pulmonary edema,bleeding above the diaphragm.

Hydrostatic balloon condomcatheter-It is a sterile rubbercatheter fitted with a condomplaced into the uterus throughthe vagina and inflated with 250-500 ml of saline. To keep catheterin place vagina must be packedwith gauze. In a recent study 21, 22

conducted in Bangladesh, atonicPPH was controlled within 15minutes following use ofcondom catheter along withuterotonics. The catheter wasremoved after 24-48 hours,depending on the initial amountof blood loss. Even if surgerywould eventually be requiredNIASG and condom cathetercan gain useful time for transportto a hospital where definitivetherapy would be available.


Conclusion-Post partumhaemorrhage remains a leadingcause of maternal mortality.Effectiveness of activemanagement of third stage oflabour in preventing PPH hasbeen established in the literature.Anticipation and step wiseapproach in managing PPH mayavoid serious morbidities andmortality.References1. Abouzahn C. Global burden

of maternal death anddisability. Br Med Bull 2003;67: 1-11.

2. Deldy GA3, Paine AR,George NC, Velasco C.Estimating blood loss: canteaching significantlyimprove visual estimation?Obstet Gynaecol 2004; 104:601-6.

3. Cunningham FG, Leveno KJ,Bloom SL, Obstetrichaemorrhage. In: WilliamsObstetrics. 22nd ed. NewYork: McGraw –Hill 2005; P-809-54

4. Alexander J, Thomas P,Sanghera J. Treatment forsecondary PPH. TheCochrane database ofSystemic reviews 2002; Issue1. Ant. No. CD002867. DOI:10. 1002/14651858.

5. Stonew RW, Paterson CM.Risk factors for majorobstetrics haemorrhage. EurJ Obstet Gynecol Reprod.Biol 1993; 48: 15-8.

6. Prendiville WJ, Elbourne D,McDonald S. Active versusexpectant management in thethird stage of labor(Cochrane review). In theCochrane Library, eds

chickesten (UK): John Wileyand sons, Ltd., 2003, issue 4.

7. Kundodyiwa TW, Majoko F,Rusa Kanikos. Misoprostolversus oxytocin in the thirdstage of labor. Int. J GynaecolObstet 2001; 75: 235-241.

8. Gulmezogluam, Forna F,Villar J, Hofmeyer GJ.Prostaglandins for preventionof post partum haemorrhage(Cochrane review). In theCochrane library, edsChickesten (UK): John Wileyand sons, Ltd., 2004.

9. Sharma S. El-Refaey H.Prostaglandins in theprevention and managementof post partum haemorrhage.Best Pract. Res Clin ObstetGynaecol 2003; 17: 811-823.

10. Mousa H, Alfivenc Z.Treatment for Primarypostpartum haemorrhage(Cochrane review). In theCochrane Library,edschichesten (UK): JohnWiley and Sons, Ltd; 2004.Issue 1.

11. Allam MS, B lynch C. The Blynch and other uterinecompression suturetechnique. Int. J GynaecolObstet 2005; 89: 236-41.

12. Rebarber A. Lon ser R,Jacksons et al. The safety ofintraoperative autologousblood collection andautotransfusion duringcaesarean section. Am JObstet Gynaecol 1998; 179:715-20.

13. Silver RM, Landon MB,Rouse DT et al. Maternalmorbidity associated withmultiple repeat caesarean

delivery. Obstet Gynaecol2006; 107: 1226-32.

14. Huntingtons JL, Irving Fe etal. Abdominal reposition inacute inversion of thepuerperal uterus. Am JObstet Gynecol 1928; 15: 34-40.

15. Haultain FW. The treatmentof chronic uterine inversionby abdominal hysterotomywith a successful case. Br.Med J 1901; 2: 974-6.

16. James AH. Von Willebranddisease. Obstet Gynecol Surv2006; 61: 136-45.

17. TS4 VD. New and underusedtechnologies to reducematernal mortality. Lancet2004; 363: 75-76.

18. Miller S, Lester F, HensleighP. Prevention and treatmentof postpartum haemorrhage:New advances for lowresource settings. J MidwiferyWomen’s Health 2004; 49 :283-292.

19. Hensleigh PA. Antishockgarment providesresuscitation and hemostasisfor obstetric haemorrhage. BrJ Obstet Gynaecol 2002; 109:1377-1384

20. Brees C, Hensleigh P, MillerS, Pelligra R. Non-inflatableanti shock garment (NI-ASG) provides resuscitationand hemostasis for obstetrichaemorrhage. A series of 14cases 2004; proceedings ofpreventing PPH: fromResearch to practice.Bangkok, Thailand, Jan 20-24.

21. Akhter S, Begum MR, KabirZ et al. Use of a condom tocontrol massive PPH


Table 1

Technique Advantages & limitations

Bilateral uterine Quicker, easy to perform & similar suturesartery ligation within utero-ovarian ligament.

Internal iliac artery Difficult technique, generally reserved forligation the experienced gynecologist & less

successful than considered.

B lynch suture* Exerts even pressure to compress uterinecavity and decreases bleeding.

Multiple square Eliminates uterine cavity space bysuturing* suturing both walls.

* New techniques for which experiences are limited.

Table 2

Product Volume Contents Effect (per unit)(ml perunit )

Packed red 240 RBCs, WBCs, plasma Increasescells haematocrit (3%) &

Hb (1gm.dl)

Platelets 50 Platelets, RBCs, Increase plateletWBCs, plasma count

(5000-10000.cu.mm/unit)

Fresh frozen 250 Fibrinogen, Increase fibrinogenplasma antithrombin III, (10 mg/dl )

factors V & VIII

Cryoprecipitate 40 Fibrinogen, factors Increase fibrinogenVIII & XIII, Von- ( 10mg/dl )Willebrand factor

(Internet). Medscape.Available from: http://www. Medscape.com /viewarticle / 459894-print.

22. Akhter S. Innovations in thetreatment of PPH, 2004.Proceedings of preventingPPH from research topractice. Bangkok,Thailand, Jan 20-24.


deliveries. It is estimated thatover 85% of women who havespontaneous vaginal birth willsustain same form of perinealtrauma and of these 60 – 70%will require repair. RCOG 2000reports International variation inepisiotomy rate namely 8% inNetherlands, 20% in Englandand Wales, 50% in USA and 99%in Eastern European countries.Anal sphincter injuries arereported in 11% of vaginaldeliveries with midlineepisiotomy 2.5% withmediolateral episiotomy but 33%of women sustain occult analsphincter injury (Sultan 1997).Ifthe perineal laceration are notappropriately repaired due toincorrect classification long termcomplication can occur. Sultan(1999) has proposed thefollowing classification which hasbeen incorported in guidelines ofRoyal College of Obstetricians &Gynaecologists and Internationalclassification (Norton et al 2002).

First degr ee - Lacerationinvolving vaginal epitheliumor perineal skin only.Second degree-Involvement ofperineal muscles but not analsphincter.Third degree - Disruption ofanal sphincter muscles andthis is further classified into -Grade 3a-<50% thickness ofexternal sphincter torn; Grade

3b->50% of thickness ofexternal sphincter torn; Grade3c-Internal sphincter also tornFourth degree-A third degreetear with disruption of analepithelium.

An isolated rectal tear withoutinvolvement of the anal sphincteris rare and should not be includedin the above classification. Anyinjury to the anterior part of thelabia, anterior vagina, urethra orclitoris is classified as an anteriorperineal tear.This classification enables toidentify full extent of injury toperform an appropriate repair. Ithas prognostic significance fromevidences that repair of isolatedinternal anal sphincter defects inpatients with fecal incontinenceis associated with favourableoutcome.Risk factors for 3rd degreeperineal repair include

Fetal macrosomia OR (Oddratio) 1.9Failure of labour to progressin 2nd stage OR 10.8Induction of labour (OR 1.9)Non reassuring fetal heartpattern OR 11.7Mediolateral epis 2.8%Vaccum extraction 8.2%Forceps deliveries 26.7%

EpisiotomyEpisiotomy is a surgical incisionmade in perineum and cuts thevaginal mucosa, perineal musclesand skin to enlarge the vaginalorifice during the last part of the

second stage of labour. It is thecommonest operation requiringrepair in the obstetrics. It is ofthree typesMedian - Starts in the midline ofthe fourchete and extend in themiddle of the perineum.Drawbacks is extension to analsphincter is common. Advantageis associated with less bleeding,pain and wound breakdown.Mediolateral - Starts at themidpoint of the lower vulvar rimand should be inclined to left orright the side of midline by about15° - 20°. Main advantage is thatit avoids the risk of potentialextension of the incision to theexternal and sphincter and mayreduce the likelihood of a severeperineal tear (Riskin – Mashiahet al 2000). It is associated withmore bleeding and pain.J-shaped - Incision is initiallydirected downward towards theanal sphincter but terminal partof the incision is directedlaterally. Aim is to combine theadvantage of both medial andmedio lateral episiotomy.Episiotomy was popular in 70sand 80s and rational behind theroutine episiotomy was that itcause less pain, heals better, haveless chances of extending to 3rd

or 4th degree tear and lessdyspareuria compared to raggedperineal tear. However, evidencebased studies showed itepisiotomy cause morehaemorrhage, equal pain and

9ReviewArticle

I njuries to genital tract arecommon both in assisted aswell as spontaneous

Recent advances in identification and management of genital tracttrauma – perineal tear, episiotomy complications

Anju Huria, Lajya Devi,Department of OBG, Government Medical College, Chandigarh

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