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EMERGENCY LOWER CEASAREAN SECTION DUE TO OLIGOHYDRAMNIOS AND PRESUMED FETAL DISTRESS WITH ONE PREVIOUS SCAR NAME: NURUNNABILAH BINTI MUHAMMAD BAKARUDDIN IDENTIFICATION NUM: 940320035932

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Page 1: gynaecology case write up

EMERGENCY LOWER

CEASAREAN SECTION DUE TO

OLIGOHYDRAMNIOS AND

PRESUMED FETAL DISTRESS

WITH ONE PREVIOUS SCAR

NAME:NURUNNABILAH BINTI MUHAMMAD BAKARUDDIN

IDENTIFICATION NUM: 940320035932

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Demographic details

Name : Zaizuriatiey bt. Aziz

Age : 23 years old

Sex : Female

RN : 30967

Race : Malay

Religion : Islam

Ward : 2

Address : KG. Pondok Hidayah, Tanah Merah

D.O.A : 29/10/2015 (1430)

Occupation : housewife

E.D.D : 8/11/2015

L.M.P : Unsure of date

Chief complain :

Referred from Klinik Kesihatan Batu 30 for oligohydroamnions with one previous scar to

Hospital Tanah Merah for further management.

History Of Present Illness :

Zaizuriatiey bt. Aziz is a 23 years old malay women of gravida 3 para 2 at 38 weeks + 4 days

period of gestation with one previous scar referred from KK Batu 30 due to oligohydroamnions with

amniotic fluid index(AFI) of 6.81.The problem noticed during follow up scanning on 29/10/2015 and

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referred to Hospital Tanah Merah. She was admitted at HTM on that day itself. Upon admission, there

is no leaking of liquor or show. The cervical dilatation is 1cm and fetal movement is slow. There is no

contraction at that time and the patient is not in labour yet.

Antenatal History

She noticed she was pregnant when she missed period about a month but unsure the exact days that she missed it. She also mention that she missed pill of oral contraceptive (ocp) for a day. After that she bought urine pregnancy test and the result are positive. She went for checkup scan on 15 march 2015 to confirm her pregnancy. At that time, the scan shows that she has pregnant for 7 weeks period of gestation(POG). During the checkup, her first antenatal blood pressure was 110/80, pulse 84 beats/min, BMI 33.4 and hb is 7.2. she noticed the first fetal movement at 21 weeks of geststion. This pregnancy is unplanned but wanted the pregnancy

She had hyperemesis gravidarum with decrease oral uptake up to 20 weeks of gestation. She also had anemia secondary to alpha thalasemia trait that being diagnose since early pregnancy. She always felt lethargic, and pallor was noted. She also complaint that she was passing out black colour stool. On 18/3/2015, the pheripheral blood film was carried out and the result was anemia with red cell changes probably secondary thalasemia with recurrent iron deficiency anemia. RBC morphology shows microcytic hypocromic cell with target cell, cigar cell as well as teardrop cells. Then, on 22/4/2015 the a-thalasemia DNA analysis was done to ruled out thalasemia and the result was positive result. She has been admitted from 4/5/2015 until 6/5/2015 for blood transfusion. Her blood group is group A with rhesus positive.

She was taking modified glucose tolerance test at 35 weeks of gestation( 29/9/2015) due to risk of maternal obesity but the result was normal. She also had been injected with anti tetanus toxoid for 2 times along the pregnancy. she had done 6 ultrasound scan but she don’t remember when was it done. The findings was normal it seems.

Past Obstetrics History

NUMBER OF CHILDREN

SEX WEIGHT MODE OF DELIVERY

TERM BREAST FEEDING

1ST (2010)

-Hospital Machang

BOY 2.8 KG SVD FULL TERM

EXCLUSIVE UNTIL 6 MONTH

2ND (2013) GIRL 3.1KG EMERGENCY LOWER SEGMENT

FULL TERM

EXCLUSIVE UNTIL 2

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-Hospital Tanah Merah

CEASERIAN SECTION(EMLSCS)

-PRESUMED FETAL DISTRESS

YEARS

Past Gaenacological History

She attained menarche at 13 years old, irregular cycle with duration 7 days . 3 to 4 pads per day. She has mild dysmenorhea. She denied any vaginal discharge and dyspareunia. She had done pap smear on 2013 and the result was normal. She took oral contraceptive pills since 2010. She took OCP after the 1st baby was born for 2 years . then after the 2nd baby, she took again the OCP for 2 years also.

Past Medical History

There was no significant past medical and surgical history mentioned by patient.

Drug history

Iron supplement for anemia and folic acid

Patient stated that she had no known allergy to drugs, medication and food.

Family History

There is no running disease in the family

Social History

Patient stated that she had not taken any alcohol and illicit drugs. she is a non smoker. She had good diet habits and exercise occasionally. She lives with with her husband and he Is a smoker. She lives in one storey house.

Systemic Review

There is no significant systemic reviews.

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Physical Examination:

On general observation, The patient is alert, conscious and laying comfortably on bed with one pillow. She is not in pain. Patient is obese. She is also oriented to time, place, person and responsive to questions.

Vital signs: Blood pressure:120/72

Pulse : 100 beats/min

Temperature : 37 degree Celsius

Respiratory rate : 20/min

There is no clubbing and signs of peripheral cyanosis observed from this patient. Her facial appearance is pale. The conjunctiva was pale due to sign of anemia and her sclera was white. There was no discharge from eye ear and nose. Noticed there is angular stomatitis. Oral hygiene is good and the tongue was pink moist and normal contour. There is no peri auricular, cervical and supraclavicular lymph node enlargement and also patient has no pre tibia edema.

LOCAL EXAMINATION

Respiratory system:

Inspection :No sign of surgical scar found on chest. Normal movement of chest and the

respiratory rate is noted which is 20..

Palpitation :Trachea in the right position not deviated. Chest spring was done to check for any

fracture. Normal vocal fremitus.

Auscultation :Normal breath sound, no any crepitus or rhonchi was heard. Normal vocal

resonance.

Cardiovascular system:

Inspection :Chest wall was symmetrical and absence of any deformities and surgical scar.

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Palpitation :Apex beat was felt and not shifted. There is no parasternal heave and trill felt.

Auscultation :Normal rate and rhythm of heart sound, S1 and S2 are heard. Murmurs or

pericardial rubbing was not heard.

Abdomen :

Inspection:

The abdomen is distended with gravid uterus. There is linea nigra striae gravidarum that shows the

evidence of pregnancy. Striae albicans also seen which is sign of previous pregnancy. the umbilicus is

centrally located and flattened. Noted also pfanneisteil scar sign of previous ceaser. The scar look well

and no keloid. At that moment, the fetal movement not seen.

Palpation: Superficial palpation was done on all 9 quadrants and shows the abdomen soft and non

tender. There is negative sign of abnormal mass present on the abdomen. Then, upper part of pubic

symphysis till uppermost of the fundus was located to measure symphysis-fundal height (SFH), it was

37cm which is corespond to the date. After that Leopold’s maneuver was done. During this

examination, fundus grip was done, soft , broad surface was felt and non ballotable that indicate

buttock of fetus. During the lateral grip, firm smooth surface was felt at the right side which indicate

the fetal back and the limbs at left side. On the pelvic grip, hard surface, round was felt and ballotable

that indicate the head of fetus. The engagement is 5/5. The fetal was obviously felt due to

oligoamnions. The amniotic fluid is less than normal(non adequate).

Auscultation :Pinard stethoscope was placed over the fetal anterior shoulder to hear the fetal heart.

Normal fetal heart was heard and regular rhythm.

Nervous system:

Cranial nerves and peripheral nerves are intact. Both upper and lower limbs show normal tone, power

and reflexs.

Vaginal examination

Cervix 2cm, medium and midline with os opening 1cm. membrane intact and station -2

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DIFFERENTIAL DIAGNOSIS

Isolated oligohydramnios Umbilical cord compression Fetal distress PPROM

INVESTIGATION

FULL BLOOD COUNT Haemoglobin 72( 90-140), haematocrit 21.7(33-39) ,mean cell volume 56.8(70—86), mean cell haemoglobin 19.3(23-31). These 4 readings show lower level than normal that indicate the patient has anemia. Otherwise WBC and platelet shows normal level.

PERIPHERAL BLOOD FILM(PBF) RBC morphology shows microcytic hypochromic cell with target cells, cigar cell and tear drop cells. -impression: anemia with red cell changes probably secondary to Thalassaemia/haemoglobinopathy with concurrent iron deficiency anemia.

a-THALASSAEMIA DNA ANALYSIS ( MULTIPLEX POLYMERASE CHAIN REACTION- BASED TEST)Result: compound heterozygous for alpha thalassaemia 3.7 and South East Asian deletions identified. In keeping with Hb H disease(deletional type)

MODIFIED GLUCOSE TOLERANCE TEST (MGOTT) -to ruled out gestational diabetes mellitus due to risk of maternal obesityResult: fasting blood sugar 4.4( 3.9- 6.1) Glucose 2 hour 5.2 ( 6.0-7.8) lowThe result shows normal level

ULTRASOUND

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-Ultrasound helps to confirm the diagnosis while also helping to make the differential diagnosis. It is often used for observing the fetal kidney and bladder to rule out the possibility of cystic dysplasia, renal agenesis and ureteral obstruction.The test is also useful for checking the fetal growth to eliminate the possibility of IUGR (intrauterine growth restriction) responsible for oliguria. A specific form of ultrasound named the Doppler ultrasound [4] is used for assessing placental insufficiency, in case it is suspected. The diagnostic criteria include: Amniotic fluid levels lower than 5 cm Absence of a 2-3 cm deep fluid pocket The total amniotic fluid volume below 500mL between 32nd and 36th gestational

MANAGEMENT AND PROGRESSPatient was referred from KK Batu 30 on 29/10/2015(38 weeks+4 days POG)for

further management of oligohydramnions with AFI 6.84 with one previous scar on 2013 due to presumed fetal distress . Upon admission(2.30 pm),there is no contraction and the engagement is 3/5 with os opening 1cm.The patient was planned for bishop score and induction of labour on the next morning if still not delivered . she entered the ward at 3.00pm and at 6.00 pm the patient complain of contraction which is 2 in 10. On the next morning(30/10/2015, 38weeks +5 days POG) 6.40 am the bishop score was done and the assessment result was 4/13 with dilatation of os 1cm, length of cervix 2 cm, station -2 with medium consistency of cervix and posterior position. The condition of cervix is unfavourable so the induction of labour was done by giving prostine 1.5mg. 6 hours later, there is still no contraction, no leaking and no show and good fetal movement with os opening progressed to 2cm. At 2.40 pm,informed by the staffnurse that patient complaint of leaking. there is dribbling but no gushing of liquor, clear and no foul smelly. During examination, no pooling of liquor with minimal show and the cough reflex is negative. The patient was planned for early morning speculum to ruled out PROM. At 4.35 pm, noted patient had abdominal pain. She complained that she had pain at the old scar with each contraction. It is a throbbing pain with scoring of 6/10. The patient was given IM Nubain which is pain killer to relieve the pain. It is important to ruled out scar dehissence. The CTG start and if the CTG is not reactive, keep in view for EMLSCS. The CTG was reactive.

The early morning speculum was done as planned at 4.30am and no leaking liquor noted. There is also no scar tenderness and not irritable. At 6.45 am., the second prostine is inserted as planned. Next review after 6 hour, the os opening still 2 cm and the patient complain of leaking at 1.30pm. plan at that time, if the cervix is favourable, to do artificial rupture membrane and if not favourable, insert 3rd prostine. A GSH to confirm to reassess Bishop score.

On 1/11/2014, at 6.45, the os opening progress to 3cm with irregular contraction pain. CTG at that suspicious so reassess Bishop score and artificial rupture membrane was done due to favourable cervix. At 7.15am, the patient sent to the labour room. At 9.50am, the patient had pain at previous scar . at 10.45 am, the CTG repeated and it is reactive. After 7 hours in latent phase, the contaction is 3 in 10 at that time. The CTG shows pathological with no acceleration and poor variability. It is important to presume fetal distress and at 1.30pm, the patient went to operation theater for Emergency Lower Segment Ceaserian Section(EMLSCS).

PRE-OP

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First, counsel and explain to about the operation and after that take consent from patint. In this case, the patient had given medication which are Zantac( Ranitidine)an histamine H2-blocker, and citrates. The blood pressure at that time is 140/84 with pulse pressure 122 beat/min. the time start for operation is at 2.40pm and completed at 4.00 pm. The operation occur at OT1. The analgesic used is spinal block.

INTRA-OPThe type of Ceasarean section is lower segment with Pfannensteil skin incision. The

lower segement is clean and well healed with no adhesion. The engagement is 2/5 with OP positon. One baby boy delivered at 3.03pm with birth weight of 3.2 kg. the head circumference is 33cm and apgar score is 9/10. The total blood loss is 500ml. the baby triage for thin MSL.

POST-OPIV Ptocin and SC Heparin is inserted to the patient. The patient need to use stockinette

for prevent blood clot and pulmonary embolism. The patient is advised for birth spacing at least 18 month and go for Elective Lower Ceaserian Section for next delivery.

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DISCUSSION

My patient’s name Zaizuriatiey bt. Aziz admitted due to oligohydramnions with one previous scar in previous pregnancy. She also have severe anemia due to a-Thalassemia trait. The patient end up to have emergency lower ceaserian section in this pregnancy. So, there are a few things that needed to be discuss in order the know why the patient indicates for ceaserian section. Some of the issues arised during the progression of labour is that failure of induction, failure of trial of scar, oligohydramnions , fetal distress(pathological CTG) , meconium stained liquour. I will also discuss about the severe anemia due to a-Thalasemia that complicates the whole pregnancy.

First, the major issue is oligohydramnions that causes this patient to be admitted for induction of labour. Oligohydramnions is refer to reduction of amniotic fluid that has amniotic fluid index less than 5th centile of gestation. This fluid plays a vital role in proper fetal development while its deficiency can lead to oligohydramnios sequence or Potter sequence characterized by an irregular appearance of the fetus or neonate. The onset of oligohydramnios usually occurs during the later part of the third trimester, often when one is overdue.It is maybe suspected antenatally following a history of clear fluid leaking from vagina and represent PPROM. Clinically, during the abdominal palpation,the fetal pole maybe very obviously felt and hard with a small for dates uterus. In many cases, oligohydramnios is idiopathic with experts still trying to find out the exact cause responsible for the problems. The fetal urine mainly forms the amniotic fluid during the later stages of pregnancy. So, reduction in fetal urine production due to some pregnancy irregularity, such as obstruction of the fetal urinary tract, can lead to oligohydramnios. Signs of low amniotic fluid levels during the first or second trimester may indicate some fetal abnormalities. Amniotic fluid is important in the development of fetal organs, especially the lungs. Too little fluid for long periods may cause abnormal or incomplete development of the lungs called pulmonary hypoplasia.

There is several common contributing factor of oligohydramnios.For fetal causes,leaky or Ruptured Amniotic Membranes which is sometimes, the amniotic fluid leaks out through a small tear or hole in the amniotic membranes, leading to Oligohydramnios. This can occur at any stage of pregnancy but is most common as one approaches delivery. Second factor of fetal causes is fetal abnormalities, absence of the kidney or any other kidney abnormality (renal agenesis, polycystic kidney) in the baby can also hamper urine production.Genetic factors is also one of the factors under the fetal causes. Inheriting abnormal genes in an autosomal recessive or autosomal dominant pattern.

Other than fetal causes, plancenta also play an important role that contribute too oligohydramnios. Placenta causes include the Placental abruption in which placental abnormalities, like a partial abruption, which causes the placenta to peel away from the inner uterus wall, may lead to amniotic fluid deficiency. Any irregularity in the placental blood and nutrient supply can prevent the baby from producing urine which may lead to serious complications. In addition, women pregnant with twins or multiples are at a higher risk of low amniotic fluid levels. Twin-to-twin transfusion

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syndrome (a condition where one twin experiences severe amniotic fluid deficiency while the other has excessive amounts of fluid) can also cause oligohydramnios. Lastly, using NSAIDs like indometacin and certain ACE (angiotensin-converting enzyme) inhibitors can also causes oligohydramnios.

Several problems can occur from Oligohydramnios. Oligohydramnios occurring during the first and the second trimester is more likely to cause serious complications than when it occurs during the third trimester. Problems that usually arise in first and second trimester are birth defects that cause malformation or complete absence of some external or internal organs in the newborn. Examples are the hip dysplasia, club foot. Premature birth, miscarriage, Stillbirth, death of the baby shortly after birth are other problems that occurs if oligohydramnios start in first and second trimester. In third trimester, problems that occurs is fetal growth restrictions and complications like an umbilical cord compression during labor or at the time of birth (the umbilical cord is responsible for carrying oxygen and food to the fetus, so its compression prevents the baby from getting enough nutrition and oxygen) and lastly can lead to cesarean delivery (a surgical method to bring the baby out through a cut in the mother’s abdomen and uterus). (1)

Same as this case which is the mother had problem of oligohydramnios that diagnosed in last third trimester.The fetus also distress with thin meconium stained liquor and pathological CTG and end up with caeserian section. For causes of oligoghydramnios in this case , most probably isolated oligohydramnios(amniotic fluid index of less than 5cm and has not been shown to be associated with poor materal and fetal outcomes). It is because the mother does not have any symptoms of oligohydramnios and she knew it during follow up scan. She had no leaking and UTI symptoms. There is also no noted fetal anomalies. The correlation between the oligohydramnios and fetal distress is maybe due to umbilical cord compression. Umbilical cord compression can be caused by reason that results in the cord becoming compressed, with the most common being umbilical cord prolapse. An umbilical cord prolapse occurs when an infant’s umbilical cord slips ahead, usually right before birth. As the cord slips into the birth canal, it can become compressed and flattened. If an umbilical cord become compressed, oxygen, blood flow, and nutrients can be cut off from the baby, resulting in brain damage and in severe cases, fetal death. For severe cases of umbilical cord prolapse, an emergency C-section may be necessary, and is often carried out just as soon as fetal distress is detected.

FETAL COMPROMISE IN LABOUR

Fetal compromise may present as fresh meconium staining to the amniotic fluid and abnormal CTG. Intervention for ‘presumed fetal compromise” is therefore more accurate than ‘fetal distress’. In many cases, babies deliverd by Ceasarean section for presumed fetal compromise are found to be in good condition. The risk factor for fetal compromised is placental insufficiency, prematurity, postmaturity, multiple pregnancy, augmentation with oxytocin, uterine hyperstimulation, cord prolapsed, uterine rupture or dehiscence and maternal diabetes.

Recognition of fetal compromised is meconium staining of amniotic fluid is considered significant when it is either thick, dark green, bright green or black. Thin and light meconium more likely to represent fetal gut maturity than fetal compromise. However, when any meconium is seen in the liquor, consideration should be given to starting continuous EFM with CTG and this is mandatory if meconium is thick and dark. CTG sign of fetal compromise is fetal tachycardia, loss of baseline variability, recureent late decelerations. In this case, the CTG shows poor variabily and no acceleration.

Management of fetal compromise is that when the CTG become suspicious, it is reasonable to continue observation on CTG. If the CTG become pathological, it is important to carry out an immediate vaginal examnination to exclude malpresentation and cord prolapsed to assess progress of labour. (If cervix is fully dilated, it is maybe possible to deliver the baby vaginally through forceps or

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ventouse. Alternatively, if the cervix is not fully dilated, a fetal blood sampling can be considered. This is usually only possible when the cervix is dialted 3cm or more. A normal result will permit labour to continue although it may needed to be repeated every 30-60 minutes if CTG is abnormal persist or worsen. An abnormal result mandates immediate delivery by Caesarean section if cervix is not fully dilated. (4)

TRIAL OF SCAR

In the first half of the 20th century, if patients had one caesarean section, then subsequent pregnancies were likely to be delivered in the same way. However, current medical evidence indicates that 60%-80% of women can achieve vaginal delivery after a previous lower uterine segment caesarean delivery. Patients who attempt a VBAC (vaginal birth after caesarean) but fail and require an emergency repeat caesarean section have the greatest morbidity. Uterine rupture is the most catastrophic complication of a trial of labor (TOL) after previous caesarean delivery. In such cases, prompt intervention is necessary to minimize both maternal and neonatal complications. Other complications include scar dehiscence, febrile illness, infections, thromboembolic events and bleeding due to morbidly adherent placenta. For women with a prior uterine scar, repeat elective caesarean birth or TOL for vaginal birth after caesarean birth (VBAC) are risk-free.

The American College of Obstetricians and Gynecologists (ACOG) updated their guidelines concerning vaginal delivery after previous caesarean section. The ACOG Committee on Obstetrics: Maternal and Fetal Medicine stated; “the concept of routine repeat caesarean birth should be replaced by a specific indication for a subsequent abdominal delivery and in the absence of a contraindication, a woman with one previous caesarean delivery with a low transverse incision should be counseled and encouraged to attempt labor in her current pregnancy’(3). Enthusiasm for vaginal birth after caesarean section has waned. As a result, the caesarean birth rate is again on the rise. There is now a large obstetric population with caesarean sections and most of these have been done for non-recurrent conditions. In developing countries such as Pakistan, the parity is high and restriction of family size is not generally accepted due to social, religious or psychological beliefs. Therefore, in Pakistan, the overall rate of caesarean section should be reduced by a sound indication for the first caesarean section and then encouragement for vaginal birth after a caesarean section to reduce operative morbidity and mortality.Current obstetric opinion is that the lower segment caesarean section is not a contraindication for the use of oxytocin for induction and augmentation of labor, however, the role of prostaglandin is controversial.in this case, the patient had trial of scar but failed at the end due to fetal distress.

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INDUCTION OF LABOUR

Favourable (>5cm) unfavourable(<5cm)

ARM Prostin(2dose) c-sec

IV Syntocinon(oxytocin) cervix favourable unfavourable

Can try 2 more dose of Prostine. If failed, c-sec

A Bishop’s Score refers to a group of measurements used to determine whether a woman may have a successful vaginal delivery and whether labor ought to be induced. Bishop’s Score is based on station, dilation, effacement, position and consistency. Indication of induction of labour is that case of fetal IUGR, GDM at 38-39 weeks, post-EDD, risk of placental insuffieciency, abnormal lie and hemolytic disease. , PROM and placenta abruption.

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Method of induction by 3 ways. First is by non pharmacological method which is by membrane sweeping. For pharmacological method, the vaginal PGE2 is usually used and misoprostol and mifepristone are only used in case of intrauterine death. For surgical, artificial rupture membrane is done. Complication of induction of labour is that failed, prematurity(wrong date), sepsis, hypertonicity of uterus, uterine rupture and cord prolapsed. In this case, the patient undergo failure of induction and the management is a further attempt to induce labour and caesarean section. The patient had 2 times induction of labour by prostine. Prostine helps dilate the opening of the uterus (cervix) in a pregnant woman. Belongs to a class of drugs called prostaglandins.

Anemia secondary to a-Thalasemia.

Thalassemi is a form of inherited autosomal recessive blood disorder characterized by abnormal formation of hemoglobin.The abnormal hemoglobin formed results in improper oxygen transport and destruction of red blood cells. Thalassemia is caused by variant or missing genes that affect how the body makes hemoglobin, the protein in red blood cells that carries oxygen. People with thalassemia make less hemoglobin and have fewer circulating red blood cells than normal, which results in mild or severe microcytic anemia.

Thalassemia can cause complications, including iron overload, bone deformities, and cardiovascular illness. However, this same inherited disease of red blood cells may confer a degree of protection against malaria (specifically, malaria caused by the protozoan parasite Plasmodium falciparum), which is or was prevalent in the regions where the trait is common. This selective survival advantage of carriers (known as heterozygous advantage) may be responsible for perpetuating the mutation in populations. In that respect, the various thalassemias resemble another genetic disorder affecting hemoglobin, sickle-cell disease.

The α-thalassemias involve the genes HBA1 and HBA2,inherited in a Mendelian recessive fashion. Two gene loci and so four alleles exist. It is also connected to the deletion of the 16p chromosome. α Thalassemias result in decreased alpha-globin production, therefore fewer alpha-globin chains are produced, resulting in an excess of β chains in adults and excess γ chains in newborns. The excess β chains form unstable tetramers (called hemoglobin H or HbH of 4 beta chains), which have abnormal oxygen dissociation curves. he most severe form of alpha thalassemia major causes stillbirth (death of the unborn baby during birth or the late stages of pregnancy). (2)

This case of anemia, the patient had several times of blood transfusion and also taking iron supplement given by the hospital. The patient had been diagnosed of Alpha Thalasemia by full blood count, pheripheral blood and thalasemia DNA analysis. CONCLUSIONFor this case, the patient had oligohydramnios with one previous scar complicates with anemia indicated for emergency lower ceasarean section due to presumed fetal distress.

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REFERENCE

INTERNET DOCUMENTS1)PREGMEDhttp://www.pregmed.org/oligohydramnios.htm2)MEDLINE PLUShttps://www.nlm.nih.gov/medlineplus/ency/article/000587.htm

ELECTRONIC JOURNAL ARTICLE3)Aliya Islam, Ambreen Ehsan, Saadia Arif, Javeria Murtaza, and Ayesha Hanif. Evaluating trial of scar in patients with a history of caesarean section, The American Journal of Medicine , 2011 Apr; 3(4): 201–205.

ENTIRE BOOK:4) OBSTETRIC TEN TEACHERS, PHILIP N BAKER AND LOUISE C KENNY, 19TH EDITION, NEW YORK, CRC PRESS