Patient’s presentation is classic for uterine rupture, were she developed sudden abdominal pain followed by cessation of contractions, termination of urge to push and vaginal bleeding.
Abdominal examination shows no fetal cardiac activity and signs of fluid collection like fluid thrill and shifting dullness. The fluid collected will be blood, which usually enters the peritoneum after the rupture of the uterus. In such patients vaginal examination will reveal a range of cervical dilatation with evidences of cephalopelvic disproportion.
Anterior lower transverse segment is the most common site for spontaneous uterine rupture. Patient in the case presenting with tachycardia and hypotension is in shock due to blood loss and will require urgent resuscitation.

Placenta previa presents with painless bleeding from the vagina and Placental abruption will present with painful vaginal bleeding with tender and tense uterine wall, however, in contrary to that of uterine rupture, uterine contractions will continue in both these cases.

Shoulder dystocia is more likely to present in a prolonged labour with a significant delay in the progress of labour. However, in this case, there is no mention of shoulder dystocia.

Disseminated intravascular coagulation (DIC) is a condition which is causes due to abnormal and excessive generation of thrombin and fibrin in the circulating blood which results in bleeding from every skin puncture sites. It results in increased platelet aggregation and consumption of coagulation factors which results in bleeding at some sites and thromboembolism at other sites. Placental abruption, or retained products of conception in the uterine cavity are the causes for DIC.

Obstetric complications during or following a cesarean section delivery include:
-Increased risk of maternal mortality.
-Increased need for cesarean sections in the subsequent pregnancies.
-Increased risk for damage to adjacent visceral organs especially bowels and bladder.
-Increased risk of infections.

Increased risk for formation of adhesions is a complication after cesarean section and this is the correct response for the given question.

Due to the previous history of caesarean section, uterine rupture would be the most likely cause of bleeding in this patient who is at a prolonged active phase of first stage of labour.

Maternal manifestations of uterine rupture are highly variable but some of its common features includes:
– Constant abdominal pain, where the pain may not be present in sufficient amount, character, or location suggestive of uterine rupture and may be masked partially or completely by use of regional analgesia.
– Signs of intra abdominal hemorrhage is a strong indication. Although hemorrhage is common feature, but signs and symptoms of intra-abdominal bleeding in cases of uterine rupture especially in those cases not associated with prior surgery may be subtle.
– Vaginal bleeding is not considered as a cardinal symptom as it may be modest, despite major intra-abdominal hemorrhage.
– Maternal tachycardia and hypotension
– Cessation of uterine contractions
– Loss of station of the fetal presenting part
– Uterine tenderness
As seen in this case, fetal bradycardia is the most common and characteristic clinical manifestation of uterine rupture, preceded by variable or late decelerations, but there is no other fetal heart rate pattern pathognomonic of rupture. Furthermore, fetal heart rate changes alone have a low sensitivity and specificity for diagnosing a case as uterine rupture.
Pain and persistent vaginal bleeding despite the use of uterotonic agents are characteristic for postpartum uterine rupture. If the rupture extends into the bladder hematuria may also occur.
A definite diagnosis of uterine rupture can be made only after laparotomy. Immediate cesarean section should be performed to save both the mother and the baby in cases where uterine rupture is suspected.

Group B Streptococcus (GBS) or Streptococcus agalactiae is a Gram-positive bacteria which colonizes the gastrointestinal and genitourinary tract. In the United States of America, GBS is known to be the most common infectious cause of morbidity and mortality in neonates. GBS is known to cause both early onset and late onset infections in neonates, but current interventions are only effective in the prevention of early-onset disease.

The main risk factor for early-onset GBS infection is colonization of the maternal genital tract with Group B Streptococcus during labour. GBS is a normal flora of the gastrointestinal (GI) tract, which is thought to be the main source for maternal colonization.

The principal route of neonatal early onset GBS infection is vertical transmission from colonized mothers during passage through the vagina during labour and delivery.

Intravenous penicillin G is the treatment of choice for intrapartum antibiotic prophylaxis against Group B Streptococcus.

Patient mentioned in the case has developed thyrotoxicosis during pregnancy. TSH level should be tested, and if the result shows any suppressed or elevated TSH level, then it is mandatory to check for free T4 level.

The finding of ketonuria in this patient indicates profound dehydration and electrolyte loss. Immediate investigation with baseline serum electrolytes, urea, and creatinine is recommended for aid In intravenous resuscitation and rehydration.

All other assessments listed are appropriate, however, baseline electrolyte concentration is important before initiating intravenous resuscitation.

Other causes that can lead to vomiting in early pregnancy include normal pregnancy, multiple pregnancies, molar pregnancies, or urinary tract infection. Urine culture is necessary to exclude urinary tract infection, pelvic ultrasound to confirm singleton or multiple pregnancy and rule out a molar pregnancy.

An erect abdominal Xray may help to rule out an organic intestinal obstruction in this patient. Her history of an appendectomy predisposes this patient to adhesions leading to small bowel obstruction. However, it is not the immediate assessment in this case.

Before the advent of ultrasound, a quantitative hCG analysis was indicated to assess the presence of molar pregnancy. However, ultrasound is now preferred to confirm this diagnosis.

This patient presenting with oligohydramnios in her third trimester and had reported an episode of sudden gush of fluid secondary to ruptured membrane which she had mistaken to be “urinary incontinence”.  Hence, the most likely cause of oligohydramnios in this patient will be premature preterm rupture of membrane (PPROM).

An amniotic fluid volume which is less than expected for gestational age is called as Oligohydramnios and is typically diagnosed by ultrasound examination. This condition can be qualitatively described as reduced amniotic fluid volume and quantitatively as amniotic fluid index ≤5 cm or a single deepest pocket <2 cm. Oligohydramnios either can be idiopathic or may have a maternal, fetal or placental cause. Fetal prognosis in this case depends on several factors like the underlying cause, the severity of loss ie. reduced versus no amniotic fluid state and the gestational age at which oligohydramnios occurred. As an adequate volume of amniotic fluid is critical for the normal fetal movements, for fetal lung development and for cushioning the fetus and umbilical cord from uterine compression, so pregnancies complicated with oligohydramnios are at higher risk for fetal deformation, pulmonary hypoplasia and umbilical cord compression.
Oligohydramnios is also associated with an increased risk for fetal or neonatal death, which can either be related to the underlying cause of reduction in amniotic fluid volume or due to the sequelae caused due to reduced amniotic fluid volume. The amniotic fluid volume reflects the balance between fluid production and movement of fluid out of the amniotic sac and the most common mechanisms behind oligohydramnios are fetal oliguria/anuria or fluid loss due to rupture of membranes; also reduction in the amount of lung fluid or increased swallowing do not play major roles in this. Idiopathic cases as in idiopathic oligohydramnios, may be due to alterations in the expression of water pores like aquaporin 1 and aquaporin 3, present in fetal membranes and placenta.

Causes of oligohydramnios
a) Maternal causes includes:
– Medical or obstetric conditions associated with uteroplacental insufficiency like preeclampsia, chronic hypertension, collagen vascular disease, nephropathy, thrombophilia.
– Intake of medications like angiotensin converting enzyme inhibitors, prostaglandin synthetase inhibitors, trastuzumab.
b) Placental causes are:
– Abruption of placenta
– Twin polyhydramnios-oligohydramnios sequence which is the Twin to twin transfusion
– Placental thrombosis or infarction
c) Fetal cases leading to oligohydramnios are:
– Chromosomal abnormalities
– Congenital abnormalities which are associated with impaired urine production
– Growth restriction
– Demise
– Post-term pregnancy
– Ruptured fetal membranes
– Infections
– Idiopathic causes

During First trimester: Etiology of oligohydramnios during the first trimester is often unclear. As the gestational sac fluid is primarily derived from the fetal surface of the placenta via transamniotic flow from the maternal compartment and secretions from the surface of the body of the embryo reduced amniotic fluid prior to 10 weeks of gestation is rare.

During Second trimester: Fetal urine begins to enter the amniotic sac and fetus begins to swallow amniotic fluid by the beginning of second trimester, therefore, during this period any disorders related to the renal/urinary system of the fetus begins to play a prominent role in the etiology of oligohydramnios. Some of such anomalies include intrinsic renal disorders like cystic renal disease and obstructive lesions of the lower urinary tract like posterior urethral valves or urethral atresia. Other common causes of oligohydramnios in the second trimester are maternal and placental factors and traumatic or nontraumatic rupture of the fetal membranes.

During Third trimester: Oligohydramnios which is first diagnosed in the third trimester is often associated with PPROM or with conditions such as preeclampsia or other maternal vascular diseases leading to uteroplacental insufficiency. Oligohydramnios frequently accompanies fetal growth restriction as a result of uteroplacental insufficiency.

Most common risk factors for spontaneous abortion are considered to be:
– Age above 35 years.
– Smoking.
– High intake of caffeine.
– Uterine abnormalities like leiomyoma, adhesions.
– Viral infections.
– Thrombophilia.
– Chromosomal abnormalities.
Conditions like subclinical thyroid disorder, subclinical diabetes mellitus and retroverted uterus are not found to cause spontaneous abortions.
The term retroverted uterus is used to denote a uterus that is tilted backwards instead of forwards.

As they respond differently to different drugs, a thorough distinguishing must be done between the two major groups of epilepsies while approaching a woman, who wishes to become pregnant while on antiepileptic drugs.

Partial epilepsies will respond to most of the antiepileptic drugs, but in case of idiopathic generalized epilepsies, especially in juvenile myoclonic epilepsy, seizure can be controlled only with a reasonably low dose of sodium valproate. Although lamotrigine may be helpful but substitution of sodium valproate with lamotrigine is not the right choice. This is because lamotrigine is not as effective as sodium valproate and will sometimes worsens myoclonic seizures in juvenile myoclonic epilepsy.

Topiramate and levetiracetam are found to be effective in idiopathic generalized epilepsy, while carbamazepine, phenytoin and gabapentin may worsen some seizure types, especially in myoclonic and absence seizures. For some women with idiopathic generalized epilepsies, there will be no effective alternative to sodium valproate as cessation of sodium valproate will lead to recurrence of the generalized seizures, especially juvenile myoclonic epilepsy. Hence, it is not advisable to discontinue the drug in auch patients.

On the other hand, sodium valproate have the highest reported teratogenicity potential among antiepileptic drugs and the Australian Pregnancy Register has reported the risk to be as high as 16% if used in first trimester. Sodium valproate should be avoided in women of reproductive age and if a patient on the medication is willing to become pregnant, she should be well informed about the risk of teratogenicity and the decision must be left to her. If she decides to accept the risks and continue with pregnancy, the lowest possible effective dose should be prescribed to her.

If the dose of sodium valproate has been reduced to minimum during pregnancy to reduce the possible teratogenesis, it is recommended to re-establish the prepartum effective dose before the onset of labor. This is because, it is the time with increased risk for seizures, especially in patients with idiopathic generalised epilepsy who are very sensitive to sleep deprivation. Valproate therapy is found to be safe during breastfeeding.

Rheumatoid arthritis and its prognosis during pregnancy are highly unpredictable, as the disease can improve in 75% of the cases and gets worse in 25%. During conception and pregnancy, it is advisable to avoid those rheumatoid arthritis medications which possess high risk in causing congenital disabilities. Most common such contraindicated remedies include methotrexate and leflunomide.
Drugs like Prednisone, Non-steroidal anti-inflammatory drugs and TNF inhibitors are also not considered safe during pregnancy, so if required these should be used under specialist supervision.

Sulfasalazine and Antimalarials such as hydroxychloroquine are safe and can be used without much complications during pregnancy. In this given case, the patient should be advised to stop methotrexate and to continue sulfasalazine during pregnancy.