Volume 1 Issue 5, May 2014

Gupta AS

Congenital Heart Block Due To Maternal Autoantibodies
Khadkikar R, Prasad M,  Jain N, Chauhan AR.

Snake Bite During Pregnancy
Valvi D, Karnik ND, Samant PY, Parulekar SV.

Huge Ovarian Dysgerminoma Masquerading As a Subserosal Fibroid in Pregnancy
Bakre T, Patil LY, Gupta AS.

An Unusual Case of Hyperemesis Gravidarum
Gupta AS

Successful Management of Diabetic Ketoacidosis in Pregnancy
Channawar S, Madhva Prasad M, Jain N, Chauhan AR.

Conservative Management of Placenta Accreta
Chakre S, Warke H, Mayadeo NM, Pardeshi S.

Acute Uterine Inversion - A Catastrophic Event
Panchbudhe S, More V, Mali K, Satia MN.

Determination of Viability of Ovary in Torsion of Ovarian Cyst
Parulekar SV

Innovative Surgical Technique for Uterine Conservation in Giant Cervical Fibroid
Pawde A, Saxena N, Channawar S, Chauhan AR.


Gupta AS
The editors are back with the next issue. This issue brings together a few cases wherein pathological correlation with clinical features sprung up some interesting surprises. Such surprises makes clinical practice challenging and encourages a dialogue between the clinician and the pathologist. Clinical medicine when correlated with histopathological results improves the overall diagnostic and management outcomes. It gives direction to the clinician and helps in making the final diagnosis.
Clinicopathological correlation is a term that defines the relationship between the clinical and the pathological findings of a patient. It is not an etiological cause of the disease. A consultation between the clinician and the pathologist allows the objective review of symptoms, signs, laboratory investigations, imaging techniques and histopathology, results of the disease condition and its course. Clinicians reach a provisional diagnosis when they evaluate the patient’s history, and examination findings. This diagnosis is then confirmed or refuted, by the laboratory results, imaging techniques, the histopathologic examination and finally the autopsy results in the event of the death of the patient. This correlation is a positive correlation wherein the clinical and the pathological findings sync with each other. However, when they don't correlate then it is negative clinicopathological correlation. This is all the more important as the clinical dilemmas can be resolved. 
It is gratifying to the clinician when the pathologist collaborates his clinical diagnosis.
There is a case of a pregnant patient with a dysgerminoma. The preoperative clinical and MRI diagnosis was that of a subserosal fibroid uterus. Surgery revealed it to be an ovarian neoplasm and the gross and typical round or polygonal tumor cells arranged in nests, sheets and cords with pleomorphic hyperchromatic nuclei, thick nuclear membrane, prominent eosinophilic nucleoli and moderate vacuolated cytoplasm within these cells clinched the diagnosis of a dysgerminoma.
The pathologist needs to review the clinician’s notes and then correlate the histopathology or the autopsy findings prior to writing his report. This clinicopathological summary report should be presented in a concise, simple, and easy to understand language detailing the positive and the relevant negative relationship between the clinical and the pathological findings. These reports aid in constructing the sequence of the disease process in an individual, especially when this is the summary report of an autopsy. Unrelated findings should also be highlighted. This will update the knowledge of the clinician and aid in improving the quality of healthcare.
When the clinician and the pathologist join hands then the patient, the medical world and academia all stand to benefit. I have great pleasure in presenting the May issue of our journal to our readers who are ever willing to learn from others’ experiences.

Congenital Heart Block Due To Maternal Autoantibodies

Author Information
Khadkikar Rashmi*, Prasad Madhva**,  Jain Neha**, Chauhan AR***
(* Assistant Professor, ** Resident, ***, Additional Professor. Department of Obstetrics and Gynecology, Seth G.S. Medical College and K.E.M Hospital, Mumbai, India.)


Congenital heart block (CHB) is associated with maternal antibodies to Ro (SSA) and La (SSB) that cross the placenta and damage the AV node of fetus. An asymptomatic 27-year-old primigravida, diagnosed with second degree fetal heart block was investigated and found positive for antinuclear antibodies (ANA), anti-Ro and anti-La antibodies.  Fetal echocardiography (2D-echo) showed no structural defect but bradycardia. The patient was started on dexamethasone 8mg/day. She had preterm premature rupture of membranes (PPROM) at 34 weeks and underwent emergency cesarean section (LSCS). The baby was born with complete heart block but was managed conservatively in view of low birth weight. The infant is now 5 months old and permanent pacemaker implantation is planned.


The occurrence rate of CHB is approximately 2 to 3% of all pregnancies born to women with autoantibodies. The recurrence rate with a previous affected child is 18 to 20%.[1] CHB is most commonly diagnosed between 18 and 24 weeks of gestation, and may be first, second or third degree (complete). In pregnant women with autoimmune conditions, maternal autoantibodies cross the placenta and cause inflammation and fibrosis of AV node, causing block in signal conduction leading to congenital heart block. However, though the fetus is affected due to maternal anti-Ro/SSA and anti-La/SSB antibodies, the mother herself may be asymptomatic.

Case report

A 27 year old primigravida was referred at 28 weeks’ gestation in view of fetal bradycardia (fetal heart rate [FHR] of 78 beats/ min) and 2D-echo showing second degree heart block (intermittent type II) with early diastolic dysfunction, without evidence of hydrops fetalis. Detailed malformation scan was normal, liquor was adequate and there was no placental abnormality. She had no clinical features of autoimmune disorder or any known medical or surgical illness, except hypothyroidism for which she was on thyroid hormone supplementation.
In view of these findings, she was investigated: ANA, Anti-Ro, anti-La antibody tests were positive,   anti-dsDNA was negative. Consultations with a rheumatologist, a neonatologist and a cardiologist were obtained. Maternal therapy was started with tablet Dexamethasone 4 mg and tablet Hydoxychloroquine twice daily which was continued till delivery.
The patient was followed up weekly (FHR on auscultation varied between 60 -70/min) with USG for fetal viability and growth, and fetal 2D-Echo every 15 days. Degree of heart block progressed despite medications, and at 33 weeks there was complete heart block (FHR 50/min). She was counseled regarding need of pacemaker post-delivery.
Patient had premature rupture of membranes at 34 weeks of gestation. In view of impossibility of fetal heart monitoring during labor, emergency LSCS was performed. Male child of 1820 g was born with Apgar of 9/10 and was managed conservatively in neonatal ICU. Post delivery, ECG was suggestive of complete heart block with narrow QRS escape rhythm. Conservative management was continued in view of prematurity and low birth weight. Four months post-delivery, the infant was started on diuretics and was advised permanent pacemaker implantation as ECG showed complete heart block with ventricular rate of 43/min.

Figure 1: Fetal 2D Echocardiography

Figure 2: Postnatal ECG


Neonatal lupus is diagnosed by the presence of bradycardia in a fetus or newborn without structural cardiac abnormalities. Other manifestations of neonatal lupus are skin rashes, liver function abnormalities and cytopenias. These non-cardiac manifestations resolve after maternal antibodies are cleared from circulation (6 to 8 months after birth) but the conduction system disease is irreversible. The mother may have SLE or Sjogren's syndrome or may be asymptomatic, as in our case.[2]
CHB associated with neonatal lupus is a form of passively acquired autoimmune disease in which maternal autoantibodies cross the placenta and injure the previously normal fetal heart. Anti-Ro and anti-La antibodies have direct arrhythmogenic activity; the onset of bradycardia is between 16 and 24 weeks of gestation, corresponding to placental transfer of maternal IgG antibodies. These antibodies bind to fetal cardiocytes and inhibit the normal physiological removal of apoptotic cells, resulting in inflammatory reaction and fibrosis of the conduction system. Though these antibodies are directly involved in the pathogenesis of CHB, environmental, fetal, maternal, and genetic factors also predispose to this condition.[3]
Most patients are diagnosed antenatally with first and second degree heart block which should be managed with steroids and monitored for improvement or worsening to irreversible complete heart block, where steroids may not be effective. Fetal heart rate is a prognostic indicator of the disease; a critical level of less than 55/min, along with myocardial dysfunction and presence of hydrops fetalis (due to increase in ventricular size as an adaptation to persistent bradycardia), are risk factors for high mortality (85%) in neonatal period.[4] 
Fetal 2D echo is recommended in second trimester in mothers affected with autoimmune disorders and those with previous child affected with neonatal lupus. Conversely, presence of autoantibodies in mother should be suspected with fetal congenital heart block in the absence of any cardiac structural abnormality.
No guidelines for treatment of CHB exist though various therapeutic regimens are proposed: β-sympathomimetic drugs to increase the FHR; plasmapheresis and steroids to target the antibody-mediated inflammation; and digoxin or frusemide to prevent hydrops. The use of glucocorticoids in fetal second degree heart block may increase the chances of reverting to first degree heart block rather than progressing to third degree heart block. Dexamethasone may also improve fetal survival in complete heart block. After birth, therapy includes medical management, along with pacing in those infants who do not respond to medical treatment alone.[4]
In conclusion, multidisciplinary team approach by level III sonologist, obstetrician, neonatologist and pediatric cardiologist is valuable in management of this rare condition.


1.      Buyon JP, Heibert R, Copel J, et al. Autoimmune-associated congenital heart block: Mortality, morbidity, and recurrence rates obtained from a national neonatal lupus registry. J Am Coll Cardiol.1998; 31:165.
2.      Tincani A, Rebaioli CB, Taglietti M and Shoenfeld Y. Heart involvement in systemic lupus erythematosus, anti-phospholipid syndrome and neonatal lupus. Rheumatology 2006; 45(suppl 4): iv8-iv13.
3.      Friedman DM, Duncanson LJ, Glickstein J and Buyon JP. A review of congenital heart block. Images Paediatr Cardiol. 2003 Jul- Sep; 5(3): 36-48.
4.      Friedman DM, Rupel A, Glickstein J and Buyon JP. Congenital heart block in neonatal lupus: the pediatric cardiologist's perspective. Indian J Pediatr 2002 Jun; 69(6): 517-22.


Khadkikar R, Prasad M,  Jain N, Chauhan AR. Congenital Heart Block Due To Maternal Autoantibodies. JPGO 2014 Volume 1 Number 5 Available from: http://www.jpgo.org/2014/05/congenital-heart-block-due-to-maternal.html

Snake Bite During Pregnancy

Author Information
Durga Valvi*, Parulekar SV**, Karnik ND***, Samant PY****
 (* Assistant Professor, ** Professor and Head of Department, **** Additional Professor Department of Obstetrics and Gynecology, *** Professor, Department of Medicine. Seth GS Medical College and KEM Hospital, Mumbai, India.)


Snake bite envenomation is uncommon during pregnancy. Severity of obstetric consequences depends on the degree of envenomation. We report a case of G2P1L1 with 36 weeks of pregnancy who presented with history of snake bite.  The patient developed severe coagulopathy and neuroparesis.  The patient recovered after successful treatment with antivenom, antibiotics and transfusion of blood products.


In studies from South Africa, India, and Sri Lanka, pregnant women have accounted for 0.4% to 1.8% of hospitalized snakebite victims.[1] Snake venoms are primarily composed of mixture of protein and polypeptides with various properties. The composition of snake venom varies with the age and species the of snake, geographic locality and the time of year.[2]  Other factors which influence the effect of venom on humans include the quantity of venom injected, age and health of the victim.[3]  Venomous snake bite in the pregnant woman may lead to a poor outcome in both the fetus and the mother. Poisoning by members of the Crotalidae family during pregnancy carries fetal wastage rate of 43% and a maternal mortality rate of 10%. Pit viper venom contains a procoagulant that defibrinates the blood and bite by these viper cause a bleeding diathesis.[4]  Venom procoagulant activates intravascular coagulation and produce consumption coagulopathy by fibrinogen depletion.

Case Report

A patient G2P1L1 with 36 weeks of pregnancy presented with snake bite on right index finger in her village. The patient had swelling and severe pain at site of bite, weakness in all limbs proximally, bodyache, and giddiness. She received 10 vials of polyvalent antivenom at a peripheral medical facility and was transferred to our hospital.
On physical examination, the patient was conscious, oriented, and hemodynamically stable. Power of all four limbs was grade-4, knee jerks were brisk and plantar reflexes were extensor. On abdominal examination her uterus was 32 weeks’ size and relaxed, and fetal heart sounds were normal and regular. On vaginal examination the cervix was uneffaced and the os was closed. On local examination there was a blister at bite mark and bluish black discoloration of hand.

Figure 1. Site of snake bite on the right index finger.

On admission laboratory investigations were: Hemoglobin 11.6 g/dL, White blood count 32,000/cmm, Platelets 0.24 million/ml, Clotting time more than 20 min, INR was 1.25, Liver and Renal function tests were normal.  The patient was admitted in intensive care unit and started on antivenom injections and antibiotics.  On the second day her clotting time was increased to more than 1 hour and INR was more than 10.  The Patient  received 6 units of fresh frozen plasma and 2 units of cryoprecipitate.  Antivenom was continued in a dose of 5 vials twice daily for next 3 days. She needed 2 units of fresh frozen plasma daily for next 5 days to maintain PT/INR   and clotting within normal limits. The patient went into labor on day 3. Nifedepine was administered in a dose of 10 mg PO q6h for tocolysis in view of severe coagulopathy.  Both clotting time and INR were decreased to normal level by day 5. Fetal non stress test was reactive. Routine obstetric scan was normal. The patient's neuromuscular  weakness recovered totally by day 5. She was discharged on day 9. Two weeks later patient was delivered 2.7 kg alive female baby vaginally. The postpartum period was uneventful.


Snakebite in pregnancy is a rare event and seems to be related to the fact that pregnant women are homebound, avoiding outdoor activities.  The obstetrics consequences are severe and related to severity of the envenomation.  The common adverse obstetrical events in snake bite cases are antepartum hemorrhage, abruption of the placenta, postpartum hemorrhage, premature labor, decreased fetal movements, and intrauterine fetal death.  Snake venom is a mixture of complex biochemical compounds inducing potentially uterotonic  substances that may have direct effect on uterine muscle or act indirectly by releasing or potentiating effect of bradykinin which causes preterm labor.[7,8]

Nifedepine can be given for tocolysis in snake bite patient but magnesium sulfate is contraindicated in neurotoxic snake envenomation. Our patient had severe coagulopathy hence Nifedepine was started to delay labor to avoid potential massive intrapartum and postpartum hemorrhage.Bottom of Form
The adverse obstetrical events may occur because of the following pathophysiology.
  1. Direct effect of venom on the fetus
  2. Fetal hypoxia due to maternal shock
  3. Venom induced uterine contractions
  4. Placental bleeding due to coagulopathy[7]

Early gestational age at the time of snakebite and  delay in treatment may result in an unfavorable prognosis for pregnancy due to a slight decrease of platelets in early pregnancy.[6]Top of Form  The effect of antivenom on the fetus remains unclear but anaphylactic reactions caused by antivenom  may have an adverse effect on the mother or fetus.[1]  The venom can cause systemic poisoning in the fetus even without evidence of envenomation in the mother.[5]
Incoagulable blood suggest viper bite and rules out elapid bite. In our case, the exact identity of snake could not be ascertained but neurotoxicity  associated with severe coagulopathy was suggestive of Russel Viper bite. Neurotoxic symtoms in Russel Viper are believed to be due to presence of presynaptic toxin.
Neostigmine is an anticholinesterase used in neurotoxic snake bite but it is effective against post synaptic toxins such as those of cobra and there is some doubt against presynaptic toxins. Neostigmine is a category C drug. It could cause preterm labor if given intravenously, but potential benefits may warrant use of the drug in pregnancy despite potential risk.[9] Our patient responded to antivenom and blood component replacement therapy.  She did not need Neostigmine as her neuromuscular paralysis was mild and responded to above treatment itself.

ReferencesBottom of Form

1.      Seneviratne SL, de Silva CE, Fonseka M, Pathmeswaran A,Gunatilake SB, de Silva HJ. Envenoming due to snake during pregnancy. Trans R Soc Trop,Med Hyg. 2002;96:272-274.
2.      Gold B, Dart R, Barish R.Bites of venomous snakes. N Eng J Med. 2002;345: 347-356.
3.      David P.Principal actions of venoms and their symtoms. In: Bauchot R, ed. Snakes: A Natural History.New York: Sterling Publishing Co ; 2006: pp 208-209.
4.      Dunnihoo DR,  Rush BM, Wise RB, Brooks GG, Otterson WN. Snake bite poisoning in pregnancy.A review of the literature. J Reprod Med 1992 ;37(7):653-8.
5.      Mcnally SL., Reitz CJ.  Victims of snakebite. A 5-years study at Shongwe Hospital, Kangwane, 1978-1982. S Afr Med J, 1987, 72, 855-60.
6.      Rezende J. Obstetricia. 4.ed. Rio de Janeiro: Guanabara Koogan, 1987: 649-63.
7.      Habib AJ, Abubaker SB, Doufa S, Noabi A, Yusuf PO. Envenoming after Carpet Viper bite during Pregnancy. Timely use of asv Improves maternal and fetal outcomes; Tropical Med Int Health. 2008;13: 1172-1175.
8.      Langley RL. A Review of venomous animal bites and stings in pregnant patient; Wilderness and Environmental medicine.2004; 15: 207-215.
9.      Neostigmine Pregnancy and Breastfeeding Warnings. Available at: http://www.drugs.com/pregnancy/neostigmine.html


Valvi D, Karnik ND, Samant PY, Parulekar SV. Snake Bite During Pregnancy. JPGO 2014 Volume 1 Number 5 Available from: http://www.jpgo.org/2014/05/snake-bite-during-pregnancy.html

Huge Ovarian Dysgerminoma Masquerading As a Subserosal Fibroid in Pregnancy

Author Information
Bakre Tejashree *, Patil Lalita Y**, Gupta AS.
(* Second Year Resident, *** Professor. Department of Obstetrics and Gynecology, ** Assistant Professor, Department of Pathology; Seth G.S. Medical College and K.E.M Hospital, Mumbai, India.)


A 20 year old primigravida with 19 weeks of pregnancy came with pain in abdomen, dysuria and frequent urination. She was diagnosed as a case of Gastro Intestinal Stromal Tumor (GIST) of the descending colon on ultrasonography (USG). Magnetic resonance imaging (MRI) & Doppler sonography diagnosed the mass as a sub-serosal fibroid of the uterus. During emergency lower segment cesarean section (LSCS) at term the ovarian origin of the mass was discovered.


Dysgerminoma is the commonest malignant ovarian germ cell  tumor diagnosed in pregnancy.[1,2,3] These tumors can however be misdiagnosed as sub-serosal fibroids or tumors of the colon. At times modalities like Doppler and MRI can also lead to misdiagnoses.[4]  Such masses are then diagnosed  accidentally. Here we present a case of left ovarian dysgerminoma misdiagnosed as fibroid during antenatal period resulting in delay of her definitive treatment.

Case Report

A 20 year old primigravida with 19 weeks of gestation presented with complaints of dull aching pain in left lumbar region and dysuria for 15 days.  On examination her vital parameters were stable, chest was clear, abdominally uterus was 20 weeks in size and relaxed. An 11 x 8 cm sized non tender mass separate from uterus and hard in consistency was palpated in left lumbar region. On vaginal examination a firm, non tender mass was felt high up in the left fornix. An ultrasound examination revealed a 19 weeks size normal intrauterine fetus and a large hyperechoic, well defined, highly vascular mass measuring 11cm x 8 cm x 8 cm in the left lumbar region.  USG differential diagnosis was GIST of the descending colon or a left subserosal fibroid of the uterus. MRI of the pelvis and abdomen was suggestive of a large subserosal or broad ligament fibroid but possibility of GIST could not be ruled out. The patient was closely followed by obstetrician and gastroenterologist. Rest of antenatal period was unremarkable. The patient underwent an emergency LSCS under spinal anesthesia at term in view of thick meconium stained liquor in latent stage of labor. Intraoperatively, after birth of a term fetus a large lobulated mass, hard in consistency, smooth surfaced, measuring 25 x 20 x 8 cm arising from the left ovary and free from the bowel was seen.  A thick leash of blood vessels was seen extending from the base of the mass to the left cornua of the uterus and into the mesosalpinx.

Figure 1. Large left ovarian tumor with a thick leash of vessels during Cesarean section.
M: is the mass. Arrow shows the thick leash of blood vessels in the mesoovarium.

The surgeon deferred the excision of the mass due to its high vascularity and the thick leash of blood vessels seen in its pedicle.  Tumor markers like LDH, AFP and β-HCG were sent, chest radiograph was obtained. Tumor markers (LDH-2290 U/L and β -HCG – 26 mIU/L) were elevated. Exploratory laparotomy was performed after puerperium. Peritoneal washings were sent for cytology. A left ovarian mass lobulated, bosselated 19 x15 x5 cm in size was seen. A left salpingo-oophorectomy was done and the tumor was sent for frozen section.Cut surface was solid, greyish white, firm, fleshy, and bulging.  Frozen section was suggestive of a malignant ovarian tumor probably a mixed germ cell tumor.

Figure 2a. Left large ovarian neoplasm. M is the mass; Black arrow is the vascular pedicle and the green arrow shows the normal uterus.

Figure 2b. Gross: Large, lobulated 19 x15 x5 cm, solid mass.

Figure 3. Cut surface: Solid, greyish-white, fleshy with bulging cut surface.

Opposite ovary and uterus were inspected which were grossly normal. Peritoneum of the cul de sac, liver, omentum, under surface of the diaphragm, colon, bowel mesentery, spleen,  bladder peritoneum, pelvic and para aortic lymph nodes were evaluated and found to be grossly normal. As the patient was young and desirous of further child bearing only unilateral salpingo-oophorectomy was done. Peritoneal cytology showed presence of malignant cells (FIGO stage 1c). Final histopathology report confirmed the tumor to be an ovarian dysgerminoma. The patient was referred to an oncology center for adjuvant treatment.

Figure 4. H&E 40X: Shows tumor cells are arranged in nests, sheets and cord separated by fibrous septae. C are the tumor cells and S are the fibrous septae.

Figure 5. H&E 100X: Shows stromal lymphocytic infiltration (L) and few mitotic figures were seen.

Figure 6. H&E 400X: Shows large round to polygonal cells with high N:C ratio, pleomorphic hyperchromatic nuclei, thick nuclear membrane, prominent eosinophilic nucleoli and moderate vacuolated cytoplasm.


Dysgerminoma accounts for only 1-2% of all malignant ovarian tumors. Dysgerminoma occurs mainly in children and young women.[3] The average age is 22 years, and 90 percent of the patients are less than 30 years of age. About 20 percent of malignant ovarian tumors detected during pregnancy are dysgerminomas. Differential  diagnosis of a pelvic mass in pregnancy include uterine leiomyomas,  overdistended urinary bladder, ovarian neoplastic cysts, GIST,  impacted feces,  large hydrosalpinx and retroperitoneal tumor. [5]
This case is interesting as it posed diagnostic challenges ranging from GIST to subserosal leiomyoma and finally dysgerminoma. USG is the primary imaging modality.[6] However not only USG but also MRI misdiagnosed the dysgerminoma as a fibroid uterus in our case.  MRI  has around 98% sensitivity for detecting ovarian origin of a mass.[4,7] However there have been reports of mistaking a malignant ovarian tumor for pedunculated uterine fibroid with areas of cystic degeneration as in our case.[4] Such adnexal masses are then diagnosed for first time during LSCS.  Tumor markers elevated in a case of a dysgerminoma are most commonly LDH and occasionally β-HCG, when the dysgerminoma has components of syncytiotrophoblasts. Raised AFP is less common. Preoperative evaluation of all of the tumor markers is advisable in patients with suspected germ cell tumor or dysgerminoma.[5] A MRI diagnosis of fibroid uterus misguided us and so tumor markers were not studied in the antenatal period. Had these tumor markers been done the diagnosis would have been established and the patient could have been operated in the antenatal period itself, or along with LSCS. The tumor may then have been staged as FIGO stage 1a. For patients with stage Ia dysgerminoma, unilateral salpingo-oophorectomy conserving the uterus and opposite ovary is accepted treatment in a young patient desirous of preserving her fertility. The initial treatment of these patients is surgery, which includes unilateral salpingo-oophorectomy. Frozen section is performed. Multiple biopsies from the peritoneum, omentum, and contralateral ovary, and pre- and paraaortic lymph nodes are taken and studied. Peritoneal washings are subjected for cytological analysis.[8] The frozen section pathologic diagnosis in our case was mixed germ cell tumor as the pathologist studied only representative section. In such cases it is best to defer definitive surgery. Fortunately, the accuracy of frozen section diagnosis of ovarian tumors is more than 90%.[9]  Incompletely staged patients or those with higher stage tumors (1c and above) should probably receive adjuvant treatment  like radiation therapy or chemotherapy. [10]

1.        Smith HO, Berwick M, Verschraegen CF, Wiggins C, Lansing L, Muller CY, et al. Incidence and survival rates for female malignant germ cell tumors. Obstet Gynecol. 2006;107(5):1075-85.
2.        Lee KH, Lee IH, Kim BG, Nam JH, Kim WK, Kang SB, et al. Clinicopathologic characteristics of malignant germ cell tumors in the ovaries of Korean women: a Korean Gynecologic Oncology Group Study. Int Journal of Gynecol Cancer. 2009;19(1):84-7.
3.        Zaloudek C . Current Issues Part Two ,Case 13 Dysgerminoma Available at: http://pathology.ucsf.edu/uploads/376/182_CZ%20Current%20Issues%202012%20Part%202.pdf
4.        Anwar S, Rehan B, Hameed G   MRI for the diagnosis of ultrasonographically indeterminate pelvic masses- Journal of Pakistan Medical Association, 2014; February: 171-174.
5.        Michener C M,  HuhW K. Available at: http://emedicine.medscape.com/article/253701-overview/
6.        Munir S S, Misbah S And Dawood A D. The Evaluation Of Pelvic Mass. Biomedica Vol.26, Jan. – Jun. 2010/Bio-14.
7.        Yoon K, Chang Y, Guisera L, et al. Ovarian dysgerminoma in pregnancy. Korean J Obstet Gynecol 2011;54(4):218-222.
8.        Dark GG , Bower M, Newlands ES, Paradinas F, Rustin GJS. Surveillance Policy for Stage I Ovarian Germ Cell Tumors. J Clin Oncol 1997;15, No 2: 620-624.
9.        Leiserowitz GS. Managing Ovarian Masses During Pregnancy: Obstet Gynecol Survey 2006: 61, No 7:463-470.
10.    Medical Protocol  Ovarian Germ Cell Tumour (Ogct) – Management Guidelines Protocol No: ME-O1 (Version No: 1) http://www.mccn.nhs.uk/userfiles/documents/ Ovarian% 20 germ%20cell%20protocol%20(final%20version).pdf


Bakre T, Patil LY, Gupta AS. Huge Ovarian Dysgerminoma Masquerading As a Subserosal Fibroid in Pregnancy. JPGO 2014 Volume 1 Number 5 Available from: http://www.jpgo.org/2014/05/huge-ovarian-dysgerminoma-masquerading.html

An Unusual Case of Hyperemesis Gravidarum

Author Information
Gupta AS.
(Professor. Department of Obstetrics and Gynecology, Seth G.S. Medical College and K.E.M Hospital, Mumbai, India.)


An interesting case of hyperemesis gravidarum with elevated hepatic aminotransferases is reported. Despite complete cessation of vomiting the patient’s liver aminotransferases kept rising. All investigations to detect any underlying liver disease were futile. She eventually responded to oral administration of a multivitamin.


Hyperemesis gravidarum is pernicious vomiting of pregnancy that can lead to dehydration, ketoacidosis of starvation, alkalosis, electrolyte imbalance, weight loss, altered liver or renal function and Wernicke’s encephalopathy.[1] It can result in deficiency of vitamins and nutrients due to reduced intake or poor absorption. B complex vitamins are important coenzymes in enzymatic reactions. They are required for normal energy metabolism, thiamine more than the others. Wernicke encephalopathy is a well documented complication of thiamine deficiency in patients of hyperemesis gravidarum.

Case Report

Twenty one year old Gravida 1 presented with a complaint of hyperemesis gravidarum at 8 weeks of pregnancy. She had had persistent vomiting for one week.  She was admitted, kept nil by mouth and was infused with intravenous crystalloids including Ringer lactate solution. Doxylamine and pyridoxine were administered at 8 hour intervals orally with sips of water. On admission her pulse rate was 96/min., BP was 90/60 mm of Hg, tongue was moist, respiratory rate was 18/min. Her uterus was anteflexed, soft and corresponding to 8 weeks size. Her laboratory parameters were as follows: Hb 11.5 g/dl, WBC 7600/mm3. TSH was 1.35 μIU/mL, random blood sugar was 110 mg%, uric acid 3.2 mg%, BUN 11 mg%, serum creatinine 0.8 mg%, SGOT 115 U/L, SGPT 91 U/L, serum electrolytes within normal limits. Urinary ketones were small. After admission the patient had no further episodes of vomiting and she was started on dry carbohydrate diet after 24 hours and oral doxylamine and pyridoxine were continued three times a day. As her liver enzymes were marginally elevated they were repeated. Her serial serum hepatic aminotransferases levels are shown in the table below.

Serial laboratory serum hepatic aminotransferases levels

2nd Jan 14
Day 1
Day 3
Day 6
Day 9
Day 12
Day 15
Day 17
Day 81

Her serum bilirubin, creatinine, BUN, electrolytes, coagulation profile were normal on serial measurements. The liver enzymes showed a rising trend. The patient had no further episodes of vomiting. Her condition was stable and she was tolerating dry solids orally. She was continued on oral doxylamine and pyridoxine three times a day. A coexisting liver disorder was suspected. A gastroenterologist’s opinion was obtained. As per his advise, viral markers, ultrasound (USG) abdomen, ANA, Anti-ds DNA and Anti smooth muscle antibody testing (ASMA) were obtained. All viral markers (HbsAg, HCV, HIV, IgM HbcAb, and IgM HEV) were negative. Autoimmune markers like ANA, Anti-ds DNA, and ASMA (Interglandular Actin Fibers, Muscularis Mucosa, Muscle layers of blood vessels) were all negative. USG abdomen was normal. Liver was normal in size and echo texture. Hepato- portal color Doppler was also normal. Hepatic veins were normal. Middle and lower hepatic vein had common ostia. Right hepatic vein was normal. Spleen was normal. As the liver enzymes showed a rising trend over 12 days and all tests indicating any other liver pathology were negative we were in a dilemma about terminating her pregnancy. However before that we decided to give a multivitamin orally. The contents of that multivitamin were vitamin B1 10mg, vitamin B2 10 mg, Nicotinamide 100 mg, vitamin B6 3 mg, calcium pantothenate 50 mg, Folic acid 1.5 mg, vitamin B12 15 mcg, vitamin C 150 mg. We gave her one tablet of this multivitamin daily and then repeated the liver enzymes after 3 days. The liver enzymes gradually decreased and normalized over the next 15 days. The patient was discharged after a stay of 19 days. The pregnancy is ongoing and is uncomplicated.


Nausea vomiting is common is the first trimester of pregnancy. Incidence of hyperemesis gravidarum is about 0.1-2% pregnancies.[1] Of these about 50% patients have evidence of liver dysfunction as evidenced by deranged liver aminotransferases.[2] The liver enzymes normalize after vomiting resolves. If liver dysfunction persists an underlying liver pathology is to be evaluated.[3] In our patient despite having no vomiting her liver enzymes kept deteriorating. All investigations to detect any underlying viral, autoimmune or ischemic pathology were done but no cause for the rising aminotransferases could be found. B group of vitamins act as a cofactor in many of the chemical reaction in the liver. Use of thiamine for prevention of Wernicke’s encephalopathy is well documented.[4] B complex vitamins have a wide role in enzymatic, non enzymatic regulatory roles. Thiamine is an important cofactor in energy metabolism and is naturally present in the liver.[5] One of the hypothesis of alteration of liver function in patients of hyperemesis is the affect on the fatty acid oxidation in the mitochondria. Starvation also results in increase in circulating fatty acids due to increased lipolysis.[2] Thiamine pyrophosphate, a derivative of thiamine, is required for the carbohydrate metabolism and the Kreb’s cycle. Deficiency of this vitamin may increase the fatty acid metabolism.[6] Niacin is supposed to reduce the triglyceride and secretion of very low density and low density lipoproteins.[7] Riboflavin is believed to be involved in the biosynthesis of coenzyme A reducing  the oxidative stress.[8] Administration of the B complex tablet in this case  may have corrected the energy metabolism and reduced the fatty acid metabolism allowing the liver enzymes to correct themselves. It may be worth trying to administer a multivitamin tablet in cases of hyperemesis gravidarum patients who fail to recover their liver function despite cessation of vomiting.  This may be because the deficiency of the one or more components of the B group of vitamins, especially where they are not stored in the body like thiamine, may persist due to inadequate dietary intake even after vomiting stops. However, we noted a significant decline in the liver enzymes on continuous administration of the B complex tablet in our patient.


B complex administration in intractable elevation of liver aminotransferases is worth a trial especially in those cases of hyperemesis gravidarum whose liver function continues to deteriorate even after control of vomiting and no other cause for the abnormal liver function is detected.


1.      Kuşcu N K, Koyuncu F; Hyperemesis gravidarum: current concepts and management. Postgrad Med J 2002;78:76-79 doi:10.1136/pmj.78.916.76
2.      http://emedicine.medscape.com/article/254751-workup
3.      Hay JE. Liver disease in pregnancy. Hepatology. Mar 2008;47(3):1067-76. [Medline].
4.      Galvin R  , Bråthen G, Ivashynka A, Hillbom M, Tanasescu R, Leone MA; EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. Eur J Neurol. 2010 Dec;17(12):1408-18.
5.      Lonsdale D; A review of the biochemistry, metabolism and clinical benefits of thiamin(e) and its derivatives, Evid Based Complement Alternat Med. Mar 2006; 3(1): 49–59.
6.      Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H Freeman; 2002. Section 17.1, The Citric Acid Cycle Oxidizes Two-Carbon Units. Available from: http://www.ncbi.nlm.nih.gov/books/NBK22427/
7.      Kamanna VS1, Kashyap ML.Mechanism of action of niacin.Am J Cardiol. 2008 Apr 17;101(8A):20B-26B.
8.      Moĭseenok AG, Gurinovich VA, Omel'ianchik SN, Slyshenkov VS.; Coenzyme A biosynthesis as universal mechanism of conjugation of exogenous and multiple pantothenic acid functions[Article in Russian],Ukr Biokhim Zh. 2004 Jul-Aug;76(4):68-81. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19621759


Gupta AS. An Unusual Case of Hyperemesis Gravidarum. JPGO 2014 Volume 1 Number 5 Available from: http://www.jpgo.org/2014/05/an-unusual-case-of-hyperemesis.html

Successful Management of Diabetic Ketoacidosis in Pregnancy

Author Information
Sarita Channawar*, Madhva Prasad**, Neha Jain***, Anahita R. Chauhan****
(* Assistant Professor, **Registrar, *** Second Year Resident, **** Additional Professor Department of Obstetrics and Gynecology, Seth G.S. Medical College and K.E.M Hospital, Mumbai, India.)


Diabetic ketoacidosis (DKA) is a complication seen in type 1 diabetes mellitus (DM) but can also occur in pregnancies complicated by type 2 DM or gestational diabetes mellitus (GDM). DKA is a medical emergency with high maternal and fetal mortality, and requires treatment in an intensive care setting. Prompt recognition and resuscitative therapy improves medical and obstetric outcomes. This report of DKA in a case of GDM provides insight into pathophysiology and successful management.


Normal pregnancy is characterized by a state of decreased insulin sensitivity, accelerated lipolysis and ketogenesis.[1, 2, 3, 4] The concentration of serum ketones is estimated to be two to four times greater than in nonpregnant state.[1, 5] Despite these changes, the incidence of DKA in pregnant diabetics is only 1 to 3%.[2, 3] Fetal mortality rates of 30 to 90% in the past have now decreased to 9% due to improvements in neonatal and diabetic management.[2, 3]

Case History

A 22 year old primigravida with 34+6 weeks of gestation was referred to our tertiary care center with giddiness, polyuria, polydipsia, candidial vagina discharge and deranged blood sugars (fasting blood glucose 280 mg/dl and post-meal value 410 mg/dl a few days back). She had stable vital signs, 34 weeks’ sized relaxed gravid uterus with cephalic presentation and normal fetal heart sounds. She had been diagnosed by her primary care obstetrician as GDM one month earlier and referred to us; however she did not report nor was she on any treatment. Recent sonography revealed oligohydramnios (amniotic fluid index 7 cm) but no fetal malformations.
A diagnosis of DKA was made. She was urgently hospitalized. Her hemoglucotest (HGT) on admission was 590 mg%, urinary sugars were 3+, urinary ketones 2+, venous blood gas (VBG) analysis showed pH of 7.32, bicarbonate of 17.3 meq/L, sodium of 125 meq/L and potassium of 3.9 meq/L. She was initially hydrated with normal saline (NS) 1liter over 1 hour, followed by 500 ml NS with 20 ml potassium chloride (KCl) over the next hour, and continued on 500 ml NS with 10 ml KCl over next 4 hours. Insulin therapy was initiated with bolus dose of 16 units human insulin subcutaneously followed by insulin drip (50 units in 500 ml NS at 70 ml/h). Monitoring was performed with hourly HGT, 4 hourly urinary sugars/ketones, and 6 hourly serum electrolytes and VBG. The patient stabilized on insulin drip: blood sugar value was 314 mg% after 3 hours, which reduced over 10 hours to 115mg%. Urine ketones also disappeared. Hence insulin drip was discontinued. Fetal heart rate monitoring was done while on insulin drip and was normal. She was converted to high doses of subcutaneous regular and isophane human insulin (20 + 30 units respectively), and maintained on thrice daily doses which were tapered gradually, along with diabetic diet, so as to maintain her blood glucose levels within normal range. The patient was managed jointly with the endocrinologist. She remained hospitalized, blood sugars were monitored six times a day and insulin was continued with good glycemic control. Fetal assessment was done clinically with daily fetal movement count, nonstress test on alternate days and weekly Doppler studies, all of which were normal. Labor was induced electively at 37 weeks’ gestation; however emergency LSCS was done for failed induction and she delivered a healthy female weighing 2.6 kg. Postoperatively her blood sugars were normal; and insulin was not required. She was managed on diabetic diet and oral hypoglycemic agent Metformin 250 mg twice daily for 10 days, after which it was omitted and she was discharged.


Diabetic ketoacidosis is a life-threatening, acute metabolic state due to insulin deficiency. Hence all patients with diabetes in pregnancy including GDM patients should be monitored for DKA. Low levels of insulin cause increased gluconeogenesis while decreasing glucose uptake and utilization. Increased levels of counter-regulatory hormones (glucagon, cortisol, catecholamines and growth hormone) accelerate the development of ketoacidosis by increasing gluconeogenesis, glycogenolysis, ketogenesis and insulin resistance. Insulin deficiency also leads to high anion gap metabolic acidosis. Hyperglycemia and hyperosmolality in patients with DKA produce the characteristic osmotic diuresis causing intravascular volume depletion; if not corrected by intravenous fluids and insulin, DKA can rapidly progress to a state of poor tissue perfusion, diminished cardiac and renal function, multisystem failure and death. A number of physiological changes during pregnancy influence carbohydrate and fat metabolism.[2, 3, 4] 
  1. Placental lactogen and increased cortisol contribute to increased insulin resistance, particularly later in pregnancy.
  2. Pregnant women have respiratory alkalosis with decreased serum bicarbonate concentrations and reduced capacity to buffer organic acids.
  3. Pregnancy being an accelerated state of starvation, overnight fast can increase lipolysis and ketone body concentrations 2-4 times greater than in nonpregnant state.[1, 5]
  4. Predisposing factors for DKA include stress of labor, cessation of insulin therapy, use of β-sympathomimetic agents and emesis with accompanying dehydration.
  5. Both fetus and placenta utilize large quantities of glucose resulting in lower maternal fasting glucose levels.[2, 3, 4 ]

Hence DKA in pregnancy can develop more rapidly and at lower serum glucose concentrations often causing delay in the diagnosis.[2, 3, 4] Several cases of “normoglycemic” DKA have been reported, although in almost every case glucose has exceeded 130 mg/dl. Our patient had levels of 590 mg%, low bicarbonate concentration, positive anion gap and VBG pH of 7.3 suggestive of acidosis; possibly starvation ketosis contributed to development of high anion gap metabolic acidosis. Management principles in DKA include aggressive volume replacement, intravenous insulin therapy, correction of acidosis and electrolyte abnormalities, and management of precipitating factors, as well as monitoring of maternal-fetal response to treatment. Nonreassuring fetal heart rate pattern may be seen due to associated fetal hypoxemia and acidosis, but correction of maternal metabolic abnormalities should be a priority and delivery considered only after maternal stabilization if indicated. Prevention strategies include education of diabetic pregnant women about the risks of DKA, precipitating factors, and the importance of timely reporting of signs and symptoms. A multidisciplinary approach including obstetrician, endocrinologist, intensivist and neonatologist is necessary for good outcome.


1.      Carroll MA, Yeomans ER. Diabetic ketoacidosis in pregnancy. Crit Care Med 2005;33: S347–S353.
2.      Kamalakannan D, Baskar V, Barton DM, Abdu TAM. Diabetic ketoacidosis in pregnancy. Postgrad Med J 2003;79: 454–457.
3.      American College of Obstetricians and Gynecologists. ACOG practice bulletin No. 60: pregestational diabetes. Obstet Gynecol 2005;105:675–685.
4.      Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI et al. Management of hyperglycemic crises in patients with diabetes. Diabetes Care 2001;24:131–153
5.      Sibai BM, Viteri OA. Diabetic ketoacidosis in pregnancy. Obstet Gynecol 2014;123(1): 167-78.


Channawar S, Madhva Prasad M, Jain N, Chauhan AR. An Unusual Case of Hyperemesis Gravidarum. JPGO 2014 Volume 1 Number 5 Available from:  http://www.jpgo.org/2014/05/successful-management-of-diabetic.html