Your SlideShare is downloading. ×
Nonimmune  hydrops  fetalis .  Dr B M Rakshit
Upcoming SlideShare
Loading in...5

Thanks for flagging this SlideShare!

Oops! An error has occurred.


Introducing the official SlideShare app

Stunning, full-screen experience for iPhone and Android

Text the download link to your phone

Standard text messaging rates apply

Nonimmune hydrops fetalis . Dr B M Rakshit


Published on



Published in: Health & Medicine

1 Like
  • Be the first to comment

No Downloads
Total Views
On Slideshare
From Embeds
Number of Embeds
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

No notes for slide


  • 1. NONIMMUNE HYDROPS FETALIS Dr Bibek Mohan Rakshit MD; MRCOG; DNB; MNAMS Associate Professor (Gynaecology & Obstetrics) Burdwan Medical college and Hospital
  • 2. BACKGROUND Nonimmune Hydrops Fetalis (NIHF) is now responsible for 90% of all hydrops.  It has an estimated incidence of 1/1500 to 1/3800 births.  The pathogenesis of NIHF is not clear, but it is associated with numerous potential mechanisms and underlying disorders.  NIHF has an obvious poor prognosis for the fetus, but can also have maternal consequences as well with a 10% incidence of Mirror syndrome.  Newzealand maternal fetal medicine network
  • 3. DEFINITION....... NIHF is established by the ultrasound findings of at least two of the following  Ascites  Pleural effusion: ANY fluid abnormal  Pericardial effusion: > than 2mm  Skin edema: > than 5mm on chest and scalp  Polyhydramnios: Max pocket > 8cm, or AFI > 24cm
  • 4. DIFFERENTIAL DIAGNOSIS Immune hydrops  Isolated fluid collection  Ascites  Pleural effusion  Pericardial effusion  Skin Oedema  Polyhydramnios or placentomegaly. 
  • 5. ETIOLOGY.....  Aneuploidy  Cardiovascular abnormalities        Structural Functional Arrhythmias Tachyarrythmia Bradyarrhythmia Vascular  Shunt or Thrombosis Thoracic abnormalities       CCAM Diaphragmatic hernia Masses Pulmonary sequestration Chylothorax Airway obstruction •
  • 6. Non cardiac/thoracic anomalies    Lymphatic Gastrointestinal Genitourinary Neurological/Decreased movement Anaemia  Decreased production     Increased loss     Parvovirus Infiltration/Storage diseases Myeloproliferative/ congenital leukaemia Intrinsic cell abnormality (alpha-thalassemia, G6PD, membrane…) Hemangioma Haemorrhage/abruption
  • 7.  Infectious disease  toxo, syphilis, varicella, adenovirus, coxsackie Metabolic storage disease  Placental  TTTS/TRAP  Trauma  Cord anomalies  Chorio-angioma   MATERNAL DISEASE Idiopathic  Decreasing significance with knowledge
  • 8. PRESENTATION     35% incidental finding Size > dates Decreased fetal movement Mirror Syndrome in mother
  • 9. IMPORTANT HISTORY  Personal and family history to look for inheritable disorders associated with     Alpha thalassemia Metabolic disorders Genetic syndromes Infectious exposures  Parvovirus Consanguinity  Previous baby with hydrops 
  • 10. EVALUATION..... Detailed ultrasound  Anatomy  MCA PSV  Echocardiogram
  • 11. LABORATORY INVESTIGATIONS Mother  Blood group and RBC antibody screen  Baseline BP and urinalysis  FBC and film screen for thalassemia  Parvo, toxo, rubella, syphillis,  HSV(if recent primary infection) Kleihauer-Betke  LFT, urea,urate,electrolytes 
  • 12. Infant     Amniocentesis Karyotype PCR for TORCH pathogens Storage for further testing Cordocentesis RBC for anaemia Metabolic/genetic tests UTERINE VENOUS PRESSURE
  • 13. PROGNOSIS The overall perinatal mortality rate is 50 – 98%.  There has been no significant change over past 15 years.  Mortality rates will vary according to     Gestation (earlier has worse prognosis) Pleural effusions (worse prognosis) Underlying etiology
  • 14. MANAGEMENT OPTIONS Termination  Selective therapeutic intervention if possible Ongoing pregnancy with hydrops  Monitor for PET/Mirror syndrome  Consider neonatal palliation 
  • 15. INTERVENTION If for active intervention Monitor with CTG’s or BPP’s 2. Delivery at tertiary care center 3. Consider risks of:      birth trauma PPH non reassuring fetal heart dystocia caesarean Low recurrence if no inheritable disorder identified
  • 16. SOGC CLINICAL PRACTICE GUIDELINES Recommendations .. 1. All patients with fetal hydrops should be referred promptly to a tertiary care centre for evaluation. Some conditions amenable to prenatal treatment represent a therapeutic emergency after 18 weeks. (II-2A) 2. Fetal chromosome analysis and genetic microarray molecular testing should be offered where available in all cases of non-immune fetal hydrops. (II-2A) 3. Imaging studies should include comprehensive obstetrical ultrasound (including
  • 17. 4.Investigation for maternal–fetal infections, and alphathalassemia in women at risk because of their ethnicity, should be performed in all cases of unexplained fetal hydrops. (II-2A) 5. To evaluate the risk of fetal anemia, Doppler measurement of the middle cerebral artery peak systolic velocity should be performed in all hydropic fetuses after 16 weeks of gestation. In case of suspected fetal anemia, fetal blood sampling and intrauterine transfusion should be offered rapidly. (II2A) 6. All cases of unexplained fetal hydrops should be referred to a medical genetics service where available. Detailed postnatal evaluation by a medical geneticist should be performed on all cases of newborns with unexplained non-immune hydrops. (II-2A)
  • 18. 7. Autopsy should be recommended in all cases of fetal or neonatal death or pregnancy termination. (II-2A) Amniotic fluid and/or fetal cells should be stored for future genetic testing. (II-2B) 8. SOGC GUIDELINES.....2013