1. R2 陳柏嵩
Case discussion

2. General data Name： XX之子 Chart Number： 177612xx Bed No： 4P203
Date of Admission： 2016/08/26
Occupation： 無
Ethnicity： 台灣-福佬人

3. Chief complain Fetal distress with polyhydramnios

4. Present illness
The patient was born at GA 32+5 weeks by 27 years old mother. Polyhydramnios was noted since GA 21 week. His mother had no GDM, no PIH, nor other adverse event was noted.
She visited our OBS/GYN OPD for evaluation of C/S
Due to fetal distress with absence of end-diastolic velocity of umbilical artery, C/S was arranged on the next day.

6. Past history
Birth History: G1P1,CS,GA: 32+5 weeks, BBW: 1692, DOIC(-), PROM(-)
APGAR score: 7->9
Growth and Development:
BW: 1692 gm (10th-25th percentile)
BL: 42.8 cm (50th-75th percentile)
Mother had no medication history

7. Family history
No family history of hereditary disease

8. Review of system
HEENT：no deformity of eyes. Ears, nose, mouth, throat, and neck
Respiratory System：cough(-), hemoptysis(-),wheezing(-),dyspnea(-)
C-V System：varicose vein(-),orthopnea(-),pedal edema(-)
G-I System：vomiting(-),belching(-),diarrhea(-),constipation(-)
G-U System：polyuria(-), hematuria(-),abnormal urine color(-)
Neuromuscular System：　
Motor：muscle atrophy(-),involuntary movementbilateral shoulders and hips atrophy(-)　　
Extremities：swelling(-),edema(-),deformity(-),stiffness(-)
Skin：pigmentation(-),itching(-),petechiae(-)

9. Physical examination T: 36.5°C P: 114/min R: 32/min BP: 69/38mmHg
HEENT:
Anterior fontanel: 2 f.b.;
Posterior fontanel: <1 f.b.
Fracture: no
Epicanthic eyefold, Broad flat face spaced
Chest:
Breath pattern: smooth,
Bilateral symmetric expansion
Breathing sound: bilateral clear AND symmetric, no crackle
HEART:
Heart sound: regular heart sound, mild murmur
Abdomen: Soft, ovoid,
normoactive bowel sound
Anogenitalis:
Hydrocele: no
Cryptorchidism: no Epispadias
Extremities:
Dislocation OF Hip: no;
Palm crease, big toes widely
Skin: Vesicles: no
Neuro: Moro`s reflex: yes; Grasp reflex: yes; Rooting reflex: yes

10. Lab data

12. Tentative diagnosis Polyhydraminos Suspected Down syndrome
Duodenal, Esophageal, or Intestinal atresia
Anencephaly
Massive unilateral dysplastic kidneys
Suspected Down syndrome
Prematurity, 32+5 weeks
Polycythemia
Primary gastrointestinal obstruction (eg, duodenal, esophageal, or intestinal atresia)
Neuromuscular disorders (eg, anencephaly)
Secondary obstruction of the gastrointestinal tract (eg, massive unilateral dysplastic kidneys)

14. Treatment course 8/26, OG decompression, Cardiac echo
8/29, Abdominal echo
8/30, Operation
Ascites fluid about 30 cc golden yellow color
Atresia located 2nd to 3rd portion area without fibrous band
Duodenoduodenostomy

15. Duodenal atresia
discussion

16. Epidermiology
Congenital duodenal obstruction occurs in /100,000 live births
Intrinsic defect of bowel formation
Extrinsic compression by abnormal neighboring structure, duplication cysts, or congenital bands associated with malrotation
Duodenal atresia complicates 1/10,000 live births and accounts for 25-40% of all intestinal atresias

17. Comorbidity Approximately 50% are premature
Nearly half have chromosome abnormalities; trisomy 21 up to 1/3 of patients
Esophageal atresia , 5-10%
Malrotation, 20-30%
Renal anomalies,5-15%
Skeletal malformation, 5%
Anorectal anomalies, 5%
Congenital heart disease , 30%
Annular pancreas, 30%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Esophageal atresia , 5-10%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Congenital heart disease , 30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Malrotation, 20-30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Annular pancreas, 30%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Renal anomalies,5-15%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
Anorectal anomalies, 5%
skeletal malformations (5%), and anorectal anomalies (5%).
Nearly half of patients with duodenal atresia have chromosome abnormalities; trisomy 21 is identified in up to one third of patients.
Skeletal malformation, 5%
Skeletal malformation, 5%
Skeletal malformation, 5%
Skeletal malformation, 5%
Skeletal malformation, 5%
Skeletal malformation, 5%
Skeletal malformation, 5%
Skeletal malformation, 5%
Skeletal malformation, 5%
Skeletal malformation, 5%
Skeletal malformation, 5%
Skeletal malformation, 5%
Skeletal malformation, 5%

18. Symptoms/Sign Bilious vomiting History of polyhydramnios
without abdominal distention, usually noted on the 1st day of life
History of polyhydramnios
In half the pregnancies
Fluid may be bile stained
Jaundice is present in one third of the infants.
Fluid may be bile stained due to intrauterine vomiting

19. Diagnosis “ Double bubble” sign
gas-filled stomach and proximal duodenum
Contrast studies are occasionally needed
Exclude malrotation and volvulus because intestinal infarction can occur within 6-12 hr
Contrast studies are generally not necessary and may be associated with aspiration.
Prenatal identification of duodenal atresia is associated with decreased morbidity and fewer hospitalization days
Prenatal diagnosis of duodenal atresia is readily made by fetal ultrasonography, which reveals a sonographic double-bubble.

20. Treatment Nasogastric or orogastric decompression
Echocardiography, renal ultrasound, and radiology of the chest and spine
The typical surgical repair for duodenal atresia is duodenoduodenostomy
Definitive correction of the atresia is usually postponed for life threatening anomalies
Long-term prognosis is excellent, approaching 90% survival in most series.