Case Presentation: Antenatal USS significance? · Case Presentation ... The presence of IUGR or elevated maternal serum alpha-fetoprotein in the second trimester in association with

Case

Presentation:

Antenatal USS

significance? By

Thomas Cromarty

ST2

Introduction

Case Presentation

South Africa bites to break it up

Topic learning

Summary

Background 35+3, Primigravida

SROM 36hrs

Steroids (bethamthosone) 2nd dose 13.3 0500

Born @ 2249

Grade I Meconium

No maternal High Temp/Tacchycardia

Mat WCC 21.6, CRP 49. (Erythromycin PO x2)

CMV and CF negative

A/N Bloods – Rubella susceptible (otherwise NAD)

Mum non smoker, no alcohol

Asthma

Surestart

Background

Antenatal Scans 25week

Dilated loop of bowel with maximum diameter of 14mm

Some echogenic bowel noted

31week

Normal growth

No polyhydramnios

Bowel dilation 10.9mm Some areas of echogenic bowel

EDF +ve

Due to see the surgeons on Monday and fetal medicne @ 36 weeks

Delivery

Born by SVD in a good condition

No resus required

HR>100 throghout

Regular Respiration <1min

Normal palate, anus, spine

PREM, PROM, Raised Mat CRP

IV ABX for presumed sepsis

LBW and Mec obs

GI Management

Neonatal and SHO & Reg reviewed Hx

No documentation of FU/Mx

Reg discussed with Surgical Reg ~ 00.00

Continue with normal neonatal care

Feed early as per usual

No dysmorphic features

Transitional Care Unit Day 1

Feeding well via bottle, some small vomits

PU

Otherwise examines well systemically

Soft, non distended, non tender, BS +ve

R/v at 24 hours old Completed hypoglycaemia protocol

3 hourly bottle feeds, few small vomits

NBO

Normal examination

TCU

Day 2 (36 hours of age)

NBO

1x green vomit

Vomiting after each feed (milky)

Abdo exam

?tinkling bowel sounds?

AXR @ 37 hours age

There is gross dilatation of the stomach, duodenum and proximal jejunum. There is no gas seen distally. Appearances are in keeping with Jejunal atresia. No evidence of perforation.

Referred to Surgical Team

Day 2

Admitted to SCBU @ 40 hours of age.

NBM

NGT on free drainage

Surgical r/v

Day 3 - Surgical r/v

2x mucous plugs passed following PR

Testes descended bilaterally

?Small Bowel Atresia

Repeat Xray (no change)

Surgery @1300 on 16.3.14

(62 hours of age)

Fresh blood in abdomen (15-20ml)

Very Dilated twisted duodenojejunal loop (blind ending)

Apple peel atresia with nonviable (proximal part)

Absent Right & Transverse colon/Appedix/IC valve

Descending (Left)colon patent but curled

Ladd’s band twisting the D2-D3 creating a blind end.

• Non viable

bowel

removed

• Bowel

untwisted &

straightened

• Anastomoses

A-B & C-D.

Small bowel

length – 55cm

No Ileo-caecal

valve

Post op complication

Not passed urine since operation (12 hrs)

Catheter passed, balloon inflated but ?not in

bladder.

Balloon deflated and fresh blood into

catheter. Catheter removed.

Post op information

Operation D3

Triple ABX (Gent, Co-Amox, Metroni)

TPN initiated (Standard initially)

PICC Day 5 (Prescribed TPN Day 6)

Extubated Day 7 to SVIA

Day 9 – completed 5/7 triple ABX

Trophic feeds 1ml hourly initiated Day 11

BO with Meconium on Day 12

Day 14 – Up to 3ml hourly

2x Vomits with green aspirates (up to 8mls)

Day 15 – Returned to low reflux

Echogenic Bowel First described in 1985

Poorly understood, Consequences for parents, obstetricians, radiologists,

neonatologists and paediatric surgeons.

Definition:

Foetal bowel with homogenous areas of

echogenicity equal to or greater than

surrounding bone. It can be focal or

multifocal.

There is associated considerable debate as

there is much intraobserver variability. Difficult to introduce objective measures

Echogenic Bowel

Timing

Physiological midgut herniation in the first

trimester precludes assessment of foetal

bowel in the first trimester.

In normal foetuses, it is a rare finding in T2 and

resolves with no adverse sequelae.

<20/40 usually transient, disappearing on

serial scans during the next few weeks

Foetal bowel is often echogenic in the third

trimester and is not considered to be clinically

significant.

It is often considered a soft sign for

aneuploidic anomalies.

Incidence

Echogenic bowel is present in 0-6% to 1-4% of

all second trimester foetuses.

Foetal small bowel becomes progressively

more visible by ultrasound scan during the

second trimester as relatively ‘bright’

meconium accumulates within its lumen from

about 16 weeks’ gestation.

Persistently hyper echogenic small bowel in

the third trimester is more likely to reflect

underlying pathology even though a normal

outcome is still possible.

Differential Diagnosis

35% of foetuses with echogenic bowel will

have underlying pathology (65% Normal)

1. Foetal aneuploidy Most commonly Trisomy 21: (bowel

hypotonia)

Includes Trisomy 13,18 and the sex

chromosomes

Isolated finding in 9% of foetuses with

aneuploidy.

2. Non chromosomal

Cystic fibrosis risk 2%: (meconium)

Congenital infection: CMV, Toxoplasmosis,

Parvovirus

Intra-amniotic bleeding: swallowing of blood Congenital malformations of the bowel: atresia,

perforation, meconium.

3. IUGR and increased risk perinatal morbidity and mortality: (mesenteric ischemia)

4. Other: foetal alcohol syndrome, alpha

thalassaemia homozygous

Differential Diagnosis

Relevant PMHx

Past obstetric history and any anomalies

Any family history of note. In particular

cystic fibrosis, aneuploidy, syndromes

History of bleeding (swallowed blood)

Viral/bacterial illness

A prior risk for aneuploidy

Scanning: Isolated or Other

Structural Anomalies

Detailed review of anatomy, growth and

placenta

Assess markers for aneuploidy Other major structural abnormality

Nuchal thickening Short femur / humerus

Intracardiac echogenic foci

Hypoplastic/absent nasal bone

Mild foetal pyelectasis Choroid plexus cyst

Assess markers of infection

Microcephaly, ventriculomegaly,

calcifications

Hydrops

IUGR

Scanning: Isolated or Other

Structural Anomalies

Investigation Amniocentesis

Karyotype

PCR for virology: Toxoplasma, Rubella,

Parvovirus, CMV DNA analysis: Cystic fibrosis

Maternal factors Virology screen : Toxoplasma, Rubella,

Parvovirus, CMV

Maternal AFP (associated IUGR)

Parental cystic fibrosis carrier status

screening detects 80% of carriers.

Not all mutations can be identified and this

does not exclude the possibility.

Main Causes (5)

Mechanism: Hypoperistalsis and/or decreased fluid content of the

meconium.

Foetal aneuploidy mostly Trisomy 21 (trisomy

18/13, Turner’s syndrome and triploidy)

It is thought to be due to decreased bowel motility

with increased water absorption from the meconium.

There appears to be decreased microvillar enzymes

activity in the amniotic fluid of aneuploid fetuses.

Causes

Small bowel obstruction proximally

(especially duodenal atresia) can

produce hyper echogenic bowel

by reducing the meconium fluid content.

Oligohydramnios.

due to decreased amniotic fluid content of

meconium.

Causes Hirschsprung’s disease (increased

frequency in foetuses with Down

syndrome) due to hypoperistalsis.

Intra-amniotic haemorrhage Swallowed blood products result in a

hypercellular meconium, probably with small

clots within the bowel lumen which is very

echogenic.

Bowel atresia. Decreased amniotic fluid content of the

meconium.

Causes – Cystic Fibrosis 0.8% - 13.3% of foetuses with echogenic

CF

Echogenic bowel in 50% to 78%

Abnormalities in pancreatic enzyme

secretion changes in meconium

consistency.

Focal echogenic bowel with calcifications

A hyper echoic mass

Bowel dilation.

Causes - IUGR

IUGR

Most don’t have echogenic bowel.

The suggested mechanism is bowel ischemia due

to haemodynamic redistribution and subsequent

mesenteric ischemia.

The presence of IUGR or elevated maternal serum

alpha-fetoprotein in the second trimester in

association with echogenic bowel seems to be

associated with a particularly poor foetal

prognosis.

Other Rarer Causes

Viral Infections 0% to 10%

Cytomegalovirus (Most common)

Toxoplasmosis

Parvovirus Mechanism is unclear, ?caused by direct

intestinal damage from inflammation or

meconium peritonitis or indirectly by ascites,

anaemia, or growth restriction

Thalassemia

Outcomes

5 large North American Studies combined

60% had no abnormalities

Aneuploidy (3-27%)

IUGR in 15%

Rare mechanical associations

Congenital infections

Antenatal haemorrhage

CF

Management

Detailed parental history

?links with karyotype anomalies, intrauterine

infection, and CF.

Complete USS to exclude associated

structural problems

Serial ultrasound assessments

Persistently hyper echogenic bowel

Especially those with IUGR and/or

documented abnormalities of umbilical

artery blood flow are at risk of functional

neonatal intestinal obstruction.

Prognosis

Usually resolves but still requires

investigation

Better prognosis if does resolve but

underlying disease still present in 15%

Outcome in those with no prenatal

diagnosis – probably normal, no clear

evidence long-term bowel problems

Summary

Algorithm

Main causes

1. Intra-amniotic bleeding

2. Cystic Fibrosis

3. Aneuploidy

4. Congenital Infection

5. Primary GI pathology

?Associated with IUGR