Neonatal acute abdomen

2.  One of surgical emergencies in neonates
 May include
- Intestinal obstruction
- Necrotising Enterocolitis
- Intussusception
- GI perforation in a newborn

3.  Sepsis & ileus – bilious vomitting & abdominal
distension (most important non-surgical
cause)
 Intracranial lesions – Hydrocephalus &
subdural hemorrhage
 Renal Dx with uremia - renal agenesis,
polycystic Dx.

4.  Bilious vomiting – always abnormal. NB! Until
proven otherwise it’s a malrotation and/or
volvulus
 Abdominal distension (scaphoid possible)
 Delayed, scanty, or no meconium
• Polyhydramnios in mother
• Downs Syndrome
• Family history (HSD, DM mother, jejunal
atresia)

5.  High Obstruction
• Gastric outlet
• Duodenal
• Jejunal
 Low obstruction
• Distal small bowel
• Colonic
 Congenital (bowel atresias & stenoses; HSD;
Meconium Ileus)
 Acquired (pyloric stenosis, malrotation &
midgut volvulus, hernias)

6.  Intrinsic developmental defects
 Insults acquired in utero, after the formation
of normal bowel
 Abnormalities of peristalsis and/or abnormal
intestinal contents.

7. 1. Plain abdominal X-Rays.
 Complete high obstruction – no gas in distal
small bowel
 Low obstruction – many gas filled loops
(24hrs)
 May be non specific – malrotation

11. 2. Contrast enema – differentiates types of low
IO. (meconium plug, HSD)
3. Upper GI series – procedure of choice to
diagnose malrotation
4. Rectal biopsy – HSD (suction biopsy & full
thickness)

12.  Diagnose early to prevent clinical
deterioration, aspiration pneumonia, sepsis &
biochem & hematological derangements.
 Surgery …… once preliminaries done
- Resuscitation
- NGT
- Baseline labs
- Discuss with parents & consent for OT.

14.  1:1000 live births
 Risk factors
– prematurity and low birth weight. 750-1000g
have highest incidence.
- Infant related (perinatal asphyxia, congenital
heart disease. Etc)
- Maternal related (pre-eclampsia, prolonged
PROM, drugs)

16.  Inappropriate inflammatory response to an
insult -> injury & disruption of epithelial
barrier -> bacterial translocation ->
activation of host immune system -> release
of cytokines -> global & detrimental immune
response

17.  NEC may be
- Focal (isolated) disease : single area of
the bowel is necrotic or perforated
-Multifocal disease : multisegmental
disease with > 50% viable
- NEC totalis : necrosis of at least 75% of
the gut

18.  NEC - mucosal disease
that extends well into the
normal intestine
 Terminal ileum,
ascending & transverse
colon commonly affected
 The disease can occur
anywhere from stomach
to rectum

19.  Onset may be sudden or insidious in nature
 The clinical course can vary from a slow, indolent
process to one that progresses rapidly to death
in a few hours
 Nonspecific findings:
◦ lethargy,
◦ temperature instability,
◦ recurrent apnea,
◦ bradycardia,
◦ hypoglycemia, and
◦ shock

20.  More specific GI symptoms:
◦ abdominal distention (70% to 98%),
◦ blood per rectum (79% to 86%),
◦ vomiting (>70%), and
◦ Diarrhoea (4% to 26%).
◦ Gross blood in the stool is present in 25%
◦ occult blood in 22% to 59%.
 Rectal bleeding is seldom massive

21.  Bowel distension
 Pneumatosis intestinalis – intramural gas
 Portal vein gas
 Pneumoperitoneum

22.  Pneumatosis
intestinalis with air
over the liver shadow
dispersed within the
radicles of the portal
venous system

23.  Portal venous gas and
pneumatosis

24. STAGE CLINICAL X-RAY TREATMENT
I. SUSPECT
NEC
-Mild
abdominal
distention
-Poor feeding
-Emesis
-Mild ileus -Medical
workup for
sepsis
II. DEFINITE
NEC
-The above plus
-Marked
abdominal
distention
-GI bleeding
-Significant ileus
-Pneumatosis
intestinalis
-PVG
Medical
III. ADVANCED
NEC
-The above plus
-Unstable vital
signs
-Septic shock
Pneumoperitoneum Surgical

25.  Nonoperative Therapy is the initial
management
 Commence immediately upon suspicion of
the diagnosis of NEC
 The goals of medical management
include restoration of tissue perfusion,
control of infection or sepsis
careful observation for evidence of
intestinal gangrene or perforation.

26.  NEC without necrosis or perforation –
Treatment is supportive
 Keep NPO – Discontinue feeding
 Gastric tube - decompression
 Commence IVF resuscitation
 Commence Antibiotics
 Consider Empirical antifungal if clinical
course is prolonged

27. Absolute indication
1. Pneumoperitoneum
Relative indication
2. Clinical deterioration despite adequate therapy
a. Erythema and oedema of abdominal wall
b. Abdominal mass
c. Signs of peritonitis
d. Increasing acidosis
e. Persistent and progressive thrombocytopenia

29.  Idiopathic :
- 10days after URTI or GE
- Change from breast to bottle feeds
- Increase in lymphoid tissue mass (Peyers
Patches) – most likely cause
- Seasonal variation, higher in spring &
summer
- Viruses may play a role (rotavirus; associated
with vaccination)

30.  Lead Point
- Seen in older children.
- E.g Meckels diverticulum, enlarged LN,
polyps.
- Lead points initiate intussusception on a
mechanical basis
 Postoperative
- 2-5days postop, painless, observation, NG
aspiration is done. May self limit.

31.  Well nourished/ fat children 3-18months.
 Sudden onset ‘colicky’ abdominal pain,
associated vomiting.
 ‘Red currant jelly’ stool
 Dehydration/shock
 Palpable mass ‘sausage like’ (may palpate in
rectum – DRE)
 Intussusceptum may prolapse out of rectum

32. 1. Abdominal Xray :
- Signs of obstruction
- May see a mass
2. Contrast enema:
- Barium or gas may be used.
3. U/S scan.

34. Donut-like. “Target
lesion” “pseudo kidney”
Invagination seen. “

35.  Resuscitation !!! Massive third space loss
 NGT
 Antibiotics (Penicillin, Aminoglycoside,
metronidazole)
 Resuscitate before contrast enema, and prior
to reduction
 Sedation/analgesia. pethidine

36.  Reduction
- Enema reduction
- Pneumatic/ Hydrostatic reduction
Contra-indications:
Shock, septicemia, peritonitis, perforation,
Intestinal infarction, chronic obstruction.

37.  Surgical management
- When reduction unsuccessful
- Peritonitis
- Perforation

39.  THANKYOU FOR YOUR
ATTENTION!