03 Neonatal Em,AP and Intususc seminar .ppt

this presentation on neonatal EM, AP and intussception presentationthis presentation on neonatal EM, AP and intussception presentation

2. Acute Apendicitis
•Peak age 12-18 years
•Rare <5 years and extremely rare in < 3yrs
•Male > female
•Whites are more affected than blacks

3. Pathology
•Multiple etiologies
•Luminal obstruction with
–foreign body, lymphoid hyperplasia, parasites, Tumors/
•Followed by
–Increase intraluminal pressure
–lymphatic and venous congestion and edema
–impaired arterial perfusion
•Eventually leading to
–ischemia of the wall of the appendix,
–bacterial invasion with inflammatory infiltrate and
–necrosis

4. Clinical Pictures
•Malaise,
•Abdominal pain
–Initially peri umbilical and latter after 12-24hrs RUQ pain
•Nausea and vomiting
•Diarrhea and urinary incontinence
•After 30-40hrs,the risk of perforation is high
–Diffuse peritonitis
–Hypotension, oliguria, acidosis..

5. •Febrile, tachycardia….
•lie still, often with one or both hips flexed
•Peritoneal inflammation causes splinting, which reduces movement of the
anterior abdominal wall during normal breathing.
•Generalized abdominal tenderness with some rigidity.
•Local tenderness with some rigidity of the abdominal wall at RUQ is the most
reliable clinical sign of acute appendicitis that is present in school-aged
children and adolescents
•Rovsing's sign —Pain in the right lower quadrant on palpation of the left side
•Obturator sign —Pain on internal rotation of the right hip, which is seen
when the inflamed appendix lies in the pelvis
•Iliopsoas sign —Pain on extension of the right hip, which is found in
retrocecal appendicitis

6. Laboratory findings
•WBCand differcial
–Normal in early, high >20,000 after 48hrs
•CRP
•Urinalysis
•Plain abdominal x-rays may show
–sentinel loops of bowel and localized ileus,
–scoliosis from psoas muscle spasm,
–a colonic air-fluid level above the right iliac fossa (colon cutoff sign
•U/S-90 % sensitive
–wall thickness <6 mm, luminal distention, lack of compressibility, a
complex mass in the right lower quadrant, or a fecalith
•CT-gold standard-95% sensitive and specific
•MRI

7. Treatment
•Pre oprative care
–Fluid and electrolytes
–Analgesic
–Antibiotic prophylaxis
•Surgery-appendectomy
•Interval appendectomy
–For appendicitis complicated by an inflammatory mass or
abscess
–can be treated without immediate appendectomy
–Most cases of recurrent appendicitis develop within 2 yr of
the initial illness

8. Complication
•In simple acute appendicitis,complication rate of 5–10%
•In gangrenous or perforated appendicitis, the complication rate
rises to 15–30%
–wound infections and
–intra-abdominal abscesses; both are more common after perforation.
•Perforationrates are consistently >80% in children <5 yr of age.
•Mortality after appendicitis is rare (<0.3%) and seen mostly in
neonates and immunocompromised patients.
•Perforation and abscess formation can also lead to fistula
formation in adjacent organs.

9. Intussusception
•Intussusception occurs when a portion of the alimentary tract is
telescoped into an adjacent segment.
•It is the most common b/n 3 mo and 6 yr of age
–80% of the cases occur before 24 mo; it is rare in
neonates.
–Rare in neonates and immature infants
•Male: female ratio is 4:1

10. Etiology
•The cause of most intussusceptions is unknown.
•Predisposing factors-prior or concurrent respiratory adenovirus,
otitis media, gastroenteritis, Henoch-Schönlein
purpura, or upper respiratory tract
infections,rotavirus vaccine. Cystic fibrosis is another risk
factor
•In 2–8% of patients, recognizable lead points for the intussusception
are found, such as a Meckel diverticulum, intestinal polyp,
neurofibroma, intestinal duplication, hemangioma, or malignant
conditions such as lymphoma.
•Intussusceptioncan complicate mucosal hemorrhage, as
in Henoch-Schönlein purpura or hemophilia.
•Lead points are more common in children >2 yr of age.

11. Pathology
•Intussusceptions are most often ileocolic, less commonly cecocolic,
and rarely exclusively ileal.
•The upper portion of bowel, the intussusceptum, invaginatesinto
the lower, the intussuscipiens, pulling its mesentery along with it
into the enveloping loop.
•Constriction of the mesentery obstructs venous return;
engorgement of the intussusceptumfollows, with edema, and
bleeding from the mucosa leads to a bloody stool, sometimes
containing mucus.
•The apex of the intussusception can extend into the transverse,
descending, or sigmoid colon, even to and through the anus in
neglected cases.

12. Clinical features
•Typically develop the sudden onset of intermittent, severe,
crampy, progressive abdominal pain, accompanied by
inconsolable crying and drawing up of the legs toward the
abdomen.
–occur at 15 to 20 minuteintervals and become more frequent
and more severe over time.
–are comfortable and play normally between the paroxysms
of pain
•Vomiting ,initially non-bilious, but it may become bilious as the
obstruction progresses

13. •progressively the infant becomes weaker and
lethargic. Eventually develope a shock like state
with fever
–weak pulse
–shallow breathing and grunting, and
–pain may be manifested only by moaning sounds
•60% bloody stool with mucus, the currant jelly
stool

14. •In 30% ,tender sausage-shaped mass, sometimes
ill defined, which may increase in size and
firmness during a paroxysm of pain and is
–most often in the RUQ with its long axis
cephalocaudal
–in the epigastrium, the long axis is transverse.
•PR exam-blood in the finger is supportive
•Signs of intestinal obstruction
•Recurrent intussusception 5–8% and is more
common after hydrostatic than surgical
reduction.

15. Diagnosis
•Clinical/ history and physical exam/
•U/S-dognutshape or target sign or coilledspring in transverse
images
•Contrast enema
DDX
–Gastroenteritis
–Meckel’sdiverticulum
–Henoch-Schönleinpurpura

16. Treatment
•Reduction –early
•The success rate of radiologic hydrostatic reduction
under fluoroscopic or ultrasonic guidance
–≈50% if symptoms are present longer than 48 hr and
–70–90% if reduction is done in the 1st 48 hr.
•Bowel perforations occur
•Surgery
–manual operative reduction
–resection of the intussusception with end-to-end
anastomosis.

17. Prognosis
•Untreated intussusce-usually fatal
•Spontaneous reduction
•The recurrence rate
–after reduction of intussusceptions is ≈10%
–after open surgical reduction it is 2–5%;
–nonehas recurred after surgical resection.
•Corticosteroids may reduce the frequency
of recurrent intussusception.

18. Neonatal Emergencies
▫Duodenal, atresia/ stenosis
▫Malrotation& midgutvolvulus
▫Jejunal& ilealatresia/ stenosis

19. Congenital Intestinal Obstruction
Intestinal Atresia
Duodenal atresia
Ileal and jejunal atresia
Meconium Ileus
Malrotation and Volvulus
Hirschspung’s Disease
Imperforate Anus

20. Duodenal Atresia
Incidence
Most common site of neonatal intestinal obstruction
1 in 6,000 to 10,000 live births
75% of stenoses and 40% of atresias are found in
Duodenum
Multiple atresias in 15% of cases
50% pts are LBW and premature

21. Etiology
No specific genetic abnormality
Increase incidence in siblings
Has been shown to occur in several
generations of a family
Association with Trisomy 21

22. Associated Anomalies
Down Syndrome 28%
Annular pancreas 23%
Congenital heart disease 23%
Malrotation 20%
Esophageal atresia/TEF 9%
Genitourinary 8%
Anorectal 4%
Other bowel atresia 4%
None 45%

23. Pathology
Type I: The most common type is
formed by a membrane composed
of mucosa and submucosa and
obstructs the lumen.A variation is
the windsock deformity.
Type II: The atretic ends of the
duodenum are connected by a fibrous
cord.
Type III: Complete separation of the
atretic segments. Most biliary duct
anomalies are associated with this type.

24. Diagnosis
Prenatally
•Diagnosed in 32-57% of patients
•Dilated stomach bubble apparent by 3
rd
trimester
•Polyhydramnios in 32-59% of cases
Postnatally
•Symptoms usually appear within the first 24 hours
•Recognition of partial obstruction can be delayed
•Repeated bilious emesis is characteristic –85%
•Bilious emesis is a surgical emergency until proven
otherwise
•Nonbilious emesis is present when the atresia is above the
level where the bile duct enters the duodenum (papilla of
Vater)

25. Diagnosis
Radiologic studies
Plain radiograph of the abdomen
will generally confirm the
diagnosis with a finding of the
“double bubble sign
Upper GI series or barium enema
may be helpful to differentiate
from midgut volvulus

26. Management
NG tube
Intravenous fluid resuscitation
Electrolyte correction
If midgut volvulus has been ruled out, surgical
correction is not urgent
Surgery performed is a duodenoduodenostomy or
duodenojejunostomy
Can be performed laparoscopically

27. Post-operative Management
NPO
Replogle tube (10 Fr)
IV fluids /hyperalimentation
No feeds until return of bowel function

28. Complications
Early postoperative complications can be related to:
•Prematurity
•Coexisting congenital anomalies
•Parenteral nutrition
Anastomotic obstruction/stenosis
Anastomotic leak
Adhesions
Prolonged feeding intolerance
Duodenal dysmotility

29. Outcomes
Current survival rates are 90-95%
Higher mortality rates are associated with
prematurity and multiple congenital anomalies
Postoperative complications are reported to be 14-
18%

30. Jejunoileal Atresia
Incidence
Has been reported to be as high as 1/3000 live births
in the US
Wide variation in the reported incidence
Males = females
1/3 to ¼ of infants are low birth weight
Higher incidence in African-American infants
Increased risk with maternal use of
pseudoephedrinealone and in combination with
acetaminophen
Increased in mothers with migraine headaches
receiving ergotamine tartrate and caffeine

31. Etiology
Cause is unknown
Most likely associated with a late intrauterine
mesenteric vascular catastrophe
Has been associated with,
Volvulus,
Intussusception,
Internal hernia and
Constriction of the mesentery in a
tight gastroschisis or omphalocele

32. Associated anomalies
Gastroschisis/Omphalocele
Ascites
Cystic fibrosis
Malrotation and volvulus
Genitourinary

33. Pathology
Equally distributed between the jejunum (51%)
and the ileum (49%)
Atresia is usually single (>90%)
Multiple atresias more often involve the proximal
jejunum
Currently 5 classifications

34. Type I: Mucosal atresia with intact
bowel and mesenetery
TypeII: Blind ends separated by a
fibrous cord
Type III(a): Blind ends separated
by a V-shapemesenteric defect
Type III(b): Apple-peel atresia
Type IV: Multiple atresias (string
of sausages)

35. Diagnosis
Clinical Signs
•Polyhydramnios-more commonly seen in proximal
atresias
•Bilious emesis –surgical emergency until proven
otherwise
•Abdominal distension
•Jaundice
•Failure to pass meconium
Radiologic Studies
•Supine and erect abdominal films
•Contrast enema or UGI

36. Management
Replogle tube (10 Fr) to continuous suction
Intravenous fluids
Electrolyte correction
PICC line placement
Operative procedure depends on defect
•May require multiple anastomoses
•May require ostomy
•May require tapering of proximally dilated intestine

38. Postoperative Management
IV fluid resuscitation
NPO
Replogle (10 Fr) to suction
Clear liquids with return of bowel function
Advance to formula-medium chain triglyceride or
casein hydrolysate formulas should be offered
Malabsorption and diarrhea are common in infants:
•With short bowel length
•In whom the ileocecal valve has been resected
•With multiple atresias
•Apple peel atresia

39. Outcomes
Overall survival rates for jejunoileal atresia are
reported to range from 80-90%
Most common cause of early death
•Pneumonia
•Peritonitis
•Sepsis
Postoperative complications
•Intestinal obstruction at the anastomosis
•Anastomotic leak

40. Outcomes
Factors affecting morbidity and mortality
•Associated anomalies
•Short bowel syndrome
•Prematurity
•Respiratory distress

41. Intestinal Malrotation and Volvulus
Incidence
Occurs in 1/500 live births
Male to female ration is 2:1 in neonatal
presentation
No sexual predilection in patients over 1 year
As many as 40% present within the first week
50% present by 1 month
75% present by 1 year

42. Etiology
Rotation and fixation of the intestine takes place
during the first 3 months of gestation
As rotation begins, the intestine moves outside the
abdomen
At 10 weeks of gestastional age the intestine
returns to the abdomen
Normal mesenteric attachment extends from
the ligament of Treitz to the cecum
Ascending and descending colon are fixed
retroperitoneally

43. Etiology
Malrotationis when the normal process of rotation
is arrested or deviated at various stages
Anomalous fixation may also occur
Dense fibrous bands extending from the cecum
and right colon across the duodenum to the
retroperitoneum may form –Ladd’s Bands

44. Pathology
Midgut may be supported by a narrow pedicle that
contains the entire blood supply
Narrow pedicle predisposes the bowel to a clockwise
twisting from the duodenum to the transverse colon
Distension and peristalsis may initiate torsion of the
intestine on the pedicle –Volvulus
Acute midgut volvulus occurs when the blood supply to
the midgut is disrupted by the torsion
Vascular obstruction and necrosis of the complete midgut
develops rapidly
Ladd’s Bands can cause a mechanical duodenal
obstruction without vascular compromise

45. Associated Anomalies
Are found in 30 to 60% of patients
Malrotationis almost always associated with
•Diaphragmatic hernia
•Omphalocele/gastroschisis
•Prune belly syndrome
Can be associated with
•Duodenal atresia
•Ileal atresia
•Meconium ileus
•Congenital heart disease
•Imperforate anus
•Annular pancreas
•Biliary atresia

46. Diagnosis
Clinical symptoms
•Most frequent symptom is bilious emesis
•Pain and irritability in the toddler or older child
•Abdomen is soft and non-tender to palpation initially
•Becomes distended and tender with strangulation of bowel
•Stool may be bloodstained
Radiologic studies
•Abdominal radiographs may show a dilated duodenem with a
fluid level, however can be read as normal in 20% of cases
•Barium enema is unreliable –position of cecum varies

47. Diagnosis
Radiologic studies
•Upper GI series with small bowel follow
through is the most reliable –96%
specificity in one report
Dilated duodenum with a typical corkscrew
appearance
Absence of Ligament of Treitz
Small bowel on right side of abdomen
UGI may be misleading if duodenal obstruction
is complete (also seen with duodenal atresia)

48. Management
Once the diagnosis is made on a symptomatic child,
the patient should be taken to the operating room
immediately
Ladd’s procedure is performed
•Derotation of the bowel
•Division of the Ladd’s bands if present
•Widening the small bowel mesentary by lysis of
congenital adhesions
•Return the bowel to a position of nonrotation
•Appendectomy

49. Management
If ischemic bowel is present every attempt to
preserve bowel length should be made
Bowel is not surgically fixed into position
Procedure may also be done laparoscopically

50. Outcomes
Mortality rate with midgut volvulus is at least 15%
Return of bowel function is dependent upon
duration of obstruction and extent of
compromise
High incidence of short gut syndrome
Recurrent obstructions are rare
Higher incidence of intussusception post op than
with laparotomies for other reasons ~3%

51. Thank you!