1. Acute Abdominal Pain In Children
Hai Ho, M.D.
Department of Family Practice

2. Pathophysiology of pain
Visceral pain
Mechanical – stretching
Chemical – mucosa
Aching and dull, poorly localized
Parietal pain
Sharp, well-localized

3. Pathophysiology of pain
Referred pain
Somatic and visceral afferent fibers enter the spinal close to each other
Localization of pain
Bilateral – most GI tract, midline pain
Unilateral – kidney, ureter, ovary, somatic
Ascending and descending colons – bilateral innervations, but predominately unilateral neural perception

4. History
Usual: quality, location, severity, associated symptoms, aggravating/alleviating factors
Kids cannot give a history
Dangerous signs given by parents

5. My history: the red flags
Duration – acute vs. chronic
Fever – inflammation, infection
Vomiting – stasis, obstruction, dehydration
Urine output – volume depletion
Diarrhea - bloody

6. Examination Usual: inspection, auscultation, percussion, palpitation
Rectal – rectocecal appendicitis, occult blood
Pelvic – PID
Scrotal - torsion

7. Tests?
Chemistry – electrolyte abnormality, BUN/creatinine, liver function test
CBC – infection, bleeding
Plain abdominal x-ray – free air, obstruction
Urinalysis – pyuria, hematuria
Pregnancy test

8. Pyloric stenosis

9. What is pyloric stenosis?
Hypertrophy of pylorus – thickening & elongation

10. Cause of pyloric stenosis?
Unknown
Associations
Abnormal muscle innervations
Erythromycin in neonates for pertussis postexposure prophylaxis
Infant hypergastrinemia

11. Epidemiology Prevelance – 3/1000
More common in white northern European descents
Male:female = 4:1 to 6:1
Age – 1 week – 5 months but usually 3 to 6 weeks
Does not occurs at birth

12. Clinical presentation?
Abdominal pain
Nonbilious vomiting after feeding and with 91% having projectile emesis
Distinguish pyloric stenosis from GER?

13. Clinical presentation?
Abdominal pain
Nonbilious vomiting after feeding and with 91% having projectile emesis
Hungry after feeding
Weight loss
Progressive symptoms

14. Clinical presentations
Jaundice
5% of affected patients
Indirect hyperbilirubinemia due to decreased level of glucuronyl transferase

15. Examination? Abdominal distension Olive mass – RUQ, after feeding
The mass is firm, movable, approximately 2 cm in length, olive shaped, hard, best palpated from the left side, and located above and to the right of the umbilicus in the mid epigastrium beneath the liver edge.

16. Examination
Gastric peristaltic wave from left to right after feeding

17. Tests?
Chemistry
Plain abdominal x-ray
Ultrasound
UGI

18. Chemistry? Decreased chloride
Elevated bicarbonate – metabolic alkalosis
± Hypokalemia
Elevated BUN and creatinine
±Elevated indirect bilirubin

19. Abdominal x-ray
Increased gastric air or fluid suggestive gastric outlet obstruction

20. Ultrasound Pyloric length > 15-19 mm Wall thickness > 3-4 mm
Pyloric diameter >10-14 mm

21. Ultrasound
Shoulder sign - indentation of pylorus into the stomach

22. UGI
String sign
Pyloric spasm may mimic the string sign

23. Treatment? Medical resuscitation first Pyloromyotomy
IVF hydration with potassium
Correction of alkalosis because of postoperative apnea associated with general anesthesia
Pyloromyotomy
Endoscopically-guided balloon dilation – surgery is contraindicated or incomplete pyloromyotomy

24. Pyloromyotomy

25. Pyloromyotomy

26. Pyloromyotomy: laparoscopy

27. Postoperative management
May be fed within hours, early as 4 hours post-op in one study
Vomiting
Not a reason to delay feeding
GER – up to 80% post-op
Consider UGI if vomiting persists > 5 days
Vomiting post-op may be due to edema

28. Intussusception

29. What is intussusception?
Invagination of intestine into itself

30. Pathophysiology
Proximal bowel telescopes into distal segment, dragging along mesentery
Compression of mesenteric vessels & lymphatics leads to edema, ischemia, mucosal bleeding, perforation, and peritonitis

31. Ileocolic intussusception

32. Causes of intussusception?
Idiopathic –
75% of ileocolic intussusception
More likely in children < 5
The incidence of intussusception has a seasonal variation, with peaks coinciding with seasonal gastroenteritis [2].     Intussusception has been associated with the rotavirus vaccine.     Approximately 30 percent of patients experienced otitis media, flu-like symptoms, or an upper respiratory tract infection prior to the onset of intussusception. Viral infections, including enteric adenovirus [3,4] and rotavirus [5], can accentuate lymphatic tissue in the intestinal tract, resulting in hypertrophy of Peyer patches in the lymphoid-rich terminal ileum, which potentially acts as a lead point for ileo-colic intussusception.
Small bowel intussusception may occur after an episode of Henoch-Schönlein, with a bowel wall hematoma acting as the lead point. In contrast, thick inspissated stool may act as the lead point for patients with cystic fibrosis, whereas patients with celiac disease may develop small bowel intussusception caused by the dysmotility and excessive secretion or bowel wall weakness [13]. Crohn disease can cause intussusception because of inflammation and stricture formation [14].

33. Causes of intussusception
Leading point
Hyperplasia of Peyer patches in terminal ileum
Structural: small bowel lymphoma, Meckel diverticulum
Systemic: cystic fibrosis, Henoch-Schönlein, Crohn disease
The incidence of intussusception has a seasonal variation, with peaks coinciding with seasonal gastroenteritis, spring and autumn     Intussusception has been associated with the rotavirus vaccine.     Approximately 30 percent of patients experienced otitis media, flu-like symptoms, or an upper respiratory tract infection prior to the onset of intussusception. Viral infections, including enteric adenovirus [3,4] and rotavirus [5], can accentuate lymphatic tissue in the intestinal tract, resulting in hypertrophy of Peyer patches in the lymphoid-rich terminal ileum, which potentially acts as a lead point for ileo-colic intussusception.
Small bowel intussusception may occur after an episode of Henoch-Schönlein, with a bowel wall hematoma acting as the lead point. In contrast, thick inspissated stool may act as the lead point for patients with cystic fibrosis, whereas patients with celiac disease may develop small bowel intussusception caused by the dysmotility and excessive secretion or bowel wall weakness [13]. Crohn disease can cause intussusception because of inflammation and stricture formation [14].

34. Epidemiology Male:female – 3:2 Age – Most common - ileocolic
3 months to 6 years with 80% < age 2
Peak at 6-12 months
Most common - ileocolic

35. Clinical manifestations?
Intermittent, severe, crampy abdominal pain with loud cry and in curled up position
Vomiting
Appear normal between attack
Currant-jelly stool
Vomiting – bilious in later stage

36. Mixture of blood and mucus
Currant-jelly stool
Mixture of blood and mucus
Foul smelling

37. Tests? Chemistry – dehydration, electrolyte imbalance CBC – infection
X-ray: plain film & contrast or air enema
Ultrasound
CT scan – only if other tests are negative
Contrast enema – air or radiographic agent
CT cannot be used to reduce the intussusception and can be time-consuming in children who may require sedation and thus, generally is reserved for patients in whom the other imaging modalities are unrevealing

38. X-ray : plain film

39. X-ray
Contrast material between the intussusceptum and the intussuscipiens is responsible for the coil-spring appearance
Use water-soluble agent prior to barium if high risk of perforation suspected
A central linear column of barium may be visible in the compressed lumen of the intussusceptum, and a thin rim of barium may be seen trapped around the invaginating intestine in the folds of mucosa within the intussuscipiens (coiled-spring sign), especially after evacuation.

40. Ultrasound Could detect ileoileal intussusception
An advantage of ultrasonography is that it can diagnose the rare ileoileal intussusception and identify the lead point of intussusception in approximately two-thirds of cases in which underlying pathology exists
Could detect ileoileal intussusception

41. Treatment? Air or contrast reduction Surgery
Air is better than barium reduction – less perforation <1%
Not very successful if symptoms > 24 – 48 hours or with bowel obstruction
Successful rate – 75-90% with ileocolic intussusception
Surgery

42. Reduction
Barium enema reduction of intussusception can be performed if no evidence of perforation exists. The standard method of reduction is to place a reservoir of barium 1 m above the patient so that constant hydrostatic pressure is generated. With experience (and depending upon the clinical status of the patient), a physician may undertake a more aggressive reduction.
Successful reduction is indicated by the free flow of contrast into the small bowel. Reduction is complete only when a good portion of the distal ileum is filled with barium, thus excluding ileo-ileal intussusception. Other indications of successful reduction include relief of symptoms and disappearance of the abdominal mass. A characteristic sound also may be appreciated with auscultation. In occasional patients, the contrast material does not reflux freely into the small bowel even with a complete reduction, but no filling defect in the cecum is present apart from the ileocecal valve and symptoms and signs of these patients resolve.

43. Surgery Manual reduction and end-to-end anastomosis Indications
Persistent filling defects
Failed nonoperative reduction
Prolonged intussusception

44. Recurrence
10%
Not necessary an indication for surgery

45. Malrotation & Volvulus

46. Normal development
The mechanism of intestinal obstruction with incomplete rotation of the midgut (malrotation). The dotted lines show the course the cecum should have taken. Failure to rotate has left obstructing bands across the duodenum and a narrow pedicle for the midgut loop, making it susceptible to volvulus. (From Nixon HH, O'Donnell B: The Essentials of Pediatric Surgery. Philadelphia, JB Lippincott, 1961.)
The gut starts as a straight tube from stomach to rectum. The midbowel (distal duodenum to midtransverse colon) begins to elongate and progressively protrudes into the umbilical cord until it lies totally outside the confines of the abdominal cavity. As the developing bowel rotates in and out of the abdominal cavity, the superior mesenteric artery, which supplies blood to this section of gut, acts as an axis. The duodenum, on re-entering the abdominal cavity, moves to the region of the ligament of Treitz, and the colon that follows is directed to the left upper quadrant. The cecum subsequently rotates counterclockwise within the abdominal cavity and comes to lie in the right lower quadrant. The duodenum becomes fixed to the posterior abdominal wall before the colon is completely rotated. After rotation, the right and left colon and the mesenteric root become fixed to the posterior abdomen. These attachments provide a broad base of support to the mesentery and the superior mesenteric artery, thus preventing twisting of the mesenteric root and kinking of the vascular supply. Abdominal rotation and attachment are completed by 3 mo gestation.

47. Midgut volvulus

48. Volvulus
Sigmoid volvulus
Cecal volvulus

49. Clinical presentation?
Bilious emesis
Abdominal distension

50. Tests? UGI- duodenum not crossing the midline
Barium enema – malposition of cecum

51. Abdominal series Gastric and duodenal bulb distention
Little air in intestine

52. Cork-screw pattern – barium flowing through restricted bowel lumen
UGI with SBFT
Cork-screw pattern – barium flowing through restricted bowel lumen

53. Treatment: surgery
Surgical intervention is recommended for any patient with a significant rotational abnormality, regardless of age. If a volvulus is present, it is reduced and the duodenum and upper jejunum are freed of any bands and remain in the right abdominal cavity. The colon is freed of adhesions and placed in the right abdomen with the cecum in the left lower quadrant, usually accompanied by incidental appendectomy. Extensive intestinal ischemia from volvulus produces the short-gut syndrome (see Chapter ). Persistent symptoms after repair of malrotation should suggest a pseudo-obstruction–like motility disorder.