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

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Presentation on theme: "Acute Abdominal Pain In Children Hai Ho, M.D. Department of Family Practice."— Presentation transcript:

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

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

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

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 –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


26 Pyloromyotomy: laparoscopy

27 Postoperative management May be fed within 12-24 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

28 IntussusceptionIntussusception

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

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

34 Epidemiology Male:female – 3:2 Age – –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

36 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

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

40 Ultrasound Could detect ileoileal intussusception

41 Treatment? Air or contrast reduction –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

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

47 Midgut volvulus

48 Volvulus Cecal volvulus Sigmoid 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 UGI with SBFT Cork-screw pattern – barium flowing through restricted bowel lumen

53 Treatment: surgery

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