1. Disorders of the Gastrointestinal Function Chapter 31

2. GI Dysfunction Primary function off the GI tract is the absorption & metabolism of nutrients necessary to support & promote optimal growth and development An alteration in GI function can affect other body systems

3. Cleft Lip & Palate Facial malformations that occur during embryologic development More common seen in combination Incidence is 1 in 1000 live births

4. Cleft Lip & Palate Etiology –Cleft lip Due to a failure of the medial nasal & maxillary processes to join Unilateral or bilateral Associated with abnormal development of the external nose, nasal cartilage, & nasal septum

5. Cleft Lip & Palate Etiology –Cleft palate Failure of the palatal shelves to fuse Mat be the soft palate or extend into the hard palate Multifactorial inheritance Folklore

6. Cleft Lip & Palate Clinical manifestations –Feeding may not be difficult if palate intact –Extensive ones Feeding difficulties Ineffective suck Saliva & feedings may leak into the nasal cavity Speech can be delayed or hypernasal Recurrent OM Psychologic difficulties

7. Cleft Lip & Palate Diagnostic tests –Apparent at birth Medical management –Cleft lip Z-plasty – performed at 1 or 2 months of age –Cleft palate Repaired before 1 year of age

8. Cleft Lip & Palate Nursing interventions –Ensure adequate nutrition –Prevent aspiration –Special feeding devices are used –Frequent burping –Promote bonding

9. Cleft Lip & Palate Nursing –Post op Protect the integrity of the suture line –Cleft lip – position on side & back only –SRDs –NPO & then fed with Breck feeder –Suture line gently cleansed with a saline soaked cotton swab –Infant chair or on right side –Aspiration of oral & nasopharyngeal cavities

10. Cleft Lip & Palate Post op –Cleft palate Allowed to lie on abdomen Analgesics Liquids by cups Straws, pacifiers, and eating utensils are avoided Advanced to a blenderized diet

11. Cleft Lip & Palate Patient teaching –Educate –Refer parents to Cleft Palate Foundation & March of Dimes Prognosis –Some degree of speech impairment –Recurrent OM –Hearing impairment

12. Dehydration Body loses more fluid than it absorbs or when it absorbs less water than it excretes Total fluid intake is less than the total fluid output Mild – 5% Moderate – 10% Severe – 15%

13. Dehydration Etiology –Result of a number of disease processes that cause abnormal losses through the skin, respiratory, renal, & (most commonly) GI systems

14. Dehydration Clinical manifestations –Skin – Cold, dry, gray, loss of turgor –Mucous membranes - Dry –Eyes – Sunken –Fontanels – Sunken –Behavior - Lethargic –Pulse – Rapid, weak –Blood pressure – Low –Respirations - Rapid

15. Dehydration Diagnostic tests –Observed clinical manifestations –Determine severity Serum sodium Serum glucose Serum bicarbonate BUN –Weighing daily

16. Dehydration Medical management –Same as diarrhea Nursing –Clinical assessment –I&O –Vital signs & so forth –Teach parents – more vulnerable to fluid & electrolyte imbalances

17. Dehydration Prognosis –Shock – severe depletion –Favorable with effective management

18. Diarrhea & Gastroenteritis One of the most common disorders affecting children Can see fluid deficits & electrolyte imbalances Disturbance in intestinal motility, characterized by an increase in frequency, fluid content, & volume of stools Acute or chronic Infectious or non infectious

19. Diarrhea Etiology –Most common – bacterial or viral invasions –Bacterial Salmonella Shigella Campylobacter jejuni Yersinia enterocolitica Rotavirus Giardia lamblia –Infants have a greater susceptibility –More serious –More prone Malnourished Debilitated Immunocompromised

20. Diarrhea Etiology –Poor hygiene –Contaminated food or water –Warm weather –Crowded & substandard living conditions –Large quantities of fruit juices –Food sensitivities –Antibiotics –Formula intolerance

21. Diarrhea Pathogen invades the intestinal mucosa, the resulting enterotoxins stimulate an inflammatory response Water & electrolytes are secreted & there is an invasion & destruction of the epithelial cells of the GI mucosa

22. Diarrhea Clinical manifestations –Cool, pale skin –Lethargy –Sunken eyes –Sunken fontanelles –Poor skin turgor –Rapid pulse & respirations –Low blood pressure –Normal or elevated temperature –Irritability progressing to lethargy –Weight loss –Vomiting –Malodorous stools Watch for dehydration

23. Diarrhea Medical management –Restore fluid & electrolyte imbalances –Treat underlying cause –AAP – no longer recommends withholding food or fluids for 24 hrs or administering the BRAT diet –Oral rehydration solution – small amounts

24. Diarrhea Medical management –Oral maintenance solution –Number of stools & fluid content have decreased – advanced to full strength formula –Rehydration complete offer solid foods Non irritating foods – bananas, rice, applesauce, cereal, vegetable juice, crackers, pretzels, & toast (modified BRAT diet)

25. Diarrhea Severe diarrhea –Hospitalization & IV therapy Saline solution with 5% dextrose Add potassium as needed - check kidney function Continue until diarrhea improves Detect & treat underlying cause

26. Diarrhea Nursing/Patient teaching –Assessment I&O Promotion of rehydration Correction of electrolyte imbalances Nutrition Prevention of the spread Support Nursing diagnoses –Fluid volume, deficit –Skin integrity, impaired –Anxiety Avoid use of anti diarrheals Wash hands Proper disposal/cleaning of soiled diapers & linens

27. Diarrhea Prognosis –Mild or moderate – managed at home –Severe – hospitalization –Excellent

28. Constipation Passage of hardened stools associated with failure of complete evacuation of the colon with defecation Primary disorder or in association with other disorders

29. Constipation Etiology –Any age –Newborn – failure to pass meconium may indicate – intestinal atresia or stenosis, Hirschprung’s disease, meconium ileus, or meconium plug –Formula fed infants – high fat or protein content or inadequate fluid in the formula

30. Constipation Etiology –Children – environmental factor (meds) or learned repression of the urge to defecate –Continuous repression results in dilation of the rectum, reduced sensation of the need to defecate, decreased muscle tone in the lower rectum

31. Constipation Clinical manifestations –Infancy – hard stools & fresh blood in the stools –Children – cramping, abdominal pain, anal fissures, pain on defecation, loss of appetite, & irritability Diagnostic test –Careful history –Examination of anus & rectum

32. Constipation Medical management –Newborn – alleviate the problem Modifying formula –Older infants – adding food with bulk –Manually dilate the sphincter –Mild laxatives or enemas – to completely empty the rectum Instituting dietary modifications –Treatment of chronic constipation Complete evacuation & toilet retraining therapy

33. Constipation Nursing/Patient teaching –Careful history –Educate on diet modifications –Educate on normal stool patterns –Discuss their expectations & attitudes –Avoid honey & corn syrup in infants

34. Constipation Prognosis –Simple measures ordinarily correct –Successful resolution Depends on age & underlying cause Counseling & bowel retraining

35. Gastroesophageal Reflux Effortless regurgitation of the gastric contents into the esophagus Usually begins within 1 week of birth Immediately after feeding or when infant is laid down Most common cause of vomiting in infancy

36. GER Etiology –Primarily due to an incompetent lower esophageal sphincter –Gastric contents are allowed to regurgitate into the esophagus

37. GER Clinical manifestations –Vomiting or spitting up –Aspiration can lead to respiratory signs & aspiration pneumonia –Growth & weight gain are a problem –Continuous irritation of the esophageal lining – esophageal ulceration Anemia Hematemesis Blood in stools

38. GER Diagnostic tests –History & growth measurements –Barium esophagography –Esophageal probe – measure pH –Upper endoscopy –Esophageal Scintigraphy

39. GER Medical management –Small, frequent feedings thickened with infant cereal –Positioning –Pharmacologic intervention Cimetidine, ranitidine, famotidine Metoclopramide –Nissen fundoplication Wrapping the fundus of the stomach around the distal esophagus to prevent reflux

40. GER Nursing/Patient teaching –Recognition of these infants –Provide care for infant needing surgery –Emotional reassurance –Educate parents

41. GER Mild GER –Normal function by 6 to 7 weeks –90% improve by 1 year of age – require only medical therapy Severe –Unsuccessfully treated Esophageal strictures Recurrent respiratory distress with aspiration pneumonia

42. Hypertrophic Pyloric Stenosis Obstructive disorder in which the gastric outlet is mechanically obstructed by a congenitally hypertrophied pyloric muscle Most common reason for an abdominal operation during the first 6 months of life Males 3-4 times more likely to be affected

43. HPS Etiology –Cause – unknown –Increased incidence in siblings & offspring of affected persons –Muscle becomes diffusely enlarged as the result of hypertrophy & hyperplasia –Difficult for the stomach to empty –4-6 weeks – vomit almost immediately after feedings –Grows more forceful & projectile

44. HPS Clinical manifestations –Regurgitation that progresses to projectile vomiting –Lethargy, weight loss, poor skin turgor, sunken fontanelles, & loss of subcutaneous tissue –Dehydration

45. HPS Diagnostic tests –Examination of the abdomen Visible peristaltic waves – move from left to right across the epigastric region Palpation of an olive shaped mass - right of the midline –Upper GI radiographic –Ultrasound

46. HPS Medical management –Surgical relief – done as soon as diagnosed –Pyloromyotomy – surgically splitting the pylorus muscle down to the submucosa, allowing for a larger lumen

47. HPS Nursing Interventions –Assist with diagnosis –Provide adequate nutrition –Manage preop & postop care Correct any metabolic disturbances & dehydration Prevent complications postop –Supporting the family Caused by a structural problem

48. HPS Prognosis –Recover completely & rapidly –Postoperative complications Persistent pyloric obstruction Wound dehiscence 15% have GER

49. Intussusception Most common cause of intestinal obstruction in children between 3 months and 6 years of age Twice as common in males Generally cause is not known

50. Intussusception Etiology –Result of telescoping one portion of the intestine into another –Most common site – ileocecal valve –Passage of intestinal contents becomes obstructed –Hallmark sign – currant jelly stools Mucosa of intestinal walls rub against each other, blood & mucus from the mucosa leak into the intestinal lumen

51. Intussusception Serious complications –Peritonitis –Intestinal ischemia –Infarction –Perforation –Shock Condition untreated – death can occur within 2 to 5 days

52. Intussusception Clinical manifestations –Sudden onset of severe abdominal pain –Vomiting & lethargy –Within 12 hours – pass currant jelly stools

53. Intussusception Diagnostic tests –History & physical signs –Definitive – barium enema – reveal obstruction to the flow of barium –Digital exam – reveals blood & mucus

54. Intussusception Medical management –Hydrostatic reduction using barium Force exerted by flowing barium may successfully force the telescoped portion of bowel into the correct position –Surgical treatment Manual reduction of the invagination & if needed resection of non viable bowel with end to end anastomosis

55. Intussusception Nursing intervention –Obtain a thorough history & observe physical signs –Educate on diagnostics and if possible surgery –After watch for the return of normal bowel movements/watched for 24 hours –Postoperative VS Operative site Assess for return of bowel sounds

56. Intussusception Prognosis –Many patients treated with hydrostatic reduction –If untreated – 90% will worsen or die –Treated – serious complications & death are rare

57. Hirschsprung’s Disease Megacolon –Functional intestinal obstruction caused by the absence of parasympathetic ganglion cells in a portion of the colon –Predominance in males –More common in children with Trisomy 21 –Small number follow a familial pattern

58. Hirschsprung’s Etiology –Absence of innervation to a segment of the bowel –Most cases – lower portion of the sigmoid colon just above the anus affected –No peristaltic waves in affected portion to propel fecal contents - causes an intestinal obstruction & distention of the bowel proximal to the defect

59. Hirschsprung’s Clinical manifestations –Vary according to age –Neonates Diagnosed early with failure to pass meconium Partial or complete intestinal obstruction – abdominal distention, vomiting & poor feeding –Infants History of constipation or intermittent constipation & diarrhea –Infants Dehydration, failure to thrive, abdominal distention, & fever –Older child Chronic constipation – abdominal distention, ribbon like, foul smelling stools, poor wt gain, malnourishment, anemia, palpable fecal mass, & visible peristalsis

60. Hirschsprung’s Diagnostic tests –History –Clinical manifestations –Barium enema

61. Hirschsprung’s Medical management –Immediate treatment Surgical removal of affected portion Two stages –1 st - Placement of temporary colostomy – in portion of normal colon just proximal to the defect –Period of rest – to regain tone –2 nd – excising the affected segment –Pull the normal innervated segment down through the anus, anastomosing it to the anal canal –Soave endorectal pull through – performed when child reaches 20 pounds

62. Hirschsprung’s Nursing interventions –Assist parents –Educate –Preoperative Restore nutritional status – low fiber, high protein, high calorie diet May need daily enemas & stool softeners Abdominal girths Prepare & educate parents

63. Hirschsprung’s Postoperative –VS & BS –Passage of flatus & stools –Operative site –NG removed with peristalsis –Regular diet for age –Colostomy care

64. Hirschsprung’s Prognosis –Most require surgery –Stabilize & then do colostomy – very successful –After closure – able to attain satisfactory defecatory function