GASTROINTESTINAL DYSFUNCTION IN CHILDREN.pptx

explaining the gastrointestinal dysfunction in children

1. GASTROINTESTINAL DYSFUNCTION IN CHILDREN

2. Presented to: Mam ZAHRA AZIZ Presented by : GROUP 6

3. GROUP MEMBER’S NAME

4. OBJECTIVES: At the end of the presentation the learners will be able to:

5. Structural Defects Cleft lip Cleft lip is a birth defect in which a baby's upper lip doesn't form completely and has an opening in it . Cleft pala t Cleft palate is a birth defect in which a baby's palate (roof of the mouth) doesn't form completely and has an opening in it. These birth defects are called oral clefts or orofacial clefts.

6. Conti… Clefts of the lip (CL) and palate (CP) are facial malformations that occur during embryonic development and are the most common congenital deformities . They may appear separately or, more often, together . The palate can be divided as: Primary Palate Secondary palate

7. Conti…. The palate can be divided into the primary and secondary palates. The primary palate consists of the medial portion of the upper lip and the portion of the alveolar ridge that contains the central and lateral incisors. The secondary palate consists of the remaining portion of the hard palate and all of the soft palate .

8. E tiology Genetic Environmental factors Teratogenic agents(Alcohol, cigarette smoking etc,) Maternal drugs use(Anticonvelcents , steroids etc) Folic acid deficiency

9. Pathophysiology Cleft deformities represent a defect in cell migration that results in a failure of the maxillary and premaxillary processes to come together between the fourth and tenth weeks of embryonic development . Although often appearing together, CL and CP are distinct malformations embryologically, occurring at different times during the developmental process.

10. Diagnostic Evaluation CL and CL/P are apparent at birth. CP is less obvious than CL and may not be detected immediately without a thorough assessment of the mouth . CPis identified through visual examination of the oral cavity or when the examiner places a gloved finger directly on the palate. Clefts of the hard and soft palate form a continuous opening between the mouth and the nasal cavity.

11. Therapeutic Management Management is directed toward closure of the cleft(s), prevention of complications, and facilitation of normal growth and development in the child . Treatment of the child with CL and CP involves the cooperative efforts of a multidisciplinary health care team, including pediatrics, plastic surgery, orthodontics, speech/language pathology, audiology and nursing .

12. Surgical Management C/L Surgical techniques( Chieloplasty ): Fisher repair The Millard rotational C/P Surgical technique( Palatoplasty ): Veau-Wardill-Kilner V-Y pushback Furlow double-opposing Z- plasty

13. Fisher Repair An anatomic subunit approximation t echnique Millard rotational advancement technique The design of rotation-advancement flap is based on a curved line (rotation) on the non-cleft side in order to balance the lip height discrepancy.

14. Surgical Correction of Cleft Palate Veau-Wardill-Kilner V-Y pushback procedure Used for incomplete clefts of the hard and soft palate. It include lengthening and repositioning of the palate. Furlow double-opposing Z- plasty Furlow described a doubled reversed Z- plasty technique to close palatal defects.

15. Prognosis The prognosis for patients with Cleft Lip is excellent; improvements to physical appearance positively impact the life of the child. Routine monitoring to ensure progress and healthy development is necessary.

16. Nursing Care Management The immediate nursing problems for an infant with CL/P deformities are related to feeding. Parents of newborns with clefts place high priority on learning how to feed their infants CP/CL reduces the infant's ability to suck, which interferes with breastfeeding and traditional bottle feeding. Modifications to positioning, bottle selection, and feeder supportive techniques can help infants with CP feed efficiently. By positioning an infant with CP in an upright position with the head supported by the caregiver's hand or cradled in the arm; this position allows gravity to assist with the flow of the liquid so that it is swallowed .

17. Conti…. Maintain adequate nutrition Positioning Tools for feeding0(pigeon bottles and Cleft Palate Nurser). Promote family coping Reduce family anxiety Provide family teaching

18. Preoperative Care In preparation for surgical repair, parents may be taught to use alternative feeding systems (e.g., syringes) several days before surgery. For CL, many surgeons allow babies to return to their typical feeding system. For CP, some surgeons require that the child be off the bottle and drinking from an open cup or sippy cup.

19. Postoperative Care The major efforts in the postoperative period are directed toward protecting the operative site . Apply petroleum jelly to the operative site. Elbow immobilizers may be used to prevent the infant from rubbing or disturbing the suture line. Analgesics Avoid the use of suction Avoid placing any objects such as straws into the mouth. Feeding is resumed when tolerated. Give soft or mashed foods for 3 weeks

20. ESOPHAGEAL ATRESIA AND TRACHEOESOPHAGEAL FISTULA

21. D efinition Congenital esophageal atresia (EA) and tracheoesophageal fistula (TEF) are rare malformations that represent a failure of the esophagus to develop as a continuous passage and a failure of the trachea and esophagus to separate into distinct structures. These defects may occur as separate entities or in combination.

22. Pathophysiology Esophageal atresia (EA) is a rare birth defect in which a baby is born without part of the esophagus (the tube that connects the mouth to the stomach). Instead of forming a tube between the mouth and the stomach, the esophagus grows in two separate segments that do not connect . TE fistulas occur due to abnormal septation of the caudal foregut during the fourth and fifth weeks of embryonic development. Normally, the trachea forms as a diverticulum of the foregut and develops a complete septum that separates the esophagus from the trachea.

23. Diagnostic Evaluation Chest Radiographic studies Bronchoscopic examination

24. Clinical Manifestations of Tracheoesophageal Fistula Fistula Excessive frothy mucus from nose and mouth Three Cs of tracheoesophageal fistula (TEF): Coughing Choking Cyanosis Apnea Increased respiratory distress during feeding Abdominal distention

25. Therapeutic Management The treatment of patients with EA and TEF includes: Maintenance of a patent airway P revention of pneumonia G astric or blind pouch decompression S upportive therapy S urgical repair of the anomaly D eprived of oral intake, IV fluids are initiated, and the infant is positioned to facilitate drainage of secretions and decrease the likelihood of aspiration.

26. Prognosis The survival rate is nearly 100% in otherwise healthy children. Most deaths are the result of extreme prematurity or other lethal associated anomalies. Potential complications (leak, strictures caused by tension or ischemia, respiratory compromise and gastroesophageal reflux)after the surgical repair of EA and TEF.

27. Nursing Care Management Nursing responsibility for detection of this serious malformation begins immediately after birth. Preoperative Care: The nurse carefully suctions the mouth and nasopharynx and places the infant in an optimum position to facilitate drainage and avoid aspiration . Until surgery, the blind pouch is kept empty by intermittent or continuous suction. Nursing interventions include respiratory assessment, airway management, thermoregulation, fluid and electrolyte management, and parenteral nutrition (PN) support.

28. Conti…. Often the infant must be transferred to a hospital with a specialized care unit and pediatric surgical team. The nurse advises the parents of the infant's condition and provides them with necessary support and information . Postoperative Care: Postoperative care for these infants is the same as for any high-risk newborn Pain management Gastrostomy feedings may be initiated and continued until the esophageal anastomosis is healed.

29. Conti… The nurse must carefully observe the initial attempt at oral feeding to make certain the infant is able to swallow without choking. Oral feedings are begun with sterile water, followed by frequent small feedings of breast milk or formula . Until the infant is able to take a sufficient amount by mouth, oral intake may need to be supplemented. I nfants are not discharged until they can take oral fluids well.

30. Special Problems Upper respiratory tract complications are a threat to life in both the preoperative and the postoperative periods . Pneumonia Respiratory distress resulting from atelectasis P neumothorax L aryngeal edema Temperature instability

31. Liver Abscess A liver abscess is a collection of pus in the liver caused by bacteria, fungi, or parasites. It may occur as a single lesion or as multiple lesions of different sizes.

32. Incidence & Epidemiology Liver – organ most subject to the development of abscesses 13% of total intra abdominal abscesses 48% of all visceral abscess Mortality - 5-30% of cases Most common causes of death include sepsis, multi organ failure, and hepatic failure Equal male to female ratio

33. Types Of Liver Abscess There are three major forms of liver abscess, classified by etiology Pyogenic liver abscess Which is most often poly microbial, accounts for 80% of hepatic abscess cases. A moebic liver abscess D ue to entamoeba histolytic, accounts for 10% of cases. Fungal abscess Most often due to candida species, accounts for less than 10% of cases.

34. Most common species involved are Streptococcus milleri Pseudomonas E. coli Klebsiella pneumoniae Proteus vulgaris Bacteroides Opportunistic Pathogens (Staphylococcus )` Common Causative Agents

35. Pathophysiology

36. Clinical Manifestation Fever with Chills Abdominal pain Anorexia Weight loss Nausea , Vomiting Right shoulder pain / irritable cough Cough and Dyspnea Hepatomegaly Tenderness Rebound tenderness Jaundice (late)

37. CBC Increased WBC, usually Neutrophilic Leukocytosis . Raised ESR ( erythrocyte sedimentation rate). LFTs, Liver function studies Diagnosis

38. Conti…. Elevation of alkaline phosphatase Hypoalbuminemia Elevations of transaminase and bilirubin levels ( variable ) Blood cultures are positive in roughly 50% of cases. Stool analysis, Stools can contain cysts or trophozoites of E. histolytica. USG guide percutaneous aspiration and drainage and biliary tree examination CT Scan MRI

39. Treatment and Management Medi cine can help to treat the infection caused by bacteria,fungi or a parasite. Percutaneous Needle aspiration : it is a procedure to drain fluid with in needle. Catheter drainage:It is a procedure to drain fluid through a catheter inserted into an incision. Surgery maybe needed if the abcess is large or burst.

40. Nursing Management Pain Management : Alleviation or reduction in pain. Nutrition Management : Assisting with or providing a balanced dietary intake of foods and fluids. Infection Protection Monitor vitals Monitor intake and output Monitor for growth Monitor lab results

41. Complications Return of Abscess Widespread infection in abdomen. Overwhelming sepsis. Rupture of the abscess into adjacent structures (pleural, peritoneal and pericardial spaces). Prognosis Pyogenic liver abscess , mortality rate is 5-30%. Condition such as DM, HIV, malignancy, affect prognosis . Amoebic liver abscess , Mortality rates have fallen to 1-3%.

42. BILIARY ATRESIA

43. Closure of a normal body opening or tubular structure . What is Atresia ?

44. Definition Biliary atresia is a condition in which the normal hepatic biliary system is disrupted. Progressive damage of extrahepatic and intrahepatic bile ducts which occur secondary to inflammation, leading to fibrosis, biliary cirrhosis, and eventual liver failure. Definition

45. Biliary atresia affects approximately 1 in 10,000- 15,000 births Biliary atresia seems to affect girls more than boys. There does not appear to be any link to medications taken during pregnancy. Incidence

46. The causes of biliary atresia are not known, but may include: Infection by a virus. Infectious agent Reovirus Rotavirus retrovirus Cytomegalovirus Human papilloma virus Inflammation and scarring caused by problems with the immune system Exposure to harmful chemicals Mutations (changes) in the genes. (Biliary atresia is not inherited from the baby’s parents.) Etiology

47. The biliary system is the network of tiny tubular structures and ducts that drain bile from the liver to the small intestine, where it helps the digestive process PATHOPHYSIOLOGY Bile is a liquid secreted by liver cells, made up of cholesterol, bile salts and waste products.Biliary atresia progressively destroys the bile ducts that carry bile from the liver to the intestine, beginning outside the liver and later affecting bile ducts inside the liver .

48. The damaged ducts prevent the draining of bile from the liver; as a result, bile trapped inside the liver causes damage and scarring that can lead to cirrhosis .

49. Symptoms of Biliary Atresia Jaundice Earliest manifestation and most striking feature of disorder
• First observed in sclera
• Usually not apparent until 2 to 3 weeks old after resolution of neonatal jaundice. Stools lighter than expected or white or tan

50. Hepatomegaly and abdominal distention common
Splenomegaly occurs later
Poor fat metabolism results in:
• Poor weight gain
• Failure to thrive
Pruritus
Irritability; difficulty comforting infant

51. Blood Tests - For liver function abnormalities. X-rays Of The Abdomen- Look for an enlarged liver and spleen. Abdominal Ultrasound- To find out whether there is a small gall bladder or none at all. A nuclear test-HIDA scan- Determines the flow of bile. In this scan, a radioactive dye is injected into the infant's vein. The dye acts like bilirubin. If the baby has biliary atresia, the liver will take up the dye but it will not be able to flow through the damaged biliary system into the small intestine. Diagnostic Evaluation

52. Liver Biopsy. Cholangiography . This is done by injecting contrast material through the gallbladder. To find the communication between the biliary tree and the gastrointestinal tract. Duodenal intubation To perform this study, a nasogastric tube is placed in the distal duodenum. The absence of bilirubin in aspirated fluid suggests obstruction.

53. There is no cure for biliary atresia. The main treatment is a surgery called the Kasai procedure. In this surgery, the surgeon removes the damaged bile ducts from outside the liver and replaces them with a piece of the patient’s small intestine. The small intestine will then drain the liver directly to the small intestine. Management And Treatment

54. This surgery is successful in most cases of biliary atresia. The chances of successful Kasai procedure is done before 30 to 45 days of age. However, if it is not successful, the child will likely need a liver transplant. The child may need a liver transplant even if the surgery is successful, depending on when the surgery is performed.

55. Nutrition and Biliary Atresia Adding medium-chain triglyceride (MCT) oil to foods and liquids or infant formulas. MCT adds extra calories that will help child grow. High-calorie liquid feedings may be recommended if child is too ill to eat normally. Feedings are given through a NG tube Although digestion may return to normal after surgery, extra vitamins or MCT oil may be needed.

56. Prognosis Untreated BA results in progressive cirrhosis and death in most children by 10 years old. The Kasai procedure improves the prognosis but is not a cure. Biliary drainage can often be achieved the surgery is done before the intrahepatic bile ducts are destroyed, and the success rate decreases to 20% if surgery is performed in an infant greater than 3 months old. Long-term survival rates of 75% to 90% have been reported in children who receive the Kasai procedure.

57. Nursing Care Management Include support of the family before during and after the surgical procedure and education.regarding the treatment plan. Administration of nutritional therapy, including special formulas, vitamin and mineral supplements. The risk of complications of BA, such as cholangitis, portal hypertension, GI bleeding, and ascites, should be explained to the caregivers

58. Intussusception is the most common cause of intestinal obstruction in children between 5 months old and 3 years old. Intussusception is more common in males than in females and is more common in children younger than 2 years old. Although specific intestinal lesions occur in a small percentage of the children, generally the cause is not known. More than 90% of intussusceptions do not have a pathologic lead point, such as a polyp, lymphoma, or Meckel diverticulum. The idiopathic cases may be caused by hypertrophy of intestinal lymphoid tissue secondary to viral infection. Intussusception

59. Intussusception occurs when a proximal segment of the bowel telescopes into a more distal segment, pulling the mesentery with it. The mesentery is compressed and angled, resulting in lymphatic and venous obstruction. As the edema from the obstruction increases, pressure within the area of intussusception increases. When the pressure equals the arterial pressure, arterial blood flow stops, resulting in ischemia and the pouring of mucus into the intestine. Venous engorgement also leads to leaking of blood and mucus into the intestinal lumen, forming the classic currant jelly–like stools. Pathophysiology

60. On the base of segment: CLASSIFICATION

61. Ileocecal valve ( ileocolic : The most common site is the ileocecal valve ( ileocolic ), where the ileum invaginates into the cecum and then further into the colon. Ileoileal : Other forms include ileoileal (one part of the ileum invaginates into another section of the ileum).

62. Colocolic Colocolic (one part of the colon invaginates into another area of the colon) intussusceptions, usually in the area of the hepatic or splenic flexure or at some point along the transverse colon.

63. Sudden acute abdominal pain Child screaming and drawing the knees onto the chest Child appearing normal and comfortable between episodes of pain Vomiting Lethargy Passage of red, currant jelly–like stools (stool mixed with blood and mucus) Tender, distended abdomen Palpable sausage-shaped mass in upper right quadrant Empty lower right quadrant (Dance sign) Eventual fever, prostration, and other signs of peritonitis Clinical Manifestations:

64. Frequently, subjective findings which are described as clinical signs lead to the diagnosis , which can be confirmed by: ultrasonography. A rectal examination reveals mucus, blood, and occasionally a low intussusception itself. Diagnostic Evaluation:

65. Conservative treatment consist of: Radiologist guide pneumoenema (air enema). Ultrasound guide hydrostatic (saline) enema. I.v fluids NG decompression and Antibiotic therapy If these procedures are not successful the child my require surgical intervention. Surgery involve manually reducing the invagination, when indicated, resecting any nonviable intestine. Therapeutic management:

66. Nonoperative reduction is successful in approximately 65% to 75% of cases ( Gourlay , 2013). Surgery is required for patients in whom the hydrostatic enema is unsuccessful. With early diagnosis and treatment , serious complications and death are uncommon. Prognosis:

67. As soon as the possible diagnosis is made, the nurse should prepares the parents for: Immediate need for hospitalization The non surgical technique of hydrostatic reduction The possibility of surgery. Explain the basic defect of intusuception . Telescoping rod Principle of reduction Nursing Management:

68. Physical care of the child doesn’t different from that for any child undergoing abdominal surgery. The usual preoperative procedures such as maintenance of NPO status, routine laboratory testing (CBC and urinalysis), Signed Parental consent and preanesthetic sedation are performed by the nurse. Fluid replacement and restoration of electrolytes may be required in such children before surgery. The nurse monitors all stools before surgery. Conti…

69. It includes the observation of: vital signs blood pressure intact sutures and dressing Observe for passage of water soluble contrast and the stool patterns. A recurrence of intussusception is treated with the conservative reduction techniques but a laparotomy is considered for multiple recurrences. PoStProcedure care:

70. Definition: Hirschsprung disease is also known as Congenital Aganglionic Megacolon . Hirschsprung disease is a congenital anomaly that results in mechanical obstruction from inadequate motility of part of the intestine. It accounts for about one fourth of all cases of neonatal intestinal obstruction. The incidence is 1 in 5000 live births (Liang, Ji, Yuan, et al, 2014). It is four times more common in males than in females and follows a familial pattern in a small number of cases.

71. The pathology of Hirschsprung disease relates to the absence of ganglion cells in the affected areas of the intestine, resulting in a loss of the rectosphincteric reflex and an abnormal microenvironmen of the cells of the affected intestine. The term congenital aganglionic megacolon describes the primary defect, which is the absence of ganglion cells in the myenteric plexus of Auerbach and the submucosal plexus of Meissner. Pathophysiology:

72. Pathophysiology:

73. In 80% of cases, the aganglionosis is restricted to the internal sphincter, rectum, and a few centimeters of the sigmoid colon and is termed short-segment disease.

74. Most children with Hirschsprung disease are diagnosed in the first few months of life. Clinical manifestations vary according to the age when symptoms are recognized and the presence of complications, such as enterocolitis . A neonate usually is seen with: Distended abdomen Feeding intolerance with bilious vomiting Delay in the passage of meconium. Typically, 99% of normal term infants pass meconium in the first 48 hours of life, but fewer than 10% of infants with Hirschsprung disease do so. Diagnostic Evaluation:

75. History is an important part of diagnosis. It includes: Chronic pattern of constipation On examination : Rectum is empty of feces Internal sphincter is tight Leakage of stool Accumulated gas may occur . To confirm the diagnosis rectal biopsy is performed. Conti…

76. Newborn Period: Failure to pass meconium within 24 to 48 hours after birth Refusal to feed Bilious vomiting Abdominal distention Clinical Manifestations of Hirschsprung Disease:

77. Infancy: Failure to thrive
Constipation
Abdominal distention
Episodes of diarrhea and vomiting
Signs of enterocolitis Explosive, watery diarrhea
Fever
Appears significantly ill Cont …

78. Childhood: Constipation
Ribbonlike, foul-smelling stools
Abdominal distention
Visible peristalsis
Easily palpable fecal mass
Undernourished, anemic appearance Cont …

79. Therapeutic management: Majority of children with Hirschsprung Disease require surgery rather than medical therapy with frequent enemas. Surgical management consist primarily of the removal of the aganglionic portion of the bowel to relieve obstruction, restore normal motility and preserve the function of external anal sphincter. Transanal Soave endorectal pull through procedure Simpler operations, an Anorectal myomectomy may be indicated in very short segment disease.

80. Some children may experience: Stricture Recurrent enterocolitis Prolapse Perianal abscess While after the pull through procedure majority of the children achieve fecal continence. Complications:

81. Promote skin integrity. When performing routine colostomy care. Give careful attention to the area around the colostomy; record and report redness, irritation, and rashy appearances of the skin around the stoma; prepare the skin with skin-toughening preparations that strengthen it and provide better adhesion of the appliance. Promote comfort Observe for signs of pain, such as crying, pulse and respiration rate increases, restlessness, guarding of the abdomen, or drawing up the legs; administer analgesics as ordered; additional nursing measures that can be used are changing the child’s position, holding the child when possible, stroking, cuddling, and engaging in age-appropriate activities. Nursing care management

82. Maintain fluid balance
Accurate intake and output determinations and reporting the character, amount, and consistency of stools help determine when the child may have oral feedings; to monitor fluid loss, record and report the drainage from the NG tube every 8 hours. Provide family teaching: Show the family caregiver how to care for the colostomy at home; discuss topics such as devices and their use, daily irrigation, and skin care; the caregivers should demonstrate their understanding by caring for the colostomy. Conti…