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Gastrointestinal Disorders. Embryonic Development Failure to fuse = cleft lip and palate Failure to differentiate = duodenal stenosis Atresia or abnormal.

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Presentation on theme: "Gastrointestinal Disorders. Embryonic Development Failure to fuse = cleft lip and palate Failure to differentiate = duodenal stenosis Atresia or abnormal."— Presentation transcript:

1 Gastrointestinal Disorders

2 Embryonic Development Failure to fuse = cleft lip and palate Failure to differentiate = duodenal stenosis Atresia or abnormal closing of structure:  Esophogeal atresia  Anal-rectal malformation  Biliary atresia

3 Fetal Development Fistula is an abnormal connection  Tracheal esophageal fistula  Anal-rectal malformations with fistula Incomplete or abnormal placement  Mal-rotation  Diaphragmatic hernia

4 Prenatal History Birth weight Prematurity History of maternal infection Polyhydramnios Down Syndrome

5 Health History Congenital anomalies Growth or feeding problems Economic status Food preparation General hygiene Family history of allergies

6 Present Illness Onset and duration of symptoms Weight loss or gain Recent changes in diet

7 Vomiting  Reflexive = infection or allergy  Central = central nervous system Head trauma Meningitis CNS tumor

8 Nursing Assessment Abdominal distention  Abdominal circumference Abdominal pain  Acute / diffuse / localized Abdominal assessment  Inspect / auscultation / palpation / measure

9 Measuring Abdominal Girth Bowden Text

10 Diagnostic Tests Flat plate of abdomen  Fluid  Gas  Structural changes Barium swallow or UGI  Strictures  Foreign body  Motility disorder

11 Diagnostic Tests Ultrasound  Visualize organs  Cysts  Abscess  appendicitis CT scan = tumors, abscess, obstruction 24 hour probe = Gastro esophogeal reflux Biopsy of liver, esophagus, stomach, intestine

12 Stool and Blood White blood cells Ova and Parasite Bacterial cultures Blood

13 Failure to Thrive Inadequate growth resulting from inability to obtain or use calories required for growth.

14 Cleft Lip and Palate Most common craniofacial anomaly 1 in 700 births Males 3 to 1 Higher in Asians Familial history Often diagnosed in utero by ultrasound

15 Cleft Lip Incomplete fusion of the primitive oral cavity Obvious at birth Infant may have problems with sucking Surgery in 2 to 3 months Goals of surgery Close the defect Symmetrical appearance of face

16 Feeding

17 Cleft Lip Plasticsurgery.org

18 Cleft Lip Plasticsurgery.org

19 Post Surgery Care Airway management Pain control Position in infant seat – upright position Elbow restraints Wound care as ordered by MD Minimizing crying Feeding techniques

20 Cleft Lip Repair

21 Cleft Palate Cleft palate occurs when the palatine plates fail to migrate and fuse between the 7 th and 12 th week of gestation. Diagnosed by looking into infants mouth.

22 Cleft Palate Pedisurg.com

23 Cleft Palate Pedisurg.com

24 Cleft Palate Repair Babies should be weaned from bottle or breast prior to the surgical procedure. Done around 1 year of age after teeth have erupted and before the child is talking to promote better speech outcomes Poor speech outcomes if done after 3 years of age.

25 Palate Repair Pre-surgery feeding  Alternate nipple design  Breast feeding consultant  ESSR Enlarge / stimulate / swallow / rest

26 ESSR TIP 18-2: Bowden Text

27 Devices For Feeding  Lamb’s nipple  Flanged nipple  Special nurser  Syringe with rubber tubing

28 Post Surgery Repair Position on side NPO for 48 hours Suction with bulb syringe only Avoid injury to palate with syringes, straws, cups etc.

29 Long Term Referrals Hearing Speech Dental Psychological Team approach to care

30 Esophageal Atresia Esophagus ends in a blind pouch. Infant has a lot of mucous at birth. The rationale for giving sterile water for the first feed.

31 E.A. Tracheo- esophageal Fistula 85 to 90% of defects Failure of the esophagus to recanalize between 4 th and 6 th week of development. Bowden Text

32 Esophageal atresia (or Oesophageal atresia) is a congenital medical condition (birth defect) which affects the alimentary tract.birth defectalimentary tract It causes the esophagus to end in a blind- ended pouch rather than connecting normally to the stomach.esophagusstomach It comprises a variety of congenital anatomic defects that are caused by an abnormal embryological development of the esophagus. It is characterized anatomically by a congenital obstruction of the esophagus with interruption of the continuity of the esophageal wall.esophagus

33 Esophageal atresia (EA) is a birth defect in which part of your baby’s esophagus is missing. Instead of forming a tube between the mouth and the stomach, the esophagus grows in two separate segments that do not connect. Children with esophageal atresia almost always have another birth defect called tracheoesophageal fistula, or TEF (a fistula is an abnormal connection). The esophagus and trachea should be two separate, unconnected tubes, but in TEF, they're connected. There are four types of esophageal atresia:

34 Type A  The upper and lower segments of the esophagus end in pouches, like dead-end streets that don’t connect.  TEF is not present. Type B  The lower segment ends in a blind pouch.  TEF is present on the upper segment.  This type is very rare. Type C  The upper segment ends in a blind pouch.  TEF is present on the lower segment.  This is the most common type. Type D  TEF is present on both upper and lower segments.  This is the rarest form of EA/TEF.

35

36 Clinical Manifestations Excessive drooling / frothy mucus Inability to pass NG tube Choking and cyanosis with feeding High risk for aspiration of HCL from stomach causing a chemical pneumonia.

37 X-ray Findings

38 Pre-surgery Care NPO Up in infant seat or HOB elevated Continuous suction G-tube to decompress stomach

39 Post Surgery Care

40 Post Operative Care Respiratory support Gastric decompression Chest Tube Gentle suctioning TPN until taking PO’s Antibiotics

41 Long Term Complications 5 to 15% experience leaking at operative site. Aspiration Dysphagia / difficulty swallowing Stricture of esophagus  Coughing  Regurgitation

42 Pyloric Stenosis Most common cause of gastric outlet obstruction in infants. 1 in 500 More common in males 3 weeks to 2 months of age History of regurgitation and non-bilious vomiting shortly after feeding. Vomiting becomes projectile

43 Pyloric Stenosis Ball & Bindler

44 Clinical Manifestations Projectile vomiting Visible peristaltic waves Olive shape mass in the upper abdomen to right of the midline Electrolyte imbalance

45 Management Pre-surgery NPO / document any emesis IV therapy / Correct electrolyte imbalance Comfort infant and caretakers

46 Feeding Post-operatively Give 10 ml oral electrolyte solution after recovered from anesthesia Start pyloric re-feeding protocol. Increase feeding volumes from clear fluids to dilute to full-strength formula. Keep feeding record Assess for vomiting Discharged when taking full-strength formula

47 Hernias A hernia is a protrusion of an organ or part of an organ through the wall of the cavity in which it is contained.

48 Inguinal Hernia

49 Inguinal hernia is the most common congenital anomaly requiring surgical repair in infants: 80% It is a protrusion of peritoneal sac into the processus vaginalis Most common in males and pre-term infants.

50 Inguinal Hernia

51 Hydrocele

52 Caused by peritoneal fluid communication with the scrotal area through a patent processus vaginalis. Often will resolve on its own unless associated with an inguinal hernia.

53 Umbilical Hernia More common in African American infants.

54 Diaphragmatic Hernia Congenital diaphragmatic hernia is the protrusion of abdominal contents into the chest cavity through a defect in the diaphragm.  1 in 5,000 births  Mortality rate is 40 to 50%

55 Diaphragmatic Hernia

56 Clinical Manifestations Chest appears barrel-like Abdomen is sunken Bowel sounds in chest Breath sound decreased Severe respiratory distress

57 Diaphragmatic Hernia

58 X-ray Diaphragmatic Hernia

59 Treatment Ventilator support Chest tube Umbilical artery catheter NG tube Surgical correction when stable

60 Long Term Problems Gastro Esophogeal Reflux Respiratory infections Obstructions

61 Abdominal Defects Omphalocele Gastroschisis

62 Intussusception Telescoping of part of intestine into an adjacent distal portion.

63 History Child appears with intermittent pain which is colicky, severe Child will often draw legs up Episodes occur 2-3 times / hour Vomiting is prominent feature – bile stained vomiting a late sign Bowel movements – bloody / mucous Classic current jelly stool is a late sign

64 Clinical Manifestation  Severe abdominal pain  Inconsolable crying  Draw knees up  Currant jelly-like stool is a late sign

65 Diagnostic X-ray

66 Management Reduce the obstruction before the bowel becomes necrotic.  Contrast Enema is diagnostic in 95% of cases and therapeutic curative in most cases.  Surgical reduction is radiologic reduction is not achieved.

67 Surgical Intervention IV fluids + antibiotics pre-operatively. Manual reduction is attempted. If bowel perforation is noted during operative procedure a temporary colostomy may be needed.

68 Hirschsprung Disease Congenital abnormality caused by reduced motility in colon.

69 Definition Lack of ganglion cells in colon prevents bowel from transmitting peristaltic waves needed to move fecal material.

70 Clinical Manifestations No meconium in the first 24 hours. History of constipation or fecal mass. Distended abdomen.

71 Diagnosis and Treatment Rectal biopsy Removal of the aganglionic portion of the colon. 1 st stage surgery is often a colostomy 2 nd stage is pull-through surgery to connect the working colon to a point near the anus.

72 Typical X-ray

73 Colostomy at Birth

74 Pull-through Surgery

75 Surgery Surgical repair done between 12 and 18 months

76 Long Term Complications Anal stricture Incontinence of stool Short bowel syndrome

77 Appendicitis

78 Pathophysiology Inflammation of the vermiform appendix. Obstruction at base blocks outflow of mucus. Pressure builds up Blood vessels are compressed. Perforation and rupture

79 Clinical Manifestations Abdominal pain Generalized to localized Mc Burney’s point Rebound tenderness Loss of appetite Vomiting Low grade fever

80 Appendectomy

81 Ruptured Appendix Child develops high fever after a period of feeling better.

82 Perforation Alert: With perforation of appendix, abdominal pain is suddenly relieved, but as peritonitis develops, it returns, along with signs of generalized acute abdomen. Child will guard area of pain Abdominal distension High fever May appear dehydrated

83 Interventions for Perforation Extra fluids may be needed – a bolus of normal saline NG may be inserted to decompress the stomach IV antibiotics prior to surgical procedure Fever control

84 Post Operative Care  NPO  IV therapy  IV Antibiotics

85 Nursing Interventions Monitor I & O Assess for bowel sounds Dressing change as ordered Ambulate ! Ambulate ! Ambulate ! Cough and deep breath Pain Management

86 Inflammatory Bowel Disease A virus or bacteria interacts with the body’s immune system to trigger an inflammatory reaction in the intestinal wall.

87 Inflammatory Bowel Disease Refers to two chronic diseases that cause inflammation of the intestines.  Ulcerative Colitis  Crohn’s Disease

88 Causes Most likely a genetic link that affects the immune system.

89 Ulcerative Colitis Inflammatory disease of the large intestine. The inner lining or mucosa becomes inflamed, swells and ulcers develop. Affects the lining of the bowel. Most severe in the rectal area and anus.

90 Crohn’s Disease Differs from ulcerative colitis in the areas of the bowel affected. Most often affects the small intestine and parts of the large intestine. Inflammation that extends deeper into the layers of the intestinal wall than ulcerative colitis.

91 Clinical Manifestations Diarrhea Rectal bleeding Abdominal pain Weight loss Anemia

92 Diagnostic Tests Erythrocyte sedimentation rate ESR Stool for gross or occult blood Colonoscopy evaluation and biopsy Genetic marker / family history

93 Drug Therapy Corticosteroids during acute phase Mesalazine – anti-inflammatory drug for mild to moderate cases. Immunosuppression drugs: Azathioprine, methotrexate, 6-mercaptopurine Remicade has been approved in severe cases

94 Long Term Surgical removal of bowel if not managed by medical management. Complications:  Alteration in body image due to steroids  Arthritis  Osteoporosis  Increase risk of colorectal cancer

95 Gastro-esophageal Reflux GER Incompetence of lower esophogeal sphincter, which allows return of stomach contents into esophagus.

96 GER Common condition involving regurgitation, or “spitting-up” which is the passive return of gastric contents retrograde into the esophagus. Peaks between one to four months. Usually resolved by 12 months.

97 Clinical Manifestations GER Regurgitation of formula after feeding No weight loss

98 Conservative Management GER Positioning: upright, semiprone after feeding to promote gravity resistance to reflux Dietary: thicken feedings Feeding modifications: small feedings with frequent burping to decrease gastric distention

99 GERD: Gastro-esophageal Reflux Disease Infant older than 6 months, infant / child with congenital or neurological problems. GER not relieved by simple measures. Clinical Manifestations: Regurgitation of feedings with slow growth / poor weight gain Esophagitis = excessive crying Apnea / Respiratory problems Anemia

100 Diagnostic Work-up for GERD Upper GI series Esophageal pH monitoring Endoscopic exam

101 Pharmacologic Therapy Medications to reduce symptoms including antacids or histamine-2 blocking agents Histamine 2 blocker: cimetadine Reglan or metaclopramide to enhance gastric emptying

102 Surgical Management: GERD Fundoplication Pedisurg.com

103 Celiac Disease Malabsorption caused by a permanent intolerance to dietary gluten. 1 in 3000 in USA 1 in 300 in European countries Genetic predisposition

104 Celiac Disease Small villi lining the intestine are damaged by the Body’s immune system. Celiac.com

105 Assessment Chronic diarrhea Foul smelling, greasy stools Abdominal distention Anemia Muscle wasting

106 Management Gluten free diet Limit the intake of wheat, barley, rye containing foods

107 Management

108 Dietary Restrictions

109 Lactose Intolerance Inability to digest significant amounts of lactose. Lactose that is not broken down can cause abdominal distention and bloating. Lactose tablets to help breakdown lactose containing foods.


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