Pediatrics Digestive System Part 2 2025 PDF

DIGESTIVE SYSTEM (PART 2) Dr. Ann Flor Somera Abad, Balmores, Clarete, Gabot, Talla Outline Diagnostics I. I. Foreign Bodies...

DIGESTIVE SYSTEM (PART 2) Dr. Ann Flor Somera Abad, Balmores, Clarete, Gabot, Talla Outline Diagnostics I. I. Foreign Bodies o Abdominal plain film II. II. Bezoars o Ultrasound III. III. Peptic Ulcer Disease o CT examination IV. IV. Inflammatory Bowel Disease Treatment V. V. Chronic Ulcerative Colitis o Removal- endoscopy, surgical VI. VI. Crohn Disease VII. VII. Acute Gastroenteritis Peptic Ulcer Disease in Children VIII. VIII. Zinc Supplementation Imbalance between cytoprotective and IX. IX. Acute Appendicitis cytotoxic factors in the stomach and duodenum X. X. Pancreatitis Primary peptic ulcers- chronic, often duodenal XI. XI. Cholestasis Secondary- acute, often gastric XII. XII. Biliary Atresia Clinical Manifestations: o Vary with the age of the patient o School-age children and adolescents- Legends epigastric pain and nausea Book Lecture Prev. Trans Remember Other o Older children- dyspepsia, epigastric abdominal pain or fullness o Infants and younger children- feeding difficulty, vomiting, crying episodes, Foreign Bodies in the Stomach and Intestine hematemesis, or melena Ages of 6 months and 6 years o Neonatal period- gastric perforation Coins- most commonly ingested foreign body in o pain- dull or aching children o nocturnal pain- other children Meats or food impactions- adolescents and o acute or chronic outlet obstruction can adults occur- extensive inflammation and 90% of foreign bodies are opaque edema Radiologic examination- type, number, and Diagnosis: location o Esophagogastroduodenoscopy Conservative management- indicated for most o Biopsy foreign bodies that have passed through the Treatment: esophagus and entered the stomach o Acute hemorrhage- hemodynamic 4-6 days- most objects pass through the stability intestine o High-dose intravenous PPI therapy Surgical removal is necessary- symptoms or o 2 goals: ulcer healing and elimination of signs of obstruction or perforation or if the the primary cause foreign body fails to progress for several weeks o Are relief of symptoms and prevention Retrieve/remove of complications o Older children and adults- oval objects o First line drugs – PPIs and H2 receptor larger than 5cm in diameter or 2cm in antagonists thickness o Cytoprotective agents o Thin long objects >6cm in length fail to o H. pylori- antibiotics in combination negotiate the pylorus or duodenal with a PPI sweep o Infants or toddlers- objects >3cm in Inflammatory Bowel Disease length or >20mm in diameter Genetic and environmental influences Caused by dysregulated or inappropriate Bezoars immune response to environmental factors in a Accumulation of exogenous matter in the genetically susceptible host stomach or intestine Attributable to alterations in the microbiome Composed of food or fiber Most have been found in females Chronic Ulcerative Colitis Trichobezoars Localized to the colon and spares the upper GI Phytobezoars tract Lactobezoars Begins in the rectum and extends proximally for a variable Proctitis Pancolitis  Clinical Manifestations: o Gastric or duodenal involvement- o Blood, mucus and pus in stool and recurrent vomiting and epigastric pain diarrhea o Penetrating disease- demonstrated by o Constipation- proctitis fistula formation o Tenesmus, urgency, cramping ▪ Enteroenteric or enterocolonic abdominal pain fistulas, enterovesical fistulas, o Onset ranges from insidious with enterovaginal, gradual progression of symptoms to enterocutaneous fistulas acute and fulminant o Abscess – intraabdominal, hepatic or Fulminant colitis- fever, severe anemia, splenic abscess, anorectal, psoas hypoalbuminemia, leukocytosis, and more then abscess 5 bloody stools per day for 5 days o Extraintestinal manifestation – oral Iron deficiency aphthous ulcers, peripheral arthritis, Secondary amenorrhea erythema nodosum, digital clubbing, Clinical course is marked by remission and episcleritis, renal stones and gallstones relapse Diagnosis: Diagnosis: o Endoscopy o Make a firm diagnosis only when there ▪ Esophagogastroduodenoscopy is evidence of chronicity on colonic ▪ Ileocolonoscopic biopsy o Radiologic Studies o Anemia (either iron deficiency or the ▪ Plain films anemia of chronic disease) or ▪ Upper GI contrast hypoalbuminemia ▪ CT and MR enterography o Elevated sedimentation rate and C- Treatment: reactive protein o 5-aminosalicylates o Barim enema ▪ Mild terminal ileal disease or o Flexible sigmoidoscopy- confirm the mild Crohn disease diagnosis o Antibiotics/Probiotics Treatment: o Corticosteroids o Controlling symptoms and reducing the o Immunomodulators- azathioprine, risk of recurrence mercaptopurine, methotrexate o Aminosalicylate- mild or mild-to- o Biologic Therapy- Infliximab, moderate colitis Adalimumab o 5-ASA preparations (Mesalamine, o Enteral Nutritional Therapy Balsalazide) o Surgery: o Probiotics- adults ▪ localized disease of small o Corticosteroids- moderate to severe bowel pancolitis ▪ colon that is unresponsive to o Immunomodulators- azathioprine, 6- medical treatment mercaptoprine ▪ bowel perforation fibrosed o Colectomy – surgical stricture with symptomatic partial small bowel obstruction, Crohn Disease (Regional Enteritis, Regional Illeitis, and intractable bleeding Granulomatous Colitis) Acute Gastroenteritis in Children Involves region of the alimentary tract from the mouth to the anus Many of these infections are foodborne illness Inflammatory process tends to be eccentric and Rotavirus- most common cause of AGE among segmental, often with skip areas children throughout the world >50% - involves ileum and colon (ileocolitis) 4th most common cause of child deaths worldwide 20% - exclusively colonic disease Associated with malnutrition, stunting, 30% - upper GI involvement (esophagus, micronutrient deficiencies, and significant stomach, duodenum) deficits in psychomotor and cognitive Clinical Manifestations: development o Small bowel disease- obstructive Risk Factors: pattern (most commonly with right o Young age lower quadrant pain) o Immunodeficiency o Colonic disease- symptoms resulting o Measles from inflammation (diarrhea, bleeding, o Malnutrition cramping) o Lack of exclusive or predominant o Fever, malaise, and easy fatigability breastfeeding o Growth failure with delayed bone maturation and delayed sexual Clinical Manifestation: development o Passage of 3 or more abnormally loose o Primary or secondary amenorrhea or liquid stools per day o Perianal disease is common o Viral diarrhea o Bacterial  o Protozoal o Improved Water and Sanitary Facilities Clinical Manifestations of Diarrhea: and Promotion of Personal and o Related to the infecting pathogen and Domestic Hygiene the dose or inoculum o Nature of the infecting pathogen Acute Appendicitis Complications: Most common acute surgical condition in o Related to delays in diagnosis and children and a major cause of childhood delays in the institution of appropriate morbidity therapy Higher perforation rate than adults o Be life-threatening in infants and young 1-2 per 10,000 children from birth to 4 yr of age children 19-28 per 10,000 children younger than ager 14 o Inappropriate therapy can lead to yr prolongation of the diarrheal episodes, Peak incidence between the ages of 10 and 18 with consequent malnutrition and yr complications such as secondary Begins with luminal obstruction; inspissated infections and micronutrient fecal material, lymphoid hyperplasia, ingested deficiencies foreign body, parasites, and tumors have been Diagnosis: implicated o Based on clinical recognition Obstruction of the appendiceal lumen initiates a o Evaluation of its severity by rapid progressive cascade including: assessment o Increasing intraluminal pressures from o Confirmation by appropriate laboratory bacterial proliferation and continued investigations secretion of mucus Treatment: o Elevated intraluminal pressure o Oral Rehydration Therapy o Lymphatic and venous congestion and o Preferred mode of rehydration and edema replacement of ongoing loses o Impaired arterial perfusion o Intravenous resuscitation include: o Ischemia of the wall of the appendix ▪ age < 6 months o Bacterial invasion of the appendiceal ▪ prematurity wall ▪ chronic illness o Necrosis ▪ 38 C < 3 mos age Clinical Features ▪ >39 C if 3-36 mos of age o 6 mos of age with acute diarrhea – oral zinc o Anorexia – classic and consistent (20 mg/day) in some form for 10-14 days finding Treatment: o Diarrhea and urinary symptoms o Probiotics- Lactobacillus, o Perforation- diffuse abdominal pain Bifidobacterium, Saccharomyces and rapid development of toxicity boulardii evidence by dehydration and signs of o Antimotility agents- no role sepsis including hypotension, oliguria, o Antiemetics- ondansetron acidosis, and high-grade fever o Racecatodril Physical Examination: Prevention: o 7mm) o Magnetic resonance thick-walled appendix, cholangiopancreatography and inflammatory streaking of endoscopic retrograde surrounding mesenteric fat, cholangiopancreatography and a pericecal phlegmon or Treatment: abscess o Relieve pain and restore metabolic o MRI homeostasis Differential Diagnosis o fluid, electrolyte, and mineral balance o Gastrointestinal should be restored and maintained o Gynecologic o nasogastric suction  o antibiotics 3rd type o proton pump inhibitors o Most common variant o Non-patency of the entire etxrahepatic Cholestasis biliary system and intrahepatic bile NEONATAL CHOLESTASIS ducts at the hilum prolonged elevation of the serum levels of conjugated bilirubin beyond the 1st 14 days of Idiopathic Neonatal Hepatitis life Familial incidence of approximately 20% jaundice that appears after 2 weeks of age, More common in infants who are premature or continues to progress, or does not resolve at small for gestational age this time should be evaluated and a conjugated Percutaneous liver biopsy – most valuable bilirubin level determined procedure in the evaluation of neonatal infectious, genetic, metabolic, or undefined hepatobiliary diseases and provides the most abnormalities giving rise to mechanical reliable discriminatory evidence obstruction of bile flow or to functional impairment of hepatic excretory function and Biliary Atresia bile secretion Fetal onset has an increased incidence of other abnormalities INTRAHEPATIC CHOLESTASIS Persistently acholic stools suggest biliary Neonatal Hepatitis obstruction o Idiopathic neonatal hepatitis Palpation of the liver might find an abnormal o Disease of unknown cause size or consistency Aagenaes Syndrome Abdominal ultrasound o Associated with lymphedema of the o Triangular cord sign- represents a cone lower extremities shaped fibrotic mass cranial to the o Episodic cholestasis with elevation of bifurcation of the portal vein serum aminotransferases, alkaline o Hepatobiliary scintigraphy with phosphatase, and bile acids technetium-labeled iminodiacetic acid Zellweger (cerebrohepatorenal) syndrome derivatives o By progressive degeneration of the ▪ Sensitive but not specific test liver and kidneys for biliary atresia o Severe, generalized hypotonia and markedly impaired neurologic function MANAGEMENT OF BILIARY ATRESIA: with psychomotor retardation Exploratory laparotomy and direct Neonatal Iron Storage Disease (neonatal cholangiography to determine the presence hemochromatosis, gestational alloimmune and site of obstruction liver disease) Direct drainage- few patients with a correctable o Rapidly progressive disease lesion characterized by increased iron Hepatoportoenterostomy (Kasai) procedure – deposition in the liver, heart, and for patients in whom no correctable lesion is endocrine organs without increased found iron stores in the reticuloendothelial The success rate for establishing good bile flow system after the Kasai operation is much higher (90%) o Patients have multiorgan failure and if performed before 8 weeks of life shortened survival Biliary Atresia Obliterative Cholangiopathy Cystic- Choledochal cysts Noncystic- different variants of biliary atresia Cystic biliary atresia o Uncommon variant of biliary atresia (about 10-20% of cases) o Has a relatively favorable prognosis particularly with early surgery Noncystic biliary atresia – 3 types 1st type o Correctable biliary atresia o 7% of the cases o Patency of the proximal extrahepatic bile ducts with atresia of the distal bile duct 2nd type Reference: o 15% of the cases Doc Somera’s PPT o There is atresia of the common hepatic Nelson Book for Pediatrics 21st edition duct at different levels