10. ac. diarrhoea, vomiting & rec abd pain

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10. ac. diarrhoea, vomiting & rec abd pain

  1. 1. DIARRHEABy: Syed Ariff Amir Syed Awaly
  2. 2. TOPICS Definition Epidemiology Types of diarrhea Causes Acute Diarrhea
  3. 3. DEFINITION According to WHO - passage of 3 or more loose or liquid stools per day, or more frequently than is normal for the individual.
  4. 4. EPIDEMIOLOGY Diarrheal diseases continue to be a major cause of morbidity and mortality in children in developing nations. In the year 2000, diarrheal diseases claimed an estimated 1.4 to 2.5 million lives; they are among the leading causes of death in children in developing countries In developed nations , they are an important cause of hospital admission although mortality rates may be lower. About 9% of all hospitalizations of children younger than 5 years were reported to be a result of diarrhea.
  5. 5. TYPES OF DIARRHEA
  6. 6. CAUSES OF DIARRHEA IN INFANT ACUTE Common causes: Gastroenteritis Systemic infection Antibiotic associated Rare causes: Primary disaccharidase deficiency Hirschsprung’s toxic colitis Adrenogenital syndrome CHRONIC Common causes: Post-infectious secondary lactase deficiency Cow’s milk/ soy protein intolerance Toddler’s diarrhea Coeliac disease Cystic fibrosis AIDS enteropathy Rare causes: Primary immune deficiency Familial villous atrophy Secretory tumor Short bowel syndrome
  7. 7. CAUSES OF DIARRHEA IN CHILDREN ACUTE Common causes: Gastroenteritis Food poisoning Systemic infection Antibiotics associated Rare cause: Toxic ingestion CHRONIC Common causes: Post-infectious secondary lactase deficiency Irritable bowel syndrome Coeliac disease Lactose intolerance Giardiasis Inflammatory bowel disease AIDS enteropathy Rare causes: Acquired immune defect Secretory tumor Pseudo-obstruction
  8. 8. ACUTE DIARRHEA
  9. 9. ETIOLOGY Protozoal Giardiasis Food poisoning Drugs NSAIDs Antibiotics Viral Rotavirus Norovirus Bacterial Vibrio cholera E. coli Salmonella* Shigella* Campylobacter* Clostridium defficile* * Associated with bloody diarrhoea
  10. 10. ASSESSMENT 1). History Foods ingested ??? Duration & frequency of diarrhea Presence of blood or steatorrhoea Abdominal pain Tenesmus Ask whether family @ community members have been affected
  11. 11. ASSESSMENT 2). Physical Examination Assess degree of dehydration by :- Skin tugor Pulse and BP measurement Monitoring of urine output and ongoing stool loses
  12. 12. ASSESSMENT 3). Investigation FBC Serum electrolyte Blood and urine culture Stool inspection for blood and examination for ova, cysts and parasites Chest X-ray
  13. 13. DEHYDRATION Asses based on :- 1.General condition 2. Sunken eyes 3. Offer the child drink 4. Skin turgor Classification: - 1. Mild dehydration (<5%) 2. Moderate dehydration (5-10%) 3. Severe dehydration (>10%)
  14. 14. MANAGEMENT First, assess the state of dehydration & then choose the treatment plan A, B or C PLAN A (mild diarrhea) Give extra fluid Breastfeed frequently Give ORS and cooled boiled water Plus food-based fluid (not exclusively breastfed) *10ml/kg of ORS after each loose stool
  15. 15. 2. Continue Feeding Feed as usual on demand Avoid food high in simple sugar as osmotic load may worsen the diarrhea 3. When to Return (to clinic/hospital) Not able to drink Becomes sicker Develops fever Has blood in stool
  16. 16. PLAN B (moderate diarrhea) Give recommended amount of ORS 4- hourly * Approximat amount of ORSs required = weight (in kg) x 75 After 4 hours Reassess the child Select appropriate treatment Begin feeding the child Explain the 3 rules of PLAN A
  17. 17. PLAN C (severe diarrhea) Start IV or IO fluid immediately. Give 100ml/kg Ringers Lactate @ normal saline devided as :- - 1st give 20ml/kg as fast as possible. Repeat boluses until perfusion has improved - Give the remaining fluid 5 hrs (age < 1 year) or 2 ½ hrs (age >1 year) Reassess the child after every bolus Reassess the child every 1-2 hour during rehydration Give ORS as soon as the child can drink. Classify the degree of dehyration Choose appropriate treatment
  18. 18. Maintenance Fluid Therapy Volume of fluid required < 6 months age : 150 ml/kg/day 6 to 1 year : 120 ml/kg/day >1 year : 1st 10 kg = 100 ml/kg 10- 20 kg = + 50 ml/kg for the subsequent kg > 20 kg = + 20 ml/kg for the subsequent kg
  19. 19. Antimicrobial Treatment Indicators:- Toxic looking Severe dehydration Blood in stool Types of Antibiotics:- Ampicilin Trimethoprim (TMP) Sulfamethoxazole
  20. 20. VOMITING
  21. 21. Chief Complaint: “Sally has a fever and is vomiting.” History of Present Illness A 4-year-old female is brought to the emergency dept. by her parents. She started complaining of abdominal pain 3 hrs ago and then had an onset of vomiting episodes x 4. No blood noted in the emesis or bile appearance. Temperature taken at home one half hour ago, temperature was 38.2 C. Mother has also commented on Sally’s increased level of thirst over the past week, and has attributed Sally’s new onset of night time bedwetting to her increased consumption of fluids. CASE SCENARIO
  22. 22. Vomiting is a coordinated, sequential series of events that leads to forceful oral emptying of gastric contents. DEFINITION
  23. 23. –Duration, frequency, bilious material, abdominal pain, diarrhea, hematemesis, hematochezia, melena, headache, fever, dysuria, weight loss, urine output –Sick contacts, cough, rhinorrhea, neck stiffness Family history: Genetic disease Hx of vomiting
  24. 24. –Vital signs, weight, mucous membranes, nasal discharge, breath sounds, rashes –Abdominal pain/distension, hepatosplenomegaly, abdominal masses, Murphy/obturator/psoas sign –Skin turgor, capillary refill –Neuro exam including funduscopy for papilledema Physical exam
  25. 25. Bilateral vomition centers in the reticular formation of the medulla integrate signals triggers vomition.Thevomition centers receive afferent signals from four major sources: The chemoreceptor trigger zone -bilateral set of centers in the brainstem lying under the floor of the fourth ventricle. The chemoreceptor trigger zones function as emetic chemoreceptors for the vomition centers - chemical abnormalities in the body (e.g. emetic drugs, uremia, hypoxia and diabetic ketoacidosis) are sensed by these centers, which then send excitatory signs to the vomition centers. Visceral afferents from the gastrointestinal tract (vagus or sympathetic nerves) Visceral afferents from outside the gastrointestinal tract - this includes signals from bile ducts, peritoneum, heart and a variety of other organs. Afferents from extramedullary centers in the brain - certain psychic stimuli (odors, fear), vestibular disturbances (motion sickness) and cerebral trauma Physiology of vomiting
  26. 26. Nausea - unpleasant psychic experience. Retching phase - abdominal muscles undergo a few rounds of coordinated contractions together with the diaphragm and the muscles used in respiratory inspiration. Expulsive phase - intense pressure is formed in the stomach brought by enormous shifts in both the diaphragm and the abdomen. The vigorous contractions of these muscles last much longer than a normal period of muscular contraction. The pressure is then suddenly released when the upper esophageal sphincter relaxes resulting in the expulsion of gastric contents. VOMITING PHASES
  27. 27. VOMITING Manifested by nausea, pallor and diaphoresis, followed by forceful gagging and retching. REGURGITATION Effortless and not preceded by nausea. But , the unpleasant sensations of gastric contents in mouth during regurgitation, may trigger gagging and true vomiting.
  28. 28. Gastric secretions are highly acidic. Recent food Malodorous. Blood “coffee ground vomiting"(as the iron in the blood is oxidized) Bile Fecal vomiting-consequence of intestinal obstruction or a gastrocolic fistula non-productive emesis or dry heaves-vomiting reflex continues for an extended period with no appreciable vomitus Contents
  29. 29. Bright red-bleeding from the oesophagus Dark red vomit with liver-like clots- profuse bleeding in the stomach (e.g.; perforated ulcer) Coffee ground-like vomit-less severe bleeding in the stomach-gastric acid has had time to change the composition of the blood Yellow vomit-bile indicates that the pyloric valve is open and bile is flowing into the stomach from the duodenum. Color
  30. 30. FBC U & E Creatinine Stool serology Abdominal X-Ray Surgical opinion if obstruction Exclude systemic disease INVESTIGATIONS
  31. 31. Aspiration of vomit Under normal circumstances the gag reflex and coughing will prevent this from occurring. The individual may choke and asphyxiate or suffer an aspiration pneumonia. Dehydration and electrolyte imbalance Tears in GIT If these tears are limited to the inner lining of esophagus, they are called Mallory-Weiss tears-Passing of bright red or dark blood in the vomitus. Tears through the entire wall of the esophagus resulting in perforation and the escape of stomach contents outside the gut- “Boerhaave’s syndrome Painful bruises or tears in the abdominal wall muscles. Dentistry Recurrent vomiting may lead to destruction of the tooth enamel due to the acidity of the vomit and also can degrade tissue of the gum. If prolonged, weight loss or malnutrition may occur. Complications
  32. 32. Stabilize patient and fluid resuscitation as initial therapy with electrolyte correction Surgical consultation if obstruction suspected Oral rehydration with small amounts of liquids if tolerated Treat infections if indicated Remove toxins and allergens Surgical interventions for volvulus, Hirschprung, intracranial masses, pyloric stenosis, other anatomic causes Correct metabolic derangements Lifelong gluten-free diet for celiac disease Rare use of antiemetics/promotility agents for chemotherapy, motion sickness, postsurgery, gastroesophageal reflux disease Treatment
  33. 33. ABDOMINAL PAIN Acute and recurrent
  34. 34. ABDOMINAL PAIN DEFINITION Pain– feeling of distress, suffering, caused by stimulation of specialized nerve endings. Abdomen – the part of body lying between the thorax and pelvis, containing the abdominal cavity & viscera CATEGORIES Referred pain Painful sensation in a body region distant from true source of pain Caused by activation of spinal cord somatic sensory cell bodies by intense signaling from visceral afferent nerves located at the same level. Somatic pain overlying body structures are injured Described as MSK pain Pain is sharp, intense, discrete & localized Visceral pain nerves within gut detect injury,affecting soft organ n&body tissue ‘’discomfort’’ and poorly localized
  35. 35. Acute Abdominal Pain Can signal presence of dangerous intra-abdominal process -Eg: appendicitis, bowel obstruction Or originate from extraintestinal sources -Eg: lower lobe pneumonia or urinary tract stone
  36. 36. Diagnostic Approach history onset- sudden or gradual, episodes, association w meals, history of injury Nature – sharp vs dull, colicky or constant, burning Location – epigastric, periumbilical,generalized, R or L lower quardrant, change in location over time Fever – presence suggests appendicitis or other infection Extraintestinal symptoms – cough, dyspnea, dysuria, urinary frequency, flank pain Course of symptoms – worsening or improving, changes in nature or location of pain
  37. 37. PHYSICAL EXAMINATION General – growth & nutrition, general appearance, hydrational status, degree of discomfort, body position Abdominal – tenderness, distention, bowel sounds, rigidity, guarding, mass Genitalia – testicular torsion, hernia, PID, ectopic pregnancy Surrounding structures – breath sounds, rales(crepitation), wheezing, flank tenderness, tenderness of abd. wall structures, ribs, costochondral joints Rectal examination – perianal lesions, stricture, tenderness, fecal impaction, blood
  38. 38. LABORATORY CBC, C-Reactive protein, ESR – evidence of infection/ inflammation AST, ALT, GGT, Bilirubin – biliary or liver dss Amylase, lipase - pancreatitis Urinalysis – UTI, bleeding d/t stone, trauma or obstruction Pregnancy test (older females) – ectopic pregnancy
  39. 39. RADIOLOGY Plain flat & upright abdominal films – bowel obstruction, appendiceal fecalith, free intraperitoneal, kidney stones CT scans – rule out abscess, appendicitis, Crohn dss, pancreatitis, gallstones, kidney stones Barium enema - Intussusception, malrotation Ultrasound – gallstones, appendicitis, intussusception, pancreatitis, kidney stones. ENDOSCOPY Upper endoscopy – suspected PU/ esophagitis
  40. 40. DIFFERENTIAL DIAGNOSIS
  41. 41. DISTINGUISHING C.FEATURES
  42. 42. APPENDICITIS
  43. 43. APPENDICITIS Clinical Features Lower abdominal pain- right iliac fossa,Nausea and vomiting,loss of appetite,Diarrhoea,Dysuria Physical Findings quiet ,dehydrated.Tenderness on palpation or percussion ,discomfort, Guarding signifies peritonitis, Rectal examination is only required if other diagnosis are suspected e.g. ovarian or adnexal pathology.
  44. 44. INTUSSUSCEPTION invagination of one portion of intestine into another with involving the ileocaecal junction peak age group being 2 months to 2 years Clinical Features Pain - Sudden onset ,severe intermittent cramping pain lasting seconds to minutes vomiting –undigested food ,Stools- dark red and mucoid (redcurrant jelly) Physical Findings well- looking/ drowsy/ dehydrated abdominal mass may be difficult to palpate in a distended abdomen Abdominal distension is a late sign
  45. 45. MANAGEMENT APPENDICITIS Laparoscopic surgery INTUSSUSCEPTION Barium enema in early intussusception Surgery
  46. 46. RECURRENT ABD. PAIN DEFINITION CRITERIA At least 3 bouts of significant abd. pain over 3 months Severe phase lasting at least 3 mins Usually in children above 3 yr old. Occurrence of multiple episodes of abdominal pain over at least 3 months that are severe enough to cause some limitation of activity
  47. 47. DIAGNOSTIC APPROACH When taking history, pediatrician should ask about the warning signs for underlying diseases If any warning signs are presents, further investigation is necessary. Even if they are absent, some laboratory evaluation is warranted.
  48. 48. Vomiting fever Bilious emesis Abnormal screening lab. study Growth failure Weight loss Pain awakening child from sleep Location away from periumbilical region Blood in stools or emesis Delayed puberty WARNING SIGNS!
  49. 49. INVESTIGATIONS FOLLOW UP CBC ESR Amylase, lipase Urinalysis Abdominal ultrasound Trial of 3- day lactose-free diet CT scan Celiac disease serology Barium upper GI Endoscopy Colonoscopy
  50. 50. DIFF. DIAGNOSIS OF RAP Functional abdominal pain* - IBS* Chronic pancreatitis Gallstones Peptic disease - duodenal ulcer, gastric ulcer, esophagitis Lactose intolerance* Fructose malabsorption Inflammatory bowel disease* - crohn’s disease, ulcerative colitis Constipation* Obstructive uropathy Congenital intestinal malformation – stricture or web, malrotation, duplication cyst Celiac disease*
  51. 51. FUNCTIONAL A.P. Pain that characteristically occurs daily or nearly every day Not assoc. with or relieved by eating/ defecation Assoc. with sig. loss of ability to function normally. These kids have personality traits that include tendency towards anxiety & perfectionism – results in stress Parents noted that child enjoys going to school, but the pain often worst at the start of school day & before returning to school after vacations.
  52. 52. Irrittable Bowel Syndrome cramping, abdominal pain, bloating, constipation, and diarrhea. Pain begin with a change in stool frequency /consistency. A stool pattern fluctuating between diarrhea and constipation. Relief of pain with defecation Symptom are link to gut motility Modulated by psychosocial factor such as stress and anxiety.
  53. 53. MANAGEMENT Treat underlying conditions Allows children to resume with daily activities Reassures that the although pain is there, will not harm the children physically (in case of FAP) IBS-can control symptoms with diet, stress management, and prescribed medications.

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