1. Modul Gastro Fakultas Kedokteran UNTAN Pontianak, 8 Maret 2012
Dr. Rini Andriani, Sp A
Fakultas Kedokteran UNTAN

2. Anatomy

3. GASTROINTESTINAL EMERGENCIES
Gastrointestinal Bleeding
Acute Abdomen

4. GASTROINTESTINAL BLEEDING
Blood loss from the gastrointestinal (GI) tract occurs in four ways:
1. Hematemesis
2. Hematochezia
3. Melena
4. Occult bleeding

5. GASTROINTESTINAL BLEEDING
   1.    Initial evaluation :  
Assess airway, breathing, and circulation and hemodynamic stability.   
Perform physical examination, looking for evidence of bleeding.   
Verify bleeding with rectal examination and/or testing of stool or emesis for occult blood.
Obtain baseline laboratory tests.
Consider the following laboratory studies: Complete blood count (CBC), prothrombin time/partial thromboplastin time (PT/PTT), blood type and cross-match, reticulocyte count, blood smear, blood urea nitrogen/creatinine, electrolytes, and a panel to assess for disseminated intravascular coagulation.   

6. GASTROINTESTINAL BLEEDING
   1.    Initial evaluation :  
Consider gastric lavage to differentiate upper from lower GI bleeding and to assess for ongoing bleeding.   
Provide specific therapy based on assessment and site of bleeding.   
Begin initial fluid resuscitation with normal saline or lactated Ringer's solution.
Consider transfusion if there is continued bleeding, symptomatic anemia, and/or a hematocrit level <20%. Initiate intravenous acid suppression therapy, preferably with a proton pump inhibitor (PPI).

7. DIFFERENT DIAGNOSIS OF GI BLEEDING
Age
Upper GI
Lower GI
Neonates (0-30 days)
Swallowed maternal blood
Gastritis
Necrotizing enterocolitis
Malrotation and midgut volvulus
Anal fissure
Hirschprung disease
Infant (>30 days – 1 year)
Esophagitis
Peptic ulcer disease
Allergic proctocolitis
Intususception
Meckel’s diverticulum
Lymphonodular hyperplasia
Intestinal duplication
Infectious colitis
Preschool (1-5 year)
Esophageal varices
Epistaxis
Juvenile polyp’s 
Hemolytic-uremic syndrome
Henoch-Schönlein purpura
School age and adolescent
Inflammatory bowel disease
Juvenile polyps
Hemorrhoids

8. Acute Abdomen

9. ACUTE ABDOMEN Appendicitis perforated ulcer Pancreatitis
1.    Differential diagnosis: GI Source   
Appendicitis
perforated ulcer
Pancreatitis
Meckel diverticulitis
Intussusception
Cholecystitis
malrotation with volvulus
Choledocholithiasis
inflammatory bowel disease
Constipation
gastroenteritis   
Gastritis
bowel obstruction
mesenteric lymphadenitis
irritable bowel syndrome
Abscess
Hepatitis

10. ACUTE ABDOMEN 1. Differential diagnosis:
Renal source: Urinary tract infection, pyelonephritis, nephrolithiasis.   
Gynecologic source: Ectopic pregnancy, ovarian cyst/torsion, pelvic inflammatory disease.   
Oncologic source: Wilms tumor, neuroblastoma, rhabdomyosarcoma, lymphoma.   
Other sources: Henoch-Schönlein purpura, pneumonia, sickle cell anemia, diabetic ketoacidosis, juvenile rheumatoid arthritis.   

11. ACUTE ABDOMEN 2. Diagnosis:
a.    History: Course and characterization of pain, diarrhea, melena, hematochezia, fever, last oral intake, menstrual history, vaginal discharge/bleeding, urinary symptoms, and respiratory symptoms. Assess past GI history, travel history, and diet.   

12. ACUTE ABDOMEN 2. Diagnosis: b. Physical examination:
(1)  General: Vital signs, toxicity, rashes, arthritis, jaundice.   
(2)  Abdominal: Moderate to severe abdominal tenderness on palpation, rebound/guarding, rigidity, masses, change in bowel sounds.   
(3)  Rectal: Include testing stool for occult blood.   
(4)  Pelvic: Discharge, masses, adnexal/cervical motion tenderness.   

13. ACUTE ABDOMEN 3. Studies: a. Radiology:
First obtain plain abdominal radiographs to assess for obstruction, constipation, free air, gallstones, and kidney stones, and chest radiographs to check for pneumonia.
Consider abdominal/pelvic ultrasonography
Consider endoscopy     

14. ACUTE ABDOMEN
3. Studies: b. Laboratory: Electrolytes, chemistry panel, CBC, liver and kidney function tests, coagulation studies, blood type and screen/cross-match, urinalysis, amylase, lipase

15. ACUTE ABDOMEN 4.Management: a. Immediate:
Patient should be placed on nothing by mouth (NPO) status.
Begin rehydration.
Consider nasogastric decompression, serial abdominal examinations, surgical/gynecologic/GI evaluation as indicated, pain control, and antibiotics as indicated.   
b.    Definitive: Surgical or endoscopic exploration as warranted.

16. Malrotation
Duodenum to right of spine
Failure of midgut to rotate into normal anatomic position during development
Colon and cecum in left
Duodenum on right side
Bilious vomiting
Peritoneal (Ladd) bands cause partial bowel obstruction
High risk for...
Cecum in left abdomen

17. Midgut volvulus !
SURGICAL
EMERGENCY
Twisting of bowel around its mesentery and vascular supply
Leads to ischemia, infarction, perforation, necrosis
Presentation: lethargy, abdominal distention, bloody stools

18. Malrot/Midgut Volvulus
UERMMMC Department Of Radiology
Malrot/Midgut Volvulus
Cross Table Lateral
“DOUBLE BUBBLE SIGN”
Supine

19. Malrotation/Midgut Volvulus
UERMMMC Department Of Radiology
Malrotation/Midgut Volvulus

20. Malrotation/Midgut Volvulus
UERMMMC Department Of Radiology
Malrotation/Midgut Volvulus S d

21. UERMMMC Department Of Radiology
Spiraling of
contrast material

22. ! Duodenal atresia Obliteration of lumen Neonatal bilious vomiting
Failure to recanalize
Neonatal bilious vomiting
Associations
Prematurity
Congenital heart defects
Trisomy 21
Double bubble sign !
Complete small bowel obstruction
SURGICAL
EMERGENCY

23. Duodenal Atresia “DOUBLE BUBBLE SIGN” UERMMMC Department Of Radiology
Cross Table Lateral
“DOUBLE BUBBLE SIGN”
Supine

24. Duodenal Atresia S D UERMMMC Department Of Radiology
Distended Stomach & Duodenum
No gas distally

25. Gastric Atresia UERMMMC Department Of Radiology Cross Table Lateral
Supine

26. Gastric Atresia UERMMMC Department Of Radiology Distended Stomach
No gas distally

27. Jejunal Atresia “TRIPLE BUBBLE SIGN” UERMMMC Department Of Radiology
Cross Table Lateral
“TRIPLE BUBBLE SIGN”
Supine

28. Jejunal Atresia S D J UERMMMC Department Of Radiology
Distended stomach, duodenum, and jejunal segement
No gas distally

29. Stomach/duodenum – Bleeding
Presentation –
Haematemesis +/-
Melaena
Severity
Increased CR
Fall BP
Causes
DU, erosions, GU
Treatment – control bleeding
transfusion

30. Stomach/duodenum – Perforation
Presentation –
abdominal pain
rigidity
peritonism, shock
Air under diaphragm on X-ray
Treatment
antibiotics, resuscitate
repair

31. Pancreas Acute pancreatitis Constant pain, vomiting, shock Causes
Gallstones, or
Alcohol
Diagnosis
Serum amylase
elevation, US
complications
pseudocyst, phlegmon
abcess

32. Small Intestine Meckel’s Diverticulum rare
diverticulum of terminal ileum
can be lined by gastric epithelium
can perforate
can present like appendicitis

33. Meckel’s diverticulum
Remnant of omphalomesenteric duct
Painless rectal bleeding
Less commonly: intuss., volvulus, perforation
Diagnosis
CT scan
Nuclear medicine scan
Endoscopy
Treatment
Surgical resection

34. Small Intestine Intestinal obstruction May arise due to
adhesions, hernia, tumour
Presentation
colicky abdominal pain,
vomiting, constipation
Treatment
resuscitate/operate

35. Intussusception Telescoping of one segment of bowel into another
Ileocolonic most common
6 mos – 3 years old
Progressive course
Intermittent acute abd. pain
Vomiting
Bloody stools (currant jelly)
Fever, lethargy
Palpable sausage-shaped mass in upper abdomen

36. Intussusception Management
Abdominal X-ray: obstruction
Contrast enema
Diagnostic confirmation
Therapeutic in 75% of cases
Hydrostatic pressure reduces the intussusception
Surgeon must be involved directly
If enema reduction fails
Small bowel intussusceptions require surgical reduction

37. Intussusception
Terminal ileum telescoped into cecum

38. Small Intestine Mesenteric infarct Sudden occlusion of small
bowel arterial supply
Sudden onset of abdominal pain, shock
Peritonitis
Treatment
resuscitate/operate

39. Hirschsprung’s disease
Congenital absence of ganglion
cells in distal rectum
- and varying distance proximally
Lack of peristalsis causes colonic
obstruction
Abdominal distention
Failure to pass meconium
Fever and diarrhea suggest “toxic megacolon” !
SURGICAL
EMERGENCY

40. Hirschsprung’s Suction rectal bx
AXR: obstructive pattern
Suction rectal bx
Absence of ganglion cells in myenteric plexus
Barium enema: Dilated proximal colon with transition zone

41. Hirschsprung’s Surgical treatment Colostomy
Pull-through and removal of
aganglionic segment
Hirschsprung’s

42. Inguinal hernia Common surgical problem Painless scrotal bulge
More common in male and premature infants
Intestinal segment entering into scrotum through processus vaginalis
Does not resolve spontaneously
Painless scrotal bulge
Increases in size with crying/straining
Management
Reducible: refer to surgery for repair
Incarcerated: immediate surgical consult

43. Umbilical hernia Incomplete closure of umbilical ring fascia
More common in premature and African-American infants
Usually close by 2-4 yrs
Refer to surgery if:
Larger than 1.5 cm at 2 yrs
Present after 4 yrs
Supraumbilical

44. Indications for Surgical Consultations in Children with Acute Abdominal Pain
Severe or increasing abdominal pain with progressive signs of deterioration
Bile-stained or feculent vomitus
Involuntary abdominal guarding/rigidity
Rebound abdominal tenderness
Marked abdominal distension with diffuse tympany
Signs of acute fluid or blood loss into the abdomen
Significant abdominal trauma
Suspected surgical cause for the pain
Abdominal pain without an obvious etiology

45. OBJECTIVES
Recognize
Diagnose
Consult surgery

47. Major Symptom and Signs of GI Disorders
Dysphagia
Regurgitation
Vomiting
Anorexia
Diarrhea
Constipation
Abdominal Pain
GI Bleeding
Abdominal distention and mass

48. Differential Diagnosis of Acute Abdominal Pain by Predominant Age
Birth to one year
Infantile colic
Gastroenteritis
Constipation
Urinary tract infection
Intussusception
Volvulus
Incarcerated hernia
Hirschsprung's disease
Two to five years
Gastroenteritis
Appendicitis
Constipation
Urinary tract infection
Intussusception
Volvulus
Trauma
Pharyngitis
Sickle cell crisis
Henoch-Schönlein purpura
Mesenteric lymphadenitis

49. Six to 11 years
Gastroenteritis
Appendicitis
Constipation
Functional pain
Urinary tract infection
Trauma
Pharyngitis
Pneumonia
Sickle cell crisis
Henoch-Schönlein purpura
Mesenteric lymphadenitis
12 to 18 years
Appendicitis
Gastroenteritis
Constipation
Dysmenorrhea
Mittelschmerz
Pelvic inflammatory disease
Threatened abortion
Ectopic pregnancy
Ovarian/testicular torsion

50. Abdominal Pain
Individual children differ greatly in their perceptive of and tolerance for abdominal pain.
The more specific the pain and the more suggestive of a particular diagnosis, the more likely it will have an organic basis.

51. Abdominal Pain
Two types of nerve fibers transmit painful stimuli in the abdomen.
A fibers (sharp, localize pain)  skin, muscle
C fibers (poor localized, dull pain)  visera, peritoneum.

52. Abdominal Pain
Visceral pain tends to be experienced in the dermatome from which the affected organ receives innervation.
Painful stimuli originating in the liver, pancreas, biliary tree, stomach, and upper bowel are felt in the epigastrium.
Pain from the distal small bowel, cecum, appendix, or proximal colon is felt at the umbilicus.

53. Abdominal Pain
Pain from distal large bowel, urinary tract, or pelvic organs is usually suprapubic.
In the gut, the usual stimulus provoking pain is tension or stretching

55. Evaluation of vomiting
Type
Etiology
Evaluation
Typically bilous
Obstruction
Intussusception
Malrotation
Volvulus
Pancreatitis
Intestinal dysmotility
Incarcerated inguinal hernia
Intestinal Atresia, stenosis
Review feeding and medication history.
NG/OG tube for decompression if GI obstruction is suspected.
If bilious and/or hematemesis, consider surgical consultation.
Plain abdominal film with upright or cross-table lateral views to rule out obstruction, free air.
Upper GI series to rule out pyloric stenosis, obstruction, anomalies snd evaluate GI motility.

56. Evaluation of vomiting
Type
Etiology
Evaluation
Typically non billous
Overfeeding
GERD
Milk-protein sensitivity
Infection (GU, respiratory, GIT)
Peptic disease
Drugs
Electrolytes imbalance
Eating disordes
Necrotizing enterocolitis
Metabolic abnormality
Pyloric stenosis
CNS abnormality
Considered feeding modification
AVOID antiemetics unless specific, benign etiology is suspected
Either billous or nonbillous
Ileus
Appendicitis

57. GASTROESOPHAGEAL REFLUX DISEASE
Gastroesophageal reflux (GER) is passage of gastric contents into the esophagus
Gastroesophageal reflux disease (GERD) is defined as symptoms or complications of GER.

58. GERD …diagnosis
History and physical examination: Usually sufficient to reliably diagnose GER, identify complications, and initiate management.
Esophageal pH monitoring: Valid and reliable method of measuring acid reflux
Esophageal impedance monitoring: Combined with esophageal pH monitoring; by nature of its ability to detect both acid as well as nonacid reflux, impedance pH monitoring has greater sensitivity than pH monitoring alone in the detection of GER.
Upper GI series: Neither sensitive nor specific for GER but may be useful for the evaluation of anatomic abnormalities.

59. TREATMENT OPTIONS Diet:
Milk-thickening agents (e.g., cereal) may decrease frequency of vomiting.
Trial of hypoallergenic formula (e.g., protein hydrolysate) in formula-fed infants.
Lifestyle: Children and adolescents with GERD should avoid caffeine, chocolate, and spicy foods that provoke symptoms. Obesity, exposure to tobacco smoke, and alcohol are also associated with GER.
Acid-suppressant therapy: PPIs and histamine-2 receptor antagonists (H2RAs) are effective in relieving symptoms and promoting mucosal healing when acid reflux is present. PPIs are superior to H2RAs for this purpose.
Prokinetic therapy:
Literature supports use of erythromycin; if use of a prokinetic agent is warranted, erythromycin in combination with acid suppression should be considered. Current literature insufficient to either support or oppose use of metoclopramide for GERD in infants, it should not be considered a treatment option.

60. Diarrhea

61. Definition
Usual stool output is 10 g/kg/day in children and 200 g/day in adults.
Diarrhea is characterized by passage of loose or watery stools. The volume of fluid lost through stools can vary from 10 mL/kg/day (approximately normal) to >200 mL/kg/day.
Acute diarrhea is >3 loose or watery stools per day.
Chronic diarrhea is diarrhea lasting more than 14 days.

62. Etiology
Diarrhea may be infectious or malabsorptive, and the mechanism is either osmotic or secretory.
Underlying etiology should be determined to further assist in management.

63. Etiology
Osmotic diarrhea: Stool volume depends on diet and decreases with fasting (fecal ion gap ≥100 mOsm/kg).
Secretory diarrhea: Stool volume is increased and does not vary with diet (fecal ion gap <100 mOsm/kg).

64. Management Oral rehydration therapy (ORT): Diet:
Mainstay of initial management regardless of etiology.
Parenteral hydration is indicated in severe dehydration, hemodynamic instability, or failure of ORT.
Diet:
Breast-feeding should continue
regular diet should be restarted as soon as the patient is rehydrated, unless found to be the source of the diarrhea

65. Management
Other:
Nonspecific antidiarrheal agents (e.g., adsorbents such as kaolin-pectin), antimotility agents (e.g., loperamide), antisecretory drugs, and toxin binders (e.g., cholestyramine) have limited data regarding efficacy.
If infectious, antimicrobial therapy may be indicated.
If malabsorptive disorder (e.g., celiac disease, inflammatory bowel disease), therapy should be tailored to that disease process (e.g., gluten-free diet, steroids).
Zinc elemental (2 mg/kg/d) for 14 days.
Probiotics

66. OVERALL GOALS OF FLUID AND ELECTROLYTE MANAGEMENT
Estimate Fluid and electrolyte
Deficits
Maintenance requirements
Ongoing losses
Select and administer appropriate fluids
Select fluids for the following:   
1.    Initial replacement: Always with isotonic fluid (i.e., normal saline or lactated Ringer's solution).   
2.    Maintenance requirements and ongoing losses.

67. HOLLIDAY-SEGAR METHOD
Water
Body Weight
mL/kg/day
mL/kg/hr
Electrolytes (mEq/100 mL H2O)
First 10 kg
100 ∼4
Na+ 3
Second 10 kg 50 ∼2
Cl- 2
Each additional kg 20 ∼1
K+ 2
Note The Holliday-Segar method is not suitable for neonates < 14 days old; generally, it overestimates fluid needs in neonates compared with the caloric expenditure method.

68. STANDARD VALUES FOR USE IN BODY SURFACE AREA METHOD
1500 mL/m2/24 hr
Na+
30–50 mEq/m2/24 hr K+
20–40 mEq/m2/24 hr
Based on the assumption that caloric expenditure is related to BSA ( Tabel 11-3 ). It should not be used for children <10 kg. See BSA nomogram in Formulary Adjunct.

69. DEFICIT THERAPY
The most precise method of assessing fluid deficit is based on pre-illness weight. If this is not available, clinical observation may be used, as described subsequently.
Fluid deficit (L) = pre-illness weight (kg) - illness weight (kg)
% Dehydration = (pre-illness weight - illness weight)/pre-illness weight × 100%

70. CLINICAL OBSERVATIONS IN DEHYDRATION[*]
Older Child
3% (30 mL/kg)
6% (60 mL/kg)
9% (90 mL/kg)
Infant
Examination
5% (50 mL/kg)
10% (100 mL/kg)
15% (150 mL/kg)
Dehydration
Mild
Moderate
Severe
Skin turgor
Normal
Tenting
None
Skin (touch)
Dry
Clammy
Buccal mucosa/lips
Moist
Parched/cracked
Eyes
Deep set
Sunken
Tears
Present
Reduced
Fontanelle
Flat
Soft
CNS
Consolable
Irritable
Lethargic/obtunded
Pulse rate
Slightly increased
Increased
Pulse quality
Weak
Feeble/impalpable
Capillary refill
∼2 sec
>3 sec
Urine output
Decreased
Anuric
For the same degree of dehydration, clinical symptoms are generally worse for hyponatremic dehydration than for hypernatremic dehydration.

71. ELECTROLYTE COMPOSITION OF VARIOUS BODY FLUIDS[*]
Na+ (mEq/L)
K+ (mEq/L)
Cl- (mEq/L)
Gastric
20–80
5–20
100–150
Pancreatic
120–140
5–15
90–120
Small bowel
100–140
90–130
Bile
80–120
Ileostomy
45–135
3–15
20–115
Diarrhea
10–90
10–80
10–110
Burns[†]
140 5
110
Sweat
 Normal
10–30
3–10
10–35
 Cystic fibrosis
50–130
5–25
50–110
This table is useful in determining ongoing electrolyte losses in dehydration.
3–5 g/dL of protein may be lost in fluid from burn wounds.

72. Contoh perhitungan kebutuhan cairan
Anak Budi, berat badan 8,5 kg dengan dehidrasi berat dengan tanda-tanda syok hipovolemik (tanpa penyakit penyerta)
1. Kebutuhan cairan rumatan:
Berdasarkan Holliday Segar:
8,5 kg x 100 ml/kg/ 24 jam = 850 ml/24 jam
2. Kebutuhan cairan defisit dehidrasi berat 10-15%
(= ml/kg)
Disini tidak diketahui BB sebelum sakit sehingga di perkirakan defisit sebesar 10% = 100 ml/kg
8,5 kg x 100 ml/kg = 850 ml
Disini defisit cairan harus dikoreksi segera, dengan adanya tanda syok hipovolemik defisit dapat diberikan:
30 ml/kg = 255 ml dalam waktu 30 menit
70 ml/kg = 595 ml dalam waktu 2 jam 30 menit
Target defisit terkoreksi dalam waktu 3 jam.
3. Kebutuhan akan kehilangan cairan yang terus berlangsung (on going losses)
10 ml/kg/ x BAB cair
5ml/kg/ x muntah
Dalam hal ini monitoring pasien sangat penting. Dapat dilakukan tiap 4 jam, dilakukan pencatatan frekuensi muntah dan diare, sehingga jumlah cairan yang hilang dapat digantikan per oral dengan cairan rehidrasi oral, atau ditambahkan ke dalam cairan rumatan.

73. Thank you