Transcript gastrointestinal emergencies

Pontianak, 8 Maret 2012
Dr. Rini Andriani, Sp A
Fakultas Kedokteran UNTAN
Anatomy
1. Gastrointestinal Bleeding
2. Acute Abdomen
GASTROINTESTINAL BLEEDING
 Blood loss from the gastrointestinal (GI) tract
occurs in four ways:
 1. Hematemesis
 2. Hematochezia
 3. Melena
 4. Occult bleeding

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.
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).

DIFFERENT DIAGNOSIS OF GI BLEEDING
Age
Upper GI
Neonates (0-30 days)
Swallowed maternal blood
Gastritis
Infant (>30 days – 1 year)
Gastritis
Esophagitis
Peptic ulcer disease
Preschool (1-5 year)
Gastritis
Esophagitis
Peptic ulcer disease
Esophageal varices
Epistaxis
School age and adolescent
Esophageal varices
Peptic ulcer disease
Epistaxis
Gastritis
Lower GI
Necrotizing enterocolitis
Malrotation and midgut volvulus
Anal fissure
Hirschprung disease
Anal fissure
Allergic proctocolitis
Intususception
Meckel’s diverticulum
Lymphonodular hyperplasia
Intestinal duplication
Infectious colitis
Juvenile polyp’s
Meckel’s diverticulum
Lymphonodular hyperplasia
Hemolytic-uremic syndrome
Henoch-Schönlein purpura
Infectious colitis
Anal fissure
Inflammatory bowel disease
Infectious colitis
Juvenile polyps
Anal fissure
Hemorrhoids
ACUTE ABDOMEN
1.
Differential diagnosis: GI Source
Appendicitis
Pancreatitis
Intussusception
malrotation with volvulus
inflammatory bowel
disease
Gastritis
bowel obstruction
mesenteric lymphadenitis
irritable bowel syndrome
Abscess
Hepatitis
perforated ulcer
Meckel diverticulitis
Cholecystitis
Choledocholithiasis
Constipation
gastroenteritis
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.
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.
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.
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
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
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.
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
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
UERMMMC Department Of Radiology
Malrot/Midgut Volvulus
Cross Table Lateral
“DOUBLE BUBBLE SIGN”
Supine
UERMMMC Department Of Radiology
Malrotation/Midgut Volvulus
UERMMMC Department Of Radiology
Malrotation/Midgut Volvulus
S
S
d
d
UERMMMC Department Of Radiology
Spiraling of
contrast material
Duodenal atresia
 Obliteration of lumen
 Failure to recanalize
Double
bubble sign
 Neonatal bilious vomiting
 Associations
 Prematurity
 Congenital heart defects
 Trisomy 21
!
SURGICAL
EMERGENCY
Complete
small bowel
obstruction
UERMMMC Department Of Radiology
Duodenal Atresia
Cross Table Lateral
“DOUBLE BUBBLE SIGN”
Supine
UERMMMC Department Of Radiology
Duodenal Atresia
S
D
•Distended Stomach & Duodenum
•No gas distally
UERMMMC Department Of Radiology
Gastric Atresia
Cross Table Lateral
Supine
UERMMMC Department Of Radiology
Gastric Atresia
•Distended Stomach
•No gas distally
UERMMMC Department Of Radiology
Jejunal Atresia
Cross Table Lateral
“TRIPLE BUBBLE SIGN”
Supine
UERMMMC Department Of Radiology
Jejunal Atresia
S
D
J
•Distended stomach, duodenum, and jejunal segement
•No gas distally
Stomach/duodenum – Bleeding
Presentation –
Haematemesis +/Melaena
Severity
Increased CR
Fall BP
Causes
DU, erosions, GU
Treatment – control bleeding
transfusion
Stomach/duodenum – Perforation
Presentation –
abdominal pain
rigidity
peritonism, shock
Air under diaphragm on X-ray
Treatment
antibiotics, resuscitate
repair
Pancreas
Acute pancreatitis
Constant pain, vomiting,
shock
Causes
Gallstones, or
Alcohol
Diagnosis
Serum amylase
elevation, US
complications
pseudocyst, phlegmon
abcess
Small Intestine
Meckel’s Diverticulum
rare
diverticulum of
terminal ileum
can be lined by gastric
epithelium
can perforate
can present like
appendicitis
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
Small Intestine
Intestinal obstruction
May arise due to
adhesions, hernia, tumour
Presentation
colicky abdominal pain,
vomiting, constipation
Treatment
resuscitate/operate
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
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
Intussusception
Terminal ileum telescoped
into cecum
Small Intestine
Mesenteric infarct
Sudden occlusion of small
bowel arterial supply
Sudden onset of abdominal pain, shock
Peritonitis
Treatment
resuscitate/operate
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
Hirschsprung’s
AXR:
obstructive
pattern
Barium enema:
Dilated
proximal colon
with transition
zone
Suction rectal bx
Absence of
ganglion cells
in myenteric
plexus
Hirschsprung’s
Surgical treatment
1. Colostomy
2. Pull-through and removal of
aganglionic segment
Inguinal hernia
 Common surgical problem
 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
Umbilical hernia
 Incomplete closure of
umbilical ring fascia
 More common in
premature and AfricanAmerican infants
 Usually close by 2-4 yrs
 Refer to surgery if:
 Larger than 1.5 cm at 2 yrs
 Present after 4 yrs
 Supraumbilical
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
 OBJECTIVES
 Recognize
 Diagnose
 Consult surgery
Major Symptom and Signs of GI Disorders
 Dysphagia
 Regurgitation
 Vomiting
 Anorexia
 Diarrhea
 Constipation
 Abdominal Pain
 GI Bleeding
 Abdominal distention and mass
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












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
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.
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.
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.
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
Evaluation of vomiting
Type
Etiology
Typically bilous Obstruction
Intussusception
Malrotation
Volvulus
Pancreatitis
Intestinal dysmotility
Incarcerated inguinal hernia
Intestinal Atresia, stenosis
Evaluation
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.
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
Either billous or
nonbillous
Ileus
Appendicitis
AVOID antiemetics
unless specific, benign
etiology is suspected
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.
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.
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.
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.
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.
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).
Management
 Oral rehydration therapy (ORT):
 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
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
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.
HOLLIDAY-SEGAR METHOD
Water
Body Weight
First 10 kg
Second 10 kg
Each
additional kg
mL/kg/day
100
50
mL/kg/hr
∼4
∼2
Electrolytes
(mEq/100 mL
H2O)
Na+ 3
Cl- 2
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.
STANDARD VALUES FOR USE IN BODY SURFACE AREA METHOD
H2O
Na+
K+
1500 mL/m2/24 hr
30–50 mEq/m2/24 hr
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.
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)/preillness weight × 100%
CLINICAL OBSERVATIONS IN DEHYDRATION[*]
3% (30 mL/kg)
Older Child
6% (60 mL/kg)
9% (90 mL/kg)
Examination
5% (50 mL/kg)
Infant
10% (100 mL/kg)
15% (150 mL/kg)
Dehydration
Skin turgor
Skin (touch)
Buccal mucosa/lips
Mild
Normal
Normal
Moist
Moderate
Tenting
Dry
Dry
Severe
None
Clammy
Parched/cracked
Eyes
Tears
Fontanelle
CNS
Normal
Present
Flat
Consolable
Deep set
Reduced
Soft
Irritable
Sunken
None
Sunken
Lethargic/obtunded
Pulse rate
Normal
Slightly increased
Increased
Pulse quality
Normal
Weak
Feeble/impalpable
Capillary refill
Urine output
Normal
Normal
∼2 sec
Decreased
>3 sec
Anuric
For the same degree of dehydration, clinical symptoms are
generally worse for hyponatremic dehydration than for
hypernatremic dehydration.
ELECTROLYTE COMPOSITION OF VARIOUS BODY FLUIDS[*]
Fluid
Gastric
Pancreatic
Small bowel
Bile
Ileostomy
Diarrhea
Burns[†]
Sweat
Normal
Cystic fibrosis
Na+ (mEq/L)
20–80
120–140
100–140
120–140
45–135
10–90
140
K+ (mEq/L)
5–20
5–15
5–15
5–15
3–15
10–80
5
Cl- (mEq/L)
100–150
90–120
90–130
80–120
20–115
10–110
110
10–30
50–130
3–10
5–25
10–35
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.
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%
(= 100-150 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.