Pediatric GI Emergencies and Imaging Modalities
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Transcript Pediatric GI Emergencies and Imaging Modalities
Pediatric GI Emergencies and
Imaging Modalities
Brett Wiesley, MD
Monica Patel, MD
October 6th, 2004
Overview
Topics:
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Pyloric Stenosis
Malrotation
Appendicitis
Intussusception
GI Foreign Body
NEC
Hirschsprung’s Dz
Meckel’s Diverticulum
Outline:
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History
Pathophysiology
Clinical
DDx
Physical Findings
Imaging
Protocols
Management
Hypertrophic Pyloric Stenosis
HISTORY:
Most common obstruction in infants >1mo.
1:250 live births
Males > Females 4:1
White > Black
Some familial patterning
Hypertrophic Pyloric Stenosis
Pathophysiology
Born with normal pylorus – hypertrophy
developes as time progresses
Unknown etiology
Progresses to Gastric Outlet Obstruction
Vomiting = loss of H+, Cl Eventually = Hypochloremic, Hypokalemic
Metabolic Acidosis
Hypertrophic Pyloric Stenosis
Clinical
Present in 2nd – 6th week of life
Gradually progressive emesis
becomes Projectile (remains non-bilious)
Vigorous appetite, rapid feedings
projectile regurgitation of entire volume
Late findings = marasmus (protein-calorie
malnutrition)
Hypertrophic Pyloric Stenosis
DDx
GERD
Malrotation (would be bilious)
Toxic Ingestions
Increased ICP
Sepsis
Remember: only > 2 weeks life & gradual
Hypertrophic Pyloric Stenosis
Physical Findings
Palpable Pylorus “olive”
– Placing NGT facilitates exam
– “pathognomonic”
Hypertrophic Pyloric Stenosis
Radiologic Imaging
Hypertrophic Pyloric Stenosis
New AMC Protocol for Pyloric Stenosis
Hypertrophic Pyloric Stenosis
Management
Fluid & Electrolyte replacement & Labs
– Initial IVF bolus (20ml/kg)
– D5 ½ NS @ 1.5-2.0 maintenance
– K+ replacement is common
Surgical Consultation & Confirmatory Imaging
– Can be done on a semi-elective basis
– Procedure: Pyloromyotomy (open or laproscopic)
– Remember: it’s a chronic progressive disease
Malrotation
History
1:500 live births
Male > Female 2:1
75% will develop volvulus
– ¾ of these in first month
Bilious Emesis is hallmark (75%)
3-15% Mortality
Malrotation
Pathophysiology
Embryologic: GI tract rotates around SMA
– Duodenum fixed by ligament of trietz LUQ
– Cecum fixed into RLQ
– The 2 separated & connected by the mesentery
In Malrotation:
– Incomplete rotation = short stalk
– Duodenum & Cecum reside closely suspended
by their vascular attachment (the SMA)
– Twisting = bowel ischemia & necrosis w/in 1-2hrs
Malrotation
Clinical
“Classic” = sudden onset bilious vomiting &
abdominal distention
– However, high obstruction may = no distention
Infants generally appear ill (possibly shock)
May be intermittant suddenly more intense
Bilious Emesis = possibility of acute
obstruction
Distended ABD & ill = malrotaion/volvulus
until proven o/w
Malrotation
DDx
GERD
Pyloric Stenosis
NEC
Toxic Ingestions
Malrotation
Radiologic Imaging
Malrotation
New AMC protocols for Malrotation
Malrotation
Management
Labs (cbc, bmp)
Fluid Replacement
– Repeated 20ml/kg IVF bolus until VS stabilized
Emergent Pediatric Surgical Consultation
NGT (for ABD decompression)
ill-appearing: may require triple Abx
Appendicitis
History
1 in 15 individuals will develop in lifetime
Peak 9 – 12 y/o (uncommon in <5 y/o)
Overall Mortality < 1%
– Unruptured = 0.1%
– Ruptured = 3-5%
Rate of Rupture inversely related to age
– When < 2 y/o at least 90% have perforated
Appendicitis
Pathophysiology
Appendix is a blind pouch
– Obstruction bacterial proliferation
Edema
Vasocongetion
Inflamm
Ischemia
Infarction
Necrosis
PERFORATION
Adults have thicker appy wall & omentum
– Children do not, & rupture
peritonitis quicker
Appendicitis
Clinical History
Gradual progression of symptoms over 4-24hrs
1st: ABD pain (vague, crampy, periumbilical)
2nd: N/V progressive & accompanied by Anorexia
3rd: ABD pain worsens (severe, constant, & in RLQ)
4th: Fever is late (possibly not until in the ED)
Watch for ‘Multiphasic Course”
1st: Classic ABD pain
Sudden Resolution
Days Later: F/C, ABD pain (acute appy w/ rupture
&
formation of an abscess)
Appendicitis
Clinical Exam
TTP @ McBurney’s Point
Pain w/ mov’t, patient lying still (unable jump)
– Even tapping heels or rocking bed
Hypoactive/Absent bowel sounds
+ Rovsing’s Sign (LLQ palp = tender in RLQ)
+ Psoas Sign = (Hyperextension of Rt. Thigh)
+ Obturator Sign = Internal rot. of flexed R thigh
Appendicitis
DDx
Mesenteric Adenitis
– Usually diffuse ABD pain, but may localized right
middle/lower quadrant. Lack Fever, & no true
peritoneal signs. Usually follows viral illness.
Non-accidental trauma
Munchhausen Syndrome
OB/GYN if female
Torsion (testicle or ovary)
Appendicitis
Radiologic Imaging
Appendicitis
New AMC protocols
Appendicitis
Management
If you suspect Appendicitis
– NPO, IVFs, Analgesia & antiemetics
– CBC w/ diff, urinalysis (icon)
– Broad Spectrum Abx (if perforation suspected)
– Early pediatric surgical consultation
– Arrange imaging modality of choice
xray, US, CT
– Admission
Intussusception
History
Most common obstruction in < 2 y/o
Highest b/w 5 – 12 months
Siblings = 15-20 x greater relative risk
Untreated Intussusception = HIGH mortality
Intussusception
Pathophysiology
Theory: a lead point causes telescoping of
one segment into another.
– Edema
Venous
Ischemia
Peritoneal Irritat
In young kids the lead point is often the result
of enlarged Peyer’s patches after a viral
infection.
> 5 y/o generally have an identifiable lesion
– HSP, Meckel’s, Lymphoma, Polyps, Surgical
Scars, CF
Intussusception
Clinical
Classic triad = ABD pain, N/V & bloody stools
– <33% have all 3
– 75% have 2 findings
– 13% have 0 – 1 findings
Intussusception
Clinical
Cyclical Episodes of Severe ABD pain
– Last ~10-15min, inconsolable, occur ~Q15min
– Often draw legs up to ABD and scream in pain
Blood in Vomit or Diarrhea
– “currant jelly” stool (mucus & blood)
Palpation of “sausage-like” mass in RUQ
– The sausage + empty RLQ (cecum moved) is
known a Dance’s Sign = pathognomonic
Not commonly associated with high fever
Intussusception
DDx
Volvulus
Torsion
– Both Dz with sudden onset of pain
Appendicitis
Constipation
Pancreatitis
– All Dz with slow progressive onset of pain
Intussusception
Radiologic Imaging
Intussusception
New AMC protocols
Intussusception
Management
Initial Stabilization
– IVFs (with 20ml/kg boluses)
– NPO
– NGT (if needed for severe distention)
Prompt pediatric surgical consultation
Abx: If truly ill-appearing
– broad spectrum (zosyn/unasyn)
Imaging Modalities
Surgery needed if reduction fails or perforated
Intussusception
Management
Admission for Observation
– 7–10% of radiologic reductions recur
– 2-5% of surgical reductions recur
– Recurrence usually happens w/in 24hrs
GI Foreign Body
History
Majority due to toddlers putting FB in mouth
Increased Risk Due to:
– Lack of coordination in swallowing
Coins most common (food in adults)
High occurrence in children with MR
GI Foreign Body
Pathophysiology
FB become lodged in areas of narrowing:
– Upper esophageal sphincter
– Aortic arch/tracheal bifurcation
– Lower esophageal sphincter
C6-T1
T4-T6
T10-T11
80-90% objects into stomach pass w/o diff.
GI Foreign Body
Clinical
May be witnessed
Child may present with drooling / dry heaves
Respiratory distress = in airway
Increased risk for Perforation:
– Dysphagia, pain, resp. distress, fever
Button Batteries:
– Esophageal = remove (erosions/mediastinitis)
– Stomach or Beyond = pass w/o diff.
unless stuck @ pylorus
GI Foreign Body
Radiologic Imaging
GI Foreign Body
Management
Removal
– Object in esophagus
– Button battery in esophagous
– Large or Sharp object in stomach
Observation & Follow-up
– Most all objects in stomach
Other techniques
– Advancing object into stomach
– Endoscopy (watch airway)
NEC
History
NEC
Pathophysiology
NEC
Clinical
NEC
Radiologic Imaging
NEC
Management
Hirschsprung’s Disease
History
Hirschsprung’s Disease
Pathophysiology
Hirschsprung’s Disease
Clinical
Hirschsprung’s Disease
Radiologic Imaging
Hirschsprung’s Disease
Management
Meckel’s Diverticulum
History
Meckel’s Diverticulum
Pathophysiology
Meckel’s Diverticulum
Clinical
Meckel’s Diverticulum
Radiologic Imaging
Meckel’s Diverticulum
Management