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
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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
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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
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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
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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
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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
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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.
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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
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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
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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