Can occur in children less than age of 2, but typically presents with peritonitis or sepsis…

At the age of 6 weeks gestation, elongating intestines prolapse into the yolk sac. At 10 weeks, the midgut rotates Counter clockwise 270 degs

(ampicillin aminoglycoside or third-generation cephalosporin, and clindamycin or metronidazole. Vancomycin if indicated

The acute abdomen in the pediatric population. Pete Tilney DO, EMT-P Albany Medical Center Albany NY

Overview: The pediatric abdomen. Abdominal emergencies are often a diagnostic challenge in a child. Some abdominal emergencies are age specific. As a competent clinical EM physician, we must be able to initiate a proper differential diagnosis of the etiologies of abdominal pain in a child.

The Approach: Initial Assessment. What is the patient’s age and gender? What are the patient’s vital signs? Are they febrile? Is the process occurring obstructive or non-obstructive? Are the complaints isolated to the abdomen? Is the child ill appearing?

History: Verbal or non-verbal patient. Events leading up to ED visit Past Medical History Fever at any time leading up to evaluation? OPQRST… Feeding? Bowel/ Bladder Habits. Bloody? Constipation or diarrhea? Vomitus? Bloody? Bilious?

Physical: EXPOSE! EXPOSE! EXPOSE! EXPOSE! Not only do an abdominal exam, complete a thorough head to toe assessment. Complete a rectal and/ or genital exam if indicated. Children are notorious for being unable to qualify pain and identify location of pain.

EXPOSE!

Abdominal Quadrants

Case #1 “My one month old is vomiting…no seriously, he is vomiting across the room.” Increasing projectile vomiting for the last several weeks. V/S demonstrates tachycardia, tachypnea. What is the diagnosis?

Pyloric Stenosis Also known as hypertrophic pyloric stenosis or gastric outlet obstruction Most common obstruction in infants >1mo. 1:250 live births Males > Females 4:1 White > Black Some familial patterning  up to 20% prevalence. First male.

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

Pyloric Stenosis- Clinical Presentation Present in 2nd – 6th week of life Gradually progressive emesis Becomes Projectile (remains non-bilious) Vigorous appetite, rapid feedings, projectile regurgitation of entire volume (arc projection) Late findings = marasmus (protein-calorie malnutrition). Constipation can also occur.

Pyloric Stenosis Figure 1. Transverse sonographic image in a patient with proven hypertrophic pyloric stenosis demonstrates the target sign and heterogeneous echo texture of the muscular layer (pylorus is deep to the anechoic gallbladder). Image courtesy of Emedicine.

Pyloric Stenosis Physical Findings Palpable Pylorus “olive.” (if you feel this, let everyone know). Peristaltic waves left to right… Evidence of dehydration. Tachycardia. “lethargy” Dry mucous membranes.

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 Can be done on a semi-elective basis Procedure: Pyloromyotomy (open or laproscopic) Remember: it’s a chronic progressive disease

Case #2 “My child has eaten a ‘P’.”

Case #2 My child has eaten a letter “P” We were playing scrabble and well, I turned my head away…

GI Foreign Body H and P 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

Foreign Body

Foreign Body

GI Foreign Body Pathophysiology FB become lodged in areas of narrowing: Upper esophageal sphincter C6-T1 Aortic arch/tracheal bifurcation T4-T6 Lower esophageal sphincter T10-T11 80-90% objects into stomach pass w/o diff.

GI Foreign Body 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 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)

Case # 3 “You will never believe this one…”

Appendicitis

Appendicitis

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 and Inflammation  Ischemia  Infarction  Necrosis  PERFORATION Adults have thicker appy wall & omentum Children do not and thus rupture faster  PERITONITIS!!

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 with Sudden Resolution Days Later: Focal and crampy, ABD pain (acute appendicitis 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 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

Images of Appendicitis

Upper and Lower GI Bleeding Multiple Etiologies and Diagnoses Can be difficult to determine causes of minimal or moderate GI bleeding. Repeated Episodes need evaluation including GI studies, endoscopy, etc… Etiologies can vary based on age.

Etiologies of GIB in the neonatal population (under 2 months). Upper GIB Bleeding Diathesis Swallowed maternal blood Vascular malformation Lower GIB Congenital duplications Intussusception Meckel diverticulum Necrotizing Enterocolitis Swallowed maternal blood Vascular Malformation Volvulus

Etiologies of GIB in the infant population (2 months to 2 years) Upper GIB Bleeding diathesis Foreign Body Gastroenteritis Vascular malformation Mallory Weiss tear Lower GIB Anal Fissure HUS HSP IBS Meckel’s Diverticulum Polyps Milk allergy

Etiologies of GIB in the toddler population (over 2 years) Upper GIB Esophageal varices Foreign body Gastroenteritis Mallory Weiss tear PUD Vascular malformation Varices Gastritis Lower GIB Colitis HUS HSP IBS Meckel’s Polyps

Case #4 1 year old male comes in with intermittent abdominal pain lasting 15 mins and then resolves. Oh by the way, the diaper is red…

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. 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, Foreign Bodies

Intussusception Classic triad = ABD pain, N/V & bloody stools <33% have all 3 75% have 2 findings 13% have 0 – 1 findings

Intussusception Physical Exam Blood in Vomit or Diarrhea “currant jelly” stool (mucus & blood)

Intussusception Physical Exam Cyclical Episodes of Severe ABD pain Last ~10-15min, inconsolable, occur ~Q15min Often draw legs up to ABD and scream in pain 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 Radiologic Imaging

Intussusception Management Initial Stabilization IVFs (with 20ml/kg boluses) NPO NGT (if needed for severe distention) Prompt pediatric surgical consultation Air enema preferred over barium 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

Case #5 Through the translator phone, “ My child was fine until a few hours ago. He has been throwing up constantly yellow liquid…”

Malrotation History 1:500 live births Male > Female 2:1 75% will develop volvulus (Life Threatening) ¾ of these in first month Bilious Emesis is hallmark (75%) 3-15% Mortality Progression of symptoms to ischemic or gangrenous bowel can be a few hours

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 intermittent then suddenly more intense without warning. Streaks of blood in stool can be common Bilious Emesis = perhaps acute obstruction Distended ABD & ill = malrotaion/ volvulus until proven o/w

Malrotation Infants: Sudden onset of an acute abdomen with accompanying shock… Rigid/ discolored abdomen. Bloody vomiting/ or stools. Older children Constant pain Most older children have a previous history of midgut volvulus.

Malrotation Be aware: Duodenal stenosis, atresia and Intussusception can all present similarly!!! Consider your differential carefully.

Malrotation Management Labs to identify electrolyte abnormalities and have pre-op labs available. Fluid Replacement Repeated 20ml/kg IVF bolus until VS stabilized Emergent Pediatric Surgical Consultation NGT (for ABD decompression) This is a clinical diagnosis initially.

Malrotation Images

Case #6 While in the PICU, a nurse presents a bloody diaper from a neonate who is scheduled to go to the OR tomorrow for a repair of a “PDA.”

Necrotizing enterocolitis (NEC) The most common GI medical/surgical emergency occurring in neonates. Affects close to 10% of infants who weigh less than 1500 g, Mortality rates of 50% or more depending on severity. More common in premature infants, it can also be observed in term and near-term babies. Unknown etiology

Necrotizing Enterocolitis Presenting symptoms may include: Abdominal distention, decreased bowel sounds Delayed gastric emptying (increased gastric residuals) Vomiting Hematochezia Visible intestinal loops Change in stool pattern A palpable abdominal mass Erythema of the abdominal wall

NEC Nonspecific systemic signs and symptoms: increased apnea bradycardia lethargy temperature Patients with fulminant necrotizing enterocolitis: Profound apnea Rapid cardiovascular and hemodynamic collapse Shock

NEC Radiographic findings: show ileus and/or pneumatosis intestinalis. Severe disease can show portal venous gas with or without ascites

NEC Management IV rehydration and fluid resuscitation NPO Antibiotics (amp, gent, cefotaxime, etc) If the child has advanced stages of NEC TPN Inotropic support Ventilator support Surgical consultation should be obtained.

Thanks