A Bowel Inside a Bowel: Intussusception

The Case

A 14 month-old female with no significant PMH who presented to the Emergency Department with vomiting. Per mom, patient was well yesterday, but today has been refusing food, crying and vomiting. Patient has had no known sick contacts and her vaccinations are up to date. A review of systems was performed and was otherwise negative.

Physical Exam

Vital signs were within normal limits. Patient was listless with decreased responsiveness, but not in distress. No evidence of respiratory compromise. Abdominal exam was unremarkable, with no focal tenderness and no guarding, rigidity or rebound. During the time the examiner was present in the room, the patient had one episode of crying inconsolably and then vomiting.

An abdominal ultrasound was performed and the diagnosis was revealed to be Intussusception


Ultrasound has been shown to be 97.9% sensitive and 97.8% specific for diagnosing ileocolic intussusception. To evaluate for intussusception, start with the high frequency low penetration linear transducer. In most young children this transducer will provide adequate depth. In an older child, you may have to use the higher penetration curvilinear transducer. If available, use warm gel to minimize patient discomfort and thereby increasing your changes of obtaining clear images. Begin in the transverse plane and slide your probe up to the right upper quadrant, across, and then down the left side, interrogating for the intussusception (Figure 1).

Figure 1: Suggested path of the ultrasound transducer to evaluate for intussusception.  (https://www.acep.org/how-we-serve/sections/emergency-ultrasound/news/september-2018/pediatric-emergency-ultrasound-deep-dive-on-pocus-for-intussusception/)

Figure 1: Suggested path of the ultrasound transducer to evaluate for intussusception.


Most of the intussusceptions will be found on the right hand side, and are described as a “target sign” when you are viewing the intestinal intussusception in transverse or the “sandwich sign” in long axis.  The “lawn-mower” approach can be used, similar to the approach for SBO, and graded compression along your path can help move bowel gas out of the way to better evaluate the intestine. The hyperechoic rings are the mucosa and muscularis and the hypoechoic portion is the submucosa.  

Case Discussion

Intussusception is the most common abdominal emergency in early childhood, with the majority of cases occurring in patients <2 years of age. It occurs when the bowel telescopes in on itself and gets stuck. The peristaltic waves of the bowel causes waves of pain in the patient. The classic triad is described as pain, vomiting and bloody stools. Ultrasonography is the preferred diagnostic modality to evaluate for intussusception, given the high sensitivity and specificity (97.9% and 97.8% respectively) when performed by a skilled clinician. Ultrasound also has a high negative predictive value (approaching 99.7%) and can rule out intussusception in a majority of patients. Intussusception presents on ultrasound as a peripheral hypoechoic ring surrounding a central echogenic focus described as either a "target sign” or a “doughnut sign.” (Figure 2a) The visualized doughnut represents the layers of the intestinal wall that have invaginated into themselves. Color doppler can be applied to evaluate for tissue ischemia. (Figure 2b) The most common type of intussusception, ileocolic (as in this case) is usually found in the right lower quadrant. There is usually associated focal tenderness in the right lower quadrant (though this patient was non-tender). Treatment of a non-perforated intussusception typically consists of reduction via air enema, but sometimes operative management is indicated.

Figure 2: Ultrasound image of intussusception

Figure 2: Ultrasound image of intussusception

FPIES: Expanding the Differential for Hypotension in the Pediatric Patient


An 8-month-old male, full term, infant with no significant past medical history presents to the ED for nausea, vomiting, and non-bloody diarrhea for the past several hours. His family has slowly been introducing new foods into his diet. There are no known sick contacts. He is well-appearing, hemodynamically stable, and tolerating PO in the ED. After some observation, the patient was discharged with the diagnosis of viral gastroenteritis.

Six days later, the same patient presented with profuse vomiting, diarrhea, and profound lethargy. He was found to be tachycardic and hypotensive. He was taken to the critical care area for altered mental status, unstable vital signs, and undifferentiated shock. His exam was notable for lethargy, pallor, and a distended abdomen. Initial labs showed a metabolic acidosis, eosinophilia, and thrombocytosis. Stool studies and UA were unrevealing. Abdominal plain films were normal.


FPIES - What is it?

As many ED practitioners are aware, food allergies are common in the first 2 years of life, with a prevalence cited between 1-10% of the population. Most food allergies are IgE-mediated hypersensitivity reactions. Food protein-induced enterocolitis (FPIES) is a syndrome characterized by a severe non-IgE mediated food hypersensitivity reaction. FPIES is important to keep on the differential as the syndrome often goes unrecognized or is misdiagnosed at the initial (or subsequent) presentation. (1)

FPIES is characterized by profound and repetitive vomiting, and occasionally diarrhea, 1-4 hours after exposure to the causal protein. In the acute setting, this can manifest as dehydration and lethargy. More than 15% of FPIES patients will require admission for hemodynamic instability secondary to dehydration. In the chronic setting, pediatric patients can present as failure to thrive and/or unexplained weight loss. The most common food triggers in FPIES are cow milk's and soy. FPIES may be induced by solid food, including grains, meat and poultry, eggs, vegetables and fruit, seafood, and legumes. (1,3)

Though the underlying mechanism of FPIES is not clearly understood, it differs from other allergen mediated reactions as it is not triggered by an (IgE)-mediated hypersensitivity. Preliminary research indicates that there is inflammation within the lamina propria and epithelium in both the small and large intestine secondary to increased tumor necrosis factor-alpha (TNF-α) expression by activated T cells. Downstream, this causes increased intestinal permeability which contributes to pathogenesis of FPIES. (4, 8)

Figure A.

Figure A.


Patients with acute presentations tend to be sicker and may develop pallor, hypotension/shock, and/or hypothermia. Failure to thrive and weight loss are seen in patients with chronic FPIES.

  • Lethargy (70%)

  • Pallor (70%)

  • Dehydration

  • Hypotension (15%)

  • Hypothermia (25%)

  • Abdominal distension


Labs often reveal anemia, hypoalbuminemia, and an elevated white blood cell count with a left shift. Eosinophilia is often seen in chronic FPIES. Thrombocytosis was found in 65 percent of acute FPIES. Metabolic acidosis (mean pH 7.03) and methemoglobinemia have been reported in both acute and chronic FPIES. Transient methemoglobinemia was reported in about one-third of acute FPIES infants with some requiring methylene blue treatment. Methemoglobinemia may be caused by severe intestinal inflammation and reduced catalase activity resulting in increased nitrites. (5)

Diagnostic imaging studies are not part of the standard FPIES workup, but some older studies have analyzed trends. Although findings are nonspecific, it is important to be familiar with them as often these infants get imaging as part of their workup.

Findings include:

  • Air fluid levels

  • Nonspecific narrowing and thumb-printing of rectum and sigmoid colon

  • Thickening of plicae circulares in duodenum and jejunum

  • Excess luminal fluid

  • Rarely intramural gas (which can lead to misdiagnosis of NEC)

Resolution of radiographic abnormalities after dietary restriction has been documented. (1, 3, 5)


Given the clinical picture of FPIES is nonspecific, the ED physician can arrive at the diagnosis more quickly by obtaining a brief dietary history. This especially holds true if the patient has been seen multiple times in the ED prior for similar complaints. In infants, the causes of acute repetitive vomiting and severely altered mental status includes a broad differential diagnosis. Sepsis, infectious gastroenteritis, head injury, toxicologic, gut malrotation, intussusception, NEC, pyloric stenosis, as well as other metabolic and cardiogenic causes can present similarly. In patients with such symptoms, allergy as a cause is sometimes not considered by ED physicians. Diagnosis of FPIES is based on the recognition of clinical manifestations, exclusion of alternative causes, and a physician-supervised oral food challenge (OFC). Diagnosis is often made in the inpatient or primary care setting, and is based on presence of a major criterion as well as three minor criteria as seen below.

Below are some quick and dirty rules to differentiate FPIES from other diagnoses:

Food protein-induced proctocolitis: Infants are well-appearing and thriving, unlike acute FPIES children. Present with blood streaked stools in first months of life.

Anaphylaxis: Time to symptoms is much shorter (usually minutes vs. 2-4 hours). Have constellation of associated symptoms not seen in FPIES: rash, respiratory distress/stridor. Symptoms resolve with IM epinephrine.

Infections/Sepsis: Usually present febrile (or less often hypothermic) and often with a history of sick contacts. Labs showing leukocytosis with a left shift/bandemia (vs eosinophilia in FPIES). There may be a presence of respiratory symptoms if sepsis 2/2 to PNA, viral URI. Septic patients typically do not improve with IVF alone (unlike FPIES patients).

Necrotizing enterocolitis: Systemic and abdominal symptoms seen in NEC that are not typical of FPIES include apnea, respiratory failure, temperature instability, intramural gas on abdominal radiograph. NEC is usually at a much earlier age, and often within the first few days of life.

Intestinal obstruction: There are reports of ex-laps being performed when acute FPIES was mistaken for ileus. Obstruction often presents with more pronounced distention and history of decreased to no stool output (FPIES infants can have normal stool output and/or diarrhea).

Intussusception: While the classic teaching is currant jelly stools, this is rarely present. Vomiting/discomfort waxing and waning over protracted period of time, and pain may be more predominant.

Pyloric Stenosis: Usually between 2 weeks and 2 months of life before the introduction of solid foods. There may be an olive-shaped mass in epigastrium, and ultrasound confirms the diagnosis.

Metabolic disorders: May have other features, such as hypoglycemia, hematologic abnormalities (ex, anemia, neutropenia, thrombocytopenia), liver dysfunction (hepatomegaly, jaundice), renal disease, and developmental delay.

Data shows that of FPIES patients presenting to the ED, 34% of patients undergoing abdominal imaging, 28% undergoing a septic evaluation, and 22% having a surgical consultation. Misdiagnosis and delays in diagnosis for children with food protein-induced enterocolitis syndrome were common, leading many children to undergo unnecessary investigations. (6, 7, 9)


The patient mentioned in the case earlier was subsequently admitted to the PICU for further workup and resuscitation. After many diagnoses were ruled out, and in conjunction with thorough dietary review, it was found that the patient had both of these episodes after exposure to sweet potato. The diagnoses of FPIES was made and patient was discharged to home in good health with rheumatology follow up.

For acute presentations, patients often require admission for fluid resuscitation, symptom management, and parent education. For chronic FPIES patients, it is sometimes reasonable to discharge patient to home, but this should always be done in conjunction with primary care doctor as well as expectant management and education. Often times, labs can be drawn in the emergency setting as a conduit to help the patient’s PCP rule out other causes (such as IgE-mediated allergies). (2, 3)

Faculty Reviewer: Dr. Jane Preotle



  1. Nowak-Węgrzyn A, Katz Y, Mehr SS, Koletzko S. Non-IgE-mediated gastrointestinal food allergy. J Allergy Clin Immunol 2015; 135:1114.

  2. Nowak-Węgrzyn A, Chehade M, Groetch ME, et al. International consensus guidelines for the diagnosis and management of food protein-induced enterocolitis syndrome: Executive summary-Workgroup Report of the Adverse Reactions to Foods Committee, American Academy of Allergy, Asthma & Immunology. J Allergy Clin Immunol 2017; 139:1111.

  3. Mehr S, Kakakios A, Frith K, Kemp AS. Food protein-induced enterocolitis syndrome: 16-year experience. Pediatrics 2009; 123:e459.

  4. Caubet JC, Nowak-Węgrzyn A. Current understanding of the immune mechanisms of food protein-induced enterocolitis syndrome. Expert Rev Clin Immunol 2011; 7:317.

  5. Sicherer SH, Eigenmann PA, Sampson HA. Clinical features of food protein-induced enterocolitis syndrome. J Pediatr 1998; 133:214.

  6. Ruffner MA, Ruymann K, Barni S, et al. Food protein-induced enterocolitis syndrome: insights from review of a large referral population. J Allergy Clin Immunol Pract 2013; 1:343.

  7. Coates RW, Weaver KR, Lloyd R, et al. Food protein-induced enterocolitis syndrome as a cause for infant hypotension. West J Emerg Med 2011; 12:512.

  8. Sampson HA, Anderson JA. Summary and recommendations: Classification of gastrointestinal manifestations due to immunologic reactions to foods in infants and young children. J Pediatr Gastroenterol Nutr 2000; 30 Suppl:S87.

  9. Jayasooriya S, Fox AT, Murch SH. Do not laparotomize food-protein-induced enterocolitis syndrome. Pediatr Emerg Care 2007; 23:173.

  10. Figure A: Berin, M. Cecilia. Immunopathophysiology of food protein-induced enterocolitis syndrome. Journal of Allergy and Clinical Immunology, Volume 135. Issue5. 1108-1113

Orbital Floor Blowout Fracture


A 16-year-old male presents with head trauma. The patient was in gym class when another classmate ran into him, kneeing him in the left eye. There was no loss of consciousness. On presentation, the patient complains of headache, dizziness, nausea, visual disturbance, and photophobia. He has vomited several times. On review of systems, the patient also endorses double vision and numbness over the left cheek. The patient’s mother notes he is alert but is slow to respond to questions.  He has no prior history of facial fractures.

Physical Exam

BP 130/70, HR 58, RR 20, SpO2 99% on RA, Temp 98.6 F

The patient is alert and oriented.  He appears uncomfortable but is in no acute distress.

HEENT exam with left periorbital ecchymosis and edema, with tenderness to palpation. Diminished sensation to light touch over cheek and upper lip. Nasal bridge swelling and tenderness, with subtle nasal deviation to the right. No septal hematoma. Symmetric smile.

Pupils are equal, round, and reactive to light. No hyphema or subconjunctival hemorrhage. Left eye with decreased up-gaze as compared to the right. Extraocular movements of the left eye are painful.

The neck has normal range of motion. There is no cervical midline tenderness to palpation.

The patient’s history and examination are significant for trauma to the left eye and face. His examination reveals bony tenderness, with decreased sensation to light touch, and evidence of inferior rectus entrapment as evidenced by abnormal extraocular movements. These findings are concerning for orbital blow-out fracture. There is also concern for nasal bone fracture given nasal bridge swelling, tenderness, subtle deviation, and epistaxis. Given patient’s nausea, vomiting, dizziness, and slowed responses to questions (as per patient’s mother), intracranial injury was also considered.

The patient underwent a CT of the brain and face, with thin (1mm) cuts through the orbits (Figure 1).

Figure 1: Axial CT of the face (bone window) with fracture through the left orbital floor, with herniation of the orbital fat (“teardrop” sign) and inferiorly displaced inferior rectus muscle

Figure 1: Axial CT of the face (bone window) with fracture through the left orbital floor, with herniation of the orbital fat (“teardrop” sign) and inferiorly displaced inferior rectus muscle


Figure 2: Anatomy of the orbit (https://en.wikipedia.org/wiki/File:Orbital_bones.png)

Figure 2: Anatomy of the orbit (https://en.wikipedia.org/wiki/File:Orbital_bones.png)

The orbit is composed of six bones. The frontal bone forms the superior orbital rim and the roof of the orbit. The sphenoid bone and the zygomatic bone form the lateral wall of the orbit. The maxilla and the zygomatic bone form the infraorbital rim and floor of the orbit. Finally, the maxilla and ethmoid bones form the medial wall of the orbit (Figure 2).

Housed within, or within in close proximity to the bony orbit are the globe, six extra-ocular muscles, the infraorbital and supraorbital nerves, lacrimal duct system, medial and lateral canthal ligaments, and 4 pairs of sinuses (Neuman).

A blowout fracture is a fracture through any of the orbital walls, with an inferior fracture through the floor being the most common (Knipe). It is caused by direct force to the orbit. In children, nearly 50% of these injuries occur during sports, with the direct blow usually coming from a ball or another player (Hatton).

A trap door fracture is a sub-type of the orbital floor fracture. It is a linear fracture that inferiorly displaces and then recoils back to near-anatomic position. With this movement there is concern for entrapment of orbital fat and inferior rectus muscle, resulting in ischemia, restriction of ocular movement, and visual disturbance (Hacking). The trap door fracture is predominantly seen in the pediatric population, owing to increased elasticity of the orbital floor (Chung, Grant).

Clinically, a patient will present with periorbital edema and ecchymosis. Altered sensation or numbness over the cheek, upper lip, and upper gingiva is suggestive of infraorbital nerve injury. Proptosis of the eye is suggestive of orbital hematoma. A posteriorly displaced globe (enophthalmos) is suggestive of increased orbital volume secondary to fracture. An inferiorly displaced globe (orbital dystopia) is a result of muscle and fat prolapse into the maxillary sinus. Restricted and/or painful extraocular movements are suggestive of muscle entrapment (Neuman).

In children, a phenomenon called the oculocardiac reflex can occur. Stimulation of the ophthalmic division of the trigeminal nerve due to traction or pressure on the extraocular muscles or globe results in excitation of the vagus nerve, leading to bradycardia, nausea, and syncope. In severe cases, asystole can occur (Sires).

CT of the face, with thin (1mm) cuts through the orbit is the primary modality used for identification of orbital blowout fractures. Plain radiographs of the face and orbits are no longer the gold standard as they have poor sensitivity and specificity.  Trap door fractures may be occult, but any evidence of soft tissue herniation into the maxillary sinus (also known as the “teardrop” sign) should raise suspicion for a clinically significant fracture.

These injuries can be severe, and are often more significant in the pediatric population than the adult population, owing to associated soft tissue and muscular injuries. Almost half of children with this injury will require surgery, most frequently due to entrapment. Nearly half of pediatric patients will have ocular injuries (globe rupture, hyphema, retinal tear) and nearly one third of patients will have a second facial fracture (Hatton). 

Urgent ophthalmology and facial surgery consultations are indicated for orbital floor fractures with concern for entrapment (Chung).

Symptomatic treatment includes:

  • Head of bed elevation

  • Ice

  • Sinus precautions: no nose blowing, sneeze with the mouth open, no straw use or sniffing

  • Analgesia and anti-emetics as needed


For orbital fractures with extension into a sinus, the use of prophylactic antibiotics has limited data and often varies by institution (Neuman).

Corticosteroids are recommended for patients with diminished extraocular movements to reduce swelling and expedite improvement in diplopia (Neuman).

For orbital blowout fractures with evidence of entrapment and/or oculocardiac reflex, repair should be performed within 24-48 hours. Delayed repair (more than 2 weeks after injury) can be considered if mild-moderate diplopia is not spontaneously improving, or patient has worsening of enopthalmos > 2mm after initial edema and inflammation has resolved.  Other indications for surgical repair include large fracture (involvement of greater than 50% of the orbital floor) or multiple fractures (Chung).



The patient was admitted for observation overnight in the setting of persistent nausea, vomiting, borderline bradycardia, and diplopia. He was placed on oral prednisone, as well as anti-inflammatory medication. Overnight his symptoms and heart rate improved, although he had persistent diplopia, with diminished upward gaze of the left eye. He was discharged home on hospital day 1, with plan for ophthalmology and facial surgery follow-up for operative planning.

Faculty Reviewer: Dr. Jane Preotle



  1. Chung, Stella Y., and Paul D. Langer. “Pediatric Orbital Blowout Fractures.” Current Opinion in Ophthalmology, vol. 28, no. 5, 2017, pp. 470–476., doi:10.1097/icu.0000000000000407.

  2. Grant, John H., et al. “Trapdoor Fracture of the Orbit in a Pediatric Population.” Plastic and Reconstructive Surgery, vol. 109, no. 2, 2002, pp. 490–495., doi:10.1097/00006534-200202000-00012.

  3. Hacking, Craig. “Trapdoor Fracture.” Radiopaedia.org, radiopaedia.org/articles/trapdoor-fracture.

  4.  Hatton, Mark P., et al. “Orbital Fractures in Children.” Ophthalmic Plastic and Reconstructive Surgery, vol. 17, no. 3, 2001, pp. 174–179., doi:10.1097/00002341-200105000-00005. 

  5. Knipe, Henry, and Frank Gaillard.  “Orbital Blowout Fracture.” Radiopaedia.org, radiopaedia.org/articles/orbital-blowout-fracture-1.

  6. Neuman, Mark, and Richard G Bachur. “Orbital Fractures.” UpToDate, www.uptodate.com/contents/orbital-fractures.

  7. Sires, Bryan S. “Orbital Trapdoor Fracture and Oculocardiac Reflex.” Ophthalmic Plastic & Reconstructive Surgery, vol. 15, no. 4, 1999, p. 301., doi:10.1097/00002341-199907000-00014.

  8. Soll, D. B., and B. J. Poley. “Trapdoor Variety of Blowout Fracture of the Orbital Floor.” Plastic and Reconstructive Surgery, vol. 36, no. 6, 1965, p. 637., doi:10.1097/00006534-196512000-00017.