Pediatrics

FPIES: Expanding the Differential for Hypotension in the Pediatric Patient

CASE

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.

DISCUSSION

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.

CLINICAL FEATURES

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

LAB AND IMAGING FINDINGS

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)

THE DIFFERENTIAL: HOW DO THEY DIFFER?

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)

DISPOSITION AND CASE CONCLUSION

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

 

REFERENCES

  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

Hey Kiddo, Take a Seat…

Case 1:

A 13-month-old boy arrives by EMS after a motor vehicle accident. He was a rear passenger, restrained in a front-facing car seat when the vehicle struck a utility pole at high speed. Initially, he was responsive and crying, but became unresponsive and lost vital signs en-route to the ED. In the trauma bay, ROSC is achieved after a brief period of CPR and airway management. His imaging is notable for significant fractures at C1/C2 as well as complex ligamentous disruption; he requires emergent surgical intervention for his spinal injuries, and suffers a severe anoxic brain injury.

Case 2:

Two boys, a 4-month-old and a 3-year-old, arrive by EMS after a low speed, T-bone motor vehicle accident with airbag deployment. Both patients were restrained rear passengers, the 4-month-old in a rear-facing seat, and the 3-year-old in a front-facing seat. In the ED, exam is significant only for some mild abrasions, and both are discharged after a period of observation. The car seats involved in the accident are brought to the ED, and family attempts to use them to transport the children home.

Case 3:

A 5-year-old girl arrives by EMS unresponsive after a front-end collision. She was restrained in her front-facing car seat, when the vehicle struck a telephone pole. Per EMS providers, the seat was not properly restrained within the vehicle. She is apneic with obvious, severe head injuries and asymmetric pupils, with imaging confirming multiple skull fractures and intracranial hemorrhage. Despite maximal interventions, she succumbs to her injuries.

 

Case 4:

A new mother brings her 31-day-old infant for evaluation of vomiting. An exam is performed and is reassuring, consistent with likely reflux, and she is discharged home with close pediatrician follow up in the coming days. On the way out of the exam room, she asks if her car seat is safe to use, as it was a hand-me-down from another family member, and she is not sure if this seat is “expired.”

The Facts:

Unintentional injuries remain a leading cause of death in children. While the number of fatalities from motor vehicle collisions has declined, it remains the cause of death in 1 out of 4 children ages 1-13 [1]. Car safety seats (CSS) have been demonstrated to reduce the risk of injury and death in children, and are credited with saving the lives of 328 children under age 4 in 2016 [2]. Currently, laws exist in all 50 states and Washington D.C. governing the use of child safety seats. The use of car safety seats has been well studied by multiple agencies, including the National Highway Traffic Safety Administration, the Center for Disease Control and Prevention, the Insurance Institute for Highway Safety, and the American Academy of Pediatrics.

We have a duty to our pediatric patients and their families to be familiar with the current recommendations for car safety seats, and provide education and resources when necessary to help prevent morbidity and mortality. In two of the above cases, provider knowledge about these recommendations is critical, and allows rapid intervention on discharge to prevent possible further injuries. As unfortunately common to practitioners in the emergency department, the remaining two cases help reinforce the need for a high index of suspicion for injuries when children present with a history consistent with improper restraint.

 

Current Recommendations [3,10]:

The American Academy of Pediatrics recently released a policy statement published November 2018, highlighting the current recommendations for child safety seats. A summary of recommendations along with a useful flow chart is shown below*:

  • All infants and toddlers should ride in a rear-facing car seat as long as possible, until they reach the height or weight limit listed by the car seat manufacturer

    • It is important to check which type of seat is used rear-facing: infant-only seats have a much lower height and weight limit than convertible or 3-in-1 car seats

  • All children that have outgrown the height or weight limit on a rear-facing seat should ride in a forward-facing seat with a harness until they reach the height/weight limit listed by the manufacturer

  • When children outgrow the height or weight limit of a forward-facing seat, they should use a booster seat until the vehicle lap and shoulder belt fits appropriately, typically when they reach a height of 4 feet 9 inches, and between the age of 8-12

  • When children are old/tall enough to use the vehicle seat belt alone, they should always use both a lap and shoulder belt

  • All children under age 13 should remain restrained in the back seat for optimal protection

*Modified from Table 1: Summary of Best Practice Recommendations, Durbin and Hoffman, Pediatrics, Vol 145 No 5, November 2018

Algorithm to guide implementation of best practice recommendations for optimal child passenger safety:

From: Durbin and Hoffman,  Pediatrics,  Vol 145 No 5, November 2018

From: Durbin and Hoffman, Pediatrics, Vol 145 No 5, November 2018

For the visual learners, the CDC has a graphical representation of the seats with corresponding ages[9]:

Picture2.png

In Rhode Island, specific laws were enacted in 2017, outlining the proper restraint of passengers in vehicles, including children, with a pertinent summary below [4]:

  • All children under age 8, less than 57 inches in height (4 feet 9 inches), and less than 80 pounds should be restrained in a rear sitting position in an approved child restraint system

  • All infants and toddlers less than 2 years of age, or weighing less than 30 pounds, should be restrained in a rear-facing car seat

  • All children 2 years of age or older who outgrow rear-facing car seats should use a forward-facing car seat with harness, up to the maximum allowed by the car seat manufacturer

Frequently Asked Questions:

I have a car seat and am not sure it is installed properly, or am expecting a new baby and not sure how to install my car seat. Where can I go to make sure this is done correctly?

  • There are several options to ensure a child safety seat is installed correctly. The easiest way to do this is to simply search through the National Child Passenger Safety Certification webpage, listed below for a car seat check station. Several options exist, including locating a local agency that will perform a car seat check/installation teaching (most often a local police or fire department), attending a child safety event, or locating a specific inspection station not included in the above [5]. Many children’s hospitals, such as Hasbro Children’s Hospital, also have staff certified for safe car seat installation.

I received a car seat as a hand-me down from another family member, but heard car seats expire. Is this true, and how can I tell if this seat is okay?

  • This is an important, sometimes overlooked fact of child safety seats. While both vehicle and car seat technology have dramatically improved the safety of children riding in vehicles, there are limitations of the seats. Most car seats carry an expiration date 6 years after the manufacture date (although this may vary slightly based on seat construction) [6]. The primary reason for this is the wear and tear placed on the seats themselves, including temperature variation, spills, and physical wear from use of the seat. It is also important to recognize that new technology is continually being produced, which quickly makes older seats less superior in safety. Find the label on the child’s seat, which will list both the manufacture date and expiration date. An example of a label can be found below, as seen in a blog post about this topic from Cincinnati Children’s Hospital [7]:

Picture3.png
  • An additional checklist is provided in the “Additional Resources” section below that should be reviewed before purchasing, and using a used car seat

My child was involved in a car accident in a car seat. Is this seat safe to use after the accident?

  • The National Highway Traffic Safety Administration has some guidelines for when a car seat should be replaced. In cases of minor accidents, a car seat does not necessarily have to be replaced, but the accident must meet all of the following criteria [8]:

    • Vehicle was driven away from crash site

    • Vehicle door nearest car seat was not damaged

    • No passengers in the vehicle sustained injuries

    • No airbag deployment in the vehicle

    • The car seat has no obvious damage

  • If there is any doubt about the severity of the accident, or of the integrity of the car seat, the safest option is to replace the seat

Is there anything else I should do after purchasing a car seat to help ensure it remains up-to-date?

  • Like all new technology, product failures sometimes happen, requiring replacement parts or adjustments. After purchasing a car seat, it is important to register the seat with the appropriate manufacturer to ensure prompt notification of any recall notices in a timely manner. Most manufacturers provide a card that can be submitted, which can also be done online through the specific manufacturer’s page, or using the finder link on the National Highway Traffic Safety Administration website.

Additional Resources:

 

* A special thank you to the providers, nurses, staff, and most importantly, patients/families at Hasbro Children’s Hospital, and to my faculty reviewer, Dr. Jane Preotle

Faculty Reviewer: Jane Preotle, MD

References:

  1. Insurance Institute for Highway Safety, Highway Loss Data Institute, accessed at: https://www.iihs.org/iihs/topics/t/child-safety/fatalityfacts/child-safety, posted December 2017.

  2. US Department of Transportation, National Highway Traffic Safety Administration, “Quick Facts 2016”, accessed at: https://crashstats.nhtsa.dot.gov/Api/Public/ViewPublication/812451

  3. Durbin, DR, Hoffman, BD; “Child Passenger Safety”, AAP Council on Injury, Violence, and Poison Prevention Policy Statement, Pediatrics, Volume 142, No. 5, November 2018

  4. Rhode Island State Police, Department of Public Safety, “Seat belt laws and car seat recommendations”, accessed at: http://risp.ri.gov/safety/vehiclesafety/seatbelts.php

  5. National Child Passenger Safety Certification webpage, accessed at: https://cert.safekids.org/get-car-seat-checked

  6. National Safety Commission Alert, published October 2011, accessed at: http://alerts.nationalsafetycommission.com/2011/10/child-safety-seats-have-expiration-date.html

  7. Cincinnati Children’s Blog, “Car seat expiration dates: have you checked yours?”, published online June 22, 2015, accessed at: https://blog.cincinnatichildrens.org/safety-and-prevention/car-seat-expiration-dates-have-you-checked-yours/

  8. National Highway Traffic Safety Administration, “Car seat use after a crash”, accessed at: https://www.nhtsa.gov/car-seats-and-booster-seats/car-seat-use-after-crash

  9. Centers for Disease Control and Prevention, Child  Passenger Safety summary page, accessed at: https://www.cdc.gov/features/passengersafety/index.html

  10. Car Seats: Information for Families, accessed at: https://www.healthychildren.org/English/safety-prevention/on-the-go/Pages/Car-Safety-Seats-Information-for-Families.aspx

Orbital Floor Blowout Fracture

CASE

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

DISCUSSION

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).

 

CASE CONCLUSION

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

 

REFERENCES & FURTHER READING

  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.