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Pediatric Emergency Medicine (PEM) Pearls

Created in 2015, this series is hosted by Dr. Jessica Chow and Dr. Josh Bukowski who are authors and editors for this series which focuses on evidence-based care in the realm of pediatric emergency medicine.

 

PEM Pearls: Approach to Spontaneous Intracranial Hemorrhage in Pediatric Patients

pediatric intracranial hemorrhage on MRI

Case:

A 6-year-old female with a past medical history of immune thrombocytopenia presents to the Emergency Department (ED) for concerns of dysarthria that started the day prior to arrival. The patient’s mother denies any recent trauma, including head injury.

Vitals and Physical Exam

  • Blood pressure 109/80
  • Pulse 121 beats/minute
  • Respiratory rate 22 breaths/minute
  • Oxygen saturation 100% on room air
  • Temperature 36.8ºC

Her physical exam is remarkable for a mild right-sided facial droop with forehead sparing and dysarthria.

Initial Work-Up

The patient’s ED workup shows the following:

  • Point-of-care glucose: Normal
  • Platelet count: 0 platelets/liter
  • Hemoglobin: 9.8 g/dL
  • Head CT: Frontal lobe hemorrhage

Background

Although rare, pediatric intracranial hemorrhage (ICH) contributes to almost half of all childhood strokes and can cause lifelong disability and death [1]. One 3-center prospective study on pediatric ICH noted a 9% mortality rate with ⅓ of survivors having “significant disability” at 2-year follow-up [2]. Primary predictors of adverse outcomes from pediatric ICH involve the following [2-4]:

  • Hemorrhagic lesion volume
  • Presence of hydrocephalus and/or herniation
  • Altered mental status

Multiple studies consistently point to vascular causes such as arteriovenous malformation as a leading risk factor for spontaneous pediatric ICH followed by hematological pathologies including coagulation deficiencies [5-7].  No matter the cause, the sequelae of pediatric ICH can be devastating making early detection and immediate intervention essential for better outcomes. Unfortunately, given children often present with vague and non-specific symptoms, there is often a delay in presentation to care and in diagnosis [8]. Unfortunately, in contrast to adults, there are no set guidelines for the management of pediatric ICH despite its associated morbidity and mortality.

Clinical Findings

Although headache is the most common presenting symptom, other symptoms can vary [6,8,9]. In one study, children <6 years old were more likely to present with symptoms such as seizures and altered mental status, while children ≥6 years presented more with focal deficits, headache, vomiting, and altered mental status [9].

Presenting Symptom/FindingIncidence
Headache46-80%
Vomiting21-64%
Altered mental status37-50%
Seizures37-54%
Focal deficits (hemiparesis and aphasia)16-50%
Table 1. Incidence rates of common symptoms and findings in pediatric patients with a spontaneous intracranial hemorrhage (adapted from Boulouis G, et al [7].) 

Differential Diagnosis

Given how rare pediatric ICH is, consider other diagnoses when a patient presents with focal deficits, altered mental status, and/or vague symptoms such as headache and weakness.

  1. Bell’s palsy
  2. Cerebral venous thrombosis
  3. Complicated migraines
  4. Drug intoxication/exposure
  5. Inborn error of metabolism
  6. Intracranial mass
  7. Ischemic stroke
  8. Metabolic derangements (hypoglycemia, hyponatremia)
  9. Non-accidental trauma
  10. Posterior Reversible Encephalopathy Syndrome (PRES)
  11. Seizures with Todd’s paralysis

Approach for the ED Provider

Key history questions:

  1. When did the symptoms start?
  2. Does the child or anyone in the family have any history of bleeding disorder?
  3. Have you noticed excessive bruising from minimal trauma?
  4. Has the child had any recent illnesses?

Key physical exam findings:

  1. Is there any bruising, gum bleeding, or signs of non-accidental trauma?
  2. In infants, is the fontanelle bulging or flat?
  3. Are there any focal neurologic findings such as facial droop, pupil asymmetry, etc?
  4. Are there any signs of increased intracranial pressure (i.e., papilledema)?

Workup to initiate:

Emergency medicine physicians should have strong suspicion for ICH particularly in the setting of a pediatric patient presenting with acute onset of headache, vomiting, altered mental status, seizure, and/or focal deficits.

  1. Emergent neuroimaging: CT or MRI is essential in order to distinguish between ischemic versus hemorrhagic causes. CT is often the first imaging study completed due to ease of access. If no acute intracranial process is noted, MRI is warranted to evaluate for ischemic stroke or other etiology.
  2. Laboratory studies:
    • Point-of-care glucose
    • Comprehensive metabolic panel
    • Ammonia (if concerned for inborn error of metabolism)
    • Comprehensive blood count
    • Prothrombin time with INR, partial thromboplastin time
    • Urine drug screen (if concerned for drug exposure contributing to symptoms)

Management:

If a patient has a confirmed ICH, consultation with neurosurgery is required. Immediate transfer may be necessary if your facility does not have neurosurgical services. Further management includes:

  1. Reversing coagulopathy [7,10,11]:
    • If the patient has an underlying coagulopathy, consider intravenous vitamin K and/or fresh frozen plasma.
    • Pediatric patients with hemophilia require immediate factor replacement (factor VIII or IX).
    • Patients on anticoagulation need anticoagulation reversal with the appropriate reversal agents.
  2. Neuroprotective supportive measures (prevent worsening brain injury): 
    • Monitor the patient closely with frequent neurologic checks for any signs of deterioration.
    • Maintain euglycemia as hyperglycemia is associated with worse outcomes [7].
    • Maintain normothermia. Use external cooling measures or antipyretics to manage hyperthermia [10].
    • Treat clinical and subclinical seizures with antiepileptics. Consider EEG monitoring to detect subclinical status [7].  The benefits of prophylactic administration of antiepileptics is unknown in this population [10].
    • Avoid hypotension [7, 10]. There are no established guidelines for hypertension management in pediatric ICH; blood pressure goals should be discussed with the neurosurgical team and blood pressure variability should be avoided.
  3. Treatment of increased intracranial pressure:  If the patient has a change in mental status or develops focal deficits, an increase in intracranial pressure should be suspected [10,11].
    • Treat hypotension, hypercapnia, and hypoxia.
    • Elevate the head of the bed to 30 degrees.
    • Ensure appropriate pain control.
    • Sedation may be necessary but be wary of resultant hypercapnia and consider intubation if patients require a lot of sedation or become too somnolent following medication.
    • In patients with acute deterioration or concern about impending herniation, consider hyperventilation if the patient is intubated and/or treatment with a hyperosmolar agent like mannitol or hypertonic saline.
    • Some patients may need acute interventions such as an external ventricular drain or operative decompression with clot removal.
    • Steroids have not been shown to be beneficial [10].

Case Resolution

The patient was transferred to a tertiary care center. Further imaging confirmed an intraparenchymal hemorrhage in the left frontal lobe and right parietal lobe with midline shift. No underlying lesions or vascular malformation were seen.

Management: The patient was admitted to intensive care and received tranexamic acid and a platelet transfusion. She was monitored by neurosurgery but no surgical interventions were needed. For her idiopathic thrombocytopenia, she received steroids and IV immunoglobulin.

Hospital Course: Her deficits and platelet count improved during her stay, and she was discharged on hospital day 5 with outpatient neurology and hematology follow-up.

Outpatient: Repeat imaging 3 weeks after discharge showed resolution of the midline shift and decrease in hemorrhage size.

Pearls

  • Consider pediatric ICH in patients presenting with focal deficits, altered mental status, and/or generalized symptoms such as headache, seizures, and weakness.
  • Management of pediatric ICH is focused on maintaining physiological homeostasis and preventing further brain injury.
  • Call your neurosurgical team early for consultation and evaluation or transfer your patient to the appropriate tertiary care center.

Read more pediatric EM blog posts in the PEM Pearls series.

References

  1. Baldovsky MD, Okada PJ. Pediatric stroke in the emergency department. J Am Coll Emerg Physicians Open. 2020;1(6):1578-1586. Published 2020 Oct 6. doi:10.1002/emp2.12275. PMID: 33392566
  2. Porcari GS, Beslow LA, Ichord RN, Licht DJ, Kleinman JT, Jordan LC. Neurologic Outcome Predictors in Pediatric Intracerebral Hemorrhage: A Prospective Study. Stroke. 2018;49(7):1755-1758. doi:10.1161/STROKEAHA.118.021845 PMID: 29895534
  3. Guédon A, Blauwblomme T, Boulouis G, et al. Predictors of Outcome in Patients with Pediatric Intracerebral Hemorrhage: Development and Validation of a Modified Score. Radiology. 2018;286(2):651-658. doi:10.1148/radiol.2017170152 PMID:29023219
  4. Jordan LC, Kleinman JT, Hillis AE. Intracerebral hemorrhage volume predicts poor neurologic outcome in children. Stroke. 2009;40(5):1666-1671. doi:10.1161/STROKEAHA.108.541383 PMID: 19286576
  5. Ciochon UM, Bindslev JBB, Hoei-Hansen CE, et al. Causes and Risk Factors of Pediatric Spontaneous Intracranial Hemorrhage-A Systematic Review. Diagnostics (Basel). 2022;12(6):1459. Published 2022 Jun 13. doi:10.3390/diagnostics12061459 PMID: 35741269
  6. Al-Jarallah A, Al-Rifai MT, Riela AR, Roach ES. Nontraumatic brain hemorrhage in children: etiology and presentation. J Child Neurol. 2000;15(5):284-289. doi:10.1177/088307380001500503 PMID: 10830193
  7. Boulouis G, Blauwblomme T, Hak JF, et al. Nontraumatic Pediatric Intracerebral Hemorrhage. Stroke. 2019;50(12):3654-3661. doi:10.1161/STROKEAHA.119.025783 PMID: 31637968
  8. Yock-Corrales A, Mackay MT, Mosley I, Maixner W, Babl FE. Acute childhood arterial ischemic and hemorrhagic stroke in the emergency department. Ann Emerg Med. 2011; 58:156–163. doi: 10.1016/j.annemergmed.2010.10.013 PMID: 21310508
  9. Lo WD, Lee J, Rusin J, Perkins E, Roach ES. Intracranial Hemorrhage in Children: An Evolving Spectrum. Arch Neurol. 2008;65(12):1629–1633. doi:10.1001/archneurol.2008.502 PMID: 19064750
  10. Ferriero DM, Fullerton HJ, Bernard T, et al. Management of stroke in neonates and children. A scientific statement from the American Heart Association/American Stroke Association. Stroke. 2019;50:e51-e96. doi: 10.1161/STR.0000000000000183 PMID: 30686119
  11. Tsze D and Steele D. Neurosurgical Emergencies, Nontraumatic. In: Fleisher G and Ludwig S,. eds. Textbook of Pediatric Emergency Medicine, 6e. Lippincott Willimas and Wilkins. 2010. Accessed online 5/23/2024.
By |2024-06-19T23:59:23-07:00Jun 20, 2024|Expert Peer Reviewed (Clinical), Neurology, Pediatrics, PEM Pearls|
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The Febrile Infant: Incorporating the 2021 American Academy of Pediatrics guidelines

Can you trust a febrile infant?

“No” has been, and continues to be, the resounding answer over the last 40 years as researchers and clinicians work to determine the optimal evaluation and management of the well-appearing young febrile infant [1].

The goal remains to identify infants with bacterial infections in this at-risk cohort of patients while also considering the balance of cost-effectiveness on a population scale and the potential for iatrogenic harm with evaluation such as unnecessary lumbar punctures, unnecessary antibiotics, and unnecessary hospitalization. Fortunately, bacteremia and bacterial meningitis in this age group are uncommon [2]. Unfortunately, delayed or missed diagnosis can be devastating [1-3].

In the most recent 2021 Clinical Practice Guideline, the American Academy of Pediatrics (AAP) aims to provide guidance with 3 separate age-based algorithms for the evaluation and management of the well-appearing febrile infant [4]. These guidelines were made possible by the recent PECARN, Step by Step, and other studies and the invaluable information they have provided [5-7].

Who’s included?

  • Well-appearing febrile infants
    • The AAP acknowledges that clinician experience is likely the best determinate of what is “well-appearing”, further admitting that there is no measure or definition of either “experience” or “well-appearing”
  •  Febrile
    • Rectal temperatures of  38.0C or 100.4F at home in the past 24 hours or determined in a clinical setting
    • Subjective fevers at home are excluded
  •  Gestation
    • Between 37-42 weeks
    • Premature infants excluded
  • Age
    • Days 8 to 60 and have been discharged home following birth

Who is not included?

  • Preterm or infants with congenital/chromosomal abnormalities
  • Infants with focal bacterial infections
  • Cellulitis, omphalitis, septic arthritis, osteomyelitis
  •  Bronchiolitis
    • With or without a positive RSV test
  •  Immunocompromised
    • Either suspected or known deficiency
  • Immunizations in the previous 48 hours

It should also be noted that the AAP has named the following as high-risk inflammatory markers that will be referenced in the soon-to-be-discussed guidelines [4,5].

  • Temperature >101.3F (38.5C)
  • C-reactive protein (CRP) > 20 mg/L
  • Procalcitonin >0.5 ng/mL
  • Absolute neutrophil count (ANC) >4000 mm3  (or 5200 mm3 if your facility does not have procalcitonin available)

The Groups

While the AAP makes the distinction of an age 0-7 days group from the age 8-21 days, they provide no specific recommendations about emergency department (ED) management in the youngest group [4]. Despite this, these infant groups are likely best evaluated and managed similarly in the ED:

  • Urinalysis (UA) +/- urine culture if indicated by UA
  • Blood culture
  • Lumbar puncture (LP)
    • Cell count, Gram stain, glucose, protein, bacterial culture, and enterovirus PCR (if available)
  • Admission

Inflammatory markers are not required to determine ED management in this age group but may guide inpatient clinicians.

Treatment

  • Ampicillin IV or IM
  • Ceftazidime IV or IM or gentamicin IV or IM

The addition of acyclovir to IV antibiotics depends on the following risk factors which increase the likelihood of HSV:

  • Maternal genital HSV lesions or fever 48 hours before or after delivery
  • Infants with vesicles, seizures, hypothermia, mucous membrane ulcers
  • CSF pleocytosis with a negative Gram stain result
  • Leukopenia, thrombocytopenia, or elevated AST/ALT levels

Although many febrile infants in this group will still require a full evaluation for sepsis, there are some new alternatives in patients meeting certain criteria. At the minimum, all 22-28 day old infants will need:

  • UA +/- culture
  • Blood culture
  • Inflammatory markers (ANC, CRP, procalcitonin)

Further management of a well-appearing infant in this group can be based on the following pathways:

    1. If UA positive with negative inflammatory markers
      • LP may be performed but is not required
      • IV antibiotics and admission are required regardless
    2. If UA negative with negative inflammatory markers, then there are 2 options
      • Perform LP
        • If LP negative, then the patient can be given a dose of parenteral antibiotics and discharged home with close follow-up in 24 hours.
        • If LP is traumatic or pleocytosis is present, administer antibiotics and admit.
      • Defer LP
        • Antibiotics may be administered, but the patient should be admitted.
    3. If UA negative and ANY positive inflammatory marker (procalcitonin > 0.5 mg/mL, CRP >20 mg/L, ANC >4000, or temperature >101.3F), LP is required
      1. If LP positive
        • Admit with IV antibiotics
      2. If LP negative
        • Admit +/- antibiotics, OR
        • Discharge home after one dose of parenteral antibiotic with 24-hour follow-up

Treatment

  • Same antibiotic options as the day 0-21 infants

The nuances of this group’s decision tree revolve around the inflammatory markers.

Each infant in this group should have the following completed:

  • Urinalysis
  • Blood Cultures
  • Inflammatory markers (CRP, ANC, and procalcitonin)

If everything is negative (UA & inflammatory markers):

  • Infants may be discharged home without antibiotics and with close follow-up within 36 hours.

If inflammatory markers are negative:

  • Infants with a positive urinalysis and negative inflammatory markers may be treated with oral antibiotics.
    • They may be either admitted to the hospital for observation or discharged with 24-hour follow-up.
    • No LP needed.

If inflammatory markers are positive:

  • A LP may be performed if the clinician feels it necessary but is not required.
    • If performed and CSF is negative the infant may be discharged with close follow-up.
    • Given high risk of bacteremia with elevated inflammatory markers in this age group, a dose of parenteral antibiotics prior to discharge is appropriate.
  • If LP deferred:
    • Administer parenteral antibiotics, and likely admit to hospital.
    • The caveat to this is if they have viral testing completed that is positive and are well appearing.
      • Example: A 48-day-old infant presents with a fever of 100.6F, CRP of 22 mg/L, and otherwise normal procalcitonin, ANC, and UA. The mother reports that an older brother has had a runny nose. Viral PCR testing is positive for rhinovirus. Seeing as the UA is negative, the infant appears well with a positive viral test, they may go home with shared decision-making and close outpatient follow-up, despite a positive inflammatory marker (CRP 22 mg/L) [3].

Treatment

Urinary Tract Infection:

  • Ceftriaxone (IV/IM) or cephalexin/cefixime as oral options.

Concern for Bacteremia/Meningitis:

  • Ceftriaxone + vancomycin
  • May add acyclovir for the above-mentioned antiviral treatment indications.

What should be done if the viral panel is positive?

  • Children 29 days or older with fever from a documented viral source can be managed according to their clinical presentation and can go outside the algorithm.
  • This requires a documented positive viral swab and not just a presentation consistent with a viral syndrome.
  • UTI is common in this age group, and a UA should be obtained [8].

Conclusion

Over the course of nearly the last half century there has been a lack of clear evidence-based guidelines in evaluating the young febrile infant [1]. Although serious bacterial infections in these young, febrile infants are uncommon, studies show that in the first month of life, bacteremia can be present in nearly 3% of febrile infants, with bacterial meningitis occurring in about 1% [2]. The absence of consensus regarding management has led to significant costs due to hospitalizations and their associated iatrogenic complications [9]. In the movement to create new recommendations, shifting epidemiology pushed changes in previous guidelines with a new focus on the use of the now widely available inflammatory markers [10].  With the advent of multiple large-scale studies and the recent improvements in lab testing, the newly updated AAP guidelines provide recommendations on how to manage this challenging population [4-7].

Take Home Points

  • These management strategies can only be used in WELL-APPEARING infants – if they’re ill-appearing, do a complete workup.
  • Evaluation of febrile infants 0-21 days remains the same – do everything (blood culture, UA +/- culture, LP with CSF studies), give antibiotics, and admit.
  • For those infants 22-28 days, get the UA, blood culture, and inflammatory markers to guide management.
    • Not all febrile infants in the 22-28 day subset need an LP, though it should still be obtained in certain clinical circumstances, and discussed between  provider and parents in other situations
  • In infants ≤28 days, a complete workup is still needed even if a viral source is present.
  • Febrile infants 29-60 days old may be sent home after a negative workup with close follow-up.

References:

    1. Roberts KB. Young, febrile infants: a 30-year odyssey ends where it started. JAMA. 2004 Mar 10;291(10):1261-2. PMID: 15010450.
    2. Biondi EA, Lee B, Ralston SL, et al. Prevalence of Bacteremia and Bacterial Meningitis in Febrile Neonates and Infants in the Second Month of Life: A Systematic Review and Meta-analysis.JAMA Network Open. 2019 Mar; 2(3). PMID: 30901044.
    3. Baker MD, Avner JR, Bell LM. Failure of infant observation scales in detecting serious illness in febrile, 4- to 8-week old infants. Pediatrics. 1990;85(6):1040–1043. PMID: 2339027
    4. Pantell RH, Roberts KB, Adams WG, et al. Clinical Practice Guideline: Evaluation and Management of Well Appearing Febrile Infants 8 to 60 Days Old. Pediatrics. 2021;148(2):e2021052228. PMID: 34281996
    5. Kuppermann N, Dayan PS, Levine DA, et al. A Clinical Prediction Rule to Identify Febrile Infants 60 Days and Younger at Low Risk for Serious Bacterial Infections. JAMA Pediatr. 2019;173(4):342-351. PMID: 30776077
    6. Gomez B, Mintegi S, Bressan S, et al. Validation of the “Step-by-Step” approach in the management of young febrile infants. The Journal of Pediatrics. 2016 Aug; 138(2):e20154381. PMID: 27382134
    7. Nguyen THP, Young BR, Poggel LE, et al. Roseville Protocol for the Management of Febrile Infants 7-60 Days. Hosp Pediatr. 2020 Dec 17:hpeds.2020-0187. PMID: 33334815
    8. Shaikh N, Morone NE, Bost JE, Farrell MH. Prevalence of urinary tract infection in childhood: a meta-analysis. Pediatr Infect Dis J. 2008;27(4):302-308. PMID: 18316994
    9. Coyle C, Brock G, Wallihan R, Leonard JC. Cost Analysis of Emergency Department Criteria for Evaluation of Febrile Infants Ages 29 to 90 Days. J Pediatr. 2021 Apr;231:94-101.e2. doi: 10.1016/j.jpeds.2020.10.033. Epub 2020 Oct 31. PMID:33130155.

    Milcent K, Faesch S, Gras-Le Guen C, et al. Use of Procalcitonin Assays to Predict Serious Bacterial Infection in Young Febrile Infants [published correction appears in JAMA Pediatr. 2016 Jun 1;170(6):624].JAMA Pediatr. 2016;170(1):62-69. doi:10.1001/jamapediatrics.2015.3210 PMID: 26595253

By |2023-04-09T20:40:05-07:00Mar 29, 2023|Expert Peer Reviewed (Clinical), Infectious Disease, Pediatrics, PEM Pearls|
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PEM Pearls: An Approach to Infant Apnea

infant

A 2-day-old female born at 41 weeks presents to the Emergency Department (ED) for an episode of apnea. Her parents noticed she stopped breathing, went limp, and turned blue. They are not sure for how long. The infant has had decreased urine output but is otherwise well without any other symptoms. Mom has an unspecified autoimmune condition and is taking hydroxychloroquine. The pregnancy and birth were largely uneventful. Mom was positive for Group B. Strep, had prolonged rupture of membranes, and was appropriately treated with antibiotics.

Vitals: The infant’s vital signs in the ED are within normal limits except for mild tachypnea.

Initial Exam: Her exam is nonfocal.

Background

Apnea among infants occurs when an infant stops breathing for 20 seconds or longer or stops breathing, for any amount of time, with bradycardia, cyanosis, pallor, and/or hypotonia. The overall incidence of apnea is 1 in 1,000 full-term infants. Infants who are premature (<37 weeks) are at increased risk for apnea; the incidence is almost 100% in infants born less than 28 weeks. Apnea is more common in premature infants due to their immature respiratory systems and physiologic stressors often manifest as respiratory depression in infants [1].

For infants that are actively apneic, the approach is similar to any pediatric resuscitation: ABCs (see ED approach below for management). 

For infants who had an apneic episode that has since resolved, one has more time to think about the differential. 

Differential Diagnosis

Apnea can be benign and physiologic, typically lasting between 5-10 seconds and more often occurring between 2 weeks to 6 months of life. Because physiologic stressors can manifest as respiratory depression in infants, the differential for pathologic apnea is broad. The following are broad categories to consider (similar to “the misfits” mnemonic for the crashing neonate).

  1. Sepsis: UTI, pneumonia, necrotizing enterocolitis, meningitis/encephalitis 
  2. Pulmonary disease: pneumonia, pneumothorax, viral illness  
  3. Congenital heart disease 
  4. Metabolic disease: glucose, inborn errors of metabolism, electrolytes 
  5. Intracranial abnormalities
  6. Non-accidental trauma 
  7. Toxins: carbon monoxide, botulism, maternal opioid use 

It’s important to note that apnea in infants may qualify as a BRUE (brief, resolved, unexplained event). However, in this case, the infant is less than 60 days old. This is NEVER a low-risk BRUE [2]. 

Approach for the ED Provider

For the emergency provider, considering all of this can be overwhelming. Our job is to collect pertinent data, stabilize the infant, and start empiric treatment in order for the inpatient teams to further investigate the exact cause of the apnea. The following is a simplified ED approach: 

Key history questions:

  1. How was the delivery: Was meconium present? Was there prolonged rupture of membranes? 
  2. How was the pregnancy: Did mom get prenatal care? Were there any abnormal results with prenatal testing? What are mom’s medical conditions? Did mom get any treatment during her pregnancy (e.g. PCN for syphilis)?
  3. How is the infant feeding, stooling, and urinating? Are there any other symptoms? 

Key workup to initiate (in bold are items we wouldn’t typically send for adult workups and may be forgotten by ED providers who do not primarily care for children):

  1. VBG, CBC, CMP, ammonia (for metabolic conditions), blood culture, urinalysis, lumbar puncture (if concerned about sepsis)
  2. Respiratory viral panel, pertussis (if endemic and/or area with low vaccination rates)
  3. ECG, chest X-ray (if hypoxic or abnormal clinical exam)
  4. Pre and post-ductal oxygen saturation and four-point blood pressure (for heart disease, primarily coarctation of the Aorta)

Key physical exam findings (undress the patient fully):

  1. Are there bruises or other signs of abuse? 
  2. What is the fontanelle size? How do the pupils appear?
  3. Is there wheezing, rhonchi, or rales on lung auscultation? Are breath sounds equal? Is there increased work of breathing?
  4. Is there abdominal distension or guarding?
  5. Are there rashes? Is there edema in the extremities?

Management for infants currently apneic: ABCs.

  1. Establish access, connect to monitors, and get a full set of vitals (including rectal temperature).
  2. Support the airway. Start with oxygenation and ventilation. Utilize noninvasive pressure ventilation with continuous positive airway pressure (CPAP) or High Flow Nasal Canula (HFNC). Consider intubation if there is no improvement, however, do not jump immediately to intubation as an infant’s respiratory status can quickly change with respiratory support. 
  3. Start CPR if there is no pulse or the pulse is less than 60 beats per minute.
  4. Begin intravenous fluids at 10-20ml/kg (be careful if you have concerns about heart failure). 
  5. Obtain a point of care glucose (and if available, venous blood gas). Consider naloxone if opioid ingestion is possible.

Management for the infants who are not currently apneic: 

  1. Monitor vital signs and support respiration as needed (e.g. nasal cannula, CPAP).
  2. Give empiric antibiotics if there is a concern for sepsis. Remember, avoid ceftriaxone in neonates less than 28 days due to concern for kernicterus. Instead, use ampicillin and gentamicin. Add vancomycin if concerned about MRSA.
  3. Nutritional support – remember that infants have low glucose stores. Start maintenance fluids (D10W (if <28 days) or D5NS +/- KCl).
  4. The NICU may want you to start caffeine and/or theophylline in the ED for treatment for apnea of prematurity.

Disposition is mainly to the Neonatal Intensive Care Unit (NICU).

Case Resolution

While in the ED, the infant desaturates to the 80s with improvement on HFNC. She has a full sepsis workup and is started on empiric antibiotics (ampicillin/gentamicin) and antivirals (acyclovir). The infant is found to have hypoglycemia and metabolic acidosis. Her neurologic, cardiac, and infectious workups are unremarkable and she doesn’t have any apneic/cyanotic episodes while hospitalized. She is discharged home with suspected hypoglycemia from poor feeding as the cause.

Conclusion

  • The workup for apnea in infants is broad and not limited to pulmonary pathology.
  • Remember your ABCs, ask key history questions (prenatal, intrapartum, postpartum), send key diagnostics (including ammonia and pertussis), and collect key physical exam findings (including pre and post-ductal saturation and four-point blood pressure).
  • Call your NICU team early.
  • You will likely not arrive at the cause of the apnea in the ED, but your early workup and empiric treatment (e.g. CPAP, antibiotics) are critical in caring for these infants.

Read more pediatric emergency medicine topics as part of the PEM Pearls Series on ALiEM.

References

  1. Kondamudi NP, Khetarpal S. Apnea In Children. [Updated 2022 Jul 18]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. https://www.ncbi.nlm.nih.gov/books/NBK441894/ .Accessed September 21, 2022.
  2. Tieder JS, Bonkowsky JL, Etzel RA, et al. Brief Resolved Unexplained Events (Formerly Apparent Life-Threatening Events) and Evaluation of Lower-Risk Infants [published correction appears in Pediatrics. 2016 Aug;138(2):]. Pediatrics. 2016;137(5):e20160590. PMID 27244835 

Read more pediatric emergency medicine topics as part of the PEM Pearls Series on ALiEM.

By |2022-09-21T15:16:27-07:00Sep 26, 2022|Pediatrics, PEM Pearls|
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PEM Pearls: To Scan or Not to Scan? CT Abdomen in Children with Blunt Torso Trauma

blunt torso traumaAn 18-month-old female with no past medical history is brought in by ambulance after a motor vehicle collision (MVC) at highway speed, restrained in an appropriate car seat. Mom was also brought in after delayed extrication with an obvious femur deformity. EMS reports that the patient had emesis on the scene, was fearful but calm, and has been moving all extremities.

Vitals per EMS: HR 120, BP 100/60, RR 30, SpO2 99%, Temp 36.5 C

Initial Exam:

  • General: crying
  • Neuro: Glasgow Coma Scale (GCS) of 13 (eyes shut unless talked to, crying spontaneously, moving all extremities)
  • MSK: atraumatic chest, erythema on the left leg
  • Abdomen: without tenderness

Blunt Torso/Abdominal Trauma

An intra-abdominal injury (IAI) is considered to be any radiographically or surgically apparent injury to an intra-abdominal structure (urinary tract, gastrointestinal tract, spleen, liver, pancreas, gallbladder, adrenal gland, vasculature, and fascia). An intra-abdominal injury requiring intervention (IAI-I) is any IAI that causes death or requires an intervention such as laparotomy, angiographic embolization, blood transfusion, or even admission for intravenous fluids [1].

Despite our curiosity and desire to diagnose all injuries, emergency medicine teams must focus on recognizing IAI-I and tailor their workup accordingly given the negative consequences of excessive workup and treatment of stable IAIs (e.g., unnecessary splenectomies, hepatectomies, increased length of stay, radiation, and increased medical costs/resources).

Although the incidence of pediatric blunt torso trauma in the United States was 110,525 cases in 2016, the prevalence of IAI has been quoted to be as low as 6.3%; more importantly, the prevalence of IAI-I is less than 2% [1]. Non-pediatric level 1 trauma centers were more likely to use computed tomography (CT) in pediatric trauma patients compared to pediatric trauma centers, even after adjusting for injury severity [2].

Clinical Decision Rule

The Pediatric Emergency Care Applied Research Network (PECARN) conducted a prospective study of over 12,000 children ages 0-18 years presenting to pediatric and general EDs with blunt torso trauma. Significant predictors of IAI-I were low GCS, abdominal tenderness, abdominal wall trauma, thoracic wall trauma, decreased breath sounds, and vomiting. The authors developed a prediction rule with a sensitivity of 97% (93.7, 98.9) and a negative predictive value of 99.9% (99.7, 1.00) [1]. External validation had similar sensitivity (99% 96-100%) reinforcing the utility of this clinical decision rule (CDR) in identifying low-risk individuals and decrease the use of CT [4].

In comparison to other CDRs, this rule does not include a gestalt variable but outperforms clinical gestalt with a lower miss rate (6 compared to 23) [5]. Of note, this prediction rule is not a two-way tool and was created only to determine individuals at low risk of IAI-I, rather than to assist providers in deciding who needs a CT scan.

IAI

Adapted from Holmes JF et al 2013 [1]

Reviewing the cases missed by the prediction rule in the initial study, possible clinical findings that could be captured with adjuncts, such as labs and imaging, include:

  • Gross hematuria
  • Microscopic hematuria (Red Blood Cells on Urinalysis)
  • Elevated AST/ALT
  • Rib fracture

Adjuncts

No single test effectively screens for IAI-I or IAI, but additional testing can increase the index of concern in cases that already have a higher pre-test probability (individuals who have any of the variables factored into the prediction rule). The following adjuncts can be considered for children who are not deemed very low risk.

Labs

  • Hematocrit <30% [3,7-8]
  • AST>200 U/L, ALT>125U/L [3,7, 9-10]
  • Lipase >100 U/L [9,11-12]
  • UA Gross hematuria [12-17]

Focused Assessment with Sonography for Trauma (FAST)

  • The diagnostic role of a FAST in pediatric trauma is less established than in adult trauma [18].
  • Application of FAST increases as provider suspicion for IAI increases [19].
  • As an adjunct to the clinical exam, FAST can be incorporated into decision making for selected cases of increased IAI concern [20].

Chest X-ray (CXR)

  • Injuries noted on a CXR may contribute to increased concern for IAI depending on location, mechanism, and type of injury [21].

Review of Case

Returning to our case, findings of concern include her GCS of 13 and reported emesis. Although it was a high-speed MVC and may represent a more severe mechanism, this variable was not found to be a predictor of IAI-I and should not in isolation inform your evaluation of her abdominal injury.

Application of the PECARN CDR demonstrates that the patient is not at very low risk for IAI-I. Labs and a FAST are performed and medications are given for symptom control.

The patient’s results are:

Labs:

  • HCT 35%
  • Lipase 20 U/L
  • AST 23 U/L, ALT 30 U/L
  • UA: no gross hematuria

FAST: Negative

On re-evaluation after ondansetron and acetaminophen, the patient has a GCS of 15 and is excitedly playing with her new teddy bear from the fire department while sipping apple juice. The patient is safely discharged home with her dad after a very frightening experience without unnecessary costs or radiation.

Take-Home Points

  • While blunt pediatric abdominal trauma has a high incidence, the prevalence of IAI-I is rather low.
  • The PECARN prediction rule for blunt torso trauma can identify patients that are very-low-risk for an IAI-I.
  • Notably, the mechanism of injury is not a predictable factor in determining IAI-I.
  • Clinicians should consider the use of labs, FAST, and CXR for risk stratification of patients that are not found to be very-low-risk.

Read more pediatric emergency medicine topics as part of the PEM Pearls Series on ALiEM.

References

  1. Holmes JF, Lillis K, Monroe D, et al. Identifying children at very low risk of clinically important blunt abdominal injuries. Ann Emerg Med. 2013;62(2):107-116.e2. doi:10.1016/j.annemergmed.2012.11.009. PMID: 23375510
  2. Marin JR, Wang L, Winger DG, Mannix RC. Variation in Computed Tomography Imaging for Pediatric Injury-Related Emergency Visits. J Pediatr. 2015 Oct;167(4):897-904.e3. doi: 10.1016/j.jpeds.2015.06.052. PMID: 26233603
  3. Holmes JF, Sokolove PE, Brant WE, et al. Identification of children with intra-abdominal injuries after blunt trauma. Ann Emerg Med. 2002;39(5):500-509. doi:10.1067/mem.2002.122900. PMID: 11973557
  4. Springer E, Frazier SB, Arnold DH, Vukovic AA. External validation of a clinical prediction rule for very low risk pediatric blunt abdominal trauma. Am J Emerg Med. 2019 Sep;37(9):1643-1648. doi: 10.1016/j.ajem.2018.11.031. PMID: 30502218.
  5. Mahajan P, Kuppermann N, Tunik M, et al. Comparison of Clinician Suspicion Versus a Clinical Prediction Rule in Identifying Children at Risk for Intra-abdominal Injuries After Blunt Torso Trauma. Acad Emerg Med. 2015;22(9):1034-1041. doi:10.1111/acem.12739. PMID: 26302354
  6. Nishijima DK, Yang Z, Clark JA, Kuppermann N, Holmes JF, Melnikow J. A cost-effectiveness analysis comparing a clinical decision rule versus usual care to risk stratify children for intraabdominal injury after blunt torso trauma. Acad Emerg Med. 2013;20(11):1131-1138. doi:10.1111/acem.12251. PMID: 24238315
  7. Taylor GA, Eichelberger MR, O’Donnell R, Bowman L. Indications for computed tomography in children with blunt abdominal trauma [published correction appears in Ann Surg 1992 Jul;216(1):99]. Ann Surg. 1991;213(3):212-218. doi:10.1097/00000658-199103000-00005. PMID: 1998402
  8. Taylor GA, O’Donnell R, Sivit CJ, Eichelberger MR. Abdominal injury score: a clinical score for the assignment of risk in children after blunt trauma. Radiology. 1994;190(3):689-694. doi:10.1148/radiology.190.3.8115612. PMID: 8115612
  9. Streck CJ, Vogel AM, Zhang J, et al. Identifying Children at Very Low Risk for Blunt Intra-Abdominal Injury in Whom CT of the Abdomen Can Be Avoided Safely. J Am Coll Surg. 2017;224(4):449-458.e3. doi:10.1016/j.jamcollsurg.2016.12.041. PMID: 28130170
  10. Streck CJ Jr, Jewett BM, Wahlquist AH, Gutierrez PS, Russell WS. Evaluation for intra-abdominal injury in children after blunt torso trauma: can we reduce unnecessary abdominal computed tomography by utilizing a clinical prediction model?. J Trauma Acute Care Surg. 2012;73(2):371-376. doi:10.1097/TA.0b013e31825840ab. PMID: 22846942
  11. Adamson WT, Hebra A, Thomas PB, Wagstaff P, Tagge EP, Othersen HB. Serum amylase and lipase alone are not cost-effective screening methods for pediatric pancreatic trauma. J Pediatr Surg. 2003;38(3):354-357. doi:10.1053/jpsu.2003.50107. PMID: 12632348
  12. Capraro AJ, Mooney D, Waltzman ML. The use of routine laboratory studies as screening tools in pediatric abdominal trauma. Pediatr Emerg Care. 2006;22(7):480-484. doi:10.1097/01.pec.0000227381.61390.d7. PMID: 16871106
  13. Mee SL, McAninch JW, Robinson AL, Auerbach PS, Carroll PR. Radiographic assessment of renal trauma: a 10-year prospective study of patient selection. J Urol. 1989;141(5):1095-1098. doi:10.1016/s0022-5347(17)41180-3. PMID: 2709493
  14. Morey, Allen F., et al. “Efficacy of Radiographic Imaging in Pediatric Blunt Renal Trauma.” Journal of Urology, vol. 156, no. 6, 1996, pp. 2014–2018., doi:10.1016/s0022-5347(01)65422-3.
  15. Brown SL, Haas C, Dinchman KH, Elder JS, Spirnak JP. Radiologic evaluation of pediatric blunt renal trauma in patients with microscopic hematuria. World J Surg. 2001;25(12):1557-1560. doi:10.1007/s00268-001-0149-6. PMID: 11775191
  16. Santucci RA, Langenburg SE, Zachareas MJ. Traumatic hematuria in children can be evaluated as in adults. J Urol. 2004;171(2 Pt 1):822-825. doi:10.1097/01.ju.0000108843.84303.a6. PMID: 14713834
  17. Levy JB, Baskin LS, Ewalt DH, et al. Nonoperative management of blunt pediatric major renal trauma. Urology. 1993;42(4):418-424. doi:10.1016/0090-4295(93)90373-i. PMID: 8212441
  18. Holmes JF, Gladman A, Chang CH. Performance of abdominal ultrasonography in pediatric blunt trauma patients: a meta-analysis. J Pediatr Surg. 2007 Sep;42(9):1588-94. doi: 10.1016/j.jpedsurg.2007.04.023. PMID: 17848254
  19. Menaker J, Blumberg S, Wisner DH, et al. Use of the focused assessment with sonography for trauma (FAST) examination and its impact on abdominal computed tomography use in hemodynamically stable children with blunt torso trauma. J Trauma Acute Care Surg. 2014;77(3):427-432. doi:10.1097/TA.0000000000000296. PMID: 25159246
  20. Retzlaff T, Hirsch W, Till H, Rolle U. Is sonography reliable for the diagnosis of pediatric blunt abdominal trauma? J Pediatr Surg. 2010 May;45(5):912-5. doi: 10.1016/j.jpedsurg.2010.02.020. PMID: 20438925
  21. Holmes JF, Sokolove PE, Brant WE, Kuppermann N. A clinical decision rule for identifying children with thoracic injuries after blunt torso trauma. Ann Emerg Med. 2002 May;39(5):492-9. doi: 10.1067/mem.2002.122901. PMID: 11973556

Read more pediatric emergency medicine topics as part of the PEM Pearls Series on ALiEM.

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