Pediatric Pearls – Bronchiolitis

Posted on by David Traficante 
Pathophysiology
  • Disorder that is commonly caused by a viral lower respiratory tract infection in infants
  • Characterized by acute inflammation, edema and necrosis of epithelial cells lining small airways and increased mucus production

  • Etiology
    • Coronavirus
    • Influenza
    • Rhino virus
    • Adenovirus
    • Parainfluenza virus
    • RSV (respiratory syncytial virus) – MOST COMMON!
  • Incidence – December-March
      • Most infections occur within first 2 years of life
      • About 40% experience lower respiratory infection during initial infection
      • RSV doesn’t grant permanent or long-term immunity – RE-INFECTION COMMON
      • The risk of significant viral or bacterial lower respiratory tract infection or pneumonia in an infant is low
  • Transmission
    • Direct contact with secretions
    • Young children shed virus for >2 weeks
    • 30-70% of household contacts become ill
  • Natural history
    • Begins with URI – Rhinorrhea, congestion, cough
    • Progresses to LRI in 2-6 days – Airway obstruction (tachypnea, wheezing, respiratory distress)
    • Variable and dynamic course
    • Lasts 2-4 weeks
Case

7-month-old male presents to the emergency room with his parents due to cough, runny nose, congestion and SOB that started 3 days ago.

VS: RR – 65, HR – 140, Temp – 99.1°F, O2 sat – 93% on RA

History
  • Typical Presentation of Bronchiolitis
    • Viral URI and cough with signs of lower respiratory tract infection
      • Work of breathing – grunting, nasal flaring, intercostal/subcostal retractions
      • Tachypnea
      • Wheeze
      • Coarse rales
Physical Exam
  • TIPS for a better exam
    • Upper airway obstruction can contribute to work of breathing
    • Suctioning and positioning may decrease the work of breathing and improve the quality of your examination
    • Counting respiratory rate over the course of 1 min is more accurate than shorter observations
  • Assess mental status, respiratory rate, work of breathing, oxygen status, listen to breath sounds, and assess hydration status

Diagnosis
  • DIAGNOSIS IS CLINICAL – NO LABS OR RADIOLOGICIAL STUDIES ARE NEEDED
    • When to consider CXR – if child has had >2 days of fever, an asymmetric chest exam, does not demonstrate improvement or has an unusually high O2 need
    • Diagnostic testing may be considered if:
      • Need cohorting – this is why we get testing for those we admit
      • Uncertain clinical diagnosis
      • Age <2 months
      • To assess for influenza – also needed this for those we admit
Management

Classify patient as mild, moderate, or severe based on the above physical exam

Mild Moderate Severe
1. Consider suction bulb

2. Discharge

 1. Suction bulb

2. No bronchodilators

3. Discharge or admit

 1. Suction bulb or wall

2. No bronchodilators

3. If no improvement consider starting high flow NC

4. Admit
  • Rehydration
    • IVF – moderately or severely dehydrated, secretions are thick and difficult to mobilize or severe respiratory distress
    • PO feeds – mildly to moderately dehydrated and can tolerate PO
  • Considerations for severely ill patients
    • Consider ONE TIME albuterol MDI trial if:
      • Severe respiratory distress OR
      • Increased risk for asthma
        • >12 months old, wheeze and once of the following
          • personal history of atopy or recurrent wheezing
          • strong family history of atopy or asthma
        • if responds to albuterol then consider switching to asthma pathway
      • Consider HFNC for significant hypoxia OR severe respiratory distress not improving with rigorous supportive care

 

Discharge criteria Admission criteria
–       Oxygen saturation >90%

–       Awake

–       Adequate oral intake

–       Mild/moderate work of breathing

–       Reliable caretaker

–       Able to obtain follow up care

–       MDI/spacer teaching if response to albuterol

 –       Admit if discharge criteria not met:

o   Inpatient: Requires 02 or progression expected

o   OBS: Mild disease with expected LOS < 24 hours

o   ICU: Apnea, severe distress; Requires HFNC / CPAP / intubation

–       Infants with these risk factors present early in the illness have higher risk of progression:

o   Gestational age < 34 weeks

o   Respiratory rate ≥ 70

o   Age < 3 months

 
Additional Notes
  • Differentiate infants with probable viral bronchiolitis from those with other disorders
  • The above management points to do take into consideration patients with significant medical history such as congenital heart disease, anatomic airway defects, neuromuscular disease, immunodeficiency, chronic lung disease – ADMIT, HIGH RISK!
  • The physical exam will vary from minute to minute depending on child’s position, level of alertness, response to treatment – CONSTANTLY RE-EVALUATE!
  • If patient presents within the first couple of days, they may worsen and need admission at a later point – PARENT EDUCATION IS KEY!
    • Viral illness, treated by hydration and suction
    • Signs of respiratory distress
    • How to suction
    • When to suction
    • Frequent feeds and watch hydration status
    • Cough may last 2-4 weeks, do not use OTC cough and cold medications
    • Avoid tobacco smoke
  • NOT RECOMMENDED!
    • Albuterol – Wheezing is due to the airways being clogged with debris not bronchospasm
    • Racemic epinephrine
    • Corticosteroids
    • Chest physiotherapy
    • Montelukast
    • Antibiotics
    • Hypertonic Saline
    • Routine testing
    • Chest X-rays

References

  1. http://pediatrics.aappublications.org/content/134/5/e1474
  2. http://www.chop.edu/clinical-pathway/bronchiolitis-emergent-evaluation-clinical-pathway
  3. http://www.cochrane.org/CD001266/ARI_bronchodilators-for-bronchiolitis-for-infants-with-first-time-wheezing
  4. http://www.seattlechildrens.org/healthcare-professionals/gateway/pathways/

Special thanks to Dr. Hima Khamar, MD PGY-2 for her contribution to this month’s Pediatric Pearls!

Case of the week COW #11

Posted on by Yenis Paez-Perez

CC: Can’t see for 2 months

HPI: 10 year old male with no significant past medical history presents to the Emergency Dept. complaining of painless vision loss in the right eye for 2-3 months. Patient states he has been having difficulty seeing out of his right eye for 2 months despite changing positions in class, taking on and off his glasses and using eye drops. Vision loss has become progressively worse and now he can only distinguish whether lights are on or off. Mother states she did not do anything about this problem because she thought he was kidding and she didn’t’ have money or health insurance to seek medical attention. Patient has been wearing Bifocals for myopia since the age of 6, with corrective vision lenses at age 5. Denies associated trauma. Patient moved to the U.S from Nigeria 5 years ago. He lives with his mother and sister. Vaccines are up to date.

PMH/Birth History: NSVD at 39 weeks, 1 day. Birth took place in Nigeria and mother denies any infection during or after pregnancy. Following birth, patient did not have any complications such as pneumonia, eye infections or rashes.

Social History: Denies drug abuse. Denies exposure to chemicals. Denies contact with dirt, dogs or pigs. Patient did not live on a farm. As per mother, there was no domestic abuse in the family

PHYSICAL EXAM 

Vitals within normal Limits

General: In no acute distress, appears stated age.

Head: Atraumatic, normocephalic. No deformities.

Eye: Right (OD): pupil non-reactive and remains white in color and approximately 2mm. Afferent reflex is present CN II; efferent reflex is absent. There is a complete visual field defect on the right side. Visual Acuity: Can only distinguish between light and dark. Unable to count fingers at any distance or visual objects even in motion. On Fundoscopic exam, the fundus is gray/dull, with no retina visualized. ALL CONSISTENT WITH LEUKOCORIA

Respiratory: Lungs CTA bilaterally.

Cardiac: +S1/S2, no MRG, regular rate and rhythm

Abdomen: soft NT ND

Neuro exam: CN III –XII intact. No motor, sensory, vibratory, temperature or pain deficits. Gait is steady and normal, without any difficulty. Cerebellar function intact, no dysmetria bilaterally.

Extremities: Full ROM in all extremities. 5/5 strength in all extremities

Skin: No edema, rashes, lacerations, or abrasions. Skin is warm, pink, moist and intact.

LABS

CBC: Unremarkable with        WBC: 7.1     Hemoglobin: 13.5       Platelets 211.

CMP: WNL       CRP and ESR = WNL

Tonometry: IOP approx. 17-18 x 3 times

Wood lamp: No corneal abrasion, dendritic ulcers, lesions or depositions OU

Bedside U/S: Completed within 10 minutes of arrival ( Only Right eye is shown)

Working Differential Diagnosis:

  • Retinoblastoma
  • Intraocular Mass
  • Cataract
  • Syphilis
  • Parasitic infiltrate
  • Posterior Infarct

CT Max/Facial w/o Contrast to rule out intracranial pathologies: Negative for masses; positive for homologous material in the right lobe. MRI was recommended for further evaluation

ED/Hospital course:  Ophthalmologist on call was consulted, and said there was nothing more to do. Unfortunately because his vision loss was > 2 months, no life saving surgery was imminent as the retina was already detached causing ischemia to the rods and cones within it.  Patient was to follow up in ophthalmology clinic the following day. Patient’s Pediatrician was also contacted and he referred the patient to a Pediatric Ophthalmic specialist in University Hospital, with a scheduled appointment within the same week. Approximately one week ago, patient underwent surgery and the leading diagnosis was Toxocariasis as per MRI. Biopsy results to follow. As per mother, the patient is still without vision in his right eye.

LEUKOCORIA, UNILATERAL, 10 YO MALE DIFFERENTIALS

Coats disease— is an exudative retinal vascular disorder characterized by retinal telangiectasias and subretinal exudation leading to serous retinal detachment. Presenting complaints include decreased visual acuity, strabismus, or leukocoria. The leukocoria in Coats disease is generally more yellow than white due to the presence of subretinal lipid. Coats disease is almost always unilateral and the vast majority of cases occur in boys. The majority of cases presenting with leukocoria are diagnosed between five and nine years of age, which is older than the majority of retinoblastoma patients.

Clinical examination: subretinal lipid and abnormal telangiectatic vessels US: demonstrates complete retinal detachment with massive subretinal lipid. Intraocular calcification is almost never present in Coats disease, another feature that helps to distinguish it from retinoblastoma.

The retinal photograph depicts bullous retinal detachment in the Left eye of a 1-year-old child with Coat’s disease simulating retinoblastoma. The magnetic resonance images confirm the diagnosis of retinal detachment and exclude retinoblastoma because of the absence of intraocular mass.

 

Toxocariasis — Toxocariasis, or visceral larva migrans, is an infection caused by the dog ascarid Toxocara canis or, less commonly, the cat ascarid Toxocara catis. There may be a history of living in an underdeveloped country, and exposure to dirt or undomesticated dogs. It occurs most commonly in children one to five years of age. Common presenting signs of toxocariasis are strabismus and poor vision. The ocular lesion is caused by the inflammatory response to the second-stage larva, which may localize in the one eye or both eyes

Chorioretinitis characteristic of toxoplasmosis. A pigmented scar is seen with an adjacent area of active chorioretinitis. The diagnosis of toxoplasmosis is based primarily on the appearance of the chorioretinal lesion rather than serologic studies. Courtesy of James T Rosenbaum, MD.

 Retinopathy of prematurity (ROP) — developmental vascular proliferative disorder that occurs in the incompletely vascularized retina of preterm infants and can lead to retinal detachment and permanent blindness. The most important risk factor for developing ROP is prematurity. There needs to be a history of prematurity, and/or mother mentions patient was on O2 for awhile.

Vitreous hemorrhage — Vitreous hemorrhage causes leukocoria when there is extensive organization of the blood into a clot before degradation. With time, the reddish hue of the blood is lost and the hemorrhage transforms into “whitish debris.” Etiology includes advanced ROP,  trauma (MOST common), leukemia or hemorrhagic disease of newborn

Retinablastoma– Retinoblastoma is the most common primary intraocular malignancy of childhood and accounts for 10 to 15 percent of cancers that occur within the first year of life. Retinoblastoma typically presents as leukocoria in a child under the age of two years. Untreated retinoblastoma is a deadly disease; however, with advances in treatment, survival in the contemporary era is >95 percent. Most common age group is birth- 2 years. Very uncommon in children over the age of 5, although 1-2 case reports have occurred in 18 year old males

 Pearls & Takeaways:

  • Leukocoria Requires further investigation – On exam, History and Diagnostic
  • The use of tonometry, fundoscopy and ocular ultrasound are an easy, noninvasive way to add to your ophthalmic exam. Slit-lamp exam could have been considered here
  • Ocular ultrasound is really cool and fun!
  • Advocate for your patients!  Make sure they have proper follow up with a specialist
  • If any abuse or neglect is suspected, be sure to turn on “Sherlock Holmes” senses and investigate.

 

Case presented by Dr. Sarah Bolan

 

Case of the Week COW #9

Posted on by Yenis Paez-Perez

CC: “Post Surgical Pain” ; Abdominal pain

HPI: 8 year old Male with PMH of Sickle Cell Disease (HbSC), Post-opt Day 10 for laparoscopic splenectomy for recurrent sequestration crises presents to the Emergency Department (ED) complaining of abdominal pain x 2 days. The pain is described as diffuse and worse in the RUQ. Denies exacerbating or relieving factors. Pain is associated with constipation; last Bowel movement was 7 days prior. Mother states he did have one small BM shortly after surgery. He is tolerating PO without difficulty and does report flatus. She has been giving him Oxycodone 2mg every 6 hours for pain with minimal relief. Upon review of systems, patient reports feeling hot for the past 2 days but without a recorded temperature at home. Additionally, patient complained of a non-productive cough for 2 days and has been “breathing fast” for the same duration of time.

Physical Exam:

BP 112/74    HR 129     RR 24   SpO2 93% on RA   Temp 99.9F      26.3 kg

Constitutional: Well developed, well-nourished child who is awake, alert and in moderate distress due to pain and feeling hot; making tears

HEENT: NCAT, pupils PERRLA, neck supple

Respiratory: CTA B/L, no wheezing, rales or rhonchi

Chest/Axilla: Normal symmetrical motion, no tenderness

Cardiac: +S1/S2, RRR, no MRG,

Abdomen: Scars noted over splenectomy site which are clean dry and intact, healing well without discharge; Diminished Bowel Sounds in all quadrants; soft, non-distended with mild tenderness in all 4 quadrants. No rebound or guarding.

Neuro exam: AAO x 3. No deficits

Extremities: no edema, no tenderness or swelling

Pertinent Labs:

CBC: 42.1

HBG: 12.5

HCT: 36.9

Platelets: 721

Seg: 79

Lymphs: 9

Mono: 12

Reticulocyte count: reported as normal

Pertinent Imaging and other tests:

Working Diagnosis:

Generalized abdominal pains

Elevated WBC

Abscess of spleen

ED/Hospital course:

Surgery was consulted in the ED and they believed the pain was not related to the surgery. Abdominal U/S performed at their request showed “s/p splenectomy with gallbladder sludge.” Patient had moderate improvement in his pain after Toradol 15mg IV and Morphine 2mg IV were given in the ED. Patient also received Rocephin 75mg/kg and NS 500mL IV Fluid bolus for presumed infection with the leukocytosis of 42.1.

The patient was admitted to Pediatric Step down for further evaluation and management. Overnight, he remained comfortable with stable vital signs, afebrile and saturating 94-96% on 2L NC. On Hospital day #1, patient became febrile to 103F and continued to deny chest pain, SOB or difficulty breathing. The cough remained unchanged since admission. A repeat Chest X-Ray was obtained and the patient was diagnosed with Acute Chest Syndrome and received exchange transfusion the same day (Refer to Image below) Additionally, he received Ceftriaxone, Azithromycin, Nitric oxide and IVF at ¾ maintenance ate throughout hospitalization. On Hospital Day #4 he was discharged home.

Pearls:

Acute Chest Syndrome

  • It is the leading cause of death in patients with SCD in the United States
  • Most often occurs as a single episode, but patients may have multiple attacks resulting in chronic lung disease
  • Multiple Etiologies
    • Pulmonary infections
    • Iatrogenic cause including aggressive hydration for sickle cell painful crisis ——à causing Pulmonary Edema
    • Opioid use —–à Decreased inspiratory effort——à Atelectasis
  • New infiltrate identified on Chest X-Ray with at least one of the following: Fever, cough, wheezing, tachypnea, chest pain, hypoxemia.
  • Radiographic changes often lag behind clinical features so initially the Chest X-Ray may actually be normal (as in our case)
  • Treatment
    • Supportive: Early Supplemental Oxygen, analgesics and IV Hydration up to 1.5x maintenance rate
    • Antibiotic irrespective of cultures
    • Transfusion is believed to be lifesaving; recommendations based on empirical observations and not on firm evidence
    • Exchange transfusion seems to be more advantageous, especially in patients with a hemoglobin of > 9.0
      • It decreases the concentration of sickled hemoglobin with little iron gain
    • Inhaled Nitrous Oxide is beneficial
      • Due to its vasodilatory effects –à improved ventilation/perfusion in damaged lung tissue
      • Reduced RBC and leukocyte adhesion to endothelial cells, therefore affecting disease progression
    • Hydroxyurea reduces occurrence of acute chest syndrome

Case Presented by Greg Cassidy, MD

 

References:

  1. Stapczynski, J. S., & Tintinalli, J. E. (2016). Tintinalli’s emergency medicine: A comprehensive study guide (8th ed.). New York, N.Y.: McGraw-Hill Education LLC..

 

EM Conference Pearls (9/20)

Posted on by David Traficante

Pediatric congenital heart disease

  • Congenital HD: Two types: Neonates with ductal dependent lesions and infants (2-6months) presents with CHF
  • Cyanosis presentation: When ductal-dependent lesion is required for pulmonary blood flow (Will not respond to oxygen)
  • Shock presentation: When ductal-dependent lesion is required for systemic blood flow (appear septic and not response to fluids, may get worse with fluids)
  • Hypoxic/cyanotic or shocky/acidotic baby treatment = Prostaglandin E1 (PGE1) and transfer to facility with pediatric cardiovascular surgeon.
  • PGE1 treatment may cause apnea (monitor closely and consider intubation)
  • CHF in infants = wheezing, retractions, tachypnea, sweating/crying, difficulty feeding

EBM in the ED

  • EBM = What the evidence shows in the literature + What the physician wants for the patient + what the patient wants for themselves
  • Just like we need to practice intubation, central lines –> Learning to read and interpret literature is a skill that needs to be practiced.

Aortic Dissection

  • AD: Chest pain plus disease (ex: CP + Neurodeficit)
  • If you find your self giving large amounts of strong pain meds (narcotics) while treating what is seemingly ACS…STOP..think about AD or alternative diagnosis of chest pain
  • The 3 important questions, aortic dissection is the subarachnoid hemorrhage of the torso, migrating pain, colicky pain + opioids = badness and pain that comes and goes can still be a dissection.
  • Treatment: Treat pain, HR, BP
  • Pain: Fentanyl 25 – 50 mcg bolus
  • HR: Goal of 60 bbpm
  • Esmolol 0.5 mg/kg bolus then 50 – 300 mcg/kg/min or
  • Labetalol 10 – 20 mg bolus then 0.5-2 mg/minor
  • BP control: Goal SBP =110
  • Nitroprusside 0.25 – 0.5 mcg/kg/min then titrate (CN toxicity)
  • Nicardipine 5 mg/hr
  • Warning: Giving a vasodilator without concomitant reduction in ionotropy may cause progression of dissection. Start BB first before vasodilation meds.

When kids eat coins

Posted on by terrancemcgovern

Kids eat up your money in more ways than one.  Some may eat it up in the form of $50,000 a year in college tuition and some eat it up as a meal.  For coins that get stuck in the esophagus the American Society for Gastrointestinal Endoscopy recommends watching asymptomatic patients for a period of 24 hours prior to any intervention.  Once the coins passes into the stomach most will traverse the GI tract without any complication.  There are multiple different methods of retrieving coins that are lodged in the esophagus: endoscopy, foley catheter technique, glucagon and bougienage is a method of pushing the coin into the stomach.  Classically, you use a Hurst dilator (or build your own) and advance it down the child’s esophagus to push the coin past the lower esophageal sphincter (step-by-step instructions).  Bougienage, when used on appropriate patients, is a safe modality for treating esophageal coins with only minor complications reported.  Some have reported success rates as high as 95%; however, you have to stick to the following inclusion criteria:

  1. Witnessed ingestion
  2. Foreign body is a coin
  3. Coin is seen in the esophagus on x-ray
  4. Single coin is present
  5. Ingestion < 24 hrs
  6. No previous esophagus procedure or pathology
  7. No respiratory symptoms
  8. Performed by trained personnel

If you successfully get the coin to pass into the stomach then the patient can be discharged home.  If the piggy bank doesn’t give up the coin in the next 2 weeks, then the patient will need a repeat xray to see where it is.  Check out this ACEP Now article for a more detailed discussion of bougienage.

Post by: Terrance McGovern DO, MPH (@drtmcg13)