Brown Pediatrics

Brown's Pediatric Residency Blog

Category: Critical Care

Metabolism gone wild!

Case: Last week we talked about Jane, an otherwise healthy 2-week old girl. Let’s change the story a bit to hit on another consideration in infants. Instead of simply being febrile and fussy, let’s say that she comes back to the ED, this time afebrile, but lethargic with poor cap refill. How does our differential change now?



Image Credit: Pixabay

What are the important diagnostic considerations for neonates and infants who present very ill?

  1. Infection
  2. Metabolic/Endocrinologic
  3. Trauma
  4. Cardiac
  5. Surgical emergencies

For those of you who like acronyms, consider “THE MISFITS” in neonates and young children presenting with undifferentiated shock (adapted from post on PEM Playbook)

  • Trauma
  • Heart Disease/Hypovolemia
  • Endocrine Emergencies
  • Metabolic
  • Inborn errors of metabolism (to get this acronym to work, there may be some repetition)
  • Seizures
  • Formula problems (think too little or too much water)
  • Intestinal disasters
  • Toxins
  • Sepsis (while this is last, all very sick infants/children should be evaluated/treated for sepsis)


Today we will focus on the emergency management of inborn errors of metabolism (IEM), specifically at the immediate recognition and management.



Epidemiology and Etiology

IEMs are Individually rare, but more common in aggregate- 1/5000 live births for any IEM (Ewing, 2009)

Helpful to lump metabolic deficiencies into 3 broad categories (Saudabray, 2002)

  1. Disorders leading to intoxication (think urea cycle defects)
  2. Disorders involving energy metabolism (think hypoglycemia)
  3. Errors involving synthesis or catabolism of complex molecules (e.g. lysosomal storage disorders)
    • Note: Disorders in this category are rarely treatable in emergency

How do these children present?

  • Deterioration of consciousness is one of the more common presentations of IEMs (El-Hattab, 2015)
    • Other presenting features include vomiting, seizures, apnea, hepatic failure, and cardiac disease (heart failure, cardiomyopathy, arrhythmias)
  • Specific Presentation Patterns (Ewing, 2009)
    • Hypovolemia, hyponatremia, hyperkalemia: Consider adrenal insufficiency
    • Metabolic acidosis, hyperammonemia, ketotic hypoglycemia: Consider an organic acid defect
    • Encephalopathy, respiratory alkalosis, hyperammonemia: Consider a urea cycle disorder
  • Remember, “As the neonate has an apparently limited repertoire  of responses to severe overwhelming illness, the predominant clinical signs and symptoms can be nonspecific like poor feeding, lethargy, failure to thrive, etc.” (Saudabray, 2002)

What is the immediate workup? (El-Hattab, 2015)

Image Credit: Pixabay

  • Primary Workup

    • Glucose
    • Blood Gas with Lactate
    • Serum Chemistry (including BUN/SCr)
    • Urinalysis
    • Complete Blood Count (CBC) and Differential
  • Secondary Workup

    • Specific Findings from Initial Workup and/or Exam
      • Hypoglycemia: insulin, cortisol, growth hormone, β-hydroxybutryate, plasma acylcarnitine profile, plasma amino acids and urine organic acids
      • Encephalopathy: ammonia, Liver “Function” Test (sp. ALT, AST, bilirubin)
      • Suspected galactosemia: urine reducing substances

How do you stabilize? (Note: Do not wait for labs to return to begin stabilization!)

Image Credit: Pixabay

  • ABCs (patients can present altered, apneic and/or in shock)
  • Recall the 2 main categories leading to emergencies: IEMs leading to intoxication and those resulting in energy defects (Ewing, 2009)
    1. Give Energy
      • Dextrose
        • Bolus as needed to treat hypoglycemia
        • Maintenance with D10 solutions
    2. Remove Toxins
      • Make NPO
      • Intravenous Fluids
        • D10 Half-normal saline run at 1-1.5x maintenance rate
      • Hemodialysis if indicated
        • Severe Hyperammonemia (Urea Cycle defects)

Next Steps?

Consultation with a metabolic specialist is essential!

  • Will help direct further diagnostic workup
  • Will help determine if further medical interventions (medications, vitamins, cofactors, etc)



  1. Inborn errors of metabolism present non-specifically
  2. Always consider IEM when presented with unwell neonate or infant
  3. For critically ill presentations, IEMs can be broken down into 2 main categories: Toxin Accumulation and/or Deficient Energy
    • Emergent Treatment (following ABCs) are directed at these two issues

Faculty Reviewer: Chanika Phornphutkul, MD


  • El-Hattab AW. “Inborn Errors of Metabolism.” Clinc Perinatol. 2015;1-27
  • Ewing, PH et al. “Evidence-Based Management Of Metabolic Emergencies In The Pediatric Emergency Department.” Pediatric Emergency Medicine Practice. 2009;6(10)1-16
  • Horeczko, Tim. “The Undifferentiated Sick Infant.” PEM Playbook. Accessed: 5/3/2017
  • Saudabray JM et al. ” Clinical approach to inherited metabolic disorders in neonates: an overview.” Semin Neonatol. 2002;7(1)3-15


Pass the salt…

Post Created by: Dani Halpern, MD

Case: 5yo M comes into the ED with nausea, confusion, and headache. On exam, he is sleepy but noticeable uncomfortable. He has moist mucous membranes, pupils are reactive and he has no noticeable edema. Suddenly, he begins to have a generalized tonic-clonic seizures. Amid the chaos and his mother’s crying you check a BMP and lo and behold his Na comes back as 125!


Image credit:

What is the pathophysiology of hyponatremia?

When there is an acute drop in sodium in the blood, water is pulled into the intracellular fluid so cells, especially brain cells, begin to swell. This causes meningeal irritation and the manifested symptoms of nausea, confusion, headache, vomiting and eventually, seizures.

Effects of Hyponatremia on the Brain and Adaptive Responses

Image from: Adrogue HJ et al, 2000

What is the workup of hyponatremia?

Choice of diagnostic algorithms:

  • Classic algorithm begins with an evaluation of patient’s fluid status.
    • Hypovolemic hyponatremia: ↓↓Na/↓H20 Euvolemic hyponatremia: ↔Na/↑H20   Hypervolemic hyponatremia: ↑ Na/↑↑H20
    • This is notoriously difficult to do accurately and clinicians have been shown to be very inaccurate in their assessment with sensitivities ranging from 0.5-0.8 and specificities 0.3-0.5 (Chung HM et al, 1987)
  • Alternative algorithm: (Milionis HJ et al, 2002).

Application of Alternative Algorithm

(Adapted from Milionis HJ et al, 2002)

Step 1: Verify this is an accurate level and is not spuriously low

Step 2: Obtain serum osmolality: (normal 275-290)

  • Low serum osmolality: True hyponatremia
  • Normal serum osmolality: Results from either large volumes of isotonic fluid lacking sodium (most common = mannitol), or in cases of hyperparaproteinemia or hyperlipidemia/triglyceridemia, that latter cases being referred to as “pseudohyponatremia” (see below for illustration). This is only seen in labs that use flame photometry; newer methods using ion-specific electrode have nearly eliminated this entity (Androgue HJ et al, 2000).

  • Increased osmolality: Osmotically active substances (most commonly glucose), draw water out of cells, effectively diluting serum sodium
    • Correction is approximately 2 mEq Na for every 100 glucose is >100

Step 3: Obtain urine Osm and Urine Sodium

  • <100 mOsm/kg = Appropriate water Excretion
    • Primary polydipsia/ psychogenic water drinking
      • Adult needs to drink about 18L for noticeable decrease in Na
    • Low solute intake (e.g. malnutrition, “beer potomania”)
  • >100 mOsm/kg = impaired water excretion. Can be due to problems in 3 different locations in process of diluting urine (this is where urine sodium comes in):
    • <20 mEq/L: hypovolemia (most common cause) and other states of decreased effective arterial blood volume (e.g. cirrhosis, congestive heart failure, nephrotic syndrome (rare in the absence of concurrent renal failure or volume depletion))
    • >40 mEq/L: SIADH vs renal salt wasting (e.g. renal dysplasia, post-obstructive diuresis, post-ATN diuresis), diuretics [mostly thiazide diuretics, uncommon with loop diuretics], adrenal insufficiency, metabolic alkalosis) THIS IS WHERE CLINICAL ASSESSMENT OF VOLUME STATUS ACTUALLY MATTERS (SIADH: restrict water.  Salt wasting: give salt or stop drugs)

In summary, a diagnosis of SIADH requires SOsm < 275, Uosm >100, UNa >30 (Because the fact that urine sodium is not low suggests that the patient is not volume depleted)


Image Credit:

In general, treatment of hyponatremia must weigh the benefits of therapy against the risks of overcorrecting, namely, osmotic demyelination (Adrogue HJ et al, 2000).

General Principles

  1.  If the patient has severe symptoms (e.g. seizures, CNS depression), hypertonic saline (3-5cc/kg) should be administered (Brenkert TE et al, 2013)
  2. When correcting hyponatemia, the rate of correction should not exceed 8mmol/L on any day of treatment  (Adrogue HJ et al, 2000).
  3. Treat the underlying condition, as detailed above


And now a table for all the conditions that often get confused for one another: 

First test yourself:

SIADH Renal salt wasting Hypovolemia
Volume Status
Serum Na
Urine Na
Serum Osm
Urine Osm
Urine output




SIADH Renal salt wasting Hypovolemia
Volume Status Euvolemic Hypovolemic hypovolemic
Serum Na low low Low
Urine Na > 40 >>40 <20
Serum Osm low low low
Urine Osm > plasma Osm > plasma Osm >plasma Osm
Urine output Low high low
ADH high high high

Faculty Reviewer: R. Kremsdorf, MD


Adrogué HJ, Madias NE, and Madias NE. “Hyponatremia.” N Engl J Med. 2000;342:1581-1589

Brenkert TE et al. “Intravenous hypertonic saline use in the pediatric emergency department.” Pediatr Emerg Care. 2013 Jan;29(1):71-3.

Chung HM, Kluge R, Schrier RW, Anderson RJ. “Clinical assessment of extracellular fluid volume in hyponatremia.” Am J Med. 1987;83: 905-908

Milionis HJ, Liamis GL, Elisaf MS. “The hyponatremic patient: a systematic approach to laboratory diagnosis.” Canadian Medical Association Journal. 2002;166(8):1056-1062.

Fluid Therapy Part II: Resuscitation Fluids

Case Continued:  Clinically, you determine that Julius (2-year-old boy with an acute diarrheal illness) needs IV fluid resuscitation. Why give fluid?


Image courtesy of pixabay

When given for acute resuscitation (maintenance fluid will be addressed later), the goal of fluid administration is to reverse and correct circulatory insufficiency (Arikan et al, 2008).

  • In physiologic terms, fluid therapy rests aims to restore and/or increase oxygen delivery
    • Oxygen Delivery = CO x CaO2, where CO is the cardiac output (determined by heart rate and stroke volume) and CaO2 is the oxygen carrying capacity (determined by SaO2 and Hemoglobin).
    • The goal of administering fluids is to increase preload, which in turn increases stroke volume and ultimately oxygen delivery
      • THUS, each time fluid is administered, the goal is to increase stroke volume.
      • NOTE: the assessment of “fluid responsiveness” is a large topic, and will not be addressed later

Furthermore, many studies have illustrated an improvement in patient outcome with early administration of IVF (Mederios et al, 2015)- more on this later.

What to give: Theory  professor

Image courtesy of pixabay

  • Fluids are divided into 2 main categories: Crystalloids and Colloids
    • Colloids are defined as “fluids containing high molecular weight substances that remain in the intravascular compartment, thereby generating an oncotic pressure.” (Mitra et al, 2009)
      • Examples include: synthetic starches and albumin (natural)
    • Crystalloids are salt solutions of varying composition
      • In clinical practice, examples would include 0.9% saline solution, Ringer’s Lactate, and Hartmann’s solution (see Fluid Therapy: Part I for solution components)
        • Historical Note (Myburgh, 2014): “Normal Saline” was determined in the 1880s via experiments in lysing red blood cells, which indicated the amount of salt in human blood was 0.9%. Unfortunately, these studies were flawed and physiologically, human plasma is closer to 0.6% saline. Despite these findings, “normal” saline remains ubiquitous.
  • The choice of resuscitation fluid relies on Starling’s other formula, describing the determinants of fluid movement across semipermeable membranes (Myburgh, 2014)
    • The ideal solution would remain completely within the vascular space, with little extravasation into the interstitium
      • Based on this, colloids were initially thought to carry a theoretical benefit including: more rapid plasma expansion and correction of oncotic pressure (Medeiros et al, 2015)
  • Recent experiments into the glycocalyx layer of vascular endothelium have complicated this picture, indicating that in septic shock, damage to this layer contributes to vascular permeability, thereby limiting the benefits of colloids in actual practice

How does this theory play out in the real world?

In other words, in patients presenting with hypovolemia and/or shock, what fluid should be given to restore intravascular volume?

  • Colloids vs. Crystalloids
    • From our theoretical perspective, it would seem that colloids, though markedly more expensive, would be better
    • Pediatric-centered data is sparse, but studies comparing colloids and crystalloid in septic shock (usually dengue), fail to show convincing benefit of one solution over another (Mederios et al, 2015)
      • A recent meta-analysis of adult patients with sepsis indicates that synthetic colloids, specifically 6% HES, are associated with a higher rate of renal replacement therapy and mortality (Gattas et al, 2013)
      • Conversely, in adults, the use of albumin compared to crystalloid trends towards showing a 90 day mortality benefit  (Xu et al, 2014)
  • Chloride rich vs. balanced salt solutions
    • Recently, researchers have turned their attention to comparing chloride rich (e.g. normal saline) solutions with more physiologically balanced solutions (Ringer’s Lactate or Plasma-lyte)
      • These studies arose from observational studies showing (again, in adults) that hyperchloremia is associated with acute kidney injury (Suetrong et al, 2016)
        • In the recent SPLIT trial (randomized trial comparing NS and plasma-lyte), investigators failed to show any differences between the groups. In this study, the primary outcome was AKI, with secondary outcomes being use of RRT and in-hospital mortality (Young et al, 2015)
    • While such literature is sparse in the pediatric world, numerous case reports detail the association with normal saline and hyperchloremic metabolic acidosis (Skellett S et al, 2000).

Until further studies are performed, crystalloids should be used as first line therapy in fluid resuscitation in pediatrics, with attention paid to avoiding large volumes of chloride-rich fluids.


Now that we’ve chose a fluid, how to administer?

  • By convention, pediatric patients are given fluid boluses in 20 ml/kg aliquots. Unfortunately, the literature detailing how “20cc/kg” came to be is sparse.
  • The 2015 PALS (pediatric advanced life support) Guidelines indicate that in patients with signs of shock (diminished pulses, cool/pale/mottled skin, prolonged capillary refill, tachycardia, and altered mental status (particularly ominous), 20cc/kg should be administered over 5-10 minutes
  • In the United States, various studies have shown adherence to the PALS guidelines in children with shock is correlated with improved mortality (Carcillo et al, 2002; Han at al, 2003) and shorter length of stay (Paul et al, 2012)
  • However, the recent FEAST study (RCT Trial, population: children in sub-Saharan Africa), showed fluid bolus therapy was associated with increased mortality (Maitland et al, 2011).
    • Presently, Canadian investigators (SQUEEZE Investigators) are investigating this question (fluid sparing vs. usual care) with results of their pilot studying informing the feasibility of a multi-center trial (Parker et al, 2016).



  • Fluid, like any other intervention, has indications and contraindications
  • When deciding to give fluid boluses, determine the underlying pathophysiologic insult (sepsis vs. hypovolemia from ongoing losses) and intervene appropriately
  • Anticipate complications (fluid overload, metabolic derangements)
    • Case control studies from single institutions indicate that in the PICU setting, fluid overload is associated with higher morbidity (Sinitsky et al, 2015) and mortality (Sutawan et al, 2016).
    • Hyperchloremic metabolic acidosis with normal saline
  • Various retrospective studies show that adherence to PALS algorithm is associated with improved outcomes


Faculty Review: Lee Polikoff, MD



  • Arikan AA et al. “Pediatric Shock.” Signa Vitae. 2008;3(1)13-23
  • Carcillo JA et al. “Clinical practice parameters for hemodynamic support of pediatric and neonatal patients with septic shock.” Critical Care Med. 2002;30:1365-78
  • Gattas DJ. “Fluid resuscitation with 6% hydroxyethyl starch (130/0.4 and 130/0.42) in acutely ill patients: Systematic review of effects on mortality and treatment with renal replacement therapy.” Intensive Care Medicine. 2013;39(4)558-568.
  • Han YY et al. “Early reversal of pediatric-neonatal septic shock by community physicians is associated with improved outcome. Pediatrics. 2003;112: 793-99.
  • Maitland K et al. “Mortality after Fluid Bolus in African Children with Severe Infection.” NEJM. 2011;364:2483-2495.
  • Medeiros DN et al. “Colloids for the Initial Management of Severe Sepsis and Septic Shock in Pediatric Patients: A Systematic Review.” Pediatric Emergency Care. 2015;31(11)e11- e16.
  • Mitra S et al. “Are All Colloids Same (sic)? How to Select the Right Colloid?” Indian J Anaesth. 2009;53(5)592-607
  • Myburgh JA. “Fluid resuscitation in acute medicine: what is the current situation?” Journal of Internal Medicine. 2015;277; 58–68
  • Paul R et al. “Adherence to PALS Guidelines and Hospital Length of Stay.” Pediatrics. 2012;130(2):e273-280
  • Skellett S et al. “Chasing the base deficit: hyperchloraemic acidosis following 0.9% saline fluid administration.” Arch Dis Child. 2000; 83:514-516
  • Suetrong B et al. “Hyperchloremia and moderate increase in serum chloride are associated with acute kidney injury in severe sepsis and septic shock patients.” Critical Care. 2016; 20:315
  • Sutawan IB et al. “Association of fluid overload with mortality in pediatric intensive care unit.” Crit Care Shock. 2016;19:8-13
  • Young P et al. “Effect of a Buffered Crystalloid Solution vs Saline on Acute Kidney Injury Among Patients in the Intensive Care Unit.” JAMA. 2015
  • Xu JY et al. “Comparison of the effects of albumin and crystalloid on mortality in adult patients with severe sepsis and septic shock: a meta-analysis of randomized clinical trials.” Critical Care. 2014;18:702



Fluid Therapy: Part 1


Image courtesy of Pixabay, Public Domain Pictures

Fluid therapy is likely one of the most common interventions performed in pediatrics. Until recently, fluid therapy wasn’t given much thought, “reflecting the long held notion that fluid therapy is straightforward and of little consequence to the patient” (Osteermann, 2012). This post will be the first in a likely 3-part series that looks at fluids and acid-base in the care of pediatric patients. 


Julius is a 2 year-old boy, who presents to the ED with an acute diarrheal illness, which started 3 days prior (his older brother had a similar illness 1 week prior, and is now well). Initially, Julius was drinking well, however mom notes that over the last day he has stopped drinking and doesn’t appear to be making wet diapers. On your exam, you note him to be fatigued, with dry mucus membranes and vitals are significant for mild tachypnea and moderate tachycardia.  You recognize that he is hypovolemic and want to start fluids. What should you use? (NOTE: in this context, many would make the argument for NG fluids, however in the context of the post we are going to assume that this is not possible).


Why do we use fluids?


Image courtesy of Pixabay, Public Domain Pictures

  • Fluids are used for 2 main reasons (Davidson et al, 2013):
    • Maintain intravascular volume (“Fill the Tank”)
    • Maintain water and electrolyte homeostasis (e.g. hypo- vs. hypernatremia)


Flashback to Med School: Fluid Compartments (Davidson et al, 2013):

  • Remember that “Total Body Water” (TBW) is about 60% of lean body weight
    • Note that neonates generally have much higher TBW (~75% of body weight) and TBW decreases with age


Adapted from Davidson et al, 2013

Tonicity vs Osmolality (Khurana, 2013)


Image courtesy of Pixabay, Public Domain Pictures

  • Osmolality (Osm) = moles of solute/kg of solvent
    • Depends on number of solute particles, not the specific type of particles
      • E.g. A 1 molar solution of NaCl has an osmotic concentration of 2 Osm, as NaCl will disociate into equal parts Na+ and Cl-
      • The osmolality of human intra- and extracellular fluid is 290 milliosmoles per kg (mOsm/kg)
        • This is largely determined by sodium, chloride, and bicarbonate (and to a lesser degree, glucose and urea).
  • Tonicity
    • Describes the movement of water between 2 compartments between a semi-permeable membrane (osmotic gradient)
      • In human physiology, everything is compared with that of human plasma
    • How does this apply to fluids we infuse?
      • Water will ALWAYS travel along its concentration gradient, from areas of low Osmolality to high Osmolality
        • Hypotonic fluids will result in the net influx of water into cells
        • Hypertonic fluids will draw fluids out of cells
    • As tonicity describes movement of water, it is only influenced by substances that cannot cross membrane
      • Substances that can freely cross membranes are called “ineffective osmoles” (e.g. dextrose, urea)

As such, osmolality does not equal tonicity

  • For example, the fluid D5 1/2NS is both hyperosmolar (owing to the dextrose) and hypotonic (again owing to the dextrose).

What is in the fluid we use?

 Common Fluid Choices and Their “Ingredients”

Human Body

Normal Saline (Isotonic)

Lactated Ringer’s (Isotonic)

D5 and 0.45% NaCl (Hypotonic)

Sodium 140 meq/L 154 130 77
Potassium 4 meq/L 0 4 0
Calcium 9 mg/dl 0 2.7 0
Chloride 102 meq/L 154 109 77
Lactate 0 0 28 0
Osmolality (mOsm) 298 308 273 406


How does one choose a fluid?

  • To choose a fluid, you must answer the question: What am I treating?
    • As mentioned earlier, this generally falls along the lines of: do I need to restore intravascular volume and/or do I need to provide daily requirements of water and electrolytes?
  • This question will be explored further on our next post, please stay tuned!


  • Fluid therapy is common in pediatrics, and should be approached like any other medication: Understand indications and any contraindications
  • Fluids can be classified by their osmolality (#moles solute/weight of solvent) and by tonicity (which describes the movement of water between a selectively permeable membrane)
    • Osmolality and Tonicity are related, but not equivalent. This is due to presence of “ineffective osmoles,” which are solutes than can freely cross membranes and therefore do not influence the movement of water
      • Hypotonic fluids will result in the net influx of water into cells
      • Hypertonic fluids will draw fluids out of cells
      • There will be no net movement of water with isotonic fluids

Faculty Reviewer: Lee Polikoff, MD

Sources (for table with various [ ]’s

Davidson D et al. “Fluid Management in Adults and Children: Core Curriculum 2014.” Am J Kidney Dis. 2013; 63(4)700-

Edelson JB et al. “Intravenous Fluid Management in the Pediatric Hospital Setting: Is Isotonic Fluid the Right Approach for all Patients.” Current Treatment Options in Pediatrics. 2015; 1:90-99.

Khurana, Indu. Textbook of Human Physiology for Dental Students, 2nd Ed. Elsevier. 2013. p18.

Ostermann M. “The importance of fluid therapy: No longer an innocent bystander.” Monitor. 2012;19(6).

Image of the Week: 8/3

Created on 8/3/2016 by Vanessa Hand, MD


A 17 year-old male in obvious distress is brought the ED by his sister. She states that  this morning he woke up with a fever and a sore throat. However, over the next few hours his voice has been changing and is now more “hoarse.” She notes that during this time he also developed difficulty breathing. Below is an x-ray obtained upon presentation. What are you most concerned about?


Case courtesy of Dr Maxime St-Amant, From the case rID: 26840

 Radiology Findings: Typical findings of epiglottitis with enlarged epiglottis and aryepiglottic folds.

Diagnosis: Acute Epiglottitis


  • Combination of sore throat, dysphagia, “hot potato” voice and high fevers classically described
  • Difficulty with breathing may be most common chief complaint (Mayo-Smith et al, 1995)
  • Symptoms progress rapidly, usually over hours (Stroud et al, 2001)
  • Physical Exam Shows:
    • Vitals: Febrile, Tachypnea
    • Visibly Distressed Child; “Tripoding” position
    • Muffled or hoarse voice

Epidemiology (Shah at al, 2004)

  • Historically caused by H. Influenza type B, however vaccination has largely shifted etiology to other organisms
  • Rate dropped from 5/100,000 to 0.6-0.8/100,000 (immunized)
  • Increased age of presentation from 3 yo to 6-12 yo 

Causative Organisms

  • H. influenzae, penicillin resistant S. pneumoniae, S. Aureus, β-hemolytic strep


  • Minimize stimuli, stressful procedures
  • Maintain airway, anesthesia/ENT intubate in OR
  • Antibiotics: Ceftriaxone or Ampicillin/Sulbactam; add Vancomycin or Clindamycin if concern for MRSA

Faculty Reviewer: Brian Alverson, MD


Mayo-Smith MF et al. “Acute Epiglottitis. An 18-year experience in Rhode Island.” Chest. 1995;108(6):1640-7

Shah RK et al. “Epiglottitis in the Hemophilus influenzae Type B Vaccine Era: Changing Trends.” The Laryngoscope. 2004;114(3): 557-60

Stroud RH et al. “An update on inflammatory disorders of the pediatric airway: epiglottitis, croup, and tracheitis.” Am J Otolaryngology.  2001;22(4):268-275


We are so excited to launch the OPENPediatrics Critical Care Curriculum! The OPENPediatrics platform will have two purposes.
  1. The Guided Learning Pathway is designed to teach you the bread and butter of critical care.
  2.  The second component is a Group page that will have additional educational material outside the OPENPediatrics curriculum. We will invite each resident to the group page. We encourage residents to send any interesting data or learning material to us. We will review the material with the critical care team and then uploaded onto the group page.

How to gain accesses to the material:

  1. Go to
  2. Create a username and password. Please create a username with the email the residency uses. We will be searching for your email when designing the group page.
  3.  Click the learning tab
  4. Click Guided Learning Pathways
  5. Click on Brown Pediatric Critical Care Resident Curriculum
  6. Enroll!
Our goal is asynchronous learning that provides a solid foundation for clinical management of patients.  As such, the material can be approached in a nonlinear fashion.

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