Brown Pediatrics

Brown's Pediatric Residency Blog

Category: Hospital Medicine

This is… Lumbar Puncture

Case: Jane is a 2 week-old, previously healthy, ex- full term girl who presents to the ED from her PCPs office after being found to have a temperature of 102.5 rectally. On exam, she is fussy but consolable and has an otherwise normal exam.  In addition to blood and urine studies, you plan to perform a lumbar puncture. What would be other indications and even contraindications for an LP? What are the various techniques? Should you use local anesthesia?  


Lumbar Puncture: The basics


  • The most common indication for lumbar puncture is to diagnose meningitis (Bonadio, 2014)
    • Other indications include diagnosing: demyelinating diseases, subarachnoid hemorrhage, or idiopathic intracranial hypertension (formerly pseudotumor cerebri)


  • Suspected intracranial pressure elevation
  • Clinical/Physiological Instability (hypotension, respiratory distress, status epilepticus)
  • Coagulopathy
  • Infection of overlying skin


Basics of setup

After discussing the case with the team, you decide that Jane has no contraindications and that it is important to rule out meningitis.  What do you need, and how do you set up?

1.  Equipment

  • Most (if not all) of your equipment will be included in a commercially available tray (Figure 1 as an example).
    • In general, you will need the following
      • Spinal needle (1.5″ or 3″ depending on the patient)
      • sterile gloves and drapes
      • Povidone-Iodine scrub
      • Monometer tune (to measure CSF pressure)
      • Sterile tubes for CSF collection


Figure 1: LP Tray (Picture from Bonadio, 2014)


2. Position 

  • In the younger child, and in those you need to measure CSF pressures, the child should be placed in the lateral decubitus position
  • In older children, the seated position can also be used (Figure 2)
  • Remember, the spinal cord ends around L2. Therefore, the needle should enter the L3/4 or L4/5 disc space
    • The L3/4 disc space will be transected by the line that connects the iliac crests (as seen in Figure 2).


Figure 2: LP Landmarks (Picture from Bonadio, 2014)


Maximizing Success

As you are gathering your materials, you begin wondering what can be done to maximize the success of your procedure.

1.)  Anesthesia

  • Topical (“EMLA”) vs local (1% lidocaine infiltration)
    • Use of local anesthetic associated with an increased odds ratio (OR = 2.2) for success (Baxter, 2006)
    • Other RCTs (Pinheiro et al, 1993; Nigrovic, 2007) found that local infiltration did not increase success, but statistically decreased the amount of struggling in infants.
      • Note: Despite not finding any differences in success rates between the two methods, it is important to note that local infiltration did not lead to decreased success (concern for a loss of landmarks, etc).

2.) Early stylet removal (“Cincinnati” Method)

  • In this method, the stylet is removed after puncturing the epidermis
    • Baxter et al found a trend towards increased success in residents employing this method, but this was not statistically significant (Baxter, 2006)
    • Nigrovic et al did find an association between leaving the stylet in and with the composite outcome of traumatic or unsuccessful lumbar puncture (Nigrovic, 2007)

Conclusion: Use an anesthetic (topical or local infiltrate) and consider removing the stylet early


Now that we know what we need, where we need to go, and what helps maximize success, how do we do the procedure?


NEJM Tutorial

Another Example from EM:RAP


Faculty Reviewer: Jeff Riese, MD


  • Baxter AL et al. “Local Anesthetic and Stylet Styles: Factors Associated with Resident Lumbar Puncture Success.” Pediatrics. 2006;117(3)876-881
  • Bonadio W. “Pediatric Lumbar Puncture and Cerebrospinal Fluid Analysis.” The Journal of Emergency Medicine. 2014;46(1)141-150.
  • Nigrovic et al. “Risk Factors for Traumatic or Unsuccessful Lumbar Punctures in Children.” Annals of Emergency Medicine. 2007;49(6)762-771
  • Pinheiro JM et al. “Role of Local Anesthesia During Lumbar Puncture in Neonates” Pediatrics. 1993;91(2)379-82


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).

Trouble in Paradise



Case: George is a 5 year-old boy presenting to an Emergency Department (ED) complaining of abdominal pain and loose stools following a recent tropical vacation. How should we proceed? Is there any way that we could have prevented this?

What is traveler’s diarrhea?

    1. Classic Definition: ≥ 3 unformed stools in 24 hour period with nausea, vomiting, cramps, fever, blood in stool (Stauffer et al, 1990)
      • For infants and young children, some authors define diarrhea as ≥ 2-fold increase in unformed stool (Ashkenazi et al, 2016)
    2. Moderate diarrhea: 1-2 loose stools per 24 hour period
    3. Mild diarrhea: 1 loose stool per 24 hour period
    4. Duration (CDC, 2016)
      • Viral : 2-3 days
      • Bacterial: 3-7 days
      • Protozoal: weeks to months

Etiology (Ashkenazi et al., 2016)


Electron Microscope Image of E. Coli (Pixabay Image)

    1. Bacterial: E. Coli (ETEC, EHEC, EAEC, etc), Campylobacter jejuni, Salmonella spp., Shigella spp.,  are the most commonly seen, though Aeromonas spp. increasingly noted (CDC, 2016).
      • Of note, E. Coli (O157:H7) [associated with hemolytic uremic syndrome] has not been described in traveling children (Mackell, 2005)
    2. Viral: rotavirus, norovirus, adenovirus
    3. Parasite: Giardia (most common), Cryptosporidium, Cyclospora, entamoeba (uncommon)
    4. Etiologic agent generally identified in less than ⅓ of cases



    1. General incidence: 10-40% of travelers (Pitzinger B et al, 1991), though can affect up to 70% of travelers depending on the location they were traveling in (CDC Yellow Book)
      • Highest risk in Asia, Sub-Saharan Africa, and Latin America (Hagmann et al, 2010)
    2. Young children at the highest risk and manifest most severely (Ashkenazi et al, 2016)
    3. Children visiting family and/or friends are at higher risk as compared to tourists


    1. Microbiologic identification is generally unnecessary
    2. If fever and colitis  think Campylobacter, Shigella, EHEC
    3. Predominance of upper GI symptoms  Giardia, isospora, cyclospora
    4. If recent antimicrobials  -> C. diff
    5. If ill, send cultures for salmonella

Role for Prevention? (Connor, 2015)

  1. Choosing food and beverages wisely while traveling has been the cornerstone of advice
    • Unfortunately, studies do not show benefit to this practice (Steffen et al, 2004)
  2. Hand hygiene very important
  3. For children older than 12 years old, bismuth subsalicylate has been shown to reduce incidence of traveler’s diarrhea by 50%
    • Inconvenient dosing: 2 tabs, four times daily
  4. Prophylactic antibiotics are not generally recommended
    • May be considered in “high-risk hosts” (e.g. immunosuppressed)

His dad asks: how should he treat this?


    1. Maintaining hydration is the most important treatment
      • Use urine output as a guide (if normal urine output, diarrheal illness is mild)
    2. If evidence of dehydration: Preferentially use oral rehydration solution (Desforges, 1990)
      • WHO solution made with: Glucose (20g/L), 3 salts (3.5g/L) [sodium chloride, potassium chloride, and sodium bicarbonate]
      • Rationale for use is intestinal co-transport of glucose and sodium
    3. Role of antibiotics
      • Warranted in severe diarrhea (>4 stools in 24 hr period, fever, blood/pus in stool)
        1. Azithromycin is treatment of choice (Ashkenazi et al., 2016)
        2. Rifaxamin for children ≥ 12 years old
        3. Fluoroquinolones (Note: not FDA approved for children)


      1. Diarrheal illness in children returning from travel is not uncommon
      2. Younger children at higher risk of significant morbidity
      3. Maintaining hydration is essential; utilize oral route
      4. Antibiotics not well studied, beneficial in severe cases
      5. For all traveler’s, utilize CDC’s Website to provide resources and guidance

Online Resources

  • CDC:

Faculty Reviewer: Michael Koster, MD


Ashkenazi S et al. “Travelers’ Diarrhea in Children: What have we learnt?” The Pediatric Infectious Disease Journal. 2016;35(6)698-700.

Connor BA. “Traveler’s Diarrhea.” CDC Health Information for International Travelers 2016. Ed. G. Brunette. Oxford University Press, 2015.  Print and Online

Desforges JF. “Oral therapy for Acute Diarrhea- The Underutilized Simple Solution.” NEJM. 1990; 323:891- 894.

Hagmann S et al. “Illness in Children After International Travel: Analysis From the GeoSentinel Surveillance Network.” Pediatrics. 2010. 125(5)e1072-e1080

Mackell S. “Traveler’s Diarrhea in the Pediatric Population: Etiology and Impact.” Clin Infect Dis. 2005;41(Suppl 8)S547-S552.

Pitzinger B et al. “Incidence and clinical features of traveler’s diarrhea in infants and children.” The Pediatric Infectious Disease Journal. 1991;10(10)

Stauffer WM et al. “Traveling with Infants and Small Children. Part III: Traveler’s Diarrhea.” Journal of Travel Medicine. 2002;9(3):141-50

Steffen R et al. “Epidemiology of Travelers’ Diarrhea: Details of a Global Survey.” J Travel Med. 2004;11(4)231-238.



“Water, water, everywhere…”



Case: Zoe is a 10 day old ex- full term female, born to a G1P0 →1 presenting with feeding difficulties. Per her mother, she is exclusively breastfed and had initially had been doing “ok” but for the last couple days, has been more sleepy than usual and not feeding as well. She also notes that during this time, her eyes have become a bit more yellow.


On exam, you note an infant in no distress, but she sleeps comfortably through your exam. Jaundice is appreciated. Vitals are normal, but you note she has lost 12% of her birth weight. Her HEENT is notable for a sunken anterior fontanelle. Her exam is otherwise benign. Concerned for hyperbilirubinemia and dehydration, you order a complete metabolic panel, which, among other abnormalities, is significant for a serum sodium of 165 meq/L.


Why is her sodium so high?

Diagnosis: Severe neonatal hypernatremic dehydration



  • In this case, the most likely etiology is ineffective breastfeeding (also termed lactation failure), which is a rare, but increasing cause of hypernatremic dehydration (Mortiz et al, 2002)
  • In all humans (not just neonates), hypernatremia results from one of two mechanisms: inadequate access to free water and/or an inability to concentrate urine
  • Breastfeeding failure leads to inadequate fluid intake, but is also related to the higher concentration of sodium in breast milk (Morton, 1994)


How do patients present? (Moritz et al, 2005)

scaleOver 70% of patients had > 10% weight loss


Signs at Presentation

% Of Infants (n=70)

Jaundice 81
Poor PO Intake 61
Decreased Urine Output 36
Fever 20

Table Adapted from Moritz et al, 2005


How common is this problem?

  • Neonatal hypernatremic dehydration is rare. A review of admissions to a major children’s hospital found that over 4 years, 1.9% of term and near term infants were admitted for hypernatremic dehydration (Mortiz et al., 2005)
  • Most commonly affects primiparous mothers


How should we treat?

  • The goal of treatment is to lower serum sodium in a slow and controlled fashion
  • Conventional teaching states that sodium should not be lowered faster than 0.5mEq/hr and in fact, recent studies suggest that correction faster than 0.5mEq/L/hr is independently associated with poor neurologic outcomes and seizures (Bolat et al, 2013)
  • Specifics (based on protocol detailed in Bolat et al)
    • Emergency Phase
      • Correct shock immediately (within 30 mins) with 10-20 cc/kg 0.9% saline
    • Rehydration Phase
      • Calculated Free Water Deficit
      • Composition of fluid for rehydration is dependent on serum sodium; remember, in patients with high serum concentrations, “normal saline” will be hypotonic (154 meq/L)
      • Serum sodium should be decreased by 0.5meq/L/hr over the first 24-48 hours
      • If a patient is urinating, add 40 meq potassium to fluids


What are the neurological outcomes?

  • In the aforementioned study (Bolat et al, 2013), researchers found that presenting serum sodium >160 meq/L was an independent predictor of mortality (OR: 1.9) and correction faster than 0.5 meq/hr was independently associated with an increased risk of seizures (OR: 4.3)
  • At 6 months of age, patients were screened with the Denver Developemental Screening Test II. Serum sodium > 165 meq/L on presentation was associated with worse outcome.


  • Neonatal hypernatremic dehydration is a rare complication of exclusive breastfeeding, primarily seen with primiparous mothers and  can have devastating consequences
  • Clinicians need to be aware of this complication and ensure infants  who are exclusively breastfed are followed closely to ensure adequate breastfeeding and weight gain
  • If hypernatremic dehydration is encountered, it is imperative to 1.) treat shock initially and 2.) ensure that serum sodium is NOT corrected faster than 0.5 meq/hour

Resident Reviewer: Marie Carillo, MD


  • Ahmed A et al. “Complications Due to Breastfeeding Associated Hypernatremic Dehydration.” Journal of Clinical Neonatology. 2014;3(3):153-157
  • Bolat F et al. “What Is the Safe Approach for Neonatal Hypernatremic Dehydration?” Pediatric Emergency Care. 2013;29(7):808-813
  • Moritz ML et al. “Breastfeeding-Associated Hypernatremia: Are We Missing the Diagnosis?” Pediatrics. 2005;116(3):e343-e347
  • Moritz ML et al. “Disorder of Water Metabolism in Children: Hyponatremia and Hypernatremia.” Pediatrics in Review. 2002;23(11):371-380
  • Morton J. “The Clinical Usefulness of Breast Milk Sodium in the Assessment of Lactogenesis” Pediatrics. 1994;93(5):802-806

EKG Basics

Created on 8/4/2016 by Hiral Mehta, MD


Griffin is a 5 y/o boy who comes into the ER. Parents state that earlier today he began complaining of his “heart running fast” and his chest hurting. His cardiac exam is unremarkable. You decide to get an EKG as part of your work up.

What should I know when interpreting a pediatric EKG?

EKGs are simple, relatively straightforward to obtain, and provide a great deal of important information- if you are able to interpret them!

First: Lead placement

There are several different types of lead set ups. Intuitively, more leads generally provide more information. Remember, EKGs are vector representations of electrical depolarization. The more “viewpoints” you have, the more information you can gather.


5 Lead-ECG: This is what we generally have on our hospitalized kids who are on CRM (cardio-respiratory monitoring).



Think “smoke (black) over fire (red), snow (white) over grass (green)” and “white on right”.

12-lead EKG: This is the standard 12 lead EKG that we order. In pediatrics, we use the “V4R lead” to better assess the right ventricular potentials because the RV extends to the right of the sternum in children. This gets confusing- you should still use the leads that the machine labels “V1”-”V6” in that order (R->L anatomically), but start V1 further to the right (and relabel the EKG when it prints out).


How do I interpret this EKG?

Good general guidelines: have a systematic approach. Look at as many EKGs as possible to start getting a sense of what is “normal”, especially at various ages. One standard approach is to think through EKGs as an approach of “rate, rhythm, and axis” but really, everyone tends to develop their own methodology.

It is helpful to think of the EKG as a “graph” of electrical activity on the “Y-axis” and time on the “X-axis.” (For more in depth explanation, please see videos at end of the post). 

  • The standard speed of paper is 25mm/sec, but it is always helpful to make sure EKG strips you are looking at are run at the standard speed
  • A “small box” is 0.04 seconds on the time axis and 0.1mV on the electrical axis
  • A “big box” is 0.2 seconds on the time axis and 0.5mV on the electrical axis
Basic components of Interpretation:


  1. For regular rhythms (more below on how to determine this), Rate = 300/ #of big boxes between 2 consecutive R waves
  2. For faster rhythms (infants), Rate = 1500/ #small boxes between 2 consecutive R waves
  3. For irregular rhythms, Rate = number of complexes on rhythm strip (usually lead II), multiplied by 6


  1. P waves: absent or present?
  2. Relationship between p- waves and QRS
    1. For sinus rhythm, there is a 1-1 relationship between p waves and QRS
  3. Regular vs Irregular (are intervals consistent across the rhythm strip)?
    1. If Irregular, is it regularly irregular (classically A-flutter) or irregularly irregular (classical atrial fibrillation)
  4. QRS morphology
    1. Narrow (sinus or junctional origin)
    2. Wide (ventricular origin)

Axis: There are multiple ways of determining the “axis.” Below highlights 1 of these methods. “Normal” axis changes with age, with infants having a “rightward” axis. As children grow older, the axis becomes more leftward.


Waves and Intervals:



  • P wave- represents atrial depolarization
  • QRS complex- represents ventricular depolarization
  • T wave- represents ventricular repolarization

(Note: In case you were wondering, there is an atrial repolarization wave, but it is “hidden” in the QRS complex).

Note: Remember, standard speed of paper is 25mm/sec, therefore, a “small box” is 0.04 seconds on the time axis and 0.1mV on the electrical axis and a “big box” is 0.2 seconds on the time axis and 0.5mV on the electrical axis


PR interval: This reflects conduction from the SA node AV node.

  • Normally thought of as 0.12- 0.2 sec (one “big box”) for adults; however in children it varies with age and HR.

QRS interval: Represents ventricular depolarization. The Q wave reflects depolarization from L -> R across the interventricular septum, the R wave reflects depolarization through the thick ventricular walls, and the S wave reflects depolarization of the Purkinje fibers. Again, normal intervals vary by age.

QT interval: Represents the time it takes for ventricular depolarization and repolarization. This is one of the intervals that can’t really be obtained just by reading off what the EKG machine calculates, since QT varies with the HR and the individual RR intervals. This will be expanded upon in a future topic, but for now:

  • The calculated “corrected QT” interval (QTc) is most commonly derived with Bazett’s Formula:
    • QTc=QT√RR
    • Use the RR interval preceding the QT interval that you’re looking at. This formula is most accurate for HRs 60-100!
    • Infants normally have a longer QTc (under 6 months, QTc of <490 msec is considered normal). Children older than 6 months should have a QTc <440msec.
    • MD Calc


For reference, here is a table with some normal EKG values for children (adapted from Sharieff et al, 2006):



Videos From around the web:

Basics of EKG leads

The Limb Leads

The Precordial Leads


Faculty Reviewer: Sara Ford, MD

Resident Reviewer: Brian Lee, MD


“ECG Basics.”

“Paediatric ECG Interpretation.”

Sharieff GQ, Rao SO. The pediatric ECG. Emerg Med Clin North Am 2006;24:196.


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

Image of the Week: 7/8

As you are starting your morning ED shift, your first patient is a 2-year-old boy, previously healthy,  who is coming in with 5 days of fevers at home. Fevers have occurred daily and have been as high as 39.5ºC. His mother states that during this time he has been more fussy than usual and has been not been eating or drinking very well. Vital signs demonstrate a temperature of 38.9ºC, HR of 150, RR is 20. His BP is 110/60.  On exam, he is fussy and appears ill. His conjunctiva are injected and you appreciate limbic sparing.  Oropharyngeal exam is shown below. You also note a diffuse macular rash. What are you most concerned about?



Kole A, Chandakole D. N Engl J Med 2015;373:467-467.


Answer: The picture above shows a strawberry tongue with fissured lips, which in conjunction with 5 days of fever, rash and bilateral conjunctival injection is concerning for Kawasaki Disease (KD). KD is an acute vasculitis of still unknown etiology affecting primarily infants and children. KD  affects coronary arteries, and without IVIG, 20% of children will go on to have coronary artery aneurysms (Newburger et al). Diagnosis of KD is primarily clinical, and requires 5 or more days of fever in conjunction with 4/5 clinical criteria (see below). For those children with persistent fever, but who lack all 4 criteria (child mentioned in case has 3), diagnosis utilizes lab and ECHO findings (listed below). In children with classic Kawasaki, as well as those with incomplete disease, the mainstay of acute management is IVIG paired with high-dose aspirin. For more information, please review the attached references.


Diagnostic Criteria of Kawasaki Disease (requires at least 5 days of fever)

  1. Changes in extremities: Acute: Erythema and edema of hands and feet Convalescent: Desquamation of fingertips
  2. Polymorphous exanthema
  3. Bilateral, painless bulbar conjunctival injection without exudate
  4. Changes in lips and oral cavity: Erythema and cracking of lips, strawberry tongue, diffuse injection of oral and pharyngeal mucosae
  5. Cervical lymphadenopathy (≥1.5 cm in diameter), usually unilateral

Diagnostic Criteria for children who have at least 5 days of fever and only 2-3 findings mentioned above:

  1.  Obtain Labs: CRP/ESR, CBC, LFTs, and UA
  2. If CRP < 3 mg/dl AND ESR <40
    1. If fever continues, re-evaluate
    2. If fever defervesces, no follow-up required (EXCEPTION: in children who develop desquamation, an ECHO should be obtained).
  3. If CRP ≥ 3 mg/dl and/or ESR ≥40, obtain ECHO 
    1. If > 3 supplementary lab findings (See Below), treat with IVIG and high dose ASA
    2. If < 3 supplementary Findings
      1. ECHO positive (see below for criteria) –> TREAT
      2. ECHO Negative
        1. If fever resolves, Kawasaki is unlikely
        2. If fever persists, obtain 2nd ECHO, consult specialist

Important Lab or Imaging Findings

  1. Supplementary Lab Findings (Need 3 or more)
    1. LFTs: Albumin ≤ 3 g/dL or elevated ALT (> 50 units/L)
    2. CBC: WBC ≥ 15,000 or PLT≥ 450,000 after 7 days, or anemia for age [normochromic, normocytic]
    3. UA: ≥10WBC per HPF
  2. ECHO findings
    1. Any of the Following
      1. z score of LAD or RCA ≥2.5
      2. coronary arteries meet Japanese Ministry of Health criteria for aneurysms
      3. ≥3 other suggestive features exist:
        1. perivascular brightness
        2. lack of tapering
        3. decreased LV function
        4. mitral regurgitation
        5. pericardial effusion,
        6. zscores in LAD or RCA of 2–2.5

From: AHA Scientific Statement on Kawasaki Disease 2004.

Faculty Reviewer: Erica Chung, MD



  • “Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease.” Circulation. 2004; 110(17)2747-2771
  • Son MB and Newburger JW. “Kawasaki Disease.” Pediatrics in Review. 2013; 24(4)151-161
  • Newburger JW et al. “Kawasaki Disease.” Journal of the American College of Cardiology. 2016;67(14)1738-49.

Diagnosis: Acute Hematogenous Osteomyelitis

What is It?

Osteomyelitis is an infection of the bones that occurs either via hematogenous spread (most common in children), bacterial spread from local (contiguous) infections (cellulitis or septic arthritis), or traumatic inoculation. Long bones are more likely to be affected, with the femur being the most commonly affected bone (see below).

NEJM osteo


Skeletal Distribution of Acute Osteomyelitis in Children. From: Peltola H, Pääkkönen M. N Engl J Med 2014;370:352-360.


  1. Who is affected?
    • In developed countries, annual incidence is 8 out of 100,000 children. In developing countries, the incidence is much higher
    • Boys are affected twice as much as girls
  2. Who are the major pathogenic players?
    • Skin organisms predominate!
      • S. aureus is the most common etiologic agent
        • S. aureus possess virulence factors making it especially good at infecting bone
      • S. pyogenes 
    • Other common organisms
      • S. pneumoniae, H. influenza (though less common given vaccination; often affects joints, as compared to bones)
      • Kingella Kingae (most common in children under 4)
    • Sickle Cell disease
      • Consider Salmonella (though staph/strep still more common)
    • Neonatal Osteomyelitis
      • The organisms listed above still cause infections, but can also see: GBS, coag. negative Staph, Enterobacteriaceae

Clinical Presentation and Management

  1. Clinical Presentation 
    • Most common findings in children with osteomyelitis are pain of affected area and loss of function, however 2 distinct clinical syndromes have been described:
      • Children presenting with fever, localized pain, who appear acutely ill (likely septic)
      • A more indolent course, with gradual onset of pain and concurrent loss of function. In this presentation, the child may be afebrile or have low-grade fevers
    • As the lower extremity is more commonly affected, a common presentation is a child with a limp
    • Always consider osteomyelitis when dealing with a fever of unknown origin
    • Neonatal osteomyelitis is more likely to be associated with septic arthritis as well as be multi-focal
  2. Diagnosis
    • Physical Exam: As above, there are two main presentations, but most commonly children will demonstrate:
      • Fever
      • Localized erythema, swelling, inability to bear weight
    • Lab Studies
      • Serum Inflammatory Markers (CRP/ESR)
      • Blood Cultures (large studies show blood cultures positive in 48% [Peltola et al.])
      • CBC (may show mild-moderate leukocytosis, although normal white count does not exclude the diagnosis)
    •  Imaging
      • MRI is the most sensitive modality (Sensitivity: 88-100%, Specificity: 75-100%. [Song et al.])
      • Bone Scintigraphy
      • Plain Radiographs: Early in disease will show soft tissue swelling. (Sensitivity: 43-75%; Specificity: 75-83%)
    •  Microbiologic Data
      • Blood cultures as above
      • Bone biopsy, debridement
      • Abscess drainage, if applicable
  3. Treatment:
    • Choice of antibiotic: Empiric therapy in children should adequately cover S. aureus based on local susceptibility patterns (If suspecting osteomyelitis in a neonate, also need to consider Gram-negative organisms).
      • First Generation Cephalosporin (e.g. cefazolin)
      • Anti-staph Penicillin (nafcillin, oxacillin, etc)
      • Clindamycin (if suspecting MRSA and local resistance to clindamycin is low)
      • Vancomycin
      • Linezolid
    • Choice between IV and PO antibiotics
      • Historically, AHOM treated with long courses of IV antibiotics
      • Recent data suggests that a 2-4 day course of IV antibiotics, followed by oral antibiotics is as efficacious as IV therapy alone in uncomplicated cases (Peltola et al)
    • Duration of therapy
      • Historically, treatment duration ranged from 4-8 weeks
      • Recent data suggests that 3 week courses may be appropriate in carefully selected patients (Peltola et al, Song et al).
  4.  Conclusions
    • In pediatric patients, osteomyelitis is most often a hematogenous infection
    • S. aureus and S. pyogenes are the most common etiologic agents
      1. However, in small children, always consider Kingella spp.
    • Most common presenting complaints are fever and loss of function (lower extremities affected more commonly than upper extremities)
    • MRI is the most sensitive diagnostic modality
    • Initial Treatment is aimed at Staph and Strep, while consulting local susceptibility patterns
    • In uncomplicated cases following initial IV treatment, oral regimens have been shown to be as effective as IV regimens.
Case Presentation Radiographic Findings:
  • Altered marrow signal intensity of the distal left femur with low T1 and hyper intense T2 and PDFS signals. A focal destruction of the posteromedial distal femoral cortex is noted with elevated periosteum and periosteal reaction as well as subperiosteal 3.0 x 1.2 cm. cystic collection is noted with low T1 and hyper intense PDFS signal intensity.
  • Inflammatory changes with oedema signal and mild muscle enlargement are seen within the distal thigh and periarticular musculature with hypointense T1 and hyperintense T2 and PDFS signal.
  • Normal both hip joints with no evidence of significant joint effusion or septic arthritis.
  • The findings are those of distal femoral osteomyelitis with subperiosteal abscess and inflammatory myositis of the distal thigh muscles.


Faculty Reviewer: Michael Koster, MD



  1. Akakpo-Numado GK et al. “Current Bacterial Causes of Osteomyelitis in Children with Sickle Cell Disease” Sante 2008;18(2)67-70
  2. Conrad DA. “Acute Hematogenous Osteomyelitis.” Peds in Review 2010;31(11)
  3. Pääkkönen M, Peltola H. “Antibiotic treatment for acute hematogenous osteomyelitis of childhood: Moving towards shorter courses and oral administration.” International Journal of Antimicrobial Agents 2011;38:273-280
  4. Peltola H, Pääkkönen M, Kallio P, Kallio MJ. Short- versus long-term antimicrobial treatment for acute hematogenous osteomyelitis of childhood: prospective, randomized trial on 131 culture-positive cases. Pediatr Infect Dis J 2010;29:1123-1128
  5. Peltola H, Pääkkönen M. “Acute Osteomyelitis in Children.” N Engl J Med 2014;370:352-360.
  6. Song KM, Sloboda JF. “Acute Hematogenous Osteomyelitis in Children.” J Am Acad Orthop Surg 2001;9(3)166-75

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