Tag Archives: pediatrics

Can’t Intubate Can’t Ventilate

Originally published at Pediatric EM Morsels on May 20, 2016. Reposted with permission.

Follow Dr. Sean M. Fox on twitter @PedEMMorsels


“Can’t Intubate Can’t Ventilate” is one of the frightening statements that causes massive surges of adrenaline in everyone. Unfortunately, most neural synapses don’t function well with that large surge of adrenaline, and it is, therefore, imperative to contemplate how to manage this scenario before it arises.  We have previously discussed Transtracheal Ventilation and have several videos to view, but let us review this important topic briefly once more. Can’t Intubate Can’t Ventilate: How Do I Oxygenate?


Can’t Intubate Can’t Ventilate: Anatomy Matters!

  • With larger children and adults, the can’t intubate can’t ventilate scenario often leads to the Cricothyrotomy.
  • In younger children and infants, the differences in anatomy make a traditional cricothyrotomy challenging.
  • In infants and young children:
    • Generous proportions of subcutaneous adipose tissue (chunky little babies are cute…) obscures landmarks.
    • The Hyoid bone is more prominent than the thyroid cartilage.
    • The Thyroid notch is often not palpable.
    • The Cricothyroid membrane is:
      • More horizontally positioned vs its typical vertical position
      • Small!
        • Around 8 years of age it is 1/2 the height and width of an adult’s
        • In neonates, the size is not sufficient enough to insert any commonly used rescue device. [Navsa, 2005]
  • The altered anatomy makes location of the cricothyroid membrane more difficult (if at all possible) and the small size may make it impossible to pass a large cric-tube through.


Can’t Intubate Can’t Ventilate: Go Transtracheal

  • Transtracheal ventilation has been used successfully in children as well as adults. [Frerk, 2015; Cote, 2009]
  • It may not “secure” an airway, but it will provide the patient with oxygen while you sort out the problem (and change your pants).
  • It is also easier than placing an IV in a child!
    • Locate the trachea!
      • If you are able to locate the cricothyroid membrane and it is large enough you can use it
      • Potential to use this catheter later to convert to a guidewire-assisted percutaneous cricothyrotomy. [Boccio, 2015]
    • Load a large gauge needle/catheter (14 gauge), ideally one that is reinforced(as simple peripheral IV catheters are prone to kink and become obstructed) onto a fluid-filled syringe.
    • Aspirate as you enter the skin at a 30-45 degree angle aimed caudally.
    • When you aspirate bubbles, you are in the airway! Advance the catheter and retract the needle.
    • Boom… done. High-Fives all around! {oh wait… we need oxygen!}


Can’t Intubate Can’t Ventilate: The Hard Part

  • The most difficult aspect of the procedure is not waiting too long to do it and leading to hypoxic insult.
  • The next most difficult aspect is figuring out how to connect oxygen to the tiny catheter you just placed in the neck.
  • This is where contemplation of how to do this before you need to do it is important, because most of us are not going to successfully “MacGyver it” on the fly.
  • Oxygen Connection Options

    1. Commercial products
      • Have flow regulators that are easy to use. [Cote, 2009]
      • Connect easily via Lure-lock to the catheter.
      • Many have pressure regulators as well.
      • Con = Expensive.
    2. Oxygen Tubing and High Flow O2 from Wall 
      • Not as optimal as commercial products, but may be best you have available.
      • Turn flow up all of the way. [Bould, 2008]
      • Need to “MacGyver” a flow regulator and a connector
        • Flow Regulator
          • Cut large holes (several) in side of oxygen tubing.
          • Need large/multiple holes to allow air flow to egress easily and not add to PEEP. [Sasano, 2014]
          • May also use Y-connector to another oxygen tube.
        • Connector
          • 3-way stop cock can be used to fit into distal end of oxygen tubing and Lure-lock onto the catheter.
          • Need to ensure 3 way valve is open to flow!
    3. Self-Inflating Ventilation Bag [Sasano, 2014]
      • Not as optimal as commercial products, but may be best you have available.
      • 3.0 ETT bag connector
        • Remove from ETT
        • Insert distal end into catheter
      • 7.5 ETT bag connector
        • Remove from ETT
        • Insert into proximal end of 3 mL syringe (after removing the plunger).
        • Use Lure-lock on syringe to connect to catheter
      • Will need to disengage the bag’s pop-off valve.
  • Oxygenate!
    • Occluding the flow regulator will lead to airflow into the trachea (inspiration).
    • Uncovering the flow regulator will allow air flow from oxygen source and patient to escape (expiration).
    • Inspiration : Expiration = 1 second :  4 seconds
    • Use longer expiration phases for completely occluded upper airway (ex, 1:9)
      • Patient will tolerate hypercapnia better than barotrauma/pneumothorax.


Moral of the Morsel

  • Do not let the first time you think about transtracheal ventilation be when you realize you need to do it.
  • Know what equipment you have available.
    • If you have a commercial product, know how to use it and where it is.
    • If you don’t have a commercial product, make your MacGyver survival bag and keep it handy with the tools you need, so you don’t need to recall how to do it in the time of need.



Boccio E1, Gujral R2, Cassara M3, Amato T4, Wie B5, Ward MF6, D’Amore J7. Combining transtracheal catheter oxygenation and needle-based Seldinger cricothyrotomy into a single, sequential procedure. Am J Emerg Med. 2015 May;33(5):708-12. PMID: 25791154. [PubMed] [Read by QxMD]

Frerk C1, Mitchell VS2, McNarry AF3, Mendonca C4, Bhagrath R5, Patel A6, O’Sullivan EP7, Woodall NM8, Ahmad I9; Difficult Airway Society intubation guidelines working group. Difficult Airway Society 2015 guidelines for management of unanticipated difficult intubation in adults. Br J Anaesth. 2015 Dec;115(6):827-48. PMID: 26556848. [PubMed] [Read by QxMD]

Bould MD1, Bearfield P. Techniques for emergency ventilation through a needle cricothyroidotomy. Anaesthesia. 2008 May;63(5):535-9. PMID: 18412654. [PubMed][Read by QxMD]

PEM Playbook – Altered Mental Status in Children

Originally published at Pediatric Emergency Playbook on May 1,
2016 – Visit to listen to accompanying podcast. Reposted with permission.

Follow Dr. Tim Horeczko on twitter @EMTogether


How do you approach the child who may be altered?

Altered mental status in children can be subtle.  Look for age-specific behaviors that range from irritability to anger to sleepiness to decreased interaction.

In the altered child, anchoring bias is your biggest enemy.  Keep your mind open to the possibilities, and be ready to change it, when new information becomes available.

For altered adults, use AEIOU TIPS (Alcohol-Epilepsy-Insulin-Overdose-Uremia-Trauma-Infection-Psychosis-Stroke).

Try this for altered children: remember that they need their VITAMINS!

V – Vascular (e.g. arteriovenous malformation, systemic vasculitis)

I – Infection (e.g. meningoencephalitis, overwhelming alternate source of sepsis)

T – Toxins (e.g. environmental, medications, contaminated breast milk)

A – Accident/abuse (e.g. non-accidental trauma, sequelae of previous trauma)

M – Metabolic (e.g. hypoglycemia, DKA, thyroid disorders)

I – Intussusception (e.g. the somnolent variant of intussusception, with lethargy)

N – Neoplasm (e.g. sludge phenomenon, secondary sepsis, hypoglycemia from supply-demand mismatch)

S – Seizure (e.g. seizure and its variable presentation, especially subclinical status epilepticus)

Case One: Sleepy Toddler

16-month-old who chewed on his grandmother’s clonidine patch

Clonidine is an alpha-2 agonist with many therapeutic indications including hypertension, alcohol withdrawal, smoking cessation, perimenopausal symptoms.  In children specifically, clonidine is prescribed for attention deficit hyperactivity disorder, spasticity due to cerebral palsy and other neurologic disorders, and Tourette’s syndrome.

The classic clonidine toxidrome is altered mental status, miosis, hypotension, bradycardia, and bradypnea.  Clonidine is on the infamous list of “one pill can kill”.

Treatment is primarily supportive, with careful serial examinations of the airway, and strict hemodynamic monitoring.

Naloxone can partially counteract the endogenous opioids that are released with clonidine’s pharmacodynamics.

Start with the usual naloxone dose of 0.01 mg/kg, up to the typical adult starting dose of 0.4 mg.

In clonidine overdose, however, you may need to increase the naloxone dose (incomplete and variable activity) up to 0.1 mg/kg.  Titrate to hemodynamic stability and spontaneous respirations, not full reversal of all CNS effects.

Case Two: In Bed All Day

A 7-year-old with fever, vomiting, body aches, sick contacts.  Altered on exam.

Should you get a CT before LP?

If you were going to perform CT regardless, then do it.

Adult guidelines: age over 60, immunocompromised state, history of central nervous system disease, seizure within one week before presentation, abnormal level of consciousness, an inability to answer two consecutive questions correctly or to follow two consecutive commands, gaze palsy, abnormal visual fields, facial palsy, arm drift, leg drift, and abnormal language.

Children: if altered, and your differential diagnosis is broad (especially if you may suspect tumor, bleed, obvious abscess).

Influenza is often overlooked as a potential cause of altered mental status.  Many authors report a broad array of neurological manifestations associated with influenza, such as altered mental status, seizures, cranial nerve abnormalities, hallucinations, abnormal behavior, and persistent irritability.  All of this is due to a hypercytokinemic state, not a primary CNS infection.

Case Three: “Terrible Teenager”

14-year-old brought in for “not listening” and “acting crazy”; non-complaint with medications for systemic lupus erythematosus (SLE).

SLE is rare in children under 5. When school-age children present with SLE, they typically have more systemic signs and symptoms.  Teenagers present like adults.  All young people have a larger disease burden with lupus, since they have many more years to develop complications.

Lupus cerebritis: high-dose corticosteroids, and possibly IV immunoglobulin.  Many will need therapeutic plasma exchange (TPE), a type of plasmapheresis, where the patient’s plasma is replaced with donor plasma, to remove auto-antibodies and cytokines.


  • In altered mental status, keep your differential diagnosis open
  • Pursue multiple possibilities until you are able to discard them
  • Be ready to change your mind completely with new information
  • Make sure your altered child gets his VITAMINS (Vascular, Infectious, Toxins, Accident/Abuse, Metabolic, Intussusception, Neoplasm, Stroke)


Beckman HB, Frankel RM. The effect of physician behavior on the collection of data. Ann Intern Med 1984; 101:692.

Fujita K, Nagase H, Nakagawa T et al. Non-convulsive seizures in children with infection-related altered mental status. Pediatrics International. 2015; 57(4):659–664.

Gallagher J, Luck RP, Del Vecchio M. Altered mental status – a state of confusion. Paediatr Child Health. 2010 May-Jun; 15(5): 263–265.

Hasbun R, Abrahams J, Jekel J, Quagliarello VJ. Computed tomography of the head before lumbar puncture in adults with suspected meningitis. N Engl J Med. 2001; 345(24):1727-33.

Oliver WJ, Shope TC, Kuhns LR. Fatal Lumbar Puncture: Fact Versus Fiction—An Approach to a Clinical Dilemma. Pediatrics. 2003; 112(3)

Schwartz J et al. Guidelines on the Use of Therapeutic Apheresis in Clinical Practice—Evidence-Based Approach from the Writing Committee of the American Society for Apheresis: The Sixth Special Issue. Journal of Clinical Apheresis. 2013; 28:145–284.

Zorc JJ. A lethargic infant: Ingestion or deception? Pediatr Ann 2000; 29: 104–107

This post and podcast are dedicated to Teresa Chan, HBSc, BEd, MD, MS, FRCPC for her boundless passion for and support of #FOAMed, for her innovation in education, and for her dedication to making you and me better clinicians and educators.  Thank you, T-Chan.



Altered Mental Status

Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP

Ear, Nose, and Throat Foreign Bodies

Authors: Brooke Moungey, MD (Senior EM Resident at the University of Wisconsin) and Christopher Stahmer, MD (Clinical Assistant Professor at the University of Wisconsin) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital)

It is a busy day in the emergency department (ED) when a 35-year old male presents with an insect in his right ear. In the next room, a 3-year old girl presents with her mother after having placed a plastic bead in her left nostril. And just then, a 2-year-old boy is brought in to the ED by his parents because he had just swallowed a coin.

With all the possible tools and techniques for foreign body removal, choosing a method that is most likely to be successful for your patient can sometimes be a daunting task. In addition, it can be challenging when trying to determine if a patient will be cooperative and whether analgesia or sedation will be required.

Here are a few tips to help you remove those foreign bodies like a pro and get your patient safely on his or her way.

Foreign Bodies of the Ear Canal:

While foreign bodies in children often include a wide range of objects such as toys, rocks, beads, crayons, and cotton swabs, foreign bodies in adults are most commonly insects.

There is a wide array of tools available to assist in removal and this can often be confusing for providers as these tools are not created equal for all types or locations of foreign bodies.

  • You should always check for tympanic membrane (TM) perforation. If this is present, the patient should not undergo removal in the ED and should be referred to otolaryngology (ENT) for removal.
  • In general, you should avoid sharp instruments if you are not getting adequate visualization of the foreign body. Additionally, sharp objects should not be used if the patient is not cooperative with your exam so that accidental TM damage can be avoided.
  • Side effects of these removal techniques include tissue damage such as abrasions, lacerations or TM perforations. These techniques can also push the object further back in the ear canal and make removal even more difficult.
  • There are several different types of otoscopes. Some include those with removable lenses and operating otoscopes that allow tools to pass through the otoscope head while directly visualizing foreign bodies.


Alligator forceps and curettes:

Curettes are best for foreign bodies that can be well visualized but are small enough that the curette can be pushed beyond the object and pulled from behind. Forceps can also be used to directly grasp objects but are less effective when used for round objects or larger objects.  They are more effective for soft or irregularly shaped objects that can be grasped firmly to prevent pushing them further out of reach.



Can be done using a 20 mL syringe and 16 gauge angiocatheter filled with water or normal saline. A plastic basin may be used to catch the fluid. This technique can be helpful for a variety of foreign body shapes and sizes and is safe for normal TMs. However, irrigation should not be used in patients with a history of TM perforation or instrumentation including myringotomy tubes. This method should not be used for foreign bodies made of organic material as they will soak up the fluid and expand. This will cause further difficulty with extraction. Irrigation should also never be used if the foreign body is a button battery.



Suction tpically requires 100 mmHg or more of negative pressure with a soft-tipped plastic suction catheter placed against the object. The side port can be occluded to capture the object and pull it out. Tip: Best for hard, round foreign bodies.



Can be placed on the end of a cotton-tipped applicator that is advanced into the ear canal and pressed against the foreign body until dry. The foreign body can then be pulled out.  Be very cautious as glue can be accidentally applied to the ear canal or TM itself and cause tissue damage.

Tip: Best used to extract round objects which are well visualized.



Can be used for removing metal foreign bodies. It works best for smaller metal objects and those in the more distal portion of the ear canal.


Can be manually extracted with forceps or a curette, or irrigated out of the ear canal as previously described.   However, live bugs often cause significant patient discomfort with attempted removal. This can be prevented by using a syringe and angiocatheter to fill the ear canal with viscous lidocaine and allowing it to sit for 15 minutes prior to removal.  Mineral oil is also an alternative to viscous lidocaine.


A small amount of viscous lidocaine can be a helpful local anesthetic. However, sedation may be needed in younger pediatric patients. Several common options include:

  • Intranasal midazolam 0.3-0.5 mg/kg
  • Oral midazolam 0.5 mg/kg
  • Ketamine IV 1 mg/kg or IM 2-3 mg/kg

Take Away Points:

  • Referral to ENT will be necessary if extraction in the ED fails, the foreign body has been in place long enough to cause acute otitis media or other surrounding infection, or if there is a TM perforation.
  • Antibiotics will be necessary for abrasions or lacerations of the ear canal, even if extraction is successful. Prescribe ofloxacin 0.3% otic drops 10 drops once daily for 7 days.
  • Use different tools and techniques to your advantage to successfully address different types of foreign bodies in the ear canal.
  • When one foreign body is found, check for additional foreign bodies in the ears, nose and mouth (especially in pediatric patients).
  • Never apply a liquid to a button battery.

Nasal foreign bodies:

Nasal foreign bodies are most commonly found in pediatric patients and often include many of the same objects as foreign bodies in the ear canal. Once the foreign body is located, there are several easy techniques to remove them without additional instrumentation.

  • Side effects of these removal techniques include abrasions, lacerations, and epistaxis. Another side effect is potentially moving the object further back, which will increase the risk of aspiration or ingestion.
  • A nasal speculum is beneficial to aid in visualizing the object.


Positive pressure:

If the patient can assist with removal, then nose blowing while sitting forward and occluding the other nostril is often effective.  If the child is unable to participate in nose-blowing the “big kiss” technique is an alternative. With this technique, have the parent blow into the child’s mouth while occluding the patent nostril.  This can also be modified to apply high flow supplemental oxygen or a Bag Mask Valve (BVM) into the mouth while again occluding the patent nostril.  Please use caution due to a risk of barotrauma if oxygen or a BVM is used.


Balloon catheters:

Small balloon catheters such as a Fogarty or Katz extractor can be attached to a 5 mL syringe. Check the balloon function and then advance the deflated catheter tip into the nostril until the entire balloon is past the foreign body. Then inflate the balloon until it fills the space behind the object and pull the balloon catheter out along with the object.



Can also be used similarly to foreign bodies of the ear canal. However, they are more effective for nasal foreign bodies if advanced past the object and then used to pull the object forward. If they are used to directly grasp the object, then the object can be pushed further back, which may lead to aspiration, ingestion, or more a difficult extraction.


Lidocaine or phenylephrine spray can be used to prevent swelling and pain, but should be rarely used due to the risk of causing sneezing and associated aspiration or ingestion of the object.  Both of these medications should be avoided in the case of button batteries.

Sedation options are similar to those as listed above for ear foreign bodies; however, no intranasal medications such as intranasal midazolam should be used due to risk of aspirating/ingesting the object.

Take Away Points:

  • Referral to ENT will be necessary if ED extraction fails, extraction causes uncontrolled epistaxis or if the foreign body is aspirated.
  • When possible, avoid anesthetic sprays and intranasal medications to prevent aspiration or ingestion.
  • Non-invasive techniques with positive pressure and the assistance of the child and/or parents are often most successful for nasal foreign bodies.
  • Always look for other foreign bodies and never apply liquids to a button battery.

Foreign Bodies of the Throat:

In adults, these foreign bodies often represent food boluses, fish bones, and dentures. In children, they may include a number of objects from coins and button batteries to food, toys, and crayons. If a patient presents with stridor or respiratory distress, it is best to leave him or her in a position of comfort while getting airway equipment ready and gathering resources such as anesthesia and ENT, if available. Airway intervention may become necessary at any time and can include attempting to remove the foreign body with Magill forceps if visible or intubating the patient with an attempt to force the object into the right mainstem bronchus to relieve a complete obstruction.


For patients who are not in respiratory distress, radio-opaque foreign bodies can be located in the esophagus or trachea/bronchus with AP and lateral neck X-rays and an abdominal x-ray can often be used to identify objects in the stomach or further along the GI tract. If the object is radiolucent and suspected to have been aspirated due to respiratory symptoms, then bilateral decubitus X-rays may show air trapping in the affected side such that the lung does not deflate appropriately when the affected side is down. Inspiratory and expiratory films may also show air trapping on the affected side during expiration and pushing of the mediastinum to the opposite side. Any objects located in the respiratory tract will likely have to be removed by bronchoscopy.

Esophageal Foreign Bodies:

Objects that are blunt and small (<2.5 cm wide) may be pushed forward into the stomach as they will likely be small enough to pass the pylorus and pass from the GI tract on their own. This is typically done with application of lidocaine spray to the oropharynx and advancement of a bougie which the patient swallows and is then advanced until the object is dislodged. If this is not an option or this method fails then endoscopy will be needed for removal. Any objects that are sharp, regardless of their location in the GI tract, or too large to pass the pylorus must also be removed by endoscopy. If there are signs the object has caused a perforation, then surgery will likely be indicated for definitive care.

Button batteries:

Regardless of whether the button battery is located in the respiratory tract or GI tract, this is a medical emergency and the battery should be removed by endoscopy or bronchoscopy within 6 hrs of aspiration to prevent necrosis or perforation.

Food bolus:

Administration of glucagon is unlikely to be of benefit as its use in clearing a food bolus is likely related to causing retching and emesis, which can also increase the risk of perforation or tearing of the esophageal mucosa. Food boluses can also be pushed forward into the stomach or removed by endoscopy as listed above for blunt objects in the esophagus.

Take Home Points:

  • Most foreign bodies of the throat will be aspirated or ingested and will likely require bronchoscopy, endoscopy or surgery for appropriate treatment. Thus, get your specialty services on board early.
  • Button batteries as a foreign body in any location are an emergency and every effort should be made to remove them as quickly as possible, preferably within 6 hrs of ingestion.
  • Small blunt foreign bodies (<2.5 cm) and food boluses can be pushed forward into the stomach and passed safely.
  • Always evaluate your patient for signs of perforation even after the foreign body has been removed.

References / Further Reading

-Baker MD. Foreign bodies of the ears and nose in childhood. Pediatr Emerg Care 3: 67, 1987.

-Botma M, Bader R, Kubba H. “A parent’s kiss”: evaluating an unusual method for removing nasal foreign bodies in children. J Laryngol Otol 114: 598, 2000.

-Figueiredo RR, Azevedo AA, Kos AO, Tomita S. Complications of ENT foreign bodies: a retrospective study. Rev Bras Otorrinolaringol (English ed) 74: 7, 2008.

-Kadish HA, Corneli HM. Removal of nasal foreign bodies in the pediatric population. Am J Emerg Med 15: 54, 1997.

-Kalan A, Tariq M. Foreign bodies in the nasal cavities: a comprehensive review of the aetiology, diagnostic pointers, and therapeutic measures. Postgrad Med J 76: 484, 2000.

-Marin JR, Trainor JL. Foreign body removal from the external auditory canal in a pediatric emergency department. Pediatr Emerg Care 22: 630, 2006.

-Marx JA, Hockberger RS, Walls RM. Rosen’s Emergency Medicine Concepts and Clinical Practice, 8e. Chapter 60.

-Roberts JR, Custalow CB, Thomsen, TW, Hedges JR. Roberts and Hedges’ Clinical Procedures in Emergency Medicine, 6e. Chapter 63.

-Tintinalli JE, Stapczynski JS, Ma OJ, Kline DM, Cydulka RK, Meckler GD, The American College of Emergency Physicians. Tintinalli’s Emergency Medicine, A Comprehensive Study Guide, 7e. Chapters 80, 119, 143.

-Triadafilopoulos G, Saltzman JR, Travis AC. Ingested Foreign Bodies and Food Impactions in Adults. www.uptodate.com

PEM Playbook – Big Labs, Little People: Troponin, BNP, D-Dimer, and Lactate

Originally published at Pediatric Emergency Playbook on April 1,
2016 – Visit to listen to accompanying podcast. Reposted with permission.

Follow Dr. Tim Horeczko on twitter @EMTogether

It’s a busy shift.  Today no one seems to have a chief complaint.

Someone sends a troponin on a child.  Good, bad, or ugly, how are you going to interpret the result?

And while we’re at it – what labs do I need to be careful with in children – sometimes the normal ranges of common labs can have our heads spinning!

Read on for bread-and-butter pediatric blood work and further, to answer the question – what’s up with troponin, lactate, d-dimer, and BNP in kids?


A fundamental tenet of emergency medicine:

We balance our obligation to detect a dangerous condition with our suspicion of the disease in given patient.

Someone with a cough and fever may simply have a viral illness, or he may have pneumonia.  Our obligation is to evaluate for the pneumonia.  It’s ok if we “miss” the diagnosis of a cold. It could be bad if we don’t recognize the pneumonia.

How do we decide?  Another fundamental concept:

The threshold.

Depending on the disease and the particular patient, we have a threshold for testing, and a threshold for treating.  Every presentation – and every patient for that matter – has a complicated interplay between what we are expected to diagnose, how much we suspect that particular serious diagnosis, and where testing and treating come into play.

What’s wrong with “throwing on some labs”?

Easy to do right?  They are but a click away…

Often a good history and physical exam will help you to calibrate your investigational thresholds.  This is especially true in children – the majority of pediatric ambulatory visits do not require blood work to make a decision about acute care.  If your patient is ill, then by all means; otherwise, consider digging a bit deeper into the history, get collateral information, and make good use of your general observation skills.

First, a brief word about basic labs.

The punchline is, use a pediatric reference.

If you don’t have a trusted online reference available during your shift, make sure you have something like a Harriett Lane Handbook accessible to you. Don’t rely on your hospital’s lab slip or electronic medical record to save you, unless you are sure that they use age-specific pediatric reference ranges to flag abnormal values. Believe it or not, in this 21st century of ours, some shops still use adult reference ranges when reporting laboratory values on children.

Notable differences in basic chemistries

Potassium: tends to run a bit higher in infants, because for the first year of life, your kidneys are inefficient in excreting potassium.

BUN and creatinine: lower in children due to less muscle mass, and therefore less turnover (and usually lack of other chronic disease)

Glucose: tends to run lower, as children are hypermetabolic and need regular feeding (!)

Alkaline phosphatase: is always high in normal, growing children, due to bone turn over (also found in liver, placenta, kidneys)

Ammonia: high in infancy, due to immature liver, trends down to normal levels by toddlerhood

ESR and CRP: low in healthy children, as chronic inflammation from comorbidities is not present; both increase steadily with age

Thyroid function tests: all are markedly high in childhood, not as a sign of disease, but a marker of their increased metabolic activity

Big Labs


Reliably elevated in myocarditis, and may help to distinguish this from pericarditis (in addition to echocardiography)

Other causes of elevated troponin in children include: strenuous activity, status epilepticus, toxins, sepsis, myocardial infarction (in children with congenital anomalies).  Less common causes of troponemia are: Kawasaki disease, pediatric stroke, or neuromuscular disease.

Don’t go looking, if you won’t do anything with the test.

Brain natriuretic peptide (BNP)

In adults, we typically think of a BNP < 100 pg/mL as not consistent with symptoms caused by volume overload.

Luckily, we have data in children with congenital heart disease as well.  Although each company’s assay reports slightly different cut-offs, in general healthy pediatric values match healthy adult values.

One exception is in the first week of life, when it is high even in healthy newborns, due to the recent transition from fetal to newborn circulation.

Use of BNP in children has been studied in both clinic and ED settings. Cohen et al. in Pediatrics used BNP to differentiate acute heart failure from respiratory disease in infants admitted for respiratory distress. They compared infants with known CHF, lung disease, and matched them with controls.

Later, Maher et al. used BNP in the emergency department to differentiate heart failure from respiratory causes in infants and children with heart failure and those with no past medical history.

The bottom line is:

BNP reliably distinguishes cardiac from respiratory causes of shortness of breath in children with a known diagnosis of heart failure.


To cut to the chase: d-dimer for use as a rule-out for pulmonary embolism has not been studied in children.

The only data we have in using d-dimer in children is to prognosticate in established cases. It is only helpful to track therapy for children who have chronic clots.

This is where our adult approach can get us into trouble. Basically, think of the d-dimer in children like it doesn’t even exist. It’s not helpful in our setting for our indications.   An adult may have an idiopathic PE – in fact, up to a third of adults with PE have no known risk factor, which makes decision tools and risk stratification important in this population.

Children with PE almost always have a reason for it.


There is at least one identifiable risk factor in up to 98% of children with pulmonary embolism. The majority have at least two risk factors.

If you’re suspecting deep venous thrombosis, perform ultrasonography, and skip the d-dimer.

If you’re worried about PE, go directly to imaging. In stable patients, you may elect to use MR angiography or VQ scan, but most of us will go right to CT angiography. Radiation is always a concern, but if you need to know, get the test.

This is yet another reminder that your threshold is going to be different in children when you think about PE – they should have a reason for it. After you have excluded other causes of their symptoms, if they have risk factors, and you are still concerned, then do the test you feel you need to keep this child safe.

You are the test.

Risk factors only inform you, and you’ll have to just pull the trigger on testing in the symptomatic child with risk factors.


A sick child with sepsis syndrome?

The short answer – yes.

In the adult literature, we know that a lactate level above 4 mmol/L in patients with severe sepsis was associated with the need for critical care. This has been studied in children as well, and an elevated lactate in children – typically above 4 – was a predictor of prolonged ICU course and mortality in septic patients.

The acute recognition and treatment of sepsis is first and foremost, clinical.

Our goal is to promote perfusion and provide oxygen to the tissues. Laboratory testing is not a substitute for clinical assessment – it should be used as an extension of your assessment.  There are two main reasons for an elevated lactate: the stress state and the shock state.

The stress state is due to hypermetabolism and an increase in glycolysis, as an example, in early sepsis. The shock state is due to tissue hypoxia, seen in septic shock. The confusion and frustration with lactate is that we often test the wrong people for it.

We could use it to track treatment, and see if we can clear the lactate; decreased lactate levels are associated with a better outcome in adults. Serial clinical assessments are even more useful to gauge your success with treatment.

We should use lactate to detect occult shock. Children compensate so well for shock, that subtle tissue hypoxia may not be detected until later. It may inform your decision for level of care, intensive care versus some other lower level.

Have you every been in this situation:

“Why, oh why, did we send a lactate?”

There are times when a lactate is ordered – maybe by protocol or maybe accidentally – or maybe in retrospect, the patient didn’t need it. Here is a quick mnemonic to remember the reasons for an elevated lactate: LACTATES


Lliver – any liver disease affects how lactate is metabolized by the Cori cycle
Aalbuterol (or for our international friends, salbutamol), beta-agonists like albuterol, increase lactate production via cyclic amp
C“can’t breathe” – respiratory distress and increased work of breathing shifts the ratio of aerobic and anerobic repiration
Ttoxins – all kinds of wonder drugs and recreational drugs do it – look up your patient’s list if you’re suspicious
Aalcohol, not an infrequent offender
Tthiamine deficiency – think of this in your cachectic or malnourished patients
Eepinephrine – a by-product of the Cori cycle, how lactate is metabolized. Difficult to interpret lactates when a patient is on an epinephrine drip.
Sseizure or shock – most commonly septic, but can be any type: cardiogenic, bstructive, hypovolemic, distributive.

Bottom line: high serum lactate levels have been associated with morbidity and mortality in children with sepsis and trauma, the two best-studied populations.

A summary of how labs can help you – or hurt you – in pediatric emergency medicine:

  1. Have a good reference for normal values and always be skeptical of how your lab reports them.
  2. Troponin testing is great for the child with suspected cardiogenic shock, myocarditis, or in unwell children with congenital heart disease.
  3. BNP in children can be used just like you do in adults – to get a sense of whether the presenting symptoms are consistent with heart failure.
  4. D-dimer is mostly a waste of time in the PED.
  5. Lactate can be useful in the right patient – use it to risk-stratify the major trauma patient or the patient with sepsis that may be suffering from occult shock.
  6. And lastly, make sure that you are mindful of your threshold for testing, and our threshold for treatment. If will vary by disease and by the patient at hand.



Gupta SK, Naheed Z. Chest Pain in Two Athletic Male Adolescents Mimicking Myocardial Infarction. Pediatr Emer Care. 2014;30: 493-495.

Kelley WE, Januzzi JL, Christenson RH. Increases of Cardiac Troponin in Conditions other than Acute Coronary Syndrome and Heart Failure. Clinical

Chemistry. 2009; (55) 12:2098–2112.

Kobayashi D, Aggarwal S, Kheiwa A, Shah N. Myopericarditis in Children: Elevated Troponin I Level Does Not Predict Outcome. Pediatr Cardiol. 2012; 33:1040–1045.

Koerbin G, Potter JM, Abhayaratna WP et al. The distribution of cardiac troponin I in a population of healthy children: Lessons for adults. Clinica Chimica Acta. 2016; 417: 54–56.

Liesemer K, Casper TC, Korgenski K, Menon SC. Use and Misuse of Serum Troponin Assays in Pediatric Practice. Am J Cardiol. 2012;110:284 –289.

Newby KL et al. for the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents. ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations. J Am Coll Cardiol. 2012; 60(23): 2427-2463.

Schwartz MC, Wellen S, Rome JJ et al. Chest pain with elevated troponin assay in adolescents. Cardiology in the Young; 2013. 23: 353–360.


Auerbach SR, Richmond ME, Lamour JM. BNP Levels Predict Outcome in Pediatric Heart Failure Patients Post Hoc Analysis of the Pediatric Carvedilol Trial. Circ Heart Fail. 2010;3:606-611.

Cohen S, Springer C, Avital A et al. Amino-Terminal Pro-Brain-Type Natriuretic Peptide: Heart or Lung Disease in Pediatric Respiratory Distress? Pediatrics. 2005;115:1347–1350.

Fried I, Bar-Oz B, Algur N et al. Comparison of N-terminal Pro-B-Type Natriuretic Peptide Levels in Critically Ill Children With Sepsis Versus Acute Left Ventricular Dysfunction. Pediatrics. 2006; 118(4): 1165-1168.

Koch A, Singer H. Normal values of B type natriuretic peptide in infants, children, and adolescents. Heart. 2003;89:875–878.

Maher KO, Reed H, Cuadrado A et al. , B-Type Natriuretic Peptide in the Emergency Diagnosis of Critical Heart Disease in Children. Pediatrics. 2008;121:e1484–e1488.

Mir TS, Marohn S, Laeer S, Eistelt M. Plasma Concentrations of N-Terminal Pro-Brain Natriuretic Peptide in Control Children From the Neonatal to Adolescent Period and in Children With Congestive Heart Failure. Pediatrics. 2002;110(6)1:6.

Mir TS, Laux R, Hellwege HH et al. Plasma Concentrations of Aminoterminal Pro Atrial Natriuretic Peptide and Aminoterminal Pro Brain Natriuretic Peptide in Healthy Neonates: Marked and Rapid Increase After Birth. Pediatrics. 2003;112:896–899.


Goldenberg NA, Knapp-Clevenger RA, Manco-Johnson MJ. Elevated Plasma Factor VIII and d-Dimer Levels as Predictors of Poor Outcomes of Thrombosis in Children for the Mountain States Regional Thrombophilia Group. Pediatrics. 2003;112:896–899.

Manco-Johnson MJ. How I treat venous thrombosis in children. Blood. 2006; 107(1)21-31.

Naqvi M, Miller P, Feldman L, Shore BJ. Pediatric orthopaedic lower extremity trauma and venous thromboembolism. J Child Orthop. 015;9:381–384.

Parasuraman S, Goldhaber SZ. Venous Thromboembolism in Children. Circulation. 2006;113:e12-e16.

Strouse JJ, Tamma P, Kickler TS et al. D-Dimer for the Diagnosis of Venous Thromboembolism in Children. N Engl J Med. 2004;351:1081-8.


Andersen LW, Mackenhauer J, Roberts JC et al. Etiology and therapeutic approach to elevated lactate. Mayo Clin Proc. 2013; 88(10): 1127–1140.

Bai et al. Effectiveness of predicting in-hospital mortality in critically ill children by assessing blood lactate levels at admission. BMC Pediatrics. 2014; 14:83.

Scott HF, Donoghue AJ, Gaieski DF et al. The Utility of Early Lactate Testing in Undifferentiated Pediatric Systemic Inflammatory Response Syndrome. Acad Emerg Med. 2012; 19:1276–1280.

Shah A, Guyette F, Suffoletto B et al. Diagnostic Accuracy of a Single Point-of-Care Prehospital Serum Lactate for Predicting Outcomes in Pediatric Trauma Patients. Pediatr Emer Care. 2013; 29:715-719.

Topjian AA, Clark AE, Casper TC et al. for the Pediatric Emergency Care Applied Research Network. Early Lactate Elevations Following Resuscitation From Pediatric Cardiac Arrest Are Associated With Increased Mortality. Pediatr Crit Care Med. 2013; 14(8): e380–e387.

This post and podcast are dedicated to Daniel Cabrera, MD for his vision and his leadership in thinking ‘outside the box’.


Troponin     |     BNP     |     D-Dimer     |     Lactate

Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP

Cystic Fibrosis: ED Management, Pearls and Pitfalls

Authors: Stephanie Tassin, MD (EM Resident at SAUSHEC) and Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital)


Cystic fibrosis (CF) is a life-shortening, autosomal recessive disease that affects multiple organ systems via mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) chloride channel. In short, a defective CFTR channel prevents mucous and exocrine glands from secreting chloride. Without chloride, water cannot follow, and the end result is thick, hyperviscous secretions in the lung, sinuses, pancreas, intestines, and biliary system [1].  In the sweat glands, chloride reabsorption is impaired, leading to excess sodium chloride loss. With excessive sweating, this can lead to hyponatremic hypochloremic dehydration. It also has detrimental effects on the reproductive, musculoskeletal, and urinary systems, but these are rarely relevant in the Emergency Department (ED) [2].

CF affects 1 in 3,200 Caucasian births and is primarily thought of as a Caucasian disease, though it is also seen in other ethnicities at lower frequencies. As of 2014, less than 2/3 of cases are detected by newborn screening, so providers must keep it on their differential, especially in young children with recurrent pulmonary infections, sinus infections, failure to thrive, and constipation or meconium ileus [2].

Case 1

A 22 year old female with cystic fibrosis presents to you complaining of increasing shortness of breath over the last week. Her chronic cough has gotten worse recently and it is productive of occasionally blood-tinged and green sputum. She reports low-grade fevers at home as well as fatigue, headache, and anorexia. She just moved to town and has no medical records in your system. Vital signs include blood pressure (BP) 110/64, heart rate (HR) 110, respiratory rate (RR) 34, oxygen saturation (SpO2) 92% on room air, temperature (T) 100.1°Farenheit (F) orally. Her examination is remarkable for coarse breath sounds with scattered expiratory wheezes, a slightly increased work of breathing, and clubbing of her fingernails. Her chest x-ray is shown below.



You put her on oxygen by nasal cannula and give her a small intravenous (IV) fluid bolus, but you wonder what to do next. You do not see a lot of patients with CF, but you see a lot of chronic obstructive pulmonary disease (COPD), and she looks almost exactly like a patient with a COPD exacerbation. Do you just treat her like COPD with nebulizer treatments, steroids, antibiotics, and bi-level positive pressure ventilation (BiPAP)? What antibiotics do you use? Is there anything else you can offer?

CF Pulmonary Exacerbations

Progressive pulmonary disease accounts for 85% of the mortality in CF[3]. From a young age, the CF patient is colonized with a predictable spectrum of bacteria that persist and cause chronic infection and inflammation [1]. Typically, this causes a persistent, productive cough and an obstructive pattern on pulmonary function tests. This may progress to chronic bronchitis and bronchiectasis with occasional exacerbations. These pulmonary exacerbations are generally characterized by increasing dyspnea, tachypnea, changes in sputum production, increased adventitious lung sounds, malaise, anorexia, and a decrease in pulmonary function [3, 4, 5].

The majority of pulmonary exacerbations are caused by clonal expansion of existing strains of bacteria, rather than an acquisition of new bugs [6]. Still, other causes of pulmonary distress must be kept on the differential in cystic fibrosis patients. Allergic bronchopulmonary aspergillosis (ABPA) should be suspected in patients with significant wheezing. Though it will likely not be diagnosed in the emergency department [6], it is reasonable to start steroids in these patients as discussed below. Spontaneous pneumothorax can occur, especially in older patients with advanced disease. Recurrence is also common [7].  Minor hemoptysis is also common in CF, especially during a pulmonary exacerbation. Beyond checking the international normalized ratio (INR) to rule out any contributing vitamin K deficiency, this generally only requires reassurance. A complete blood count (CBC) is rarely needed unless in circumstances concerning for anemia.

In patients with suspected pulmonary exacerbations, plain chest radiographs should be ordered to exclude pneumothorax. Other findings such as mucous plugging, peribronchial thickening, and air space disease are common but not specific for an acute exacerbation [8].


Early in life, the most common bugs cultured from the lungs are Staphylococcus aureus and non-typeable Haemophilus influenzae [9]. Pseudomonas aeruginosa is also often isolated early and is the most significant pathogen in CF. Once established, P. aeruginosa is essentially impossible to eradicate due to a combination of genetic adaptations, biofilm formation, and an optimal environment in CF airways.  Burkholderia cepacia complex is less common, but is still occasionally seen and can rapidly lead to necrotizing pneumonia, sepsis, and death. Other common organisms include S. maltophilia, and A. xylosoxidans, which tend to be less virulent.  Aspergillus spp. is isolated from more than 25% of patients but it rarely causes invasive infection outside of the immunocompromised post-transplant patient. However, allergic bronchopulmonary aspergillosis (ABPA) can cause significant illness and it is a diagnosis to keep in mind if your patient presents with significant wheezing [9].


Early recognition and treatment of pulmonary exacerbations has been associated with slower long-term decline in lung function [10]. Pulmonary exacerbations are treated with antibiotics and supportive measures aimed at airway clearance. In cases of ABPA, which is usually not diagnosed in the ED, patients may present with asthma-type symptoms and are usually treated with steroids [9].

Management is summarized in Table 1.

 Table 1

Management Considerations in CF Pulmonary Disease
1. Antipseudomonal antibiotics (high doses): Aminoglycoside + β-lactam

2. Bronchodilator – either MDI or nebulized albuterol

3. Nebulized 7% saline, 4mL

4. BiPAP if needed

5. Only use steroids if there are significant asthma-type symptoms (i.e. wheezing)


In general, antibiotic choices should be tailored to the patient’s previous culture results if known. For mild exacerbations or presumed viral upper respiratory infections not requiring inpatient admission, it is reasonable to discharge patients on an oral antibiotic such as amoxicillin-clavulanate that will cover both H. influenza and S. aureus. If the patient has a known history of Pseudomonas infection, an anti-pseudomonal fluoroquinolone such as ciprofloxacin may be used (1 month – 5 years: 15mg/kg max 750mg/dose BID, 5-18 years: 20mg/kg BID). Recommended duration of treatment is 2 weeks [5]. Patients should continue to use their regular nebulized anti-pseudomonal antibiotic. In these cases, sputum should be sent for culture prior to starting therapy. If there is no improvement on oral antibiotics, there should be a low threshold to admit for intravenous treatment [6].

For more severe exacerbations or those failing outpatient therapy, treatment is usually aimed at Pseudomonas unless the previous cultures identify a different pathogen as the likely culprit. For presumed Pseudomonas infection in a patient with a severe exacerbation, double antibiotic therapy is preferred with two anti-pseudomonal drugs with different mechanisms of action. This is most often accomplished with an aminoglycoside and β-lactam [5]. While results of previous cultures are useful to determine which bug is most likely causing an exacerbation, antibiotic sensitivities for Pseudomonas in particular are not useful for selecting antibiotics and have no effect on patient outcomes [6, 11].

Of the aminoglycosides, tobramycin is most frequently used and has been extensively studied [12, 13]. Amikacin is also used but is used less often. Gentamicin is avoided in CF due to an increased risk of nephrotoxicity [12].  The CF Foundation recommends that aminoglycosides be administered in once daily doses rather than TID to maximize efficacy and minimize nephrotoxicity [3]. Of the β-lactams, ceftazidime is most commonly used among accredited CF centers, followed by cefepime, piperacillin-tazobactam, meropenem, ticarcillin-clavulanate, and aztreonam [14].

Note that patients with CF require larger doses of antibiotics (often larger doses than are FDA-approved) due to a larger volume of distribution, increased renal clearance, and the increased minimal inhibitory concentration (MIC) of Pseudomonas [12, 15]. Many providers, even in CF Foundation-accredited care centers, continue to prescribe inadequate doses of anti-pseudomonal antibiotics despite published dosing guidelines [16]. The best available evidence, based on the pharmacokinetics, pharmacodynamics, tolerability, and efficacy of different regimens, supports the dosing regimens listed below in Table 2 [15].

Table 2 – Antibiotic Choices in CF Exacerbation

Aminoglycoside Dose
Tobramycin 10 mg/kg/day in one daily dose
Amikacin 30-35 mg/kg/day in one daily dose
β-lactam Dose
Ceftazidime 200-400 mg/kg/day div every 6-8 hr (max 8-12 g/day)
Cefepime 150-200 mg/kg/day div every 6-8 hr (max 6-8 g/day)
Pip-tazo 350-600 mg/kg/day div Q4H (max 18-24 g/day piperacillin)
Meropenem 120 mg/kg/day div Q8H
Ticarcillin-clavulanate 450-750 mg/kg/day Q6H (max 24-30 g/day ticarcillin)
Aztreonam 200-300 mg/kg/day div Q6H (max 8-12 g/day)

For infections caused by bugs other than Pseudomonas, culture and susceptibility testing usually guide antibiotic choice. Staphylococcus aureus is a common pathogen in CF and can be treated according to local resistance patterns.  Other typical bugs, notably B. cepacia complex, S. maltophilia, and A. xylosoxidans, tend to be very antibiotic-resistant, so treatment should be guided by culture and susceptibility testing [17].

Patients with CF have variable responses to bronchodilators. Approximately 50% of these patients will have some degree of bronchial hyperresponsiveness [9]. Given the relatively benign side effect profile of beta-agonists, nebulized treatments in the ED may assist in airway opening. Bronchodilators may not be the mainstay of treatment of pulmonary exacerbations, but it is helpful when administered prior to treatment with nebulized hypertonic saline, as discussed below.

Mucolytics (hypertonic saline)

Inhaled hypertonic saline (HS) has been shown to improve the properties of sputum and acutely increase mucociliary clearance in patients with CF. Unlike the other major mucolytic used for CF called DNase I (Dornase alpha), HS appears to be beneficial during an acute exacerbation, especially when followed by chest physiotherapy [9, 10]. A nebulized dose of 4mL of 7% saline has been shown to improve symptoms and lung function when compared to a control treatment with 0.12% saline. Patients treated with the 7% saline nebs during their hospitalization are more likely to return to their pre-exacerbation FEV1 with a number needed to treat of 6 [10]. It is generally well tolerated, but it does have the potential to cause a transient airflow obstruction. For this reason, patients should be treated with a bronchodilator immediately prior to hypertonic saline [18].

Positive pressure ventilation

As in COPD, non-invasive positive pressure ventilation is an attractive treatment option for severe pulmonary exacerbations. Several observational studies have looked at the use of NPPV in these situations and concluded that it may be useful, especially if used early during an acute exacerbation. It is at the very least preferable to invasive ventilation due to the high mortality rates seen in patients with CF who get intubated[19].


Progression of lung disease in CF is largely mediated by chronic inflammation, so it makes sense that corticosteroids should provide some benefit [20].  Unfortunately, although treatment of CF with long-term corticosteroids has shown some improvement in lung function, the risks and significant side effect profile preclude their utility on a regular basis. Theoretically, short-term use of steroids during an acute pulmonary exacerbation should have a more acceptable risk-benefit profile. Only two small studies (n=44) have looked at the use of steroids during an acute exacerbation and showed a small trend towards improvement in lung function at follow up [20, 21]. In the larger of the studies, 3 of the 12 patients in the prednisone group had to be withdrawn from the study either from hypertension or hyperglycemia [20]. The CF Foundation concludes there is insufficient evidence to recommend routine use of steroids during an acute exacerbation [3].  Though they are not recommended for routine use, they may provide more benefit in patients with predominant asthma-type symptoms or suspected ABPA [9]. Close consultation with the patient’s pulmonologist if possible is needed to discuss steroid treatment.

Your patient reports growing Pseudomonas from multiple cultures in the past, so you decide to treat her with cefepime and tobramycin. You also give her an albuterol treatment immediately followed by a 7% saline neb. You had considered BiPAP, but her respiratory rate and work of breathing improve following treatment. She is admitted to the hospital for continued IV antibiotics and airway clearance therapy.

Case 2

A 12 year old male with cystic fibrosis presents with 3 weeks of progressively worsening crampy right lower quadrant (RLQ) abdominal pain and now non-bilious vomiting and oral fluid intolerance. He had a few episodes of diarrhea yesterday but has since had no bowel movement. He takes pancreatic enzyme replacement therapy and has chronic constipation, for which he uses polyethylene glycol (PEG) 3350 daily. His vital signs are normal for his age except for a heart rate of 120 beats per minute (bpm). His examination is significant for dry mucous membranes and abdominal distention with RLQ tenderness, but no rigidity or guarding. You think you feel a small mass in the RLQ. His abdominal x-ray is shown below:


Distal Intestinal Obstruction Syndrome

Distal Intestinal Obstruction Syndrome (DIOS), previously known as “meconium ileus equivalent,” is an entity unique to CF that is caused by partial or complete obstruction of the ileocecum by inspissated fecal material [22]. It is seen in all age groups, though it is more common in adults and is almost always seen in patients with pancreatic insufficiency [23].


DIOS commonly presents with progressive, cramping abdominal pain that usually located in the RLQ or peri-umbilical region. Pain may be acute, but it often precedes the actual obstruction by several weeks or even months. Patients may have abdominal distension first, however.  Though DIOS is commonly seen with constipation, it may also be seen with diarrhea or even normal bowel movements [23]. On examination, the inspissated material can usually be felt in the RLQ, although a palpable mass may be present for years without causing obstructive symptoms [24].


A plain abdominal radiograph is the first line imaging test that should be obtained. It will typically show an accumulation of “bubbly” or “granular” fecal material in the distal ileum [23]. The triad of characteristic abdominal pain, palpable RLQ mass, and distal ileal fecal material on x-ray is usually sufficient to diagnose DIOS. If symptoms or radiographic findings are atypical, or if there is no improvement with treatment, additional imaging such as ultrasound or CT scan should be obtained to evaluate mimics such as appendicitis or intussusception [24].

Differential Diagnosis

It may be difficult to distinguish impending DIOS from chronic constipation by history alone. Constipation usually has a more gradual onset of symptoms with fecal material distributed throughout the colon, as opposed to being localized to the right lower quadrant [22]. However, these entities often coexist and except in severe cases, initial treatment is the same.

Appendicitis should also be on the differential, but unfortunately is sometimes difficult to evaluate. Chronically inspissated mucoid contents may lead to a distended appendix that is difficult to distinguish from an acutely inflamed appendix. This can often lead to a delay in diagnosis of appendicitis, resulting in increased rates of appendiceal perforation and abscess formation in patients with CF.  Other causes of bowel obstruction must also be considered such as adhesions, malignancy, or intussusception. Intussusception occurs in about 1% of CF patients and is a common mimic but can also be a complication of DIOS [24].


First, correct any fluid or electrolyte abnormalities and treat any associated infections. After that, treatment is fairly straightforward and involves laxatives administered either orally, by nasogastric tube, or by enema. Patients with incomplete obstructions usually respond to oral therapy with any PEG bowel prep solution such as GoLytely®, Klean-Prep®, or Movicol®. Another option for oral therapy is Gastrografin diluted in water or juice (50mL in 200mL for kids under 6 years, and 100mL in 400mL for everyone else). Therapy is continued until symptoms resolve and bowel movements are clear. Thus, admission may be required [24].
For patients with complete obstruction, PO intolerance, or failure of oral therapy, a nasogastric tube should be placed for decompression, followed by a Gastrografin enema. Since Gastrografin is radiopaque, these enemas can be both diagnostic and therapeutic and may be used to monitor progress [23, 24, 25]. However, these enemas can cause significant fluid shifts as well as intestinal ischemia, perforation, and necrosis, so they should only be administered by an experienced radiologist. These patients all require admission with a low threshold for surgical consultation [24, 26].
You suspect an incomplete obstruction, but he remains PO intolerant. You place an IV to draw labs and give him a 20 cc/kg bolus of LR. After correcting his electrolytes, you place a nasogastric tube for decompression and to administer GoLytely for bowel irrigation. He has a small bowel movement and slight improvement in pain. He is admitted to pediatrics for continued bowel irrigation.


-CF is not limited to Caucasians and over 33% of cases are missed by newborn screening programs [2].

-Pulmonary exacerbations must be treated early and aggressively to slow the decline in lung function [10].

Treatment of pulmonary exacerbations:

  1. Antipseudomonal antibiotics (high doses): Aminoglycoside + β-lactam
  2. Bronchodilator – either MDI or nebulized albuterol
  3. Nebulized 7% saline, 4mL
  4. BiPAP if needed’
  5. Only use steroids if there are significant asthma-type symptoms (i.e. wheezing)


-Diagnosed by classic history, mass in the RLQ, and localized fecal material on plain abdominal film [22].

-Don’t miss appendicitis or intussusception. Get an ultrasound and/or CT scan if needed [24].

-Correct fluids and electrolytes first [24].

-If PO tolerant, may treat from above with PEG solution (e.g. GoLytely®) or Gastrografin diluted 1:4 in water or juice. Patients may require an NG tube in order to consume enough of the laxative [24].

-If PO intolerant or with bilious vomiting (i.e. complete obstruction), decompress the stomach with a nasogastric tube. Call radiology for a Gastrografin enema [24].

-Treat until bowel movements are clear and watery [24].


References / Further Reading

  1. Rowe SM, Miller S, Sorscher EJ. Cystic Fibrosis. N Engl J Med 2005; 352:1992-2001.
  2. Cystic Fibrosis Foundation Patient Registry: Annual Data Report to the Center Directors, 2014. https://www.cff.org/2014_CFF_Annual_Data_Report_to_the_Center_Directors.pdf/ (Accessed on June 30, 2016).
  3. Flume PA, Mogayzel PJ, Robinson KA, et al. Cystic fibrosis pulmonary guidelines: treatment of pulmonary exacerbations. Am J Respir Crit Care Med. 2009 Nov 1;180(9):802-8.
  4. Bilton D, Canny G, Conway S, et al. Pulmonary exacerbation: towards a definition for use in clinical trials. Report from the EuroCareCF Working Group on outcome parameters in clinical trials. J Cyst Fibros 2011; 10: Suppl. 2, S79-S81.
  5. Smyth A, Elborn JS. Exacerbations in cystic fibrosis: 3 – Management. Thorax 2008; 63: 180-184.
  6. Bhatt JM. Treatment of pulmonary exacerbations in cystic fibrosis. Eur Respir Rev. 2013 Sep 1;22(129):205-16. PMID 23997047.
  7. Flume PA. Pneumothorax in cystic fibrosis. Current Opinion in Pulmonary Medicine 2011. 17(4):220-225.
  8. Greene KE, Takasugi JE, Godwin JD, et al. Radiographic changes in acute exacerbations of cystic fibrosis in adults: a pilot study. Am J Roentgenol 1994; 163(3):557-62.
  9. Gibson RL, Burns JL, Ramsey BW. Pathophysiology and Management of Pulmonary Infections in Cystic Fibrosis. Am J Respir Crit Care Med 2003; 168:918-951.
  10. Dentice, RL, Elkins MR, Middleton PG, et al. A randomized trial of hypertonic saline during hospitalization for exacerbation of cystic fibrosis. Thorax 2016; 71:141-147.
  11. Hurley MN, Ariff AH, Bertenshaw C, et al. Results of antibiotic susceptibility testing do not influence clinical outcome in children with cystic fibrosis. J Cyst Fibros 2012; 11:288-292.
  12. Talwalkar JS, Murray TS. The Approach to Pseudomonas aeruginosa in Cystic Fibrosis. Clin Chest Med 2016; 37:69-81.
  13. Young DC, Zobell JT, Stockmann C, et al. Optimization of Anti-Pseudomonal Antibiotics for Cystic Fibrosis Pulmonary Exacerbations: V. Aminoglycosides. Pediatric Pulmonology 2013; 48:1047-1061.
  14. Fischer DR, Namanny H, Zobell JT. Follow-up survey of the utilization of anti-pseudomonal beta-lactam antibiotics at U.S. cystic fibrosis centers. Pediatr Pulmonol. 2016 Jul; 51(7):668-9.
  15. Zobell JT, Young DC, Waters CD, et al. Optimization of Anti-Pseudomonal Antibiotics for Cystic Fibrosis Pulmonary Exacerbations: VI. Executive Summary. Pediatric Pulmonology 2013; 48:525-537.
  16. Zobell JT, Waters CD, Young DC, et al. Optimization of Anti-Pseudomonal Antibiotics for Cystic Fibrosis Pulmonary Exacerbations: II. Cephalosporins and Penicillins. Pediatric Pulmonology 2013; 48:107-122.
  17. Doring G, Flume P, Heijerman H, et al. Treatment of lung infection in patients with cystic fibrosis: Current and future strategies. Journal of Cystic Fibrosis 11 (2012):461-479.
  18. Elkins MR, Robinson M, Rose BR, et al. A controlled trial of long-term inhaled hypertonic saline in patients with cystic fibrosis. N Engl J Med 2006; 354:229.
  19. Fauroux B. Why, when and how to propose noninvasive ventilation in cystic fibrosis? Minerva Anestesiol 2011; 77:1108-1114.
    20. Dovey M, Aitken ML, Emerson J, McNamara S, Waltz DA, Gibson RL. Oral corticosteroid therapy in cystic fibrosis patients hospitalized for pulmonary exacerbations: a pilot study. Chest 2007;132:1212-1218.
  20. Tepper RS, Eigen H, Stevens J, Angelicchio C, Kislin J, Ambrosius W, Heilman D. Lower respiratory illness in infants and young children with cystic fibrosis: evaluation of treatment with intravenous hydrocortisone. Pediatr Pulmonol 1997;24:48-51.
  21. Houwen RH, van der Doef HP, Sermet I, et al. Defining DIOS and constipation in cystic fibrosis with a multicenter study on the incidence, characteristics, and treatment of DIOS. J Pediatr Gastroenterol Nutr 2010; 50:38
  22. Houwen RH, van der Doef HP, Sermet I, et al. Defining DIOS and constipation in cystic fibrosis with a multicenter study on the incidence, characteristics, and treatment of DIOS. J Pediatr Gastroenterol Nutr 2010; 50:38.
  23.  Khoshoo V, Udall JN Jr. Meconium ileus equivalent in children and adults. Am J Gastroenterol 1994; 89(2): 153.
  24. Colombo C, Ellemunter H, Houwen R, et al. Guidelines for the diagnosis and management of distal intestinal obstruction syndrome in cystic fibrosis patients. J Cyst Fibros 2011; 10 Suppl 2:S24.
  25. Nash EF, Ohri CM, Stephenson AL, and Durie PR. Abdominal pain in adults with cystic fibrosis. European Journal of Gastroenterology & Hepatology 2014, 26:129-136.
  26. Voynow JA, Mascarenhas M, Kelly A, Scanlin TF. Cystic Fibrosis. In: Grippi MA, Elias JA, Fishman JA, Kotloff RM, Pack AI, Senior RM, Siegel MD. Eds. Fishman’s Pulmonary Diseases and Disorders, Fifth Edition. New York, NY: McGraw-Hill; 2015. http://accessmedicine.mhmedical.com/content.aspx?bookid=1344&Sectionid=81189522. Accessed August 06, 2016.

FOAMed Resource Series Part III: Pediatrics

Author: Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Welcome to Part III of the FOAMed Resource Series. Part I evaluated the ECG (http://www.emdocs.net/foamed-resource-series-part-ecg/), and Part II evaluated US resources (http://www.emdocs.net/foamed-resource-series-part-ii-ultrasound/) Today’s post will evaluate Pediatric EM FOAMed. Many providers are not as comfortable with pediatric patients as compared to adults. After all, we are commonly taught “kids are not just little adults.” Though many challenge this notion, pediatric EM can be challenging.

These websites and podcasts were chosen based on useful education pearls, validity of content, impact on clinical practice, and clear citation of references and authors. This serves as an overview of several top education pediatric resources. If you have found other great resources, please mention them in the comments below!

  1. http://pemplaybook.org

Screen Shot 2016-09-08 at 10.41.50 PM

One of the finest for pediatric EM content, Dr. Tim Horeczko’s Pediatric Emergency Playbook is an amazing resource. This podcast and blog provides reviews on key conditions in the pediatric ED including headache, approach to shock, and multisystem trauma. Each post and podcast is chock-full of useful tips, tricks, and lessons. The Pediatric Emergency Playbook is one of the best resources on this list.

  1. http://www.pemed.org

Screen Shot 2016-09-08 at 10.41.10 PM

PEM ED, or “Pediatric Emergency Medicine an Education and Directional Podcast,” is a great podcast with show notes from Dr. Andy Sloas. This resource provides content in three different formats for podcasts: specialist interview, lecture, or a case presentation. Most podcasts are 20-30 minutes, though some of the more in-depth content reaches up to an hour. This podcast, with show-notes for each cast, provides the nuts and bolts evaluation and management of many conditions in the pediatric ED.

  1. http://pedemmorsels.com

Screen Shot 2016-09-08 at 10.52.13 PM

Pediatric EM Morsels is a site run by Dr. Sean Fox that provides almost weekly posts on a multitude of conditions. Each submission is presented in bullet form with references and the most recent literature. The site contains content from EM topic areas ranging from critical care to dermatology going back to 2010. For those of you on the run with only a couple of moments, this resource will give you the must-know information.

  1. http://dontforgetthebubbles.com

Screen Shot 2016-09-08 at 10.42.21 PM

Don’t Forget the Bubbles (DFTB) is a pediatric blog created and run by Tessa Davis, Henry Goldstein, Ben Lawton, and Andrew Tagg. This resource is now in its third year. DFTB contains an amazing variety of content including clinical topics, ECG library, radiology interpretation, quick reference sheets, podcast of the week, and literature reviews.

  1. http://empem.org

Screen Shot 2016-09-08 at 10.44.11 PM

The podcast and blog empem provides one of the most comprehensive resources on this list. Podcasts range from 10 minutes to one hour, with the majority of content from Drs. Colin Parker, Susan Fairbrother, Kate Bradman, and Rachel Rowlands. If you enjoy podcasts and pediatric EM, this is a great resource for in-depth understanding of pediatric EM.

  1. https://pemgeek.com

Screen Shot 2016-09-01 at 2.42.37 AM

PEMgeek is a great site for those beginning their journey into FOAMed, as this blog provides a “concentrated stream of the best free, open access pediatric education material from around the web.” The site comes from a Paediatric registrar in London. This blog also contains links to reviews of other topics and clinical guidelines.

  1. http://pemcincinnati.com/blog/

Screen Shot 2016-09-08 at 10.50.49 PM

PEMBlog from Dr. Brad Sobolewski covers a wide variety of topics, with blog posts, videos, and podcast (PEM Currents). The site contains literature reviews in the form of “reading lists,” quick reviews in “briefs,” and core content in the form of “starter packs.”

  1. http://www.pemacademy.com

Screen Shot 2016-09-08 at 10.50.33 PM

PEM Academy is an online blog with several great features. The “Hot Seat” provides cases with questions based on clinical dilemmas found in the pediatric ED. Comments from readers and post authors are enlightening and enjoyable to follow. ECG modules take learners through several pediatric-based ECGs. “Article of the Week” is a section updated weekly with a new study selected by PEM faculty, with a short discussion. The “Best Evidence” section contains links to literature evaluating the facts behind what we do in the ED. Finally, an US section contains cases and videos for US use in the ED.

That’s it for this week’s FOAMed resources. Next up, we’re covering toxicology resources. See you then!

Seizures in the First Year of Life

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident at SAUSHEC, USAF) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Case 1:

A nine month-old female presents to the emergency department (ED) with an increased work of breathing. The patient’s mother states that she developed a cough three days prior.  Her past medical history is unremarkable and the patient’s immunizations are up to date.

Initial vital signs (VS) in the ED: Heart rate (HR) 166 beats per minute (bpm), respiratory rate (RR) 42/minute (min), Oxygen saturation 96% on room air (RA), Temperature (T) of 103.1° Fahrenheit (F). As you walk into the room, you note the patient exhibiting generalized tonic-clonic motions, which resolve approximately one minute after onset.  After rechecking the patient’s airway, breathing and circulation (ABCs), you verify that the patient is stable and you quickly move on to the next patient.

Case 2:

The nurse is triaging a well-appearing three week-old infant.  The baby’s VS are within normal limits.  However, the nurse pulls you aside to express her concern regarding the patient’s repetitive tongue movements and directional eye motions she witnessed prior to your arrival.

If you are scanning your memory bank for information regarding the evaluation and treatment of these pediatric seizures, look no further.  This post will discuss the epidemiology of pediatric seizures, and offer a review of the evaluation and treatment of seizures occurring within the first year of life.

Epidemiology of Pediatric Seizures

Seizures are the most common neurologic emergency of childhood, representing approximately 1.5% of pediatric emergency department (ED) visits annually.1-3  Each year, nearly 150,000 children in the United States experience new onset seizure activity and an estimated 25,000 to 40,000 of these are afebrile. In addition, up to 10% of these patients suffer from status epilepticus.1-5 Among individuals with unprovoked afebrile seizures, approximately 70% are idiopathic and nearly 88% experience a recurrence within two years of the initial event.5

Evaluation & Treatment

In all patients presenting with a chief complaint of seizure, a comprehensive history and physical examination should be performed.  The patient history should center on events immediately prior to seizure onset (cyanosis, LOC), length of the seizure, a description of seizure activity, the presence of bowel or bladder incontinence, evidence of a postictal period, and the presence or absence of a family history of seizure disorder.

Important historical information should be obtained in patients under the age of one year. This includes birth history (pre-term/term, maternal infection), immunizations, change in diet or formula (change in preparation), any time spent unsupervised (accidental ingestions), and home remedies or medications utilized to treat maladies.1,2,5

 If the patient has a known seizure disorder, details should be obtained regarding seizure frequency, any alterations in medication regimens such as missed doses, and changes in seizure pattern (s).5,6

Physical examination in infants should focus on:

Neurologic:  developmental stages appropriate for age (milestones: 2 months = social smile, coos, tracks faces; 4 months = babbles, reaches for toy, holds head unsupported, etc)7
HEENT: head circumference, bulging or sunken fontanelles, retinal hemorrhages (may indicate increased intracranial pressure (ICP) +/- non-accidental trauma (NAT) versus volume depletion

Cardiac: capillary refill >2 seconds (sec)

Abdominal: hepatosplenomegaly => metabolic derangement/glycogen storage disease

Integumentary: café-au-lait spots => neurofibromatosis; vitiliginous lesions => tuberous sclerosis; port-wine stains => Sturge-Weber Syndrome; excessive bruising => NAT5

 The evaluation and treatment of pediatric seizures within the first year of life varies according to seizure classification.

 Febrile Seizures

The American Academy of Pediatrics defines a febrile seizure as seizure activity associated with a temperature ≥ 100.4 °F or 38 °C, occurring in patients 6 through 60 months of age, in the absence of central nervous system (CNS) infection, metabolic abnormalities or a history of afebrile seizure.1-4  The incidence of simple febrile seizures peaks at 18 months of age.1

Risk Factors for Febrile Seizures

While the pathophysiology of seizures occurring in the setting of elevated core temperatures is poorly understood, several risk factors have been identified:

  • Family history of febrile seizures (no susceptibility gene identified, but family history reported in 25-40% of patients).1,8
  • Viral infections: human herpes virus (HHV) 6 and influenza.1,8
  • Vaccinations: diphtheria, tetanus toxoids, and whole cell pertussis (DTP), and measles, mumps, and rubella (MMR)1,8

To help aid in physician decision-making regarding the need for diagnostic testing and treatment, febrile seizures are identified as simple versus complex.

Table 1 summarizes the characteristics of simple and complex seizures.

Seizure Type
Simple Complex
Duration < 15 minutes ≥15 minutes
Motion Generalized, Tonic-Clonic Focal
Mental Status Return to baseline Persistent alteration in mental status
Episodes 1 episode within 24 hours > 1 episode within 24 hours

Neonatal seizures can be subtle and difficult to detect.  Generalized tonic-clonic and myoclonic activity is rarely seen in patients of this age group given their premature central nervous systems.1  Much more commonly, patients under 28 days of age present with motor automatisms (ocular deviations, repetitive limb movements, repetitive oral movements) or changes in heart rate, and/or respiratory rate (apneic episodes).6

Evaluation and Treatment of Simple Febrile Seizures

In 2011, the American Academy of Pediatrics (AAP) released an updated guideline for the management of simple febrile seizures.  In the setting of a simple febrile seizure, the AAP recommends the following:10

  • A lumbar puncture (LP) should be performed in pediatric patients presenting with meningeal signs or in any child whose history and/or examination suggest meningitis or intracranial infection (Level B recommendation based on overwhelming evidence from observational studies).
  • In infants 6-12 months of age who presents with a seizure and fever, a LP is an option when the child is deficient in Haemophilus influenza type b (Hib) or Streptococcus pneumoniae immunizations, or when immunization status is unknown (Level D recommendation that is based on expert opinion and case reports).
  • A LP is an option in a pediatric patient pre-treated with antibiotics, as antibiotics may mask signs and symptoms of meningitis (Level D recommendation based on expert opinion and case reports).
  • An electroencephalogram (EEG) should not be performed in a neurologically healthy child with a simple febrile seizure (Level B recommendation based on overwhelming evidence from observational studies).
  • Routine laboratory studies should not be routinely performed for the sole purpose of identifying the cause of a simple febrile seizure (Level B recommendation based on overwhelming evidence from observational studies).
  • Neuroimaging should not be performed in the setting of a simple febrile seizure (Level B recommendation based on overwhelming evidence from observational studies).

Note: The AAP’s recommendations are based on an academic review of literature published from 1996-2009.  Perhaps the most commonly cited studies include:

Green SM, Rothrock SG, Clem KJ, Zurcher RF, Mellick L. Can seizures be the sole manifestation of meningitis in febrile children? Pediatrics. 1993;92(4):527–534.

This is a retrospective review of 503 consecutive cases of meningitis in pediatric patients aged 2 months to 15 years seen at two referral hospitals over a 20 year period. None of the 503 patients noted to have meningitis manifested with seizure as a sole symptom.

Kimia AA, Capraro AJ, Hummel D, Johnston P, Harper MB. Utility of lumbar puncture for first simple febrile seizure among children 6 to 18 months of age. Pediatrics. 2009;123(1):6–12.

  • Retrospective cohort review of patients aged 6 to 18 months who were evaluated for first simple febrile seizure in a pediatric emergency department between October 1995 and October 2006: no patient was diagnosed as having bacterial meningitis (number undergoing LP: 360)

Ultimately, evaluation of a febrile patient experiencing a simple febrile seizure should focus on identifying the underlying etiology of the fever. Laboratory studies and imaging should be ordered at physician discretion and according to institutional policy.  Please review the Philadelphia, Rochester, & Boston criteria for further information on how to identify febrile infants who are at risk for serious bacterial infections.  Despite thorough evaluation, approximately 30% of patients experiencing a simple febrile seizure will leave the ED without an identified etiology.11

Evaluation of Complex Febrile Seizures

Given the heterogeneity of patient presentations and relatively little knowledge regarding their etiologies, no standard algorithm or clinical practice guideline exist for the evaluation and management of complex febrile seizures.1,4

 However, a recent retrospective, cohort review by Kimia et al. did present data on this patient population:

  • From 1995 to 2008, 526 pediatric ED patients aged 6 to 60 months (median age 17 months) were evaluated for a first complex febrile seizure. Of the 526 patients, 340 underwent LP. Ultimately, 3 patients were discovered to have acute bacterial meningitis (0.5% of patients experiencing a complex febrile seizure). An additional patient was hospitalized and treated with antibiotics based upon a positive blood culture result.

In terms of complex febrile seizures, further studies are warranted.  Determining the need for neuroimaging, lumbar puncture, laboratory studies, and EEG must be determined on a case-by-case basis.4 CT can be considered if there is a concern for increased ICP or a mass, while MRI may demonstrate hippocampal injury or temporal sclerosis in the setting of febrile seizures. A neurology consultation and admission are likely in the best interest of any of these patients.

Afebrile Seizures

The differential diagnosis for new onset afebrile seizures within the first year of life is broad (Table 2).  The emergency physician primarily plays a role in stabilizing patients and in initiating preliminary evaluation.

Etiologies of New-Onset Afebrile Seizures
Time of Onset  
24 Hours Direct Drug Effects Intraventricular Hemorrhage
  Hypoxic-ischemic Encephalopathy Laceration of Tentorium or Falx
  Intrauterine Infection Pyridoxine Dependency
  Subarachnoid Hemorrhage (SAH)
24-72 Hours Cerebral Contusion/Subdural Glycogen Synthase Deficiency
Cerebral Dysgenesis Glycine Encephalopathy
Cerebral Infarction Pyridoxine Dependency
Drug Withdrawal SAH
Hypoparathyroidism Tuberous Sclerosis
Intracranial Hemorrhage (ICH) Urea-cycle Disturbances
Intraventricular Hemorrhage  Electrolyte Disturbances
72 Hours – 1 Week Familial Neonatal Seizures Kernicterus
Cerebral Dysgenesis Methylmalonic Acidemia
Cerebral Infarction Nutritional Hypocalcemia
Hypoparathyroidism Propionic Acidemia
ICH Tuberous Sclerosis
Urea-cycle Disturbances  Electrolyte Disturbances
> 1 Week Adrenoleukodystrophy Gm1 Gangliosidosis Type 1
Cerebral Dysgenesis HSV Encephalitis
Fructose Dysmetabolism Ketotic Hyperglycinemias
Gaucher Type 2 Maple Syrup Urine Disease
Tuberous Sclerosis Urea-cycle Disturbances
Electrolyte Disturbances

New-Onset Neonatal Afebrile Seizures5,6

Based upon patient presentation and a comprehensive history and physical examination, the following laboratory studies/imaging may or may not be warranted:6

  • Inborn errors of metabolism: accucheck, ammonia levels, serum organic acids, urine organic acids, metabolic panel, lactate, pyruvate
  • NAT/cerebral anomalies: Cerebral US vs. CT vs. MRI, skeletal survey
  • Meningitis/meningoencephalitis: LP
  • Toxic ingestions: serum heavy metal screen, serum toxicology levels

It is important to note that experts recommend emergent neuroimaging in the following patient populations:13,14

  • Patients with a prolonged seizure (> 15 minutes)
  • Focal seizure in patients < 33 months
  • Patients with a persistent postictal focal deficit
  • Patients with alterations in baseline mental status post seizure activity
  • Patients with conditions pre-disposing to intracranial pathology (sickle cell, bleeding diathesis, neurocutaneous disorder, HIV, hydrocephalus, VP shunt, or closed head injury)

Ultimately, the decision between outpatient and inpatient evaluation should be based upon the clinical scenario and in consultation with a neurologist.  In general, stable, well-appearing children who have experienced a first unprovoked seizure and are in the low risk category (not requiring emergent neuroimaging as detailed above), may undergo outpatient evaluation if expedited follow-up for EEG is arranged.1,5

All patients experiencing a new-onset afebrile seizure should undergo EEG evaluation as soon as possible because EEG abnormalities may predict seizure recurrence.5 Overall, the recurrent seizure rate in this group is 54% and the majority of seizures recur within two years of the initial event.1  Patients with developmental delays or those with an abnormal EEG are more likely to eventually develop an epileptiform disorder.15

 Seizure Treatment

Addressing the patient’s airway and providing benzodiazepines are the mainstays of ED management.  The authors Abend and Loddenkemper provide an excellent example of a protocol created for the management of pediatric seizures:16

 PIC1 seizures

 PIC2 seizures

A quick word on status epilepticus: As mentioned previously, nearly 10% of all pediatric patients with new-onset seizure activity present to the ED in status epilepticus, which is defined as seizure activity > 5 minutes without return to mental status baseline.1  Unlike adults in which cerebral vascular accidents (CVAs) are the most common etiology of status epilepticus, febrile seizures are the most common etiology in pediatric patients, representing 1/3 of all episodes.17


Seizure Mimics

There are a number of seizure mimics that can present during the first year of life:

  • Neonatal reflexes – the startle reflex can often be misinterpreted as seizure activity.1
  • Benign sleep myoclonus – migrating myoclonic movements that do not wake the child.18
  • Shuddering attacks – rapid shivering of the head, shoulders, and trunk.19
  • Sandifer syndrome – arching of the back, crying, and writhing secondary to severe gastroesophageal reflux.1
  • Breath holding spells – seen in 5% of pediatric patients 6 months – 5 years of age (presentation variable but often times mistaken for a seizure or brief resolved unexplained event).1

 These seizure mimics are diagnoses of exclusion.  Every effort should be made to obtain an accurate history of events to aid in clinical decision-making.

Seizure Syndromes Unique to Patients in the First Year of Life

The differential diagnosis of a patient experiencing an unprovoked afebrile seizure in the first year of life should include the following:

Syndrome Onset Characteristics
Benign Convulsions Associated with Gastroenteritis 6-60 months Generalized seizures accompanying gastroenteritis, in the absence of electrolyte derangements.  Often associated with Shigella and rotavirus infection.20
Benign Familial Neonatal Convulsions First days of life; self-resolves within 1 year. Behavioral arrest, eye deviation, tonic stiffening, myoclonic jerks.  Associated with a positive family history.9
Benign Idiopathic Neonatal Convulsions First days of life; self-resolves within 15 days. “Fifth day fits” – clonic movements, apnea, positive family history.  May represent 5% of all seizures in term infants.21
Infantile Spasms 4-18 months Jerking of extremities, head, neck and trunk; typically in clusters.  Associated with neurologic conditions (95% have developmental delay).  Spontaneously resolve, however the majority develop new seizures.22

Seizure Syndromes Unique to Pediatric Patients1


The emergency physician’s role in addressing seizures in the first year of life is to stabilize the patient and initiate an appropriate evaluation based upon an accurate history and physical examination.  While decision rules exist for simple febrile seizures, the evaluation of a complex febrile seizure and a new onset afebrile seizure must be weighed carefully.  While seizure mimics do exist, the emergency physician must always rule out any life threatening conditions first.

Key Pearls

  • Simple febrile seizure = Fever evaluation.
    • Meningeal symptoms => LP
    • 6-12 months of age with no immunization record/concern for meningitis => LP
    • Received antibiotics and concern that treatment is masking symptoms => LP
  • Complex febrile seizure = No clinical decision rules.
    • Some evidence to suggest that, although rare, we may be missing acute bacterial meningitis (3 of 340 patients in the Kimia, et al.12 study)
    • Further studies required; evaluation should be catered to the clinical scenario.
  • Afebrile seizure = No clinical decision rules, again cater to clinical scenario.
    • Focal seizure < 33 months, prolonged seizure duration, prolonged neuro deficit or co-morbidities => emergent neuroimaging.
    • All patients get an EEG (expedited outpatient if well-appearing and no focal neuro).
      • Up to 54% have recurrent seizures.
    • Seizure treatment = ABCs, benzos => fosphenytoin => sedation with continuous EEG +/- anticonvulsant
    • Seizure mimics exist, but so do seizure syndromes.
      • Your history and physical examination are vital.

References / Further Reading

  1. Agarwal M, and Fox S. Pediatric seizures. Emerg Med Clin N Am 31 (2013):733-754.
  2. Taylor C, Piantino J, Hageman J, Lyons E, Janies K, Leonard D, Kelley K, Fuchs S. Emergency department management of pediatric unprovoked seizures and status epilepticus in the state of Illinois. J Child Neurol. 2015; 30(11):1414-1427.
  3. Carapetian S, Hageman J, Lyons E, Leonard D, Janies K, Kelley K, Fuchs S. Emergency department evaluation and management of children with simple febrile seizures. Clin Pediatr. 2014; 54(10):992-998.
  4. Patel A, and Vidaurre J. Complex febrile seizures: a practical guide to evaluation and treatment. J Child Neurol. 2013; 28(6):762-767.
  5. Sharieff G, Hendry P. Afebrile pediatric seizures. Emerg Med Clin N Am 29 (2011); 95-108.
  6. Granelli S, and McGrath J. Neonatal seizures: diagnosis, pharmacologic interventions, and outcomes. J Perinat Neonat Nurs. 2004; 18(3):275-287.
  7. Learn the Signs. Act Early: Developmental milestones. Centers for Disease Control and Prevention. 2016. Available from: http://www.cdc.gov/ncbddd/actearly/index.html
  8. Graves R, Oehler K, Tingle L. Febrile seizures: risks, evaluation, and prognosis. Am Fam Physician. 2012; 85(2):149-153.
  9. Zupanc M. Neonatal seizures. Pediatr Clin North Am. 2004; 51:961-978.
  10. Clinical practice guideline – febrile seizures: guideline for the neurodiagnostic evaluation of the child with a simple febrile seizure. American Academy of Pediatrics. Pediatrics. 2011; 127(2):389-394.
  11. Colvin J, Jaffe D, Muenzer J. Evaluation of the precision of emergency department diagnoses in young children with fever. Clin Pediatr. 2012; 156:469-472.
  12. Kimia A, Ben-Joseph EP, Rudloe T, et al. Yield of lumbar puncture among children who present with their first complex febrile seizure. Pediatrics. 2010;126(1):62–69.
  13. Sharma S, Riviello J, Harper M, et al. The role of emergent neuroimaging in children with new-onset afebrile seizures. Pediatrics. 2003; 111:1-5.
  14. Warden C, Brownstein E, Del Beccaro M. Predictors of abnormal findings of computed tomography of the head in pediatric patients presenting with seizures. Ann Emerg Med. 1997; 29: 518-523.
  15. Shinnar S, Berg A, Moshe S, et al. The risk of seizure recurrence after a first unprovoked afebrile seizure in childhood: an extended follow-up. Pediatrics. 1996; 98:216-225.
  16. Abend N, Loddenkemper T. Pediatric status epilepticus management. Curr Opin Pediatr. 2014; 26(6): 668-674.
  17. Stafstrom C. Neonatal seizures. Pediatr Rev. 1995; 16:248-255.
  18. Alam S, Lux A. Epilepsies in infancy. Arch Dis Child. 2012; 97:985-992.
  19. Tibussek D, Karenfort M, Mayatepek E, et al. Clinical reasoning: shuddering attacks in infancy. Neurology. 2008; 70:338-41.
  20. Verrotti A, Nanni G, Agostinelli S, et al. Benign convulsions associated with mild gastroenteritis: a multicenter clinical study. Epilepsy Res. 2011; 93:107-114.
  21. Vining E. Pediatric seizures. Emerg Med Clin North Am 1994; 12:973-988.
  22. Hancock E, Osborne J, Edwards S. Treatment of infantile spasms. Cochrane Database Syst Rev. 2008; (4):CD001770

PEM Playbook – Multisystem Trauma in Children Part II: Massive Transfusion, Trauma Imaging, and Resuscitative Pearls

Originally published at Pediatric Emergency Playbook on March 1,
2016 – Visit to listen to accompanying podcast. Reposted with permission.

Follow Dr. Tim Horeczko on twitter @EMTogether


A 5-year-old boy was playing with his older brother in front of their home when he was struck by a car. He sustained a femur fracture, splenic laceration, and blunt head trauma – the so-called Waddell’s triad.

On arrival, he was in compensated shock, with tachycardia. He needs blood.

He decompensates…

How do we manage his hemodynamics and when do we perform massive transfusion?

Pediatric Massive Transfusion

40 mL/kg of blood products given at any time within the first 24 hours.

Adolescents and Adult Massive Transfusion

6-8 units of packed red blood cells (PRBCs)

  • Adults have about 5 L of circulating blood.
  • Not including plasma, one could replace all circulating erythrocytes with about 10 units of PRBCs
  • The best ratio of PRBCs:Plasma:Platelets is unknown, but consensus is 1:1:1.
  • 1 unit of PRBCS is typically 300 mL of volume.

The typical initial transfusion of PRBCs in children is 10 mL/kg.

Massive transfusion in children is defined as 40 mL/kg of any blood product.

Once you start to give a child with major trauma the second 10 mL/kg dose of PRBCs – start thinking about other blood components, and ask yourself whether you should initiate your massive transfusion protocol.

The goal is to have the products ready to use in the case of the dynamic trauma patient.

The Thromboelastogram (TEG)

TEG directly measures the four components of clot formation. When there is endolethial damage and bleeding, the sequence that your body takes to address it is as follows:

  1. Platelets migrate and form a plug
  2. Clotting factors aggregate and reinforce the platelets
  3. Fibrin arrives an acts like glue
  4. Other cells migrate and support the clot.

R time – reaction time – the initial line in the tracing that shows time to beginning of clot formation.

  • Treated with platelets

K factor – kinetics of the clot –how much the clot allows the pin to move, or the amplitude.

  • Treated with cryoprecipitate

Alpha angle – the slope between the R and K measurements – reflects how quickly the fibrin glue is working.

  • Treated with cryoprecipitate

Ma – maximum amplitude – reflects the overall strength of the clot.

  • Treated with platelets

LY30 – the clot lysis at 30 min – is the decrease in strength of the clot’s amplitude at 30 min.

  • Treated with an antifibrinolytics (tranexamic acid)

Shape Recognition

Red wine glass: a normal tracing with a normal reaction time and a normal amplitude. That patient just needs support and monitoring.

Champagne glass: a coagulopathic TEG tracing – thinned out, with less amplitude. This patient needs specific blood products.

Puffer fish or blob: a hyperfibrinolytic tracing. That patient will needs clot-stablizer.

TEG – like the FAST – can be repeated as the clinical picture changes.

The Trauma Death Spiral

Lethal triad of hypothermia, acidosis, and coagulopathy.

Keep the patient perfused and warm.

Each unit of PRBCs contains 3 g citrate, which binds ionized calcium, causing hypotension. In massive transfusion, give 20 mg/kg of calcium chloride, up to 2 g, over 15 minutes. Calcium chloride is preferred, as it is ionically readily available – just use a larger-bore IV and watch for infiltration. Calcium gluconate could be used, but it requires metabolism into a bioavailable source of calcium.

Prothrombin complex concentrate (PCC)

Prothrombin complex concentrate (PCC) is derived from pooled human plasma and contains 25-30 times the concentration of clotting factors as FFP. Four-factor PCCs contain factors II, VII, IX and X, while 3-factor PCCs contain little or no factor VII.

The typical dose of PCC is 20-50 units/kg

In the severely hemorrhaging patient – you don’t have time to wait for the other blood products to thaw – PCC is a powder that is reconstituted instantly at the bedside.

Tranexamic acid (TXA)

Tranexamic acid (TXA), is an anti-fibrinolytic agent that functions by stopping the activation of plasminogen to plasmin, and the degradation of fibrin. The Clinical Randomisation of an Antifibrinolytic in Significant Hemorrhage (CRASH-2) investigators revealed a significant decrease in death secondary to bleeding when TXA was administered early following trauma.

Based on the adult literature, one guideline is to give 15 mg/kg loading dose of TXA with a max 1 g over 10 minutes followed by 2 mg/kg/h for at least 8 h or until bleeding stops.

Resuscitative Pearls

Our goal here is damage control. Apply pressure whenever possible. Otherwise, resuscitate, identify the bleeding source, and slow or stop the bleeding with blood products or surgery.

How Children are Different in Trauma

In adults, we speak of “permissive hypotension” (also called “balanced resuscitation” or “damage control resuscitation”). The idea is that if we bring the adult patient’s blood pressure up to normal, we may be promoting clot rupture. To avoid this, we target a MAP of 65 and look for clinical signs of sufficient perfusion. Adults tolerate hypotension relatively well, and is sufficient until we send them to the OR or interventional radiology suite.

In children, this is simply not the case. Hypotension in children is a sign of pre-arrest. Remember, they compensate with an increased systemic vascular resistance and tachycardia to maintain blood pressure.

We should not allow children to become hypotensive – severe tachycardia alone should prompt us to resuscitate.

In other words, permissive hypotension is not permissible for children.

FAST is not sensitive enough to rule-out abdominal trauma.

Fox et al. in Academic Emergency Medicine found a sensitivity of 52%; with a 95% confidence interval [CI] = 31% to 73%.

Often children even with high-grade splenic and liver lacerations can be managed non-operatively. If they are supported adequately, they are observed in the ICU and can avoid surgery in many cases. Unfortunately, a negative FAST cannot help with detecting or grading the laceration for non-operative management. In other words, feel free to use ultrasound – especially for things that we in the ED will react to and intervene on – but CT may help to manage the traumatized child non-operatively.

General Guideline for Imaging in Pediatric Trauma

CT Head and Neck, non-contrast: in concerning mechanisms of injury, patients that are difficult to assess (especially those under 3 months), those with a GCS of 13 or lower.

CT Chest, IV contrast: for suspicion of vascular injury that needs exploration, especially in penetrating trauma. Otherwise, chest xray will tell you everything you need to know in children – especially in blunt trauma. Hemo or pneumothoraces are readily picked up by US or CXR. Rib fractures on CXR predict pulmonary contusions. If you are concerned about great vessel injury, then CT Chest may be helpful; otherwise consider omitting it.

CT Abdomen and Pelvis, IV contrast: helpful in grading splenic and liver lacerations with goal to manage non-operatively. Abdominal tenderness to palpation, significant bruising, or a seat belt sign are concerning and would generally warrant a CT. Also, consider in liver function test abnormalities, or hematuria.

Extremity injuries: in general can be evaluated with physical exam and plain films. However, some injuries in high-risk anatomically complex areas such as the hand and wrist, tibial plateau, and midfoot may be missed by plain films, and CT may be helpful here.

Remember: you can help to mitigate post-traumatic stress and risk for adult healthcare aversion.


  1. Massive transfusion in children is at 40 mL/kg of total blood products. Think about it if you are giving your second transfusion to the traumatized child.
  2. Do everything you can to support perfusion and avoid the death spiral of hypothermia, coagulopathy, and acidosis. Keep the child perfused with blood as needed, correct coagulopathy, avoid too much crystalloid, and make sure to use the least high-tech of all of these interventions – keep him dry and covered with warm blankets.
  3. Do a careful physical exam, and use CT selectively with an end-point in mind – the default is not the pan-scan – evaluate possible injuries depending on your suspicions from history, physical, and lab tests.
  4. Become familiar with the relatively new modalities in trauma such as TXA, cryoprecipitate and the emerging technology of thromboelestogram – red wine is good for you, champagne is weak, and a puffer fish is trouble.

Selected References

Dehmer JJ, Adamson WT. Massive transfusion and blood product use in the pediatric trauma patient. Semin Pediatr Surg. 2010 Nov;19(4):286-91. doi: 10.1053/j.sempedsurg.2010.07.002.

Fox JC, Boysen M, Gharahbaghian L, Cusick S, Ahmed SS, Anderson CL, Lekawa M, Langdorf MI. Test characteristics of focused assessment of sonography for trauma for clinically significant abdominal free fluid in pediatric blunt abdominal trauma. Acad Emerg Med. 2011 May;18(5):477-82.

Harvey V, Perrone J, Kim P. Does the use of tranexamic acid improve trauma mortality? Ann Emerg Med. 2014 Apr;63(4):460-2.

Holscher CM, Faulk LW, Moore EE, Cothren Burlew C, Moore HB, Stewart CL, Pieracci FM, Barnett CC, Bensard DD. Chest computed tomography imaging for blunt pediatric trauma: not worth the radiation risk. J Surg Res. 2013 Sep;184(1):352-7.

Nosanov L, Inaba K, Okoye O, Resnick S, Upperman J, Shulman I, Rhee P, Demetriades D. The impact of blood product ratios in massively transfused pediatric trauma patients. Am J Surg. 2013 Nov;206(5):655-60.

Ryan ML, Van Haren RM, Thorson CM, Andrews DM, Perez EA, Neville HL, Sola JE, Proctor KG. Trauma induced hypercoagulablity in pediatric patients. J Pediatr Surg. 2014 Aug;49(8):1295-9.

Scaife ER, Rollins MD, Barnhart DC, Downey EC, Black RE, Meyers RL, Stevens MH, Gordon S, Prince JS, Battaglia D, Fenton SJ, Plumb J, Metzger RR. The role of focused abdominal sonography for trauma (FAST) in pediatric trauma evaluation. J Pediatr Surg. 2013 Jun;48(6):1377-83.

This post and podcast are dedicated to Larry Mellick, MS, MD, FAAP, FACEP. Thank you for your dedication to medical education, and sharing your warm bedside manner, extensive knowledge and talents, and your patient interactions with the world.


Massive Transfusion on WikEM

Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP