Pediatric Difficult Airway

Pediatric Difficult AirwayRespiratory illness, sepsis, and trauma are three important entities afflicting children that may lead to needing to manage a child’s airway. Airway management in the ED is a complex interplay of patient factors, clinical illness status, and provider factors that, through our thorough training we become proficient at navigating. We have discussed many airway concepts previously (ex, ETT Depth, Cuffed ETTs, Apneic Oxygenation, Delayed Sequence Intubation, Noninvasive Ventilation, Heliox, and Transtracheal Ventilation) but one topic that deserves specific attention is the notion of a Difficult Airway:


Difficult Airway: Basics

  • Defining “Difficult Airway” is challenging, so studies are not strictly comparable (we all know it after we have dealt with it though).
  • Some separate “Difficult Airway” from “Difficult Intubation.” [Belanger, 2015]
    • Difficult Airway – unable to provide adequate gas exchange despite BVM, airway adjuncts, or combination of the two.
    • Difficult Intubation – 3 or more attempts by an experienced clinician
  • The incidence of difficult intubations in children vary from <0.1% to 9% [Graciano, 2014; Heinrich, 2012]
  • Difficult intubations is associated with higher incidence of oxygen desaturations below 80% and adverse events. [Graciano, 2014]


Difficult Airway: Important Differences

Anatomic and physiologic differences influence how the oral, pharyngeal, and tracheal axes align as well as how the respiratory mechanics function and how the child compensates to physiologic stress.

The differences are most prominent in children < 2 years of age and more adult anatomy evolves as children progress to 8 years of age.

Anatomic Differences:

  • Relatively larger head (particularly occiput)
    • Need for shoulder roll instead of head elevation to align external auditory meatus with sternal notch (which helps align the three axes).
  • Smaller and compressible nasal passages
    • More easily occluded by mucous
    • Easily obstructed by poorly positioned facemask.
  • Relatively larger tongue
    • More difficult to control with laryngoscope blade.
    • Occupies more mouth and posterior pharyngeal space.
  • Larynx location is more cranial
    • Adult’s larynx located around C4-5
    • Child’s larynx located around C3-4, but can be even higher (C2-3).
    • Makes for more of an “anterior” airway and acute angle from pharyngeal axis to tracheal axis.
  • Epiglottis is longer and more floppy
    • Softer cartilage and more pliable tissues
    • Can be more difficult to retract away from glottic opening.
  • Trachea is more compressible
    • Softer cartilage and more pliable tissues
    • Can be easily compressed by a “helpful” person performing cricoid pressure (don’t let this happen).
  • Ribs are horizontal
    • Contribute less to the work of breathing
    • Diaphragm does most of the work of breathing.
  • Low functional residual capacity
    • Due to smaller airways and less dead space
    • Smaller reservoir from which the apneic child can draw oxygen
  • Smaller number of alveoli
    • Less oxygen absorption surface area.


Physiologic Differences:

  • Higher metabolic rate
    • Consumes oxygen at more than twice the adult rate
    • Combined with low functional residual capacity, leads to rapid desaturations.
  • Low glycogen stores


Difficult Airway: Predictive Factors

  • Adult-based tools (ex, LEMON, Mallampati, thyromental distance) are not predictive in young children. [Belanger, 2015]
  • There are patient factors that are associated with difficult intubation. [Karsli, 2015; Belanger, 2015]
    • History of difficult airway (duh) [Graciano, 2014]
    • Less than 1 year of age
    • Signs of Upper Airway Obstruction (duh) [Graciano, 2014]
    • Congenital/Genetic Syndromes w/ altered anatomy
    • Physiologic stress [Graciano, 2014]
      • Hypotension, ventilation failure, etc


Difficult Airway: Assume the Worst

  • Most pediatric airways can be secured by experienced clinicians, but the potential for discovering a difficult airway after meds have been pushed is a perilous position to be in. [Belanger, 2015]
  • Absence of predictive factors for difficult airway does not mean it will be an easy airway. [Karsli, 2016; Graciano, 2014]
    • One study found 1 in 5 Difficult Airway cases were NOT anticipated. [Karsli, 2016]


Moral of the Morsel

  • Pediatric patients are a special population and warrant special considerations.
  • Anatomy and Physiology matter! There are numerous differences that need to be considered… even when it is “easy.”
  • Anticipate the Worst! 1 out of 5 is a concerning number – All pediatric patients should be considered to have a Difficult Airway until you successfully intubate them… then you can hit the “easy” button.
  • There are no “easy airways” in the ED, regardless of age. Patients that require intubation in the ED have, be definition, stressed physiologic systems and, as such, should be considered difficult until proven otherwise.



Karsli C1, Pehora C2, Al-Izzi A2, Mathew P2. A retrospective review of pediatric difficult airways: once easy, not always easy. Can J Anaesth. 2016 Jun;63(6):776-7. PMID: 26767657. [PubMed] [Read by QxMD]
Karsli C1. Managing the challenging pediatric airway: Continuing Professional Development. Can J Anaesth. 2015 Sep;62(9):1000-16. PMID: 26243378. [PubMed] [Read by QxMD]

Belanger J, Kossick M. Methods of identifying and managing the difficult airway in the pediatric population. AANA J. 2015 Feb;83(1):35-41. PMID: 25842632. [PubMed] [Read by QxMD]

Black AE1, Flynn PE, Smith HL, Thomas ML, Wilkinson KA; Association of Pediatric Anaesthetists of Great Britain and Ireland. Development of a guideline for the management of the unanticipated difficult airway in pediatric practice. Paediatr Anaesth. 2015 Apr;25(4):346-62. PMID: 25684039. [PubMed] [Read by QxMD]

Graciano AL1, Tamburro R, Thompson AE, Fiadjoe J, Nadkarni VM, Nishisaki A. Incidence and associated factors of difficult tracheal intubations in pediatric ICUs: a report from National Emergency Airway Registry for Children: NEAR4KIDS. Intensive Care Med. 2014 Nov;40(11):1659-69. PMID: 25160031. [PubMed] [Read by QxMD]

Heinrich S1, Birkholz T, Ihmsen H, Irouschek A, Ackermann A, Schmidt J. Incidence and predictors of difficult laryngoscopy in 11,219 pediatric anesthesia procedures. Paediatr Anaesth. 2012 Aug;22(8):729-36. PMID: 22340664. [PubMed] [Read by QxMD]

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Hypocalcemia and Neonates

Neonatal HypocalcemiaUnquestionably, a lot of electrolyte panel laboratory studies get ordered reflexively and have little true clinical utility. The healthy kid (or adult for that matter) with vomiting and diarrhea for two days does not typically benefit from the “Chem 200” {recall, dehydration is a clinical diagnosis}. Labs are useful when they help answer specific questions that they are capable of answering (ex, is the kid hypoglycemic? Not, is the kid dehydrated). That being said, certain populations have varying risks for electrolyte disturbances – one notable one is the neonate (goes along with “never trust a neonate.“). Let us look at one interesting issue – Hypocalcemia in the Neonate.


Hypocalcemia: Basics

  • Calcium forms:
    • Majority of total body calcium is stored in bone.
    • ~40% of serum calcium is protein-bound and not active.
    • ~50% of total serum calcium is ionized (Ca2+) and is biologically active.
    • Total body calcium may remain stable, but the amount of ionized calcium can be altered by chelation and protein binding.
      • Increases in phosphate, citrate, bicarbonate will chelate calcium decreasing ionized calcium.
      • Free fatty acids and an Alkaline pH increases Ca2+ binding to proteins.
      • Acidotic pH decreases Ca2+ binding to proteins.
  • Calcium homeostasis is complex! [Kelly, 2013]
    • Parathyroid Hormone (PTH) directly increased serum calcium levels.
      • Influences bone (release of Ca) and kidneys (absorb Ca)
    • PTH indirectly causes increased GI absorption of Ca via Vitamin D.
    • Calcitonin lowers Ca by targeting bone, renal, and GI tissues.
    • PTH levels are influence by:
      • Elevated Ionized Ca – lowers PTH.
      • Elevated magnesium levels – also inhibit PTH secretion.
        • Interestingly, severely deficient magnesium levels can also inhibit PTH secretion.
      • Severe burns and sepsis can also reduce PTH.
  • Fluctuations in ionized calcium is responsible for symptoms.


Hypocalcemia in the Neonate

  • Neonates are particularly at risk for hypocalcemia.[Thornton, 2013]
    • Fetal skeleton has a high demand for calcium and phosphorus.
    • The mother provides additional calcium to the fetus.
      • The fetus is hypercalcemic relative to the mother.
      • The high serum Ca2+ in the fetus leads to low PTH.
      • Once born, the maternal calcium source is cut off (literally).
      • The parathyroid gland has a blunted response initially, and calcium levels fall.
      • Gestational age is associated with the infant’s parathyroid gland’s ability to respond appropriately (prematurity leads to greater risk).
        • Hypocalcemia is a common consideration in the NICU.
  • Neonatal Hypocalcemia is classified as either Early or Late.
    • Early:
      • Occurs within first 3 days of life.
      • Immature parathyroid gland produce low levels of PTH.
      • Immature kidneys are less responsive to PTH.
      • More commonly seen with:
        • Premature infants
        • Low birth weight infants
        • Infants born to mothers with diabetes
        • Infants born to mothers with hypercalcemia
        • Perinatal asphyxia
    • Late:
      • Occurs after first 3 days of life
      • Classically due to excessive phosphate load (ex, drinking too much cow’s milk, phosphate enemas)
      • Other causes include:
        • Congenital defects in PTH production, secretion, or action
          • DiGeorge sequence – triad of absence of thymus, congenital hypoparathyroidism, and cardiac anomalies.
          • Isolated hypoparathyroidism can be caused by several gene mutations.
          • Pseudohypoparathyroidism – target tissue is resistant to PTH (so PTH level is high, but Calcium is low).
        • Magnesium deficiency
          • Infants who are small for gestation age are at risk.
        • Vitamin D deficiency


Hypocalcemia: Presentation

  • In general, hypocalcemia leads to neuomuscular irritability.
    • Tetany
    • Muscle cramps
    • Fatigue
    • Irritability
    • Distal extremity paresthesias
    • Circumoral numbness (in older patients able to report this)
    • Prolonged QTc
  • Severe hypocalcemia can lead to:
    • Bronchospasm (may mimic asthma)[Kelly, 2013]
    • Focal or Generalized Seizures
      • Neonatal Seizures should not be approached similarly to other seizures.
      • An etiology is found in ~90% of neonatal seizures. [Thornton, 2013]
  • Hypocalcemia can be seen in the critically ill patient as well. [Kelly, 2013]


Hypocalcemia: Treatment

  • Two most common calcium solutions for acute IV administration:
    • 10% Calcium Gluconate
      • 10 mL ampule has 90 mg of elemental calcium.
      • Lower osmolality
      • Can be given peripherally.
    • 10% Calcium Chloride
      • 10 mL ampule has 272 mg of elemental calcium. (that’s 3 times as much!)
      • Hyperosmolar – better to give via Central access (or in a CODE)
    • Bolus of calcium can transiently increase calcium levels, but serum levels will fall again after ~30 min.
  • Magnesium depletion is a common associated finding in the critically ill – consider magnesium administration as well.


Moral of the Morsel



Kelly A1, Levine MA. Hypocalcemia in the critically ill patient. J Intensive Care Med. 2013 May-Jun;28(3):166-77. PMID: 21841146. [PubMed] [Read by QxMD]

Thornton MD1, Chen L, Langhan ML. Neonatal seizures: soothing a burning topic. Pediatr Emerg Care. 2013 Oct;29(10):1107-10. PMID: 24084610. [PubMed] [Read by QxMD]

Walton DM1, Thomas DC, Aly HZ, Short BL. Morbid hypocalcemia associated with phosphate enema in a six-week-old infant. Pediatrics. 2000 Sep;106(3):E37. PMID: 10969121. [PubMed] [Read by QxMD]

Lynch RE1. Ionized calcium: pediatric perspective. Pediatr Clin North Am. 1990 Apr;37(2):373-89. PMID: 2184403. [PubMed] [Read by QxMD]

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Pyoderma Gangrenosum

Pyoderma GangrenosumMany of us enjoy the aspect of medicine that requires our refined detective skills to not only find clues in the haystacks of chief complaints and presentations, but also use those clues to deduce a diagnosis. It is one of the unique characteristics of emergency medicine; however, when those clues are of dermatologic origin, they can be quite tricky. We have discussed several aspects of skin lesions previously (ex, Pediatric Rash, Erythema Multiforme, Scalded Skin Syndrome, Molluscum, Eczema Herpeticum, Atopic Dermatitis), but let us look at one skin eruption that looks scary and is a great clue to other problems: Pyoderma Gangrenosum.


Pyoderma Gangrenosum: What is it?

  • This is a great example of a skin condition that can distract from the real problem.
    • First described in 1916 (by a French Dermatologist, Louis Brocq) [Soleimani, 2016]
      • Described as a rapidly progressive ulcer with a vertical ridge at the border, as sharp as a cliff.
      • Had necrotic base with geometric edges.
    • In 1930, Mayo Clinic group called it “pyoderma gangrenosum,” associating it with gangrene caused by strep infection.
  • Despite its appearance, it is not due to infection.
    • It is on the spectrum of neutrophilic and autoinflammatory dermatoses. [Soleimani, 2016]
    • Often initially misidentified as a pyogenic disease process.
  • Characteristics:
    • Pain is the major symptom. [Schoch, 2017]
    • Appearance:
      • May begin as pustules surrounded by erythema. [Schoch, 2017]
      • Develop into the hallmark lesion: [Soleimani, 2016]
        • Violaceous ulcer with overhanging/undermined, well-defined borders.
        • Base is necrotic
          • Contains granulation tissue and blood.
          • May have purulent exudate.
        • May involve subcutaneous and muscle layers.
    • Can develop at sites of trauma
      • Incidental bumps (also know as Pathergy) [Kechichian, 2017; Schoch, 2017]
      • Surgical sites
        • If not appreciated as pyoderma gangrenosum, surgeons may be consulted to debride….
        • Debridement can worsen the lesion! [Soleimani, 2016]
      • Can occur spontaneously also.
    • Enlarge concentrically. [Kechichian, 2017]
    • Location:
      • Often on the lower extremities
        • Most common presentation is disseminated ulcerative lesions on legs. [Kechichian, 2017]
      • Kids have a higher involvement of the head and neck than adults. [Schoch, 2017]
  • It is uncommon.
    • Which makes our vigilance necessary!
    • Approximately 4% of cases occur in children. [Schoch, 2017; Kechichian, 2017]


Pydorema Gangrenosum: Think of…

  • While it may look like it is overtly infected, it is actually a sterile lesion.
  • More than 50% of lesions are associated with an underlying systemic illness: [Kechichian, 2017; Kechichian, 2017; Soleimani, 2016]
    • Gastrointestinal
      • Inflammatory bowel disease is the most frequent association in children
    • Rheumatologic / Autoimmune
      • ex, juvenile rheumatoid arthritis, arteritis
    • Infectious
      • ex, HIV, chronic hepatitis
    • Hematologic / Malignancy
      • ex, leukemias, monoclonal gammopathy
    • Odd ball:
      • Pyogenic Arthritis, Pyoderma gangrenosum and Acne (PAPA) Syndrome [Kechichian, 2017]
    • Idiopathic – actually accounts for ~50% of cases [Kechichian, 2017]


Pyderma Gangrenosum: Diagnosis

  • Diagnosis is often delayed. [Kechichian, 2017]
  • It is a diagnosis of exclusion. [Kechichian, 2017]
  • There is no specific serologic or radiographic markers for it. [Soleimani, 2016]
  • Biopsy often performed to rule out other causes (ex, malignancy, infection, vasculitis).
    • Neutrophilic dermal infiltration demonstrated.
  • Other conditions to consider (abridged): [Soleimani, 2016]
    • Infection
    • Cutaneous anthrax
    • Atypical myobacterium
    • Traumatic ulceration
    • Cutaneous malignancy
    • Vascular insufficiency
    • Behcet’s disease
    • Vasculitis


Pyoderma Gangrenosum: Treatment

  • There is no current gold standard of care. [Kechichian, 2017]
  • Treatment is generally aimed at the underlying condition. [Kechichian, 2017]
  • Main therapy is systemic steroids or other immunosuppressants/modulators. [Schoch, 2017; Soleimani, 2016]
    • Most children have a good response to systemic steroids.
    • Anti-tumor necrosis factor alpha agents are being used.
    • Sulfasalazine is commonly used.
    • Topical tacrolimus has also been used.
    • If you are sending patient to a dermatologist, may want to withhold these medications as they may affect the ability to make the diagnosis.
  • Surgical interventions are generally avoided, but…
    • Can be helpful after the disease has been better controlled. [Soleimani, 2016]
    • Biopsy, debridement, and grafting have been utilized.


Moral of the Morsel

  • Not all “ugly” wounds are infected. It is important to consider infection, but if the kid has been on “100 courses” of antibiotics and not getting better… please think of another cause and Pydoderma Gangrenosum!
  • A post-surgical ulcer that hasn’t responded to antibiotics may be pyoderma gangrenosum.
  • Pyoderma Gangrenosum is just the “tip of the iceberg” (or ulcer of the inflammatory disease). Think about the potential associated conditions (particularly inflammatory bowel disease in children).



Schoch JJ1, Tolkachjov SN1, Cappel JA1, Gibson LE1,2, Davis DM1. Pediatric Pyoderma Gangrenosum: A Retrospective Review of Clinical Features, Etiologic Associations, and Treatment. Pediatr Dermatol. 2017 Jan;34(1):39-45. PMID: 27699861. [PubMed] [Read by QxMD]

Kechichian E1,2, Haber R1,2, Mourad N1,2, El Khoury R1,2, Jabbour S2,3, Tomb R2,4. Pediatric pyoderma gangrenosum: a systematic review and update. Int J Dermatol. 2017 May;56(5):486-495. PMID: 28233293. [PubMed] [Read by QxMD]

Soleimani T1, Sasor SE2, Spera L3, Eppley BE2, Socas J2, Chu MW2, Tholpady SS4. Pediatric pyoderma gangrenosum: is it just big wounds on little adults? J Surg Res. 2016 Nov;206(1):113-117. PMID: 27916349. [PubMed] [Read by QxMD]

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