Parotitis and Sialadenitis

sialadenitisCaring for children in the ED can be challenging for certain.  Managing the critically ill child requires a lot of skill and action (ex, Can’t Intubate, Can’t Ventilate and Hypercyanotic Spell).  Remaining vigilant for the subtly sick takes a lot of energy and contemplation (ex, Subtle Signs of Heart Failure, Osteosarcoma, and Inborn Errors in the ED).  While these two groups make our job challenging, often I find the relatively “simple” conditions to be surprisingly challenging;  they can generate a number of questions that perhaps I wasn’t ready to answer.  As many of us (in the USA anyway) salivate over our Thanksgiving meals, let us consider the “seemingly simple” condition of Sialadenitis and Parotitis.


Sialadenitis: Basics

  • Sialadenitis = inflammation of the salivary glands.
  • Saliva is important! It plays a role in:
    • Digestion, lubrication, and taste
    • Tooth intergrity
    • Defense against bacterial (secretion of IgA)
  • There are Numerous Salivary Glands
    • Parotid Gland
      • Largest of the glands
      • Stensen duct travels parallel to the zygoma, ~1cm inferior to it, and exist opposite the 2nd mandibular molar. [Francis, 2014]
      • Produces two-thirds of stimulated salivation.
      • Lower rate of secretion.
      • Produces primarily serous, watery saliva
      • More likely to become inflamed due to infectious and autoimmune reasons.
    • Submandibular Gland
      • 2nd largest of the glands
      • Wharton duct exists the floor of the mouth near the frenulum of the tongue. [Francis, 2014]
      • Produces two-thirds of the constant salivation.
      • Produced mixture of mucinous and watery saliva.
        • Mucinous saliva aids in lubrication, mastication, and swallowing.
      • More likely to become inflamed by obstructive processes, like stones.
    • Sublingular Glands
      • Multiple smaller glands.
      • Have very small ducts without a dominant duct. [Francis, 2014]
    • Minor Salivary Glands
      • Scattered in the oral cavity and oral pharynx.


Sialadenitis: Causes

  • Variety of factors can lead to sialadenitis and often due to multi-factorial processes leading to a “salivary gland inflammatory cycle”.  [Francis, 2014]
    • Sequence of events that decrease saliva flow, increase inflammation, generate ductal dysfunction, and increase mucinous saliva.
    • Predisposing factors = infection, structural abnormality, immune factors, dehydration.
  • Infectious
    • Viral
      • Mumps
        • Vaccination has made this much less common, but outbreaks do occur.
        • Systemic illness… so look for other systems that may be involved.
      • EBV
      • HIV
      • Parainfluenza
    • Bacterial
      • Staph, Strep, H. flu, E. coli, Bacteroides
      • Most commonly occurs in the Parotid Gland. [Francis, 2014]
  • Immunologic
    • Sjogren Syndrome [Baszis, 2012]
      • Chronic inflammatory disease of the exocrine glands.
      • Dry mouth and dry eyes are common.
    • HIV
      • Can cause bilateral involvement (think of this with bilateral parotitis)
      • Often glands are NOT tender.
    • IgA deficiency
    • Juvenile rheumatoid arthritis
    • Ankylosing spondylitis
    • Sarcoidosis [Banks, 2013]
    • Ulcerative colitis
    • Bulimia Nervosa Sialadenosis (unclear etiology, but may be first presentation)
  • Trauma
    • Local obstruction from stones
      • Relatively uncommon in children.
      • Submandibular gland involved in majority of cases (higher amount of mucoid saliva production).
    • Penetrating injuries
    • Blunt injuries
    • Radiation injury


Sialadenitis: Presentation

  • Swelling, pain, fever, and erythema of the affected gland.
  • Trimus and Pain with mastication
  • Purulence may be expressed from the associated duct.  [Francis, 2014]
  • Inspissated mucus may also mimic purulence.


Sialadenitis: Recurrent?

  • Recurrent or chronic sialadenitis has been associated with several autoimmune disorders.   [Francis, 2014; Baszis, 2012]
  • Causes are, again, likely must-factorial (structural, infectious, obstruction, inflammatory, etc).
  • Juvenile Recurrent Parotitis is a common cause.
    • True incidence is unknown, but thought to be the second most common cause of salivary disease in children worldwide (after Mumps).  [Francis, 2014; Patel, 2009]
    • Has two peaks in age of presentation: ages 2-6 years and at age of puberty.
    • Self-limited and resolves spontaneous after puberty.  [Francis, 2014]
  • Diagnostic sialendoscopy can be useful to help diagnose and manage. [Ramakrishna, 2015]


Sialadenitis: Management

  • Diagnosis is primarily a clinical one!  (It’s awesome when you don’t need to order tests!)
  • Treatment is typically conservative:  [Francis, 2014]
    • Pain management 
    • Adequate hydration
      • Dehydration exacerbates inflammatory process.
      • Dehydration makes mucoid saliva more prominent.
    • Warm massage
    • Sialogogues
    • Treat underlying autoimmune / inflammatory disorder.
    • Appropriate antibiotics
      • While bacterial infection may not have initiated the condition, it is difficult to deny the possibility of its involvement.
      • If able to express material from duct, send purulence / inspissated mucus for Gram Stain and Culture.  [Francis, 2014]
      • Antistaphylococcal penicillinases-resistant antibiotics should be started while awaiting culture results.
    • Patients with co-morbidities, fever, or leukocytosis may benefit from inpatient, IV antibiotics. [Stong, 2005]
  • If medical therapies fail, or there is concern for localized complication: [Stong, 2005]
    • May need to image:
      • Ultrasound
        • Considered 1st line option by many.
        • Can help evaluate the gland and abscess formation.
        • May illustrate a stone, but may still miss smaller stones. [Francis, 2014]
      • CT
        • Likely needed if surgical options need to be considered.
    • Surgical options:
      • Stone retrieval and ballon dilation
      • Lithotripsy
      • Gland excision – has become less common
      • Sialendoscopy – has become preferred option


Moral of the Morsel

  • The “seemingly simple” conditions occurring in a complex organism (like us Humans) can be less than straight forward.
  • Don’t dismiss sialadenitis as a simple infection and throw antibiotics at it. It is multifactorial and may not merely be an antibiotic deficiency. Keep other etiologies in mind, especially when educating families about it.
  • Recurrent parotitis / sialadenitis warrants additional consideration and referral.



Ramakrishna J1, Strychowsky J1, Gupta M1, Sommer DD1. Sialendoscopy for the management of juvenile recurrent parotitis: a systematic review and meta-analysis. Laryngoscope. 2015 Jun;125(6):1472-9. PMID: 25393103. [PubMed] [Read by QxMD]

Francis CL1, Larsen CG2. Pediatric sialadenitis. Otolaryngol Clin North Am. 2014 Oct;47(5):763-78. PMID: 25128215. [PubMed] [Read by QxMD]

Banks GC1, Kirse DJ, Anthony E, Bergman S, Shetty AK. Bilateral parotitis as the initial presentation of childhood sarcoidosis. Am J Otolaryngol. 2013 Mar-Apr;34(2):142-4. PMID: 23102965. [PubMed] [Read by QxMD]

Baszis K1, Toib D, Cooper M, French A, White A. Recurrent parotitis as a presentation of primary pediatric Sjögren syndrome. Pediatrics. 2012 Jan;129(1):e179-82. PMID: 22184654. [PubMed] [Read by QxMD]

Saarinen RT1, Kolho KL, Kontio R, Saat R, Salo E, Pitkäranta A. Mandibular osteomyelitis in children mimicking juvenile recurrent parotitis. Int J Pediatr Otorhinolaryngol. 2011 Jun;75(6):811-4. PMID: 21489642. [PubMed] [Read by QxMD]

Patel A1, Karlis V. Diagnosis and management of pediatric salivary gland infections. Oral Maxillofac Surg Clin North Am. 2009 Aug;21(3):345-52. PMID: 19608051. [PubMed] [Read by QxMD]

Stong BC1, Sipp JA, Sobol SE. Pediatric parotitis: a 5-year review at a tertiary care pediatric institution. Int J Pediatr Otorhinolaryngol. 2006 Mar;70(3):541-4. PMID: 16154645. [PubMed] [Read by QxMD]

Orvidas LJ1, Kasperbauer JL, Lewis JE, Olsen KD, Lesnick TG. Pediatric parotid masses. Arch Otolaryngol Head Neck Surg. 2000 Feb;126(2):177-84. PMID: 10680869. [PubMed] [Read by QxMD]

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Road Rash

Road Rash Friction InjuryCertainly, pediatric rashes can be a challenge (and we have discussed my “Approach to the Pediatric Rash” previously).  One “rash,” however, deserves particular attention as it is not a Rash at all: it is a Burn!  Let’s remain vigilant for that benign sounding rash that may not be benign at all: Road Rash.


Road Rash : Basics

  • Accidental Injury is the leading cause of mortality for children.
    • See Childhood Injury
    • Motor Vehicle Accidents are the most common cause.
    • Fire/Burn is the 5th most common cause of injury.
  • “Road Rash” is a Friction Burn.
    • It is the most common non-thermal burn.
    • Patients 0-20 years of age account for 40% of cases. [Agrawal, 2008]
    • Often overlooked initially [Castana, 2009; Agrawal, 2008]
      • Many times associated with other injuries that may distract providers.
        • 35% had associated fractures
        • 10% had head injuries
      • Severity may be under-appreciated by providers – classifying it as “road rash” rather than burn.
  • “Road Rash” – difficult to know its true incidence.
    • Often embedded with diagnosis of abrasion or burn.
    • More minor versions may not even be documented.
    • Patients with minor versions may not seek medical attention.
    • Friction burns are not included in burns surveys. [Agrawal, 2008]


Road Rash: Physics Matters

  • Friction is a non-conservative, resistive force
  • Occurs when two surfaces move against each other
  • Is a function of the coefficient of friction of the objects
    • Skin moving against other surfaces has a high coefficient of friction
  • Frictional forces generate both:
    • Structural injury 
    • Thermal injury
  • Other influencers:
    • Velocity of the moving objects – the greater, the more severe the burn
    • Surface temperature – the hotter, then more severe (ex, asphalt in afternoon is hotter and generates more damage)


Road Rash: The Culprits

  • Most often occurs with motor vehicle accidents. [Agrawal, 2008]
    • Ejected passengers from car accidents
    • Motorcycle passengers
    • Bicycle riders
  • Other common causes:
    • Exercise Treadmills (fast moving belts) [Friedrich, 2007; Collier, 2004]
      • Many injuries reported and has lead to Injury Prevention strategies.
      • Can be severe injuries – one study had 46% with Full Thickness burns [Collier, 2004]
    • Sanders and Grinders (again, fast moving surfaces)
    • Domestic Vacuum cleaners (particularly those with rotating brushes) [Grob, 2003]


Road Rash: Severity

  • Road Rash / Friction Burn severity is determined by the depth (just like Thermal Burns):
    • Epidermal: Painful, red
    • Superficial Dermal: Painful, pink
    • Deep Dermal: Reduced pain, blotchy, No Cap Refill 
    • Full Thickness: No sensation, white or black, No cap refill
    • Deep Structures (Muscle, Tendon, Bone, etc) [Bailey, 2011]
  • Most of the cases in the literature are Superficial Dermal or deeper. [Castana, 2009]
    • Likely somewhat do to reporting bias, but still highlights the fact there is a lot of significant non-thermal burn.
    • Often had secondary infections and scar formation.
  • Can also be complicated by Traumatic Tattooing [Vrints, 2014]
    • Forceful impregnation of dirt, asphalt, gravel, glass into dermis.
    • After re-epithelization, becomes a permanently discolored area (black or blue).
    • Best strategy to prevent tattooing is to remove all of the foreign bodies before the region re-epithelializes.


Moral of the Morsel

  • Don’t be complacent with “road rash!”
  • Characterize and describe “road rash” like the burn that it is!
  • Treat “road rash” like a Burn! – because it is.
    • Assess the severity of the burn.
    • Don’t forget the fluid resuscitation!
    • Don’t forget the tetanus prophylaxis!
    • Consult your plastic surgeons or burn specialists to help determine best management (Close follow-up? Surgical debridement? Skin grafting?)



Vrints I1, Den Hondt M, Van Brussel M, Nanhekhan L. Immediate debridement of road rash injuries with Versajet® hydrosurgery: traumatic tattoo prevention? Aesthetic Plast Surg. 2014 Apr;38(2):467-70. PMID: 24584860. [PubMed] [Read by QxMD]

Menon S1, Ward D, Harvey JG, Hei EL, Holland AJ. Friction burns in children: does laser Doppler imaging have a role? J Burn Care Res. 2012 Nov-Dec;33(6):736-40. PMID: 22878493. [PubMed] [Read by QxMD]

Bailey JK1, Park C, Yakuboff KP. Fourth-degree burn of the brain from friction burn of scalp: an unusual injury from a golf cart. J Burn Care Res. 2011 Jul-Aug;32(4):e146-8. PMID: 21747331. [PubMed] [Read by QxMD]

Castana O1, Dagdelenis J, Rempelos G, Paneris P, Anagiotos G, Diplas D, Alexakis D. Traumatic injuries with deep abrasion: “a burn”. Ann Burns Fire Disasters. 2009 Mar 31;22(1):44-7. PMID: 21991151. [PubMed] [Read by QxMD]

Agrawal A1, Raibagkar SC, Vora HJ. Friction burns: epidemiology and prevention. Ann Burns Fire Disasters. 2008 Mar 31;21(1):3-6. PMID: 21991101. [PubMed] [Read by QxMD]

Friedrich JB1, Muzaffar AR, Hanel DP. Pediatric hand friction burns from treadmill contact. Hand (N Y). 2007 Dec;2(4):188-93. PMID: 18780051. [PubMed] [Read by QxMD]

Han T1, Han K, Kim J, Lee G, Choi J, Lee J, Jang Y, Oh S. Pediatric hand injury induced by treadmill. Burns. 2005 Nov;31(7):906-9. PMID: 15990237. [PubMed] [Read by QxMD]

Maguiña P1, Palmieri TL, Greenhalgh DG. Treadmills: a preventable source of pediatric friction burn injuries. J Burn Care Rehabil. 2004 Mar-Apr;25(2):201-4. PMID: 15091149. [PubMed] [Read by QxMD]

Collier ML1, Ward RS, Saffle JR, Edelman LS, Morris SE, Lundy C. Home treadmill friction injuries: a five-year review. J Burn Care Rehabil. 2004 Sep-Oct;25(5):441-4. PMID: 15353938. [PubMed] [Read by QxMD]

Grob M1, Josty IC, Soldin MG, Dickson WA. Paediatric friction hand injuries caused by domestic vacuum cleaners-a review from one unit. Burns. 2003 Nov;29(7):714-6. PMID: 14556731. [PubMed] [Read by QxMD]

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Endocarditis in Children

EndocarditisMany conditions may present subtly in children (ex, Inborn Errors of Metabolism, HUS, Pneumonia), but the subtle presentations of cardiac disease are often the most attention grabbing. We have previously discussed Subtle Signs of Heart Failure and Myocarditis.  Let us take a moment to appreciate another significant cardiac condition that may present in subtle fashions and requires our vigilance: Endocarditis in Children.


Endocarditis in Children: Basics

  • Rare, but deadly!
    • Difficult to know the exact occurrence of infective endocarditis in children.
    • Estimates range from 0.05 to 0.78 cases per 1,000 pediatric admissions. [Baltimore, 2015]
    • Overall frequency of endocarditis in children is increasing, though.
    • Unfortunately, mortality remains high: 5-10% [Tseng, 2014; Day, 2009]
  • Epidemiology has changed over past 80 years. [Baltimore, 2015; Elder, 2015; Tseng, 2014]
    • Rheumatic Heart Disease was once a significant factor, but now relatively rare.
    • Post-operative Congenital heart disease is now the leading associated condition in endocarditis cases.
      • Much improved survival for children with CHD leads to longer timespans for children to be affected.
      • Postoperative infective endocarditis is a long-term risk after correction of complex CHD, especially if there are residual defects or prosthetic material.
      • Increased prevalence of septal or vascular occluders and coils increases risk also.
    • Central Indwelling Lines also used more commonly now and increase risk.
  • S. aureus has become more prevalent over the past few decades. [Baltimore, 2015; Esposito, 2015; Yock-Corrales, 2013; Wei, 2010; Day, 2009]
  • Streptococci viridans group still remains an important cause.


Infective Endocarditis: Presentation

  • Symptoms are often vague and indolent: [Baltimore, 2015]
    • Prolonged fever
    • Rigors, diaphoresis
    • Fatigue, weakness
    • Arthralgias, myalgias
    • Weight loss
  • Occasionally, may present with acute illness with rapidly developing symptoms.
  • Clinical findings relate to 4 underlying phenomena: [Baltimore, 2015]
    1. Bacteremia / Fungemia
      • >85% of cases present with fever [Wei, 2010]
    2. Valvulitis
      • New murmur may be appreciated.
      • May develop overt heart failure.
      • In children with CHD, may not appreciate change in murmur, but there may be decreased oxygenation.
    3. Immunologic Responses
    4. Embolic
      • Extra-cardiac findings (Janeway lesions, Roth Spots, Osler Nodes, etc) are less commonly found in children than adults.
      • May see renal abnormalities (ex, glomerulonephritis, infarct).
        • Hematuria is one of the more common findings. (~53% of cases had microscopic hematuria) [Wei, 2010]
        • Can be due to embolic or immune complex deposition.
      • Embolic disease can also lead to injury to brain, lung, GI tract, or heart. [Wei, 2010]
      • Mycotic aneurysms have also been reported.
  • The Modified Duke Criteria
    • The current recommendations to help make the diagnosis of endocarditis is to use the Modified Duke Criteria. [Baltimore, 2015Baddour, 2005]
    • Divides cases into 3 categories and has Major and Minor Criteria:
      • Definite Infective Endocarditis
      • Possible Infective Endocarditis
      • Rejected
    • See TABLE 3 and TABLE 4 in Circulation 2015 for Modified Duke Criteria (too complex to replicate here).


Endocarditis in Children w/ Normal Hearts

  • While less common, endocarditis can occur in structurally normal hearts (~8-10% of cases) [Baltimore, 2015; Day, 2009]
    • One study had much higher percentage of previously healthy children developing endocarditis (35.4%) [Lin, 2012]
    • Average interval from symptom onset to diagnosis in these children was 18-31 days. [Lin, 2012]
  • Usually involves the aortic or mitral valves
  • Indwelling intravascular catheters are major risk factor for many of these patients.
  • Staphylococcus aureus bacteremia is the leading culprit. [Day, 2009]
  • Methicillin-resistant S. aureus has also become a common causative agent. [Esposito, 2015]
  • Neonates and Premature infants with normal hearts who develop endocarditis are at high risk for mortality. [Day, 2009]


Moral of the Morsel

  • Persistent fever always warrants our appreciation and contemplative minds! Don’t just dismiss it as another Virus.
  • Fever in child with structurally abnormal heart should absolutely grab your attention, even long after any repair. May need to discuss specific lesion and repair and potential risk of endocarditis with the cardiologist.
  • Central lines are useful, but come with a lot of risk as well.
  • Got hematuria? Don’t just blame the kidney… think about the heart also!



Esposito S1, Mayer A1, Krzysztofiak A2, Garazzino S3, Lipreri R4, Galli L5, Osimani P6, Fossali E7, Di Gangi M8, Lancella L2, Denina M3, Pattarino G4, Montagnani C5, Salvini F9, Villani A2, Principi N1, Italian Pediatric Infective Endocarditis Registry. Infective Endocarditis in Children in Italy from 2000 to 2015. Expert Rev Anti Infect Ther. 2016;14(3):353-8. PMID: 26708337. [PubMed] [Read by QxMD]

Baltimore RS, Gewitz M, Baddour LM, Beerman LB, Jackson MA, Lockhart PB, Pahl E, Schutze GE, Shulman ST, Willoughby R Jr; American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young and the Council on Cardiovascular and Stroke Nursing. Infective Endocarditis in Childhood: 2015 Update: A Scientific Statement From the American Heart Association. Circulation. 2015 Oct 13;132(15):1487-515. PMID: 26373317. [PubMed] [Read by QxMD]
Baddour LM, Wilson WR, Bayer AS, Fowler VG Jr, Tleyjeh IM, Rybak MJ, Barsic B, Lockhart PB, Gewitz MH, Levison ME, Bolger AF, Steckelberg JM, Baltimore RS, Fink AM, O’Gara P, Taubert KA; American Heart Association Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young, Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and Stroke Council. Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy, and Management of Complications: A Scientific Statement for Healthcare Professionals From the American Heart Association. Circulation. 2015 Oct 13;132(15):1435-86. PMID: 26373316. [PubMed] [Read by QxMD]

Elder RW1, Baltimore RS2. The Changing Epidemiology of Pediatric Endocarditis. Infect Dis Clin North Am. 2015 Sep;29(3):513-24. PMID: 26311357. [PubMed] [Read by QxMD]

Tseng WC1, Chiu SN, Shao PL, Wang JK, Chen CA, Lin MT, Lu CW, Wu MH. Changing spectrum of infective endocarditis in children: a 30 years experiences from a tertiary care center in Taiwan. Pediatr Infect Dis J. 2014 May;33(5):467-71. PMID: 24378945. [PubMed] [Read by QxMD]

Yock-Corrales A1, Segreda-Constenla A, Ulloa-Gutierrez R. Infective endocarditis at Costa Rica’s children’s hospital, 2000-2011. Pediatr Infect Dis J. 2014 Jan;33(1):104-6. PMID: 23989105. [PubMed] [Read by QxMD]

Lin YT1, Hsieh KS, Chen YS, Huang IF, Cheng MF. Infective endocarditis in children without underlying heart disease. J Microbiol Immunol Infect. 2013 Apr;46(2):121-8. PMID: 22727890. [PubMed] [Read by QxMD]

Wei HH1, Wu KG, Sy LB, Chen CJ, Tang RB. Infectious endocarditis in pediatric patients: analysis of 19 cases presenting at a medical center. J Microbiol Immunol Infect. 2010 Oct;43(5):430-7. PMID: 21075710. [PubMed] [Read by QxMD]

Day MD1, Gauvreau K, Shulman S, Newburger JW. Characteristics of children hospitalized with infective endocarditis. Circulation. 2009 Feb 17;119(6):865-70. PMID: 19188508. [PubMed] [Read by QxMD]

Baddour LM, Wilson WR, Bayer AS, Fowler VG Jr, Bolger AF, Levison ME, Ferrieri P, Gerber MA, Tani LY, Gewitz MH, Tong DC, Steckelberg JM, Baltimore RS, Shulman ST, Burns JC, Falace DA, Newburger JW, Pallasch TJ, Takahashi M, Taubert KA; Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease; Council on Cardiovascular Disease in the Young; Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia; American Heart Association; Infectious Diseases Society of America. Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America. Circulation. 2005 Jun 14;111(23):e394-434. PMID: 15956145. [PubMed] [Read by QxMD]

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Negative Pressure Pulmonary Edema and Croup

Negative Pressure Pulmonary Edema and CroupCaring for patients is very humbling. I once described the EM Mindset as being one that requires Humble Arrogance (See – requiring humility to know you can’t know it all and arrogance to believe that your skills can make a difference in another’s life.  Certainly, this requires a continual assessment of the balance between the two extremes.  Sometimes that balance is easy, but other times we don’t even recognize the disequilibrium until our patients alert us to it. Recently, a patient reminded me that, while most croup is rather benign, it can become complicated. Let us use my recent humbling experience to refresh our memories about Negative Pressure Pulmonary Edema and Croup.


Croup: What is Usual

  • Usually caused by a virus
  • Usually 1-2 episodes per year
  • Usually seen in the Fall and Winter months
  • Usually affects children 6 mos – 3 years with peak at 2 years
  • Usually short in duration (1-2 days)
  • Usually standard therapies effectively treat the condition.
  • Usually does NOT require hospitalization.


Croup: What is Feared

  • Airway Obstruction
    • Obviously, this is the major emergent condition that needs to be avoided.
    • This is why stridor garners so much attention in the ED.
  • Negative Pressure Pulmonary Edema
    • Occurs as a result of the airway obstruction and leads to pulmonary edema and hypoxia. [Chen, 2010]
    • May be present even after obstruction has resolved.


Negative Pressure Pulmonary Edema

  • Also referred to as “Post-Obstructive Pulmonary Edema”
  • Can be caused from severe, sudden upper airway obstruction (Type I)
    • Cases reported due to laryngospasm, epiglottis, croup, aspirated FB’s, and angioedema. [Chen, 2010]
    • Even seen in agitated patient after biting down on endotracheal tube. [Bhattacharya, 2016]
    • Can also develop after surgery (especially ENT T&A surgery) for upper airway obstruction. (Type II) [Sonsuwan, 2014; Mehta, 2006]
  • Forced inspiration against a closed or obstructed glottis generates excessive negative intrathoracic pressures [Bhattacharya, 2016]
    • Known as Muller Maneuver.
    • -140 cm H2O compared to baseline of -4 cm H2O
  • This increases venous return to right heart and increases pulmonary venous pressures.
  • Additionally, low cardiac output leads to increased high afterload pressures.
  • These combine to cause increased hydrostatic pressures –> fluid moves from pulmonary vasculature to the interstitial space –> Pulmonary Edema –> Hypoxia
  • Acute airway obstruction can also lead to hypoxia, which further causes pulmonary vasoconstriction, pulmonary hypertension, and right heart failure.
  • Usually occurs within minutes of airway obstruction; often resolves within 12-24 hours. [Bhattacharya, 2016Chen, 2010]



  • May present with obvious signs of upper airway obstruction (stridor, increased work of breathing/retractions, hoarseness, drooling).
    • May also present after the episode of obstruction resolved (so, perhaps you took appropriate actions to fix the problem with positioning, medications, or intubation).
  • Signs of Pulmonary Edema [Chen, 2010]
    • Hypoxemia
    • Frothy sputum in nonintubated patient or edema fluid in endotracheal tube.
    • Bilateral infiltrates on CXR



  • Early recognition is important (remember, hypoxia in a patient with “croup” is odd).
  • Beta-agonists may help improve fluid clearance. [Bhattacharya, 2016]
  • Supplemental oxygenation
  • May need Positive Pressure Ventilation
  • Use of diuretics
    • Still controversial [Chen, 2010]
    • May be beneficial, if patient is not hypotensive. [Bhattacharya, 2016]
  • May require Prone Positioning or even ECMO.


Moral of the Morsel

  • Even the Simple can become Complicated! Remain Vigilant!
  • Even the Common can cause Humility.
  • Not all that has stridor has croup: don’t bark up the wrong tree.
  • Not all croup is simple: if there is hypoxia, think about negative pressure pulmonary edema.



Bhattacharya M1, Kallet RH1, Ware LB2, Matthay MA3. Negative-Pressure Pulmonary Edema. Chest. 2016 Oct;150(4):927-933. PMID: 27063348. [PubMed] [Read by QxMD]

Zhonghua Er Ke Za Zhi. 2014 Jul;52(7):531-4. PMID: 25224060. [PubMed] [Read by QxMD]

Dubey PK1. Post extubation negative pressure pulmonary edema due to posterior mediastinal cyst in an infant. Ann Card Anaesth. 2014 Apr-Jun;17(2):161-3. PMID: 24732622. [PubMed] [Read by QxMD]

Sonsuwan N1, Pornlert A2, Sawanyawisuth K3. Risk factors for acute pulmonary edema after adenotonsillectomy in children. Auris Nasus Larynx. 2014 Aug;41(4):373-5. PMID: 24746668. [PubMed] [Read by QxMD]

Bajwa SS1, Kulshrestha A. Diagnosis, prevention and management of postoperative pulmonary edema. Ann Med Health Sci Res. 2012 Jul;2(2):180-5. PMID: 23439791. [PubMed] [Read by QxMD]

Chen IC1, Chen KH, Tseng CM, Hsu JH, Wu JR, Dai ZK. Croup-induced postobstructive pulmonary edema. Kaohsiung J Med Sci. 2010 Oct;26(10):567-70. PMID: 20950784. [PubMed] [Read by QxMD]

Anasthesiol Intensivmed Notfallmed Schmerzther. 2006 Feb;41(2):64-78. PMID: 16493558. [PubMed] [Read by QxMD]

Mehta VM1, Har-El G, Goldstein NA. Postobstructive pulmonary edema after laryngospasm in the otolaryngology patient. Laryngoscope. 2006 Sep;116(9):1693-6. PMID: 16955006. [PubMed] [Read by QxMD]

Ead H1. Review of laryngospasm and noncardiogenic pulmonary edema. Dynamics. 2003 Fall;14(3):9-12. PMID: 14725141. [PubMed] [Read by QxMD]

Lang SA1, Duncan PG, Shephard DA, Ha HC. Pulmonary oedema associated with airway obstruction. Can J Anaesth. 1990 Mar;37(2):210-8. PMID: 2178789. [PubMed] [Read by QxMD]

Travis KW, Todres ID, Shannon DC. Pulmonary edema associated with croup and epiglottitis. Pediatrics. 1977 May;59(5):695-8. PMID: 857236. [PubMed] [Read by QxMD]

The post Negative Pressure Pulmonary Edema and Croup appeared first on Pediatric EM Morsels.

Spinal Needle Stylet Hokey Pokey

Spinal Needle StyletCertainly, one of the most common procedures in the Ped ED is the lumbar puncture.  We have discussed efforts to ensure that our first attempt is our best attemptgood positioning and analgesia are critical.  We have also discussed how to deal with the result when the LP was traumatic.  Additionally, we have covered the complication of Post-LP Headaches. One question we should ask though is… are we undermining our own success rate?  Do we need to keep replacing the Spinal Needle Stylet? Does playing the LP Hokey Pokey help or hurt us?


Anatomy Matters

  • One major goal of the Lumbar puncture is to obtain an atraumatic tap (AKA “Champagne Tap”)
    • An aside – What “Champagne tap” means is often debated
      • Does it just reference Zero RBCs, or does it also have to have No leukocytes?
      • Is it for every LP you do? Or just the first time you do one? 
      • Who is to say?  Generally the person buying the bottle of champagne is the one to make “the rules.”
    • Having an atraumatic tap will make interpretation and management more clear. (Clear fluid => clear decisions)
    • See Traumatic Tap Morsel for reasons why you should NOT adjust your CSF results in an attempt to interpret CSF with lots of RBCs.
  • Landmarks: [Bonadio, 2014]
    • Superior Iliac Crest
    • Supracristal line
      • Horizontal line connecting superior portion of superior iliac crests.
      • Intersects the spinal column at the L3-L4 interspace.
    • Whether in the lateral decubitus position or the seated position (See Morsel as to why you may want to favor the seated position), ensure the spinal column and the supracristal line are perpendicular to each other.
  • Spinal Cord terminates around level of L1.
  • Venous plexus
    • Surrounds the dura lining.
    • Ventral to the subarachnoid space the plexus is extensive.
    • Important not to “over-shoot” the subarachnoid space as you will likely encounter the extensive venous plexus that is ventral to it. [Bonadio, 2014]
    • Using a stylet can cause you to inadvertently over-shoot, as you blindly advance the needle and may advance through the lumbar cistern and enter the venous plexus that is ventral to it.


Spinal Needle Stylet: Why Use It?

If using a stylet may make it more likely to have a traumatic LP, then why use it at all?

  • There are cases of intraspinal epidermoid tumors arising related to LPs. [Ziv, 2004]
  • The hollow tip of a needle can, potentially, carve out a plug of epidermis or dermis and then translocate that into the subarachnoid space.
  • The stylet converts a hollow bore needle into a solid one, thus, preventing a plug of skin being carved out and transplanted.


Spinal Needle Stylet: Not a Dance

  • Obviously, if we want to avoid creating a complication like epidermoid tumors, we need to use the spinal needle stylet; however, this often has lead to an interesting dance:
    • Inserting the stylet, advancing the needle, removing the stylet, checking for CSF, reinserting the stylet, advancing again, and repeating
    • “You put the stylet in. You put the stylet out. You put the stylet in and … you hope you get CSF and not blood” (ok, not the best dance song).
  • Two main issues exist with the “Stylet Hokey Pokey:”
    • 1st – The “pop” sensation of piercing the inner ligaments is not as prominent in children as adults, so having the stylet in position can lead to over-inserting the needle and entering the ventral venous plexus… and turning champagne into fruit punch.
    • 2nd – The stylet is, itself, sharp. Repeatedly reinserting it also increases the potential for inadvertently sticking your self with it.


Spinal Needle Stylet: Best of Both Worlds

  • There is a way to both minimize the risk of causing epidermoid tumor AND minimize risk of a traumatic LP. [Bonadio, 2014; Baxter, 2006; Strupp, 1997]
    • Appropriately position the child and ensuring adequate analgesia and sterile prep.
    • Insert the spinal needle through the epidermis and dermis with the stylet in place.
    • Once through the dermal layers (< 1cm), remove the stylet and advance slowly without the stylet.
    • Stop once CSF is seen to flow into the hub of the spinal needle.
    • Rejoice.
  • The stylet should be reinserted prior to removing the spinal needle completely to help minimize post-LP headaches.



Bonadio W1. Pediatric lumbar puncture and cerebrospinal fluid analysis. J Emerg Med. 2014 Jan;46(1):141-50. PMID: 24188604. [PubMed] [Read by QxMD]

Baxter AL1, Fisher RG, Burke BL, Goldblatt SS, Isaacman DJ, Lawson ML. Local anesthetic and stylet styles: factors associated with resident lumbar puncture success. Pediatrics. 2006 Mar;117(3):876-81. PMID: 16510670. [PubMed] [Read by QxMD]

Ziv ET1, Gordon McComb J, Krieger MD, Skaggs DL. Iatrogenic intraspinal epidermoid tumor: two cases and a review of the literature. Spine (Phila Pa 1976). 2004 Jan 1;29(1):E15-8. PMID: 14699293. [PubMed] [Read by QxMD]

Strupp M, Brandt T. Should one reinsert the stylet during lumbar puncture? N Engl J Med. 1997 Apr 17;336(16):1190. PMID: 9102578. [PubMed] [Read by QxMD]
Bonadio WA1, Smith DS, Goddard S, Burroughs J, Khaja G. Distinguishing cerebrospinal fluid abnormalities in children with bacterial meningitis and traumatic lumbar puncture. J Infect Dis. 1990 Jul;162(1):251-4. PMID: 2355199. [PubMed] [Read by QxMD]

Bonadio WA, Smith DS, Metrou M, Dewitz B. Estimating lumbar-puncture depth in children. N Engl J Med. 1988 Oct 6;319(14):952-3. PMID: 3419463. [PubMed] [Read by QxMD]

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