Perichondritis: Not Just Simple Cellulitis

Background: Perichondritis is an infection of the connective tissue of the ear that covers the cartilaginous auricle or pinna, excluding the lobule (Caruso 2014). The term perichondritis is itself a misnomer, as the cartilage is almost always involved, with abscess formation and cavitation (Prasad 2007). Perichondritis can be a devastating disease, and if left improperly treated, the infection can worsen into a liquefying chondritis resulting in disfigurement and/or loss of the external ear (Noel 1989) (Martin 1976). Unfortunately, misdiagnosis and mistreatment is common. In one small retrospective review, the overwhelming majority of patients presenting to a large general hospital were prescribed antibiotics without appropriate antimicrobial coverage, resulting in a significant number of patients developing chondral deformities or “cauliflower ear” (Liu 2013).

Causes: A number of causes of perichondritis have been identified, with one study of 85 patients suggesting the most common causes including minor trauma, burns, and ear piercing (Prasad 2005). Notably, damage to the cartilage is not a necessary prerequisite—infection can occur if the overlying meatal skin is subjected to even trivial trauma, such as a scratch with an infected fingernail. In a significant percentage of cases, no significant cause can be identified (Prasad 2007) (Levin 1995).  Nonetheless, several authors postulate that a growing incidence of perichondritis may be associated with the rising popularity of high chondral ear piercing, which causes stripping of the perichondrium and microfracture of the avascular cartilage while directly introducing infection (Prasad 2007) (Liu 2013).  Perichondritis has been noted to be the presenting symptom of a number of disease processes marked by immunosuppression, including HIV-associated Non-Hodkin’s Lymphoma, relapsing polychondritis, and—not uncommonly—diabetes (Caruso 2014) (Levin 1995).

The most common microorganism responsible for perichondritis is Pseudomonas Aeruginosa, a gram-negative rod with intrinsic antibiotic resistance mechanisms (Caruso 2014) (Wu 2011). In one retrospective analysis of 61 patients with perichondritis, Pseudomonas was identified in 95% of cases. Co-infection with E. Coli was identified in half of cases, and Staph Aureus in 7% of patients. Because of the varying antibiotic sensitivities of these causative organisms, culture swab is recommended in all cases (Prasad 2005).

Diagnosis and Management: The diagnosis of perichondritis is clinical via physical exam. Patients initially experience dull pain, which gradually develops into severe otalgia with a purulent discharge (Noel 1989). Early cases are marked by erythema, swelling, and tenderness of the auricle without notable fluctuance (Chun 2013). The lobule remains unaffected, helping to distinguish perichondritis from otitis externa (Kullar 2012). A nidus of infection may be able to be identified within the superior fossae, though often will be absent. Complete clinical examination should exclude tenderness or fluctuance of the mastoid process of the temporal bone, as well as facial, orbital, or middle ear involvement.

Perichondritis in an 8-year-old boy. No traumatic etiology was identified.

Management of perichondritis includes antibiotic therapy with anti-pseudomonal activity and consideration of incision and drainage by ENT specialists in the case of fluctuance in order to remove necrotic cartilage (Caruso 2014). Generally, appropriate outpatient antibiotic coverage would dictate oral therapy with ciprofloxacin or another fluoroquinolone, however the overall susceptibility of Pseudomonas has decreased steadily from 86% in 1994 to 76% in 2000, a result that has been significantly correlated to the increased use of fluoroquinolones (Wu 2011). Local antibiograms demonstrating antibiotic susceptibilities should guide empiric therapy, however. As high rates of oral antibiotic treatment failure have been documented, some patients may require a course of intravenous antibiotics or treatment in a monitored setting in order to ensure symptom improvement (Rees 2016). Indeed, as any lesion involving the pinna can have drastic and alarming cosmetic complications, some authors routinely recommend hospital admission for urgent specialist evaluation and parenteral therapy, particularly among pediatric patients (Prasad 2005).

Perichondritis in a 16-year-old girl. An infected high chondral piercing is visible near the scaphoid fossa.

Traditionally, fluoroquinolones have been avoided in pediatric patients due to fears of arthropathy, however recent literature suggests that risk is abundantly low. In one meta-analysis of 16,184 pediatric patients given systemic ciprofloxacin, the risk of musculoskeletal adverse events attributed to therapy was 1.6%, half of which were arthralgias which resolved upon drug withdrawal (Adefurin 2011). In another comprehensive review of the literature from 1980 to 2007, four large retrospective studies failed to identify a significant link between musculoskeletal injury and fluoroquinolone treatment (Forsythe 2007). Ultimately, there are no studies demonstrating significant growth disturbance due to ciprofloxacin use, suggesting that a short course in reasonable and safe in pediatric populations in the context of appropriate monitoring and follow-up (Liu 2013).

Take-Home Points:

  • Perichondritis is a pseudomonal infection of the outer ear marked by tenderness and erythema and distinguished by a spared lobule.
  • Misdiagnosis or mistreatment can result in devastating patient outcomes.
  • Treatment of perichondritis includes a foundation of anti-pseudomonal antibiotic therapy with or without surgical intervention.
  • Urgent specialist evaluation and hospital admission should be considered when abscess or necrosis are suspected or patient follow-up may be challenging.
  • Fluoroquinolone therapy appears safe in pediatric populations in the context of appropriate monitoring and follow-up.


  1. Caruso, Andria M., Macario Camacho Jr, and Scott Brietzke. “Recurrent auricular perichondritis in a child as the initial manifestation of insulin-dependent diabetes mellitus: A case report.” ENT: Ear, Nose & Throat Journal 93.2 (2014). (PMID: 24526489)
  2. Prasad, H. Kishore C., et al. “Perichondritis of the auricle and its management.” The Journal of Laryngology & Otology 121.6 (2007): 530-534. (PMID: 17319983)
  3. Noel, Stella Boustany, et al. “Treatment of Pseudomonas aeruginosa auricular perichondritis with oral ciprofloxacin.” The Journal of dermatologic surgery and oncology. 15.6 (1989): 633-637. (PMID: 2723226)
  4. Martin, A.J. Yonkers, C.T. Yarington. Perichondritis of the ear Laryngoscope, 86 (1976), pp. 664-673 (PMID: 933656)
  5. Liu, Z. W., and P. Chokkalingam. “Piercing associated perichondritis of the pinna: are we treating it correctly?.” The Journal of Laryngology & Otology 127.5 (2013): 505-508. (PMID 23442437)
  6. Levin, Roger J., David H. Henick, and Alan F. Cohen. “Human immunodeficiency virus-associated non-Hodgkin’s lymphoma presenting as an auricular perichondritis.” Otolaryngology–Head and Neck Surgery 112.3 (1995): 493-495. (PMID: 7870459)
  7. Wu, Douglas C., et al. “Pseudomonas skin infection.” American journal of clinical dermatology 12.3 (2011): 157-169. (PMID: 21469761)
  8. Prasad KC, Karthik S, Prasad SC. A comprehensive study on lesions
  9. of the pinna. Am J Otolaryngol 2005;26(1):1-6. (PMID: 15635573)
  10. Chun, Robert, and Opeyemi Daramola. “Clinical Anatomy for the Pediatrician.” Otolaryngology for the Pediatrician 1 (2013): 3.
  11. Kullar, Peter, and Philip D. Yates. “Infections and foreign bodies in ENT.” Surgery (Oxford) 30.11 (2012): 590-596. (PMID: 27057069)
  12. Rees, Chris A., Daniel M. Rubalcava, and Corrie E. Chumpitazi. “A child with a painful swollen ear.” Archives of disease in childhood 101.9 (2016): 859. (PMID: 27102760)
  13. Adefurin A, Sammons H, Jacqz-Aigrain E, Choonara I. Ciprofloxacin safety in paediatrics: a systematic review. Arch Dis Child 2011;96:874–80 (PMID: 27185119)
  14. Forsythe, Clinton T., and Michael E. Ernst. “Do fluoroquinolones commonly cause arthropathy in children?.” Canadian journal of emergency medicine 9.6 (2007): 459-462. (PMID: 18072993)

Post Peer Reviewed By: Salim Rezaie (Twitter: @srrezaie)

The post Perichondritis: Not Just Simple Cellulitis appeared first on R.E.B.E.L. EM - Emergency Medicine Blog.

Apneic Oxygenation (ApOx): A Review of the Evidence in Critical Care & Emergency Medicine

Background: Apneic oxygenation (ApOx) is the passive flow of oxygen into the alveoli during apnea.  This passive movement occurs due to the differential rate between alveolar oxygen absorption and carbon dioxide excretion producing a mass flow of gas from the upper respiratory tract into the lungs.  Another important component of this maneuver is maintaining a patent airway so that supplemental oxygen administered through the nares is able to be delivered to the alveoli.  This practice has been a game changer in emergency airway management for many providers.  However, there are still some naysayers that believe in the sickest patients ApOx may not be so beneficial. This post is a review of two recent systematic reviews/meta-analyses published in the critical care and ED/retrieval settings on the use of ApOx.

Review #1: Pavlov I et al [1]:

What They Did:

  • Systematic review and meta-analysis of studies using apneic oxygenation performed in critical care settings


  • Primary: Effect of apneic oxygenation on incidence of clinically significant hypoxemia during emergency endotracheal intubation
  • Secondary:
    • Incidence of Increasingly Severe Hypoxemia (SpO2 <90%, SpO2 <80%, SpO2<70%)
    • Incidence of Death of Any Cause During 28 Days Following endotracheal Intubation


  • Clinically Significant Hypoxemia: Any fall of SpO2 to a level at which any further drop will lead to a near-exponential drop in SpO2. Conventionally this has been defined as SpO2 <90%


  • Studies of ApOx performed in an adult critical care setting (i.e. emergency department, intensive care unit, prehospital emergency transport)


  • Studies that did not have control groups (Authors included observational studies to increase the power of their review. Observational studies don’t really have control groups .They have exposed and non-exposed groups.)


  • 9 studies (n = 1953) included in analysis
    • 4 RCTs
    • 5 Observational Trials
  • Pooled absolute risk of clinically significant hypoxemia (7 studies included):
    • Usual Care: 27.6%
    • ApOx: 19.1%
    • ApOx reduced the relative risk of hypoxemia by 30%
    • ApOx reduced the absolute risk of hypoxemia by 8.5%
  • Mortality (3 studies included)
    • Usual Care: 44.8%
    • ApOx: 34.8%
    • Relative Risk of Death 0.77 (95% CI 0.59 – 1.02) – Barely NOT Statistically Significant


  • Meta-analysis conformed with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and Meta-Analyses of Observational Studies in Epidemiology (MOOSE) guidelines
  • No disagreements between reviewers arose on which studies to include in the review
  • Risk of bias in randomized controlled trials was assessed with the Cochrane Collaboration Tool and the Risk of Bias Assessment tool for Non-Randomized Studies (RoBANS) for observational studies
  • Despite all 4 RCTs using median or mean lowest SpO2 during intubation as the main outcome, the authors of this paper used proportion of patients who experience hypoxemia during intubation
  • No heterogeneity between studies making conclusions more reliable


  • Strategy of ApOx (Standard Cannula vs High-Flow Nasal Cannula) and reported outcomes of studies differed
  • Paucity of studies evaluating the individual secondary outcomes
  • Standard care was contaminated with ventilation or some form of ApOx in three of the eight studies, hence diluting the benefit of ApOx


  • ApOx reduced the incidence of clinically significant hypoxemia by 30% during emergency intubation in critically ill patients which was consistent in all sub-group analyses studied
  • The reduction in mortality with the use of ApOx was not statistically significant and should be interpreted as preliminary and hypothesis generating
  • Potential mechanisms of why ApOx would reduce mortality:
    • Higher rate of successful intubation on first attempt, reduced risk of adverse events (i.e. critical desaturation, or aspiration due to repeated bag valve mask reoxygenation)
    • Hypoxemia demands reoxygenation attempts that may be accompanied by iatrogenic hyperventilation with resulting hypocapnia

Author Conclusion: “Apneic oxygenation significantly reduces the incidence of hypoxemia during emergency endotracheal intubation.  These findings support the inclusion of apneic oxygenation in everyday clinical practice.”

Review #2: Binks MJ et al [2]

What They Did:

  • Systematic review of six databases for all relevant studies on apneic oxygenation


  • Primary: Desaturation (SpO2 <93 – 95%) and Critical desaturation (SpO2 <80%)
  • Secondary: First pass success rate of intubation in the ED and during retrieval


  • Studies evaluating apneic oxygenation during intubation in the ED and during retrieval


  • Studies not using apneic oxygenation in the ED or retrieval setting


  • 6 Trials included (n = 1822)
    • Significant reduction in incidence of desaturation (SpO2 <93 – 95%)
      • RR = 0.76
      • p = 0.002
    • Significant reduction in incidence of critical desaturation (SpO2 <80%)
      • RR = 0.51
      • p = 0.01
    • Significant improvement in first pass intubation success rate
      • RR = 1.09
      • p = 0.004


  • All studies assessed for level of evidence and risk of bias
  • First systematic review and meta-analysis to investigate use of apneic oxygenation during intubation in the ED and retrieval settings


  • There was only one high quality RCT; All other studies included were low quality evidence (i.e. 3 low quality prospective comparative trials, 1 retrospective comparative trial and 1 retrospective observational trial)
  • Significant heterogeneity between studies
  • Study protocols differed in their methods of pre-oxygenation (i.e. some used positive pressure ventilation)
  • Lack of all-cause 30 day mortality analysis


  • In the second study, relative risk reduction was used, however many of us prefer absolute risk reduction. We went ahead and calculated this:
    • Desaturation: ARR 5.9% with a NNT = 16.8 to avoid one desaturation event
    • Critical Desaturation: ARR 11.9% with a NNT = 8.9 to avoid one critical desaturation event
    • First Pass Intubation: ARR 6.2% with a NNT = 16.1 to avoid not getting first pass intubation

Author Conclusion: “Apneic oxygenation may reduce patient hypoxemia during intubation performed in the ED and during retrieval.  It also improves intubation first-pass success rate in this setting.”


In patients with SHUNT PHYSIOLOGY (PNA, Pulmonary Edema), oxygenation will not help as much as PEEP, as this will help recruit atelectatic alveoli to over come the shunt.

There are several interventions that are possible to overcome this shunt physiology:

  • Intervention 1 (My Go To Intervention): ApOx + BVM + Peep Valve
  • If O2 Sat NOT >=95% change to BVM set at 15L + PEEP Valve set up to 10 – 15cmH20
  • For all causes of hypoxia NC 15LPM + BVM at 15LPM + PEEP Valve 15cmH20 = Best PreOx, ApOx, & ReOx Currently Available
  • Important Note: Don’t ventilate with this setup (Apneic CPAP Recruitment of atelectatic alveoli)

  • Intervention 2: Delayed Sequence Intubation
  • Weingart SD et al. Delayed Sequence Intubation: A Prospective Observational Study. Ann Emerg Med 2015; 65(4): 349 – 55. PMID: 25447559
  • Procedural Sedation with the procedure being preoxygenation
  • 1mg/kg IV ketamine –>PreOx –> Paralyze –> ApOx –> Intubate

Clinical Take Home Point:  Use of Apneic Oxygenation (ApOx)  in adult patients requiring emergency intubation, without shunt physiology, in critical care settings, the ED, and retrieval settings is a low cost, low complexity maneuver, and reduces the incidence of hypoxemia and increases first pass intubation rates based on limited studies. Further prospective, randomized trials would be ideal but, in the absence of better evidence, this intervention should be part of everyday clinical practice during emergency intubation, unless future high quality randomized controlled trials prove otherwise.


  1. Pavlov I et al. Apneic Oxygenation Reduces the Incidence of Hypoxemia During Emergency Intubation: A systematic Review and Meta-Analysis. Am J Emerg Med 2017; [Epub Ahead of Print] PMID: 28647137
  2. Binks MJ et al. Apneic Oxygenation During Intubation in the Emergency Department and During Retrieval: A Systematic Review and Meta-Analysis. Am J Emerg Med 2017; S0735 – 6757 (17): 30497. PMID: 28684195
  3. Oliveira L et al. Effectiveness of Apneic Oxygenation During Intubation: A systematic Review and Meta-Analysis. Ann Emerg Med 2017 [epub ahead of print]

For More on This Topic Checkout:

Post Peer Reviewed By: Anand Swaminathan (Twitter: @EMSwami)

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Occult Causes of Non-Response to Vasopressors

Intro: Vasoactive substances are powerful therapeutic medications that can boost a patient’s blood pressure and perfusion to target organs. They are often used in resuscitation to support tissue perfusion though their benefits are mostly unproven and may be harmful in certain circumstances (i.e. hypovolemia, hemorrhage). The cognitive response to hypotension should not be reaching for a pressor. The primary therapy for any sick hypotensive patient is treatment of the underlying pathology.

While many patients will respond to these medications, we occasionally encounter non-responder-patients who despite substantial doses do not show hemodynamic parameter improvements. Absence of response can result from a number of causes including misidentification of the underlying pathology (i.e. I missed the massive PE or pericardial tamponade thinking the patient was in septic shock). Premature diagnostic closure can lead us to simply push on with higher doses of pressors and adding additional pressors. However, there should be a cognitive pause at this point where the clinician reassesses the situation, considers alternate causes and therapeutics. Below is a list of pathologic conditions that complicate other diagnoses and are frequently missed as causes of non-response to vasopressors. This is the list I consider during my cognitive pause.


  1. Diagnostic: Blood gas, basic metabolic panel
  2. Therapeutic
    1. Reverse underlying cause if possible.
    2. Sodium bicarbonate is unlikely to be helpful thought it may be used as a drip as a bridge to continuous veno-venous hemodialysis (CVVHD)
    3. CVVHD may be an option


  1. Diagnostic
    1. Clinical diagnosis
    2. TSH with T3/T4 reflex
      1. Results often delayed
      2. May be false negative in acute decompensation
  2. Therapeutic: Levothyroxine (may need to give empirically if labs delayed)


  1. Can present as hypotension alone
  2. Diagnostic: History
  3. Therapeutic: Epinephrine, Methylene blue, ECMO (in refractory cases)

Adrenal Insufficiency/Failure

  1. Diagnostic
    1. Clinical
    2. Depressed cortisol level
    3. Hyperkalemia with hyponatremia
  2. Therapeutic
    1. Stress dose steroids (hydrocortisone 100-200 mg IV)
    2. Empiric treatment often necessary


  1. Diagnostic
    1. Ionized serum calcium (iCa2+)
    2. Prolonged QTc interval
  2. Therapeutic: Calcium salts (CaCl or CaGluconate)

Occult or Ongoing Blood Loss

  1. Occult Sources: GI Hemorrhage, Retroperitoneal bleed
  2. Therapeutic
    1. Operative or interventional control if source amenable
    2. Reverse anticoagulation if relevant,
    3. Transfuse to buy time to locate bleeding


  1. Occult causes: Beta blocker overdose, calcium channel blocker overdose, TCA overdose
  2. Therapeutic: Hyperinsulinemia Euglycemia Therapy (HIET), ECMO, bicarbonate (for TCA overdose)

Second Cause of Shock

  1. Patients can have multiple concurrent causes of shock (Hickum’s dictum)
  2. Make sure to search for a secondary cause of shock
  3. Rapid Ultrasound for Shock and Hypotension (RUSH) protocol extremely useful when considering multiple causes of shock


Thank you to Reuben Strayer (Twitter: @emupdates), Haney Mallemat (Twitter: @CriticalCareNow) and Salim Rezaie (Twitter: @srrezaie) for helping develop this post.

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