All posts by Sean M. Fox

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

transtracheal-ventilation-attachments

“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

  • This is THE MOST IMPORTANT PROCEDURE TO KNOW!
  • 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.

 

References

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]

Septic Arthritis

Originally published at Pediatric EM Morsels on August 28, 2015. Reposted with permission.

Follow Dr. Sean M. Fox on twitter @PedEMMorsels

We have discussed several entities that may lead to a child limping. We have covered osteomyelitis, plantar punctures, and toddler’s fractures.  We have also touched upon Osgood Schlatter’s Disease, SCFE, osteosarcoma and even Growing Pains. Now let us review a topic that always crosses our minds when considering the painful extremity: Septic Arthritis.

Septic Arthritis: Basics

  • Septic arthritis is an infection in the joint space and synovial fluid.
  • Can occur by hematogenous spread of bacteria or direct inoculation.
  • High Risk populations = children less than 2 years of age, immunocompromised, and patients without functional spleens
  • Complications:
    • Capsule damage
    • Chronic arthritis
    • Osteonecrosis
    • Growth Arrest
    • Sepsis

Septic Arthritis: Presentation

  • Fever
    • Although no/low fever noted in up to 20% of cases!
  • Joint pain, swelling, and erythema
    • Pain with passive range of motion!
    • Limps or refuses to bear weight on limb.
  • 80% of cases in children involve the lower limbs
    • Knee involved in 40% of cases
    • Hip involved in 20% of cases

Septic Arthritis: The Bugs

  • Staph aureus = most common organism across all ages
    • MRSA has become more prevalent [Young, 2011]
    • Group B Strep is 2nd most common
  • Special Population considerations:
    • Infants:
      • E. Coli
    • Young Children (<4 years)
      • Klingella kingae (notoriously difficult to culture)
      • Hemophilus influenza B has become less prevalent since HiB vaccination.
    • Immunocompromised:
      • Klingella kingae
      • Streptococcus pneumoniae (especially with HIV infection)
    • Sickle Cell Disease:
      • Salmonella (although, S. Aureus is still most common)
    • Sexually Active:
      • N. Gonorrhea – most common cause of polyarticular infections in sexually active patients

Septic Arthritis vs. Toxic Synovitis

  • Despite the name, toxic synovitis is the self-limited, benign inflammation of the joint that gets treated symptomatically.
  • Unfortunately, the presentation of toxic synovitis can be difficult to differentiate from septic arthritis, particularly when involving the hip joint.
    • Atraumatic 
    • Acute pain
    • Limp / refuses to bear weight
    • Fever
  • The treatment strategies and potential outcomes are quite different for the two conditions, so differentiating between them is critical… although challenging. (again, your job isn’t easy)

Septic Arthritis: Kocher’s Criteria

  • In 1999, Kocher et al published retrospective data from cases that presented to their facility from 1979-1996 due to “acutely irritable hip.”
  • Through a logistic regression analysis of 168 patients, they devised a probabilityalgorithm to help differentiate between septic arthritis and toxic synovitis.
  • There was no single lab test that was able to differentiate between the two entities. [Kocher, 1999]
  • Kocher’s Criteria: [Kocher, 1999]

    • Predictors associated with risk of Septic Arthritis
      • Fever
      • Non-weight-bearing
      • ESR = 40 or more
      • Serum WBC = 12,000 or more
    • Probability of Septic Arthritis based on number of Predictors
      • 0 Predictors – <0.2 %
      • 1 Predictor – 3.0%
      • 2 Predictors – 40.0%
      • 3 Predictors – 93.1%
      • 4 Predictors – 99.6%
  • Use this information wisely… not blindly.
    • May not apply to your patient.
      • Not hip pain?
      • Any underlying high-risk factors?
      • Clinical Decision Rules typically have diminished performance in different populations other than the derivation group. [Kocher, 2004]
    • Must balance the risk of false-positives vs false-negatives.
      • At what point does risk of missing septic arthritis outweigh the morbidity of joint aspiration? [Kocher, 1999].
        • 0 or 1 Predictors – close follow-up / observation
        • 2 Predictors – Aspiration via fluoroscopy/ultrasound
        • 3 or 4 Predictors – Aspiration in OR with likely arthrotomy and drainage.

Morals of the Morsel

  • Septic Arthritis needs to be higher on your differential than Toxic Synovitis.
  • Appreciate the diagnostic challenge inherent in the evaluation.
  • NO SINGLE TEST WILL DIAGNOSE OR RULE-OUT SEPTIC ARTHRITIS. [Dodwell, 2013]
  • Anticipate what tool (ex, Kocher Criteria) your consultants will likely use, but know their limitations.
  • 2 Predictors is more reassuring than 3, but still comes with increased risk.
    • Having Fever and being Non-Weight Bearing with normal labs can still be associated with Septic Arthritis!
  • Your pretest probability has to be taken into account, like always.
  • Don’t forget to give some analgesics!  
    • The child who is now weight-bearing after NSAIDs just became less concerning and it may be better to arrange close followed-up rather than ordering a bunch of non-specific lab tests.

References

Montgomery NI1, Rosenfeld S. Pediatric osteoarticular infection update. J Pediatr Orthop. 2015 Jan;35(1):74-81. PMID: 24978126. [PubMed] [Read by QxMD]

Dodwell ER1. Osteomyelitis and septic arthritis in children: current concepts. Curr Opin Pediatr. 2013 Feb;25(1):58-63. PMID: 23283291. [PubMed] [Read by QxMD]

Gill KG1. Pediatric hip: pearls and pitfalls. Semin Musculoskelet Radiol. 2013 Jul;17(3):328-38. PMID: 23787987. [PubMed] [Read by QxMD]

Young TP1, Maas L, Thorp AW, Brown L. Etiology of septic arthritis in children: an update for the new millennium. Am J Emerg Med. 2011 Oct;29(8):899-902. PMID:20674219. [PubMed] [Read by QxMD]

Yuan HC1, Wu KG, Chen CJ, Tang RB, Hwang BT. Characteristics and outcome of septic arthritis in children. J Microbiol Immunol Infect. 2006 Aug;39(4):342-7. PMID:16926982. [PubMed] [Read by QxMD]

Kocher MS1, Mandiga R, Zurakowski D, Barnewolt C, Kasser JR. Validation of a clinical prediction rule for the differentiation between septic arthritis and transient synovitis of the hip in children. J Bone Joint Surg Am. 2004 Aug;86-A(8):1629-35. PMID: 15292409.[PubMed] [Read by QxMD]

Mastoiditis

Originally published at Pediatric EM Morsels on October 12, 2015. Reposted with permission.

Follow Dr. Sean M. Fox on twitter @PedEMMorsels

Acute Mastoiditis – Conservative Management

2 Morsels ago (Yes you can mark the passage of time in “Morsels”) [HSP and Testicular Pain] we addressed some common themes of the Ped EM Morsels.  This week will highlight one of these themes again – Clinical Examination is more important in determining patient management than a collection of test results.

We all very comfortable with diagnosing and managing Acute Otitis Media (AOM). We are also aware of potential complications of AOM and the need to vigilantly search for patients at risk for complications (Cochlear Implants) and signs of complications (Gradeningo’s Syndrome).  But once you discover a complication what needs to be done?  Acute Mastoiditis is the most common complication of AOM – how do you diagnose it and how does the ENT physician manage it?

Incidence of Mastoiditis

  • Interestingly, there are numerous papers that have been published over the past decade looking at whether the incidence of Mastoiditis has been altered with the increased use of Watchful Waiting / Delayed Antibiotic Strategies.  There is conflicting data, but recently a true population study demonstrated that there has “not been a significant change in the incidence of acute mastoiditis in the pediatric population of the United States” (Pritchett, May 2012)
  • Internationally, this fact appears to be true also (Groth, 2011)
  • Kids 1 – 4 years of age have highest number of cases.

Diagnose Mastoiditis

It is a Clinical Diagnosis!

  •  AOM on otoscopy with
    • Inflammatory changes over the Mastoid Area (tenderness, erythema, edema, abscess)
    • Protruded Auricle

“But it means that there is extension of the infection and, therefore, we should get a CT to ensure that it is not extending into the brain! Plus the ENT doctor is going to ask what the CT shows before saying “hello”… so I might as well get the test.”

What does the ENT literature say?

  • Is CT necessary to diagnosis Acute Mastoiditis when it is clinically suspected?
    • Simple answer = NO
    • In rare cases of “masked mastoiditis,” where there is no evidence of AOM, a CT would be needed.
    • If you have AOM and postauricular edema or erythema than you have just made the diagnosis.
  • Is CT necessary to routinely rule out further complications of Mastoiditis?
    • Simple answer = NO
    • But your exam needs to be thorough.
  • When is a CT scan indicated?
    • When the patient has clinical signs of CNS involvement (ex. stupor, altered mental status).
    • When there is evidence of cranial nerve involvement (ie. Gradeningo’s Syndrome).
    • When there is a history of cholesteatoma.
  • Why does this limited approach to CT make sense?
    • There has been a change in practice making the management of Mastoiditis more conservative and less aggressive.
      • Parental Antibiotics combined with myringotomy and incision and drainage of subperiosteal abscess has proven to be as efficacious as traditional mastoidectomy.
      • The Conservative approach leads to no greater complication rates and yields earlier hospital discharge.
    • These kids are not going home… they will be in the hospital and observed. CT scans can be done later if:
      • Condition deteriorates.
      • Persistent high fevers after 48-72 hours of therapy.
      • Local progression of disease.

 

SO, IF YOU THINK THAT THE CHILD CLINICALLY HAS MASTOIDITIS AND HAS AN OTHERWISE NORMAL NEUROLOGIC EXAM, GIVE THE KID IV ANTBIOITCS, PAIN MEDICATIONS, AND CALL THE ENT PHYSICIAN.  DISCUSS HOW YOU ARE AWARE THAT THEIR OWN LITERATURE WOULD BE AGAINST THE UNNECESSARY IRRADIATION OF THE PATIENT AND… AWAIT COLLEGIAL CONVERSATION THAT WILL ENSUE.
 
Pritchett CV, Thorne MC. Incidence of Pediatric Acute Mastoiditis. Arch Otolaryngol Head Neck Surg. May 2012; 138(5): pp. 451-455.
Bakhos D, Trijolet JP, Morieniere S, Pondaven S, Al zahrani M, Lescanne E. Conservative Management of Acute Mastoiditis in Children. Arch Otolaryngol Head Neck Surg. Apr 2011; 137(4): pp. 346-350.
Groth A, Enoksson F, Hermansson A, Hultcrantz M, Stalfors J, Stenfeldt. Acute Mastoiditis in children in Sweden 1993-2007 – No increase after new guidelines. International Journal of Pediatric Otorhinolaryngology. Dec 2011; 75(12): pp. 1496-1501
Tamir S, Schwartz Y, Peleg U, Perez R, Sichel JY. Acute Mastoiditis in Children: Is Computer Tomography Always Necessary? Annals of Otology, Rhinology, and Laryngology. 2009; 118(8): pp. 565-569.

Seizure Mimics

Originally published at Pediatric EM Morsels on May 1, 2015. Reposted with permission.

Follow Dr. Sean M. Fox on twitter @PedEMMorsels

Screen Shot 2016-03-31 at 12.59.44 PM

Few things will frighten parents more than seeing their child appear to shake all over.  Fortunately, many times seizure activity is due to benign causes like simple febrile seizures.  Unfortunately, our job is quite difficult and we need to deal with other more troublesome entities like complex febrile seizures or neonatal seizures.  Of course we also need to consider entities that may provoke seizures, like hypoglycemiaAVMs, or pyridoxine deficiency.  While juggling all of the potential causes of seizures, we also need to pause and ask ourselves a simple question: was this even a seizure?  Perhaps we are dealing with a Seizure Mimic!

Seizure Numbers

  • Seizures are the most common pediatric neurologic emergency.
  • Seizures affect 4-10% of children during their lifetime.  (Hauser, 1994)
  • ~10% of new onset seizures present to the ED in status epileptics. (Singh, 2010)

 

Some Seizure Mimics

Since seizures are the most common neurologic emergency encountered in pediatric patients, it is reasonable to have it on the Ddx list of any child presenting with odd movements and/or behavior; however, there are also other significant conditions that should be considered in that situation! Here are some that could alter your initial management!

  • Arrhythmias
    • Long QT and torsades
    • VTach
    • Anytime there is poor cardiac output impairing cerebral perfusion, you can see motor activity / hypoxic convulsions.
  • Breath-Holding Spells
    • Actually not associated with inspiratory hold. The child typically screams/cries and exhales fully.
    • They can loose postural tone and have motor activity.
    • Up to 15% will have generalize hypoxic convulsions. (DiMario, 2001)
  • Syncope
    • Commonly encountered in teenagers
    • May have eye-rolling, incontinence, and motor twitching.
    • There are many causes of syncope (don’t forget the pregnancy test!) to consider… like Hair Grooming Syncope.
  • Sandifer Syndrome
    • Gastroesophageal reflux may cause generalized stiffness or posturing.
    • Can have apnea also.
    • Often occurs 20-30 min after a meal.
  • Dystonic Reactions
    • Always look at the medication list!!
  • Migraine Syndromes
    • Basilar Migraine
    • Familial Hemiplegic Migraine
  • Sleep-Related Phenomena
    • Benign sleep myoclonus
    • Periodic sleep jerks
    • Narcolepsy

 

Moral of the Morsel:

“NOT ALL THAT SHAKES IS A SEIZURE!

 

References

Luat AF, Kamat D, Sivaswamy L. Paroxysmal nonepileptic events in infancy, childhood, and adolescence. Pediatr Ann. 2015 Feb 1;44(2):e18-23. PMID: 25658214[PubMed] [Read by QxMD]

Agarwal M1, Fox SM. Pediatric seizures. Emerg Med Clin North Am. 2013 Aug;31(3):733-54. PMID: 23915601[PubMed] [Read by QxMD]

Singh RK1, Stephens S, Berl MM, Chang T, Brown K, Vezina LG, Gaillard WD. Prospective study of new-onset seizures presenting as status epilepticus in childhood. Neurology. 2010 Feb 23;74(8):636-42. PMID: 20089940[PubMed] [Read by QxMD]

DiMario FJ Jr1. Paroxysmal nonepileptic events of childhood. Semin Pediatr Neurol. 2006 Dec;13(4):208-21. PMID: 17178351[PubMed] [Read by QxMD]

Ovarian Torsion

Originally published at Pediatric EM Morsels on January 24, 2015. Reposted with permission.

Follow Dr. Sean M. Fox on twitter @PedEMMorsels

Torsion

We all know that abdominal pain is a common complaint that in the ED.  The differential is vast and includes some terrible conditions (ex, Intussusception,Necrotizing Enterocolitis, Malrotation) as well as rather common conditions (ex,Constipation).  Naturally, we have all been taught to think “outside the box” and know to consider conditions outside the abdominal cavity (ex, Pneumonia, Testicular Torsion). When we are thinking outside of the box, make sure we keep Ovarian Torsion on our DDx list for the young girls.

Ovarian Torsion Basics

  • It is rare (Estimated at ~4.9 cases per 100,000).
  • Caused by the ovary rotating around its supportive ligaments.
  • Leads to occlusion of the lymphatics and vascular structures.
  • Most commonly occurs on the right side (great, another appendicitis mimic).
  • 58% of the time the ovary has no obvious pathology as the cause of the torsion.
  • Risk of torsion is related to size of mass or cyst if known; 4-5cm is significant.

Ovarian Anatomy Matters

  • The ovary receives blood from two sources – the ovarian and uterine arteries.
  • As the ovary twists, it will first compromise lymphatic drainage, leading to swelling.
  • This can then compromise venous flow, worsening engorgement.
  • Since there are two arterial supplies, even with significant and prolonged torsion,there still may be arterial flow.
    • This is important to remember when considering the ultrasound results!

Ovarian Torsion in Kids

  • Children account for only 15% of all of the cases of Ovarian Torsion.
  • Has been described in all age groups.
    • < 1 year of age – 16% of cases
    • 1 – 8 years of age – 18% of cases
    • 9 – 14 years of age – 52% of cases
    • 15 – 19 years of age – 14 % of cases
  • Younger children often reported has being more likely to have neoplasm, but actually most likely to have normal ovaries.
  • Infants may have been diagnosed in utero with ovarian cysts by ultrasound.  Ask about this when evaluating abdominal pain.

Ovarian Torsion Presentation

  • Classically, presents with sudden onset of severe, unilateral pain that is constant.
  • Unfortunately, the pain can be intermittent for spontaneous torsion and detorsion.
  • Vomiting that occurs with pain is concerning for it (60% of patients have been documented with this).
  • Younger children, obviously, are more difficult to diagnose.
  • Ovarian Torsion has many mimics and is, therefore, often missed at first.
  • Appendicitis and Ovarian Torsion overlap in presentation and are difficult to distinguish on exam.
    • One study found Ovarian Torsion cases had a lower WBC, CRP, and Alvarado Score.
    • While I am not a huge advocate for these tests for appendicitis, they may be helpful when considering other entities.
    • Or, if your evaluation for appendicitis is negative, you can also make yourselfreconsider Ovarian Torsion.
  • Duration of symptoms

    • Prolonged symptoms do not predict poor outcome.
      • Salvage rates are equal to oophorectomy rates despite prolonged times.
    • Do not diminish your concern because it has been 48 or even 72 hours.
      • The initial diagnosis is difficult to make and may have been missed.
      • The ovary still may be salvageable.

The Ultrasound!

  • This is the diagnostic study of choice currently, but it has limitations!
  • In prepubescent and nonsexually active females, transabdominal U/S is useful.
    • A full bladder can help with the image quality.
  • Transvaginal U/S is preferred for older, sexually active females.
  • Because the Ovary has two blood supplies, the U/S may show normal arterial flow.
    • 2/3 of patients with ovarian torsion have had normal blood flow.
  • Most common finding is an enlarged ovary or adnexal mass.
  • The ovary can also show multiple cortical follicles.
  • Rarely is the “whirlpool sign” seen – twisted vessels in the ovarian pedicle.
  • The U/S is often abnormal with enlargement or obvious cyst(s); however, DO NOT rely on arterial blood flow.

Moral of the Morsel:

Ovarian Torsion is another entity that requires us to be vigilant and reconsider our DDx.  Do not allow diagnostic momentum obscure the possibility of the ovary being the primary issue.  Also, if your history and your exam make you concerned for it, do not allow “normal doppler blood flow” to remove ovarian torsion from your differential.

References

Schmitt ER, Ngai SS, Gausche-Hill M, Renslo R. Twist and shout! Pediatric ovarian torsion clinical update and case discussion. Pediatr Emerg Care. 2013 Apr;29(4):518-23; quiz 524-6. PMID: 23558274. [PubMed] [Read by QxMD]

Delgado A, Sobolewski B, Kurowski EM. A tale of 2 torsions: ovarian torsion in infants and toddlers. Pediatr Emerg Care. 2013 Mar;29(3):374-6. PMID: 23462396. [PubMed][Read by QxMD]

ECMO in the Ped ED

Originally published at Pediatric EM Morsels on November 13, 2015. Reposted with permission.

Follow Dr. Sean M. Fox on twitter @PedEMMorsels

ECMO

Remaining vigilant for the child with a subtle presentation of a severe illness is part of our job in the Ped ED; however, sometimes, the illness is not subtle and the child requires critical actions (ex, Damage Control Resuscitation, Mechanical Ventilation,Optimize Chest Compressions)  .  Often, it is best to consider these critical actions prior to needing to do them so there is no delay. One such, potentially life-saving, critical action is Extracorporeal Membrane Oxygenation (ECMO).  Recently there was a nice review of Pediatric ECMO [Gehrmann, 2015] that deserves further contemplation. Below are some highlights from that article:

ECMO: Basics

  • ECMO utilizes an external circuit to oxygenate blood and remove carbon dioxide.
  • It has been successfully used in the NICU for respiratory failure since 1970’s.
  • ECMO is not a therapy to correct a medical condition; it is used to support a patient while definitive strategies are able to correct the problem, or “time heals the wounds.”
  • ECMO essentially buys a patient some time.
  • Used for patients who have reversible cardiac or respiratory failure.
    • In the NICU that includes:
      • Meconium aspiration
      • Persistent fetal circulation
      • Congenital diaphragmatic hernia
      • Pulmonary hypertension of the newborn
  • Basic circuit has:
    • Vascular cannulas for access – one to extract blood and one to replace it.
    • Pump and Tubing
    • Gas-exchanger – to add the oxygen and extract the carbon dioxide.
    • Heat exchanger – to ensure that the blood returns to the patient at safe temperature.

ECMO: VA vs VV

  • The circuit can be completed through two modes: Venoarterial (VA) orVenovenous (VV).
  • Venoarterial
    • Accesses major vein (ex, IJ, Femoral Vein) and major artery (ex, Carotid)
    • Able to provide circulatory support as well as oxygenation.
    • Can be used for patients with primary heart failure.
  • Venovenous
    • Access two major veins (ex, IJ, Femoral Vein) or uses a double-lumen catheter to access one major vein (ex, IJ).
      • Advantage over VA is the lack of needing to access and repair major artery.
      • Less risk for ischemic injury or thromboembolic complications.
    • Provides oxygenation, but because oxygenated blood returns to venous side, the oxygenation level will be lower compared to VA.
    • Does not provide circulatory support and cannot be used for heart failure.
    • Well suited for reversible acute respiratory failure.

ECMO: in the Ped ED

  • ECMO is the last option when standard management has failed and:
    • the condition causing cardiopulmonary failure is reversible or
    • the organ transplantation is an option.
  • While it is the last option, considering it at the last minute will not help, as it requires time to coordinate with the teams and time to gain access and set up the system.
  • Common conditions ECMO is used for:
    • Newborns and infants:
    • Children and Adolescents
      • Pneumonia
      • Status asthmaticus
      • ARDS
      • Submersion injury
      • Acute chest syndrome
      • Traumatic pulmonary contusion
      • Myocarditis
      • Intractable dysrhythmias
      • Beta blocker / calcium channel blocker poisoning
      • Hypothermia – as a means to rewarm
      • Cardiac arrest
        • E-CPR (Extracorporeal Cardiopulmonary Resuscitation)
          • ECMO as a rescue therapy for cardiac arrest.
          • American Heart Association lists it as an option for In-Hospital Cardiac Arrest if condition is thought to be reversible or amenable to heart transplantation.
          • Effectiveness is higher when started within 30 min after cardiac arrest. [Tajik, 2008]
          • Proper patient selection is important, although there are no clear guidelines.

Moral of the Morsel

  • ECMO is not commonly needed in the ED, but on the rare occasion that it will be helpful, the means to initiate it need to already been known, as time is critical.
  • Having a protocol in place (hopefully, never to be needed) to help with patient selection and streamline the activation of the “ECMO Team” may literally save a child’s life.

References

Gehrmann LP1, Hafner JW2, Montgomery DL3, Buckley KW4, Fortuna RS5. Pediatric Extracorporeal Membrane Oxygenation: An Introduction for Emergency Medicine Physicians. J Emerg Med. 2015 Oct;49(4):552-60. PMID: 25980372. [PubMed] [Read by QxMD]

Tajik M1, Cardarelli MG. Extracorporeal membrane oxygenation after cardiac arrest in children: what do we know? Eur J Cardiothorac Surg. 2008 Mar;33(3):409-17. PMID:18206379. [PubMed] [Read by QxMD]

Posner JC1, Osterhoudt KC, Mollen CJ, Jacobstein CR, Nicolson SC, Gaynor JW.Extracorporeal membrane oxygenation as a resuscitative measure in the pediatric emergency department. Pediatr Emerg Care. 2000 Dec;16(6):413-5. PMID: 11138884.[PubMed] [Read by QxMD]

Pediatric Rash

Originally published at Pediatric EM Morsels on October 16, 2015. Reposted with permission.

Follow Dr. Sean M. Fox on twitter @PedEMMorsels

Erythema-Multiforme

“Rash” seems to be a ubiquitous complaint some days in the Ped ED.  Knowing that the skin is the largest organ, it seems only appropriate that we should take these complaints seriously. Unfortunately, often I feel a little inadequate when trying to decipher the code of the Pediatric Rash.  Below is a simple approach I use to help ensure I don’t over-diagnose viral exanthem.

Pediatric Rash Step 1: Sick or Not Sick

  • This speaks for itself.
  • Sick? 
    • Treat aggressively!
    • The skin findings may help clue you in to the source of the sickness, but don’t let pontification of the unusual rash delay your rapid administration of necessary care!
  • Not Sick?
    • Don’t be cavalier, just yet!
    • Not appearing sick is reassuring, but kids can be deceptive!
    • Remain vigilant and move to Step 2.

Pediatric Rash Step 2: Evidence of Badness?

  • Naturally, our default is always to be concerned for badness and, thus, we need tolook for evidence of serious, systemic illness first.
  • Finding any of the following characteristics does not necessarily define “badness” as being present, but it should make you think more carefully of that possibility.
  • Actively look for:
    • Petechiae
      • Is this ITP?
      • Are these petechiae associated with coughing/vomiting and above the nipple line or are they below the nipple line and concerning forMeningococcemia?
    • Purpura
      • Does this fit the “illness script” of HSP?
      • Platelet disorders? TTP?
      • DIC?
      • Unfortunately, must also consider Abuse.
    • Vesicles
      • HSV
      • Chickenpox (yes, it is still around)
    • Bullae
      • Burns to Bullous Impetigo. Lots to consider.
    • Target Lesions
      • Erythema Multiforme?
      • Spectrum of Stevens Johnson Syndrome / Toxic Epidermal Necrolysis?
      • Erythema Marginatum concerning for Rheumatic Fever?
    • Urticaria
    • Desquamation
  • If none of these characteristics exist, move to Step 3.

Pediatric Rash Step 3: Look at the Mucous Membranes Again!

  • Let’s be honest, looking in a kid’s mouth can be challenging, but this step is very important!
    • For instance, ITP with Wet Purpura (mucous membrane involvement) may be a clue to greater risk of spontaneous bleeding.
    • Certainly, finding Koplick’s Spots would alter your plans.
    • Even finding herpangina or gingivostomatits may impact your plan!
  • While wiping the sweat off of your brow and allowing the parent’s muscle fatigue to resolve, move onward to step 4.

Pediatric Rash Step 4: Look for “Common Pediatric Rashes”

  • If Steps 1-4 have not lead to a diagnosis or a high level of concern, then move onward to step 5.

Pediatric Rash Step 5: Admit You Aren’t Sure

  • This is the hardest part… admitting to the family that you are not sure what the cause of the rash is can be challenging.
  • We are not admitting defeat… we are appropriately avoiding the addition of an incorrect “label” (diagnosis) to the patient.
    • Announce your reassurance in the lack of the concerning characteristics…
    • Acknowledge that rashes often evolve over time…
      • In the next several hours to days, your ability to make a more accurate diagnosis may change.
      • Give good anticipatory guidance on what specific things they need to monitor for and encourage repeat evaluation in the next 12-24 hours.

References

Pediatric Chest Pain

Originally published at Pediatric EM Morsels on May 15, 2015. Reposted with permission.

Follow Dr. Sean M. Fox on twitter @PedEMMorsels

Chest-Pain-2

Children like to pretend to be grown-ups.  Unfortunately, sometimes they develop grown-up problems (Cholelithiasis, Kidney Stones, and Hypertension).  Additionally, often kids will complain of symptoms that warrant great concern in adults, but often engender apathy when considered in children. Chest Pain is a great example of one of these complaints.

Chest Pain: Hysteria vs Vigilance

  • The odds are in favor of being reasonable
    • Only ~1-6% of chest pain in children is due to a cardiac cause
    • GI cause – 2-11% of chest pain
    • Musculoskeletal – 2-11% of chest pain
    • No Identifiable cause – 21-45% of the time!
  • Yet, our job requires vigilance for find the rare dangers!

Culprits to Consider

Chest Pain: Evaluation

  • The goal is to balance risk of the rare with risk of over-testing.
  • Reasonable screen for cardiac etiology [Kane, 2010]:
    • Chest Pain with Exertion?
    • High-risk family history (ex, unexplained sudden death)?
    • Abnormal exam (ex, murmurs, hepatomegaly)?
    • Abnormal ECG
  • Reasonable screen for pulmonary etiology:
    • CXR
      • Obviously useful… but perhaps leads to unnecessary imaging.
    • If pneumothorax is your primary concern, consider the Bedside Ultrasound
      • There are plenty of studies  that demonstrate that U/S is more sensitive than supine CXR in the setting of adult trauma.
        • U/S – ~90% sensitive
        • Supine CXR – ~50% sensitive
        • Erect CXR has increased sensitivity (~90%), naturally.
      • U/S is naturally operator dependent… and in this case the operator is you… so are you dependable?

Moral of the Morsel

  • For the young patient presenting with chest pain, be vigilant, but be reasonable.
  • Screen for badness with:
    • Thorough history and directed physical exam
    • ECG
    • Ultrasound and/or CXR.

References

Angoff GH1, Kane DA, Giddins N, Paris YM, Moran AM, Tantengco V, Rotondo KM, Arnold L, Toro-Salazar OH, Gauthier NS, Kanevsky E, Renaud A, Geggel RL, Brown DW, Fulton DR. Regional implementation of a pediatric cardiology chest pain guideline using SCAMPs methodology. Pediatrics. 2013 Oct;132(4):e1010-7. PMID: 24019419.[PubMed] [Read by QxMD]

Friedman KG1, Kane DA, Rathod RH, Renaud A, Farias M, Geggel R, Fulton DR, Lock JE, Saleeb SF. Management of pediatric chest pain using a standardized assessment and management plan. Pediatrics. 2011 Aug;128(2):239-45. PMID: 21746719. [PubMed][Read by QxMD]

Kane DA1, Fulton DR, Saleeb S, Zhou J, Lock JE, Geggel RL. Needles in hay: chest pain as the presenting symptom in children with serious underlying cardiac pathology.Congenit Heart Dis. 2010 Jul-Aug;5(4):366-73. PMID: 20653703. [PubMed] [Read by QxMD]

Son MB1, Sundel RP. Musculoskeletal causes of pediatric chest pain. Pediatr Clin North Am. 2010 Dec;57(6):1385-95. PMID: 21111123. [PubMed] [Read by QxMD]

Selbst SM1. Approach to the child with chest pain. Pediatr Clin North Am. 2010 Dec;57(6):1221-34. PMID: 21111115. [PubMed] [Read by QxMD]

Lichtenstein DA1, Mezière G, Lascols N, Biderman P, Courret JP, Gepner A, Goldstein I, Tenoudji-Cohen M. Ultrasound diagnosis of occult pneumothorax. Crit Care Med. 2005 Jun;33(6):1231-8. PMID: 15942336. [PubMed] [Read by QxMD]