• First steps:
  • Place on capnography
  • Continuous albuterol nebulizer
    • 10 mg/hr for 5-10kg
    • 15 mg/hr for 10-20kg
    • 20 mg/hr for >20kg 
    • Max dose 30 mg/kg
  • Consider a DuoNeb (ipratropium/albuterol)
    • 1.5 mg inhaled over the first hour of therapy
    • Followed by 0.5 mg may be nebulized Q4-6 hours. 
    • 2-3 doses are recommended
  • Get IV access
  • IV Steroids 
    • Methylprednisolone
    • Dexamethasone
  • IV Magnesium sulfate 
    • Dosing 25-75 mg/kg
    • Max dose 2g 
  • IVF
    • Lots of losses with tachypnea 
    • Want to pump up that preload incase things go south 
  • Call RT
• Briefly consider other diagnoses:
  • Heart Failure
  • Anaphylaxis
  • Aspiration
  • Tracheal stenosis
  • Inhaled foreign body
  • PE
  • Hyperventilation syndrome
  • Pneumothorax
  • Vocal cord dysfunction

• Magnesium 
  • Multicenter retrospective cohort study analyzed clinical data from 7 EDs from 2012 to 2017. We described use of IV Mg in children aged 2-17 years treated for acute asthma and its effect on blood pressure
    • ~6,500 kids received IV Mg-–about 10.5% of the total visits 
    • Average time to administration was 154 minutes 
    • 11.1% of patients were able to be discharged home after administration
    • 6.8% became hypotensive
  • Intravenous and Nebulized Magnesium Sulfate for Treating Acute Asthma in Children: A Systematic Review and Meta-Analysis
    • PubMed, Cochrane Library, and EMBASE databases 
    • Ten randomized and quasi-randomized trials (6 IV, 4 nebulized) were identified.
    • IV Mg sulfate treatment is associated with significant improvement in pulmonary function (standardized mean difference, 1.94; 95% CI, 0.80-3.08; P = 0.0008) and hospital admission (RR, 0.55; 95% CI, 0.31-0.95; P = 0.03). 
    • Nebulized Mg sulfate treatment shows no significant effect on respiratory function or hospital admission 
  • High-Dose Magnesium Sulfate Infusion for Severe Asthma in the Emergency Department Efficacy Study
    • All patients of 6–16 years old who failed to improve after 2 hours of standard therapy for asthma.
    • Patients either received a high-dose prolonged infusion or a bolus infusion
    • 50 mg/kg over 1 hour (bolus) 
    • Prolonged magnesium sulfate infusion of 50 mg/kg/hr for 4 hours 
    • Asthma severity was assessed via asthma scores and peak expiratory flow rates at 0-2-6 hours. 
    • Primary outcome was discharge to home at 24 hours.
    • 38 total patients; 19 in each group
    • There was a significant difference in the patients discharged at 24 hours: 47% in high-dose prolonged magnesium sulfate infusion (9/19) versus 10% (2/21) in the bolus group 
  • IV magnesium sulfate in the treatment of acute severe asthma: a multicenter randomized controlled trial
    • Primary efficacy end point was FEV1 at 240 min, & the data analysis was intent to treat.
    • final FEV1 was 51.1% predicted in the magnesium-treated group and 53.9% predicted in the placebo-treated group (mean difference, - 2.9%, 95% CI, - 9.4 to 3.7; p = not significant). Overall, the use of magnesium sulfate did not improve hospital admission rates.
    • Administration of 2 g of IV magnesium sulfate improves pulmonary function when used as an adjunct to standard therapy in patients with very severe, acute asthma.
  • Magnesium sulphate in acute severe asthma in children (MAGNETIC): a randomised, placebo-controlled trial
    • Randomized placebo-controlled, multi-center, parallel trial in the UK
    • Enrolled kids (2–16 years) with severe acute asthma who did not respond to standard inhaled treatment 
    • nebulised albuterol and ipratropium bromide with either :
      • 2·5 mL of isotonic MgSO 4 
      • 2·5 mL of isotonic saline (placebo group) 
    • An asthma severity score was measured on three occasions at 20-min intervals. 
    • Nebulized isotonic MgSO did not show a clinically significant improvement in mean ASS in children with acute severe asthma. 
    • However, the greatest clinical response was seen in children with more severe attacks (SaO 2<92%) at presentation and those with preceding symptoms lasting less than 6 h.
• Ipratropium 
  • DuoNeb dosing:
    • 1.5 mg inhaled over the first hour of therapy
    • Followed by 0.5 mg may be nebulized Q4-6 hours. 
    • 2-3 doses are recommended
  • Efficacy and safety of ipratropium bromide/albuterol compared with albuterol in patients with moderate-to-severe asthma: a randomized controlled trial
    • Looked at differences with use of each as “as needed” controller medications
    • 226 patients, ≥18 years old, with inadequately controlled, moderate-to-severe asthma were randomized
    • Found significant improvement in the ipratropium bromide/albuterol group after 4 weeks
  • The Use of Ipratropium Bromide for the Management of Acute Asthma Exacerbation in Adults and Children: A Systematic Review
    • Dr. S. Aaron , M.Sc., M.D., F.R.C.P.C. &Shawn D. Aaron , M.Sc., M.D., F.R.C.P.C.
    • There is a modest statistical improvement in airflow obstruction when ipratropium is used as an adjunctive to beta2-agonists for the treatment of acute asthma exacerbation. In pediatric asthma exacerbation, use of ipratropium also appears to improve clinical outcomes
  • Randomized Trial of the Addition of Ipratropium Bromide to Albuterol and Corticosteroid Therapy in Children Hospitalized Because of an Acute Asthma Exacerbation Norma Goggin, MD, MRCP; Colin Macarthur, MB, ChB, PhD; Patricia C. Parkin, MD, FRCPC
    • The addition of 2 to 3 doses of inhaled ipratropium bromide to β2-agonist therapy in the emergency department treatment of children with severe asthma improves lung function and reduces the hospital admission rate. The role of ipratropium bromide in the treatment of children hospitalized following emergency department treatment has not been well studied
• Capnography
  • Normal range is 35 - 45 mmHg
  • Will be diminished in severe asthmatics as they are not moving air
  • In asthmatics the wave form changes from the typical box-shape we’re used to to more of a shark fin or wave shape
  • This up slope represents changes in Phase II 
    • Phase II: the expiratory upstroke, a sharp incline in which CO2 levels increase dramatically 
  • https://www.acepnow.com/article/how-to-use-end-tidal-capnography-to-monitor-asthmatic-patients/
    • Each portion of the lung is associated with its own ventilation-perfusion ratio (V:Q) that subsequently determines its respective PaCO2. 
    • During expiration in an asthma exacerbation, the areas of the lung with less bronchoconstriction have a lower PaCO2 and will preferentially be expired first. 
    • The regions of the lung with a greater degree of obstruction will have a higher PaCO2 and will have delayed emptying. 
    • The desynchronization of alveolar emptying causes changes within the capnogram waveform; the slope of Phase II decreases, the slope of Phase III increases as the more highly obstructed alveoli expire their retained CO2 in a delayed fashion, and these changes in the slope result in an increased α angle

• Recheck:
  • Next steps:
    • Continue continuous nebs
    • Subcutaneous terbutaline 
  • Systemic beta 2 agonist 
    • 10 mcg/kg IV loading dose over 10 minutes
    • 0.5 mcg/kg/min
    • Can increase dose q30 min to max dose of 10 mcg/kg/min
    • Can cause elevations in troponin
  • If there hasn’t been improving, consider IM epinephrine instead
    • Same as anaphylaxis dose 
    • 0.01 mg/kg of 1mg/ml (1:1000) IM for peds‐ Max dose 0.5 mg
    • 0.3-0.5 for adults 
• Aminophylline
  • Drug combination of theophylline and ethylenediamine
  • Used for reversible airway obstructions but also thigh cellulite cream….
  • Phosphodiesterase Inhibitor, Adenosine receptor antagonist, &  Histone deacetylase activator
  • Dosing:
    • 6 mg/kg loading dose
    • 0.5-1 mg/kg/hr
  • Recommended starting dose
    • 1-9 years: 1 mg/kg/hr
    • 10-16 years old: 0.8 mg/kg/hr 
  • Narrow therapeutic index and is associated with a wide range of adverse effects
  • Does an aminophylline injection in addition to bronchodilators for an asthma attack improve lung function and other outcomes or cause harm?
  • 2012 Cochrane Review - aminophylline is not significantly better than other bronchodilator drugs, and has more adverse effects. 
• Heliox
  • Lack of Benefit of Heliox During Mechanical Ventilation of Subjects With Severe Air-Flow Obstruction
    • Ann Allergy Asthma Immunol. 2014 
    • Respiratory Care, 2018
    • In mechanically ventilated subjects with severe air-flow obstruction, administration of heliox had no effect on indices of dynamic hyperinflation (plateau pressure and total PEEP) and resulted in only a small reduction in PaCO2
  • Heliox-driven β2-agonists nebulization for children and adults with acute asthma: a systematic review with meta-analysis
    • Eleven trials from 10 studies 
    • Heliox presented a statistically significant difference for mean percentage of change in peak expiratory flow (17.2%; 95% confidence interval 5.2-29.2, P = .005). 
    • Post hoc subgroup analysis showed that patients with severe and very severe asthma showed a significant improvement in peak expiratory flow compared with those with mild to moderate acute asthma. 
    • Heliox-driven nebulization also produced significant decreases in the risk of hospitalizations (odds ratio 0.49, 95% confidence interval 0.31-0.79, P = .003) 
    • Severity of exacerbations (pediatric studies; standard mean difference -0.74, 95%% confidence interval -1.45 to -0.03, P = .04)
  • Heliox for nonintubated acute asthma patients
    • Cochrane review 2016
    • Pooling of the eight trials showed no significant group differences 
    • There was significant heterogeneity among the studies. 
    • Heliox use did improve pulmonary function only in the subgroup of patients with the most severe baseline pulmonary function impairment; however, this conclusion is based on a small number of studies. 
    • There were no significant differences between groups when adults versus children or high versus low heliox dose 
    • At the end of treatment, participants treated with heliox showed no significant different risk of admission to hospital (RR 0.83, 95%CI 0.66-1.08, P = 0.17, I(2) = 0%)

• Noninvasive Ventilation
  • Decreases WOB -> larger tidal volumes
  • The MoA of NIV in status asthmaticus seems to be based on its bronchodilator effect, which induces alveolar recruitment.
  • PEEP through NIV helps overcome the patient’s intrinsic PEEP resulting in bronchodilation
    • Bronchodilation -> increased airflow -> re-expansion of areas previously collapsed with atelectasis -> improvement of V/Q mismatch -> decreased work of breathing
  • IPAP can help unload some of the work of accessory inspiratory muscles and increase tidal volumes 
    • May improve distribution of aerosolized meds into the deep portions of airway 
  • Goal is to use BiPAP to stave off intubation but if it doesn’t work change the patient’s course it still provides an excellent way to preoxygenate
  • Remember: : PEEP and FiO2 will help your oxygenation, while pressure support will help you ventilate.
  • Settings to Maximize Inspiratory Support
    • Inspiratory pressure start around 7-8 but can increase slowly up to 15
    • PEEP 3-5 cmH2O which is low, only enough to match patient's auto-PEEP
    • IPAP = EPAP or PEEP + Pressure Support
    • IPAP > 20-25 is enough pressure to over come the lower esophageal sphincter  gastric insufflation -> vomiting 
  • High inspiratory flow rate 
  • Low I:E ratio (eg 1:5) and prolonged expiratory phase
  • Once you’ve placed the patient on BiPAP and allowed them to chill out they should be pulling reasonably large TVs around 5cc/kg of ideal body weight
    • If the TV is low they may not be ventilating 
  • If the patient cannot tolerate BiPAP you can always put them on HFNC while they are getting continuous nebs to help reduce dead space 
  • Several studies have shown NIV can be safe and effective in pediatric patients with severe asthma
    • There is one study showing increased PICU admissions in moderate asthmatics who were treated with BiPAP
    • Small sample size
    • Could not distinguish if admissions were secondary to worsening condition (eg BiPAP led to air stacking) or because of treatment momentum (floors don’t take kids on BiPAP and may be nervous to take a kid who was even treated with BiPAP while in the ED) 
  • Noninvasive ventilation in status asthmaticus in children: levels of evidence 
    • Rev Bras Ter Intensiva. 2015 Oct-Dec; 27(4): 390–396. doi: 10.5935/0103-507X.20150065
    • Search, selection and analysis were conducted for all original articles on asthma and NIV in children (up to 18 years old) published until September 1, 2014 
    • Serval observational studies and two non-blinded randomized control trials 
    • The results suggest that noninvasive ventilation is applicable for the treatment of status asthmaticus in most pediatric patients unresponsive to standard treatment. However, the available evidence cannot be considered as conclusive, as further high-quality research is likely to have impacts on and change the estimates of effects.
  • Clinical Outcomes After Bilevel Positive Airway Pressure Treatment for Acute Asthma Exacerbations
    • Christopher Golden, BS, MS, OTD1; Meng Xu, MPH2; Cristina M. Estrada, MD3; et alDonald H. Arnold, MD, MPH3 JAMA Pediatr. 2015;169(2):186-188. doi:10.1001/jamapediatrics.2014.2767
    • 933 children and adolescents aged 5 to 17 years who were admitted to the Vanderbuilt pediatric emergency department with acute asthma exacerbations.
    • Primary predictor variable was BiPAP treatment (yes or no) among participants who did not have signs of respiratory failure.
    • Outcomes included hospital admission, admission to the pediatric intensive care unit (PICU), hospital length of stay, and time to spacing of albuterol inhalation to every 4 hours (hereinafter referred to as time to albuterol Q4h) (a metric of exacerbation resolution) based on severity scoring by respiratory therapists.
    • The results indicate that BiPAP treatment of children and adolescents with acute asthma exacerbations who have no signs of impending respiratory failure is associated with a greater likelihood of hospital and PICU admission and no apparent benefit in decreased length of stay or time to albuterol Q4h. 
    • The study is limited because it cannot resolve whether these findings are a consequence of clinical momentum after positive pressure ventilation or of increased air trapping and ventilation-perfusion mismatch, derangements that worsen an exacerbation
  • Bilevel Positive Airway Pressure ventilation efficiently improves respiratory distress in initial hours treating children with severe asthma exacerbation
    • Chun-Min Kang 1, En-Ting Wu 1, Ching-Chia Wang 1, Frank Lu 1, Bor-Luen Chiang 2, Ting-An Yen 3PMID: 31806384 DOI: 10.1016/j.jfma.2019.11.013
      
    • We included data of 46 admissions from 33 different patients (24 with BiPAP and 21 without BiPAP.) The BiPAP group had significantly higher initial RR as well as higher severity scores compared with the other group (p < 0.001). The RR improved significantly in the following time intervals in BiPAP group. There was no significant difference in HR between groups in any of the time intervals. The serum pCO2 levels decreased significantly after initiation of ventilation support in the BiPAP group, and SpO2 levels improved significantly for both groups.
• Agitated Asthmatics 
  • Ketamine
    • Use dissociative dosing—generally frowned upon with use of NIV bc we’d like the patient to tell us if there is something wrong with the mask or be able to take it off if they start to vomit BUUUUUT you’re going to be in the room watching these patients closely until they turn the corner so it should be ok
    • Does not affect respiratory drive
    • Theoretical bronchodilation with large doses, however, has never directly been liked to improved outcomes in asthmatic patients 
  • Dexmedetomidine 
    • Usually start low and titrate up slowly…but may want to consider the reverse in these patients bc it can take awhile to work
    • Alpha 2 antagonists can relax smooth muscle --> directly improving the patient’s condition 
    • Can induce bradycardia 
  • Some thoughts? 
    • Consider Dex when the patient is doing okay but needs help relaxing
    • Consider Ketamine when the patient is severely agitated ripping off their mask that need to relax quickly or if preparing to intubate but want to try NIV as a last ditch effort to prevent having to go down that route
      • In that case you are using ketamine like you would of any other delayed sequence intubation and if it happens ot turn them around that’s great, if not you just provided some great pre-oxygenation 
  • Opioids
    • Can decrease respiratory drive... which is suboptimal
    • IF you don’t have any other option I’d stick to small doses of fentanyl bc it is quick on/quick off
  • Benzos 
    • Bad for the same reason as opioids so again avoid if possible 
    • You really shouldn’t be giving these meds if you have dex or ketamine available 

• Intubation
  • About 1/4 of kids intubated for asthma have complications (pneumothorax, impaired Preload, cardiovascular collapse) because of increased intrathoracic pressures.
    
  • If the patient that you just intubated for his/her asthma becomes unstable / hypotensive, the first thing you should do is disconnect the ventilator and allow the patient to exhale (likely that intrathoracic pressures have increased preventing venous return to the right heart). Consider pneumothorax after that.
  • Consider delayed sequence intubation with ketamine and BiPAP as we discussed
  • If you have to BVM the patient keep RR low (10-12)
  • Optimize pre-intubation hemodynamics
  • Pressure bag IVF or start pressures if need be
    • if you haven’t already started them on an epi drip to assist with bronchodilation this may be the time to do so
  • Use as large of a tube as you can to minimize airway resistance
  • Paralyze with a longer acting agent (aka roc over sux), allows you to take control over your respiratory mechanics 
  • Consider calling the ECMO team early for these patients 
  • If the patient becomes hypotensive after intubation consider S-H-I-T:
    • Stacking (hyperinflation)
    • Hypovolemia
    • Induction drugs
    • Tension pneumothorax
  • Ventilator Settings:
    • Respiratory rate of 12 breaths/minute
    • Inspiratory time (I-time) of 1 second
    • Inspiratory pressure of 40 cm, with a PEEP of 5 cm
    • TV of 6-8 cc per kg of IDEAL body weight 
    • You can start with an FiO2 of 100% per usual but should be able to titrate down quickly 
    • Allow for permissive hypercapnia BUT monitor pH closely 
  • Barotrauma will cause more problems than moderate hypercapnia will in an intubated patient
• Plateau Pressure
  • Check plateau pressure NOT peak pressure
  • Done by preforming an inspiratory pause on the vent 
  • >30 is bad 
  • Represents the pressure that is applied by the mechanical ventilator to the small airways and alveoli
  • High plateau pressures = higher risks of barotrauma
  • To reduce PP you can:
  • Decreasing the tidal volume
  • Decrease PEEP
  • Decrease flow 
  • Increasing the patient's sedation or paralyze the patient (on beneficial in the acute setting) ​

• Quick Differential: DIMES
  • D – drugs (digoxin, CCB, beta blockers, cholinergic drugs, TCAs, Clonidine)
  • I – ischemia (heart and brain)/ infection (sepsis, Lyme disease) 
  • M – metabolic (hypothyroid, hypoglycemia, hypothermia) 
  • E – electrolytes (hyperkalemia, hypokalemia, hypercalcemia, hypocalcemia, hypermagnesemia) 
  • S – sinus dysfunction (SSS, AV block) 
• Meds: 
  • 3g calcium gluconate (treats hyperK & increases inotropy) 
  • Atropine ? 
    • 0.5 – 1 mg q5min, max dose 3 mg 
    • peds = 0.02 mg/kg
    • Only effective in 28% of patients with symptomatic bradycardia 
    • Atropine shuts down the vagus nerve to remove parasympathetic stimulation to the heart….not effective for many types of bradycardia 
    • Atropine will NOT work in someone who has had a heart transplant, dat vagus nerve has already been cut. 
  • Epinephrine bolus 
    • 20-40 mcg IV (EMCRIT recommended dose using push dose epi) 
    • peds 0.01 mcg/kg in 1:10,000 concentration (code dose concentration) 
    • Epi acts on myocardia muscles, the SA node, and the AV node -> effective against a wider range of underlying pathologies and can help out your BP 
  • Epinephrine drip 2-10 mcg/min 
  • Dopamine drip 2-10 mcg/kg/min 
  • Isoproterenol is a pure beta agonist that can go through a peripheral line 
    • Last ditch med: isoproterenol reported to work really well but $$$$
    • Can also be used in refractory Torsades to shorten QTc (Thanks Dr. Littmann)
  • CONFIRM PACING BY PALPATING A PULSE (or using pulse ox pulse rate NOT rhythm strip on monitor) 
• Overdoses to consider:
  • Beta blocker OD: glucagon and high dose insulin + dextrose 
  • CCB overdose: high dose insulin + dextrose
    • CCB OD -> hyperglycemia
    • Consider in patients who are not known to be diabetic but present with lab values consistent with DKA + bradycardia + hypotension 
    • The level of hypoglycemia can serve as a marker of severity of shock 
  • Digoxin OD: Digibind
    • Potassium level correlates with level of toxicity 
    • 20 viiles for a coding patient! 
    • Dosing formula on MedCalc using serum level & amount ingested  (mg ingested x 0.8 x 2) 
• Pacing:
  • Transcutaneous Pacing:
    • https://www.youtube.com/watch?v=1fjmyog37Fo – Peds example, smoooooth voice
    • https://www.youtube.com/watch?v=5qfIRPxoHuw – adult example 
    • https://www.youtube.com/watch?v=UInoEPPjwKo – how to set up the box 
  • Transvenous Pacing:
    • https://www.youtube.com/watch?v=OMtuaBV8C2k – Set up
    • https://www.youtube.com/watch?v=00-T8PcbStE – Procedure
    • https://www.youtube.com/watch?v=9dgZfX7OK_k – trouble shooting

OB Trauma

• Physiologic changes of pregnancy: physiologic anemia, decreased SVR, increased HR, increased RR, and pelvic vessel engorgement 
• Traumatic complications: placental abruption, preterm labor (PTL), uterine rupture, and pelvic fx
• Abruption triad = abd pain, large for dates uterus, vaginal bleeding
• Perform cervical check to eval for PTL
• Obtain Type and Screen and KB test
• Give Rhogam if mom is Rh neg. 50 mcg if <12 wks, 300mcg if > 12 wks
• Check fetal HR after E-FAST, nml is 120-160

 
-Travis Barlock

----
See also Slides from Dr. Michael Gibbs on this subject - http://www.mededmasters.com/obgyn.html

Topic: Superior Vena Cava Syndrome
Definition: 

• Any condition leading to obstruction of blood flow through the SVC

Pathophysiology: 

• Pathology in adjacent anatomy (lung, lymph node, thymus, mediastinum) or within the SVC itself obstructs venous return to the right atrium. As the SVC is compressed, venous collaterals form alternative pathways returning blood to the right atrium which can dilate over several weeks. As a result, upper body venous pressure increases, which in extreme cases lead to airway congestion and venous cerebrovascular congestion and edema. Hemomdynamic compromise is most often by direct compression of the heart, not from SVC obstruction. 

Risk factors:

• Indwelling device through the SVC (Central line, dialysis catheter, pacemaker)
• Lung cancer
• Lymphoma
• Thymoma

Presentation:

• Signs – plethoric appearance, dilated neck and chest veins, swollen face/neck/chest
• Symptoms – congestive symptoms (head fullness, swelling), cardiopulmonary symptoms (chest pain, dyspnea, stridor, hoarseness), and neurologic symptoms (headache, confusion, obtundation, visual disturbances)

Work-up​:

• Is the patient unstalbe? Do they have severe SVC?
  • If yes, secure airway, support breathing, support circulation
  • Consult vascular/cardiothoracic surgery
• Patient is stable
  • Confirm diagnosis and evaluate for malignant obstruction
    • CBC, CMP, PT/INR, CXR, CT chest w/contrast
  • Does the patient have a malignant obstruction or thrombosis?
    • Yes -> consult heme/onc and admit
    • No -> observe in ED

References:

1. García Mónaco R, Bertoni H, Pallota G, et al. Use of self-expanding vascular endoprostheses in superior vena cava syndrome. Eur J Cardiothorac Surg 2003; 24:208.
   
2. Rice TW, Rodriguez RM, Light RW. The superior vena cava syndrome: clinical characteristics and evolving etiology. Medicine (Baltimore) 2006; 85:37.
   
3. Schraufnagel DE, Hill R, Leech JA, Pare JA. Superior vena caval obstruction. Is it a medical emergency? Am J Med 1981; 70:1169.
   
4. Wilson LD, Detterbeck FC, Yahalom J. Clinical practice. Superior vena cava syndrome with malignant causes. N Engl J Med 2007; 356:1862.

Skin and Soft Tissue Infections
 
Epidemiology 

• Cellulitis 2.3 million visits in the ED annually
• 15% get admitted
• Up to 30% of diagnosed cellulitis is really a “cellulitis mimic”

 
Important Aspects of your History

• Travel? Water exposure?
• Recent trauma or bug bite?
• Recent antibiotics?
• Immunocompromised? Diabetes w/ complications (neuropathy, sugar uncontrolled, etc)?

 
The Mimics

• Venous stasis
• PAD
• DVT or superficial thrombophlebitis
• Dermatosclerosis
• Diabetic myonecrosis
• Lymphedema
• Contact dermatitis
• Necrotizing fasciitis 

 
Workup

• Good history and physical exam
• Always ultrasound to look for purulence or abscess
• Labs largely unhelpful

 
Treatment

• Simple cellulitis w/out purulence = Keflex (consult local antibiogram)
• Cellulitis w/ purulence = Keflex plus Staph Aureus coverage
• Abscess – Drain and only give antibiotics in special circumstances

 
“Special” cellulitis

• Perichondritis
  • Needs coverage for pseudomonas
• Bites – think Pasteurella
  • Augmentin
• Water exposure
  • Vibrio– doxycycline
  • Aeromonas– Rocephin, Bactrim, or a fluoroquinolone. 
• Orbital cellulitis
  • IV abx, CT scan
• Unvaccinated children
  • H. influenzacellulitis associated with 90% bacteremia
• Abscess
  • Needs drainage
  • Bactrim if abscess > 5cm, patient immunocompromised, in axilla or groin

 
 
Necrotizing fasciitis +/- Toxic Shock Syndrome 

• When patient presents in extremis, the diagnosis is easy
• Helpful physical exam findings
  • Pain out of proportion
  • Pain outside the margin of the rash
  • Bullae, skin necrosis, pallor, hypoesthesia, crepitus are late findings
• Labs are unhelpful and cannot be relied upon until it is too late
• Resuscitate and give Vancomycin, Zosyn, and Clindamycin
  • Clindamycin needed for decreased toxin release in setting of toxic shock syndrome. Always give with first wave of antibiotics if you are treating necrotizing fasciitis
• Imaging is not universally helpful
• Very tough diagnosis, you need a high index of suspicion
• Consult surgery quickly if suspicious, you will need source control 

Republished with Permission from www.PedEMMorsels.com

Difficult Airway: Basics

• Defining “Difficult Airway” is challenging, so studies are not strictly comparable (we all know it after we have dealt with it though).
• Some separate “Difficult Airway” from “Difficult Intubation.” [Belanger, 2015]
  • Difficult Airway – unable to provide adequate gas exchange despite BVM, airway adjuncts, or combination of the two.
  • Difficult Intubation – 3 or more attempts by an experienced clinician

• The incidence of difficult intubations in children vary from <0.1% to 9%[Graciano, 2014; Heinrich, 2012]
• Difficult intubations is associated with higher incidence of oxygen desaturations below 80% and adverse events. [Graciano, 2014]

Difficult Airway: Important Differences
Anatomic and physiologic differences influence how the oral, pharyngeal, and tracheal axes align as well as how the respiratory mechanics function and how the child compensates to physiologic stress.
The differences are most prominent in children < 2 years of age and more adult anatomy evolves as children progress to 8 years of age.

Anatomic Differences:

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

Physiologic Differences:

• Higher metabolic rate
  • Consumes oxygen at more than twice the adult rate
  • Combined with low functional residual capacity, leads to rapid desaturations.
• Low glycogen stores
  • High metabolic rate and low glycogen stores leads to hypoglycemia.
  • Hypoglycemia is a common SYMPTOM of the critically ill child.

Difficult Airway: Predictive Factors

• Adult-based tools (ex, LEMON, Mallampati, thyromental distance) are notpredictive in young children. [Belanger, 2015]
• There are patient factors that are associated with difficult intubation. [Karsli, 2015; Belanger, 2015]
  • History of difficult airway (duh) [Graciano, 2014]
  • Less than 1 year of age
  • Signs of Upper Airway Obstruction (duh) [Graciano, 2014]
  • Congenital/Genetic Syndromes w/ altered anatomy
    • Down Syndrome
    • Pierre Robin Sequence 
    • Treacher Collins
    • Cleft Palate
    • Mucopolysaccharidosis (ex, Hunter, Hurler)
  • Physiologic stress [Graciano, 2014]
    • Hypotension, ventilation failure, etc

Difficult Airway: Assume the Worst

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

Moral of the Morsel

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

Taking care of children in the ED isn't just diagnosing viruses - child abuse/neglect is more prevalent than we'd like to think:
            - 2-10% of children presenting to the ED are victims of abuse or neglect
            - children that are abused often have multiple healthcare visits before it is recognized
 
Child maltreatment includes neglect and abuse
Neglect
- failure to meet the most basic needs of a child (food, shelter, supervision, nurturance)
- can be educational, psychological, emotional, medical neglect, or supervisory
            - by far the most common type of maltreatment - about ⅔ of cases
            - very difficult to identify diagnose
Abuse
- includes physical abuse, sexual abuse, emotional abuse, and medical child abuse
* medical child abuse is the current term for Munchausen Syndrome by proxy
- physical abuse (also referred to as non-accidental trauma or NAT) is often the most recognizable type of abuse
- makes up 16% of maltreatment cases
 
Providers should be mindful of sentinel injuries - injuries without a plausible explanation
            - knowing basic developmental milestones can be helpful
                        4-5 months - rolling over
                        6 months - sitting unassisted
                        9 months - pulling to a stand and walking
                        12 months - walking
 
**soft tissue injuries - bruising in children who cannot cruise, or in high risk areas
            - normal childhood bruises occur on surfaces that take impact when the child falls
                        bruising on the knees and shins isn’t alarming
                        bruising on areas like the back, buttocks, thighs, abdomen is concerning
- TEN-4 FACES P can help you identify injuries that suggest potential abuse
            * bruising on the Trunk, Ears, or Neck in a child less than 4 years old
* ANYbruising on a child less than 4 months
* injuries/bruising to the Frenulum, Auricular area, Cheek, Eyes, Sclera or
* Patterned bruising is a red flag
 
**skeletal injuries are the second most common presentation of abuse - certain fractures should raise your suspicion for abuse
- rib fractures (make sure you check that CXR ordered to look for pneumonia)
- any fracture in a child that cannot walk
- long bone fractures in an infant or toddler
 
**abusive head trauma (formally known as “shaken baby syndrome”)
                  - this is the most common cause of death following abuse
                  - 30% of cases are missed initially – remember to consider it in cases of excessive fussiness or altered mental status
 
**chest and abdominal injuries
            - the abdomen can hide injuries and hold a lot of blood - you won’t always see bruising
            - elevated liver enzymes or lipase should raise your concern for occult intra-abdominal injury
 
What can you do to help prevent a missed diagnosis of abuse?

• Perform a “top-toe” exam on every patient and examine their skin for bruising (this means everyone should be in a gown)
• Make sure the explanation of the injury makes sense developmentally – “those who don’t cruise rarely bruise”
• If you’re concerned about possible abuse, initiate a screening work up or admit the child to a service that can complete an abuse evaluation
• Remember that you are a mandated reporter – involve Social Work early, even if you plan to refer the child to another hospital for evaluation.​

ACEP Now. The Recognition of Child Abuse. May 1, 2012.
 
Colbourne M, Clarke MS. Child Abuse and Neglect. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e New York, NY: McGraw-Hill; 2016. http://accessmedicine.mhmedical.com.libproxy.lib.unc.edu/content.aspx?bookid=1658&sectionid=109435341. Accessed May 15, 2019.
 
Christian CW. The Evaluation of Suspected Child Abuse.  PEDIATRICS. 2015; 135 (5): e1337-e1354.
 
Glick JC, Lorand MA, and Bilka KR. Physical Abuse of Children.  Pediatrics in Review. 2016; 37(4): 146-158.
 
Lindberg DM, Beaty B, Juarez-Colunga E, et al. Testing for Abuse in Children With Sentinel Injuries. PEDIATRICS. 2015; 136(5): 831-838.
 
Petska HW and Sheets LK. Sentinel Injuries Subtle Findings of Physical Abuse. Pediatric Clinics of North America. 2014; 61(5): 923-935.
 
Ravichandiran N, Schuh S, Bejuk M, et al. Delayed Identification of Pediatric Abuse-Related Fractures.  PEDIATRICS. 2009; 125 (1): 60-66. 
 
Sheets LK, Leach ME, Koszewski IJ, et al.  Sentinel Injuries in Infants Evaluate for Child Physical Abuse. PEDIATRICS. 2013; 131(4): 701-107.
 
Teeuw AH, Derkx BHF, Koster WA, et al. Detection of child abuse and neglect in the emergency room. European Journal of Pediatrics. 2012; 171: 877-885.
 
Teeuw AH, Hoytema van Konijnenburg EM, Sieswerda-Hoogendoorn T, et al.  Parents’ Opinions About a Routine Head-to-Toe Examination of Children as a Screening Instrument for Child Abuse and Neglect in Children Visiting the Emergency Department.  Journal of Emergency Nursing. 2016; 42(2): 128-138.

MG Pathophysiology & Symptoms

• Autoimmune neuromuscular junction disease
• Antibodies to muscle fiber ACh receptors -> decrease function and # of ACh receptors available for neurotransmission -> decreased muscle stimulation -> weakness 
• Weakness worse with exertion and at the end of the day 
• Other symptoms: Ptosis, diplopia, weakness of proximal muscle groups, neck extensors and facial/bulbar muscles

 

MG Crisis (MC) Causes 

• MC = MG patient in respiratory distress 
• 15-20% of MG patients will undergo crisis requiring emergency intervention 
• Any form of physical or emotional stress can trigger MC
• Infection most common cause
• Other precipitants: surgery, pregnancy, childbirth, tapering steroids, medications (LOTS of them), conditions that change drug tolerance 

 
Drugs to avoid in MG Patients: 

• Fluoroquinolones, Ketolides, Botulinum toxin, D-Penicillamine

 
Drugs that should be used with caution: 

• Aminoglycosides, metronidazole, macrolides
• Beta-blockers, dihydropyridine calcium channel blockers (ex. amplodipine), quinidine, quinine 
• Corticosteroids & ACTH
• Interferons, Mg, narcotic analgesics (ex. morphine), phenothiazines, sedatives & hypnotics 
• Depolarizing & non-depolarizing neuromuscular blocking agents (succinylcholine-like, curare-like – need to use at lower doses) 

 

Evaluation

• Most come to the ED with  known MG diagnosis  
• Assess respiratory status – look for accessory muscle use, retractions, abnormal lung sounds, ability to clear secretions
• NOTE: Accessory muscle use can be blunted or absent in MC because of muscle fatigue 
• Focused review of systems: Neuro symptoms (ex. weakness/diplopia) that improve with rest; recent infections, toxins, drug exposures, trauma, stress
• Pay attention to current medication list (and any recently added meds) 
• Cholinergic crisis is rare but similar in presentation. Distinguish by assessing for autonomic and cholinergic symptoms like bradycardia, diarrhea, emesis, miosis, urination; etc. 

 
Focused 30-second Neuro Exam

• Test: Extraocular muscles, pupil reactivity, sensation in each extremity, Babinski & patellar reflexes, strength against resistance (arms, legs & head) 
• Observe for weakness, ptosis, grossly increased secretions, signs of respiratory failure

 

Airway Management

• Indications for Intubation: 

- NIF score less than -20 
- Vital capacity less than 10-20 mL/kg
- Single-breath test (unable to count past 20) 
- Unable to clear secretions

• Don’t just rely on thresholds – assess overall respiratory status (respiratory rate, work of breathing, oxygenation, phonation) 
• For borderline patients, consider noninvasive PPV like BiPap - shown to reduce need for ventilator support and time in the ICU 
• Depolarizing agents can last 2-4 times longer in MG patients. Succinylcholine can have unpredictable response so try to avoid
• Consider nondepolarizing agents like vecuronium or rocuronium, but at lower doses (still need to be cautious!). Start at one-third to one-half the standard dose. 
• Can also try awake intubation with propofol, fentanyl or ketamine 
• Avoid pyridostigmine during a crisis as it increases secretions and make airway management difficult! 

 
 
Management After Stabilization

• Look for underlying cause
• Infectious work-up: CXR, CBC, urinalysis, blood culture
• Other tests: BMP, tox screen, CK levels, EKG, beta-hcg 
• ABG useful for vent management, but not great as diagnostic tool – CO2 level and O2 sat usually change much later in myasthenic crisis 
• Discontinue meds that could cause exacerbation, replace electrolyte imbalances, treat any underlying infection (double-check to make sure antibiotic is safe in MG patients)  
• Call Neurology 
• Admit to ICU, where PLEX or IVIG will be initiated 

 
 
Sources:
Bird, S.J. & Levine, J.M (2019). Myasthenic crisis. In A.F. Eicheler & G. Finlay (Ed.), UpToDate.Retrieved February 27, 2019, from https://www.uptodate.com/contents/myasthenic-crisis
 
Howard, J.F. (2009). Myasthenia Gravis: A manual for the health care provider. Myasthenia Gravis Foundation of America, Inc.
 
Jowkar, A. (2010).  Neuromuscular topics for Neuroscience ICU RNs. Presentation, University of North Carolina at Chapel Hill.
 
Roper, J., Fleming M.E., Long. B. et al. (2017). Myasthenia Gravis and Crisis: Evaluation and Management in the Emergency Department. The Journal of Emergency Medicine, 53(5): 843-853. http://dx.doi.org/10.1016/j.jemermed.2017.06.099
 
Tintinalli, J. E., Stapczynski, J. S., Ma, O. J. et al. (2016). Tintinalli's emergency medicine: A comprehensive study guide(Eighth edition.). New York: McGraw-Hill Education.