Adult and Pediatric Respitory Emergency by nikeborome

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									  Adult and Pediatric
Respiratory Emergency
   Christopher Martella, DO
   Adult and Pediatric Respiratory
• Discuss the differential diagnosis of Adult
  and Pediatric Respiratory Emergencies
• Pathophysicology
• Epidemiology
• History
• Physical findings
• Treatments
          Adult and Pediatric Respiratory
•   DDX in Adults
•   HEENT Angiodema Anaphylaxis Pharyngeal infections Deep neck
    infections Foreign body Neck trauma
    Chest wall Rib fractures Flail chest
    Pulmonary COPD exacerbation Asthma exacerbation Pulmonary embolism
    Pneumothorax Pulmonary infection ARDS Pulmonary contusion or other
    lung injury Hemorrhage
    Cardiac ACS ADHF Flash pulmonary edema High output failure
    Cardiomyopathy Arrhythmia Valvular dysfunction Cardiac tamponade
    Neurological Stroke Neuromuscular disease
•   Toxic/metabolic Organophosphate poisoning Salicylate poisioning CO
    poisoning Toxic ingestion Diabetic ketoacidosis Sepsis Anemia Acute chest
    syndrome Miscellaneous Hyperventilation Anxiety Pneumomediastinum
    Lung tumor Pleural effusion Intra-abdominal process Ascites Pregnancy
    Massive obesity
              Adult and Pediatric Respiratory
•   DDX in children
     – Respiratory tract Infection Epiglottitis Retropharyngeal abscess Peritonsillar abscess Croup
        Tracheitis Bronchiolitis Pneumonia Asthma Anaphylaxis Foreign body Upper airway Lower
        airway Esophageal
     – Biologic or chemical weapons
     – Chest wall/thoracic Chest wall deformity (eg, thoracic dystrophy, flail chest) Air leak (eg,
        tension pneumothorax) Mass lesion (eg, pulmonary sequestration, malignancy)
     – Cardiovascular Heart failure Cyanotic heart disease Pericarditis Cardiac tamponade
     – Nervous system Depressed ventilation (from ingestion, injury, or infection) Hypotonia (poor
        pharyngeal tone, ineffective respiratory effort) Loss of airway protective reflexes (aspiration)
     – Gastrointestinal Splinting from abdominal pain Abdominal distention Aspiration as the result
        of gastroesophageal reflux
     – Metabolic/endocrine Acidosis (eg, diabetic ketoacidosis, severe dehydration, sepsis)
        Hyperthyroidism Hypothyroidism
     – Hematologic Decreased oxygen carrying capacity (eg, severe anemia, methemoglobinemia)
     – Trauma Blunt or penetrating (eg, pneumothorax, pulmonary contusion) Inhalational injury
        (eg, airway burn, smoke inhalation)
• Time of onset
• Current medications
• Recent use of beta 2 agonists
• Risk factors for severe disease is ED
  visits, hospitalizations, ICU admits
  intubations, repeated courses of oral
  glucocorticoids, hx of intubation and food
Physical findings
  Use of accessory muscles
  Brief fragmented speech
  Inability to lie supine
  Cyanosis, depressed mental status, inability to maintain
  respiratory effort
  Pulmonary Index in pediatrics patients
  I to E ratio
  Pulus paradoxus
Clinical finding
   Hypoxia -nearly all asthma patients have hypoxia as a result of
       V/Q mismatch. Beta 2 agonist may worsen this mismatch by
       causing pulmonary vasodilation in areas of the lung that are
       poorly ventilated
  Marked hypoxia PO2<60 SaO2<90
       Infrequent but potential cause of complications and death.
       Recommendations for continuous Pulse ox monitoring for
       patients with PEFR <40 % of baseline
  Hypercapnia (ABG)
     Asthma patients are usually tachynic therefore normal or high
     PaCO2 could be an ominous sign
  Chest x-ray rarely helpful unless patient with fever suspected PTX
  Labs not helpful
Treatment for Adult patient
• Oxygen to maintain SaO2 >92%
• Inhaled beta agonist Albuterol 2.5-5.0 mg neb x 3 q 20
  minutes then 1-4 hours as needed or MDI w/ spacer 4
  puffs q 10 min or 8 puffs q 20 min for up to 4 hours then
  1-4 hours as needed
• Critically ill patients continuous neb 10-15 mg over one
• IV hydration NSS bolus to replace insensible losses
Nebs vs MDI essentially no difference and MDI maybe
Ipratopium 500mcg neb q 20 minutes for
three doses, then as needed or 8 puffs via
MDI q 20 min then as needed for up to 3
Usually reserved for severe obstruction
failing to improve despite beta agonists
Systemic glucocorticoids

  Speeds rate of recovery with patients with persistent
  wheezing despite intensive bronchodilator therapy likely
  secondary to airway flow obstruction due to airway
  inflammation and intraluminal mucous plugging

  Current guidelines encourage early systemic
  glucocorticoids for all patients who have a moderate
  (PEFR of < 70%) or severe exacerbation ( PEFR<40%)
Systemic glucocorticoids
  Optimal dose unknown

  Corticosteroids: give methylprednisolone 60-125 mg IV or
  prednisone 40-60 mg po; alternatives include: dexamethasone 6-10
  mg IV or hydrocortisone 150-200 mg IV; steroids may be given IM or
  orally if IV access is unavailable

  PO absorbed rapidly with similar bioavailability to IV
  IV dosing can be used for vomiting or severely ill patients
  IM as effective as PO
  Duration rough guide 10-14 days for severe attacks
  Tapering is not necessary
• Magnesium
• IV MGSO4 has a bronchodilator activity possibly
  due to inhibition of calcium influx into airway
  smooth muscle cells
• Routine use does not seem to confer significant
  benefit beyond beta agonists and systemic
  glucocorticoids, MgSO4 is suggested for
  patients who have life-threatening exacerbations
• Dose 2 gm over 20 minutes
• Nonstandard therapies
  – Helium-oxygen
  – Leukotriene receptor antagonist
  – BiPAP
  – Terbutaline 0.25 mg SC q 20 minx 3 doses
  – Epinephrine 0.2-0.5 ml 1 :1000 SC
  Ineffective therapies
    Inhaled glucocorticoids
    Empiric antibiotics
Treatment in Peds
  Similar approach to adults
  Levalbureol vs Racemic albuterol
  Parental beta 2-agonist Epinephrine and
• Parental beta 2-agonist Epinephrine and Terbutaline

      May be superior to inhaled beta 2-agonists for children with
      severe exacerbations and poor inspiratory flow or anxious
      young children who are uncooperative with or have suboptimal
      response to initial aerosolized therapy.

      The intramuscular route may provide for more rapid drug
      absorption, although direct       comparisons are lacking. In
      this setting, terbutaline may be expected to produce fewer
      adverse effects than epinephrine.
Heart failure (HF) is a common clinical syndrome
 representing the end-stage of a number of
 different cardiac diseases. It can result from any
 structural or functional cardiac disorder that
 impairs the ability of the ventricle to fill with or
 eject blood. There are two mechanisms by which
 reduced cardiac output and HF occur:
     Systolic dysfunction
     Diastolic dysfunction.
The New York Heart Association's classification:
     Class I describes a patient who is not limited
     with normal physical activity by symptoms.
     Class II occurs when ordinary physical
     activity results in fatigue, dyspnea, or other
     Class III is characterized by a marked
     limitation in normal physical activity.
     Class IV is defined by symptoms at rest or
     with any physical activity.
•   Frequency
     – United States
         • More than 3 million people have congestive heart failure (CHF), and more than 400,000
           new patients present yearly. The prevalence rate of CHF is 1-2%.

•   Mortality/Morbidity
     – Approximately 30-40% of patients with congestive heart failure (CHF)
       are hospitalized every year.
     – CHF is the leading diagnosis-related group (DRG) among hospitalized
       patients older than 65 years.
     – 5-year mortality rate after diagnosis was reported in 1971 as 60% in
       men and 45% in women. In 1991, data from the Framingham heart
       study showed the 5-year mortality rate for CHF essentially remaining
       unchanged, with a median survival of 3.2 years for males and 5.4 years
       for females.
     – The most common cause of death is progressive heart failure, but
       sudden death may account for up to 45% of all deaths. Patients with
       coexisting insulin-dependent diabetes mellitus have a significantly
       increased mortality rate.
• Race
  – Blacks are 1.5 times more likely to die of CHF than whites are.
    Nevertheless, black patients appear to have similar or lower in-
    hospital mortality rates than white patients.
• Sex
  – Prevalence is greater in males than in females in patients aged
    40-75 years.
  – No sex predilection is noted among patients older than 75 years.
• Age
  – Prevalence of CHF increases with increasing age and affects
    about 10% of the population older than 75 years.
• Causes
    – The most common cause of heart failure is coronary artery disease,
    – Other disease processes include
       • hypertension,
       • valvular heart disease
       • congenital heart disease
       • myocarditis and infectious endocarditis.

• CHF is often precipitated by cardiac ischemia or dysrhythmias,
  cardiac or extracardiac infection, pulmonary embolus, physical or
  environmental stresses, changes or noncompliance with medical
  therapy, dietary indiscretion, or iatrogenic volume overload.

• One also must consider systemic processes such as pregnancy and
  hyperthyroidism as precipitants of CHF.
•   History
•   Anxiety
•   Dyspnea at rest
•   Dyspnea upon exertion: This has been found to be the most sensitive
    symptom reported, yet the specificity for dyspnea is less than 60%.
•   Orthopnea and paroxysmal nocturnal dyspnea the sensitivity for orthopnea
    and PND is only 20-30% but specificity 74-80%.
•   Cough: Cough that produces pink, frothy sputum is highly suggestive of
    congestive heart failure (CHF).
•   Edema
•   Nonspecific symptoms
     –   Weakness
     –   Lightheadedness
     –   Abdominal pain
     –   Malaise
     –   Wheezing
     –   Nausea
• Physical Findings for the vet with Acute
  decompensated heart failure (ADHF)
   – Displaced Apical Pulse most sensitive and specific of all physical findings
     of Systolic HF. Apical impulse laterally displaced past midclavicular line
   – Peripheral edema, jugular venous distention, and tachycardia are highly
     predictive of congestive heart failure (CHF). specificity of physical examination
     reported at 90%
   – Tachypnea, using accessory muscles of respiration, has been observed.
   – Hypertension may be present.
   – Pulsus alternans (alternating weak and strong pulse indicative of depressed left
     ventricle [LV] function) may be observed.
   – The skin may be diaphoretic or cold, gray, and cyanotic.
   – Jugular venous distention (JVD) is frequently present.
   – Wheezing or rales may be heard on lung auscultation.
   – Cardiac auscultation may reveal aortic or mitral valvular abnormalities (S3 or S4).
   – Lower extremity edema may also be noted, especially in the subacute process.
Work up
  Labs Chem 7, CBC, Cardiac enzymes, BNP
  ABG levels may be of benefit in evaluation of hypoxemia,
       ventilation/perfusion (V/Q) mismatch, hypercapnia, and
  ECG nonspecific tool but may be useful in diagnosing concomitant
       cardiac ischemia, prior myocardial infarction (MI), cardiac
       dysrhythmias, chronic hypertension, and other causes of left
       ventricular hypertrophy
  ECHO Emergency transthoracic echocardiography may help
       identify regional wall motion abnormalities as well as
       globally depressed or myopathic left ventricular function.
       ECHO may help reveal cardiac tamponade, pericardial constriction, and
         pulmonary embolus.
       ECHO is also useful in revealing valvular heart disease, such as mitral or aortic
         stenosis or regurgitation.
Work up
  CXR Chest radiography is the most useful tool diagnostic tool. A recent
  study showed that 1 out 5 patients admitted to the hospital with CHF lacked
  signs of congestion on chest radiograph.
    – Cardiomegaly may be observed with a cardiothoracic ratio greater than 50%.
      Pleural effusions may be present bilaterally or if they are unilateral more
      commonly observed on the right.
    – Early CHF may manifest as cephalization of pulmonary vessels, generally
      reflecting a pulmonary capillary wedge pressure (PCWP) of 12-18 mm Hg. As
      the interstitial fluid accumulates, more advanced CHF may be demonstrated by
      Kerley B lines (PCWP is 18-25 mm Hg).
    – Pulmonary edema is observed as perihilar infiltrates often in the classic butterfly
      pattern, reflecting a PCWP of more than 25 mm Hg.
    – Several limitations to chest radiography are observed when attempting to
      diagnose CHF. Classic radiographic progression is often not found, and as much
      as a 12-hour radiographic lag from onset of symptoms may occur. In addition,
      radiographic findings frequently persist for several days despite clinical recovery.
• Treatment depends on
  – Acuity of presentation
  – Volume status
  – Systemic perfusion
• As always in Every ER lecture ABC’s
  – Noninvasive positive pressure Ventilation
  – Endotracheal intubation
Treatment Acute Decompensated Heart Failure
  HOSPITALIZATION — Hospital admission is recommended for patients with ADHF
  with the following clinical conditions:
   –   Hypotension
   –   Worsening renal function
   –   Altered mentation
   –   Dyspnea at rest
   –   Also consider hospitalization for:
         Worsened congestion, even if without dyspnea; typically reflected by a weight gain of ≥5kg
         Signs and symptoms of pulmonary or systemic congestion, even in the absence of weight
         Major electrolyte disturbance
         Associated comorbid conditions such as pneumonia, pulmonary embolus, diabetic
         ketoacidosis, or symptoms suggestive of TIA or stroke
         Repeated ICD firings
         Previously undiagnosed HF with signs and symptoms of systemic or pulmonary congestion
         High BNP levels
         Poor compliance or ability to manage symptoms as an outpatient
• Acute Pulmonary edema with normal or elevated
  – Sublingual NTG 0.4 mg q minute until reduction of BP or
    improvement of symptoms. IV NTG gtt can be used with rapid
    titration to 200ug/min or higher
  – IV Nitroprusside or Nesirtidemay can be used as an alternative
  – Diuretics IV Furosemide (40mg ) or bumetanide(1-3 mg)
    Ethacrynic acid (50mg) for sulfa allergy
  – Morphine 2-5 mg IV venodialtor
  – Contraindication to Vasodilators Right Ventricular MI, AS,
    Hypertrophic Cadiomyopathy
     • Goal of therapy in HCM with Pulmonary edema is to decreasing outflow
       gradient by slowing the hear in the ICU
• Decompensated HF
  – Stable vitals, adequate oxygenation with
    symptoms i.e. SOB, DOE, JVD orthopnea and
  – Usually do well with Diuresis, O2 and BP
Beta-blockers, particularly carvedilol, have been shown to improve
  symptoms in patients with moderate-to-severe heart failure.
  However, the role of beta-blockers in the acute setting is currently
  unclear; limit use until hemodynamic studies indicate that further
  deterioration is not possible.

Digoxin has no place in the treatment of acute HF

Potassium sparring diuretics such as Spironolactone are generally
   reserved for class III or IV HF, aggressive use could result in
Nitroprusside Cardiac steal syndrome
Angiotensin-Coverting Enzyme Inhibitor
• Drugs to aviod
  – Calcium channel blockers may result pulm
    edema and cardigenic shock secondary to
    negative inotropic effects
  – NSAIDS inhibits effects of ACEI and diuretics
  – Antiarrhythmics HFf patients are sensitive to
    pro-arrhythic and cardiodepressent effects
• Pediatric
  – Most common cause is Congenital Heart
    Disease and dx in first 4 weeks of life
  – Masquerades or co-exists with pneumonia or
  – Symptoms poor feeding, weak cry, grunting
    and nasal flaring, diaphoresis, lethargy, poor
    weight gain, Murmur
           DDX of CHF based upon age
Age        Spectrum
1 min      anemia, acidosis, hypoxia, hypoglycemia,
1 hour     hypocalcemia, sepsis
1 day      PDA
1 week     hypoplastic L verntricle
2 weeks    Coarctation
1 month    VSD
3 months   SVT
1 year     Myocarditis, Cardiomyopathy, severe anemia
10 year    Rheumatic fever
             Pulmonary Embolus
DEFINITIONS — PE refers to obstruction of the pulmonary
  artery or one of its branches by material (eg, thrombus,
  tumor, air, or fat) that originated elsewhere in the body

  Acute or Chronic
  Submassive or Massive              which is defined as causes hypotension,
  defined as a systolic blood pressure <90 mmHg or a drop in systolic blood
  pressure of ≥40 mmHg from baseline for a period >15 minutes

NATURAL HISTORY — Untreated PE is associated with a
  mortality rate of approximately 30 percent. Recurrent embolism is
  the most common cause of death.
         Pulmonary Embolus
 RV dysfunction — RV dysfunction due to PE
 predicts increased PE-related mortality
 Brain natriuretic peptides (BNP) — An
     elevated BNP or N-terminal pro-brain
     natriuretic peptide (NT-proBNP) predicts RV
     dysfunction and mortality, according to
     three meta-analyses
RV thrombus have a higher 14-day mortality
           Pulmonary Embolus
PATHOPHYSIOLOGY — Most PE arise from thrombi in the
  deep venous system of the lower extremities. However,
  they may also originate in the right heart or the pelvic,
  renal, or upper extremity veins.

  It is estimated that 50 to 80 percent of iliac, femoral, and
  popliteal vein thrombi

  Fortunately, most calf vein thrombi resolve
  spontaneously and only 20 to 30 percent extend into the
  proximal veins if untreated
           Pulmonary Embolus
 Dyspnea most common symptoms were at rest or with exertion (73
 Pleuritic pain (44 percent)
 cough (34 percent)
 >2-pillow orthopnea (28 percent)
 Calf or thigh pain (44 percent)
 Calf or thigh swelling (41 percent)
 Wheezing (21 percent)
 Tachypnea (54 percent)
 Tachycardia (24 percent),
 Rales (18 percent),
 Recreased breath sounds (17 percent),
 Accentuated pulmonic component of the second heart sound (15 percent)
             Pulmonary Embolus
• Laboratory — Routine laboratory findings are nonspecific. They
  include leukocytosis, an increased ESR, and an elevated serum
  LDH or AST (SGOT) with a normal serum bilirubin.

• Arterial blood gas (ABG) measurements and pulse oximetry have a
  limited role in diagnosing PE
    – The typical arterial blood gas findings are not always seen
        • Hypoxemia can be minimal or absent. A PaO2 between 85
          and 105 mmHg exists in approximately 18 percent of patients
          with PE.
        • Up to 6 percent may have a normal alveolar-arterial gradient
          for oxygen.

   Troponins, BNP, ECG, CXR
   Lower Extremity Ultrasound
                 Pulmonary Embolus
•   D-dimer — D-dimer is a degradation product of cross-linked fibrin. It can be
    detected in serum using a variety of different assays:
     –   Enzyme-linked immunosorbent assay (ELISA) (results in >8 hrs)
     –   Quantitative rapid ELISA (results in 30 min)
     –   Semi-quantitative rapid ELISA (results in 10 min)
     –   Qualitative rapid ELISA (results in 10 min)
     –   Quantitative latex agglutination assay (results in 10 to 15 min)
     –   Semi-quantitative latex agglutination assay (results in 5 min)
     –   Erythrocyte agglutination assay (SimpliRED) (results in 2 min)

     Angiography — Pulmonary angiography is the definitive diagnostic technique or
       "gold standard" in the diagnosis of acute PE. It is performed by injecting contrast
       into a pulmonary artery branch after percutaneous catheterization, usually via the
       femoral vein. A filling defect or abrupt cutoff of a small vessel is indicative of an
       embolus. A negative pulmonary angiogram excludes clinically relevant PE.

     Spiral CT 98 percent of patients with PE were detected by CT-PA

     The frequency of negative CT-PA among patients without PE was more consistent,
       around 90 percent
           Pulmonary Embolus
• Wells criteria
   – PE is unlikely (score ≤4) or likely (score >4). The
     modified Wells Criteria include the following :
      • Clinical symptoms of DVT (3 points)
      • Other diagnoses less likely than PE (3 points)
      • Heart rate >100 (1.5 points)
      • Immobilization ≥3 days or surgery in previous four weeks (1.5
      • Previous DVT/PE (1.5 points)
      • Hemoptysis (1 point)
      • Malignancy (1 point)
        Pulmonary Embolus
• Common questions asked by clinicians
  when a patient presents with PE include:
  – Which anticoagulant should I administer?
    How much? How long?
  – Should I administer thrombolytic therapy?
  – Should an inferior vena caval filter be placed?
  – Is embolectomy indicated?
  – Can I withhold therapy and follow the patient
        Pulmonary embolus
• Risk of death from PE untreated is 30%
• Risk of bleeding complication is 3 %
• Options
  – SC Low Molecular weight Heparin
  – IV Unfractionated Heparin
  – SC Unfractionated Heparin
  – SC Fondaparinux
         Pulmonary Embolus
• Warfarin
  – Highly effective for preventing recurrent PE
  – Can be intiated on same day of Hepatin and
    should not be started prior to heparin because
    of three fold increase in incidence of recurrent
  – Should be overlapped with Heparin for a
    minimum of 5 days until INR reaches 2-3 for
    at least 24 hours
           Pulmonary Embolus
                  Duration of Therapy
• First Episode
   – Reversible Risk factor i.e. immobilization, surgery and
     trauma Warfarin for 3 months
   – Unprovoked
       • Studies have shown benefit for . Then 3 month
         therapy in patient with PE or DVT and other
         studies have shown no benefit
       • 2008 ACCP antithrombotic and Thrombolytic
         therapy quidelines recommended 3 months of
         therapy because the study that recommeded 3
         months of therapy was speciffically for PE
        Pulmonary embolus
• Reccurrent PE
• Indefinate Warfarin therapy for patinets
  with 2 or more episodes of PE or PE
           Pulmonary Embolus
  – Improves important physiologic parameters, such as RV function
    and pulmonary perfusion.
  – However, no clinical trial has been large enough to conclusively
    demonstrate a mortality benefit.
  – Thrombolytic therapy is associated with an increased risk of
    major hemorrhage.
  – Persistent hypotension due to PE (ie, massive PE) is the most
    widely accepted indication for thrombolytic therapy.
  – Some clinicians believe that thrombolysis should be considered
    on a case-by-case basis in certain other clinical circumstances,
    such as severe hypoxemia, large perfusion defects, right
    ventricular dysfunction, free-floating right atrial or ventricular
    embolus, and patent foramen ovale
         Pulmonary Embolus
• IVC FILTERS — Inferior vena caval (IVC) filters
  provide a screen in the inferior vena cava,
  allowing blood to pass through while preventing
  large emboli from traveling from the pelvis or
  lower extremities to the lung.
• Indications —
  – Absolute contraindication to anticoagulation (eg,
    active bleeding)
  – Recurrent PE despite adequate anticoagulant therapy
  – Complication of anticoagulation (eg, severe bleeding)
  – Hemodynamic or respiratory compromise that is
    severe enough that another PE may be lethal
             Pulmonary Embolus
• EMBOLECTOMY — Embolectomy (ie, removal of the emboli) can
  be performed using catheters or surgically. It should be considered
  when a patient's presentation is severe enough to warrant
  thrombolysis (eg, persistent hypotension due to PE), but this
  approach either fails or is contraindicated.

• WITHHOLDING THERAPY — The diagnosis of PE almost
  invariably leads to treatment with anticoagulants or IVC filter
  placement. However, one retrospective analysis that used data from
  two prospective studies suggested that patients with PE who are
  hemodynamically stable, have adequate cardiopulmonary reserve,
  and have a contraindication to anticoagulation, can be safely
  observed without treatment if serial lower extremity venous
  ultrasounds are negative over 14 days. Although intriguing, the data
  are clearly insufficient to recommend this approach.
• Croup (laryngotracheitis) is a respiratory
  illness characterized by inspiratory stridor,
  barking cough, and hoarseness.
  – It typically occurs in children six months to
    three years of age
  – Caused by parainfluenza virus.
  – Corticosteroids and nebulized
    epinephrine have become the cornerstones of
• Westley croup score
  – Level of consciousness: Normal, including sleep = 0;
    disoriented = 5
  – Cyanosis: None = 0; with agitation = 4; at rest = 5
  – Stridor: None = 0; with agitation = 1; at rest = 2
  – Air entry: Normal = 0; decreased = 1; markedly
    decreased = 2
  – Retractions: None = 0; mild = 1; moderate = 2; severe
     • Mild croup is defined by a Westley croup score of
     • Moderate croup is defined by a Westley croup
       score of 3 to 7.
     • Severe croup is defined by a Westley croup score
       of ≥8.
• MILD CROUP — Children with mild symptoms,
  defined by a Westley croup score of ≤2, should
  be treated symptomatically with humidity, fever
  reduction, and oral fluids. Many such children
  can be managed by phone, provided that none
  of the criteria for further evaluation described
  above are present.
  – Randomized controlled trials have demonstrated that
    treatment with a single dose of oral
    dexamethasone (0.15 to 0.6 mg/kg, maximum dose
    10 mg) may reduce the need for reevaluation, shorten
    the course, improve duration of the child's sleep, and
    reduce parental stress
• MODERATE TO SEVERE CROUP — Westley croup score 3 to 7,
  stridor and retractions at rest without agitation should be evaluated
  in the emergency department or office
• Supportive care for children with moderate/severe croup includes
  administration of humidified air or humidified oxygen
• The child with severe croup must be approached cautiously, as any
  increase in anxiety may worsen airway obstruction.
• Nebulized epinephrine should be added as quickly as possible
   – Racemic epinephrine is administered as 0.05 mL/kg per dose
      (maximum of 0.5 mL) of a 2.25 percent solution diluted to 3 mL
      total volume with normal saline. It is given via nebulizer over 15
   – - L-epinephrine is administered as 0.5 mL/kg per dose
      (maximum of 5 mL) of a 1:1000 dilution. It is given via nebulizer
      over 15 minutes.
• Dexamethasone (0.6 mg/kg, maximum of 10 mg), by the least
  invasive route possible: has a foul taste. The intravenous
  preparation is more concentrated (4 mg per mL) and can be given
  orally mixed with syrup. A single dose of nebulized budesonide is
  another option
• Observation
•   Hospitalization
•   Indications — Children with moderate/severe croup whose condition
    worsens or fails to improve as expected after treatment with nebulized
    epinephrine and corticosteroids should be admitted to the hospital for
    repeated doses of nebulized epinephrine, observation, and supportive care.
    Poor response to nebulized epinephrine in conjunction with high fever and
    toxic appearance should prompt consideration of bacterial tracheitis
    Additional factors that influence the decision regarding admission include :
     – Need for supplemental oxygen
     – Moderate retractions and tachypnea, indicating increased work of
        breathing, which may lead to respiratory fatigue and failure
     – Degree of response to initial therapies
     – "Toxicity" or clinical picture suggesting serious secondary bacterial
     – Poor oral intake and degree of dehydration
     – Young age, particularly younger than six months
     – Ability of the family to comprehend the instructions regarding recognition
        of features that indicate the need to return for care
     – Ability of the family to return for care (eg, distance from home to care
        site, weather/travel conditions)
     – Recurrent visits to the ED within 24 hours
• Epiglottitis is inflammation of the
  epiglottis and adjacent supraglottic
  structures. Without treatment, epiglottitis
  can progress to life-threatening airway
• Infectious epiglottitis is a cellulitis of the
  epiglottis, aryepiglottic folds, and other
  adjacent tissues
  – Children — Haemophilus influenzae type b (Hib) is
    the most common infectious cause of epiglottitis in
    children. Although the incidence of Hib epiglottitis
    declined after Hib was added to the routine infant
    immunization schedule in the United States and other
    developed countries, Hib epiglottitis still occurs, even
    in immunized children
  – Adults — In adults, epiglottitis has been associated
    with a broad range of bacteria, viruses, combined
    viral-bacterial infections, fungi, and noninfectious
•   Incidence — The epidemiology of epiglottitis changed after the addition of
    the Hib conjugate vaccine to the routine infant immunization schedule in the
    United States and other developed countries . Important changes included:
     – A decrease in the average annual incidence of epiglottitis in children.
     – An increase in the median age of epiglottitis in children (from
        approximately 36 months to 70 to 139 months) .
     – An increase in the average annual incidence of epiglottitis in adults.
     – The annual incidence of epiglottitis among children immunized against
        Hib ranges from 0.6 to 0.78 cases per 100,000. The annual incidence of
        epiglottitis in adults appears to be increasing, from <1 case per 100,000
        in 1986 to two to three per 100,000 in the early to mid-2000s .
•   The reason for the increased incidence of epiglottitis in adults is not clear.
    Possible explanations include an increase in cases of non-Hib epiglottitis
    and increased diagnosis of milder cases secondary to greater physician
    awareness and increased availability of flexible nasopharyngoscopy
• Clinical features
   – The clinical features of epiglottitis differ with age,
     severity, and etiology. Young children classically
     present with respiratory distress, anxiety, and the
     characteristic "tripod" or "sniffing" posture
   – However, the presentation may be subtle . Older
     children, adolescents, and adults may present with a
     severe sore throat but relatively normal
     oropharyngeal examination.
   – Children — Abrupt onset and rapid progression
     (within hours) of dysphagia, drooling, and distress
     ("the three D's") are hallmarks of epiglottitis in
• Symptoms:
• Children
   – Difficulty breathing (80 percent)
   – Stridor (80 percent)
   – Muffled or hoarse voice (79 percent)
   – Pharyngitis (73 percent)
   – Fever (57 percent)
   – Sore throat (50 percent)
   – Tenderness of anterior neck (38 percent)
   – Cough (30 percent)
   – Difficulty swallowing (26 percent)
   – Change in voice (20 percent)

• Symptoms
• Adults
   – Sore throat or odynophagia (90 to 100 percent)
   – Fever ≥37.5ºC (26 to 90 percent)
   – Muffled voice (50 to 80 percent)
   – Drooling (15 to 65 percent)
   – Stridor or respiratory compromise (approximately 33
   – Hoarseness (20 to 40 percent)
• Examination
  – Examining children — Examination of a child in whom
    epiglottitis is a consideration should occur in a setting
    where the airway can be secured immediately if
    necessary (eg, the operating room, emergency
    department, or intensive care unit).
  – Examination efforts should be individualized
    according to the severity of illness of the child. There
    are rare reports of cardiorespiratory arrest during
    attempts to visualize the epiglottis. These arrests
    have been attributed to functional airway obstruction
    (resulting from increased respiratory effort secondary
    to increased anxiety) and/or aggravation of airway
    obstruction caused by supine positioning.
• Examination
  – Examination of the oral cavity and oropharynx in
    patients with epiglottitis is normal in the majority of
  – Pooled secretions may be noted.
  – The laryngotracheal complex may be tender to
    palpation, particularly in the region of the hyoid bone
  – Laboratory features — Laboratory studies should not
    be performed in patients with suspected epiglottitis
    until the airway is secured. Laboratory evaluation
    should include complete blood count with differential,
    blood culture, and epiglottal culture (in intubated
• Radiographic features —
   – Soft-tissue lateral neck radiographs can confirm the diagnosis of
     epiglottitis but are not necessary in many cases. Radiographs
     are most helpful in the evaluation of children in whom epiglottitis
     is a possibility but other conditions are more likely
   – Radiographic features of epiglottitis include:
       • An enlarged epiglottis protruding from the anterior wall of the
         hypopharynx (the "thumb sign". In adults with epiglottitis, the width
         of the epiglottis is usually >8 mm.
       • Loss of the vallecular air space, a finding that may be
       • Thickened aryepiglottic folds. In adults with epiglottitis, the width of
         the aryepiglottic folds is usually >7 mm.
       • Distended hypopharynx (nonspecific).
       • Straightening or reversal of the normal cervical lordosis
• DIAGNOSIS — Diagnosis of epiglottitis is made
  by visualization of the epiglottis or demonstration
  of epiglottal swelling on lateral neck radiographs.
  Cultures of the blood and/or surface of the
  epiglottis identify the microbial pathogen.

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