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Status Asthmaticus

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INTRODUCTION Section 2 of 10

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Background: Status asthmaticus is a medical emergency inwhich asthma symptoms are refractory to initialbronchodilator therapy in the emergency department.Patients report chest tightness, rapidly progressive shortness

of breath, dry cough, and wheezing. Typically, patientspresent a few days after the onset of a viral respiratoryillness, following exposure to a potent allergen or irritant, orafter exercise in a cold environment. Frequently, patientshave underused or have been underprescribed anti-inflammatory therapy. Illicit drug use may play a role in pooradherence to anti-inflammatory therapy. Patients may haveincreased their beta-agonist intake (either inhaled ornebulized) to as often as every few minutes.

Pathophysiology: Inflammation in asthma is characterizedby an influx of eosinophils during the early-phase reactionand a mixed cellular infiltrate composed of eosinophils, mastcells, lymphocytes, and neutrophils during the late-phase (orchronic) reaction. The simple explanation for allergicinflammation in asthma begins with the development of apredominantly helper T2 lymphocytedriven, as opposed tohelper T1 lymphocytedriven, immune milieu, perhapscaused by certain types of immune stimulation early in life.This is followed by allergen exposure in a geneticallysusceptible individual. Specific allergen exposure (eg, dustmites) under the influence of helper T2 lymphocytes leads toB-lymphocyte elaboration of immunoglobulin E (IgE)antibodies specific to that allergen. The IgE antibodyattaches to surface receptors on airway mucosal mast cells.One important question is whether atopic individuals withasthma, in contrast to atopic persons without asthma, have adefect in mucosal integrity that makes them susceptible topenetration of allergens into the mucosa.

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Subsequent specific allergen exposure leads to cross-bridging of IgE molecules and activation of mast cells, withelaboration and release of a vast array of mediators. Thesemediators include histamine; leukotrienes C4, D4, and E4;

and a host of cytokines. Together, these mediators causebronchial smooth muscle constriction, vascular leakage,inflammatory cell recruitment (with further mediator release),and mucous gland secretion. These processes lead toairway obstruction by constriction of the smooth muscles,edema of the airways, influx of inflammatory cells, andformation of intraluminal mucus. In addition, ongoing airwayinflammation is thought to cause the airway hyperreactivitycharacteristic of asthma. The more severe the airwayobstruction, the more likely ventilation-perfusion mismatchingwill result in impaired gas exchange and hypoxemia.

Frequency:

In the US: The prevalence and severity of asthmacases are on the rise (see Asthma). Also increasingare the occurrences of asthma hospitalization andmortality resulting from status asthmaticus. Statusasthmaticus is usually more common among personsin low socioeconomic groups, regardless of race, andparticularly in people who live alone.

Internationally: Similar to the US data, asthmamortality rates are increasing.

Mortality/Morbidity:

Patients who delay medical treatment, particularlytreatment with systemic steroids, have a greaterchance of dying.

Patients with other preexisting conditions (eg,restrictive lung disease, congestive heart failure, chest

deformities) are at particular risk of death from statusasthmaticus.

Patients who smoke regularly have chronicinflammation of the small airways and are at particularrisk of death from status asthmaticus.

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Race:

A recent study by Hanania et al noted that althoughasthma is more common among African American

and Hispanic persons, this prevalence may be theresult of socioeconomic factors rather than race.

African American and Hispanic persons in the UnitedStates, in association with lower socioeconomicfactors, have less access to regular specialist medicalcare, which leads to an increased risk of statusasthmaticus.

In the United States, particularly in large cities,illiteracy and lower educational competence are more

prevalent in African American and Hispanic families,and children in these families have increasedmorbidity from asthma.

Sex:

Status asthmaticus is slightly more common in malesthan in females.

Age:

Status asthmaticus can occur in persons of any agegroup, including infants and geriatric patients.Mortality rates are higher in very young children andelderly adults.

Children younger than 2 years, and sometimes thoseolder, may have respiratory syncytial virus (RSV)infections that can result in severe attacks ofwheezing that mimic status asthmaticus. Also, RSVinfections can predispose patients to asthma later inlife.

CLINICAL Section 3 of 10


History:
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Patients with status asthmaticus have severe dyspneathat has developed over hours to days.

Frequently, patients have a prior history of

endotracheal intubation and mechanical ventilation,frequent emergency department visits, and previoususe of systemic corticosteroids.

Patients usually present with audible wheezing.

Physical:

Patients are usually tachypneic upon examinationand, in early stages of status asthmaticus, may havesignificant wheezing. Initially, wheezing is heard only

during expiration, but, later, wheezing occurs duringboth expiration and inspiration.

The chest is hyperexpanded, and accessory muscles,particularly the sternocleidomastoid, scalene, andintercostal muscles, are used. Later, asbronchoconstriction worsens, patients' wheezing maydisappear, which may indicate severe airflowobstruction.

Normally, the pulsus paradoxus (ie, the difference in

systolic blood pressure between inspiration andexpiration) does not exceed 15 mm Hg. In patientswith severe asthma, a pulsus paradoxus of greaterthan 25 mm Hg usually indicates severe airwayobstruction.

Causes:

In persons with acute asthma, bronchospasms occuras a result of one or more inciting factors that mayinclude, but are not limited to, a viral upper or lower

respiratory tract infection, significant allergic responseto an allergen (eg, pollen, mold, animal dander, housedust mites), exposure to an irritant, or vigorousexercise in a cold environment.

Precipitating factors can include infection, allergen orirritant exposure, poor adherence to the medicalregimen, strenuous exercise, and a rapid decrease in


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long-term oral steroid therapy.

Inflammation can be the result of infection;lymphocyte, mast cell, eosinophilic, and neutrophilicresponses; and airway epithelial damage.

DIFFERENTIALS Section 4 of 10


Pulmonary Hypertension, Primary

Other Problems to be Considered:

Congestive heart failureCroupStridorUpper airway obstructionOrthopnea

WORKUP Section 5 of 10

Author InformationIntroductionClinicalDifferentialsWorkupTreatmentMedicationFollow-upMiscellaneousBibliography

Lab Studies:

Obtain a CBC count and differential to evaluate for infectious causes (eg,pneumonia, viral infections such as croup), allergic bronchopulmonaryaspergillosis, and Churg-Strauss vasculitis.

Obtain an arterial blood gas (ABG) value to assess the severity of the asthmaattack and to substantiate the need for more intensive care. ABGdeterminations are indicated when the peak expiratory flow (PEF) rate orforced expiratory volume in one second (FEV1) is less than or equal to 30% ofthe predicted value or when the patient shows evidence of fatigue orprogressive airway obstruction despite treatment. ABG values are importantto help determine the severity of the asthma attack. The 4 stages of bloodgas progression in persons with status asthmaticus are as follows:

o The first stage is characterized by hyperventilation with a normal

partial pressure of oxygen (PO2).

o The second stage is characterized by hyperventilation accompanied

by hypoxemia (ie, a low partial pressure of carbon dioxide [PCO2] and
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low PO2).

o The third stage is characterized by the presence of a false-normalPCO2; ventilation has decreased from the hyperventilation present inthe second stage. This is an extremely serious sign of respiratory

muscle fatigue that signals the need for more intensive medical care,such as admission to the ICU and, probably, intubation withmechanical ventilation.

o The last stage is characterized by a low PO2 and a high PCO2, which

occurs with respiratory muscle insufficiency. This is an even moreserious sign that mandates intubation and ventilatory support.

Imaging Studies:

Obtain a chest radiograph to evaluate for pneumonia, pneumothorax,

congestive heart failure, and signs of chronic obstructive pulmonary disease,which would complicate the patient's response to treatment or reduce thepatient's baseline spirometry values.

Other Tests:

The most important and readily available test to evaluate the severity of anasthma attack is the measurement of PEF. PEF monitors are commonlyavailable to patients for use at home, and they provide patients with asthmawith a guideline for changes in lung function as they relate to changes insymptoms. In most patients with asthma, a decrease in peak flow as a

percent of predicted value correlates with changes in spirometry values.

According to the guidelines of the National Heart, Lung, and BloodInstitute/National Asthma Education and Prevention Program, severe asthmaexacerbation is usually associated with a PEF rate or FEV1 of less than 50%of the predicted value. Also, hospitalization is generally indicated when thePEF or FEV1 after treatment is greater than 50% of the predicted value butless than 70% of the predicted value. Hospitalization in the ICU is indicatedwhen the PEF value or FEV1 is less than 50% of predicted.

A drop in the FEV1 to less than 25% of the predicted value indicates a severe

airway obstruction.

A patient with an FEV1 of greater than 60% of the predicted value may betreated in an outpatient setting, depending on the clinical situation. However,if the patient's FEV1 or PEF rate drops to less than 50% of predicted,admission to the hospital is recommended.

Pulse oximetry and spirometry values should be used to monitor the


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progression of asthma. As the results indicate improvement, treatment maybe adjusted accordingly.

o If a portable spirometry unit is not available, a PEF rate of 20% or less

of the predicted value (ie, usually


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for 30 seconds or more, signaling increased airway reactivity.

o Peripheral airway inflammation and obstruction are signaled byincreased resistance at low (5 cycles/s) oscillation frequencies that aredecreased at higher oscillation frequencies (15 or 20 cycles/s). In

association with the fall in resistance from 5 to 15 cycles per second,the magnitude of respiratory reactance in peripheral airwayinflammation and obstruction increases.

o Careful attention must be paid to whether patients have their lips fully

closed around the mouthpiece. Patients with acute dyspnea may feelconstrained breathing through a mouthpiece and may reflexively opentheir mouths to increase airflow during late inspiration. This isanalogous to flaring alae nasi with dyspnea and results incharacteristic airflow leak patterns. This causes underestimation oftrue airflow resistance. IOS tests with such airflow leak patterns must

be repeated after reassuring the patient and ensuring closure of thelips around the mouthpiece.

Histologic Findings: Autopsy results from patients who died from statusasthmaticus of brief duration (ie, developed within hours) show neutrophilicinfiltration of the airways. In contrast, results from patients who developed statusasthmaticus over days show eosinophilic infiltration. Autopsy results also showextensive mucus production and severe bronchial smooth muscle hypertrophy.However, the predominant response, based on results from bronchoalveolar lavagestudies, is eosinophilic in nature. The eosinophil itself can lead to epithelialdestruction through its own degrading products (eg, cationic proteins). This

destruction can result in inflammation and, later, a neutrophilic response.

Staging: The 4 stages of status asthmaticus are based on ABG progressions instatus asthma.

Patients in stage 1 or 2 may be admitted to the hospital, depending on the severityof their dyspnea, their ability to use accessory muscles, and their PEF values orFEV1 after treatment (>50% but


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these patients may benefit from ipratropium treatment via a handheldnebulizer in the emergency setting as an adjunct to beta-agonists.

Stage 2

o

This stage is similar to stage 1, but patients are hyperventilating andhypoxemic.o Such patients may still be discharged from the emergency department,

depending on their response to bronchodilator treatment, but willrequire systemic corticosteroids.

Stage 3

o These patients are generally ill and have a normal PCO2 due torespiratory muscle fatigue. Their PCO2 is considered a false-normalvalue and is a very serious sign of fatigue that signals a need for

expanded care. This is generally an indication for elective intubationand mechanical ventilation, and these patients require admission tothe ICU.

o Parenteral corticosteroids are indicated, as is continued aggressive

use of an inhaled beta2-adrenergic bronchodilator.o These patients may benefit from theophylline.

Stage 4

o This is a very serious stage in which the PO2 is low and the PCO2 is

high, signifying respiratory failure.

o These patients have less than 20% lung function or FEV1 and requireintubation and mechanical ventilation.

o Patients in stage 4 should be admitted to the ICU. Switching from

inhaled beta-2 agonists and anticholinergics to metered-dose inhalers(MDIs) via mechanical ventilator tubing is indicated.

o Parenteral steroids are essential, and theophylline may be added, aswith patients in stage 3.

TREATMENT Section 6 of 10


Medical Care: After confirming the diagnosis and assessing the severity of theasthma attack, direct treatment toward controlling bronchoconstriction andinflammation.

Bronchodilator treatment with beta-2 agonistso The first line of therapy is bronchodilator treatment with a beta-2
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agonist, typically albuterol.o Handheld nebulizer treatments may be administered either

continuously (10-15 mg/h) or by frequent timing (eg, q5-20min),depending on the severity of the bronchospasm.

o The dose of albuterol for intermittent dosing is 0.3-0.5 mL of a 0.5%

formulation mixed with 2.5 mL of normal saline. Many of thesepreparations are available in a premixed form with a concentration of0.083%.

o Studies have also shown an excellent response to well-supervised use

of albuterol via an MDI with a chamber. The dose is 4 puffs, repeatedat 15- to 30-minute intervals as needed. Most patients respond within1 hour of treatment.

o Recently, the US Food and Drug Administration approved the use of

the R isomer of albuterol known as levalbuterol, for treating patientswith acute asthma. This isomer has fewer effects on the heart rhythm(ie, tachyarrhythmia) and is associated with fewer occurrences of

tremors, while having the same or greater clinical bronchodilatoreffects as racemic albuterol.o The decreased prevalence of adverse effects with this new medication

may allow physicians to use nebulizer therapy in patients with acuteasthma more frequently with less concern over the adverse effects ofother bronchodilators (eg, albuterol, metaproterenol). The dose oflevalbuterol is either a 0.63-mg vial for children or a 1.26-mg vial foradults.

o These drugs, especially albuterol, are safe to use during pregnancy.

Nonselective beta-2 agonists

o Patients whose bronchoconstriction is resistant to continuoushandheld nebulizer treatments with traditional beta-2 agonists may becandidates for nonselective beta-2 agonists (eg, epinephrine [0.3-0.5mg] or terbutaline [0.25 mg]) administered subcutaneously. However,systemic therapy has no proven advantage over aerosol therapy withselective beta-2 agents.

o Exercise caution in patients with other complicating factors (eg,

congestive heart failure, history of cardiac arrhythmia).o Intravenous isoproterenol is not recommended for the treatment of

asthma because of the risk of myocardial toxicity.

Ipratropium treatmento Ipratropium, which comes in premixed vials at 0.2%, can be synergistic

with albuterol or other beta-2 agonists.o Ipratropium is administered every 4-6 hours.o Because children appear to have more cholinergic receptors, they are

more responsive to parasympathetic stimulation than adults.

Oxygen monitoring


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o Monitoring the patient's oxygen saturation is essential during the initial

treatment.o ABG values are usually used to assess hypercapnia during the

patient's initial assessment.o Oxygen saturation is then monitored via pulse oximetry throughout the

treatment protocol. Oxygen therapy

o Oxygen therapy is essential. It can be administered via a nasal canula

or mask, although patients with dyspnea often do not like masks.o With the advent of pulse oximetry, oxygen therapy can be easily

titrated to maintain the patient's oxygen saturation above 92% (>95%in pregnant patients or those with cardiac disease).

Glucocorticosteroidso Steroids are the most important treatment for status asthmaticus.

o The usual dose is oral prednisone at 1-2 mg/kg/d.

o In the authors' experience, methylprednisolone provides excellentefficacy when given intravenously at 1 mg/kg/dose every 6 hours.

o Some authorities report that pulse therapy with steroids at a high dose

(eg, 10-30 mg/kg/d as a single dose) is associated with a more rapidresponse and shorter hospitalization and has similar adverse effects;however, this is not standard therapy. Adverse effects of pulsetherapy, in the authors' experiences, are minimal and comparable tothe traditional doses of intravenous steroids. The adverse effects mayinclude hyperglycemia, which is usually reversible once steroid therapyis stopped; increased blood pressure; weight gain; increased striaeformation; and hypokalemia. Long-term adverse effects depend on the

duration of steroid therapy after the patient leaves the hospital.o Steroid treatment for acute asthma is necessary but has potential

adverse effects. The serum glucose value must be monitored, andinsulin can be administered on a sliding scale if needed. Monitoring apatient's electrolyte levels, especially potassium, is essential.Hypokalemia can cause muscle weakness, which may worsenrespiratory distress and cause cardiac arrhythmias.

Nebulized steroidso The use of nebulized steroids for treating status asthmaticus is

controversial. Recent data comparing nebulized budesonide withprednisone in children suggest that the latter therapy is more effective

for treating status asthmaticus.o No good scientific evidence supports using nebulized dexamethasone

or triamcinolone via a handheld nebulizer. In fact, in the authors'experiences, more adverse effects, including a cushingoid appearanceand irritative bronchospasms, have occurred with these nebulizers.

Fluid replacement: Intravenous fluids are administered to restore euvolemia. Antibiotics

o The routine administration of antibiotics is discouraged.


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o Patients are administered antibiotics only when they show evidence of

infection (eg, pneumonia, sinusitis).

Aminophyllineo Conflicting reports on the efficacy of aminophylline therapy have made

it controversial.o Starting intravenous aminophylline may be reasonable in patients who

do not respond to medical treatment with bronchodilators, oxygen,corticosteroids, and intravenous fluids within 24 hours.

o Recent data suggest that aminophylline may have an anti-

inflammatory effect in addition to its bronchodilator properties.o The loading dose is usually 5-6 mg/kg, followed by a continuous

infusion of 0.5-0.9 mg/kg/h.o Physicians must monitor a patient's theophylline level. Traditionally,

the level was targeted to the higher end of the local therapeutic range;however, many authorities suggest that the lower portion of the range

(ie, >5 but


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Corticosteroids are essential in the treatment of patients with status asthmaticus.The mechanism of action of corticosteroids can include a decrease in mucusproduction, an improvement in oxygenation, a reduction in beta-agonists ortheophylline requirements, and the activation of properties that may prevent latebronchoconstrictive responses to allergies and provocation. Corticosteroids can

decrease bronchial hypersensitivity, reduce the recovery of eosinophils and mastcells in bronchioalveolar lavage fluid, and decrease the number of activatedlymphocytes. Corticosteroids also help regenerate the bronchial epithelial cells.

The exact mode of corticosteroid action is not well understood. Their anti-inflammatory effect depends, at least partially, on inhibiting phospholipase A2,which can lead to prostaglandin inhibition and leukotriene synthesis.Corticosteroid action usually requires at least 4-6 hours from administrationbecause it requires protein synthesis before it initiates anti-inflammatory effects.Because of this, patients with status asthmaticus must depend on othersupportive measures (eg, beta-2 agonists, oxygen, adequate ventilation) in their

initial treatment while awaiting the action of corticosteroids.

Theophylline preparations are also used in patients with status asthmaticus.Usually, theophylline is given parenterally, but it can also be given orally,depending on the severity of the attack and the patient's ability to takemedications. This class of drugs can induce tachycardia and decrease theseizure threshold (especially in children); therefore, therapeutic monitoring ismandatory.

Typical theophylline levels range from 10-20 mcg/mL; however, adverse effectscan occur even with therapeutic levels. A safer range is 10-15 mcg/mL, although

seizures have occurred even with levels below 10 mcg/mL. Theophylline alsohas significant drug interactions with medications such as ciprofloxacin, digoxin,and warfarin (Coumadin). These interactions may decrease the rate oftheophylline clearance by interfering with P-450 site metabolism. On the otherhand, phenytoin (Dilantin) and cigarette smoking can increase the rate ofmetabolism of theophylline and, therefore, can decrease the therapeutic level ofthe drug.

Manage the theophylline dose in persons who previously smoked but quit fewerthan 6 months ago as if they are still smoking. Patients who smoke or those onphenytoin require higher loading and maintenance doses of theophylline. Otheradverse effects can include nausea, vomiting, and palpitations.

The usual loading dose of theophylline is 6 mg/kg, followed by maintenancedoses of 1 mg/kg/h in the emergent setting. In patients who smoke, themaintenance dose may be higher and the loading dose may be slightly higher.Patients on phenytoin should also receive increased maintenance doses oftheophylline. Patients with liver disease or elderly patients may require amaintenance dose as low as 0.25 mg/kg/h.


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Theophylline can induce bronchodilation, stimulate the central respiratory cycle,reduce diaphragmatic muscle fatigue, and relax vascular smooth muscles. Themechanism of action includes an increased cyclic adenosine monophosphateconcentration by the inhibition of phosphodiesterase; however, this usuallyoccurs when the concentration of theophylline is toxic. Therefore, the true

mechanism of action of theophylline is still unclear, but a possible explanation forthe bronchodilatation may be related to adenosine antagonism. Theophylline isavailable in multiple preparations, both short- and long-acting. For patients withstatus asthmaticus, short-acting preparations are preferred; however, parentalpreparations are even better.

The addition of the anticholinergic ipratropium, which comes in premixed vials at0.2%, sometimes results in additional bronchodilation beyond that achieved withalbuterol.

Drug Category: Beta-adrenergic agonists -- Relieve reversible

bronchospasm by relaxing smooth muscles of the bronchi.

Drug Name

Albuterol (Ventolin, Proventil) -- Use forbronchospasms refractory to epinephrine.Relaxes bronchial smooth muscles byaction on beta-2 receptors, with littleeffect on cardiac muscle contractility.First DOC because it can quickly reverseasthma bronchoconstriction. Availableinhaled via MDI or HHN and orally forthose too young to use nebulizer.

Reserve oral dosing for preventative orlonger-acting use.

Adult Dose

PO: 2-4 mg PO tid/qid; not to exceed 32mg/dInhaler: 1-2 puffs q4-6h; not to exceed 12puffs/dNebulizer: Dilute 0.5 mL (2.5 mg) of 0.5%inhalation solution in 1-2.5 mL of NS;administer 2.5-5 mg q4-6h, diluted in 2-5mL sterile saline or water

Pediatric Dose PO2-5 years: 0.1-0.2 mg/kg tid; not toexceed 12 mg/d5-12 years: 2 mg tid/qid; not to exceed 24mg/d>12 years: Administer as in adultsInhaler


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>12 years: Administer as in adultsNebulizer5 years: Administer as in adults

Contraindications Documented hypersensitivity

Interactions

Beta-adrenergic blockers antagonizeeffects; inhaled ipratropium may increaseduration of bronchodilatation;cardiovascular effects may increase withMAOIs, inhaled anesthetics, TCAs, andsympathomimetic agents

PregnancyC - Safety for use during pregnancy has

not been established.

Precautions

Caution in hyperthyroidism, diabetesmellitus, and cardiovascular disordersAdverse effects include irritability,particularly in children; tachycardia(patients with baseline cardiacabnormalities have decreased thresholdfor tachyarrhythmia); and electrolyteabnormalities (eg, hypokalemia)Ventilation of areas that are not wellperfused may lead to ventilation-

perfusion mismatch, which can beproblematic in severe asthmaIn outpatient setting, inappropriate use(ie, overuse of MDIs) can lead toparadoxical response of increasedbronchial obstruction and may inducestatus asthmaticus

Drug Name

Levalbuterol (Xopenex) -- Moderatelyselective beta2-receptor agonist. Activeenantiomer of racemic albuterol and morepotent than racemic mixture. Decreasedoccurrence of adverse effects may allowuse of more frequent nebulizer therapy inpatients with acute asthma with lessconcern over adverse effects of otherbronchodilators (eg, albuterol,metaproterenol).

Adult Dose 0.63-1.25 mg nebulized q6-8h; may be


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given more frequently during emergentsituations

Pediatric Dose

>12 years: Administer as in adults


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intervalsOnce patient is stabilized, use lowesteffective dose

Pediatric Dose

Powder in caps for use with Spinhaler>5 years: 20 mg inhaled qid at regular

intervalsMDI5 years: 2 puffs (800 mcg/puff) qid atregular intervalsNebulizer2-12 years: 20 mg inhaled qid at regularintervals>12 years: Administer as in adultsOnce patient is stabilized, use lowesteffective dose

ContraindicationsDocumented hypersensitivity; severerenal or hepatic impairment

Interactions None reported

PregnancyC - Safety for use during pregnancy hasnot been established.

Precautions

Do not use with severe renal or hepaticimpairment; exercise caution whenwithdrawing drug because symptomsmay recur

Drug Category: Corticosteroids -- Maintenance medications that decreaseinflammatory mediators to limit airway remodeling. Must be taken regularly to bebeneficial. Glucocorticoids do not relieve acute bronchospasm, and short-actingbronchodilators must be available. Multiple formulations are available that are notequivalent on a per-dose or per-mcg basis. Inhaled corticosteroids are one of themost important developments in asthma management because they decreaseinflammation. These agents are proven to improve lung function (FEV1 andairway hyperactivity) and decrease symptoms, exacerbation frequency, and theneed for rescue inhalers.

Drug Name

Methylprednisolone (Solu-Medrol) -- Fortreatment of inflammatory and allergicreactions. By reversing increasedcapillary permeability and suppressingPMN activity, may decreaseinflammation. Other corticosteroids maybe used in equivalent dosages.

Adult Dose Loading dose: 125-250 mg IV


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Maintenance dose: 4 mg/kg/d IV individed doses q4-6h

Pediatric DoseLoading dose: 2 mg/kg IVMaintenance dose: 4 mg/kg/d IV individed doses q6h

ContraindicationsDocumented hypersensitivity; viral,fungal, or tubercular skin infections

Interactions

Coadministration with digoxin mayincrease digitalis toxicity secondary tohypokalemia; estrogens may increaselevels; phenobarbital, phenytoin, andrifampin may decrease levels (adjustdose); monitor patients for hypokalemiawhen taking concurrently with diuretics

Pregnancy

C - Safety for use during pregnancy has

not been established.

Precautions

Hyperglycemia, edema, osteonecrosis,peptic ulcer disease, hypokalemia,osteoporosis, euphoria, psychosis,growth suppression, myopathy, andinfections are possible complications ofglucocorticoid use

Drug Category: Bronchodilators-- Act to decrease muscle tone in both smalland large airways in lungs, thereby increasing ventilation.

Drug Name

Theophylline (Aminophyllin) -- Potentiates exogenouscatecholamines and stimulates endogenous catecholaminerelease and diaphragmatic muscular relaxation, which, inturn, stimulates bronchodilation. For bronchodilation, neartoxic (>20 mg/dL) levels are usually required.

Adult Dose5.6 mg/kg loading dose (based on aminophylline) IV over 20min, followed by maintenance infusion of 0.1-1.1 mg/kg/h

Pediatric Dose

6 weeks to 6 months: 0.5 mg/kg/h loading dose IV in first 12h (based on aminophylline), followed by maintenanceinfusion of 12 mg/kg/d thereafter; may administercontinuous infusion by dividing total daily dose by 24 h6 months to 1 year: 0.6-0.7 mg/kg/h IV in first 12 h asloading dose, followed by maintenance infusion of 15mg/kg/d; may administer as continuous infusion, as above>1 year: Administer as in adults

Contraindications Documented hypersensitivity; uncontrolled arrhythmia,peptic ulcers, hyperthyroidism, uncontrolled seizure


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disorders

Interactions

Aminoglutethimide, barbiturates, carbamazepine,ketoconazole, loop diuretics, charcoal, hydantoins,phenobarbital, phenytoin, rifampin, isoniazid, andsympathomimetics may decrease effects; allopurinol, beta-

blockers, ciprofloxacin, corticosteroids, disulfiram,quinolones, thyroid hormones, ephedrine, carbamazepine,cimetidine, erythromycin, macrolides, propranolol, andinterferon may increase effects

PregnancyC - Safety for use during pregnancy has not beenestablished.

Precautions

Caution in peptic ulcer, hypertension, tachyarrhythmia,hyperthyroidism, and compromised cardiac function; do notinject IV solution faster than 25 mg/min; patients diagnosedwith pulmonary edema or liver dysfunction are at greater

risk of toxicity because of reduced drug clearance

Drug Category:Anticholinergics-- Thought to work centrally by suppressingconduction in vestibular cerebellar pathways. May have inhibitory effect onparasympathetic nervous system.

Drug Name

Ipratropium bromide (Atrovent) -- Synthetic ammoniumcompound very structurally similar to atropine. May provideadditive benefit to inhaled beta-2 agonists when treatingsevere acute asthma exacerbations. Also may bealternative bronchodilator for patients unable to tolerate

inhaled beta-2 agonists. Children may be more responsiveto parasympathetic inhibition than adults because childrenappear to have more cholinergic receptors.

Adult DoseMDI: 2 puffs (18 mcg/puff) qidNebulizer: 500 mcg tid/qid

Pediatric Dose

MDI3-14 years: 1-2 puffs (18 mcg/puff) tid/qid>14 years: Administer as in adultsNebulizer


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Pregnancy B - Usually safe but benefits must outweigh the risks.

PrecautionsNot indicated for emergent episodes of bronchospasm;caution in narrow-angle glaucoma, prostatic hypertrophy,and bladder neck obstruction

FOLLOW-UP Section 8 of 10Author InformationIntroductionClinicalDifferentialsWorkupTreatmentMedicationFollow-upMiscellaneousBibliography

Further Inpatient Care:

Sedatives

o Patients may benefit from sedatives in very small doses and under

controlled, monitored settings. Sedatives should be used judiciously, if at all. For example, lorazepam (0.5 or 1 mg

intravenously) could be used for patients who are very anxious andare undergoing appropriate and aggressive bronchodilator therapy.

o More powerful agents (eg, oxybutynin) can be administered tointubated patients to achieve sedative, amnestic, and anxiolyticeffects.

Mechanical ventilation

o Consider mechanical ventilation as a last resort in patients with

status asthmaticus.o

Mechanical ventilation in patients with asthma requires carefulmonitoring because these patients have high end-expiratorypressure and, therefore, are at very high risk for pneumothorax.

o Mechanical ventilation, when used in patients with asthma, is

usually required for less than 72 hours; however, in occasionalpatients with severe bronchospasm, mechanical ventilation can beprolonged. In these situations, consultation with a pulmonologist oranother expert in mechanical ventilatory techniques is likely useful.

Other treatments

o

Other treatments have been used, but none is well proven inpatients with severe acute asthma.o A combination of helium and oxygen known as heliox (ie, 30/70

mixture) has been used, but this treatment should only beconsidered in patients who are able to take deep breaths becausethe treatment is dependent on inspiratory flow.

o Intravenous magnesium sulfate can be tried, especially in pregnantwomen, as an adjunct to beta-2 bronchodilator therapy.
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o Nitrate oxide has recently been tried in a child with refractory

asthma. The future role of this therapy remains to be determined.o Leukotriene modifiers are useful for treating chronic asthma but not

acute asthma. This treatment may be beneficial if used via anebulizer, but it remains experimental.

Hydrationo Hydration, such as normal saline at a reasonable rate (eg, 150

mL/h), is essential.o Special attention to the patient's electrolyte status is important.

o Hypokalemia may result from either steroid use or beta-agonistuse. Correcting hypokalemia helps wean an intubated patient withasthma. Hypophosphatemia may result from poor oral intake and isalso an important consideration when weaning such patients.

Intravenous antibiotics

o Intravenous antibiotics are important in patients with acute asthmaonly if they have evidence of an infection (eg, pneumonia, sinusitis).

o In some situations, sinus imaging using CT scanning or plain

radiography may be essential to help rule out chronic sinusitis.

Further Outpatient Care:

Instruct patients to use of inhalers appropriately, to be compliant withtherapy, and to practice stress-avoidance measures. Stress factors (ie,triggers of asthma attacks) include pet dander, house dust, and mold.Strongly discourage patients from smoking; this practice should be

avoided at all costs. Finally, appropriate follow-up is important, as ischecking the patient's peak flow meter and FEV1 at home or in the office,respectively.

Children with asthma commonly present with normal FEV1, and,accordingly, more sensitive lung function testing should be undertakenwith regular IOS assessments. Medication titration may be usefully guidedby IOS resistance and reactance values.

Deterrence/Prevention:

Status asthmaticus can be prevented if patients are compliant with theirmedications and they avoid stress factors; however, it can occur evenwhen patients are compliant and doing well as outpatients. In suchsituations, search for an occult infection (eg, RSV in children but rarely inadults; occult sinus infection).

Prevention of status asthmaticus may be aided by monitoring forcedoscillation test results rather than spirometry findings. This is particularly


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true for children younger than 12 years; however, adults with reactiveairways may be undertreated if the criterion for stability and normality is aspirometric FEV1 greater than 80% of the predicted value.

Complications:

Pneumothorax may complicate acute asthma, either because of increasedairway pressure or as a result of mechanical ventilation. Superimposedinfection can also occur in intubated patients. Patients may require a chesttube for pneumothorax or aggressive antibiotic therapy for asuperimposed infection.

Prognosis:

In general, unless a complicating illness such as congestive heart failureor chronic obstructive pulmonary disease is present, with appropriate

therapy status asthmaticus has a good prognosis. A delay in initiatingtreatment is probably the worst prognostic factor. Delays can result frompoor access to health care on the part of the patient or even delays inusing steroids. Patients with acute asthma should use steroids early andaggressively.

Patient Education:

One important aspect of patient education is that asthma is a disease ofairway inflammation; it is not simply bronchospasms. Airway inflammationis a continuing process that renders patients with asthma vulnerable to

acute bronchospasms. Symptoms are more dependent onbronchospasms than on inflammation; thus, symptoms may becomeminimal in the presence of continued peripheral airway inflammation.Because patients often wish to discontinue inhaled corticosteroids whenthey are free of acute bouts of wheezing, educating them regarding theneed for controller medications to minimize peripheral airway inflammationis important.

Patients can be shown the results of forced oscillation testing that occurwith peripheral airway inflammation and obstruction. Review the testresults with patients and show them the improvement with inhaled

corticosteroids and the deterioration when they are not compliant with anti-inflammatory medications. This information may materially enhancepatients' awareness of the need for continuing treatment, despite anabsence of wheezing.

For excellent patient education resources, visit eMedicine's AsthmaCenter. Also, see eMedicine's patient education articles, Asthma, AsthmaFAQs, and Understanding Asthma Medications.
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MISCELLANEOUS Section 9 of 10


Medical/Legal Pitfalls:

Failure to initiate steroid therapy or intubation with mechanical ventilation

Failure to obtain sinus imaging or to monitor the patient's electrolytebalance

Failure to admit a wheezing patient with a normal PCO2: Such patientstypically have respiratory muscle fatigue and require hospital admission.

Failure to treat expediently, especially with bronchodilators

Failure to educate patients upon discharge about the appropriate use oftheir inhalers, the importance of therapy compliance, and the efficacy ofstress-avoidance measures

Special Concerns:

Treat pregnant women with acute asthma in the same aggressive manneras nonpregnant women. Respiratory acidosis can be detrimental to boththe fetus and the mother. Use special abdominal shielding during chestradiography or sinus imaging.

Treat children with acute asthma in manner similar to that for adults,except when children are mechanically ventilated, because their chestsare more compliant and require special attention.

BIBLIOGRAPHY Section 10 of 10


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Ducharme FM, Davis GM: Measurement of respiratory resistance in the

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