Asthma

Description

Asthma describes bronchial hyper-reactivity with reversible airflow obstruction in response to various stimuli. Despite its reversible nature, chronic airway inflammation is a hallmark.
A reactive airway, or bronchial hyper-responsiveness, is also seen in chronic bronchitis, emphysema, allergic rhinitis, and respiratory infections.

Epidemiology

Incidence

7% of US population, increasing yearly

Prevalence

1/2 of all cases develop before the age of 10 years
1/3^rd occur after the age of 40 years
2:1 male:female preponderance up to the age of 30 years, then equalizes

Morbidity

Perioperative occurrence is seen in 0.17–2.4% of asthmatics.
40,000 missed school or work days each day
30,000 asthma attacks daily
5,000 ER visits daily
1,000 hospital admissions daily

Mortality

5000/year

Etiology/Risk Factors

Allergens
Pharmacologic agents (aspirin, beta-blockers, NSAIDS, sulfa)
Infections (viral airway infections increase airway resistance even in non-asthmatics, possibly due to a cholinergic mechanism in the bronchial smooth muscles)
Exercise (post-exercise)
Emotional stress
Cold weather
Abnormal autonomic nervous system regulation
Endotracheal tube, mucus, saliva (anesthetic related)
Pregnant patients administered prostaglandins for abortion or operative delivery

Physiology/Pathophysiology

The above-mentioned triggers can elicit bronchial smooth muscle contraction. Additionally, vagal and sympathetic factors directly modulate airway tone (1,2,3).
Acutely, inflammatory edema and mucus plugging exacerbate airflow limitation. Chronically, airway remodeling, thickening, and abnormal communications occur in the epithelium of the injured airway and in the pulmonary mesenchyma; changes are permanent and can result in progressive damage (1,2,3).
Immunologic–inflammatory pathways involve lymphocytes, eosinophils, neutrophils, mast cells, leukotrienes, and cytokines (1,2,3).
Bronchoconstriction increases (3):
- Work of breathing
- Air trapping
- V/Q mismatch (reduced ventilation that causes shunting)
- Pulmonary vascular resistance (PVR)
- Right ventricle afterload
- Residual volume (RV)
- Functional residual capacity (FRC)
- Total lung capacity (TLC)
- Oxygen consumption
- Carbon dioxide production
Bronchoconstriction decreases:
- Airflow
- FEV₁
- Expiratory reserve volume (ERV)
- Inspiratory reserve volume (IRV)
- FEV₁/FVC
- FEV_25-75%
- Dynamic compliance of lungs
Accessory muscles are recruited to preserve tidal volume (TV) despite increased ERV (from increased FRC and air trapping) (1,2).
Initially, hyperventilation causes respiratory alkalosis. Over time, increased air trapping and respiratory muscle fatigue increase CO₂ retention; therefore, normalization of PaCO₂ reflects decompensation. Extreme air trapping can restrict cardiac filling and "pulmonary tamponade" that can result in pulse-less electrical activity.

Anesthetic GOALS/GUIDING Principles

Assess severity of disease, optimize pulmonary function, and treat acute exacerbation
The anesthetic plan should prevent, suppress, and blunt airway hyper-reactivity; stimuli that do not ordinarily evoke airway responses can precipitate life-threatening bronchoconstriction in the asthmatic.
Diagnose and treat perioperative bronchoconstriction

Diagnosis ⬆ ⬇

Symptoms

Shortness of breath
Chest tightness
Cough

History

Age of onset
Triggers
Treatment history
- Frequency of exacerbations
- Nighttime awakenings
- Rescue inhaler use
- Steroids pulse dose
- ER visits
- Hospitalizations
- ICU admissions
- Intubations

Signs/Physical Exam

Expiratory wheezing
Accessory muscle use
Tachypnea
Diminished or inaudible breath sounds

Medications

"Controller" to modify airway environment
- Inhaled steroids
- Theophylline
- Leukotriene modifiers
- Cromolyn
"Rescue" for acute bronchospasm (quick onset)
- Beta-adrenergic agonists
- Anticholinergics

Diagnostic Tests & Interpretation

Labs/Studies

Pulmonary function tests can aid with diagnosis, and objectively assess severity and response to treatment (FEV, FEV₁/FVC)
CXR (hyperventilation, pneumonia, CHF)
EKG (acute right heart failure, PVCs)
Eosinophilia
ABGs (pCO₂ and pO₂)

CONCOMITANT ORGAN DYSFUNCTION

77% have gastroesophageal reflux disease (GERD); control of GERD may improve asthma symptoms.

Circumstances to delay/Conditions

Acute exacerbation
Chronic sinus infection
Upper respiratory infection
Pneumonia

Classifications

Based on symptoms, nighttime awakenings, short-acting beta-agonist symptoms, interference with normal activity, lung function, oral steroid use
- Mild
- Moderate
- Marked
- Severe/status asthmaticus

Treatment ⬆ ⬇

PREOPERATIVE PREPARATION

Premedications

Consider beta-agonists (MDI, nebulizer)
Consider a steroid stress dose (avoid Addisonian crisis if recent therapy and major surgery)
Consider a steroid pulse dose (avoid perioperative exacerbation in severe disease, or major surgery)
Anxiolysis

INTRAOPERATIVE CARE

Choice of Anesthesia

Consider regional anesthesia to avoid airway instrumentation and stage II emergence (increased risk for bronchoconstriction)
Consider LMA, which sits supraglottically and is associated with less airway irritation than ETT

Monitors

Standard ASA monitors
Consider augmenting the ETCO₂ waveform to improve detection of obstruction; a slow rise to the peak indicates expiratory obstruction.
Consider an arterial line in high-risk patients to allow for ABG monitoring

Induction/Airway Management

Laryngoscopy, intubation, suctioning, and cold inspired gases can exacerbate hyper-reactivity.
Patient should be "deep" prior to airway instrumentation. Ensure that an adequate dosage of induction medications and neuromuscular blockade have been administered, as well as an appropriate amount of time for onset. Induction medications should be titrated to blunt bronchial smooth muscle responsiveness, and NMBD should be titrated to block coughing, gagging, or bucking. Although these are skeletal muscle phenomenon, when provoked, they can precipitate irritant receptors and airway hyper-reactivity.
Consider bag mask ventilating with volatile agents (potent bronchodilators) for 2–3 minutes prior to airway instrumentation
Ketamine is the only bronchodilating IV induction agent; propofol and etomidate blunt airway reflexes to a greater extent than thiopental.
Lidocaine blunts airway response to irritation. However, caution is advised when topically applied; spraying can cause irritation and precipitate bronchospasm.
Succinylcholine has histamine release; however, studies have not shown this to be clinically relevant.
When considering a RSI, the risk of aspiration needs to be weighed against the risk of bronchoconstriction from airway manipulation prior to the patient being "deep."

Maintenance

Keep the patient "deep" or adequately anesthetized. Otherwise, innocuous stimuli can result in increased airway resistance (saliva, mucus, ETT).
I:E ratio should be reduced (increased time for exhalation to avoid air trapping; similar to phenomenon of "pursed lip breathing" in patients with emphysema).
Humidify, warm inspiratory gases
Fluid hydration to soften mucus secretions

Extubation/Emergence

Consider "deep" extubation (removing airway while anesthetic is sufficient to suppress hyper-reactivity)
When it is unwise to extubate before the patient is fully awake, consider suppressing airway reflexes (IV lidocaine, bronchodilators, epinephrine IV/SQ, dexmedetomidine).
Neostigmine may bronchoconstrict if not administered with adequate antimuscarinics.
Antimuscarinics can thicken secretions.

Follow-Up ⬆ ⬇

Bed Acuity

Vigilance for bronchospasm
Consider supplemental oxygen (nasal cannula, face mask)
Consider scheduled bronchodilator treatments
Incentive spirometry and deep breathing
Early mobilization
Good pain control
Control GERD

Complications

Intraoperative bronchospasm is diagnosed by:
- Increased peak inspiratory pressures (PIP)
- ETCO₂ sloping
- Expiratory wheezing
Treatment consists of:
- Deepening the anesthetic with inhaled volatile agents. Volatile agents are potent bronchodilators and cause direct bronchial smooth muscle cell dilation by altering intracellular calcium regulation. However, if there is little or no airway movement, this may not be effective.
- Deepening the anesthetic with intravenous agents. Propofol does not bronchodilate, but it can suppress airway reflexes.
- Inhaled beta-agonists. Albuterol causes bronchodilation, but may require several puffs (8–10) to ensure delivery through a long narrow ETT. There are several devices available that can facilitate delivery.
- Steroids intravenously. Administration should not preclude more immediate therapy.
- Epinephrine (IV bolus, SQ, drip); sympathomimetic that decreases bronchospasm via beta-2 agonist.
- Theophylline may be considered; however, it is more common for symptom control and prevention. Additionally, it has a narrow therapeutic index and levels need to be monitored if continued postoperatively.
- Heliox can promote laminar airflow, but reduces FIO₂, and has not been shown to be therapeutic.
- Magnesium (drowsiness and NMBD potentiation)
- Avoid histamine-releasing medications (e.g. morphine, vancomycin)

References ⬆ ⬇

Woods BD , Sladen RN. Perioperative considerations for the patient with asthma and bronchospasm. Br J Anaesth. 2009;103(S1):i57–i65.
Fanta CH. Asthma. N Engl J Med. 2009;360:1002–1014.
Tirumalasetty J , Grammer LC. Asthma, surgery, and general anesthesia: A review. J Asthma. 2006;43(4):251–254.

Additional Reading ⬆ ⬇

Asthma and Allergy Foundation of America
Burburan SM , Xisto DG , Ferreira HC , et al. Lung mechanisms and histology during sevoflurane anesthesia in a model of chronic allergic asthma. Anesth Analg. 2007;104(3):631–637.
Overview of Changes to Asthma Guidelines. www.aafp.org

See Also (Topic, Algorithm, Electronic Media Element)

Ventilation Perfusion Matching
Ventilation Perfusion Mismatching
Pulmonary Function Tests
Functional Residual Capacity
End Tidal Co2
I:E Ratio
Deep Extubation
Laminar Flow

Codes ⬆ ⬇

ICD9

493.90 Asthma,unspecified type, unspecified
493.92 Asthma, unspecified type, with (acute) exacerbation

ICD10

J45.901 Unspecified asthma with (acute) exacerbation
J45.909 Unspecified asthma, uncomplicated

Clinical Pearls ⬆ ⬇

Assess the severity of disease in order to plan an appropriate anesthetic technique.
Stimuli that do not ordinarily evoke airway responses can precipitate life-threatening bronchoconstriction in asthmatics. Ensure that the patient is adequately induced prior to airway manipulation, as well as remains adequately anesthetized during the surgery; consider a "deep" extubation.
Intraoperative bronchoconstriction presents as increased PIP, a sloping ETCO₂ waveform, and wheezing.
All that wheezes is not asthma; rule out other causes prior to treating for bronchospasm.
Asthma increases the risk of bronchospasm, hypoxemia, hypercapnia, inadequate cough, atelectasis, and pulmonary infection following surgery.

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Basics ⬇