8. Obstructive vs Restrictive disorders
Obstructive Restrictive
Limitation of airflow usually
resulting from an increase in
resistance caused by partial or
complete obstruction at any level
Reduced expansion of lung
parenchyma accompanied by
decreased total lung capacity.
COPD – Emphysema, chronic
bronchitis; bronchiectasis,
asthma
ARDS, Interstitial lung disease,
such as idiopathic pulmonary
fibrosis,Sarcoidosis, Scoliosis
Neuromuscular disease –
muscular dystrophy
9. Bronchial Asthma
Definition:
Chronic inflammatory disease of airways that is characterized
by increased responsiveness of lower airways to multiple
stimuli; episodic, and with reversible obstruction; may range in
severity from mild without limitation of patient’s activity to
severe and life-threatening.
Severe obstruction persisting for days or weeks is known as
status asthmaticus.
(--Harrison’s Manual of Medicine-16thEd.)
10. Prevalence
Asthma affects 300 million persons worldwide and accounts for 1 of every
250 deaths worldwide
Prevalence in India – 3%
*Global Burden of Asthma Report, GINA May 2004
12. Etiology
Multifactorial and heterogeneous disease
Exact cause not completely understood
Four categories based on pathophysiology:
Extrinsic (allergic or atopic),
Intrinsic (idiosyncratic, non-allergic, or non-atopic),
Drug-induced,
Occupational asthma
17. Clinical Features
Dyspnea, coughing and expiratory wheezing
May be worse at night and patients typically awake in the
early morning hours
Onset usually is sudden, with peak symptoms occurring
within 10 to 15 minutes.
Tenacious mucus that is difficult to expectorate
Prodromal symptoms may precede an attack
with itching under the chin,
discomfort between the scapulae, or
inexplicable fear
19. Diagnosis
Compatible clinical history plus either/or:
FEV1 ≥ 15% (and 200 ml) increase following administration of a
bronchodilator/trial of corticosteroids
> 20% diurnal variation on ≥ 3 days in a week for 2 weeks on PEF diary
FEV1 ≥ 15% decrease after 6 mins of exercise
20. Other investigations
Bronchial provocation tests with the suspected agent
Skin prick tests
Sputum Eosinophilia
Exhaled nitric oxide levels
Radiological examination – Generally unhelpful. May point to
alternative diagnoses.
HRCT scan may be useful to detect bronchiectasis
21. *National Asthma Education and Prevention Program Guidelines for the Diagnosis and Management of Asthma: 2007 Report
22. Management
Aims of Asthma Therapy
Minimal (ideally no) chronic symptoms, including nocturnal
Minimal (infrequent) exacerbations
No emergency visits
Minimal (ideally no) use of a required β2-agonist
No limitations on activities, including exercise
Peak expiratory flow circadian variation <20%
(Near) normal PEF
Minimal (or no) adverse effects from medicine
25. β2 sympathomimetics
Effects of β2
-Adrenergic
Agonists on
Airways
Relaxation of
airway
smooth
muscle
(proximal and
distal airways)
Inhibition of
mast cell
mediator
release
Inhibition of
plasma
exudation and
airway edema
Increased
mucociliary
clearance
Increased
mucus
secretion
Decreased
cough
No effect on
chronic
inflammation
29. Omalizumab
A recombinant humanized monoclonal antibody that recognizes IgE
Forms complexes with circulating free IgE
Prevents the binding of IgE to the high- and low-affinity receptors on cell
membranes
Impedes the recognition of the allergen by the effector cells
Inhibits their allergen-induced activation
33. Acute Severe Asthma/ Status asthmaticus
Coughing, wheezing, shortness of breath, and chest wall recession (indrawing
in the flesh between the ribs and sternum)
Inability to complete a sentence in one breath,
Use of accessory muscles,
Respiratory rate >30/min,
Pulse >120/min
Presence of pulsus paradoxus severe asthma; PEFR < 60% of the predicted
or best.
Silent chest type asthma.
34. Acute Severe Asthma/ Status asthmaticus
Silent chest
Cyanosis
Feeble respiratory effort
Bradycardia
Hypotension and PEFR <30% of the predicted or best.
Patient may be exhausted, confused and lapses into coma.
ABG normal or high PaCO2 (more than 45 mm Hg), severe hypoxia
(PaO2 <60 mm Hg) and a low pH.
35. Acute Severe Asthma/ Status asthmaticus
40% to 60% oxygen is administered. Achieve sPO2 >95%
Salbutamol 5 mg or terbutaline 10 mg via oxygen driven nebulizer – 2-
4 puffs every 20 min for first hour
Mild exacerbation – 2-4 puffs every 3-4 hours
Moderate exacerbation – 6-10 puffs every 1-2 hrs
Ipratropium 0.5 mg may also be added to the salbutamol nebuliser
solution and repeated every 6 hours.
Prednisolone tablet 0.5-1 mg/kg(30 to 60 mg) or hydrocortisone
hemisuccinate 200 mg through intravenous route – to reverse
inflammation and speed recovery
If unresponsive, 2 gm Magnesium sulphate iv
36. Acute Severe Asthma/ Status asthmaticus
If any patient does not respond to treatment,
Suspect pneumonitis or pneumothorax.
Chest radiograph is useful.
Patient should be closely monitored with
PEFR every 15 to 30 minutes after starting the treatment, and
Pulse oximetry to maintain oxygen saturation above 90%.
Oxygen saturation < 90%, an arterial blood gas analysis should be
done and repeated every 2 hours.
Assisted mechanical ventilation may be required
37. Therapies not recommended*
Sedatives (strictly avoid)
Mucolytic drugs – may worsen cough
Chest physiotherapy – may increase patient discomfort
Hydration with large volumes of fluids for adults and older
children
Antibiotics
Epinephrine – indicated for acute treatment of anaphylaxis and
angioedema not asthma attacks
*GINA Pocket Guide for Asthma management and Prevention; 2012
38.
39. Updating patients health history at every visit about these following
factors will help identify the risk of an acute exacerbation:
Frequency of asthmatic attacks
Precipitating agents
Types of pharmacotherapy used
Length of time since an emergency visit owing to acute asthma
Before Treatment
40. Dental treatment can invoke a significant decrease in pulmonary
function among asthmatic patients.
As a general rule, elective dentistry should be performed only on asthmatic
patients who are asymptomatic or whose symptoms are well-controlled.
The symptomatic person should not be treated, and the presence of asthmatic
symptoms such as coughing and wheezing necessitate reappointment.
Before Treatment
41. During Treatment
The most likely times for an acute exacerbation are:
During and immediately after local anesthetic administration.
With stimulating procedures such as extraction, surgery,
pulp extirpation.
42. During Treatment
At each visit make sure:
Confirm that they have taken their most recent scheduled dose of medication
The patient’s own metered-dose inhaler bronchodilator should be on hand at
each visit to minimize the risk of an attack
Patient’s appointment should be in the late morning or the late afternoon
If the asthmatic patient does not use a bronchodilator, make sure the emergency
kit has both a bronchodilator and oxygen
43. During Treatment
Prophylactic dose of β2 agonist bronchodilator could prevent diminished
lung function during dental treatment.
H1-blocking antihistamines– useful in blunting the bronchoconstrictor
response with a pretreatment dose.
Promethazine and diphenhydramine have the benefit of being antiemetic
and sedative as well as antihistaminic
44. During Treatment
Anxiety is a known asthma trigger thus the dental environment is a common site for
an acute asthmatic attack. Therefore, it should be ascertained that the patient has
taken his or her most recent scheduled dose of antiasthma medication before
treatment
Substantive stress-management techniques should be used
Attempt to lessen fear of dental treatment by gentle handling and reassurance.
45. During Treatment
N2O in patients with mild-to-moderate asthma can prevent acute stress related
symptoms. However, because of its potential for causing airway irritation, N2O is
contraindicated for use in patients with severe asthma. It is advisable to obtain a
medical consultation before administering N2O to such patients
Patients with severe persistent asthma and those who are prone to severe abrupt
episodes of airway obstruction are best given dental treatment in the hospital
46. During Treatment
Check for:
i. Improper positioning of suction tips
ii. Avoid prolonged supine positioning.
iii. Bacteria-laden aerosols from plaque or carious lesions and ultrasonically
nebulized water also can be asthma triggers in the dental setting.
iv. Additionally, aeroallergens such as tooth-enamel dust and methyl methacrylate
have been reported to trigger asthmatic attacks.
47. Be aware that some patients may have an adverse reaction to
nonsteroidal anti-inflammatory drugs.
Avoid use of erythromycin in patients taking theophylline.
Avoid use of phenobarbitals in patients taking theophylline.
Analgesic of choice for these patients is acetaminophen.
After Treatment
48. Acute Asthmatic Attack on Dental
Chair
Discontinue the dental procedure
Allow the patient to assume a comfortable position.
Calm the patient.
Begin basic life support A, B,C,Ds activity as needed.
Administer β2 agonists via inhaler or nebulizer.
Administer oxygen 6-10 liters via face mask, nasal hood or cannula.
49. Acute Asthmatic Attack on Dental
Chair
If no improvement is observed and symptoms are worsening, administer epinephrine
subcutaneously (1:1,000 solution, 0.01 mg/kg of body weight to a maximum dose of 0.3 mg).
Hydrocortisone sodium succinate 100-200 mg iv
Alert emergency medical services-109.
Maintain a good oxygen level until the patient stops wheezing and/or medical assistance
arrives.
Escort patient to hospital as needed.
50. Drugs to be avoided, since they may precipitate an asthmatic attack
Aspirin (also increases serum zafirlukast levels) and other NSAIDs
Barbiturates (e.g. methohexitone)
Beta-blockers
Cyanoacrylates
Drugs causing histamine release directly
Mefenamic acid
Morphine and some other opioids
Pancuronium
Pentazocine
Suxamethonium
Tubocurarine
51. Little and Falace’s Dental Management of the Medically Compromised Patient, 8th Ed.
52. During GA the most important consideration is to prevent reflex
stimulation of airways by laryngoscopy and intubation.
Induction: Although Ketamine has the best bronchodilator
property therefore, theoretically most preferred agent but due to
its side effects not used practically.
Propofol is the most commonly employed agent (because of
bronchodilator property).
Thiopentone can induce bronchoconstriction therefore should be
avoided.
General anesthetic considerations
* Ajay Yadav. Short Textbook of Anesthesia 5th Ed.; 2012
53. Maintenance:
Oxygen, nitrous oxide and sevoflurane.
Sevoflurane is considered as agent of choice.
Halothane most bronchodilator
Sensitizes myocardium; increases the risk of arrhythmias in
patients on β agonist and Aminophylline
Halothane should be avoided
General anesthetic considerations
* Ajay Yadav. Short Textbook of Anesthesia 5th Ed.; 2012
54. Relaxant:
As Benzylisoquinoline compounds by releasing histamine can
produce bronchospasm
Vecuronium should be used.
Cis-atracurium does not release histamine so, can be safely used.
General anesthetic considerations
* Ajay Yadav. Short Textbook of Anesthesia 5th Ed.; 2012
Each bronchopulmonary segment break down into small lobules. Each lobule wrapped in elastic c.t. & contains lymphatic vessel, an arteriole, a venule & branch from terminal bronchiole which subdivides into microscopic respiratory bronchioles.
Respiratory bronchioles divide into subdivide into several alveolar ducts, around the circumference of alveolar ducts are numerous alveoli and alveolar sacs.
Lumen is lined with respiratory epithelium (i.e. pseudostratified columnar ciliated with goblet cells). Goblet cells produce mucous to trap airborne dust particles and pathogens, which are then swept towards the oral cavity via the mucociliary escalator to be coughed or swallowed. The lamina propria has a meshwork of reticular and elastic fibres containing lymphocytes, which provide immunological defence against invading pathogens.
External to the lamina propria, the lumen is encircled with criss-crossing bands of smooth muscle, which constrict the lumen and shorten the airway via contraction, thereby regulating bronchial airflow. (Note: muscularis lies external to submucosa in extrapulmonary (primary) bronchi)
Contains loose connective tissue (CT) and mixed glands, including light-staining mucous glands, whose thick moist secretions coat and protect the luminal surface, and dark-staining serous glands, whose watery proteinaceous secretions flush out the lumen. Externally there are irregular hyaline cartilage plates that provide structural support. (Note: extrapulmonary bronchi contain 8-10 C-shaped hyaline cartilage rings per bronchus)
Rings of cartilage are replaced by plates of cartilage that finally disappear in the bronchioles
As cartilage decreases, amount of smooth muscle increases
Epithelium changes from pseudostratified ciliated to simple cuboidal in terminal bronchioles
IL4 – stimulate IgE production; IL5 – activates eosinophils; IL13– stimulates mucus production
Airway remodeling– hypertrophy of bronchial smooth muscle; deposition of subepithelial collagen
LT—C4,D4,E4– potent mediators– prolonged bronchoconstriction, in. vascular permeability, in mucin secretion
Ach– from intrapulmonary motor nerves – airway smooth muscle constriction by direct + of muscarinic receptors
Histamine – bronchospasm, in vascular permeability
PGD2—bc & vd; PAF:aggregation of platelets release of histamine;
Eotaxin– airway epithelium—chemoattractant and activator of eosinophils
Major basic protein of eosinophils – epi. Damage & more airway constriction
FEV1 – volume of air exhaled during first second of a forced exhalation after a maximum inhalation
FVC – maximum volume of air a person can exhale after deep inhalation
PEFR – maximal rate that a person can exhale during a short maximal expiratory effort after a full inspiration (height in cms – 80)x5
Peak flow meters are inexpensive and widely available,
Provide a simple and straightforward method of confirming the diagnosis.
Ideally patients should be instructed to record peak flow readings after rising in the morning and before retiring in the evening.
A diurnal variation in PEF (the lowest values typically being recorded in the morning) of more than 20% is considered diagnostic.
Radiological examination --Generally unhelpful.
May point to alternative diagnoses.
Acute asthma is accompanied by hyperinflation, and lobar collapse may be seen if mucus has occluded a large bronchus. Flitting infiltrates, on occasion accompanied by lobar collapse, suggest asthma complicated by allergic bronchopulmonary aspergillosis (ABPA).
Upper airway obstruction by a tumor or laryngeal edema can mimic severe asthma, but patients typically present with stridor localized to large airways. The diagnosis is confirmed by a flow-volume loop that shows a reduction in inspiratory as well as expiratory flow, and bronchoscopy to demonstrate the site of upper airway narrowing.
Persistent wheezing in a specific area of the chest may indicate endobronchial obstruction with a foreign body.
Left ventricular failure may mimic the wheezing of asthma but basilar crackles are present in contrast to asthma.
Eosinophilic pneumonias and systemic vasculitis, including Churg-Strauss syndrome and polyarteritis nodosa, may be associated with wheezing.
Chronic obstructive pulmonary disease (COPD) is usually easy to differentiate from asthma as symptoms show less variability, never completely remit, and show much less (or no) reversibility to bronchodilators.
Bronchodilation is promoted by cAMP. Intracellular levels of cAMP can be increased by B-adrenoceptor agonists, which increase the rate of its synthesis by adenylyl cyclase (AC); or by phosphodiesterase (PDE) inhibitors such as theophylline, which slow the rate of its degradation. Bronchoconstriction can be inhibited by muscarinic antagonists and possibly by adenosine antagonists
Usually given by inhalation to reduce side effects.
Short-acting β2-agonists (SABAs) – albuterol and terbutaline (duration of action of 3–6 hours). Rapid onset of bronchodilation, therefore, used as needed for symptom relief.
Increased use of SABAs indicates that asthma is not controlled.
Useful in preventing EIA if taken prior to exercise.
SABAs are used in high doses by nebulizer or via a metered-dose inhaler with a spacer.
Long-acting β2-agonists (LABAs) – salmeterol and formoterol, (duration of action over 12 hours) given twice daily by inhalation. LABAs have replaced the regular use of SABAs, but LABAs should not be given in the absence of ICS therapy as they do not control the underlying inflammation. They do, however, improve asthma control and reduce exacerbations when added to ICS, which allows asthma to be controlled at lower doses of corticosteroids.
Does not bind to cell-bound IgE
Therefore, does not trigger cell activation by crosslinking of the IgE molecules on cell membranes.
Omalizumab reduces the allergen induced late asthmatic response, airway hyperresponsiveness and sputum eosinophilia
Reduces both asthma exacerbations and corticosteroid requirement
Agent may have a long-term anti-inflammatory effect
1- mild, intermittent asthma, a short-acting B2-agonist
2- any patient who: has experienced an exacerbation of asthma in the last 2 years; uses inhaled β2-agonists three times a week or more;reports symptoms three times a week or more; is awakened by asthma one night per week.
ICS given twice daily. It is usual to start with an intermediate dose [e.g., 200 (µg) bid of (beclomethasone dipropionate)
3- poorly controlled despite regular use of ICS; a thorough review of the patient should be made with particular regard to adherence and inhaler technique
Leukotriene receptor antagonists (e.g. montelukast 10 mg daily). Theophyllines may be useful in some patients but their unpredictable metabolism, propensity for drug interactions and prominent side-effect profile have limited their use
4- In adults the dose of ICS may be increased to 2000 μg BDP/BUD daily
5- prednisolone(OD in the morning) in the lowest amount necessary to control symptoms. Patients on long-term corticosteroid tablets (> 3 months) or receiving more than three or four courses per year will be at risk of systemic side-effects
With normal bbreathing, the airways of the lungs are full open as in this cross-section of an airway.
In asthmatics, smooth muscle becomes thicker; during an attack, in response to an allergen or trigger, airway smooth muscle may contract leading to airway narrowing
During bronchial thermoplasty, a small flexible tube is advance into the airway through a standard flexible bronchoscope through mouth or nose. No incision required. The device has an expandable basket at the tip & when it is expanded, 4 arms of basket come in contact with & snugly fit against wall of airway. Controlled radiofrequency energy delivered for about 10 sec to heat the airway smooth muscle 1/3rd of targeted lung areas are treated during a single session. Total of 3 procedures for complete t/t. once the session is completed, device along with bronchoscope is removed. Controlled heat delivered reduces the amount of airway smooth muscle; thus reducing the ability of airway walls to contract in response to irritatin, infection or inflammation.
Pulsus Paradoxus In normal individuals the systolic blood pressure falls by 2 to 4 mm Hg with normal inspiration and 10 mm Hg with deep inspiration. When systolic pressure falls more than 10 mm Hg during inspiration, the pulse is called as pulsus paradoxus. Pulsus paradoxus may also be present in other conditions such as cardiac tamponade, constrictive pericarditis, and superior vena cava obstruction.
If the condition worsens, airways become further narrowed and the movement of air decreases. In such situations, sometimes wheezing ceases. It indicates that the airways are extremely narrowed and very little air is moving in and out. This is also called silent chest type asthma
Aminophylline 250-500 mg diluted in 20-50 ml glucose(5% sol) iv over 20-30 mins- previously used but outdated now
No additional benefit; may produce more adverse effects hence, restrict use to resistant cases
Indication Mechanical Ventilation
Mechanical ventilation is indicated when the spontaneous ventilation is inadequate to sustain life. Initially, some patients may respond to non-invasive ventilation (NIV), therefore a trial of NIV for a period of 1 to 2 hours is a logical approach in selected patients.
Indications
Absolute indication: Cardio-pulmonary arrest, deteriorating consciousness
Relative indications: Hypercapnia, acidosis, progressive deterioration with increasing distress or physical exhaustion
Complications
Hypotension, barotrauma and nosocomial pneumonia
For severe and unstable asthma, consultation with the patient’s physician is advised.
40% to 60% oxygen is administered. Achieve sPO2 >95%
Salbutamol 5 mg or terbutaline 10 mg via oxygen driven nebulizer – 2-4 puffs every 20 min for first hour
Mild exacerbation – 2-4 puffs every 3-4 hours
Moderate exacerbation – 6-10 puffs every 1-2 hrs
Ipratropium 0.5 mg may also be added to the salbutamol nebuliser solution and repeated every 6 hours.
Prednisolone tablet 0.5-1 mg/kg(30 to 60 mg) or hydrocortisone hemisuccinate 200 mg through intravenous route – to reverse inflammation and speed recovery
If unresponsive, 2 gm Magnesium sulphate iv
3 doses of bronchodilator fail to resolve the acute episode, additional steps of management to be considered
If 1:10,000 concentration, then 3 ml iv (1:1000 never administered iv)
Vascular B2 receptors are more sensitive than A receptors
Side effects of ketamine:
HR,CO, BP elevated due to sympathetic stimulation
Dangerous for hypertensives, IHD, those with raised intracranial pressure
Good for hypovolemic patients