Airway obstruction is a potentially life
threatening situation. Airway emergencies tend to progress rapidly and are associated with a high degree of morbidity and mortality. It is not often that general practitioners are required to deal with airway related emergencies. It is therefore vital that when general practitioners encounter this problem, they are able to recognise it, have an understanding of the underlying issues and are able to manage it appropriately. This article is intended to be an overview of acute upper airway emergencies that a general practitioner may encounter; especially conditions where timely emergency intervention may be lifesaving.
Background
What is airway obstruction?
Airway obstruction is a partial or complete blockage of the airway, site of which can be in the pharynx, larynx or the trachea. The upper airway consists of passages extending from the anterior nares down to and including the larynx. The lower airway consists of the trachea and the bronchi. Normal airway functions require a patent airway and most airway emergencies result from obstruction to airflow. Obstruction can result from either internal obstruction by oedema, spasm or foreign body or from external compression or distortion. Airway obstruction prevents gas exchange with resultant hypoxia and hypercarbia. Inability to relieve the obstruction can result in lack of oxygen to the brain resulting in brain damage or death.
Subacute and chronic causes of airway obstruction are usually congenital or are associated with underlying disease processes such as tumours (thyroid goitres, upper and lower airway malignancies), chronic obstructive airway diseases and asthma and radiotherapy. These develop over a period of hours or days and will allow for time to get the patient to a hospital or a specialist treatment centre. Acute airway obstruction on the other hand, is a life threatening emergency and requires immediate intervention.
Aetiology and Pathophysiology
Common causes of acute upper airway obstruction which a general practitioner is most likely to encounter are listed in Table 1.
Foreign body inhalation : In adults, foreign bodies are usually inhaled bits of food. In children, the most commonly inhaled food is peanuts. Children also commonly choke on many non organic items, such as coins, beads and fragments of toys. A large foreign body like a coin or a marble will tend to lodge in the pharynx or trachea and cause immediate and severe respiratory distress, while smaller foreign bodies like peanuts may lodge in the bronchus and after an initial episode of coughing, may occasionally go undetected for a period of time. In the USA about 500 children die each year due to foreign body inhalation and the National Safety Council estimates that a total of 2900 deaths occur annually in the United States because of foreign body aspiration.1,2
Angio-oedema : Angio-oedema is a local well defined non-pitting oedema of acute onset, involving the skin and subcutaneous tissues of the lips, face, neck, tongue, uvula, and larynx. The oedema is caused by an increase in capillary leakage as a result of inflammatory mediators. This can be a manifestation of type I allergic reactions (anaphylaxis) or as a consequence of deficiency in C1 esterase inhibitor, an enzyme that damps down complement activation
Angio-oedema can be hereditary and non hereditary. Hereditary angio-oedema is a rare autonomic dominant disorder which results from a deficiency of C1 esterase inhibitor enzyme and is characterised by recurrent attacks of angio-oedema in affected individuals. The causes of non hereditary angio-oedema are variable and include acquired C1 esterase inhibitor deficiency (malignancies especially lymphoproliferative disorders), idiopathic, allergic reactions (antibiotics, food, inhalants), immune complex diseases, and drug reactions. Angio-oedema may be caused by a considerable number of drugs particularly antibiotics, aspirin and non steroidal anti-inflammatory drugs, radio-contrast media, ACE inhibitors and angiotensin II receptor antagonists. Of the above, the two most likely encountered forms of angio-oedema are the allergic reactions- anaphylaxis/ anaphylactoid reactions and the ACE inhibitor related angio-oedema. It is important to understand the differences in aetiology as they respond to different therapeutic regimes.
ACE inhibitors related angio-oedema is one of the most common causes of non- hereditary angio-oedema and is thought to account for 25- 39% of the cases.3 Angio-oedema of the face and neck is rare with a reported incidence of 0.1- 0.2%, but is a potentially life threatening complication of ACE inhibitor therapy. The incidence of reported cases of angio-oedema is increasing in parallel with the use of ACE inhibitors which continue to gain popularity and today are one of the most widely used class of antihypertensive drugs. Clinical presentation is variable and unpredictable. The symptoms in most cases are mild and regress spontaneously even when the patient continues to take ACE inhibitors, however up to 20% of cases may present with acute onset of swelling with dyspnoea, dysphagia, dysphonia and stridor with rapid progression to life threatening airway obstruction. It is this variability in presentation that makes the diagnosis of ACE inhibitor related oedema difficult. Despite extensive literature on the subject, many physicians fail to recognize this association and attribute the angio-oedema to an allergy or to other drugs, even after multiple recurrences. Recognition of the true drug-induced nature of the angio-oedema is important as withdrawal of the drug may prevent a later life threatening attack, even in patients on long term therapy.
Anaphylaxis : Anaphylaxis is a serious, rapid-onset, allergic reaction which is associated with swelling of the tongue, pharynx, larynx and tracheal mucosa. Severe anaphylaxis is characterized by life-threatening upper airway obstruction in association with rash, bronchospasm and/or hypotension. Diagnosis can be difficult, with skin features being absent in up to 20% of people. Anaphylaxis must be considered as a differential diagnosis for any acute-onset respiratory distress, bronchospasm, hypotension or cardiac arrest. Onset can be within minutes and anaphylaxis in general practice is seen in association with antibiotics (especially penicillin), nuts (especially peanuts), bee and wasp stings, latex and drugs such as aspirin and other non-steroidal anti inflammatory drugs. There have been reported cases of misdiagnosis, where allergic reactions have been confused with foreign body inhalation and with ACE inhibitor related angio-oedema.4,5 It is important to differentiate anaphylaxis resulting in angio-oedema and airway obstruction from other causes of angio-oedema as the former condition responds rapidly to treatment.
Infections : There are certain infections which are associated with a high incidence of airway compromise.
Diphtheria remains endemic in developing countries and there is a slow resurgence of cases in the developed countries. Jayashree et al reviewed forty eight children admitted to the paediatric intensive care unit with a diagnosis of diphtheria.6 Upper airway obstruction was the commonest complication seen in nearly 70% of the patients and resulted in 11% of the deaths. Airway obstruction can result from laryngeal involvement with formation of a laryngeal membrane or more commonly as a result of extensive oedema and necrosis of the soft tissues of the oropharynx with bleeding into the airway.
Epiglottitis is an acute inflammation in the supraglottic region of the oropharynx with inflammation of the epiglottis. Acute bacterial epiglottitis can cause rapid airway obstruction as the epiglottis swells and occludes the airway. Acute epiglottitis is preventable by vaccination against H. influenzae bacteria. Historically, acute epiglottitis was most common in children aged 2-4 years old, however with the introduction of the Hib vaccine and the accompanying dramatic reduction in H influenzae type B invasive disease, epiglottitis has become rare in children. It is now increasingly being diagnosed in adults and has a high risk of a fatal outcome.7
Croup or laryngotracheobronchitis may lead to a fairly rapid decrease in airway diameter and marked respiratory distress.
Ludwig’s angina is a potentially life-threatening, rapidly expanding, diffuse inflammation of the submandibular and sublingual spaces that occurs most often in young adults with dental infections. Swelling of the tissues occurs rapidly and may block the airway or prevent swallowing of saliva. Before the advent of antibiotics, the mortality associated with Ludwig’s angina approached 50%. Today, mortality rates are in the range of 8–10%. The most common cause of death is respiratory compromise.
Retropharyngeal and peritonsillar abscess are rapidly expanding abscesses and can block the airway and cause respiratory distress. In all cases of infections resulting in airway obstruction, recognition of the true nature of the problem with urgent referral to a specialist unit may be life saving.
Burns and Inhalation Injuries : Heat produces an immediate injury to the airway mucosa, resulting in oedema, erythema, and ulceration. In most cases, thermal injury is confined to the upper airways, because the trachea usually shields the lung from thermal loads. However, secondary airway involvement can occur after inhalation of steam as it has a greater thermal capacity than dry air. Inhalation of toxins and/or smoke may further compound the problem. Upper airway oedema is the earliest consequence of inhalation injury and is commonly seen during the first 6 to 24 hours after injury. Patients who are at a risk of airway obstruction following burns and inhalation injuries need a thorough initial assessment of the risk to their airway and then regular assessments with a low threshold for early intervention.
Poisonings : Ingestion of corrosive substances such as organophosphorus compounds, acids, household cleaning substances such as Dettol and kerosene and inhalation of compounds such as chlorine gas can result in laryngeal spasm, oedema and rapid airway obstruction.8,9
Airway trauma : Blunt trauma or penetrating trauma can cause disruption of the trachea or major bronchi resulting in air leaks. Air leaks from the major airways can result in soft tissue and subcutaneous emphysema which can either be benign or can compress the airway or cause a pneumothorax or pneumo-mediastinum.
The unconscious patient : Loss of consciousness results in an inability to maintain a patent airway due to an absence of or a decrease in the upper airway muscle tone and protective airway reflexes. Airway obstruction in an unconscious patient is usually due to the posterior displacement of the tongue producing obstruction at the oropharyngeal level and more commonly in the nasopharynx where the soft palate approximates the posterior pharynx. Air can move either through the oral or pharyngeal cavity during inspiration and the soft palate does not cause obstruction. Obstruction occurs mainly during expiration, especially when the mouth and lips are closed.
Recognition of airway obstruction
Airway obstruction may be partial or complete.
Features of respiratory obstruction are
- Noisy breathing
- snoring
- inspiratory stridor
- crowing or noisy respiration dysphonia
or aphonia,
- choking, or drooling
- gagging or feeble cough.
Respiratory distress
It is characterized by dyspnoea and use of accessory muscles of respiration. It can be partial or complete. Partial is more noisy and can have changing signs and symptoms. Complete airway obstruction is silent as there is no movement of air. Cyanosis should not be used as an early sign of obstruction as this usually occurs late and is difficult to detect. Loss of consciousness, bradycardia, hypotension, cardiac arrest and death is inevitable if the obstruction is not relieved within 2-5 minutes of the onset.
Management of airway obstruction
An accurate assessment of the cause and of the severity of the obstruction, allows the attending doctor to determine the need for immediate intervention or of urgent transfer to a specialist centre. It is important to note that in cases of partial obstruction, injudicious interventions may convert it into a complete obstruction, e.g. crying and anxiety in a child with epiglottitis and partial airway obstruction can result in progression to a complete airway obstruction.10
Measures and remedies - They depend on the severity and available facilities
Resuscitation without equipment
A) Foreign body dislodgement or removal
* Adults- the Heimlich manoeuvre can be performed upon the choking patient.
* Children over 1 year of age, a series of 5 abdominal thrusts (a children’s version of the Heimlich manoeuvre)
* Infants under 1 year of age, a combination of 5 back blows (with the flat of the hand) and 5 abdominal thrusts (with 2 fingers on the upper abdomen)
B) Maintenance of Airway Patency-It consists of laying the patient on their side and the triple airway manoeuvre. This consists of a head tilt/chin lift, jaw thrust and open mouth which when done together is one the most reliable method to maintain a patent upper airway. This movement tenses the muscles in the floor of the mouth and prevents obstruction as a result of tongue fall and the approximation of pharyngeal tissues.
Resuscitation with equipment
1) Oxygen therapy
2) Airway insertion (may induce vomiting)
3) Ambu bag and mask ventilation
3) Emergency intubation
4) Cricothyroidotomy
5) Tracheostomy
Details and training opportunities of these resuscitation manoeuvres are provided by a wide variety of resuscitation bodies such as the Adult and Paediatric resuscitation councils and it is in interest of all general practitioners to familiarise themselves with the treatment guidelines.
ANAPHYLAXIS-Cornerstones of management
IM adrenaline Airway
(0.3-0.5 mg in adults) support with O2
Intravenous fluid Ventilation when
indicated In severe
In resistant cases, adrenaline may require to be repeated or to be administered intravenously. Antihistamines (IV/IM chlorpheniramine 10-20 mg) and corti-costeroids (IV/IM hydrocortisone 100-200 mg) may also be of benefit in this situation.
ACE inhibitor related oedema
* Withdrawal of the inciting agent
* Assessment of the degree of airway oedema and its management
* Role of adrenaline (nebulised or intramuscular), regular corticosteroids and
* Antihistamines is unproven. However they are used when intubation facilities may not be at hand
It is a non progressive angio-oedema and often resolves in 24-48 hour.3
Airway obstruction which results from infection, trauma or burns is likely to be rapidly progressive in nature and early recognition of the condition with urgent transfer to the appropriate centre may be lifesaving.
Summary
It is important for a general practitioner to be aware of conditions which may present as acute airway obstruction, as this will allow them to deal with it effectively. Recognising the severity of airway obstruction is the key to its management. Regular training in basic airway management and resuscitation skills is essential and may prove to be life saving.
References
1. Skoulakis CE, Doxas PG, Papadakis CE, et al. Bronchoscopy for foreign body removal in children. A review and analysis of 210 cases. International J Pediatric Otorhino-laryngology 2000; 53 : 143- 8.
2. National Safety Council: Accident Facts Itsaca, Illinois 1992; 32.
3. Rai MR, Amen F, Idrees F. Angiotensin-converting enzyme inhibitor related angioedema and the anaesthetist. Anaest Hesia 2004; 59 :
283-9.
4. Kolenc KM, Dobbin KR. Angioedema caused by ACE inhibitor mistaken for allergic reaction. J Emergency Nursing 1996; 22 : 228-31.
5. Nguyen AD, Gern JE. Food allergy masquerading as a foreign body obstruction. Annals of Allergy, Asthma and Immunology. 2003; 90 (2) : 271-2.
6. Jayashree M, Shruthi N, Singhi S. Predictors of outcome in patients with diphtheria receiving intensive care. Indian Pediatrics 2006; 43 :
155-60.
7. Hayward H, McParland P, Schuster-Bruce M, et al. Upper airway obstruction in a young adult. Internetional J Clinical Practice 2003; 57 : 55-6.
8. Tibballs J, Cathie R, Buist M, et al. Upper airway obstruction caused by ingestion of concentrated acetic acid. Anesthesia and Intensive Care 2006; 34 : 379-81.
9. Graham CA. Stridor after ingestion of dettol and domestos. European J Emergency Medicine 2004; 11 : 52-4.
10. Ghirga G, et al. Bag-mask ventilation as a temporizing measure in acute infectious upper airway obstruction: does it really work? Pediatric Emergency Care 2001; 17 (60) : 444-6.
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