Upper airway obstruction
Upper airway obstruction is defined as occlusion or narrowing of the upper airways leading to compromise in ventilation. Airway obstruction that is initially partial, may worsen and develop into a life-threatening emergency, which can be fatal without appropriate treatment.
The upper airway is defined as the airway segment above the main carina (i.e. above the lower end of the trachea). The upper airway consists of the following compartments:
■ the nose (functional during nasopharyngeal breathing)
■ the mouth (which functions as an airway during
oropharyngeal breathing)
■ the pharynx
■ the larynx
■ the trachea.
CC BY 3.0 File:Blausen 0872 UpperRespiratorySystem.png. Blausen.com staff (2014). "Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. - Own work
The mouth and nose are rarely
the site of upper airway obstruction, because of their parallel anatomic
arrangement, except in cases of massive facial trauma.
Acute upper airway
obstruction can result from aspiration of a foreign body, viral or bacterial
infections (retropharyngeal abscess, epiglottitis, croup, bacterial tracheitis),
anaphylaxis, angioedema, trauma to the larynx, burns to the face or neck, inhalation injury (smoke, chlorine). Acute upper airway
obstruction is a medical emergency that requires prompt intervention. Reactions
to allergens (e.g., bee stings, peanuts, sea-food, medications), infections
(epiglottitis), or inhaled irritant particles and gases (smoke inhalation) may
cause acute edema of the pharynx and larynx. In addition, a common cause of acute
upper airway obstruction is a foreign body lodged in the airway.
Obstruction of the upper
airway may occur acutely, resulting in respiratory distress of sudden onset
which can lead to death within minutes, in case of complete obstruction, or
it may develop chronically, causing progressive dyspnea and exercise
intolerance. The sudden onset of respiratory distress and stridor should generally
suggest an acute upper airway obstruction. Chronic obstruction, during its
course, may also lead to acute respiratory distress when a critical narrowing
of the airway develops. This can occur through the progression of the primary cause of the
obstruction or as a result of mucus plugging or bleeding.
Clinical manifestations of upper airway obstruction
Symptoms and signs, depending
on the location and the severity of the obstruction, usually include cough,
hoarse voice or muffled voice, dyspnea (the patient often is unable to finish
sentences), tachypnea, stridor, agitation or confusion, and tachycardia. In severe
cases, without prompt treatment, the clinical picture, due to fatigue of the
respiratory muscles and hypoxia, may progress to bradycardia, bradypnea, and
cardiac arrest.
Stridor is an important
clinical finding which suggests upper airway obstruction. It is a high-pitched musical
sound which usually occurs during inspiration, it is heard loudest in the neck
and sometimes it can be confused with wheezing. If the site of the obstruction is
below the thoracic inlet, both inspiratory and expiratory stridor may be present.
On the contrary, wheezing, occurs
predominantly during expiration, becoming louder at end-expiration. Wheezing is a
sign of diffuse lower airway narrowing, usually as a result of asthma or COPD.
The voice may be a clue to the
site of upper airway obstruction. Hoarseness may be a sign of a laryngeal
abnormality in the glottis (the part of the larynx consisting of the vocal
cords and the opening between them). Muffling of the voice without hoarseness
may suggest a supra-glottic process (an obstruction above the glottis).
In cases of mild upper airway
obstruction, the manifestations include cough and hoarse voice but no
respiratory distress.
Upper airway obstruction of
moderate severity manifests with moderate respiratory distress (moderate tachypnea,
mild intercostal and subcostal retractions), agitation, and stridor.
Clinical features of severe
upper airway obstruction include severe respiratory distress (severe tachypnea,
severe intercostal and subcostal retractions, and nasal flaring), stridor, cyanosis, or SpO2 < 90%, tachycardia, and agitation or lethargy. Cardiac arrest may
follow in the most severe cases.
Treatment of upper airway obstruction
Examine the patients in the
position in which they are the most comfortable.
Evaluate the severity of the
obstruction according to the clinical features described above and monitor SpO2,
heart and respiratory rate, and the patient’s mental status. In cases with a
severe obstruction seek immediate help from a clinician experienced in airway
management (an anesthesiologist or otolaryngologist or both).
Administer oxygen
continuously: if respiratory distress is present, or if the SpO2 < 94% to
maintain the SpO2 between 94 and 98%. If a pulse oximeter is not available
administer at least 5 liters of oxygen /minute.
Maintain adequate IV hydration.
Secure the airway if needed
(by endotracheal intubation, cricothyroidotomy, or tracheotomy) in cases of
severe obstruction and recognize and treat the underlying cause. Treatment for
the underlying cause may consist of IV antibiotics for bacterial infections
such as epiglottitis and bacterial tracheitis, drainage and antibiotics for a
retropharyngeal abscess, humidified oxygen, dexamethasone, and nebulized
adrenaline for severe croup, epinephrine corticosteroids, and antihistamines
for an anaphylactic reaction).
In an unconscious patient with
upper airway obstruction, first try to ventilate with a head-tilt or jaw thrust
maneuver (the latter if there is a suspicion of a possible neck injury) and the
placement of an oral airway. If these measures fail, direct laryngoscopy with
the aid of a gum bougie introducer may often permit successful passage of a
small diameter endotracheal tube over the bougie introducer through the
glottis.
In a patient with severe upper
airway obstruction, when endotracheal intubation fails or is not possible,
prompt placement of a surgical airway is indicated. This is achieved by
emergency tracheostomy or emergency cricothyroidotomy (or cricothyrotomy).
Cricothyroidotomy may provide adequate short-term airway control if a
tracheostomy cannot be performed immediately.
Percutaneous cricothyroidotomy
A
cricothyroidotomy or cricothyrotomy is an emergent procedure performed when
there is a need to secure the airway and orotracheal
intubation is not possible or has been unsuccessfully attempted. Percutaneous cricothyroidotomy can be performed by physicians without surgical experience
more easily than a surgical cricothyroidotomy, in order to establish an airway.
The technique is based on the Seldinger technique (similar to the technique
used to insert a central venous line). Special kits for percutaneous cricothyroidotomy
are available, that contain the necessary equipment (a scalpel, a catheter over a needle, a syringe, a guidewire, and an airway catheter and its dilator).
Clean
and drape the patient’s neck. Lubricate the dilator and insert it through the
airway catheter. Lubricate the airway catheter and dilator after it has been
assembled into a unit. Identify the anatomical landmarks. The cricothyroid
membrane is located between the thyroid cartilage superiorly and the cricoid
cartilage inferiorly and it can be identified by palpation of these two surrounding
cartilages. With a #11 scalpel blade make a stab incision just through the skin
over the center of the cricothyroid membrane. Attach a 5 mL syringe containing
saline to the catheter-over-the-needle and insert it slowly at a 30° to 45° angle through the skin incision into the center of the cricothyroid membrane, aiming inferiorly (towards the feet). Advance the catheter-over-the-needle
while simultaneously aspirating with the syringe. Stop advancing the catheter-over-the-needle
when it enters the airway. When the catheter enters the airway you will feel a
loss of resistance and you will see air bubbles in the syringe. Then hold the
syringe securely and advance the catheter over the needle until the hub of the
catheter is at the skin. Hold the catheter hub against the skin of the neck while
removing the needle and syringe. Then advance the guidewire through the
catheter into the trachea. Hold the guidewire securely and remove the catheter
over the guidewire. Do not stop holding the guidewire in order to prevent it
from completely entering the patient’s airway. Insert into the trachea the airway
catheter with the dilator in it as a unit over the guidewire. The insertion of the airway catheter-dilator unit over the guidewire is performed with a
semicircular motion. Perform this insertion gently to prevent causing injury or
perforation of the posterior tracheal wall. Advance the airway catheter-dilator unit until the flange reaches the
skin of the neck. Hold the airway catheter securely and remove the guidewire
and dilator as a unit, keeping the airway catheter in place. Start ventilation
of the patient and secure the airway catheter.
Simple percutaneous insertion of an angiocatheter
into the cricothyroid membrane
Another
technique, that is easy and can be performed fast, especially indicated in
children less than10 years of age, is to insert a 12-16 gauge catheter-over-the-needle
(angiocatheter) percutaneously into the cricothyroid membrane. Attach a 5 or 10
mL syringe containing 5 mL of sterile saline to the catheter-over-the-needle (angiocatheter).
Insert the angiocatheter through the skin into the inferior aspect of the
cricothyroid membrane (preferably through the lower left quadrant of the
cricothyroid membrane because this region is least likely to contain
cricothyroid arteries and veins). The angiocatheter is inserted with an
inferior direction (towards the patient’s feet) at a 30° to 45° angle to the
skin. Aspirate continuously with the syringe as the angiocatheter is advanced.
The catheter is advanced until you feel a loss of resistance and air bubbles
are visible in the syringe. These both signify that the angiocatheter has
entered the trachea. Hold the needle securely and advance the catheter until its
hub is at the skin. Then remove the needle and syringe. Attach again the
syringe without the needle to the catheter and aspirate once again to reconfirm
that the catheter is within the trachea. Hold the catheter hub firmly at the
skin, remove the syringe and attach the oxygen tubing to the catheter. Ventilate
the patient and continue until a more secure airway (e.g. a tracheostomy) is
established.
Oxygenation
and ventilation of the patient can be achieved by several methods. One method
is to insert the adapter piece from a #3.0 endotracheal tube to the catheter
hub and then connect it directly to a bag-valve device or a ventilator. Another
method is to connect the high-flow oxygen tubing directly to the hub of the
catheter. This method requires cyclic ventilation for 1-2 seconds followed by
exhalation for 4- 5 seconds.
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Treatment of some specific etiologies of acute airway obstruction
Angioedema is nonpitting,
nonpruritic swelling of the deep layers of the skin and mucosal tissues
occurring in a localized area of the body, preferentially involving the face
(lips, the area around the eyes), tongue, larynx, extremities,
gastrointestinal tract (with abdominal pain). Angioedema can often accompany
allergic reactions. Angioedema is caused by the following mechanisms:
■ an allergic mechanism (mast
cells release histamine in response to IgE-mediated hypersensitivity reactions
due to severe food allergies or in response to certain drugs such as aspirin,
opiates, iodinated contrast agents).
■ activation of the complement
system.
■ accumulation of
bradykinin has been implicated as the probable mechanism of angioedema caused
by ACE-inhibitors which occurs in 0,1-0,5 % of the patients receiving these
drugs, usually shortly after treatment initiation. (In rare cases it may appear
later, even years after treatment initiation).
Angioedema can be, acquired,
drug-induced, hereditary or idiopathic. Hereditary angioedema is an autosomal
dominant disease resulting from inadequate levels or reduced function of the C1
esterase inhibitor. This changes the activation of the complement system.
Angioedema can cause acute airway obstruction due to tissue swelling. Usually, it can be relieved with subcutaneous epinephrine, corticosteroids, and antihistamines, except from the hereditary type, in which these drugs have much less effect. The above treatment (antihistamines, corticosteroids, and epinephrine) is effective for allergic, histamine-mediated angioedema. Epinephrine (adrenaline) is administered if airway obstruction or hypotension is present. The dosage of epinephrine in acute angioedema or anaphylaxis is the following: Epinephrine (adrenaline) 1:1,000 solution (i.e. 1mg/ml): In adults: 0.2 to 0.5 mL (0.2 to 0.5 mg). In children: 0.01 mg / kg. It is administered subcutaneously or intramuscularly, usually into the upper arm. The injection site may be gently massaged to facilitate absorption. Depending on the patient’s response you may repeat this dose 2-3 times at intervals of 10 -15 minutes.
Antihistamines also provide relief of symptoms in anaphylaxis or in allergic angioedema, e.g., diphenhydramine (Benadryl), 1-2 mg / kg in children (maximum 50 mg) or 25-50 mg in adults, intravenously or intramuscularly.
For hereditary angioedema, there are other more specific
treatments (icatibant, C1 esterase inhibitor replacement).
In patients presenting with
angioedema, the likelihood of the need for intubation (preferably fiberoptic
intubation) or tracheostomy is increased if the tongue, or larynx is involved
and if stridor or drooling occurs.
Aspiration of a foreign body
Upper airway
obstruction due to a foreign body aspiration may occur in a child 6 months-5 years playing with a small object or
eating. Foreign body aspiration can also occur in an adult while eating because
of carelessness or under the influence of drugs or alcohol or in a person who
has had a stroke, which may impair the ability to swallow.
If the person is coughing do
not intervene, only encourage coughing which may expel the foreign body from
the respiratory tract. Maneuvers to relieve obstruction should be performed
promptly only if the patient cannot speak or cough.
For children over 1 year and
adults:
The Heimlich maneuver is
performed to relieve obstruction with the rescuer standing behind the patient.
Place a closed fist on the epigastrium (above the navel and below the ribs).
Place the other hand over the fist and press hard into the epigastrium with a
quick, upward thrust (1-5 times). This maneuver is performed with the intention
to compress the lungs from below and dislodge the foreign body.
For children <1 year:
Place the infant face down
across your forearm (which rests on your leg) supporting the infant’s head with
your hand. With the heel of the other hand, perform one to five slaps on the
back, between shoulder plates. If unsuccessful, turn the
infant on its back. Perform five forceful sternal compressions as in
cardiopulmonary resuscitation: Place 2 or 3 fingers in the center of the
infant’s chest just below the nipples and press down approximately one-third
the depth of the chest (about 3 to 4 cm).
In a patient who is unable to
cough, repeat these maneuvers that aim to relieve the obstruction, until the foreign
body is expelled and spontaneous breathing (coughing, talking, crying) is
resumed. If the patient loses consciousness perform cardiopulmonary resuscitation
(give ventilations and chest compressions).
If effective ventilations are
not possible, then urgent endotracheal intubation may be performed with a small
diameter tube by an experienced physician. If this is also not possible, an emergency tracheostomy or cricothyroidotomy must be performed very promptly to
save the patient’s life.
Laryngotracheobronchitis (croup) is
a viral inflammation of the respiratory tract affecting children 3 months-3
years old. The most common presenting features include characteristic barking
cough and stridor which is inspiratory or biphasic. The child is usually restless,
and developing respiratory distress is often accompanied by flaring of ala
nasae and development of intercostals recession. Most cases can be sufficiently
managed with humidification, corticosteroids, and nebulized adrenaline, whereas
intubation is uncommonly required to secure the airway.
Epiglottitis
It is
an acute, rapidly progressive bacterial infection of the epiglottis and adjacent
structures that can result in complete obstruction of the upper airway. Epiglottis
is an important structure at the base of the tongue preventing food from entering
the trachea. Causative organisms include
group A Streptococcus (GAS), Streptococcus pneumoniae, Haemophilus
parainfluenzae, and Staphylococcus aureus. In children, the cause is Hemophilus
influenzae but it has become rare because of the widespread vaccination against
this microorganism.
Patients
present with severe sore throat, fever, systemic toxicity, and often inspiratory
stridor accompanied by respiratory distress with tachypnea and chest wall
retractions. Drooling may be present. When there is a clinical suspicion of epiglottitis,
avoid direct visualization of the throat in the examination room (i.e., with a
tongue blade) because this carries the risk of precipitating complete airway
obstruction. The examination should be performed in a controlled environment (e.g.,
an operating room) with direct fiberoptic laryngoscopy. This may be performed
for diagnosis and also for the placement of an endotracheal tube.
Treatment
of epiglottitis
●In cases
with respiratory distress, airway protection is required (endotracheal
intubation or if this is not possible tracheostomy). Such measures for airway
protection are needed in about 10-15% of cases. Signs and symptoms associated
with a need for intubation include respiratory distress, stridor, inability to
swallow, and drooling.
● Medications:
Administration of dexamethasone should be considered (reduces the edema of the pharynx and the
epiglottis and may help to avoid airway obstruction). IV antibiotics for 7-10
days, comprise the main treatment (ampicillin/sulbactam or a second- or
third-generation cephalosporin).
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