ACUTE UPPER AIRWAY RESTRICTION

Diagnosis
Causes:
1. Acute

foreign object (e.g. food bolus)

Periglottic infection (epiglottitis, pharyngeal abscess)
Laryngospasm (mechanical irritation, anaphylaxis)
Asthma (variant)
Inflammation secondary to thermal or caustic injury
Post extubation glottis edema
Trauma
Obstructive sleep apnea
Neuromuscular dysfunction (pathologic or pharmacologic)

2. Chronic

bilateral midline vocal cord paralysis

Granulation tissue, stricture, or chondromalacia (post
Intubation, tracheostomy, trauma)
Indwelling small diameter endotracheal or tracheostomy tube
Rheumatoid disease of the arytenoid cartilage
Tumor of the larynx, trachea thyroid
Mediastinal fibrosis

Manifestations:
Patients may be symptom free until the orifice reaches a critical dimension. Dyspnea then progresses
disproportionately to further decrements in size. The symptoms of upper airway disease may be difficult to
distinguish from lower airway disease. However, the following are particularly suggestive:
1. Inspiratory limitation of airflow
2. Stridor
This shrill inspiratory crowing noise is most heard commonly with extrathoracic obstruction. In an
adult, stridor at rest usually indicates a narrow aperture (less than 3 mm). Occasionally, stridor is
mimicked by secretions pooled in the airway.
3. Difficulty in clearing central airway secretions
4. Cough of a brassy or bovine character
5. Altered voice
Hoarseness may be the only sign of a laryngeal tumor or unilateral vocal cord paralysis (frequently
associated with processes that cause obstruction). Bilateral vocal cord paralysis causes obstruction
but usually meet near the midline, so that the voice may be breathy or soft, but otherwise normal.
Only short phrases may be spoken before the next breath, and the patient may sense dyspnea when
conversing.
6. Marked accentuation of dyspnea by exertion or hyperventilation
During vigorous inspiratory efforts, negative intratracheal pressures and turbulent inspiratory airflow
tend to narrow a variable extrathoracic aperture. Exertion is stressful because obstruction worsens
rather than improves during inspiration, as it does in asthma and COPD.
7. Change in symptoms with neck movement

Diagnostic Work-Up
1. Laryngoscopy (mirror, direct, fiberoptic)
2. CT scans or lateral tomograms of the neck and trachea
3. Pulmonary function tests, to include flow volume loops with and without helium- oxygen, maximal
voluntary ventilation, and diffusing capacity
In general , upper airway obstruction (UAO) impairs inspiratory flow more than expiratory flow; impairs
peak flow, maximal voluntary ventilation (MVV), ans airway resistance disproportionately to FEV1; and
responds extraordinarily well to a low density gas (helium-oxygen) but not to bronchodilators.
In general, asthma and COPD have just the opposite characteristics. However, asthma can have a
significant upper airway component. Occasionally, stridor will be the only presenting sign of asthma,
Often, these patients benefit from anxiolytics as well as bronchodilators. Unlike the diffuse obstructive
diseases which alter lung volume, distribution of airflow, and diffusing capacity, UAO alone leaves the
parenchyma normal.
The flow-volume loop contour depends upon: 1) the fixed or variable nature of the obstruction and 2) the
intrathoracic or extrathoracic location. A fixed lesion inside or outside the thorax blunts maximal
inspiration and maximal expiration to a similar degree, giving a squared-off loop. A variable extrathoracic
lesion, surrounded by atmospheric pressure is pulled inward when subjected to negative inspiratory
airway pressure but dilated by positive airway pressure. Conversely, a variable intrathoracic lesion,
surrounded by a pleural pressure more negative than airway pressure, dilates on inhalation. On exhalation
the lesion is pushed inward to critically narrow the airway.
PFT results suggestive of UAO include:
Preserved Inspiratory vital capacity with severe reduction of FEV1
FEV1/Peak flow ratio greater than 0.6
MVV less than 30%FEV1
FIV1/FEV1 less than 0.9
Inspiratory Vmax50 less than expiratory Vmax50
Helium augmentation of Vmax50 greater than 50%
The validity of these criteria depends on the position, nature and severity of obstruction; none by itself
should be considered diagnostic of UAO.

Management
Acute Obstruction:
Keep patient under continual surveillance in the ICU if possible.
Keep succinylcholine, a 14 gauge needle for cricothyroid puncture, and tracheostomy tray at bedside for
emergent use.

Administer an IV bronchodilator if bronchospasm is present.

If there is inflammatory obstruction, avoid stimulation but do not sedate heavily.
Postextubation glottic edema and thermal injury edema usually peak within 12-24 hrs. and then recede
over the next 48-72 hrs.
If the patient does not struggle to breathe and maintains acceptable arterial blood gases, the following
supportive measures may help temporarily while attention is directed to the primary cause:
Nurse in head-up positions
Racemic epinephrine by aerosol
Intravenous corticosteroids (uncertain benefit)
Helium-oxygen by mask
Endotracheal intubation or tracheostomy may be necessary if ventilatory failure ensues or secretions
cannot be cleared.
Chronic Obstruction:
The primary cause dictates therapy.
Tracheostomy is usually necessary.

PNEUMOTHORAX
Free air in the pleural cavity between the visceral and parietal pleura

Etiology and Pathophysiology:

1. Traumatic pmeumothorax
a. Open pneumothorax penetrating chest wound that creates a pleurocutaneous fistula between
outside air and pleural space that permits the air to rush in causing lung to collapse
b. Closed pneumothorax- e.g. stab wound; chest wall becomes airtight after penetration or it may
continue to receive air (e.g. fractured rib punctures lung). Air may also leak from ruptured
bronchus or perforated esophagus into the mediastinum and then rupture into the pleural
space.
c. Pulmonary barotrauma- mechanically ventilated patients
2. Spontaneous Pneumothorax air enters pleural space in the absence of antecedent trauma during the
course of pulmonary disease or in previously healthy individual. The most common cause in an
apparently healthy person 20-30 years old, most commonly in right lung is rupture of emphysematous
bulla at right apex. Other causes are asthma, eosinophilic granuloma, lung abscess, bronchopleural
fistula, TB. Most occur without exertion; some occur during diving or high altitude flying; may also
occur as a compliucation of interstitial pulmonary air leak and pneumomediastinum.
In 1 and 2 communication between the bronchial tree and the bronchial space usually stops leaking
and heals quickly as the lung collapses.but it may remain open.
3. Tension (positive Pressure ) Pneumothorax occurs when a check valve mechanism in a
bronchopleural fistula permits air to enter, but not to leave the pleural space, causing pressure within
the space to rise above atmospheric resulting to complete lung collapse and shift of the mediastinum
to opposite side.

4. Induced pneumothorax- artificial pneumothorax now rarely used as a diagnostic procedure to outline
masses or replace fluid for better x-ray visualization of intrathoracic structures
Signs and Symptoms:
Symptoms vary according to size of pneumothorax and extent of the disease and range from minimal
disturbance to severe dyspnea, shock, circulatory collapse.
1. Sudden, sharp chest pain, dyspnea, occasional dry, hacking cough at onset
2. Referred pain to shoulder, chest, abdomen
3. Symptoms tend to be less severe in slowly seveloping pneumothorax and subside as accommodation to
altered physiologic state occurs.
Physical findings also depend on the size of the pneumothorax.
1. Small collection no detectable signs or diminution of voice and breath sounds may be the only
abnormality
2. Large collections tympany on percussion, diminished or absent tactile fremitus, diminished motion
on the affected side, mediastinal shift as detectable by displacement of cardiac area of dullness.
Hypoxemia is minimal or absent in previously well individual with spontaneous pneumothorax but may
be severe and associated with hypercapnia in a patient with lung disease.
Chest X-Ray
Air without lung markings peripherally but limited by a sharp pleural margin with lung marking medially
indicating position of the collapsed lung
Small pneumothorax may be better seen on expiratory x-ray.
Treatment:
1. Small spontaneous pneumothoraces require no special treatment; air resorbed after a few days
2. Larger lesions may take 2-4 weeks = course can be shortened by introduction of a chest tube with
water-sealed drainage, application of a suction if there is a persistent bronchopleural fistula, and rapid
expansion of the lung
3. Tension pneumothorax quick removal of air is life saving (tube thoracostomy)
4. Recurrent pneumothorax requires surgical intervention thoracotomy with oversewing or excision of
bullae and roughening of the pleura; in the presence of extensive bullous disease, parietal pleurectomy
is done.

NEAR DROWNING
Severe oxygen deprivation caused by submersion in water; but not resulting in death
Pathophysiology:
1. Victims sustain significant hypoxemia because of aspiration and laryngospasm with consequent
danger of respiratory failure and hypercapnia
2. Acute reflex laryngospasm may result in asphyxia without aspiration of water

3. Aspiration of water and particulate matter may cause chemical pneumonitis which leads to patchy
atelectasis
4. Perfusion of non-aerated, atelectatic areas leads to intrapulmonary shunting of blood and aggravates
hypoxemia
5. With large amounts of water aspirated, there can be massive atelectatic areas in the lung resulting to
stiff, non-compliant lungs and respiratory failure
6. Hypoxemia+tissue hypoxia often result in pulmonary edema and cerebral edema
Treatment:
1. The key factors for survival without permanent injury appear to be the duration of submersion, water
temperature, age of the individual, speed of resuscitation.
2. Survival depends on prompt correction of hypoxemia and acidosis and correction of electrolyte
imbalance
3. CPR should be promptly started and defibrillation may be necessary
4. Attempts should be made to drain water from the lungs in freshwater victims because the hypotonic
fluid passes rapidly into the circulation. Sea water draws plasma into the lungs, and the
Trendelenberg position may promote drainage.
5. Hospitalization is mandatory, since consciousness is not synonymous with recovery and delayed death
from hypoxia can occur
6. Intensive pulmonary care to achieve adequate arterial blood gas and acid base levels plus
supplemental oxygen should be emphasized
7. IV sodium bicarbonate is usually indicated since metabolic acidosis usually accompanies hypoxia
8. Manual hyperinflation to re-expand atelectatic alveoli with inhaled or IV isoproterenol to reduce
bronchospasm
9. Consider antibiotocs or corticosteroids on case to case basis
10. Pluid and electrolyte solutions required for correction of significant electrolyte imbalance; see if blood
expanders are indicated
11. RBC replacement to increase the oxygen carrying capacity of blood and forced diuresis to facilitate
excretion of free plasma Hb may be necessary in the presence of massive hemolysis
12. Mechanical ventilation in those who develop ARDS