Emphysema is characterised by loss of elasticity of the lung tissue; destruction of structures supporting the alveoli; and destruction of capillaries feeding the alveoli. The result is that the small airways collapse during expiration, leading to an obstructive form of lung disease (air is trapped in the lungs in obstructive lung diseases). Features are: shortness of breath on exertion--particularly when climbing stairs or inclines (and later at rest), hyperventilation and an expanded chest. As emphysema progresses, clubbing of the fingers may be observed, a feature of longstanding hypoxia.

Emphysema patients are sometimes referred to as "pink puffers". This is because emphysema sufferers may hyperventilate to maintain adequate blood oxygen levels. Hyperventilation explains why emphysema patients do not appear cyanotic as chronic bronchitis (another COPD disorder) sufferers often do; hence they are "pink" puffers (adequate oxygen levels in the blood) and not "blue" bloaters (cyanosis; inadequate oxygen in the blood).

Diagnosis

Diagnosis is by spirometry (lung function testing), including diffusion testing. Other investigations might include X-rays, high resolution spiral chest CT-scan, bronchoscopy (when other lung disease is suspected, including malignancy), blood tests, pulse oximetry and arterial blood gas sampling.

Pathophysiology

The scientific definition of emphysema is:

"Permanent destructive enlargement of the airspaces distal to the terminal bronchioles without obvious fibrosis".

Hence, the definite diagnosis is made by a pathologist. However, we can easily ascertain clinical diagnosis by history, clinical examination, chest radiography and lung function tests.

In normal breathing, air is drawn in through the bronchial passages and down into the increasingly fine network of tubing in the lungs called the alveoli, which are many thousands of tiny sacs surrounded by capillaries. These absorb the oxygen and transfer it into the blood. When toxins such as smoke are breathed into the lungs, the particles are trapped by the hairs and cannot be exhaled, leading to a localised inflammatory response. Chemicals released during the inflammatory response (trypsin, elastase, etc.) are released and begin breaking down the walls of alveoli. This leads to fewer but larger alveoli, with a decreased surface area and a decreased ability to take up oxygen and lose carbon dioxide. The activity of another molecule called alpha 1-antitrypsin normally neutralizes the destructive action of one of these damaging molecules.

After a prolonged period, hyperventilation becomes inadequate to maintain high enough oxygen levels in the blood, and the body compensates by vasoconstricting appropriate vessels. This leads to pulmonary hypertension. This leads to enlargement and increased strain on the right side of the heart, which in turn leads to peripheral edema (swelling of the peripherals) as blood gets backed up in the systemic circulation, causing fluid to leave the circulatory system and accumulate in the tissues.

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Surgical emphysema following tonsillectomy
From Ear, Nose & Throat Journal, 10/1/05 by Nitesh Patel

Abstract

Complications of tonsillectomy have been well documented. However, subcutaneous emphysema of the neck following tonsillectomy has rarely been described. We report a case of this complication in a young man who forcefully performed Valsalva's maneuver following a tonsillectomy.

Introduction

The most common complications of tonsillectomy are hemorrhage, infection and, secondary to anesthesia, cardiac arrhythmia, laryngeal trauma, and aspiration of blood or mucus. (1) Only rarely is tonsillectomy complicated by subcutaneous emphysema (2-6) or pneumomediastinum. (4-7) We describe a case of subcutaneous emphysema that developed in a patient who had performed repeated Valsalva's maneuvers following a tonsillectomy.

Case report

A 31-year-old man with a long-standing history of recurrent tonsillitis was admitted for tonsillectomy surgery. Findings on the physical examination were unremarkable. The tonsillectomy was performed with general anesthesia through a laryngeal mask. The tonsils were removed by bipolar diathermy dissection, and hemostasis was achieved by bipolar cautery. The operation was uneventful, and the patient recovered promptly from anesthesia.

During the 6 hours following surgery, the patient developed mild dyspnea and a gradual swelling of the neck. On examination, we noted gross subcutaneous emphysema of the neck (figure 1). We also observed that the dyspnea was mild while the patient lay flat. Of interest was the fact that the patient performed Valsalva's maneuver during the examination. He explained that he had done so repeatedly since his recovery from anesthesia in an attempt to ventilate his right ear. Examination of the right ear revealed a middle ear effusion. The extent of the swelling was marked with ink, and the patient was advised to stop performing the maneuver. A lateral neck x-ray revealed that a large amount of air had accumulated in the soft tissues of the neck (figure 2). A chest x-ray detected no evidence of pneumothorax or pneumomediastinum.

[FIGURES 1-2 OMITTED]

The patient was started on broad-spectrum antibiotics and kept under close observation. No swelling beyond the marked area occurred during 2 days of observation, and the patient was discharged. At a follow-up visit 1 week later, the swelling had resolved.

Discussion

Subcutaneous emphysema can occur as a result of either (1) a pressure difference across a break in an epithelial surface or (2) the release of gas by organisms into an enclosed space. (3) Subcutaneous emphysema of the neck, with or without pneumomediastinum, is usually caused by the disruption of the esophagus or the tracheobronchial tree. (6) However, it can also occur after disruption of the oral or pharyngeal mucosa. This disruption could be secondary to surgical or anesthetic trauma or a pathologic process such as erosion by disease. (3)

Subcutaneous emphysema following tonsillectomy is rare. When it has occurred, most authors believe that the likely site of air entry is through the tonsillar fossa. (2,4-7) A small tear in the tonsillar muscle bed might have afforded the entry point in our patient. In a case described by Podoshin et al, histologic examination detected some striped-muscle bundles attached to the tonsil, which indicated damage to the tonsillar bed. (5) Other sites, however, should also be suspected because a laceration of the posterior pharyngeal wall secondary to intubation or a Boyle Davis gag may occasionally be the cause. (2) A chest x-ray should always be obtained in these cases because a pneumothorax would suggest a deeper origin than a break in the oropharyngeal mucosa. (3)

Air can be forced into the fascial planes of the neck and along the trachea into the mediastinum, thereby causing a pneumomediastinum. (6) In pneumomediastinum, gas can escape into the abdominal cavity through diaphragmatic apertures and cause pneumoperitoneum following a tonsillectomy. (7) High intrapharyngeal pressures caused by coughing, vomiting, convulsions, or air infusion have been described as mechanisms by which air is forced into the tissues of the neck. (4) Our case is unique in that the likely cause was the repeated performance of Valsalva's maneuver. It is interesting to note that in 1885, Silvester advocated that sailors use Valsalva's maneuver to prevent drowning. (8) He demonstrated that a 10-lb dog inflated with air into its subcutaneous tissues could float in water. He suggested that in order to improve their chance of not drowning, sailors should bite the inside of their cheek and inflate themselves via Valsalva's maneuver!

Treatment is expectant and involves frequent careful assessment of the extent of the subcutaneous emphysema and the airway. It is possible that organisms will be implanted throughout the mucosal breach, and therefore broadspectrum antibiotics should be used prophylactically. (2)

References

(1.) Cummings GO. Mortalities and morbidities following 20,000 tonsil- and adenoidectomies. Laryngoscope 1954;64:647-55.

(2.) Hampton SM, Cinnamond MJ. Subcutaneous emphysema as a complication of tonsillectomy. J Laryngol Otol 1997;111:1077-8.

(3.) Smelt GJ. Subcutaneous emphysema: Pathological and anaesthetic, but not surgical. J Laryngol Otol 1984;98:647-54.

(4.) Braverman I, Rosenmann E, Elidan J. Closed rhinolalia as a symptom of pneumomediastinum after tonsillectomy: A case report and literature review. Otolaryngol Head Neck Surg 1997;116:551-3.

(5.) Podoshin L, Persico M, Fradis M. Posttonsillectomy emphysema. Ear Nose Throat J 1979;58:73-6, 81-2.

(6.) Prupas HM, Fordham SD. Emphysema secondary to tonsillectomy. Laryngoscope 1977;87:1134-6.

(7.) Vos GD, Marres EH, Heineman E, Janssens M. Tension pneumoperitoneum as an early complication after adenotonsillectomy. J Laryngol Otol 1995;109:440-1.

(8.) Silvester HR. Life saving from drowning by self-inflation. Lancet 1885;2:418.

Nitesh Patel, FRCS; Gerald Brookes, FRCS

From the Department of Otolaryngology, Royal National Throat, Nose, and Ear Hospital, London.

Reprint requests: Dr. Nitesh Patel, 33 Cedar Rise, Southgate, London N14 5NJ, UK. Phone: 44-208-361-0696; fax: 44-709-212-0197; e-mail: nitesh.hema@talk21.com

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