In: Dental treatment9 Jan 2010
Pneumothorax can be caused by 1 of the following 4 mechanisms: (1) extrathoracic trauma (ie, closed-chest compressions), (2) spontaneous rupture of alveoli, (3) disruption of fascial planes in the neck (ie, traumatic intubation), or (4) abnormally high intrathoracic pressure (ie, valsalva from protracted coughing). Tension pneumothorax occurs when there is continuous loss of air from the lung into the pleural space with no escape route. This results in a shift of the mediastinal contents to the opposite side.
In this case, there was no need for closed-chest compressions, essentially eliminating the first cause of pneumothorax. Spontaneous rupture of alveoli is uncommon but not rare. It is estimated that 20,000 new cases occur each year, more frequently in tall, thin males, sometimes having a history of smoking or inhalation drug abuse.
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Dyspnea, tachycardia, and chest pain are common symptoms. Chest-tube decompression is usually recommended if the lung collapse is greater than 15-25%. Spontaneous healing can occur in less serious cases at the rate of 1.25% per day. A patient with a history of spontaneous pneumothorax has a recurrence rate dependent on the type of treatment received. Simple needle aspiration has a recurrence rate of 20-50%, whereas chest-tube thoracocentesis results in 10-20% recurrence.
Blind nasal tracheal intubation was successful after 1 attempt utilizing moderate pressure applied to the cricoid cartilage (Sellick maneuver). The tube did not appear to engage any resistance from either the piriform sinus or vallecula, which could lacerate the hypophar-ynx. Traumatic laryngoscopy can cause a delayed entry of air into the fascial planes, first producing a pneumomediastinum and then pneumothorax. The most likely cause of pneumothorax in this case is from elevated airway pressures that could have occurred in one of several ways. Controlled ventilation was utilized intermittently. At the beginning of the case, a ventilator was used to control respiration for 10 minutes, during which dental x-rays were taken. The patient was then allowed to breathe spontaneously. Inspired pressures were not elevated (ie, greater than 25 mm Hg) at any time. If pneumothorax occurred during this period, symptoms probably would have developed earlier.
There were no subtle warning signs of awakening (ie, eyes opening, brow furrowing, swallowing, or bodily movement). In the recovery room, the patient began to cough and buck on the endotracheal tube. Although partially restrained, he was able to extubate himself. It was surmised that coughing produced a rupture of alveoli from elevated airway pressure. Various precautionary methods are available to minimize the abrupt awakening of an intubated patient. Those might include ex-tubation while asleep, narcotic sedatives, intravenous or inhaled lidocaine, and application of lidocaine on or in the endotracheal tube cuff. The use of a laryngeal mask airway (LMA) eliminates entering the trachea and therefore the tracheal irritation. But an LMA was not used in this case.
The occurrence of spontaneous pneumothorax can never be predicted but needs to be considered whenever a patient has been on a ventilator or had a traumatic intubation. One should begin to suspect a pneumothorax when oxygenation decreases and airway pressures increase during controlled ventilation. Auscultation may reveal diminished unilateral or bilateral breath sounds. However, this may also be the case with a bron-chospasm, so other clinical signs need to be considered to confirm the diagnosis. Distended neck veins not previously noticed may appear as indicating signs of venous congestion. Associated cervico-facial soft tissue emphysema may develop quickly, especially if nitrous oxide is in use. Tracheal deviation may be observed as well as an altered end tidal C02 pattern on the monitor, indicating a slow rise in expired C02. The ECG may show a rightward shift in the frontal or horizontal axis, a diminution in precordial voltage, and precordial T-wave inversion.
In an outpatient setting like a dental office, a CXR is not generally available. Therefore, a prompt clinical diagnosis is necessary and early treatment may be life-saving if a significantly large pneumothorax exists. As intrathoracic pressure increases, a mediastinal shift causes an impairment of venous return and decreased cardiac output that further compromises oxygenation and blood pressure stability. If hypotension had occurred, intravenous fluids and/or direct acting beta adrenergic agents would have been required to increase cardiac output. kamagra uk
Oxygen saturation was decreased and the blood pressure was stable, but the attempts at mask ventilation were becoming more difficult. Direct laryngoscopy and nasal intubation were easily completed. Nasal intubation was the chosen route because (1) displacement caudally (into the mainstem bronchus) or cephalad (accidental extubation) are less likely than with oral intubation and (2) nasal RAE tubes are easier to stabilize than oral tubes, especially for transport.
Needle thoracentesis should be performed as soon as possible after pneumothorax is suspected. Nitrous oxide as well as air can rapidly fill the thorax. Thoracentesis should be performed at least 2-3 inches lateral to the sternum to avoid the internal mammary artery. The midclavicular line at the second or third intercostal space above the nipple is the most desired location. The largest bore needle available is recommended, but even an 18 gauge, which was the largest available, is sufficient. Entry into the intrapleural cavity is achieved by penetration of the skin at a 90° angle. If a rib is contacted, the needle should be deflected off the superior surface to avoid lacerating an intercostal artery or vein. A sudden loss of resistance and air escape are indicators of accurate placement and confirmation of the diagnosis. With the heart displaced to the right, the needle is not likely to penetrate the pericardium and produce tem-panode. If it does contact the heart, cardiac arrhythmias may also occur. erectalis 20
In this case, 600 mL of air were tapped followed by placement of a water-trap seal connecting a 3-way stop clock and an IV extension set. An underwater seal may be the best choice for several reasons. The patency of the extension set is more easily verified by the presence of bubbles during lung inflation. A bottle of saline or sterile water can be utilized and placed below the level of the chest. Additionally, if wall suction were used instead, negative vacuum through a small needle may get obstructed by soft tissue or blood and go unrecognized.
It was the consensus of the hospital physicians that the etiology of this pneumothorax was probable due to a bleb or bullae. Destruction of lung parenchyma causes formation of an air-filled, thin-walled space within the lung. Walls of bullae may be connective tissue septae, compressed lung, or pleura. A bleb connotes subpleural collection of air within layers of visceral pleura due to ruptured alveoli. Preoperative risks include smoking, especially for those smokers with chronic obstructive pulmonary disease (COPD) and those with pulmonary hypertension and right ventricular failure. While a ruptured diaphragm is another possible cause of pneumothorax, it would also produce a pneumoperitoneium and require more surgical intervention and not the quick resolution as in this case. eriacta tablets
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