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 حالات اكلينيكيه ...... فكروا معايا

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hosseny



المساهمات : 93
تاريخ التسجيل : 07/09/2007

مُساهمةموضوع: حالات اكلينيكيه ...... فكروا معايا   الأربعاء سبتمبر 19, 2007 4:01 am




BACKGROUND
A 27-year-old man presents with progressive dyspnea following an initial scuba-diving training session. He states that he felt normal and did not have any difficulty breathing immediately following the training dive; however, approximately 1 hour after the dive, he began to feel some mild chest tightness directly under his breastbone. Over the next 8 hours, his chest tightness progressed to difficulty breathing with a frequent, nonproductive cough. He states that any physical exertion worsens his shortness of breath, whereas drinking cool water improves it. The patient remembers that he accidentally held his breath as he ascended from a depth of approximately 12 ft to a depth of 10 ft of freshwater in a swimming pool. He explains that he had been instructed to not hold his breath on ascent; however, he had become distracted and did not realize he was ascending.
On physical examination, the patient is an anxious-appearing, healthy young man with mildly labored breathing. He has a pulse of 71 bpm, a blood pressure of 129/85 mm Hg, a respiratory rate of 16 breaths/min, and an oxygen saturation of 98% while breathing room air. Auscultation of the lungs reveals clear breath sounds. There is no dullness to percussion throughout the lung fields. His speech is normal; his neck is without fullness, jugular venous distention, tracheal deviation, or subcutaneous emphysema. There is no pedal or extremity edema present. The heart sounds are normal. The neurologic examination reveals no deficits. The remainder of the physical examination yields no abnormalities.

A chest radiograph is unrevealing. A computed tomography (CT) scan of his chest is obtained (see Images 1-4).

What is the cause of this patient’s dyspnea?
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hosseny



المساهمات : 93
تاريخ التسجيل : 07/09/2007

مُساهمةموضوع: رد: حالات اكلينيكيه ...... فكروا معايا   الأربعاء سبتمبر 19, 2007 4:04 am

ANSWER

Pneumomediastinum: The CT scans reveal abnormal mediastinal gas or pneumomediastinum. The lungs are otherwise well expanded without evidence of pneumothorax, pneumopericardium, subcutaneous emphysema, or other abnormality. Pneumomediastinum is 1 of 5 conditions that can result from pulmonary barotrauma or pulmonary overinflation syndrome (the others being arterial gas embolism, pneumothorax, subcutaneous emphysema, and pneumopericardium). The underlying pathologic process of pulmonary barotrauma occurs when gas expansion in the lungs ruptures the lung tissues and dissects into the adjoining tissue. Once lung tissues rupture, the trapped gas, which is at a relatively high pressure, will seek an area of relatively lower pressure. In this case, the escaping air from the lung ultimately resided in the mediastinum. Carolan and Vaughan stated that “the generally accepted explanation for the development of PM [pneumomediastinum] is that free air tracks from ruptured peribronchial vascular sheaths toward the hilum of the lung. From there, it extends proximally to the mediastinum.”2 Although we understand the various factors that predispose a person to pulmonary barotrauma, the actual injury mechanism is not well understood.3

The underlying physics are well understood. Pulmonary barotrauma while diving is directly related to Boyle’s law, which states that, at a constant temperature, the volume of a gas varies inversely with its pressure. As a result of Boyle’s law, gas inhaled while a diver is at depth will expand as the diver ascends towards the surface. In general, the expanding gas is allowed to escape through the glottis as the diver breathes while ascending. If a diver’s glottis is closed, as in breath-holding, the expanding gas causes pulmonary over-pressurization. Air trapping caused by asthma, chronic obstructive pulmonary disease (COPD), and blebs can predispose a diver to pulmonary barotrauma.

The clinical presentation, diagnosis, and treatment of pneumomediastinum can vary greatly. The most common presenting signs and symptoms are chest pain, dyspnea, dysphonia, and the presence of other conditions that can result from pulmonary barotrauma. The diagnosis of pneumomediastinum is dependent upon imaging studies. Chest radiography is the most common method used to diagnose this condition. This imaging modality may be insensitive; however, it is still useful as a first-line modality that can also detect other coexisting injuries, such as pneumothorax. In the event that pneumomediastinum is suspected but not detected on chest radiography, a CT scan should be performed. In this case, the chest radiography was normal; however, a significant amount of mediastinal air was noted on the CT scan.

The treatment of pneumomediastinum is dependent upon the clinical presentation. Most cases of pneumomediastinum will resolve spontaneously, and no further therapy is necessary other than administration of supplemental oxygen to hasten the process of mediastinal air absorption. The increased amount of consumable oxygen and decreased amount of inspired inert gas (ie, nitrogen) help to provide an increased gradient for trapped air to return into solution. In the case of a very large amount of trapped mediastinal air, a patient may present with respiratory compromise secondary to poor ventilation or with cardiovascular compromise secondary to increased intrathoracic pressure and decreased venous return. In either situation, immediate surgical intervention is warranted. There have been reports of percutaneous drainage being effective; however, mediastinoscopy and thoracotomy remain the primary treatments.2

The following conditions can also occur as a result of pulmonary barotrauma:

The potential space between the lung and chest wall provides an area where escaping trapped air resulting from pulmonary barotrauma can eventually cause a pneumothorax. The most common presenting signs and symptoms of a traumatic pneumothorax are chest pain, dyspnea, tachycardia, decreased or absent breath sounds, increased resonance on percussion, decreased chest wall movement, and, in the case of a tension pneumothorax, tracheal deviation, jugular venous distention, hypotension, and cyanosis.1 Tension pneumothorax is an emergency that requires immediate intervention. A needle thoracentesis can be a temporizing measure; however, definitive treatment will require the placement of a thoracostomy tube. In the case of a simple or nontension pneumothorax, the treatment may range from observation with spontaneous resolution to the placement of a thoracostomy tube (depending upon the clinical presentation of the patient).


An arterial gas embolism (AGE) is the result of lung tissue rupture with injury to the pulmonary vasculature. This type of injury shunts air into the pulmonary venous circulation, which is then distributed to end organs, such as the brain, through systemic circulation. The most common signs and symptoms of an AGE are cranial nerve deficits, paralysis or weakness, poor coordination, sensory abnormalities, and unconsciousness. Additionally, the signs and symptoms of an AGE will manifest very quickly following pulmonary barotrauma. In fact, more than 98% of AGEs manifest within 10 minutes following the initial trauma. An AGE requires immediate action because it closely resembles a stroke or an end-organ infarction. The length of time it takes to get a patient to definitive treatment is directly correlated to the amount of end-organ tissue ischemia and irreversible hypoxic injury at presentation. A patient should be immediately placed on 100% oxygen, if available, for transport to the nearest hyperbaric oxygen treatment facility. Hyperbaric oxygen therapy will force any remaining gas within the systemic arterial system back into solution, thus restoring normal blood flow. Additionally, hyperbaric oxygen helps supply oxygen to ischemic areas that would otherwise progress into irreversible hypoxic injury.

Jouriles stated that “pneumopericardium is caused most commonly by an increase in intra-alveolar pressure above atmospheric pressure, resulting in rupture of alveoli. Air dissects into the hilum and mediastinum, through the pericardial reflection on the pulmonary vessels, and into the pericardium.”4 Like other conditions that can arise from pulmonary barotrauma, pneumopericardium can range from clinically insignificant to life-threatening. A hemodynamically stable patient with pneumopericardium can be observed as the condition resolves. Anecdotally, a brief treatment of 100% oxygen may speed up the reabsorption of gas from the pericardium. If a pneumopericardium results in hemodynamic instability, an emergency pericardiocentesis is indicated.

Subcutaneous emphysema arises when air dissects the pulmonary interstitium and ultimately resides in the subcutaneous tissues. The diagnosis of subcutaneous emphysema can be made via physical examination or with ancillary studies (ie, chest radiography or CT scanning). On physical examination, the skin will have notable crepitus on palpation. Additionally, the locally affected area will appear full. The presence of air within the subcutaneous tissues on chest radiography or CT scans is diagnostic of subcutaneous emphysema. Unlike other conditions that arise from pulmonary barotrauma, subcutaneous emphysema is benign. Subcutaneous emphysema is unlikely to be an isolated finding after pulmonary barotrauma; therefore, a complete physical examination and ancillary studies are warranted to evaluate for the presence of AGE, pneumothorax, pneumopericardium, or pneumomediastinum.
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