Chest
Pulmonary Embolism
December 05, 2009, 19:44
Pulmonary Embolism
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care
Introduction
Pulmonary embolus is a common condition occurring in about 1 in 50 hospital admissions. Because of difficulties in positively ruling the diagnosis in or out, many physicians hesitate the raise the possibility that a pulmonary embolus may be present in a particular case though the mortality of an untreated pulmonary embolus may approach 30%.
Pathophysiology
95% of pulmonary emboli originate as lower extremity deep venous thrombi. A recent study demonstrated that about 50% of patients with DVT could be shown to have an unmatched perfusion defect by V/Q scan and of these 66% of these defects resolved after anticoagulation suggesting that these were acute pulmonary emboli. 10% of pulmonary emboli result in some degree of pulmonary infarction. It is not clear whether pulmonary embolic mortality is strictly related to pulmonary vascular obstruction (i.e. hemodynamic effects) or whether humoral or gas-exchange factors predominate. It would not be surprising if the dominate pathology varied among patients. Note that since normal patients are able to at least double their cardiac output (and thus their pulmonary blood flow) without significantly elevating their pulmonary artery pressure, that at least 50% of the pulmonary circulation would need to be obstructed by a pulmonary embolus before significant hemodynamic compromise resulting from mechanical obstruction would occur. This, of course, assumes that the pulmonary circulation is normal before the embolus occurs. Pulmonary embolic disease converts normal lung units into dead space units. This results in V/Q mismatches (i.e. areas of normal ventilation with reduced perfusion). This alteration in V/Q mismatching result in hypoxemia and results in a need for an increased minute volume to maintain the same PaCO2 level. If the mismatch is significant one would expect tachypnea and hypoxia to develop as a result of this mismatch.
Signs/Symptoms
Most symptoms of pulmonary embolus emanate directly from the pathophysiology. Some (hypoxia) relate from the creation of deadspace while others (right atrial enlargement on the EKG) result from increased pulmonary artery pressure from mechanical obstructive phenomena. Common findings in pulmonary embolus include:
hypoxia and respiratory alkalosis
EKG evidence of RV overload such as right ventricular hypertrophy or right atrial enlargement.
Increased deadspace as shown by Vd/Vt measurement (rarely measured).
Pleural effusion, frequently bloody.
Hypoperfusion on chest radiograph.
Unmatched perfusion defects on V/Q scan.
Positive pulmonary angiogram (gold standard).
Tachycardia (this is frequently the only objective finding).
Chest pain and dyspnea (very common).
Diagnostic Work-up
Once the possibility of pulmonary embolus has been raised, a diagnostic work-up must be conducted to either confirm or deny the diagnosis. Given the high rate of pulmonary embolus in patients with deep venous thrombosis, it could be argued that all patients with DVT should be worked up for PE as well. In most cases, the treatment for DVT will be the same as the treatment for PE therefore diagnosis of either will result in treatment though it would be useful in future management to know whether PE has occurred. The two main methods used to evaluate for PE are V/Q lung scanning and pulmonary arteriography. The pulmonary angiogram is the 'gold standard' for diagnosing or ruling out a pulmonary embolus. The risks are the risks of a central venous line plus the risk of IV contrast. The usual algorithm though is to start with a V/Q scan except in cases where the V/Q is non-diagnostic (this is frequent) or in cases where one would expect the V/Q scan to be difficult to interpret. The V/Q scan is really two tests, one to evaluate ventilation and one to evaluate perfusion. The ventilation test involves the patient breathing a radioactive tracer gas and sitting under the gamma camera to evaluate whether ventilation is normal in areas of the lung that may be shown to have abnormal perfusion on a perfusion scan. A high probability V/Q scan would be one that showed a segmental defect in perfusion without a matching defect in ventilation. V/Q scans in patients with significant ventilation defects are difficult to interpret and even in a low probability scan, the incidence of pulmonary embolus may be as high as 25%. A recent study demonstrated that V/Q scanning had a sensitivity of 98% with a specificity of only 10% if one considers low probability scans to be positive scans. If you decide that only high probability scans are positive then the sensitivity drops to 41% with a specificity of 97%. Because of this diagnostic uncertainty in ruling out PE (i.e. low sensitivity), a V/Q scan really needs to be very normal, not just low probability, to avoid doing a pulmonary arteriogram to rule out PE if clinical suspicion is high unless the plan is to just treat the patient emperically. If a V/Q scan is positive, however, treatment can begin. A recent studies (Hull) suggest that the combination of clinical suspicion (prior probability) and the V/Q scan agreeing with that clinical suspicion would be 95% sensitive and 95% specific. Unfortunately the basis of this estimate of clinical suspicion was not standardized or defined in the paper. Since 95% of pulmonary emboli originate from the legs, a venogram or venous doppler study can be used to detect the DVT and treatment can proceed if this is positive even though there is a possibility of a PE without a DVT (5%) and you could have a DVT without PE (around 50% of the time). The need for further work-up for PE in the patient with a DVT would depend on how seriously ill the patient was and whether further therapy specific for the PE was considered (i.e. thrombolytic therapy or embolectomy). The echocardiogram is frequently useful in evaluating the patient with suspected pulmonary embolus. In some cases residual clot can be imaged in the right ventricle or right atrium (a finding that suggests a high likelihood of another embolus soon) and right ventricular overload can be demonstrated if it is present.
Chemical Tests for PE
Recently there has been work done to try to develop assays for serum and urine markers of pulmonary embolic disease. So far, these tests have a fairly high degree of sensitivity but have a fairly low specificity which means that they can be used to rule out a pulmonary embolus but they cannot be used to confirm one. This is still very useful, however, as they tests can be used as evidence to avoid an expensive, and perhaps risky, work up in patients who fail to show the markers. One test, the D-dimer test, measures the level of a product of fibrin degradation. A serum D-dimer concentration of less than 500 ug/l has a negative predictive value of 98% meaning that less than 2% of persons with a D-dimer level below 500 will be later found to have a pulmonary embolus. The sensitivity of this test remained high even 3 and 7 days after presentation. The RMH laboratory (1991) provides the D-dimer test on demand for a cost of $42 (a CBC is $48) and a testing time of under one hour. A recent paper (Leitha et al) has cast some controversy on the utility of the D-dimer test showing a sensitivity closer to 50% for predicting a high-probability V/Q scan if 500 ng/ml is the cut-off and 84% if the cut-off is 120 ng/ml. It should be noted, however, that V/Q scans may remain abnormal for some time (perhaps months or longer in some cases) after an acute event so a study using a V/Q scan as the end-point might not be valid as a test of the accuracy of the D-dimer study as a screening test for pulmonary embolus. In any case, realized that this use of the D-dimer study is likely to be the subject of further study before its utility is generally accepted. There is more than one methodology of D-Dimer test in common use in laboratories. Only the quantitative measurement techniques are really sensitive enough to be of much utility in ruling out a PE.
Treatment
Most pulmonary emboli are treated with systemic anti-coagulation. This means IV heparin followed by coumadin. Note the table below on how to actually administer these drugs. There have been some trials of thrombolytic therapy and thus far the results are promising but it remains to be seen whether morbidity and mortality are improved by this therapy. Thrombolysis is probably indicated for patients with hemodynamic compromise from a pulmonary embolus in the absense of contraindications and will possibly gain acceptance as treatment for all symptomatic emoboli in the future. Embolectomy is a therapy of last resort and most patients who might benefit from it are very sick and many die before the diagnosis is even certain.
References
Hyers TM, Hull RD, Weg JG: Antithrombotic Therapy for Venous Thromboembolic Disease, Chest 95:2, February 1989 supplement.
The PIOPED investigators: Value of Ventilation/Perfusion Scan in Acute Pulmonary Embolism, Results of the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED), JAMA 263:20, May 1990.
Bone RC: Ventilation/Perfusion Scan in Pulmonary Embolism, 'The Emperor is Incompletely Attired', JAMA 1990; 263:20.
Bell WR: The Clinical Features of Submassive and Massive Pulmonary Emboli, AM J MED 1977; Vol. 62.
Hull RD: Diagnostic Value of Ventilation-Perfusion Lung Scanning in Patients with Suspected Pulmonary Embolism, Chest 1991; 88:6.
Tulchinsky, M, Zeller JA, Reba RC: Urinary Fibrinopeptide A in Evaluation of Patients with Suspected Acute Pulmonary Embolism, Chest 1991; 100:394-98.
Bounameaux H, Cirafici P, De Moerloose P, et al: Measurement of D-dimer in plasma as diagnostic aid in suspected pulmonary embolism, Lancet 1991; 337:196-200.
Kelly MA, Carson JL, Palevsky HI, Schwartz JS: Diagnosing Pulmonary Embolism: New Facts and Strategies, Annals of Internal Medicine 1991; 114: 300-306.
Hull RD, Hirsch J, Carter CJ, et al: Diagnostic value of ventilation-perfusion lung scanning in patients with suspected pulmonary embolism, Chest 1985; 88: 819-28.
Hull RD, Hirsh J, Carter CJ, et al: Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan, Ann Intern Med 1983; 98: 891-9.
Leitha T, Speiser W, Dudczak R: Pulmonary Embolism, Efficacy of D-dimer and thrombin-antithrombin III complex determinations as screening tests before lung scanning, Chest 1991; 100:1536-41.
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care
Introduction
Pulmonary embolus is a common condition occurring in about 1 in 50 hospital admissions. Because of difficulties in positively ruling the diagnosis in or out, many physicians hesitate the raise the possibility that a pulmonary embolus may be present in a particular case though the mortality of an untreated pulmonary embolus may approach 30%.
Pathophysiology
95% of pulmonary emboli originate as lower extremity deep venous thrombi. A recent study demonstrated that about 50% of patients with DVT could be shown to have an unmatched perfusion defect by V/Q scan and of these 66% of these defects resolved after anticoagulation suggesting that these were acute pulmonary emboli. 10% of pulmonary emboli result in some degree of pulmonary infarction. It is not clear whether pulmonary embolic mortality is strictly related to pulmonary vascular obstruction (i.e. hemodynamic effects) or whether humoral or gas-exchange factors predominate. It would not be surprising if the dominate pathology varied among patients. Note that since normal patients are able to at least double their cardiac output (and thus their pulmonary blood flow) without significantly elevating their pulmonary artery pressure, that at least 50% of the pulmonary circulation would need to be obstructed by a pulmonary embolus before significant hemodynamic compromise resulting from mechanical obstruction would occur. This, of course, assumes that the pulmonary circulation is normal before the embolus occurs. Pulmonary embolic disease converts normal lung units into dead space units. This results in V/Q mismatches (i.e. areas of normal ventilation with reduced perfusion). This alteration in V/Q mismatching result in hypoxemia and results in a need for an increased minute volume to maintain the same PaCO2 level. If the mismatch is significant one would expect tachypnea and hypoxia to develop as a result of this mismatch.
Signs/Symptoms
Most symptoms of pulmonary embolus emanate directly from the pathophysiology. Some (hypoxia) relate from the creation of deadspace while others (right atrial enlargement on the EKG) result from increased pulmonary artery pressure from mechanical obstructive phenomena. Common findings in pulmonary embolus include:
hypoxia and respiratory alkalosis
EKG evidence of RV overload such as right ventricular hypertrophy or right atrial enlargement.
Increased deadspace as shown by Vd/Vt measurement (rarely measured).
Pleural effusion, frequently bloody.
Hypoperfusion on chest radiograph.
Unmatched perfusion defects on V/Q scan.
Positive pulmonary angiogram (gold standard).
Tachycardia (this is frequently the only objective finding).
Chest pain and dyspnea (very common).
Diagnostic Work-up
Once the possibility of pulmonary embolus has been raised, a diagnostic work-up must be conducted to either confirm or deny the diagnosis. Given the high rate of pulmonary embolus in patients with deep venous thrombosis, it could be argued that all patients with DVT should be worked up for PE as well. In most cases, the treatment for DVT will be the same as the treatment for PE therefore diagnosis of either will result in treatment though it would be useful in future management to know whether PE has occurred. The two main methods used to evaluate for PE are V/Q lung scanning and pulmonary arteriography. The pulmonary angiogram is the 'gold standard' for diagnosing or ruling out a pulmonary embolus. The risks are the risks of a central venous line plus the risk of IV contrast. The usual algorithm though is to start with a V/Q scan except in cases where the V/Q is non-diagnostic (this is frequent) or in cases where one would expect the V/Q scan to be difficult to interpret. The V/Q scan is really two tests, one to evaluate ventilation and one to evaluate perfusion. The ventilation test involves the patient breathing a radioactive tracer gas and sitting under the gamma camera to evaluate whether ventilation is normal in areas of the lung that may be shown to have abnormal perfusion on a perfusion scan. A high probability V/Q scan would be one that showed a segmental defect in perfusion without a matching defect in ventilation. V/Q scans in patients with significant ventilation defects are difficult to interpret and even in a low probability scan, the incidence of pulmonary embolus may be as high as 25%. A recent study demonstrated that V/Q scanning had a sensitivity of 98% with a specificity of only 10% if one considers low probability scans to be positive scans. If you decide that only high probability scans are positive then the sensitivity drops to 41% with a specificity of 97%. Because of this diagnostic uncertainty in ruling out PE (i.e. low sensitivity), a V/Q scan really needs to be very normal, not just low probability, to avoid doing a pulmonary arteriogram to rule out PE if clinical suspicion is high unless the plan is to just treat the patient emperically. If a V/Q scan is positive, however, treatment can begin. A recent studies (Hull) suggest that the combination of clinical suspicion (prior probability) and the V/Q scan agreeing with that clinical suspicion would be 95% sensitive and 95% specific. Unfortunately the basis of this estimate of clinical suspicion was not standardized or defined in the paper. Since 95% of pulmonary emboli originate from the legs, a venogram or venous doppler study can be used to detect the DVT and treatment can proceed if this is positive even though there is a possibility of a PE without a DVT (5%) and you could have a DVT without PE (around 50% of the time). The need for further work-up for PE in the patient with a DVT would depend on how seriously ill the patient was and whether further therapy specific for the PE was considered (i.e. thrombolytic therapy or embolectomy). The echocardiogram is frequently useful in evaluating the patient with suspected pulmonary embolus. In some cases residual clot can be imaged in the right ventricle or right atrium (a finding that suggests a high likelihood of another embolus soon) and right ventricular overload can be demonstrated if it is present.
Chemical Tests for PE
Recently there has been work done to try to develop assays for serum and urine markers of pulmonary embolic disease. So far, these tests have a fairly high degree of sensitivity but have a fairly low specificity which means that they can be used to rule out a pulmonary embolus but they cannot be used to confirm one. This is still very useful, however, as they tests can be used as evidence to avoid an expensive, and perhaps risky, work up in patients who fail to show the markers. One test, the D-dimer test, measures the level of a product of fibrin degradation. A serum D-dimer concentration of less than 500 ug/l has a negative predictive value of 98% meaning that less than 2% of persons with a D-dimer level below 500 will be later found to have a pulmonary embolus. The sensitivity of this test remained high even 3 and 7 days after presentation. The RMH laboratory (1991) provides the D-dimer test on demand for a cost of $42 (a CBC is $48) and a testing time of under one hour. A recent paper (Leitha et al) has cast some controversy on the utility of the D-dimer test showing a sensitivity closer to 50% for predicting a high-probability V/Q scan if 500 ng/ml is the cut-off and 84% if the cut-off is 120 ng/ml. It should be noted, however, that V/Q scans may remain abnormal for some time (perhaps months or longer in some cases) after an acute event so a study using a V/Q scan as the end-point might not be valid as a test of the accuracy of the D-dimer study as a screening test for pulmonary embolus. In any case, realized that this use of the D-dimer study is likely to be the subject of further study before its utility is generally accepted. There is more than one methodology of D-Dimer test in common use in laboratories. Only the quantitative measurement techniques are really sensitive enough to be of much utility in ruling out a PE.
Treatment
Most pulmonary emboli are treated with systemic anti-coagulation. This means IV heparin followed by coumadin. Note the table below on how to actually administer these drugs. There have been some trials of thrombolytic therapy and thus far the results are promising but it remains to be seen whether morbidity and mortality are improved by this therapy. Thrombolysis is probably indicated for patients with hemodynamic compromise from a pulmonary embolus in the absense of contraindications and will possibly gain acceptance as treatment for all symptomatic emoboli in the future. Embolectomy is a therapy of last resort and most patients who might benefit from it are very sick and many die before the diagnosis is even certain.
References
Hyers TM, Hull RD, Weg JG: Antithrombotic Therapy for Venous Thromboembolic Disease, Chest 95:2, February 1989 supplement.
The PIOPED investigators: Value of Ventilation/Perfusion Scan in Acute Pulmonary Embolism, Results of the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED), JAMA 263:20, May 1990.
Bone RC: Ventilation/Perfusion Scan in Pulmonary Embolism, 'The Emperor is Incompletely Attired', JAMA 1990; 263:20.
Bell WR: The Clinical Features of Submassive and Massive Pulmonary Emboli, AM J MED 1977; Vol. 62.
Hull RD: Diagnostic Value of Ventilation-Perfusion Lung Scanning in Patients with Suspected Pulmonary Embolism, Chest 1991; 88:6.
Tulchinsky, M, Zeller JA, Reba RC: Urinary Fibrinopeptide A in Evaluation of Patients with Suspected Acute Pulmonary Embolism, Chest 1991; 100:394-98.
Bounameaux H, Cirafici P, De Moerloose P, et al: Measurement of D-dimer in plasma as diagnostic aid in suspected pulmonary embolism, Lancet 1991; 337:196-200.
Kelly MA, Carson JL, Palevsky HI, Schwartz JS: Diagnosing Pulmonary Embolism: New Facts and Strategies, Annals of Internal Medicine 1991; 114: 300-306.
Hull RD, Hirsch J, Carter CJ, et al: Diagnostic value of ventilation-perfusion lung scanning in patients with suspected pulmonary embolism, Chest 1985; 88: 819-28.
Hull RD, Hirsh J, Carter CJ, et al: Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan, Ann Intern Med 1983; 98: 891-9.
Leitha T, Speiser W, Dudczak R: Pulmonary Embolism, Efficacy of D-dimer and thrombin-antithrombin III complex determinations as screening tests before lung scanning, Chest 1991; 100:1536-41.
Pneumothorax
December 05, 2009, 19:43
Pneumothorax
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care
Definition
A pneumothorax is a collection of gas that is in the pleural space within the chest but outside of the lungs. The pleural space is a potential space bounced by the visceral and parietal pleura. This potential space exists to allow the chest wall to exert a suction to oppose the normal elastic recoil of the lungs. If this potential space is filled by air, this opposition is lost and a collapse of the involved lung occurs.
Classification
A pneumothorax is called spontaneous if it occurs in the absence of any trauma to the chest. It is considered to be primary when there is no obvious lung disease. A traumatic pneumothorax is normally caused by penetrating chest trauma but could be a result of barotrauma from a ventilator. A tension pneumothorax is one in which there is positive pressure in the pleural space sufficient to cause patient compromise.
Etiology
There are many causes of pneumothorax. Air enters the pleural space either from outside the chest (penetrating trauma), from lung parynchyma, or from the esophagus in cases of perforation. Obstructive lung diseases, either intrinsic, or resulting from foreign body airway obstruction, can lead to pneumothorax by allowing for inadequate exhalation of inspired gas. This can start out as "Auto-PEEP" which may damage lung tissues resulting in air leaks or can result from a "ball-valve" effect where an obstruction can be bypassed by enlarging airway diameter on inspiration but cannot be bypassed during exhalation when airway diameter is smaller. Such an obstruction could be caused by mucus plugging or by a foreign body in an airway. Pleural diseases can cause a pneumothorax by direct disruption of the pleura. Marfan syndrome patients are more susceptible to pneumothorax possibly due to a combination of abnormal connective tissue and by greater pleural pressure changes during breathing that result from the Marfan body habitus. This occurs mostly in young tall thin males.
Tension Pneumothorax
A tension pneumothorax results from situations where air can enter the pleural space but cannot leave. An example might be a stab wound to the chest that punctures the lung. While there is a hole in the chest, a knife wound tends to seal itself in the chest wall thus trapping any air leaked from the lung injury in the chest cavity. A gun shot wound is less likely to result in a tension pneumothorax as the leaked air can exit the chest via the entry wound in the chest wall. Most tension pneumothoraces are traumatic and many of these are iatrogenic and occur on patients who are receiving mechanical ventilation where positive airway pressures facilitate leakage of air into the pleural space. A tension pneumothorax is life threatening because there is more complete collapse of the affected lung and because the positive pressure exerts several adverse effects on the cardiovascular system including tamponade of the mediastinal structures and kinking of the great vessels at their point of entry to the thorax caused by mediastinal shift.
Diagnosis
A pneumothorax by have either an insidious or dramatic onset. Typical symptoms include pleuritic chest pain and dyspnea. Tachycardia and severe hypotension are the only noticeable findings in a mechanically ventilated patient or a patient who is otherwise unable to provide a history. There may be evidence of tracheal deviation and a deviated PMI if there is tension with mediastinal shift. Breath sounds will normally be absent or diminished but you may be able to hear breath sounds transmitted from the contralateral lung in some patients. In some cases, transillumination of the chest with a bright light source will light up the hemithorax of a patient with a pneumothorax though this technique is limited to pediatric patients or those with a thin chest wall. A chest x-ray, preferably with a lateral view or one taken during exhalation is normally the most definitive test to diagnose a pneumothorax but in some cases of tension pneumothorax, a patient may succumb before there is time to obtain one so it is necessary to consider treating an as-yet unconfirmed pneumothorax if the clinical situation dictates.
Radiographic diagnosis
The classic finding of pneumothorax on a chest x-ray is to see a peripheral lung margin with lucency between the lung margin and the chest wall. With a tension pneumothorax there will be mediastinal shift away from the affected side. It must be remembered, however, that the chest is a 3-dimensional structure and that the free air of a pneumothorax may be loculated anterior or posterior to lung or even interposed between the diaphragm and the lung. For this reason, presence of lung markings on a single view chest x-ray does not rule out a pneumothorax. One should be suspicious of any unusual lucencies in the chest and additional views should be obtained, perhaps even including CT scans of the chest in some cases.
Treatment
Not all pneumothoraces require specific therapy. In asymptomatic or mildly symptomatic patients, serial chest x-rays can be obtained to allow for spontaneous resorption of a small pneumothorax. Resorption can be accelerated by placing a patient on 100% oxygen to wash nitrogen from the pleural space with a resultant decrease in the size of the collected free gas. There has been some success reported with needle thoracentesis of spontaneous pneumothoraces though recurrences of pneumothorax are not unusual with this technique and a repeat procedure or chest tube may be required. If a patient is being mechanically ventilated there is a higher risk of progression to a tension pneumothorax and in these cases a chest tube should be used to evacuate any free air and allow time for the original air leak to heal.
Chest Drainage Systems
In an emergency, the initial treatment of a pneumothorax, tension or otherwise, is to place a large bore IV needle into the pleural space to decompress any tension and/or to remove free air to allow the lung to re-expand. Free air will normally collect anteriorly in a supine patient so the needle would be placed into the chest, over a rib, normally in the 2-4th rib interspace between the anterior axillary and mid-clavicular lines. In many cases, a patient will improve as soon as tension is released with a needle procedure though some patients will not improve until their lung has been re-expanded. Once a chest tube has been inserted in the pleural space (anteriorly if possible) a system is needed that will allow air and fluids out of the chest without allowing air to leak back into the chest. In some cases, it may be desirable to allow for suction to be applied to the pleural space to facilitate removal of air or fluids. A Heimlich valve can be used to satisfy the first requirement and consists essentially of a one-way valve that is attached directly to a chest tube. A make shift Heimlich valve can be produced by attaching the finger of a surgical glove over the end of a chest tube and placing a small hole in the end of the glove finger. The glove finder would tend to allow gasses to escape but would collapse in response to negative pressure in the pleural space.
A 3-bottle or Atrium or Pleurovac drainage system can provide valuable information about the patient's pleural pressure and the presence of absence of an active air leak (bronchopleural fistula for example). The first chamber (White on a Pleurovac) is a simple trap to catch any fluids drained from the chest tube. The second chamber (Pink on a Pleurovac) is the underwater seal or water seal chamber. This chamber exists to provide the one-way valve that will allow air to exit the chest but not to enter it. Note that the tube from the drainage chamber is immersed under water about 2 cm deep. Any pressure in the pleural space greater than 2 cm H2O will result in bubbles forming in this chamber. If you see bubbles in this chamber then there is air coming from the chest tube or connecting tubing. Note that a hole in the chest tube that is outside of the chest will result in heavy bubbling in this chamber so not all leaks are from the pleural space. The third chamber (Blue on a Pleurovac) is the suction control chamber. If the "S" connection is attached to wall suction and there is bubbling from the vent tube, then the level of negative pressure applied to the pleural space is equal to the depth that the vent tube is placed under water. 20 cm H2O would be a typical level of suction. Some chest drainage systems substitute a needle valve suction regulator for the suction control chamber. To measure the pleural pressure, one can pinch off the suction tubing "S" and read the water level in the underwater seal chamber (second chamber).
Prevention
Iatrogenic pneumothoraces can be prevented in some but not all cases. If a thoracentesis is to be performed, use of ultrasound guidance can help in avoiding lung injury and avoidance of pleural adhesions which may be likely to result in a pneumothorax if punctured. The biggest danger in an iatrogenic pneumothorax is in not recognizing that one has occurred. Listening to breath sounds before an invasive procedure starts will make it much easier to tell if a pneumothorax exists afterwards. In high risk patients (i.e. high airway pressures and/or unstable hemodynamics) plan ahead by having large bore needles, stop cocks, and syringes available before the procedure is started so there will be minimal delay in draining a life-threatening pneumothorax.
References
Connors AF, Altose MD: Textbook of Pulmonary Diseases, p.1592, Little Brown, Boston, 1989.
Bevelaqua FA and Aranda C: Management of spontaneous pneumothorax with small lumen catheter manual aspiration. Chest 1982; 81:693-694.
Gustman P, Yerger L, Wanner A: Immediate Cardiovascular Effects of Tension Pneumothorax, ARRD 1983; 127:171-174.
Haake R, Schlichtig R, Ulstad DR: Barotrauma Pathophysiology, Risk Factors, and Prevention, CHEST 1987, 91:608-613.
Conces DJ et al: Treatment of Pneumothoraces Utilizing Small Caliber Chest Tubes, CHEST 1988, 94:55-60.
Jenkinson, SG: Pneumothorax, Clinics in Chest Medicine, 1985, 6:153-161.
Ohata M, Suzuki H: Pathogenesis of Spontaneous Pneumothorax, CHEST 1980, 77:771-776.
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care
Definition
A pneumothorax is a collection of gas that is in the pleural space within the chest but outside of the lungs. The pleural space is a potential space bounced by the visceral and parietal pleura. This potential space exists to allow the chest wall to exert a suction to oppose the normal elastic recoil of the lungs. If this potential space is filled by air, this opposition is lost and a collapse of the involved lung occurs.
Classification
A pneumothorax is called spontaneous if it occurs in the absence of any trauma to the chest. It is considered to be primary when there is no obvious lung disease. A traumatic pneumothorax is normally caused by penetrating chest trauma but could be a result of barotrauma from a ventilator. A tension pneumothorax is one in which there is positive pressure in the pleural space sufficient to cause patient compromise.
Etiology
There are many causes of pneumothorax. Air enters the pleural space either from outside the chest (penetrating trauma), from lung parynchyma, or from the esophagus in cases of perforation. Obstructive lung diseases, either intrinsic, or resulting from foreign body airway obstruction, can lead to pneumothorax by allowing for inadequate exhalation of inspired gas. This can start out as "Auto-PEEP" which may damage lung tissues resulting in air leaks or can result from a "ball-valve" effect where an obstruction can be bypassed by enlarging airway diameter on inspiration but cannot be bypassed during exhalation when airway diameter is smaller. Such an obstruction could be caused by mucus plugging or by a foreign body in an airway. Pleural diseases can cause a pneumothorax by direct disruption of the pleura. Marfan syndrome patients are more susceptible to pneumothorax possibly due to a combination of abnormal connective tissue and by greater pleural pressure changes during breathing that result from the Marfan body habitus. This occurs mostly in young tall thin males.
Tension Pneumothorax
A tension pneumothorax results from situations where air can enter the pleural space but cannot leave. An example might be a stab wound to the chest that punctures the lung. While there is a hole in the chest, a knife wound tends to seal itself in the chest wall thus trapping any air leaked from the lung injury in the chest cavity. A gun shot wound is less likely to result in a tension pneumothorax as the leaked air can exit the chest via the entry wound in the chest wall. Most tension pneumothoraces are traumatic and many of these are iatrogenic and occur on patients who are receiving mechanical ventilation where positive airway pressures facilitate leakage of air into the pleural space. A tension pneumothorax is life threatening because there is more complete collapse of the affected lung and because the positive pressure exerts several adverse effects on the cardiovascular system including tamponade of the mediastinal structures and kinking of the great vessels at their point of entry to the thorax caused by mediastinal shift.
Diagnosis
A pneumothorax by have either an insidious or dramatic onset. Typical symptoms include pleuritic chest pain and dyspnea. Tachycardia and severe hypotension are the only noticeable findings in a mechanically ventilated patient or a patient who is otherwise unable to provide a history. There may be evidence of tracheal deviation and a deviated PMI if there is tension with mediastinal shift. Breath sounds will normally be absent or diminished but you may be able to hear breath sounds transmitted from the contralateral lung in some patients. In some cases, transillumination of the chest with a bright light source will light up the hemithorax of a patient with a pneumothorax though this technique is limited to pediatric patients or those with a thin chest wall. A chest x-ray, preferably with a lateral view or one taken during exhalation is normally the most definitive test to diagnose a pneumothorax but in some cases of tension pneumothorax, a patient may succumb before there is time to obtain one so it is necessary to consider treating an as-yet unconfirmed pneumothorax if the clinical situation dictates.
Radiographic diagnosis
The classic finding of pneumothorax on a chest x-ray is to see a peripheral lung margin with lucency between the lung margin and the chest wall. With a tension pneumothorax there will be mediastinal shift away from the affected side. It must be remembered, however, that the chest is a 3-dimensional structure and that the free air of a pneumothorax may be loculated anterior or posterior to lung or even interposed between the diaphragm and the lung. For this reason, presence of lung markings on a single view chest x-ray does not rule out a pneumothorax. One should be suspicious of any unusual lucencies in the chest and additional views should be obtained, perhaps even including CT scans of the chest in some cases.
Treatment
Not all pneumothoraces require specific therapy. In asymptomatic or mildly symptomatic patients, serial chest x-rays can be obtained to allow for spontaneous resorption of a small pneumothorax. Resorption can be accelerated by placing a patient on 100% oxygen to wash nitrogen from the pleural space with a resultant decrease in the size of the collected free gas. There has been some success reported with needle thoracentesis of spontaneous pneumothoraces though recurrences of pneumothorax are not unusual with this technique and a repeat procedure or chest tube may be required. If a patient is being mechanically ventilated there is a higher risk of progression to a tension pneumothorax and in these cases a chest tube should be used to evacuate any free air and allow time for the original air leak to heal.
Chest Drainage Systems
In an emergency, the initial treatment of a pneumothorax, tension or otherwise, is to place a large bore IV needle into the pleural space to decompress any tension and/or to remove free air to allow the lung to re-expand. Free air will normally collect anteriorly in a supine patient so the needle would be placed into the chest, over a rib, normally in the 2-4th rib interspace between the anterior axillary and mid-clavicular lines. In many cases, a patient will improve as soon as tension is released with a needle procedure though some patients will not improve until their lung has been re-expanded. Once a chest tube has been inserted in the pleural space (anteriorly if possible) a system is needed that will allow air and fluids out of the chest without allowing air to leak back into the chest. In some cases, it may be desirable to allow for suction to be applied to the pleural space to facilitate removal of air or fluids. A Heimlich valve can be used to satisfy the first requirement and consists essentially of a one-way valve that is attached directly to a chest tube. A make shift Heimlich valve can be produced by attaching the finger of a surgical glove over the end of a chest tube and placing a small hole in the end of the glove finger. The glove finder would tend to allow gasses to escape but would collapse in response to negative pressure in the pleural space.
A 3-bottle or Atrium or Pleurovac drainage system can provide valuable information about the patient's pleural pressure and the presence of absence of an active air leak (bronchopleural fistula for example). The first chamber (White on a Pleurovac) is a simple trap to catch any fluids drained from the chest tube. The second chamber (Pink on a Pleurovac) is the underwater seal or water seal chamber. This chamber exists to provide the one-way valve that will allow air to exit the chest but not to enter it. Note that the tube from the drainage chamber is immersed under water about 2 cm deep. Any pressure in the pleural space greater than 2 cm H2O will result in bubbles forming in this chamber. If you see bubbles in this chamber then there is air coming from the chest tube or connecting tubing. Note that a hole in the chest tube that is outside of the chest will result in heavy bubbling in this chamber so not all leaks are from the pleural space. The third chamber (Blue on a Pleurovac) is the suction control chamber. If the "S" connection is attached to wall suction and there is bubbling from the vent tube, then the level of negative pressure applied to the pleural space is equal to the depth that the vent tube is placed under water. 20 cm H2O would be a typical level of suction. Some chest drainage systems substitute a needle valve suction regulator for the suction control chamber. To measure the pleural pressure, one can pinch off the suction tubing "S" and read the water level in the underwater seal chamber (second chamber).
Prevention
Iatrogenic pneumothoraces can be prevented in some but not all cases. If a thoracentesis is to be performed, use of ultrasound guidance can help in avoiding lung injury and avoidance of pleural adhesions which may be likely to result in a pneumothorax if punctured. The biggest danger in an iatrogenic pneumothorax is in not recognizing that one has occurred. Listening to breath sounds before an invasive procedure starts will make it much easier to tell if a pneumothorax exists afterwards. In high risk patients (i.e. high airway pressures and/or unstable hemodynamics) plan ahead by having large bore needles, stop cocks, and syringes available before the procedure is started so there will be minimal delay in draining a life-threatening pneumothorax.
References
Connors AF, Altose MD: Textbook of Pulmonary Diseases, p.1592, Little Brown, Boston, 1989.
Bevelaqua FA and Aranda C: Management of spontaneous pneumothorax with small lumen catheter manual aspiration. Chest 1982; 81:693-694.
Gustman P, Yerger L, Wanner A: Immediate Cardiovascular Effects of Tension Pneumothorax, ARRD 1983; 127:171-174.
Haake R, Schlichtig R, Ulstad DR: Barotrauma Pathophysiology, Risk Factors, and Prevention, CHEST 1987, 91:608-613.
Conces DJ et al: Treatment of Pneumothoraces Utilizing Small Caliber Chest Tubes, CHEST 1988, 94:55-60.
Jenkinson, SG: Pneumothorax, Clinics in Chest Medicine, 1985, 6:153-161.
Ohata M, Suzuki H: Pathogenesis of Spontaneous Pneumothorax, CHEST 1980, 77:771-776.
Hemothorax
December 05, 2009, 19:42
Hemothorax
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care
Definition
A hemothorax is a collection of blood in the pleural space. It is classified according to the amount of blood. 350 ml or less is considered minimal, 350-1500 ml is moderate, and greater than 1500 ml is considered massive. In many cases, blood in the pleural cavity will be diluted by other pleural fluid. In these cases, the pleural fluid hematocrit can be used to diagnose a hemothorax using a hematocrit of greater than half the serum hematocrit as diagnostic of hemothorax.
Presentation
The presentation of hemothorax is related primarily to the acuity in that a chronic or slowly accumulating hemothorax may be asymptomatic while an acute hemothorax may present with shock, anemia, and respiratory compromise relating to compression of the lung and mediastinum by pressurized blood resembling the presentation of a tension pneumothorax.
Etiology
Trauma is an important cause of hemothorax. Hemothorax may result from either blunt or penetrating trauma of the chest but can also result from trauma to the abdomen such as from a ruptured spleen or liver. A ruptured ectopic pregnancy, bleeding from recent abdominal or pelvic surgery, or a ruptured abdominal aneurysm can also cause a hemothorax. Blood most commonly comes from systemic chest-wall vessels but can get to the pleural space from the pulmonary and/or bronchial vasculature. Other diagnostic considerations for hemothorax include malignancy (lung or pleural), or a pulmonary embolus or infarct. An unusual iatrogenic cause of hemothorax is from insertion of a central IV line through a vascular structure and into the pleural cavity.
Treatment
Chest tube drainage is the primary therapy for a hemothorax and 85% of cases will resolve spontaneously with only this treatment. If blood loss continues at a rate higher than 100-200 ml / hour then a thoracotomy should be considered remembering that a hemothorax could originate in the abdomen.
References
Lewis FR, Krupski WC, Trunkey DD: Management of the Injured Patient In Way LW (Ed.), Current Surgical Diagnosis & Treatment, Lange Medical Publications, 1983. Pp 194-5.
Conners AF, Altose MD: Pleural Anatomy, Pleural Fluid Dynamics, and the Diagnosis of Pleural Disease In Baum GL, Wolinsky E (Ed.), Textbook of Pulmonary Diseases, 4th edition, Little, Brown and Company, 1989. p 1569.
Ganji H, Vidrine A: Ectopic Pregnancy presenting as hemothorax, American Journal of Surgery 1970 December; 120(6) 807-9.
Pratt JH, Shamblin WR: Spontaneous hemothorax as a direct complication of hemoperitoneum, Annals of Surgery 1968 June; 167(6) 867-72.
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care
Definition
A hemothorax is a collection of blood in the pleural space. It is classified according to the amount of blood. 350 ml or less is considered minimal, 350-1500 ml is moderate, and greater than 1500 ml is considered massive. In many cases, blood in the pleural cavity will be diluted by other pleural fluid. In these cases, the pleural fluid hematocrit can be used to diagnose a hemothorax using a hematocrit of greater than half the serum hematocrit as diagnostic of hemothorax.
Presentation
The presentation of hemothorax is related primarily to the acuity in that a chronic or slowly accumulating hemothorax may be asymptomatic while an acute hemothorax may present with shock, anemia, and respiratory compromise relating to compression of the lung and mediastinum by pressurized blood resembling the presentation of a tension pneumothorax.
Etiology
Trauma is an important cause of hemothorax. Hemothorax may result from either blunt or penetrating trauma of the chest but can also result from trauma to the abdomen such as from a ruptured spleen or liver. A ruptured ectopic pregnancy, bleeding from recent abdominal or pelvic surgery, or a ruptured abdominal aneurysm can also cause a hemothorax. Blood most commonly comes from systemic chest-wall vessels but can get to the pleural space from the pulmonary and/or bronchial vasculature. Other diagnostic considerations for hemothorax include malignancy (lung or pleural), or a pulmonary embolus or infarct. An unusual iatrogenic cause of hemothorax is from insertion of a central IV line through a vascular structure and into the pleural cavity.
Treatment
Chest tube drainage is the primary therapy for a hemothorax and 85% of cases will resolve spontaneously with only this treatment. If blood loss continues at a rate higher than 100-200 ml / hour then a thoracotomy should be considered remembering that a hemothorax could originate in the abdomen.
References
Lewis FR, Krupski WC, Trunkey DD: Management of the Injured Patient In Way LW (Ed.), Current Surgical Diagnosis & Treatment, Lange Medical Publications, 1983. Pp 194-5.
Conners AF, Altose MD: Pleural Anatomy, Pleural Fluid Dynamics, and the Diagnosis of Pleural Disease In Baum GL, Wolinsky E (Ed.), Textbook of Pulmonary Diseases, 4th edition, Little, Brown and Company, 1989. p 1569.
Ganji H, Vidrine A: Ectopic Pregnancy presenting as hemothorax, American Journal of Surgery 1970 December; 120(6) 807-9.
Pratt JH, Shamblin WR: Spontaneous hemothorax as a direct complication of hemoperitoneum, Annals of Surgery 1968 June; 167(6) 867-72.