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A One-Sided Affair?
roentgenogram of the month A One-Sided Affair?* jan H. Zwaveling, M.D.; and Steven] M. Cans, M.D.
A 78-year-old woman was admitted to the hospital
with respiratory failure and coma. She had a history of non-insulin-dependent diabetes mellitus, moderate impairment of renal function (serum creatinine level, 2. 7 mgldl), and mild anemia (hemoglobin level, 10.3 gldl). The patient was well until the day of admission, when she developed a nonproductive cough and progressive shortness of breath. There was no history of substernal or abdominal pain, nor of preexisting respiratory disease. Her condition worsened in the course of the day, and when the paramedics were called, she was in a coma with gasping respiration and bradycardia of 20 beats per minute. Endotracheal intubation and external cardiac massage were performed, and the patient was ventilated with a manual resuscitator (Ambu-bag). On arrival at the hospital, the patient was comatose and apparently in respiratory failure. Frothy sputum was coming up the endotracheal tube. The blood pressure was 130/60 mm Hg, the heart rate was 90 beats per minute, and the rectal temperature was 34.9°C (94.8°F). Auscultation of the heart revealed a gallop rhythm. Coarse rales were noted over the entire right lung. The sounds over the left lung were normal. Bowel sounds were normal, and no abdominal mass was palpated. The hands and feet were cold. Arterial blood gas pressures while breathing room air were as follows: Pa0 2 , 49.4 mm Hg; PaC0 2 , 47.0 mm Hg; and oxygen saturation, 63.7 percent. The arterial pH was 7.026, and the plasma HC0 3 - concentration was 11.6 mEq/L. A chest roentgenogram taken on admission is shown in Figure 1. An ECG showed sinus tachycardia at a rate of 130 beats per minute, multiple ventricular premature beats, and nonspecific ST-segment abnormalities in the precordial leads. A tentative diagnosis of pneumonia and sepsis was made, and treatment was instituted accordingly with mechanical ventilation, erythromycin, gentamicin, and cefuroxime. Mechanical ventilation with 100 percent oxygen and PEEP at 15 cmH 20 resulted in a Pa0 2 of 54.1 mm Hg and a saturation of 79.4 percent, *From the Departments of Reanimation and Clinical Toxicology and ofPulmonary Medicine, University Hospital Utrecht, Utrecht, the Netherlands.
FIGt:RE
FIGt'RE
1
2
CHEST I 95 I 3 I MARCH, 1989
673
chest x-ray film, an initial diagnosis of pneumonia could not be maintained because of absence of fever, negative cultures, and complete resolution of the pulmonary infiltrates within 48 hours. The combination of recent myocardial infarction, high pulmonary
FICI RE 3
suggestive of considerable pulmonary shunting. Bronchoscopy was performed and showed large amounts of pinkish fluid in the lungs and diffuse edema with increased vascular injection of the bronchial mucosa. Cultures of blood, sputum, and urine remained negative. Because of anuria of supposed prerenal origin, the patient was volume-loaded with plasma from a CVP of 10 mm Hg to a CVP of 15 mm Hg. Subsequently, the blood pressure fell to 100 mm Hg systolic, and she was started on therapy with dopamine. A Swan-Ganz flow-directed catheter was introduced. The pulmonary capillary wedge pressure was 30 mm Hg. The initial diagnosis had to be reconsidered, and a new diagnosis of high-pressure pulmonary edema was made. Treatment was started with furosemide, nitroglycerin, and dobutamine. Within 48 hours the chest x-ray film cleared almost entirely, beginning from the subpleural space (Fig 2 and 3), and the F I o 2 could be reduced to 0.30 with P E E P of 7.5 cm H 2 0 . Urinary output rose to normal, as did the body temperature. The patient could be weaned from the ventilator in the following days. A follow-up E C G was consistent with an anterior myocardial infarction. The creatine phosphokinase level in the serum rose to a peak of 1,437 units/ml on the second day. Diagnosis: Myocardial infarction edema and forward failure
with
pulmonary
In this patient with unilateral abnormalities on the 674
capillary wedge pressure, and rapid improvement with diuretics strongly suggested pulmonary edema due to elevated microvascular pressure as the cause of respiratory failure in this patient. Cardiogenic pulmonary edema usually presents as a bilateral "butterfly" or "bat wing" configuration, leaving the periphery of the lungs relatively clear.1 Unilateral distribution is uncommon. 2 In reviewing the subject, Calenoff and associates3 proposed 18 conditions associated with unilateral pulmonary edema. Conditions favoring edema at the side opposite a lung with impaired perfusion were termed "contralateral," and conditions favoring accumulation of excess water at the diseased side were termed "ipsilateral." The contralateral type of pulmonary edema may be caused by unilateral conditions like local emphysema, congenital absence of a pulmonary artery, the SwyerJames syndrome, unilateral pulmonary embolus, or prior lobectomy. In these conditions the diseased lung is protected from developing pulmonary edema because of its decreased perfusion, resulting in contralateral edema only. Instances of the ipsilateral type of condition are pulmonary contusion, unilateral aspiration, bronchial obstruction, unilateral veno-occlusive disease, and rapid removal of fluid or air from the pleural cavity. The edema caused by rapid thoracocentesis is often called "reexpansion edema." Its mechanism is still unclear. Gravity (the "down lung syndrome") has also been implicated as a cause of ipsilateral pulmonary edema, for instance, in fluid-overloaded patients with a preference for a lateral decubitus position4 or in patients who have undergone surgery in a similar position.5 The dependent lung receives more perfusion than the nondependent lung, resulting in increased capillary pressure with a consequent increase of fluid transudation. 6 A contralateral type of pulmonary edema in our patient was unlikely; there was no history of pleural or pulmonary disease, and a perfusion scan showed normal distribution of pulmonary blood flow. Most of the ipsilateral type of causes could be ruled out as well; there was no history of trauma or of instrumentation of the pleura or pulmonary vessels, and bronchoscopy showed no signs of massive aspiration. We believe that the most likely cause of unilateral pulmonary edema in this patient was prolonged lateral Roentgenogram of the Month Gans) decubitus in the presence position of cardiac prior tofailure. admission to (Zwaveling, the hospital decubitus in the presence position of cardiac prior Roentgenogram tofailure. admissio of the CHEST I 95 I 3 I MARCH, 1989
673 CHEST
REFERENCES 1 Pare JAP, Fraser R G . Synopsis of diseases of the chest. Philadelphia: W B Saunders Co, 1983 2 Nessa C B , Rigler L G . The roentgenological manifestations of pulmonary edema. Radiology 1941; 37:35-46 3 Calenoff L, Kruglik G D , Woodruff A. Unilateral pulmonary edema. Radiology 1978; 126:19-24
4 Woodring J H , Witt W S , Stelling C B . Unilateral pulmonary edema. J Ky Med Assoc 1983; 81:362-64 5 Snoy FJ, Woodside J R . Unilateral pulmonary edema (down lung syndrome) following urological operation. J Urol 1984; 132:77677 6 Baraka A, Moghrabi R, Yazigi A. Unilateral pulmonary oedema/ atelectasis in the lateral decubitus position. Anaesthesia 1987; 42:171-74
CHEST / 95 / 3 / MARCH, 1989
6 75
A 78-year-old woman was admitted to the hospital
with respiratory failure and coma. She had a history of non-insulin-dependent diabetes mellitus, moderate impairment of renal function (serum creatinine level, 2. 7 mgldl), and mild anemia (hemoglobin level, 10.3 gldl). The patient was well until the day of admission, when she developed a nonproductive cough and progressive shortness of breath. There was no history of substernal or abdominal pain, nor of preexisting respiratory disease. Her condition worsened in the course of the day, and when the paramedics were called, she was in a coma with gasping respiration and bradycardia of 20 beats per minute. Endotracheal intubation and external cardiac massage were performed, and the patient was ventilated with a manual resuscitator (Ambu-bag). On arrival at the hospital, the patient was comatose and apparently in respiratory failure. Frothy sputum was coming up the endotracheal tube. The blood pressure was 130/60 mm Hg, the heart rate was 90 beats per minute, and the rectal temperature was 34.9°C (94.8°F). Auscultation of the heart revealed a gallop rhythm. Coarse rales were noted over the entire right lung. The sounds over the left lung were normal. Bowel sounds were normal, and no abdominal mass was palpated. The hands and feet were cold. Arterial blood gas pressures while breathing room air were as follows: Pa0 2 , 49.4 mm Hg; PaC0 2 , 47.0 mm Hg; and oxygen saturation, 63.7 percent. The arterial pH was 7.026, and the plasma HC0 3 - concentration was 11.6 mEq/L. A chest roentgenogram taken on admission is shown in Figure 1. An ECG showed sinus tachycardia at a rate of 130 beats per minute, multiple ventricular premature beats, and nonspecific ST-segment abnormalities in the precordial leads. A tentative diagnosis of pneumonia and sepsis was made, and treatment was instituted accordingly with mechanical ventilation, erythromycin, gentamicin, and cefuroxime. Mechanical ventilation with 100 percent oxygen and PEEP at 15 cmH 20 resulted in a Pa0 2 of 54.1 mm Hg and a saturation of 79.4 percent, *From the Departments of Reanimation and Clinical Toxicology and ofPulmonary Medicine, University Hospital Utrecht, Utrecht, the Netherlands.
FIGt:RE
FIGt'RE
1
2
CHEST I 95 I 3 I MARCH, 1989
673
chest x-ray film, an initial diagnosis of pneumonia could not be maintained because of absence of fever, negative cultures, and complete resolution of the pulmonary infiltrates within 48 hours. The combination of recent myocardial infarction, high pulmonary
FICI RE 3
suggestive of considerable pulmonary shunting. Bronchoscopy was performed and showed large amounts of pinkish fluid in the lungs and diffuse edema with increased vascular injection of the bronchial mucosa. Cultures of blood, sputum, and urine remained negative. Because of anuria of supposed prerenal origin, the patient was volume-loaded with plasma from a CVP of 10 mm Hg to a CVP of 15 mm Hg. Subsequently, the blood pressure fell to 100 mm Hg systolic, and she was started on therapy with dopamine. A Swan-Ganz flow-directed catheter was introduced. The pulmonary capillary wedge pressure was 30 mm Hg. The initial diagnosis had to be reconsidered, and a new diagnosis of high-pressure pulmonary edema was made. Treatment was started with furosemide, nitroglycerin, and dobutamine. Within 48 hours the chest x-ray film cleared almost entirely, beginning from the subpleural space (Fig 2 and 3), and the F I o 2 could be reduced to 0.30 with P E E P of 7.5 cm H 2 0 . Urinary output rose to normal, as did the body temperature. The patient could be weaned from the ventilator in the following days. A follow-up E C G was consistent with an anterior myocardial infarction. The creatine phosphokinase level in the serum rose to a peak of 1,437 units/ml on the second day. Diagnosis: Myocardial infarction edema and forward failure
with
pulmonary
In this patient with unilateral abnormalities on the 674
capillary wedge pressure, and rapid improvement with diuretics strongly suggested pulmonary edema due to elevated microvascular pressure as the cause of respiratory failure in this patient. Cardiogenic pulmonary edema usually presents as a bilateral "butterfly" or "bat wing" configuration, leaving the periphery of the lungs relatively clear.1 Unilateral distribution is uncommon. 2 In reviewing the subject, Calenoff and associates3 proposed 18 conditions associated with unilateral pulmonary edema. Conditions favoring edema at the side opposite a lung with impaired perfusion were termed "contralateral," and conditions favoring accumulation of excess water at the diseased side were termed "ipsilateral." The contralateral type of pulmonary edema may be caused by unilateral conditions like local emphysema, congenital absence of a pulmonary artery, the SwyerJames syndrome, unilateral pulmonary embolus, or prior lobectomy. In these conditions the diseased lung is protected from developing pulmonary edema because of its decreased perfusion, resulting in contralateral edema only. Instances of the ipsilateral type of condition are pulmonary contusion, unilateral aspiration, bronchial obstruction, unilateral veno-occlusive disease, and rapid removal of fluid or air from the pleural cavity. The edema caused by rapid thoracocentesis is often called "reexpansion edema." Its mechanism is still unclear. Gravity (the "down lung syndrome") has also been implicated as a cause of ipsilateral pulmonary edema, for instance, in fluid-overloaded patients with a preference for a lateral decubitus position4 or in patients who have undergone surgery in a similar position.5 The dependent lung receives more perfusion than the nondependent lung, resulting in increased capillary pressure with a consequent increase of fluid transudation. 6 A contralateral type of pulmonary edema in our patient was unlikely; there was no history of pleural or pulmonary disease, and a perfusion scan showed normal distribution of pulmonary blood flow. Most of the ipsilateral type of causes could be ruled out as well; there was no history of trauma or of instrumentation of the pleura or pulmonary vessels, and bronchoscopy showed no signs of massive aspiration. We believe that the most likely cause of unilateral pulmonary edema in this patient was prolonged lateral Roentgenogram of the Month Gans) decubitus in the presence position of cardiac prior tofailure. admission to (Zwaveling, the hospital decubitus in the presence position of cardiac prior Roentgenogram tofailure. admissio of the CHEST I 95 I 3 I MARCH, 1989
673 CHEST
REFERENCES 1 Pare JAP, Fraser R G . Synopsis of diseases of the chest. Philadelphia: W B Saunders Co, 1983 2 Nessa C B , Rigler L G . The roentgenological manifestations of pulmonary edema. Radiology 1941; 37:35-46 3 Calenoff L, Kruglik G D , Woodruff A. Unilateral pulmonary edema. Radiology 1978; 126:19-24
4 Woodring J H , Witt W S , Stelling C B . Unilateral pulmonary edema. J Ky Med Assoc 1983; 81:362-64 5 Snoy FJ, Woodside J R . Unilateral pulmonary edema (down lung syndrome) following urological operation. J Urol 1984; 132:77677 6 Baraka A, Moghrabi R, Yazigi A. Unilateral pulmonary oedema/ atelectasis in the lateral decubitus position. Anaesthesia 1987; 42:171-74
CHEST / 95 / 3 / MARCH, 1989
6 75