Postgraduate Medicine
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Recurrent postictal pulmonary edema R. Brent Archibald & John D. Armstrong Jr To cite this article: R. Brent Archibald & John D. Armstrong Jr (1978) Recurrent postictal pulmonary edema, Postgraduate Medicine, 63:1, 210-213, DOI: 10.1080/00325481.1978.11714739 To link to this article: http://dx.doi.org/10.1080/00325481.1978.11714739
Published online: 07 Jul 2016.
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Citing articles: 10 View citing articles
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Date: 26 August 2017, At: 05:05
case
Downloaded by [Australian Catholic University] at 05:05 26 August 2017
report recurrent postictal pulmonary ede ma
• A 32-year-old man was seen in the emergency room of University of Utah Hospital, Salt Lake City, on August 13, 1972, after a grand mal seizure with immediate dyspnea and copious frothy, bloody sputum. Since discontinuing anticonvulsant medication (phenytoin) three months previously, he bad had seizures weekly. The attacks of grand mal epilepsy had begun after a head injury when he was 4 years old. He was otherwise in good health, with no known cardiopulmonary disease. He denied using alcohol. Temperature was 98.8 F, pulse rate 100/ min, and respiration rate 24/min. The tongue was not lacerated, and no oropharyngeal lesions were seen on indirect laryngoscopy. Diffuse raies and rhonchi were audible, but no cardiac murmurs or gallops were beard. The WBC count was Il ,400/cu mm, with normal differentiai and adequate platelet counts. Blood gas levels, with the patient breathing 3.5 liters/min of oxygen, were: Pao2 54 mm Hg (normal in Salt Lake City 68 mm), Paco2 36 mm Hg, and pH 7.39. An ECG showed right axis deviation ( + 100°) and incomplete
right bundle-branch block. Patchy air-space infiltrates involving the upper lobes of the lungs were seen on chest films made with a portable unit in the emergency room. The patient was admitted t9 the hospital and started on a regimen of phenytoin, 300 mg/ day orally. He continued to have bloody sputum for the next five hours. A chest film made at 7:30PM showed increased infiltrates in both lungs (figure la). The bouse staff made a diagnosis of aspiration pneumonia, and treatment was begun with hydrocortisone, 100 mg intravenously, and ampicillin, 2 gm intravenously every six hours. The next morning, the patient was much improved clinically and was afebrile. A chest film made at Il :30 AM showed nearly complete clearing (figure lb). Later that day, he had a grand mal seizure without respiratory complications. He refused medical care and left the hospital against medical advice. Skull films and a brain scan made on an outpatient basis showed no abnormalities; on an EEG, however, a seizure focus in the right frontal area was seen. Pulmonary findings on a chest film made on September 21 were normal. The patient continued to be uncooperative and took anticonvulsant medication irregularly. On August 12, 1973, he again bad a grand mal seizure followed by frothy, bloody sputum and tachypnea. When seen in the emergency room, he was dyspneic. Other findings were: pulse rate 88/min, respiration rate 24/min, temperature 99 F, and blood pressure 122/84 mm Hg. Bilateral raies and rhonchi were audible, but no cardiac abnormality or jugular vein distention was noted. The WBC count was 12,400/cu mm, with a normal differentiai count. Blood gas levels, with the patient breathing room air, were:
210
POSTGRADUATE MEDICINE • January 1978 • Vol. 63 • No. 1
R. Brent Archibald, MD John O. Armstrong, Jr, MD University of Utah Medical Center Salt Lake City
Downloaded by [Australian Catholic University] at 05:05 26 August 2017
Figure 1. Chast films of patient with postictal pulmonary edema.
a.
Bilateral interstitial and patchy air-space infiltrates in upper and middle lobes.
b. Remarkable clearing 16 hours later.
PaÛ2 36 mm Hg, Paco2 32 mm Hg, and pH 7.45. ECG findings were normal, but a chest film showed fluffy air-space infiltrates in the upper lobe of the le ft lung and the upper and middle lobes of the right lung. The patient refused treatrnent except for nasally adrninistered oxygen and intermittent positive pressure breathing. The next day, he was clinically irnproved and a chest film showed partial clearing. However, he continued to have bilateral raies and to produce srnall arnounts of blood-tinged sputurn. The raies bec ame more pronounced following two more seizures and were accornpanied by tachypnea and a temperature of 100.5 F. On August 15, a chest film showed virtual clearing, and arterial blood gas levels, with the patient breathing roorn air, were essentially normal. Following discharge from the
hospital, he continued to take anticonvulsant medication irregularly and consequently bad one or two seizures rnonthly. He was next seen on February 6, 1975, when he carne to the ernergency roorn after experiencing a grand mal seizure on a city bus. He was cyanotic and severely dyspneic and was producing copious frothy, bloody sputurn, but aspiration bad not been noted. Pulse rate was 120/rnin, respiration rate 44/ min, blood pressure 110/80 mm Hg, and temperature 100 F. Other abnormal findings were as follows: generalized raies and rhonchi, Pao2 32 mm Hg and Paco2 28 mm Hg; right axis deviation of+ 100° and s waves in leads 1 and V4 _6 ; and bilateral patchy air-space infiltrates, especially in the upper lobe of the right lung. The diagnosis of postictal pulrnonary ederna
Vol. 63 • No. 1 • January 1978 • POSTGRADUATE MEDICINE
211
case report ...............................................
Downloaded by [Australian Catholic University] at 05:05 26 August 2017
ln postictal edema, treatment of aspiration pneumonia-unless the condition has definitely been ruled out-may be prudent.
was made. The patient was given oxygen nasal! y, and within three hours showed significant improvement. He refused hospitalization.
Discussion In most cases of postictal pulmonary edema the seizure disorder has been present for many years and it often is poorly controlled. The edema follows one or severa} seizures or status epilepticus and has been associated only with the grand mal type of seizure. Symptoms include dyspnea, tachypnea, and cough with production of various quantities of mucoid fluid, which may be copious and frankly hemorrhagic. The patients usually are otherwise in good health, with no evidence of cardiac or pulmonary disease. Twenty-six cases of pulmonary edema associated with grand mal seizures have been reported in the English literature. 1·2 The presentation of postictal pulmonary edema varies from asymptomatic (detectable only on chest films) to fulminant with death immediately after the seizure. 1 While the distribution of edema seen radiographically is variable and unpredictable, predominance of upper lobe involvement has been reported. 3 •4 Our patient had bilateral upper and middle lobe edema with similar distribution in each ofthree documented episodes over 2Y2 years. Uncomplicated pulmonary edema may clear significantly within severa} to 48 hours and completely in three to five days. The ECG is usually normal, but a wide range of abnormalities may be seen. 5 The major condition to be considered in differentiai diagnosis is aspiration pneumonia, a critical illness in which lung clearing often takes two to three weeks. 6 In acute cases, exclusion of this diagnosis may be impossible. Supportive therapy is usually ail that is required for postictal edema: oxygen administration and, perhaps, intermittent positive pressure breathing. In most instances, the hemodynamic causes of the edema no longer
212
operate when seizure activity ceases, obviating the use of morphine, diuretics, and digitalis. However, treatment of aspiration pneumonia-unless the condition has definitely been ruled out-may be prudent. The mechanism by which generalized seizures produce pulmonary edema is unknown. Grand mal seizures have been associated with systemic hypertension, increased cerebral blood flow, and increased intracranial pressure. 7 These responses could result directly from involvement of sympathetic centers in the generalized seizure discharge or possibly indirectly from protective responses triggered by neuronal hyperactivity to assure adequate cerebral blood flow and oxygen de livery. Results of several studies in animais are pertinent. Bean and co-workers 8 have reported that pulmonary edema associated with drug-induced seizures in rats can be prevented by administration of sympatholytics; however, the hemodynamic mechanisms involved have not been clarified. In reporting results of experiments with chimpanzees, Ducker and associates 9 have suggested that protective responses to primary increases in intracranial pressure may be capable of stimulating sufficie nt venoconstriction, venous return, myocardial inotropic response, and occasionally, peripheral arteriolar constriction to cause left ventricular failure leading to pulmonary ede ma. More recently, Moss and associates10 have proposed that direct pulmonary vascular reflexes occurring as a result of hypothalamic ischemia may provide an additional mechanism.
Summary A 32-year-old man with a long history of grand mal seizures but otherwise good health had recurrent episodes of postictal pulmonary edema when he failed to take anticonvulsant medication regularly. This case illustrates most of the features observed in other reported cases of postictal pulmonary edema. Symptoms include dyspnea and cough with production of various quantities of mucoid
POSTGRADUATE MEDICINE • January 1978 • Vol. 63 • No. 1
Downloaded by [Australian Catholic University] at 05:05 26 August 2017
fluid that may be copious and frankly hemorrhagic. Blood pressure is normal, and temperature may be normal also but is frequently elevated to 100 or 101 F. No cardiac irregularities are heard on auscultation, and the ECG is often normal, but a wide range of abnormalities may be seen. Considerable arterial hypoxemia may occur, and leukocytosis (II ,000 to 14,000 cells per cubic millimeter) is common. Raies and rhonchi are audible, and chest films often show bilateral upper and middle lobe infiltrates. The patient is usually clinically improved within 24 hours and the pulmonary edema completely cleared in three to five days. • Address reprint requests to John D. Armstrong, MD, Department of Radiology, University of Utah Medical Center, Salt Lake City, UT 84132.
References 1. Greene R, Plat! R, Matz R: Postictal pulmonary edema. NY State 1 Med 75:1257-1261, 1975 2. Malik SK, Zalinsky H, Graham DY: Pulmonary edema following generalized convulsions (postictal). 1 Assoc Physicians lndia 21:795-798, 1973 3. Fe Iman AH: Neurogenic pulmonary ede ma: Observations in 6 patients. Am 1 Roentgenol Radium Ther Nucl Med 112:393-396, 1971 4. Richards P: Pulmonary edema and intracraniallesions. Br Med 1 2:83-86. 1963 5. Abildskov JA, Millar K, Burgess MJ, et al: The electrocardiogram and the central nervous system. Prog Cardiovasc Dis 13:210-216. 1970 6. Mendelson CL: The aspiration of stomach contents into the lungs during obstetric anesthesia. Am 1 Obstet Gynecol 52:191-205. 1946 7. White PT. Grant P, Mosier J, et al: Changes in cerebral dynamics associated with seizures. Neurology Il :354361, 1961 8. Bean JW, Zee D, Thom B: Pulmonary changes with convulsions induced by drugs and oxygen at high pressure. 1 Appl Physiol21:865-872, 1966 9. Ducker TB, Simmons RL, Anderson RW: Increased intracranial pressure and pulmonary edema. Part 3. The effect of increased intracranial pressure on the cardiovascular hemodynamics of chimpanzees. J Neurosurg 29:475-483, 1968 10. Moss G. Staunton C, Stein AA: Cerebral etiology of the "shock Jung syndrome ... 1 Trauma 12:885-890, 1972 POSTGRADUATE \1EDICI~E
invites submission of brief case reports, especially those related to ambulatory medical care. Illustrations and references should be inc luded only wh en essential.
Vol. 63 • No. 1 • January 1978 • POSTGRADUATE MEDICINE
213
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Recurrent postictal pulmonary edema R. Brent Archibald & John D. Armstrong Jr To cite this article: R. Brent Archibald & John D. Armstrong Jr (1978) Recurrent postictal pulmonary edema, Postgraduate Medicine, 63:1, 210-213, DOI: 10.1080/00325481.1978.11714739 To link to this article: http://dx.doi.org/10.1080/00325481.1978.11714739
Published online: 07 Jul 2016.
Submit your article to this journal
View related articles
Citing articles: 10 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ipgm20 Download by: [Australian Catholic University]
Date: 26 August 2017, At: 05:05
case
Downloaded by [Australian Catholic University] at 05:05 26 August 2017
report recurrent postictal pulmonary ede ma
• A 32-year-old man was seen in the emergency room of University of Utah Hospital, Salt Lake City, on August 13, 1972, after a grand mal seizure with immediate dyspnea and copious frothy, bloody sputum. Since discontinuing anticonvulsant medication (phenytoin) three months previously, he bad had seizures weekly. The attacks of grand mal epilepsy had begun after a head injury when he was 4 years old. He was otherwise in good health, with no known cardiopulmonary disease. He denied using alcohol. Temperature was 98.8 F, pulse rate 100/ min, and respiration rate 24/min. The tongue was not lacerated, and no oropharyngeal lesions were seen on indirect laryngoscopy. Diffuse raies and rhonchi were audible, but no cardiac murmurs or gallops were beard. The WBC count was Il ,400/cu mm, with normal differentiai and adequate platelet counts. Blood gas levels, with the patient breathing 3.5 liters/min of oxygen, were: Pao2 54 mm Hg (normal in Salt Lake City 68 mm), Paco2 36 mm Hg, and pH 7.39. An ECG showed right axis deviation ( + 100°) and incomplete
right bundle-branch block. Patchy air-space infiltrates involving the upper lobes of the lungs were seen on chest films made with a portable unit in the emergency room. The patient was admitted t9 the hospital and started on a regimen of phenytoin, 300 mg/ day orally. He continued to have bloody sputum for the next five hours. A chest film made at 7:30PM showed increased infiltrates in both lungs (figure la). The bouse staff made a diagnosis of aspiration pneumonia, and treatment was begun with hydrocortisone, 100 mg intravenously, and ampicillin, 2 gm intravenously every six hours. The next morning, the patient was much improved clinically and was afebrile. A chest film made at Il :30 AM showed nearly complete clearing (figure lb). Later that day, he had a grand mal seizure without respiratory complications. He refused medical care and left the hospital against medical advice. Skull films and a brain scan made on an outpatient basis showed no abnormalities; on an EEG, however, a seizure focus in the right frontal area was seen. Pulmonary findings on a chest film made on September 21 were normal. The patient continued to be uncooperative and took anticonvulsant medication irregularly. On August 12, 1973, he again bad a grand mal seizure followed by frothy, bloody sputum and tachypnea. When seen in the emergency room, he was dyspneic. Other findings were: pulse rate 88/min, respiration rate 24/min, temperature 99 F, and blood pressure 122/84 mm Hg. Bilateral raies and rhonchi were audible, but no cardiac abnormality or jugular vein distention was noted. The WBC count was 12,400/cu mm, with a normal differentiai count. Blood gas levels, with the patient breathing room air, were:
210
POSTGRADUATE MEDICINE • January 1978 • Vol. 63 • No. 1
R. Brent Archibald, MD John O. Armstrong, Jr, MD University of Utah Medical Center Salt Lake City
Downloaded by [Australian Catholic University] at 05:05 26 August 2017
Figure 1. Chast films of patient with postictal pulmonary edema.
a.
Bilateral interstitial and patchy air-space infiltrates in upper and middle lobes.
b. Remarkable clearing 16 hours later.
PaÛ2 36 mm Hg, Paco2 32 mm Hg, and pH 7.45. ECG findings were normal, but a chest film showed fluffy air-space infiltrates in the upper lobe of the le ft lung and the upper and middle lobes of the right lung. The patient refused treatrnent except for nasally adrninistered oxygen and intermittent positive pressure breathing. The next day, he was clinically irnproved and a chest film showed partial clearing. However, he continued to have bilateral raies and to produce srnall arnounts of blood-tinged sputurn. The raies bec ame more pronounced following two more seizures and were accornpanied by tachypnea and a temperature of 100.5 F. On August 15, a chest film showed virtual clearing, and arterial blood gas levels, with the patient breathing roorn air, were essentially normal. Following discharge from the
hospital, he continued to take anticonvulsant medication irregularly and consequently bad one or two seizures rnonthly. He was next seen on February 6, 1975, when he carne to the ernergency roorn after experiencing a grand mal seizure on a city bus. He was cyanotic and severely dyspneic and was producing copious frothy, bloody sputurn, but aspiration bad not been noted. Pulse rate was 120/rnin, respiration rate 44/ min, blood pressure 110/80 mm Hg, and temperature 100 F. Other abnormal findings were as follows: generalized raies and rhonchi, Pao2 32 mm Hg and Paco2 28 mm Hg; right axis deviation of+ 100° and s waves in leads 1 and V4 _6 ; and bilateral patchy air-space infiltrates, especially in the upper lobe of the right lung. The diagnosis of postictal pulrnonary ederna
Vol. 63 • No. 1 • January 1978 • POSTGRADUATE MEDICINE
211
case report ...............................................
Downloaded by [Australian Catholic University] at 05:05 26 August 2017
ln postictal edema, treatment of aspiration pneumonia-unless the condition has definitely been ruled out-may be prudent.
was made. The patient was given oxygen nasal! y, and within three hours showed significant improvement. He refused hospitalization.
Discussion In most cases of postictal pulmonary edema the seizure disorder has been present for many years and it often is poorly controlled. The edema follows one or severa} seizures or status epilepticus and has been associated only with the grand mal type of seizure. Symptoms include dyspnea, tachypnea, and cough with production of various quantities of mucoid fluid, which may be copious and frankly hemorrhagic. The patients usually are otherwise in good health, with no evidence of cardiac or pulmonary disease. Twenty-six cases of pulmonary edema associated with grand mal seizures have been reported in the English literature. 1·2 The presentation of postictal pulmonary edema varies from asymptomatic (detectable only on chest films) to fulminant with death immediately after the seizure. 1 While the distribution of edema seen radiographically is variable and unpredictable, predominance of upper lobe involvement has been reported. 3 •4 Our patient had bilateral upper and middle lobe edema with similar distribution in each ofthree documented episodes over 2Y2 years. Uncomplicated pulmonary edema may clear significantly within severa} to 48 hours and completely in three to five days. The ECG is usually normal, but a wide range of abnormalities may be seen. 5 The major condition to be considered in differentiai diagnosis is aspiration pneumonia, a critical illness in which lung clearing often takes two to three weeks. 6 In acute cases, exclusion of this diagnosis may be impossible. Supportive therapy is usually ail that is required for postictal edema: oxygen administration and, perhaps, intermittent positive pressure breathing. In most instances, the hemodynamic causes of the edema no longer
212
operate when seizure activity ceases, obviating the use of morphine, diuretics, and digitalis. However, treatment of aspiration pneumonia-unless the condition has definitely been ruled out-may be prudent. The mechanism by which generalized seizures produce pulmonary edema is unknown. Grand mal seizures have been associated with systemic hypertension, increased cerebral blood flow, and increased intracranial pressure. 7 These responses could result directly from involvement of sympathetic centers in the generalized seizure discharge or possibly indirectly from protective responses triggered by neuronal hyperactivity to assure adequate cerebral blood flow and oxygen de livery. Results of several studies in animais are pertinent. Bean and co-workers 8 have reported that pulmonary edema associated with drug-induced seizures in rats can be prevented by administration of sympatholytics; however, the hemodynamic mechanisms involved have not been clarified. In reporting results of experiments with chimpanzees, Ducker and associates 9 have suggested that protective responses to primary increases in intracranial pressure may be capable of stimulating sufficie nt venoconstriction, venous return, myocardial inotropic response, and occasionally, peripheral arteriolar constriction to cause left ventricular failure leading to pulmonary ede ma. More recently, Moss and associates10 have proposed that direct pulmonary vascular reflexes occurring as a result of hypothalamic ischemia may provide an additional mechanism.
Summary A 32-year-old man with a long history of grand mal seizures but otherwise good health had recurrent episodes of postictal pulmonary edema when he failed to take anticonvulsant medication regularly. This case illustrates most of the features observed in other reported cases of postictal pulmonary edema. Symptoms include dyspnea and cough with production of various quantities of mucoid
POSTGRADUATE MEDICINE • January 1978 • Vol. 63 • No. 1
Downloaded by [Australian Catholic University] at 05:05 26 August 2017
fluid that may be copious and frankly hemorrhagic. Blood pressure is normal, and temperature may be normal also but is frequently elevated to 100 or 101 F. No cardiac irregularities are heard on auscultation, and the ECG is often normal, but a wide range of abnormalities may be seen. Considerable arterial hypoxemia may occur, and leukocytosis (II ,000 to 14,000 cells per cubic millimeter) is common. Raies and rhonchi are audible, and chest films often show bilateral upper and middle lobe infiltrates. The patient is usually clinically improved within 24 hours and the pulmonary edema completely cleared in three to five days. • Address reprint requests to John D. Armstrong, MD, Department of Radiology, University of Utah Medical Center, Salt Lake City, UT 84132.
References 1. Greene R, Plat! R, Matz R: Postictal pulmonary edema. NY State 1 Med 75:1257-1261, 1975 2. Malik SK, Zalinsky H, Graham DY: Pulmonary edema following generalized convulsions (postictal). 1 Assoc Physicians lndia 21:795-798, 1973 3. Fe Iman AH: Neurogenic pulmonary ede ma: Observations in 6 patients. Am 1 Roentgenol Radium Ther Nucl Med 112:393-396, 1971 4. Richards P: Pulmonary edema and intracraniallesions. Br Med 1 2:83-86. 1963 5. Abildskov JA, Millar K, Burgess MJ, et al: The electrocardiogram and the central nervous system. Prog Cardiovasc Dis 13:210-216. 1970 6. Mendelson CL: The aspiration of stomach contents into the lungs during obstetric anesthesia. Am 1 Obstet Gynecol 52:191-205. 1946 7. White PT. Grant P, Mosier J, et al: Changes in cerebral dynamics associated with seizures. Neurology Il :354361, 1961 8. Bean JW, Zee D, Thom B: Pulmonary changes with convulsions induced by drugs and oxygen at high pressure. 1 Appl Physiol21:865-872, 1966 9. Ducker TB, Simmons RL, Anderson RW: Increased intracranial pressure and pulmonary edema. Part 3. The effect of increased intracranial pressure on the cardiovascular hemodynamics of chimpanzees. J Neurosurg 29:475-483, 1968 10. Moss G. Staunton C, Stein AA: Cerebral etiology of the "shock Jung syndrome ... 1 Trauma 12:885-890, 1972 POSTGRADUATE \1EDICI~E
invites submission of brief case reports, especially those related to ambulatory medical care. Illustrations and references should be inc luded only wh en essential.
Vol. 63 • No. 1 • January 1978 • POSTGRADUATE MEDICINE
213
