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Pulmonary edema in the pregnant patient with mitral stenosis
PULMONARY
CAPTAIN
EDEMA
IN THE
PREGNANT STENOSIS
MICHAEL PETERSAND MEDICAL CORPS,ARMYOF
PATIENT
WITH
nIITRAL
CAPTAINSIDNEY L. PENNER THE UNITEDSTATES
I
NJUDICIOUS administration of intravenous fluids is a not uncommon cause of acute pulmonary edema. Patients with mitral stenosis are particularly susceptible to this hazard, especially during pregnancy. Two cases, recently under our care, clearly exemplify this danger. CASE REPORTS CASE l.-Mrs. E. M. T. H., a 29-year-old primigravida, was first seen in the prenatal clinic June 13, 1944. She gave a definite history of chorea and heart disease in childhood and stated that her father, a physician, had urged her to be careful of her heart. Routine examination however, was normal and the patient felt quite well throughout the pregnancy, having gained thirty-five pounds in weight. At no time did she experience any dyspnea, orthopnea, edema, or other evidence of limited cardiac reserve. Labor began Jan. 4, 194.5, and was prolonged by a persistent occiput-posterior position and uterine inertia. After fifty-two hours of fairly hard labor, she was delivered by mid-forceps, under spinal anesthesia, with the use of Kjelland’s forcepts for rotation. During this prolonged labor it was thought advisable to give the patient supplementary fluids. Accordingly. she received five separate intravenous infusions, each of l,fIkIO cc. of 5 per cent glucose in saline, at twelve-hour intervals. The last of these infusions was given one hour before delivery. In the delivery room she received 1 unit (250 CC.) of plasma before delivery and 5 )O cc. of titrated blood afterward. She appeared well for the next ten hours, after which she complained of gradually increasing dvspnen. Examination revealed slight cyanosis with difficult breathing. RBles kvere present throughout 28 per minute. The both lungs. The temperature was 99.2”F.; pulse, lq?; and respirations, white celf count was 12,700. .\ clinical diagnosis of pneumonia was made and she was treated with penicillin, sulfadiazine, and oxygen for forty-eight hours without definite improvement. X-ray examination of the chest showed mottled infiltration of both lung fields, some fluid in the The radiologic interpretation was congestive left costophrenic sinus, and enlargement of the heart. heart failure. \Vhen seen h>, a medical consultant, a to-and-fro mitral murmur was heard at There \vas no enlargement of the apex. Xloist rgles were present throughout both lung fields. the liver, no noticeable distension of the neck or peripheral veins, and no demonstrable peripheral Digitalis was prescribed, the fluid intake was restricted to I ,57(! CC. daily, and oxygen edema. therapy was continued. The penicillin and sulfadiazine were discontinued. From this time, improvement was rapid and at the end of sixty hours all clinical evidences of pulmonary edema had disappeared. The mitral systolic and diastolic murmurs gradually diminished in intensity so that two weeks later a rumbling mid-diastolic murmur could be elicited X-ray examination showed normal lung fields and an essentially only by careful auscultation. normal cardiac silhouette. Six weeks after delivery no murmurs at all could be elicited. She has remained well sine. ---From the Cardiovascular Received for publication
Section. March
Army Yervico 19. 1946.
528
Forcns
R&ma1
Hospital,
Fort
Benning,
Ga.
PETERS
AND
PENNER:
PULMONARYEDEMA
IN
PREGNANT
PATIENT
520
Summary.-A young woman with “silent” mitral stenosis of long standing had never experienced any cardiac symptoms. Pulmonary edema developed ten hours after a long, hard labor, during which she received intravenous fluids. CASE 2.--Mrs. J, H. H., a 27-year-old secundigravida. was lirst seen in the prenatal clinic in .April, 1945, during the third month of pregnancy. She gave a history. of chorea at 8 years of age with annual recurrences until she was 18 years old. She had never known of heart disease and six years previously had gone through a normal pregnancy’ without difficulty. Examination in the cardiac clinic disclosed a localized rumbling diastolic murmur at the apes. The clinical diagnosis of mitral stenosis was confirmed by x-ray’ examination \rhich showed straightening of the left upper heart border in the postero-anterior view and pressure b!, the left auricle on the barium-filled esophagus in the left lateral view. Her course was uneventful until July 4, 1945, u-hen she was admitted to the hospital because of acute pyelonephritis. The night of admission she received 1,000 cc. of 5 per cent glucose in saline without untoward effect. The nest morning another infusion of 5 per cent glucose in saline was started. lifter fifteen minutes of moderately rapid flow, she suddenly developed severe dyspnea. On examination she was dyspneic and cyanotic and coughed frequently. There were numerous loud Sties in both lungs. S-ray examination showed disseminated densities throughout both lung tields which suggested congestive failure. This emergcnc\’ was treated promptly by the use of alternating tourniquets on all four extremities and by the administration of morphine, atropine. oxygen. and digitalis, \I?thin three hours she \vas fairly. comfortable so that the tourniquets \vere removed. Ten hours later she experienced a mild relapse. .\gain, rapid relief was obtained by the use of the tourniquets. There were no further recurrences of pulmonary edema and the nevt day she felt perfectly, comfortable. .At the end of two weeks she was allowed out of bed for short periods and three weeks later was delivered by classical cesarean section under local anesthesia xvithout untoward effects.
Summary.-A young woman in the eighth month of pregnancy, with classical manifestations of mitral stenosis, but who had never been in failure nor had experienced any limitation of activities, suddenly developed acute pulmonary edema in the course of an intravenous infusion of 5 per cent glucose in saline. She responded quickly to therapy and was delivered five weeks later by a classical cesarean section. DISCUSSION
The dynamic equilibrium in the pulmonary circulation of pregnant patients with mitral stenosis is easily upset. Both the physiologic hydremia of pregnancy and the mechanical obstruction by the narrowed mitral diaphragm tend to cause pulmonary engorgement. Intravenous fluids may thus lead to acute pulmonary edema more readily than in normal individuals. It is suggested that special precautions be taken in such patients as to the route of administration, rate of flow, and total quantity of parenteral fluids. The two cases reported here emphasize the fact that good exercise tolerance and inconspicuous physical findings may give a false sense of security. SUMMARY
The occurrence of pulmonary edema, in association with pregnancy, in two young women with mitral stenosis is reported. Neither patient had had any previous cardiovascular symptoms. In both patients the pulmonary edema followed the parenteral administration of large amounts of fluid.
CAPTAIN
EDEMA
IN THE
PREGNANT STENOSIS
MICHAEL PETERSAND MEDICAL CORPS,ARMYOF
PATIENT
WITH
nIITRAL
CAPTAINSIDNEY L. PENNER THE UNITEDSTATES
I
NJUDICIOUS administration of intravenous fluids is a not uncommon cause of acute pulmonary edema. Patients with mitral stenosis are particularly susceptible to this hazard, especially during pregnancy. Two cases, recently under our care, clearly exemplify this danger. CASE REPORTS CASE l.-Mrs. E. M. T. H., a 29-year-old primigravida, was first seen in the prenatal clinic June 13, 1944. She gave a definite history of chorea and heart disease in childhood and stated that her father, a physician, had urged her to be careful of her heart. Routine examination however, was normal and the patient felt quite well throughout the pregnancy, having gained thirty-five pounds in weight. At no time did she experience any dyspnea, orthopnea, edema, or other evidence of limited cardiac reserve. Labor began Jan. 4, 194.5, and was prolonged by a persistent occiput-posterior position and uterine inertia. After fifty-two hours of fairly hard labor, she was delivered by mid-forceps, under spinal anesthesia, with the use of Kjelland’s forcepts for rotation. During this prolonged labor it was thought advisable to give the patient supplementary fluids. Accordingly. she received five separate intravenous infusions, each of l,fIkIO cc. of 5 per cent glucose in saline, at twelve-hour intervals. The last of these infusions was given one hour before delivery. In the delivery room she received 1 unit (250 CC.) of plasma before delivery and 5 )O cc. of titrated blood afterward. She appeared well for the next ten hours, after which she complained of gradually increasing dvspnen. Examination revealed slight cyanosis with difficult breathing. RBles kvere present throughout 28 per minute. The both lungs. The temperature was 99.2”F.; pulse, lq?; and respirations, white celf count was 12,700. .\ clinical diagnosis of pneumonia was made and she was treated with penicillin, sulfadiazine, and oxygen for forty-eight hours without definite improvement. X-ray examination of the chest showed mottled infiltration of both lung fields, some fluid in the The radiologic interpretation was congestive left costophrenic sinus, and enlargement of the heart. heart failure. \Vhen seen h>, a medical consultant, a to-and-fro mitral murmur was heard at There \vas no enlargement of the apex. Xloist rgles were present throughout both lung fields. the liver, no noticeable distension of the neck or peripheral veins, and no demonstrable peripheral Digitalis was prescribed, the fluid intake was restricted to I ,57(! CC. daily, and oxygen edema. therapy was continued. The penicillin and sulfadiazine were discontinued. From this time, improvement was rapid and at the end of sixty hours all clinical evidences of pulmonary edema had disappeared. The mitral systolic and diastolic murmurs gradually diminished in intensity so that two weeks later a rumbling mid-diastolic murmur could be elicited X-ray examination showed normal lung fields and an essentially only by careful auscultation. normal cardiac silhouette. Six weeks after delivery no murmurs at all could be elicited. She has remained well sine. ---From the Cardiovascular Received for publication
Section. March
Army Yervico 19. 1946.
528
Forcns
R&ma1
Hospital,
Fort
Benning,
Ga.
PETERS
AND
PENNER:
PULMONARYEDEMA
IN
PREGNANT
PATIENT
520
Summary.-A young woman with “silent” mitral stenosis of long standing had never experienced any cardiac symptoms. Pulmonary edema developed ten hours after a long, hard labor, during which she received intravenous fluids. CASE 2.--Mrs. J, H. H., a 27-year-old secundigravida. was lirst seen in the prenatal clinic in .April, 1945, during the third month of pregnancy. She gave a history. of chorea at 8 years of age with annual recurrences until she was 18 years old. She had never known of heart disease and six years previously had gone through a normal pregnancy’ without difficulty. Examination in the cardiac clinic disclosed a localized rumbling diastolic murmur at the apes. The clinical diagnosis of mitral stenosis was confirmed by x-ray’ examination \rhich showed straightening of the left upper heart border in the postero-anterior view and pressure b!, the left auricle on the barium-filled esophagus in the left lateral view. Her course was uneventful until July 4, 1945, u-hen she was admitted to the hospital because of acute pyelonephritis. The night of admission she received 1,000 cc. of 5 per cent glucose in saline without untoward effect. The nest morning another infusion of 5 per cent glucose in saline was started. lifter fifteen minutes of moderately rapid flow, she suddenly developed severe dyspnea. On examination she was dyspneic and cyanotic and coughed frequently. There were numerous loud Sties in both lungs. S-ray examination showed disseminated densities throughout both lung tields which suggested congestive failure. This emergcnc\’ was treated promptly by the use of alternating tourniquets on all four extremities and by the administration of morphine, atropine. oxygen. and digitalis, \I?thin three hours she \vas fairly. comfortable so that the tourniquets \vere removed. Ten hours later she experienced a mild relapse. .\gain, rapid relief was obtained by the use of the tourniquets. There were no further recurrences of pulmonary edema and the nevt day she felt perfectly, comfortable. .At the end of two weeks she was allowed out of bed for short periods and three weeks later was delivered by classical cesarean section under local anesthesia xvithout untoward effects.
Summary.-A young woman in the eighth month of pregnancy, with classical manifestations of mitral stenosis, but who had never been in failure nor had experienced any limitation of activities, suddenly developed acute pulmonary edema in the course of an intravenous infusion of 5 per cent glucose in saline. She responded quickly to therapy and was delivered five weeks later by a classical cesarean section. DISCUSSION
The dynamic equilibrium in the pulmonary circulation of pregnant patients with mitral stenosis is easily upset. Both the physiologic hydremia of pregnancy and the mechanical obstruction by the narrowed mitral diaphragm tend to cause pulmonary engorgement. Intravenous fluids may thus lead to acute pulmonary edema more readily than in normal individuals. It is suggested that special precautions be taken in such patients as to the route of administration, rate of flow, and total quantity of parenteral fluids. The two cases reported here emphasize the fact that good exercise tolerance and inconspicuous physical findings may give a false sense of security. SUMMARY
The occurrence of pulmonary edema, in association with pregnancy, in two young women with mitral stenosis is reported. Neither patient had had any previous cardiovascular symptoms. In both patients the pulmonary edema followed the parenteral administration of large amounts of fluid.