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Two cases of patent ductus arteriosus in preterm newborns who were operated on are reported. Several physiopathologic and clinical aspects of importance for the diagnosis and treatment of this entity are pointed out.
Seven hundred and forty-four cases of patent ductus arteriosus were diagnosed at The Hospital for Sick Children, Toronto, in the 20-year period from 1947 to 1966. Of these 705 have been treated surgically. It is concluded that operation is best performed between 6 and 12 months of age. Isolated ductus arteriosus is rarely a cause of congestive heart failure, and is more likely to be so in the presence of the rubella syndrome. Failure associated with the anomaly in the neonatal period can usually be successfully managed by medical treatment. Spontaneous closure after one month of age is not to be expected. Surgical treatment at the appropriate time prevents the subsequent development of Eisenmenger's complex.
This paper reviews patent and information data on the methods of cardiac location using ultrasound dopplercardiography, as well as on the design and development of onboard equipment to be used for medical monitoring of aircraft and spacecraft crewmembers inflight. It is emphasized that dopplercardiography, being a very informative, noise-proof and relatively simple technique, holds high promise for operational medical monitoring.
The surgical treatment of patent ductus arteriosus (PDA) in adults as in children, usually comprises section and suture, but a certain number of technical precautions must be taken. The aortic wall is often fragile due to atheromatous lesions which are more common with increasing age. Associated hypertension may add to the fragility. Controlled medicated hypotension and reinforcement of sutures with a piece of pericardium may be useful in reducing the risk of haemorrhage. It is sometimes necessary to use partial femoro-femoral cardiopulmonary bypass circuit. The presence of an aneurysm at the aortic end of a calcified ductus necessitates the same precautions. When PDA is complicated by pulmonary hypertension, the surgical indication can only be considered when the left-to-right shunt remains voluminous and when pulmonary artery pressures fall significantly during catheter or peroperative trials of closure. The operative risk in these cases increases with age. Cardiopulmonary bypass may also be very useful in these cases. Secondary repermeabilisation of an operated ductus, and cases complicated by endocarditis require an endopulmonary approach under cardiopulmonary bypass because of the fragility of the ductus region and difficulty in controlling haemorrhage. This technique is also preferred when an associated intracardiac malformation is to be corrected. Between 1965 and 1981, 37 patients were operated in the department of thoracic and cardiac surgery at the Pitié Hospital. The ages ranged from 20 to 65 years with a mean of 34 years. Cardiopulmonary bypass was necessary in 5 cases, (partial in 4, and total in 1 case of endoaortic closure).(ABSTRACT TRUNCATED AT 250 WORDS)
Over a 10 year period, 185 patients have been treated for patent ductus, including nine premature infants with a respiratory distress syndrome. Thirty-five other infants have had duct obliteration during the neonatal period, the incidation for surgery being intractable heart failure. Six of 18 adults had calcification or aneurysm in the duct region. three of these required extracorporeal circulation for duct control and closure. The remaining patients were from 1 to 18 years of age and underwent elective duct obliteration. Double ligation of the duct is regarded as the simplest, safest, and quickest technique generally applicable. Special techniques are required for fragile, broad, calcified, hypertensive, and conical ducts.
A 5-month-old cat with patent ductus arteriosus (PDA) and probable small ventricular septal defect had severe cardiomegaly and congestive heart failure. The cat improved slightly with medical therapy and markedly after surgical closure of the ductus. A 4th left intercostal space thoracotomy gave good exposure. The external anatomy of the PDA was similar to that of a short, wide PDA in dogs; however, the internal aortic orifice was situated more cranial than in dogs, as evidenced by preoperative cardiac catheterization. Examination 1 year later showed marked reductions in heart size and electrocardiographic amplitude. The cat was 1 of 3 with clinically diagnosed PDA at the University of Pennsylvania from 1968 to 1980. The prevalence of PDA in 14,224 cats (0.2/1,000) was significantly less than in 68,049 dogs (4.7/1,000).
Despite a considerable amount of investigation, controversy continues concerning the use of indomethacin in inducing the closure of patent ductus arteriosus. This controversy may be attributable to differences in dosage, route of administration, postnatal age at treatment and the variable pharmacokinetics of the drug in premature infants. The pharmacokinetics and clinical efficacy of i.v. administered indomethacin in five premature infants with PDA were evaluated. There was considerable intersubject variability in the half life of elimination (63.1 +/- 38 h). This variability was mainly due to clearance (0.0086 +/- 0.0069 l/h/kg) rather than to distribution volume variability (0.54 +/- 0.27 l/kg). A reduction of half life was observed after the second dose, probably due to a maturation process. A permanent closure of the ductus was obtained in two patients after the first dose and in two patients after the second dose. The side-effects observed in our infants were transient and no long-term complication was attributable to this drug.
Among 71 patients with proved patent ductus arteriosus (PDA) as a sole anomaly, 13 were diagnosed as having "atypical PDA" because of a lack of a continuous murmur. Of these, 10 had find-pulmonary hypertension and were the materials of the present study, in which the phonocardiographic findings were correlated with the findings by other techniques including pulsed Doppler echocardiography. Six cases with equal pulmonary arterial and aortic pressures showed a diastolic murmur alone. The murmur started with the pulmonic component of the second heart sound and continued throughout diastole. All cases showed inspiratory augmentation or presystolic accentuation of the diastolic murmur. Pulsed Doppler echocardiograms disclosed that the murmur was produced by pulmonary regurgitation in five of six cases and by a left-to-right shunt via the ductus plus pulmonary regurgitation in one case. A to-and-fro murmur was observed in three cases. Pulmonary artery pressure was significantly lower than that of the systemic artery in two of three cases. These hemodynamic findings and pulsed Doppler echocardiograms indicated that the murmur of the two cases was produced by both a left-to-right shunt through the ductus and pulmonary regurgitation. A systolic murmur only was seen in one case and the cause of this murmur was not clear. In four of five cases with grade IV and V murmur, division or plugging of the ductus was performed with uneventful clinical course in three and sudden death in one. On the other hand, four of five cases with grade II and III murmur showed Eisenmenger reaction and the surgery was not attempted. The second heart sound showed normal splitting in eight cases, abnormally wide splitting in one case and was single in one case.
The diagnosis, surgery and results of a case of patent ductus arteriosus in a dog are presented. The case was treated successfully in a private practice.
Abnormal ventricular septal motion is usually observed after open heart surgery, but its mechanism is not fully understood. Our previous study suggested that a sudden reduction of left ventricular (LV) volume overload after corrective surgery would be one mechanism, showing that postoperative abnormal septal motion is more frequent in patients who have preoperative LV volume overload. The purpose of this study was to investigate further the direct effect of LV volume alone on the ventricular septal motion in 22 patients who underwent non-surgical closure of a patent ductus arteriosus (PDA) by the Porstmann's method. The non-surgical closure of a PDA reduced LV diastolic diameter (LVDd) from 55.7 +/- 7.3 mm to 48.1 +/- 5.2 mm (P less than 0.001), and LV systolic diameter (LVDs) from 36.3 +/- 7.0 mm to 34.1 +/- 7.0 mm (p less than 0.01). Septal motion decreased in amplitude from 8.5 +/- 2.4 mm to 3.8 +/- 3.4 mm (p less than 0.01) and eight (36%) patients developed abnormal septal motion, while LV posterior wall excursions remained unchanged. When compared these eight patients with 14 without abnormal septal motion, the magnitude of postoperative LVDd reduction (delta LVDd) and its ratio to preoperative volume (delta LVDd/pre op LVDd) were significantly greater in patients with abnormal septal motion. Thus sudden reduction in LV volume overload alone could induce abnormal septal motion without altering other factors such as adhesion of the pericardium.(ABSTRACT TRUNCATED AT 250 WORDS)
In 20 infants or children with an isolated or complicated patent ductus arteriosus (PDA), we qualitatively and quantitatively studied pulsatile flow dynamics of the ductus, descending thoracic aorta and pulmonary artery by means of a catheter-tip electromagnetic flow velocity probe. They were divided into four groups according to ductal shunt states as follows: 14 patients with a continuous left-to-right (L-R) shunt (Group I), three patients with a bidirectional but a dominant L-R shunt (Group IIA), two patients with a bidirectional but dominant right-to-left (R-L) shunt (Group IIB), and one patient without a significant ductal flow (Group III). In Group I, the ductal flow was pulsatile and showed continuous L-R shunting. The timing of a peak flow velocity was coincident with the peak aortic pressure at the mid-ductus, and it shifted to diastolic phase as the flow sensor approached the pulmonary end of the ductus arteriosus. In Group IIA, the peak velocity of a L-R shunt flow was located at mid-diastole and a transiently reversed R-L shunt flow was seen during systole. Two patients of Group IIB showed that the peak flow velocity of a dominantly reversed shunt was at mid-diastole, while a low grade L-R shunt flow was seen over a wide range of diastolic period. One patient of Group III who underwent operation for aortic arch interruption did not show any significant ductal flow because of a narrow PDA. In most cases of the present study, a diastolic backflow reflecting a L-R ductal shunt during diastole was demonstrated both in the descending thoracic aorta and main pulmonary artery. The peak flow velocity of the thoracic aorta was correlated with the ductal L-R shunt ratio determined by the Fick method (r = 0.46), and the diastolic regurgitant flow fraction of the thoracic aorta was increased in patients with a larger L-R shunt or with a reversed shunt. Therefore, it was suggested that a net forward flow of the thoracic aorta is reduced in these patients. On the other hand, the quantitative evaluation of a pulmonary flow during systole was found unreliable and expected to be underestimated because of the occurrence of turbulence at the site of the main pulmonary artery by the confluence of ejection stream from the right ventricle and a shunted flow from the aorta.(ABSTRACT TRUNCATED AT 400 WORDS)
Selected parameters of renal function were studied in premature infants with a significant patent ductus arteriosus who were treated with intravenous indomethacin according to a specific protocol. Urine volume, glomerular filtration rate, urine sodium, and the fractional excretion of sodium were analyzed in 17; osmolar, sodium, and free water clearances in 8; and indomethacin pharmacokinetics in 7 premature infants. All renal function parameters analyzed decreased during indomethacin therapy: urine volume and glomerular filtration rate returned to normal, while urine sodium, fractional excretion of sodium, and the osmolar, sodium, and free water clearances remained low 24 hours after cessation of therapy. The water retention, shown by the reduced free water clearance, had no apparent deleterious effects, probably because of the infants' low fluid intake. Indomethacin pharmacokinetic parameters (clearance, area under the curve) may account in part for the variability of the fractional excretion of sodium, glomerular filtration, and urine flow rate.
In the course of a double-blind controlled trial of intravenous indomethacin therapy in premature infants with patent ductus arteriosus, plasma glucose was evaluated in 47 infants before and at 24, 48, and 72 hours following the medication. Twenty-two infants were assigned to the control group and 25 were in the indomethacin group. Significantly lower plasma glucose was noted at 24 (P less than 0.01) and 48 (P less than 0.05) hours in the indomethacin group as compared to the control group. There was a significant inverse correlation between the plasma glucose and the corresponding plasma indomethacin concentration (P less than 0.05) and between the plasma glucose and the corresponding plasma indomethacin concentration-time integral (P less than 0.01) at 24, 48, and 72 hours after drug administration, suggesting that the decreased plasma glucose may be related to indomethacin therapy. The results of this study indicate that endogenous prostaglandin may play a role in glucose homeostasis in premature infants.
23 premature infants were placed on a randomized double-blind study to evaluate the effectiveness of indomethacin in closing a patent ductus arteriosus. Infants received 0.2 mg/kg indomethacin or placebo by gavage. In the treatment group, 7 patients responded out of a total of 12, while in the placebo group, 2 responded out of a total of 11. Indomethacin plasma levels were obtained in 6 patients in the treatment group. Plasma levels showed marked variability in peak level (60-3,100 ng/ml), time to peak level (0.5-6 h) and t1/2 (1 to greater than 24 h).
In the course of a double-blind trial of intravenous indomethacin therapy in premature infants with patent ductus arteriosus, renal function and urinary kallikrein were studied in 21 infants following one dose of either saline placebo or indomethacin. Ten infants were assigned to the control group and 11 were in the indomethacin group. Significantly lower urine output, fraction excretion of sodium, fraction excretion of chloride, and urinary kallikrein were noted by 45%, 59%, 63%, and 51%, respectively, in the indomethacin group as compared to the control group. There was a concomitant decrease in serum sodium concentration (P less than .05) at 24 hours following indomethacin therapy. No significant difference in glomerular filtration rate was seen between the control group and the indomethacin-treated infants.
Serum digoxin (DIG) levels, timed urine and M-mode echocardiograms were performed in 9 low birth weight infants with left-to-right shunting due to patent ductus arteriosus treated with DIG (40 micrograms/kg in 3 and 20 micrograms/kg in 6). Half the DIG was given initially and a quarter at 8-hourly intervals. Serum DIG levels at 24 h (1.8-7.0 ng/ml) were similar in both dose groups. One infant in the 40 micrograms/kg dose group developed Wenckebach phenomenon. Left atrial to aortic root ratio fell within 30 min and remained reduced during the ensuing 24 h (p less than 0.025). There were no significant changes in the other echocardiographic measurements. Half-life of distribution and elimination of DIG were 1.04 +/- 0.46 and 15.25 +/- 0.36 h. The alpha-phase volumes of distribution (VD) differed between the 40 and 20 micrograms/kg dose groups (2.28 +/- 0.05 vs. 1.33 +/- 0.66 liters/kg, p less than 0.025). The beta-phase VD (4.25 +/- 0.61 and 2.76 +/- 0.99, respectively) were similar. Mean urinary DIG clearance was 13.1 +/- 3.2 ml/min/1.73(2).
Patent ductus arteriosus is the most common shunting congenital cardiac anomaly in the cat. If it is treated surgically, early in the course of the disease, the prognosis is good.
Eighteen patients with ventricular septal defect or patent ductus arteriosus were studied to investigate the effects of an increase of pulmonary hypertension. In general group II showed similar results as previously reported in patients with atrial septal defect without pulmonary hypertension. In group I, we found an increased frequency of functional abnormalities in the small airways. We do not have a definitive explanation for the origin of these differences.