Anemia in the newborn: a diagnostic approach.
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Biomedical subjects
Publications and source records attributed to L R Smith.
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Estimation of effective renal plasma flow (ERPF) can be made easily, inexpensively, and accurately by means of a single plasma concentration determination, sampled 44 min after injection of 131I-orthoiodohippurate (OIH). We originally established predictive regression equations based on a series of patients with a wide variety of diseases and a few normal potential kidney donors. The equation best fitting that data was parabolic in form and assumed a negative slope when high ERPF rates were encountered. This problem has been corrected by deriving new equations (parabolic and exponential) based on an expanded series which includes a large number of subjects with high ERPF. Errors of estimation are lower than those of the more classic para-aminohippuric acid (PAH) clearances and well within the exigencies of clinical practice.
A new formula is presented for the prediction of urinary excretion at approximately 35 min after injection of 131I-orthoiodohippurate, derived from a large series of normal kidney donors, before and after unilateral nephrectomy, and a few patients with diseases in which there was no evidence of urinary tract obstruction. The best formula was: Expected percent dose excretion at 35 min = 79.3[1-e--(0.004798 X ERPF)] with a standard error of estimate (Sy.x) of 5.2% dose. This value has been particularly useful in clinical practice in the calculation of an excretion index (actual/expected percent dose excretion) which separates various post-transplantation entities and various nephrourologic processes.
To compare the relative merits of conventional and axial RAO/LAO angiography, we performed biplane left ventricular (LV) cineangiograms in 36 patients in both the conventional 30-degree RAO/60-degree LAO projection and in the axial 45-degree RAO/60-degree LAO/25-degree cranial projection, in random sequence. LV volumes were calculated by a computerized system utilizing modification of the area-length method. Eng-diastolic volume, end-systolic volume, and ejection fraction correlated closely between the two projections (r = 0.93, 0.95, and 0.86, respectively). The axial 60-degree LAO view projected the LV apex inferiorly, the LV outflow tract superiorly, reduced LV foreshortening, and "uncovered" the LV outflow tract in all cases. Segmental wall motion abnormalities of the ventricular septum, apex, and posterior wall were better evaluated by the axial 60-degree LAO view in patients with regional asynergy in these zones. The 45-degree RAO, compared to the 30-degree RAO view, allowed a true tangential view of the mitral valve and provided a large "clear area" between the mitral valve and descending aorta, which improved the ability to quantify mitral regurgitation. Thus, axial oblique LV angiography improves evaluation of LV regional wall motion and mitral valve function without compromising LV volume quantitation.
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Fifty patients undergoing isolated coronary artery bypass grafting procedures using a clear, cold cardioplegic solution, topical hypothermia, and reduced systemic flow for intraoperative myocardial protection were evaluated for myocardial injury by serial plasma creatine kinase-MB isoenzyme (CK-MB) measurements and electrocardiograms. Forty-one (82%) of the patients had three-vessel disease. Preoperative left ventricular contractility determined angiographically was normal in 13 patients (26%), mildly abnormal in 26 (52%), and moderately or severely abnormal in 11 (22%). The number of arteries grafted ranged from 2 to 6 (mean, 3.5). The mean duration of aortic clamping was 38.6 +/- 1.6 minutes. There were no hospital deaths. Enzymatic and electrocardiographic (ECG) evidence of myocardial infarction occurred in 1 patient. Nonspecific ECG changes occurred in 16 patients (32%), and th electrocardiograms were unchanged in the remaining 33 patients (66%). In the 49 patients without ECG evidence of infarction, the mean peak plasma CK-MB value, which occurred 6 hours after the onset of cardiopulmonary bypass, was 7.9 +/- 0.8 IU/L (standard error of the mean) and the mean integrated area 158 +/- 19.5 IU/L X hours. There was no correlation between these CK-MB values and the extent of disease, number of arteries grafted, or the duration of myocardial ischemia. These data document a low incidence of perioperative myocardial injury with this technique, and can serve as a baseline for comparison with other techniques for intraoperative myocardial protection in this setting.
Cardiopulmonary bypass (CPB) alters systemic hemodynamics and affects several biochemical systems involved in cardiovascular regulation. We investigated the changes in levels of circulating epinephrine (E) and norepinephrine (NE) and related them to events during CPB. Twenty-eight patients undergoing various surgical procedures were studied. Plasma E and NE were determined by radioenzymatic assay at eight stages of the operation. A ninefold increase in arterial E (from 75 +/- 13 to 708 +/- 117.3 pg/ml) occurred from prebypass (stage 1) measurements to the end of aortic cross-clamping (stage 4). The values at stage 4 were significantly higher (p less than 0.05) than at all other stages. E decreased rapidly, to 360 +/- 84.3 pg/ml, after myocardial and pulmonary reperfusion (stage 5). Arterial NE increased twofold from stage 1 to stage 4 (from 426 +/- 66.9 to 825 +/- 84.2, p less than 0.05). The increase in NE from initial CPB values (stage 2) to 30 minutes of aortic cross-clamping (stage 3) was associated with an increase in mean blood pressure (r = 0.51, p = 0.02). The peak increases in catecholamines occurred when the heart and lungs were excluded from the circulation, which suggests that either or both contributed to the increase. Because the increase in E was markedly greater than that in NE, the predominant humoral response to CPB appears to be adrenomedullary release of E. This significant increase in catecholamines could jeopardize myocardial protective measures during CPB.
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Individual variation occurs in time to induction of anaesthesia with intravenous drugs. Less free drug is available to cross the blood-brain barrier when the drug is highly protein bound. Since this may prolong time to sleep, we correlated the induction time, serum albumin and total protein concentrations, and doses of midazolam, which is a highly protein bound intravenous anaesthetic. There is a poor correlation (r = 0.062) between induction time and serum protein, a weak (r = 0.542) but statistically significant (p = 0.026) correlation between induction time and serum albumin, and a highly significant (p = 0.003) negative correlation (r = 0.579) between drug dose and induction time. The administration of the appropriate dose of midazolam for induction, therefore, appears to affect induction time more significantly than does the serum albumin concentration.
In rat experiments, the relative potency an safety of thiopentone, diazepam and etomidate were assessed using different indices of anaesthesia - loss of righting reflex, prevention of movement and heart rate responses to an noxious stimulus. Log-probit dose-response curves for these end-points and for lethal effect were determined. Etomidate proved to be more potent than thiopentone or diazepam; its relative potency figures varied from 5 to 18 with the use of different end-points of anaesthesia. According to the ED50 level of response for the loss of righting reflex and increased of heart rate, diazepam was more potent than thiopentone. At the same time it was less potent in the prevention of movement response. Etomidate has an extremely large standard safety margin (SSM) regarding the loss of righting reflex; with the use of movement response or heart rate response, the SSM for etomidate was close to that of thiopentone. With diazepam, SSM for movement response and heart rate response was negative (anaesthetic dose-response curve partially overlaps the lethal curve); it was positive for the loss of righting reflex. The extreme variability in assessment of relative potency and safety with different end-points of anaesthesia probably indicates that the indices used reflected various components of anaesthesia. It seems likely that for the proper assessment of the potency of intravenous anaesthetics, one index of potency is not sufficient. Several indices of potency corresponding to different components on general anaesthesia must be used.
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Total and individual plasma free fatty acids (FFA) were measured on admission and over the next 4 days in 24 patients admitted to the hospital with chest pain and suspected acute myocardial infarction (AMI). In a prospective randomized fashion, the patients were either given an infusion of 300 gm of glucose, 50 units of insulin, and 80 mEq of KCl per liter at a rate of 1.5 ml/kg/hr over the initial 48 hours of hospitalization, or they served as controls receiving conventional therapy. Eleven patients were in the control group and 13 were in the glucose-insulin-potassium (G-I-K) group. Twenty-one of the patients had an AMI by CK-MB rise and ECG changes (in the G-I-K group three did not evolve AMI). The total plasma FFA were 840 +/- 134 microM/L in the controls and 933 +/- 160 microM/L in the G-I-K group initially (prestudy). Total FFA rapidly fell in the G-I-K group and then rebounded when G-I-K was stopped. In contrast, total FFA values fell gradually in the control group over the 4-day period. The individual FFA had similar percentages initially in the two groups. In the control group the percent of individual plasma FFA was unchanged over the period studied, although there was some mild random day-to-day fluctuation. In contrast in the G-I-K group linoleic acid fell both during and after the infusion was stopped (26.8% to 19.1% P less than 0.001). Arachidonic acid doubled in percentage of the total FFA value during G-I-K infusion (3.1% to 6.5%, P less than 0.002) and returned to the control value when it was stopped. Thus G-I-K infusion during AMI reduces the total level of plasma FFA while increasing the percent of arachidonic and decreasing the percent of linoleic acid, observations proposed to reflect improved membrane stability of the ischemic myocardium.
The efficacy, safety, and tolerability of lofexidine, a centrally acting imidazoline derivative, were compared to that of clonidine in a randomized double-blind trial in 28 patients with moderate essential hypertension. The study consisted of a washout phase, a placebo phase, a drug titration phase (0.2 to 1.6 mg/day, with hydrochlorothiazide added at 0.4 mg daily for supine and erect diastolic blood pressure above 90 mm Hg), and a maintenance phase lasting 3 mo. During the titration phase supine systolic and diastolic pressures fell in lofexidine patients from 143 +/- 4/98 +/- 3 to 122 +/- 3/81 +/- 2 mm Hg and in clonidine patients from 154 +/- 6/101 +/- 2 to 124 +/- 4/81 +/- 2 mm Hg (P less than 0.01), and erect systolic and diastolic pressures fell in lofexidine patients from 143 +/- 3/105 +/- 2 to 116 +/- 3/85 +/- 2 mm Hg and in clonidine patients from 156 +/- 6/104 +/- 2 to 117 +/- 4/82 +/- 2 mm Hg (P less than 0.01). Maximal doses of lofexidine and clonidine in combination with hydrochlorothiazide had equivalent antihypertensive effects, but when the effects of lofexidine and clonidine were compared at each dose level, larger doses of lofexidine patients in either the supine or erect position during the titration phase but heart rate fell in the clonidine patients (P less than 0.05) over the same period. Dry mouth and drowsiness were reported in both groups but were both less frequent and less severe in the lofexidine group than the clonidine group.
Since coronary revascularization improves prognosis in some patients with multivessel disease, can the potential benefits be extended to "prophylaxis" in selected postinfarction patients as well? These investigators sought the answer on the basis of patient characteristics, types of surgery, survival data, and mode of death in the postinfarction population of 129 patients who had early angiography.
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Hemodynamic responses to induction of anesthesia with midazolam maleate and diazepam were compared in patients with ischemic heart disease. While breathing 100% oxygen, 10 patients (group M) received midazolam maleate, 0.2 mg/kg, and 10 patients (group D) received diazepam, 0.5 mg/kg. In addition, 10 patients (group MN) breathing 50% nitrous oxide in oxygen received midazolam, 0.2 mg/kg. Patients in group M had a small but statistically significant (p less than 0.05) decrease (vs awake control values) in systemic and pulmonary arterial blood pressure, pulmonary arterial occluded pressure, stroke index, and left and right ventricular stroke work indices. Patients in group D experienced statistically significant decreases in systemic blood pressure. The only statistically significant differences between groups M and D occurred 5 minutes followed drug administration: heart rates were higher and systemic pressures and left ventricular stroke work indices were lower following midazolam. Hemodynamic changes following midazolam and nitrous oxide were similar to those observed in patients given midazolam and 100% oxygen. Patients in all three groups responded to endotracheal intubation with transient increases in blood pressure, heart rate, and systemic vascular resistance, but the hemodynamic values spontaneously returned toward control levels within 2 to 5 minutes. Although differing somewhat, midazolam, like diazepam, provided rapid, hemodynamically stable induction of anesthesia in patients with ischemic heart disease.