A study of surgeons' postural muscle activity during open, laparoscopic, and endovascular surgery.

BACKGROUND: Different surgical procedures impose different physical demands on surgeons and high prevalence rates of neck and shoulder pain have been reported among general surgeons. Past research has examined electromyography in surgeons mainly during simulated conditions of laparoscopic and open surgery but not during real-time operations and not for long durations. The present study compares the neck-shoulder muscle activities in three types of surgery and between different surgeons. The relationships of postural muscle activities to musculoskeletal symptoms and personal factors also are examined. METHODS: Twenty-five surgeons participated in the study (23 men). Surface electromyography (EMG) was recorded in the bilateral cervical erector spinae, upper trapezius, and anterior deltoid muscles during three types of surgical procedures: open, laparoscopic, and endovascular. In each procedure, EMG data were captured for 30 min to more than 1 h. The surgeons were asked to rate any musculoskeletal symptoms before and after surgery. RESULTS: The present study showed significantly higher muscle activities in the cervical erector spinae and upper trapezius muscles in open surgery compared with endovascular and laparoscopic procedures. Muscle activities were fairly similar between endovascular and laparoscopic surgery. The upper trapezius usually has an important role in stabilizing both the neck and upper limb posture, and this muscle also recorded higher activities in open compared with laparoscopic and endovascular surgeries. Surgeons reported similar degrees of musculoskeletal symptoms in open and laparoscopic surgeries, which were higher than endovascular surgery. CONCLUSIONS: The present study showed that open surgery imposed significantly greater physical demands on the neck muscles compared with endovascular and laparoscopic surgeries. This may be due to the lighter manual task demands of these minimally invasive surgeries compared with open procedures, which generally required more dynamic movements and more forceful exertions.

Major malformations in infants of IDDM women. Vasculopathy and early first-trimester poor glycemic control.

From animal and in vitro studies, it has been suggested that high environmental glucose, ketone, or insulin concentrations and low glucose or insulin concentrations may be etiologic factors for congenital malformations (CMs) in infants of diabetic mothers (IDMs). Transplacental passage of antibody-bound insulin has been demonstrated in humans. Controversy exists regarding the pathophysiology of CMs in human insulin-dependent diabetes mellitus (IDDM) pregnancies. We hypothesized that CMs in IDMs are associated with maternal vasculopathy, poor first-trimester glycemic control (i.e., hyper- and/or hypoglycemia), advanced White class, and high insulin requirements. We studied 165 first pregnancies of women with IDDM from 1978 to 1986. The goals of glucose control were a fasting blood glucose of less than 100 mg/dl and a 90-min postprandial blood glucose of less than 140 mg/dl. Insulin requirements, body weight, and pre- and postprandial blood glucose were recorded at weekly clinic visits. Maternal blood HbA1 was measured on entry and every 4 wk to confirm that adequate glycemic control was achieved. Women who enrolled in the project were interviewed during gestation by a geneticist/dysmorphologist who obtained genetic and environmental histories using a standard questionnaire. All live-born infants and stillbirths were examined. Each live-born infant was assessed systematically by two independent examiners, a neonatologist and a geneticist/dysmorphologist; examination with standardized checklists was performed in the newborn nursery as soon after birth as was practical. In first pregnancies in the study, there were 13 IDMs with major CMs (7.9%).(ABSTRACT TRUNCATED AT 250 WORDS)

Sequential bone mineral content in small preterm infants with and without fractures and rickets.

Seventy-four infants with birth weights 1009 +/- 28 grams and gestational age 28.6 +/- 0.3 weeks (M +/- SEM) were studied prospectively to test the hypotheses that bone mineral content (BMC) measured by photon absorptiometry, would be: (1) lower in very low birth weight (VLBW) infants with radiographic evidence of fractures and/or rickets (F/R), and (2) will continue to be lower over the first year when compared to VLBW infants without F/R. BMC and bone width (BW) of the distal one-third of left radius and ulna were measured at 5 weeks (n = 8), 14 weeks (n = 61), 26 weeks (n = 58), 40 weeks (n = 59), and 1 year (n = 52). Standardized radiographs of both forearms, and weight, length, and head circumference were also determined at each study age. Investigators and technicians involved in the photon absorptiometry measurements were unaware of the radiographic findings and vice versa. Twenty-three of 74 infants were found to have F/R. BMC of studied infants remained markedly below our previously determined range of "intrauterine bone mineralization," even at 26 weeks after birth. There was no significant difference in BMC or BW between infants with and without F/R, either at the time of confirmation of F/R or during early follow-up; however, BMC was lower at greater than or equal to 6 months and BW was lower at greater than or equal to 9 months in infants with F/R. We suggest that the extremely low BMC measurements in early infancy predispose all VLBW infants to fractures and rickets.

Effects of growth hormone replacement therapy on 1,25-dihydroxyvitamin D and calcium metabolism.

To elucidate the changes in mineral metabolism and blood concentrations of calciotropic hormones which accompany GH therapy, we studied 12 GH-deficient children for 5 days before and for 1 week after high dose (5 IU/day) GH therapy, and again at 1 month, 3 months, and 1 yr of replacement therapy (0.1 IU/kg to a maximum dose of 2 IU three times weekly). All responded with acceleration of height velocity, and bone ages advanced appropriately. Fasting serum ionized calcium levels did not change: 4.11 +/- 0.06 (SEM) mg/dl before, 4.19 +/- 0.05 for the week of high dose therapy, and 4.20 +/- 0.14 during replacement therapy. Likewise, fasting serum parthormone did not vary: 38.9 +/- 2.6 muleq/ml before to 44.1 +/- 9.2 at 1 yr. Twenty four-hour nephrogenous cyclic AMP (NcAMP) did not vary over the first week (1.2 +/- 0.7 nmol/dl glomerular filtrate before, 1.3 +/- 0.4 after 1 week), but increased to 5.3 +/- 1.9 after 1 yr (alpha less than 0.001). The response of ionized calcium and parathormone to a standardized disodium EDTA infusion of 50 mg/kg also did not change. The mean fasting serum calcitonin level was not different before therapy (29.4 +/- 2.8 pg/ml), after 1 week (21.5 +/- 1.8), or after 1 yr (42.4 +/- 11.0). However, the mean serum 1,25-dihydroxyvitamin D concentration rose from 33.1 +/- 3.3 pg/ml before therapy to 68.3 +/- 12.3 on the seventh day of high dose therapy (alpha less than 0.01), returning to pretherapy values by 1 month. We conclude that high dose GH therapy in GH-deficient children raises 1,25-dihydroxyvitamin D concentration acutely, but that long term, physiological replacement therapy does not cause such an effect. Because NcAMP excretion rose in the absence of an increase in serum parathormone concentration, we conclude that GH sensitizes the kidney to a cAMP-mediated effect of parathormone.

Hypocalcemia and pregnancy-induced hypertension produced by low-calcium diet.

Recent studies from our laboratory in fasting pregnant ewes with twin gestation have implicated low serum calcium concentration in the etiology of hypertension in pregnancy. We hypothesized that the reduction in serum calcium concentration produced by feeding of a calcium-deficient diet in twin gestation would lead to a significant increase in maternal arterial blood pressure, vascular resistance, and protein in the urine and decreased uterine blood flow. Twenty-five instrumented ewes were used in the present study. After surgery a calcium-deficient diet and deionized water (calcium ion free) were provided ad libitum to 19 animals. Blood pressure, cardiac output, heart rate, and uterine blood flow were monitored every other day. Six control animals were provided with standard Rumilab diet and tap water (group 1). Animals on a low-calcium diet (group 2) were subdivided according to the blood ionized calcium response to low dietary calcium intake. Non-hypocalcemic animals were assigned to group 2a (n = 10), and hypocalcemic animals (calcium concentration below two standard deviations from the control group) were assigned to group 2b (n = 9). In group 2b calcium concentration decreased from 1.03 +/- 0.04 mmol/L on day 110 of gestation to 0.77 +/- 0.03 mmol/L by day 125 of gestation. Arterial blood pressure increased significantly from 76 +/- 2 to 91 +/- 2 mm Hg, and uterine blood flow decreased from 950 +/- 53 to 579 +/- 48 mL/min. Urinary protein increased from 1.7 +/- 0.3 to 10.5 +/- 1.2 g/L.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of different vitamin A intakes on very-low-birth-weight infants.

Formula-fed infants with birth weights < or = 1500 g (n = 61) were stratified by 250-g birth-weight ranges and randomly assigned to receive one of three preterm infant formulas (vitamin A contents of 820 IU, 1640 IU, or 2900 IU/MJ; 1 RE = 3.3 IU vitamin A activity) when subjects tolerated 0.314 MJ.kg-1.d-1. Experimental formula feedings were continued until infants weighed approximately 2 kg or until hospital discharge. Vitamin A status as indicated by serum retinol and retinol-binding protein (RBP) concentrations significantly decreased during experimental formula feeding at the lowest vitamin A intake. All subjects fed the formula providing the lowest vitamin A intake had hyporetinolemia (< 0.70 mumol/L, or < 20 micrograms/dL), which occurred less frequently (P < 0.05) with the intermediate (6 of 20) and the high (6 of 21) vitamin A intakes. Other outcome measures, including increases in weight, length, and head circumference, and ventilatory support and oxygen therapy, were not different among groups. After the end of the experimental formula-feeding period, all infants were fed standard infant formulas with a vitamin A content of 715 IU/MJ. In a subset of 19 of these infants, subsequent vitamin A status was monitored at ages 6-12 mo and was found to be comparable with that of older children and adults, regardless of the vitamin A content of the formula fed during hospitalization.(ABSTRACT TRUNCATED AT 250 WORDS)

Mineral homeostasis during lactation- relationship to serum 1,25-dihydroxyvitamin D, 25-hydroxyvitamin D, parathyroid hormone and calcitonin.

During lactation maternal losses of calcium and phosphorus through human milk average 220 to 340 and 110 to 170 mg/day, respectively. The present study reports maternal serum concentrations of vitamin D metabolites, parathyroid hormone, calcitonin, calcium, magnesium, and phosphorus during the first 6 months of lactation. Serum calcium and magnesium concentrations increased during the first 6 months of lactation. Serum 1,25-(OH)2 vitamin D was increased at 6 months of lactation compared to values in nonpregnant nonlactating controls. During this same period, serum parathyroid hormone decreased slightly and serum calcitonin remained unchanged. Our data do not support the observation that lactation represents a state of physiological hyperparathyroidism. On the contrary, our results suggest that lactating women are able to adequately compensate for the losses of calcium and phosphorus during the early months of lactation, although increased serum 1,25-(OH)2 vitamin D concentrations may be necessary to maintain calcium homeostasis with lactation beyond 6 months.

Pediatric familial type II hyperlipoproteinemia: therapy with diet and colestipol resin.

Effects of a low-cholesterol, polyunsaturate-rich diet and a synthetic organic bile sequestrant polymer (U26,597A, colestipol) were studied in 21 children, heterozygous for familial hypercholesterolemia. Total cholesterol, beta-lipoprotein cholesterol, and triglyceride were measured twice on habitual diet, monthly for six months on a low-cholesterol diet, and monthly for six months on low-cholesterol diet plus 10 gm of colestipol per day. Total cholesterol (mean +/- 1 SD) was 295 +/- 37 on habitual diet, 278 +/- 29 on low-cholesterol diet, and fell significantly to 242 +/- 29 mg/100 ml on diet plus colestipol. Low-density lipoprotein (LDL) cholesterol was 234 +/- 37 on habitual diet, 220 +/- 28 on low-cholesterol diet, and fell significantly to 179 +/- 26 mg/100 ml on diet plus drug. Plasma triglyceride levels on habitual diet were 79 +/- 31, remained unchanged on low-cholesterol diet, 86 +/- 22, and were unaffected by low-cholesterol diet plus drug, 85 +/- 17 mg/100 ml. On diet alone, plasma LDL was not normalized (less than 170 mg/100 ml) in any of the 21 children, and cholesterol fell to within normal limits (less than 230 mg/100 ml) in only one child. The combination of diet plus colestipol resin normalized total and LDL cholesterol in 52% of the children. Cholesterol was lowered to a "moderately elevated" range of 230 to 250 mg/100 ml in an additional 14% of the children and LDL was lowered to a range of 170 to 190 mg/100 ml in an additional 29%. In 33% of the children, cholesterol remained greater than 250 mg/100 ml despite diet plus colestipol, while LDL was greater than 190 mg/100 ml in 19%. Colestipol is an effective and well-tolerated cholesterol lowering compound which, in conjunction with diet, may prove to be very useful in the treatment of children heterozygous for familial hypercholesterolemia.

Blood sampling through umbilical catheters.

An in vitro study testing the reliability of chemical determinations on blood samples withdrawn through an umbilical catheter is described. Blood samples were withdrawn through three different sizes of umbilical catheters containing a solution of dextrose, sodium bicarbonate, and potassium. Using either a 5 French or a 3 1/2 French catheter, accurate results were obtained for pH, sodium, potassium, and glucose when measurements were made after an initial 4-ml blood sample was discarded. With an 8 French catheter, accurate results were obtained for pH, sodium, and potassium but plasma glucose determinations remained inaccurate after 6 ml of blood was discarded.

Therapy of familial hypercholesterolemia in childhood: diet and cholestyramine resin for 24 to 36 months.

In 16 children heterozygous for familial hypercholesterolemia, two- to three-year therapy with diet and cholestyramine resin (16 gm/day) was assessed in terms of effectiveness, practicality, and safety. All 16 children had previously taken a low-cholesterol (less than 300 mg/day), polyunsaturate-rich (P/S ratio, 1.5:1) diet and choeltyramine resin (12 gm/day) for 12 months. In this study, the cholestyramine resin dose was increased to 16 gm/day, and follow-up was maintained through months 13 through 18, 19 through 24, 25 through 30, and 31 through 36. Eleven children had good drug adherence (four packs of cholestyramine per day) and five children had fair adherence (two to three packs per day). Plasma total cholesterol and low-density lipoprotein (LDL) cholesterol levels were not significantly lowered on the drug-plus-diet regimen as compared to diet alone in five children with fair drug adherence. For children with good drug adherence, mean plasma cholesterol level was lowered below levels achieved on diet alone by 13% (months 13 through 18), 12% (months 19 through 24), 12% (months 25 through 30), and 11% (months 31 through 36) (P less than .05). Reduction in plasma cholesterol level was no greater with 16 than with 12 gm of cholestyramine per day. There were no group changes in mean plasma triglyceride levels. Cholestyramine resin, when added to diet and maintained for two to three years effects a significant reduction in total and LDL cholesterol levels in about 60% of children heterozygous for familial hypercholesterolemia. Continued reinforcement of both diet and drug adherence is necessary in the face of gradual increments in plasma cholesterol level with time.

Decreased bone mineral content in small-for-gestational-age infants compared with appropriate-for-gestational-age infants: normal serum 25-hydroxyvitamin D and decreasing parathyroid hormone.

Bone mineral content was determined by photon absorptiometry, adapted for use in neonates, in 23 small-for-gestational-age (SGA) infants of 31 to 42 weeks of gestational age, for 12 weeks. At birth, term SGA infants had lower bone mineral content than term appropriate-for-gestational-age (AGA) infants; postnatal increase in bone mineral content was slow and lagged significantly behind that of term AGA infants. Preterm SGA infants had bone mineral content that was similar to that of preterm AGA infants at birth; postnatal bone mineral content was similar to that of preterm AGA infants, but was decreased compared with the expected intrauterine bone mineral content. Serum 25-hydroxyvitamin D concentrations and parathyroid hormone levels were the same for SGA and AGA infants. Serum 25-hydroxyvitamin D concentrations decreased slightly with postnatal age and remained within normal limits. Serum parathyroid hormone concentrations decreased in both SGA and AGA infants and reached undetectable levels at 10 to 12 weeks of age.

Calcium-regulating hormones and minerals from birth to 18 months of age: a cross-sectional study. I. Effects of sex, race, age, season, and diet on vitamin D status.

The influence of sex, race, age, season, and diet (cow's milk formula v human milk) on the vitamin D and vitamin D-binding protein status in infants less than 18 months of age was investigated in this cross-sectional, prospective study of 198 infants. No differences by sex were observed in serum 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D, or vitamin D-binding protein concentrations. By race, black infants had significantly elevated serum 1,25-dihydroxyvitamin D levels relative to white infants. By age, vitamin D-binding protein concentrations increased with increasing age. By season, serum 25-hydroxyvitamin D concentrations were low in winter, whereas 1,25-dihydroxyvitamin D and vitamin D-binding protein were high in winter compared with summer. By diet, formula-fed infants had higher serum concentrations of all measured vitamin D metabolites and vitamin D-binding protein than human milk-fed infants. Thus, race, age, season, and diet exert, individually or in combination, different and significant effects on vitamin D metabolites; these should be considered in assessing infant vitamin D status.

Plasma and dietary phytosterols in children.

Plasma phytosterol (plant sterol) levels were studied in 26 infants on various commercial formulas, in 36 infants on breast or cow's milk formulas, in 101 normal and 22 hypercholesterolemic children on a free diet, and in 32 hypercholesterolemic children on a low-cholesterol diet. Commercial formulas, poor in animal fats and enriched with vegetable oils, and low-cholesterol, phytosterol-rich diets generally elevated total plasma phytosterol levels in infants and hypercholesterolemic children from normal mean levels of 2 mg/100 ml to about 9 mg/100 ml. The implications of long-term three- to five-fold elevations of the plasma phytosterols (campesterol, stigmasterol, beta-sitosterol) in infancy and childhood are unknown. Watchful prospective analysis of plasma phytosterol levels may be useful, particularly in regards to otherwise unanticipated long-term effects of cholesterol-poor, phytosterol rich diets.

Calcium-regulating hormones and minerals from birth to 18 months of age: a cross-sectional study. II. Effects of sex, race, age, season, and diet on serum minerals, parathyroid hormone, and calcitonin.

The influence of sex, race, age, season, and diet (cow's milk formula v human milk) on serum minerals and calcium-regulating hormones in infants less than 18 months of age is described in this study of 198 infants. No sex differences were observed in calcium, magnesium, phosphorus, parathyroid hormone, or calcitonin concentrations. Black infants had decreased serum phosphorus concentrations compared with white infants. There was a decrease in serum ionized calcium and phosphorus levels with age. During winter, there were significant increases in serum calcium and magnesium and decreases in serum phosphorus, parathyroid hormone, and calcitonin levels. Formula-fed infants had increased serum phosphorus and decreased ionized calcium concentrations compared with infants fed human milk. Thus, race, age, season, and diet appear to exert significant effects on serum minerals and calcium-regulating hormones in infancy. Interpretation of these mineral and hormone concentrations in normal or diseased states should be based on normative data specific to race, age, season, and diet.

Serum vitamin D metabolites and bone mineralization in young children with chronic low to moderate lead exposure.

One hundred five children (49 male, 99 black) with known lead exposure indices from birth and adequate nutrient intake of calcium, phosphorus, and vitamin D were studied at 1 of 3 ages (21, 27, or 33 months) to determine the effects of chronic low to moderate lead exposure on circulating concentrations of vitamin D metabolites and bone mineral content as determined by photon absorptiometry. Univariate multiple regression analyses showed no direct relationship of blood lead levels to vitamin D metabolites or bone mineral content. Structural equation analyses which took into account potential covariates of age, season, race, and sex showed estimated declines in serum concentrations of total calcium (from 9.72 to 9.61 mg/dL), phosphorus (from 5.4 to 4.67 mg/dL), and 25-hydroxyvitamin D (from 27.24 to 25.8 ng/mL) and estimated increases in concentrations of parathyroid hormones (from 73.03 to 83.14 microL Eq/mL), 1,25-dihydroxyvitamin D (from 62.39 to 62.69 pg/mL), and bone mineral content (from 222.66 to 234.91 mg/cm) over the observed range of average lifetime blood lead concentrations (4.76 to 23.61 micrograms/dL, geometric mean 9.74 micrograms/dL). However, the only statistically significant effect of average lifetime blood lead concentration was that for phosphorus, and the multivariate test of the combined effects of lead on these six outcomes was not statistically significant (P = .2). It is concluded that significant alterations in vitamin D metabolism, calcium and phosphorus homeostasis, and bone mineral content are not present in children whose nutritional status is adequate and who experience low to moderate lead exposure.

Cholesterol-free diet and the physiologic hyperlipidemia of pregnancy in familial hypercholesterolemia.

Longitudinal studies of the effects of a cholesterol-free diet and a less rigid 300 mg/day low cholesterol diet, both with a polyunsaturated to saturated fatty acid ratio of 1.8/1, were carried out preconception, during gestation, and postpartum in a women heterozygous for familial hypercholesterolemia. On the cholesterol-free diet, during weeks 8-14 of gestation, plasma cholesterol was lowered 25% (from 310 to 230mg/dl), and plasma low density lipoprotein cholesterol (C-LDL) (from 240 to 160 mg/dl), 33%. The 25% reduction in plasma cholesterol was slightly more than previously reported decrements of 19% in 14 normal women during pregnancy, also receiving a cholesterol-free diet. The 300 mg cholesterol diet was not as hypocholesterolemic as the cholesterol-free diet. Its maintenance throughout gestation limited the within-pregnancy increments of total plasma cholesterol and C-LDL to 21% (352-426 mg/dl) and 14% (286-326 mg/dl) respectively. Both the cholesterol-free and the 300 mg cholesterol diet were well tolerated, and should be nutritionally adequate for pregnant women, since they contain more than the recommended amounts of high quality protein, vitamins, minerals, and calories for pregnant women. Cholesterol restricted diets during pregnancy in familial hypercholesterolemics should reduce the physiologic hypercholesterolemia of pregnancy, and potentially reduce the increased risk of coronary heart disease relative to the degree and duration of elevations of total and LDL cholesterol.

Neonatal familial hypobeta-lipoproteinemia.

A kindred with four generation vertical transmission of familial hypobeta-lipoproteinemia was ascertained by measurement of low levels of cord blood low density lipoprotein cholesterol (C-LDL) in a propositus neonate. Measurement of cord blood C-LDL in conjunction with family studies allows the neonatal diagnosis of familial hypobetalipoproteinemia.

Black-white similarities in cord blood lipids and lipoproteins.

Cord blood lipoproteins were quantitated in 117 neonates (58 white, 50 black) to assess for potential early expression of racial lipid distinctions. In comparison of black and white neonates there were no differences in total cholesterol (TC), high-density lipoprotein cholesterol (C-HDL), low-density lipoprotein cholesterol (C-LDL), C-HDL/C-LDL, or C-HDL/TC. Cord blood triglycerides were slightly higher in black neonates (p = 0.02). Unlike certain adult black-white comparisons and within the limits of "genicity" as expressed by cord blood lipoproteins, there were no racial differences in C-HDL, C-LDL, and total cholesterol.

Neonatal familial hyperalphalipoproteinemia.

A kindred with four-generation vertical transmission of familial hyperalphalipoproteinemia was ascertained by measurement of elevated levels of cord blood high-density lipoprotein cholesterol (C-HDL) in a neonatal propositus. Quantitation of cord blood C-HDL coupled with family studies and longitudinal follow-up allows the diagnosis of familial hyperalphalipoproteinemia in infancy.

Decreased amniotic fluid magnesium concentration in diabetic pregnancy.

Amniotic fluid samples from 21 diabetic pregnant women were pair-matched for gestational age with 21 samples obtained from nondiabetic women, and analyzed for magnesium concentration. Mean +/- standard deviation amniotic fluid magnesium concentration (mg/dL) was 0.86 +/- 0.21 in the diabetic group and 1.06 +/- 0.22 in the control group (P less than .001). It is concluded that in the diabetic pregnancy, a state of fetal magnesium deficiency exists. This deficient state may contribute to neonatal hypocalcemia in infants of diabetic mothers.