Impact of early human milk on sepsis and health-care costs in very low birth weight infants.

OBJECTIVE: To study the incidence of sepsis and neonatal intensive care unit (NICU) costs as a function of the human milk (HM) dose received during the first 28 days post birth for very low birth weight (VLBW) infants. STUDY DESIGN: Prospective cohort study of 175 VLBW infants. The average daily dose of HM (ADDHM) was calculated from daily nutritional data for the first 28 days post birth (ADDHM-Days 1-28). Other covariates associated with sepsis were used to create a propensity score, combining multiple risk factors into a single metric. RESULT: The mean gestational age and birth weight were 28.1 ± 2.4 weeks and 1087 ± 252 g, respectively. The mean ADDHM-Days 1-28 was 54 ± 39 ml kg(-1) day(-1) (range 0-135). Binary logistic regression analysis controlling for propensity score revealed that increasing ADDHM-Days 1-28 was associated with lower odds of sepsis (odds ratio 0.981, 95% confidence interval 0.967-0.995, P=0.008). Increasing ADDHM-Days 1-28 was associated with significantly lower NICU costs. CONCLUSION: A dose-response relationship was demonstrated between ADDHM-Days 1-28 and a reduction in the odds of sepsis and associated NICU costs after controlling for propensity score. For every HM dose increase of 10 ml kg(-1) day(-1), the odds of sepsis decreased by 19%. NICU costs were lowest in the VLBW infants who received the highest ADDHM-Days 1-28.

Breast pump suction patterns that mimic the human infant during breastfeeding: greater milk output in less time spent pumping for breast pump-dependent mothers with premature infants.

OBJECTIVE: The objective of this study was to compare the effectiveness, efficiency, comfort and convenience of newly designed breast pump suction patterns (BPSPs) that mimic sucking patterns of the breastfeeding human infant during the initiation and maintenance of lactation. STUDY DESIGN: In total, 105 mothers of premature infants ≤34 weeks of gestation were randomly assigned to 1 of 3 groups within 24 h post-birth. Each group tested two BPSPs; an initiation BPSP was used until the onset of lactogenesis II (OOL-II) and a maintenance BPSP was used thereafter. RESULT: Mothers who used the experimental initiation and the standard 2.0 maintenance BPSPs (EXP-STD group) demonstrated significantly greater daily and cumulative milk output, and greater milk output per minute spent pumping. CONCLUSION: BPSPs that mimic the unique sucking patterns used by healthy-term breastfeeding infants during the initiation and maintenance of lactation are more effective, efficient, comfortable and convenient than other BPSPs.

Calculating postnatal growth velocity in very low birth weight (VLBW) premature infants.

OBJECTIVE: Currently, there is no standardized approach to the calculation of growth velocity (GV; g kg (-1) day(-1)) in hospitalized very low birth weight (VLBW) infants. Thus, differing methods are used to estimate GV, resulting in different medical centers and studies reporting growth results that are difficult to compare. The objective of this study was to compare actual GV calculated from infant daily weights during hospitalization in a Neonatal Intensive Care Unit (NICU) with estimated GV using two mathematical models that have been shown earlier to provide good estimated GVs in extremely low birth weight (ELBW) infants: an exponential model (EM) and a 2-Point model (2-PM). STUDY DESIGN: Daily weights from 81 infants with birth weights (BWs) of 1000 to 1499 g were used to calculate actual GV in daily increments from two starting points: (1) birth and (2) day of life (DOL) of regaining BW. These daily GV values were then averaged over the NICU stay to yield overall NICU GV from the two starting points. We compared these actual GV with estimated GV calculated using the EM and 2-PM methods. RESULTS: The mean absolute difference between actual and EM estimates of GV showed <1% error for 100% of infants from both starting points. The mean absolute difference between actual and 2-PM estimates showed <1% error for only 38 and 44% of infants from birth and regaining BW, respectively. The EM was unaffected by decreasing BW and increasing length of NICU stay, whereas the accuracy of the 2-PM was diminished significantly (P<0.001) by both factors. CONCLUSION: In contrast to the 2-PM, the EM provides an extremely accurate estimate of GV in larger VLBW infants, and its accuracy is unaffected by common infant factors. The EM has now been validated for use in all VLBW infants to assess growth and provides a simple-to-use and consistent approach.

Activation of blood platelets after percutaneous transluminal coronary angioplasty and coronary artery bypass graft surgery.

We have evaluated the activation of platelets in blood samples taken from patients with stable angina undergoing balloon angioplasty (percutaneous transluminal coronary angioplasty [PTCA]) (n=11) or coronary artery bypass grafting (CABG) under hypothermic (n=11) or normothermic conditions (n=11). We have found that surface expression of P-selectin on platelets in whole blood from PTCA patients upon thrombin treatment was significantly reduced, as compared with control platelets from healthy subjects. This effect was partially reversed when platelets washed from the same blood sample were used, but even then P-selectin expression was significantly lower in PTCA patients than it was in control subjects. There was a significant increase in basal expression of P-selectin in blood platelets taken from patients who underwent CABG under normothermic conditions (warm blood cardioplegia) as opposed to hypothermic patients (cold crystalloid cardioplegia). These platelets retain the ability to respond to agonists, although to a much lower extent than do those from healthy control donors. The surface exposure of P-selectin on resting and thrombin-treated platelets isolated from CABG surgery patients was not different from that of the control platelets. The adhesion to fibrinogen of resting and thrombin-treated platelets from patients who underwent balloon angioplasty as well as CABG surgery under normothermic and hypothermic conditions was significantly reduced when compared with the fibrinogen of the control platelets. These results suggest that the function of platelet fibrinogen receptor is impaired in patients with stable angina pectoris and that PTCA and CABG surgery activates platelets.

[Myocardial revascularization for sudden cardiac death in patients after previous coronary angioplasty]. / Rewaskularyzacja serca w trybie naglym u chorych po przebytej koronaroplastyce.

UNLABELLED: PTCA was introduced into our hospital in June 1991. Since then till the end of 1996 emergency CABG operations were performed in fourteen patients. They were indicated because of acute myocardial ischaemia and hemodynamic deterioration that was the result of the dissection and occlusion of a coronary artery during angioplasty. There were 11 male and 3 female patients in this group aged 34 to 65 average 50 years. Twenty-three grafts were performed in total (18 saphenous, 5 using internal mammary artery), that is 1.6 graft per patient. A female patient died of myocardial infarction on the first postoperative day. All other patients survived and are under outpatient clinic's care. Over the analysed 6 years' period of time 1079 PTCAs were performed. The low rate of the unsuccessful procedures (1.3%) that required the emergency CABG is noteworthy. Since 1995, when the implantation of stents was introduced into our hospital, there were only 2 such procedures (0.4% of all PTCAs). CONCLUSIONS: The CABG operation performed shortly after a dissection and occlusion of the coronary artery underwent angioplasty usually prevents myocardial infarction and saves the patient's live. The introduction of implantation of the stents significantly diminished a number of patients who required an emergency CABG operation.

Beyond cold cardioplegia.

One hundred fifteen consecutive patients were operated on for myocardial revascularization or valvular disease or both with continuous antegrade and retrograde aerobic warm (37 degrees C) blood cardioplegia. Mean cross-clamp time was 56.3 +/- 21 minutes (+/- standard deviation). Mean reperfusion time was 18.4 +/- 11.8 minutes (range, 5 to 81 minutes). Five patients (4.3%) died, and 15 (13%) needed inotropic support. Two (1.7%) required intraaortic balloon support. Two patients (1.7%) had evidence of perioperative myocardial infarction, and 98 (85%) returned spontaneously to normal sinus rhythm. Sixteen patients had a cross-clamp time greater than 80 minutes. All 16 of them had an uneventful postoperative course except for 1 patient who required inotropic drugs. This method of myocardial protection is now used for all open heart procedures in our institution.

[Surgical mitral valvuloplasty in the treatment of mitral valve diseases]. / La place de la plastie mitrale chirurgicale dans le traitement des maladies de l'orifice mitral.

Mitral valve repair surgery, in presence of a pure mitral leakage or one associated to a stenosis, is not only possible but has been well codified for a decade. According to damage, there are two methods of operation: valvular mobilization surgery and valvular motion amplitude reduction surgery. They are usually associated to annuloplasty with a Carpentier prosthetic ring. The incidence of late mortality is of 0.6 p. 100 pt/yr, that is to say 91.7 p. 100 at 13 years. This late survival rate is about 20 p. 100 better than for a valvular replacement. Reoperations rate is 1.6 p. 100 pt/yr. The incidence of thromboembolic event occurrence is low: 0.5 p. 100 pt/yr. The ideal indications for mitral valve repair are represented by damage of prolapse from a degenerative origin for which results are better and more constant. For rheumatic damage, the valvular repair indication depend on the valvular tissue elasticity and area. The presence of calcification and extensive fibrosis remain on principle counter-indications.

Mitral valve repair: results and the decision-making process in reconstruction. Report of 275 cases.

From January 1975 to June 1988, 275 patients underwent mitral valve repair for mitral regurgitation, pure (148 patients) or associated with mitral stenosis (127 patients). Patients with pure mitral stenosis were excluded from this study. The cause of mitral regurgitation was rheumatic in 180 patients (aged 28.6 +/- 1.2 years, mean +/- standard error of the mean) and degenerative in 84 patients (aged 54.7 +/- 1.5 years). Fifty-nine percent of the patients were in New York Heart Association classes III and IV before the operation. Intraoperative assessment of the mitral valve led us to identify four major mechanisms of mitral regurgitation: (1) restriction of leaflet motion by fibrosis (group I, 63 patients); (2) enhancement of leaflet motion by leaflet and chordal extension and prolapse (group II, 139 patients), (3) combination of both (group III, 64 patients); and (4) isolated dilatation of the anulus (group IV, 10 patients). One hundred sixty-one patients had isolated mitral disease and 114 had associated aortic or tricuspid valve disease, or both. The hospital mortality rate was 4.0%. Follow-up was 96% complete and totaled 1247.47 patient-years. At 13 years' follow-up, the survival rate was 93.0% +/- 6.8% in group I, 90.0% +/- 6.0% in group II, and 96.6% +/- 4.6% in group III. Freedom from reoperation was 78.1% +/- 21.0%, 83.2% +/- 18.9%, and 79.6% +/- 16.2%, respectively. Freedom from embolism was 94.7% for the whole series. In patients with isolated mitral valve repair, the cumulative morbidity was significantly higher in groups I (6.3 +/- 2.0%/pt-yr) and III 6.3% +/- 1.7%/pt-yr) than in group II (2.5% +/- 0.9%/pt-yr, p less than 0.05). Multivariate analysis identified age and associated tricuspid valve disease as significant predictors of reoperation (p less than 0.01 for both factors). These results suggest that conservative surgery should be used with caution in group I and III patients. In contrast, indications for mitral valve repair should be extended in group II patients. This observation has important clinical implications since, in Western countries, valve prolapse tends to be a major cause of mitral regurgitation.