Re: poród w szpitalu "Parkitka"
A poniżej masz napisane coś zgoła innego.
Chyba nie czytałeś lub nie zrozumiałeś tego o czym pisałem wcześniej?
W badaniach, na które się powołujesz najbardziej przekonał mnie argument o zmniejszeniu krwawienia po obrzezaniu...
Czy nie pomyliłeś przypadkiem strefy geograficznej?
Z tego co mi wiadomo, u nas nie obrzezuje się dzieci. Chyba, że w Twojej parafii stosuje się takie praktyki?
Thromb Haemost. 1999 Mar;81(3):456-61.
Vitamin K deficiency bleeding (VKDB) in infancy. ISTH Pediatric/Perinatal Subcommittee. International Society on Thrombosis and Haemostasis.
Sutor AH, von Kries R, Cornelissen EA, McNinch AW, Andrew M.
Universitäts-Kinderklinik, Freiburg, Germany. firstname.lastname@example.org
TERMINOLOGY: Replace the term "Hemorrhagic Disease of the Newborn" (HDN) by "Vitamin K Deficiency Bleeding" (VKDB), as neonatal bleeding is often not due to VK-deficiency and VKDB may occur after the 4-week neonatal period.
DEFINITION: VKDB is bleeding due to inadequate activity of VK-dependent coagulation factors (II, VII, IX, X), correctable by VK replacement.
DIAGNOSIS: In a bleeding infant a prolonged PT together with a normal fibrinogen level and platelet count is almost diagnostic of VKDB; rapid correction of the PT and/or cessation of bleeding after VK administration are confirmative. WARNING SIGNS: The incidence of intracranial VKDB can be reduced by early recognition of the signs of predisposing conditions (prolonged jaundice, failure to thrive) and by prompt investigation of "warning bleeds". CLASSIFICATION: VKDB can be classified by age of onset into early (<24 h), classical (days 1-7) and late (>1 week <6 months), and by etiology into idiopathic and secondary. In secondary VKDB, in addition to breast feeding, other predisposing factors are apparent, such as poor intake or absorption of VK. VK-PROPHYLAXIS:
BENEFITS: Oral and intramuscular VK (one dose of 1 mg) protect equally well against classical VKDB but intramuscular VK is more effective in preventing late VKDB. The efficacy of oral prophylaxis is increased with a triple rather than single dose and by using doses of 2 mg vitamin K rather than 1 mg. Protection from oral doses repeated daily or weekly may be as high as from i.m. VK. VK-PROPHYLAXIS: RISKS: VK is involved in carboxylation of both the coagulation proteins and a variety of other proteins. Because of potential risks associated with extremely high levels of VK and the possibility of injection injury, intramuscular VK has been questioned as the routine prophylaxis of choice. Protection against bleeding should be achievable with lower peak VK levels by using repeated (daily or weekly) small oral doses rather than by using one i.m. dose. BREAST FEEDING MOTHERS TAKING COUMARINS: Breast feeding should not be denied. Supervision by pediatrician is prudent. Weekly oral supplement of 1 mg VK to the infant and occasional monitoring of PT are advisable.
CONCLUSION: VKDB as defined is a rare but serious bleeding disorder (high incidence of intracranial bleeding) which can be prevented by either one i.m. or multiple oral VK doses.
Paediatr Perinat Epidemiol. 2008 Nov;22(6):562-8.
Neonatal jaundice: a risk factor for infantile autism?
Maimburg RD, Vaeth M, Schendel DE, Bech BH, Olsen J, Thorsen P.
Department of Epidemiology, Institute of Public Health, University of Aarhus, Aarhus, Denmark. email@example.com
In a previous study, we found that infants transferred to a neonatal ward after delivery had an almost twofold increased risk of being diagnosed with infantile autism later in childhood in spite of extensive controlling of obstetric risk factors. We therefore decided to investigate other reasons for transfer to a neonatal ward, in particular hyperbilirubinaemia and neurological abnormalities. We conducted a population-based matched case-control study of 473 children with autism and 473 matched controls born from 1990 to 1999 in Denmark. Cases were children reported with a diagnosis of infantile autism in the Danish Psychiatric Central Register. Conditional logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals [CI] and likelihood ratio tests were used to test for effect modification. We found an almost fourfold risk for infantile autism in infants who had hyperbilirubinaemia after birth (OR 3.7 [95% CI 1.3, 10.5]). In stratified analysis, the association appeared limited to term infants (>or=37 weeks gestation). A strong association was also observed between abnormal neurological signs after birth and infantile autism, especially hypertonicity (OR 6.7 [95% CI 1.5, 29.7]). No associations were found between infantile autism and low Apgar scores, acidosis or hypoglycaemia. Our findings suggest that hyperbilirubinaemia and neurological abnormalities in the neonatal period are important factors to consider when studying causes of infantile autism.