[The newborn infant and vitamin K].
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Biomedical subjects
Publications and source records attributed to W Künzer.
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Haemorrhages were observed in four wholly breastfed infants beyond the neonatal period. These infants were observed within a period of 8 weeks and showed the following characteristics: 1. Onset of bleedings was unexpected and without prior indication. 2. They were of a serious nature and involved the CNS in two children. 3. In all cases infants between 4 and 6 weeks of life were affected. 4. All infants had been wholly breastfed. 5. All were male. 6. There was a prompt improvement after administration of vitamin K or after blood or blood derivatives. Although preliminary own investigations do not indicate general lowering of vitamin-K-dependent coagulation factors in wholly breastfed infants in the postneonatal period, these 4 cases observed within a short time confirm the necessity to consider vitamin K deficiency in haemorrhages in infants in the postneonatal period. Diagnostic steps have to be initiated immediately.
In a prospective study serum C-reactive protein (CRP) was measured in 100 premature infants. All babies were suspected of having bacterial infection (septicemia - meningitis) because of complications during pregnancy and/or during the perinatal period. CRP was measured with the radial immunodiffusion technique. 6/6 babies with bacterial infections proved by positive cultures from blood and/or CSF showed elevated levels of CRP already within 24 h after the first appearance of clinical symptoms suggesting sepsis. In 11 of 21 cases most probably suffering from septicemia CRP rose within a period of 82 h after the appearance of clinical signs. Even extremely immature infants were able to react with elevated CRP concentrations. Peak values of CRP were independent of birth weight. On the other hand, only 2 of 73 babies without clinical or laboratory findings of infection had slightly elevated amounts of CRP for a short time. Therefore it is suggested that increased levels of serum CRP are a valuable parameter for the early diagnosis of severe bacterial infections in premature infants.
An enzyme linked immunoassay was developed using the microtiter system to measure platelet-associated IgG (PAIgG). The specificity of the assay was demonstrated in 6 children with acute idiopathic thrombocytopenic purpura (ITP): Elevated values of PAIgG (25-800 fg IgG/platelet) corresponded with low platelet counts. Complete remission was accompanied by normalization of PAIgG levels. Since immune destruction of platelets may be encountered in the development of neonatal postexchange thrombocytopenia, platelet counts and PAIgG levels were determined in pre- and postexchange samples from the recipient and in samples from the donor's blood. Eight double-volume exchange transfusions were studied in 7 newborns. Various patterns of interaction between donor and recipient were observed. Five donors proved to be thrombocytopenic, 3 of them had correspondingly high PAIgG levels, indicating immune destruction of donor platelets prior to transfusion. Three newborns had pre-existing immune thrombocytopenia before the exchange. Significant falls in platelet counts with concomitant rises in PAIgG were found following 2 out of 8 exchange transfusions. The quantitation of PAIgG by means of a micro enzyme linked immuno-assay is reliable and helpful in the detection of immune-mediated thrombocytopenia in all pediatric age-groups.
Applying a rotatory sector-scanner, in 437 infants between the 29th gestational week and 18th month of life, a sonographic study was performed in order to look for an intracranial haemorrhage. The recording was performed real-time, using the anterior fontanelle as an acoustic window. In 42 infants we saw signs of an intracranial haemorrhage, which was confirmed 11 times anatomically and 11 times by CAT. Advantages and disadvantages of the method are discussed.
During the course of severe coagulopathy in an infant suffering from septicaemia and shock, antithrombin III levels were determined repeatedly before and during substitution therapy with human antithrombin. By mathematical analysis of these data, using a biexponential function, the plasma elimination half-life of the antithrombin III was estimated to be 7.5-10.5 h. Compared with known plasma half-lives of radioactively labelled antithrombin III in adults the increase was five-to ten-fold. This indicates that the significantly decreased levels of antithrombin III in this case of coagulopathy were at least partly due to an accelerated consumption of antithrombin III. The estimation of the plasma elimination half-life of antithrombin III helps to differentiate decreased production from increased consumption in cases of severe coagulopathy. Thus, a more precise diagnosis of disseminated intravascular coagulation can be made whilst taking advantage of substitution therapy and avoiding the hazards of radioactive tracer proteins.
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The diagnosis of neonatal isoimmune thrombocytopenia is based upon the exclusion of other causes of thrombocytopenia in the newborn, and on successful treatment by transfusion of compatible, preferably maternal, platelets, If isoimmunization is suspected, detection of antiplatelet isoantibodies should be attempted using specific serological methods. This case report nevertheless illustrates that failure to confirm isoimmunization serologically does not exclude the diagnosis of neonatal isoimmune thrombocytopenia.
A premature infant of 31 weeks gestational age weighing 1650 g developed pronounced generalized bleeding following exchange transfusion for rhesus-incompatibility. As a consequence there was continuous leakage into a subcutaneous haematoma that had been caused by accidental puncture of the infant's flank during diagnostic amniocentesis. The ensuing massive and prolonged loss of blood required replacement by infusions of heparinized fresh blood over several days. The most conspicuous detail in the longitudinal study of haemostasis was hyperfibrinolysis with values for Fibrin-Fibrinogen Split Products exceeding 1280 micrograms/ml. This situation could be treated effectively with epsilon-amino-capronic acid. We suggest that anti-fibrinolytic agents can be recommended under cover of heparin for treating those rare cases in which hyperfibrinolysis predominates and clinical criteria of disseminated intravascular thrombosis are missing. We would, however, strongly discourage the uncritical use of antifibrinolytic agents whenever Fibrin-Fibrinogen-Split Products are detected.
The simultaneous occurrence of severe bacterial, especially urinary tract infections and cholostatic icterus in newborn and young infants, is a wellknown phenomenon. Since the pathogenetic principle is unknown, such types of icterus are described as "idiopathic", "septic" or "septic-toxic". However, in recent years an increasing number of pointers seems to indicate that cholostatic jaundice, being a polyaetiological syndrome, can be closely linked in respect of time and cause, with disseminated intra vascular coagulation. It would suggest itself to assume that pathogenetically speaking a severe infection (or some other triggering cause) may lead to shock which, in turn, produces an intravascular consumption reaction, resulting in severe disturbances of microcirculation in the liver and hence in disordered liver function which is clinically manifest in the form of a cholastatic icterus. Among the patients treated at the Unversity Paediatric Hospital at Freiburg, a total of 31 mostly male children--30 babies and one schoolchild--was seen in whom this causal chain is highly likely.
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A new senitive and specific micromethod for determination of UDP-glucuronic acid is described Extracts from 2.5 mg of liver are incubated with twice washed guinea pig microsomes (as a source of UDP-glucuronyl transferase) and [14C]p-nitrophenol. The content of UDP-glucuronic acid is calculated from the [14C]p-nitrophenyl glucuronide/[14C]p-nitrophenol radioactivity ratio and the known amount of introduced [14C]p-nitrophenol. These values are corrected for losses of UDP-glucuronic acid by a calibration experiment, containing in addition to the aforementioned constituents, a known amount of UDP-glucuronic acid. The mean concentration of UDP-glucuronic acid in mice liver was found to be 171 mumol/kg wet weight.
Using the paper-radioimmunosorbens test (PRIST) normal values were obtained from 200 non-allergic children. The IgE level was aged-dependent, in part with significant differences between various age groups. These normal values were compared with those in children with seborrhoeic dermitis, constitutional neurodermatitis, parasitoses, urticaria, Quincke oedema, Schönlein-Henoch purpura, pityriasis rosea, multiform exudative erythema, erythema nodosum and infantile papular acrodermatitis. Half-life of IgE in neonates was 16.2 hours.
Among twelve patients with homozygous alpha1-antitrypsin deficiency (Pi-type Z), five cases of infantile liver disease were diagnosed. The course of the disease was extremely variable; only one patient died of liver cirrhosis at the age of fourteen. In four cases the clinical, biochemical and histological (2 cases) findings became normal over a follow-up period of one to fifteen years. The results of these observations demonstrate that in alpha1-antitrypsin deficiency even when associated with proven liver disease the prognosis need not be unfavorable.
Hypercoagulation and intravascular coagulation developed a nearly 12-year-old girl with a one-year history of typical anorexia. Because of extreme cachexia she had been treated with numerous drugs elsewhere, among them ACTH an infusions of amino-acids. At the end of the second week of hospitalisation acute venous thrombosis of the right leg developed which was treated with heparin. Severe disseminated intravascular coagulopathy and thrombosis of the right leg were diagnosed on admission, the previously administered heparin was neutralised and streptokinase given for 60 hours, heparin was then given for several days, and the cachexia then treated. Both the local and general condition of the patient having been cured, the emotional state has also very much improved during the last year.
Seven patients with classic hemophilia A had alteration of primary hemostasis after treatment with lyophilized antihemophilic globulin (LAHG). The following test results, which were normal before treatment, became abnormal after treatment: bleeding time, bleeding intensity, and platelet adhesiveness. In two patients, the fibrin-fibrinogen-degradation products increased to more than 40 microgram/ml. In three patients, the bleeding symptoms became worse with LAHG therapy although no inhibitor against Factor VIII was demonstrated. In one of these patients, the bleedings symptoms disappeared when the use of LAHG was discontinued and prednisone was given; at the same time, the altered primary hemostasis returned to normal. In the remaining two patients, prednisone did not have any effect. In these two patients, however, the bleeding stopped, and the bleeding time became normal immediately after freshly prepared blood-group compatible cryoprecipitate was given.
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