[Meetings on cost savings and techniques reduce time spent with patients!].
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Cost Savings↗
Biomedical subjects
A Larsson
Publications and source records attributed to A Larsson.
[Better intensive care saves more lives].
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Critical Care↗
Analysis of oligonucleotide probe affinities using surface plasmon resonance: a means for mutational scanning.
A novel strategy for real-time analysis of oligonucleotide probe hybridization based on detection by surface plasmon resonance is described. The design of the analysis, exploiting the rapid dissociation kinetics of short oligonucleotides from their hybridization templates, allows monitoring in genuine sensor mode of equilibrium hybridization responses, circumventing the need for regeneration between sample cycles. Applied to a model system comprising oligonucleotide probes and different immobilized hybridization targets the effects of temperature, probe length, and nucleotide substitutions in template were investigated. The procedure described was observed to have an efficient discriminatory power with respect to end-mismatch situations. Affinity determinations of octamer probes showed good correlation between calculated Tm-values and probe affinities. From affinity data collected at different temperatures thermodynamic parameters were determined, which correlated well with data obtained from theoretical calculations. The technique, modified to a simplified form, allowed detection of single nucleotide substitutions in a target template, suggesting that procedures for confirmatory DNA sequencing can be envisioned.
Biotin↗
[Pulmonary artery catheterization is not without risks].
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Catheterization, Swan-Ganz↗
Engineering of Fc(1) and Fc(3) from human immunoglobulin G to analyse subclass specificity for staphylococcal protein A.
A system for production of recombinant Fc fragments of human IgG in Escherichia coli has been developed to allow for structural and functional studies of human Fc. The genes for the Fc fragments of human IgG subclasses 1 and 3, designated Fc(1) and Fc(3), were cloned from a human spleen cDNA library. The interactions to Staphylococcal protein A (SpA), a bacterial Fc receptor, that interacts with human IgG-Fc(1), but not with human IgG-Fc(3), were analyzed. To corroborate the involvement of amino acid residues in Fc, responsible for these differences in binding, two Fc variants were constructed; Fc(1(3)) and Fc(3(1)), each containing an isotypic dipeptide substitution. Production levels in E. coli of 1-10 mg/l of secreted Fc proteins, covalently linked as dimers, were routinely obtained. SpA-binding analyses of all four Fc variants using biosensor technology, showed that Fc(1) and Fc(3(1)) interact with SpA, while Fc(3) and Fc(1(3)) lack detectable SpA binding. The rendered SpA binding of the Fc variant Fc(3(1)), is concluded to result from the introduced dipeptide substitution (R435H, F436Y). The results demonstrate that the Fc expression system efficiently can be used in Fc engineering.
Amino Acid Sequence↗
Growth failure, encephalopathy, and endocrine dysfunctions in two siblings, one with 5-oxoprolinase deficiency.
UNLABELLED: Two female siblings, born to consanguineous parents, presented with a similar phenotype characterized by severe growth and developmental failure, dysmorphic features, thyroid and gonadal dysfunction, autistic traits and hand stereotypes resembling Rett syndrome. In the elder patient, analysis of urinary organic acids disclosed a very high excretion of 5-oxoproline (4.2 to 8.1 mol/mol creatinine) and enzyme assays of leucocyte extracts revealed a profound deficiency of 5-oxoprolinase. However, normal urinary organic acid profiles were found in the younger child. In view of their distinct dysmorphic features and severe growth deficiency, these siblings cannot be considered as Rett Syndrome variants. The Dubowitz and carbohydrate-deficient glycoprotein syndromes were also excluded clinically and biochemically respectively. We conclude that these patients suffer from a hitherto undescribed autosomal recessive disorder, unrelated to the 5-oxoprolinase deficiency of the elder sib. CONCLUSION: The present findings give evidence that 5-oxoprolinase deficiency is not associated with a distinct morbid phenotype.
Brain Diseases↗
Genetic and linkage analysis of familial congenital hypothyroidism: exclusion of linkage to the TSH receptor gene.
Congenital hypothyroidism affects 1/3000-4000 newborns. The causes of this group of disorders are still largely unknown. Although most cases are sporadic some families have several affected children and/or consanguineous parents, suggesting autosomal recessive inheritance. Furthermore, there is a murine strain (hyt) with congenital hypothyroidism and autosomal recessive inheritance, whose phenotype appears to be identical with the corresponding human disease. In the hyt mouse, the disease is caused by a mutation in the thyroid-stimulating hormone receptor (TSHR) gene, making this gene a likely candidate also for the human disease. The human TSHR gene was mapped on radiation hybrid panels and closely linked flanking markers D14S287 and D14S616 were identified. On the Genebridge 4 panel, D14S287 was found to be located 8.5 cR (corresponding to 2.3 cM) proximal to the TSHR gene, and D14S616 was found to be located 4.4 cR (1.2 cM) distal to the TSHR gene. These markers were analyzed in 23 families, most of them with two or more children affected by congenital hypothyroidism and some with appreciable consanguinity of the parents. Assuming homogeneity, the two-point lod score at theta = 0.1 was -4.8 for D14S287 and -5.8 for D14S616, and thus linkage to the TSHR gene was excluded. Even when the data were analyzed with allowance for heterogeneity, there was no evidence of linkage. Our conclusion is that if mutation of the TSHR gene causes familial congenital hypothyroidism in humans, it affects only a small proportion of the cases.
Adult↗
Inhibition of complement activation by soluble recombinant CR1 under conditions resembling those in a cardiopulmonary circuit: reduced up-regulation of CD11b and complete abrogation of binding of PMNs to the biomaterial surface.
The influence of soluble recombinant CR1 (sCR1) on complement activation, and its indirect effects on the coagulation system and cellular responses were assessed in two models for the study of blood/surface and blood/air interactions, as are encountered in e.g. cardiopulmonary bypass circuits. The concentrations of C3a and sC5b-9 and the amount of bound C3/C3 fragments were analyzed as indicators of complement activation. Thrombin-antithrombin complexes, the platelet count, surface-ATP, beta-thromboglobulin, and the expression of CD11b on leukocytes were the parameters analyzed to reflect coagulation and cellular responses. In addition, immunochemical analyses of the phenotypes of surface-bound leukocytes and platelets were performed. Recombinant sCR1, at doses ranging between 0.1-0.25 mg/ml, was found to completely inhibit the generation of sC5b-9, and of C3a by two thirds; the binding of C3 and/or C3 fragments to the surface was almost entirely abolished. As a result of the inhibition of complement activation, the expression of CD11b on PMNs, and the binding of these cells to the biomaterial surface was almost completely lost. In contrast, the thrombin-antithrombin complexes, the platelet count, and the adherence of platelets to the surface, as reflected by the ATP binding and the release of beta-thromboglobulin, were not affected. These data show that complement activation, in association with extra-corporeal treatment, causes activation and binding of PMNs to the biomaterial and that these effects can be completely abolished by the addition of soluble recombinant sCR1.
Biocompatible Materials↗
Analysis of the T-cell receptor V beta usage in monozygotic and dizygotic twins living in a Plasmodium falciparum endemic area in west Africa.
To investigate the influence of genetic and/or environmental factors in the development and shaping of the human peripheral T cell repertoire the authors studied the T-cell receptor (TCR) V beta usage in 10 adult monozygous (Mz) and nine dizygous (Dz) twin pairs living in a Plasmodium falciparum endemic area in West Africa. The TCR repertoire was determined using a small panel of anti-V beta specific monoclonal antibodies (MoAbs) using conventional immunofluorescence assays. The results revealed that the V beta repertoire was similar to that recently described for a Caucasian population using a similar panel of antibodies. The frequencies of particular V beta genes tested were influenced neither by anti-malarial antibody titres nor by parasite densities, indicating that the P. falciparum parasite is not a dominating factor in determining the peripheral T cell repertoire. All donors were human leucocyte antigen (HLA) class I and II typed; no association was found between the expression of any V beta genes and MHC haplotype. The V beta usage was more concordant within the Mz than within the Dz pairs. For a group comprising four HLA class II identical individuals, the average within-pair difference was significantly greater than for the whole Mz group, but similar to that seen for the total Dz group. Thus, the data suggest that genetic, rather than environmental, factors have a profound effect on the shaping of the human circulating T cell repertoire and that the major genetic factors are encoded by non-HLA class II genes.
Adolescent↗
Iodine nutrition in Sudan: determination of thyroid-stimulating hormone in filter paper blood samples.
In this study we examined the technique of measuring thyroid-stimulating hormone (TSH) on filter paper blood samples for use in evaluating the iodine nutrition status of newborns and adults living in iodine-deficient areas. Filter paper blood samples were obtained between the 5th and 7th day after birth from 103, 43 and 103 term newborns living in Khartoum (mild iodine deficiency), Kosti (moderate iodine deficiency) and Darfur (severe iodine deficiency), respectively. TSH was measured with a commercial assay and the levels were compared with those obtained with the same method in 1147 samples from term Swedish newborns, obtained on the 3rd to the 5th day of life. The mean (95% confidence interval) TSH levels of the three Sudanese groups and the Swedish group were 7.1 (4.8-9.4), 8.3 (6.6-10.1), 11.9 (0.9-22.9) and 4.51 (3.8-5.3) mU l-1, respectively. The mean TSH for all three Sudanese groups was higher than the Swedish mean (p < 0.001). TSH levels determined in filter paper blood samples from adults living in an iodine-deficient area showed a correlation (p < 0.001; r = 0.55) to levels in corresponding serum samples (range 0.52-14.1 mU l-1, median 3.4 mU l-1). No significant correlation was found, however, between blood spot levels and serum levels within the reference range (< 5 mU l-1). A modification of the commercial procedure consisting in using three instead of two monoclonal antibodies did not sufficiently improve the assay for measurements of TSH within the reference range. Thus, there is a need to develop the filter paper technique further to make it a useful test for monitoring iodine deficiency in populations expected to have TSH levels close to the reference range. In the examination of neonates, however, with their birth-induced surge of TSH, the current assay promises to be a convenient tool for discovering iodine deficiency within a community.
Filtration↗
Missense mutations in the human glutathione synthetase gene result in severe metabolic acidosis, 5-oxoprolinuria, hemolytic anemia and neurological dysfunction.
Severe glutathione synthetase (GS) deficiency is a rare genetic disorder with neonatal onset. The enzymatic block of the gamma-glutamyl cycle leads to a generalized glutathione deficiency. Clinically affected patients present with severe metabolic acidosis, 5-oxoprolinuria, increased rate of hemolysis and defective function of the central nervous system. The disorder is inherited in an autosomal recessive mode and, until recently, the molecular basis has remained unknown. We have sequenced 18 GS alleles associated with enzyme deficiency and we detected missense mutations by direct sequencing of cDNAs and genomic DNA. In total, 13 different mutations were identified. Four patients were found to be compound heterozygotes and two individuals were apparently homozygous. Reduced enzymatic activities were demonstrated in recombinant protein expressed from cDNAs in four cases with different missense mutations. The results from biochemical analysis of patient specimens, supported by the properties of the expressed mutant proteins, indicate that a residual activity is present in affected individuals. Our results suggest that complete loss of function of both GS alleles is probably lethal. It is postulated that missense mutations will account for the phenotype in the majority of patients with severe GS deficiency.
Acidosis↗
A delivery system for inhalation of nitric oxide evaluated with chemiluminescence, electrochemical fuel cells, and capnography.
OBJECTIVE: To evaluate a system for delivery of inhaled nitric oxide. DESIGN: Prospective, laboratory study. SETTING: Engineering laboratory. SUBJECTS: A standard ventilator (Servo Ventilator 300), supplemented with extra gas modules for nitric oxide delivery. INTERVENTIONS: Two ventilator-integrated gas modules, delivering < or = 10 parts per million (ppm) or < or = 100 ppm of nitric oxide, were used in adult and neonatal modes during volume-controlled ventilation. Set nitric oxide concentration and FIO2 were systematically changed and compared with the measured concentration. Short-term mixing was tested in adult, pediatric, and neonatal modes by substituting nitric oxide with CO2, and measuring the delivered concentration by a fast-response CO2 analyzer during five successive respiratory cycles. Long-term mixing was tested with the administration of 25 ppm of nitric oxide for 7 days. MEASUREMENTS AND MAIN RESULTS: Delivered concentration of nitric oxide and nitrogen dioxide were simultaneously measured at the Y-place by two methods-chemiluminescence and electro-chemical fuel cells. The maximum absolute difference between set and measured concentrations of nitric oxide in the adult mode was 0.6 ppm at a set concentration of 10 ppm and 2.7 ppm at a set concentration of 100 ppm. In the neonatal mode, the maximal difference was 3.1 ppm at a set concentration of 100 ppm. Nitrogen dioxide concentration increased with increasing concentration of nitric oxide and oxygen to 2.6 ppm (as measured by the chemiluminescence analyzer) and 3.6 ppm (as measured by the electro-chemical fuel cell), at a setting of 100 ppm of nitric oxide with an FIO2 of 0.90 in the neonatal mode (2 L/min). During the short-term test of mixing stability throughout the respiratory cycles, a constant set CO2 concentration varied maximally by +/-6.2% from the set value in the neonatal mode, whereas the variance was by +/-6.5% in pediatric mode, and by +/-8.0% in the adult mode. During the long-term test, nitric oxide concentration varied maximally by +/-2.6% (as measured by the chemiluminescence analyzer) and by +/-2.3% (as measured by the electrochemical fuel cell). CONCLUSIONS: An accurate precision in delivered nitric oxide concentration was achieved during intermittent flow ventilation, and this accuracy was independent of tested ventilator settings. The delivery system administered an almost stable concentration throughout a respiratory cycle and during long-term delivery. If the mixing point is in the inspiratory part of the ventilator, valid measurement of nitric oxide and nitrogen dioxide delivery concentrations are possible. Both techniques for measuring nitric oxide and nitrogen dioxide have drawbacks.
Administration, Inhalation↗
Selection of collimator for rCBF studies and evaluation of triple-headed SPET using noise-resolution plots.
We investigated the effect of collimator selection on image quality in regional cerebral blood flow (rCBF) studies of the brain performed with 99Tc(m)-HMPAO. A triple-headed SPET system (GE/CGR Neurocam) was used, together with three sets of parallel-hole collimators - general-purpose (GP), high-resolution (HR) and ultra-high-resolution (UHR). Two image quality parameters were used to describe the image quality, namely, noise and resolution. Noise was measured in experimental and Monte-Carlo simulated SPET studies of a cylinder phantom of uniform activity as the pixel root mean square error (RMS) and as the coefficient of variation (CV) of quantitative rCBF values. Resolution was measured as full-width at half-maximum in experimental SPET studies of a line-source. Plots of noise versus resolution for the different collimators were obtained by varying the cut-off frequency of the Hanning filter applied in the reconstruction of transaxial slices. From these noise-resolution plots, we were able to determine which collimator gave the best resolution for a specific noise level. A lowest reasonable noise level may be established by comparison with the inter-observer CV of the quantification method.
Brain↗
Costs of the treatment of leg ulcers: initiating a quality assurance process.
Reports on a study which aimed to initiate a quality assurance process among health care personnel in Sweden. An epidemiological survey concerning treatment of leg ulcers in a defined region in Sweden was conducted and the costs of treating leg ulcers at different levels of care were analysed. The epidemiological survey provided the data necessary to calculate the socio-economic costs for the treatment of leg ulcers. The weekly cost was found to be about 24 times higher for hospital inpatients than it was for patients treated at home. The quality assurance process has continued through an interdisciplinary regional consensus conference and the establishment of a consensus programme in the region, with targets and general suggestions for the care and treatment of leg ulcers. To maintain high quality in leg ulcer treatment in the region, an interdisciplinary reference group has been established with members from different clinics at the hospital and members from the primary health care.
Cost of Illness↗
Hemodilution significantly decreases tolerance to isoflurane-induced cardiovascular depression.
BACKGROUND: Hemodilution is used to reduce the need for allogenic blood transfusion. The aim of this study was to evaluate to what extent acute extreme normovolemic hemodilution affects the circulatory response to isoflurane. METHODS: Ten midazolam-fentanyl-pancuronium anesthetized pigs were exposed to isoflurane at end-tidal concentrations of 0, 0.5, 1.0, 1.5 and 2%, before and after extreme normovolemic hemodilution (hematocrit 33 +/- 3% and 11 +/- 1%, respectively). Systemic and myocardial hemodynamics and oxygen delivery and consumption were measured. RESULTS: At zero end-tidal isoflurane concentration, hemodilution caused an increase in cardiac output (from 157 +/- 12 to 227 +/- 39 ml kg min-1, P < 0.01) a decrease in systemic vascular resistance (from 39 +/- 7 to 18 +/- 5 mmHg.L-1.min-1, P < 0.01) a decrease in mean arterial blood pressure (MAP) (from 130 +/- 13 to 91 +/- 13 mmHg, P < 0.01) and a decrease in systemic oxygen delivery (from 23.1 +/- 2.7 to 11.8 +/- 1.7 ml.kg-1.min-1, P < 0.01). When the end-tidal isoflurane concentration was increased from 0 to 2% after hemodilution, cardiac output decreased by 86 +/- 37 ml.kg-1.min-1, as compared with 36 +/- 20 ml.kg-1.min-1 (P < 0.01) before hemodilution. Likewise, systemic vascular resistance decreased with increasing isoflurane concentrations; at 2%, the decrease was 7 +/- 4 mmHg.L-1.min-1 after hemodilution and 18 +/- 5 mmHg.L-1.min-1 before hemodilution (P < 0.01). At an end-tidal isoflurane concentration of 2%, MAP had decreased to 43 +/- 6 mmHg after hemodilution, and to 61 +/- 15 mmHg before hemodilution (P < 0.01). After hemodilution, isoflurane concentrations above 1% decreased systemic oxygen delivery enough to cause delivery-dependent oxygen consumption and hyperlactemia; and at 2% isoflurane, myocardial blood flow became insufficient, as indicated by myocardial lactate production. CONCLUSIONS: isoflurane-induced cardiovascular depression had adverse effects on cardiac output and oxygen delivery during extreme hemodilution because: 1) The vasodilatory effect of isoflurane was insufficient to compensate for the myocardial depression, and also contributed to a critically low arterial blood pressure; 2) A decrease in cardiac output produced delivery-dependent oxygen consumption and hyperlactemia; and 3) A decrease in myocardial blood flow caused myocardial ischemia which may have exacerbated the myocardial depression.
Anesthesia↗
Vitamin A exerts potential therapeutic effects in the endotoxaemic pig.
BACKGROUND: Pretreatment with an injection of vitamin A has beneficial effects on cardiac and pulmonary functions in normally bred endotoxaemic pigs. The present study was performed in order to elucidate whether the response of an ongoing infusion of E. coli can be modulated by a single injection of vitamin A. METHODS: Sixteen healthy (not vitamin A-depleted) pigs were anaesthetized, monitored, mechanically ventilated and subjected to an infusion of E. coli endotoxin (10 micrograms.kg-1.h-1). This infusion resulted within 30 min in a progressive haemodynamic derangement. When the mean pressure in the pulmonary artery was twice the baseline value, vitamin A (460 IU.kg-1) or a corresponding volume of vehicle was injected intravenously. After sacrificing the animals, the right lung was excised and weighed, and biopsy specimens were taken from the left lung for microscopical examination. RESULTS: Mean arterial blood pressure was significantly less affected (P < 0.01) between the 1st and 6th hour in endotoxaemic pigs treated with vitamin A than in those given vehicle. The mean lung weight in the vitamin A-treated pigs was significantly lower than that in the vehicle group (164 +/- 5.3 vs 199 +/- 19.8 g; P < 0.01). Microscopical examination showed significantly less oedema (0.93 +/- 0.17 vs 2.00 +/- 0.26; P < 0.01) and microatelectasis (0.56 +/- 0.17 vs 1.75 +/- 0.31; P < 0.01) in the vitamin A group. Endotoxaemia was also accompanied by an initial, steep decline in neutrophil counts in all animals; this decrease was significantly less pronounced (P < 0.05) in vitamin A-injected pigs than in the vehicle-injected group. The major difference was a more rapid restitution in the vitamin A group. CONCLUSION: Several manifestations of endotoxaemia were expressed less in the vitamin A group. Thus, vitamin A may turn out to be a tool in the management of endotoxaemia.
Animals↗
Nitrous oxide reduces inspired oxygen fraction but does not compromise circulation and oxygenation during hemodilution in pigs.
BACKGROUND: The use of nitrous oxide (N2O) during hemodilution has been questioned. Nitrous oxide reduces the inspired oxygen fraction (F1O2), depresses myocardial function and may reduce cardiac output (CO) and systemic oxygen delivery (DO2SY). The aim of this study was to evaluate the importance of the effects of nitrous oxide on systemic and myocardial circulation and oxygenation during extreme, acute, normovolemic hemodilution. METHODS: Ten midazolam-fentanyl-pancuronium anesthetized pigs were exposed to 65% N2O before and after extreme isovolemic hemodilution (hematocrit 33 +/- 1% and 10 +/- 1%, respectively). Systemic and myocardial hemodynamics, oxygen delivery and consumption and blood lactate were measured before (at F1O2 1.0 and 0.35) and during N2O exposure. RESULTS: Hemodilution caused an increase in CO from 137 +/- 43 to 229 +/- 32 ml.kg-1.min-1 (P < 0.01), a decrease in systemic vascular resistance (from 42 +/- 14 to 20 +/- 4 mmHg.L-1.min-1, P < 0.05), a decrease in mean arterial blood pressure (from 119 +/- 19 to 100 +/- 26 mmHg, P < 0.05) and a decrease in DO2SY from 21.1 +/- 6.9 to 13.7 +/- 2.1 ml.kg-1.min-1 (P < 0.01). Cardiac venous blood flow increased by 135% (P < 0.01) and cardiac venous saturation from 25 +/- 6 to 41 +/- 5% (P < 0.05). After hemodilution, changing F1O2 from 1.0 to 0.35 reduced arterial blood oxygen content from 59.4 +/- 3.7 to 52.3 +/- 5.1 ml.L-1 (P < 0.01), mixed venous saturation (SvO2) from 75 +/- 9 to 47 +/- 7% (P < 0.05) and DO2SY from 13.7 +/- 2.1 to 11.9 +/- 2.3 ml.kg-1.min-1 (P < 0.05). Dissolved oxygen at F1O2 = 1.0 and F1O2 = 0.35 constituted 25.4 +/- 3.1% and 10.1 +/- 1.5%, respectively, of systemic oxygen delivery after hemodilution, compared with 10.7 +/- 1.2% and 3.9 +/- 0.5% before hemodilution (P < 0.01). Left ventricular oxygen delivery and consumption were unchanged. Exposure to N2O did not affect mean arterial blood pressure or systemic vascular resistance before or after hemodilution. After hemodilution during N2O-exposure, CO and DO2SY decreased by 9% (P < 0.01 and P < 0.05, respectively), but no changes in SvO2, systemic oxygen uptake or arterial lactate were observed. The effect of N2O on myocardial oxygenation was similar before and after hemodilution; cardiac venous blood flow, left ventricular oxygen delivery and uptake decreased, but no animals showed left ventricular lactate production. CONCLUSION: Nitrous oxide did not compromise systemic and myocardial circulation and oxygenation during acute normovolemic hemodilution in pigs. Possible adverse effects from the use of nitrous oxide during hemodilution seem to be related to a reduced F1O2, reducing the safety margin for systemic oxygen delivery.
Animals↗
Routine oxytocin in the third stage of labour: a placebo controlled randomised trial.
OBJECTIVE: To compare intravenous oxytocin administration (Partocon 10 IU) with saline solution in the management of postpartum haemorrhage in the third stage of labour. DESIGN: A double-blind, randomised controlled trial involving 1000 parturients with singleton fetuses in cephalic presentation and undergoing vaginal delivery, randomly allocated to treatment with oxytocin (n = 513) or 0.9% saline solution (n = 487). SETTING: Labour ward at a central county hospital. MAIN OUTCOME MEASURES: Mean blood loss (total, and before and after placenta delivery); frequencies of blood loss > 800 mL, need of additional oxytocic treatment, postpartum haemoglobin < 10 g/dL; and duration of postpartum hospitalisation. RESULTS: As compared with saline solution, oxytocin administration was associated with significant reduction in mean total blood loss (407 versus 527 mL), and in frequencies of postpartum haemorrhage > 800 mL (8.8% versus 5.2%), additional treatment with metylergometrine (7.8% versus 13.8%), and postpartum Hb < 10 g/dL (9.7% versus 15.2%), and a nonsignificant increase in the frequency of manual placenta removal (3.5% versus 2.3%). There was no group difference in the mean duration of postpartum hospitalisation (4.6 versus 4.5 days, respectively). CONCLUSIONS: Administration of intravenous oxytocin in the third stage of labour is associated with an approximately 22% reduction in mean blood loss, and approximately 40% reductions in frequencies of postpartum haemorrhage (> 500 mL or > 800 mL) and of postpartum haemoglobin < 10 g/dL. Identification of risk groups for oxytocin treatment does not seem worthwhile. Oxytocin is a cheap atoxic drug and should be given routinely after vaginal delivery.
Adult↗