Relevant bibliographies by topics / Asphyxia, therapy

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Academic literature on the topic 'Asphyxia, therapy'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Asphyxia, therapy"

1

Gathwala, Geeta, Atul Khera, and Ishwar Singh. "Magnesium therapy in birth asphyxia." Indian Journal of Pediatrics 73, no. 3 (March 2006): 209–12. http://dx.doi.org/10.1007/bf02825482.

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Dang, Xiaoping, Xiaojian Hu, Yuancui Meng, Yan’e Yang, Lingfang Zheng, Qiong Zhang, Nan Dang, Jing Hao, Liang Zheng, and Feng Ni. "The Diagnostic Value of Cystatin C and Mild Hypothermia Therapy Based on Immunoturbidimetry Enhanced by Nanospheres in Asphyxia Neonate." Journal of Chemistry 2020 (December 10, 2020): 1–10. http://dx.doi.org/10.1155/2020/1549795.

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In order to evaluate the early diagnosis value of CysC and the influence of mild hypothermia on the renal damage of asphyxia neonates, the serum cystatin C (CysC) levels of asphyxia neonates and normal neonates were measured by the nanomicrosphere-enhanced immunoturbidimetric method. The treatment was carried out, and the influence of mild hypothermia treatment on the renal damage of asphyxia neonates was analyzed. The results showed that the indicators of the asphyxia group were significantly higher than those of the control group, and the severe asphyxia group was significantly higher than that of the mild asphyxia group, which was statistically significant p < 0.05 ; the heart rate of patients in the mild hypothermia treatment group decreased gradually with the decrease in body temperature. And compared with the control group, there was a significant difference ( p < 0.05 ); after symptomatic treatment, the two groups of ALT, AST, BUN, and SCR were improved to varying degrees, and the difference was statistically significant compared with before treatment ( p < 0.05 ). Studies have shown that serum CysC level can be used as an indicator to detect glomerular filtration function and early asphyxia newborns, and it is sensitive and specific for early diagnosis of kidney damage. At the same time, it can be used to monitor clinical renal function and determine the status of asphyxia newborns.
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Ford, Lisa M. "Results of antagonists in perinatal cerebral asphyxia therapy." Pediatric Neurology 6, no. 6 (November 1990): 363–66. http://dx.doi.org/10.1016/0887-8994(90)90001-h.

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Lear, Christopher A., Joanne O. Davidson, Georgia R. Mackay, Paul P. Drury, Robert Galinsky, Josine S. Quaedackers, Alistair J. Gunn, and Laura Bennet. "Antenatal dexamethasone before asphyxia promotes cystic neural injury in preterm fetal sheep by inducing hyperglycemia." Journal of Cerebral Blood Flow & Metabolism 38, no. 4 (April 7, 2017): 706–18. http://dx.doi.org/10.1177/0271678x17703124.

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Antenatal glucocorticoid therapy significantly improves the short-term systemic outcomes of prematurely born infants, but there is limited information available on their impact on neurodevelopmental outcomes in at-risk preterm babies exposed to perinatal asphyxia. Preterm fetal sheep (0.7 of gestation) were exposed to a maternal injection of 12 mg dexamethasone or saline followed 4 h later by asphyxia induced by 25 min of complete umbilical cord occlusion. In a subsequent study, fetuses received titrated glucose infusions followed 4 h later by asphyxia to examine the hypothesis that hyperglycemia mediated the effects of dexamethasone. Post-mortems were performed 7 days after asphyxia for cerebral histology. Maternal dexamethasone before asphyxia was associated with severe, cystic brain injury compared to diffuse injury after saline injection, with increased numbers of seizures, worse recovery of brain activity, and increased arterial glucose levels before, during, and after asphyxia. Glucose infusions before asphyxia replicated these adverse outcomes, with a strong correlation between greater increases in glucose before asphyxia and greater neural injury. These findings strongly suggest that dexamethasone exposure and hyperglycemia can transform diffuse injury into cystic brain injury after asphyxia in preterm fetal sheep.
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Kántor, Tibor, Bianca Grigorescu, Gabriel Popescu, Attila Ferencz, Örs Nagy, János Jung, and István Gergely. "Traumás asphyxia maradandó látásvesztéssel." Orvosi Hetilap 158, no. 22 (June 2017): 864–68. http://dx.doi.org/10.1556/650.2017.30750.

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Abstract: Traumatic asphyxia is a rare condition that occurs after compressive thoracoabdominal trauma, which is characterized by subconjunctival hemorrhage, cervicofacial cyanosis, edema and petechiae. Serious life-threatening thoracic and abdominal injuries may coexist. After conservatory treatment in most cases complete recovery is achieved, but in isolated cases permanent neurological lesions may occur. We present the case of the 39-year-old male patient who suffered a compressive thoracoabdominal trauma. The physical examination showed the characteristic “ecchymotic mask”. After surgical treatment of the abdominal injuries and intensive therapy the patient was discharged with permanent vision loss. The high retrograde venous pressure in the head and neck may be associated with neuronal ischemia, which can lead to irreversible optic nerve atrophy. It is therefore important to carry out an early, routine and complete ophtalmologic examination, especially in the intubated and poorly cooperative patients. Orv Hetil. 2017; 158(22): 864–868.
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Loboda, A. M., O. I. Smiyan, S. V. Popov, V. O. Petrashenko, and D. A. Loboda. "PECULIARITIES OF ELECTROLYTIC BALANCE IN THE BLOOD OF NEWBORNS WITH KIDNEY DAMAGE DUE TO ASPHYXIA." Eastern Ukrainian Medical Journal 7, no. 4 (2019): 341–50. http://dx.doi.org/10.21272/eumj.2019;7(4):341-350.

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Introduction. The study of the concentration of main electrolytes in serum of blood and erythrocytes in neonates with impaired renal function due to asphyxia is important, because it allows determining violations of their content and balance, tactics of infusion and diuretic therapy. The purpose of the work is explore the features of the content and balance of electrolytes (sodium, potassium, calcium, magnesium) in serum and red blood cells of newborns with disturbance kidney function due to asphyxia. Materials and methods. The study involved 200 term infants with signs of disturbance kidney function: 100 children who have suffered severe asphyxia, 100 children – with moderate asphyxia. Comparison group consisted of 20 infants without asphyxia at birth. The content of electrolytes determined by emission photometry, also expected ratios in pairs Na/K and Ca/Mg and transmembrane ratio of trace elements. Results and discussion. The critical period of formation electrolyte imbalances in neonates with impaired renal function due to moderate asphyxia is the early neonatal period, in case of severe asphyxia – all neonatal period. The feature of ischemic renal impairment in newborns is the development of serum hypernatremia and hyperkalemia, hypocalcemia and hypomagnesemia, decrease the ratio of Na/K and increase Ca/Mg. Red blood cell pool of macroelements in case of neonatorum ischemic nephropathy is characterized by the growth of sodium level and deficiency of potassium, calcium and magnesium, as well as growth transmineralisation Na/K ratio and decrease Ca/Mg. Growth transmembrane ratios relative to sodium and magnesium reflects their transport into the cell, and reducing ratios relative potassium and calcium indicates the predominance of these electrolyte transport in the extracellular fluid. Changes in serum and intracellular electrolyte content and balance must be considered during infusion therapy in infants with impaired renal function due to asphyxia.
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Parfenova, Helena, Massroor Pourcyrous, Alex L. Fedinec, Jianxiong Liu, Shyamali Basuroy, and Charles W. Leffler. "Astrocyte-produced carbon monoxide and the carbon monoxide donor CORM-A1 protect against cerebrovascular dysfunction caused by prolonged neonatal asphyxia." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 4 (October 1, 2018): H978—H988. http://dx.doi.org/10.1152/ajpheart.00140.2018.

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Neonatal asphyxia leads to cerebrovascular disease and neurological complications via a mechanism that may involve oxidative stress. Carbon monoxide (CO) is an antioxidant messenger produced via a heme oxygenase (HO)-catalyzed reaction. Cortical astrocytes are the major cells in the brain that express constitutive HO-2 isoform. We tested the hypothesis that CO, produced by astrocytes, has cerebroprotective properties during neonatal asphyxia. We developed a survival model of prolonged asphyxia in newborn pigs that combines insults of severe hypoxia, hypercapnia, and acidosis while avoiding extreme hypotension and cerebral blood flow reduction. During the 60-min asphyxia, CO production by brain and astrocytes was continuously elevated. Excessive formation of reactive oxygen species during asphyxia/reventilation was potentiated by the HO inhibitor tin protoporphyrin, suggesting that endogenous CO has antioxidant effects. Cerebral vascular outcomes tested 24 and 48 h after asphyxia demonstrated the sustained impairment of cerebral vascular responses to astrocyte- and endothelium-specific vasodilators. Postasphyxia cerebral vascular dysfunction was aggravated in newborn pigs pretreated with tin protoporphyrin to inhibit brain HO/CO. The CO donor CO-releasing molecule-A1 (CORM-A1) reduced brain oxidative stress during asphyxia/reventilation and prevented postasphyxia cerebrovascular dysfunction. The antioxidant and antiapoptotic effects of HO/CO and CORM-A1 were confirmed in primary cultures of astrocytes from the neonatal pig brain exposed to glutamate excitotoxicity. Overall, prolonged neonatal asphyxia leads to neurovascular injury via an oxidative stress-mediated mechanism that is counteracted by an astrocyte-based constitutive antioxidant HO/CO system. We propose that gaseous CO or CO donors can be used as novel approaches for prevention of neonatal brain injury caused by prolonged asphyxia. NEW & NOTEWORTHY Asphyxia in newborn infants may lead to lifelong neurological disabilities. Using the model of prolonged asphyxia in newborn piglets, we propose novel antioxidant therapy based on systemic administration of low doses of a carbon monoxide donor that prevent loss of cerebral blood flow regulation and may improve the neurological outcome of asphyxia.
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Locci, Emanuela, Giovanni Bazzano, Roberto Demontis, Alberto Chighine, Vassilios Fanos, and Ernesto d’Aloja. "Exploring Perinatal Asphyxia by Metabolomics." Metabolites 10, no. 4 (April 4, 2020): 141. http://dx.doi.org/10.3390/metabo10040141.

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Brain damage related to perinatal asphyxia is the second cause of neuro-disability worldwide. Its incidence was estimated in 2010 as 8.5 cases per 1000 live births worldwide, with no further recent improvement even in more industrialized countries. If so, hypoxic-ischemic encephalopathy is still an issue of global health concern. It is thought that a consistent number of cases may be avoided, and its sequelae may be preventable by a prompt and efficient physical and therapeutic treatment. The lack of early, reliable, and specific biomarkers has up to now hampered a more effective use of hypothermia, which represents the only validated therapy for this condition. The urge to unravel the biological modifications underlying perinatal asphyxia and hypoxic-ischemic encephalopathy needs new diagnostic and therapeutic tools. Metabolomics for its own features is a powerful approach that may help for the identification of specific metabolic profiles related to the pathological mechanism and foreseeable outcome. The metabolomic profiles of animal and human infants exposed to perinatal asphyxia or developing hypoxic-ischemic encephalopathy have so far been investigated by means of 1H nuclear magnetic resonance spectroscopy and mass spectrometry coupled with gas or liquid chromatography, leading to the identification of promising metabolomic signatures. In this work, an extensive review of the relevant literature was performed.
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Prakash, Raj, M. R. Savitha, and B. Krishnamurthy. "Neurodevelopmental Outcome at 12 Months of Postnatal Magnesium Sulphate Therapy for Perinatal Asphyxia." Journal of Nepal Paediatric Society 36, no. 3 (April 16, 2017): 256–62. http://dx.doi.org/10.3126/jnps.v36i3.15565.

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Introduction: Postnatal magnesium therapy has been proposed as a novel neuroprotective agent for perinatal asphyxia. A few studies reported short term neurological benefit with magnesium. It is uncertain whether magnesium therapy has any long term effect on neurodevelopment.Material and Methods: We randomly assigned 120 term asphyxiated infants to receive either magnesium sulphate infusion or placebo postnatally in first 48 hours of life. Babies were treated as per the standard treatment protocol for asphyxia. Short term outcome at discharge was previously reported and a follow up evaluation at 12 months was done. The primary outcome was a composite of death or disability, developmental delay and neuromotor tone abnormality at 12 months.Results: Out of 120 infants, 69 infants had moderate-severe hypoxic-ischemic encephalopathy (HIE) during initial NICU stay. Among 69 infants with moderate-severe HIE, 41 infant could be followed up. Out of 41 infants, 22 were in magnesium group and 19 in placebo group. Of 22 infants assigned to magnesium therapy, 3(13.6%) died or survived with neurodevelopmental disability as compared with 5 of 19 infants (26.3%) assigned to placebo (p=0.32). The developmental outcome evaluated found developmental delay in 3 of 22 infants in magnesium group vs 5 of 19 infants in placebo group (p=0.32). Ameil-Tisonneuromotor tone assessment revealed tone abnormality in 3 of 22 infants in study group vs 4 of 19 infants in placebo group (p=0.53).Conclusion: Magnesium therapy for perinatal asphyxia may not result in favourable long term neurodevelopmental outcome, though no significant adverse effect has been documented.J Nepal Paediatr Soc 2016;36(3):256-262
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Manole, Mioara D., Patrick M. Kochanek, Lesley M. Foley, T. Kevin Hitchens, Hülya Bayır, Henry Alexander, Robert Garman, et al. "Polynitroxyl Albumin and Albumin Therapy after Pediatric Asphyxial Cardiac Arrest: Effects on Cerebral Blood Flow and Neurologic Outcome." Journal of Cerebral Blood Flow & Metabolism 32, no. 3 (November 30, 2011): 560–69. http://dx.doi.org/10.1038/jcbfm.2011.165.

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Postresuscitation cerebral blood flow (CBF) disturbances and generation of reactive oxygen species likely contribute to impaired neurologic outcome after pediatric cardiac arrest (CA). Hence, we determined the effects of the antioxidant colloid polynitroxyl albumin (PNA) versus albumin or normal saline (NS) on CBF and neurologic outcome after asphyxial CA in immature rats. We induced asphyxia for 9 minutes in male and female postnatal day 16 to 18 rats randomized to receive PNA, albumin, or NS at resuscitation from CA or sham surgery. Regional CBF was measured serially from 5 to 150 minutes after resuscitation by arterial spin-labeled magnetic resonance imaging. We assessed motor function (beam balance and inclined plane), spatial memory retention (water maze), and hippocampal neuronal survival. Polynitroxyl albumin reduced early hyperemia seen 5 minutes after CA. In contrast, albumin markedly increased and prolonged hyperemia. In the delayed period after resuscitation (90 to 150 minutes), CBF was comparable among groups. Both PNA- and albumin-treated rats performed better in the water maze versus NS after CA. This benefit was observed only in males. Hippocampal neuron survival was similar between injury groups. Treatment of immature rats with PNA or albumin resulted in divergent acute changes in CBF, but both improved spatial memory retention in males after asphyxial CA.
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Dissertations / Theses on the topic "Asphyxia, therapy"

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Power, David John Donovan. "Asphyxia neonatorum in a developing world situation : a study of the impact of asphyxia neonatorum in term infants on the pattern of handicap in the Ciskei; an evalution of its epidemiology and a trial of the efficacy of current therapy." Doctoral thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/27190.

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This study addresses the problem of asphyxia neonatorum in a developing African community in the Mdantsane region of Ciskei. It also documents asphyxia as a prominent cause of childhood handicap, examines aspects of its epidemiology and evaluates the effectiveness of a regimen of phenobarbitone and dexamethasone in limiting subsequent neurological deficit in asphyxiated neonates. Analysis of neonatal deaths at Cecilia Makiwane Hospital over an 18-month period showed that asphyxia accounted for one third of all neonatal deaths. In particular, asphyxia caused two thirds of deaths in infants over 2 Kg birth weight. From a hospital register of handicapped children, 211 had cerebral palsy. Asphyxia was the cause of cerebral palsy in 33% of these children. Spastic quadriplegia, the type of cerebral palsy most often resulting from the cerebral damage associated with asphyxial hypoxic-ischaemic insults, was by far the largest diagnostic category (57%). Asphyxia therefore appears to be the single largest cause of significant handicap in Ciskei. In view of the underdeveloped support services to parents in most developing areas, the problem of asphyxia is of considerable importance. In the study of the epidemiology of asphyxia, details of pregnancy and labour were obtained for 163 asphyxiated term infants and 2758 non- asphyxiated term infants whose mothers had delivered in the hospital. The factors positively associated with asphyxia were: low gravidity and parity, failure to book for antenatal care, the occurrence of antenatal disorders, the occurrence of fetal distress, a prolonged first stage of labour and delivery by caesarean section or vacuum extraction. Maternal age and the actual number of antenatal visits were not associated with asphyxia. The causes of asphyxia assigned by the specialist obstetrician in charge were cephalopelvic disproportion (CPD) (39%), utero-placental pathologies (22%), other (8%), and "unknown" where he could find no abnormality in pregnancy and labour (27%). From these findings it appears that the steps that need to be taken for prevention include: active recruitment of patients to book for antenatal care, more active detection and management of cephalopelvic disproportion and basic research to elucidate the causes of the "unknown" group whom it is speculated have undetected utero-placental pathology.
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Books on the topic "Asphyxia, therapy"

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Sutton, Caitlin D., and Olutoyin A. Olutoye. Anesthesia for Ex Utero Intrapartum Therapy. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0052.

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Fetuses with congenital head and neck anomalies which will result in impaired spontaneous respiration and difficulty in securing the airway after delivery may suffer asphyxia at birth. The ex utero intrapartum therapy (EXIT) offers such affected babies a chance at survival by allowing airway manipulations to occur after partial delivery of the baby, while the baby remains on utero-placental support. This very unique procedure requires extensive planning and multidisciplinary coordination with a multiplicity of specialties including maternal fetal medicine, pediatric surgery, pediatric otolaryngology, pediatric anesthesiology, neonatology, and pediatric cardiology. The preoperative planning takes place several days prior to the procedure and also involves meeting with the family. It is the intricacies of multidisciplinary team that require EXIT procedures to take place in certain highly specialized tertiary care fetal centers.
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Neonatal Neural Rescue: A Clinical Guide. Cambridge University Press, 2013.

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3

Gausche-Hill, Marianne, Guy Haskell, and Mariann M. Manno. Pediatric Advanced Life Support: Pearls of Wisdom (Conforms to the Am Heart Assn Guidelines 2000). Boston Medical Publishing, 2001.

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H, Haskell Guy, and Gausche-Hill Marianne, eds. Pediatric advanced life support: Pearls of wisdom : conforms to the American Heart Association guidelines 2000. Boston: Boston Medical Pub. Corp., 2001.

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Book chapters on the topic "Asphyxia, therapy"

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Wilkins, Pamela A. "Perinatal Asphyxia Syndrome." In Robinson's Current Therapy in Equine Medicine, 732–36. Elsevier, 2015. http://dx.doi.org/10.1016/b978-1-4557-4555-5.00175-8.

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VAALA, W. "Perinatal Asphyxia Syndrome in Foals." In Current Therapy in Equine Medicine, 644–49. Elsevier, 2003. http://dx.doi.org/10.1016/b978-0-7216-9540-2.50182-1.

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Butler, Gary, and Jeremy Kirk. "Hypoglycaemia." In Paediatric Endocrinology and Diabetes, 253–72. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198786337.003.0007.

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• Hypoglycaemia is defined as ‘A plasma glucose concentration low enough to cause symptoms and/or signs of impaired brain function’. • Cut-offs are contentious, ranging from <2.2 to <4.0 mmol/L, and are dependent on age, diagnosis, and also availability/usage of alternative metabolic fuels such as ketones. • May be transient or persistent, dependent on diagnosis. • Causes broadly due to: ◦ decreased glucose including prematurity, inborn errors of metabolism, hypopituitarism, adrenal insufficiency (primary and secondary), and prolonged fasting ◦ increased glucose utilization including infant of diabetic mother, hyperinsulinaemia, perinatal asphyxia, and various syndromes, e.g. Beckwith–Wiedemann. • Endocrine causes of hypoglycaemia include growth hormone deficiency, adrenal insufficiency (primary and secondary), and (?) hypothyroidism. • Metabolic disorders cause hypoglycaemia via impaired: ◦ mobilization of glucose stores ◦ gluconeogenesis ◦ alternative energy sources ◦ liver function. • Hyperinsulinaemic hypoglycaemia presents with increased glucose requirements (>8 mg/kg/minute) and non-ketotic hypoglycaemia. Diagnosis confirmed by demonstrating raised/detectable insulin/C-peptide during hypoglycaemia. Genotyping may assist with not only diagnosis but direct therapy (medical and surgical).
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Fadeeva, Tat'iana Sergeevna. "Connective tissue dysplasia: new horizons of the problem." In Дисплазия соединительной ткани: новые горизонты проблемы. Publishing house Sreda, 2019. http://dx.doi.org/10.31483/r-22132.

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The work raises questions of predicting the complications of pregnancy and childbirth and adverse conditions in the fetus in the presence of UCTD in the expectant mother, who also need to be studied, especially from the standpoint of mathematical modeling of the disease. It is also necessary to develop a common tactic for providing medical and social assistance and treatment and diagnostic services to pregnant women suffering from UCTD, which will make the outcome of childbirth more favorable and improve the subsequent prognosis for mother and newborn. In the literature there is practically no assessment of the course of pregnancy and the outcome of childbirth, depending on the severity of UCTD. Little is known about the role of a connective tissue metabolism marker - hydroxyproline, trace elements (magnesium) and vitamins (D3) in pregnant women suffering from UCTD, and the medical tactics regarding such patients are not clearly defined. Despite numerous successes in the study of the causes of complications during pregnancy and childbirth in women suffering from UCTD, a unified approach to their management during the prenatal stage has not yet been developed. Therefore, the search for possible predictors for the timely prediction of adverse pregnancy and childbirth outcome in such patients is becoming increasingly important. This will make it possible to develop an optimal organizational and methodological base and subsequently improve the prognosis for women and their offspring. Thus, in contrast to the existing standard approach, we have proposed a comprehensive management of patients suffering from UCTD, including the timely identification of patients from the risk group, clarification of their condition using such markers as magnesium and hydroxyproline, additional intake of magnesium and vitamin D preparations. Optimal plan managing the period of gestation, childbirth, and a pathogenetically reasoned set of treatment and preventive measures for women with UCTD, will not only improve the outcomes of pregnancy and childbirth, but also contribute to the health of the future generation. 1. UCTD affects the course of pregnancy, childbirth and the condition of the newborn. The degree of exposure is largely determined by the severity of the underlying disease. In severe UCTD, the prevalence of spontaneous miscarriage and preterm labor was significantly higher, and endometritis and severe anemia were more common in the postpartum period. Severe asphyxia on the Apgar scale at the 1st and 5th minutes, congenital heart defects, morphofunctional immaturity, conjugation jaundice and convulsive syndrome were more common in the fetus. 2. A low content of magnesium and hydroxyproline is associated with the occurrence of complications during childbirth and a decrease in the anthropometric characteristics of the newborn. Taking magnesium preparations reliably affects the concentration of this trace element and hydroxyproline in the blood of pregnant women suffering from UCTD. 3. Therapy with magnesium preparations is an effective tool in patients suffering from UCTD, as it helps to improve well-being during pregnancy, improves the course of the postpartum period and reduces the prevalence of chronic fetal hypoxia. 4. Vitamin D and magnesium supplements have a beneficial effect on pregnancy and the fetus, reducing the prevalence of pre-eclampsia and chronic intrauterine hypoxia of the fetus, reducing the incidence of morphofunctional immaturity and conjugation jaundice of the newborn. 5. The created computer program “STEP DST” can be applied in the clinical practice of obstetrician-gynecologists and health care organizers. The obtained individual forecast of the probability of development of complications of reproduction allows us to outline the optimal plan for managing the period of gestation, childbirth and the postpartum period, to prescribe a pathogenetically based set of therapeutic and preventive measures for women suffering from UCTD.
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Reports on the topic "Asphyxia, therapy"

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Thompson, Andrew, Justin Williams, Vikhyat Bebarta, Bryan Jordan, Doug Alfar, Chris Hanson, Andiry Batchinsky, Stephen Paulson, and John McManus. Does Glucagon Improve Survival in a Porcine (Sus Scrofa) of Adult Asphyxial Cardiac Arrest in Addition to Standard Epinephrine Therapy? Fort Belvoir, VA: Defense Technical Information Center, January 2012. http://dx.doi.org/10.21236/ada554968.

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