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Neurocritical Care Dec 2012Drowning is a leading cause of accidental death. Survivors may sustain severe neurologic morbidity. There is negligible research specific to brain injury in drowning... (Review)
Review
Drowning is a leading cause of accidental death. Survivors may sustain severe neurologic morbidity. There is negligible research specific to brain injury in drowning making current clinical management non-specific to this disorder. This review represents an evidence-based consensus effort to provide recommendations for management and investigation of the drowning victim. Epidemiology, brain-oriented prehospital and intensive care, therapeutic hypothermia, neuroimaging/monitoring, biomarkers, and neuroresuscitative pharmacology are addressed. When cardiac arrest is present, chest compressions with rescue breathing are recommended due to the asphyxial insult. In the comatose patient with restoration of spontaneous circulation, hypoxemia and hyperoxemia should be avoided, hyperthermia treated, and induced hypothermia (32-34 °C) considered. Arterial hypotension/hypertension should be recognized and treated. Prevent hypoglycemia and treat hyperglycemia. Treat clinical seizures and consider treating non-convulsive status epilepticus. Serial neurologic examinations should be provided. Brain imaging and serial biomarker measurement may aid prognostication. Continuous electroencephalography and N20 somatosensory evoked potential monitoring may be considered. Serial biomarker measurement (e.g., neuron specific enolase) may aid prognostication. There is insufficient evidence to recommend use of any specific brain-oriented neuroresuscitative pharmacologic therapy other than that required to restore and maintain normal physiology. Following initial stabilization, victims should be transferred to centers with expertise in age-specific post-resuscitation neurocritical care. Care should be documented, reviewed, and quality improvement assessment performed. Preclinical research should focus on models of asphyxial cardiac arrest. Clinical research should focus on improved cardiopulmonary resuscitation, re-oxygenation/reperfusion strategies, therapeutic hypothermia, neuroprotection, neurorehabilitation, and consideration of drowning in advances made in treatment of other central nervous system disorders.
Topics: Asphyxia; Critical Care; Emergency Medical Services; Heart Arrest; Humans; Near Drowning; Resuscitation
PubMed: 22956050
DOI: 10.1007/s12028-012-9747-4 -
The Journal of Physiology Mar 2017Premature fetuses and babies are at greater risk of mortality and morbidity than their term counterparts. The underlying causes are multifactorial, but include exposure... (Review)
Review
Premature fetuses and babies are at greater risk of mortality and morbidity than their term counterparts. The underlying causes are multifactorial, but include exposure to hypoxia. Immaturity of organs and their functional control may impair the physiological defence responses to hypoxia and the preterm fetal responses, or lack thereof, to moderate hypoxia appear to support this concept. However, as this review demonstrates, despite immaturity, the preterm fetus responds to asphyxia in a qualitatively similar manner to that seen at term. This highlights the importance in understanding metabolism versus homeostatic threat when assessing fetal responses to adverse challenges such as hypoxia. Data are presented to show that the preterm fetal adaptation to asphyxia is triphasic in nature. Phase one represents the rapid institution of maximal defences, designed to maintain blood pressure and central perfusion at the expense of peripheral organs. Phase two is one of adaptive compensation. Controlled reperfusion partially offsets peripheral tissue oxygen debt, while maintaining sufficient vasoconstriction to limit the fall in perfusion. Phase three is about decompensation. Strikingly, the preterm fetus generally performs better during phases two and three, and can survive for longer without injury. Paradoxically, however, the ability to survive can lead to longer exposure to hypotension and hypoperfusion and thus potentially greater injury. The effects of fetal sex, inflammation and drugs on the triphasic adaptations are reviewed. Finally, the review highlights the need for more comprehensive studies to understand the complexity of perinatal physiology if we are to develop effective strategies to improve preterm outcomes.
Topics: Adaptation, Physiological; Animals; Anti-Inflammatory Agents; Asphyxia; Fetal Hypoxia; Fetus; Glucocorticoids; Homeostasis; Humans; Infant, Newborn; Infant, Premature
PubMed: 28094441
DOI: 10.1113/JP272999 -
American Journal of Physiology.... Aug 2018Magnesium sulfate (MgSO) is recommended for preterm neuroprotection, preeclampsia, and preterm labor prophylaxis. There is an important, unmet need to carefully test... (Comparative Study)
Comparative Study
Magnesium sulfate (MgSO) is recommended for preterm neuroprotection, preeclampsia, and preterm labor prophylaxis. There is an important, unmet need to carefully test clinical interventions in both sexes. Therefore, we aimed to investigate cardiovascular and neurophysiological adaptations to MgSO during normoxia and asphyxia in preterm male and female fetal sheep. Fetuses were instrumented at 98 ± 1 days of gestation (term = 147 days). At 104 days, unanesthetized fetuses were randomly assigned to intravenous MgSO ( n = 12 female, 10 male) or saline ( n = 13 female, 10 male). At 105 days fetuses underwent umbilical cord occlusion for up to 25 min. Occlusions were stopped early if mean arterial blood pressure (MAP) fell below 8 mmHg or asystole occurred for >20 s. During normoxia, MgSO was associated with similar reductions in fetal heart rate (FHR), EEG power, and movement in both sexes ( P < 0.05 vs. saline controls) and suppression of α- and β-spectral band power in males ( P < 0.05 vs. saline controls). During occlusion, similar FHR and MAP responses occurred in MgSO-treated males and females compared with saline controls. Recovery of FHR and MAP after release of occlusion was more prolonged in MgSO-treated males ( P < 0.05 vs. saline controls). During and after occlusion, EEG power was lower in MgSO-treated females ( P < 0.05 vs. saline controls). In conclusion, MgSO infusion was associated with subtle sex-specific effects on EEG spectral power and cardiac responses to asphyxia in utero, possibly reflecting sex-specific differences in interneuronal connectivity and regulation of cardiac output.
Topics: Adaptation, Physiological; Animals; Arterial Pressure; Asphyxia; Brain; Brain Waves; Cardiovascular System; Disease Models, Animal; Electroencephalography; Female; Fetal Movement; Gestational Age; Heart Rate, Fetal; Hemodynamics; Magnesium Sulfate; Male; Neuroprotective Agents; Prenatal Diagnosis; Sex Factors; Sheep, Domestic
PubMed: 29561649
DOI: 10.1152/ajpregu.00390.2017 -
AJNR. American Journal of Neuroradiology 1992To determine the CT and MR characteristics of the brains of infants who have suffered profound asphyxia and correlate those characteristics with pathophysiologic...
PURPOSE
To determine the CT and MR characteristics of the brains of infants who have suffered profound asphyxia and correlate those characteristics with pathophysiologic processes.
METHODS
MR and CT scans of 16 patients who suffered profound hypoxic-ischemic injury in the perinatal (12 patients) and postnatal (4 patients) periods were retrospectively reviewed in a search for characteristic imaging features.
RESULTS
Injury in the perinatal period: subacute MR showed short T1 and T2 in the ventral lateral thalami, posterolateral lentiform nuclei, posterior mesencephali, and hippocampi; MR 1 to 16 years after injury showed atrophy or T2 prolongation in the aforementioned regions, the lateral geniculate nuclei and perirolandic cerebral cortex. Asphyxia later in infancy: subacute MR showed T2 prolongation in the corpus striatum and most of the cerebral cortex (perirolandic sparing); MR weeks to months later showed atrophy of the aforementioned areas, the lateral geniculate nuclei and hippocampi. Acute CT in both groups showed basal ganglia hypodensity.
CONCLUSIONS
The injury patterns observed in neonates and infants with profound hypoxic-ischemic injury vary with the age of the patient at the time of the injury. The change in pattern of damage is suggested to be the result of structural and physiologic changes in the maturing brain. The patterns appear to be consistent and are well demonstrated by MR.
Topics: Adolescent; Age Factors; Asphyxia; Asphyxia Neonatorum; Child; Child, Preschool; Follow-Up Studies; Humans; Infant; Infant, Newborn; Magnetic Resonance Imaging; Retrospective Studies; Tomography, X-Ray Computed
PubMed: 1590198
DOI: No ID Found -
British Medical Journal May 1979
Topics: Asphyxia; Bedding and Linens; Epilepsy, Tonic-Clonic; Humans
PubMed: 109162
DOI: 10.1136/bmj.1.6172.1218 -
American Family Physician Aug 2021
Topics: Asphyxia; Deglutition Disorders; Humans
PubMed: 34383454
DOI: No ID Found -
Tijdschrift Voor Psychiatrie 2007Asphyxia is one of the most serious types of antipsychotic-induced extrapyramidal symptoms. (Review)
Review
BACKGROUND
Asphyxia is one of the most serious types of antipsychotic-induced extrapyramidal symptoms.
AIM
To study the prevalence, course, diagnostics and treatment of asphyxia and dysphagia caused by the use of antipsychotics.
METHOD
The relevant literature was retrieved via Medline (1960-2005), using combinations of the (mesh) terms 'antipsychotic agents', 'dystonia', 'parkinson disease', 'secondary', 'dyskinesias', 'drug-induced', 'asphyxia' and the key words 'dysphagia' en 'respiratory'.
RESULTS
Asphyxia caused by the use of antipsychotics can occur because of spasms of the respiratory muscles or because of an increased risk of choking (dysphagia). These phenomena can occur shortly after patients have started to take antipsychotics, for some time or even for a long time after. Patients who choke frequently or take rapid, irregular breaths interspersed with groans or sighs need to be observed closely. Risk factors are high doses of and long-term use of antipsychotics. Clinical examination of the gag reflex and the respiration contributes very little to an unequivocal diagnosis of swallowing disorders. However, swallowing disorders can be identified reliably by means of videofluoroscopy. Treatment that involves an adjustment of a patient's medication can often be effective.
CONCLUSION
Timely recognition of asphyxia is vital for the prevention of a life-threatening complication arising from the use of antipsychotics.
Topics: Airway Obstruction; Antipsychotic Agents; Asphyxia; Deglutition Disorders; Dyskinesia, Drug-Induced; Humans; Prevalence; Risk Factors
PubMed: 17929227
DOI: No ID Found -
Archives of Disease in Childhood Dec 1994Infants and young children may be exposed to a variety of dangerous situations when left sleeping in cots, chairs, or beds. A review of 30 cases of accidental asphyxia...
Infants and young children may be exposed to a variety of dangerous situations when left sleeping in cots, chairs, or beds. A review of 30 cases of accidental asphyxia occurring in infants and young children who had been left to sleep unattended was undertaken from the necropsy and consultation files of the Adelaide Children's Hospital. Causes of death included hanging from loose restrainers, clothing, or a curtain cord (12 cases), positional asphyxia/wedging from slipping between a mattress and bed/cot sides or wall, or from moving into a position where the face was covered and the upper airway occluded (16 cases), and suffocation from plastic bed covers (two cases). Cases of co-sleeping in bed with an adult and of non-accidental asphyxia were not included in this review. As the pathological findings were on occasion identical to those that are typically found in sudden infant death syndrome, adequate death scene examination was vital in several cases to allow identification of lethal sleeping environments and to enable steps to be taken to minimise the risk of future deaths due to similar situations. For example, two cases in which infants asphyxiated in rocking cradles led to the investigation of the cradles and to formulation of specific safety recommendations regarding the angle of tilt. Two infants who died after becoming wedged between the back of a couch and a co-sleeping parent in one case and cushions in the other, would indicate that this also represents a potentially lethal sleeping position. Other dangerous situations involved infant car seat restraints, seats with loose harnesses, cots with movable sides or projecting pieces, thin plastic mattress/pillow coverings, and beds with spaces between the mattress and cot side or wall. Lack of supervision at the time of death was a feature of each case.
Topics: Accidents, Home; Asphyxia; Cause of Death; Child, Preschool; Death, Sudden; Female; Humans; Infant; Infant Equipment; Male; Posture; Sleep; South Australia
PubMed: 7726607
DOI: 10.1136/adc.71.6.497 -
Apoptosis : An International Journal on... Oct 2020Each year, 1 million children die due to perinatal asphyxia; however, there are no effective drugs to protect the neonatal brain against hypoxic/ischemic damage. In...
Each year, 1 million children die due to perinatal asphyxia; however, there are no effective drugs to protect the neonatal brain against hypoxic/ischemic damage. In this study, we demonstrated for the first time the neuroprotective capacity of 3,3'-diindolylmethane (DIM) in an in vivo model of rat perinatal asphyxia, which has translational value and corresponds to hypoxic/ischemic episodes in human newborns. Posttreatment with DIM restored the weight of the ipsilateral hemisphere and normalized cell number in the brain structures of rats exposed to perinatal asphyxia. DIM also downregulated the mRNA expression of HIF1A-regulated Bnip3 and Hif1a which is a hypoxic marker, and the expression of miR-181b which is an indicator of perinatal asphyxia. In addition, DIM inhibited apoptosis and oxidative stress accompanying perinatal asphyxia through: downregulation of FAS, CASP-3, CAPN1, GPx3 and SOD-1, attenuation of caspase-9 activity, and upregulation of anti-apoptotic Bcl2 mRNA. The protective effects of DIM were accompanied by the inhibition of the AhR and NMDA signaling pathways, as indicated by the reduced expression levels of AhR, ARNT, CYP1A1, GluN1 and GluN2B, which was correlated with enhanced global DNA methylation and the methylation of the Ahr and Grin2b genes. Because our study provided evidence that in rat brain undergoing perinatal asphyxia, DIM predominantly targets AhR and NMDA, we postulate that compounds that possess the ability to inhibit their signaling are promising therapeutic tools to prevent stroke.
Topics: Animals; Animals, Newborn; Apoptosis; Asphyxia; Brain; DNA Methylation; Hippocampus; Humans; Hypoxia-Inducible Factor 1, alpha Subunit; Indoles; Infant, Newborn; Male; Membrane Proteins; MicroRNAs; Mitochondrial Proteins; N-Methylaspartate; Neuroprotective Agents; Oxidative Stress; Rats; Receptors, Aryl Hydrocarbon; Receptors, N-Methyl-D-Aspartate
PubMed: 32816128
DOI: 10.1007/s10495-020-01631-3 -
Molecular Neurobiology May 2018Perinatal asphyxia results from the action of different risk factors like complications during pregnancy, preterm delivery, or long and difficult labor. Nowadays, it is... (Review)
Review
Perinatal asphyxia results from the action of different risk factors like complications during pregnancy, preterm delivery, or long and difficult labor. Nowadays, it is still the leading cause of neonatal brain injury known as hypoxic-ischemic encephalopathy (HIE) and resulting neurological disorders. A temporal limitation of oxygen, glucose, and trophic factors supply results in alteration of neural cell differentiation and functioning and/or leads to their death. Among the affected cells are oligodendrocytes, responsible for myelinating the central nervous system (CNS) and formation of white matter. Therefore, one of the major consequences of the experienced HIE is leukodystrophic diseases resulting from oligodendrocyte deficiency or malfunctioning. The therapeutic strategies applied after perinatal asphyxia are aimed at reducing brain damage and promoting the endogenous neuroreparative mechanisms. In this review, we focus on the biology of oligodendrocytes and discuss present clinical treatments in the context of their efficiency in preserving white matter structure and preventing cognitive and behavioral deficits after perinatal asphyxia.
Topics: Animals; Asphyxia; Cell Transplantation; Humans; Leukoencephalopathies; Myelin Sheath; Nerve Regeneration; Oligodendroglia
PubMed: 28660484
DOI: 10.1007/s12035-017-0647-7