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Objective Methods Results Significance Sudden unexpected death in epilepsy (SUDEP) results in more years of potential life lost than any neurological condition with the exception of stroke. It is generally agreed that SUDEP happens due to some form of respiratory, cardiac, and electrocerebral dysfunction following a seizure; however, the mechanistic cause of these perturbations is unclear. One possible explanation lies with adenosinergic signaling. Extracellular levels of the inhibitory neuromodulator adenosine rapidly rise during seizures, a countermeasure that is necessary for seizure termination. Previous evidence has suggested that excessive adenosinergic inhibition could increase the risk of SUDEP by silencing brain areas necessary for life, such as the respiratory nuclei of the brainstem. The goal of this investigation was to further clarify the role of adenosine in seizure‐induced respiratory and electrocerebral dysfunction.To determine the role of adenosine in postictal physiological dysregulation, we pharmacologically manipulated adenosine signaling prior to amygdala‐kindled seizures in mice while recording electroencephalogram (EEG), electromyogram, and breathing using whole body plethysmography. The adenosinergic drugs used in this study included selective and nonselective adenosine receptor antagonists and inhibitors of adenosine metabolism.We found that high doses of adenosine receptor antagonists caused some seizures to result in seizure‐induced death; however, counterintuitively, animals in these conditions that did not experience seizure‐induced death had little or no postictal generalized EEG suppression. Inhibitors of adenosine metabolism had no effect on postictal breathing but did worsen some postictal electrocerebral outcomes.The unexpected effect of high doses of adenosine antagonists on seizure‐induced death observed in this study may be due to the increase in seizure severity, vasoconstriction, or phosphodiesterase inhibition caused by these drugs at high doses. These findings further clarify the role of adenosine in seizure‐induced death and may have implications for the consumption of caffeine in epilepsy patients and the prevention of SUDEP. [ABSTRACT FROM AUTHOR]

Although animal models have helped to elaborate meaningful hypotheses about the pathophysiology of sudden and unexpected death in epilepsy (SUDEP), specific prevention strategies are still lacking, potentially reflecting the limitations of these models and the intrinsic difficulties of investigating SUDEP. The interpretation of preclinical data and their translation to diagnostic and therapeutic developments in patients thus require a high level of confidence in their relevance to model the human situation. Preclinical models of SUDEP are heterogeneous and include rodent and nonrodent species. A critical aspect is whether the animals have isolated seizures exclusively induced by a specific trigger, such as models where seizures are elicited by electrical stimulation, pharmacological intervention, or DBA mouse strains, or whether they suffer from epilepsy with spontaneous seizures, with or without spontaneous SUDEP, either of nongenetic epilepsy etiology or from genetically based developmental and epileptic encephalopathies. All these models have advantages and potential disadvantages, but it is important to be aware of these limitations to interpret data appropriately in a translational perspective. The majority of models with spontaneous seizures are of a genetic basis, whereas SUDEP cases with a genetic basis represent only a small proportion of the total number. In almost all models, cardiorespiratory arrest occurs during the course of the seizure, contrary to that in patients observed at the time of death, potentially raising the issue of whether we are studying models of SUDEP or models of periseizure death. However, some of these limitations are impossible to avoid and can in part be dependent on specific features of SUDEP, which may be difficult to model. Several preclinical tools are available to address certain gaps in SUDEP pathophysiology, which can be used to further validate current preclinical models. [ABSTRACT FROM AUTHOR]

Brain ischemia induces slow voltage shifts in the cerebral cortex, including waves of spreading depolarization (SD) and negative ultraslow potentials (NUPs), which are considered as brain injury markers. However, different electrode materials and locations yield variable SD and NUP features. Here, we compared terminal cortical events during isoflurane or sevoflurane euthanasia using intracortical linear iridium electrode arrays and Ag/AgCl-based electrodes in the rat somatosensory cortex. Inhalation of anesthetics caused respiratory arrest, associated with hyperpolarization and followed by SD and NUP on both Ir and Ag electrodes. Ag-NUPs were bell shaped and waned within half an hour after death. Ir-NUPs were biphasic, with the early fast phase corresponding to Ag-NUP, and the late absent on Ag electrodes, phase of a progressive depolarizing voltage shift reaching −100 mV by two hours after death. In addition, late Ir-NUPs were more ample in the deep layers than at the cortical surface. Thus, intracortical Ag and Ir electrodes reliably assess early manifestations of terminal brain injury including hyperpolarization, SD and the early phase of NUP, while the late, giant amplitude phase of NUP, which is present only on Ir electrodes, is probably related to the sensitivity of Ir electrodes to a yet unidentified factor related to brain death. [ABSTRACT FROM AUTHOR]

Background: Chiari malformation type 1 (CM1) is a structural abnormality in the skull and cerebellum, causing cerebellar tonsils to shift downward. Decompression of the posterior fossa is a common surgical method to relieve symptoms and prevent neurological deterioration. After posterior fossa decompression (PFD), individuals with CM1 were more likely to have respiratory arrest. Here, we present, for the first time, a comprehensive overview of the potential risk factors and causes of respiratory arrest following PFD. Methods: A review of the literature highlighting the risk factors for postoperative respiratory arrest in CM1 patients was conducted in the databases of PubMed, Medline, and Google Scholar. Results: Patients with syringomyelia and CM1 are at increased risk for respiratory arrest due to a number of factors, including impaired respiratory mechanics, central respiratory center dysfunction from edema or ischemia, intraoperative brain stem ischemia, and delayed gastric emptying from autonomic dysfunction. Occipitalization of the first cervical vertebra, basilar impression, and fusion of C2‑C3 are all risk factors for respiratory arrest. Conclusion: Implications for CM1 patient care and prospects for further investigation of postoperative respiratory arrest’s causes and risk factors were discussed. [ABSTRACT FROM AUTHOR]

Background: Chiari malformation type 1 (CM1) is a structural abnormality in the skull and cerebellum, causing cerebellar tonsils to shift downward. Decompression of the posterior fossa is a common surgical method to relieve symptoms and prevent neurological deterioration. After posterior fossa decompression (PFD), individuals with CM1 were more likely to have respiratory arrest. Here, we present, for the first time, a comprehensive overview of the potential risk factors and causes of respiratory arrest following PFD. Methods: A review of the literature highlighting the risk factors for postoperative respiratory arrest in CM1 patients was conducted in the databases of PubMed, Medline, and Google Scholar. Results: Patients with syringomyelia and CM1 are at increased risk for respiratory arrest due to a number of factors, including impaired respiratory mechanics, central respiratory center dysfunction from edema or ischemia, intraoperative brain stem ischemia, and delayed gastric emptying from autonomic dysfunction. Occipitalization of the first cervical vertebra, basilar impression, and fusion of C2-C3 are all risk factors for respiratory arrest. Conclusion: Implications for CM1 patient care and prospects for further investigation of postoperative respiratory arrest's causes and risk factors were discussed.

In a code blue, healthcare staff play crucial roles in swiftly responding to medical emergencies, such as cardiac or respiratory arrest. The roles include a code blue leader coordinating the response, primary nurses initiating CPR and managing the patient's airway, residents or physician assistants providing advanced medical care, and additional team members assisting as directed. Other roles include runners retrieving equipment, recorders documenting interventions, family liaisons providing support, security ensuring safety, and post-code teams stabilizing patients and offering emotional support. Effective communication, teamwork, and adherence to protocols are vital for successful outcomes. [ABSTRACT FROM AUTHOR]

Opioids are the mainstay for the management of moderate to severe pain. However, their acute use is associated with several side effects, ranging from nausea, itching, sedation, hypotension to respiratory depression, and death. Also, chronic use of these drugs can lead to the development of tolerance, dependence, and eventually addiction. The most serious side effect, lethality due to opioid-induced overdose, has reached the level of national emergency, i.e., the opioid crisis, which is now the forefront of medicine. In a detailed review (Novel Synthetic Opioids: The Pathologist's Point of View), Frisoni and colleagues have discussed the side effects of novel licit and illicit fentanyl derivatives, as well as the related compounds which are more potent and faster acting than morphine and other conventional opioids (Frisoni, et al., 2018). These drugs affect the central nervous system (CNS) and can promote the development of addiction due to the quick rush they induce because of their faster entry into the brain. These drugs also arrest the cardiovascular and pulmonary systems, increasing the chance of respiratory arrest, leading to opioid-induced overdose morbidity and mortality. The respiratory arrest induced by opioids can be potentiated by other CNS depressants, such as alcohol or benzodiazepines, and therefore may occur more frequently in polydrug users. Therefore, the use of these newer fentanyl derivatives as well as other fast acting opioids should be avoided or limited to specific cases and must be kept out of the reach of children and adolescents who are more vulnerable to become addicted or overdose themselves.

Background: Nicotiana glauca is a plant known to cause acute toxicity upon ingestion or dermal exposure due to the nicotinic alkaloid, anabasine. Nicotinic alkaloids cause toxicity by acting as agonists on nicotinic-type acetylcholine receptors (nAChRs). Initial stimulation of these receptors leads to symptoms such as tachycardia, miosis, and tremors. The effects of high doses of nicotinic alkaloids are biphasic, and eventual persistent depolarization of nAChRs at the neuromuscular junction occurs. This causes apnea, paralysis, and cardiovascular collapse.Case Report: In this report, we present a case of respiratory arrest due to nicotinic alkaloid poisoning from the ingestion of Nicotiana glauca. The diagnosis was suspected after the patient’s family gave a history of the patient ingesting a plant prior to arrival. They were able to also provide a physical sample of the plant.Conclusion: The phone application, “Plant Snap”, determined the plant species and helped confirm the diagnosis. This case describes how modern technology and thorough history taking can combine to provide the best possible patient care.

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A 13.9 kg, 4‐year‐old, male cocker spaniel dog was scheduled for cystotomy. Premedication consisted of intravenous medetomidine (5 µg/kg), induction with propofol (1 mg/kg, intravenous) and anaesthesia maintenance with isoflurane in O2 100%. A medetomidine constant‐rate infusion (1 µg/kg/h) was administered throughout. A bilateral quadratus lumborum block with 3 ml of 0.5% bupivacaine (each side) was performed, and intermittent positive‐pressure ventilation was initiated. At the end of the surgery, medetomidine constant‐rate infusion and intermittent positive‐pressure ventilation ceased. The patient remained in apnoea and developed severe hypercapnia (end‐tidal carbon dioxide: 12 kPa). Thirty minutes after isoflurane discontinuation, respiratory muscles movement started. Three days before, the dog underwent a mini‐hemilaminectomy (similar anaesthetic protocol) without complications. Epidural/spinal migration from the right quadratus lumborum block was suspected, although the definitive cause of transient respiratory arrest after bilateral quadratus lumborum block could not be ascertained. We advise caution when performing quadratus lumborum if previous neighbouring spinal surgery was performed. [ABSTRACT FROM AUTHOR]

Objective: Sudden Unexpected Death in Epilepsy (SUDEP) accounts for 20% of mortality in those with recurrent seizures. While risk factors, monitoring systems, and standard practices are in place, the pathophysiology of SUDEP is still not well understood. Better knowledge of SUDEP and its potential mechanisms of action is crucial to reducing risk in this patient population and developing potential treatment options. Clinical studies and animal models of SUDEP suggest that diminished post-ictal respiratory control may be the dominant mechanism contributing to mortality. Recently, it was demonstrated that the depletion of the neuropeptide galanin in the amygdala occurs in human SUDEP. The amygdala plays a key role in the central integration of respiratory signaling; the depletion of galanin may represent a critical change that predisposes individuals to SUDEP. Materials and methods: To evaluate the impact of enhancing galaninergic signaling to potentially protect against SUDEP, we studied seizure-induced respiratory arrest (S-IRA) following central (intracerebroventricular, intraamygdala) and systemic (intraperitoneal, subcutaneous) administration of galanin analogs. Seizure naïve and seizure experienced (fully kindled) mice were tested. Results: Central and systemically administered galanin analogs protect against S-IRA in naïve C57Bl/6J mice. Differential efficacy between receptor subtypeselective analogs varied based on the route of administration. Sub-chronic systemic administration at doses that reduced 6 Hz seizures also protected against S-IRA. Acute treatment benefits also extended to fully kindled mice experiencing tonic extension. Significance: These data demonstrate that galanin analogs may be protective against post-ictal respiratory collapse. [ABSTRACT FROM AUTHOR]

ObjectiveSudden Unexpected Death in Epilepsy (SUDEP) accounts for 20% of mortality in those with recurrent seizures. While risk factors, monitoring systems, and standard practices are in place, the pathophysiology of SUDEP is still not well understood. Better knowledge of SUDEP and its potential mechanisms of action is crucial to reducing risk in this patient population and developing potential treatment options. Clinical studies and animal models of SUDEP suggest that diminished post-ictal respiratory control may be the dominant mechanism contributing to mortality. Recently, it was demonstrated that the depletion of the neuropeptide galanin in the amygdala occurs in human SUDEP. The amygdala plays a key role in the central integration of respiratory signaling; the depletion of galanin may represent a critical change that predisposes individuals to SUDEP.Materials and methodsTo evaluate the impact of enhancing galaninergic signaling to potentially protect against SUDEP, we studied seizure-induced respiratory arrest (S-IRA) following central (intracerebroventricular, intra-amygdala) and systemic (intraperitoneal, subcutaneous) administration of galanin analogs. Seizure naïve and seizure experienced (fully kindled) mice were tested.ResultsCentral and systemically administered galanin analogs protect against S-IRA in naïve C57Bl/6J mice. Differential efficacy between receptor subtype-selective analogs varied based on the route of administration. Sub-chronic systemic administration at doses that reduced 6 Hz seizures also protected against S-IRA. Acute treatment benefits also extended to fully kindled mice experiencing tonic extension.SignificanceThese data demonstrate that galanin analogs may be protective against post-ictal respiratory collapse.

Brain ischemia induces slow voltage shifts in the cerebral cortex, including waves of spreading depolarization (SD) and negative ultraslow potentials (NUPs), which are considered as brain injury markers. However, different electrode materials and locations yield variable SD and NUP features. Here, we compared terminal cortical events during isoflurane or sevoflurane euthanasia using intracortical linear iridium electrode arrays and Ag/AgCl-based electrodes in the rat somatosensory cortex. Inhalation of anesthetics caused respiratory arrest, associated with hyperpolarization and followed by SD and NUP on both Ir and Ag electrodes. Ag-NUPs were bell shaped and waned within half an hour after death. Ir-NUPs were biphasic, with the early fast phase corresponding to Ag-NUP, and the late absent on Ag electrodes, phase of a progressive depolarizing voltage shift reaching −100 mV by two hours after death. In addition, late Ir-NUPs were more ample in the deep layers than at the cortical surface. Thus, intracortical Ag and Ir electrodes reliably assess early manifestations of terminal brain injury including hyperpolarization, SD and the early phase of NUP, while the late, giant amplitude phase of NUP, which is present only on Ir electrodes, is probably related to the sensitivity of Ir electrodes to a yet unidentified factor related to brain death.

Basic life support (LBS) is a set of interventions aimed at restoring and maintaining vital organ functions in victims of cardiac and respiratory arrest. Knowledge and skills in doing LBS can be improved by training. This literature review was carried out to determine the effect of LBS training on increasing the knowledge and skills of adolescents in performing first aid in cases of cardiac or respiratory arrest. Articles published in 2010-2020 were found through Google Scholar and the Garuda portal. The results of the 5 articles that were reviewed showed significant changes in the knowledge and skills of adolescents before and after being given training. This suggests that LBS training can improve the level of knowledge and skills of adolescents in performing first aid in cases of cardiac or respiratory arrest. [ABSTRACT FROM AUTHOR]

Studies have shown that up to 63% of pediatric intensive care unit patients admitted with acute respiratory or cardiorespiratory illness require mechanical ventilation. Mechanical ventilator support can be divided into three phases: initiation, escalation, and resolution. Noninvasive ventilation is typical during the initiation phase in the management of acute pediatric respiratory failure. The major advancements in the use of noninvasive ventilation involve the emergence of high‐flow nasal cannula and how widespread the use of high‐flow nasal cannula has become in pediatric critical care practice. When high‐flow nasal cannula fails, escalation to continuous positive airway pressure or bi‐level positive airway pressure is the next step in respiratory care progression. Careful clinical assessment is necessary to avoid delayed escalation between forms of noninvasive support or escalation to intubation and invasive mechanical ventilation. Advancements in conventional mechanical ventilation are centered on optimizing ventilator settings and customizing monitoring with the overarching goal to reduce complications of mechanical ventilation, such as ventilator‐induced lung injury. New mechanical ventilator strategies integrating esophageal pressure monitoring, volumetric capnography, and neurally adjusted ventilator assist help to optimize conventional ventilator support. Nonconventional modes of ventilation in the intensive care unit are high‐frequency modes and airway pressure release ventilation. Extracorporeal pulmonary support via extracorporeal membrane oxygenation or paracorporeal lung assist devices provides rescue options when conventional and nonconventional methods fail. During resolution of a course of mechanical ventilator support, reliable weaning strategies and extubation readiness testing are lacking in pediatric critical care. Further, timing of tracheostomy, risk reduction in ventilator‐induced lung injury, and decreased sedation requirements in pediatric patients requiring mechanical ventilation in the pediatric intensive care unit are areas of ongoing research. [ABSTRACT FROM AUTHOR]

Permethrin (PER) is widely employed as the most frequently used type I synthetic pyrethroid insecticide. Despite its worldwide application, reports of pediatric toxicity following permethrin administration are scarce. The present report describes the case of a 12‐year‐old girl with cardiac and respiratory arrest resulting from self‐induced oral toxicity by permethrin. [ABSTRACT FROM AUTHOR]

Some evidence suggests that both hypothermia and anesthesia can exert similar effects on metabolism and ventilation. This study examined the synergistic effects of anesthesia and hypothermia on ventilation in spontaneously breathing adult mice under three different conditions, that is, (1) pentobarbital group (n = 7) in which mice were anesthetized with intraperitoneal pentobarbital of 80 mg/kg, (2) sevoflurane‐continued group (n = 7) in which mice were anesthetized with 1 MAC sevoflurane, and (3) sevoflurane‐discontinued group (n = 7) in which sevoflurane was discontinued at a body temperature below 22˚C. We cooled mice in each group until breathing ceased and followed this with artificial rewarming while measuring changes in respiratory variables and heart rate. We found that the body temperature at which respiration arrested is much lower in the sevoflurane‐discontinued group (13.8 ± 2.0˚C) than that in the sevoflurane‐continued group (16.7 ± 1.2˚C) and the pentobarbital group (17.0 ± 1.4˚C). Upon rewarming, all animals in all three groups spontaneously recovered from respiratory arrest. There was a considerable difference in breathing patterns between sevoflurane‐anesthetized mice and pentobarbital‐anesthetized mice during progressive hypothermia in terms of changes in tidal volume and respiratory frequency. The changes in the respiratory pattern during rewarming are nearly mirrored images of the changes observed during cooling in all three groups. These observations indicate that adult mice are capable of autoresuscitation from hypothermic respiratory arrest and that anesthesia and hypothermia exert synergistic effects on the occurrence of respiratory arrest while the type of anesthetic affects the breathing pattern that occurs during progressive hypothermia leading to respiratory arrest. [ABSTRACT FROM AUTHOR]

The impairments of cerebral blood flow microcirculation brought on by cardiac and respiratory arrest were assessed with multi‐modal diagnostic facilities, utilising laser speckle contrast imaging, fluorescence spectroscopy and diffuse reflectance spectroscopy. The results of laser speckle contrast imaging show a notable reduction of cerebral blood flow in small and medium size vessels during a few minutes of respiratory arrest, while the same effect was observed in large sinuses and their branches during the circulatory cessation. Concurrently, the redox ratio assessed with fluorescence spectroscopy indicates progressing hypoxia, NADH accumulation and increase of FAD consumption. The results of diffuse reflectance spectra measurements display a more rapid grow of the perfusion of deoxygenated blood in case of circulatory impairment. In addition, consequent histopathological analysis performed by using new tissue staining procedure developed in‐house. It shows notably higher reduction of size of the neurons due to their wrinkling within brain tissues influenced by circulation impair. Whereas, the brain tissues altered with the respiratory arrest demonstrate focal perivascular oedema and mild hypoxic changes of neuronal morphology. Thus, the study suggests that consequences of a cessation of cerebral blood flow become more dramatic and dangerous compare to respiratory arrest. [ABSTRACT FROM AUTHOR]

The purpose of this study was to clarify whether or not body armor would protect the body of a swine model using a blast tube built at National Defense Medical College, which is the first such blast tube in Japan. Seventeen pigs were divided into two groups: the body armor group and the non-body armor group. Under intravenous anesthesia, the pigs were tightly fixed in the left lateral position on a table and exposed from the back neck to the upper lumbar back to the blast wave and wind with or without body armor, with the driving pressure of the blast tube set to 3.0 MPa. When the surviving and dead pigs were compared, blood gas analyses revealed significant differences in PaO2, PaCO2, and pH in the super-early phase. All pigs injured by the blast wave and wind had lung hemorrhage. All 6 animals in the body armor group and 6 of the 11 animals in the control group survived for 3 hours after injury. Respiratory arrest immediately after exposure to the blast wave was considered to influence the mortality in our pig model. Body armor may have a beneficial effect in protecting against respiratory arrest immediately after an explosion. [ABSTRACT FROM AUTHOR]

This case report involving an early salvaged patient with a myotonic dystrophy typ 1 outlines the interdisciplinary method to control an unexpected acute life-threatening complication in gastrointestinal procedures in infancy. The only way to guarantee the patient's safety in such a scenario is an exact and interdisciplinary planning and following the guidelines to rescue the foreign body.

Objective: To investigate the code blue application at a training and research hospital in Turkey. Methods: The code blue declaration forms and the hospital database with 238 complete records between January 2016 and July 2017 were collected. The form involved individual characteristics, the reason for issuing the code blue call, the unit and block where the code was given, time and location related properties such as working time and arrival duration, properties regarding the intervention process such as its type, duration or result. The 24-hour and 30-day long survival data of the patients to whom cardiopulmonary resuscitation was implemented were obtained from the hospital database, or from their relatives. The influencing factors of arrival duration were analyzed. Results: The median duration of arrival was 2.14 (2.00-3.02) min. Code blue applications were performed more frequently in Departments of General Surgery, Internal Medicine, Orthopaedics, and Cardiology Clinics. Half of the code blue calls were due to cardiac arrest; the other half was due to shortness of breath or respiratory distress, syncope, and respiratory arrest. Three-out- of four code blue calls were treated with orotracheal intubation and cardiopulmonary resuscitation, or only orotracheal intubation or only medical treatment; one-fourth of the calls were not intervened. Altogether, 72.36% of the code blue calls patients were intervened; 69.35% of them were made both orotracheal intubation and cardiopulmonary resuscitation, and 20.5% of them were made only orotracheal intubation and 10.55% of them made only medical treatment. It was found that giving the code blue day or night had no effect on the time to reach the area where the code was given. Similarly, it was found that giving the code blue within daytime or night shift had no effect on the time to reach the area where the code was given. (P>0.05). The survival rates were 39.1% within the first 24 h and 18.1% within the first 30 d. Conclusions: Applications of code blue should be analyzed at regular intervals as clinical quality indicators. Reasons for wrong calls should be determined. The duration of reaching locations where calls are made should also be decreased.

Abstract Some evidence suggests that both hypothermia and anesthesia can exert similar effects on metabolism and ventilation. This study examined the synergistic effects of anesthesia and hypothermia on ventilation in spontaneously breathing adult mice under three different conditions, that is, (1) pentobarbital group (n = 7) in which mice were anesthetized with intraperitoneal pentobarbital of 80 mg/kg, (2) sevoflurane‐continued group (n = 7) in which mice were anesthetized with 1 MAC sevoflurane, and (3) sevoflurane‐discontinued group (n = 7) in which sevoflurane was discontinued at a body temperature below 22˚C. We cooled mice in each group until breathing ceased and followed this with artificial rewarming while measuring changes in respiratory variables and heart rate. We found that the body temperature at which respiration arrested is much lower in the sevoflurane‐discontinued group (13.8 ± 2.0˚C) than that in the sevoflurane‐continued group (16.7 ± 1.2˚C) and the pentobarbital group (17.0 ± 1.4˚C). Upon rewarming, all animals in all three groups spontaneously recovered from respiratory arrest. There was a considerable difference in breathing patterns between sevoflurane‐anesthetized mice and pentobarbital‐anesthetized mice during progressive hypothermia in terms of changes in tidal volume and respiratory frequency. The changes in the respiratory pattern during rewarming are nearly mirrored images of the changes observed during cooling in all three groups. These observations indicate that adult mice are capable of autoresuscitation from hypothermic respiratory arrest and that anesthesia and hypothermia exert synergistic effects on the occurrence of respiratory arrest while the type of anesthetic affects the breathing pattern that occurs during progressive hypothermia leading to respiratory arrest.

Introduction. Respiratory failure is the most common cause of cardiac arrest in pediatrics. Recognizing and managing it adequately is critical. Simulation is used to improve medical skills. The objective of this study was to establish the proportion of pediatric residents who recognized a respiratory arrest in a child at a simulation center. Methods. This was an observational study in 77 residents. A simulation of a patient with respiratory distress that progressed to respiratory arrest was used. Results. Among the 77 participants, 48 recognized respiratory arrest (62.3%). The mean time to recognize respiratory arrest was 38.16 seconds. Conclusion. Respiratory arrest was recognized by 62.3% of participants. Among those who did so, the average time was 38.16 seconds. Severe failures were noted in some of the expected interventions., (Sociedad Argentina de Pediatría.)

Acute spinal cord injury is a devastating event associated with substantial morbidity worldwide. The pathophysiology of spinal cord injury involves the initial mechanical trauma and the subsequent inflammatory response, which may worsen the severity of neurologic dysfunction. Interventions have been studied to reduce the extent of primary injury to the spinal cord through preventive measures and to mitigate secondary insult through early specialized care. Management, therefore, is multifold, interdisciplinary, and begins immediately at the time of injury. It includes the trauma triage, acute management of the circulatory and respiratory systems, and definitive treatment, mainly with surgical decompression and stabilization.

Abstract Background Pregnancy constitutes a significant factor in thyroid hypertrophy and can rarely progress to respiratory distress. We describe case of pregnant woman with acute respiratory distress following a tracheal compression due to goiter, quickly resulting in respiratory arrest, requiring emergency orotracheal intubation and thyroidectomy. Case presentation A pregnant woman with a growing goiter was referred to the hospital with a respiratory difficulty. During the examination, we found a large homogeneous goiter. The patient showed signs of respiratory exhaustion with bradypnea and pulmonary auscultation revealing decreased ventilation of the two pulmonary fields. The evolution quick led to respiratory arrest. The patient was rapidly intubated, which saved her. A thoracic computed tomography was performed and revealed a large goiter, compressing the trachea in its thoracic area and oppressing the vascular structures. Obstetrical ultrasound was normal. Thyroidectomy was decided after the patient’s preparation. After 24 h, the patient was successfully extubated without incident and the postoperative period was uneventful. Conclusion Airway obstruction during pregnancy secondary to goiter is rare but can be fatal. Early diagnosis might have avoided the evolution towards the respiratory failure. Prevention requires early surgery preferably before pregnancy or in our case a surgery in the second trimester.

Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death amongst patients whose seizures are not adequately controlled by current therapies. Patients with SCN8A encephalopathy have an elevated risk for SUDEP. While transgenic mouse models have provided insight into the molecular mechanisms of SCN8A encephalopathy etiology, our understanding of seizure-induced death has been hampered by the inability to reliably trigger both seizures and seizure-induced death in these mice. Here, we demonstrate that mice harboring an Scn8a allele with the patient-derived mutation N1768D (D/+) are susceptible to audiogenic seizures and seizure-induced death. In adult D/+ mice, audiogenic seizures are non-fatal and have nearly identical behavioral, electrographical, and cardiorespiratory characteristics as spontaneous seizures. In contrast, at postnatal days 20–21, D/+ mice exhibit the same seizure behavior, but have a significantly higher incidence of seizure-induced death following an audiogenic seizure. Seizure-induced death was prevented by either stimulating breathing via mechanical ventilation or by acute activation of adrenergic receptors. Conversely, in adult D/+ mice inhibition of adrenergic receptors converted normally non-fatal audiogenic seizures into fatal seizures. Taken together, our studies show that in our novel audiogenic seizure-induced death model adrenergic receptor activation is necessary and sufficient for recovery of breathing and prevention of seizure-induced death.

Sudden Unexpected Death in Epilepsy (SUDEP) is the leading cause of death in young adults with uncontrolled seizures. First aid guidance to prevent SUDEP, though, has not been previously published because the rarity of monitored cases has made the underlying mechanism difficult to define. This starkly contrasts with the first aid guidelines for sudden cardiac arrest that have been developed based on retrospective studies and expert consensus and the discussion of resuscitation challenges in various American Heart Association certificate courses. However, an increasing amount of evidence from documented SUDEP cases and near misses and from animal models points to a consistent sequence of events that starts with sudden airway occlusion and suggests a mechanistic basis for enhancing seizure first aid. In monitored cases, this sudden airway occlusion associated with seizure activity can be accurately inferred from inductance plethysmography or (depending on recording bandwidth) from electromyographic (EMG) bursts that are associated with inspiratory attempts appearing on the electroencephalogram (EEG) or the electrocardiogram (ECG). In an emergency setting or outside a hospital, seizure first aid can be improved by (1) keeping a lookout for sudden changes in airway status during a seizure, (2) distinguishing thoracic and abdominal movements during attempts to inspire from effective breathing, (3) applying a simple maneuver, the laryngospasm notch maneuver, that may help with airway management when aggressive airway management is unavailable, (4) providing oxygen early as a preventative step to reduce the risk of death, and (5) performing cardiopulmonary resuscitation before the limited post-ictal window of opportunity closes. We propose that these additions to first aid protocols can limit progression of any potential SUDEP case and prevent death. Risk stratification can be improved by recognition of airway occlusion, attendant hypoxia, and need for resuscitation.

Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death amongst patients whose seizures are not adequately controlled by current therapies. Patients with SCN8A encephalopathy have an elevated risk for SUDEP. While transgenic mouse models have provided insight into the molecular mechanisms of SCN8A encephalopathy etiology, our understanding of seizure-induced death has been hampered by the inability to reliably trigger both seizures and seizure-induced death in these mice. Here, we demonstrate that mice harboring an Scn8a allele with the patient-derived mutation N1768D (D/+) are susceptible to audiogenic seizures and seizure-induced death. In adult D/+ mice, audiogenic seizures are non-fatal and have nearly identical behavioral, electrographical, and cardiorespiratory characteristics as spontaneous seizures. In contrast, at postnatal days 20–21, D/+ mice exhibit the same seizure behavior, but have a significantly higher incidence of seizure-induced death following an audiogenic seizure. Seizure-induced death was prevented by either stimulating breathing via mechanical ventilation or by acute activation of adrenergic receptors. Conversely, in adult D/+ mice inhibition of adrenergic receptors converted normally non-fatal audiogenic seizures into fatal seizures. Taken together, our studies show that in our novel audiogenic seizure-induced death model adrenergic receptor activation is necessary and sufficient for recovery of breathing and prevention of seizure-induced death. [ABSTRACT FROM AUTHOR]

A 39-year-old male, who attempted suicide by hanging, developed chronic myoclonus with intact cognitive function. Chronic post-hypoxic myoclonus is a rare syndrome that may develop after a respiratory arrest and it presents as late onset and persistent purposeful myoclonus with preserved or slightly impaired cognitive function. Increasing critical care nurses’ awareness of chronic post-hypoxic myoclonus will lead to earlier diagnosis of this rare syndrome. [ABSTRACT FROM AUTHOR]

Sudden Unexpected Death in Epilepsy (SUDEP) is the leading cause of death in young adults with uncontrolled seizures. First aid guidance to prevent SUDEP, though, has not been previously published because the rarity of monitored cases has made the underlying mechanism difficult to define. This starkly contrasts with the first aid guidelines for sudden cardiac arrest that have been developed based on retrospective studies and expert consensus and the discussion of resuscitation challenges in various American Heart Association certificate courses. However, an increasing amount of evidence from documented SUDEP cases and near misses and from animal models points to a consistent sequence of events that starts with sudden airway occlusion and suggests a mechanistic basis for enhancing seizure first aid. In monitored cases, this sudden airway occlusion associated with seizure activity can be accurately inferred from inductance plethysmography or (depending on recording bandwidth) from electromyographic (EMG) bursts that are associated with inspiratory attempts appearing on the electroencephalogram (EEG) or the electrocardiogram (ECG). In an emergency setting or outside a hospital, seizure first aid can be improved by (1) keeping a lookout for sudden changes in airway status during a seizure, (2) distinguishing thoracic and abdominal movements during attempts to inspire from effective breathing, (3) applying a simple maneuver, the laryngospasm notch maneuver, that may help with airway management when aggressive airway management is unavailable, (4) providing oxygen early as a preventative step to reduce the risk of death, and (5) performing cardiopulmonary resuscitation before the limited post-ictal window of opportunity closes. We propose that these additions to first aid protocols can limit progression of any potential SUDEP case and prevent death. Risk stratification can be improved by recognition of airway occlusion, attendant hypoxia, and need for resuscitation. [ABSTRACT FROM AUTHOR]

Sudden unexpected death in epilepsy (SUDEP) claims the lives of one in every thousand epileptic patients each year. Autonomic, cardiac, and respiratory pieces to a mechanistic puzzle have not yet been completely assembled. We propose a single sequence of causes and effects that unifies disparate and competitive concepts into a single algorithm centered on ictal obstructive apnea. Based on detailed animal studies that are sometimes impossible in humans, and striking parallels with a growing body of clinical examples, this framework (1) accounts for the autonomic, cardiac, and respiratory data to date by showing the causal relationships between specific elements, and (2) highlights specific kinds of data that can be used to precisely classify various patient outcomes. The framework also justifies a “near miss” designation to be applied to any cases with evidence of obstructive apnea even, and perhaps especially, in individuals that do not require resuscitation. Lastly, the rationale for preventative oxygen therapy is demonstrated. With better mechanistic understanding of SUDEP, we suggest changes for detection and classification to increase survival rates and improve risk stratification.

Background and Objective: Obstructive Sleep Apnea is a disease that causes respiratory arrest in sleep and reduces sleep quality. The diagnosis of the disease is made by the physician in two stages by examining the patient records taken with the polysomnography device. Because of the negative aspects of this process, new diagnostic processes and devices are needed. In this article, a new approach to sleep staging, which is one of the diagnostic steps of the disease, was proposed. An artificial intelligence‐based sleep/awake system detection was developed for sleep staging processing. Photoplethysmography (PPG) signal and heart rate variable (HRV) were used in the study. PPG records taken from patient and control groups were cleaned by the digital filter. The HRV parameter was then derived from the PPG signal. Then, 40 features from HRV signal and 46 features from PPG signal were extracted. The extracted features were classified by reduced machine learning techniques with F‐score feature selection method. In order to evaluate the performances of the classifiers, the sensitivity and specificity values, the accuracy rates for each class were computed in the test set and receiver operating characteristic curve prepared. In addition, area under the curve (AUC), Kappa coefficient and F‐score were calculated. According to the results obtained, the system can be realised with 91.09% accuracy rate using 11 PPG and HRV and with 90.01% accuracy rate using 14 HRV features. These success rates are quite enough for the system to work. When all these values are taken into consideration, it is possible to realise a practical sleep/awake detection system. This article suggests that the PPG signal can be used to diagnose obstructive sleep apnea by processing with artificial intelligence and signal processing techniques. [ABSTRACT FROM AUTHOR]

The mechanism(s) for sudden death in epilepsy (SUDEP) remain(s) unknown, but seizure spread to brainstem areas serving autonomic and respiratory function is critical. In a rat model, we established a mechanism for SUDEP that involves seizure‐induced laryngospasm and obstructive apnea lasting until respiratory arrest. We hypothesized that DBA/2J mice, which display lethal audiogenic seizures, would be protected from death by implanting a tracheal T‐tube as a surrogate airway. In a 2 × 2 design, mice were implanted with either open or closed tracheal T‐tubes and treated with either low‐dose ketamine/xylazine to moderate thoracic spasm during the tonic seizure phase or no drug. Animals receiving both treatments had the highest survival rate, followed by animals receiving the open tube without ketamine/xylazine. The odds ratio for survival was >20 higher with an open T‐tube (odds ratio = 24.14). The impact of open tracheal tubes indicates that the mechanism of death in DBA/2J mice involves seizure‐induced upper airway obstruction until respiratory arrest. These results, our rat work, and our demonstration of inspiratory effort‐based electromyographic signals and electrocardiographic abnormalities in rats and humans suggest that seizure‐induced laryngospasm and obstructive apnea directly link seizure activity to respiratory arrest in these sudden death examples. [ABSTRACT FROM AUTHOR]

This case report involving an early salvaged patient with a myotonic dystrophy typ 1 outlines the interdisciplinary method to control an unexpected acute life-threatening complication in gastrointestinal procedures in infancy. The only way to guarantee the patient's safety in such a scenario is an exact and interdisciplinary planning and following the guidelines to rescue the foreign body. [ABSTRACT FROM AUTHOR]