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ABSTRACT Neurogenic pulmonary edema (NPE) is acute pulmonary edema triggered by an injury to the central nervous system. NPE associated with epileptic seizures is less common and not well known to recur. We report a case of a 51‐year‐old woman with NPE with recurrent epileptic seizures. The patient was brought to our hospital with two episodes of clonic convulsions. Imaging studies obtained on admission showed bilateral infiltration in the upper lobes of both lungs. The patient was discharged after receiving antiepileptic drugs. NPE may recur with epileptic seizures.

Objective To explore the role of catecholamine and its intermediate metabolites in the development of neurogenic pulmonary edema in the intensive care unit (ICU). Methods Clinical data were collected from 32 patients diagnosed with neurogenic pulmonary edema in the ICU between January 2020 and December 2023, forming the study group. Another 32 ICU patients from the same period who did not develop neurogenic pulmonary edema were selected as the control group. A retrospective analysis was conducted on the clinical data of both groups, comparing differences in blood gas indices, hemodynamic parameters, relevant laboratory indicators, inflammatory factors, and levels of cate-cholamines and their intermediate metabolites. Results Compared to the control group, the study group showed significant increases in partial pressure of carbon dioxide in arterial blood (PaCO2), fraction of inspiration O2(FiO2), artery alveolar oxygen partial pressure gradient (AaDO2), respiratory rate (RR), pulmonary artery wedge pressure (PAWP), interleukin-6 (IL-6), tumor necrosis factor (TNF-α), total catecholamines, epinephrine, metanephrine, normetanephrine, and norepinephrine, while partial pressure of oxygen in arterial blood (PaO2), arterial oxygen saturation (SaO2), arterial/alreolar oxygen tension ratio (a/APO2), PaO2/FiO2, and interferony (IFN - γ) were significantly decreased (P<0.05). No significant difference was observed in central venous pressure (CVP) levels between the groups (P>0.05). Correlation analysis indicated that epinephrine, norepinephrine, metanephrine, total catecholamines, and normetanephrine were positively correlated with PaCO2, FiO2, and AaDO2, and negatively correlated with PaO2, SaO2, a/APO2, and PaO2/FiO2(P<0.05). Conclusion Catecholamines and their intermediate metabolites are signifi- cantly elevated in ICU patients with neurogenic pulmonary edema and are correlated with blood gas indices, playing an important role in the occurrence and progression of the disease. [ABSTRACT FROM AUTHOR]

Introduction: Neurogenic pulmonary edema is a rare and potentially life-threatening condition that can present as severe pulmonary edema after significant neurologic insults. This is the first documented instance that shows a plausible causal link between cannabis consumption, psychogenic polydipsia, and the subsequent development of neurogenic pulmonary edema associated with status epilepticus secondary to acute hyponatremia. Case Report: We report a case of a 34-year-old female who presented to the emergency department altered and postictal after a witnessed new-onset seizure. She developed significant respiratory distress that required intubation. Her sodium was 121 millimoles per liter (mmol/L), from 137 mmol/L 36 hours prior on routine outpatient labs. Further history revealed excessive water ingestion after eating a cannabis edible prior to the seizure. Conclusion: This case highlights the importance of recognizing neurogenic pulmonary edema in connection with psychogenic polydipsia, severe hyponatremia, and status epilepticus subsequent to cannabis consumption. [ABSTRACT FROM AUTHOR]

Abstract Background Human records describe pulmonary edema as a life-threatening complication of electric shock. Successful management requires prompt recognition and intensive care. However, in companion animals, electrocutions are rarely reported, even though domestic environments are full of electrical devices and there is always the possibility of accidental injury. Therefore, it is important for veterinarians to know more about this condition in order to achieve successful patient outcomes. Case presentation A 3-month-old male Labrador Retriever was presented with a history of transient loss of consciousness after chewing on a household electrical cord. On admission, the puppy showed an orthopneic position with moderate respiratory distress. Supplemental oxygen via nasal catheter was provided, but the patient showed marked worsening of respiratory status. Point-of-care ultrasound exams suggested neurogenic pulmonary edema due to electrical shock close to the central nervous system and increased B-lines without evidence of cardiac abnormalities. Mechanical ventilation of the patient was initiated using volume-controlled mode with a tidal volume of 9 to 15 ml/kg until reaching an end-tidal carbon dioxide ≤ 40 mm Hg, followed by a stepwise lung-recruitment maneuver in pressure-controlled mode with increases of the peak inspiratory pressure (15 to 20 cm H2O) and positive end-expiratory pressure (3 to 10 cm H2O) for 30 min, and return to volume-controlled mode with a tidal volume of 15 ml/kg until reaching a peripheral oxygen saturation ≥ 96%. Weaning from the ventilator was achieved in six hours, and the patient was discharged two days after admission without neurological or respiratory deficits. Conclusions We present a rather unusual case of a neurogenic pulmonary edema subsequent to accidental electrocution in a dog. Timely diagnosis by ultrasound and mechanical ventilation settings are described. Our case highlights that pulmonary edema should be considered a potentially life-threatening complication of electrical shock in small animal emergency and critical care medicine.

Background Human records describe pulmonary edema as a life-threatening complication of electric shock. Successful management requires prompt recognition and intensive care. However, in companion animals, electrocutions are rarely reported, even though domestic environments are full of electrical devices and there is always the possibility of accidental injury. Therefore, it is important for veterinarians to know more about this condition in order to achieve successful patient outcomes. Case presentation A 3-month-old male Labrador Retriever was presented with a history of transient loss of consciousness after chewing on a household electrical cord. On admission, the puppy showed an orthopneic position with moderate respiratory distress. Supplemental oxygen via nasal catheter was provided, but the patient showed marked worsening of respiratory status. Point-of-care ultrasound exams suggested neurogenic pulmonary edema due to electrical shock close to the central nervous system and increased B-lines without evidence of cardiac abnormalities. Mechanical ventilation of the patient was initiated using volume-controlled mode with a tidal volume of 9 to 15 ml/kg until reaching an end-tidal carbon dioxide≤40 mm Hg, followed by a stepwise lung-recruitment maneuver in pressure-controlled mode with increases of the peak inspiratory pressure (15 to 20 cm H2O) and positive end-expiratory pressure (3 to 10 cm H2O) for 30 min, and return to volume-controlled mode with a tidal volume of 15 ml/kg until reaching a peripheral oxygen saturation≥96%. Weaning from the ventilator was achieved in six hours, and the patient was discharged two days after admission without neurological or respiratory deficits. Conclusions We present a rather unusual case of a neurogenic pulmonary edema subsequent to accidental electrocution in a dog. Timely diagnosis by ultrasound and mechanical ventilation settings are described. Our case highlights that pulmonary edema should be considered a potentially life-threatening complication of electrical shock in small animal emergency and critical care medicine. [ABSTRACT FROM AUTHOR]

Subarachnoid hemorrhage (SAH) is a common occurrence among patients with altered mental status who arrive at the emergency department (ED), particularly for emergency physicians. However, the combination of neurogenic pulmonary edema (NPE) followed by SAH is generally considered a rare condition in the ED setting. Chest radiographs in these patients often reveal lung infiltrations, which are frequently misinterpreted by many emergency physicians as resulting from chest compression during cardiopulmonary resuscitation or aspiration due to altered mental status. This case report highlights a patient with SAH who developed NPE, with the aim to raise awareness among emergency department physicians about NPE and provide comprehensive insights regarding its management, as well as clinical, prognostic and diagnostic information. [ABSTRACT FROM AUTHOR]

Abstract Acute brain injury (ABI) covers various clinical entities that may require invasive mechanical ventilation (MV) in the intensive care unit (ICU). The goal of MV, which is to protect the lung and the brain from further injury, may be difficult to achieve in the most severe forms of lung or brain injury. This narrative review aims to address the respiratory issues and ventilator management, specific to ABI patients in the ICU.

Neurogenic pulmonary edema (NPE) is a life-threatening and severe complication in patients with spontaneous subarachnoid hemorrhage (SAH). The prevalence of NPE varies significantly across studies due to differences in case definitions, study populations, and methodologies. Therefore, a precise estimation of the prevalence and risk factors related to NPE in patients with spontaneous SAH is important for clinical decision-makers, policy providers, and researchers. We conducted a systematic search of the PubMed/Medline, Embase, Web of Science, Scopus, and Cochrane Library databases from their inception to January 2023. Thirteen studies were included in the meta-analysis, with a total of 3,429 SAH patients. The pooled global prevalence of NPE was estimated to be 13%. Out of the eight studies (n = 1095, 56%) that reported the number of in-hospital mortalities of NPE among patients with SAH, the pooled proportion of in-hospital deaths was 47%. Risk factors associated with NPE after spontaneous SAH included female gender, WFNS class, APACHE II score ≥ 20, IL-6 > 40 pg/mL, Hunt and Hess grade ≥ 3, elevated troponin I, elevated white blood cell count, and electrocardiographic abnormalities. Multiple studies showed a strong positive correlation between the WFNS class and NPE. In conclusion, NPE has a moderate prevalence but a high in-hospital mortality rate in patients with SAH. We identified multiple risk factors that can help identify high-risk groups of NPE in individuals with SAH. Early prediction of the onset of NPE is crucial for timely prevention and early intervention. [ABSTRACT FROM AUTHOR]

Neurogenic pulmonary edema (NPO) is a rare and underdiagnosed clinical entity, occurring within minutes to hours of central nervous system damage. The pathogenesis of NPO is not completely understood, systemic vasoconstriction, as a consequence of higher levels of catecholamines, associated to systemic inflammatory response lead to increase capillary permeability and result in pulmonary edema. Hypoxemic respiratory failure following a catastrophic neurological event, which cannot be attributed to other causes is the main characteristic of NPO. Management is essentially based on the control of the triggering neurologic condition in order to quell the sympathetic discharge. We report the case of female who presented hypoxemic respiratory distress following a subarachnoid hemorrhage. Clinical examination and radiological investigations led to the diagnosis of neurogenic pulmonary edema. [ABSTRACT FROM AUTHOR]

Recombinant tissue plasminogen activator (r-tPA) is the first-line drug for the treatment of acute ischemic stroke, despite it may lead to a variety of complications in some cases. In patients with extensive stroke, infarction of the brain can cause suppression of the respiratory center in the brain leading to neurogenic pulmonary edema that potentially causes respiratory failure. Its etiology is either due to a neurogenic or non-neurogenic process. Nevertheless, the definite pathophysiology of these circumstances remains unclear. In this study, we reported four cases of post-thrombolytic ischemic stroke patients who suffer from pulmonary edema with different symptoms and onset times as well as we discuss the possible explanation behind these different outcomes.

This paper summarized the nursing management for a patient with intracerebral hemorrhage due to ruptured cerebral arteriovenous malformation and neurogenic pulmonary edema. Based on the monitoring of postoperative vital signs of the patient, efforts were made in the following aspects: Early identification and intervention on normal perfusion pressure breakthrough syndrome; Ensuring the effective cerebral perfusion pressure during control of blood pressure and intracranial pressure; Early identification and nursing of neurogenic pulmonary edema; Enhancing the postoperative airway, fluid and volume management; Providing lung protective ventilation strategy; Carrying out awakenings and awareness recovery for the patient with chronic disorders of consciousness. (本文总结1例脑动静脉畸形破裂出血并发神经源性肺水肿患者的护理体会。术后在严密监测神志、瞳孔、生命体征变化基础上, 对正常灌注压突破综合征进行早期识别及干预, 在控制性降压及颅内压的同时保证有效的脑灌注压; 做好神经源性肺水肿的早期识别及护理, 在扩容的同时预防肺水肿进一步加重; 做好患者的呼吸道管理及容量管理, 给予正确的肺保护通气策略, 细化出入量; 对慢性意识障碍进行促醒康复, 促进患者早日康复。)

Background In this study, we aimed to investigate the prevalence, timing, risk factors, and outcomes of acute respiratory distress syndrome (ARDS) in patients with aneurysmal subarachnoid hemorrhage (aSAH). Methods PubMed and four other databases were searched for randomized controlled trials (RCTs) and observational studies of patients 18 years or older through October 20, 2021. Study quality was assessed, using the Cochrane Risk of Bias tool for RCTs and the Newcastle-Ottawa scale for cohort and case-control studies. High-grade aSAH was defined as a Hunt-Hess grade ≥3 and/or a modified Fisher score ≥3. A good neurological outcome was defined as a Glasgow outcome scale score ≥4. Random-effects meta-analyses were conducted to estimate the pooled outcome prevalence and 95% confidence interval (CI). Results Eleven observational studies (n=6,107) met the inclusion criteria. Overall, 15% of the patients (95% CI, 10.5–20.0; I2=97.8%) developed ARDS after aSAH, with a mean time of 3 days (95% CI, 1.9–3.7; I2=54%). Overall survival at discharge was 80% (95% CI, 75–86; I2=96%), and 67% of aSAH patients (95% CI, 54.9–78.9; I2=94%) had a good neurological outcome at any time. The aSAH cohort without ARDS had a higher rate of survival than those with ARDS (79% vs. 49%, P=0.028). Male sex, patients with a high-grade aSAH, patients who developed pneumonia, and systemic inflammatory response syndrome during hospital admission were at a higher risk of developing ARDS. Conclusion In this meta-analysis, approximately one in six patients developed ARDS after aSAH, with a mean time of 3 days from the initial presentation, and ARDS was associated with increased mortality.

Abstract Background Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune inflammatory disease predominantly found in women of child-bearing age. Neurogenic pulmonary edema (NPE) is a recalcitrant complication that occurs after injury to the central nervous system and has an acute onset and rapid progression. Limbic encephalitis is an inflammatory encephalopathy caused by viruses, immune responses, or other factors involving the limbic system. NPE caused by SLE is rare. Case presentation Here, we report a case of a 21-year-old woman with SLE who experienced five episodes of generalized tonic–clonic seizure after headache and dyspnea. Anti-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) 2 antibody was tested positive in the serum and cerebrospinal fluid. Electrocardiography (EEG) indicated paroxysmal or sporadic medium amplitude theta activity. In addition, chest computed tomography (CT) showed multiple diffuse consolidations and ground-glass opacities. We finally considered a diagnosis of NPE and AMPAR limbic encephalitis. The patient's symptoms improved obviously after methylprednisolone pulse therapy and antiepileptic treatment. Conclusions NPE can be a complication of neuropsychiatric lupus erythematosus (NPSLE). AMPAR2 antibodies may be produced in NPSLE patients, especially in those with high polyclonal IgG antibody titers. More basic and clinical studies are required to confirm these observations and elucidate the pathogenicity of encephalitis-related autoantibodies in SLE patients.

Objective: To review various types of noncardiogenic pulmonary edema (NCPE) in cats and dogs. Etiology: NCPE is an abnormal fluid accumulation in the lung interstitium or alveoli that is not caused by cardiogenic causes or fluid overload. It can be due to changes in vascular permeability, hydrostatic pressure in the pulmonary vasculature, or a combination thereof. Possible causes include inflammatory states within the lung or in remote tissues (acute respiratory distress syndrome [ARDS]), airway obstruction (post‐obstructive pulmonary edema), neurologic disease such as head trauma or seizures (neurogenic pulmonary edema), electrocution, after re‐expansion of a collapsed lung or after drowning. Diagnosis: Diagnosis of NCPE is generally based on history, physical examination, and diagnostic imaging. Radiographic findings suggestive of NCPE are interstitial to alveolar pulmonary opacities in the absence of signs of left‐sided congestive heart failure or fluid overload such as cardiomegaly or congested pulmonary veins. Computed tomography and edema fluid analysis may aid in the diagnosis, while some forms of NCPE require additional findings to reach a diagnosis. Therapy: The goal of therapy for all types of NCPE is to preserve tissue oxygenation and reduce the work of breathing. This may be achieved by removing the inciting cause (eg, airway obstruction) and cage rest in mild cases and supplemental oxygen in moderate cases and may require mechanical ventilation in severe cases. Prognosis: Prognosis is generally good for most causes of veterinary NCPE except for ARDS, although data are scarce for some etiologies of NCPE. [ABSTRACT FROM AUTHOR]

The brain-lung interaction can seriously affect patients with traumatic brain injury, triggering a vicious cycle that worsens patient prognosis. Although the mechanisms of the interaction are not fully elucidated, several hypotheses, notably the “blast injury” theory or “double hit” model, have been proposed and constitute the basis of its development and progression. The brain and lungs strongly interact via complex pathways from the brain to the lungs but also from the lungs to the brain. The main pulmonary disorders that occur after brain injuries are neurogenic pulmonary edema, acute respiratory distress syndrome, and ventilator-associated pneumonia, and the principal brain disorders after lung injuries include brain hypoxia and intracranial hypertension. All of these conditions are key considerations for management therapies after traumatic brain injury and need exceptional case-by-case monitoring to avoid neurological or pulmonary complications. This review aims to describe the history, pathophysiology, risk factors, characteristics, and complications of brain-lung and lung-brain interactions and the impact of different old and recent modalities of treatment in the context of traumatic brain injury.

Abstract We report a case of neurogenic pulmonary edema (NPE) caused by middle cerebral artery infarction involving the right insular cortex. Hyperactivity of the insular cortex, which regulates sympathetic function, can cause NPE. The NPE should be considered in the differential diagnosis of dyspneic patients with insular cortex infarction.

We report a 60-year-old woman who presented to the emergency department after experiencing a witnessed unknown onset bilateral tonic clonic seizure (GTCS) that culminated in cardiac arrest. A neurology consultant uncovered a years-long history of frequent episodic staring followed by confusion and expressive aphasia, which strongly suggested that she suffered from epilepsy. Thus, her cardiac arrest and subsequent resuscitation met criteria for a near-sudden unexpected death in epilepsy (SUDEP) diagnosis. Serial bloodwork demonstrated transient troponin I elevations and leukocytoses, while a brain MRI revealed global cerebral anoxic injury and a small acute right cerebellar ischemic infarction. A review of her medical record uncovered a hospitalization sixteen months earlier for a likely GTCS whose workup showed similar troponin I elevations and leukocytoses, and surprisingly, a different small acute right cerebellar ischemic infarction in the same vascular territory. To our knowledge, this is the first report of subcortical ischemic infarctions occurring concurrently with GTCSs in a near-SUDEP patient. Aside from illustrating the key role of inpatient neurologists in the diagnosis of near-SUDEP, this manuscript discusses the potential significance of postictal ischemic infarctions, transient asymptomatic troponin elevations, and transient non-infectious leukocytoses in epilepsy patients with cardiovascular risk factors.

During physiological stress responses such as vigorous exercise, emotional states of fear and rage, and asphyxia, the nervous system induces a massive release of systemic catecholamines that prepares the body for survival by increasing cardiac output and redirecting blood flow from non-essential organs into the cardiopulmonary circulation. A curious byproduct of this vital response is a sudden, transient, and redistributive leukocytosis provoked mostly by the resultant shear forces exerted by rapid blood flow onmarginated leukocytes. Generalized convulsive seizures, too, result in catecholamine surges accompanied by similar leukocytoses, the magnitude of which appears to be rooted in semiological factors such as convulsive duration and intensity. This manuscript reviews the history, kinetics, physiology, and clinical significance of post-convulsive leukocyte elevations and discusses their clinical utility, including a proposed role in the scientific investigation of sudden unexpected death in epilepsy (SUDEP). [ABSTRACT FROM AUTHOR]

Background: Neurogenic stunned myocardium (NSM) is characterised by an acute onset cardiac dysfunction following an acute neurological insult which mimics acute coronary syndrome. Case details: A 12-year-old male child was admitted to the neuro-intensive care unit (NICU) following midline suboccipital craniotomy and resection of recurrent medulloblastoma. Postoperatively, in NICU, he developed tachycardia and hypotension, which was unresponsive to fluid challenge requiring norepinephrine infusion. Intraoperatively, during tumour resection from the dorsal medulla, episodes of hypertension and bradycardia were observed. Intraoperative blood loss was adequately managed with a stable hemodynamic profile without postoperative anaemia. An electrocardiogram showed sinus tachycardia with T wave inversion, and blood investigation revealed elevated cardiac troponin T levels. Point of care ultrasound (POCUS) of heart and lung showed features of NSM. Infusion dobutamine was added to achieve a target mean arterial pressure of 65 mm Hg with concomitant furosemide infusion and fluid restriction. Daily POCUS assessment of cardiac contractility and volume status was done. The patient was weaned from vasoactive drugs and ventilator following improvement of cardiac function and was discharged from NICU after 17 days. Conclusion: NSM results from the excessive release of catecholamines following stimulation of trigger zones in the brain. To date, a handful of cases of pediatric NSM following primary brain tumour are reported where hydrocephalus resulted in trigger zone activation. In this presented case, direct brain stem stimulation during tumour resection might have triggered NSM. Irrespective of the cause, timely diagnosis and execution of supportive management in our patient resulted in a positive outcome. [ABSTRACT FROM AUTHOR]

A 6-year-old castrated male Labradoodle was referred in uncompensated hypovolemic shock, with a 72-h history of lethargy, vomiting and diarrhea that had acutely worsened with subsequent development of profuse hemorrhagic diarrhea in the last 24 h after a visit to the groomer. In most respects this case was classic for a patient with a primary hypoadrenocortical crisis. After initial attempts to address hypovolemia and refractory hypotension, no clinical improvement was seen, and the respiratory rate had increased acutely to 80 bpm with crackles detected on thoracic auscultation and serosanguineous fluid began draining from the nose and mouth. An arterial blood gas sample while breathing room air revealed moderate hypoxemia (PaO2 59.9: RI 95–100 mmHg), an elevated alveolar-arterial (A-a) gradient at 54.7 (RI < 15 mmHg) and a PaO2:FiO2 ratio of 285 mmHg. Thoracic radiographs revealed severe bilateral alveolar lung pattern largely limited to the perihilar and caudodorsal lung fields. The radiographic findings, along with signs of ongoing hypovolemia, the lack of evidence of typical long-standing acquired cardiac disease, and the rapid resolution of the pulmonary edema without the need for diuretics or long-term cardiac medications supported non-cardiogenic pulmonary edema. The proposed cause of the non-cardiogenic pulmonary edema was speculated to be neurogenically mediated. Oxygen supplementation along with mineralocorticoid and glucocorticoid replacement therapy was sufficient for the management of the non-cardiogenic pulmonary edema in this case.

During physiological stress responses such as vigorous exercise, emotional states of fear and rage, and asphyxia, the nervous system induces a massive release of systemic catecholamines that prepares the body for survival by increasing cardiac output and redirecting blood flow from non-essential organs into the cardiopulmonary circulation. A curious byproduct of this vital response is a sudden, transient, and redistributive leukocytosis provoked mostly by the resultant shear forces exerted by rapid blood flow on marginated leukocytes. Generalized convulsive seizures, too, result in catecholamine surges accompanied by similar leukocytoses, the magnitude of which appears to be rooted in semiological factors such as convulsive duration and intensity. This manuscript reviews the history, kinetics, physiology, and clinical significance of post-convulsive leukocyte elevations and discusses their clinical utility, including a proposed role in the scientific investigation of sudden unexpected death in epilepsy (SUDEP).

We present a case of cardiogenic shock due to neurogenic stress cardiomyopathy (NSC) in a patient with nontraumatic subarachnoid hemorrhage caused by a ruptured aneurysm of the right pericallosal artery. Due to the catecholamine-resistant shock, levosimendan was administered under advanced hemodynamic control, including transpulmonary thermodilution and echocardiography. This resulted in an improved cardiac contractility and reduced demand for catecholamines. Full stabilization of hemodynamic parameters was achieved by day 5. In the discussion section we reviewed available published case reports of using levosimendan in stress cardiomyopathy treatment.

Rationale: Donor brain death-induced lung injury may compromise graft function after transplantation. Establishing strategies to attenuate lung damage remains a challenge because the underlying mechanisms remain uncertain. Objectives: The effects of tacrolimus pretreatment were evaluated in an experimental model of brain death-induced lung injury. Methods: Brain death was induced by slow intracranial infusion of blood in anesthetized pigs after randomization to tacrolimus (orally administered at 0.25 mg ⋅ kg-1 twice daily the day before the experiment and intravenously at 0.05 mg ⋅ kg-1 1 h before the experiment; n = 8) or placebo (n = 9) pretreatment. Hemodynamic measurements were performed 1, 3, 5, and 7 hours after brain death. After euthanasia of the animals, lung tissue was sampled for pathobiological and histological analysis, including lung injury score (LIS). Measurements and Main Results: Tacrolimus pretreatment prevented increases in pulmonary arterial pressure, pulmonary vascular resistance, and pulmonary capillary pressure and decreases in systemic arterial pressure and thermodilution cardiac output associated with brain death. After brain death, the ratio of PaO2 to FiO2 decreased, which was prevented by tacrolimus. Tacrolimus pretreatment prevented increases in the ratio of IL-6 to IL-10, VCAM1 (vascular cell adhesion molecule 1), circulating concentrations of IL-1β, and glycocalyx-derived molecules. Tacrolimus partially decreased apoptosis (Bax [Bcl2-associated X apoptosis regulator]-to-Bcl2 [B-cell lymphoma-2] ratio [P = 0.07] and number of apoptotic cells in the lungs [P < 0.05]) but failed to improve LIS. Conclusions: Immunomodulation through tacrolimus pretreatment prevented pulmonary capillary hypertension as well as the activation of inflammatory and apoptotic processes in the lungs after brain death; however, LIS did not improve. [ABSTRACT FROM AUTHOR]

It has been reported that neutrophil extracellular traps (NETs) involve inflammation, coagulation and cell death. Acute lung injury is also considered to be connected with NETs. Deoxyribonuclease I (DNase-1), a clinical medication for the respiratory system, has been reported to degrade cell-free DNA (cfDNA), which is the main component of NETs. Herein, we did research to clarify the therapeutic value of DNase-1 in NPE after SAH. In this model, we found that the treatment of DNase-1 remarkably decreased lung water, neutrophilic infiltration and inflammation. In addition, DNase-1 inhibited the NETs and proinflammatory subtype transition of the macrophages. Moreover, the depletion of neutrophil also verified the role of NETs in NPE. Our results suggest that DNase-1 has the potential to effectively relieve the NPE after SAH and to be a clinical drug for use after SAH. [ABSTRACT FROM AUTHOR]

Background: Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune inflammatory disease predominantly found in women of child-bearing age. Neurogenic pulmonary edema (NPE) is a recalcitrant complication that occurs after injury to the central nervous system and has an acute onset and rapid progression. Limbic encephalitis is an inflammatory encephalopathy caused by viruses, immune responses, or other factors involving the limbic system. NPE caused by SLE is rare.Case Presentation: Here, we report a case of a 21-year-old woman with SLE who experienced five episodes of generalized tonic-clonic seizure after headache and dyspnea. Anti-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) 2 antibody was tested positive in the serum and cerebrospinal fluid. Electrocardiography (EEG) indicated paroxysmal or sporadic medium amplitude theta activity. In addition, chest computed tomography (CT) showed multiple diffuse consolidations and ground-glass opacities. We finally considered a diagnosis of NPE and AMPAR limbic encephalitis. The patient's symptoms improved obviously after methylprednisolone pulse therapy and antiepileptic treatment.Conclusions: NPE can be a complication of neuropsychiatric lupus erythematosus (NPSLE). AMPAR2 antibodies may be produced in NPSLE patients, especially in those with high polyclonal IgG antibody titers. More basic and clinical studies are required to confirm these observations and elucidate the pathogenicity of encephalitis-related autoantibodies in SLE patients. [ABSTRACT FROM AUTHOR]

Recombinant tissue plasminogen activator (r-tPA) is the first-line drug for the treatment of acute ischemic stroke, despite it may lead to a variety of complications in some cases. In patients with extensive stroke, infarction of the brain can cause suppression of the respiratory center in the brain leading to neurogenic pulmonary edema that potentially causes respiratory failure. Its etiology is either due to a neurogenic or non-neurogenic process. Nevertheless, the definite pathophysiology of these circumstances remains unclear. In this study, we reported four cases of post-thrombolytic ischemic stroke patients who suffer from pulmonary edema with different symptoms and onset times as well as we discuss the possible explanation behind these different outcomes. [ABSTRACT FROM AUTHOR]

Abstract Background Neurogenic pulmonary edema is a rare but serious complication of febrile status epilepticus in children. Comprehensive screening for viral pathogens is seldomly performed in the work-up of febrile children. Case presentation A 22-month-old girl presented with her first episode of febrile status epilepticus, after which she developed acute pulmonary edema and respiratory failure. After the termination of seizure activity, the patient was intubated and managed on mechanical ventilation in the emergency room. The resolution of respiratory failure, as well as the neurological recovery, was achieved 9 h after admission, and the patient was discharged 6 days after admission without any complications. Molecular biological diagnostic methods identified the presence of human coronavirus HKU1, influenza C virus, and human parainfluenza virus 2 from the patient’s nasopharyngeal specimens. Conclusions Neurogenic pulmonary edema following febrile status epilepticus was suspected to be the etiology of our patient’s acute pulmonary edema and respiratory failure. Timely seizure termination and rapid airway and respiratory intervention resulted in favorable outcomes of the patient. Molecular biological diagnostic methods identified three respiratory viruses; however, their relevance and association with clinical symptoms remain speculative.

We report a case of neurogenic pulmonary edema (NPE) caused by middle cerebral artery infarction involving the right insular cortex. Hyperactivity of the insular cortex, which regulates sympathetic function, can cause NPE. The NPE should be considered in the differential diagnosis of dyspneic patients with insular cortex infarction. Cerebral infarction involving insular cortex can cause neurogenic pulmonary edema (NPE). The NPE should be considered in the differential diagnosis of dyspneic patients with cerebral infarction involving the insular cortex. [ABSTRACT FROM AUTHOR]

Neuroinflammation is closely associated with poor prognosis in patients with subarachnoid hemorrhage (SAH). The purpose of this study was to investigate the role of neutrophil extracellular traps (NETs), which are important regulators of sterile inflammation, in SAH. In this study, markers of NET formation, quantified by the level of citrullinated histone H3 (CitH3), were significantly increased after SAH and correlated with SAH severity. CitH3 peaked at 12 h in peripheral blood and at 24 h in the brain. Administration of the peptidyl arginine deiminase 4 (PAD4) selective antagonist GSK484 substantially attenuated SAH-induced brain edema and neuronal injury. Moreover, the benefit of NET inhibition was also confirmed by DNAse I treatment and neutrophil depletion. Mechanistically, NETs markedly exacerbated microglial inflammation in vitro. NET formation aggravated neuroinflammation by promoting microglial activation and increased the levels of TNF-α, IL-1β, and IL-6, while inhibiting NETs demonstrated anti-inflammatory effects by decreasing the levels of these proinflammatory factors. Moreover, neurogenic pulmonary edema (NPE), a severe nonneurological complication after SAH, is associated with a high level of NET formation. However, GSK484 effectively inhibited the formation of NETs in the lungs of NPE mice, thereby preventing the diffusion of neutrophilic infiltration and attenuating the swelling of the alveolar interstitium. In conclusion, NETs promoted neuroinflammation after SAH, while pharmacological inhibition of PAD4-NETs could reduce the inflammatory damage caused by SAH. These results supported the idea that NETs might be potential therapeutic targets for SAH. [ABSTRACT FROM AUTHOR]

The brain-lung interaction can seriously affect patients with traumatic brain injury, triggering a vicious cycle that worsens patient prognosis. Although the mechanisms of the interaction are not fully elucidated, several hypotheses, notably the "blast injury" theory or "double hit" model, have been proposed and constitute the basis of its development and progression. The brain and lungs strongly interact via complex pathways from the brain to the lungs but also from the lungs to the brain. The main pulmonary disorders that occur after brain injuries are neurogenic pulmonary edema, acute respiratory distress syndrome, and ventilator-associated pneumonia, and the principal brain disorders after lung injuries include brain hypoxia and intracranial hypertension. All of these conditions are key considerations for management therapies after traumatic brain injury and need exceptional case-by-case monitoring to avoid neurological or pulmonary complications. This review aims to describe the history, pathophysiology, risk factors, characteristics, and complications of brain-lung and lung-brain interactions and the impact of different old and recent modalities of treatment in the context of traumatic brain injury. [ABSTRACT FROM AUTHOR]

We present a case of severe neurogenic pulmonary edema and arrhythmia complicating management of a 7-year-old child with acute epidural hematoma and impending cerebral herniation. The underlying mechanisms for this are discussed as well as management of severe neurogenic pulmonary edema. We emphasize the need to recognize this rare complication early and institute prompt aggressive management.

Objectives: Acute respiratory distress syndrome (ARDS) in patients with traumatic brain injury (TBI) is associated with increased mortality. Information on the prevalence of ARDS and its neurological outcome after TBI is sparse. We aimed to systematically review the prevalence, risk factors, and outcome of ARDS in TBI population. Data Sources: PubMed and four other databases (Embase, Cochrane Library, Web of Science Core Collection, and Scopus) from inception to July 6, 2020. Study Selection: Randomized controlled trials (RCTs) and observational studies in patients older than 18 years old. Data Extraction: Two independent reviewers extracted the data. Study quality was assessed by the Cochrane Risk of Bias tool for RCTs, the Newcastle–Ottawa Scale for cohort and case–control studies. Good neurological outcome was defined as Glasgow Outcome Scale ≥ 4. Random-effects meta-analyses were conducted to estimate pooled outcome prevalence and their 95% confidence intervals (CI). Data Synthesis: We included 20 studies (n = 2830) with median age of 44 years (interquartile range [IQR] = 35–47, 64% male) and 79% (n = 2237) suffered severe TBI. In meta-analysis, 19% patients (95% CI = 0.13–0.27, I2 = 93%) had ARDS after TBI. The median time from TBI to ARDS was 3 days (IQR = 2–5). Overall survival at discharge for the TBI cohort was 70% (95% CI = 0.64–0.75; I2 = 85%) and good neurological outcome at any time was achieved in 31% of TBI patients (95% CI = 0.23–0.40; I2 = 88%). TBI cohort without ARDS had higher survival (67% vs. 57%, p = 0.01) and good neurological outcomes (34% vs. 23%, p = 0.02) compared to those with ARDS. We did not find any specific risk factors for developing ARDS. Conclusion: In this meta-analysis, approximately one in five patients had ARDS shortly after TBI with the median time of 3 days. The presence of ARDS was associated with worse neurological outcome and mortality in TBI. Further research on prevention and intervention strategy of TBI-associated ARDS is warranted. [ABSTRACT FROM AUTHOR]

Moderate to severe traumatic brain injury is often associated with several extracranial organ complications, which increase the morbidity and mortality. Respiratory complications such as acute lung injury, pneumonia, and acute respiratory distress syndrome (ARDS) occur most commonly, but neurogenic pulmonary edema can be life threatening. Cardiovascular complications occur frequently. However, arrhythmia, cardiogenic shock, and neurogenic stunned myocardium, though occur infrequently, can be life threatening. Coagulation abnormalities and sepsis constitute serious complications that may result in multiorgan failure. These constitute independent risk factors for mortality. Endocrine abnormalities, gastrointestinal disruptions, and other complications occur less commonly. These extracranial complications develop as a result of altered neurogenic immune response, both central and peripheral responses. Brain tissue injury releases both proinflammatory mediators taking part in tissue reparative process and anti-inflammatory cytokines that propagate inflammation. In addition, release of massive amount of catecholamines after head injury results in proliferation of myeloid depressor cells in the circulation, release of reactive oxygen species, and release of immature neutrophils into the circulation. These anti-inflammatory mediators by complex mechanisms inhibit and decrease the number of T cells and cause apoptosis. This results in decreased production and release of cytokines and reduced lymphocyte activated killer cell cytotoxicity, resulting in impaired hypersensitivity reaction. Finally, the complex interplay of various factors leads to suppression of peripheral immune response and susceptibility for infection and sepsis, and causes extracranial organ system failure with increased morbidity and mortality.

Introduction: Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema after sudden raise of intracranial pressure. NPE is the result of release of catecholamines into the circulation immediately after intracranial hemorrhage. The aim of this study is to investigate a possible correlation between the values of cardiac biomarkers on admission and incidence of NPE in patients with aneurysmal subarachnoid hemorrhage (SAH). Methods: Prospective study includes 262 patients with SAH (162 females). Clinical characteristics, serum cardiac and inflammatory biomarkers were measured on admission and on the day of development of NPE. These data were analysed by tests of statistical significance and binary logistic regression analysis in order to predict the development of NPE. Results: 19 patients (7.25%) developed NPE. Statistical analysis revealed that patients who subsequently developed NPE experienced more severe SAH. Cardiac damage was more severe in these patients, as represented by significantly higher number of patients with elevated values of all examined cardiac biomarkers (P from < 0.001 to 0.004). Multivariate regression analysis revealed that elevated troponin I (OR 4.980; 95% CI 1.27-19.49, P = 0.021) and white blood cells count (OR 22.195; 95% CI 3.99-123.50, P < 0.001) were predictors of NPE. Conclusion: Significantly higher number of patients with elevated values of cardiac biomarkers had SAH complicated with NPE. Elevated values of cardiac biomarkers might play an active role in prediction of NPE, although white blood cells count may be involved in the prediction of NPE.

Abstract Objective This study aims to discuss the correlation between serum inflammatory cytokines and neurogenic pulmonary edema (NPE) in children with severe hand–foot–mouth disease (HFMD). Methods A total of 89 patients with severe HFMD were enrolled into this study. These patients were divided into two groups, according to the presence of NPE: central nervous system disease (CNSD) group and NPE group. Serum IL-4, IL-10, IL-6, IL-17, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) levels were measured in patients by enzyme-linked immunosorbent assay at 1, 3, and 5 days after admission. Furthermore, risk factors for NPE were screened using multivariable logistic regression analysis. Results IL-6, TNF-α, IL-10, and interferon-γ (IFN-γ) levels in the NPE group were higher than in the CNSD group. TNF-α, IL-10, and IFN-γ levels reached a peak on the 3rd day of admission. Age, continuous fever, blood sugar, white blood cell count, and IL-10 were risk factors for the occurrence of NPE in severe HFMD. Conclusion The dynamic unbalance of inflammatory cytokines is related to the occurrence and progress of NPE.

Acute neurological insult can trigger a cascade of events in other organ systems such as the heart and lung. Neurogenic stunned myocardium (NSM) and Neurogenic pulmonary edema (NPE) are mostly reported after stroke, subarachnoid hemorrhage, or seizures whenever sympathetic storm and autonomic dysregulation occurs. We report here for the first time, a case of postoperative infratentorial extradural hematoma in a patient triggering NSM and NPE at the same time. The challenges involved in the management of such a patient are described in this case report. The patient was successfully managed and discharged home with no new neurological deficits. [ABSTRACT FROM AUTHOR]

Background: Neurogenic pulmonary edema is a rare but serious complication of febrile status epilepticus in children. Comprehensive screening for viral pathogens is seldomly performed in the work-up of febrile children.Case Presentation: A 22-month-old girl presented with her first episode of febrile status epilepticus, after which she developed acute pulmonary edema and respiratory failure. After the termination of seizure activity, the patient was intubated and managed on mechanical ventilation in the emergency room. The resolution of respiratory failure, as well as the neurological recovery, was achieved 9 h after admission, and the patient was discharged 6 days after admission without any complications. Molecular biological diagnostic methods identified the presence of human coronavirus HKU1, influenza C virus, and human parainfluenza virus 2 from the patient's nasopharyngeal specimens.Conclusions: Neurogenic pulmonary edema following febrile status epilepticus was suspected to be the etiology of our patient's acute pulmonary edema and respiratory failure. Timely seizure termination and rapid airway and respiratory intervention resulted in favorable outcomes of the patient. Molecular biological diagnostic methods identified three respiratory viruses; however, their relevance and association with clinical symptoms remain speculative. [ABSTRACT FROM AUTHOR]

• The chromogranin A (CHGA) level in severe hand, foot, and mouth disease (HFMD) was found to be associated with neurogenic pulmonary edema and cardiopulmonary failure. • CHGA levels correlated with disease severity and a poor prognosis of the disease. • CHGA might have a certain early predictive value with high specificity and sensitivity for mortality in cases with severe HFMD. Severe hand, foot, and mouth disease (HFMD) is associated with high mortality in children, and persistent sympathetic activation is a common presentation. The aim of this study was to prospectively investigate serum chromogranin A (CHGA) levels and their prognostic role in this condition. Serum CHGA, creatine kinase myocardial band (CK-MB), serum D-dimer, norepinephrine, blood glucose, lactate, and C-reactive protein levels, white blood cell (WBC) counts, usage of vasopressors, pediatric risk of mortality Ⅲ (PRISM-Ⅲ) scores, and viral etiology were measured upon pediatric intensive care unit (PICU) admission. The correlation between clinical outcomes and the indicators listed above were analyzed, and the ability of CHGA as a biomarker to predict mortality was evaluated. Serum CHGA levels were higher in the non-survivors group than in the survivors group (median (interquartile range): 434.8 (374.3–502.4) vs 183.3 (131.9–246.9) μg/l; p < 0.001) and were correlated with norepinephrine (r = 0.37. p < 0.001), blood glucose (r = 0.32, p = 0.001), lactate (r = 0.25, p = 0.009), WBC (r = 0.20, p = 0.039), and PRISM-Ⅲ scores (r = 0.748, p < 0.0001). Patients suffering neurogenic pulmonary edema, those infected with enterovirus A71, and those requiring more vasopressors had higher serum CHGA levels (median (interquartile range): 385 (239.9–488.8) vs 161 (115.6–222.9), 340.6 (190.6–436.0) vs 150.5 (112.1–210.0), 395.6 (209.1–487.0) vs 167.7 (110.5–240.5) μg/l, respectively; p < 0.0001). The CHGA level upon PICU admission in severe HFMD could be an independent risk factor for mortality (adjusted odds ratio 2.459, 95% confidence interval 1.054–5.906, p = 0.038) with high specificity (87.5%) and sensitivity (82.6%) (cut-off value at 339.6 μg/l). The CHGA level in severe HFMD was found to be associated with cardiopulmonary failure. If measured upon PICU admission, CHGA may provide additional prognostic information in this disease. [ABSTRACT FROM AUTHOR]

Although acute respiratory distress syndrome is the most common cause of noncardiogenic pulmonary edema, NPs also should be familiar with several other less common causes, including transfusion-related acute lung injury, neurogenic pulmonary edema, preeclampsia/eclampsia, opioid overdose, high-altitude pulmonary edema, and pulmonary embolism. This article addresses the pathophysiology, clinical presentation, diagnostics, treatment, and nursing considerations associated with each uncommon cause of noncardiogenic pulmonary edema. [ABSTRACT FROM AUTHOR]

Background: In our center, large vestibular schwannoma (VS) is typically managed by a planned partial resection through the translabyrinthine route. Here, we report on a rare complication of VS surgery and severe neurogenic pulmonary edema. Case Description: A 33-year-old male was referred to our skull-base center with a large VS. A planned partial resection was performed. The surgery was without complications and the patient showed good recovery without facial nerve dysfunction. In the evening of the 2nd day after surgery, the patient showed rapid neurological deterioration, accompanied by cardiac arrest. After the patient was resuscitated, a computed tomography (CT) was made, which showed generalized (infra- and supratentorial) brain edema and hematoma in the resection cavity. Despite rapid removal of the hematoma, there was no change in the neurological situation. The next CT scan showed a further increase of brain edema and the patient died eventually. Autopsy revealed generalized lung edema, brain edema, and Hashimoto's thyroiditis. The pathologist diagnosed neurogenic lung edema. Conclusion: Neurogenic lung edema can occur on the 2nd day after surgery and induce rapid deterioration of the patient with massive brain edema. [ABSTRACT FROM AUTHOR]

Neurogenic pulmonary edema is one of the complications of acute cerebral diseases and traumas and it is accompanied by severe respiratory failure. It is associated with a high mortality level. There are several theories about neurogenic pulmonary edema development. The theory of the double hit is the most recent causing significant discussion. The theory is based on the pulmonary injury due to systemic inflammatory response when the glial tissue of the injured brain becomes the source of inflammatory mediators. A similar pathogenesis allows considering neurogenic pulmonary edema to be one of the forms of acute respiratory distress syndrome. It has diagnostic criteria common with acute respiratory distress syndrome, which are identified during acute cerebral injury and not associated with the other etiological factors. Currently, there are no effective prevention and treatment of neurogenic pulmonary edema. Support of respiratory exchange through artificial pulmonary ventilation is a major tool used for its management, which is recommended to be performed in compliance with protective ventilation principles. And some particular approaches of the preventive ventilation can be applied only with neuromonitoring.

Abstract Neurogenic pulmonary edema (NPE) is a non‐cardiogenic pulmonary edema that is caused by an acute central nervous system injury and usually develops rapidly after an injury. Although several episodes of NPE resolve spontaneously, the condition may cause unexpected death among patients with epilepsy.

Abstract When observing diffuse ground‐glass opacities in both lungs, physicians should consider several diseases, including heart failure, interstitial lung diseases, and pulmonary infections. However, brain diseases rarely cause lung infiltration. We present an instructive case of neurologic pulmonary edema showing a pathological link between the brain and the lung.

Background: Generalized epileptic convulsions frequently exhibit transient respiratory symptoms and non-infectious leukocytosis. While these peri-ictal effects appear to arise independently from one another, the possibility that they stem from a common ictal pathophysiological response has yet to be explored. We aimed to investigate whether peri-ictal respiratory symptoms and postictal leukocytosis coexist.Methods: We performed a single center retrospective chart review of 446 patients brought to our emergency department between January 1, 2017 and August 23, 2018 for the care of generalized epileptic convulsions with or without status epilepticus. We included 152 patients who were stratified based on the presence (PeCRC+) or absence (PeCRC–) of overt periconvulsive respiratory compromise (PeCRC). In addition, patients were stratified based on the presence or absence of postconvulsive leukocytosis (PoCL), defined as an initial postconvulsive white blood cell (WBC) count ≥ 11,000 cells/mm3. Triage vital signs, and chest x ray (CXR) abnormalities were also examined.Results: Overt PeCRC was observed in 31.6% of patients, 43% of whom required emergent endotracheal intubations. PoCL was observed in 37.5% of patients, and was more likely to occur in PeCRC+ than in PeCRC– patients (79.2 vs. 18.2%; OR = 17.0; 95% CI = 7.2–40.9; p < 0.001). Notably, the magnitude of PoCL was proportional to the severity of PeCRC, as the postconvulsive WBC count demonstrated a negative correlation with triage hemoglobin oxygen saturation (R = −0.22; p < 0.01; CI = −0.48 to −0.07). Moreover, a receiver operating characteristic analysis of the WBC count's performance as predictor of endotracheal intubation reached a significant area under the curve value of 0.81 (95% CI = 0.71–0.90; p < 0.001). Finally, PeCRC+ patients demonstrated frequent CXR abnormalities, and their postconvulsive WBC counts correlated directly with triage heart rate (R = 0.53; p < 0.001).Conclusion: Our data support the existence of an ictal pathophysiological response, which induces proportional degrees of PoCL and PeCRC. We suggest this response is at least partially propelled by systemic catecholamines.

Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by acute onset after central nervous system injury. Here, we investigated the clinical features of NPE in patients with subarachnoid hemorrhage (SAH). We retrospectively analyzed a total of 350 patients with SAH who were treated at our hospital from April 2014 to September 2017. Patient demographics, aneurysm size and location, clinical characteristics, and patient outcomes were reviewed and compared between an NPE and a non-NPE group. Sixteen patients (4.6%) presented with NPE at admission. Ten of these (62.5%) recovered from NPE immediately, and ventilatory support was withdrawn within 2 days from onset. A univariate analysis showed that patients with NPE were younger (P = 0.04), had a higher rate of vertebral artery dissection (P < 0.01), more severe World Federation of Neurosurgical Societies (WFNS) grades (P = 0.01), and lower systolic blood pressure on admission (P = 0.01). A multivariate analysis revealed significant differences in the frequency of vertebral artery dissection (odds ratio 4.83, 95% confidence interval 1.50–15.56, P < 0.01) and in WFNS grades (odds ratio 3.73, 95% confidence interval 1.02–13.66, P = 0.04) between the groups. No significant group differences were found in other factors including heart rate, radiographic sign (Fisher grade), aneurysm size and location, blood sample tests on admission, and neurologic outcomes. Vertebral artery dissection and severe WFNS grade on admission were confirmed as significant risk factors for NPE. However, neurologic outcomes at discharge did not differ between groups, suggesting that poor outcomes due to NPE could be reduced by appropriate diagnosis and treatment. [ABSTRACT FROM AUTHOR]

Background: Generalized epileptic convulsions frequently exhibit transient respiratory symptoms and non-infectious leukocytosis. While these peri-ictal effects appear to arise independently from one another, the possibility that they stem from a common ictal pathophysiological response has yet to be explored. We aimed to investigate whether peri-ictal respiratory symptoms and postictal leukocytosis coexist. Methods: We performed a single center retrospective chart review of 446 patients brought to our emergency department between January 1, 2017 and August 23, 2018 for the care of generalized epileptic convulsions with or without status epilepticus. We included 152 patients who were stratified based on the presence (PeCRC+) or absence (PeCRC–) of overt periconvulsive respiratory compromise (PeCRC). In addition, patients were stratified based on the presence or absence of postconvulsive leukocytosis (PoCL), defined as an initial postconvulsive white blood cell (WBC) count ≥ 11,000 cells/mm3. Triage vital signs, and chest x ray (CXR) abnormalities were also examined. Results: Overt PeCRC was observed in 31.6% of patients, 43% of whom required emergent endotracheal intubations. PoCL was observed in 37.5% of patients, and was more likely to occur in PeCRC+ than in PeCRC– patients (79.2 vs. 18.2%; OR = 17.0; 95% CI = 7.2–40.9; p < 0.001). Notably, the magnitude of PoCL was proportional to the severity of PeCRC, as the postconvulsive WBC count demonstrated a negative correlation with triage hemoglobin oxygen saturation (R = −0.22; p < 0.01; CI = −0.48 to −0.07). Moreover, a receiver operating characteristic analysis of the WBC count's performance as predictor of endotracheal intubation reached a significant area under the curve value of 0.81 (95% CI = 0.71–0.90; p < 0.001). Finally, PeCRC+ patients demonstrated frequent CXR abnormalities, and their postconvulsive WBC counts correlated directly with triage heart rate (R = 0.53; p < 0.001). Conclusion: Our data support the existence of an ictal pathophysiological response, which induces proportional degrees of PoCL and PeCRC. We suggest this response is at least partially propelled by systemic catecholamines. [ABSTRACT FROM AUTHOR]

Data on the frequency and clinical relevance of neurogenic pulmonary edema (NPE) following epileptic seizures are limited. The aim of the present study was to analyze computed tomography (CT) examinations in patients with previous seizures. Incidence of NPE and related clinical factors were retrospectively assessed in patients admitted because of epileptic seizures who underwent thoracic CT imaging as part of emergency diagnostics. Between January 2010 and January 2016, we included all patients admitted with the International Classification of Diseases (ICD) diagnosis code of epileptic seizure or epilepsy and who underwent CT imaging, including visualization of the lungs, as part of emergency diagnostics. Of the 47 included patients, 26 patients had suffered from generalized convulsive seizures (GCS), 17 patients had focal seizures with impaired and 4 without impaired consciousness. Signs of NPE were present in 5 out of 47 patients; all 5 patients had GCS prior to thoracic CT scan (i.e., 19% of patients with GCS). In four out of five cases, a single seizure was described; in one case, the seizure was only partially witnessed, but the indirect clinical signs strongly suggested a GCS. Related factors such as the initial respiratory rate or the initial pCO2 value were not significantly different in patients with and without signs of NPE. The highly selected and biased patient group warrants caution in the interpretation of the study results. Our data, however, confirm that signs of NPE appear to be rather frequent in patients with GCS. Its clinical significance as regards morbidity and sudden death in epilepsy is discussed. • Neurogenic pulmonary edema (NPE) may be involved in seizure-related complications and SUDEP. • Signs of NPE in computed tomography (CT) examinations were retrospectively assessed in patients admitted for acute seizures. • NPE was detected in 5 out of 47 patients • All 5 NPE patients had suffered from generalized convulsive seizures (GCS) prior to thoracic CT scan. • Signs of respiratory distress were not significantly more frequent in the group with NPE than in den group without NPE. [ABSTRACT FROM AUTHOR]

Diverse acute neurological injuries may cause acute cardiopulmonary events including neurogenic pulmonary edema (NPE) and neurogenic stunned myocardium (NSM). The mechanism is probably mediated by sympathetic nervous system activation. Focal central nervous system (CNS) lesions, such as demyelinating lesions in multiple sclerosis (MS), may also cause cardiopulmonary disturbances. We aim to review the acute cardiopulmonary events associated with MS relapses. We performed a literature search using PubMed, and selected case reports of acute cardiac and/or pulmonary events related to MS exacerbations. We grouped these events into three categories: 1) NPE with normal cardiac function; 2) NSM and Takotsubo cardiomyopathy (TTC); 3) coexisting myocardial dysfunction and pulmonary edema. In some cases, cardiac and pulmonary symptoms preceded the onset of neurological symptoms. The majority of cases were associated with acute demyelinating lesions located in the medulla. Acute brainstem MS relapses, with demyelinating lesions affecting the medulla, may cause acute cardiac and pulmonary events presumably secondary to sympathetic hyperstimulation. Specific regions in the medulla that regulate cardiac function, systemic blood pressure and pulmonary hydrostatic pressure seem to be responsible for these events. [ABSTRACT FROM AUTHOR]

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