Neurogenic Pulmonary Edema In Patients Research Articles

Pathophysiology and Management of Neurogenic Pulmonary Edema in Patients with Acute Severe Brain Injury.

Acute brain injury (ABI) consists of any acquired insult to the brain and is a significant cause of morbidity and mortality worldwide. Approximately 20% to 30% of patients with ABI develop a lung injury called neurogenic pulmonary edema (NPE), and its development often results in poor outcomes. This article provides a narrative review of the evidence regarding proposed mechanisms of injury, diagnosis, and treatment of NPE in the critical care setting. PubMed and Ovid databases were searched for observational or prospective studies relevant to the diagnosis and treatment of NPE. Overall, studies showed that although the specific mechanisms responsible for NPE remain uncertain, putative mechanisms include vaso- and venoconstriction, catecholamine release with resultant pulmonary vasoconstriction called the "blast injury theory," increased vagal tone, and increased capillary permeability. Diagnosis involves identifying signs of pulmonary edema in patients who experienced a neurologic insult. Management strategies aim to address both brain and lung injury, and treatment modalities appear to work best when balanced toward maintaining a normal physiologic state. In summary, NPE is an often underdiagnosed but important sequela of ABI, which may result in additional long-term morbidity. It is therefore an important entity for providers to recognize and tailor their clinical approach toward.

Clinical Features of Neurogenic Pulmonary Edema in Patients with Subarachnoid Hemorrhage

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 Ten of these (62.5%) recovered from NPE immediately, and ventilatory support was withdrawn within 2 days from onset.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.

Risk factors for neurogenic pulmonary edema in patients with severe hand, foot, and mouth disease: A meta-analysis

ObjectiveTo investigate the risk factors for neurogenic pulmonary edema (NPE) in patients with severe hand, foot, and mouth disease (HFMD) and to provide evidence for the prevention and treatment of NPE. MethodsSeveral databases were searched (from inception to 2017) to identify case–control studies on risk factors for NPE among patients with severe HFMD. Data were analyzed via meta-analysis. The combined odds ratio (OR) and 95% confidence interval (CI) were calculated using fixed-effects and random-effects models, and a sensitivity analysis and evaluation of publication bias was also performed. ResultsA total of 14 studies involving 557 cases (severe HFMD with NPE) and 1450 controls (severe HFMD) were included. Results for the categorical variables were as follows: hyperglycemia (OR 10.25, 95% CI 4.82–21.76), tachycardia (OR 6.21, 95% CI 3.02–12.75), hypertension (OR 3.79, 95% CI 2.90–4.95), respiratory rhythm abnormality (OR 7.86, 95% CI 2.46–25.12), drowsiness (OR 8.11, 95% CI 4.26–15.44), vomiting (OR 8.96, 95% CI 3.83–20.96), limb tremors (OR 8.96, 95% CI 3.83–20.96), atypical rash (OR 4.27, 95% CI 2.83–6.45). No significant publication bias was found for the different factors. ConclusionsDrowsiness ranks first among risk factors for NPE in children with severe HFMD, followed by vomiting, tachycardia, hypertension, breathing rhythm changes, limb tremors, atypical rash, and hyperglycemia.

Could cardiac biomarkers predict neurogenic pulmonary edema in aneurysmal subarachnoid hemorrhage?

Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema after a significant central nervous system (CNS) insult. NPE occurs as a result of release of catecholamines into the blood immediately after aneurysm rupture. The aim of this study is to investigate the connection between the value of cardiac biomarkers on admission and incidence of NPE in patients with aneurysmal subarachnoid hemorrhage (SAH). A total of 262 SAH patients (162 women, 100 men) were prospectively included in the study. Clinical characteristics, electrocardiographic (ECG) changes, serum cardiac and inflammatory biomarkers were measured on admission and on the day of development of NPE. These data were analyzed in order to predict the development NPE. Nineteen patients (7.25%) developed NPE. Comparison revealed that patients who subsequently developed NPE, sustained more severe SAH. Cardiac damage was more severe in these patients, as represented by significantly higher mean values of all examined cardiac biomarkers (P = 0.000), except for troponin I value that was significantly lower (P = 0.000). Multivariate regression analysis revealed that elevated troponin I (OR, 4.980; 95% CI, 1.27-19.49; P = 0.021) and white blood cell count (OR, 22.195; 95% CI, 3.99-123.50; P = 0.000) are predictors of NPE. Significantly higher values of cardiac biomarkers were observed in SAH patients complicated with NPE. Elevated values of cardiac biomarkers appear to play an active role in prediction of NPE, although white blood cell count may be involved in the prediction of NPE. There is an influence of SAH therapy on predictors of NPE.

Role of PiCCO monitoring for the integrated management of neurogenic pulmonary edema following traumatic brain injury: A case report and literature review.

Neurogenic pulmonary edema (NPE) is occasionally observed in patients with traumatic brain injury (TBI); however, this condition is often underappreciated. NPE is frequently misdiagnosed due to its atypical clinical performance, thus delaying appropriate treatment. A comprehensive management protocol of NPE in patients with TBI has yet to be established. The current study reported the case of a 67-year-old man with severe TBI who was transferred to our intensive care unit (ICU). On day 7 after hospitalization, the patient suddenly suffered tachypnea, tachycardia, systemic hypertension and hypoxemia during lumbar cistern drainage. Intravenous diuretics, tranquilizer and glucocorticoid were administered due to suspected left heart failure attack. Chest radiography examination supported the diagnosis of pulmonary edema; however, hypotension and hypovolemia were subsequently observed. Pulse index continuous cardiac output (PiCCO) hemodynamic monitoring and bedside echocardiography were performed, which excluded the diagnosis of cardiac pulmonary edema, and thus the diagnosis of NPE was confirmed. Goal-directed therapy by dynamic PiCCO monitoring was then implemented. In addition, levosimendan, an inotropic agent, was introduced to improve cardiac output. The patient had complete recovered from pulmonary edema and regained consciousness on day 11 of hospitalization. The current case demonstrated that PiCCO monitoring may serve a central role in the integrated management of NPE in patients with TBI. Levosimendan may be a potential medicine in treating cardiac dysfunction, along with its benefit from improving neurological function in NPE patients.

Heart Rate Variability Predicts Neurogenic Pulmonary Edema in Patients with Subarachnoid Hemorrhage

An alternation of sympathetic and vagal nervous activity has been suggested to be one possible mechanism of neurogenic pulmonary edema (NPE) in patients with subarachnoid hemorrhage (SAH). The study aimed to explore if sympathovagal modulation assessed by frequency domains of heart rate variability (HRV) is associated with impending NPE in patients with SAH. Two hundred forty-eight consecutive spontaneous SAH adult patients were included in this single-center cohort study. A continuous 10-min electrocardiography for HRV analysis was recorded. The patients were stratified into NPE and non-NPE based on serially clinical and radiologic findings within 24h. Seven frequency domains of HRV were compared between these 2 groups. Compared to the non-NPE (n=212), the NPE (n=36) had significantly higher mean arterial pressure, higher World Federation of Neurological Surgeons (WFNS) class, higher Hunt-Hess scale, lower total power (TP), lower very low-frequency component, lower low-frequency component, lower normalized low-frequency component (LF%), higher normalized high-frequency component, and lower low-frequency component/high-frequency component ratio. Multiple logistic regression model identified WFNS class (OR 4.048; 95% CI 1.589-10.311), LF% (OR 0.933; 95% CI 0.910-0.958), and TP (OR 0.995; 95% CI 0.992-0.998) as the significant variables associated with occurrence of NPE. The area under receiver operating characteristic curves of LF% and TP were found to be 0.838 (95% CI 0.774-0.901) and 0.653 (95% CI 0.557-0.749), respectively. Loss of cardiac variability and depressed sympathovagal modulation, represented by TP and LF%, may predict the development of NPE in the early stage in patients with SAH.

ECG abnormalities predict neurogenic pulmonary edema in patients with subarachnoid hemorrhage

ObjectiveThe study aims to assess if electrocardiographic (ECG) abnormalities could predict the development of neurogenic pulmonary edema (NPE) within 24 hours in cases of spontaneous subarachnoid hemorrhage (SAH). MethodsWe studied prospectively a cohort of 269 adult patients with nontraumatic SAH in an emergency department of a university-affiliated medical center. A 12-lead ECG was taken for these patients. The patients were stratified into NPE and non-NPE based on serially clinical and radiologic findings. The ECG abnormalities were compared between these 2 groups of patients. ResultsCompared with the non-NPE (n = 229), the NPE (n = 40) had significantly higher World Federation of Neurological Surgeons class (P < .001), higher Hunt-Hess scale (P < .001), and higher prevalence of diabetes mellitus (P = .033). In addition, the percentage of ECG morphological abnormality was significantly higher in NPE, in which nonspecific ST- or T-wave changes (NSSTTCs) are significantly higher. Multiple logistic regression model identified World Federation of Neurological Surgeons class (95% confidence interval [CI], 2.6-13.3; P < .001), abnormal Q or QS wave (95% CI, 1.1-9.1; P = .038), and NSSTTCs (95% CI, 1.2-7.5; P = .016) as the significant variables associated with NPE. ConclusionsElectrocardiographic abnormalities, especially abnormal Q or QS wave and NSSTTCs, may predict the development of NPE within 24 hours in adult patients with spontaneous SAH.

Dynamic changes in serum inflammatory cytokines and their association with neurogenic pulmonary edema in patients with severe hand-foot-mouth disease

Objective To investigate the dynamic changes in the serum inflammatory cytokines and their association with neurogenic pulmonary edema (NPE)in the patients with severe hand-foot-mouth disease (HFMD). Methods Eighty-nine patients with severe HFMD from March 2010 to December 2012 were recruited in the study.The patients were divided into NPE group and central nervous system diseases(CNSD) group according whether they had NPE.The cytokines, including interleukin (IL)-4, IL-6, IL-10, IL-17, tumor necrosis factor-α(TNF-α) and interferon-γ(IFN-γ)were evaluated by using enzyme-linked immunosorbent assay on day 1, 3 and 5 after admission to hospital.Risk factors for NPE involvement during hospital stay were analyzed with multivariate Logistic regression analysis. Results (1)Compared with the CNSD group, the serum levels of IL-6(Ftime=1.876, P=0.177, Ftime*group=2.192, P=0.145, Fgroup=7.855, P=0.007), TNF-α(Ftime=13.133, P=0.001, Ftime*group=0.291, P=0.592, Fgroup=3.644, P=0.042), IL-10(Ftime=14.580, P=0.001, Ftime*group=2.612, P=0.078, Fgroup=16.823, P=0.000), INF-γ(Ftime=3.093, P=0.045, Ftime*group= 0.513, P=0.600, Fgroup=20.141, P=0.000)were significantly higher than those in NPE group.(2)The serum levels of TNF-α, IL-10, INF-γ rose to the peak on the third day.(3) By using multivariate Logistic regression analysis, age (OR=3.383, 95% CI: 1.173-4.759), days of fever (OR=4.925, 95%CI: 1.758-3.794), hyperglycaemia (OR=3.465, 95%CI: 1.303-5.220), leucocytosis (OR=7.579, 95%CI: 2.530-12.704)and elevation of IL-10 (OR=1.228, 95%CI: 1.007-1.523) were entered into equation.In the risk evaluation model, these variables remained independent predictors for NPE. Conclusions Abnormal cytokine productions appear to be responsible for the pathogenesis of NPE, and might be an effective tool for predicting NPE in infants with severe HFMD. Key words: Hand-foot-mouth disease; Cytokine; Dynamic change; Neurogenic pulmonary edema

Neurogenic Pulmonary Edema in Patients with Nontraumatic Intracerebral Hemorrhage

Neurogenic pulmonary edema (NPE) is a well-recognized phenomenon after intracranial insult. In this study, we evaluated the predictors for NPE and its association with outcome in patients with intensive care unit-treated nontraumatic intracranial hemorrhage. This was a prospective, observational clinical study in a university-level intensive care unit. Clinical characteristics, level of consciousness, and Acute Physiology and Chronic Health Evaluation (APACHE) II score were recorded on admission and the findings of primary head computed tomography were reviewed. A chest radiograph and arterial blood gas analysis were taken serially and NPE was determined as acute bilateral infiltrates in chest radiograph and hypoxemia. Echocardiography and cardiac and inflammatory markers were recorded. The 1-year outcome was assessed using the Glasgow Outcome Scale. NPE developed in 38 (35%) of the 108 patients included. Predictors for NPE were higher APACHE II score (≥20, odds ratio 6.17, P = 0.003) and higher interleukin-6 plasma concentration (>40 pg/mL, odds ratio 5.62, P = 0.003). Of patients with 0, 1, or 2 predictors mentioned above, 4%, 37%, and 65% had NPE, respectively. NPE was associated with a higher 1-year mortality (37% vs 14%, P = 0.007, respectively), but with an unchanged functional outcome after 1 year (Glasgow Outcome Scale score 1-3, 53% vs 51%, P > 0.9). Predictors for NPE are the severity of disease defined by APACHE II scores and higher levels of systemic inflammatory mediators. NPE is associated with a higher 1-year mortality, but not with a poorer 1-year functional outcome.

Abstract 56: Association between Increased Plasma Catecholamine Levels and Neurogenic Pulmonary Edema in Patients with Subarachnoid Hemorrhage

Background: Neurogenic pulmonary edema (NPE) occurs relatively frequently after aneurysmal subarachnoid hemorrhage (SAH), and excessive release of catecholamines (epinephrine/norepinephrine) has been indicated as its principal cause. The objective of this study is to evaluate the relative contribution of each catecholamine in pathogenesis of NPE. Methods: Records of 77 SAH patients (23 men/54 women) whose plasma catecholamine levels were measured within 48 h of SAH onset were retrospectively analyzed. Results: Eight patients (10%) were diagnosed with NPE. Plasma epinephrine (366.9±347.4 vs. 130.3±167.4 pg/mL, p =0.001) and norepinephrine (3481.1±1678.9 vs. 835.5±688.9 pg/mL, p &lt;0.001) levels were significantly higher in the NPE+ group than NPE- group. Demographic comparison revealed that the severity of SAH and cardiac damage/dysfunction was significantly more profound in the NPE+ group. Multivariate logistic regression analysis revealed that increased norepinephrine levels were predictive of NPE (OR, 1.002; 95% CI, 1.001-1.004), but epinephrine levels were not. Linear regression analysis showed that plasma epinephrine and norepinephrine levels were positively correlated. Receiver operating characteristic (ROC) curves showed that threshold values predictive of NPE existed for both catecholamines, and sensitivity/specificity was higher for norepinephrine. After quadrichotomization of patients based on the results of ROC curves, patients whose plasma epinephrine/norepinephrine levels exceeded the threshold values were significantly more likely to experience NPE. Conclusions: Norepinephrine rather than epinephrine appears to play a more active role in pathogenesis of SAH-induced NPE, although both catecholamines may be involved. Since the number of SAH patients complicated by NPE is relatively small, a multi-center study may be required to clarify the issue.

Neurogenic Pulmonary Edema in Patients With Subarachnoid Hemorrhage

Neurogenic pulmonary edema (NPE), leading to cardiopulmonary dysfunction, is a potentially life-threatening complication in patients with aneurysmal subarachnoid hemorrhage (SAH). We sought to assess the clinical presentation and risk factors for the development of NPE after SAH. The database contained prospectively collected information on 477 patients with SAH. Baseline characteristics, clinical and radiologic severity of the bleeding, localization of the ruptured aneurysm, and clinical outcome of patients with NPE were compared with those of patients without NPE. Further, in patients with NPE, intracranial pressure, serum cardiac biomarkers, and hemodynamic parameters during the acute phase were evaluated retrospectively. The incidence of NPE was 8% (39 of 477 patients). Most patients with NPE were severely impaired and all of them presented with radiologically severe hemorrhage. The incidence of NPE was significantly higher in patients with ruptured aneurysm in the posterior circulation. Elevated intracranial pressure was found in 67%, pathologically high cardiac biomarkers in up to 83% of patients with NPE. However, no patient suffered from persistent cardiac dysfunction. Compared with patients without NPE, patients with NPE showed poor neurologic outcome (Glasgow outcome scale 1 to 3 in 25% vs.77% of patients). In conclusion, patients with NPE have a high mortality rate more likely due to their severity grade of the bleeding. Morbidity and mortality due to cardiopulmonary failure might be reduced by appropriate recognition and treatment. The awareness of and knowledge about occurrence, clinical presentation, and treatment of NPE, are essential for all those potentially confronted with patients with SAH in the acute phase.

Respiratory manifestations of systemic disease

Many nonpulmonary diseases may present with respiratory manifestations or may involve the lungs later in the disease course. The mechanisms by which such involvement occurs are almost as diverse as the diseases themselves and include the following. Hematogenous spread of disease is one of the most common mechanisms of lung involvement, for example, lung involvement by metastatic malignant disease. Cytotoxic factors from another anatomic location may be deposited in the alveolar basement membranes and cause pulmonary damage, for example, pulmonary hemorrhage associated with Goodpasture's syndrome. The pulmonary vasculature may prominently manifest generalized disease, as frequently occurs in Wegener's granulomatosis. Toxins accumulated as a result of disease in another organ system may damage the alveolar capillaries and result in pulmonary edema, as can occur in patients with severe azotemia due to renal failure. Depletion of lung surfactant as a consequence of disease in another organ system may produce alveolar collapse and respiratory failure; a disease that can have this effect is acute pancreatitis. The lungs may be the first organs to exhibit, through unknown mechanisms, underlying systemic diseases such as the collagenoses. Humoral factors released in another anatomic site may cause pulmonary problems; for example, bronchospasm may develop in patients with carcinoid of the intestine as a result of serotonin released by the tumor. Injury to another organ system can produce lung damage by complex mechanisms; an excellent example is the occasional development of neurogenic pulmonary edema in patients with trauma to the brain.(ABSTRACT TRUNCATED AT 250 WORDS)