2009;11:417–26, 13. Macmillan CS, Grant IS, Andrews PJ. Reprints will not be available from the authors. Neurogenic pulmonary edema in patients with subarachnoid hemorrhage. Written informed consent was obtained from the patient or a legal surrogate in all cases. This website uses cookies. CRP was measured using an immunoturbidimetric method (Advia 1800 Chemistry System; Siemens Healthcare Diagnostics Inc., Deerfield, IL) and a result >60 mg/L was defined as being elevated. Wartenberg KE, Schmidt JM, Claassen J, Temes RE, Frontera JA, Ostapkovich N, Parra A, Connolly ES, Mayer SA. Contribution: This author helped analyze the data. Clin Chem. Neurogenic pulmonary edema. 2008;57:499–506, 16. 2011;107:581–6, 21. PMID: 22429697. Neurogenic pulmonary oedema (NPO) is the most frequent manifestation of hydrostatic pulmonary oedema and develops after a severe neurological insult. It is still unclear whether anesthesia with isoflurane is closely related to pulmonary edema induced by surgical maneuvers, such as the acute respiratory distress syndrome, 32 where the involvement of neuropeptide Y and VEGF remains unclear. High … 2007;38:2001–23, 24. Systemic inflammation mediators (interleukin [IL]-6, IL-8, IL-10, and tumor necrosis-α) were measured using the Human Cytokine/Chemokine Kit (catalog ID: MPXHCYTO-60K-04; Millipore Corporation, Billerica, MA) by the authors (TK and K-HH).31,32 Matrix metalloproteinases (MMP)-2 and MMP-9 were measured in 47 study patients as a pilot study using gelatin zymography by the authors (MS and TS).33. Stroke. In this study, we demonstrated that the systemic IL-6 concentration was an independent predictor for NPE. Contribution: This author helped analyze the data and write the manuscript. 2010;35:226–32, 32. For information on cookies and how you can disable them visit our Privacy and Cookie Policy. Instead, the APACHE II score, expressing the severity of disease on admission considering different physiologic variables, was an independent risk factor for NPE, which is an original finding. However, recent evidence suggests that increased afterload as in neurogenic pulmonary oedema may also be important in cardiogenic causes. Kalsotra A, Zhao J, Anakk S, Dash PK, Strobel HW. Hyperglycemia. The flowchart of the study is shown in Figure 1. Neurogenic pulmonary edema (NPE) is a well-recognized phenomenon after intracranial insult. We believe neither was the case. Crit Care. A subdural balloon catheter was inflated for 60 s to produce intracranial hypertension. NPE has been described after grand mal seizures and subarachnoid hemorrhage, but also after retrobulbar [4,5] and trigeminal nerve blocks [6] . Nevertheless, the differences between NPE and non-NPE patients were significant even in the smaller sample size of patients who had their inflammatory mediators examined. 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). Attestation: Pasi Ohtonen has seen the original study data, reviewed the analysis of the data, and approved the final manuscript. Attestation: Tuula Salo has seen the original study data, reviewed the analysis of the data, and approved the final manuscript. A chest radiograph and arterial blood gas analysis were recorded in each section (a chest radiograph at least once per section and arterial blood gas analyses every 6 hours). The χ2 test was used for categorical variables. Neurogenic pulmonary edema (NPE) is an acute respiratory event that has been reported to occur after a wide variety of central nervous system (CNS) insults. The 1-year mortality and functional outcome were assessed using the GOS.34 Data were collected through a telephone interview (EJ and MV [see Acknowledgments])19 with either the patient or a surrogate and dichotomized as good (GOS score 4–5: no to moderate disability) or poor (GOS score 1–3: severe disability, vegetative state, death). Tung P, Kopelnik A, Banki N, Ong K, Ko N, Lawton MT, Gress D, Drew B, Foster E, Parmley W, Zaroff J. Predictors of neurocardiogenic injury after subarachnoid hemorrhage. In the pilot zymography analyses of the representative samples (in 11 NPE and 36 non-NPE patients), there were no differences between the groups in either the amounts or the molecular forms of the gelatinases MMP-2 and MMP-9 (data not shown). Some error has occurred while processing your request. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Attestation: Toni Karhu has seen the original study data, reviewed the analysis of the data, and approved the final manuscript. N Engl J Med. Br J Anaesth. . 2010;14:R49, 43. Although elevated cTnI concentration was associated with NPE in our study, it was not an independent predictor of NPE. Severe autonomic nervous system abnormalities. Junttila EK, Koskenkari JK, Ohtonen PP, Ala-Kokko TI. This finding might be related to the small sample size. An assessment of left ventricle (LV) function and LA filling was made based on the data from transthoracic echocardiography (Vivid i™; GE Healthcare Finland), by one of the authors (EJ). Sympathetic hyperactivity during sudden intracranial hypertension leads to cardiovascular instability, myocardial dysfunction, and neurogenic pulmonary edema. 2007;51:447–55, 2. Neurosurgery. Holmer-Jensen J, Karhu T, Mortensen LS, Pedersen SB, Herzig KH, Hermansen K. Differential effects of dietary protein sources on postprandial low-grade inflammation after a single high fat meal in obese non-diabetic subjects. Your account has been temporarily locked due to incorrect sign in attempts and will be automatically unlocked in Muroi C, Keller M, Pangalu A, Fortunati M, Yonekawa Y, Keller E. Neurogenic pulmonary edema in patients with subarachnoid hemorrhage. All patients admitted to the ICU with nontraumatic intracranial hemorrhage during the study period were screened. Lehto SM, Niskanen L, Herzig KH, Tolmunen T, Huotari A, Viinamäki H, Koivumaa-Honkanen H, Honkalampi K, Ruotsalainen H, Hintikka J. Serum chemokine levels in major depressive disorder. Registered users can save articles, searches, and manage email alerts. 1975;2:749–51, 11. Physiol Res. Taken together, our results and the literature support the theory of a brain injury–triggered systemic inflammatory response as an underlying mechanism of NPE, and further studies considering the possibilities to reduce this response are required. 1. ________________________________________________________________________. NPE may develop as a result of activation of specific CNS trigger zones located in the … Pulmonary edema that develops acutely after a central nervous system insult has been recognized as a special entity called "neurogenic pulmonary edema" (NPE) . Electrolyte imbalances (hyponatremia due to cerebral salt wasting, SIADH) Goals . Summary Two young patients with head injuries subsequently developed neurogenic pulmonary oedema. 2. Neurogenic pulmonary edema is an etiological subtype of non-cardiogenic pulmonary edema, classified as a subtype of the acute respiratory distress syndrome by the Berlin definition.. 30 mins. Elevated intracranial pressure increases pulmonary vascular permeability to protein. 2004;35:548–51, 36. Hravnak M, Frangiskakis JM, Crago EA, Chang Y, Tanabe M, Gorcsan J 3rd, Horowitz MB. The most common risk factors are young age, male sex, and head or neck surgery. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference. PCT was measured using an immunochemiluminometric method (DiaSorin Liaison; DiaSorin, Saluggia, Italy) and a result >0.5 μg/L was defined as being elevated. Hemodynamic control & monitoring: Minimize transmural pressure to avoid rebleed . Neurogenic shock (hypotension & bradycardia) Neurogenic pulmonary edema. This was an observational study of patients admitted to the tertiary level ICU over a 2-year period, from December 2007 to December 2009. Get new journal Tables of Contents sent right to your email inbox, April 2013 - Volume 116 - Issue 4 - p 855-861, Neurogenic Pulmonary Edema in Patients with Nontraumatic Intracerebral Hemorrhage: Predictors and Association with Outcome, Articles in Google Scholar by Eija Junttila, MD, Other articles in this journal by Eija Junttila, MD, Consensus Guidelines for the Management of Postoperative Nausea and Vomiting, Hyperchloremia After Noncardiac Surgery Is Independently Associated with Increased Morbidity and Mortality: A Propensity-Matched Cohort Study, Anesthetic Management During Cardiopulmonary Bypass: A Systematic Review, Development of Rapidly Metabolized and Ultra-Short-Acting Ketamine Analogs, The Effect of Systemic Magnesium on Postsurgical Pain in Children Undergoing Tonsillectomies: A Double-Blinded, Randomized, Placebo-Controlled Trial, International Anesthesia Research Society. Plasma B-type natriuretic peptide levels are associated with early cardiac dysfunction after subarachnoid hemorrhage. A multivariate logistic regression model was built to identify the predictors for NPE. The results of the logistic regression model are presented as OR with 99% confidence intervals (CIs). Neurocrit Care. Mascia L. Acute lung injury in patients with severe brain injury: a double hit model. 1995;4:186–92, 7. Davison DL, Terek M, Chawla LS. NPPE is an example of a noncardiogenic pulmonary edema. In this study, the frequency of NPE in patients with nontraumatic intracranial hemorrhage as a whole was similar to reports in patients with SAH.1,3 According to the literature on patients with SAH, cardiovascular disorders are associated with the severity of hemorrhage.35,36 Contrary to this, the findings in our study demonstrated no association between NPE and severity in primary head CT findings. Gäddnäs FP, Sutinen MM, Koskela M, Tervahartiala T, Sorsa T, Salo TA, Laurila JJ, Koivukangas V, Ala-Kokko TI, Oikarinen A. Matrix-metalloproteinase-2, -8 and -9 in serum and skin blister fluid in patients with severe sepsis. Contin Educ Anaesth Crit Care Pain (2011) 11 (3): 87-92 [free full text] FOAM and web resources. Physical examination did not reveal any abnormalities. Baumann A, Audibert G, McDonnell J, Mertes PM. Interferon-β attenuates lung inflammation following experimental subarachnoid hemorrhage. Cobelens PM, Tiebosch IA, Dijkhuizen RM, van der Meide PH, Zwartbol R, Heijnen CJ, Kesecioglu J, van den Bergh WM. 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. 6. The leukocyte count was measured daily using an automated hematology analyzer (CELL-DYN Sapphire; Abbott Diagnostics, Chicago, IL) and a result <4.0 or >12.0 E9/L was defined as abnormal. This was a prospective, observational clinical study in a university-level intensive care unit. 800-638-3030 (within USA), 301-223-2300 (international) Diffuse pulmonary disease. Therefore, we started an investigation on the formation of neurogenic pulmonary edema in rats with balloon-induced acute spinal cord injury, comparing the effect of pentobarbital and xylazine–ketamine anesthesia. Lancet. 2009;11:177–82, 39. Attestation: Tero Ala-Kokko has seen the original study data, reviewed the analysis of the data, and approved the final manuscript. Hyperkalemic arrest with succinylcholine after 24 hrs . Relation of elevation in cardiac troponin I to clinical severity, cardiac dysfunction, and pulmonary congestion in patients with subarachnoid hemorrhage. Cardiac troponin I and acute lung injury after subarachnoid hemorrhage. 1984;140:490–4, 34. Cardiac troponin elevation, cardiovascular morbidity, and outcome after subarachnoid hemorrhage. In patients with SAH, the reported incidence of NPE is approximately 25%1,3 and has been reported to be associated with a worsened clinical outcome.4,5, The terminology used and the definitions of NPE vary in different studies and there is a lack of etiology-specific diagnostic markers, which make the comparisons of the findings in the different publications more difficult. . Avoid secondary spinal cord injury: Spinal cord perfusion pressure: goal MAP > 85-90 (IV fluids, vasopressors) Airway Management of Neurosurgical Patients, Fluid Management for Neurosurgical Patients, Glucose Management for Neurosurgical Patients, Anesthesia for Functional Neuroanesthesia cases, Pain Medicine Fellowship Goals and Objectives, Critical Care Fellowship Goals and Objectives. According to the multivariate logistic regression analyses, the independent predictors for NPE were higher APACHE II scores (≥20, OR 6.17, lower 99% CI 1.30, P = 0.003) and higher IL-6 concentrations (>40 pg/mL, OR 5.62, lower 99% CI 1.26, P = 0.003) (Table 3). Fisher AJ, Donnelly SC, Hirani N, Burdick MD, Strieter RM, Dark JH, Corris PA. Flowchart of the study. Crit Care. The etiology of the hemorrhage was recorded based on the data from head CT scans, CT-angiographies, digital subtraction angiographies, and operation reports. This manuscript was handled by: Gregory J. Crosby, MD. 2011;15:211–40, 25. Neurocrit Care. 73 Pulmonary Edema Zvi Vered, Saar Minha, Edo Kaluski, Nir Uriel Definition Pulmonary edema is a potentially life-threatening syndrome caused by excess fluid transition into the alveoli due to alternations in Starling’s forces. Haemodynamic changes in neurogenic pulmonary oedema: effect of dobutamine. Myocardial dysfunction, arrhythmias . Address correspondence to Eija Junttila, MD, Department of Anesthesiology and Intensive Care, Oulu University Hospital, PO Box 21, FIN-90029 OUH, Oulu, Finland. 2007;27:963–74, 19. Neurocrit Care. The Association of NPE with Cardiac Function, Filling, and Biomarkers and Inflammation Markers, Multivariate Logistic Regression Model for NPE, Data Considering ICU Stay and Outcome Comparing the Patients With and Without NPE, 1. This would imply either a very light level of anesthesia during intubation or the initiation of a neurogenic edema. With the exception of the higher APACHE II scores in NPE patients, there were no differences in clinical characteristics between the NPE and non-NPE patients. He had no previous surgery or anesthesia. You may be trying to access this site from a secured browser on the server. Acute neurogenic pulmonary edema (NPE) is an underdiagnosed yet a common clinical entity. [email protected]. Anesth Analg. Pulmonary edema due to upper airway obstruction can be observed in a variety of clinical situations. SPSS (version 15.0; SPSS Inc., Chicago, IL) and SAS (version 9.2; SAS Institute Inc., Cary, NC) software were used for statistical analysis. Cardiac injury associated with neurogenic pulmonary edema following subarachnoid hemorrhage. 1989;67:1185–91, 14. Serial measurement of extravascular lung water and blood volume during the course of neurogenic pulmonary edema after subarachnoid hemorrhage: initial experience with 3 cases. Nutr J. The main pathophysiologic mechanisms behind NPE are suggested to be increased pulmonary capillary pressure due to transient pulmonary vasoconstriction or cardiac failure after cerebral insult1,6–10 and/or increased permeability in the pulmonary capillary bed due to a disruption of the endothelial barrier by the transient increase in intravascular pressure or by inflammatory mechanisms.1,3,11–14 Some investigators use the term NPE to describe the entire phenomenon,1,5,8,11 whereas others have only used it in pulmonary edemas due to cardiac failure.3,15 At the same time, patients with NPE and without evidence of increased left atrial (LA) filling have been included in the studies examining acute lung injury.3,4,12,16. Ala-Kopsala M, Magga J, Peuhkurinen K, Leipälä J, Ruskoaho H, Leppäluoto J, Vuolteenaho O. Molecular heterogeneity has a major impact on the measurement of circulating N-terminal fragments of A- and B-type natriuretic peptides. Evidence for a hydrostatic mechanism in human neurogenic pulmonary edema. The C-statistic and Hosmer-Lemeshow goodness-of-fit for the multivariable logistic regression model were 0.818 and PH-L = 0.60, respectively. 1996;22:672–6, 8. Diringer MN, Bleck TP, Claude Hemphill J 3rd, Menon D, Shutter L, Vespa P, Bruder N, Connolly ES Jr, Citerio G, Gress D, Hänggi D, Hoh BL, Lanzino G, Le Roux P, Rabinstein A, Schmutzhard E, Stocchetti N, Suarez JI, Treggiari M, Tseng MY, Vergouwen MD, Wolf S, Zipfel GNeurocritical Care Society. Intensive Care Med. It is most frequently associated with intracranial haemorrhage, notably subarachnoid haemorrhage (SAH). Ott L, McClain CJ, Gillespie M, Young B. Cytokines and metabolic dysfunction after severe head injury. Acute neurogenic pulmonary edema: case reports and literature review. Clinical practice: acute pulmonary edema. Stroke. There have been 2 previous study reports written based on these data.19,20. Vieillard-Baron A, Charron C, Chergui K, Peyrouset O, Jardin F. Bedside echocardiographic evaluation of hemodynamics in sepsis: is a qualitative evaluation sufficient? Attestation: Eija Junttila has seen the original study data, reviewed the analysis of the data, approved the final manuscript, and is the author responsible for archiving the study files. In patients undergoing anaesthesia, causes of pulmonary oedema other than cardiogenic are encountered. NPE is a clinical syndrome where pulmonary edema occurs shortly after a serious CNS insult. Attestation: Karl-Heinz Herzig has seen the original study data, reviewed the analysis of the data, and approved the final manuscript. Crit Care Med. The data considering the mechanisms are insufficient and, for the most part, consist of experimental animal studies6,13,17,18 and case series or research reports with relatively small sample sizes,7–9,11,14 as well as some studies using retrospective data collection.4 In particular, the specific role of inflammation in the development of NPE is unknown. Neurocrit Care. [free full text] O’Leary R, McKinlay J. Neurogenic pulmonary oedema. Anal Biochem. 1999;353:1412–3, 46. Br J Anaesth. The predominant mechanism is increased negative intrathoracic pressure, although hypoxia and cardiac and neurologic factors may contribute. One explanation could be that NPE occurred more frequently in more severely ill patients (defined by APACHE II) with worse outcome.47 This finding supports the claim that the aggressive supportive therapy for cardiovascular complications in the ICU may eliminate the negative impact of these complications on the outcome.48 It is notable, however, that such aggressive therapy, particularly excessive fluid resuscitation, may result in pulmonary edema and even worsen the outcome.49. Temes RE, Tessitore E, Schmidt JM, Naidech AM, Fernandez A, Ostapkovich ND, Frontera JA, Wartenberg KE, Di Tullio MR, Badjatia N, Connolly ES, Mayer SA, Parra A. Exclusion criteria included an intracranial hemorrhage resulting from tumor, arteriovenous malformation or recent head/neck operation for a reason other than intracranial hemorrhage, age younger than 18 years, and an ICU admission delay from hospital admission >48 hours. Dickstein K, Cohen-Solal A, Filippatos G, McMurray JJ, Ponikowski P, Poole-Wilson PA, Stromberg A, van Veldhuisen DJ, Atar D, Hoes AW, Keren A, Mebazaa A, Nieminen M, Priori SG, Swedberg KESC Committee for Practice Guidelines. Cardiovascular and pulmonary complications of aneurysmal subarachnoid hemorrhage. In addition, the increased production of intracranial inflammatory mediators43 and their release into the systemic circulation,44 as well as elevated levels of proinflammatory mediators in lung tissue,17,45 have been reported. Neurogenic pulmonary edema associated with pediatric status epilepticus. . Introduction. UMEM Education Pearls — Non-Cardiogenic Pulmonary Edema For immediate assistance, contact Customer Service: Psychoneuroendocrinology. 2005;112:2851–6, 38. 2012 Dec 12;16(2):212. Crit Care. This results in the disruption of gas exchange, tissue hypoxemia, respiratory acidosis, organ hypoxemia, and ultimately organ failure. Acta Anaesthesiol Scand. 2008;29:2388–442, 29. The diagnosis of neurogenic pulmonary edema is based on the occurrence of edema after a neurologic event/insult and the exclusion of other plausible causes. , Jendelová P, Syková E. mechanisms of neurogenic pulmonary edema ( NPE ) is an example a! Hypertension leads to cardiovascular instability, myocardial dysfunction, and manage email alerts Perioperative Medicine: Research reports, Characteristics. Elevated intracranial pressure increases pulmonary vascular permeability to protein, VAP, CHF, ). Elevated intracranial pressure increases pulmonary vascular permeability to protein = arteriovenous malformation these data.19,20 MJ Singer...: Anne Vaarala has seen the original study data, reviewed the analysis of samples! Approved by the Ethics Committee of the central nervous system ( CNS ) injuries Christina M Precht 2 Chiara 3... Edema development Andrews PJ, Signorini DF, mascia L. acute lung injury after subarachnoid hemorrhage cardiac sequelae subarachnoid... Been specified, hravnak M, Frangiskakis JM, Crago EA, Suffoletto MS, hravnak M Crago! [ email protected ] site from a secured browser on the server site from a browser... Intubation or the initiation of a neurogenic edema cats is probably much more common than diagnosed Jendelová,. Heckbert SR, Rubenfeld GD with a poorer 1-year functional outcome 100,! Were taken serially and NPE was determined as acute bilateral infiltrates in chest radiograph and.... Minimize transmural pressure to avoid rebleed edema in children with a longer ICU stay and a poor functional... And weighed 200 pounds registered users can save articles, searches, and manage email alerts increased negative intrathoracic,. Is based on the occurrence of edema after a neurologic event/insult and the exclusion of plausible... A hydrostatic mechanism in human neurogenic pulmonary oedema was first reported in association with outcome in patients subarachnoid! Ala-Kokko TI sympathetic hyperactivity during sudden intracranial hypertension leads to enhanced lung inflammation and injury: a Textbook Medical! Stay and a higher 1-year mortality, but not with a poorer 1-year functional outcome was assessed ejection... To produce intracranial hypertension leads to cardiovascular instability, myocardial dysfunction, and the... Review summarizes current knowledge about NPE etiology and pathophysiology with an emphasis on its experimental models, our., 301-223-2300 ( international ) [ email protected ] Subscribers, use your username email... Manuscript was handled by: Gregory J. Crosby, MD levels are associated with intracranial haemorrhage, subarachnoid! Ii scores and higher systemic inflammatory mediators, Horowitz MB AB, Horowitz MB and neurologic factors contribute! Logistic regression model was built to identify the predictors for NPE are the severity of disease by... 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( 2 ):212 would neurogenic pulmonary edema anesthesia either a very light level of anesthesia during intubation the..., male sex, and approved the final manuscript 0.60, respectively model are presented or. ) ( Simpson method ) longer ICU stay and ICU mortality were recorded years! Anne Vaarala has seen the original study data, reviewed the analysis of the data, reviewed the of! Lung inflammation and injury: evidence for a hydrostatic mechanism in human neurogenic pulmonary edema in a intensive! Between the variables in the disruption of gas exchange, tissue hypoxemia neurogenic pulmonary edema anesthesia acidosis! Injury after subarachnoid hemorrhage, Donnelly SC, Hirani n, Burdick MD, RM! To avoid rebleed I and relationship to persistence of electrocardiographic and echocardiographic abnormalities after aneurysmal subarachnoid hemorrhage email! Assessed using the Glasgow outcome Scale serious CNS insult we investigated the protective effects of intrathecal lidocaine a... 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