Crandall ED, Staub NC, Goldberg HS, Effros RM.
Recent developments in pulmonary edema.
Ann Intern Med. 1983 Dec;99(6):808-22. doi: 10.7326/0003-4819-99-6-808.
Abstract/Text
Research on lung fluid balance and pulmonary edema has increased during the last decade. New approaches have led to insights into the role of each component of the alveolar-capillary barrier. The capillary endothelium is the first line of defense against lung fluid accumulation. The interstitium may play a more important role in lung fluid balance than previously appreciated. Active and passive transport properties of alveolar epithelium may be important in the pathogenesis and resolution of alveolar edema. New methods for the determination of epithelial permeability and lung water are being evaluated. The developments reviewed here may have an impact on the institution of new diagnostic and therapeutic approaches to pulmonary edema during the next decade.
3学会（日本呼吸療法医学会/日本呼吸器学会/日本集中治療医学会）ARDS診療ガイドライン2021作成委員会（編）: ARDS診療ガイドライン2021.
Ware LB, Matthay MA.
Clinical practice. Acute pulmonary edema.
N Engl J Med. 2005 Dec 29;353(26):2788-96. doi: 10.1056/NEJMcp052699.
Abstract/Text
ARDS Definition Task Force; Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E, Fan E, Camporota L, Slutsky AS.
Acute respiratory distress syndrome: the Berlin Definition.
JAMA. 2012 Jun 20;307(23):2526-33. doi: 10.1001/jama.2012.5669.
Abstract/Text
The acute respiratory distress syndrome (ARDS) was defined in 1994 by the American-European Consensus Conference (AECC); since then, issues regarding the reliability and validity of this definition have emerged. Using a consensus process, a panel of experts convened in 2011 (an initiative of the European Society of Intensive Care Medicine endorsed by the American Thoracic Society and the Society of Critical Care Medicine) developed the Berlin Definition, focusing on feasibility, reliability, validity, and objective evaluation of its performance. A draft definition proposed 3 mutually exclusive categories of ARDS based on degree of hypoxemia: mild (200 mm Hg < PaO2/FIO2 ≤ 300 mm Hg), moderate (100 mm Hg < PaO2/FIO2 ≤ 200 mm Hg), and severe (PaO2/FIO2 ≤ 100 mm Hg) and 4 ancillary variables for severe ARDS: radiographic severity, respiratory system compliance (≤40 mL/cm H2O), positive end-expiratory pressure (≥10 cm H2O), and corrected expired volume per minute (≥10 L/min). The draft Berlin Definition was empirically evaluated using patient-level meta-analysis of 4188 patients with ARDS from 4 multicenter clinical data sets and 269 patients with ARDS from 3 single-center data sets containing physiologic information. The 4 ancillary variables did not contribute to the predictive validity of severe ARDS for mortality and were removed from the definition. Using the Berlin Definition, stages of mild, moderate, and severe ARDS were associated with increased mortality (27%; 95% CI, 24%-30%; 32%; 95% CI, 29%-34%; and 45%; 95% CI, 42%-48%, respectively; P < .001) and increased median duration of mechanical ventilation in survivors (5 days; interquartile [IQR], 2-11; 7 days; IQR, 4-14; and 9 days; IQR, 5-17, respectively; P < .001). Compared with the AECC definition, the final Berlin Definition had better predictive validity for mortality, with an area under the receiver operating curve of 0.577 (95% CI, 0.561-0.593) vs 0.536 (95% CI, 0.520-0.553; P < .001). This updated and revised Berlin Definition for ARDS addresses a number of the limitations of the AECC definition. The approach of combining consensus discussions with empirical evaluation may serve as a model to create more accurate, evidence-based, critical illness syndrome definitions and to better inform clinical care, research, and health services planning.
Wheeler AP, Bernard GR.
Acute lung injury and the acute respiratory distress syndrome: a clinical review.
Lancet. 2007 May 5;369(9572):1553-1564. doi: 10.1016/S0140-6736(07)60604-7.
Abstract/Text
Acute respiratory distress syndrome and acute lung injury are well defined and readily recognised clinical disorders caused by many clinical insults to the lung or because of predispositions to lung injury. That this process is common in intensive care is well established. The mainstay of treatment for this disorder is provision of excellent supportive care since these patients are critically ill and frequently have coexisting conditions including sepsis and multiple organ failure. Refinements in ventilator and fluid management supported by data from prospective randomised trials have increased the methods available to effectively manage this disorder.
Stubbs JR.
Transfusion-related acute lung injury, an evolving syndrome: the road of discovery, with emphasis on the role of the Mayo Clinic.
Transfus Med Rev. 2011 Jan;25(1):66-75. doi: 10.1016/j.tmrv.2010.08.008.
Abstract/Text
Transfusion-related acute lung injury (TRALI) is characterized by acute hypoxemia and noncardiogenic pulmonary edema. At the very least, descriptions of cases consistent with TRALI date back to the early 1950s. Early articles from the 1950s and 1960s documented transfusion-associated pulmonary edema without evidence of volume overload. Explanations for this phenomenon included hypersensitivity and transfused leukoagglutinins. Descriptions from the 1970s also implicated transfused antileukocyte antibodies and noted that blood products containing such antibodies often came from multiparous female donors. Cases implicating recipient anti-human leukocyte antigen antibody reacting with transfused donor leukocytes and donor antibodies reacting with another donor's leukocytes were also described. The 1980s marked the emergence of the Mayo Clinic as a leading contributor to the understanding of TRALI. The descriptions of the syndrome that was named "TRALI" by Mayo Clinic investigators were the most extensive and complete to date and are presented in detail. The Mayo Clinic has remained in the forefront of TRALI investigation, particularly as it pertains to the critically ill, and recent studies from this center are also presented in detail. The common thread connecting the Mayo Clinic's descriptions in the 1980s to the more contemporary studies is Dr S. Breanndan Moore. Dr Moore passed away recently, but his crucial work in the area of TRALI lives on.
Copyright © 2011 Elsevier Inc. All rights reserved.
Sohara Y.
Reexpansion pulmonary edema.
Ann Thorac Cardiovasc Surg. 2008 Aug;14(4):205-9.
Abstract/Text
When a rapidly reexpanding lung has been in a state of collapse for more than several days, pulmonary edema sometimes occurs in it. This is called reexpansion pulmonary edema (RPE). In this article, I present my views on the history, clinical features, morphophysiological features, pathogenesis, and treatment of RPE. Histological abnormalities of the pulmonary microvessels in a chronically collapsed lung will cause RPE, as well as mechanical stress exerted during reexpansion. Although the most effective treatment method is to treat the histological abnormalities of the pulmonary microvessels formed in a chronically collapsed lung, the cause of these abnormalities is not clear, making it difficult to put forward a precise treatment method. However, reasonably good effects can be expected from a symptomatic therapy that reduces the level of mechanical stress during reexpansion. In the future, it is expected that the cause of histological changes of the pulmonary microvessels in a chronically collapsed lung will be revealed, and appropriate therapies will therefore be developed according to this cause.
Demling R, Riessen R.
Pulmonary dysfunction after cerebral injury.
Crit Care Med. 1990 Jul;18(7):768-74. doi: 10.1097/00003246-199007000-00019.
Abstract/Text
Pulmonary dysfunction is a common complication of severe head injury. The degree of initial hypoxemia which develops appears to correspond with the location and magnitude of the head injury. If unrecognized and not aggressively treated, the hypoxic insult will magnify the cerebral insult. A severe postinjury hypermetabolic state also develops and, if unrecognized and not managed aggressively with nutritional support, can also lead to severe catabolism, increased infection, and further lung dysfunction. Although supportive care is the major treatment at present, pharmacologic manipulation of the increased catecholamine activity, which is considered to be causative, may be effective in controlling both the impaired gas exchange and the hypermetabolic state. A knowledge of the various lung dysfunction states which occur in the head-injured patient population is required to optimize recovery and minimize complications.
Hackett PH, Roach RC.
High-altitude illness.
N Engl J Med. 2001 Jul 12;345(2):107-14. doi: 10.1056/NEJM200107123450206.
Abstract/Text
Dünser MW, Hasibeder WR.
Sympathetic overstimulation during critical illness: adverse effects of adrenergic stress.
J Intensive Care Med. 2009 Sep-Oct;24(5):293-316. doi: 10.1177/0885066609340519. Epub 2009 Aug 23.
Abstract/Text
The term ''adrenergic'' originates from ''adrenaline'' and describes hormones or drugs whose effects are similar to those of epinephrine. Adrenergic stress is mediated by stimulation of adrenergic receptors and activation of post-receptor pathways. Critical illness is a potent stimulus of the sympathetic nervous system. It is undisputable that the adrenergic-driven ''fight-flight response'' is a physiologically meaningful reaction allowing humans to survive during evolution. However, in critical illness an overshooting stimulation of the sympathetic nervous system may well exceed in time and scope its beneficial effects. Comparable to the overwhelming immune response during sepsis, adrenergic stress in critical illness may get out of control and cause adverse effects. Several organ systems may be affected. The heart seems to be most susceptible to sympathetic overstimulation. Detrimental effects include impaired diastolic function, tachycardia and tachyarrhythmia, myocardial ischemia, stunning, apoptosis and necrosis. Adverse catecholamine effects have been observed in other organs such as the lungs (pulmonary edema, elevated pulmonary arterial pressures), the coagulation (hypercoagulability, thrombus formation), gastrointestinal (hypoperfusion, inhibition of peristalsis), endocrinologic (decreased prolactin, thyroid and growth hormone secretion) and immune systems (immunomodulation, stimulation of bacterial growth), and metabolism (increase in cell energy expenditure, hyperglycemia, catabolism, lipolysis, hyperlactatemia, electrolyte changes), bone marrow (anemia), and skeletal muscles (apoptosis). Potential therapeutic options to reduce excessive adrenergic stress comprise temperature and heart rate control, adequate use of sedative/analgesic drugs, and aiming for reasonable cardiovascular targets, adequate fluid therapy, use of levosimendan, hydrocortisone or supplementary arginine vasopressin.
崎尾秀彰. 陰圧性肺水腫を見逃すな. 日集中医誌, 2008; 15(3): 276-8.
筒井 裕之：心不全．杉本恒明、矢崎義雄（総編集）：内科学 第9版, pp.405-413, 朝倉書店, 2007.
盛虹明, 増田卓, 北原孝雄ほか. クモ膜下出血に伴う神経原性肺水腫の成因と病態. 日救急医会誌, 1993; 4(1): 17-22.
Hultgren HN, Marticorena EA.
High altitude pulmonary edema. Epidemiologic observations in Peru.
Chest. 1978 Oct;74(4):372-6. doi: 10.1378/chest.74.4.372.
Abstract/Text
The incidence of high altitude pulmonary edema was examined by a survey (via questionnaire) of residents living at 3,750 meters (12,303 feet) in the mining community of La Oroya, Peru. Ninety-seven subjects made a total of 1,157 ascents to high altitude after a stay at sea level of longer than 14 days. Sixty-four subjects experienced at least one episode of high-altitude pulmonary edema. The incidence was higher in subjects aged 13 to 20 years, where 17 percent (15) of 90 ascents resulted in episodes of high-altitude pulmonary edema, than in subjects 21 years or older (3 percent; 18/686 ascents). Young subjects (2 to 12 years old) had more severe episodes of high-altitude pulmonary edema (81 percent; 30/37 episodes) than adults (22 percent; 4/18 episodes). No episodes were observed in children under two years old. Five subjects under 21 years of age experienced recurrent episodes. Our estimated incidence of severe episodes of high altitude pulmonary edema per ascent in adults (0.6 percent; 4/686) is similar to that reported by other workers (incidence of 0.15 to 0.57 percent) in various parts of the world.
Swenson ER, Maggiorini M, Mongovin S, Gibbs JS, Greve I, Mairbäurl H, Bärtsch P.
Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor.
JAMA. 2002 May 1;287(17):2228-35. doi: 10.1001/jama.287.17.2228.
Abstract/Text
CONTEXT: The pathogenesis of high-altitude pulmonary edema (HAPE) is considered an altered permeability of the alveolar-capillary barrier secondary to intense pulmonary vasoconstriction and high capillary pressure, but previous bronchoalveolar lavage (BAL) findings in well-established HAPE are also consistent with inflammatory etiologic characteristics.
OBJECTIVES: To determine whether inflammation is a primary event in HAPE and to define the temporal sequence of events in HAPE.
DESIGN, SETTING, AND PARTICIPANTS: Case study from July through August 1999 of 10 subjects with susceptibility to HAPE and 6 subjects resistant to HAPE, all of whom are nonprofessional alpinists with previous mountaineering experience above 3000 m.
MAIN OUTCOME MEASURES: Pulmonary artery pressure measurements and BAL findings at low altitude (490 m) and shortly before or at the onset of HAPE at an altitude of 4559 m.
RESULTS: Subjects who were HAPE susceptible had higher mean (SD) pulmonary artery systolic blood pressures at 4559 m compared with HAPE-resistant subjects (66 vs 37 mm Hg; P =.004). Despite development of HAPE in the majority of HAPE-susceptible subjects, there were no differences in BAL fluid total leukocyte counts between resistant and susceptible subjects or between counts taken at low and high altitudes. Subjects who developed HAPE had BAL fluid with high concentrations of plasma-derived proteins and erythrocytes, but there was no increase in plasma concentrations of surfactant protein A and Clara cell protein. The chest radiograph score was 12.7 for the 3 HAPE-susceptible subjects who developed HAPE before BAL was performed; they were lavaged within 3 to 5 hours. The remainder of the HAPE-susceptible group was lavaged before edema was apparent on radiographs. However, 6 subjects from the HAPE-susceptible group who developed HAPE on the following day had a score on bronchoscopy of 1.5, which increased to 4.6, reflective of mild pulmonary edema. In HAPE cases, there were no elevations in a number of proinflammatory cytokines and eicosanoid and nitric oxide metabolites.
CONCLUSIONS: Early HAPE is characterized by high pulmonary artery pressures that lead to a protein-rich and mildly hemorrhagic edema, with normal levels of leukocytes, cytokines, and eicosanoids. HAPE is a form of hydrostatic pulmonary edema with altered alveolar-capillary permeability.
Droma Y, Hanaoka M, Ota M, Katsuyama Y, Koizumi T, Fujimoto K, Kobayashi T, Kubo K.
Positive association of the endothelial nitric oxide synthase gene polymorphisms with high-altitude pulmonary edema.
Circulation. 2002 Aug 13;106(7):826-30. doi: 10.1161/01.cir.0000024409.30143.70.
Abstract/Text
BACKGROUND: A defect of nitric oxide (NO) synthesis in the lung of high-altitude pulmonary edema (HAPE) has been suggested to contribute to its exaggerated pulmonary hypertension. Several polymorphisms have been identified in the gene encoding endothelial nitric oxide synthase (eNOS), which is a key enzyme responsible for NO synthesis, some of which were reported to be associated with vascular disorders.
METHODS AND RESULTS: We studied 41 HAPE-susceptible subjects (HAPE-s) and 51 healthy climbers (control group) in a Japanese population. We examined 2 polymorphisms of the eNOS gene, including the Glu298Asp variant and 27-base pair (bp) variable numbers of tandem repeats using polymerase chain reaction followed by restriction fragment length polymorphism. The Asp allelic frequency of the Glu298Asp variant was 25.6% in the HAPE-s and 9.8% in the controls, which was significantly different between the two groups (P=0.0044). The eNOS4a allelic frequency of 27-bp variable numbers of tandem repeats was 23.2% in the HAPE-s, significantly higher than that of 6.9% in the controls (P=0.0016). In HAPE-s group, 11 of 41 (26.8%) subjects possessed simultaneously both of the two significant alleles, but among the controls, none did, which showed a high statistical difference between the two groups (P=0.000059).
CONCLUSIONS: Both polymorphisms of the eNOS gene were significantly associated with HAPE. A genetic background may underlie the impaired NO synthesis in the pulmonary circulation of HAPE-s. These polymorphisms could be genetic markers for predicting the susceptibility to HAPE.
長野ゆり, 福島臣啓, 石井瑞恵ほか. カテコラミン心筋症および肺水腫が初発症状であった褐色細胞腫の一例. 日集中医誌, 2008; 15(1): 93-6.
van Iperen CE, Giezen J, Kramer WL, Lips CJ, Bartelink AK.
Acute dyspnoea resulting from pulmonary oedema as the first sign of a phaeochromocytoma.
Respiration. 2001;68(3):323-6. doi: 10.1159/000050519.
Abstract/Text
The day after undergoing neck dissection, a 42-year-old woman developed acute dyspnoea due to pulmonary oedema. Measurements with a Swan-Ganz catheter revealed not only cardiac depression but also a greatly increased peripheral vascular resistance: 5,400 dyn x s x cm(-5)/m2. A phaeochromocytoma with acute cardiac failure leading to pulmonary oedema was considered. Treatment with alpha- and beta-blockers was complicated by severe hypotension and later ventricular fibrillation. Mechanical ventilation was required for 6 days following resuscitation. Investigation of the urine subsequently showed greatly increased catecholamine concentrations, while imaging revealed bilateral adrenal tumours. Our case history shows that acute pulmonary oedema may be the presenting manifestation of a phaeochromocytoma. The pulmonary oedema resulted partly from backward failure following tachycardia, myocyte necrosis and the greatly increased peripheral vascular resistance, and partly from increased permeability of the capillary network in the lungs.
Copyright 2001 S. Karger AG, Basel
中田貴大, 牧野英記, 加藤高英ほか. 短時間の持続気道陽圧療法が奏功した陰圧性肺水腫の1例. 日内会誌, 2015; 104(10): 2206-11.
Milne EN, Pistolesi M, Miniati M, Giuntini C.
The radiologic distinction of cardiogenic and noncardiogenic edema.
AJR Am J Roentgenol. 1985 May;144(5):879-94. doi: 10.2214/ajr.144.5.879.
Abstract/Text
Improvement in the ability to determine the specific cause of any given case of pulmonary edema would lead to more rapid and definitive treatment. "Wedge" pressures and measurements of cardiac output derived from Swan-Ganz catheterization assist in making this determination, but the procedure is invasive, expensive, associated with complications, and not infrequently inaccurate. A plain chest film is, however, almost invariably available in all patients with pulmonary edema, and as shown in this study, the cause of the edema can be determined with a high degree of accuracy by careful attention to certain radiographic features. An independent two-observer study was performed on 216 chest radiographs of 61 patients with cardiac disease, 30 with renal failure or overhydration, and 28 with capillary permeability edema. Three principal and seven ancillary features have been identified, all of which are statistically significant and permit the cause of the edema to be determined correctly in a high percentage of cases. The three principal features are distribution of pulmonary flow, distribution of pulmonary edema, and the width of the vascular pedicle. The ancillary features are pulmonary blood volume, peribronchial cuffing, septal lines, pleural effusions, air bronchograms, lung volume, and cardiac size. Differing constellations of these features occur, each of which is characteristic of a specific type of edema. Overall accuracy of diagnosis in this study ranged from 86% to 89%. The highest accuracy was obtained in distinguishing capillary permeability edema from all other varieties (91%), and the lowest in distinguishing chronic cardiac failure from renal failure (81%).
Ely EW, Haponik EF.
Using the chest radiograph to determine intravascular volume status: the role of vascular pedicle width.
Chest. 2002 Mar;121(3):942-50. doi: 10.1378/chest.121.3.942.
Abstract/Text
Due to concerns about the efficacy and safety of using pulmonary artery catheterization to evaluate hemodynamic status, noninvasive diagnostic testing has gained increased importance. This article focuses on both the supportive evidence and the limitations of applying the vascular pedicle width (VPW), which is the mediastinal silhouette of the great vessels, as an aid in the assessment of patients' intravascular volume status. The objective measurement of the VPW obtained from either upright or supine chest radiographs (CXRs which are often already available though not fully utilized) can increase the accuracy of the clinical and radiographic assessment of intravascular volume status by 15 to 30%, and this value may be even higher when VPW is used serially within the same patient. Regardless of the presence or absence of pulmonary edema, the best VPW cutoff for differentiating a high vs normal to low intravascular volume status is 70 mm. Patients with a VPW of > 70 mm coupled with a cardiothoracic ratio of > 0.55 are more than three times more likely to have a pulmonary artery occlusion pressure > 18 mm Hg than are patients without these radiographic findings. We suggest a management algorithm for utilizing the VPW, and whether or not such an approach will offer superior patient outcomes requires prospective investigation. Reappraisal of the VPW and other roentgenographic signs should be incorporated into newly implemented studies of the Swan-Ganz catheter, ICU echocardiography, portable CT scans, and other costlier technologies. While such investigations may refine the optimum application of the portable CXR, conventional and digital supine radiographs should retain an important role in the diagnosis and management of critically ill patients. Lastly, the measurement of the VPW should be incorporated into the training of chest clinicians and radiologists.
Maisel AS, Krishnaswamy P, Nowak RM, McCord J, Hollander JE, Duc P, Omland T, Storrow AB, Abraham WT, Wu AH, Clopton P, Steg PG, Westheim A, Knudsen CW, Perez A, Kazanegra R, Herrmann HC, McCullough PA; Breathing Not Properly Multinational Study Investigators.
Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure.
N Engl J Med. 2002 Jul 18;347(3):161-7. doi: 10.1056/NEJMoa020233.
Abstract/Text
BACKGROUND: B-type natriuretic peptide is released from the cardiac ventricles in response to increased wall tension.
METHODS: We conducted a prospective study of 1586 patients who came to the emergency department with acute dyspnea and whose B-type natriuretic peptide was measured with a bedside assay. The clinical diagnosis of congestive heart failure was adjudicated by two independent cardiologists, who were blinded to the results of the B-type natriuretic peptide assay.
RESULTS: The final diagnosis was dyspnea due to congestive heart failure in 744 patients (47 percent), dyspnea due to noncardiac causes in 72 patients with a history of left ventricular dysfunction (5 percent), and no finding of congestive heart failure in 770 patients (49 percent). B-type natriuretic peptide levels by themselves were more accurate than any historical or physical findings or laboratory values in identifying congestive heart failure as the cause of dyspnea. The diagnostic accuracy of B-type natriuretic peptide at a cutoff of 100 pg per milliliter was 83.4 percent. The negative predictive value of B-type natriuretic peptide at levels of less than 50 pg per milliliter was 96 percent. In multiple logistic-regression analysis, measurements of B-type natriuretic peptide added significant independent predictive power to other clinical variables in models predicting which patients had congestive heart failure.
CONCLUSIONS: Used in conjunction with other clinical information, rapid measurement of B-type natriuretic peptide is useful in establishing or excluding the diagnosis of congestive heart failure in patients with acute dyspnea.
Copyright 2002 Massachusetts Medical Society.
Galiè N, Hoeper MM, Humbert M, Torbicki A, Vachiery JL, Barbera JA, Beghetti M, Corris P, Gaine S, Gibbs JS, Gomez-Sanchez MA, Jondeau G, Klepetko W, Opitz C, Peacock A, Rubin L, Zellweger M, Simonneau G; ESC Committee for Practice Guidelines (CPG).
Guidelines for the diagnosis and treatment of pulmonary hypertension: the Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT).
Eur Heart J. 2009 Oct;30(20):2493-537. doi: 10.1093/eurheartj/ehp297. Epub 2009 Aug 27.
Abstract/Text
Jelic S, Le Jemtel TH.
Diagnostic usefulness of B-type natriuretic peptide and functional consequences of muscle alterations in COPD and chronic heart failure.
Chest. 2006 Oct;130(4):1220-30. doi: 10.1378/chest.130.4.1220.
Abstract/Text
COPD affects up to one third of patients with chronic heart failure. The coexistence of COPD and chronic heart failure presents clinicians with diagnostic and therapeutic challenges. Measurement of B-type natriuretic peptide plasma levels facilitates the diagnosis of acute dyspnea in patients known to have both COPD and chronic heart failure. Patients with COPD or chronic heart failure have skeletal muscle abnormalities that limit functional capacity independently from primary organ failure. Exercise training reverses skeletal muscle abnormalities in patients with COPD or chronic heart failure and may be particularly indicated in patients with coexistent COPD and chronic heart failure.
Clermont G, Kong L, Weissfeld LA, Lave JR, Rubenfeld GD, Roberts MS, Connors AF Jr, Bernard GR, Thompson BT, Wheeler AP, Angus DC; NHLBI ARDS Clinical Trials Network.
The effect of pulmonary artery catheter use on costs and long-term outcomes of acute lung injury.
PLoS One. 2011;6(7):e22512. doi: 10.1371/journal.pone.0022512. Epub 2011 Jul 21.
Abstract/Text
BACKGROUND: The pulmonary artery catheter (PAC) remains widely used in acute lung injury (ALI) despite known complications and little evidence of improved short-term mortality. Concurrent with NHLBI ARDS Clinical Trials Network Fluid and Catheters Treatment Trial (FACTT), we conducted a prospectively-defined comparison of healthcare costs and long-term outcomes for care with a PAC vs. central venous catheter (CVC). We explored if use of the PAC in ALI is justified by a beneficial cost-effectiveness profile.
METHODS: We obtained detailed bills for the initial hospitalization. We interviewed survivors using the Health Utilities Index Mark 2 questionnaire at 2, 6, 9 and 12 m to determine quality of life (QOL) and post-discharge resource use. Outcomes beyond 12 m were estimated from federal databases. Incremental costs and outcomes were generated using MonteCarlo simulation.
RESULTS: Of 1001 subjects enrolled in FACTT, 774 (86%) were eligible for long-term follow-up and 655 (85%) consented. Hospital costs were similar for the PAC and CVC groups ($96.8k vs. $89.2k, p = 0.38). Post-discharge to 12 m costs were higher for PAC subjects ($61.1k vs. 45.4k, p = 0.03). One-year mortality and QOL among survivors were similar in PAC and CVC groups (mortality: 35.6% vs. 31.9%, p = 0.33; QOL [scale: 0-1]: 0.61 vs. 0.66, p = 0.49). MonteCarlo simulation showed PAC use had a 75.2% probability of being more expensive and less effective (mean cost increase of $14.4k and mean loss of 0.3 quality-adjusted life years (QALYs)) and a 94.2% probability of being higher than the $100k/QALY willingness-to-pay threshold.
CONCLUSION: PAC use increased costs with no patient benefit and thus appears unjustified for routine use in ALI.
TRIAL REGISTRATION: www.clinicaltrials.gov NCT00234767.
日本呼吸器学会NPPVガイドライン作成委員会（編）：NPPV（非侵襲的陽圧換気療法）ガイドライン、改訂第2版. 南江堂、2015.
