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Clinical Investigations in Critical Care |

Fatal Postoperative Pulmonary Edema*: Pathogenesis and Literature Review FREE TO VIEW

Allen I. Arieff, MD
Author and Funding Information

*From the Department of Medicine, University of California School of Medicine, San Francisco, CA. Supported by a grant RO1 AG 08575-01A2 from the National Institute on Aging, Department of Health and Human Services, Bethesda, MD.

Correspondence to: Allen I. Arieff, MD, Department of Medicine, University of California School of Medicine, 299 South St, Sausalito, CA 94965



Chest. 1999;115(5):1371-1377. doi:10.1378/chest.115.5.1371
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Study objectives: Pulmonary edema is a known postoperative complication, but the clinical manifestations and danger levels for fluid administration are not known. We studied (1) 13 postoperative patients (11 adult, 2 pediatric) who developed fatal pulmonary edema, and (2) one contemporaneous year of inpatient operations at two university teaching hospitals to determine the clinical manifestations, causes, epidemiology, and guidelines for fluid administration.

Design: Retrospective analysis of 13 patients with fatal postoperative pulmonary edema and one contemporaneous year of major inpatient surgery.

Patients and methods: Thirteen patients had net fluid retention of at least 67 mL/kg in the initial 24 postoperative hours and developed pulmonary edema. Ten were generally healthy while three had serious associated medical conditions.

Measurements and results: There was no measurement, laboratory value, or clinical finding predictive of impending pulmonary edema. The most common clinical manifestation following the onset of pulmonary edema was cardiorespiratory arrest (n = 8). Patients had metabolic acidosis (pH = 7.15 ± .33), hypoxia (Po2 = 45 ± 18 mm Hg), and normal electrolytes. The diagnosis of pulmonary edema was established by chest radiograph and confirmed by autopsy and pulmonary artery pressure (21 ± 4 mm Hg). The mean net fluid retention was 7.0 ± 4.5 L (90 ± 36 mL/kg/d) and exceeded 67 mL/kg/d in all patients. Autopsy revealed pulmonary edema with no other cause of death. Among 8,195 major operations, 7.6% developed pulmonary edema with a mortality of 11.9%. Extrapolation to the 8.2 million annual major surgeries in the United States yields a projection of 8,000 to 74,000 deaths.

Conclusions: Pulmonary edema can occur within the initial 36 postoperative hours when net fluid retention exceeds 67 mL/kg/d. There are no known predictive warning signs and cardiorespiratory arrest is the most frequent clinical presentation. The monitoring systems currently in use neither detect nor predict impending pulmonary edema, and as yet, there are no known panic values for excessive fluid administration or retention.

Abbreviations: TURP = transurethral resection of the prostate

Pulmonary edema is a reported postoperative complication,1but the etiology and mortality are not known.25 Although the usual clinical manifestations of pulmonary edema have been described extensively, the presentation of postoperative pulmonary edema is not known. There are several possible etiologic factors that may lead to postoperative pulmonary edema. Available evidence suggests that the disorder will be most common in patients who have preexisting heart disease. Fluid overload with high hydrostatic pressures resulting in left ventricular dysfunction would probably be the most common sequence1,6 and some of these patients would likely have suffered myocardial infarction5,7or renal failure. Other groups of patients with postoperative pulmonary edema would be those with neurogenic (noncardiogenic) pulmonary edema secondary to postoperative hyponatremic encephalopathy,8 head trauma,9pheochromocytoma,10or other causes.1112 ARDS is often an important differential consideration.1315

One frequent reason for administration of large volumes of postoperative fluids is to compensate for apparent fluid losses for which there is no clinically accessible method to accurately evaluate. Such loss includes “third space” losses, evaporative losses, blood loss, and insensible loss. Replacement is generally based on clinical approximations.1617

Currently, there is little information available concerning the maximum postoperative volume of fluid that can be administered safely. In a postoperative patient who does not have serious cardiovascular, hepatic, or renal disorders, the quantity of fluid necessary to induce pulmonary edema would vary according to such factors as age; body weight; tissue turgor; cardiovascular, pulmonary, and renal function; plasma vasopressin levels; plasma proteins; and the volume of the“ third space.”3 The differential diagnosis of postoperative pulmonary congestion includes hyponatremic encephalopathy, pulmonary capillary leak syndromes (ARDS), pneumonia, sepsis, and volume overload,1820 as well as other noncardogenic causes of pulmonary edema.4,8,1011 Furthermore, it is unclear from the literature what the usual clinical manifestations of postoperative pulmonary edema are, or if it can result in death or serious morbidity in patients without heart disease or renal failure.18,2122 In the current study, we present 13 fatal cases of postoperative pulmonary edema in generally healthy individuals in whom the pulmonary edema was secondary to excessive fluid administration.

There were 13 study patients who, from 1991 to 1996, had postoperative pulmonary edema documented by clinical criteria and characteristic findings on chest radiograph. The diagnosis was confirmed by autopsy in nine patients and by pulmonary artery catheterization in four. Demographic features are shown in Table 1. There were four men and nine women, and the average age (± SD) was 38 ± 21 years. The operations are shown in Table 1. All but one operation (patient 9) were elective. All patients were seen in consultation at university teaching hospitals (n = 9) or affiliated community hospitals (n = 4). From a review of the literature, a net fluid retention of 2.2 L/d can lead to pulmonary edema,1,3,16 so patients were considered for study only if their net fluid retention was at least 2.2 L during the initial 24 postoperative hours. In four patients, the pulmonary capillary wedge pressure was measured by means of a pulmonary artery catheter. In the“ Results” and “Discussion” sections, “cholecystectomy” refers to an open abdominal procedure rather than a laparoscopic one.3

The medical condition leading to hospitalization is shown in Table 1. Three patients had severe associated medical conditions: multiple traumatic injuries; acute pancreatitis; acute glomerulonephritis. However, all 13 patients were in stable condition and admitted to the hospital for elective surgical procedures, including tonsillectomy, knee-joint replacement, endometrial ablation, and sacral laminectomy. Only one patient had known heart disease (aortic valvular insufficiency), and 12 of 13 had normal results of heart examination on preoperative physical examination, chest radiograph, and ECG.

Every patient received IV fluids preoperatively, during surgery, and postoperatively. The intake and output values are shown in Table 2 and are the totals from admission to the hospital to the time pulmonary edema was initially diagnosed. The fluid retention index is the net fluid retention for the initial 24 postoperative hours in milliliters per kilogram per day. The output values were extracted from the inpatient records and represent the sum of urine, estimated blood loss, and tube drainage. IV fluid intake was also extracted from the inpatient records. The predominant intraoperative IV fluid was Ringers lactate (130 mmol/L of sodium), others being blood, blood products, or 154 mmol/L NaCl. No patient received IV hypotonic fluid intraoperatively. Three patients had endoscopic surgery and received parenteral intraoperative hypotonic irrigating fluids by absorption through the cauterized operative bed, either the uterus or prostate.23 The irrigating fluids were either 200 mmol/L glycine or 165 mmol/L sorbitol. In the three patients who had endoscopic surgery, the intake was determined as the sum of IV fluids plus irrigating fluids, while output was the sum of urine volume, estimated blood loss, and collected drainage of irrigating fluid from the operative field. The operative drainage was collected in stainless steel vessels. Tube drainage was collected in a polyethylene bag by gravity and the volume was measured by means of the gradations on the bags. Three patients had indwelling Foley catheters postoperatively, while in the other 10 patients, urine was collected by spontaneous voiding. The postoperative fluids consisted of either Ringer’s lactate, 154 mmol/L NaCl, or 77 mmol/L NaCl. Pulmonary edema occurred within three postoperative days (range of 3 to 66 h).

Epidemiologic Studies

The records of major inpatient surgery for one contemporaneous year (1993) from two university teaching hospitals were evaluated for (1) the incidence and mortality of pulmonary edema, and (2) the incidence of other major postoperative complications in patients with pulmonary edema (pulmonary embolus, pneumonia, acute renal failure, GI bleeding, stroke, myocardial infarction, and hyponatremia). We examined only major surgical procedures; diagnostic procedures and minor surgery were not tabulated.24A computer search of hospital records for the 8,195 hospital inpatients operated on in 1993 was done using a database (SAS; Cary, NC) to determine which surgical patients had postoperative pulmonary edema and their outcome.25 The incidence of seven other postoperative complications—pulmonary embolus, pneumonia, acute renal failure, GI bleeding, stroke, myocardial infarction, and hyponatremia (plasma sodium < 130 mmol/L)—were also tabulated. Outcome was determined only as death or discharge from the hospital within 30 days of the episode of pulmonary edema.5 Patients dying with pulmonary edema plus one of the other seven postoperative complications were subtracted from the total deaths with pulmonary edema to estimate the number of patients who died from pulmonary edema only. In addition to the information on patients with pulmonary edema, the overall postoperative mortality was determined.

Postoperative Patients With Fatal Pulmonary Edema

All results are presented as mean ± SD. In eight patients, the initial manifestation of pulmonary edema was cardiopulmonary arrest requiring emergent intubation (Table 1). One patient had intraoperative chest pain, three had acute florid pulmonary edema, and one had acute renal failure. The diagnosis of acute pulmonary edema was established by a diagnostic chest radiograph accompanied by typical physical findings of bilateral rales, a third heart sound, and copious pink frothy sputum in three patients (Table 1). Two patients died before the diagnosis of pulmonary edema was established and in these patients, the diagnosis was established at autopsy. The five patients not presenting with cardiorespiratory arrest were intubated and had a chest radiograph that demonstrated findings of diffuse pulmonary edema.

At the time of respiratory arrest or when pulmonary edema was first diagnosed (n = 11), arterial blood gases revealed a mixed metabolic-hypercapnic acidosis (Table 2), with pH = 7.15 ± 0.33, Pco2 = 58 ± 37 mm Hg, and bicarbonate = 18.5 ± 4.8 mmol/L. All patients had hypoxemia, with Po2 = 45 ± 18 mm Hg. These values are similar to those previously reported in patients with cardiogenic pulmonary edema.26

IV Fluids

The average amount of IV fluid administered for the initial 27 postoperative hours was 9.9 ± 6.0 L (171 ± 103 mL/kg) (Table 2). The mean patient weight was 58 ± 18 kg and using available tables, the calculated total body water was 29.8 ± 8.9 L.27 The average net fluid retention was 7.04 ± 4.5 L over the initial 27 ± 20 postoperative hours, a quantity of retained fluid equal to 24% of the total body water or 12.2% of body weight. The fluid retention index (Table 2) was 90 ± 36 mL/kg/d, almost three times the “normal” value (Table 3) of 38 mL/kg/d. The net fluid retention corresponded to an increase of 24% of total body water or 12.2% of body weight (Table 2). Thus, the quantity of administered fluid was clearly excessive.,1,17,2829 The reasons for the excessive quantities of administered fluid were not readily apparent. Recording of intake and output was ordered in all 13 patients. The orders were carried out, but in all patients, totals could be ascertained only by tedious searching of multiple sources: operative records, nurses notes, graphic records, physicians orders, and billing records. However, the excessive net fluid intake that was charted was not appreciated by the physicians caring for any of the patients until after pulmonary edema was diagnosed. In no instance was any physician notified that his or her patient had been administered or retained an excessive amount of fluid. Postoperative weights were ordered in all patients, but they were not actually obtained in any patient before the onset of pulmonary edema. Eight patients suffered cardiopulmonary arrest, and in all eight, the net excess of administered fluid was not appreciated until after the arrest. In eight patients, the diagnosis of pulmonary edema was confirmed at autopsy (Table 1). All eight had pulmonary edema, with no other cause of death. In particular, fat emboli were not present and none had acute myocardial infarction. In these eight patients, lung weights were 906 ± 154 g (right) and 726 ± 171 g (left), more than twice the expected normal values.30

Epidemiologic Studies of Postoperative Pulmonary Edema

During 1993, there were 8,195 major inpatient operations performed at two university teaching hospitals. The overall operative and postoperative mortality from all causes was 3.88% (302 patients). There were a total of 621 cases of postoperative pulmonary edema, an incidence of 7.6%. Among the 621 cases of pulmonary edema, 74 patients (11.9%) died. Those patients with pulmonary edema were then evaluated for the occurrence of other comorbid conditions that would be expected either to increase the chances of developing pulmonary edema or increase its mortality. The conditions were as follows: acute myocardial infarction, acute renal failure, acute GI bleeding, stroke, pneumonia, pulmonary embolus, and hyponatremia (plasma sodium < 130 mmol/L). When the patients with pulmonary edema plus one other comorbid postoperative complication were subtracted from the total, there were 204 patients remaining who had pulmonary edema without any of the other comorbid conditions (2.6%), of whom 8 (3.9%) died. In the United States in 1993, there were 8.2 million major inpatient surgical procedures.24 If the pulmonary edema figures were extrapolated from those 8.2 million operations, there would be a projected 622,000 annual cases of postoperative pulmonary edema in the United States, with 74,000 deaths. Even if all patients with comorbid factors are subtracted, there would still be projected 213,200 annual cases of postoperative pulmonary edema that had no other postoperative complications, totaling 8,315 deaths. Thus, the projected range of deaths from postoperative pulmonary edema would be 8,300 to 74,000 per year.

These data demonstrate that in generally healthy individuals undergoing elective surgery, pulmonary edema may be the initial clinical manifestation of fluid overload. If the pulmonary edema is not recognized and treated promptly, the patients may not survive. Although most textbooks of surgery recognize that excessive postoperative fluid administration can cause pulmonary edema, essentially no guidelines are available as to the quantity of fluid that may lead to such a complication.17 There are many reasons for administration of large quantities of both intraoperative and postoperative fluids.3Some of the more common reasons are as follows: (1) hypotension following induction of anesthesia; (2) fluid sequestration in the alleged “third space” during surgery; (3) maintainance of BP after traumatic injury;4,13 (4) excessive blood loss; and (5) postoperative fever with increased insensible loss.

Intraoperatively, hypotension may develop after the onset of anesthesia, requiring fluids and vasopressor therapy. In patients with cardiac disease, the afterload reduction secondary to the effects of anesthesia on sympathetic tone may improve myocardial performance transiently and allow the administration of large quantities of IV fluids. However, the return of vascular resistance to normal as the anesthetic recedes can result in congestive heart failure and pulmonary edema due to the relative fluid overload.16

The net fluid retention in these patients was > 7 L/d (Table 2). There are a number of different modalities and formulas for the calculation of postoperative fluid requirements in adults17,28,31(Table 3). These include maintenance requirements estimated at 2,500 mL/d, 30 to 35 mL/kg/d, or 1 mL/calorie/d. In addition, blood losses and tube drainage (nasogastric, chest tube, Penrose drain) are replaced and 1 to 3 L of extra fluid may be administered after a major complicated procedure in order to make up for estimated evaporative and third space losses. Operative fluid losses by evaporation are usually estimated at 150 mL/h. Using any of the aforementioned criteria, these 13 patients should have received from 2.5 to 5.5 L in the initial 36 postoperative hours. Based on any of the commonly used formulas for determining postoperative fluid requirements, the quantity administered (9.9 ± 6 L; Table 2) was excessive. In general, most textbooks recommend that the patients’ actual losses be assessed at the bedside, and fluid administration should be based on estimated maintenance requirements plus estimated losses.,17,29,32 A gain in fluid above 20% of total body water has been classified as fluid overload.1 Assuming that the patients’ net fluid retention was associated with a corresponding gain in body weight, the mean weight gain was 12.2%, a quantity that is by itself associated with a mortality of 19%.1

The “third space” is an area in the body that is occupied by fluids but is not in equilibrium with the bloodstream and thus hemodynamically inactive. Examples of the third space include burns, traumatized operative bed, and traumatically injured tissues. There is no bedside method to measure third space losses, and replacement is usually based on clinical approximation. However, the postoperative sequestered extracellular fluid has been estimated to vary from an imperceptible minimum to as much as 3 L.17 Ranges of 5 to 17 mL/kg/h of surgery after cholecystectomy or similar procedure during the initial postoperative day are typical estimated replacement values, with 500 to 1,000 mL/d being about average.3132 Fluids in the third space may return to the vascular compartment several days after surgery because of the changes in physiology resulting in intravascular reaccumulation, which may result in pulmonary edema. In addition, operative blood loss is usually estimated by the operating surgeon to be 15 to 40% less than the isotopically measured blood loss from that patient.17 Although insensible loss is typically about 600 mL/d for an adult, postoperative hyperventilation, fever, and hypermetabolism may increase this substantially (1,500/d).17 However, in the postoperative patient who is not eating, there is ordinarily no net insensible loss,16 and this fact is often neglected when considering replacement, resulting in additional fluid excess. Additional surgical fluid losses that are difficult to calculate are the following: additional insensible fluid losses by evaporation from the exposed peritoneal (or pleural) surfaces; and evaporative losses by virtue of operative drapes and from the administration of dry inhaled gases. Actual data are limited, but during laparotomy, the loss is about 150 mL/h or about 300 mL for an uncomplicated cholecystectomy.3335

Most protocols for postoperative fluid therapy recommend about 30 to 35 mL/kg/d plus estimated losses. For a 65-kg individual following cholecystectomy, the total for the initial postoperative day might thus be calculated as 2,275 mL (35 mL/kg maintenance) + 600 mL (insensible loss) + 1,000 mL (third space loss) + 300 mL (evaporative loss) = 4.2 L.

Virtually all protocols for postoperative fluid management recommend frequent monitoring of the patient’s volume status, utilizing such readily available clinical parameters as BP, heart rate, urine output, auscultation of the lungs, changes in body weight, and calculation of net fluid retention.17,28,3132 If fluid retention is noted to be excessive, then the rate of administration can be decreased. In the current series, values for heart rate, BP, pulse, and urine output were generally recorded in the nurses notes or graphic sheets. However, not a single patient had a postoperative weight recorded before pulmonary edema was diagnosed and after discharge from the recovery room, auscultation of the lungs by a physician was never recorded in any patient. These observations suggest that among physicians caring for these patients, the index of suspicion concerning possible consequences of excessive fluid administration was not high. Since to our knowledge there are no established guidelines for “panic values” or their equivalent for fluid retention, the nursing staff did not alert physicians as to possible excessive fluid retention. When postoperative pulmonary edema has occurred in generally healthy individuals, the mortality has often been in excess of 50%, as occurred in the present study.1,3

The parameters that are included in the physician’s calculation of replacement plus maintenance fluids include estimations of parameters shown in Table 3. All of the five parameters not only represent“ estimates,” but it is generally agreed that the estimates vary widely among different physicians.17 It would appear to be important that “panic” values for fluid retention be established for different categories of surgical procedures.

Postoperative pulmonary edema has been a reported complication in generally healthy postoperative subjects receiving known amounts of IV fluids.16 Among 161 postoperative patients, 27% of those retaining 2.2 L per 24 h developed pulmonary edema.16 However, since a number of these patients also had postoperative hyponatremic encephalopathy, the pulmonary edema may have been neurogenic in some cases. In the present study, neurogenic pulmonary edema secondary to postoperative hyponatremic encephalopathy should not have occurred, because the plasma sodium level was normal (135 ± 6 mmol/L).

The incidence of postoperative pulmonary edema is uncertain. In generally elderly, mostly male patients and those with heart disease, the incidence was 2.3 to 4.8%, less than the 7.6% in the current study.5,2122 In 14,707 generally low-risk female patients undergoing hysteroscopic hysterectomy, the incidence was only 0.2%.36 In none of these studies were mortality figures available.5,2122,36 There may have been patients in the current study who had undocumented silent postoperative myocardial ischemia.7 Major causes of perioperative morbidity and mortality are myocardial infarction and ischemia.18,2122 In response, there is now ever more sophisticated perioperative monitoring of cardiac function.7 However, fluid monitoring is generally carried out in an unsophisticated manner, and this appears to have contributed to the mortality from pulmonary edema (Table 3).

In three patients, pulmonary edema occurred following endoscopic procedures, in which the operative field was irrigated with copious quantities of fluid. Although the staff attempted to evaluate intake and output, such a task is technically difficult. Monitoring of fluid retention during transurethral resection of the prostate (TURP) can be accomplished by the ethanol method or monitoring of body weight,3738 and a device is available for fluid monitoring during hysteroscopic hysterectomy,39but such procedures are not in wide use. The most widely accepted method of monitoring intravascular volume status is by pulmonary artery catheter, but this procedure has been criticized recently because of associated morbidity.4041 The incidence of pulmonary edema following hysteroscopic hysterectomy (endometrial ablation) is < 1% and the number of deaths is not known.36,42The incidence of pulmonary edema following TURP is unknown, but there are at least five reported cases with one death.4345 In 25 patients undergoing TURP, the volume of irrigating fluid absorbed (± SD) was found to be 2.1 ± 0.9 L.38 In five patients undergoing hysteroscopic hysterectomy who developed fluid overload, the volume of irrigating fluid absorbed was 5 to 7 L.23 Retention of such volumes of fluid can lead to pulmonary edema in otherwise healthy subjects16(Table 2), emphasizing the necessity for monitoring net fluid retention during such procedures.

For editorial comment see page 1224.

Table Graphic Jump Location
Table 1. Patients With Pulmonary Edema
* 

PCWP = pulmonary capillary wedge pressure; M = male; F = female.

Table Graphic Jump Location
Table 2. Laboratory Values
Table Graphic Jump Location
Table 3. Fluid Losses During and After Surgery
Lowell, JA, Schifferdecker, C, Driscoll, DF, et al (1990) Postoperative fluid overload: not a benign problem.Crit Care Med18,728-733. [PubMed] [CrossRef]
 
van Hoozen, BE, van Hoozen, CM, Alberton, TE Pulmonary considerations and complications in the neurosurgical patient: pulmonary edema. Youmans, JR eds.Neurological surgery1996,624-626 WB Saunders. Philadelphia, PA:
 
Roth, E, Lax, LC, Maloney, JV Ringer’s lactate solution and extracellular fluid volume in the surgical patient: a critical analysis.Ann Surg1969;169,149-164. [PubMed]
 
Finn, JC, Rosenthal, MH Pulmonary edema in trauma and critically ill patients.Semin Anesth1989;8,265-274
 
Khuri, SF, Daley, J, Henderson, W, et al The National Veterans Administration surgical risk study: risk adjustment for the comparative assessment of the quality of surgical care.J Am Coll Surg1995;180,519-531. [PubMed]
 
Katz, AM Cardiomyopathy of overload.N Engl J Med1990;322,100-110. [PubMed]
 
Mangano, DT, Browner, WS, Hollenberg, M, et al Association of perioperative myocardial ischemia with cardiac morbidity and mortality in men undergoing noncardiac surgery.N Engl J Med1990;323,1781-1788. [PubMed]
 
Ayus, JC, Arieff, AI Pulmonary complications of hyponatremic encephalopathy: noncardiogenic pulmonary edema and hypercapnic respiratory failure.Chest1995;107,517-521. [PubMed]
 
Becker, DP, Gade, GF, Young, HF, et al Diagnosis and treatment of head injury in adults: fluids and electrolytes. Youmans, JR eds.Neurological surgery1990,2113-2115 WB Saunders. Philadelphia, PA:
 
Suga, K, Tsukamoto, K, Nishigauchi, K, et al Iodine-123-MIBG imaging in pheochromocytoma with cardiomyopathy and pulmonary edema.J Nucl Med1996;37,1361-1364. [PubMed]
 
Malik, AB Mechanisms of neurogenic pulmonary edema.Circ Res1985;57,1-18. [PubMed]
 
Frim, DM, Wollman, L, Evans, AB, et al Acute pulmonary edema after low-level air embolism during craniotomy.J Neurosurg1996;85,937-940. [PubMed]
 
Falk, JL, Rackow, EC, Weil, MH Colloid and crystalloid fluid resuscitation. Shoemaker, WC Ayres, S Grenvik, A eds.Textbook of critical care1989,1055-1073 WB Saunders. Philadelphia, PA:
 
Baumgartner, F, Omari, B, Lee, J, et al Survival after trauma pneumonectomy: the pathophysiologic balance of shock resuscitation with right heart failure.Am Surg1996;62,967-972. [PubMed]
 
Christenson, JT, Aeberhard, JM, Badel, P Adult respiratory distress syndrome after cardiac surgery.Cardiovasc Surg1996;4,15-21. [PubMed]
 
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Giesecke, AH, Egbert, LD Perioperative fluid therapy—crystalloids. Giesecke, AH Egbert, LD eds.Anesthesia1986,1313-1328 Churchill-Livingstone. New York, NY:
 
Roberts, JP, Roberts, JD, Skinner, C Extracellular fluid deficit following operation and its correction with Ringer’s lactate: a reassessment.Ann Surg1985;202,1-8. [PubMed]
 
Baggish, MS, Sze, EH Endometrial ablation: a series of 568 patients treated over an 11 year period.Am J Obstet Gynecol1996;174,908-913. [PubMed]
 
Lyon, RP, St Lezin, M, Thomas, C, et al Monitoring of body weight during transurethral resection of the prostate: preliminary report.J Endourol1994;8,161-163. [PubMed]
 
Hahn, RG, Ekengren, JC Patterns of irrigating fluid absorption during transurethral resection of the prostate as indicated by ethanol.J Urol1993;149,502-506. [PubMed]
 
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Figures

Tables

Table Graphic Jump Location
Table 1. Patients With Pulmonary Edema
* 

PCWP = pulmonary capillary wedge pressure; M = male; F = female.

Table Graphic Jump Location
Table 2. Laboratory Values
Table Graphic Jump Location
Table 3. Fluid Losses During and After Surgery

References

Lowell, JA, Schifferdecker, C, Driscoll, DF, et al (1990) Postoperative fluid overload: not a benign problem.Crit Care Med18,728-733. [PubMed] [CrossRef]
 
van Hoozen, BE, van Hoozen, CM, Alberton, TE Pulmonary considerations and complications in the neurosurgical patient: pulmonary edema. Youmans, JR eds.Neurological surgery1996,624-626 WB Saunders. Philadelphia, PA:
 
Roth, E, Lax, LC, Maloney, JV Ringer’s lactate solution and extracellular fluid volume in the surgical patient: a critical analysis.Ann Surg1969;169,149-164. [PubMed]
 
Finn, JC, Rosenthal, MH Pulmonary edema in trauma and critically ill patients.Semin Anesth1989;8,265-274
 
Khuri, SF, Daley, J, Henderson, W, et al The National Veterans Administration surgical risk study: risk adjustment for the comparative assessment of the quality of surgical care.J Am Coll Surg1995;180,519-531. [PubMed]
 
Katz, AM Cardiomyopathy of overload.N Engl J Med1990;322,100-110. [PubMed]
 
Mangano, DT, Browner, WS, Hollenberg, M, et al Association of perioperative myocardial ischemia with cardiac morbidity and mortality in men undergoing noncardiac surgery.N Engl J Med1990;323,1781-1788. [PubMed]
 
Ayus, JC, Arieff, AI Pulmonary complications of hyponatremic encephalopathy: noncardiogenic pulmonary edema and hypercapnic respiratory failure.Chest1995;107,517-521. [PubMed]
 
Becker, DP, Gade, GF, Young, HF, et al Diagnosis and treatment of head injury in adults: fluids and electrolytes. Youmans, JR eds.Neurological surgery1990,2113-2115 WB Saunders. Philadelphia, PA:
 
Suga, K, Tsukamoto, K, Nishigauchi, K, et al Iodine-123-MIBG imaging in pheochromocytoma with cardiomyopathy and pulmonary edema.J Nucl Med1996;37,1361-1364. [PubMed]
 
Malik, AB Mechanisms of neurogenic pulmonary edema.Circ Res1985;57,1-18. [PubMed]
 
Frim, DM, Wollman, L, Evans, AB, et al Acute pulmonary edema after low-level air embolism during craniotomy.J Neurosurg1996;85,937-940. [PubMed]
 
Falk, JL, Rackow, EC, Weil, MH Colloid and crystalloid fluid resuscitation. Shoemaker, WC Ayres, S Grenvik, A eds.Textbook of critical care1989,1055-1073 WB Saunders. Philadelphia, PA:
 
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