Decreased Plasma Oncotic Pressure Research Articles

Kwashiorkor - New evidence in the puzzle of oedema formation.

Kwashiorkor, a type of severe malnutrition associated with oedema, has been known for centuries but its mechanism remains elusive.1 The low level of plasma albumin and the associated decreased plasma oncotic pressure has been for years the main explanation of oedema of kwashiorkor: an excess fluid flow from the capillaries to the interstitium was assumed to result from an imbalance of Starling's forces.2 This mechanism seems plausible, as a low level of plasma albumin is a hallmark of kwashiorkor3 and the Starling's principle shows that plasma oncotic pressure, largely determined by plasma albumin, is amongst the factors influencing fluid flow from the capillaries towards the interstitium.

TO STUDY PROFILE OF PATIENTS WITH PLEURAL EFFUSION AT TERTIARY CARE CENTRE.

Pleural effusion is the condition characterized by an abnormal collection of uid in pleural space resulting from excess uid production or decreased absorption(1–3). It is due to pleural uid accumulation inside pleural space. The major mechanism include: increased interstitial uid in the lungssecondary to increased pulmonary capillary pressure (i.e., heart failure) or permeability (i.e., pneumonia); decreased intrapleural pressure (i.e., atelectasis); decreased plasma oncotic pressure (i.e., hypoalbuminemia); increased pleural membrane permeability and obstructed lymphatic ow (e.g., pleural malignancy or infection); diaphragmatic defects (i.e., hepatic hydrothorax); and thoracic duct rupture (i.e., chylothorax)(4).

MASKED SEPSIS DUE TO ACUTE CHOLECYSTITIS IN A PATIENT WITH CARDIOPULMONARY DISEASE LEADING TO SEPTIC SHOCK: A CASE REPORT

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Sepsis is a primary cause of death in nearly 23.5% of chronic heart failure patients. The relationship between acute cholecystitis and cardiovascular disease is vague but there have been few studies suggesting cholecystocardiac link. Here we describe a similar case that presented as pulmonary edema and myocardial ischemia. CASE PRESENTATION: 81-year-old male with past medical history of myocardial infarction, chronic obstructive pulmonary disease, hypothyroidism, hypertension, hyperlipidemia presented to the emergency department with worsening exertional dyspnea for the past 3 days. On physical examination he was afebrile, tachycardic, hypoxic requiring 4L oxygen. Chest auscultation revealed bibasilar rales. Electrocardiogram showed ST segment depression in lateral leads and troponins were elevated at 1.56. Labs showed mild leukocytosis, BNP 1658, Creatinine 1.8 and normal hepatic panel. Chest X-Ray suggested pulmonary edema for which he was diuresed. He was started on heparin drip. Echocardiogram showed reduced ejection fraction of 40%. Cardiac catheterization showed multivessel disease and moderate pulmonary hypertension. Coronary artery bypass surgery was recommended. Next day he developed mild periumbilical pain, which later moved to his right upper quadrant. CT abdomen showed cholelithiasis with pericholecystic inflammation. Cholescintigraphy confirmed acute cholecystitis. Patient started becoming more dyspneic and pulmonary edema worsened. He became hypotensive and febrile. Sepsis bundle was initiated including blood cultures, broad spectrum antibiotics and intravenous fluids. Patient was intubated and transferred to critical care unit. He required multiple pressors. Continuous hemodialysis was started for metabolic acidosis. Blood cultures revealed gram negative bacteremia. Unfortunately, the patient could not be saved. DISCUSSION: Gallbladder edema may be a response to the ischemia caused by cardiac instability. The exact mechanism linking acute cholecystitis to extracholecystic diseases is unknown, but it is likely due to an increase in portal venous pressure along with a decrease in plasma oncotic pressure. Chronic cardiopulmonary diseases and aging can cause immune-senescence that may increase the risk of sepsis which sometimes does not meet SIRS criteria. These patients, especially when on betablockers, cannot meet increased metabolic demands. Irritation and spasticity of the gallbladder can create reflex stimuli through the autonomic pathways, which leads to temporary alteration in coronary blood flow. CONCLUSIONS: Acute cholecystitis may coexist with or be misdiagnosed as a cardiovascular disorder. Looking for signs of end organ dysfunction or subtle vital sign irregularities may help identify older patients who are on their way to decompensation and allow us to intervene earlier with appropriate investigations and treatment which may lead to the prevention of fatal events. Reference #1: Ozeki M, Takeda Y, Morita H, et al. Acute cholecystitis mimicking or accompanying cardiovascular disease among Japanese patients hospitalized in a Cardiology Department. BMC Res Notes. 2015;8:805. Published 2015 Dec 19. doi:10.1186/s13104-015-1790-8 Reference #2: Walker AMN, Drozd M, Hall M, et al. Prevalence and Predictors of Sepsis Death in Patients With Chronic Heart Failure and Reduced Left Ventricular Ejection Fraction. J Am Heart Assoc. 2018;7(20):e009684. doi:10.1161/JAHA.118.009684 Reference #3: Meelu OA, Baber U, Theodoropoulos K, Mennuni MG, Kini AS, Sharma SK. Acute cholecystitis and myocardial infarction: a case study with coronary involvement. Clin Case Rep. 2016;4(8):793-796. Published 2016 Jul 13. doi:10.1002/ccr3.621 DISCLOSURES: No relevant relationships by Aditya Bansal, source=Web Response No relevant relationships by Hina Farrukh, source=Web Response No relevant relationships by sreeja sompalli, source=Web Response

Fatal reversal of the cholecystocardiac link

Abstract Patients presenting to the emergency department with right upper quadrant pain are usually placed on a list of critical, yet limited differential diagnoses. Of these diagnoses, cholecystitis is fairly common. Although most cases of cholecystitis are relatively straight-forward, there are numerous extracholecystic conditions which have been known to cause acute acalculous cholecystitis. Examples include systemic infections, acute and chronic renal failure, systemic lupus erythematosus, and congestive heart failure. These conditions lead may lead to diffuse gallbladder wall thickening through a number of hypothesized mechanisms, including an increase in portal venous pressure, and a decrease in plasma oncotic pressure. The right upper quadrant pain caused by this gallbladder wall thickening however, is usually a late complaint, after the primary etiology has made itself clear. We report the case of a 6 year old female who presented to the emergency department with acute right upper quadrant pain and vomiting. Apart from the gastrointestinal system, examination of all other systems (including cardiovascular) was negative. An ultrasound was done and the diagnosis of acute acalculous cholecystitis was made. The patient did not respond to treatment, and after additional investigations, evidence of congestive heart failure with bilateral pulmonary effusions was seen. It was concluded that the patient's heart failure, although not apparent on initial examinations, was the etiology behind her initial gallbladder thickening and abdominal pain. This case reports an important etiology to be aware of in patients presenting with right upper quadrant pain which is unresponsive to treatment methods. Multiple extracholecystic disease entities such as congestive heart failure, must be placed in the list of differential diagnoses by the caring physician.

Subclinical pulmonary congestion is prevalent in nephrotic syndrome.

In patients with nephrotic syndrome (NS), the lung is considered an organ protected from the risk of edema. However, data on objectively measured lung water in NS patients is lacking. Here we measured lung water by an ultrasound (US) technique as well as by transthoracic impedance in 42 asymptomatic patients with active NS, in 14 stage G5D CKD patients on chronic hemodialysis, and in 21 healthy individuals. In patients with active NS, the median number of US-B lines (a metric of lung water) after 5 min in a supine position was significantly higher (12; interquartile range: 7-25) compared with that in healthy individuals (4; 2-9) but similar to that in hemodialysis patients (23; 10-39). The difference between NS patients and healthy individuals was significantly amplified (16; 10-35 vs. 4; 2-9) after 60 min of supine resting and significantly attenuated after 5 min of standing (10; 7-25 vs. 3; 1-6). Posture-dependent changes in lung water in patients with active NS were significantly accentuated compared with both hemodialysis patients and healthy individuals. After NS remission, the number of US-B lines was significantly reduced to 5 (4-18) at 5 min and to 6 (5-22) at 60 min approaching the normal range. Lung congestion in patients with active NS was confirmed by transthoracic impedance. Thus, asymptomatic pulmonary congestion is pervasive in patients with NS. A clinical trial is needed to assess the utility of lung US for the management of patients with NS.

Reactive Oxygen Species and NFkB Increase Peritoneal Filtration and Generate Ascites in Nephrotic Syndrome

Clinical and experimental observations suggest that nephrotic ascites is not accounted for by hypoalbuminemia but by changes of the capillary endothelium permeability. We investigated the mechanism of these changes in puromycin aminonucleoside (PAN) nephrotic rats. The peritoneal filtration coefficient (Kf) was estimated by the slope of the regression line connecting the trans‐peritoneal gradient of osmotic pressure which was varied experimentally to the trans‐peritoneal water flux measured by osmotic dilution.Kf doubled and expression of aquaporin 1 (AQP1) increased in peritoneum of PAN rats. PAN rats displayed peritoneal oxidative stress attested by ROS accumulation and dysregulation of NADPH oxidase and ROS detoxifying enzymes expression. The ROS scavenger N‐acetyl cysteine (NAC) prevented the increase in Kf and in AQP1 expression. It also reduced by half the volume of ascites without changing renal sodium handling, albuminuria or hypoalbuminemia. PAN rats peritoneum also displayed activation of NFkB attested by increased nuclear labeling with anti‐p50 antibody. Activation of NFkB was blunted in NAC‐treated PAN rats. JSH‐23, an inhibitor of NFkB transcriptional activity, mimicked all the effects of NAC.These results show that nephrotic syndrome is associated with increased filtration coefficient of the peritoneal barrier which stems in part from increased expression of AQP1. These changes are triggered by oxidative stress and subsequent activation of NFkB. They account for at least half of increased filtration rate, the remaining stemming possibly from decreased plasma oncotic pressure.

The characteristic of Indonesia's pre-eclampsia: From obstetric intensive care with ventilator until epidemiologic and its molecular biology profile of pulmonary edema in severe pre-eclampsia.

Pulmonary edema is among the least frequently diagnosed criteria for severe pre-eclampsia. A higher incidence of pulmonary edema was noted in older patients, multigravidas, and patients with underlying chronic hypertension that developed prior to delivery. The development of pulmonary edema was also associated with the administration of excess colloid or crystaloid infusion. Two hundreds and thirty millions people occupying Indonesia as tropical and coastal country gave rise the problem of highly maternal mortality rate of 225/100,000 deliveries where pre-eclampsia and eclampsia as most possible cause. Over 5years from the year 2005 through 2009 our 160 eclampsia study observed about significantly correlation between typical estafet referred case and maternal mortality (Odds ratio 19.1 and P=0.065). Specifically those referred eclampsia cases arriving lately to our tertiary hospital, complication of pulmonary edema also apparently became determinant factor to uphold the increased maternal mortality (Odds ratio 6.1 and P=0.083) We found at our teaching hospital Dr. Soetomo Surabaya as referral center along the year 2012, 477 pre-eclampsia-eclampsia cases which complicated by 27 cases of pulmonary from which we apply obstetric intensive care unit for tightly monitoring treatment. The majority use of ventilator were applied on 22 cases (81.4%), that most approximately 16 cases (72%) need 48h under ventilator use and the remaining 6 cases was not untill 5days of extubation. The etiology of pulmonary edema in preeclamptic patients involves multi-factors; abnormal COP-PWCP gradient, increased pulmonary capillary permeability, and left ventricular failure were identified causes. It has been well known that the pathogenesis of pulmonary edema in severe pre-eclampsia-eclampsia initiated by capillary alveolar leakage that leading increased capillary permeability and extravascular fluid oncotic as well as decreased plasma oncotic pressure. In severe pre-eclampsia appear that another circumstance directing its worst state of inhibited angiogenesis related pulmonary edema. The study confirmed that the decreased serum albumin of ⩽3g% and its content of amino acid essentiale acitvate endoplasmic reticulum stress response in which indicated by increasingly produced GRP (Glucose Related-Protein) 78. It may affect the decreased VEGFR and may also be inhibiting angiogenesis and hypoxia as well. At such moment apparently pulmonary edema patient get worsening clinical sign.

The Diagnosis and Management of Pleural Effusions in the ICU

Pleural effusions are common in critically ill patients. Most effusions in intensive care unit (ICU) patients are of limited clinical significance; however, some are important and require aggressive management. Transudative effusions in the ICU are commonly caused by volume overload, decreased plasma oncotic pressure, and regions of altered pleural pressure attributable to atelectasis and mechanical ventilation. Exudates are sequelae of pulmonary or pleural infection, pulmonary embolism, postsurgical complications, and malignancy. Increases in pleural fluid volume are accommodated principally by chest wall expansion and, to a lesser degree, by lung collapse. Studies in mechanically ventilated patients suggest that pleural fluid drainage can result in improved oxygenation for up to 48 hours, but data on clinical outcomes are limited. Mechanically ventilated patients with pleural effusions should be semirecumbant and treated with higher levels of positive-end expiratory pressure. Rarely, large effusions can cause cardiac tamponade or tension physiology, requiring urgent drainage. Bedside ultrasound is both sensitive and specific for diagnosing pleural effusions in mechanically ventilated patients. Sonographic findings of septation and homogenous echogenicity may suggest an exudative effusion, but definitive diagnosis requires pleural fluid sampling. Thoracentesis should be carried out under ultrasound guidance. Antibiotic regimens for parapneumonic effusions should be based on current pneumonia guidelines, and anaerobic coverage should be included in the case of empyema. Decompression of the pleural space may be necessary to improve respiratory mechanics, as well as to treat complicated effusions. While small-bore catheters inserted under ultrasound guidance may be used for nonseptated effusions, surgical consultation should be sought in cases where this approach fails, or where the effusion appears complex and septated at the outset. Further research is needed to determine the effects of pleural fluid drainage on clinical outcomes in mechanically ventilated patients, to evaluate weaning strategies that include pleural fluid drainage, and to better identify patients in whom pleural effusions are more likely to be infected.

Nephrotic Syndrome in Dogs: Clinical Features and Evidence-Based Treatment Considerations

Nephrotic syndrome (NS), defined as the concurrent presence of hypoalbuminemia, proteinuria, hyperlipidemia, and fluid accumulation in interstitial spaces and/or body cavities, is a rare complication of glomerular disease in dogs, cats, and people. Affected animals frequently have markedly abnormal urine protein:creatinine ratios because of urinary loss of large amounts of protein; however, hypoalbuminemia-associated decreased plasma oncotic pressure is insufficient to explain fluid extravasation in most laboratory models, and, instead, either aberrant renal tubule retention of sodium with resultant increase in hydrostatic pressure or a systemic increase in vascular permeability may be the primary defects responsible for development of NS. Factors associated with NS in people (including "nephrotic-range" serum albumin concentration and urine protein concentration, and particular glomerular disease subtypes) have been assumed previously to also be important in dogs, although descriptions were limited to those patients included in case series of glomerular disease, and sporadic case reports. However, case-control comparison of larger cohorts of dogs with nephrotic versus nonnephrotic glomerular disease more recently suggests that predisposing factors and concurrent clinicopathologic abnormalities differ from those typically encountered in people with nephrotic syndrome, although case progression and negative effect on patient outcome are similar. This article briefly reviews major current theories and supporting evidence on the pathogenesis of NS, followed by an overview on the clinical features of this syndrome in dogs with glomerular disease. The authors also offer evidence-based and experience-based treatment recommendations that are based on minimizing the suspected dysregulation of the renin-angiotensin-aldosterone axis in affected dogs.

NOVEL OVINE MODEL OF METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS-INDUCED PNEUMONIA AND SEPSIS

Methicillin-resistant Staphylococcus aureus (MRSA)-related pneumonia and/or sepsis are a frequent serious menace. The aim of the study was to establish a standardized and reproducible model of MRSA-induced septic pneumonia to evaluate new therapies. Sheep were operatively prepared for chronic study. After 5 days' recovery, tracheostomy was performed under anesthesia, and smoke injury was induced by inhalation of cotton smoke (48 breaths, <40 degrees C). Methicillin-resistant S. aureus (AW6) (approximately 2.5x10(11) colony-forming units) was instilled into the airway by a bronchoscope. After the injury, animals were awakened and maintained on mechanical ventilation by 100% oxygen for first 3 h, and thereafter, oxygen concentration was adjusted according to blood gases. The sheep were resuscitated by lactated Ringer solution with an initial rate of 2 mL kg(-1) h(-1) that was further adjusted according to hematocrit. Study groups include (1) sham (noninjured, nontreated; n=6), (2) S+MRSA (exposed to smoke inhalation and MRSA, nontreated; n=6), and (3) smoke (exposed to smoke inhalation alone; n=6). Injured (S+MRSA) animals showed the signs of severe sepsis-related multiple organ failure 3 h after insult. Cardiovascular morbidity was evidenced by severe hypotension, with increased heart rate, cardiac output, left atrial pressure and severely decreased systemic vascular resistance index, and left ventricle stroke work index. Pulmonary dysfunction was characterized by deteriorated gas exchange (PaO2/FIO2 and pulmonary shunt) and increased ventilatory pressures. The S+MRSA group showed significantly greater lung tissue water content, myeloperoxidase activity, and cytokine production compared with uninjured sham animals. Microvascular hyperpermeability was evidenced by marked fluid retention (fluid net balance), decreased plasma protein with decreased plasma oncotic pressure, and increased pulmonary microvascular pressure. All these changes were accompanied by 6- to 7-fold increase in plasma nitrite/nitrate and increased production of reactive nitrogen species in lung. The smoke inhalation alone had a little or no effect on these variables. This model closely mimics hyperdynamic human sepsis. The excessive production of NO may be extensively involved in the pathogenic process.

Isoflurane Inhibits Compensatory Intravascular Volume Expansion After Hemorrhage in Sheep

After hemorrhage, blood volume is partially restored by transcapillary refill, a process of spontaneous compensatory intravascular volume expansion that we hypothesized would be inhibited by anesthesia. Six chronically instrumented sheep were subjected to four randomly ordered experiments while conscious or during anesthesia with isoflurane. After plasma volume measurement (indocyanine green), 15% or 45% of the blood volume was withdrawn. To quantify transcapillary refill, mass balance and kinetic calculations utilized repeated measurements of hemoglobin concentration, assuming that transcapillary refill would dilute hemoglobin concentration. After 15% hemorrhage, mean arterial blood pressure remained stable in both conscious and isoflurane-anesthetized sheep (normotensive hemorrhage) but decreased after 45% hemorrhage (hypotensive hemorrhage). After either normotensive or hypotensive hemorrhage, transcapillary refill occurred more rapidly during the first 40 min than during the next 140 min (P < 0.001). In conscious sheep, at 180 min, 57% and 42% of the bled volume had been restored after normotensive and hypotensive hemorrhage, respectively, in contrast to only 13% and 27% (P < 0.001) in isoflurane-anesthetized sheep. A novel kinetic model implicated hemodynamic factors in rapid, early transcapillary refill and decreased plasma oncotic pressure in subsequent slower filling. We conclude that isoflurane inhibits transcapillary refill after both normotensive and hypotensive hemorrhage in sheep.

Inducible nitric oxide synthase dimerization inhibitor prevents cardiovascular and renal morbidity in sheep with combined burn and smoke inhalation injury.

Inducible nitric oxide synthase (iNOS) is implicated in the pathogenesis of acute respiratory distress syndrome (ARDS). ARDS treatment is frequently complicated by significant extrapulmonary comorbidity. This study was designed to clarify the role of iNOS in mediating extrapulmonary comorbidity in sheep after combined burn and smoke inhalation injuries using a potent and highly selective iNOS dimerization inhibitor, BBS-2. Twenty-two female sheep were operatively prepared. After 5 days of recovery, tracheostomy was performed under ketamine-halothane anesthesia. Sheep were given a 40% total body surface third-degree burns and insufflated with cotton smoke (48 breaths, <40 degrees C). Sheep were divided into four groups: noninjured and nontreated (sham group; n = 6), noninjured but treated with BBS-2 (sham/BBS-2 group; n = 4), injured but nontreated (control group, n = 6), and injured but treated with 100 microg.kg-1.h-1 BBS-2 (BBS-2 group; n = 6). Evaluation was in a laboratory intensive care unit setting for 48 h. The sham group had stable cardiopulmonary and systemic hemodynamics. Control animals showed multiple signs of morbidity. Decreased left ventricular stroke work index and stroke volume index with elevated left atrial pressure indicated myocardial depression. Systemic vascular leak was evidenced by robust hemoconcentration, decreased plasma oncotic pressure, and increased transvascular fluid flux into the lymphatic system. Finally, severely impaired renal function (urinary output) was associated with adverse net fluid balance. Treatment with BBS-2 prevented all these morbidities without adversely effecting cardiovascular hemodynamics such as cardiac index and mean arterial pressure. The results identify a major role for iNOS in mediating extrapulmonary comorbidity in a clinically relevant and severe trauma model and support the use of highly selective iNOS inhibitors as novel treatments in critical care medicine.

Mechanisms of water exchanges: the Starling equation

This review considers the main mathematical models used in the understanding of transvascular fluid exchanges and oedema formation. Models by Starling, Kedem-Katchalsky and Wiederhielm are briefly described. The main factors which determine the value of the physical parameters involved in these models are the osmotic and interstitial pressures in plasma and tissue. With regard to the regulation of interstitial osmotic pressure, the importance of the presence of mucopolysaccharidic gel in the interstitial compartment creating an exclusion volume for proteins diffusing from plasma is underlined, as well as the importance of lymphatic flow, a parameter neglected in several models of transcapillary exchanges. Consequences of variations in venous hydrostatic pressure, plasma oncotic pressure, endothelial permeability are discussed using the described models. In case of changes combining an increase in venous pressure and permeability and a decrease in plasma oncotic pressure, the importance of correcting venous pressure relatively to protein supply is discussed.

Pathophysiology of pulmonary edema.

Pulmonary edema is a frequent and common cause of death in patients in critical care settings. It is seen as a complication of myocardial infarcts, hypertension, pneumonia, smoke inhalation, and high-altitude pulmonary edema. Pulmonary edema occurs when there are alterations in Starling forces and capillary permeability, opposition to lymphatic flow in the lungs, decreased plasma oncotic pressure, central nervous system lesions, and following some types of strenuous exercise. Pulmonary edema presents initially with crackles, wheezing, and dry cough and progresses to tachypnea, dyspnea, orthopnea, pink frothy sputum, and cyanosis. Treatment involves supportive therapy, reduction in blood volume, and oxygen therapy.

Edematous disorders

The pathogenesis of renal sodium and water retention in cardiac failure, cirrhosis, and the nephrotic syndrome may be explained by the unifying hypothesis of body fluid volume regulation. According to this hypothesis, underfilling of the arterial vascular compartment initiates a sequence of events, including activation of various neurohormonal vasoconstrictor systems, which results in enhanced renal sodium and water reabsorption, the failure to escape from the sodium-retaining effect of aldosterone, and renal resistance to atrial natriuretic peptide. In patients with low-output cardiac failure, a decrease in cardiac output results in arterial underfilling. Peripheral arterial vasodilation diminishes the fullness of the arterial vascular compartment in patients with high-output cardiac failure and cirrhosis. In the nephrotic syndrome, the decrease in plasma oncotic pressure due to hypoalbuminemia initiates arterial underfilling. The factors that are responsible for the peripheral arterial vasodilation in patients with cirrhosis remain obscure. Diuretics are initially effective in reducing the excess of total-body sodium and water in edematous patients. Loop diuretics, with or without metolazone or a thiazide diuretic, are quite useful in patients with heart failure. In cirrhosis and the nephrotic syndrome, the specific aldosterone antagonist spironolactone, alone or in combination with other diuretics, has proven to be highly efficacious. However, in all instances, the emergence of diuretic resistance represents a major limitation of diuretic therapy for the edematous patient. This diuretic resistance may be mediated by further activation of vasoconstrictor, antinatriuretic neurohormones.

Is a decrease in plasma oncotic pressure enough to explain the edema of pregnancy?

The balance of fluid across capillaries is given by the Starling equation. Because the plasma protein concentration (one of its components) is decreased in pregnancy, we decided to explore the question as to whether hypoproteinemia with intact protein mass (produced by blood volume expansion) or hypoproteinemia with decreased total protein mass (produced by removal of circulating proteins) alters the oncotic pressure differences across capillaries. We calculated the oncotic pressure difference obtained in seven nonpregnant ewes during periods of normoproteinemia and hypoproteinemia; the influence of fluid infusion under both conditions was also observed. There was an increase in the oncotic pressure difference across the capillary wall during hypoproteinemia produced by a decrease in the total protein mass (p less than 0.01); however, the response to hypoproteinemia produced by fluid infusion was similar (p greater than 0.1). The venous pressure (used as an index of interstitial fluid pressure changes) did not differ in either hypoproteinemia or fluid infusion. Capillary permeability was decreased during hypoproteinemia, as evidenced by a higher lymph/protein ratio of labeled albumin during the control period (p less than 0.05). In conclusion, during a state of decreased plasma protein concentration similar to that of pregnancy, the difference in the oncotic pressure and hydrostatic pressure forces acting to prevent transfer of fluid to the interstitium is increased. Therefore other factors that influence fluid transfer across the capillaries must be investigated to explain the edema of pregnancy.

The Acute Cerebral Effects of Changes in Plasma Osmolality and Oncotic Pressure

Although it is generally accepted that a decrease in plasma oncotic pressure may result in the formation of peripheral edema, the effect of a hypo-oncotic state on brain water content is less well known. Therefore, utilizing the technique of hollow-fiber plasma-pheresis to manipulate plasma composition, the authors examined the effects of acute changes in either plasma osmolality or colloid oncotic pressure on the EEG, regional cerebral blood flow, intracranial pressure, and brain tissue specific gravity (as a measure of cerebral water content) in anesthetized, neurologically normal New Zealand white rabbits. Animals in which either osmolality or oncotic pressure was decreased by plasma replacement with an appropriate solution were compared with a group of control animals in which both of these variables were maintained constant. Animals in which plasma osmolality was decreased by 13 +/- 6 mOsm/kg (from a baseline value of 295 +/- 5 mOsm/kg) showed evidence of a significant increase in cortical water content (approximately 0.5%), whereas a 65% reduction in oncotic pressure (from 20 +/- 2 mmHg to 7 +/- 1 mmHg) failed to produce any change. There were no significant differences in mean arterial pressure, central venous pressure, regional cerebral blood flow, or the EEG between any of the groups. Although intracranial pressure increased in all groups, the largest increase (8.1 +/- 4.4 mmHg) occurred in those animals whose osmolality was reduced. The increase in intracranial pressure in animals rendered hypo-oncotic was no different from the "control" group (2.4 +/- 0.9 mmHg vs. 3.0 +/- 1.5 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

Les échanges transcapillaires de liquides: Un programme en Basic

Transcapillary fluid exchanges are analysed with the Wiederhielm's model programmed in this study in Basic language. The physiological variable which are taken in account are : arterial and venous capillary pressures, interstitial pressure and the colloid osmotic pressure of plasma and tissue proteins. This model shows the relationship between filtration, reabsorption, plasma leakage and the lymph flow. Edema resulting from venous and lymphatic obstruction or from a decrease in plasma oncotic pressure are simulated.

Management of Fluid Retention in Patients With Advanced Cancer

SODIUM retention and fluid accumulation manifested as edema are common in cancer patients.¹This is usually secondary to pooling of fluids in a third space as occurs in ascites, pleural effusion, dependent edema secondary to obstruction of the inferior vena cava or lymphatics, peritonitis, or ileus. This abnormal accumulation of extracellular fluid is physiologically unavailable and results in a decreased effective circulating blood volume. Hyponatremia is common, but on a "dry weight" basis there is extra body sodium. A state of chronic protein depletion is common in cancer patients because of loss of protein into the malignant effusions and repeated drainage of these protein-rich fluids, loss of protein in diarrhea and external fistulae (especially pancreatic), decreased food intake and malnutrition, and hypercatabolism as a result of sepsis. Hypoalbuminemia with consequent decreased plasma oncotic pressure leads to a decreased plasma volume and facilitates the escape of fluid to these third

Plasma oncotic pressure and plasma protein concentration in patients following thermal injury.

Plasma oncotic pressure (POP), albumin and total protein were measured in 14 patients with thermal injuries varying extent from 16 to 90% of the body surface. The patients were treated with large amounts of balanced salt solutions in the initial phase. There was an abrupt, pronounced decrease in POP to about 51% of the normal during the first 24 h. Despite the low POP values (minimum 0.78 kPa) and marked peripheral oedema, no patient had overt pulmonary oedema. Clinical and roentgenological evidence of pulmonary dysfunction during the initial period was only seen in conjunction with lung burn or aspiration pneumonitis. Oedema-preventing mechanism and inability to detect interstitial pulmonary oedema are discussed as possible explanations. There was no significant correlation between decrease in POP and mortality, but low POP values seemed to persist longer in the patients who died.