DOCSLIB.ORG

Transcapillary Colloid Osmotic Gradient and Body Fluid Volumes in Renal Failure

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Transcapillary Colloid Osmotic Gradient and Body Fluid Volumes in Renal Failure View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 29 (1986), pp. 895—900 Transcapillary colloid osmotic gradient and body fluid volumes in renal failure PER FAUCHALD Medical Department B, The National Hospital of Norway, Oslo, Norway Transcapillary colloid osmotic gradient andbodyfluid volumes In renal treatment, below which the patient often will suffer sympto- failure. The aim was to study the transcapillary fluid balance in dialysis matic hypotension [6, 7]. patients during and after ultrafiltration. Plasma and subcutaneous The aim of the study was to examine to what extent the interstitial fluid (wick technique) colloid osmotic pressure, plasma volume (I'25-albumin space) and extracellular fluid volume (radiosulfate edema—preventing mechanisms of reduced interstitial colloid space) were measured in nine patients on maintenance hemodialysis osmotic pressure and increased transcapillary colloid osmotic before (pre-dialysis state) and after (dry-weight state) ultraffitration. In gradient are activated in patients with chronic renal failure on the pre-dialysis state, interstitial colloid osmotic pressure was reduced maintenance hemodialysis. A secondary aim was to study the compared to normal controls (12.7 3.5versus 15.8 2.7mmHg, mean values SD) andtranscapillary colloid osmotic gradient increased changes in plasma colloid osmotic pressure and plasma volume (15.3 3.0versus 12.8 2.7mmHg). Ultrafiltration resulted in a during ultrafiltration. In order to accomplish these objectives, parallel decrease of plasma volume and interstitial fluid volume of 19 to colloid osmotic pressure in plasma and interstitial fluid and 20%, and an increase in mean interstitial colloid osmotic pressure of 3.4 body fluid volumes (plasma volume and extracellular fluid mmHg and in mean transcapillary colloid osmotic gradient of 1.9volume) were measured in a pre-dialysis fluid state and after mmHg. The mean ultrafiltration rate was 21.9 1.9mllmin and the plasma refilling rate was 16.5 2.7mI/mm. It is concluded that the ultrafiltration to a dry-weight state. In addition, plasma colloid changes in plasma and interstitial fluid colloid osmotic pressure tend to osmotic pressure was followed during ultrafiltration. preserve plasma volume and limit the interdialytic increase in intersti- tial fluid volume. Material Patients Nine patients (2 females and 7 males, mean age 65.6 years, range of 61 to 70 years old) with chronic renal failure were studied. Patient 1 was anephric and the other patients had Patients with chronic renal failure on maintenancecreatinine clearance less than 5 mI/mm. Diagnosis and clinical hemodialysis commonly show abnormalities in body fluid com-information are given in Table 1. The body weight and the position [1—5]. In addition to increases in extracellular fluidlaboratory values in Table 1 are data from day 1 (before volume, alterations in the partition of volumes between thetreatment). Patient 2 had moderate edema in the ankle region on intravascular and the interstitial spaces are reported in chronicday 1, the other patients did not have edema. None of the renal failure [1, 2, 5]. Intermittent fluid overload and the needpatients had congestive heart failure, nephrotic syndrome, for fluid withdrawal during dialysis frequently create clinicaldiabetes mellitus or liver disease. They were all established on complications [6—8]. Plasma volume depletion is an importanthemodialysis treatment for at least eight weeks and were factor in the pathogenesis of symptomatic hypotension whichinvestigated as outpatients. Six of the patients were treated with occurs in approximately 25% of hemodialysis treatments [6—11].furosemide (mean dosage 590 mg/day, range 160 to 1000 With the tendency to at least intermittent fluid overload,mg/day) and four patients were on antihypertensive treatment activation of local edema—preventing factors [12], such as(Table 1). All medication was continued in unchanged dosage reduced interstitial colloid osmotic pressure, could be expectedduring the investigation. in dialysis patients. Hildebrandt et al [13] recently found Normal subjects Colloid osmotic pressure in plasma and evidence for reduced extravascular albumin mass in patients oninterstitial fluid were measured in 16 normal subjects (four chronic hemodialysis. Reduced subcutaneous interstitial colloidfemales and 12 males, mean ageS! years, range of 33 to 72 years osmotic pressure has been found in patients with fluid overloadold) [14]. Plasma and extracellular fluid volume were measured due to nephrotic syndrome, heart failure and hepatic cirrhosisin another group of 19 normal subjects (11 females and eight [14—16]. males) aged 22 to 54 years (mean 36 years) [14]. Dry weight or ideal weight for a given dialysis patient is Informed consent was obtained in each case. The protocol defined as the weight obtained at the end of hemodialysiswas approved by the Ethical Committee, Norwegian Council for Science and the Humanities. Received for publication April 18, 1985, Methods and in revised form July 8, 1985 Design of the study Plasma and extracellular fluid volume © 1986 by the International Society of Nephrology were measured in the morning under fasting condition and in 895 896 Fauchald Table 1. Clinical and laboratory data of the patientsa. Body Body Serum Serum Serum Duration of Antihypertensive Patient Clinical Age height weight MAP Hct urea creatinine albumine dialysis diuretic no, diagnosis(years)Sex (cm) (kg) (mmHg) (%)(mmolell) (Mmolell) (gil) (months) treatment I TBC 62 M 173 70.5 120 25 22.4 1149 33 12 none 2 CON 70 M 162 76.4 107 31 26.1 415 31 5 F+A 3 NSC 61 M 178 75.0 110 28 24.0 1060 32 6 F+A 4 CON 63 F 157 51.0 117 28 23.0 884 41 25 F+A+C 5 CON 67 M 178 65.8 95 27 36.8 946 36 41 none 6 CGN 69 M 176 82.0 105 24 33.0 955 38 4 F 7 CON 67 F 169 59.5 125 22 23.7 1061 31 4 C 8 PCK 61 M 170 62.4 107 25 26.1 1140 36 17 F 9 CPN 70 M 163 60.9 103 30 29.7 990 37 31 F a Abbreviationsare: TBC, renal tuberculosis; CON, chronic glomerulonephritis; NSC, nephrosclerosis; PCK, polycystic kidney disease; CPN, chronic pyelonephritis; MAP, mean arterial blood pressure; F, furosemide; A, aipha-methyldopa; C, captopril. the supine position. All subjects were recumbent for at least 30 were accepted, red wicks being excluded. Wick fluid was mm before the injections were given. The measurements of isolatedby centrifugation under mineral oil [19] and colloid plasma and interstitial colloid osmotic pressure were performedosmotic pressure was measured by the osmometer mentioned in patients and normal subjects in the supine position and at theearlier. All the interstitial fluid pressure values represent the same time of the day. Both patients and normal subjects weremean of at least two (two to four) separate measurements of ambulatory until the blood test for plasma colloid osmoticwick fluid from two to four wicks. pressure was drawn. Plasma volume Plasma volume (PV) was determined as the In the patients, body fluid volumes and colloid osmoticinitial '251-albumin distribution space as previously described pressure in plasma and subcutaneous interstitial fluid were[14]. Values are given as ml per kg lean body mass (mllkg measured on day 1 in pre-dialysis state (48 to 72 hours afterLBM). hemodialysis). On days 2 and 3, ultrafiltration was performed in Blood volume (BV) BV was calculated from PV and hemato- order to bring the patient as near to dry-weight as possible, andcrit using a Fcell ratio (ratio of whole body hematocrit to large was followed by hemodialysis without transmembrane pressurevessel hematocrit) of 84% in normal subjects and 81% in the for two hours. Plasma colloid osmotic pressure was measureddialysis patients [11. Values are given as ml per kg lean body before, during and after ultrafiltration. The measurements per-mass (mllkg LBM). formed on day 1 were then repeated on day 4 in exactly the Extracellular fluid volume Extracellular fluid volume was same manner. measured by intravenous administration of radiosulfate as Ultrafiltration procedure Ultrafiltration treatment was per-previously described [14]. Values are given as ml per kg lean formed using a Oambro AK-b proportioning system with abody mass (mllkg LBM). Oambro-Lundia plate filter (11.5 t)(OambroIndustries, Bar- Interstitial fluid volume Interstitial fluid volume equals extra- rington, Illinois, USA). Ultrafiltrate was collected during treat-cellularfluid volume minus plasma volume and the values are ment and the volume measured. Infusions were not given given as ml per kg lean body mass (mllkg LBM). during ultrafiltration. Blood samples were collected from the Leanbody mass LBM wascalculated from body height and arterial blood line at the start, and after 30, 60, and 120 mm, and weightusing the formulas given by Womersley et al [21]. at end of ultrafiltration for measurements of plasma colloid Plasma refilling rate (PRR) PRR represent a measure of the osmotic pressure and hematocrit. fluid volume transport from the interstitium to the intravascular Colloidosmoticpressure A colloid osmometer (Departmentspace during ultrafiltration and the values are given as mllmin. ofPhysiology, University of Bergen, Norway) made for 5 gliter PRR was calculated using the following equation: samples with Amieon PM3O membranes was used [17]. The coefficient of variation within assays was 4.3% (N=12)and PRR =(UF-volume—PV)IUF-time between assays 4.9% (N=10). Interstitialcolloid osmotic pressure Subcutaneousinterstitial fluid was collected by the wick technique [18—20], Under where UF-volume is ultrafiltrate volume in ml, PV is the aseptic conditions four double nylon wicks (containing 600 calculated change in plasma volume during ultrafiltration in ml, filaments,diameter 1 mm) soaked in saline were sewn into and UF-time is the duration of ultrafiltration in mm. APV was subcutaneous tissue on the side of the thorax in a length of 5 to calculated as: 8 cm.
Load more

Recommended publications
  • Albumin in Health and Disease: Protein Metabolism and Function*
    Article #2 CE An In-Depth Look: ALBUMIN IN HEALTH AND DISEASE Albumin in Health and Disease: Protein Metabolism and Function* Juliene L. Throop, VMD Marie E. Kerl, DVM, DACVIM (Small Animal Internal Medicine), DACVECC Leah A. Cohn, DVM, PhD, DACVIM (Small Animal Internal Medicine) University of Missouri-Columbia ABSTRACT: Albumin is a highly charged, 69,000 D protein with a similar amino acid sequence among many veterinary species. Albumin is the major contributor to colloid oncotic pressure and also serves as an important carrier protein. Its ability to modulate coagulation by preventing pathologic platelet aggrega- tion and augmenting antithrombin III is important in diseases that result in moderately to severely decreased serum albumin levels. Synthesis is primar- ily influenced by oncotic pressure, but inflammation, hormone status, and nutrition impact the synthetic rate as well. Albumin degradation is a poorly understood process that does not appear to be selective for older mole- cules.The clinical consequences of hypoalbuminemia reflect the varied func- tions of the ubiquitous albumin protein molecule. he albumin molecule has several characteristics that make it a unique protein. Most veterinarians are aware of the importance of this molecule in maintain- Ting colloid oncotic pressure, but albumin has many other less commonly recog- nized functions as well. The clinical consequences of hypoalbuminemia are reflections of the many functions albumin fulfills. Understanding the functions, synthesis, and *A companion article on degradation of the albumin molecule can improve understanding of the causes, conse- causes and treatment of quences, and treatment of hypoalbuminemia. hypoalbuminemia appears on page 940. STRUCTURE Email comments/questions to Albumin has a molecular weight of approximately 69,000 D, with minor variations [email protected], among species.
    [Show full text]
  • Renal Sodium Handling in Minimal Change Nephrotic Syndrome
    Arch Dis Child: first published as 10.1136/adc.59.9.825 on 1 September 1984. Downloaded from Archives of Disease in Childhood, 1984, 59, 825-830 Renal sodium handling in minimal change nephrotic syndrome A-B BOHLIN AND U BERG Department of Paediatrics, Karolinska Institute, Huddinge Hospital, Stockholm, Sweden SUMMARY Renal sodium handling was studied in 23 children at three different stages of the minimal change nephrotic syndrome-the oedema forming state, proteinuric steady state, and remission. Clearances of inulin and para-aminohippuric acid and urinary sodium excretion were determined basally, after intravenous infusion of isotonic saline and hyperoncotic albumin, and after furosemide injection. Absolute and fractional basal sodium excretion were significantly lower in oedema forming patients than in proteinuric patients in steady state, and non-proteinuric patients. In contrast to proteinuric patients in steady state and non-proteinuric patients, the oedema forming patients failed to respond to isotonic saline infusion with increased sodium excretion. After diuretic blockade with furosemide, the fractional sodium excretion of the oedema forming patients increased to values no different from those of the non-proteinuric patients, whereas the fractional sodium excretion of the steady state patients increased to significantly higher values. The plasma aldosterone concentration was within normal limits in 11 of 14 proteinuric patients, and did not correlate with the basal sodium excretion. Thus, sodium copyright. retention in the minimal change nephrotic syndrome was found only in oedema forming patients, and since this is not related to the plasma aldosterone concentration it may be caused by an intrarenal mechanism, probably sited in distal parts of the nephron.
    [Show full text]
  • Determinants of Glomerular Filtration in Experimental Glomerulonephritis in the Rat
    Determinants of glomerular filtration in experimental glomerulonephritis in the rat. D A Maddox, … , T M Daugharty, B M Brenner J Clin Invest. 1975;55(2):305-318. https://doi.org/10.1172/JCI107934. Research Article Pressures and flows were measured in surface glomerular capillaries, efferent arterioles, and proximal tubules of 22 Wistar rats in the early autologous phase of nephrotoxic serum nephritis (NSN). Linear deposits of rabbit and rat IgG and C3 component of complement were demonstrated in glomerular capillary walls by immunofluorescence microscopy. Light microscopy revealed diffuse proliferative glomerulonephritis, and proteinuria was present. Although whole kidney and single nephron glomerular filtration rate (GFR) in NSN (0.8 plus or minus 0.04 SE2 ml/min and 2 plus or minus 2 nl/min, respectively) remained unchanged from values in 16 weight-matched NORMAL HYDROPENIC control rats (0.8 plus or minus 0.08 and 28 plus or minus 2), important alterations in glomerular dynamics were noted. Mean transcapillary hydraulic pressure difference (deltaP) averaged 41 plus or minus 1 mm Hg in NSN versus 32 plus or minus 1 in controls (P LESS THAN 0.005). Oncotic pressures at the afferent (piA) end of the glomerular capillary were similar in both groups ( 16 mm /g) but increased much less by the efferent end (piE) in NSN (to 29 plus or minus 1 mm Hg) than in controls (33 plus or minus 1, P less than 0.025). Hence, equality between deltaP and piE, denoting filtration pressure equilibrium, obtained in control but not in NSN rats. While glomerular plasma flow rate was slightly higher […] Find the latest version: https://jci.me/107934/pdf Determinants of Glomerular Filtration in Experimental Glomerulonephritis in the Rat D.
    [Show full text]
  • Glomerulonephritis Management in General Practice
    Renal disease • THEME Glomerulonephritis Management in general practice Nicole M Isbel MBBS, FRACP, is Consultant Nephrologist, Princess Alexandra lomerular disease remains an important cause Hospital, Brisbane, BACKGROUND Glomerulonephritis (GN) is an G and Senior Lecturer in important cause of both acute and chronic kidney of renal impairment (and is the commonest cause Medicine, University disease, however the diagnosis can be difficult of end stage kidney disease [ESKD] in Australia).1 of Queensland. nikky_ due to the variability of presenting features. Early diagnosis is essential as intervention can make [email protected] a significant impact on improving patient outcomes. OBJECTIVE This article aims to develop However, presentation can be variable – from indolent a structured approach to the investigation of patients with markers of kidney disease, and and asymptomatic to explosive with rapid loss of kidney promote the recognition of patients who need function. Pathology may be localised to the kidney or further assessment. Consideration is given to the part of a systemic illness. Therefore diagnosis involves importance of general measures required in the a systematic approach using a combination of clinical care of patients with GN. features, directed laboratory and radiological testing, DISCUSSION Glomerulonephritis is not an and in many (but not all) cases, a kidney biopsy to everyday presentation, however recognition establish the histological diagnosis. Management of and appropriate management is important to glomerulonephritis (GN) involves specific therapies prevent loss of kidney function. Disease specific directed at the underlying, often immunological cause treatment of GN may require specialist care, of the disease and more general strategies aimed at however much of the management involves delaying progression of kidney impairment.
    [Show full text]
  • Glomerular Filtration I DR.CHARUSHILA RUKADIKAR Assistant Professor Physiology GFR 1
    Glomerular filtration I DR.CHARUSHILA RUKADIKAR Assistant Professor Physiology GFR 1. Definition 2. Normal value 3. Variation 4. Calculation (different pressures acting on glomerular membrane) 5. Factors affecting GFR 6. Regulation of GFR 7. Measurement of GFR QUESTIONS LONG QUESTION 1. GFR 2. RENIN ANGIOTENSIN SYSTEM SHORT NOTE 1. DYNAMICS OF GFR 2. FILTRATION FRACTION 3. ANGIOTENSIN II 4. FACTORS AFFECTING GLOMERULAR FILTRATION RATE 5. REGULATION OF GFR 6. RENAL CLEARANCE TEST 7. MEASUREMENT OF GFR Collecting duct epithelium P Cells – Tall, predominant, have few organelles, Na reabsorption & vasopressin stimulated water reabsorption I cells- CT and DCT, less, having more cell organelles, Acid secretion and HCO3 transport CHARACTERISTICS OF RENAL BLOOD FLOW 600-1200 ml/min (high) AV O2 difference low (1.5 mL/dL) During exercise increases 1.5 times Low basal tone, not altered in denervated / innervated kidney VO2 in kidneys is directly proportional to RBF, Na reabsorption & GFR Not homogenous flow, cortex more & medulla less Vasa recta hairpin bend like structure, hyperosmolarity inner medulla Transplanted kidney- cortical blood flow show autoregulation & medullary blood flow don’t show autoregulation, so no TGF mechanism Neurogenic vasodilation not exist 20% of resting cardiac output, while the two kidneys make < 0.5% of total body weight. Excretory function rather than its metabolic requirement. Remarkable constancy due to autoregulation. Processes concerned with urine formation. 1. Glomerular filtration, 2. Tubular reabsorption and 3. Tubular secretion. • Filtration Fluid is squeezed out of glomerular capillary bed • Reabsorption Most nutrients, water and essential ions are returned to blood of peritubular capillaries • Secretion Moves additional undesirable molecules into tubule from blood of peritubular capillaries Glomerular filtration Glomerular filtration refers to process of ultrafiltration of plasma from glomerular capillaries into the Bowman’s capsule.
    [Show full text]
  • Significance of Protein in Edema Fluids I C
    i Significance of Protein in Edema Fluids I C. L. Witte, M. H. "f itte, A. E. Dumont Departments of Surgery, University of Arizona College of Medicine, Tucson, Arizona and "'ewYorkl.Jniversity_School of Medicine, New York, N. Y. Lymphology 4 (1971), 29-31 The partition of extracellular fluid between plasma and tissues is largely regulated by the balance of hydrostatic an~ colloid osmotic (oncotic) pressure gradients across capillary membranes. Normally ~ small excess of tissue fluid forms, enters lymphatics and returns to the bloodstream. When an imbalance develops between the rate of lymph production and the rate of its return to the systemic venous circulation, edema.or effusion appear. Accumulation of edema, however, is not uniform in amount and composition throughout the body and depend, on the forces governing capillary filtration, regional differences in capillary permeabiFty, lymph flow and the specific factor tending to per­ petuate the edema. Obstruction td lymph return or disruption of capillary integrity (e.g. I infiltrating cancer or inflammation) promote effusion or edema high in protein content (so-called "exudate"). On the other hand, increased hydrostatic pressure in semiperme­ able capillaries promotes excess lymph and ultimately edema or effusion low in protein content (so-called "transudate"). iThe hepatic sinusoid is unique in its free permeability to plasma protein. Hepatic venous outflow obstruction, accordingly, produces excess hepatic and thoracic duct lymphi and eventually ascitic fluid, high in protein. In his monograph on The Fluids of the Body (1), Starling reasoned that increased capillary hydrostatic pressure Jas initially off set by a fall in tissue oncotic pressure. As the gradient in hydrostatic pressure rises in semipermeable capillary beds a progres­ sively more dilute capillary filtrate forms in tissues.
    [Show full text]
  • 13-CAPILLARY CIRCULATIOJN.Pdf
    Very important Extra information * Guyton corners, anything that is colored with grey is EXTRA explanation Capillary Circulation Objectives : • Describe the structure of capillary wall: endothelial cells, basement membrane, intercellular clefts, vesicles, pores. • Blood brain barrier to water soluble agents. • Describe structure of liver and renal capillaries. • Compare and contrast diffusion and filtration. • State the Starling forces acting on the capillary wall: capillary blood pressure, interstitial fluid pressure, plasma protein colloid osmotic pressure, interstitial fluid colloid osmotic pressure. • Describe net loss of fluid from capillaries and discuss role of lymphatics. • Discuss importance of filtration giving clinical situations. • Define odema, state its causes and discuss its mechanisms. * We recommend studying Histology of Capillaries before this lecture 2 Contact us : [email protected] Functions of the circulation Serve the requirements of the tissues: 1- Transport nutrients & remove waste products. 2- Transport hormones, enzymes, body heat, electrolytes …etc. 3- Maintain normal homeostasis for optimal survival &function of cells. 3 Functional Parts of the circulation It is divided to : 1. Aorta : (Elastic recoil) 2. Arteries : Transport blood Rapidly under high pressure to the tissues (muscular, low resistance vessels) (Thick) 3. Arterioles : Can close the arteriole completely or dilate it several folds they alter blood flow to the capillaries in Response to needs(Thick). -Arterioles & small arteries are called (Resistance vessels) (high resistance vessels). 4. Capillaries: Have numerous Capillary pores and very large surface area (exchange blood vessels) for exchange of gases, nutrients, waste products etc. (Very thin wall with unicellular layer of endothelial cells and very small internal diameter). -Blood flow is intermittent (discontinuous) , turn on and off every few seconds or minutes (vasomotion), determined by oxygen demand.
    [Show full text]
  • 4 Edema in Childhood
    Kidney International, Vol. 51, Suppl. 59 (1997). pp. S-100-S-104 (1) Red Hypo Ne] Liv Edema in childhood Ma Pre Sev SATOSHI HISANO, SEUNGHOON HAHN, NANCY B. KUEMMERLE, JAMES CM. CHAN, (2) Incr. and NATALE G. DESANTO Cardi He: h Pediatric Nephrology Division, Virginia Commonwealth University's Medical College of Virginia, Richmond, Virginia, USA, and Divisione di Nefrologia Art dell' Adulto e del Bambino, Seconda Universita'degli Studi di Napoli, Naples, Italy Renal Act ACt Idiops Fan Edema in childhood. There are two types of edema: localized edema sympathetic nervous system (SNS) activity; and (3) antidiuretic Nor and generalized edema. The causes ofgeneralized edema in childhoodare hormone (ADH) release [4-6]. These forces and perhaps as yet diverse. Formation of generalizededema involves retention of sodium and Prej unidentified factors give rise to the consequential water and water in the kidney. The treatment of generalized edema depends on the (3) Incre primary etiology. Supportive nutritional and medicaltherapies are needed sodium retention, which promotes the development of edema, Allerg to prevent further edema. These and related features of edema in The sodium and water retention leads to further decreased Vascu childhood are discussed in this review. den plasma oncotic pressure, setting up a vicious cycle perpetuating dise the edema formation. The movement of water from intracellular space to interstitial space by itself also contributes to the devel­ opment of edema formation [1, 3]. Edema can be defined as the presence of excess fluid in the In contrast, the mechanism of "overfilling edema" is expanded interstitial space of the body. Edema is divided into two types, extracellular volume that results from primary renal sodium localized edema and generalized edema.
    [Show full text]
  • Mechanisms and Management of Nephrotic Edema
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 45 (1994),pp.266—281 NEPHROLOGY FORUM Mechanisms and management of nephrotic edema Principal discussant: MICHAEL H. HUMPHREYS University of California San Francisco, San Francisco, California showed a normal heart size and regular rhythm; heart sounds were distant through a thickened chest wall, but no murmurs or gallops were Editors heard, The abdomen was nontender without evidence of hepatic or JORDAN J. COHEN splenic enlargement. The stool was guaiac positive. The extremities JOHN T. HARR1NGTON showed no clubbing, but massive anasarca was present, with pitting edema of all extremities as well as the abdominal and thoracic wall. The NICOLAOS B. MADIAS penis and scrotum were edematous, and paraphimosis was evident, Neurologic examination was normal except for a slowed relaxation Managing Editor phase of the deep-tendon reflexes. CHERYL J. ZUSMAN Laboratory values on admission were: hematocrit, 29.5; white blood cell count, 16,700/mm3 with a left shift; and a platelet count of 212 x 103/mm'. The serum sodium concentration was 145 mEq/liter; potas- sium, 4.3 mEq/liter; chloride, 121 mEq/liter; total CO2. 16 mmol/liter; State University of New York at Stony Brook BUN, 65 mg/dl; and serum creatinine, 5.5 mgldl. The serum albumin and concentration was 0.6 g/dl; calcium, 6.9 mg/dl; phosphorus, 5.4 mg/dl; and magnesium, 1.8 mg/dl. The erythrocyte sedimentation rate was 139 Tufts University School of Medicine mm/hr, and the serum cholesterol was 554 mg/dl.
    [Show full text]
  • 3- Pathophysiology of Ascites.Pdf
    § § ﻻ ﯾﻤﺘﻄﻲ اﻟﻤﺠﺪ ﻣﻦ ﻟﻢ ﯾﺮﻛﺐ اﻟﺨﻄﺮ ... وﻻ ﯾﻨﺎل اﻟﻌﻠﻰ ﻣﻦ ﻗﺪم اﻟﺤﺬرا و ﻣﻦ اراد اﻟﻌﻼ ﻋﻔﻮا ﺑﻼ ﺗﻌﺐ ... ﻗﻀﻰ و ﻟﻢ ﯾﻘﺾ ﻣﻦ إدراﻛﮭﺎ وطﺮا Important Doctor's notes Extra explanation Introduction : ★ Ascites is of Greek derivation ("askos") and refers to a bag or sack and describes pathologic fluid accumulation within the peritoneal cavity. ★ Most patients (85%) with ascites have cirrhosis. ★ The most common causes of cirrhosis at the present time are chronic viral hepatitis and alcoholic liver disease. PERITONEAL CAVITY ★ It is a potential space between the parietal peritoneum and visceral peritoneum; the two membranes separate the organs in the abdominal cavity from the abdominal wall. ★ Derived from the coelomic cavity of the embryo. ★ Largest serosal sac in the body and secretes approximately 50 ml of fluid per day. PERITONEAL FLUID ★ Normal, lubricating fluid found in the peritoneal cavity. ★ The fluid is mostly water with electrolytes, antibodies, white blood cells, albumin, glucose and other biochemicals. : ★ Reduce the friction between the abdominal organs as they move around during digestion. Usually we have a small amount of fluid in the peritoneal cavity, which prevents ulceration and friction. But if the fluid is more then normal it's ascites. و(̵˂MORE 12 PAGES U CAN DO IT (๑˃̵ᴗ CAUSES OF Infection Nephrotic Pancreatic or Cirrhosis CHF Malignancy (TB) biliary ascites ASCITES: MOST COMMON syndrome ★ Essential hypertension will not lead to ascites , in long term it will lead to heart failure which cause PATHOGENESIS OF ASCITES: ascites ! PATHOGENESIS 3-Increase in the 2-Decreased colloid 1-Increased permeability of osmotic pressure.
    [Show full text]
  • The Physiological Proof That Starling's Law for the Capillary-Interstitial Fluid Transfer Is Wrong
    CRIMSONpublishers http://www.crimsonpublishers.com Research Article Open Acc Res Anatomy ISSN: 2577-1922 The Physiological Proof that Starling’s Law for the Capillary-Interstitial Fluid Transfer is Wrong: Advancing the Porous Orifice (G) Tube Phenomenon as Replacement Khaled A Ghanem1 and Ahmed N Ghanem2* 1Mansoura University Hospital, Egypt 2Retired Consultant Urologist, Egypt *Corresponding author: Ahmed N Ghanem, Retired Consultant Urologist, No1 President Mubarak Street, Mansoura 35511, Egypt, Tel: 001020883243; Email: Submission: October 16, 2017; Published: November 13, 2017 Abstract Objective: Material and To reportmethods: physiological evidence that the capillary works as a porous orifice (G) tube proving that Starling’s law is wrong. The G tube has a negative side pressure (SP) exerted on its wall. The G tube is akin to capillary and when enclosed in a chamber (C), akin to interstitial fluid space, demonstrating the G-C circulation. Here we report the results of experiments on the hind limb of sheep; first when the fluid is passed through the artery and later when passed through the vein. We monitored the occurrence of oedema of the limb comparing the two circulations.Results: The inflow pressure induces negative SP in the G tube which is responsible for absorption and G-C phenomenon: an autonomous magnetic field-like G-C circulation occurs between fluid in the G tube’s lumen and a surrounding fluid compartment C. The hind limb acted as normal without oedema and has a negative interstitial (ISF) pressure when the fluid is passed through the artery i.e. acting like the G tube. There was gross oedema with increaseConclusion: in weight of the limb when the fluid was passed through the vein acting like Poiseuille’s tube.
    [Show full text]
  • Edema: Diagnosis and Management KATHRYN P
    Edema: Diagnosis and Management KATHRYN P. TRAYES, MD, and JAMES S. STUDDIFORD, MD, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania SARAH PICKLE, MD, Rutgers Robert Wood Johnson Medical School, New Brunswick, New Jersey AMBER S. TULLY, MD, Cleveland Clinic, Cleveland, Ohio Edema is an accumulation of fluid in the interstitial space that occurs as the capillary filtration exceeds the limits of lymphatic drainage, producing noticeable clinical signs and symptoms. The rapid development of generalized pitting edema associated with systemic disease requires timely diagnosis and management. The chronic accumulation of edema in one or both lower extremities often indicates venous insufficiency, especially in the presence of dependent edema and hemosiderin deposition. Skin care is crucial in preventing skin breakdown and venous ulcers. Eczematous (stasis) dermatitis can be managed with emollients and topical steroid creams. Patients who have had deep venous thrombosis should wear compres- sion stockings to prevent postthrombotic syndrome. If clinical suspi- cion for deep venous thrombosis remains high after negative results are noted on duplex ultrasonography, further investigation may include magnetic resonance venography to rule out pelvic or thigh proximal venous thrombosis or compression. Obstructive sleep apnea may cause bilateral leg edema even in the absence of pulmonary hyperten- sion. Brawny, nonpitting skin with edema characterizes lymphedema, which can present in one or both lower extremities. Possible secondary causes
    [Show full text]