Hypo Albumina Emi A

7/28/2019 Hypo Albumina Emi A

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,lHYPOALBUMINAEMIA

Background

Albumin, the body's predominant serum-binding protein, has several important functions, asfollows:

Albumin comprises 75-80% of normal plasma colloid oncotic pressure and 50% ofprotein content. When plasma proteins, especially albumin, no longer sustain sufficient

colloid osmotic pressure to counterbalance hydrostatic pressure, edema develops.

Albumin transports various substances, including bilirubin, fatty acids, metals, ions,hormones, and exogenous drugs. One consequence of hypoalbuminemia is that drugs that

are usually protein bound are free in the plasma, allowing for higher drug levels, more

rapid hepatic metabolism, or both.

Alterations in albumin level affect platelet function.Albumin.

Reference serum values range from 3.5-4.5 g/dL, with a total body content of 300-500 g.

Synthesis occurs only in hepatic cells at a rate of approximately 15 g/d in a healthy person, but

the rate can vary significantly with various types of physiologic stress. The half-life of albumin isapproximately 21 days, with a degradation rate of approximately 4% per day.

Hypoalbuminemia is a common problem among persons with acute and chronic medical

conditions. At the time of hospital admission, 20% of patients have hypoalbuminemia.

Hypoalbuminemia can be caused by various conditions, includingnephrotic syndrome, hepaticcirrhosis,heart failure, and malnutrition; however, most cases of hypoalbuminemia are caused by

acute and chronic inflammatory responses.

Serum albumin level is an important prognostic indicator. Among hospitalized patients, lower

serum albumin levels correlate with an increased risk of morbidity and mortality.

The presentation, physical examination findings, and laboratory results associated with

hypoalbuminemia depending on the underlying disease process.
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Pathophysiology

Serum albumin levels are dependent on the rate of synthesis, the amount secreted from the liver

cell, the distribution in body fluids, and the level of degradation. Hypoalbuminemia results froma derangement in one or more of these processes.

Synthesis

Albumin synthesis begins in the nucleus, where genes are transcribed into messenger ribonucleicacid (mRNA). The mRNA is secreted into the cytoplasm, where it is bound to ribosomes,

forming polysomes that synthesize preproalbumin. Preproalbumin is an albumin molecule with a

24 amino acid extension at the N terminus. The amino acid extension signals insertion of

preproalbumin into the membrane of the endoplasmic reticulum. Once inside the lumen of theendoplasmic reticulum, the leading 18 amino acids of this extension are cleaved, leaving

proalbumin (albumin with the remaining extension of 6 amino acids). Proalbumin is the principal

intracellular form of albumin. Proalbumin is exported to the Golgi apparatus, where the

extension of 6 amino acids is removed prior to secretion of albumin by the hepatocyte. Oncesynthesized, albumin is secreted immediately; it is not stored in the liver.

Distribution

Tracer studies with iodinated albumin show that intravascular albumin is distributed into theextravascular spaces of all tissues, with the majority being distributed in the skin. Approximately

30-40% (210 g) of albumin in the body is found within the vascular compartments of the muscle,

skin, liver, gut, and other tissues.

Albumin enters the intravascular space via 2 pathways. First, albumin enters this space by

entering the hepatic lymphatic system and moving into the thoracic duct. Second, albumin passesdirectly from hepatocytes into the sinusoids after traversing the Space of Disse.

After 2 hours, 90% of secreted albumin remains within the intravascular space. The half-life ofintravascular albumin is 16 hours. Daily losses of albumin from the intravascular space are

approximately 10%. Certain pathological conditions, such as nephrosis, ascites, lymphedema,

intestinal lymphangiectasia, and edema, can increase the daily loss of albumin from the plasma.

Albumin distributes into the hepatic interstitial volume, and the concentration of colloids in this

small volume is believed to be an osmotic regulator for albumin synthesis. This is the principal

regulator of albumin synthesis during normal periods without stress.

Degradation

Degradation of albumin is poorly understood. After secretion into the plasma, the albumin

molecule passes into tissue spaces and returns to the plasma via the thoracic duct. Taggedalbumin studies suggest that albumin may be degraded within the endothelium of the capillaries,

bone marrow, and liver sinuses. Albumin molecules apparently degrade randomly, with no

differentiation between old and new molecules.


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Epidemiology

Frequency

United States

Hypoalbuminemia is more frequent in older patients who are institutionalized, patients who arehospitalized with advanced stages of disease (eg, terminal cancer), and malnourished children.

Mortality/Morbidity

Low serum albumin levels are an important predictor of morbidity and mortality. A meta-analysis of cohort studies found that, with every 10 g/L decrease in serum albumin, mortality

was increased by 137% and morbidity increased by 89%. Patients with serum albumin levels of

less than 35 at 3 months following discharge from the hospital have a 2.6 times greater 5-yearmortality than those with a serum albumin levels greater than 40.

Hypoalbuminemia has also been studied as an important prognostic factor among subsets of

patients, such as patients with severesepsis, burns, and regional enteritis (Crohn disease).

Whether or not hypoalbuminemia is merely a marker of severe protein malnutrition, which itself

is a cause of increased morbidity and mortality or an independent risk factor for death, is unclear.

Race

No race predilection exists.

Sex

No sex predilection exists.

Age

Hypoalbuminemia affects persons of all age groups, depending on the underlying cause.

Hypoalbuminemia Clinical Presentation

Author: Ruben Peralta, MD, FACS; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM more...

Overview Presentation Workup
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Treatment Medication Follow-up

Updated: Apr 15, 2010

History Physical Causes Show All

History

The potential underlying causes of hypoalbuminemia are numerous. Patients' histories vary

significantly depending on the underlying disease state.

Gather past medical history for a history of liver or renal failure,hypothyroidism, malignancy,and malabsorption.

Evaluate the patient for appropriate dietary intake. Seek potential causes of acute or chronic inflammation that could explain the low albumin

levels.

Physical

Abnormal physical examination findings may be found in multiple organ systems depending onthe underlying disease. The findings listed below suggest the potential underlying disease

processes rather than the underlying hypoalbuminemia per se.

Head, eyes, ears, nose, and throat - Facial edema, macroglossia, parotid swelling,conjunctival icterus, temporal wasting

Integumentary - Loss of subcutaneous fat, delayed wound healing, dry coarse skin,painful dermatoses, peripheral edema, thin hair, spider angiomas, palmar erythema,

changes due to surgery and burns, jaundice

Cardiovascular - Bradycardia, hypotension, cardiomegaly Respiratory - Decreased respiratory expansion due to pleural effusion and weakened

intercostal muscles

Gastrointestinal - Hepatosplenomegaly, ascites Musculoskeletal - Muscle wasting, growth retardation in children, atrophy of the

interosseus hand muscles

Neurological - Encephalopathy, asterixis Genitourinary - Testicular atrophy Endocrine - Gynecomastia, hypothermia, thyromegaly Other - Various other signs related to associated specific nutrient deficiencies
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Causes

Hypoalbuminemia can result from decreased albumin production, defective synthesis because of

ahepatocyte damage, deficient intake of amino acids, increased losses of albumin via GI or renalprocesses, and, most commonly, acute or chronic inflammation. Some of the many causes are as

follows:

Protein malnutrition: Deficient protein intake results in the rapid loss of cellularribonucleic acid and disaggregation of the endoplasmic reticulumbound polysomes and,

therefore, decreased albumin synthesis. Albumin synthesis can decrease by more thanone third during a 24-hour fast. Albumin synthesis may be stimulated by amino acids

produced in the urea cycle, such as ornithine.

Defective synthesis: In patients with cirrhosis, synthesis is decreased because of the lossof hepatic cell mass. Also, portal blood flow is often decreased and poorly distributed,leading to maldistribution of nutrients and oxygen. The flow of substrate may affect

certain functions of the liver, including protein synthesis, which is decreased in patients

with cirrhosis who lack ascites. Albumin synthesis may actually increase in patients withcirrhosis who have ascites, possibly because of a change in hepatic interstitial colloid

levels, which may act as an overriding stimulus for albumin production. Although

synthesis is increased, the concentration of albumin is decreased because of dilution.

Extravascular protein losso Nephrotic syndrome: This can produce hypoalbuminemia by massive proteinuria,

with 3.5 g or more of protein lost within 24 hours. Albumin is filtered by the

glomerulus and catabolized by the renal tubules into amino acids that arerecycled. In patients with chronic renal disease, in whom both glomerular and

tubular diseases are present, excessive protein filtration may lead to both

increased protein loss and increased degradation. Only at higher rates of

albuminuria (>100 mg/kg/d) and only when the diet is adequate is albuminsynthesis increased.

o Protein-losing enteropathy: Under normal conditions, less than 10% of the totalalbumin is lost through the intestine. This fact has been confirmed by comparingalbumin labeled with chromium-51, which helps measure intestinal losses, to

albumin labeled with iodine-125, which helps measure overall degradation. In

cases of protein-losing enteropathy related to bacterial overgrowth,hypoalbuminemia is exacerbated by peripheral factors that inhibit albumin

synthesis by mechanisms similar to those observed with burns, trauma, infection,and carcinoma.

o Extensive burns: The skin is the major site for extravascular albumin storage andis the major exchangeable albumin pool needed to maintain plasma levels.Hypoalbuminemia results from direct losses of albumin from tissue damage, from

compromised hepatic blood flow due to volume loss, and from inhibitory tissue

factors (eg, tumor necrosis factor, interleukin-1, interleukin-6) released at the burnsites.

o Lymphatic blockage or mucosal disease: Diseases that result in protein loss fromthe intestine are divided into 2 main types. The first is lymphatic blockage, whichcan be caused by constrictive pericarditis, ataxia telangiectasia, and mesenteric


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blockage due to tumor. The second is mucosal disease with direct loss into the

bowel, which is observed with (1) inflammatory bowel disease and sprue and (2)

bacterial overgrowth, as in blind loop syndrome after intestinal bypass surgery.

Hemodilution: In the presence of ascites from any cause, the serum albumin level is not agood index of the residual synthetic capacity of the liver unless actual radioisotopic

measurements of production are used. With ascites, synthesis may be normal or evenincreased, but serum levels are low because of the larger volume of distribution. This istrue even for ascites due to cirrhosis.

Congestiveheart failure: The synthesis of albumin is normal in patients with congestiveheart failure. Hypoalbuminemia results from an increased volume of distribution.

o Oncotic pressure increase: The serum oncotic pressure partially regulates albuminsynthesis. The regulation site may be the oncotic content in the hepatic interstitial

volume because albumin synthesis is inversely related to the content of this

volume. Conditions that increase other osmotically active substances in the serumtend to decrease the serum albumin concentration by decreasing synthesis.

Examples include elevated serum globulin levels in hepatitis and

hypergammaglobulinemia. Acute and chronic inflammation: Albumin levels that are low because of acute

inflammation should normalize within weeks of resolution of the inflammation.

Persistent hypoalbuminemia beyond this point should prompt an investigation for an

ongoing inflammatory process. The cytokines (TNF, IL-6) released as part of theinflammatory response to physiologic stress (infection, surgery, trauma) can decrease

serum albumin by the following mechanisms:

o Increased vascular permeability (allowing albumin to diffuse into theextravascular space)

o Increased degradationo Decreased synthesis (among other mechanisms, by activating TNF-a, which

decreases transcription of the albumin gene)

Causes

Hypoalbuminemia can result from decreased albumin production, defective synthesis because of

hepatocyte damage, deficient intake of amino acids, increased losses of albumin via GI or renal

processes, and, most commonly, acute or chronic inflammation. Some of the many causes are asfollows:

Protein malnutrition: Deficient protein intake results in the rapid loss of cellularribonucleic acid and disaggregation of the endoplasmic reticulumbound polysomes and,

therefore, decreased albumin synthesis. Albumin synthesis can decrease by more thanone third during a 24-hour fast. Albumin synthesis may be stimulated by amino acids

produced in the urea cycle, such as ornithine.

Defective synthesis: In patients with cirrhosis, synthesis is decreased because of the lossof hepatic cell mass. Also, portal blood flow is often decreased and poorly distributed,

leading to maldistribution of nutrients and oxygen. The flow of substrate may affectcertain functions of the liver, including protein synthesis, which is decreased in patients

with cirrhosis who lack ascites. Albumin synthesis may actually increase in patients with
http://www.medscape.com/resource/heartfailurehttp://www.medscape.com/resource/heartfailurehttp://www.medscape.com/resource/heartfailurehttp://www.medscape.com/resource/heartfailure


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cirrhosis who have ascites, possibly because of a change in hepatic interstitial colloid

levels, which may act as an overriding stimulus for albumin production. Although

synthesis is increased, the concentration of albumin is decreased because of dilution.

Extravascular protein losso Nephrotic syndrome: This can produce hypoalbuminemia by massive proteinuria,

with 3.5 g or more of protein lost within 24 hours. Albumin is filtered by theglomerulus and catabolized by the renal tubules into amino acids that arerecycled. In patients with chronic renal disease, in whom both glomerular and

tubular diseases are present, excessive protein filtration may lead to both

increased protein loss and increased degradation. Only at higher rates ofalbuminuria (>100 mg/kg/d) and only when the diet is adequate is albumin

synthesis increased.

o Protein-losing enteropathy: Under normal conditions, less than 10% of the totalalbumin is lost through the intestine. This fact has been confirmed by comparingalbumin labeled with chromium-51, which helps measure intestinal losses, to

albumin labeled with iodine-125, which helps measure overall degradation. In

cases of protein-losing enteropathy related to bacterial overgrowth,hypoalbuminemia is exacerbated by peripheral factors that inhibit albumin

synthesis by mechanisms similar to those observed with burns, trauma, infection,

and carcinoma.

o Extensive burns: The skin is the major site for extravascular albumin storage andis the major exchangeable albumin pool needed to maintain plasma levels.

Hypoalbuminemia results from direct losses of albumin from tissue damage, from

compromised hepatic blood flow due to volume loss, and from inhibitory tissuefactors (eg, tumor necrosis factor, interleukin-1, interleukin-6) released at the burn

sites.

o Lymphatic blockage or mucosal disease: Diseases that result in protein loss fromthe intestine are divided into 2 main types. The first is lymphatic blockage, whichcan be caused by constrictive pericarditis, ataxia telangiectasia, and mesenteric

blockage due to tumor. The second is mucosal disease with direct loss into the

bowel, which is observed with (1) inflammatory bowel disease and sprue and (2)bacterial overgrowth, as in blind loop syndrome after intestinal bypass surgery.

Hemodilution: In the presence of ascites from any cause, the serum albumin level is not agood index of the residual synthetic capacity of the liver unless actual radioisotopicmeasurements of production are used. With ascites, synthesis may be normal or even

increased, but serum levels are low because of the larger volume of distribution. This is

true even for ascites due to cirrhosis.

Congestiveheart failure: The synthesis of albumin is normal in patients with congestiveheart failure. Hypoalbuminemia results from an increased volume of distribution.

o Oncotic pressure increase: The serum oncotic pressure partially regulates albuminsynthesis. The regulation site may be the oncotic content in the hepatic interstitial

volume because albumin synthesis is inversely related to the content of thisvolume. Conditions that increase other osmotically active substances in the serum

tend to decrease the serum albumin concentration by decreasing synthesis.

Examples include elevated serum globulin levels in hepatitis andhypergammaglobulinemia.
http://www.medscape.com/resource/heartfailurehttp://www.medscape.com/resource/heartfailurehttp://www.medscape.com/resource/heartfailurehttp://www.medscape.com/resource/heartfailure


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Acute and chronic inflammation: Albumin levels that are low because of acuteinflammation should normalize within weeks of resolution of the inflammation.

Persistent hypoalbuminemia beyond this point should prompt an investigation for anongoing inflammatory process. The cytokines (TNF, IL-6) released as part of the

inflammatory response to physiologic stress (infection, surgery, trauma) can decrease

serum albumin by the following mechanisms:o Increased vascular permeability (allowing albumin to diffuse into the

extravascular space)

o Increased degradationo Decreased synthesis (among other mechanisms, by activating TNF-a, which

decreases transcription of the albumin gene)

Imaging Studies

Liver ultrasound for evidence of cirrhosis Small bowel barium series for mucosal abnormalities typical of malabsorption syndromes Imaging studies as appropriate to seek infectious causes of inflammation and

hypoalbuminemia (eg, chest radiography)

Echocardiogram for congestive heart failure

Procedures

Liver biopsyto confirm cirrhosis Kidney biopsy to help evaluate etiology of nephrosis

Histologic Findings

When hypoalbuminemia is due to cirrhosis, liver biopsy findings show a

loss of hepatic architecture, fibrosis, and nodular regeneration. The

pattern of injury and special stains can help determine the etiology of

cirrhosis. Hypoalbuminemia Treatment & Management

Author: Ruben Peralta, MD, FACS; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM more...When hypoalbuminemia is due to nephrotic syndrome secondary to a primary renal disorder, light

microscopy may show sclerosis (focal glomerulosclerosis), mesangial immunoglobulin A

(immunoglobulin A nephropathy), or no changes (minimal change disease). Electron microscopy may

show subepithelial immunoglobulin G deposits (membranous glomerulonephritis)

Overview Presentation Workup
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Treatment Medication Follow-up


Medical Care Surgical Care Consultations Diet Activity Show All

Medical Care

Treatment should focus on the underlying cause of hypoalbuminemia. See the Medication

section below.

To help optimize fluid resuscitation with colloids in patients who are critically ill, volume statusmay be monitored with a central venous, pulmonary artery catheter or other minimal invasive

techniques. (See the eMedicine articleDistributive Shock).

In patients who are critically ill, low calcium levels can be simply due to hypoalbuminemia,which has no clinical significance because the active fraction (ionized) is not affected. However,

to prevent missing a second hypocalcemic disorder, measure the ionized calcium level whenever

the albumin level is low.

Surgical Care

Surgery is considered only when indicated for the underlying cause.

Consultations

Depending on the clinical situation, multiple consultations may be necessary.

Gastroenterologist Intensivist Nephrologist Surgeon Endocrinologist Registered dietitian
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Diet

Support the underlying cause with adequate nutrition

(sufficient high biological value protein and energy intake

for anabolism). Activity

Recommendations depend on the severity of the underlying disease.

Hypoalbuminemia Medication

Author: Ruben Peralta, MD, FACS; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM more...

Overview Presentation Workup Treatment Medication Follow-up


Medication Summary

Hypoalbuminemia is a common phenomenon in patients with serious illness. Treatment shouldfocus on the underlying cause rather than simply replacing albumin. Exogenous albumin is not

used for the purpose of raising serum albumin levels.

Indications and the use of albumin administration in critically ill patients is an area ofcontroversy; studies to clarify these issues are ongoing.

[1]

o Although prior meta-analysis of small studies suggested that albumin infusions may beharmful (increasing the mortality rate by 6% as compared with crystalloid), a large

multicenter clinical trial (SAFE) documented that, except in patients with neurotrauma,

albumin infusions did not measurably affect outcome.[2]

In patients with neurotrauma,

these trials found a small, but significant, increase in mortality as compared with

crystalloid therapy.o Outcomes are similar regardless of baseline serum albumin concentration; albumin

administration for patients with hypoalbuminemia has no added benefit. Based on

these studies of patients with septic shock, the benefit of colloid versus crystalloid

administration for critically ill patients is not clearly demonstrated. Furthermore, the

relative amount of albumin that can be effectively replenished by infusion is minimal,

considering the normal albumin turnover rate.
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These findings are in contrast to prior studies that also found no difference or increasedmortality among those receiving albumin. Preliminary studies, including a favorable study by

Dubois (2006), examined the effect of albumin on organ function in critically ill patients, but

additional work is needed in this area.[3]

Limited indications for albumin supplementation exist, and considerable clinical judgment isrequired when albumin is administered. Albumin has been used as one part of regimens

designed to prevent hepatorenal syndrome in patients with cirrhosis; however, this is

controversial and survival benefit has not been clearly established. However, in general, albumin

is not given specifically to treat hypoalbuminemia, which is a marker for serious disease.

Like crystalloids, colloids produce a dilutional effect on hemoglobin and clotting factors.Clinicians need to monitor the appropriate parameters to safeguard against iatrogenic

complications.

Considering fluid resuscitation more generally, recent investigation found that 6% hydroxyethylstarch used for resuscitation in patients with severe sepsis was associated with a significant

increase in acute renal failure, calling this approach into question.

The most effective method of minimizing hypoalbuminemia and restoring serum oncoticpressure is by creating a positive nitrogen balance. This is usually accomplished by enteral

protein feeding and reversing the inflammatory state, if present. Clearly, those patients withnephrotic syndrome need the nephrosis treated as a primary problem. The importance of

enteral nutrition as an early and continued treatment for hypoalbuminemia cannot be

overemphasized.

Further Inpatient Care

The significance of hypoalbuminemia appears to be its reflection of the severity of the

underlying disease process. Therefore, follow-up care, in both inpatient and outpatient settings, is

dictated by those processes.

Patient Education

Specific dietary recommendations are based on the underlying disease.

Contributor Information and Disclosures

Author

Ruben Peralta, MD, FACS Professor of Surgery, Anesthesia and Emergency Medicine, SeniorMedical Advisor, Board of Directors, Program Chief of Trauma, Emergency and Critical Care,

Consulting Staff, Professor Juan Bosch Trauma Hospital, Dominican Republic

Ruben Peralta, MD, FACS is a member of the following medical societies:AmericanAssociation of Blood Banks,American College of Healthcare Executives,American College of
http://www.aabb.org/http://www.aabb.org/http://www.aabb.org/http://www.aabb.org/http://www.ache.org/http://www.ache.org/http://www.ache.org/http://www.facs.org/http://www.facs.org/http://www.facs.org/http://www.ache.org/http://www.aabb.org/http://www.aabb.org/


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Surgeons,American Medical Association,Association for Academic Surgery,Eastern

Association for the Surgery of Trauma,Massachusetts Medical Society,Society of Critical Care

Medicine, andSociety of Laparoendoscopic SurgeonsDisclosure: Nothing to disclose.

Coauthor(s)

Brad A Rubery, MD Consulting Staff, Department of Internal Medicine, Division of

Emergency Medicine, Gastroenterology AssociatesBrad A Rubery, MD is a member of the following medical societies:American College of

PhysiciansandAmerican Medical Association

Disclosure: Nothing to disclose.

Sarah C Langenfeld, MD Assistant Professor of Psychiatry, Department of Psychiatry,

University of Massachusetts Medical School; Attending Psychiatrist, Community HealthLink

Sarah C Langenfeld, MD is a member of the following medical societies:American Medical

Association,American Psychiatric Association, andMassachusetts Medical SocietyDisclosure: Nothing to disclose.

Specialty Editor Board

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Departmentof Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface

General HospitalSat Sharma, MD, FRCPC is a member of the following medical societies:American Academy of

Sleep Medicine,American College of Chest Physicians,American College of Physicians-

American Society of Internal Medicine,American Thoracic Society,Canadian Medical

Association,Royal College of Physicians and Surgeons of Canada,Royal Society of Medicine,Society of Critical Care Medicine, andWorld Medical Association


Francisco Talavera, PharmD, PhD Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Harold L Manning, MD Associate Professor, Departments of Medicine, Anesthesiology and

Physiology, Section of Pulmonary and Critical Care Medicine, Dartmouth Medical SchoolHarold L Manning, MD is a member of the following medical societies:American College of

Chest Physicians,American College of Physicians, andAmerican Thoracic Society


Timothy D Rice, MD Associate Professor, Departments of Internal Medicine and Pediatrics

and Adolescent Medicine, St Louis University School of Medicine

Timothy D Rice, MD is a member of the following medical societies:American Academy ofPediatricsandAmerican College of Physicians

http://www.facs.org/http://www.facs.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.aasurg.org/http://www.aasurg.org/http://www.aasurg.org/http://www.east.org/http://www.east.org/http://www.east.org/http://www.east.org/http://www.massmed.org/AM/Template.cfm?Section=Homehttp://www.massmed.org/AM/Template.cfm?Section=Homehttp://www.massmed.org/AM/Template.cfm?Section=Homehttp://www.sccm.org/http://www.sccm.org/http://www.sccm.org/http://www.sccm.org/http://www.sls.org/i4a/pages/index.cfm?pageid=1http://www.sls.org/i4a/pages/index.cfm?pageid=1http://www.sls.org/i4a/pages/index.cfm?pageid=1http://www.acponline.org/http://www.acponline.org/http://www.acponline.org/http://www.acponline.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.psych.org/http://www.psych.org/http://www.psych.org/http://www.massmed.org/AM/Template.cfm?Section=Homehttp://www.massmed.org/AM/Template.cfm?Section=Homehttp://www.massmed.org/AM/Template.cfm?Section=Homehttp://www.aasmnet.org/http://www.aasmnet.org/http://www.aasmnet.org/http://www.aasmnet.org/http://www.chestnet.org/http://www.chestnet.org/http://www.chestnet.org/http://www.acponline.org/http://www.acponline.org/http://www.acponline.org/http://www.acponline.org/http://www.thoracic.org/http://www.thoracic.org/http://www.thoracic.org/http://www.cma.ca/index.cfm/ci_id/121/la_id/1.htmhttp://www.cma.ca/index.cfm/ci_id/121/la_id/1.htmhttp://www.cma.ca/index.cfm/ci_id/121/la_id/1.htmhttp://www.cma.ca/index.cfm/ci_id/121/la_id/1.htmhttp://rcpsc.medical.org/index.php?pass=1http://rcpsc.medical.org/index.php?pass=1http://rcpsc.medical.org/index.php?pass=1http://www.rsm.ac.uk/http://www.rsm.ac.uk/http://www.rsm.ac.uk/http://www.sccm.org/http://www.sccm.org/http://www.wma.net/e/http://www.wma.net/e/http://www.wma.net/e/http://www.chestnet.org/http://www.chestnet.org/http://www.chestnet.org/http://www.chestnet.org/http://www.acponline.org/http://www.acponline.org/http://www.acponline.org/http://www.thoracic.org/http://www.thoracic.org/http://www.thoracic.org/http://www.aap.org/http://www.aap.org/http://www.aap.org/http://www.aap.org/http://www.acponline.org/http://www.acponline.org/http://www.acponline.org/http://www.acponline.org/http://www.aap.org/http://www.aap.org/http://www.thoracic.org/http://www.acponline.org/http://www.chestnet.org/http://www.chestnet.org/http://www.wma.net/e/http://www.sccm.org/http://www.rsm.ac.uk/http://rcpsc.medical.org/index.php?pass=1http://www.cma.ca/index.cfm/ci_id/121/la_id/1.htmhttp://www.cma.ca/index.cfm/ci_id/121/la_id/1.htmhttp://www.thoracic.org/http://www.acponline.org/http://www.acponline.org/http://www.chestnet.org/http://www.aasmnet.org/http://www.aasmnet.org/http://www.massmed.org/AM/Template.cfm?Section=Homehttp://www.psych.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.ama-assn.org/http://www.acponline.org/http://www.acponline.org/http://www.sls.org/i4a/pages/index.cfm?pageid=1http://www.sccm.org/http://www.sccm.org/http://www.massmed.org/AM/Template.cfm?Section=Homehttp://www.east.org/http://www.east.org/http://www.aasurg.org/http://www.ama-assn.org/http://www.facs.org/


13/13

Chief Editor

Michael R Pinsky, MD, CM, FCCP, FCCM Professor of Critical Care Medicine,Bioengineering, Cardiovascular Disease and Anesthesiology, Vice-Chair, Academic Affairs,

University of Pittsburgh School of Medicine, University of Pittsburgh Medical Center

Michael R Pinsky, MD, CM, FCCP, FCCM is a member of the following medical societies:American College of Chest Physicians, American College of Critical Care Medicine,American

Heart Association,American Thoracic Society, Association of University Anesthetists,Shock

Society, andSociety of Critical Care MedicineDisclosure: LiDCO Ltd Honoraria Consulting; iNTELOMED Intellectual property rights Board

membership; Edwards Lifesciences Honoraria Consulting; Applied Physiology, Ltd Honoraria

Consulting; Cheetah Medical Consulting fee Consulting
http://www.chestnet.org/http://www.chestnet.org/http://www.americanheart.org/presenter.jhtml?identifier=1200000http://www.americanheart.org/presenter.jhtml?identifier=1200000http://www.americanheart.org/presenter.jhtml?identifier=1200000http://www.americanheart.org/presenter.jhtml?identifier=1200000http://www.thoracic.org/http://www.thoracic.org/http://www.thoracic.org/http://www.shocksociety.org/http://www.shocksociety.org/http://www.shocksociety.org/http://www.shocksociety.org/http://www.sccm.org/http://www.sccm.org/http://www.sccm.org/http://www.sccm.org/http://www.shocksociety.org/http://www.shocksociety.org/http://www.thoracic.org/http://www.americanheart.org/presenter.jhtml?identifier=1200000http://www.americanheart.org/presenter.jhtml?identifier=1200000http://www.chestnet.org/

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