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APPROACH TO PATIENTS WITH EDEMA AND FLUID RETENTION

I. DEFINITION

EDEMA- derived from the Middle English word “YDEMA’’ which comes from the Greek word “SWELLING”- accumulation of fluid in bodily tissues or a body cavity- “Excess Fluid in the Interstitial Space” (about 2L)- Most edema are Non-Life Threatening - Some are Life Threatening such as Pulmonary Edema; Cerebral Edema- most commonly found in: feet and legs- earlist manifestation: periorbital area

II. FORMS AND CLASSIFICATIONS

1. LOCALIZED vs. GENERALIZED

LOCALIZEDa. Occurs in one part of the body b. Can be confined to specific organs

such as lips, lungs (pulmonary edema) or eyes (periorbital edema)

c. Originating from an inflammation or hypersensitivity is usually readily identified

d. Lymphadenema- Restriction of lymphatic flow resulting in

increased protein concentration in the interstitial fluid

- Circumstance that aggravates retention of fluid

e. Localized edema due to venous or lymphatic obstruction maybe caused by:

- Thrombophlebitits (thrombus in the vein)- Chronic lymphadenitis - Resection of regional lymph nodes

(filariasis)

GENERALIZEDa. Widespread edema “anasarca”b. Anasarca with generalized

edema suffer from:- advanced cardiac

disorders- Renal disorders

- Hepatic disorderc. Examples of generalized

edema:- Edema of heart failure- edema of nephrotic syndrome- Edema of cirrhosis

2. PITTING vs. NON- PITTING

1.) PITTING- Pressing on the edematous area levels an

indention- MOST COMMON!!!

2.) NON-PITTTNG- Pressing on the edematous area that does

not leave an indention

- (+) umbilical protrution- E.g.: hypothyroidism and filariasis

3. LOCATION

1. Ascites2. Anasarca 3. Hydrothorax4. Pulmonary Edema- edema in

the lung parenchyma (VERY LIFE THREATENING!)

5. Cerebral Edema- edema in the brain (VERY LIFE THREATENING!)

6. Cellular Edema- edema in the different cells of the body

4. GRADING OF EDEMA

Grade-1 Edema = confined to both feet (Bipedal Edema) Grade-2 Edema = reaches the level of the kneeGrade-3 Edema = reaches the level of the abdomen Grade-4 Edema = Generalized Edema (also known as Anasarca)

5. TWO BASIC STEPS TO EDEMA FORMATIONa. Alteration of Capillary

Hemodynamics

Subject: MedicineTopic: Approach to Patient with Edema & Fluid RetentionLecturer: Dr. Eugene CastilloDate of Lecture: Aug. 5, 2011Transcriptionist: Portal TriadPages: 6

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b. Na+ and Water Retention

5.A. Principles in Edema

o Safety Factors against development of Edema: there must be atleast 10-15mmHg Increase in gradient favoring filtration

o Two Factors for Edema Formation: Increase in Pif and Decrease

in Pif occurs as fluid moves into Interstitium

Increase in Pif enhances Lymph Flow

5.B. Starling’s Law

o Hydrostatic Pressure = Water Pressureo Oncotic Pressure = Albumin Pressure

Net Filtration = Kf (Hydrostatic Pressure Gradient – Oncotic Pressure Gradient)

= Kf (Pcap – Pif) – (Pp – Pif)

**Any Alteration of the Components of Starling’s Law = EDEMA!

Schematic representation of the hemodynamic factors controlling fluid movement across the capillary wall in skeletal muscle.

ETIOLOGY OF EDEMA I. INCREASED CAPILLARY HYDROSTATIC PRESSURE (Most Common)

A. Increased Blood Volume due to Renal Na + Retention

1. Heart Failure

2. Primary Renal Na+ Retnetion

Renal Failure Drugs: Minoxidil, Diazoxide,

Calcium-Channel Blockers (Nifedipine)

Non-Steroidal Anti-Inflammatory Drugs, Fludrocortisone, Estrogens

Refeeding Edema Hepatic Cirrhosis Idiopathic Edema

*** Anti- Hypertensive drugs esp. Calcium- Channel Blockers are usually the drugs that cause edema to the patients

3. Pregnancy and Premenstrual Edema

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B. Venous Obstruction

1. Hepatic Cirrhosis or Hepatic Venous Obstruction2. Acute Pulmonary Edema3. Local Venous Obstruction

Symptoms exhibited when there’s an increased capillary hydrostatic pressure

1. Asyptomatic2. Chronic

- Jugular Vein Distention (sign of heart failure)

- Ascites- Leg Edema

3. Acute - Jugular Vein Distention (sign of heart

failure)- Neck Muscle Retraction- Air Hunger (use of accessory muscles in

breathing)- Look of Acute Distress (panic or fear)- Wide eyes- Cyanosis on lips

II. DECREASED PLASMA ONCOTIC PRESSURE -involves pressure exerted by proteins

which are mostly synthesized in the liver -due to significant decrease in Albumin

LevelA. Protein Loss

1. Nephrotic Syndrome

-due to massive losses of protein into the Urine

-this promotes a net movement of fluid into the Interstitium, causes Hypovolemia, and Initiates the edema forming sequence of events including activation of the RAAS (Renin-Angiotensin- Aldosterone System)**Hallmark = PROTEINURIA OF

GREATER THAN 15 GRAMS PER DAY

2. Protein-Losing Enteropathy

B. Reduced Albumin Synthesis

1. Liver Disease2. Malnutrition

III. INCREASED CAPILLARY PERMEABILITY

- causes Life Threatening Edemas

1. Burns: swelling of upper airways ( (+) stridor, a wheezing sound during respiration) which causes pulmonary edema

2. Trauma3. Inflammation4. Allergic Reactions: from the foods we eat5. Adult Respiratory Distress Syndrome:

patient should be administered with epinephrine or adrenaline

6. Idiopathic Edema7. Malignant Ascites

IV. INCREASED INTERSTITIAL ONCOTIC PRESSURE

1. Lymphatic Obstruction2. Increased Capillary Permeability3. Hypothyroidism

FIVE COMMON CAUSES OF EDEMA

Cardiac Renal Hepatic Endocrine Idiopathic

**These are the Five Differential Diagnosis when patient comes to you with Edema**

I. CARDIAC EDEMA

A. Pathophysiology of Cardiac Edema (Forward Hypothesis)

Forward hypothesis of Heart Failure = reduction of cardiac output due to Cardiac Failure is the primary event (it stimulates the RAA System which will lead to salt and water retention

reduction of Cardiac Output is the primary event

**Renin-Angiotensin-Aldosterone System any condition which reduces blood volume

stimulates Renin-Angiotensin-Aldosterone

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results in Water Retention and Na+

retentionB. Frank-Starling Curves

Stroke Volume (SV) is related to Left Ventricular End Diastolic Pressure (LVEDP) in normal subjects and in patients with Heart Failure

Normal Person = Increase in Heart Volume (LVEDP) will cause Heart to Increase Stroke Volume

Heart Failure = Increase in Volume of the Heart will NOT cause Increase in Stroke Volume (because there is no longer increase in contractility in the heart muscles) ***PLS CHECK LAST PAGE FOR GRAPH!!!

II. LIVER EDEMA

***PLS CHECK LAST PAGE FOR DIAGRAM!!!

III. RENAL DISEASE In Underfilling, there is a decrease in blood volume due to Hypoalbuminemia, Peripheral Vasodilation

and Increase in Sinusoidal Pressure In Overflow, there is Sodium and Water Retention which leads to an increase in Plasma Volume then to

Ascites

PHYSICAL AND LABORATORY FINDINGS-this table shows how to different the five causes of Edema (MEMORIZE!)

-four parameters used to diagnose the Etiology of Edema

o Pulmonary Edema Left Sided Heart Failureo Central Venous Pressure Right Sided Heart Failure o Ascites Hepatic Cirrhosis o Proteinuria Nephrotic Syndrome

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I. LEFT SIDED HEART FAILURE Pulmonary Edema (Congestion) is MOST

PROMINENT Central Venous Pressure (JVP) is variable There is no Proteinuria There is also Left Ventricular Hypertrophy

or Cardiomegaly There is also extra Heart Sounds (S3 and S4)

II. RIGHT-SIDED HEART FAILURE

MOST PROMINENT feature is the Increase in Central Venous Pressure (CVP) or Jugular Vein Pressure

The Jugular Veins are very prominent There is also ascites, and we may or may

not have proteinuria

III. LIVER CIRRHOSIS MOST PROMINENT manifestation = Ascites When a patient has Ascites as the form of

Edema, always consider Liver Cirrhosis

IV. NEPHROTIC SYNDROME MOST PROMINENT feature = Proteinuria

(more than 3g per day)

V. IDIOPATHIC EDEMA Iit is a “waste basket” diagnosis Pedal Edema is MOST PROMINENT When there is no other diagnosis for the

edema, then it is Idiopathic Edema (when all others are ruled out)-classically, patient is a female in 30-40’s

Treatment of Edema: “Diuretics are the mainstay”CLASSIFICATION of DIURETICS:

Loop Diuretics:Furosemide (BEST EXAMPLE), Bumetanide,

Ethacrynic A.

Distal Tubule and Connecting Segment Thiazides, Chlothalidone, Metolazone

Cortical Collecting Tubule Spironolactone, Amiloride, Triamterene

**Potassium Sparing- patients with Hepatic Encephalopathy (low potassium; hypokalemia)

For liver cirrhosis because of complication of hepatic encephalopathy where the pathophysiology is excess in serum

ammonium level could be aggravated by hypokalemia

Such diuretics will promote non-retention of serum ammonia, thus lowering serum ammonium levels in the case of liver cirrhosis

Hepatic encephalopathy can lead to coma, seizures, or loss of consciousness

Complications of Diuretic Therapy• Volume depletion

-excess water loss-severe dehydration renal failure-hypovolemia -Clinical Manifestation: poor skin turgor, hypotension, tachycardia, inc. pulse rate

• Azotemia-earliest manifestation of renal failure; patients with gout can have this-increase in urea, creatinine, BUN levels-also known as uremia because they are excreted in the kidneys-Renal Failure results from increased creatinine levels

• Metabolic alkalosis-except with DCT diuretics-Bicarbonate retention

• Hypokalemia -low potassium• Hyperkalemia & Metabolic acidosis• Hyperuricemia - excess in uric acid that

could lead to gout• Hyponatremia - low sodium• Hypomagnesemia - low magnesium

*** Harrison’s Internal Medicine, 17th ed

• Figure 36-1, p233 • Table 36-2, p235

End of Transcription

1 Corinthians 13:13 And now these three remain: faith, hope and love. But the greatest of these is love.

*Kindly check the PPT for the pictures*Break a leg in the sportsfest, 2014!

SPECIAL GREETINGS TO:

AIRA DE LOS SANTOS.. happy birthday!!!! Wishing you all the best god bless u!!!!

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***FRANK-STARLING CURVES

*** II. LIVER EDEMA

Plasma volume

Renal Na+ and water

retention

“Overflow”

Ascites

Hypo - albuminemia

Peripheral Vasodilation

Splanchnic pooling

“Underfilling”

Ascites

Effective circulating volume

Renal Na+ and water retention

Further Ascites

Hepatic disease“Underfilling” & “Overflow” Theory

Sinusoidalpressure

SV, mL Severe Heart Failure

50

10 20

00

LVEDP, mmHg

NormalA

B

C

100

50

10 20

00

NormalA

B

C50

10 20

00

NormalA

B

C50

10 20

00

NormalA

B

C50

10 20

00

NormalA

B

C50

10 20

00

NormalA

B

C