Daniel Eshetu

Definition

Pathogenesis

Localized vs Generalized

Edematous states; CHF, the Nephrotic state and decompensated cirrhosis.

EDEMA is defined as a clinically apparentincrease in the interstitial fluid volume whichmay expand by several liters before theabnormality is evident.

ANASRCA refers to gross generalized edema.

ASCITES & HYDROTHORAX refer toaccumulation of excess fluid in the pleural andperitoneal space respectively and areconsidered special forms of edema.

EDEMA may be localized or generalizeddepending on its cause and mechanisms.

Pathogenesis: one third of total body water is in theECF compartment and 75% of the latter is interstitialfluid with the rest in the plasma compartment.

Starling forces: refers to the forces that regulatemovement of fluid between the two compartments ofthe ECF.

Hydrostatic pressure in the vascular compartment andoncotic pressure in the interstitial space drive fluidout of the vessels at the arteriolar end of the capillarywhile hydrostatic pressure in the interstitial spaceand the plasma oncotic pressure promote movementof fluid into the vessel. Fluid also returns to thecapillaries through the lymphatics.

Disturbances in the Starling forces leading to themovement of fluid from the vascular space intothe interstitium or a body cavity are responsiblefor edema.

Edema due to increased capillary pressure mayoccur in conditions like congestive heart failurewhile a reduction in the plasma oncotic pressuremay be responsible for edema in malnutrition,liver disease and the nephrotic state.

Edema may also occur when the capillaryendothelium is damaged (mechanical, viral/bacterial, drugs, etc) allowing leaks through thecapillary wall.

In states of generalized edema(CHF, cirrhosis & thenephrotic syndrome) the reduced effective arterialvolume plays a central role in the initiation and/orperpetuation of edema.

↓effective arterial volume stimulates the reninangiotensin aldosterone (RAA) system, thesympathetic nervous system, release of Endothelinand secretion of arginine vasopressin(AVP). Allthese result in the retention of salt and water torestore the effective arterial volume.

The natriuretic peptides, ANP,BNP and CNPare released in edematous states tocounteract the hormones causing Naretention.

ANP and BNP are found increased in thecirculation BUT are not sufficient to preventedema formation.

There is also resistance to the effects of thenatriuretic peptides in the edematous states

Clinical causes of edema

A. Localized edema

- Obstruction of venous drainage of a limb :increase in hydrostatic pressure proximal tosite of obstruction.

- Obstruction of lymphatic drainage of alimb: inability to return the fluid in theinterstitial space to the circulation.

B. Generalized edema

Congestive heart failure: the impairedsystolic emptying of the ventricle(s) and orimpaired ventricular relaxation promotesan accumulation of blood in the venouscirculation at the expense of the arterialside. The resultant ↓ in effective arterialblood volume initiates the cascade of eventsleading to edema. The raised venouspressure also contributes to edema.

The Nephrotic Syndrome: the primary alterationis a decrease in the colloid oncotic pressure dueto loss of large quantities of protein in the urine.The ↓ colloid oncotic pressure initiates edemabut subsequently the ↓effective arterial volumeperpetuates edema. Reduced kidney functionalso contributes to edema in the nephrotic state.

In Other hypoalbumniemc states: severemalnutrition, GI losses of protein and severechronic liver disease, the mechanisms of edemaare similar to those in the nephrotic state.

Cirrhosis: is characterized in part by hepaticvenous outflow blockade which expands thesplanchnic blood volume and hepatic lymphformation. Intrahepatic hypertension acts as astimulus for renal Na retention and ↓effectivearterial blood volume. Hypoalbuminemia (dueto ↓ hepatic synthesis and systemicvasodilatation) contributes to edemaformation in cirrhosis.

Drug induced edema: several drugs are knownto cause edema through differentmechanisms. Mechanisms include

renal vasoconstriction (NSAIDs &cyclosporine)

arterial vasodilatation ( calcium channelblockers)

augmented renal Na absorption(steroids) and

capillary damage( Interluekin 2)

Differential diagnosis of edema:

History: recent weight gain, facial puffiness,abdominal distension, leg swelling, dyspnea,orthopnea, paroxysmal nocturnal dyspnea(PND).

Physical exam : BP, auscultation at lung basesfor crackles & for evidence of hydrothorax ,JVP, precordial exam, Abdominal exam(liversize, shifting dullness, etc),peripheraledema(grading)

CONGESTIVE HEART FAILURE

CIRRHOSIS NEPHROTIC SYNDROME

Facial swelling + - +++

Abdominal distension

++ ++++ ++

Orthopnea /PND +++ _ _

Elevated JVP Yes No No

Hepatomegaly Yes No No

Ascites ++ ++++ ++

Hydrothorax ++++ + ++

Treatment of Edema

I ) Specific treatment of the underlying disorder

II) Treatment of the edema state

Salt and Water restriction

Diuretics : Thiazides, loop diuretics or potassium sparing diuretics.

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