Approach To Patient With Generalized Body Oedema

Approach to patient with generalized body oedema
: BY
4TH STAGE Medical student
Supervised by
: DR
INTERNAL MEDICINE
2020
GENERALIZED EDEMA
Oedema is caused by an excessive accumulation of fluid within the
interstitial space. Clinically, this can be detected by persistence of an
indentation in tissue following pressure on the affected area (pitting
oedema). Non-pitting oedema is typical of lymphatic obstruction and
may also occur as the result of excessive matrix deposition in tissues –
for example, in hypothyroidism or scleroderma. There are various
possible causes. Pitting oedema tends to accumulate in the ankles
during the day and improves overnight as the interstitial fluid is
reabsorbed. In developed countries, the most common causes of oedema
are local venous problems and heart failure, but it is important to
identify other causes. Generalized edema refers to fluid accumulation
that affects the whole body rather than particular organs or body
areas. Cardiac, renal, hepatic, or nutritional disorders are responsible for
a large majority of patients with generalized edema. Consequently, the
differential diagnosis of generalized edema should be directed toward
.identifying or excluding these several conditions
CLINICAL CAUSES OF EDEMA

A weight gain of several kilograms usually precedes overt
manifestations of generalized edema. Anasarca refers to gross,
generalized edema. Ascites and hydrothorax refer to accumulation of
excess fluid in the peritoneal and pleural cavities, respectively, and are
considered special forms of edema.. Edema may be present when the
ring on a finger fits more snugly than in the past or when a patient
complains of difficulty putting on shoes, particularly in the evening.
Edema may also be recognized by puffiness of the face, which is most
.readily apparent in the periorbital areas
APPROACH TO THE PATIENT

An important first question is whether the edema is localized or
generalized. If it is localized, the local phenomena that may be
responsible should be identified. If the edema is generalized, one should
determine if there is serious hypoalbuminemia, e.g., serum albumin
<3.0 g/dl. If so, the history, physical examination, urinalysis, and other
laboratory data will help evaluate the question of cirrhosis, severe
malnutrition, or the nephrotic syndrome as the underlying disorder. If
hypoalbuminemia is not present, it should be determined if there is
evidence of heart failure severe enough to promote generalized edema.
It is usually gravity-dependent and so especially seen around the ankles,
or over the sacrum in patients lying in bed. The most common causes of
lower limb swelling are chronic venous disease and lymphoedema. In
general, if the jugular venous pressure (JVP) is not elevated, then
oedema is not cardiogenic. Finally, it should be ascertained as to
whether or not the patient has an adequate urine output or if there is
significant oliguria or anuria
Heart Failure
In heart failure, the impaired systolic emptying of the ventricle(s)
and/or the impairment of ventricular relaxation promotes an
accumulation of blood in the venous circulation at the expense of the
effective arterial volume. In addition, the activation of the sympathetic
nervous system and the RAAS acts in concert to cause renal
vasoconstriction and reduction of glomerular filtration and salt and
water retention. Sodium and water retention continue, and the increment
in blood volume accumulates in the venous circulation, raising venous
and intracapillary pressure resulting in edema. The presence of overt
cardiac disease, as manifested by cardiac enlargement and/or ventricular
hypertrophy, together with clinical evidence of cardiac failure, such as
dyspnea, basilar rales, venous distention, and hepatomegaly, usually
indicates that edema results from heart failure. Noninvasive tests such as
electrocardiography, echocardiography, and measurements of BNP (or
NTproBNP) are helpful in establishing the diagnosis of heart disease. The
edema of heart failure typically occurs in the dependent portions of the
.body
History
Dyspnea with exertion prominent—often associated with orthopnea—or
.paroxysmal nocturnal dyspnea
Physical examination Elevated jugular venous pressure, ventricular
S3 gallop; occasionally with displaced or dyskinetic apical pulse;
.peripheral cyanosis, cool extremities, small pulse pressure when sever
LABORATORY FINDINGS
Elevated urea nitrogen to creatinine ratio common; serum sodium often -

.diminished; elevated natriuretic peptides
Hepatic Cirrhosis
This condition is characterized in part by hepatic venous outflow
obstruction, which in turn expands the splanchnic blood volume, and
hepatic lymph formation. Intrahepatic hypertension acts as a stimulus
for renal sodium retention and causes a reduction of effective arterial
blood volume. These alterations are frequently complicated by
hypoalbuminemia secondary to reduced hepatic synthesis of
albumin, as well as peripheral arterial vasodilation. These effects
reduce the effective arterial blood volume, leading to activation of the
sodium- and water-retaining mechanisms described above. The
concentration of circulating aldosterone often is elevated by the failure of
the liver to metabolize this hormone. Initially, the excess interstitial fluid
is localized preferentially proximal (upstream) to the congested portal
venous system, causing ascites. In later stages, particularly when there is
severe hypoalbuminemia, peripheral edema may develop. A sizable
accumulation of ascitic fluid may increase intraabdominal pressure and
impede venous return from the lower extremities and contribute to the
.accumulation of the edema
HISTORY
Dyspnea uncommon, except if associated with significant degree of

ascites; most often a history of ethanol abuse
PHYSICAL EXAMINATION
Frequently associated with ascites; jugular venous pressure normal or
low; blood pressure lower than in renal or cardiac disease; one or more
additional signs of chronic liver disease (jaundice, palmar erythema,
Dupuytren’s contracture, spider angiomata, male gynecomastia; asterixis
.and other signs of encephalopathy) may be present
LABORATORY FINDINGS
If sever reduction in serum albumin , cholesterol, other hepatic proteins

(transferrin, fibrinogen); liver enzymes elevated, depending on the cause
and acuity of liver injury; tendency toward hypokalemia, respiratory
.alkalosis; macrocytosis from folate deficiency
Nephrotic Syndrome and Other Hypoalbuminemic States

The primary alteration in the nephrotic syndrome is a diminished colloid
oncotic pressure due to losses of large quantities (≥3.5 g/d) of protein
into the urine, and hypoalbuminemia (<3.0 g/ dL). As a result of the
reduced colloid osmotic pressure, the sodium and water that are
retained cannot be confined within the vascular compartment, and
total and effective arterial blood volumes decline. This process initiates
the edema-forming sequence of events described above, including
activation of the RAAS. The nephrotic syndrome may occur during the
course of a variety of kidney diseases, including glomerulonephritis,
diabetic glomerulosclerosis, and hypersensitivity reactions. The edema
is diffuse, symmetric, and most prominent in the dependent areas;
.periorbital edema is most prominent in the morning
HISTORY
Usually chronic: may be associated with uremic signs and symptoms,

including decreased appetite, altered (metallic or fishy) taste, altered
sleep pattern, difficulty concentrating, restless legs, or myoclonus;
dyspnea can be present, but generally less prominent than in heart failure
or Childhood diabetes mellitus; plasma cell dyscrasias in nephortic
. syndrome
PHYSICAL EXAMINATION
Elevated blood pressure; hypertensive retinopathy; nitrogenous fetor;
pericardial friction rub in advanced cases with uremia in chronic renal
.failure , Periorbital edema; hypertension
LABORATORY FINDINGS
Elevation of serum creatinine and cystatin C; albuminuria; hyperkalemia,

metabolic acidosis, hyperphosphatemia, hypocalcemia, anemia (usually
normocytic in chroinic renal failure or Proteinuria (≥3.5 g/d);
hypoalbuminemia; hypercholesterolemia; microscopic hematuria in
. nephrotic syndrome
Drug-Induced Edema A large number of widely used drugs can cause

edema . Mechanisms include renal vasoconstriction (NSAIDs and
cyclosporine), arteriolar dilation (vasodilators), augmented renal sodium
.reabsorption (steroid hormones), and capillary damage
Edema of Nutritional Origin

A diet grossly deficient in calories and particularly in protein over a
prolonged period may produce hypoproteinemia and edema. The latter
may be intensified by the development of beriberi heart disease, which
also is of nutritional origin, in which multiple peripheral arteriovenous
fistulae result in educed effective systemic perfusion and effective arterial
blood volume, thereby enhancing edema formation. Edema develops or
becomes intensified when famished subjects are first provided with an
adequate diet. The ingestion of more food may increase the quantity of
sodium ingested, which is then retained along with water. So-called
refeeding edema also may be linked to increased release of insulin,
which directly increases tubular sodium reabsorption. In addition to
hypoalbuminemia, hypokalemia and caloric deficits may be involved
.in the edema of starvation
Refernces
Harrison's principles of internal medicine, 20th edition
Davidson's principles and practice of medicine 22ND
edition
Macleod clinical examination 14TH Edition

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Approach to patient with generalized body oedema

4TH STAGE Medical student

CLINICAL CAUSES OF EDEMA

APPROACH TO THE PATIENT

Elevated urea nitrogen to creatinine ratio common; serum sodium often -

Dyspnea uncommon, except if associated with significant degree of

If sever reduction in serum albumin , cholesterol, other hepatic proteins

Nephrotic Syndrome and Other Hypoalbuminemic States

Usually chronic: may be associated with uremic signs and symptoms,

Elevation of serum creatinine and cystatin C; albuminuria; hyperkalemia,

Drug-Induced Edema A large number of widely used drugs can cause

Edema of Nutritional Origin

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