APPROACH TO A PATIENT WITH

OEDEMA

Presented by
 ZAWEDDE NANCY
 AGEIMO PAUL
 SSEGONJA ALEXANDER
 RUTAREMWA KENNETH
 OBJECTIVES

 Case presentation
 To define edema
 Classification of edema
 To explain the Pathophysiology of edema
 To explain the causes of edema
 To outline the complications of edema
 Clinical presentation of a patient with edema
 To explain how a patient can be diagnosed for edema
 To explain how a patient with edema can be Managed
CASE:
N.R is 67 year old HIV negative female pt who’s been hypertensive and diabetic for more
than 10 years, but non adherent to medication due to financial constraints presented with a
3/52 hx of progressively worsening DIB exacerbated by exertion and lying flat and
relieved by sitting up. The DIB was preceded by a long standing history of generalized
body swelling that started from both lower limbs and gradually involved the entire body
inclusive of the face. She narrates a 3/52 hx of palpitations, PND, occasional productive
cough and chest pain however no hemoptysis or wheezing. She reports a reduced output
(<0.5L in a day) for the past 2/52, despite fairly good fluid intake with no associated
hematuria, suprapubic or loin pain
ROS;
GIT- She reported a mild generalized painless abdominal swelling of gradual onset for
1/52 associated with a reduced appetite for food and weight loss however no hx of
diarrhea, constipation or vomiting
. OTHER SYSTEMS; unremarkable
Past medications include lantus insulin, amlodiopine, ecorin, sildenafil, Lasix, digoxin wch
Social and occupational hx:
She lives in wakiso, is a catholic housewife with no job, is a former pipe smoker and moderate alcoholic who
quit both 8 yrs ago.
Family hx: is married with 10 children, who are all well and gives a positive family history of hypertension
and diabetes on her paternal side
On examination ,
she was sick looking, afebrile, with moderate pallor and bilateral lower limb edema however with no jaundice
or cyanosis, temp is 36.2 degrees Celsius, random blood sugar is 23 mmol/L, was on oxygen, cannula in situ
on the rt arm
CVS:
Her pulse was irregular and of thin volume with a tachycardia of 123 b/min, an almost normal SPO of 92%,
and high blood pressure of 188/106 mmHg, raised JVP and positive hepatojugular reflux, displaced apex
pulsation, heart sounds s1 + s2 and s3. warm extremities
P/A: there was mild non tender distention of the abdomen with a shifting dullness. Deep palpation not done
(fluid). Bowel sounds present
CNS: she was fully conscious with a GCS of 15/15 , and well oriented on place and time, soft neck, PEARL,
-ve kernings
R/S: has a tachypnea of 26/min, bilateral basal fine crakles
Differential diagnoses: CCF secondary to hypertension, acute kidney injury secondary to heart failure(low
 EDEMA
Edema is defined as a condition where there is excessive accumulation of fluid within the interstitial space more than
the lymphatic drainage CLASSIFICATION OF OEDEMA

1. According to the distribution of 2. According to the underlying

edematous fluid cause
 Localized edema this refers to edema that occurs in a
particular part of the body and may be due to lymphatic  Edema due of cardiac disease
obstruction(lymphedema), complex regional pain  Edema due to Renal disease
syndrome type 1(reflex sympathetic  Drug induced edema
dystrophy),thrombophlebitis, varicose veins , primary  Edema to due liver cirrhosis
venous valve failure,cellulitis, lipedema, compartment  Edema due to pregnancy
syndrome due to local venous hypertension  Refeeding edema
 Generalized edema refers to accumulation of interstitial  Edema due to lymphatic obstruction
fluid occurring all over the body and may be due to  Edema due to allergic reaction
cardiac ,renal,or hepatic disease or nutritional disorders
allergies,obstructive sleep apnea, pregnancy and
premenstrual due to increase in the plasma volume
 .hypoalbumuninemia may also cause generalized edema
Cont...

3)According to the gravity of edema

 Pitting edema: A type of edema characterized by residual indentation following application of pressure to site
of swelling . Common causes include fluid retention due to reduced cardiac stroke volume , impaired renal perfusion and
protein deficiency.
Pitting edema can be further graded depending on how long indentation occurs after
application of pressure
Grade 1: 2mm of indentation, rebound immediately
Grade 2: 3 to 4 mm indentation , rebound in 15 seconds
Grade 3 : 5 to 6 mm indentation , rebound in 60 seconds
Grade 4 : 8mm depression ,rebound in 2 to 3 minutes
 Non pitting edema: there is no depression . Caused mainly by lymphatic
obstruction(lympedema) and hypothyroidism (myxedema)
Pitting edema
 PATHOPHYSIOLOGY OF EDEMA

1/3 of body water is in the extracellular space, 75% of the extracellular fluid is in the
interstitial space and the rest is plasma
Starling forces i.e. colloid oncotic pressure and hydrostatic pressure act across the
capillary membrane to maintain the fluids volumes in normal balance.
 The net filtration pressure (NFP) is calculated as
 NFP = Pc − Pif −p −if
 Vascular Hydrostatic pressure & interstitial colloid oncotic pressure, promote movement of
fluid to the interstitial space while
interstialHydrostatic pressure & vascular colloid oncotic pressure, promote movement of
fluid to the vascular space
 significant Alteration
in the hydrostatic or colloid oncotic pressure gradient will lead to a
further net movement of fluid into one of the compartments of the extracellular fluid
Continued……

Edema (net movement of fluid from the intravascular to interstitial space )arises when there is;
 Decreased plasma protein level ie oncotic pressure; caused by hypoalbuminemia secondary to severe
malnutrition, liver disease, nephrotic syndrome, severe catabolic state
 Increased intracapillary hydrostatic pressure due to elevated venous pressure secondary to venous
obstruction e.g in CHF, obstruction of lymphatic flow in filariasis, malignancy and pregnancy
 Increased capillary permeability due to capillary damage ,caused by thermal or mechanical trauma,
viral and bacterial agents, drugs, hypersensitivity reaction. For example in inflammatory edema
 Increase in oncotic pressure in the interstitial space

Reduction in effective arterial volume causes reduced cardiac output and deceased systemic vascular
resistance seen in pooling of blood in splanchnic vessels in liver cirrhosis and in hypoalbuminemia
Reduction in the renal blood flow will therefore activate the RAAS system leading to secretion of
angiotensin 11 that leads to vasoconstriction of efferent arterioles ,reduces hydrostatic pressure in
peritubular capillaries and therefore increases water and sodium retention causing oedema .
Pathophysiology of the underlying causes
1. Congestive heart failure
-impaired systolic emptying causing
-reduction of the effective arterial volume
 activating the RAAS
 Non-osmotic secretion of vasopressin
 Increased secretion of endothelin vasoconstrictor which increases renal vasoconstriction
 Retention of more water and Na ions
 accumulation of blood in the venous circulation
 Causing peripheral edema
2. Nephrotic and other hypoalbuminemic states(severe nutrition deficiency, severe chronic liver
disease protein losing enteropathy)
 massive Loss of proteins
 Decreased colloid oncotic pressure
 Loss of fluid to the interstitial space
 Reduction in the effective arterial volume
 Activation of the RAAS
3.Liver cirrhosis
 Hepatic venous blockage
 Expanding splanchnic blood volume causing Intrahepatic hypertension
 Reduction of effective arterial blood volume
 Activation of the RAAS and retention of the Na ions
Other causes of edema

 Hypothyroidism (myxedema) majorly due to the deposition of hyauluronic acid

 hyperthyroidism (pretibial myxedema secondary to Graves’ disease), in which
edema is typically nonpitting.
 exogenous hyperadrenocortism; pregnancy; and administration of estrogens and
vasodilators, particularly dihydropyridines such as nifedipine.
CLINICAL PRESENTATIONS.

CLINICAL FETURES OF EDEMA DUE TO CARDIAC FAILURE:

Occurs in lower extremities.
Bilateral, painless and pitting
features of cardiac failure associated(chest pain, dyspnea).
Elevated jugular venous pressure.
Features of edema of renal origin
Associated with puffiness of the face and prominent in periorbital areas(generalized edema).
Edema is bilateral.
Associated with hematuria, proteinuria, hypertension and impaired renal function tests.
Features or edema of hepatic origin
Clinical evidence of hepatic disease e.g. jaundice, yellow eyes, dark urine, spider angioma.
Cardiac presentation
history
Dyspnea with exertion
Prominent physical exercise—
often
associated with orthopnea
when lying—
or paroxysmal nocturnal
dyspnea
examination
Elevated jugular venous
pressure,
ventricular (S3) gallop;
occasionally with displaced or
dyskinetic apical pulse;
peripheral
cyanosis, cool extremities, small
pulse pressure when
severe(ventricular dysfunction)
lab
Elevated urea nitrogen-to
creatinine
ratio common;
serum sodium often
diminished; elevated
natriuretic peptides
Hepatic presentation
history
Dyspnea uncommon, except if
associated with significant
degree of ascites;
most often a history of
ethanol abuse
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
lab
If severe, reductions 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.
 Renal presentation
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;
examiantion
Elevated blood pressure;
hypertensive retinopathy;
nitrogenous fetor; pericardial
friction rub in advanced cases
with
uremia
lab
Elevation of serum
creatinine and cystatin C;
albuminuria; hyperkalemia,
metabolic acidosis,
hyperphosphatemia,
hypocalcemia, anemia
(usually normocytic)
Nephrotic syndrome

history examination lab

Childhood diabetes Periorbital edema; Proteinuria (≥3.5 g/d);

mellitus; plasma cell hypertension hypoalbuminemia;
dyscrasias hypercholesterolemia;
microscopic hematuria
Differential diagnosis
Peripheral oedema Generalized oedema
 Cardiac failure: right or combined left and right heart  Congestive cardiac failure
failure, pericardial constriction, cardiomyopathy
 Nephrotic syndrome
 Chronic venous insufficiency: varicose veins
 Myxedema
 Hypoalbuminaemia: nephrotic syndrome, liver
disease, proteinlosing enteropathy; often widespread,  Cirrhosis
can affect arms and face
 Chronic renal failure
 Drugs:
 Sodium retention: fludrocortisone, non-steroidal
antiinflammatory drugs
 Increasing capillary permeability: nifedipine,
amlodipine
 Idiopathic: women > men
 Chronic lymphatic obstruction
APPROACH TO A PATIENT WITH
EDEMA.
HISTORY TAKING:
 Ask for the site -localized or generalized, unilateral(venous or lymphatic obstruction) or bilateral.
 Duration-is it acute(venous obstruction, cellulitis, drugs) or chronic(heart failure, kidney disease or liver
disease)
 Periodicity- like early morning puffiness(kidney disease) does it resolve as the day goes on ?
 Association- pain and warmth suggest inflammation like in DVT or cellulitis.
 Aggravating factor- edema increases on standing(heart failure)
-What is the duration of the edema (acute vs chronic)?
 -Is the edema painful ?
 -What drugs are being taken?
 -Is there history of systemic disease(Heart, liver, kidney)?
 -Is there a history of pelvic/ abdominal neoplasm or radiation?
 -Does the edema improve overnight?
History taking
Review of other systems:
 Gastrointestinal- loss of appetite, abdominal distension, yellow skin
 Cardiovascular-chest pain, dyspnea: ask if it worsens when he lies down , paroxysmal nocturnal
dyspnea.
 Genitourinary- oliguria, bloody urine, altered taste(metallic/fishy),altered sleep pattern.
Past medical history:
 Any history of chronic illness such as hypertension, DM, hypothyroidism. use of drugs that may
cause edema.
EXAMINATION.
GENERAL EXAMINATION:
 Look for jaundice, pallor, cyanosis, finger clubbing. Nutritional status.
 Site of edema and appearance of skin over it. Pitting or non pitting
SYSTEMIC EXAMINATION:
 Cardiovascular system- elevated JVP, peripheral cyanosis, cold extremities, S3
gallop:3rd heart sound, weak pulse
 GIT system- jaundice, spider naevi, splenomegaly, hepatomegaly
 RENAL- palpable enlarged kidneys, uremic frost, pale and opaque nails(leukonychia)

2) General examination and systems examination

general examination
Unilateral edema -generally due to a local cause e.g deep vein thrombosis or lymphatic obstruction
Bilateral edema-Can be due to local cause or systemic cause e.g heart failure or kidney disease
Generalized edema - Due to systemic disease ie. Kidney failure , cardiac failure and liver cirrhosis
Cont... Ascites

b)Tenderness;
Deep vein thrombosis are often tender
Lymphedema is usually non tender
c) Pitting;
Deep vein thrombosis, Venous insufficiency are usually pitting Ulceration
Myxedema lymphedema does not pit
d) Varicose veins;
Leg varicosities are often present in patients with
chronic venous insufficiency
DIFFERENTIAL DIAGNOSIS.

 Edema of renal failure/ acute glomerulonephritis

 Edema of nephrotic syndrome
 Edema of cardiac failure
 Edema of cirrhosis
 Edema of nutritional origin / refeeding edema
RADIOLOGY AND OTHER SPECIFIC
TESTS
 CHEST X ray
 Ultrasound scan
 MRI
 Echocardiography
 ECG
 Lympho scintigraphy
tests

 a) CBC- shows anemia in renal disease

 b) Urinalysis and renal function tests- help to diagnose or rule out nephrotic
syndrome or chronic kidney disease
 c) Liver function tests- if positive findings are made these can be used to focus on
liver cirrhosis, nephrotic syndrome, protein losing enteropathy or malnutrition.
 d) Serum lipid profile- nephrotic syndrome is a associated with hyperlipidemia.
Dyslipidemia is a risk factor for chronic heart disease.
 e) Ultrasound scan - for diagnosing deep vein thrombosis or chronic venous
insufficiency.
tests

) ECG, Brain Natriuretic Peptide level- these identify heart failure. BNP has a
sensitivity of 90% and a specificity of 76% for heart failure diagnosis.
g) D-dimer estimation - can be used to identify deep vein thrombosis in acute pedal
edema. In patients with increased D-dimer levels, other investigations like ultrasound
should be done
h) Lympho scintigraphy - lymphedema can be identified using radionucleotide tracer
which is injected into the first web space and the glow of lymph is monitored using
gamma camera. This gives an indirect evidence of lymphatic obstruction.
I) Echocardiography- assessment of left ventricular function in patients with
congestive heart failure, also measures artery pressure to diagnose pulmonary
hypertension in cor pulmonaleand obstruction sleep apnea syndrome.
COMPLICATIONS

 respiratory fatigue and failure due to Pleural effusions- hydrothorax

 Ascites
 Bacterial peritonitis
 Elephantiasis due to obstruction of lymphatic vessels
 Skin breakouts in the legs
Management of edema
 The management of edema is specific to the cause hence different managements
 HOME MANAGEMENT OF EDEMA
 Plenty of movement to increase circulation in the body
 Frequently raise the affected area of your body so that its above the level of the heart
 Massage the area affected by the edema
 Use bandages or compression socks t keep pressure on the edema
 Consuming less salt

MANAGEMENT OF EDEMA IN CHF AND LIVER DISEASE

 Fluid restriction
 Salt restriction
 Elevation of body parts with edema
 Diuretic therapy of furosemide and spironolactone if edema is refractory to the above measures
 Albumin infusion to correct hypoalbuminemia in liver disese
MANAGEMENT

 MANAGEMENT OF EDEMA IN RENAL DISEASE

 Salt and fluid restriction
 Diuretic therapy like Loop diuretics eg furosemide but potassium sparing diuretics
are contraindicated in risk of causing hyperkalemia
 MANAGEMENT OF EDEMA IN DVT
 Bandages and stockings are important
 Anticoagulation treatment like low molecular weight heparin and oral
anticoagulants
 MANAGEMENT
 MANAGEMENT OF EDEMA IN VENOUS INSUFFICIENCY
 Initial stages resolve with limb elevation
 In chronic states, it needs high knee compression stockings.
 In patients with peripheral vascular disease, stockings are contraindicated thus
pneumatic compression devices are used. Diuretics are of no importance in this
case and may cause metabolic derangement. Skin care with topical steroids and
emollients should be used to avoid excoriation and ulceration.

MANAGEMENT OF IDIOPATHIC EDEMA

 Responds to treatment with aldosterone antagonists like spironolactone at a starting dose of 50-100 mg daily.
 If spironolactone is ineffective, thiazides should be started and potassium levels monitored. It's better to avoid loop
diuretics.
 Other measures are low salt diet, limited fluid intake, weight loss
MANAGEMENT

MANAGEMENT OF LYMPHEDEMA
initially massaging manually gives relief
Compression bandages and stockings are important
Intermittent pneumatic compression devices
Surgical procedures like bypass or debulking
References
 Davidsin’s priciples and practice of medicine, 23rd edition; pg 395-396, 465
 Harrison’s principles of internal medicine, 20th edition pg 237-240
THANK YOU