done by Al Yaqdhan Al Atbi Senior clerkship medical student SQUH - Oman

1. EDEMA

2.  Edema: definition, pathophysiology, and causes
 Common causes:
 Heart failure
 Nephrotic syndrome
 Cirrhosis
 Premenstrual edema and pregnancy
 Drug-induced edema
 Approach to a patient presented with edema
 Management of edema
 Case senario

3. CASE
 Mr.A.B., a 68 years old man, was admitted to the hospital. He
suffers from fatigue, shortness of breath on exertion, cough,
tenderness in the right upper quadrant of the abdomen and ankle
swelling.
 On examination, he was pale and his hands were cold, his
temperature was 37C, pulse 130 beats per minute and irregular.
His jugular venous was elevated and pitting edema was present
in both feet and ankles. Crepitations were present over the lung
bases. There was enlargement of the liver beyond the costal
margin that was tender.

4. Questions
 What is the most likely diagnosis??
 What is the cause of hepatomegaly in this
patient??
 In a chest x-ray, what do you expect to see??
 What is the type of edema he have??

5. Case 2
 A 72-year-old man goes to his GP complaining of
painless swelling of both legs since 2 months ago.
The swelling started at the ankles but now his legs,
and thighs are swollen. His face is puffy in the
mornings on getting up. His weight is up by about 10
kg over the previous 3 months.
 He has noticed that his urine appears to be frothy in
the toilet. He has noted gradual increasing shortness
of breath, but denies any chest pain. He has also
developed spontaneous bruising over the past 6
months. He had HTN diagnosed 13 years ago, and MI
4 years previously. He continues to smoke 30
cigarettes a day, and drinks about 30 units of alcohol
a week. His medication consists of atenolol 50 mg
once a day.

7.  Is a palpable swelling produced by expansion of
the interstitial fluid volume.
 Edema is the medical term for swelling caused by
a collection of fluid in the small spaces that
surround the body's tissues and organs.
 It becomes evident when the interstitial fluid
increased by 2.5 – 3 L

8.  Brain: Cerebral edema
 Lung: Intra-alveolar= pulmonary edema,
 intra-pleural= pleural effusion
 Peritoneum= Ascites
 Massive and generalized edema = Anasarca

9. Starling’s law:
• Vascular system
Hydrostatic pressure
Interstitial space
Hydrostatic
pressure
Colloid oncotic pressure
pressure
(tissue tension)
Colloid oncotic

11. Mechanism
Increased
hydrostatic
pressure
Causes
Site
•Decrease arteriolar
resistance:
Calcium channel blockers
•Due to gravity, the fluid
accumulates in the
dependent parts of the
body “dependent edema”
•Venous obstruction:
•-Liver disease with portal
vein obstruction
•-acute PE
•-DVT (thrombophlebitis)
•Increase vascular
volume:
•-heart failure
•-kidney disease
•-premenstrual sodium
retention
•-pregnancy
• -environmental heat
stress
•Generalized edema is
usually the result of
increase vascular volume.
•Pitting edema

12. Mechanism
Decreased
colloidal
osmotic
pressure
Causes
Site
•Increase loss of plasma
proteins:
•Affect tissues in both
nondependent and
dependent parts of the
body (e.g. face, legs and
feet)
-protein loosing kidney disease,
e.g. nephrotic syndrome
-extensive burn
•Decrease production of
plasma proteins:
•Pitting edema
-liver disease
-Starvation, malnutrition,
malabsorbtion
Increased
capillary
permeability
Obstruction of
lymphatic flow
“lymphedema”
_Inflammation/infections
_Allergic reactions (e.g. hives,
angioneurotic edema)
_Malignancy
_Tissue injury and burn
_local: local inflammation
_generalized: sever sepsis
_infection: filariasis,
Non-pitting edema
lymphogranuloma venereum
_malignant obstruction of
lymphatic structure
_surgical removal of lymph node
_radiation injury
_congenital abnormality

13.  Heart failure
 Cirrhosis
 Nephrotic syndrome and other forms of
renal disease
 Premenstrual edema and pregnancy

14. Left heart failure
volume and
EDV pressure
in LV
Pressure in LA
Leakage of fluid
into interstitial
space.
Hydrostatic P
exceeded
oncotic P
Pulmonary
pressure
Pulmonary
oedema

15.  Shortness of breath and orthopnea.
 Chest pain in case of MI
 O/E:
 tachypneic, diaphoretic patient with wet rales and
possibly a diastolic gallop (S3) and heart murmurs.
 The diagnosis of pulmonary edema should be
confirmed by radiologic studies.

16. 
Pulmonary edema in a "butterfly distribution" due to left ventricular failure. Chest
radiograph shows large perihilar opacities in patient with enlarged cardiac silhouette.

18.  Increased venous pressure behind the right
side of the heart increased capillary
hydrostatic pressure
 Congested jugular veins
 Enlarged & tender liver
 Peripheral edemaAnasarca

19.  Increased venous pressure below the diseased liver
 Ascites  edema in the lower extremities.
 JVP is usually reduced or normal , not elevated as
in heart failure.
 Can be raised if tense ascites  upward pressure on
the diaphragm can increase the intrathoracic pressure
 Signs of portal hypertension
 (distended abdominal wall veins & splenomegaly)

20. 
Heavy proteinuria (> 3.0 g/day)

Hypoalbuminemia

Hyperlipidemia

Peripheral edema

21. 
2 factors:
1.
2.
sodium retention due to underlying renal disease
diminished transcapillary oncotic pressure gradient

Typically- periorbital
and peripheral edema,
occasionally also ascites.

The central venous pressure
is usually normal to high-normal
in the nephrotic syndrome.

22.  Retention of water and increase in weight which
occurs during or preceding menstruation.
 The etiology is poorly
understood
 The edema tends to be generalized, and resolves
during a diuresis that occurs with the onset of menses.

23.  Direct vasodilators, such as CCB which reduce the
blood pressure activate renin-angiotensinaldosterone and sympathetic nervous systems, both of
which stimulate renal sodium retention.
 The thiazolidinediones such as pioglitazone or
rosiglitazone stimulate sodium reabsorption by the
sodium channels in the luminal membrane of cortical
collecting tubule cells
 NSAID can exacerbate edema in patients with
underlying heart failure or cirrhosis.
 This effect is largely due to increased renal sodium
reabsorption in response to the inhibition of renal
vasodilatory prostaglandins.

24.  Young women (usually obese)
 No cardiac, hepatic, or renal disease
 Periodic episodes of edema (unrelated to menstrual cycle)
 Frequently accompanied by abdominal distention
 Pathogenesis- unknown (capillary leak?
diuretic-induced edema?)
 Treatment:
 low-sodium diet
 stop diuretic therapy

26.  Demographic data (age ,sex)
 (dyspnea, orthopnea, edema,PND, pain abdominal
distention)
 (fatigue, weakness)it’s relation to exertion.
 palpitations with or without lightheadedness.
 The anorexia ,nausea
 Drug history (thyroxine, cocaine, amphetamine)
 history of coronary artery disease or myocardial
infarction, and use of a loop diuretic .
 Family history of CAD (less than66yrs in F, less
than 55yrs in M) or unexplained death in young
relative
 Social history(smoking , alcohol)

27.  Where is the edema located?
 If primary complaint is:
 SOB>> Left heart failure
 Ascites >> cirrhosis
 Peripheral edema>> Rt HF, pericardial disease, renal disease,
local venous or lymphatic disease
 Is there a history of any disorder (coronary
disease, HTN, alcohol abuse)??
 drug that can cause cardiac, hepatic, or renal
disease?
 Is the edema intermittent or persistent?
 Intermittent edema is a common premenstrual symptom
 Associated symptoms

28.  Pitting vs. non-pitting
 Distribution of the edema





Localized or diffuse ?
Periorbital ?
Jugular veins ?
Ascites ?
Legs
 cardio- polumonary examination+ abdominal
examination
 Stigmata of chronic liver disease
 Physical findings of heart failure

29. Pitting edema
Non-pitting edema

30.  Pitting Edema overpressure of
monitor duration of indentation
 1 cm indentation 1+
 2 cm indentation 2+
 3 cm indentation 3+
 4 cm indentation 4+
10 seconds and

31.  Lymphedema
Post mastectomy
Lymphatic disease
Malignancy
 Pretibial myxedema
Infection
thyroid diseases

32. Heart
Liver
Kidney
Nutritional
Generalized
or

Venous obstruction
Lymphatic obstruction
Localized

36.  Chest X rays:
 Cardiomegally; Pulmonary congestion; Pleural effusion.
 Echocardiography
 Wall motion abnormalities; LV function; RV function;
Pulmonary hypertension.
 Abdominal US:
 Liver size & morphology; Hepatic veins; Presence of ascites;
Renal morphology
 24h urinary protein excretion
 Levels of liver enzymes, INR, albumin
 diagnostic paracentesis

37.  The Serum-ascites albumin gradient (SAAG) is probably
a better discriminant than older measures (transudate
versus exudate) for the causes of ascites.
 A high gradient (> 1.1 g/dL) >>>portal hypertension.
 A low gradient (< 1.1 g/dL) >>>non-portal hypertensive
etiology.

38.  high SAAG ("transudate") :
 Cirrhosis- 81% (alcoholic in 65%, viral in 10%, cryptogenic in 6%)
 Heart failure- 3%
 Hepatic Venous occlusion: Budd-Chiari syndrome or veno-occlusive
disease
 Constrictive pericarditis
 Kwashiorkor (childhood protein-energy malnutrition)
 Nephrotic syndrome
 low SAAG("exudate"):





Cancer (primary peritoneal carcinomatosis and metastasis) - 10%
Infection: TB- 2% or Spontaneous bacterial peritonitis
Pancreatitis - 1%
Serositis
Hereditary angioedema

40.  Reversal of the underlying disorder (if
possible)
 Dietary sodium restriction
 Diuretic therapy
http://www.uptodate.com/contents/general-principles-of-the-treatment-of-edema-inadults?source=search_result&search=oedema&selectedTitle=2%7E150

41.  When must edema be treated?
 What are the consequences of the removal of
edema fluid?
 How rapidly should edema fluid be removed?

42.  Pulmonary edema is the only form of
edema that is life-threatening and requires
immediate therapy.
 In most other edematous states, removal of
the excess fluid can proceed more slowly,
since it usually is of no immediate danger
to the patient

43.  Sodium and water retention by the kidney is
compensatory! raises the effective circulating volume(HF,
cirrhosis).
 Diuretic therapy may have a -ve effect on systemic
hemodynamics even though it reduces the edema!!
reduction in CO +increased secretion of the "hypovolemic" hormones
 Therefore- use diuretics, but cautiously !
monitoring the Urea(BUN) and
creatinine concentration

44.  Diuretics are administered intially fluid loss from the Intravascular
space decrease hydrostatic pressure fluid move from interstitial
space to intravascular space
 In patients with generalized edema due to heart failure, the nephrotic
syndrome, or primary sodium retention, the edema fluid can be
mobilized rapidly, since most capillary beds are involved.
 In patients with cirrhosis and ascites but no peripheral edema
 300 to 500 mL/day is the maximum amount that can be mobilized

In patients with anasarca, removal of 2 to 3 liters of edema fluid or
more in 24 hours can usually be accomplished without a clinically
significant reduction in plasma volume

45.  Start with a loop diuretic (furosemide)
 Watch for electrolyte complications:
 Hypokalemia
 Hyponatremia
Thiazides, Spironolactone
 Metabolic alkalosis
 For resistant edema Use high-dose intravenous loop diuretics
 Use combination of diuretics to act at different sites in
the nephron

46.  For patients with cirrhosis, spironolactone and a loop
diuretic is the preferred initial regimen
 Spironolactone contributes to the diuresis and
tends to raise K+
 For patient with NS, higher-than-usual doses of a
loop diuretic may be required because of:
 Binding of the loop diuretic by albumin in the
tubular lumen inactive
 because transport of the diuretic into the tubular
lumen is impaired

47.  the most efficient way
 Diagnostic & therapeutic
47
1/25/2014

48. - New onset ascites
- Hospitalization of a patient with ascites
- Clinical deterioration of an inpatient or outpatient
with ascites
- Fever
- Abdominal pain
- Abdominal tenderness
- Hepatic encephalopathy
- Peripheral leukocytosis
- Deterioration in renal function
48
1/25/2014

49.  Patients with disseminated intravascular
coagulation.
 Primary fibrinolysis.
 Patients with a massive ileus with bowel distension.
 The location of the paracentesis should be modified
in patients with surgical scars so that the needle is
inserted several centimeters away from the scar.
49
1/25/2014

50.  Ascitic fluid leak
 Bleeding
 Infection
 Mortality
50
1/25/2014

51. CASE
 Mr.A.B., a 68 years old man, was admitted to the hospital. He
suffers from fatigue, shortness of breath on exertion, cough,
tenderness in the right upper quadrant of the abdomen and ankle
swelling.
 On examination, he was pale and his hands were cold, his
temperature was 37C, pulse 130 beats per minute and irregular.
His jugular venous was elevated and pitting edema was present
in both feet and ankles. Crepitations were present over the lung
bases. There was enlargement of the liver beyond the costal
margin that was tender.

52. Heart failure is a condition in which the heart
cannot pump enough blood to the rest of the
body.
Heart failure is usually a chronic illness,
which may get worse over time

53. Reduced ventricular contractility
Myocarditis/cardiomyopathy
Myocardial infarction
HTN, aortic stenosis
Ventricular outflow obstruction
PHTN, PV stenosis
Endomyocardial fibrosis
Ventricular inflow obstruction
Mitral, tricuspid stenosis
Constrictive pericarditis
Increase metabolic demand
RV volume overload
Ventricular volume overload
VSD
LV volume overload
53
Arrhythmias
Complete heart block
AF, Tachycardia cardiomyopathy

54. Impaired ventricular function
(e.g. MI, cardiomyopathy)
Heart failure
Neurohormonal activation
Activation of renin-angiotensinAldosterone system
Activation of sympathetic
system
Vasoconstriction (increased sympathetic
Tone and angiotensin 2)
Sodium and fluid retention
(increased aldosterone and ADH)
Increased preload and afterload
Further stress on ventricular wall
And dilatation
54
Further heart failure

55. N/H changes
Favorable effect
Unfavorable effect
 HR , contractility,
vasoconstion.   V return,
preload
Arteriolar constriction 
After load  workload
 O2 consumption
 Renin-Angiotensin –
Aldosterone
Salt & water retention & venous
constriction  VR
Vasoconstriction 
after load
Peripheral edema & pulmonary
congestion
 antidiuretic hormone
circulating volume
Peripheral edema & pulmonary
congestion
 Sympathetic activity

56. Symptomes and signs of HF
Cardiomegaly
Fatigue
Gallop rhythm
Exertional dyspnoea
Tachycardia
Left Heart Failure
orthopnoea
Paroxysmal nocturnal
dyspnoea
Basal Crackles
Murmur
Raised JVP
Breathlessness
Right Heart Failure
Fatigue
Anorxia
56
Dependent pitting edema
Ascites
Pleural effusion
Tender hepatomegaly

57. Framingham Criteria for Dx of Heart Failure
 The Framingham criteria for the diagnosis of heart failure
consists of the concurrent presence of either 2 major criteria or 1
major and 2 minor criteria
 Major Criteria:








57
PND
JVP
Rales
Cardiomegaly
Acute Pulmonary Edema
Gallop
Positive hepatic Jugular reflux
↑ venous pressure > 16 cm H2O

58. Dx of Heart Failure (cont.)
Minor Criteria

LL edema
 Night cough
 Dyspnea on exertion
 Hepatomegaly
 Pleural effusion
 Tachycardia 120 bpm
 Weight loss 4.5 kg over 5 days
management
58

59. NYHA Classification - The
Stages of Heart Failure
Class
Class I (Mild)
Patient Symptoms
No limitation of physical activity. Ordinary physical
activity does not cause undue fatigue, palpitation, or
dyspnea (shortness of breath).
Class II (Mild) Slight limitation of physical activity. Comfortable at
rest, but ordinary physical activity results in fatigue,
palpitation, or dyspnea.
Class III
Marked limitation of physical activity. Comfortable at
(Moderate)
rest, but less than ordinary activity causes fatigue,
palpitation, or dyspnea.
Class IV
Unable to carry out any physical activity without
(Severe)
discomfort. Symptoms of cardiac insufficiency at
rest. If any physical activity is undertaken, discomfort
is increased.

60. Investigation
Imaging: CXR, Echo.
General diagnostic investigation
ECG
Blood test
Serum BNP
Ambulatory (24-48hrs) ECG
monitoring
Fluid balance
monitoring body wight

61. Treatment of heart failure
Treatment focuses on improving the symptoms and preventing the
progression of the disease.
Diet and lifestyle measures
Pharmacological
management

62. Diet and lifestyle measures
 Education in term of explaining the nature of the disease and





treatment.
Moderate physical activity, when symptoms are mild or moderate;
or bed rest when symptoms are severe.
Weight reduction; as obesity is a risk factor for heart failure and
left ventricular hypertrophy
Sodium restriction 60–100 mmol total daily intake. More severe
restrictions may be required in severe CHF.
Fluid restriction should be limited to 1.5 L daily or less in patients
with hyponatremia.
Influenza and pneumococcal vaccination should be considered.

63. Diuretics
ß- blockers
Vasodilators
ACE inhibitors
Inotropic agents

64. References
o http://www.uptodate.com/contents/edemaswelling-beyond-the-basics
o http://www.abouthf.org/questions_stages.htm
o http://health.nytimes.com/health/guides/disease
/heart-failure/overview.html
o http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH
0001211/
o Davidson
o Oxford handbook of clinical medicine.
o Macleod’s clinical examination,12th edition