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.
6.
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
9. Starling’s law:
• Vascular system
Hydrostatic pressure
Interstitial space
Hydrostatic
pressure
Colloid oncotic pressure
pressure
(tissue tension)
Colloid oncotic
10.
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.
17.
18. Increased venous pressure behind the right
side of the heart increased capillary
hydrostatic pressure
Congested jugular veins
Enlarged & tender liver
Peripheral edemaAnasarca
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)
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
25.
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
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
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
39.
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
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
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
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.
Edema formation — The development of edema requires an alteration in one or more of the Starling forces in a direction that favors an increase in net filtration and also inadequate removal of the additional filtered fluid by lymphatic drainage. Edema may form in response to an elevation in capillary hydraulic pressure (which increases the "Δ hydraulic pressure"), increased capillary permeability (Lp), higher interstitial oncotic pressure, a lower plasma oncotic pressure (which reduces the "Δ oncotic pressure"), or a combination of these changes (table 1). Edema can also be induced by lymphatic obstruction since the fluid that is normally filtered is not returned to the systemic circulation.
where Lp is the unit permeability (or porosity) of the capillary wall, S is the surface area available for fluid movement, Pcap and Pif are the capillary and interstitial fluid hydraulic pressures, πcap and πif are the capillary and interstitial fluid oncotic pressures, and s represents the reflection coefficient of proteins across the capillary wall (with values ranging from 0 if completely permeable to 1 if completely impermeable). The interstitial oncotic pressure is derived primarily from plasma proteins that have crossed from the capillary to the interstitium and, to a lesser degree, proteoglycans, which originate in the interstitium
Symptoms of HF include those due to excess fluid accumulation (dyspnea, orthopnea, edema, pain from hepatic congestion, and abdominal distention from ascites) and those due to a reduction in cardiac output (fatigue, weakness) that is most pronounced with exertion.Patients with atrial and/or ventricular tachyarrhythmias may complain of palpitations with or without lightheadedness.The anorexia is secondary to several factors including poor perfusion of the splanchnic circulation, bowel edema, and nausea induced by hepatic congestion.Other clinical features such as older age, history of coronary artery disease or myocardial infarction, and use of a loop diuretic are associated with increased likelihood of heart failure
? Patients with a primary complaint of shortness of breath may have left heart failure and pulmonary edema; those with ascites may have cirrhosis; and those with only peripheral edema may have right-sided heart failure, pericardial disease, renal disease, or local venous or lymphatic disease. Among patients with heart failure, the localization of edema may provide diagnostic information. Patients with left ventricular dysfunction (eg, due to ischemia, hypertension, or valvular disease) typically present with pulmonary congestion; those with cardiomyopathy may have equivalent involvement of both the right and left ventricles, often leading to the simultaneous onset of pulmonary and peripheral edema; disease mainly affecting the right ventricle or venous return to the heart causes mainly peripheral edema.Intermittent edema is a common premenstrual symptom
. Testing for pitting involves applying firm pressure to the edematous tissue for at least five secondsAlthough clinicians commonly grade pitting edema from 1+ to 4+ (mild to severe), there is no agreed upon definition of these grades. However, this type of grading scheme may help the clinician record relative changes in edema (eg, less edema after diuretic therapy). Since the degree of edema is also influenced by posture, documenting weight loss is another component of monitoring the efficacy of diuretic therapy.
lymphedema
and patients with tense ascites are often treated with therapeutic paracentesis
Surgical scars are associated with tethering of the bowel to the abdominal wall, increasing the risk of bowel perforation. Bowel perforation by the paracentesis needle occurs in approximately 6/1000 taps. Fortunately, it is generally well tolerated [5].
Cough•Fatigue, weakness, faintness•Loss of appetite•Pulse that feels fast or irregular, or a sensation of feeling the heart beat (palpitations)•Shortness of breath when active or after lie down•Swollen (enlarged) liver or abdomen•Swollen feet and ankles•Waking up from sleep after a couple of hours due to shortness of breath•Weight gain
EDEMA TREATMENT — Treatment of edema includes several components: treatment of the underlying cause (if possible), reducing the amount of salt (sodium) in your diet, and, in many cases, use of a medication called a diuretic to eliminate excess fluid. Using compression stockings and elevating the legs may also be recommended. (See "General principles of the treatment of edema in adults".)Not all types of edema require treatment. Edema related to pregnancy or menstrual cycles is not usually treated. Peripheral edema and ascites are usually treated slowly to minimize the side effects of rapid fluid loss (such as low blood pressure).
