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Oedema
 

Oedema

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done by Al Yaqdhan Al Atbi

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

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  • 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).

Oedema Oedema Presentation Transcript

  • EDEMA
  •  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
  • 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.
  • 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??
  • 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.
  •  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
  •  Brain: Cerebral edema  Lung: Intra-alveolar= pulmonary edema,  intra-pleural= pleural effusion  Peritoneum= Ascites  Massive and generalized edema = Anasarca
  • Starling’s law: • Vascular system Hydrostatic pressure Interstitial space Hydrostatic pressure Colloid oncotic pressure pressure (tissue tension) Colloid oncotic
  • 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
  • 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
  •  Heart failure  Cirrhosis  Nephrotic syndrome and other forms of renal disease  Premenstrual edema and pregnancy
  • 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
  •  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.
  •  Pulmonary edema in a "butterfly distribution" due to left ventricular failure. Chest radiograph shows large perihilar opacities in patient with enlarged cardiac silhouette.
  •  Increased venous pressure behind the right side of the heart increased capillary hydrostatic pressure  Congested jugular veins  Enlarged & tender liver  Peripheral edemaAnasarca
  •  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)
  •  Heavy proteinuria (> 3.0 g/day)  Hypoalbuminemia  Hyperlipidemia  Peripheral edema
  •  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.
  •  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.
  •  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.
  •  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
  •  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)
  •  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
  •  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
  • Pitting edema Non-pitting edema
  •  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
  •  Lymphedema Post mastectomy Lymphatic disease Malignancy  Pretibial myxedema Infection thyroid diseases
  • Heart Liver Kidney Nutritional Generalized or  Venous obstruction Lymphatic obstruction Localized
  •  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
  •  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.
  •  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
  •  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
  •  When must edema be treated?  What are the consequences of the removal of edema fluid?  How rapidly should edema fluid be removed?
  •  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
  •  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
  •  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
  •  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
  •  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
  •  the most efficient way  Diagnostic & therapeutic 47 1/25/2014
  • - 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
  •  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
  •  Ascitic fluid leak  Bleeding  Infection  Mortality 50 1/25/2014
  • 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.
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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.
  • Investigation Imaging: CXR, Echo. General diagnostic investigation ECG Blood test Serum BNP Ambulatory (24-48hrs) ECG monitoring Fluid balance monitoring body wight
  • Treatment of heart failure Treatment focuses on improving the symptoms and preventing the progression of the disease. Diet and lifestyle measures Pharmacological management
  • 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.
  • Diuretics ß- blockers Vasodilators ACE inhibitors Inotropic agents
  • 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