Pathophysiology of edema and its applied aspects

Edema

1. LAB INVESTIGATION PROTOCOL OF A PATIENT PRESENTING WITH EDEM A Speaker: Dr. Pratiksha Mishra Moderator: Dr Goutami Dasnayak

2. EDEMA : OUTLINES W hat is edema P athophysiology of edema C auses of edema M orpholog y and types of edema L aboratory investigation protocol Summary

3. Definition Edema is the accumulation of fluid in interstitial tissues due to a net movement of water into extravascular spaces. It is marked by swelling of tissues and accumulation of fluid in body cavities, commonly in subcutaneous tissues, lungs and brain.

4. 60 % of body weight is water ; Fluid (water) movement between the vascular and interstitial spaces is by two opposing forces: The hydrostatic pressure and The osmotic pressure . 2/3 rd : Intracellular 1/3 rd : Extracellular 3/4 th : Interstitial 1/4 th : Intravascular

5. Normally, outflow of fluid produced by hydrostatic pressure at the arteriolar end is balanced by inflow at the venular end. This balance when disturbed by pathologic conditions promote edema.

6. PATHOPHYSIOLOGY OF EDEMA

7. CAUSES OF EDEMA

8. MORPHOLOGY Edema is easily recognized on gross inspection. HPE shows clearing and separation of the extracellular matrix elements. Edema most commonly found in subcutaneous tissues, lungs and brain.

9. EDEMA » MORPHOLOGY » SUBCUTANEOUS EDEMA Finger pressure over affected tissue displaces the interstitial fluid, leaving a finger-shaped depression; this appearance is called pitting edema . Fig: PITTING EDEMA; showing depression

10. TYPES OF EDEMA PITTING EDEMA NON PITTING EDEMA Chronic lymphedema Myxedema Angioneurotic edema Radiation injury

11. EDEMA » MORPHOLOGY » PULMONARY EDEMA Fig: PULMONARY EDEMA Grossly, 2-3 times the normal weight C/S: Frothy, blood tinted fluid consisting of mixture f air, fluid and extravasated red cells

12. EDEMA » MORPHOLOGY » BRAIN EDEMA Brain edema can be localized or generalized With generalized edema, the sulci are narrowed as the gyri swell and become flattened against the skull. Fig: BRAIN EDEMA

13. LAB INVESTIGATION PROTOCOL Complete blood count (CBC) Urine routine microscopy and Renal function tests(RFTs) Liver f unction tests(LFTs) Serum total protein and albumin Serum lipid profile Serum TSH, fT3 AND fT4 levels

14. Following laboratory tests are useful for diagnosing systemic and localized causes of edema: CXR, ECG and Brain natriuretic peptide levels D-Dimer USG Abdomen and KUB Doppler study Lymphoscintigraphy Echocardiography

15. SERUM TOTAL PROTEIN and ALBUMIN The normal range of albumin is  3.5 to 5.5 g/ dL or 35-55 g/liter. Normal serum protein : 60-80g/L • Increased loss – Nephrotic syndrome • Decreased synthesis – Chronic liver disease • Malabsorption – Protein-losing enteropathy , e.g. Crohn’s disease and coeliac disease • Malnutrition – Kwashiorkar

16. Composition of normal urine (24 hrs) in adults 19 Sl No Parameters Values Sl No Parameters Values 1 Volume 600-2000 ml 10 Urea nitrogen 12-20 gm 2 Specific gravity 1.003-1.030 11 U r i c A c i d 250-750 mg 3 Osmolality 300-900 mOsm/kg 12 Sodium 40-200 mEq 4 pH 4.6-8.0 13 Potassium 25-125 mEq 5 Glucose < 0.5 gm 14 Chloride 110-250 mEq 6 Proteins < 150 mg 15 Calcium (low cal c i u m d i et) 50-150 mg 7 Urobilinogen 0.5-4.0 gm 16 Formiminogluta mi c ac i d (FIGlu ) < 3 mg 8 Prophobilinog en 0.2 mg 17 Red cells, epithelial cells and w hi t e blood cells ≤ 1-2 per high p o w er f ie l d 9 Creatinine M: 14-26 mg/kg F: 11-20 mg/kg

17. URINE ANALYSIS 24-hour urine collection can help identify the cause of generalized edema by showing the degree of proteinuria. 1. Edema associated with slight or no proteinuria (less than 0.5 g/24 hours): CHF , cirrhosis, hypertension, malnutrition, inferior vena cava thrombosis below the renal veins, hypothyroidism, and varicose veins .

18. 2. Edema associated with significant proteinuria (greater than 0.5 g/24 hours, generally 2 g/24 hours or more ):  G lomerular diseases, preeclampsia, tubulointerstitial disease, hypertension, and vascular diseases. 3. Edema associated with heavy proteinuria (3 g/24 hours or more): Consistent with both primary(MCD, MPGN,FSGS) and secondary(Diabetic, amyloidotic ) glomerular diseases.

19. Other preliminary blood tests Complete blood counts : To rule out anemia seen in renal failure or any other cause. Liver function tests: For liver cirrhosis Serum lipid profile: Nephrotic syndrome and Coronary heart disease Serum TSH: Hypothyroidism

20. BRAIN NATRIURETIC PEPTIDE LEVELS Secreted by  cardiomyocytes  in the  heart ventricles  in response to stretching caused by increased ventricular blood volume. BNP is more sensitive to acute changes in disease processes . BNP is a useful prognostic indicator for myocardial stress correlated with long-term  cardiovascular mortality and in acute myocardial infarction patients.

21. Heart failure is unlikely if the BNP value is less than 100  pg /mL and heart failure is very likely if the value is over 500  pg / mL. Patients with end-stage renal disease and dialysis patients usually show higher BNP and NT- proBNP in serum.

22. D DIMER LEVELS In patients who present with acute onset of unilateral upper or lower extremity swelling, a d-dimer ELISA can rule out DVT in low risk patients. But, has a low specificity, and d-dimer concentrations may be elevated in the absence of thrombosis. Normal D-Dimer levels < 0.5.

23. ULTRASONOGRAPHY OF ABDOMEN AND PELVIS Cirrhotic liver shows nodular hepatic contour, changes in volume distribution, including an enlarged caudate lobe and left lobe lateral segment, atrophy of the right and left lobe medial segments, widening of the fissures and the porta hepatis , and regenerative nodules. Chronic kidney disease shows bilateral shrunken kidneys and altered echotexture .

24. ULTRASONOGRAPHY Venous ultrasonography: Imaging modality of choice in the evaluation of suspected DVT. Compression ultrasonography with or without Doppler waveform analysis has a high sensitivity (95%) and specificity (96%) for proximal thrombosis; the sensitivity is lower for calf veins (73 %). Duplex ultrasonography used to confirm the diagnosis of chronic venous insufficiency.

25. LYMPHOSCINTIGRAPHY Lymph flow cannot be detected with ultrasonography. Indirect radionuclide lymphoscintigraphy , shows absent or delayed filling of lymphatic channels, is the method of choice for evaluating lymphedema when the diagnosis cannot be made clinically

26. MAGNETIC RESONANCE IMAGING Magnetic resonance angiography(MRA) with venography of the lower extremity and pelvis can be used to evaluate for intrinsic or extrinsic pelvic or thigh DVT. MRI may aid in the diagnosis of musculoskeletal etiologies, such as a gastrocnemius tear or popliteal cyst causing unilateral edema.

27. Others Echocardiography should be performed in patients with obesity, obstructive sleep apnea, and edema to evaluate pulmonary arterial pressures . Ankle-brachial index measured in patients with chronic venous insufficiency and cardiovascular risk factors before initiation of compression therapy, which is contraindicated in peripheral arterial disease

28. Resolve the underlying cause . Cases of heart or kidney disease, are treated with diuretics. Positioning the affected body parts to improve drainage, Compression can be used to pressurize tissue in a limb, forcing fluids; both blood and lymph, to flow out of the compressed area. EDEMA » TREATMENT

29. REFERENCES Robbins BASIC PATHOLOGY, 10 th Edition Harrison’s principles of internal medicine, 19 th edition Uptodate American academy of family physician guidelines https ://www.aafp.org/pubs/afp/issues/2013/0715/p102.html

30. QUESTION S ?? Thank You ☺