Edema and effusions

Four pressures act across the capillary wall. Capillary hydrostatic pressure (Pc, the lecture's PH) pushes fluid out; plasma oncotic pressure (πc, the lecture's PO), made mostly by albumin, holds it in. Interstitial hydrostatic and oncotic pressures are small. At the arteriolar end, hydrostatic pressure wins and fluid filters out; along the capillary hydrostatic pressure falls, and near the venular end the balance favors return. The small net excess that stays in the interstitium is carried back by lymphatics. Edema appears when filtration outruns lymph flow.

Most clinical edema combines a Starling change with renal sodium retention. Match each setting to its main mechanism; the type of fluid and where it collects follow.

Anything that raises pressure in the venous side of a capillary bed raises filtration there. In left-sided heart failure a high left atrial pressure is transmitted back to the pulmonary capillaries: fluid floods the interstitium and then the alveoli (dyspnea, orthopnea, crackles), and leaked red cells are eaten by alveolar macrophages that fill with hemosiderin (“heart failure cells”). In right-sided heart failure the systemic veins are congested: dependent pitting edema, a congested “nutmeg” liver and ascites. Portal hypertension in cirrhosis raises sinusoidal pressure and produces ascites. A deep vein thrombosis raises pressure only below the clot, so the edema is one-sided.

These are passive congestion: blood dammed back in veins, bluish-red tissue, and chronic hypoxic injury of the congested organ. They differ from active hyperemia, in which arterioles dilate and bring more blood in (exercise, inflammation), making the tissue red and warm.

Albumin supplies most of plasma oncotic pressure, so any cause of hypoalbuminemia lowers the force that holds fluid in vessels. The lecture lists four: nephrotic syndrome (albumin lost in urine, > 3.5 g/24 h), cirrhosis (less albumin made), malnutrition with low protein intake, and malabsorption (protein not absorbed). The edema is generalized, soft and pitting, and shows early where tissue is loose: around the eyes in the morning in nephrotic syndrome, in the legs by evening.

Increased vascular permeability is the edema of acute inflammation. Histamine, bradykinin and leukotrienes contract endothelial cells of venules and open gaps; more severe injury (burns, toxins, sepsis) damages endothelium directly. Protein escapes with the water, so the interstitial oncotic pressure rises and the fluid is an exudate, rich in protein and, once leukocytes arrive, in cells (pus when neutrophils dominate). The same mechanism in the lungs is ARDS (4.7).

Lymphatic obstruction leaves filtered fluid and protein in the tissue: lymphedema. Causes include axillary dissection and radiation after mastectomy, filariasis (Wuchereria bancrofti, giving elephantiasis of legs and scrotum), lymphogranuloma venereum, and tumor blocking lymphatics. In the breast, tumor in dermal lymphatics causes skin edema tethered at hair follicles: peau d'orange. Because the trapped fluid is protein-rich, it stimulates fibrosis: early lymphedema pits, chronic lymphedema becomes firm and nonpitting.

A Starling problem alone would soon stop: as fluid leaves the vessels, plasma volume falls, capillary pressure drops and the leak slows. Edema keeps accumulating because the kidney refills the circulation. In heart failure, cirrhosis and nephrotic syndrome the arterial tree is underfilled (low cardiac output, or fluid lost to the interstitium and splanchnic vasodilation in cirrhosis). Baroreceptors and the kidney respond as if the patient were bleeding: RAAS, sympathetic tone and ADH retain sodium and water. The retained fluid meets the same raised venous pressure or low oncotic pressure and leaves the vessels again.

In acute glomerulonephritis and renal failure the order is reversed: the kidney retains sodium first (low GFR), the ECF is overfilled, and blood pressure rises along with the edema.

Pitting happens when free fluid in loose tissue can be pushed aside and flows back slowly: low-protein transudates. Fluid that is bound in a glycosaminoglycan matrix (myxedema) or trapped in fibrosed, protein-rich tissue (chronic lymphedema) does not move under the finger: nonpitting edema. In pretibial myxedema of Graves disease, T-cell cytokines and TSH-receptor antibodies stimulate fibroblasts to make hyaluronic acid; in hypothyroidism, matrix accumulates in the face, tongue and skin.

The same distinction applies to effusions in body cavities. For pleural fluid, Light's criteria call it an exudate if any of these holds: fluid/serum protein > 0.5, fluid/serum LDH > 0.6, or fluid LDH > two-thirds of the upper limit of normal serum LDH. A transudative effusion points to a pressure or protein problem (heart failure, cirrhosis, nephrotic syndrome); an exudative one to a leaky or invaded pleura (pneumonia, tuberculosis, cancer).