What causes ascites and pleural effusion?

Pleural effusion is a disease with leakage in the chest cavity and no inflammatory changes in the pleura. It is a symptom of other organs or systemic diseases, usually characterized by dyspnea. 【 Etiology 】 It is often caused by heart disease, some chronic lung diseases or blood circulation disorder when venous trunk is compressed. Chronic anemia and anemia, as well as any long-term wasting disease, can also cause pleural effusion. 【 Symptoms 】 The main symptoms are dyspnea, normal body temperature and heart pitch. When tapping the chest wall, there are horizontal voiced sounds on both sides, and the position of the voiced boundary changes with the posture of the sick dog. When auscultating, alveolar sounds can't be heard in voiced areas, and sometimes bronchial breathing sounds can be heard. Often accompanied by ascites, pericardial effusion and subcutaneous edema. [Diagnosis] It is not difficult to make a diagnosis according to the general symptoms such as insufficient body heat and voiced sound at the level of percussion. But it should be distinguished from pleurisy. Pleurisy has fever, chest pain, cough and pleural fricative sound, which mostly occurs on one side. Pleurisy is exudate, which contains a lot of fibrin, protein and rivastatin. However, pleural effusion has no systemic symptoms, and the pleural fluid is a leakage fluid, which is clear and thin, containing a small amount of fibrin and protein, and Leviathan reaction is negative. [Treatment] The principle of treatment is to strengthen nursing, limit drinking water, strengthen heart and diuresis, and eliminate stagnant water. Cardiotonic diuretics can be injected subcutaneously with caffeine, sodium salicylate and cocaine, digitalis preparation and pilocarpine hydrochloride. Promote the absorption of stagnant water. You can also inject prednisone to prevent pleural adhesion and accelerate liquid absorption, and the effect is good. Removing pleural effusion When there is too much pleural effusion, it is especially difficult to breathe and there is a danger of suffocation, you can perform thoracotomy to remove pleural effusion, and then inject 25mg of cortisone ester acid. 1) Formation mechanism of ascites: Ascites is the result of multiple factors. Portal hypertension is the main cause of ascites, and the decrease of serum albumin is an important factor causing ascites (see Figure 4- 16-3). 1) Increased portal pressure: Under normal circumstances, the pressure of hepatic sinuses is very low (0-2mmHg), while the hydrostatic pressure of hepatic sinuses is increased during portal hypertension (portal pressure 10 mmhg is the basic condition for the formation of peritoneal effusion), and a large amount of fluid flows into the Disse space, resulting in excessive production of hepatic lymph. Patients with liver cirrhosis are often 20 times as many as normal people. When the thoracic duct cannot drain too much lymph, it will directly leak into the abdominal cavity from the liver capsule, forming peritoneal effusion. The increase of hepatic sinus pressure can also cause the activation of intrahepatic pressure receptors, reduce renal sodium excretion and aggravate water and sodium retention through liver-kidney reflex. 2) Visceral artery dilation: In the early stage of liver cirrhosis, splanchnic blood vessels dilate, and the effective blood volume is maintained in the normal range by increasing cardiac output and heart rate. In the progressive stage of liver cirrhosis, splanchnic artery dilatation is more obvious, which leads to the obvious decrease of effective arterial circulating blood volume and arterial pressure, thus activating sympathetic nervous system, renin-angiotensin-aldosterone system, increasing the release of antidiuretic hormone (ADH) to maintain arterial pressure, leading to renal vasoconstriction and sodium and water retention. The interaction between portal hypertension and splanchnic vasodilation changes the capillary pressure and permeability of intestine, which is beneficial to the accumulation of fluid in abdominal cavity. 3) Decreased plasma colloid osmotic pressure: The intake of patients with liver cirrhosis is reduced, the function of liver reserve is decreased, and the ability to synthesize albumin is decreased, which leads to the decrease of plasma albumin, and then the decrease of plasma colloid osmotic pressure, and a large amount of fluid enters the interstitial space, forming peritoneal effusion. 4) Other factors: the relative shortage of plasma central natriuretic peptide, the decrease of the body's sensitivity to it, the decrease of estrogen inactivation, the increase of antidiuretic hormone secretion, the decrease of prostaglandin secretion, the contraction of renal blood vessels, the decrease of renal perfusion and the redistribution of renal blood flow are all related to the formation and persistence of ascites. Abdominal effusion can be absorbed through the parietal peritoneum with a maximum rate of 900 ml/d, and the absorbed peritoneal effusion can be drained through intestinal lymphatic vessels or reabsorbed through visceral capillaries. Due to the overload of lymphatic system, the absorption of visceral capillary circulation is limited by Starlin9 force, and patients with liver cirrhosis often have peritoneal thickening, so the absorption rate is reduced. The production of ascites increases, the absorption decreases, and the ascites gradually increases. (2) Formation mechanism of spontaneous bacterial peritonitis: Spontaneous infection of ascites leads to spontaneous bacterial peritonitis (SBP) and endotoxemia without infection in abdominal cavity. In patients with liver cirrhosis, intestinal bacteria overgrow, the permeability of intestinal wall increases, and the local immune defense function of intestinal wall decreases, which causes bacterial translocation in intestinal cavity and enters the circulatory system through mesenteric lymph nodes, resulting in bacteremia. The activity of reticuloendothelial system decreases, and the opsonin, immunoglobulin, complement and albumin in peritoneal effusion decrease, which leads to the infection of peritoneal effusion.