Ascites pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]
Overview
Pathophysiology
Cirrhotic Ascites
- The main pathophysiology of ascites in cirrhotic patients consists of three interrelated mechanisms:[1]
- Portal hypertension
- Vasodilation
- Hyperaldosteronism
- There is a nitric oxide overload in cirrhotic patients from an unknown source. Therefore, they involved in hypovolemia secondary to the systemic vasodilation.[2]
- The visodialtion induced by nitric oxide would trigger the stimulation of juxta-glumerular system to upregulate antidiuretic hormone (ADH) and sympathetic drive.[3] Excess ADH causes water retention and volume overload.[4]
- Despite the normal physiology of vessels, angiotensin would not cause vasoconstriction in cirrhotic patients and vasodilation becomes perpetuated.[5]
- Portal hypertension leads to more production of lymph, to the extend of lymphatic system overload. Then, the lymphatic overflow will directed into to peritoneal cavity, forming ascites.[6]
Non-Cirrhotic Ascites
- Ascitic fluid can accumulate as a transudate or an exudate. Amounts of up to 25 liters are fully possible.
- Roughly, transudates are a result of increased pressure in the portal vein (>8 mmHg), e.g. due to cirrhosis, while exudates are actively secreted fluid due to inflammation or malignancy. As a result, exudates are high in protein, high in lactate dehydrogenase, have a low pH (<7.30), a low glucose level, and more white blood cells. Transudates have low protein (<30g/L), low LDH, high pH, normal glucose, and fewer than 1 white cell per 1000 mm³. Clinically, the most useful measure is the difference between ascitic and serum albumin concentrations. A difference of less than 1 g/dl (10 g/L) implies an exudate. Portal hypertension plays an important role in the production of ascites by raising capillary hydrostatic pressure within the splanchnic bed.
Regardless of the cause, sequestration of fluid within the abdomen leads to additional fluid retention by the kidneys due to stimulatory effect on blood pressure hormones, notably aldosterone. The sympathetic nervous system is also activated, and renin production is increased due to decreased perfusion of the kidney. Extreme disruption of the renal blood flow can lead to the feared hepatorenal syndrome. Other complications of ascites include spontaneous bacterial peritonitis (SBP), due to decreased antibacterial factors in the ascitic fluid such as complement.
References
- ↑ Giefer, Matthew J; Murray, Karen F; Colletti, Richard B (2011). "Pathophysiology, Diagnosis, and Management of Pediatric Ascites". Journal of Pediatric Gastroenterology and Nutrition. 52 (5): 503–513. doi:10.1097/MPG.0b013e318213f9f6. ISSN 0277-2116.
- ↑ La Villa, Giorgio; Gentilini, Paolo (2008). "Hemodynamic alterations in liver cirrhosis". Molecular Aspects of Medicine. 29 (1–2): 112–118. doi:10.1016/j.mam.2007.09.010. ISSN 0098-2997.
- ↑ Leiva JG, Salgado JM, Estradas J, Torre A, Uribe M (2007). "Pathophysiology of ascites and dilutional hyponatremia: contemporary use of aquaretic agents". Ann Hepatol. 6 (4): 214–21. PMID 18007550.
- ↑ Bichet, Daniel (1982). "Role of Vasopressin in Abnormal Water Excretion in Cirrhotic Patients". Annals of Internal Medicine. 96 (4): 413. doi:10.7326/0003-4819-96-4-413. ISSN 0003-4819.
- ↑ Hennenberg, M.; Trebicka, J.; Kohistani, A. Z.; Heller, J.; Sauerbruch, T. (2009). "Vascular hyporesponsiveness to angiotensin II in rats with CCl4-induced liver cirrhosis". European Journal of Clinical Investigation. 39 (10): 906–913. doi:10.1111/j.1365-2362.2009.02181.x. ISSN 0014-2972.
- ↑ Laine GA, Hall JT, Laine SH, Granger J (1979). "Transsinusoidal fluid dynamics in canine liver during venous hypertension". Circ. Res. 45 (3): 317–23. PMID 572270.