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
Pathogenesis
- 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), such as cirrhosis; while exudates are actively secreted fluid due to inflammation or malignancy.
- Exudates:
- high in protein
- High in lactate dehydrogenase
- Low pH (< 7.30)
- Low glucose level
- white blood cells
- Transudates:
- Low protein (< 30 g/L)
- Low LDH, high pH
- Normal glucose
- Fewer than 1 white cell per 1000 mm³
Serum Albumin Ascites Gradiant (SAAG)
- The most useful measure is the difference between ascitic and serum albumin concentrations.
- A difference of less than 1.1 g/dl (10 g/L) implies an exudate.
Cirrhotic Ascites
- The main pathophysiology of ascites in cirrhotic patients consists of three interrelated mechanisms, include:[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
- Peritoneal malignancy produces some protein factors into the peritoneum, which may lead to osmotic drainage of water and fluid accumulation. Tuberculosis and other forms of ascites are induced through the same mechanism and osmotic fluid shift.[7]
- Pancreatic and biliary ascites are induced through leakage of pancreatic secretions or bile into the peritoneal cavity, which may lead to inflammatory fluid shift and accumulation.
| ↑Renin-angiotensin system | ↑Sympathetic nervous system | ↑Antidiuretic hormone | |||||||||||||||||||||||||||||||
| Systemic circulation | Renal circulation | ||||||||||||||||||||||||||||||||
| Arterial vasoconstriction | ↑Tubular Na and H2O reabsorbtion | Renal vasoconstriction | |||||||||||||||||||||||||||||||
| Arterial hypertension | Na and H2O excretion | Hepatorenal syndrome | |||||||||||||||||||||||||||||||
| Fluid overload | Dilutional hyponatremia | ||||||||||||||||||||||||||||||||
| Ascites formation | |||||||||||||||||||||||||||||||||
Genetics
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
Associated Conditions
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
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.
- ↑ Goodman GM, Gourley GR (1988). "Ascites complicating ventriculoperitoneal shunts". J. Pediatr. Gastroenterol. Nutr. 7 (5): 780–2. PMID 3054040.