Causes and Pathophysiology of Ascites
Ascites is a pathological accumulation of fluid in the peritoneal cavity. Healthy men have little or no intraperitoneal fluid, but women may normally have as much as 20 mL, depending on the phase of their menstrual cycle.
When a person develops larger accumulations of fluid in the peritoneum of more than one liter, they will start to express features of ascites
In this article, we shall cover the causes and pathophysiology of ascites.
There are a number of disorders of conditions that can cause ascites but the most common of them are malignant diseases, liver cirrhosis, and heart failure. It is important to consider some primary disorders of the peritoneum and visceral organs as the possible causes of ascites even in a person with confirmed chronic liver disease.
Ascites can result from either increased portal venous pressure, low plasma proteins (hypoproteinemia), chronic peritoneal irritation, leakage of lymphatic fluid into the peritoneal cavity or fluid overload.
What are the causes of Ascites?
Increased portal venous pressure.
Conditions that cause ascites as a result of increased portal venous pressure are:
Pre hepatic causes are;
- Portal vein compression
Hypoproteinemia as a result if;
Chronic peritoneal inflammation and infection.
- Secondary infections such as tuberculosis or fungal infection.
- Secondary malignant infiltration ( carcinomatosis peritonei).
- Post irradiation.
Leakage of lymphatic fluid to the peritoneal cavity (chylous ascites). It can be;
- Surgical trauma.
- Primary and secondary malignancy.
Other causes are; Pancreatic ascites, Bilous ascites, and Urinary ascites.
As a doctor, you should be at a position of differentiating ascites from other causes of abdominal distension such as bowel obstruction, bleeding, and huge abdominal masses.
Pathophysiology of ascites
Like we have mentioned above, one of the major causes of ascites is increased portal venous pressure related to cirrhosis. In discussing the causes and pathophysiology of ascites we shall do it as per the causes because all have different mechanisms.
Increased portal venous pressure.
The presence of portal hypertension contributes to the development of ascites in patients who have cirrhosis. Apart from cirrhosis, any cause of increased resistance to hepatic or portal venous flow can lead to ascites
There is an increase in intrahepatic resistance, causing increased portal pressure. This increased pressure within the hepatic veins or post sinusoidal level increases hydrostatic pressure within the hepatic sinusoids and portal veins.
In late stages of liver cirrhosis, there is collateral vein formation, shunting of blood to the systemic circulation and also vasodilation of the splanchnic arterial system, which, in turn, results in an increase in portal venous inflow.
All these abnormalities result in increased production of splanchnic lymph. Lymphatic flow is increased proximal to the point of vascular obstruction and when the normal capacity of the lymphatic system is overwhelmed the transudate fluid moves across the surfaces of the liver, mesentery, and intestines into the peritoneal cavity.
Vasodilating factors such as a nitric oxide or atrial natriuretic hormone are responsible for the vasodilator effect.
These hemodynamic changes such as a fall in systemic arterial pressure due to splanchnic vasodilatation results in sodium retention by causing activation of the renin-angiotensin-aldosterone system with the development of hyperaldosteronism. The renal effects of increased aldosterone leading to sodium retention also contribute to the development of ascites.
Sodium retention is the consequence of a homeostatic response caused by the underfilling of the arterial circulation secondary to arterial vasodilation in the splanchnic vascular bed. Because the retained fluid is constantly leaking out of the intravascular compartment into the peritoneal cavity, the sensation of vascular filling is not achieved, and the process continues
The increased portal venous pressure in combination with splanchnic vasodilation alters normal permeability and capillary pressure. This alteration enables the movement of vascular fluid through the poles between capillary vascular endothelial cells of the portal system into the extravascular space of the liver and intestines.
Any condition that causes obstruction to hepatic venous flow may lead to ascites as a result of increasing portal venous pressure like in the case of Budd-Chiari Syndrome. The site of this obstruction can be anywhere from hepatic venules, large hepatic veins, inferior vena cava or right atrium of the heart. This is why right heart failure causes ascites.
Hypoalbuminemia and ascites
Low concentration of plasma proteins mainly albumin is known as hypoalbuminemia. Hypoalbuminemia and reduced plasma oncotic pressure also contribute to the loss of fluid from the vascular compartment into the peritoneal cavity. Hypoalbuminemia usually results because or a decreased synthetic function in a cirrhotic liver.
In a normal healthy being, there is relatively high osmotic pressure of intravascular plasma which tends to draw or pull extravascular fluid back to the intravascular compartment.
This osmotic gradient is reduced in hypoproteinemia or low protein levels in the blood so that less fluid is removed from the extravascular space. In the decreased synthetic function of the liver to synthesize albumin, the capacity of intestinal and hepatic lymphatics to remove fluid from extravascular interstitial space is exceeded and ascites eventually develops.
Malignant infiltration (Carcinomatosis Peritonei)
Abdominal cancers cause ascites as a result of inflammation, exudation, shedding of cells and in some instances bleeding.
This case usually occurs in the late stages of cancer. The most common cancers associated are gastric cancers (stomach cancer) and ovarian cancers because of their ease of spread within the peritoneum (transperitoneal spread).
Ascites due to peritoneal inflammation
Like any form of inflammation, peritoneal inflammation results in increased inflow within peritoneal blood and lymphatic vessels.
Peritoneal wall microvascular permeability increases with consequent exudation of plasma proteins and fluid into extravascular spaces.
When the ability of the lymphatics to absorb the fluid is exceeded it accumulates within the peritoneal cavity. Due to high protein in this fluid, reabsorption of the fluid is also impaired.
Another important cause of ascites is leakage of fluid into the peritoneum when intraabdominal lymphatics are transected in some cases such as abdominal surgery or trauma. Ascites develops when the rate of leakage exceeds the rate of absorption by the remaining peritoneal lymphatics.
Measurement of the protein concentration and the serum–ascites albumin gradient (SAAG) can be a useful tool to distinguish ascites of different aetiologies.
Risk factors for ascites
After having looked at the causes and pathophysiology of ascites, it is important to know the risk factors for the development of ascites.
- Long-term heavy alcohol use.
- Chronic viral hepatitis or jaundice.
- Intravenous drug use.
- Multiple sexual partners.
- Homosexual activity with a male partner, or heterosexual activity with a bisexual male.
- Transfusion with blood not tested for the hepatitis virus.
- Living or birth in an area endemic for hepatitis.
- Patients with alcoholic liver disease who alternate between heavy alcohol consumption and abstention (or light consumption) may experience ascites in a cyclic fashion.
- Obesity, hypercholesterolemia, and type 2 diabetes mellitus are recognized causes of nonalcoholic steatohepatitis, which can progress to cirrhosis.
- Patients with a history of cancer, especially gastrointestinal cancer, are at risk for malignant ascites. Malignancy-related ascites is frequently painful, whereas cirrhotic ascites is usually painless
Having gotten an understanding of the causes and pathophysiology of ascites, one should be able to have a clue on the features that a person with ascites is likely to present with.
Features of ascites
Once the amount of fluid in the peritoneum is massive more than one liter, an individual will present with the following features
- Complains of abdominal distension,
- Fullness in the flanks,
- Shifting dullness due to the accumulated free fluid on percussion and,
- when the ascites are marked there will be a fluid thrill or fluid wave.
They may also present with eversion of the umbilicus, abdominal striae or stretch marks, hernia, divarication of the recti and scrotal edema.
Patients who develop ascites due to portal hypertension usually present with dilated superficial abdominal veins.