Why ascites in chf

When ascites occurs at high altitudes in meat-type chickens, which have a high metabolic oxygen requirement, it is usually caused by primary or spontaneous pulmonary hypertension because of insufficient capacity of the pulmonary capillaries.

Cold stress, even briefly, during the first 3 wk of life is known to markedly increase predisposition to ascites syndrome. In poultry, liver damage may be caused by aflatoxin or by toxins from plants such as Crotalaria.

In broiler chickens, obstructive cholangiohepatitis caused by Clostridium perfringens infection is the most common cause of the liver damage, which results in ascites. In both meat-type ducks and breeders, amyloidosis of the liver may also cause ascites. The resultant volume and pressure overload on the right ventricle cause dilatation and hypertrophy of the right ventricular wall, valvular insufficiency, RVF, and ascites.

Bird lungs are rigid and fixed in the thoracic cavity. The capillaries can expand very little to accommodate increased blood flow. Lung size in proportion to body weight, and particularly to muscle mass, decreases as meat-type chickens grow. Increased blood flow results in primary pulmonary hypertension and cor pulmonale with sporadic cases of RVF and ascites in fast-growing broilers.

Predisposing factors that increase oxygen demand eg, cold , reduce oxygen-carrying capacity of the blood eg, acidosis, carbon monoxide , increase blood volume eg, sodium , or interfere with blood flow through the lung eg, lung pathology that narrows or occludes capillaries, increased RBC rigidity, or polycythemia with increased blood viscosity may result in flock outbreaks of pulmonary hypertension syndrome with or without ascites.

Right ventricular hypertrophy is the response to an increased workload and eventually leads to RVF if the volume or pressure load persists. Hypertrophy and dilatation of the right ventricular wall is directly related to pulmonary hypertension, and the ratio of the right ventricle to the total ventricular mass can be used as a measure of the increased pressure load on the right ventricle.

Occasionally, young broilers develop pulmonary hypertension syndrome, particularly if increased sodium or lung pathology eg, aspergillosis is involved, but mortality is greatest after 5 wk of age. There are no signs until RVF occurs and ascites develops. Clinically affected broilers are cyanotic, the abdominal skin may be red, and peripheral vessels congested.

Because growth stops as RVF develops, affected broilers may be smaller than their pen mates. However, rapid growth rate is a known predisposing factor, and sometimes the largest broilers are affected, with occurrence in males more frequent than in females. The ascites increases the respiratory rate and reduces exercise tolerance. Affected broilers frequently die on their backs. Not all broilers that die from pulmonary hypertension syndrome have ascites.

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An urgent care is a place where you can be seen more quickly and at a… Read more ». Symptoms you may first notice: Fatigue Swelling in your ankles, feet and legs Weight gain Increased need to urinate, especially at night Symptoms that indicate your condition has worsened: Irregular heartbeat A cough that develops from congested lungs Wheezing Shortness of breath, which may indicate pulmonary edema.

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There are a few of types of heart failure you need to know: Left-sided heart failure : The most common type of heart failure is left-sided heart failure. Other manifesting signs which usually signify an underlying disease condition in ascetic pets may include syncope, vomiting, obtundation, seizure, anaemia which manifests as pale mucous membrane, weakness and rapid panting.

The identification and diagnosis of the cause of ascites may not be a straightforward procedure and could be complicated due to the several causative factors. This only means that diagnosis should start with the basis of thorough physical examination of the entire body and clinical examinations. A well and sequential conduction of physical and clinical examinations serves as a pointer to the underlying cause of ascites.

However this may not always be so as diagnosis oftentimes is cumbersome. In such situations diagnosis would include a complete blood count which may reveal evidence of bacterial infection. Knowledge of the blood biochemistry including total protein, albumin, creatinine and urea, liver enzymes and coagulation profile would help in revealing cases of hypoalbuminaemia, hypoproteinaemia and hepatic and kidney diseases [ 5 ].

Cardiac diseases may be diagnosed with the aid of electrocardiograph. Cardiac auscultation detects cases of cardiac murmurs and arrhythmia. Abdominal paracentesis is a useful procedure usually carried out to reduce the fluid level and alleviate complications of dyspnea.

Paracentesis is a useful procedure in the management of ascites which is instituted in conjunction with appropriate treatment of the underlying cause. Once appropriate diagnosis is made, treatment usually comes easy by alleviating life-threatening conditions such as dyspnea and administering appropriate therapy as the case may be. The purpose of this review is primarily focused on the various causes of ascites with emphasis on the hepatic origin. Based on this premise, ascites is classified broadly into hepatic, pre-hepatic and post-hepatic origin: Pre-hepatic causes emanate from portal vein thrombosis, bacterial infection such as tuberculosis, malnutrition, hypoalbuminaemia and parasitic diseases such as strongyloidosis and entamoeba [ 6 ].

Other causes include trauma or rupture of the lymphatic vessels, blood vessels and urinary bladder, renal failure, lymphoma and neoplasm of various kinds including breast, bronchus, ovary, gastric, pancreatic or colonic neoplasms [ 7 ]. Post-hepatic causes might include congestive heart failure often linked with pulmonary hypertension, left-sided heart failure, right-sided heart failure, constrictive pericarditis, Budd-Chiari syndrome and stricture web formation in the inferior vena cava [ 8 , 9 ].

Hepatic origin emanates from various hepatic diseases including cirrhosis, portal hypertension and hepatitis. Earlier classification of ascites was centred on two broad categories, transudates and exudates, based on the total protein concentration of ascetic fluid.

Both transudates and exudates were subcategorised into modified transudates and exudates based on the level of total protein concentration in the ascetic fluid.

A more recent classification of ascites has endorsed the use of serum ascites albumin gradient SAAG in diagnosis of ascites [ 14 ]. The SAAG is derived by subtracting the ascetic fluid albumin level from the serum albumin level obtained on the same day [ 14 ].

Gradients greater than 1. Gradients less than 1. Ascites is one of the cardinal complications in liver cirrhosis in most patients [ 8 ]. Onset of ascites naturally connotes decompensated underlying liver cirrhosis which also signifies poor prognosis with short life expectancy [ 10 , 17 , 18 ].

Several factors contribute to the development of cirrhosis. The heart, for instance, plays an important role through a complex mechanism in the development of liver disease. The mechanism through which the heart and liver affect each other in the development of ascites is yet to be fully elucidated [ 14 ].

Several circulatory abnormalities observed in cirrhotic patients promulgated the peripheral arterial vasodilation hypothesis proposed in the last century [ 19 ]. The circulatory abnormalities manifest as increased cardiac output, portal hypertension, peripheral vascular resistance, arterial hypotension and splanchnic vasodilation [ 6 , 20 ]. Circulatory abnormalities from cardiac disease affect circulatory volume with a resultant decrease in tissue perfusion affecting majorly the kidney functionality [ 21 ].

Earlier in the disease, renal dysfunction is less expressed; however, with disease advancement the patient may experience difficulty in sodium excretion and consequent sodium and water retention [ 22 ]. Cirrhotic ascites basically develop from failure in renal excretion of sodium [ 22 ]. Different mechanisms also play a role in ascites in cirrhosis.

Intrinsic factors including arterial vasodilation affect the blood pressure hormones such as the renin-angiotensin-aldosterone system RAAS which stimulates sodium reabsorption from the distal nephron [ 22 ].

The sympathetic nervous system SNS induces renal constriction and sodium reabsorption from the tubules with ascites [ 23 , 24 ]. The portal vein is a major vein comprising of a group of veins which supply the visceral organs including the abdomen, pancreas, intestine, etc.

These veins bifurcate into smaller vessels in the hepatic tissue. Intrinsic factors and disease conditions such as cirrhosis result in blockage of these tiny veins in the hepatic tissue increasing the blood pressure in the veins with resultant portal hypertension.

Other causes of portal hypotension include portal vein thrombosis, schistosomosis, idiopathy, etc. Ascites develops in portal hypertension when the post-sinusoidal gradient is above 12 mmHg [ 25 ]. Portal hypertension elevates the hydrostatic pressure within the hepatic sinusoids permitting seepage of transudate into the peritoneal cavity [ 26 , 27 ].

Signs and symptoms of portal hypertension include haematuria, dysentery, bloody vomitus due to spontaneous rupture and haemorrhage from varices, encephalopathy due to abnormal liver function and thrombocytopaenia.

Factors such as abnormal increase in nitric oxide production and circulation of endogenous vasoconstriction such as catecholamines, leukotrienes and angiotensin II enhance hepatic vascular resistance and portal hypertension [ 30 , 31 ]. One of the complications of activation of RAAS and SNS in cirrhosis is the resultant renal vasoconstriction leading to decrease in renal perfusion and glomerular filtrate rate which progresses to renal impairment [ 21 , 22 , 32 , 33 ].

In hepatorenal syndrome, there are no significant morphological changes in renal histology, while the patients largely retain normal tubular function [ 5 , 21 ]. Most patients with cirrhosis have their creatinine level below 1.

Hepatorenal syndrome manifests in two different types in cirrhotic patients. Type I HRS is a fulminating form of the disease rapidly progressing to acute renal failure often precipitated by variceal bleeding, septic infection and spontaneous bacteria peritonitis with poor prognosis of days to weeks [ 22 ]. Type 2 is a more chronic form of HRS.

Most patients with this form of disease have a more stable creatinine concentration with only signs of refractory ascites due to unresponsive diuretics [ 34 , 35 ].

With advancement in cirrhosis, there is also progressive increase in sodium and water reabsorption and decrease in renal blood flow and glomerular filtration [ 36 ]. The imbalance from renal vasodilatory mechanism and the intrinsic vasoconstrictor enhances vasoconstriction and hypoperfusion and decreases GFR with ultimate result of renal failure [ 22 ].

Usually there is no laid down procedure on the steps to diagnose ascites; however a systematic approach applied in various disease conditions is advantageous in making appropriate diagnosis. A step-by-step approach normally starts with physical examination. In physical examination, the patient is examined for the presence of ticks and fleas which would contribute in physical discomfort of the pet.

Anaemia is detected by the appearance of pale mucous membrane of the eye and the gum. A distended or pulsating jugular vein in the neck region may indicate cardiovascular abnormality. Yellowish discoloration of the eye indicates jaundice and hepatic disease. Generalised lymphadenopathy may suggest lymphosarcoma and other inflammatory disease conditions.

Respiratory distress could manifest in the form of rapid panting. Such condition presents a deviation from the normal respiratory pattern, from coastal to costo-abdominal or abdominal pattern. Black tarry-coloured faeces from gastrointestinal bleeding may signify ancylostomosis and portal hypertension.

Physical examination of the trunk reveals a distended abdomen. The content of the abdomen could either be by pregnancy, abdominal masses, fluid of various consistencies or organ enlargement.

The diagnosis of ascites starts from differentiating these possibilities through various procedures. First is to carry out abdominal ballottement using clinched fist. This technique can be used to differentiate abdominal masses from fluid. It can be used with other laboratory tests such as pregnancy test to rule out pregnancy. It however has some limitations in differentiating abdominal masses from organ enlargement.

Abdominal ultrasound is a better option in differentiating abdominal contents. It has been proven effective in the detection of ascetic fluid, its site of production and differentiation of ascetic nature from transudates and exudates [ 11 ].

A recent research has shown the possibility of the use of echotexture of ascetic fluid in the detection of the cause of ascites in patients [ 11 ]. Abdominal paracentesis however is a very useful technique in differentiation of ascetic fluid [ 28 ]. A well-applied paracentesis without contamination of abdominal content is essential in differentiation of ascetic fluid.