Routine complete blood count (CBC), basic metabolic profile, liver enzymes, and coagulation should be performed. Most experts recommend a diagnostic paracentesis be performed if the ascites is new or if the patient with ascites is being admitted to the hospital. The fluid is then reviewed for its gross appearance, protein level, albumin, and cell counts (red and white). Additional tests will be performed if indicated such as microbiological culture, Gram stain and cytopathology.

The "serum-ascites albumin gradient" (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites. A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertensive as a cause.

Ultrasound investigation is often performed prior to attempts to remove fluid from the abdomen. This may reveal the size and shape of the abdominal organs, and Doppler studies may show the direction of flow in the portal vein, as well as detecting Budd-Chiari syndrome (thrombosis of the hepatic vein) and portal vein thrombosis. Additionally, the sonographer can make an estimation of the amount of ascitic fluid, and difficult-to-drain ascites may be drained under ultrasound guidance. An abdominal CT scan is a more accurate alternate to reveal abdominal organ structure and morphology.

Ascites exists in three grades:

- Grade 1: mild, only visible on ultrasound and CT

- Grade 2: detectable with flank bulging and shifting dullness

- Grade 3: directly visible, confirmed with the fluid wave/thrill test

Diagnosis is made by paracentesis (needle aspiration of the ascitic fluid). SBP is diagnosed if the fluid contains neutrophils (a type of white blood cell) at greater than 250 cells per mm (equals a cell count of 250 x10/L) fluid in the absence of another reason for this (such as inflammation of one of the internal organs or a perforation). The fluid is also cultured to identify bacteria. If the sample is sent in a plain sterile container 40% of samples will identify an organism, while if the sample is sent in a bottle with culture medium the sensitivity increases to 72–90%.

Patients with ascites underwent routine paracentesis, the incidence of active SBP ranged from 10% to 27% at the time of hospital admission.

Because it is rare and has a wide spectrum of clinical, histological, and imaging features, diagnosing lymphangiomatosis can be challenging. Plain x-rays reveal the presence of lytic lesions in bones, pathological fractures, interstitial infiltrates in the lungs, and chylous effusions that may be present even when there are no outward symptoms.

The most common locations of lymphangiomatosis are the lungs and bones and one important diagnostic clue is the coexistence of lytic bone lesions and chylous effusion. An isolated presentation usually carries a better prognosis than does multi-organ involvement; the combination of pleural and peritoneal involvement with chylous effusions and lytic bone lesions carries the least favorable prognosis.

When lung involvement is suspected, high resolution computed tomography (HRCT) scans may reveal a diffuse liquid-like infiltration in the mediastinal and hilar soft tissue, resulting from diffuse proliferation of lymphatic channels and accumulation of lymphatic fluid; diffuse peribronchovascular and interlobular septal thickening; ground-glass opacities; and pleural effusion. Pulmonary function testing reveals either restrictive pattern or a mixed obstructive/restrictive pattern. While x-rays, HRCT scan, MRI, ultrasound, lymphangiography, bone scan, and bronchoscopy all can have a role in identifying lymphangiomatosis, biopsy remains the definitive diagnostic tool.

Microscopic examination of biopsy specimens reveals an increase in both the size and number of thin walled lymphatic channels along with lymphatic spaces that are interconnecting and dilated, lined by a single attenuated layer of endothelial cells involving the dermis, subcutis, and possibly underlying fascia and skeletal muscle. Additionally, Tazelaar, et al., described a pattern of histological features of lung specimens from nine patients in whom no extrathoracic lesions were identified, which they termed "diffuse pulmonary lymphangiomatosis" (DPL).

Recognition of the disease requires a high index of suspicion and an extensive workup. Because of its serious morbidity, lymphangiomatosis must always be considered in the differential diagnosis of lytic bone lesions accompanied by chylous effusions, in cases of primary chylopericardium, and as part of the differential diagnosis in pediatric patients presenting with signs of interstitial lung disease.

The chest radiograph may appear relatively normal, even late in the disease, or may suggest hyperinflation only. As the disease progresses, the chest radiograph often demonstrates diffuse, bilateral and symmetric reticulonodular opacities, cysts, bullae or a "honeycomb" (i.e., pseudo fibrotic) appearance. Pleural effusion and pneumothorax may be apparent. Preservation of lung volumes in the presence of increased interstitial markings is a radiographic hallmark of LAM that helps distinguish it from most other interstitial lung diseases, in which alveolar septal and interstitial expansion tend to increase the lung’s elastic recoil properties and decreased lung volumes.

The high-resolution computed tomography (HRCT) chest scan is better than the chest radiograph to detect cystic parenchymal disease and is almost always abnormal at the time of diagnosis, even when the chest radiograph and pulmonary function assessments are normal. The typical CT shows diffuse round, bilateral, thin-walled cysts of varying sizes ranging from 1 to 45 mm in diameter. The numbers of cysts varies in LAM from a few to almost complete replacement of normal lung tissue. The profusion of cysts tends to be milder in patients with TSC-LAM than S-LAM, perhaps explained in part because TSC-LAM patients typically receive earlier screening. Pleural effusions are seen on CT in 12% of patients with S-LAM and 6% of patients with TSC-LAM. Other CT features include linear densities (29%), hilar or mediastinal lymphadenopathy (9%), pneumothorax, lymphangiomyoma, and thoracic duct dilation. Ground-glass opacities (12%) suggest the presence of interstitial edema due to lymphatic congestion. In patients with TSC, nodular densities on HRCT may represent multifocal micronodular pneumocyte hyperplasia (MMPH) made up of clusters of hyperplastic type II pneumocytes. MMPH may be present in males or females with TSC in the presence or absence of LAM, but not in patients with S-LAM. MMPH is not typically associated with physiologic or prognostic consequences, but one case of respiratory failure due to MMPH has been reported.

Diagnosis is through biopsy. The presence of hypoproteinemia, decreased blood lymphocytes, and decreased cholesterol support the diagnosis. Hypocalcemia (low calcium) is also seen due to poor absorption of vitamin D and calcium, and secondary to low protein binding of calcium. Medical ultrasonography may show s in the intestinal mucosa indicating dilated lacteals.

Treatment of hydrothorax is difficult for several reasons. The underlying condition needs to be corrected; however, often the source of the hydrothorax is end stage liver disease and correctable only by transplant. Chest tube placement should not occur. Other measures such as a TIPS procedure are more effective as they treat the cause of the hydrothorax, but have complications such as worsened hepatic encephalopathy.

The diagnosis is based on the combination of the symptoms. Generally, people are diagnosed with yellow nail syndrome if they have two or three of the three classical symptoms (yellow nails, lymphedema and lung problems). The nail changes are considered essential for the diagnosis, but they can be subtle.

Pulmonary function testing can show obstruction of the airways. People with pleural effusions may show evidence of restriction in lung volumes due to the fluid. Analysis of the fluid in pleural effusions generally shows high levels of protein but low levels of cholesterol and lactate dehydrogenase, but about 30% of effusions are chylous (chylothorax) in that they have the characteristics of lymph.

A lymphogram may be performed in people with lymphedema. This can show both under developed (hypoplastic) lymphatic ducts and dilated ducts. Dye may be found in the skin months after the initial test. Scintigraphy of lymph flow (lymphoscintigraphy) shows delays in drainage of lymph (sometimes asymmetrically), although this test can also be normal.

Thoracocentesis, pericardiocentesis, pleurodesis, ligation of thoracic duct, pleuroperitoneal shunt, radiation therapy, pleurectomy, pericardial window, pericardiectomy, thalidomide, interferon alpha 2b, Total Parenteral Nutrition (TPN), medium chain triglyceride (MCT) and high protein diet, chemotherapy, sclerotherapy, transplant;

When Budd–Chiari syndrome is suspected, measurements are made of liver enzyme levels and other organ markers (creatinine, urea, electrolytes, LDH).

Budd–Chiari syndrome is most commonly diagnosed using ultrasound studies of the abdomen and retrograde angiography. Ultrasound may show obliteration of hepatic veins, thrombosis or stenosis, spiderweb vessels, large collateral vessels, or a hyperechoic cord replacing a normal vein. Computed tomography (CT) or magnetic resonance imaging (MRI) is sometimes employed although these methods are generally not as sensitive. Liver biopsy is nonspecific but sometimes necessary to differentiate between Budd–Chiari syndrome and other causes of hepatomegaly and ascites, such as galactosemia or Reye's syndrome.

People with yellow nail syndrome have been found to have a moderately reduced lifespan compared to people without the condition.

Several studies have attempted to predict the survival of patients with Budd–Chiari syndrome. In general, nearly 2/3 of patients with Budd–Chiari are alive at 10 years. Important negative prognostic indicators include ascites, encephalopathy, elevated Child-Pugh scores, elevated prothrombin time, and altered serum levels of various substances (sodium, creatinine, albumin, and bilirubin). Survival is also highly dependent on the underlying cause of the Budd–Chiari syndrome. For example, a patient with an underlying myeloproliferative disorder may progress to acute leukemia, independently of Budd–Chiari syndrome.

Treatment is multifactorial. A diet very low in fat and high in high quality protein is essential. Treatment of humans can also involve the use of MCT (medium-chain triglycerides) oil and/or the drug octreotide. In dogs, fat soluble vitamins (A, D, E, and K) should be supplemented. Corticosteroid treatment may be required for life. Antibiotics can be used to treat bacterial overgrowth. With a very low serum albumin, transfusion with blood plasma or an infusion of hetastarch may be necessary to treat the signs until the diet can take effect. Lymphangiectasia is rarely cured but can remain in remission for a long time. It can be fatal when unresponsive to treatment.

Hepatic doppler ultrasound is typically utilized to confirm or suggest the diagnosis. Most common findings on liver doppler ultrasound include increased phasicity of portal veins with eventual development of portal flow reversal. The liver is usually enlarged but maintained normal echogenicity. A liver biopsy is required for a definitive diagnosis.

Hydrothorax is a type of pleural effusion in which transudate accumulates in the pleural cavity. This condition is most likely to develop secondary to congestive heart failure, following an increase in hydrostatic pressure within the lungs. More rarely, hydrothorax can develop in patients with cirrhosis or ascites. Hepatic hydrothorax is often difficult to manage in end-stage liver failure and often fails to respond to therapy.

Pleural effusions may also develop following the accumulation of other fluids within the pleural cavity; if the fluid is blood it is known as hemothorax (as in major chest injuries), if the fluid is pus it is known as pyothorax (resulting from chest infections), and if the fluid is lymph it is known as chylothorax (resulting from rupture of the thoracic duct).

In normal conditions, the peritoneum appears greyish and glistening; it becomes dull 2–4 hours after the onset of peritonitis, initially with scarce serous or slightly turbid fluid. Later on, the exudate becomes creamy and evidently suppurative; in dehydrated patients, it also becomes very inspissated. The quantity of accumulated exudate varies widely. It may be spread to the whole peritoneum, or be walled off by the omentum and viscera. Inflammation features infiltration by neutrophils with fibrino-purulent exudation.

The diagnosis of plastic bronchitis is confirmed by recovery of casts that have been coughed up or visualized during a bronchoscopy. There is no specific cytologic, pathologic or laboratory test that is diagnostic for casts due to lymphatic PB.

A diagnosis of peritonitis is based primarily on the clinical manifestations described above. Rigidity (involuntary contraction of the abdominal muscles) is the most specific exam finding for diagnosing peritonitis (+ likelihood ratio: 3.9). If peritonitis is strongly suspected, then surgery is performed without further delay for other investigations. Leukocytosis, hypokalemia, hypernatremia, and acidosis may be present, but they are not specific findings. Abdominal X-rays may reveal dilated, edematous intestines, although such X-rays are mainly useful to look for pneumoperitoneum, an indicator of gastrointestinal perforation. The role of whole-abdomen ultrasound examination is under study and is likely to expand in the future. Computed tomography (CT or CAT scanning) may be useful in differentiating causes of abdominal pain. If reasonable doubt still persists, an exploratory peritoneal lavage or laparoscopy may be performed. In patients with ascites, a diagnosis of peritonitis is made via paracentesis (abdominal tap): More than 250 polymorphonucleate cells per μL is considered diagnostic. In addition, Gram stain is almost always negative, whereas culture of the peritoneal fluid can determine the microorganism responsible and determine their sensitivity to antimicrobial agents.

Simple chest roentenograms may reveal collapse due to airway obstruction. The contralateral lung may be hyperinflated. Casts can be visualized within the major airways using computerized axial tomography scans.

Heavy T2-weighted MRI, and, as appropriate, intranodal lymphangiogram and/or dynamic contrast-enhanced MR lymphangiography may be useful for identifying pathological lymphatic tissue and/or lymphatic flow.

The risk of the development of a lymphocele is positively correlated to the extent of the removal of lymphatic tissue during surgery (lymphadenectomy). Surgery destroys and disrupts the normal channels of lymph flow. If the injury is minor, collateral channels will transport lymph fluid, but with extensive damage, fluid may accumulate in an anatomic space resulting in a lymphocele. Typical operations leading to lymphocysts are renal transplantation and radical pelvic surgery with lymph node removal because of prostatic or gynecologic cancer. Other factors that may predispose of lymphocele development are preoperative radiation therapy, heparin prophylaxis (used to prevent deep vein thrombosis), and tumor characteristics. After radical surgery for cervical and ovarian cancer studies with follow-up CT found lymphoceles in 20% and 32%, respectively. Typically they develop within 4 months after surgery.

Pleural or ascitic fluid should be sent for analysis. An elevated amylase level, usually > 1,000 IU/L, with protein levels over 3.0 g/dL is diagnostic. Serum amylase is often elevated as well, due to enzyme diffusion across the peritoneal or pleural surface. Contrast-enhanced computed tomography and endoscopic retrograde cholangiopancreatography (ERCP) may also assist in diagnosis, with the latter an essential component of treatment.

Mild disease has a risk of death of about 10% while moderate disease has a risk of death of 20%. When it occurs as a result of bone marrow transplant and multiorgan failure is present, the risk of death is greater than 80%.

It has been suggested that suction drains placed during surgery and non-peritonisation (not closing the posterior peritoneum) may reduce the possibility of lymphocele development.

Smaller lymphoceles can be managed expectantly, and many lesions will regress over time. For symptomatic lesions a number of approaches are available and include fine needle aspiration with US or CT guidance, catheter insertion and drainage (with possible use of sclerosants), and surgical drainage. Sex and masturbation may cause the lymphocele to grow if it is in the genital area. It is suggested to avoid these activities for around one to one and a half months. Some exercises may also help to shrink it.