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).

A pleural effusion is excess fluid that accumulates in the pleural cavity, the fluid-filled space that surrounds the lungs. This excess can impair breathing by limiting the expansion of the lungs. Various kinds of pleural effusion, depending on the nature of the fluid and what caused its entry into the pleural space, are hydrothorax (serous fluid), hemothorax (blood), urinothorax (urine), chylothorax (chyle), or pyothorax (pus). A pneumothorax is the accumulation of air in the pleural space, and is commonly called a "collapsed lung."

Various methods can be used to classify pleural fluid.

By the origin of the fluid:

- Serous fluid (hydrothorax)

- Blood (haemothorax)

- Chyle (chylothorax)

- Pus (pyothorax or empyema)

- Urine (urinothorax)

By pathophysiology:

- Transudative pleural effusion

- Exudative pleural effusion

By the underlying cause (see next section).

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.

Meigs syndrome may mimic other conditions, since it is tumor arising from ovaries, pathology of any organs present in the abdomen may show a similar set of symptoms. Various gynecological disorders of the uterus such as endometrial tumor, sarcoma, leiomyoma (pseudo-Meigs syndrome); fallopian tube disorders such as hydrosalpinx, granulomatous salpingitis, fallopian tube malignancy; ovarian disorders such as serous, mucinous, endometrioid, or clear cell carcinoma, Brenner tumor, granulosa cell tumor, stromal tumor, dysgerminoma, fibroma, or metastatic tumor to the ovary.

Meigs syndrome is characterized by the presence of a benign solid ovarian tumor associated with ascites and right hydrothorax that disappear after tumor removal. Non-gynecological manifestations include:

ascites, portal vein obstruction, inferior vena cava obstruction, hypoproteinaemia, thoracic duct obstruction, tuberculosis, amyloidosis, pancreatitis, ovarian hyperstimulation, pleural effusion transudative, congestive heart failure, metastatic tumors to the peritoneal surfaces, collagen-vascular disease, and cirrhosis of the liver.

These entities must be clinically excluded.

Clinical condition characterized by ovarian mass, ascites, and right-sided pleural effusion.Ovarian malignancy and the

other causes (see “Differential Diagnosis”) of pelvic mass, ascites, and pleural effusion to be considered, History of early satiety,

weight loss with increased abdominal girth, bloating, intermittent abdominal pain, dyspnea, nonproductive cough may help in differentiating potential local factor causing such symptoms.

In medicine, Meigs' syndrome, also Meigs syndrome or Demons-Meigs syndrome, is the triad of ascites, pleural effusion, and benign ovarian tumor (ovarian fibroma, fibrothecoma, Brenner tumour, and occasionally granulosa cell tumour). Meigs' syndrome resolves after the resection of the tumor. Because the transdiaphragmatic lymphatic channels are larger in diameter on the right, the pleural effusion is classically on the right side. The causes of the ascites and pleural effusion are poorly understood. Atypical Meigs' syndrome, characterized by a benign pelvic mass with right-sided pleural effusion but without ascites, can also occur. As in Meigs syndrome, pleural effusion resolves after removal of the pelvic mass.

The condition is difficult to detect and may go unnoticed, because many patients have no specific symptoms. Diagnosis is further complicated by the fact that many patients with the injury experienced multiple other serious injuries as well, so the attention of hospital staff may be distracted from the possibility of aortic rupture. In fact most cases occur along with other injuries.

A common symptom is unusually high blood pressure in the upper body and very low blood pressure in lower limbs. Another symptom is renal failure where the creatinine level shoots very high and urine output becomes negligible. In most cases, however, the doctors would misinterpret renal failure as due to issues with the kidney itself and may recommend dialysis.

Though not completely reliable, chest X-rays are the first-line treatment, initially used to diagnose this condition when the patient is unstable and cannot be sent to the CT bay. The preferred method of diagnosis used to be CT angiogram until it was found to cause complications in some people; now it is reserved for when CT scans are inconclusive.

The classical findings on a chest X-ray will be widened mediastinum, apical cap, and displacement of the trachea, left main bronchus, or nasogastric tube. A normal chest x-ray does not exclude transection, but will diagnose conditions such as pneumothorax or hydrothorax. The aorta may also be torn at the point where it is connected to the heart. The aorta may be completely torn away from the heart, but patients with such injuries rarely survive very long after the injury; thus it is much more common for hospital staff to treat patients with partially torn aortas. When the aorta is partially torn, it may form a "pseudoaneurysm". In patients who do live long enough to be seen in a hospital, a majority have only a partially torn blood vessel, with the outermost adventitial layer still intact. In some of these patients, the adventitia and nearby structures within the chest may serve to prevent severe bleeding. After trauma, the aorta can be assessed by a CT angiogram or a direct angiogram, in which contrast is introduced into the aorta via a catheter.

Traumatic aortic rupture, also called traumatic aortic disruption or transection, is a condition in which the aorta, the largest artery in the body, is torn or ruptured as a result of trauma to the body. The condition is frequently fatal due to the profuse bleeding that results from the rupture. Since the aorta branches directly from the heart to supply blood to the rest of the body, the pressure within it is very great, and blood may be pumped out of a tear in the blood vessel very rapidly. This can quickly result in shock and death. Thus traumatic aortic rupture is a common killer in automotive accidents and other traumas, with up to 18% of deaths that occur in automobile collisions being related to the injury. In fact, aortic disruption due to blunt chest trauma is the second leading cause of injury death behind traumatic brain injury.

Aortic rupture can also be caused by non-traumatic mechanisms, particularly abdominal aortic aneurysm rupture.

OHSS is divided into the categories mild, moderate, severe, and critical.

In mild forms of OHSS the ovaries are enlarged (5–12 cm) and there may be additional accumulation of ascites with mild abdominal distension, abdominal pain, nausea, and diarrhea. In severe forms of OHSS there may be hemoconcentration, thrombosis, distension, oliguria (decreased urine production), pleural effusion, and respiratory distress. Early OHSS develops before pregnancy testing and late OHSS is seen in early pregnancy.

Criteria for severe OHSS include enlarged ovary, ascites, hematocrit > 45%, WBC > 15,000, oliguria, creatinine 1.0-1.5 mg/dl, creatinine clearance > 50 ml/min, liver dysfunction, and anasarca. Critical OHSS includes enlarged ovary, tense ascites with hydrothorax and pericardial effusion, hematocrit > 55%, WBC > 25,000, oligoanuria, creatinine > 1.6 mg/dl, creatinine clearance < 50 ml/min, renal failure, thromboembolic phenomena, and ARDS.

Ovarian hyperstimulation syndrome (OHSS) is a medical condition affecting the ovaries of some women who take fertility medication to stimulate egg growth. Most cases are mild, but rarely the condition is severe and can lead to serious illness or death.

The growing mass may cause pain if ovarian torsion develops. Symptoms can be caused by a mass pressing on the other abdominopelvic organs or from metastases. If these symptoms start to occur more often or more severely than usual, especially after no significant history of such symptoms, ovarian cancer is considered. Metastases may cause a Sister Mary Joseph nodule. Rarely, teratomas can cause growing teratoma syndrome or peritoneal gliomatosis. Some experience menometrorrhagia and abnormal vaginal bleeding after menopause in most cases. Other common symptoms include hirsutism, abdominal pain, virilization, and an adnexal mass.

Early signs and symptoms of ovarian cancer may be absent or subtle. In most cases, symptoms exist for several months before being recognized and diagnosed. Symptoms can be misdiagnosed as irritable bowel syndrome. The early stages of ovarian cancer tend to be painless. Symptoms can vary based on the subtype. Low malignant potential (LMP) tumors, also known as borderline tumors, do not cause an increase in CA125 levels and are not identifiable with an ultrasound. The typical symptoms of an LMP tumor can include abdominal distension or pelvic pain. Particularly large masses tend to be benign or borderline.

The most typical symptoms of ovarian cancer include bloating, abdominal or pelvic pain or discomfort, back pain, irregular menstruation or postmenopausal vaginal bleeding, pain or bleeding after or during sexual intercourse, loss of appetite, fatigue, diarrhea, indigestion, heartburn, constipation, nausea, feeling full, and possibly urinary symptoms (including frequent urination and urgent urination).

Proteinuria is the presence of excess proteins in the urine. In healthy persons, urine contains very little protein; an excess is suggestive of illness. Excess protein in the urine often causes the urine to become foamy, although foamy urine may also be caused by bilirubin in the urine (bilirubinuria), retrograde ejaculation, pneumaturia (air bubbles in the urine) due to a fistula, or drugs such as pyridium.

There are three main mechanisms to cause proteinuria:

- Due to disease in the glomerulus

- Because of increased quantity of proteins in serum (overflow proteinuria)

- Due to low reabsorption at proximal tubule (Fanconi syndrome)

Proteinuria can also be caused by certain biological agents, such as bevacizumab (Avastin) used in cancer treatment. Excessive fluid intake (drinking in excess of 4 litres of water per day) is another cause.

Also leptin administration to normotensive Sprague Dawley rats during pregnancy significantly increases urinary protein excretion.

Proteinuria may be a sign of renal (kidney) damage. Since serum proteins are readily reabsorbed from urine, the presence of excess protein indicates either an insufficiency of absorption or impaired filtration. People with diabetes may have damaged nephrons and develop proteinuria. The most common cause of proteinuria is diabetes, and in any person with proteinuria and diabetes, the cause of the underlying proteinuria should be separated into two categories: diabetic proteinuria versus the field.

With severe proteinuria, general hypoproteinemia can develop which results in

diminished oncotic pressure. Symptoms of diminished oncotic pressure may include ascites, edema and hydrothorax.