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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.
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).
When a pleural effusion has been determined to be exudative, additional evaluation is needed to determine its cause, and amylase, glucose, pH and cell counts should be measured.
- Red blood cell counts are elevated in cases of bloody effusions (for example after heart surgery or hemothorax from incomplete evacuation of blood).
- Amylase levels are elevated in cases of esophageal rupture, pancreatic pleural effusion, or cancer.
- Glucose is decreased with cancer, bacterial infections, or rheumatoid pleuritis.
- pH is low in empyema (<7.2) and may be low in cancer.
- If cancer is suspected, the pleural fluid is sent for cytology. If cytology is negative, and cancer is still suspected, either a thoracoscopy, or needle biopsy of the pleura may be performed.
- Gram staining and culture should also be done.
- If tuberculosis is possible, examination for "Mycobacterium tuberculosis" (either a Ziehl–Neelsen or Kinyoun stain, and mycobacterial cultures) should be done. A polymerase chain reaction for tuberculous DNA may be done, or adenosine deaminase or interferon gamma levels may also be checked.
The most common causes of exudative pleural effusions are bacterial pneumonia, cancer (with lung cancer, breast cancer, and lymphoma causing approximately 75% of all malignant pleural effusions), viral infection, and pulmonary embolism.
Another common cause is after heart surgery, when incompletely drained blood can lead to an inflammatory response that causes exudative pleural fluid.
Conditions associated with exudative pleural effusions:
- Parapneumonic effusion due to pneumonia
- Malignancy (either lung cancer or metastases to the pleura from elsewhere)
- Infection (empyema due to bacterial pneumonia)
- Trauma
- Pulmonary infarction
- Pulmonary embolism
- Autoimmune disorders
- Pancreatitis
- Ruptured esophagus (Boerhaave's syndrome)
- Rheumatoid pleurisy
- Drug-induced lupus
The most common causes of transudative pleural effusions in the United States are heart failure and cirrhosis. Nephrotic syndrome, leading to the loss of large amounts of albumin in urine and resultant low albumin levels in the blood and reduced colloid osmotic pressure, is another less common cause of pleural effusion. Pulmonary emboli were once thought to cause transudative effusions, but have been recently shown to be exudative.
The mechanism for the exudative pleural effusion in pulmonary thromboembolism is probably related to increased permeability of the capillaries in the lung, which results from the release of cytokines or inflammatory mediators (e.g. vascular endothelial growth factor) from the platelet-rich blood clots. The excessive interstitial lung fluid traverses the visceral pleura and accumulates in the pleural space.
Conditions associated with transudative pleural effusions include:
- Congestive heart failure
- Liver cirrhosis
- Severe hypoalbuminemia
- Nephrotic syndrome
- Acute atelectasis
- Myxedema
- Peritoneal dialysis
- Meigs' syndrome
- Obstructive uropathy
- End-stage kidney disease
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.
Death occurs immediately after traumatic rupture of the thoracic aorta 75%–90% of the time since bleeding is so severe, and 80–85% of patients die before arriving at a hospital. Of those who live to reach a hospital, 23% die at the time of or shortly after arrival. In the US, an estimated 7,500–8,000 cases occur yearly, of which 1,000–1,500 make it to a hospital alive; these low numbers make it difficult to estimate the efficacy of surgical options. However, if surgery is performed in time, it can offer a chance of survival.
Though there is a concern that a small, stable tear in the aorta could enlarge and cause complete rupture of the aorta and heavy bleeding, this may be less common than previously believed as long as the patient's blood pressure does not get too high.
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.
Traumatic aortic rupture is treated with surgery. However, morbidity and mortality rates for surgical repair of the aorta for this condition are among the highest of any cardiovascular surgery. For example, surgery is associated with a high rate of paraplegia, because the spinal cord is very sensitive to ischemia (lack of blood supply), and the nerve tissue can be damaged or killed by the interruption of the blood supply during surgery.
A less invasive option for treatment is endovascular repair, which does not require open thoracotomy and can be safer for people with other injuries to organs.
Since high blood pressure could exacerbate an incomplete tear in the aorta or even separate it completely from the heart, which would almost inevitably kill the patient, hospital staff take measures to keep the blood pressure low. Such measures include giving pain medication, keeping the patient calm, and avoiding procedures that could cause gagging or vomiting. Beta blockers and vasodilators can be given to lower the blood pressure, and intravenous fluids that might normally be given are foregone to avoid raising it.
Alcohol consumption does not appear to be related to ovarian cancer. Other factors that have been investigated, such as smoking, low levels of vitamin D in the blood, presence of inclusion ovarian cysts, and infection with human papilloma virus (the cause of some cases of cervical cancer), have been disproven as risk factors for ovarian cancer. The carcinogenicity of perineal talc is controversial, because it can act as an irritant if it travels through the reproductive tract to the ovaries. Case-control studies have shown that use of perineal talc does increase the risk of ovarian cancer, but using talc more often does not create a greater risk. Use of talc elsewhere on the body is unrelated to ovarian cancer. Sitting regularly for prolonged periods is associated with higher mortality from epithelial ovarian cancer. The risk is not negated by regular exercise, though it is lowered.
Increased age (up to the 70s) is a risk factor for epithelial ovarian cancer because more mutations in cells can accumulate and eventually cause cancer. Those over 80 are at slightly lower risk.
Smoking tobacco is associated with a higher risk of mucinous ovarian cancer; after smoking cessation, the risk eventually returns to normal.A diet high in animal fats may be associated with ovarian cancer, but the connection is unclear. Diet seems to play a very small role, if any, in ovarian cancer risk.
Higher levels of C-reactive protein are associated with a higher risk of developing ovarian cancer.
Industrialized nations, with the exception of Japan, have high rates of epithelial ovarian cancer, which may be due to diet in those countries. Caucasian are at a 30–40% higher risk for ovarian cancer when compared to Black and Hispanic people, likely due to socioeconomic factors; white women tend to have fewer children and different rates of gynecologic surgeries that affect risk for ovarian cancer.
Cohort studies have found a correlation between dairy consumption and ovarian cancer, but case-control studies do not show this correlation. There is mixed evidence regarding the effect of red meat and processed meat in ovarian cancer.
Tentative evidence suggests that talc, pesticides, and herbicides increase the risk of ovarian cancer. The American Cancer Society notes that as of now, no study has been able to accurately link any single chemical in the environment, or in the human diet, directly to mutations that cause ovarian cancer.
Sporadic OHSS is very rare, and may have a genetic component. Clomifene citrate therapy can occasionally lead to OHSS, but the vast majority of cases develop after use of gonadotropin therapy (with administration of FSH), such as Pergonal, and administration of hCG to induce final oocyte maturation and/or trigger oocyte release, often in conjunction with IVF. The frequency varies and depends on a woman's risk factors, management, and methods of surveillance. About 5% of treated women may encounter moderate to severe OHSS. Risk factors include young age, the development of many ovarian follicles under stimulation, extreme elevated serum estradiol concentrations, the use of hCG for final oocyte maturation and/or release, the continued use of hCG for luteal support, and the occurrence of a pregnancy (resulting in hCG production).
Mortality is low, but several fatal cases have been reported.
Proteinuria may be a feature of the following conditions:
- Nephrotic syndromes (i.e. intrinsic renal failure)
- Pre-eclampsia
- Eclampsia
- Toxic lesions of kidneys
- Amyloidosis
- Collagen vascular diseases (e.g. systemic lupus erythematosus)
- Dehydration
- Glomerular diseases, such as membranous glomerulonephritis, focal segmental glomerulonephritis, minimal change disease (lipoid nephrosis)
- Strenuous exercise
- Stress
- Benign orthostatic (postural) proteinuria
- Focal segmental glomerulosclerosis (FSGS)
- IgA nephropathy (i.e. Berger's disease)
- IgM nephropathy
- Membranoproliferative glomerulonephritis
- Membranous nephropathy
- Minimal change disease
- Sarcoidosis
- Alport's syndrome
- Diabetes mellitus (diabetic nephropathy)
- Drugs (e.g. NSAIDs, nicotine, penicillamine, lithium carbonate, gold and other heavy metals, ACE inhibitors, antibiotics, or opiates (especially heroin)
- Fabry's disease
- Infections (e.g. HIV, syphilis, hepatitis, poststreptococcal infection, urinary schistosomiasis)
- Aminoaciduria
- Fanconi syndrome in association with Wilson disease
- Hypertensive nephrosclerosis
- Interstitial nephritis
- Sickle cell disease
- Hemoglobinuria
- Multiple myeloma
- Myoglobinuria
- Organ rejection:
- Ebola virus disease
- Nail patella syndrome
- Familial Mediterranean fever
- HELLP Syndrome
- Systemic lupus erythematosus
- Granulomatosis with polyangiitis
- Rheumatoid arthritis
- Glycogen storage disease type 1
- Goodpasture's syndrome
- Henoch–Schönlein purpura
- A urinary tract infection which has spread to the kidney(s)
- Sjögren's syndrome
- Post-infectious glomerulonephritis
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.
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.