The epithelium of the trachea, bronchi, or gastrointestinal tract may be involved in SJS and TEN. Ocular symptoms are the most common complication in TEN, experienced by 20–79% of those with TEN, even by those who do not experience immediate ocular manifestations. These can include dry eyes, photophobia, symblepharon, corneal scarring or xerosis, subconjunctival fibrosis, trichiasis, decreased visual acuity, and blindness. Cause
Drug reactions have been reported to cause 80–95% of TEN cases.The drugs most often implicated in TEN are:

antibiotics
sulfonamides (sulfamethoxazole, sulfadiazine, sulfapyridine)
beta-lactams (cephalosporins, penicillins, carbapenems)
nonsteroidal anti-inflammatory drugs
allopurinol
antimetabolites (methotrexate)
antiretroviral drugs (nevirapine)
corticosteroids
anxiolytics (chlormezanone)
anticonvulsants (phenobarbital, phenytoin, carbamazepine, lamotrigine, and valproic acid).TEN has also been reported to result from infection with Mycoplasma pneumoniae or dengue virus. Contrast agents used in imaging studies as well as transplantation of bone marrow or organs have also been linked to TEN development. HIV
HIV-positive individuals have 1000 times the risk of developing SJS/TEN compared to the general population. The reason for this increased risk is not clear. Genetics
Certain genetic factors are associated with increased risk of TEN. For example, certain HLA-types such as, HLA-B*1502, HLA-A*3101, HLA-B*5801, and HLA‐B*57:01 have been seen to be linked with TEN development when exposed to specific drugs. Pathogenesis
The immune systems role in the precise pathogenesis of TEN remains unclear. It appears that a certain type of immune cell (cytotoxic CD8+ T cell) is primarily responsible for keratinocyte death and subsequent skin detachment. Keratinocytes are the cells found lower in the epidermis and specialize in holding the surrounding skin cells together.
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 10% of patients with ascites which is called hepatic hydrothorax. It 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). Treatment
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. See also
Pleural effusion
Pneumothorax

References

https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/hydrothorax
Garbuzenko D.V., Arefyev N.O. Hepatic hydrothorax: An update and review of the literature. World J. Hepatol. 2017; 9 (31): 1197-1204


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