Drug-induced pulmonary disease

Author and Disclosure Information


Drugs are capable of producing a variety of adverse pulmonary responses. Part 2 deals with drugs classified by pharmacological action. A homogeneous type of reaction may be seen within a particular group of drugs. However, this section is primarily designed to provide a more accessible reference for such a large number of therapeutic agents.


Analgesic and anti-inflammatory drugs are included in the ASA triad and narcotic analgesics. Carbamazepine has already been discussed in Part 1. Narcotics produce a dose-dependent central respiratory depression. Most of the adverse pulmonary responses are caused by the illicit use of narcotic drugs and will be discussed under that section.

Overdoses of acetylsalicylic acid (ASA) can produce central respiratory stimulation and noncardiogenic pulmonary edema. Therapeutic serum levels are in the 10 to 20 mg/dl range. At levels of 35 m g/dl, respiratory alkalosis occurs. Severe hyperpnea is manifest at levels of 50 mg/dl.1 At a serum level of 45 mg/dl (about 70 tablets), noncardiogenic pulmonary edema occurs.2 The pulmonary capillary wedge pressure is normal and the chest roentgenogram takes 3 to 8 days to clear. Increased vascular permeability, pulmonary lymph flow, and lymph protein clearance have been observed in experimental studies.3

The ASA triad is characterized by asthma, nasal polyposis, and drug sensitivity. It was initially described following the use of ASA, but other medications are also capable of producing this reaction (Table 1). The first manifestation of the syndrome is vasomotor rhinitis with a watery discharge. Typically this develops in the second or . . .



Next Article: