|Year : 2021 | Volume
| Issue : 1 | Page : 48-51
A case of noncardiogenic pulmonary edema and pleural effusion following diclofenac administration
Vinod Kumar, Vasantha Kamath, Shreyashi Ganguly
Department of Medicine, MVJ Medical College and Research Hospital, Hoskote, Bengaluru, Karnataka, India
|Date of Submission||18-Dec-2019|
|Date of Acceptance||12-Jan-2020|
|Date of Web Publication||03-Feb-2021|
Dr. Shreyashi Ganguly
309, Sai Charita Green Oaks, Hormavu Main Road, Bengaluru - 560 043, Karnataka
Source of Support: None, Conflict of Interest: None
The acute manifestations of diclofenac allergy vary from mild urticaria or skin rash to severe and life-threatening complications such as ARDS, and anaphylactic shock. Very few cases of diclofenac allergy have been reported in literature especially with respect to pulmonary manifestations. We are reporting a case of a 31-year-old who presented in respiratory distress consequent to diclofenac hypersensitivity. Our patient had non-cardiogenic pulmonary oedema and bilateral minimal pleural effusion 3 days following diclofenac administration. On examination the patient was conscious, alert and oriented, PR- 88 bpm, BP- 150/100 mmHg, RR-22 cpm temperature 98.6°F with oxygen saturation of 95% on room air. Her respiratory system examination revealed a dull note on percussion and decreased vocal fremitus, decreased vocal resonance, diminished air entry in bilateral infra scapular and infra axillary areas with fine inspiratory crepitations. The diagnosis of ARDS was ruled out as the ratio of PaO2 to FiO2 was 410. After treatment with I.V diuretics, antibiotics and inhalational bronchodilators she improved over a period of 5 days. She had complete resolution of her chest symptoms and chest findings both clinically and radiologically. Pulmonary manifestations such as ARDS, eosinophilic pneumonitis, pleural effusion, eosinophilic pneumonia, pulmonary oedema, hemoptysis, pulmonary infiltrates with eosinophilia and asthmatic attacks are rare. The temporal relationship between symptom onset and drug administration is the most important piece of history while making the diagnosis. History of allergic reaction to NSAIDs should be evaluated in detail. It is therefore important that the physician keep this in mind while prescribing.
Keywords: Diclofenac, hypersensitivity, noncardiogenic pulmonary edema, pleural effusion, pulmonary manifestationsa
|How to cite this article:|
Kumar V, Kamath V, Ganguly S. A case of noncardiogenic pulmonary edema and pleural effusion following diclofenac administration. APIK J Int Med 2021;9:48-51
|How to cite this URL:|
Kumar V, Kamath V, Ganguly S. A case of noncardiogenic pulmonary edema and pleural effusion following diclofenac administration. APIK J Int Med [serial online] 2021 [cited 2021 Apr 20];9:48-51. Available from: https://www.ajim.in/text.asp?2021/9/1/48/308655
| Introduction|| |
Diclofenac is a nonsteroidal anti-inflammatory agent with specific inhibiting actions on cyclo-oxygenase (COX)-1 and COX-2 with relative equipotency. The drug has been considered safer than other nonsteroidal anti-inflammatory drugs (NSAIDs) and is extensively used as an analgesic and antipyretic in both adults and children.
The acute manifestations of diclofenac allergy vary from mild urticaria or skin rash to severe and life-threatening complications such as acute respiratory distress syndrome (ARDS) and anaphylactic shock. Very few cases of diclofenac allergy have been reported in literature, especially with respect to pulmonary manifestations. We report a case of a 31-year-old female who presented in respiratory distress consequent to diclofenac hypersensitivity.
| Case Report|| |
A 31-year-old female patient presented to the hospital with complaints of acute breathlessness, exacerbated on exertion for 4 days. This was associated with generalized swelling of body and cough with scanty, frothy expectoration. The symptoms started after being injected with an intramuscular injection of diclofenac sodium.
The patient had a history of being administered intramuscular diclofenac sodium injection for the alleviation of acute low backache 3 days berore coming to the hospital. Following that, she developed the above-mentioned symptoms.
Her past medical history was unremarkable. She was not known to have any drug allergies. There was no history of atopy nor history of prior diclofenac administration.
On examination, the patient was conscious, was alert, and was oriented; his pulse rate was 88 bpm, blood pressure was 150/100 mmHg, respiratory rate was 22 cpm, and temperature was 98.6°F with oxygen saturation of 95% on room air.
Local examination of the injection site was normal. Her respiratory system examination revealed a dull note on percussion, decreased vocal fremitus, decreased vocal resonance, and diminished air entry in the bilateral infrascapular and infraaxillary areas with fine inspiratory crepitations. The rest of her physical examination was normal.
Urine routine revealed traces of albumin, and arterial blood gas analysis showed PaO2 of 88 mmHg. Electrocardiogram and two-dimensional echo were within normal limits. Rest of the investigations are summarized in [Table 1]. Of note is the fact that the absolute eosinophil count was 100 cells/mm, ruling out eosinophilic causes of pleural effusion, and pulmonary edema occurred in the setting of normal renal functions. [Figure 1] shows the serial chest X-rays taken in this patient.
|Figure 1: On presentation, the patient had evidence of pulmonary edema with pleural effusion. With subsequent treatment over time, the patient had complete resolution of the same findings|
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The patient had presented in acute respiratory distress. After treatment with intravenous diuretics, antibiotics, and inhalational bronchodilators, she improved over a period of 5 days. She had a complete resolution of her chest symptoms and chest findings both clinically and radiologically.
| Discussion|| |
Diclofenac is a phenylacetic acid derivative belonging to the group of carboxylic acids. Diclofenac is considered to be safe with worldwide administration of 7.6 million patients/year.
The exact incidence of pulmonary adverse events following diclofenac administration is unknown. Pulmonary manifestations due to diclofenac use reported in literature are rare with very few case reports.
Our patient had noncardiogenic pulmonary edema and bilateral minimal pleural effusion 3 days following diclofenac administration. The diagnosis of ARDS was ruled out as the ratio of PaO2 to FiO2 was 410 in our patient (PaO2/FiO2 in ARDS should be <300).
The pulmonary manifestations following diclofenac administration are ARDS, pneumonitis, pleural effusion, eosinophilic pneumonia, pulmonary infiltrates with eosinophilia (PIE), asthmatic attacks, pulmonary edema, and hemoptysis. These manifestations can occur after varying intervals from the time of administration of the drug as shown in [Table 2].
|Table 2: Interval between drug administration and onset of various pulmonary manifestations|
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The history of drug administration and its recent temporal relationship with appropriate symptoms and signs are important. Other relevant etiologies need to be carefully excluded in this setting before making a diagnosis.
The pathogenetic mechanisms that are responsible for drug-induced pulmonary edema remain unknown. Postulated explanations include capillary leak syndrome, hypervolemia, or anaphylaxis. Diagnosis rests on the exclusion of other disorders that may present in a similar fashion, such as congestive heart failure, diffuse pulmonary hemorrhage, or respiratory infection. Recovery is typically rapid after drug administration is discontinued. Oxygen therapy and diuretic therapy are often prescribed for pulmonary edema.
Pleural effusion following NSAID administration is reported in two cases: one in association with pneumonitis and the other in association with eosinophilic pneumonia.
Drug-induced ARDS is a relatively rare form of ARDS, but more than 200 drugs are known to cause it. Diclofenac is one among them. The clinical features and radiographic appearance of drug-induced ARDS are generally indistinguishable from other causes of pulmonary edema and ARDS. Diagnosis is often challenging and remains a diagnosis of exclusion.
NSAIDs such as diclofenac, sulindac, ibuprofen, and naproxen can induce allergic pneumonitis. Most patients will improve after drug discontinuation, although corticosteroids may be needed for severe or persistent cases.
Diclofenac and other NSAIDs such as naproxen, fenbufen, ibuprofen, and piroxicam can cause eosinophilic pneumonia. Bronchoalveolar lavage is sufficient to diagnose eosinophilic pneumonia. Corticosteroid therapy should be indicated for more severe or refractory cases.
NSAIDs including diclofenac can cause PIE. The clinical presentation includes fever, cough, dyspnea, infiltrates on chest X-ray, and an absolute peripheral eosinophilia. Pathological examination reveals poorly defined granulomas with infiltrating eosinophils. The treatment modes are discontinuation of NSAIDs and administration of corticosteroids.
Diclofenac can cause asthmatic attacks in aspirin-sensitive patients. The proposed mechanism is removal of prostaglandins (prostaglandin E [PGEs]) (which cause bronchodilation) by prostaglandin synthetase inhibitors, leading to unopposed action of endogenous bronchoconstrictors such as histamine. Furthermore, lack of PGEs promotes the release of histamine.
Pulmonary edema and hemoptysis is reported in a scuba diver using diclofenac.
| Conclusion|| |
Diclofenac hypersensitivity has a spectrum of manifestations varying from simple isolated urticaria to severe anaphylaxis. Pulmonary manifestations such as ARDS, eosinophilic pneumonitis, pleural effusion, eosinophilic pneumonia, pulmonary edema, hemoptysis, PIE, and asthmatic attacks are rare. The temporal relationship between symptom onset and drug administration is the most important piece of history while making the diagnosis. History of allergic reaction to NSAIDs should be evaluated in detail. It is, therefore, important that the physician keep this in mind while prescribing this commonly used NSAID and also while encountering respiratory manifestations in a patient exposed to the drug in recent times.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2]