Locked lung by looped hernia: a case report
© Rahman and Panda; licensee BioMed Central Ltd. 2009
Received: 05 December 2008
Accepted: 08 January 2009
Published: 08 January 2009
Large pleural effusions are usually symptomatic. We report a patient with asymptomatic massive left sided pleural effusion with left lung collapse secondary to a traumatic diaphragmatic hernia.
A 44 year old male presented with recurrent pleural effusions over six weeks. His pleural effusion was first diagnosed incidentally on a chest X-ray after a fall. Extensive diagnostic studies were unyielding for the etiology of the effusion. A diagnostic and therapeutic video assisted thoracoscopy revealed a diaphragmatic hernia with inflamed, incarcerated omentum. After hernia repair there was no recurrence.
This case underscores the obscure presentation of an incarcerated diaphragmatic hernia presenting as massive recurrent pleural effusions.
Pleural effusion is commonly encountered in clinical practice. It can cause various respiratory symptoms, constitutional symptoms and symptoms related to underlying disease process. Though some patients may be asymptomatic with a small pleural effusion, most are symptomatic and often in significant respiratory distress, especially when the effusion is massive. Diaphragmatic hernia is an uncommon cause of pleural effusion. No incidence data are available but multiple cases are reported [1, 3–5]. In most of the reported cases the diaphragmatic hernia was trauma induced.
Our patient had an intriguing presentation of massive pleural effusion with underlying lung collapse without significant symptoms. A possible explanation for the asymptomatic presentation can be the sedentary lifestyle and good pulmonary reserve of the right lung. Establishing an etiology of this pleural effusion was puzzling. While his non-toxic clinical presentation, normal leukocyte count and pleural fluid findings were consistent with transudative effusion, the unilateral distribution of the pleural effusion was inconsistent. CT imaging of chest did not identify the diaphragmatic hernia, which may be due to small size of the hernia. Usually diaphragmatic hernia does not cause pleural effusion unless it contains incarcerated viscera [1, 2, 6]. Almost all massive pleural effusions with diaphragmatic hernia contained a strangulated omentum [1, 6]. Schreier et al reported a case of hemorrhagic pleural effusion from infarcted omentum in a non-traumatic diaphragmatic hernia . Several cases were reported on World War II and Vietnam veterans [1, 5].
Presenting symptoms are much varied, but usually pain from trauma if recent, respiratory distress, gastrointestinal symptoms and abdominal pain from intrathoracic strangulation of abdominal organ . The time interval between the onset of traumatic diaphragmatic hernia and the presentation with symptom may vary from days to years. Presentation as late as 26 years after the original accident are also reported [3, 6]. In our case the effusion developed within a week. Initial thoracentesis usually yields serosanguinous fluid especially at an early stage. A unilateral pleural effusion especially one on left side, with above clinical presentation and serosanguinous pleural fluid should make one highly suspicious for a strangulated diaphragmatic hernia. If no recent trauma is reported, trauma in the past may be the clue. A CT scan of the chest may be performed early to evaluate a hernia and to assess other possible diagnoses such as malignancy, pulmonary embolism or esophageal rupture. Pleural fluid drainage with repair of the diaphragmatic hernia is the definitive treatment.
Pleural effusion from incarcerated diaphragmatic hernia is an infrequent diagnosis. It is less often entertained as a differential diagnoses in the work up of a pleural effusion. Pathology is often obscure with a potential to miss, causing the patient recurrent morbidity and even the risk of death. Early diagnosis of this potentially curable pathology will significantly reduce patient suffering and economic burden.
The patient expired several years later from accidental poisoning. Written informed consent was obtained from the patient's mother for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
Blood Urea Nitrogen
Partial pressure of arterial Carbon dioxide
Partial pressure of arterial Oxygen
Acid Fast Bacilli
Anti Nuclear Antibody
Anti Nuclear Cytoplasmic Antibody
Anti Mitochondrial Antibody
Thyroid Stimulating Hormone
Human Immunodeficiency Virus
Rapid Plasma Reagin
White Blood Cell
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