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Clinical Infection & Immunity

Case Report

Volume 7, Number 1, March 2022, pages 27-30

A Rare Case of Complicated Hepatic Hydrothorax

A hepatic hydrothorax is a rare complication seen in cirrhotic patients. It is a pleural effusion, which is defined by accumulation of fluid in the pleural cavity in patients with decompensated liver cirrhosis but without cardiopulmonary and pleural diseases. The etiology is unknown but possibly due to portal hypertension. Its pathophysiology involves movement of ascitic fluid from the peritoneal cavity into the pleural space through diaphragmatic defects. Classically, the fluid is defined as transudative (according to Light’s criteria) and is usually seen in the context of ascites. Generally, pleural fluid that contains bacteria is characterized as exudative, meaning it contains at least one of the following Light’s criteria: lactate dehydrogenase (LDH) > 2/3 of upper limit of normal, fluid LDH/serum LDH > 0.6, or fluid protein/serum protein > 0.5. In this case, the pleural fluid did not meet any of those criteria, hence diagnosed as transudative fluid, yet it grew Gram-positive bacteria (Staphylococcus aureus), indicating hepatic hydrothorax with spontaneous bacterial empyema (SBEM). There is no definitive treatment of hepatic hydrothorax, but studies have shown that medications such as diuretics can alleviate fluid accumulation. SBEM or more recently noted as spontaneous bacterial pleuritis (SBP) is similar to spontaneous bacterial peritonitis seen in cirrhotic patients with ascites. It is thought that SBP is caused from the infected ascitic fluid, but it is not always necessary for the individual to have ascites. Since SBEM is rare (14% of cirrhotic patients), it is still being studied in depth to understand the risk factors, treatments, and possible prophylaxis for prevention. Common bacteria found in SBEM tend to be Escheria coli, Streptococcus species, Enterococcus, and Klebsiella.

A 51-year-old man with a past medical history of alcoholism presented to the emergency room after a fall. History was difficult to obtain as patient was confused. Per patient’s wife, patient had an extensive history of alcohol abuse and had been “yellow” for weeks to months. He was alert and oriented to person and place but lethargic. Physical exam was notable for jaundice, scleral icterus, abdominal distension with positive fluid wave, hepatosplenomegaly, and asterixis. His vital signs included a blood pressure of 126/84, heart rate of 121, respiratory rate of 20, temperature of 99.1, and saturating 98% on room air. There was mild leukocytosis of 12.7 with left shift (neutrophils 88.2%). Total bilirubin was 7.1, aspartate transaminase (AST)/alanine aminotransferase (ALT) was 55/21, respectively, and ammonia was 64.

Patient was originally admitted for hepatic encephalopathy secondary to decompensated cirrhosis and started on lactulose. He was noted to have a marked improvement in mental status in 36 h. Despite this, the patient developed persistent fevers and was found to have positive blood cultures exhibiting methicillin sensitive Staphylococcus aureus (MSSA). Patient had a urinalysis and urine culture that were negative, chest X-ray that showed right-sided pleural effusion (Fig. 1), and a computed tomography of the abdomen and pelvis, which showed hepatic cirrhosis with splenomegaly and mild ascites, as well as, gastroesophageal and splenic varices. An extensive workup to determine the etiology of his bacteremia was performed, including a diagnostic thoracentesis. A repeat chest X-ray showed resolution of pleural effusion without any evidence for an underlying infiltrate (Fig. 2). The fluid was sent out for analysis (Table 1), which showed a pleural fluid LDH was 55, protein was 1.0, glucose was 204 and serum levels of LDH was 283 and serum protein was 6.1. Using Light’s criteria, the conclusion was a transudative fluid with the most likely diagnosis of hepatic hydrothorax. Pleural fluid culture resulted in Gram-positive cocci in clusters within 24 h in the aerobic bottle. Of note, the fluid had a white blood cell count of 412 with 52% neutrophils, which is not necessarily diagnostic of an SBP. Nevertheless, given the nature that this individual improved in 36 h and was found to have positive blood cultures, thereafter, the possibility of a nosocomial infection cannot be excluded.

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Figure 1. An anterior-posterior portable chest X-ray representing a right-sided pleural effusion (red arrow) present upon admission. The blunting of the right costophrenic angle (unable to see a clear angle where the diaphragm meets the ribs) generally signifies fluid in the lungs.

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Figure 2. An anterior-posterior portable chest X-ray representing improvement in right-sided pleural effusion that was seen in Figure 1. This was taken after a thoracentesis was done, in order to remove fluid from the lungs. The costophrenic angle is now visible.

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Table 1. Fluid Analysis Results After Thoracentesis

Patient was initially placed on vancomycin and then antibiotics were narrowed down to nafcillin once the sensitivities revealed MSSA. Repeat blood cultures resulted negative. However, the patient did deteriorate after a period of days, including respiratory distress, and subsequently became intubated and transferred to the critical care unit. Unfortunately, patient eventually expired.

A pleural effusion is an excessive accumulation of fluid in the pleural space. Patients typically present with dyspnea, dry cough, and pleuritic chest pain. They are the most common disease among all the pleural diseases and affect 1.5 million patients per year in the USA [1]. The etiology of pleural effusions is important to know in order to treat the condition appropriately. However, in almost 20% of cases, the etiology still remains unclear [2]. Effusions can be categorized as either transudative or exudative. Transudative pleural effusions develop because there is an uneven distribution of hydrostatic and oncotic pressure across the pleura, thus leading to increased rate of pleural fluid formation [3]. They usually have low cell and protein content. Some of the most common causes of transudative pleural fluid include congestive heart failure, nephrotic syndrome, and liver cirrhosis [4]. In liver cirrhosis, the term used to describe pleural effusions is hepatic hydrothorax and occurs because of movement of ascitic fluid from the peritoneal cavity into the pleural space through diaphragmatic defects [5].

Light’s criteria are a diagnostic tool used to evaluate the etiology of pleural effusions. The criteria state that if the fluid analysis contains at least one of the following, it will be an exudative pleural effusion: LDH > 2/3 of upper limit of normal, fluid LDH/serum LDH > 0.6, or fluid protein/serum protein > 0.5 [6]. Light’s criteria are reported to be highly sensitive for exudative effusions approaching 98% [7]. However, about 20% of exudative fluid is actually transudative and can further be evaluated utilizing a serum-effusion albumin gradient greater than 1.2 g/dL, thus indicating a true transudative effusion [8].

In the case presented above, the patient likely developed a pleural effusion secondary to liver cirrhosis, thus categorized as a hepatic hydrothorax. This is defined as a pleural effusion in a patient with portal hypertension and no cardiopulmonary disease with an estimated prevalence of 5-6% in patients with liver cirrhosis [5]. Its localization is right-sided in approximately 85% of cases and left-sided in approximately 13%; whereas, only 2% of patients have fluid in the pleural cavity on both sides [9]. Hepatic hydrothorax is found in almost 5-10% of patients, constituting 2-3% of all causes of pleural effusions. There is no definitive treatment of hepatic hydrothorax, but studies have shown that medications such as diuretics can alleviate fluid accumulation [9]. SBEM or more recently noted as SBP is similar to spontaneous bacterial peritonitis seen in cirrhotic patients with ascites [10]. It is thought that SBP is caused from the infected ascitic fluid, but it is not always necessary for the individual to have ascites. Diagnosis is usually made by the following criteria: 1) positive pleural fluid culture and polymorphonuclear cell count above 250 cells/mm³; 2) more than 500 polymorphonuclear cells/mm³ if pleural fluid culture negative; 3) no evidence of pneumonia on chest radiograph or computed tomography; and 4) evidence of pleural effusion before the infectious episode or transudative pleural effusion during infection [10].

Since SBEM is rare (14% of cirrhotic patients), it is still being studied in depth to understand the risk factors, treatments, and possible prophylaxis for prevention. One study showed that low pleural fluid protein and low complement levels can be risk factors for SBEM by enhancing bacterial translocation, thus making it easier to become infected [11]. The patient did indeed have both of those criteria (C3 31, C4 11), pleural protein (1.0). Another theory states that up to 40% of cases occur without underlying spontaneous bacterial peritonitis or the presence of ascites with a possible explanation that the SBEM occurs as a result of direct infection of the pleural space via transient bacteremia [11], which this patient had. Common bacteria found in SBEM tend to be Escheria coli, Streptococcus species, Enterococcus, and Klebsiella [12]. Interestingly, in our case, both the pleural fluid and blood cultures grew MSSA, making the second theory more likely in this situation.

Of note, our patient did not meet the specific criteria with the typical cell count findings normally described in SBP. This may have been due to empiric antibiotics given upon arrival to the emergency room. Regardless, given no other evidence of infection, appropriate antibiotic therapy may have been delayed otherwise. Therapy with an intravenous third generation cephalosporin antibiotic should be commenced immediately after the diagnosis is made [12]. The patient’s treatment regimen was adequately adjusted from vancomycin to nafcillin and ceftriaxone was also added.

This case highlights that SBP is a frequent but underdiagnosed complication of hepatic hydrothorax with a poor prognosis. The delay in diagnosis of this patient is unfortunate, as he originally did not have any definitive medical history except for alcoholism and came into the hospital for a fall. It was only with imaging and history that liver cirrhosis was able to be diagnosed. It is important to acknowledge the prevalence and importance of hepatic hydrothorax that can become complicated by developing SBEM/SBP, which has a 20% mortality [12]. It is crucial how early diagnosis and knowledge of this medical condition could have possibly helped prevent the subsequent hospital course that this individual endured. It is hopeful that we will be able to address the situation appropriately moving forward and even be able to empirically treat this condition, as is similarly seen in spontaneous bacterial peritonitis prophylaxis.

Acknowledgments

None to declare.

Financial Disclosure

The authors declare that they have no financial disclosure or funding.

Conflict of Interest

The authors declare that they have no competing interests.

Informed Consent

Informed consent has been obtained from the patient’s family.

Author Contributions

Dr. Narala compiled the manuscript. Dr. Suhail had interviewed the patient and wrote the case presentation. Dr. Narala conducted research and background information and wrote the abstract, introduction, discussion, and conclusion. Dr. Diaz was the supervising attending. All authors reviewed and approved the final manuscript.

Data Availability

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

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