Anesth Analg 2004;99:1803-1804
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000138034.73465.D3
CRITICAL CARE AND TRAUMA
Hepatic Hydrothorax in the Absence of Ascites: Respiratory Failure in a Cirrhotic Patient
Jordi Serrat, MD,
Julio J. Roza, MD, and
Teresa Planella, MD
Servei d’Anestesiologia i Reanimació, Hospital General de Vic, Barcelona, Spain
Address correspondence and reprint requests to Jordi Serrat, MD, Servei d’Anestesiologia i Reanimació, Hospital General de Vic, C/ Francesc Pla s/n, 08500 Vic, Barcelona, Spain. Address e-mail to jserrat{at}hgv.es
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Abstract
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The frequency of hepatic hydrothorax in cirrhotic patients is reported to be approximately 5%. The pleural effusion is predominantly right-sided (85% of cases) but may be bilateral. Although most often accompanied by significant ascites, it can occur in its absence. We report a case of a right-sided acute hepatic hydrothorax as a result of residual motor blockade during anesthesia recovery and without previous evidence of clinical ascites. This complication should be considered by the anesthesiologist in every cirrhotic patient, with or without clinical evidence of ascites.
IMPLICATIONS: Hydrothorax is a pleural space fluid accumulation. Most pleural effusions are rarely observed. Although unusual, these effusions associated with hepatic cirrhosis and ascites have been well described. However, the case we present here showed no clinical signs of ascites before surgery. Therefore, the patient developed a right-sided hydrothorax as a result of residual motor blockade during anesthesia recovery.
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Case Report
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A 58-yr-old woman underwent a correcting right crural hernia surgery. She did not present any cardiopulmonary pathology. Her medical history included hepatic cirrhosis and a right hemidiaphragm elevation in a posteroanterior chest radiograph performed a week before surgery (Fig. 1). Interestingly, this elevation had also been detected 18 mo before our surgery; thus, we inferred this could be a chronic alteration. Our patient also presented ascites grade 1 (small volume) detected 6 wk before surgery by means of echography. From the outpatient assessment to the time of operation, the patient’s condition was unremarkable. Once in the operating room, the patient was eupneic and was placed in the decubitus position. Physical examination showed a sinus cardiac rhythm heart rate of 78 bpm, arterial blood pressure of 110/50 mm Hg, a respiration rate of 16/min, and oxyhemoglobin of 99%. Anesthesia was induced with endovenous IV midazolam 2 mg, propofol 100 mg, atracurium besilate 35 mg, and fentanyl 150 µg. The trachea was intubated with a 7.5-mm endotracheal tube and anesthesia was maintained with inhaled sevoflurane 1.5%–2%. Respiratory auscultation was normal.
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Figure 1. Posteroanterior profile chest radiograph 1 wk before surgery, showing chronic hemidiaphragm elevation.
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Surgery lasted 30 min and proceeded without complications, after which clinical signs of residual motor blockade and respiratory efforts were observed. Then, IV neostigmine 2 mg and IV atropine 1 mg were used as reversals. Neuromuscular function was then regained and a train-of-four measured >90%. Nonetheless, the patient was restless with the tracheal tube, had paradoxical respiration, and developed hemoglobin desaturation. She did not withstand either spontaneous ventilation or tracheal extubation. There was right hemithorax silence and wheezing in the lung fields on auscultation. A chest radiograph showed a massive right-sided pleural effusion affecting the middle and lower lobes, but no signs of vascular pulmonary hypertension (Fig. 2).
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Figure 2. Posteroanterior chest radiograph, decubitus position, showing massive right-sided pleural effusion.
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Thoracentesis was performed by means of a 2.7-mm thoracic catheter (Pleurocath; Plastimed, GmbH, Germany) and 1300 mL of clear fluid was drained. A chest radiograph was performed (Fig. 3). Immediately afterward, the patient regained spontaneous ventilation and gasometry improved: negative logarithm of hydrogen concentration (pH) 7.48, oxygen arterial pressure 117 mm Hg, carbon dioxide arterial pressure 23 mm Hg, oxygen saturation of 99%, base excess –3.4. Tracheal extubation was then possible. The patient was referred to the Postanesthesia Care Unit.
The pleural fluid laboratory analysis revealed a white blood cell count of 440/mm3, granulocytes 7%, lymphocytes 93%, glucose 105 mg/dL, protein 1.9 g/dL, and lactic dehydrogenate 185 U/L. The serum total protein and albumin were 5.9 g/dL and 2.8 g/dL, respectively.
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Discussion
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Hepatic hydrothorax is defined as the presence of significant pleural effusion (>500 mL) in a cirrhotic patient without primary pulmonary or cardiac disease (1–3). Such pleural effusions in the absence or eventual disappearance of ascites are very rare and may lead to diagnostic problems (4–6). The most likely explanation for this hepatic hydrothorax seemed to be that ascitic fluid passed through congenital or acquired fenestration (0.03–1.2 mm in diameter, mostly in the right centrum tendinum) in the diaphragm directly into the pleural space.
A one-way valve mechanism was created, and a pressure gradient-directed, unidirectional flow of fluid occurred through these defects into the pleural cavity (7). During the extubation procedure, it is possible that cyclical subatmospheric intrathoracic pressure developed as a consequence of the highest inspiratory efforts, and the abdominal hyperpressure caused by the abdominal cough provoked the results described above. However awkward it may initially sound that a siphon mechanism could allow ascitic fluid to pass into the pleural space, there is considerable evidence to support this hypothesis (7–11). Moreover, small diaphragmatic defects may have been the cause of some leakage and then have been resealed once the peritoneal and pleural fluid reached an equilibrium (12). Therefore, the pressure gradient diminished. The flow of the ascitic fluid into the pleural space equaled the rate of ascites production in patients with this entity (4).
In conclusion, we present a case of acute hepatic hydrothorax appearing in a cirrhotic patient, without clinical evidence of ascites, attributed to the siphon mechanism during tracheal extubation. The anesthesiologist should consider the possibility that these cases, although rare, can happen.
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Acknowledgments
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The authors thank Silvina Libran for her translation assistance.
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References
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Accepted for publication June 18, 2004.
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