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.
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).
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.
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.
The authors thank Silvina Libran for her translation assistance.
1. Lazaridis KN, Frank JW, Krouwka MJ, Kamath PS. Hepatic hydrothorax: pathogenesis, diagnosis and management. Am J Med 1999;107:262–7.
2. Morrow CS, Boyer TD. Hepatic hydrothorax. Ann Intern Med 1958;49:193–203.
3. Strauss RM, Boyer TD. Hepatic hydrothorax. Semin Liver Dis 1997;17:227–32.
4. Singer JA, Kaplan MM, Katz RL. Cirrhotic pleural effusion in the absence of ascites. Gastroenterology 1977;73:575–7.
5. Rubinstein D, McInnes IE, Dudley FJ. Hepatic hydrothorax in the absence of clinical hydrothorax: diagnosis and management. Gastroenterology 1985;88:188–91.
6. Kirsh CM, Chui DW, Yenokida GG, et al. Case report: hepatic hydrothorax without ascites. Am J Med Sci 1991;1302:103–6.
7. Alberts WM, Salem AJ, Solomon DA, et al. Hepatic hydrothorax: cause and management. Arch Intern Med 1991;151:2383–8.
8. Lieberman FL, Hidemuro R, Peters RL, et al. Pathogenesis and treatment of hydrothorax complicating cirrhosis with ascites. Ann Intern Med 1966;64:341–51.
9. Emerson PA, Davies JH. Hydrothorax complicating ascites. Lancet 1955;1:487–8.
10. Chen A, Ho YS, Tu YC, Chang TC. Diaphragmatic defects as a cause of massive hydrothorax in cirrhosis of the liver. J Clin Gastroenterol 1988;10:663–6.
11. Ross J, Farber JE. Right-sided spontaneous pneumothorax complicating therapeutic pneumoperitoneum. Am Rev Tuberc 1951;63:67–75.
12. Lieberman FL, Peters RL. Cirrhotic hydrothorax. Arch Intern Med 1970;125:114–7.