Hepatic Hydrothorax

Hepatic Hydrothorax
Pratap Sagar Tiwari, DM Resident
Department of Hepatology, NAMS

Introduction
• The pleural space is bordered by the parietal and visceral pleurae that plays an important role in
respiration by coupling the movement of the chest wall with that of the lungs in 2 ways.
• First, a relative vacuum in the pleural space keeps the visceral and parietal pleurae in close
proximity.
• Second, the small volume of pleural fluid, which has been calculated at 0.13 mL/kg of body weight
under normal circumstances, serves as a lubricant to facilitate movement of the pleural surfaces
against each other in the course of respirations.
• This small volume of fluid is maintained through the balance of hydrostatic and oncotic pressure
and lymphatic drainage, a disturbance of any of these may lead to pathological condition.
• A pleural effusion is an abnormal collection of fluid in the pleural space resulting from excess fluid
production or decreased absorption or both. As in cases in which there is inflammation with
increased permeability, fluids may exudate and form the exudative PE. On the other hand as a
result of increased fluid pressures or diminished colloid oncotic forces in the plasma, transudation
of fluid occurs .
• Transudate is extravascular fluid with low protein content and a low specific gravity (< 1.012). It has
low nucleated cell counts (less than 500 to 1000 /microlit) and the primary cell types are
mononuclear cells: macrophages, lymphocytes and mesothelial cells.

• Total cell count in the PL fluid of nonsmoking normal subjects yielded a
median of 91 x 10(3) white blood cells (WBC) per milliliter of lavage fluid
(interquartile range [IR] = 124 x 10(3) cells/ml).
• Differential cell counts yielded a predominance of macrophages (median:
75%; IR: 16%) and lymphocytes (median: 23%; IR: 18%).
• Mesothelial cells (median: 1%; IR: 2%), neutrophils (median: 0%; IR: 1%),
and eosinophils (median: 0%; IR: 0%) were only marginally present.
• There were no significant differences between males and females or
between right- and left-sided pleural fluid in total and differential cell
counts.
• In contrast, in smokers a small but statistically significant increase in pleural
fluid neutrophils (median: 1%; IR: 2%; p < 0.015) was observed.

Introduction
• The presence of PHTN and not cirrhosis is required for the development of
HH; it should be noted, however, that most patients (> 80%) with PHTN have
cirrhosis.
• HH is a less common complication of PHTN occurring in 5-15% of pts with
cirrhosis.
• Although pts with ascites can often tolerate 5-8 L of fluid in their abdomen before
becoming significantly symptomatic, a patient with a HH will develop dyspnea, and/or
hypoxia when only 1-2 L of fluid accumulate in the pleural space. This is expected given
the structural characteristics of the thoracic cavity. As a result, this complication of PHTN is
challenging for clinicians and its development warrants a LT evaluation.
HH is defined as a transudative PE, usually >500 mL in pts with PHTN
without any other underlying primary CP cause.

Incidence
• The incidence of HH varies depending on the method of detecting pleural
fluid. The incidence has been reported to be 4–6% in studies that used CXR
to diagnose PE [1-5]. However, in a series of 862 cirrhotic pts from China that
used USG to detect PE, the incidence was found to be 15% [6] .
• HH accounts for 2–3% of all PE [7,8] .
• As opposed to PE of cardiac origin that are typically bilateral, 79.5% of PE in a
pt with cirrhosis are Rt sided only, 17.5% are left sided only, and 3% are
BL.[9,10] This can be helpful in establishing the Dx of HH versus cardiac disease.
1. Johnston RF, Loo RV: Hepatic hydrothorax. Ann Intern Med 1964; 61: 385–401.
2. Lieberman FL, Peters RL: Cirrhotic hydrothorax: further evidence that an acquired diaphragmatic defect is at fault. Arch Intern Med 1970; 125: 114–117.
3. Esteve M, Xiol X, Fernadez F, Gonzalez F, Baliellas C: Treatment and outcome of hydrothorax in liver cirrhosis. J Clin Nutr Gastroenterol 1986; 1: 139–144.
4. Giacobbe A, Facciorusso D, Barbano F, Andriulli A, Frusciante V: Hepatic hydrothorax: diagnosis and management. Clin Nucl Med 1996; 21: 56–60.
5. Shu-juan J, Song Z, Li-li S, Yi L: Diagnostic and therapeutic value of thoracoscopy for pleural effusions: experience from 628 consecutive cases in China. Chin Med J 2009; 122:1227–1230.
6. Chen TA, Lo GH, Lai KH: Risk factors for spontaneous bacterial empyema in cirrhotic patients with hydrothorax. J Chin Med Assoc 2003; 66: 579–586.
7. Romero S, Candela A, Martin C, Hernandez L, Trigo C, Gil J: Evaluation of different criteria for the separation of pleural transudates from exudates. Chest 1993; 104: 399–404.
8. Light RW, Macgregor MI, Luchsinger PC,Ball WC Jr: Pleural effusions: the diagnostic separation of transudates and exudates. Ann Intern Med 1972; 77: 507–513.
9. Lazaridis KN, Frank JW, KrowkaMJ, Kamath PS. Hepatic hydrothorax: pathogenesis, diagnosis, and management. Am J Med 1999; 107(3):262–267
10. Alagiakrishnan K, Patel PJ. Left-sided hepatic hydrothorax with ascites. Int J Clin Pract 1999;53(3):225–226

Extra note
1.Ultrasound is a useful method because it allows the distinction between
effusion and lung consolidations and has a higher accuracy in detecting
pleural effusion in comparison with bedside chest X-rays (93% vs. 47%).In
fact, chest X-rays can detect the presence of pleural effusion in patients in
the orthostatic position only if the volume of the effusion is at least 200
mL,and the sensitivity of this method decreases in the supine position,
whereas ultrasound can detect effusions as small as 20 mL.
2. ultrasound is 100% sensitive for effusions >100ml.
3.A meta-analysis of four studies calculated a pooled sensitivity and
specificity of ultrasound for detection pleural effusions as 93% and 96%
respectively.

Pathophysiology
• Although the exact mechanism of HH is controversial, it is probably due to
the ascites fluid that is transported directly into the pleural space.
• A number of different mechanisms have been proposed to explain the
development of HH, including: hypoalbuminemia and a ↓in colloid osmotic
pressure (Higgins et al); leakage of plasma from hypertensive azygos veins
(Morrow et al); lymphatic leakage from thoracic duct(Eisenmenger et al);
passage of fluid from peritoneal cavity to the pleural space via lymphatic
channels in the diaphragm; and passage of fluid into the pleural space
directly via defects in the diaphragm [1-7].
1. Lieberman FL, Hidemura R, Peters RL, Reynolds TB. Pathogenesis and treatment of hydrothorax complicating cirrhosis with ascites. Ann Intern Med.
1966;64(2):341–351.
2. Johnston RF, Loo RV. Hepatic Hydrothorax; Studies to Determine the Source of the Fluid and Report of Thirteen Cases. Ann Intern Med. 1964;61:385–401.
3. Lieberman FL, Peters RL. Cirrhotic hydrothorax. Further evidence that an acquired diaphragmatic defect is at fault. Arch Intern Med. 1970;125(1):114–117.
4. Alberts WM, Salem AJ, Solomon DA, Boyce G. Hepatic hydrothorax. Cause and management. Arch Intern Med. 1991;151(12):2383–2388.
5. Daly JJ, Potts JM, Gordon L. Scintigraphic diagnosis of peritoneo-pleural communication in the absence of ascites. Clin Nucl Med. 1994;19(10):892–894.
6. Kakizaki S, Katakai K, Yoshinaga T, Takayama H, Takagi H, Nagamine T. et al. Hepatic hydrothorax in the absence of ascites. Liver. 1998;18(3):216–220.
7. Strauss RM, Boyer TD. Hepatic hydrothorax. Semin Liver Dis. 1997;17(3):227–232.

Pathophysiology …continue
• Several observations indicate that the most likely cause of PE in pts with
cirrhosis is the passage of a large amount of ascites from the peritoneal to the
pleural cavity through diaphragmatic defects.[1,2,3,4,5]
• This mechanism was 1st suggested following the observation of a
pneumothorax after injection of air into the peritoneal cavity; when air was
infused intraperitoneally in pts with HH, a CXR performed within 48 hrs
detected air above the diaphragmatic surface in the rt side of the chest.[1]
1. Lieberman FL, Hidemura R, Peters RL, Reynolds TB. Pathogenesis and treatment of hydrothorax complicating cirrhosis with ascites. Ann Intern Med 1966;64(2):341–351
2. Emerson PA, Davies JH. Hydrothorax complicating ascites. Lancet 1955;268(6862):487–488
3. Mouroux J, Perrin C, VenissacN, Blaive B, Richelme H.Management of pleural effusion of cirrhotic origin. Chest 1996;109(4): 1093–1096
4. Chen A, Ho YS, Tu YC, Tang HS, Cheng TC. Diaphragmatic defect as a cause of massive hydrothorax in cirrhosis of liver. J Clin Gastroenterol 1988;10(6):663–666
5. Zenda T, Miyamoto S,Murata S,Mabuchi H. Detection of diaphragmatic defect as the cause of severe hepatic hydrothorax with magnetic resonance imaging. Am J Gastroenterol
1998;93(11): 2288–2289

Pathophysiology…continue
• Diaphragmatic defects can be demonstrated both grossly and microscopically in
patients with HH. Microscopic examination of these defects reveals discontinuities
in the collagen bundles that make up the tendinous portion of the diaphragm.[1]
• Typically, the defects are <1 cm and tend to occur on the rt side. This rt-sided
predominance likely occurs due to the close anatomical relationship of bare areas
of the liver with the diaphragm as well as the fact that the left side of the
diaphragm is thicker and more muscular than the right.
• Huang and colleagues[2] have classified the DD into four morphological types:
Type 1: No obvious defect
Type 2: Blebs lying in the diaphragm
Type 3: Broken defects (fenestrations) in the diaphragm
Type 4: Multiple gaps in the diaphragm
1. Lieberman FL, Hidemura R, Peters RL, Reynolds TB. Pathogenesis and treatment of hydrothorax complicating cirrhosis with ascites. Ann Intern Med 1966;64(2):341–351
2. Huang PM, Chang YL, Yang CY, Lee YC. The morphology of diaphragmatic defects in hepatic hydrothorax: thoracoscopic finding. J Thorac Cardiovasc Surg 2005;130(1):141–145

Abstract: BACKGROUND:
• Until now, the pathophysiology of HH has been moot. We discuss (on the basis of gross
videothoracoscopy findings in 11 cases and the literature) the pathogenesis and clinical
presentation of this complex condition.
• METHODS: We prospectively studied 11 pts (age, 31-73 yrs; 6 m & 5 w) with RHH (CP B-C)
who underwent thoracoscopic repair of diaphragmatic defects. The DD were examined
intraoperatively.
• RESULTS: The DD stemming from HH were classified into 4 morphologic types: TI, no
obvious defect (1 pt); TII, blebs lying on the diaphragm (4 pts); TIII, broken defects
(fenestrations) in the diaphragm (8 pts); and TIV, multiple gaps in the diaphragm (1
pt). The type of DD did not correlate with the volume occupied by the PE in the
preoperative chest radiograms.
• CONCLUSIONS: The finding of this study allowed HH pathophysiology to be directly
visualized, and further studies concerning the treatment of HH might be based on these
mechanisms.

• The negative intrathoracic pressure generated during inspiration favors the
passage of fluid from the intra-abdominal to the pleural space. Thus, many pts may
have only mild or no clinically detectable ascites [ 1-4].
• HH develops when the absorptive capacity of the pleural space is exceeded. This
theory is supported by studies using 99mTc-human albumin or 99mTc-sulphur
colloid.
• The valvular mechanism of HH development has been corroborated with nuclear
medicine studies using 99mTc-human albumin or 99mTc-sulfur colloid and dye studies
that show a unidirectional passage of these markers from the abdominal to the
pleural cavity in the first 24 hours after administration.[5-8]
• Also, radioactive isotope scans confirm communication between the peritoneal
cavity and the pleural space, even in the absence of sonographic evidence of
ascites.[6]
1. Strauss RM, Boyer TD. Hepatic hydrothorax. Semin Liver Dis 1997; 17:227.
2. Cárdenas A, Arroyo V. Mechanisms of water and sodium retention in cirrhosis and the pathogenesis of ascites. Best Pract Res Clin Endocrinol Metab 2003; 17:607.
3. Lazaridis KN, Frank JW, Krowka MJ, Kamath PS. Hepatic hydrothorax: pathogenesis, diagnosis, and management. Am J Med 1999; 107:262.
4. Serrat J, Roza JJ, Planella T. Hepatic hydrothorax in the absence of ascites: respiratory failure in a cirrhotic patient. Anesth Analg 2004; 99:1803.
5. Rubinstein D, McInnes IE, Dudley FJ. Hepatic hydrothorax in the absence of clinical ascites: diagnosis and management. Gastroenterology 1985;88(1 Pt 1):188–191
6. Benet A, Vidal F, Toda R, Siurana R, De Virgala CM, Richart C. Diagnosis of hepatic hydrothorax in the absence of ascites by intraperitoneal injection of 99m-Tc-Fluor colloid. Postgrad Med J 1992;68(796):153
7. Serena A, Aliaga L, Richter JA, Calderon R, Sanchez L, Charvet MA. Scintigraphic demonstration of a diaphragmatic defect as the cause of massive hydrothorax in cirrhosis. Eur J Nucl Med 1985; 11(1):46–48
8. Kakizaki S, Katakai K, Yoshinaga T, et al.Hepatic hydrothorax in the absence of ascites. Liver 1998;18(3):216–220

• Diaphragmatic defects occur in up to 20% of the noncirrhotic population;
interestingly, despite the prevalence of these defects, a pneumothorax only
rarely develops following laparoscopic procedures.[1,2,3]
• Obviously the presence of ascites alters the pressure gradient between the
intrathoracic and intraabdominal regions. In pts with ascites, the increasing
abdominal pressure and the diaphragmatic thinning secondary to
malnutrition in some cirrhotic pts enlarge these defects. When IAP ↑, gaps
can develop between the muscle fibers of the diaphragm and lead to small
herniations of the peritoneum into the pleural space. These herniations,
pleuroperitoneal blebs, may rupture and therefore facilitate passage of fluid.
The -tive ITP favors the one-way transfer of fluid across these defects.[4,5,6]
• Interestingly, up to 20% of pts with HH have no clinically sig
ascites.[7.8.9.10.11.12]

References to the previous slide
1. Fathy O, ZeidMA, Abdallah T, et al. Laparoscopic cholecystectomy: a report on 2000 cases. Hepatogastroenterology 2003;50(52): 967–971
2. Dawson R, Ferguson CJ. Life-threatening tension pneumothorax during laparoscopic cholecystectomy. Surg Laparosc Endosc 1997; 7(3):271–272
3. Kinasewitz GT, Keddissi JI. Hepatic hydrothorax. Curr Opin Pulm Med 2003;9(4):261–265
5. Strauss RM, Boyer TD. Hepatic hydrothorax. Semin Liver Dis 1997;17(3):227–232
6. AlbertsWM, SalemAJ, Solomon DA, Boyce G. Hepatic hydrothorax: cause and management. Arch Intern Med 1991;151(12): 2383–2388
7. Jeffries MA, Kazanjian S, Wilson M, Punch J, Fontana RJ. Transjugular intrahepatic portosystemic shunts and liver transplantation in patients with
refractory hepatic hydrothorax. Liver Transpl Surg 1998;4(5):416–423
8. Siegerstetter V, Deibert P, Ochs A, Olschewski M, Blum HE, RössleM. Treatment of refractory hepatic hydrothoraxwith transjugular intrahepatic
portosystemic shunt: long-term results in 40 patients. Eur J Gastroenterol Hepatol 2001;13(5):529–534
9. Xiol X, Castellote J, Cortes-Beut R, Delgado M, Guardiola J, Sesé E. Usefulness and complications of thoracentesis in cirrhotic patients. Am J Med
2001;111(1):67–69
10.Singer JA, Kaplan MM, Katz RL. Cirrhotic pleural effusion in the absence of ascites. Gastroenterology 1977;73(3):575–577
11.Rubinstein D, McInnes IE, Dudley FJ. Hepatic hydrothorax in the absence of clinical ascites: diagnosis and management. Gastroenterology 1985;88(1 Pt
1):188–191
12.Rubinstein D, McInnes IE, Dudley FJ. Hepatic hydrothorax in the absence of clinical ascites: diagnosis and management. Gastroenterology 1985;88(1 Pt
1):188–191

Clinical Presentation
• The c/p of HH is typically dominated by S/S of cirrhosis and ascites.
• HH can present asymptomatically or with cough, dyspnea or hypoxia
depending on various factors.
• These include the volume of fluid in the pleural space and the rapidity of
the accumulation of the pleural fluid .
• A HH should be suspected in a pt with cirrhosis who develops a unilateral
(typically right-sided) PE.
• Most of these effusions tend to be small to moderate in size, with only 6% of pts
having effusions that occupy greater than half of a hemithorax.[1]
1. Keddissi J, Eid AA, Janbey EM, et al. Incidence and outcome of hydrothorax in patients with chronic liver disease. Chest 2002; 122:94S
Ascites is the most common complication of cirrhosis, and 60% of patients with compensated cirrhosis develop ascites within 10 years during the course of their disease . Ascites only
occurs when portal hypertension has developed and is primarily related to an inability to excrete an adequate amount of sodium into urine, leading to a positive sodium balance.
The development of ascites in cirrhosis indicates a poor prognosis. The mortality is approximately 40% at 1 year and 50% at 2 years .

Workup/Diagnosis
• The Dx is based on the presence of PE in pt with presence of cirrhosis with
PHTN and the exclusion of CP disease.
• In a study of 60 cirrhotic pts with PE,[1] 70% (42 pts) were found to have an
uncomplicated HH(without infection, blood or pus). Of the other 18 pts, 9
had SBEM, 2 had pleural TB, 2 had adenocarcinoma, 2 had parapneumonic
effusion, and 3 were undiagnosed exudates. When the effusion was rt sided,
80% were an UHH; but when the PE was left-sided only 35% were an UHH.
Hence the presence of a right sided PE in a cirrhotic pt should not be always
assumed to be an HH. Pleural fluid analysis is mandatory.
• A thoracentesis should be performed .
1. Xiol X, Castellote J, Cortes-Beut R, Delgado M, Guardiola J, Sesé E. Usefulness and complications of thoracentesis in cirrhotic patients. Am J Med 2001;111(1):67–69

Workup/ Diagnosis DX tests to be ordered on the pleural fluid include
cell count, Gm stain & culture, & S & fluid protein,
albumin, and LDH.[1,2]
The composition of HH is transudative in nature and
therefore similar to the ascitic fluid; it will also have
a SPAG> 1.1 as is found in ascites secondary to
PHTN.
Other tests depending on the clinical circumstances include
TG, pH, ADA and PCR for mycobacteria, amylase, and cytology
to exclude chylothorax, empyema, TB, pancreatitis, and
malignancy, respectively. These additional tests should be
considered when the fluid is an exudate or when the PE is left
sided.
2. Strauss RM, Boyer TD. Hepatic hydrothorax. Semin Liver Dis 1997;17(3):227–232

• When uncertainty exists regarding the etiology of the PE, the finding of an
elevated serum soluble Fas ligand may help distinguish a HH from one
resulting from heart failure in pts with viral hepatitis.[1]
In addition to pleural fluid analysis, other tests may also be important &
informative.
1. Pertinent laboratory tests such as hepatic panel, and brain natriuretic
peptide (BNP) should be obtained in the proper clinical setting.
2. In addition, a CT scan of the chest will exclude mediastinal, pulmonary, or
pleural lesions or malignancies.
3. Echocardiography should be performed to evaluate cardiac function.
1. Wang PS, Chen YM, Hsieh YL, Yu CF, Tsai CM, Perng RP. Pleural effusion and serum soluble fas-ligand levels are
elevated in different clinical conditions. Lung 2002;180(1):25–32

• Abstract
• Fas ligand (FasL) plays an important role in the regulation of apoptosis.
Soluble FasL (sFasL) is produced by a cleavage of FasL from the cell surface by
metalloproteinase. Whether or not sFasL exists or is elevated in the PE of
different etiologies is unknown.
• The present study is designed to determine PE and serum sFasL levels under
different clinical conditions, and ascertain if there exists a significant
difference in the levels found in different clinical conditions, and whether this
difference can be used as a tool for DD.
• Soluble FasL levels in the PE and serum of 103 pts, including 37 with
malignant PE, 24 with uncomplicated parapneumonic effusion, 8 with
bacterial empyema, 16 with TB pleurisy, and 18 with transudate effusion (8
with CHF and 10 with viral liver cirrhosis), were analyzed with ELISA assays.

• Abstract
• PE from pts with bacterial empyema (median 79.4 pg/ml) and TB pleurisy (median
31.9 pg/ml) contained significantly higher amounts of sFasL than the PE from all
other conditions studied (p <0.001). Viral liver cirrhosis had a significantly higher
serum sFasL level (median 53.6 pg/ml, p = 0.025, when compared with other
patients like CHF). Pts with CHF had the lowest serum sFasL levels when compared
with other pts (p = 0.014).
• There was no significant correlation between PE sFasL levels and other parameters,
such as effusion LDH, cell count, neutrophil, and lymphocyte percentage.
• In conclusion, soluble FasL is a useful marker for the differentiation of bacterial
empyema and TB pleurisy from other disease entities. In addition, the elevation
of serum sFasL levels in viral liver cirrhosis can also be used to differentiate
cirrhosis from CHF, in which both effusions are transudate.

Spontaneous Bacterial Empyema
• A SBEM is an infection of a preexisting HH in which pneumonia has been
excluded.
• However, this term may be confusing because there is typically no evidence
of pus or abscess in the thoracic cavity; for this reason, some authors have
proposed that it be called spontaneous bacterial pleuritis.[1] However, this name
has not gained acceptance, and most published studies referring to infections of the pleural fluid in
cirrhotics use the term SBEM.
• Infection of the pleural fluid must be considered in any pt with HH who
develops fever, pleuritic pain, encephalopathy, or unexplained
deterioration in renal function. Therefore a high index of suspicion is
essential for its diagnosis.
1. Streifler J, Pitlik S, Dux S, Garty M, Rosenfeld JB. Spontaneous bacterial pleuritis in a patient with cirrhosis. Respiration 1984;46 (4):382–385

Incidence of SBEM
• is similar to the reported incidence of SBP; 15-20% of hospitalized pts with cirrhosis
will have SBP, and in a prospective study Xiol and colleagues found a 13% incidence
of SBEM.[1-4] Interestingly up to 40% of cases of SBEM are not associated with SBP.[1]
• Some patients will not have ascites, supporting the hypothesis that enteric
microorganisms reach the pleural space through bacteremia as has been reported
in SBP.[5] This is in addition to direct spread of the infection from the peritoneal
space through the diaphragmatic defects. Because SBEM can develop without
simultaneous SBP, a thoracentesis should be performed in a patient with a clinical
suspicion for an infection even if a paracentesis has not revealed an infection.
• The MC bacteria involved are Enterobacteriaceae (Escherichia coli and Klebsiella
pneumonia), Streptococcus species and Enterococcus species. Not surprisingly, these are
also the most common bacterial causes of SBP.
1. Xiol X, Castellví JM, Guardiola J, et al. Spontaneous bacterial empyema in cirrhotic patients: a prospective study. Hepatology 1996;23(4):719–723
2. Conn HO, Fessel JM. Spontaneous bacterial peritonitis in cirrhosis: variations on a theme. Medicine (Baltimore) 1971;50(3): 161–197
3. Almdal TP, Skinhøj P. Spontaneous bacterial peritonitis in cirrhosis: incidence, diagnosis, and prognosis. Scand J Gastroenterol 1987;22 (3):295–300
4. Albillos A, Cuervas-Mons V, Millán I, et al. Ascitic fluid polymorphonuclear cell count and serum to ascites albumin gradient in the diagnosis of bacterial peritonitis. Gastroenterology
1990;98(1): 134–140
5. Garcia-Tsao G. Spontaneous bacterial peritonitis. Gastroenterol Clin North Am 1992;21(1):257–275

The diagnostic criteria for SBEM are as follows:
Positive pleural fluid culture and a PMN count > 250 cells/mm3
Negative pleural fluid culture and a PMN count > 500 cells/mm3
No evidence of pneumonia on a chest x-ray
Fluid should be inoculated at the bedside directly into a blood culture bottle. This
increases the sensitivity for the diagnosis of SBEM from 33 to 77%.[1]

Treatment for SBEM
• Rx for SBEM typically involves the use of a 3G cephalosporin.
• The use of albumin in preventing HRS is the standard of care in patients with SBP but
it has not been studied in patients with SBEM.[1] These pts should be placed on life-
long (or until a LT) prophylaxis for the prevention of SBEM or SBP with norfloxacin,
ciprofloxacin, or bactrim.
• Chest tube insertion is not indicated in the management of SBEM . Chest tube
insertion can lead to renal insufficiency, increased risk of 2ND infection, and further
protein loss.[2,3]
• A few studies have evaluated the RF for developing SBEM. Sese and colleagues found
that a low pleural fluid TP(<1.0 mg/dL) as well as a higher CPS were a/w the
development of an SBEM.[4] Simultaneous SBP is also a risk factor.[5] Mortality is as
high as 20% in patients with SBEM.[6,7]
• Just as the development of SBP is an indication for a LT evaluation, the development
of SBEM should prompt a referral to a LT center.
1. Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med 1999;341(6): 403–409
2. Runyon BA, Greenblatt M, Ming RH. Hepatic hydrothorax is a relative contraindication to chest tube insertion. Am J Gastroenterol 1986;81(7):566–567
3. Orman ES, Lok AS. Outcomes of patients with chest tube insertion for hepatic hydrothorax. Hepatol Int 2009;3(4):582–586
4. Sese E, Xiol X, Castellote J, Rodríguez-Fariñas E, Tremosa G. Low complement levels and opsonic activity in hepatic hydrothorax: its relationship with spontaneous bacterial empyema. J Clin Gastroenterol 2003;36(1):75–77
5. Chen TA, Lo GH, Lai KH. Risk factors for spontaneous bacterial empyema in cirrhotic patientswith hydrothorax. J ChinMed Assoc 2003;66(10):579–586
7. Garcia N Jr, Mihas AA. Hepatic hydrothorax: pathophysiology, diagnosis, and management. J Clin Gastroenterol 2004;38(1): 52–58

Management of Hepatic Hydrothorax
• The most important aspect of MX is evaluation for liver transplantation .
• The outcome of pts with HH undergoing LT is similar to that of pts who have LT due
to other reasons [1].
The main goal of treatment is relief of symptoms and prevention of pulmonary
complications and infections until LT can be performed, or palliative treatment in
those who are not candidates for transplantation.
The treatment approach to HH consists of measures to
Reduce the formation of ascitic fluid,
Prevent the movement of ascitic fluid across the diaphragm, and
Drain or obliterate the pleural space.
1. Xiol X, Tremosa G, Castellote J, et al. Liver transplantation in patients with hepatic hydrothorax. Transpl Int 2005; 18:672.
Patients with refractory hydrothorax treated with OLT had a mean survival of 97 months, with 82% survival at 1 year and 70% at 5 years after OLT.
Survival after OLT of the patients with noncomplicated hydrothorax is 90% at 1 year and 80% at 5 years,
Mean survival of transplanted patients with hydrothorax and SBEM after OLT was 98 months . Thus SBEM should be considered an indication for OLT.

1.Reduce the Formation of Ascitic Fluid
General Management
• Decrease salt and fluid intake
Medical Management
Diuretics
Somatostatin
Terlipressin
TIPSS
LIVER TRANSPLANT

Salt restriction and Use of Diuretics
• The primary goal of HH treatment is to achieve a -ive Na balance by restricting
sodium intake and pharmacological therapy using diuretics [1] . Sodium
intake in the diet should be <2,000 mg/day.
• A combination of L diuretics (furosemide) & ARA(spironolactone) is used to
achieve a renal excretion of at least 120 mEq Na/day [2] .
• Diuretics can be increased in a stepwise manner by doubling the dose Q5
days if there is no response to treatment, and noncompliance with diet and
medications have been excluded.
• Max doses of spironolactone & furosemide are up to 400 and 160 mg/day,
respectively [3] .
1. Al-sharif H, Sharma S: Hepatic hydrothorax – how would you manage it? Can Respir J 2005; 12: 440–442.
2. Runyon BA, Practice Guidelines Committee, American Association for the Study of Liver Diseases (AASLD): Management of adult patients with ascites due to cirrhosis. Hepatology 2004; 39: 841–856.
3. Moore KP, Wong F, Gines P, et al: The management of ascites in cirrhosis: report on the consensus conference of the International Ascites Club. Hepatology 2003; 38: 258–266.

Extra notes
1.A diet containing 88 mmol/day is currently recommended for pts with ascites.
2.Pts with ascites on no diuretics commonly have renal Na excretion of < 20 mmol/day.
Such a pt on a no-added-salt diet will retain at least 100 mmol of Na/ day and 10 L of fluid
in 2 wks (100 mmol/day x 14 days/140 mmol/L = 10 L).
3.One of the goals of treatment is to increase urinary excretion of Na so that it exceeds 78
mmol per day .
4.Only the 10%-15% of pts who have spontaneous natriuresis >78 mmol per day and can be
considered for dietary sodium restriction alone (i.e., without diuretics).
5.A random ‘‘spot’’ urine Na concentration that is > K concentration correlates well with a 24-hr Na excretion.
This urine Na/K ratio may replace the cumbersome 24-hr collection. When this ratio is >1, the pt should be
losing fluid weight. The higher the ratio, the greater the urine Na excretion.
The recommended dietary sodium intake for the general population is <100 meq/day (2.3 g of sodium or 6 g of NACL).
• Sodium chloride=table salt=40 % sodium
• 3 tea spoon =1 table spoon =14.7 ml=17 gm of salt
• 1 teaspoon= 2.3 gm sodium

• Abstract:To compare the effect of diet, cirrhotic patients with ascites were randomised into
two treatment groups: (1) a low sodium diet (21 mmol) per day or (2) an unrestricted
sodium intake. Both groups received effective doses of diuretics (spironolactone or, if
necessary, spironolactone & furosemide.
• 140pts from 12 liver units were included according to well defined criteria (group 1: 76;
group 2: 64). After an initial 4-7 d period of bed rest & salt restriction (21 mmol Na pd),
randomisation was done in each centre.
• We saw no significant difference between the 2 groups with respect to clinical and
biochemical data; mortality or withdrawal (definitive or temporary) because of biochemical
disturbances (group 1: 34%, group 2: 22%); the time for complete disappearance of
ascites was significantly shorter (p = 0.014) for the salt restricted pts. Survival (curves
plotted up to the 120th day) was not statistically different (p = 0.18), but division into
subgroups using various prognostic factors showed that survival was significantly better
for salt restricted patients without previous Gi bleeding (p = 0.02); hospitalisation time
and costs were identical in both groups. We conclude that the advantage of a normal salt
diet was not shown in this study.

Role of water restriction
• There have been no studies on the benefits or harm of water restriction on the
resolution of ascites. Most experts agree that there is no role for water
restriction in patients with uncomplicated ascites. However, water restriction
for patients with ascites and hyponatraemia has become standard clinical
practice in many centres. However, there is real controversy about the best
management of these patients, and at present we do not know the best
approach.
• Most hepatologists treat these patients with severe water restriction.
• However, based on our understanding of the pathogenesis of hyponatraemia,
this treatment is probably illogical and may exacerbate the severity of effective
central hypovolaemia that drives the non‐osmotic secretion of antidiuretic
hormone (ADH). This may result in further increases in circulating ADH, and a
further decline of renal function.

Role of water restriction
• Impaired free water clearance is observed in 25–60% of pts with ascites due
to cirrhosis,1 and many develop spontaneous hyponatraemia.2 Therefore,
some hepatologists, including the authors, advocate further plasma
expansion to normalise and inhibit stimulation of ADH release.
• Studies are needed to determine the best approach.3
• There are data emerging that support the use of specific vasopressin 2
receptor antagonists in the treatment of dilutional hyponatraemia,4,5,6 but
whether this improves overall morbidity and mortality is not yet known.
• It is important to avoid severe hyponatraemia in patients awaiting liver
transplantation as it may increase the risk of central pontine myelinolysis
during fluid resuscitation in surgery.
1. Bichet D, Szatalowicz V, Chaimovitz C. et al Role of vasopressin in abnormal water excretion in cirrhotic patients. Ann Int Med 198296413–417.
2. Gatta A, Caregaro L, Angeli P. et al Impaired renal water excretion in liver cirrhosis. The role of reduced distal delivery of sodium. Scand J Gastroenterol 198823523–528.
3. Perez‐Ayuso R M, Arroyo V, Camps J. et al Effect of demeclocycline on renal function and urinary prostaglandin E2 and kallikrein in hyponatremic cirrhotics. Nephron 19843630–37.
4. Gerbes A L, Gulberg V, Gines P. et al Therapy of hyponatremia in cirrhosis with a vasopressin receptor antagonist: a randomized double‐blind multicenter trial. Gastroenterology 2003124933–939.
5. Fernandez‐Varo G, Ros J, Cejudo‐Martin P. et al Effect of the V1a/V2‐AVP receptor antagonist, Conivaptan, on renal water metabolism and systemic hemodynamics in rats with cirrhosis and ascites. J Hepatol 200338755–761.
6. Wong F, Blei A T, Blendis L M. et al A vasopressin receptor antagonist (VPA‐985) improves serum concentration in patients with hyponatremia: a multicenter, randomized, placebo‐controlled trial. Hepatology 200337182–191.

Refractory HH
• Pts who do not respond to medical therapy are considered to have a
refractory HH. It is a clinical challenge to manage refractory HH as most of these pts have
associated renal dysfunction along with impaired liver function. Aggressive diuresis is usually
complicated by renal insufficiency and electrolyte imbalance and is poorly tolerated in these pts.
• Therapeutic thoracentesis is a safe and effective way to rapidly relieve
symptoms of dyspnea in patients with large effusions (1.5-2.0 L)[1].
However, when thoracentesis is required >1 q2-3 wk in pts on maximal
sodium restriction and optimal diuretics, it is considered refractory, and
alternative treatments should be considered.[2]
1. Xiol X, Guardiola J. Hepatic hydrothorax. Curr Opin Pulm Med. 1998;4:239–242.
2. Ivo C Ditah, Badr F Al Bawardy, Behnam Saberi, Chobufo Ditah, and Patrick S Kamath. Transjugular intrahepatic portosystemic stent shunt for medically refractory hepatic hydrothorax: A systematic review and
cumulative meta-analysis.World J Hepatol. 2015 Jul 8; 7(13): 1797–1806.

Refractory HH
• In a retrospective study of 405 pts with cirrhosis admitted over a 5-yr period, 7 of
27 (25.9%) HH patients were refractory to medical treatment [1] .
• In another prospective study of 60 cirrhotic pts, 13 (21.7%) HH patients were
considered refractory [2] .
• Approximately 21–26% of HH cases are refractory to salt and fluid restriction and
diuretics [3] and warrant consideration of additional treatment measures.
• Ideally, LT is the best Mx option for these pts [4,5] .
• Treatment measures other than LT may not only provide relief from dyspnea but
also improve pt survival and serve as a bridge to LT.
• In a study of 52 HH ps [6] , resolution of HH for at least 3 mnths was reported in 37.5% of pts with chemical
pleurodesis and in 42.9% after surgical intervention, with an overall success rate of 50%. The median
survival of pts with intervention success (22.5 mnths) was significantly longer than in those with
intervention failure (5.4 months) and supportive care (6.3 mnths).
1. Esteve M, Xiol X, Fernadez F, Gonzalez F, Baliellas C: Treatment and outcome of hydrothorax in liver cirrhosis. J Clin Nutr Gastroenterol 1986; 1: 139–144.
2. Sesé E, Xiol X, Castellote J, Rodríguez-Fariñas E, Tremosa G: Low complement levels and opsonic activity in hepatic hydrothorax: its relationship with spontaneous bacterial empyema. J Clin Gastroenterol 2003; 36: 75–77.
3. Sesé E, Xiol X, Castellote J, Rodríguez-Fariñas E, Tremosa G: Low complement levels and opsonic activity in hepatic hydrothorax: its relationship with spontaneous bacterial empyema. J Clin Gastroenterol 2003; 36: 75–77.
4. Cardenas A, Kelleher T, Chopra S: Review article: hepatic hydrothorax. Aliment Pharmacol Ther 2004; 20: 271–279.
5. Garcia N Jr, Mihas AA: Hepatic hydrothorax. Pathophysiology, diagnosis, and management. J Clin Gastroenterol 2004; 38: 52–58.
6. Liu WL, Kuo PH, Huang PM, Yang PC: Impact of therapeutic interventions on survival of patients with hepatic hydrothorax. J Formos Med Assoc 2010; 109: 582–588.

RHH
• A case report showed that IV terlipressin, which is known to be beneficial in the
HRS, might also be effective in HH [1] .
• IV octreotide has also treatment benifit [2] .
• A case of refractory HH, in which after adding the α-adrenergic agonist midodrine
to octreotide, complete resolution also been reported [3] . Octreotide can
potentiate the beneficial hemodynamic and renal effects of midodrine in
decompensated cirrhosis [4] . The hypothesis behind the use of these agents is to
reduce splanchic blood flow thereby decreasing peritoneal and pleural fluid
accumulation.
• However, there are not enough data to support the routine use of these drugs in
the management of HH.
1. Ibrisim D, Cakaloglu Y, Akyuz F, et al: Treatment of hepatic hydrothorax with terlipressin in a cirrhotic patient. Scand J Gastroenterol 2006; 41: 862–865.
2. Barreales M, Sáenz-López S, Igarzabal A, et al: Refractory hepatic hydrothorax: successful treatment with octreotide. Rev Esp Enferm Dig 2005; 97: 830–835.
3. Kalambokis G, Fotopoulos A, Economou M, Tsianos EV: Beneficial haemodynamic and renal sodium handling effects of combined midodrine and octreotide treatment in a cirrhotic patient with large hepatic hydrothorax and mild ascites. Nephrol Dial Transplant 2005;
20: 2583.
4. Kalambokis G, Economou M, Fotopoulos A, et al: The effects of chronic treatment with octreotide versus octreotide plus midodrine on systemic hemodynamics and renal hemodynamics and function in nonazotemic cirrhotic patients with ascites. Am J Gastroenterol
2005; 100: 879–885.

• Abstract: HH is a complication of cirrhosis that is uncommon and difficult to
treat. Diuretic therapy, thoracentesis, TIPS and LT are the main therapeutic
options.
• Here, we report on a 47-year-old man with DLC related to hepatitis B/D virus
infections and who had complications of HH and HRS. In this case, the HH, which
was refractory to thoracic tube drainage and octreotide treatment, could be
controlled with 5 days of terlipressin therapy associated with albumin.
• Terlipressin administration resulted in both improvement in renal function and
successful resolution of hepatic hydrothorax.
• Splanchnic vasoconstrictor agents that reduce splanchnic blood flow, increase both central
volume and effective renal blood flow. Thus they improve renal function.
• In this case, terlipressin, known to be beneficial in HRS, was also effective in the
treatment of HH probably by similar mechanisms.
• This is the first case in the literature.

Transjugular intrahepatic portosystemic shunt
• TIPS is a procedure that creates an anastomosis between the portal and the
hepatic vein. It decompresses the splanchic vascular bed, thereby decreasing
portal venous pressure.
• The efficacy of TIPS in HH has been reported in several retrospective
nonrandomized studies and case reports [1-8] .
1. Siegerstetter V, Deibert P, Ochs A, Olschewski M, Blum HE, Rössle M: Treatment of refractory hepatic hydrothorax with transjugular intrahepatic portosystemic shunt: longterm results in 40 patients. Eur J Gastro
enterol Hepatol 2001; 13: 529–534.
2. Strauss RM, Martin LG, Kaufman SL, et al: Transjugular intrahepatic portal systemic shunt for the management of symptomatic cirrhotic hydrothorax. Am J Gastroenterol 1994; 92: 1520–1522.
3. Gordon FD, Anastopoulos HT, Crenshaw W, et al: The successful treatment of symptomatic,refractory hepatic hydrothorax with transjugular intrahepatic portosystemic shunt. Hepatology 1997; 25: 1366–1369.
4. Jeffries MA, Kazanjian S, Wilson M, et al: Transjugular intrahepatic portosystemic shunts and liver transplantation in patients with refractory hepatic hydrothorax. Liver Transpl Surg 1998; 4: 416–423.
5. Chalasani N, Clark WS, Martin LG, et al: Determinants of mortality in patients with advanced cirrhosis after transjugular intrahepatic portosytemic shunting. Gastroenterology 2000;118:138–144.
6. Spencer EB, Cohen DT, Darey MD: Safety and efficacy of transjugular intrahepatic portosystemic shunt creation for the treatment of hepatic hydrothorax. J Vasc Interv Radiol 2002; 13: 385–390.
7. Wilputte JY, Goffette P, Zech F, et al: The outcome after transjugular intrahepatic portosystemic shunts (TIPS) for hepatic hydrothorax is closely related to liver dysfunction: a long-term study in 28 patients. Acta
Gastroenterol Belg 2007; 70: 6–10.
8. Dhanasekaran R, West JK, Gonzales PC, et al: Transjugular intrahepatic portosystemic shunt for symptomatic refractory hepatic hydrothorax in patients with cirrhosis. Am J Gastroenterol 2010; 105: 635–641.
The procedure was first described by Josef Rösch in 1969 at Oregon Health and Science University. It was first used in a human patient by Dr.
Ronald Colapinto, of the University of Toronto, in 1982, but did not become reproducibly successful until the development of endovascular
stents in 1985. In 1988 the first successful TIPS was realized by M. Rössle, G.M. Richter, G. Nöldge and J. Palmaz at the University of Freiburg.
The procedure has since become widely accepted as the preferred method for treating portal hypertension that is refractory to medical
therapy, replacing the surgical portocaval shunt in that role.

Transjugular Intrahepatic Portosystemic Shunt
• CI to placing a TIPS are age> 70, significant HE, large PVthrombosis, right-sided
heart failure, elevated pulmonary arterial pressures, and MELD score >18.
• This elevated MELD score is a marker for more severe hepatic dysfunction. Because TIPS shunts blood away from
the liver and reduces the effective portal perfusion to the liver, it can precipitate liver failure in patients with
already significant hepatic dysfunction.
• Relative CI to TIPS include large hepatic tumors, extensive polycystic liver
disease, HVobstruction, severe coagulopathy (INR >5) and PLT <20,000/cm 3 .
Patients with significant coagulopathy may be able to undergo TIPS if following treatment
with clotting factors or platelets [1] .
• In a carefully selected population though, TIPS can lead to significant
improvements in the complications related to PHTN.
1. Boyer TD, Haskal ZJ: The role of transjugular intrahepatic portosystemic shunt (TIPS) in the management of portal hypertension: update 2009. Hepatology 2010; 51: 1–16.

• In carefully selected patients with MELD score <15, CTP A or B and age
<60 years, TIPS can be an effective treatment of RHH and can be used as
a bridge to LT.
• The average 30-day mortality was around 18.6%. The factors associated
with mortality after TIPS for HH are age >60 years, CTP class C, high pre-
TIPS MELD >15 and high pre-TIPS creatinine levels >2 mg/dl .
• In patients with high predicted 30-day mortality rates with MELD >15 and
CTP class C, TIPS should only be performed in the absence of other
options.

• The most recently published and largest series to date was reported by
Dhanasekaran and colleagues in 2010.[1] In their study 73 pts with refractory
HH had a TIPS placed. 59% of pts had a complete response, 20% had a partial
response, and 21% had no response to TIPS placement.
• The short-term survival rates at 30, 60, and 90 days were 81, 78, and 72%,
respectively.
• The long-term survival rates at 1, 3, and 5 years were 48, 26, and 15%,
respectively.
1. Dhanasekaran R, West JK, Gonzales PC, et al. Transjugular intrahepatic portosystemic shunt for symptomatic refractory hepatic hydrothorax in
patients with cirrhosis. Am J Gastroenterol 2010; 105(3):635–641

Complication of the TIPS procedure
• The major complication of the TIPS procedure is the development or worsening of
HE.
• In the study done by Dhanasekaran et al. [1] , HE developed in 15% of the pts. The
other complications included infection in 8.2%; procedure-related bleeding in
6.8%, AKI in 2.7% and the ARDS in 2.7%.
• The incidence of HE ranged anywhere between 5 and 50% in different studies, with
an average of 26.7% [1,2-7] . This could be because of the retrospective nature of these
studies making it difficult to assess the grade of HE after TIPS.
• Shunt occlusion or thrombosis is also one of the late complications of the TIPS
procedure causing reaccumulation of pleural fluid and ascites.
• The patency of covered stents seems to be better than that of uncovered stents. In a
prospective randomized study that compared the patency rates of covered and uncovered
stents, the patency rate was found to be better with covered stents (76%) then with
uncovered stents (36%) [8] .
1. Dhanasekaran R, West JK, Gonzales PC, et al: Transjugular intrahepatic portosystemic shunt for symptomatic refractory hepatic hydrothorax in patients with cirrhosis. Am J Gastroenterol 2010; 105: 635–641.
2. Siegerstetter V, Deibert P, Ochs A, Olschewski M, Blum HE, Rössle M: Treatment of refractory hepatic hydrothorax with transjugular intrahepatic portosystemic shunt: longterm results in 40 patients. Eur J Gastro enterol Hepatol 2001; 13: 529–534.
3. Gordon FD, Anastopoulos HT, Crenshaw W, et al: The successful treatment of symptomatic, refractory hepatic hydrothorax with transjugular intrahepatic portosystemic shunt. Hepatology 1997; 25: 1366–1369.
4. Jeffries MA, Kazanjian S, Wilson M, et al: Transjugular intrahepatic portosystemic shunts and liver transplantation in patients with refractory hepatic hydrothorax. Liver Transpl Surg 1998; 4: 416–423.
5. Chalasani N, Clark WS, Martin LG, et al: Determinants of mortality in patients with advanced cirrhosis after transjugular intrahepatic portosytemic shunting. Gastroenterology 2000;118:138–144.
6. Spencer EB, Cohen DT, Darey MD: Safety and efficacy of transjugular intrahepatic portosystemic shunt creation for the treatment of hepatic hydrothorax. J Vasc Interv Radiol 2002; 13: 385–390.
7. Wilputte JY, Goffette P, Zech F, et al: The outcome after transjugular intrahepatic portosystemic shunts (TIPS) for hepatic hydrothorax is closely related to liver dysfunction: a long-term study in 28 patients. Acta Gastroenterol Belg 2007; 70: 6–10.
8. Bureau C, Pagan JCG, Layrargues GP, et al: Patency of stents covered with polytetrafluoroethylene in patients treated by transjugular intrahepatic portosystemic shunts: long-term results of a randomized multicentre study. Liver Int 2007; 27: 742–747.

2. Prevent the movement of ascitic fluid across the
diaphragm
Paracentesis
Repair of diaphragmatic defects
Continuous Positive Airway Pressure

Paracentesis
• Paracentesis is a simple and well-tolerated procedure and should be
attempted in all pts with HH prior to thoracentesis to prevent the rapid
accumulation of fluid in the pleural space .
• LVP can also provide symptomatic relief of dyspnea in patients with HH even
before thoracentesis is performed.
• A study by Angueira and Kadakia [1] demonstrated a statistically significant
symptomatic improvement within 2 h of paracentesis with an average fluid
removal of 3.5 liters.
1. Angueira CE, Kadakia SC: Effects of largevolume paracentesis on pulmonary function in patients with tense cirrhotic
ascites. Hepatology 1994; 20: 825–828.

Peritoneovesical Shunt
• A peritoneovesical shunt known as ALFA pump system is a new
investigational technique that has been approved in Europe for the
management of ascites but has not yet been approved in US [1] .
• It is implanted subcutaneously and pumps excess peritoneal fluid into the
bladder where the patient can eliminate it through normal urination.
Reduction in ascites may also decrease HH formation.
1. Wong F: Management of ascites in cirrhosis. J Gastroenterol Hepatol 2012; 27: 11–20.

Repair of Diaphragm Defects
• Evaluation for defects in the diaphragm by open thoracotomy and by videothoracoscopy
has been used to identify DD. If the defect can be identified, biologic glue or sutures can be
used to close and seal these defects.[1,2,3]
• In small, uncontrolled reports, good results have been seen in pts in whom the
fenestrations can be localized and closed.
• Milanez de Campos and colleagues[4] performed thoracoscopies in 18 pts with HH with an
overall success rate of 48%. In the 5 pts where DD were identified and closed, 4 had
resolution of the HH, and the fifth pt developed Empyema and died secondary to
pneumonia and liver failure. Morbidity (57.1%) and mortality (38.9%) were high in this
study during a f/u period of 3 mnths, raising questions about the utility of such an
approach. Although there are no head-to-head comparison studies, the mortality rate in
this thoracoscopic study can be placed in the context of the lower 90-day mortality (25%)
reported with TIPS.
2. Rubinstein D, McInnes IE, Dudley FJ. Hepatic hydrothorax in the absence of clinical ascites: diagnosis and management. Gastroenterology 1985;88(1 Pt 1):188–191
3. Mouroux J, Hébuterne X, Perrin C, et al. Treatment of pleural effusion of cirrhotic origin by videothoracoscopy. Br J Surg 1994;81 (4):546–547
4. Milanez de Campos JR, Filho LO, de Campos Werebe E, et al. Thoracoscopy and talc poudrage in the management of hepatic hydrothorax. Chest 2000;118(1):13–17

Repair of Diaphragmatic Defects
• Ibi et al. [1] reported 2 cases of RHH that were successfully treated with repair of DD with
sutures, biological glue and mesh during VATS. There was no recurrence of HH in both cases
at the 1-yr f/u.
• In a surgical series of 10 pts, Huang et al. [2] reported successful control of HH with
thoracoscopic pleural mesh onlay reinforcement to repair the diaphragmatic fenestrations.
There was no recurrence in any pt after a mean follow-up of 7.7 mnths. Two patients died
of hemorrhage from EV 2 mnths postoperatively.
1. Ibi T, Koizumi K, Hirata T, et al: Diaphragmatic repair of two cases of hepatic hydrothorax using video-assisted thoracoscopic surgery. Gen Thorac Cardiovasc Surg 2008; 56: 229–232.
2. Huang PM, Kuo SW, Lee JM: Thoracoscopic diaphragmatic repair for refractory hepatic hydrothorax: application of pleural flap and mesh onlay reinforcement. Thorac Cardiovasc
Surg 2006; 54: 47–50.

Repair of Diaphragmatic Defects
• Repair of the defects has also been combined with pleurodesis during VATS to
increase the success of the procedure.
• The success rate increased from 47.6 to 60% after repair of the DD in a study
of 18 pts with RHH [1] .
1. Milanez de Campos JR, Filho LO, de Campos Werebe E, et al: Thoracoscopy and talc poudrage in the management of hepatic hydrothorax. Chest 2000; 118: 13–17.
2. Luh SP, Chen CY: Video-assisted thoracoscopic surgery (VATS) for the treatment of hepatic hydrothorax: report of twelve cases. J Zhejiang Univ Sci B 2009 10: 547–551.
3. Cerfolio RJ, Bryant AS: Efficacy of video-assisted thoracoscopic surgery with talc pleurodesis for porous diaphragm syndrome in patients with refractory hepatic hydrothorax.Ann Thorac Surg 2006; 82: 457–459.
4. Takayama T, Kurokawa Y, Kaiwa Y, et al: A new technique of thoracoscopic pleurodesis for refractory hepatic hydrothorax. Surg Endosc 2004; 18: 140–143.
5. 84 Ferrante D, Arguedas MR, Cerfolio RJ, Collins BG, van Leeuwen DJ: Video-assisted thoracoscopic surgery with talc pleurodesis in the management of symptomatic hepatic hydrothorax. Am J Gastroenterol 2002; 97:
3172–3175.
However, these defects cannot be visualized in all pts.
• Luh&Chen [2] visualized DD in only 2 of 12 (16.7%) pts. which were repaired with sutures.
• Similarly, in other studies, DD were visualized in 12 and 22.2% of the cases, respectively [3,4] , and in some
series, DD could not be visualized at all during VATS [5] .
Although this approach appears encouraging, it is limited by the lack of visualization of the DD. However, if a
patient is taken for VATS pleurodesis then an attempt to visualize the diaphragmatic fenestrations and repair,
if possible, should be considered to increase the successful outcome of pleurodesis.

Continuous Positive Airway Pressure
• CPAP ↓ the negative pressure in the thoracic cavity, thereby decreasing the pressure
gradient between peritoneal and pleural cavities and thus preventing the flux of fluid
from the abdomen to the pleural space.
• A case of resistant HH with marked improvement following nasal CPAP treatment during
sleep has been reported [1] .
• In one study, CPAP was combined with pleurodesis to improve the success rate by
increasing +intrathoracic pressure and reversing the peritoneal-pleural pressure gradient.
• This reversing of the pressure gradient encourages the backward flow of fluid from the
pleural to the peritoneal space, thereby allowing more time for the pleural surfaces to be
dry to achieve pleurodesis [2] .
• However, further large studies are needed to validate the use of CPAP solely for the
management of RHH, but a combination of CPAP with other techniques like pleurodesis
appears promising theoretically. Also, increased risk of aspiration with the use of CPAP in
the setting of HE should be kept in mind.
1. Takahashi K, Chin K, Sumi K, Nakamura T, Matsumoto H, Niimi A, et al: Resistant hepatic hydrothorax: a successful case with treatment by nCPAP. Respir Med 2005; 99:262–264.
2. Northup PG, Harmon RC, Pruett TL, Schenk WG III, Daniel TM, Berg CL: Mechanical pleurodesis aided by peritoneal drainage: procedure for hepatic hydrothorax. Ann Thorac Surg 2009; 87: 245–250.

3.Drain the Pleural Space
Repeated thoracentesis
Indwelling pleural catheter
Pleurovenous shunt

Thoracentesis and Repeated Thoracentesis
• In pts who are symptomatic, a thoracentesis needs to be performed to relieve
the dyspnea, or hypoxia. However, when a thoracentesis is required more than once every 2 -3 wks in pts on
maximal Na restriction and optimal diuretics, alternative treatments must be considered as the procedure-related
complications, including pneumothorax and hemothorax, increase with the increased frequency of procedures.
• As a general rule, no more than 2 L of fluid should be removed because of
the risk of pulmonary edema and hypotension.[45]
• However, this "2 liter rule" was developed in pts with causes of the PE other than cirrhosis;
pts with cirrhosis may be able to tolerate the removal of larger vol of fluid.
• Given the relatively small vol of fluid removed at thoracentesis we do not
administer IV albumin to avoid circulatory dysfunction unlike its routine use
with LVP.
1. Sherman SC. Reexpansion pulmonary edema: a case report and review of the current literature. J Emerg Med 2003;24 (1):23–27

Repeated Thoracentesis
• The development of chest discomfort that has been correlated with a reduction
in pleural pressure should be a sign to terminate thoracentesis [1] .
• Coagulopathy should not be considered as a CI to thoracentesis and
paracentesis.
• A retrospective study of 608 pts undergoing thoracentesis and paracentesis did
not show any increased bleeding in pts with mild-to-moderate coagulopathy
with PT up to twice the midpoint NR, or plt count of 50–99,000/μl; authors
concluded that prophylactic plasma or plt transfusions are not necessary.
However, pts with markedly elevated S creatinine levels >6.0 mg/dl had a
significantly greater average hb loss of >2 g/dl than pts with normal S creatinine
levels. Overall, red cell transfusions were required only in 0.2% of events [2] .
1. Feller-Kopman D, Walkey A, Berkowit D, Ernst A: The relationship of pleural pressure to symptom development during therapeutic thoracentesis. Chest 2006; 129: 1556–1560.
2. McVay PA, Toy PT: Lack of increased bleeding after liver biopsy in patients with mild hemostatic abnormalities. Am J Clin Pathol 1990; 94: 747–753.

Chest Tube placement
• A chest tube should not be placed in HH pts because high chest tube output
and massive loss of fluid can lead to renal dysfunction and electrolyte
disturbances [1] .
• Because of the rapid reaccumulation of fluid in the pleural space as well as the high
output, removal of the chest tube becomes difficult once it is placed.
• A retrospective review of 17 pts with HH and placement of a chest tube
showed that 16 of 17 pts had at least one complication and 12 pts had >1
complication. 11 pts had AKI, 7 pts had pneumothorax and 5 pts had
empyemas [2] .
1. McVay PA, Toy PT: Lack of increased bleeding after liver biopsy in patients with mild hemostatic abnormalities. Am J Clin Pathol 1990; 94: 747–753.
2. Orman ES, Lok AS: Outcomes of patients with chest tube insertion for hepatic hydrothorax. Hepatol Int 2009; 3: 582–586.

Chest Tube placement
• The largest retrospective study so far that analyzed the outcome of chest tube
placement in 59 cirrhotic pts was reported by Liu et al. [1] , however it also included
pts who received chest tubes for empyema as well as pneumothorax.
• The study showed that 80% of pts had one or more complications like renal
dysfunction, electrolyte imbalances and infection.
• Mortality was 16% in CTP class B pts and up to 40% among CTP C patients.
• Deaths while having a chest tube in place were deemed by the authors to be secondary to
complications from having it in place, rather than to AE from the tube placement procedure.
• Even in cases of SBEM, pts have been treated with antibiotics alone without any
requirement of a chest tube.
1. Liu LU, Haddadin HA, Bodian CA, et al: Outcome analysis of cirrhotic patients undergoing chest tube placement. Chest 2004; 126: 142–148.
2. Xiol X, Castellví JM, Guardiola J, et al: Spontaneous bacterial empyema in cirrhotic patients: a prospective study. Hepatology 1996;23: 719–723.
Since chest tube insertion is associated with higher adverse events, as discussed before, and most cases of SBEM respond
to antibiotic therapy [2] , a chest tube should not be placed in patients with SBEM unless they meet criteria for placing a
chest tube like frank pus or pH <7.2, however which is uncommon in HH.

Indwelling Pleural Catheter
• Tunneled pleural catheter (PleurX) insertion has been shown to be effective
in the management of malignant PE with symptomatic relief of symptoms
and spontaneous pleurodesis in some pts [1] . It is placed under local
anesthesia.
1. Tremblay A, Michaud G: Single-center experience with 250 tunneled pleural catheter insertions for malignant pleural effusion. Chest 2006; 129: 362–368.

• Abstract: RHH poses a challenging therapeutic dilemma, as treatment options are limited. Herein, we
describe the case of a 48-year-old lady with advanced cirrhosis and recurrent transudative PE despite a
sodium-restricted diet, optimal diuretic therapy and transjugular intrahepatic portosystemic shunt. Given
the pt's platelet and coagulation disorders, thoracoscopic pleurodesis was deemed unsafe. Instead, a
tunneled pleural catheter (PleurX®) was inserted under local anesthesia. Pleural drainage was achieved at
the time of catheter placement and subsequently according to the patient's symptoms. Symptomatic
improvement and gradual decrease of drainage volumes were noted.
• 6 mnths following placement of PleurX, MRSA cellulitis at the insertion site
prompted catheter removal. No PE was seen on CXR at that time. Subsequent f/u
revealed spontaneous pleurodesis, as no recurrence of PE was seen over a 6-mnth
f/u period.
• Very few data are available with regard to the use of indwelling pleural catheters
for benign transudative PE, and more specifically HH. Herein, Mercky P et al
presented this novel potential indication of the indwelling pleural catheter and
illustrate the successful clinical outcome.

Pleurovenous Shunt
• A few case reports have used a PVS for the management of HH [1,2] .
• Artemiou et al. [3] showed the effectiveness of pleurovenous shunts in 12
pts with chronic nonmalignant right-sided pleural effusions.
• Out of these, 6 had HH. Patients were followed for a period of 13.3 months
(1–40 months). All shunts were patent and none of the patients required
further treatment for pleural effusion.
• However, long-term patency and complications of pleurovenous shunts
remain currently unknown.
1. Hadsaitong D, Suttithawil W: Pleurovenous shunt in treating refractory nonmalignant hepatic hydrothorax: a case report. Respir Med 2005; 99: 1603–1605.
2. Bayram AS, Köprücüoğlu M, Aygün M, Gebitekin C: Pleurovenous shunt for treating refractory benign pleural effusion. Eur J Cardiothorac Surg 2008; 33: 942–943.
3. Artemiou O, Marta GM, Klepetko W, Wolner E, Muller MR: Pleurovenous shunting in the treatment of nonmalignant pleural effusion. Ann Thorac Surg 2003; 76: 231–233.

Obliterate the pleural space (pleurodesis)
• Instillation of sclerosant through the chest tube
• Talc poudrage
• VATS and pleurodesis*
• 1) Chemical
• 2) Mechanical
* May be combined with repair of diaphragmatic defects.

Pleurodesis
• is a procedure in which the space between the visceral and parietal pleura
is obliterated with the use of an agent that acts as an irritant to cause
inflammation on the pleural surfaces.
• The irritant is administered through a chest tube or during thoracoscopy
(medical or VATS).
• Transudative PE are notoriously difficult to pleurodese due to the absence
of inflamed pleural surfaces that are required for successful adhering of
parietal and visceral surfaces together.
• In addition, the rapid fluid reaccumulation prevents the visceral and
parietal pleural surfaces from approximating long enough for the
inflammatory process to result in pleural symphysis.[1,2]
1. Falchuk KR, Jacoby I, Colucci WS, Rybak ME. Tetracycline-induced pleural symphysis for recurrent hydrothorax complicating cirrhosis: a new approach to treatment.
Gastroenterology 1977;72 (2):319–321
2. Ikard RW, Sawyers JL. Persistent hepatic hydrothorax after peritoneojugular shunt. Arch Surg 1980;115(9):1125–1127

Studies regarding pleurodesis in HH
• Pleurodesis with tetracycline or talc has been used. The irritant is
administered through a chest tube or by thoracoscopy.
• In the study described earlier by Milanez de Campos and colleagues,[1]
aerosolized talc was effective in preventing recurrence of the effusion in
only 10 patients (47.6%). Effusions recurred within 3 mnths in 43.7% of pts;
in addition there were several complications noted, including fever, chest
pain,empyema, incomplete reexpansion, pneumonia, and wound infection.
• A smaller study by Mouroux and colleagues[2] utilized VATS to repair
diaphragmatic defects in addition to pleurodesis in 8 pts with RHH.
Hydrothorax resolution occurred in the 6 pts where a defect was found
and repaired, with a follow-up of 7 to 36 months.
1. Milanez de Campos JR, Filho LO, de Campos Werebe E, et al. Thoracoscopy and talc poudrage in the management of hepatic hydrothorax. Chest 2000;118(1):13–17

• In a similar study, Ferrante and colleagues[1] performed VATS and talc
pleurodesis in 15 pts with RHH. No visual defect was found in any of these
patients. Control of symptoms and resolution of the effusion were achieved
in 11 pts (73%) in the first 30 dys after the procedure, with 8 pts remaining
asymptomatic for a median f/u of 5.5 mnths and 3 experiencing recurrence
of the PE between 45-60 days after the VATS. Unfortunately, complications
included pain around the chest tube site, low-grade fever with leukocytosis,
pleurocutaneous fistula, and Empyema.
• Takayama and colleagues[2] reported on a technique of thoracoscopic
pleurodesis using argon beam coagulation, fibrin glue, and minocycline in
nine patients with RHH. In this small study all pts showed clinical
improvement with two recurrences.
1. Ferrante D, Arguedas MR, Cerfolio RJ, Collins BG, van Leeuwen DJ. Video-assisted thoracoscopic surgery with talc pleurodesis in the management of symptomatic hepatic hydrothorax. Am J
Gastroenterol 2002;97(12):3172–3175
2. Takayama T, Kurokawa Y, Kaiwa Y, et al. A new technique of thoracoscopic pleurodesis for refractory hepatic hydrothorax. Surg Endosc 2004;18(1):140–143

• Finally Northup and colleagues[1] described a technique of a thoracoscopically
guided mechanical pleurodesis followed by talc instillation combined with
simultaneous extended percutaneous peritoneal drainage tube placement to
allow complete adherence of the pleural space. In this small series of 5 pts, no
visual defects were found. The drains were left in place for a mean of 12.6 days. Pts
were f/u to 132 days without recurrence of the PE, although 2 pts received a liver
transplant within 1 mnth of the procedure.
• The success of their procedure was based on two aspects: (1) the meticulous mechanical abrasion (up
to 30 minutes) of the entire diaphragmatic surface and (2) the addition of the peritoneal catheter aided
in decreasing the hydrostatic pressure from the peritoneal cavity driving fluid into the pleural space.
• Although VATS with pleurodesis appears promising, most reports include small
numbers of pts and are uncontrolled. Therefore, medical management and TIPS
should be attempted first, and VATS with pleurodesis should be considered only if
these measures fail.
1. Northup PG, Harmon RC, Pruett TL, SchenkWG III, Daniel TM, Berg CL. Mechanical pleurodesis aided by peritoneal drainage: procedure for hepatic hydrothorax. Ann Thorac Surg 2009;87(1):
245–250

• The most common sclerosing agent that has been used in different studies is
talc. However, a few studies have used tetracycline, OK-432 with
minocycline, Vibramycin, povoiodine and bleomycin [1,2,3] . The overall
success rate of pleurodesis in different studies, which was defined as
radiographic disappearance of pleural fluid and relief of symptoms, has been
between 47 and 100%.
• The average overall success rate was 74.7% and the average recurrence rate,
requiring repeated pleurodesis, was 24.5%. The mean duration of chest tube
drainage was 8.7 days.
1. Takayama T, Kurokawa Y, Kaiwa Y, et al: A new technique of thoracoscopic pleurodesis for refractory hepatic hydrothorax. Surg Endosc 2004; 18: 140–143.
2. Helmy N, Akl Y, Kaddah SC, et al: A case series: Egyptian experience in using chemical pleurodesis as an alternative management in refractory hepatic hydrothorax. Arch Med
Sci 2010; 6: 336–342.
3. Lee WJ, Kim HJ, Park JH, et al: Chemical pleurodesis for the management of refractory hepatic hydrothorax in patients with decompensated liver cirrhosis. Korean J Hepatol
2011; 17: 292–298.

Chemical Pleurodesis
• Chemical pleurodesis can be done by instillation of a sclerosing agent through a
chest tube as well as during medical thoracoscopy.
• A retrospective Korean study used talc, taurolidine and Viscum album in 3, 2 and
6 patients, respectively, for pleurodesis via a chest tube [1] . None of the patients
was considered for TIPS as it was not available at the institution where the study
was performed.
• The median MELD score was 16 (9–21). The overall success rate was 72.7% with a
recurrence rate of 27%. Patients who achieved success of the treatment showed
significantly better outcomes than patients who did not achieve success.
Complications included low grade fever and leukocytosis (100%), pneumonia
(9.1%), pneumothorax (36.4%), azotemia/acute renal failure (54.6%) and hepatic
encephalopathy (36.4%). The procedure-related mortality due to occurrence of
acute renal failure was 45.5%.
1. Lee WJ, Kim HJ, Park JH, et al: Chemical pleurodesis for the management of refractory hepatic hydrothorax in
patients with decompensated liver cirrhosis. Korean J Hepatol 2011; 17: 292–298.

• Only one study used medical thoracoscopy for pleurodesis [1] . However, it is
unclear why medical thoracoscopy was done when talc was used as slurry after
medical thoracoscopy.
• Pleurodesis was performed in 23 patients using talc (asbestos free), Vibramycin
and povoiodine with an overall success rate of 75%. All patients were CTP B. The
recurrence rate was 20% and mean duration of chest tube drainage was 9.8 ± 2.3
days. However, pleurodesis had to be repeated at least once in all patients .
Moreover, somatostatin was used in all pts to reduce drainage volume and
shorten the duration of chest tube removal.
• As mentioned before, somatostatin reduces splanchic blood flow and the
portosystemic pressure gradient, thereby reducing peritoneal and pleural fluid
accumulation. Somatostatin was preferred instead of TIPS in the study as per
authors somatostatin has few and minor side effects compared to TIPS.
1. Helmy N, Akl Y, Kaddah SC, et al: A case series: Egyptian experience in using chemical pleurodesis as an alternative
management in refractory hepatic hydrothorax. Arch Med Sci 2010; 6: 336–342.

• Early complications after the procedure included surgical emphysema (18.2%),
superficial wound infection (9.1%), mild thoracic pain (4.5%) and a single pt (4.5%)
with prehepatic coma 4 days after the procedure that was treated medically. Two
(10.5%) pts developed late complications. One pt treated with povoiodine
developed tense ascites. Another pt treated with talc slurry developed tense
ascites and hepatic coma at the 3-mnth fw-up that was treated with medical
therapy and was also associated with encysted right-sided PE. There was only 1
single case of mortality (5%) in a pt treated with talc slurry that occurred 14 days
after the procedure due hepatic coma. Only this study compared the success rate
of different sclerosing agents.
• The success rate was 66.7% with talc slurry, 87.5% with povo-iodine and 66.7%
with Vibramycin.
• Since the number of pleurodesis sessions was highest with talc (50% required two
attempts and 50% required three) and lowest with povo-iodine (87.5% required
two attempts and none required three), povoiodine was shown to be the sclerosing
agent with the highest success rate.

VATS and Pleurodesis
• Most of the studies used VATS to achieve pleurodesis.
• In a retrospective study of 26 patients, pleurodesis was done with VATS using
talc with an overall response of 91% [1] . Only 2 cases failed to respond with a
drainage volume of >600 ml/day. Of the 2 unsuccessful cases, 1 was
discharged and lost to follow-up and 1 died of hemorrhage and hepatic
encephalopathy 1 month after the procedure.
• The comparison of VATS using thoracoscopic talc insufflation (TTI) and
pleurodesis using talc slurry was done in a study of 21 patients [2] . The initial
success rate was 77% in the VATS group, with 1 early and 2 late recurrences.
The talc slurry group had a success rate of 37.3% and a recurrence rate of 50%.
The duration of chest tube drainage was also longer in the talc slurry group
(9.8 days) as compared to the VATS group (5.8 days). TIPS was performed in 1
patient after pleurodesis failure but without any marked improvement.
1. Lin DJ, Zhang M, Gao GX, Li B, Wang MF,Zhu L, Xue LF: Thoracoscopy for diagnosis and management of refractory hepatic hydrothorax. Chin Med J (Engl) 2006; 119:430–434.
2. Assouad J, Barthes Fle P, Shaker W, Souilamas R, Riquet M: Recurrent pleural effusion complicating liver cirrhosis. Ann Thorac Surg 2003; 75: 986–989.

VATS with Pleurodesis and Repair of
Diaphragmatic Defects
• VATS also helps in to visualize as well as repair the diaphragmatic defects with
fibrin glue or sutures in patients with refractory HH.
• In a study of 8 patients, diaphragmatic defects were repaired in 6 patients along
with VATS and talc pleurodesis [1] .
• The initial success rate was 75% with a recurrence of 25%. Out of 2 patients in
whom defects could not be visualized even after intraperitoneal dye injection, the
duration of drainage was longer and pleural effusion recurred in both. Both of
these patients died of hepatocellular insufficiency.
• In another study of 18 patients by Milanez de Campos et al. [2] , diaphragmatic
defects were seen in 5 patients and repaired in all 5. The success rate increased to
60% from 47.6% after repair of the diaphragmatic defects. The recurrence rate and
duration of chest tube drainage was higher in patients in whom the repair of the
diaphragmatic defect could not be performed.
1. Mouroux J, Perrin C, Vennisac N, Blaive B,Richelme H: Management of pleural effusion of cirrhotic origin. Chest 1996; 109:1093–1096.
2. Milanez de Campos JR, Filho LO, de Campos Werebe E, et al: Thoracoscopy and talc poudrage in the management of hepatic hydrothorax. Chest 2000; 118: 13–17.

• The most common complications associated with pleurodesis seen in different
studies included fever and mild thoracic pain, though empyema, septic shock and
hepatic encephalopathy with liver failure have also been reported.
• Persistent high volume ascitic drainage from the chest tube site causing azotemia
and renal failure is another dreaded complication when the chest tube is left for a
prolonged period.
• Mechanical pleurodesis carries a high risk of bleeding especially in patients with
advanced liver disease and coagulopathy.
• The average cumulative mortality rate in all ten studies was 30.83% and was
attributed to hepatocellular insufficiency, hemorrhage due to esophageal varices,
hepatic encephalopathy, septic shock and renal failure.
• The average 30-day mortality was 21.6%.

• Pleurodesis is an effective method for the management of refractory HH.
• Even though most of the studies have used VATS to achieve pleurodesis with a good
overall success rate, it requires the use of general anesthesia which carries substantial
risks for patients with end-stage liver disease.
• In these patients, medical thoracoscopy may be a reasonable option for symptom relief. It
is done under local anesthesia with conscious sedation.
• Somatostatin can be combined with pleurodesis to decrease the portosystemic pressure
gradient and reaccumulation of pleural fluid to achieve successful pleurodesis.
• Paracentesis performed before pleurodesis may also increase the success rate by
decreasing ascites and flux of fluid from the peritoneal to the pleural cavity, allowing
more time for the pleural spaces to be opposed to each other.
• The PleurX catheter may also be combined with pleurodesis to avoid and decrease
hospitalization in patients, as shown in a study with malignant pleural effusion [1] .
1. Reddy C, Ernest A, Lamb C, Feller-Kopman D: Rapid pleurodesis for malignant pleural effusions: a pilot study. Chest
2011; 139:1419–1423.

Advantages/disadvantages of the different treatment
modalities for HH

Treatments for hepatic hydrothorax
• All patients with confirmed HH should be referred for evaluation for LT.
• The 1ST step in MX is therapy with low sodium diet (70-90 meq/day)
and diuretics.
• If there is no response to diuretics, therapeutic thoracentesis of
approx. 2 l can be attempted followed by diuretics at lower doses.
• If no response: consider for TIPS placement. This measure may help as
a bridge to liver transplantation. However, patients should be carefully selected.
TIPS is best considered in patients younger than 60 years of age, without hepatic
encephalopathy and/or those with Child A/B cirrhosis
• For patients that cannot undergo TIPS , consideration for pleurodesis
or diaphragmatic repair by thoracoscopy should be considered.
• Chest tube placement should be avoided, as it is associated with
severe complications.
* Furosemide 40 mg/day and spironolactone 100mg/day and if there is no
response, diuretics may be increased in a stepwise fashion every 3-5 days by
doubling doses (ratio of 40mg:100mg), furosemide up to 160 mg/day and
spironolactone up to 400 mg/day.
Refractory?

EXTRA NOTES
• The lateral upright chest x-ray should be examined when a PE is suspected.
• In an upright x-ray, 175 mL of fluid blunts the costophrenic angle.
• Blunting of the costophrenic angle usually requires about 175 mL but may
take as much as 500 mL.
• Larger PE opacify portions of the hemithorax and may cause mediastinal
shift; effusions > 4 L may cause complete opacification of the hemithorax
and mediastinal shift to the contralateral side.
mercksmanual

Normal pleural fluid
• The small volume of pleural fluid, which has been calculated at 0.13 mL/kg
of body weight under normal circumstances, serves as a lubricant to
facilitate movement of the pleural surfaces against each other in the course
of respirations. 1
• Clear ultrafiltrate of plasma that originates from the parietal pleura
• A pH of 7.60-7.64
• Protein content of 1-2 g/dL
• Glucose content similar to that of plasma
• Lactate dehydrogenase (LDH) less than 50% of plasma
1. Noppen M. Normal volume and cellular contents of pleural fluid. Curr Opin Pulm Med. 2001 Jul. 7(4):180-2.
Medscape

Transudate effusion
Heart failure Bilateral effusions in 81%; right-sided in 12%; left-sided in 7%
With left ventricular failure, there is increased interstitial fluid, which crosses the
visceral pleura and enters the pleural space
Cirrhosis with ascites
(hepatic hydrothorax)
Right-sided effusions in 70%; left-sided in 15%; bilateral in 15%
Ascitic fluid migration to the pleural space through diaphragmatic defects
Effusion present in about 5% of patients with clinically apparent ascites
Hypoalbuminemia Uncommon
Bilateral effusions in > 90%
Decreased intravascular oncotic pressure causing transudation into the pleural space
Associated with edema or anasarca elsewhere
Nephrotic syndrome Usually bilateral effusions; commonly subpulmonic
Decreased intravascular oncotic pressure plus hypervolemia causing transudation into
the pleural space
Hydronephrosis Retroperitoneal urine dissection into the pleural space, causing urinothorax

Transudate effusion
Constrictive
pericarditis
Increases IV hydrostatic pressure
In some patients, accompanied by massive anasarca and ascites
due to a mechanism similar to that for hepatic hydrothorax
Atelectasis Increases negative intrapleural pressure
Peritoneal dialysis Mechanism similar to that for hepatic hydrothorax
Pleural fluid with characteristics similar to dialysate
Trapped lung Encasement with fibrous peel increasing negative intrapleural
pressure
May be exudative or borderline effusion
Systemic capillary
leak syndrome
Rare
Accompanied by anasarca and pericardial effusion
Myxedema Effusion present in about 5%
Usually transudate if pericardial effusion is also present; either
transudate or exudate if pleural effusion is isolated

Exudate pleural effusion
Pneumonia
(parapneumoni
c effusion)
May be uncomplicated or loculated and/or purulent (empyema)
Thoracentesis necessary to differentiate
Cancer
Most commonly lung cancer, breast cancer, or lymphoma but possible with any tumor
metastatic to pleurae
Typically causing dull, aching chest pain
Pulmonary
embolism
Effusion present in about 30%:
Almost always exudative; bloody in < 50%
Pulmonary embolism suspected when dyspnea is disproportionate to size of effusion
Viral infection
Effusion usually small with or without parenchymal infiltrate
Predominantly systemic symptoms rather than pulmonary symptoms
Coronary
artery bypass
surgery
Effusions left-sided or larger on the left in 73%; bilateral and equal in 20%; right-sided or
larger on the right in 7%
> 25% of the hemithorax filled with fluid 30 days postoperatively in 10% of patients
Bloody effusions related to postoperative bleeding likely to resolve
Nonbloody effusions likely to recur; etiology uk but probably with an immunologic basis

TB
Effusion usually unilateral and ipsilateral to parenchymal infiltrates if present
Effusion due to hypersensitivity reaction to TB protein
Pleural fluid TB cultures positive in < 20%
Sarcoidosis
Effusion in 1–2%
Extensive parenchymal sarcoid and often extrathoracic sarcoid
Pleural fluid predominantly lymphocytic
Uremia
Effusion in about 3%
In > 50%, symptoms secondary to effusion: Most commonly fever (50%), chest
pain (30%), cough (35%), and dyspnea (20%)
Diagnosis of exclusion
Infradiaphragmatic
abscess
Causes sympathetic subpulmonic effusion
Neutrophils predominant in pleural fluid
pH and glucose normal
HIV infection Many possible etiologic factors: Pneumonias (parapneumonic), including
Pneumocystis jirovecii pneumonia, other opportunistic infections, TB, and
pulmonary Kaposi sarcoma

RA
Effusion typically in elderly men with rheumatoid nodules and deforming arthritis
Must differentiate from parapneumonic effusion
SLE
Effusion possibly first manifestation of SLE
Common with drug-induced SLE
Diagnosis established by serologic tests of blood, not of pleural fluid
Drugs
Many drugs, most notably bromocriptine, dantrolene, nitrofurantoin, IL-2 (for treatment of
renal cell cancer and melanoma), and methysergide
Ovarian
hyperstimulation
syndrome
Syndrome occurring as a complication of ovulation induction with human chorionic
gonadotropin (hCG) and occasionally clomiphene
Effusion developing 7–14 days after hCG injection
Effusion right-sided in 52%; bilateral in 27%
Pancreatitis Acute: Effusion present in about 50%: BL in 77%; left-sided in 16%; right-sided in 8%
Effusion due to transdiaphragmatic transfer of the exudative inflammatory fluid and
diaphragmatic inflammation
Chronic: due to sinus tract from pseudocyst through diaphragm into pleural space
Predominantly chest symptoms rather than abdominal symptoms
Patients presenting with cachexia that resembles cancer

Superior vena cava
syndrome
Effusion usually caused by blockage of intrathoracic venous and lymphatic flow by cancer or
thrombosis in a central catheter
May be an exudate or a chylothorax
Esophageal rupture
Patients extremely sick,Medical emergency
Morbidity and mortality due to infection of the mediastinum and pleural space
Benign asbestos pleural
effusion
Effusion occurring > 30 yr after initial exposure
Frequently asymptomatic,Tends to come and go
Must rule out mesothelioma
Benign ovarian tumor
(Meigs syndrome)
Mechanism similar to that for hepatic hydrothorax
Surgery sometimes indicated for patients with ovarian mass, ascites, and pleural effusion
For diagnosis, disappearance of ascites and effusion postoperatively required
Yellow nail syndrome Triad of pleural effusion, lymphedema, and yellow nails, sometimes appearing decades apart
Pleural fluid with relatively high protein but low LDH
Tendency for effusion to recur,No pleuritic chest pain

Thankyou
Summary
 HH occurs in 5 to 15% of patients with cirrhosis and portal hypertension.
 The entrance of fluid into the pleural space occurs when defects develop in the
diaphragm.
 Medical management with salt restriction and diuretics is first-line therapy.
 Other treatments include thoracentesis, TIPS, VATS, and pleurodesis.
 Ultimately the only cure for hepatic hydrothorax is a liver transplant.

Hepatic Hydrothorax

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