Treatment of hepatic hydrothorax and reduction of chest tube output with octreotide

Pfammatter, Rahel; Quattropani, Christiana; Reichen, Jürg; Göke, B.; Wagner, Andreas

doi:10.1097/00042737-200108000-00019

Cited by 25 publications

(18 citation statements)

References 13 publications

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“…Although numerous case reports have been published on the topic [13,14,[16][17][18], only the study by Liu et al [7] examined the outcomes of a sizeable group of cirrhotic patients with chest tubes. Their findings were similar to ours, with an 80% complication rate and 27% mortality.…”

Section: Discussionmentioning

confidence: 99%

Outcomes of patients with chest tube insertion for hepatic hydrothorax

Orman

Lok

2009

Hepatol Int

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Purpose Case reports and small case series have reported a high rate of complications associated with chest tube placement for hepatic hydrothorax. We describe the inhospital and 3-month outcomes of patients who have had this procedure. Methods A retrospective medical record review was performed of all patients admitted to a tertiary care center over a 10-year period with a chest tube placed for hepatic hydrothorax. Demographic data and outcomes were collected and analyzed. Results Seventeen patients were identified; 12 were taking diuretics and 8 were taking multiple diuretics at the time of admission. MELD score was 14 (range = 7-34). During hospitalization, 16 had at least 1 and 12 had more than 1 complications. The most common complications were acute kidney injury (n = 11), pneumothorax (n = 7), and empyema (n = 5). Two patients died during the index admission and four others within 3 months of that admission. Six of seven patients who received TIPS survived. Conclusions Chest tube insertion for hepatic hydrothorax carries significant morbidity and mortality, with questionable benefit.

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Section: Discussionmentioning

confidence: 99%

Outcomes of patients with chest tube insertion for hepatic hydrothorax

Orman

Lok

2009

Hepatol Int

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“…Octreotide is used to reduce the portal pressure and has been reported to reduce hepatic hydrothorax in adults (9,13,14).…”

Section: Discussionmentioning

confidence: 99%

Hepatic hydrothorax in the absence of ascites in a child with autoimmune hepatitis: Successful management with octreotide and pleurodesis

Sira

Am²,

Bel-S³

et al. 2013

Turk J Gastroenterol

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confidence: 89%

Beneficial haemodynamic and renal sodium handling effects of combined midodrine and octreotide treatment in a cirrhotic patient with large hepatic hydrothorax and mild ascites

Kalambokis¹,

Fotopoulos²,

Economou³

et al. 2005

Nephrology Dialysis Transplantation

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Recently, octreotide-induced natriuresis and reduction of hepatic hydrothorax was described [2,3]. We report on a case of hepatic hydrothorax, which resolved after adding the a-adrenergic agonist midodrine to octreotide. A large sterile right hepatic hydrothorax was diagnosed in a 66-year-old female with hepatitis C virus (HCV) cirrhosis (Child class C) with mild ascites and deteriorating dyspnoea. Increasing doses of spironolactone and furosemide induced marked hyponatraemia and encephalopathy without a reduction of the pleural effusion, and repeated paracenteses were required. Diuretics were discontinued and octreotide 600 mg/day was commenced on day 1; mean arterial pressure (MAP) was 80 mmHg, cardiac output (CO) 7.32 l/min, serum urea (Ure) 7.6 mmol/l, serum creatinine (Cre) 88.4 mmol/l, serum sodium (Na) 124 mmol/l, urinary sodium (UNa) 16 mmol/day, urinary volume (UV) 1100 ml/day, glomerular filtration rate (GFR) with Tc 99m -DTPA 112 ml/min, effective renal plasma flow (ERPF) with Tc 99m -MAG3 615 ml/min, plasma active renin (PAR) 119 mU/ml, plasma aldosterone (PA) 82.5 ng/dl, plasma antidiuretic hormone (ADH) 8.5 pg/ml and plasma glucagon 298 pg/ml. On day 8, PAR, PA and plasma glucagon were 45.8 mU/ml, 39.4 ng/dl and 184 pg/ml, respectively, but ADH remained high (7.4 pg/ml). Octreotide did not improve the MAP (76 mmHg), CO (7.39 l/min) or renal function (Ure 7.3 mmol/l, Cre 97.2 mmol/l, Na 127 mmol/l, UNa 11 mmol/day, UV 850 ml/day, GFR 91 ml/min) despite an increase in ERPF (876 ml/min). The pleural effusion was not mobilized by octreotide whereas it decreased gradually after adding oral midodrine, up to 10 mg t.i.d., to octreotide. On day 17, the MAP was 98 mmHg, CO 6.02 l/min, Ure 5.2 mmol/l, Cre 79.5 mmol/l, Na 133 mmol/l, UNa 165 mmol/day, UV 2900 ml/day, GFR 138 ml/min, ERPF 866 ml/min, PAR 17.3 mU/ml, PA 17.6 ng/dl, ADH 3.5 pg/ml and plasma glucagon 192 pg/ml. Thereafter, she received octreotide 600 mg thrice weekly, midodrine 7.5 t.i.d., furosemide 40 mg/day and spironolactone 100 mg/day without recurrence of the hepatic hydrothorax until her death 4 months later.Splanchnic arterial vasodilation with reflex activation of sodium-and water-retaining systems is involved in the pathogenesis of cirrhotic ascites and related pleural effusion [1]. Chronic octreotide administration seems to disrupt the circulatory homeostasis in decompensated cirrhotics by directly inhibiting the renin-angiotensin-aldosterone axis. As a result, it improves ERPF but not systemic haemodynamics, GFR and natriuresis [4]. However, octreotide ameliorates the splanchnic arterial hyporeactivity to vasoconstrictors by suppressing glucagon secretion [5]. Indeed, recent observations suggest that octreotide could potentiate the beneficial haemodynamic and renal effects of midodrine in decompensated cirrhotics [4]. The combination of midodrine and octreotide could therefore be considered in the treatment of hepatic hydrothorax.

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Treatment of hepatic hydrothorax and reduction of chest tube output with octreotide

Cited by 25 publications

References 13 publications

Outcomes of patients with chest tube insertion for hepatic hydrothorax

Outcomes of patients with chest tube insertion for hepatic hydrothorax

Hepatic hydrothorax in the absence of ascites in a child with autoimmune hepatitis: Successful management with octreotide and pleurodesis

Beneficial haemodynamic and renal sodium handling effects of combined midodrine and octreotide treatment in a cirrhotic patient with large hepatic hydrothorax and mild ascites

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