Budd-Chiari Syndrome

Updated: Jan 24, 2017

• Author: Praveen K Roy, MD, AGAF; Chief Editor: BS Anand, MD more...
•

Practice Essentials
Budd-Chiari syndrome is an uncommon condition induced by thrombotic or
nonthrombotic obstruction of the hepatic venous outflow and is characterized by
hepatomegaly, ascites, and abdominal pain. See the image below.

Sonogram showing hepatic vein thrombus, with new vessels forming. The arrow is
pointing to the thrombus.
View Media Gallery
The prognosis is poor in patients with Budd-Chiari syndrome who remain
untreated, with death resulting from progressive liver failure in 3 months to 3 years
from the time of the diagnosis. [1] Following portosystemic shunting, however, the
5-year survival rate for patients with the syndrome is 38-87%. The actuarial 5-year
survival rate following liver transplantation is 70%. [2, 3, 4]
Signs and symptoms

Physical examination may reveal the following:

• Jaundice
• Ascites
• Hepatomegaly
• Splenomegaly
• Ankle edema
• Stasis ulcerations
• Prominence of collateral veins
The clinical variants of Budd-Chiari syndrome have been described as
follows [5, 6, 7]:
• Acute and subacute forms: Characterized by rapid development of abdominal
pain, ascites (which can cause abdominal distention), hepatomegaly, jaundice,
and renal failure.
• Chronic form: Most common presentation; patients present with progressive
ascites; jaundice is absent; approximately 50% of patients also have renal
impairment
• Fulminant form: Uncommon presentation; fulminant or subfulminant hepatic
failure is present, along with ascites, tender hepatomegaly, jaundice, and renal
failure.
See Clinical Presentation for more detail.

Diagnosis

Laboratory studies
Examination of ascitic fluid provides useful clues to the diagnosis of Budd-Chiari
syndrome, including the following:
 • Patients usually have high protein concentrations (>2 g/dL); this may not be
present in persons with the acute form of the disease
• The white blood cell (WBC) count is usually less than 500/µL
• The serum ascites–albumin gradient is usually less than 1.1 (except in the
acute forms of Budd-Chiari syndrome)
Imaging studies
• Ultrasonography
• Computed tomography (CT) scanning
• Magnetic resonance imaging (MRI)
• Venography
Biopsy
Pathologic findings in liver biopsy are (1) high-grade venous congestion and
centrilobular liver cell atrophy, and, possibly, (2) thrombi within the terminal
hepatic venules.
See Workup for more detail.

Management

Pharmacologic therapy
• Anticoagulants
• Thrombolytics
• Diuretics
Procedures and surgery
• Balloon angioplasty
• Localized thrombolysis
• Placement of a stent or transjugular intrahepatic portacaval shunt (TIPS)
• Variceal treatment
• Paracentesis
 • Portal decompression
• Percutaneous transhepatic balloon angioplasty (PTBA)
• Liver transplantation
See Treatment and Medication for more detail.
Background
Budd-Chiari syndrome is an uncommon condition induced by thrombotic or
nonthrombotic obstruction of the hepatic venous outflow and is characterized by
hepatomegaly, ascites, and abdominal pain. It most often occurs in patients with an
underlying thrombotic diathesis, including in those who are pregnant or who have
a tumor, a chronic inflammatory disease, a clotting disorder, an infection, or
a myeloproliferative disorder, such as polycythemia vera or paroxysmal nocturnal
hemoglobinuria. (See Etiology and Presentation.)
Obstruction of large- or small-caliber veins leads to hepatic congestion as blood
flows into, but not out of, the liver. Microvascular ischemia due to congestion
causes hepatocellular injury. Portal hypertension and liver insufficiency
result. [5, 6](See Pathophysiology.)
Budd-Chiari syndrome should be considered separate from veno-occlusive disease
(VOD), also known as sinusoidal obstruction syndrome, which is characterized by
toxin-induced, nonthrombotic obstruction of prehepatic veins (see the images
below). (See Presentation and Workup.)
Sonogram showing hepatic vein thrombus, with new vessels forming. The arrow is
pointing to the thrombus.

View Media Gallery

Sonogram showing hepatic vein thrombus.

Pathophysiology
Occlusion of a single hepatic vein is usually silent. Overt Budd-Chiari syndrome
generally requires the occlusion of at least 2 hepatic veins. [8] Venous congestion of
the liver causes hepatomegaly, which can stretch the liver capsule and be very
painful. Enlargement of the caudate lobe is common because blood is shunted
through it directly into the inferior vena cava (IVC).
Hepatic function can be affected to a degree, depending on the amount of stasis
and resultant hypoxia. Increased sinusoidal pressure can itself cause hepatocellular
necrosis. The literature also suggests that upregulation of specific genes in chronic
Budd-Chiari syndrome contributes to liver destruction through the stimulation of
extracellular matrix proliferation, which contributes to liver fibrosis.
The most prominent genes involved include matrix metalloproteinase 7 and
superior cervical ganglion 10 (SCG10), which are increased in expression, and
thrombospondin-1, which is decreased. [9] Overexpression of the proliferating cell
nuclear antigen gene, the c -MYC oncogene, and the tumor protein p53 gene may
also be etiologic factors for Budd-Chiari syndrome. [10]
Etiology
Most patients with Budd-Chiari syndrome have an underlying thrombotic
diathesis, although in approximately one third of patients, the condition is
idiopathic. Causes of Budd-Chiari syndrome include the following:
• Hematologic disorders
• Inherited thrombotic diathesis
• Pregnancy and postpartum [11]
• Oral contraceptives
• Chronic infections
• Chronic inflammatory diseases
• Tumors
• Congenital membranous obstruction
• Hepatic venous stenosis
• Hypoplasia of the suprahepatic veins
 • Postsurgical obstruction
• Posttraumatic obstruction
• Total parenteral nutrition (TPN): Budd-Chiari syndrome has been reported as
a complication of TPN via an IVC catheter in a neonate

Hematologic disorders

These include the following:

• Polycythemia rubra vera
• Paroxysmal nocturnal hemoglobinuria
• Unspecified myeloproliferative disorder
• Antiphospholipid antibody syndrome
• Essential thrombocytosis

Inherited thrombotic diathesis

Coagulopathies include the following:

• Protein C deficiency
• Protein S deficiency
• Antithrombin III deficiency
• Factor V Leiden deficiency

Chronic infections

These include the following:

• Hydatid cysts
• Aspergillosis
• Amebic abscess
• Syphilis
• Tuberculosis
Chronic inflammatory diseases

These include the following:

• Behçet disease
• Inflammatory bowel disease
• Sarcoidosis
• Systemic lupus erythematosus
• Sjögren syndrome
• Mixed connective-tissue disease

Tumors

These include the following:

• Hepatocellular carcinoma (HCC) [12]
• Renal cell carcinoma
• Leiomyosarcoma
• Adrenal carcinoma
• Wilms tumor
• Right atrial myxoma

Congenital membranous obstructions

These include the following:

• Type I: Thin membrane is present in the vena cava or the atrium
• Type II: A segment of the vena cava is absent
• Type III: The inferior vena cava (IVC) cannot be filled, and collaterals have
developed

Miscellaneous

Miscellaneous causes of Budd-Chiari syndrome include the following:

 • Alpha1-antitrypsin deficiency
• Dacarbazine
• Urethane
Epidemiology
Budd-Chiari syndrome is extremely rare, and the incidence is not well reported in
the literature, although a study by Rajani et al found an incidence of about 1 case
per million population per year in Sweden. Congenital membranous forms of
Budd-Chiari syndrome are the most common cause of the disease worldwide,
particularly in Asia. [13]
A retrospective (2009-2013) nation-wide, population-based study in South Korea
found a total of 424 patients with Budd-Chiari syndrome, with an average age- and
sex-adjusted prevalence of 5.29 per million population. [14] The female-to-male
ratio was 1.8, the median age was 51 years, and the annual case-fatality rate was
2.8%.[14]
No data suggest that sex affects predisposition to Budd-Chiari syndrome.
Nonetheless, in the United States the condition is predominantly seen in women
and is associated with hematologic disorders.
Age at presentation is usually in the third or fourth decade of life, although the
condition may also occur in children or elderly persons.
Prognosis
The natural history of Budd-Chiari syndrome is not well known. The following
factors, however, have been associated with a good prognosis:
• Younger age at diagnosis
• Low Child-Pugh score
• Absence of ascites or easily controlled ascites
• Low serum creatinine level
In a systematic review of 79 studies, investigators found that although univariate
analysis indicated bilirubin and creatinine levels as well as ascites might be
significant prognostic factors, multivariate analyses did not always reveal
achievement of statistical significance. [15]
The following formula has been proposed to calculate the prognostic index for
Budd-Chiari syndrome; a score of less than 5.4 is associated with a good
prognosis:
• Prognostic index = (ascites score x 0.75) + (Pugh score x 0.28) + (age x
0.037) + (creatinine level x 0.0036)
The 5-year survival rate for patients with the syndrome is 38-87% following
portosystemic shunting. The actuarial 5-year survival rate following liver
transplantation is 70%. [2, 3, 4] Long-term follow-up in adults has demonstrated 10-
year survival rates as high as 55%.
The prognosis is poor, however, in patients with Budd-Chiari syndrome who
remain untreated, with death resulting from progressive liver failure in 3 months to
3 years from the time of diagnosis. [1]
In a University of Pennsylvania retrospective study (2008-2013) comprising 47
patients with Budd-Chiari syndrome, there were no significant differences in
treatment outcomes among those receiving anticoagulation therapy alone,
transjugular intrahepatic portosystemic shunt (TIPS) placement alone, and TIPS in
conjunction with anticoagulation. [16] The investigators noted that the significant
prognostic predictors for liver transplantation were age, presence of cirrhosis, and
presence of chronic kidney disease.

Morbidity and mortality

Morbidity and mortality in Budd-Chiari syndrome are generally related to

complications of liver failure and ascites but can also be impacted by the type of
concomitant underlying disease, if any. Complications associated with Budd-
Chiari syndrome include the following:
• Hepatic encephalopathy
• Variceal hemorrhage
• Hepatorenal syndrome
• Portal hypertension
• Complications secondary to hypercoagulable state
• Complications secondary to hepatic decompensation
Bacterial peritonitis is always of concern in the patient with ascites, especially if
paracentesis is undertaken. Complications must also be considered in relation to
therapies used (eg, thrombolytics). The mortality rate can be high in patients who
develop fulminant hepatic failure.
Budd-Chiari syndrome can also lead to HCC (or oppositely, in some cases,
develop secondary to it). In a retrospective study, Liu et al found evidence that
HCC in primary Budd-Chiari syndrome is associated with blockage of the inferior
vena cava and stricture of the hepatic venous outflow tract. The investigators’
results also indicated that transcatheter arterial chemoembolization (TACE) is an
effective treatment for HCC in these patients, with a significant drop in alpha-
fetoprotein levels after TACE treatment. The study included 246 patients with
Budd-Chiari syndrome, including 14 with HCC. Ultrasonography, computed
tomography (CT) scanning, magnetic resonance imaging (MRI), and angiography
were used to determine the imaging characteristics in patients with HCC. [17]
Clinical Presentation
History
The classic triad of abdominal pain, ascites, and hepatomegaly is observed in the
vast majority of patients with Budd-Chiari syndrome, [18] but it is nonspecific. A
high index of suspicion is needed to make the diagnosis.
If the liver has had time to develop collaterals and decompress, patients can be
asymptomatic (≤20% [18] ) or present with few symptoms. As the syndrome
progresses, however, it can lead to liver failure and portal hypertension with
corresponding symptoms (eg, encephalopathy, hematemesis). The American
Association for the Study of Liver Diseases has released guidelines for the
management of acute liver failure. [19]
The clinical variants of Budd-Chiari syndrome have been described as
follows [5, 6, 7]:
• Acute and subacute forms: Characterized by rapid development of abdominal
pain, ascites, hepatomegaly, jaundice, and renal failure.
• Chronic form: Most common presentation; patients present with progressive
ascites; jaundice is absent; approximately 50% of patients also have renal
impairment
• Fulminant form: Uncommon presentation; fulminant or subfulminant hepatic
failure is present, along with ascites, tender hepatomegaly, jaundice, and renal
failure.
Patients with acute onset of obstruction typically present with acute right upper
quadrant pain. Abdominal distention can also be a significant symptom, because of
ascites. Jaundice is rarely observed.
Physical Examination
Physical examination may reveal the following findings:
• Jaundice
• Ascites
• Hepatomegaly
• Splenomegaly
• Ankle edema
• Stasis ulcerations
 • Prominence of collateral veins
Diagnostic Considerations Differentials
Conditions to consider in the differential diagnosis of Budd-Chiari syndrome
include the following:
• Right-sided heart failure
• Metastatic liver disease
• Alcoholic liver disease
• Granulomatous liver disease
• Cirrhosis
• Neonatal hemochromatosis
• Alpha1-antitrypsin deficiency
• Infectious hepatitis
• Niemann-Pick disease type C
• Perforated common bile duct
• Meconium peritonitis
• Jejunal atresia
• Intestinal perforation
• Serositis
• Eosinophilic enteritis
• Henoch-Schönlein purpura
• Parvovirus
• Central venous hyperalimentation
• Obstructive uropathy
• Congestive heart failure
• Dysrhythmia
• Chylous ascites
• Neoplasm
 • Inborn error of metabolism
• Pseudoascites: Small intestinal duplication
• Celiac disease
• Fitz-Hugh Curtis syndrome
• Constrictive pericarditis
• Nephrotic syndrome
• Syphilis
• Toxoplasmosis
Appendicitis
Biliary Atresia
Chronic Granulomatous Disease
Congenital Hepatic Fibrosis
Cystic Fibrosis
Cytomegalovirus Infection
Intestinal Malrotation
Intussusception
Multicystic Renal Dysplasia
Pancreatitis and Pancreatic Pseudocyst
Workup
Approach Considerations
Evaluate patients with Budd-Chiari syndrome for underlying predisposing
conditions, such as malignancy or hypercoagulable states, and institute appropriate
therapy.
Examination of ascitic fluid provides useful clues to the diagnosis, including the
following:
• Patients usually have high protein concentrations (>2 g/dL); this may not be
present in persons with the acute form of Budd-Chiari syndrome
 • The white blood cell (WBC) count is usually less than 500/µL
• The serum ascites–albumin gradient is usually less than 1.1 (except in the
acute forms of the disease)
Routine biochemical test results are usually nonspecific in Budd-Chiari syndrome,
although mild elevations in serum aminotransferase and alkaline phosphatase
levels are present in 25-50% of patients.
Imaging is essential for the early identification and evaluation of the disease extent
in Budd-Chiari syndrome, which aids in mitigating hepatic congestion and,
thereby, restoration of hepatic function and alleviation of portal hypertension. [20]
Imaging Studies

Ultrasonography

Thrombi can be visualized; color-flow Doppler ultrasonography, the preferred

mode, has a sensitivity and specificity of 85-90%. [21, 22] (See the images below.)

Sonogram showing hepatic vein

thrombus, with new vessels forming. The arrow is pointing to the thrombus.

View Media Gallery

Sonogram showing hepatic vein thrombus.

View Media Gallery

Computed tomography (CT) scanning

Detailed imaging studies are required to determine the precise level and degree of
obstruction. CT scanning can rarely provide such detail, unless a mechanical
obstruction, such as a locally invading tumor, is suspected. [23]

Magnetic resonance imaging (MRI)

MRI, which has a sensitivity and specificity of 90% or higher, is becoming

increasingly useful in providing less-invasive venography, angiography, and
cholangiography findings. [24] MRI may assist in differentiating acute from chronic
Budd-Chiari syndrome, because it is able to provide a larger image of the
vasculature, as well as determine if edema of the parenchyma is present (acute
form).

Venography
Catheterization and venography can clearly delineate the nature and severity of an
obstruction. Occasionally, therapeutic interventions can be undertaken at the same
time, including balloon angioplasty, localized thrombolysis, and placement of a
stent or transjugular intrahepatic portacaval shunt (TIPS). [23, 25, 26, 27]
Liver Biopsy and Histology
Percutaneous liver biopsy can be of prognostic assistance, particularly if liver
transplantation is being considered, to establish the degree of hepatocellular
damage and the presence and degree of fibrosis. [28]
Pathologic findings in liver biopsy are (1) high-grade venous congestion and
centrilobular liver cell atrophy, and, possibly, (2) thrombi within the terminal
hepatic venules. The extent of fibrosis can be determined based on biopsy findings.
The most severe findings can include fulminant hepatic failure with massive
centrilobular necrosis.
Studies have indicated, however, that early pathology related to Budd-Chiari
syndrome does not have a significant impact on survival. [29]
Treatment & Management
In patients with Budd-Chiari syndrome, aggressively seek specific therapy aimed
at correcting or alleviating the obstruction. Also treat the underlying conditions
aggressively. [30]
Although medical therapy can be instituted for short-term, symptomatic
benefit, [31]the use of such treatment alone is associated with a high 2-year mortality
rate (80-85%).

Anticoagulant therapy

Anticoagulation is needed in some patients, especially those with underlying

hematologic disorders as the cause of Budd-Chiari syndrome.
Prothrombin time and activated partial thromboplastin time should be monitored
once anticoagulation is started and should be maintained within the therapeutic
range.

Thrombolytic therapy

This therapy has been used in a few cases. Agents include streptokinase, urokinase,
recombinant tissue-type plasminogen activator (rt-PA), and other modalities.

Radiologic intervention

Systemic thrombolysis can be a high-risk endeavor; local thrombolysis performed

by an interventional radiologist is preferable.
Other available radiologic interventions include balloon angioplasty, as well as
placement of a stent or a transjugular intrahepatic portacaval shunt (TIPS). [18, 32, 33]
In a single-center retrospective study (1996-2012), Tripathi et al reported good
long-term outcomes in 67 patients with Budd-Chiari syndrome following
successful transjugular intrahepatic portosystemic stent-shunt (TIPSS) using either
polytertrafluoroethane (PTFE)-covered (n=40) or bare (n=27) stents. [34] At a mean
follow-up of 82 months, 15% of patients experienced post-TIPSS encephalopathy;
2 patients underwent transplantion, 2 patients developed hepatocellular cancer, and
6 patients had liver-related deaths. The PTFE-covered stents had significantly
better primary patency (76%) and shunt reinterventions (22%) compared to the
bare stents (27% and 100%, respectively). Survival at 6 and 12 months was at 92%
or above; that at 24 and 60 months was 80% or above; and 120-month survival was
72%. The investigators indicated that in symptomatic patients in whom hepatic
vein patency cannot be restored, TIPSS should be considered first-line therapy. [34]
In another single center retrospective study (2008-2014) of 190 patients with
Budd-Chiari syndrome who underwent endovascular procedures (hepatic vein,
collateral vein or inferior vena cava [IVC] plasty with or without stenting, or
TIPSS), venous recanalization and TIPPS were safe and effective: 153 patients
(80.5%) experienced treatment response, with 19 patients (10.0%) requiring repeat
interventions and 9 patients (4.7%) with complications. [35] Of the 190 patients, 147
had hepatic vein obstruction, 40 had IVC obstruction, and 3 had both. Thirty-eight
patients underwent hepatic vein/stenting; 3, collateral vein stenting; 40, IVC
plasty/stenting; 3, hepatic vein and IVC stenting; and 106, TIPSS. [35]
Tripathi et al reported similar findings for venous recanalization and TIPPS in 122
patients. [36]

Variceal treatment

Gastroscopy should be performed to help rule out the presence of esophageal and
gastric varices. If present, they may be obliterated with banding or sclerotherapy.
Nonselective beta blockers (eg, propranolol, nadolol) can be administered for
primary prophylaxis against variceal bleeding.

Diet

A low-sodium diet is recommended for the control of ascites.

Paracentesis

Symptomatic treatment for Budd-Chiari syndrome includes diuretics and

therapeutic paracentesis, when necessary, although paracentesis can be associated
with catastrophic complications, such as bacterial peritonitis. Consequently, the
benefits of therapeutic paracentesis must be carefully weighed against its risks.

Portal decompression
Decompression of the hepatic vasculature should be offered if portal hypertension
is the cause of the symptoms. Either surgery or a transjugular intrahepatic
portosystemic shunt (TIPS) procedure can be performed. [2, 6, 27, 37, 38, 39, 40]

Liver transplantation

Liver transplantation should be offered if decompensated liver cirrhosis is

present.[4, 41]
In a Polish retrospective study (2000-2009), the long-term clinical outcomes (eg,
patient and graft survival) following liver transplantation and anticoagulation
maintenance for Budd-Chiari syndrome were good in 25 patients with
myeloproliferative disease and recurrent thrombosis. [42]
Similar findings were reported in an Indian retrospective study (2011-2015) of 9
patients with Budd-Chiari syndrome and chronic liver disease who underwent
living donor liver transplantation. [43] The investigators noted that prevention of
recurrent thrombosis was dependent on "meticulous surgical technique, perfect and
wide outflow anastomoses, and a strict anticoagulation protocol. Moreover, the use
of synthetic (PTFE) graft for inferior vena cava interposition was safe, feasible,
and provided good reconstruction results. [43]

Consultations

Early involvement of a hepatologist can help to establish the direction of workup

and therapy. Consultation with interventional radiologists, hematologists,
oncologists, gastroenterologists, and general surgeons may be required, depending
on the situation. [44]

Follow-up and monitoring

Patients with lesions that are amenable to balloon dilatation or stents require
follow-up catheterizations and, frequently, repeat dilatations or stent replacement.
In addition, patients should have routine surveillance for hepatocellular carcinoma
(HCC). [18, 45]
Angioplasty
This procedure can help relieve obstruction caused by membranous webs. In a
study of 101 patients with Budd-Chiari syndrome, Li et al concluded that the
condition can be safely and effectively treated with percutaneous transhepatic
balloon angioplasty (PTBA). [46] The authors reported successful PTBA (performed
after hepatovenography, with or without stenting) in 92 of the study’s patients,
with all of the successful procedures resulting in significant symptom
improvement.
Complications included acute hepatic vein thrombosis, occurring during or after
the operation (n=3); sustained intraperitoneal bleeding from the transhepatic
puncture track (n=2); pulmonary embolism, which occurred during the procedure
(n=1); and intrahepatic hematoma (n=1). [46] All were managed nonsurgically.
Primary patency rates at 6-, 12-, and 24-month follow-up were 84%, 78%, and
76%, respectively (with several patients lost to follow-up); secondary patency rates
were 95%, 92%, and 84%, respectively. Despite these satisfactory midterm patient
outcomes, the authors cautioned that long-term outcomes in patients treated with
PTBA for Budd-Chiari syndrome require investigation. [46]
Diuretic Therapy
Patients with liver failure and ascites have total body sodium overload, despite
typically low serum sodium concentrations. Inducing negative sodium balance can
reduce the amount of ascites. Take special care when using diuretics, to avoid
inducing hepatorenal syndrome or creating electrolyte and fluid disturbances
through overly aggressive diuresis. Electrolyte levels should be monitored closely.
Secondary hyperaldosteronism is a part of this clinical picture, making
spironolactone typically the first-line diuretic. Chlorothiazide or furosemide is
often added, which can provide synergy and avoid hyperkalemia.
Medication Summary
Medications commonly used in patients with Budd-Chiari syndrome include
diuretics, anticoagulants, and thrombolytics. The therapeutic interventions used
(medical or otherwise) must be tailored to each patient's condition. The use of
thrombolytics should be reserved for experts familiar with the special
circumstances in which they may be appropriate. The use of anticoagulants should
be directed towards therapy of an underlying coagulopathy.
Anticoagulants, Cardiovascular

Class Summary

These agents prevent recurrent or ongoing thromboembolic occlusion.

Warfarin (Coumadin, Jantoven)

• View full drug information

Warfarin interferes with hepatic synthesis of vitamin K–dependent coagulation
factors. It is used for the prophylaxis and treatment of venous thrombosis,
pulmonary embolism, and thromboembolic disorders. Tailor the dose to maintain
an international normalized ratio (INR) in the range of 2-3.
Antifibrinolytic Agents

Class Summary

Fibrinolytic drugs are used to dissolve a pathologic intraluminal thrombus or

embolus that has not been dissolved by the endogenous fibrinolytic system. They
are also used for the prevention of recurrent thrombus formation and for the rapid
restoration of hemodynamic disturbances.
Urokinase

Urokinase is a direct plasminogen activator that acts on the endogenous fibrinolytic

system and converts plasminogen to the enzyme plasmin, which, in turn, degrades
fibrin clots, fibrinogen, and other plasma proteins. It is most often used for local
fibrinolysis of thrombosed catheters and superficial vessels. An advantage to this
agent is that it is nonantigenic. However, urokinase is more expensive than
streptokinase, limiting its use. When it is used for local fibrinolysis, urokinase is
given as a local infusion directly into the area of the thrombus, with no bolus
given. The dose should be adjusted to achieve clot lysis or patency of the affected
vessel.

Alteplase (Activase)

• View full drug information

Alteplase is a tissue plasminogen activator used in the management of acute
myocardial infarction, acute ischemic stroke, and pulmonary embolism. Its safety
and efficacy with concomitant administration of heparin or aspirin during the first
24 hours after symptom onset have not been investigated.
Diuretic Agents

Class Summary

Diuretics can be useful to reduce the amount of ascites, providing symptomatic

relief and reducing the need for paracentesis.

Spironolactone (Aldactone)

• View full drug information

Spironolactone is a potassium-sparing diuretic. It competes with aldosterone for
receptor sites in the distal renal tubules, increasing water excretion while retaining
potassium and hydrogen ions.
This agent is often preferred because of its potassium-sparing effects, particularly
in a clinical setting that includes secondary hyperaldosteronism.

Furosemide (Lasix)

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Furosemide increases the excretion of water by interfering with the chloride-
binding cotransport system, which, in turn, inhibits sodium and chloride
reabsorption in the ascending loop of Henle and the distal renal tubule.

Torsemide (Demadex)

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Torsemide increases excretion of water by interfering with the chloride-binding co-
transport system, which, in turn, inhibits sodium and chloride reabsorption in the
ascending loop of Henle and distal renal tubule. It increases excretion of water,
sodium, chloride, magnesium, and calcium. If a switch is made from intravenous to
oral administration, an equivalent oral dose should be used. Doses vary depending
on the patient's clinical condition.

Chlorothiazide (Diuril)

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A thiazide diuretic, chlorothiazide inhibits sodium-chloride symport, blocking
sodium reabsorption in the distal convoluted tubule.

Hydrochlorothiazide (Microzide)

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Hydrochlorothiazide acts on the distal nephron to impair sodium reabsorption,
enhancing sodium excretion. It has been in use for more than 40 years and is
generally an important agent for the treatment of essential hypertension.