Portal hypertension, ascites and SBP

• Portal hypertension is a sustained rise in pressure in the portal venous system, most often from cirrhosis. It drives the major decompensating complications of chronic liver disease.
• In cirrhosis it is usually sinusoidal: resistance rises in the liver and splanchnic vasodilation adds to the flow. When the hepatic venous pressure gradient (HVPG) reaches 10 mmHg, portal hypertension becomes clinically significant. ^[1]
• The pressure is decompressed through portosystemic collaterals: oesophageal varices, caput medusae, anorectal varices and retroperitoneal collaterals. A transjugular intrahepatic portosystemic shunt (TIPS) creates an artificial channel between the portal vein and a hepatic vein to lower portal pressure.
• Ascites is evaluated with diagnostic paracentesis as soon as it appears. The serum-ascites albumin gradient (SAAG) tells you whether portal hypertension is the cause; a gradient of 1.1 g/dL or more points to portal hypertension. ^{[1] [2]}
• Cirrhotic ascites is treated with sodium restriction and diuretics, usually spironolactone started at 50 to 100 mg daily with furosemide 20 to 40 mg daily, rising together while monitoring electrolytes and renal function; large-volume paracentesis needs intravenous albumin. ^{[2] [3]}
• Spontaneous bacterial peritonitis (SBP) is diagnosed when polymorphonuclear leucocytes in ascitic fluid reach 250 per microlitre or more. It is treated with a third-generation cephalosporin plus albumin in high-risk patients, with secondary and, in selected cases, primary prophylaxis. ^{[2] [3]}

By the end of this page you should be able to:

1. Explain portal venous anatomy, the sites of portosystemic anastomoses and the structural purpose of a TIPS.
2. Classify the causes of portal hypertension by site and state the HVPG threshold for clinically significant portal hypertension.
3. Trace how portal hypertension produces varices, ascites, splenomegaly, hypersplenism, portal hypertensive gastropathy and hepatic encephalopathy.
4. Perform and interpret the standard new-onset ascitic fluid work-up, including the SAAG table and its interpretation.
5. Grade and treat cirrhotic ascites, including refractory ascites, hepatic hydrothorax and hyponatraemia.
6. Diagnose SBP, prescribe empirical treatment and albumin, and decide on primary and secondary prophylaxis.
7. Distinguish secondary bacterial peritonitis from SBP.
8. Adapt care in low-resource settings where tuberculosis and schistosomal portal disease predominate.

It divides broadly by site:

• Prehepatic causes act before the liver: obstruction or excessive flow in the portal vein or splenic vein.
• Intrahepatic causes act within the liver: presinusoidal, sinusoidal (the cirrhotic pattern that accounts for the large majority of cases worldwide) or postsinusoidal.
• Posthepatic causes act after the liver: obstruction of hepatic venous outflow or elevated right heart pressures transmitted back into the liver.

A useful companion concept is clinically significant portal hypertension (CSPH), defined as an HVPG of 10 mmHg or more, which marks the pressure at which the complications of cirrhosis begin to appear with serious frequency. ^[1]

Schistosomiasis is worth singling out because it is one of the commonest causes of portal hypertension worldwide and is presinusoidal, so the liver parenchyma may be relatively preserved even when collateral channels are fully established.

The portal vein is formed by the confluence of the splenic vein and the superior mesenteric vein, behind the neck of the pancreas. It carries nutrient-rich blood from the gut, pancreas and spleen into the hepatic sinusoids. The hepatic veins then drain the liver into the inferior vena cava.

When pressure in this system rises, blood finds alternative routes back to the systemic circulation through embryological channels that reopen. These are the sites to know, because each produces a recognisable clinical sign.

These collaterals are not a cure for the pressure; they are a bypass. They bleed, they enlarge and they sustain a hyperdynamic circulation, yet portal pressure stays high.

A TIPS takes advantage of this same need to decompress. A stent is placed through the hepatic parenchyma, connecting an intrahepatic branch of the portal vein to a hepatic vein. Blood is shunted past the resistant sinusoids, lowering portal pressure; it is used for refractory ascites, variceal bleeding and, when selected, other complications of portal hypertension. ^[1] The immediate goal is a portal pressure gradient reduced to less than 12 mmHg for bleeding control, with a relative reduction of at least 50 percent from baseline. ^[1]

The HVPG is the difference between the wedged (occluded) and free hepatic vein pressures, measured at cardiac catheterisation. It estimates the sinusoidal pressure and is the gold standard for portal hypertension in cirrhosis. ^[1]

• An HVPG above 5 mmHg indicates sinusoidal portal hypertension. ^[1]
• An HVPG of 10 mmHg or more defines clinically significant portal hypertension and is the threshold at which decompression confers real benefit. ^[1]

Carvedilol and other non-selective beta-blockers, and the etiological removal of the cause of cirrhosis, can lower the HVPG and delay or prevent decompensation. ^[1]

The raised pressure is the engine behind the decompensating events:

• Varices: gastro-oesophageal (most clinically dangerous), rectal and other ectopic varices.
• Ascites: reabsorption of sodium and water in the renal tubules, driven by splanchnic arterial underfilling and neurohormonal activation, produces a transudate that accumulates in the peritoneal cavity.
• Splenomegaly and hypersplenism: congestive enlargement of the spleen consumes platelets and other cell lines, contributing to cytopenia.
• Portal hypertensive gastropathy: a mosaic, red, "snake-skin" gastric mucosa that can ooze or bleed chronically.
• Hepatic encephalopathy: portosystemic shunting bypasses hepatic detoxification, and nitrogenous substances reach the systemic circulation; renal handling, diuretics and infection are common precipitants.
• Hepatorenal syndrome and circulatory dysfunction: extreme renal vasoconstriction on a background of arterial vasodilation.

Every patient with new ascites should have a diagnostic paracentesis before treatment is finalised, and again whenever the clinical picture changes. The procedure is safe even in cirrhosis. ^[3]

Send:

• Cell count and differential (total white cell count and the polymorphonuclear leucocyte count).
• Albumin and total protein.
• Culture, inoculated at the bedside into blood culture bottles (at least 10 mL of fluid).
• Gram stain and additional tests as the suspected aetiology demands (glucose, lactate dehydrogenase, amylase, lipids, cytology, adenosine deaminase for tuberculosis, polymerase chain reaction).

In stable outpatients who are simply undergoing repeated therapeutic paracentesis, only the cell count and differential are routinely needed, and SAAG need not be remeasured. ^[2]

The SAAG is the difference between the serum albumin and the ascitic fluid albumin. It separates portal hypertensive ascites from everything else.

A gradient of 1.1 g/dL or more indicates portal hypertension as the cause of the ascites. ^{[1] [2]} A gradient below 1.1 g/dL means portal hypertension is not the mechanism.

When the gradient is 1.1 g/dL or more, the ascitic protein level refines the diagnosis: a protein of 2.5 g/dL or more suggests cardiac disease or early Budd-Chiari syndrome, while a level below 2.5 g/dL is more consistent with cirrhosis. ^[2]

Chylous ascites is a distinct milky effusion caused by disruption of the thoracic duct or intestinal lymphatics (lymphoma, trauma, cirrhosis, pancreatitis). It contains triglycerides above 110 mg/dL and is worked up with lipid analysis and treatment directed at the underlying cause.

Grade 1 ascites is mild and detectable only on imaging; grade 2 is moderate, symmetrical abdominal distension; grade 3 is large or gross ascites with marked distension. Grade 1 is managed by treating the underlying cause and restricting sodium; grades 2 and 3 need diuretics or paracentesis. ^[3]

Sodium restriction of about 2 g (2,000 mg, or less than 5 g of salt) per day is standard, supplemented by nutrition counselling so that protein intake and calorie intake are preserved. ^[2]

Diuretics work best as a combination. Spironolactone is started at 50 to 100 mg daily, with furosemide 20 to 40 mg daily, and both are increased together in roughly the 100 to 40 mg proportion while monitoring weight, serum sodium, potassium and creatinine; the usual ceiling is 400 mg of spironolactone and 160 mg of furosemide. ^{[2] [3]} Aldosterone antagonists are first-line because secondary hyperaldosteronism drives sodium retention; loop diuretics are added rather than used alone. Careful monitoring avoids excessive diuresis, which risks hypovolaemia and renal injury. Avoid non-steroidal anti-inflammatory drugs and, generally, angiotensin-converting-enzyme inhibitors: both worsen renal perfusion and can precipitate hepatorenal dysfunction. ^[3]

Large-volume paracentesis is the mainstay for tense or refractory ascites. When more than 5 litres are removed, give intravenous albumin at 6 to 8 g per litre of fluid removed. ^[2] This blunts paracentesis-induced circulatory dysfunction, which otherwise concentrates neurohormonal vasoconstrictors and can trigger renal failure. LVP plus albumin is as effective as, and faster than, diuretics for massive ascites. ^[3]

Refractory ascites is ascites that cannot be mobilised by maximal diuretic therapy or that recurs rapidly. Options beyond repeated LVP are TIPS, automated low-flow ascites pumping (where available) and liver transplantation; selected medical therapy (midodrine, vasoconstrictors) is used in some guidelines. ^[3]

Hyponatraemia in cirrhotic ascites reflects advanced dilution and is a marker of poor prognosis. Management includes careful review of diuretics, free water restriction and correction under supervision; AASLD and EASL approaches differ on thresholds, so follow local guidance and avoid overly fast correction. ^{[3] [4]}

Hepatic hydrothorax is a pleural effusion (usually right-sided) caused by transfer of ascites through diaphragmatic defects. It is managed with diuretics, therapeutic thoracentesis and, when refractory, TIPS; chest tube drainage is generally avoided because of infection and protein loss. ^[3]

SBP is a bacterial infection of ascitic fluid without an identifiable intra-abdominal source. ^[3] It arises from bacterial translocation across the gut wall, usually by a single organism, most commonly Gram-negative. In large series the usual organisms are Escherichia coli, Klebsiella species (especially K. pneumoniae) and Streptococcus species. ^[2]

Diagnostic ascitic fluid in SBP shows a polymorphonuclear leucocyte count of 250 per microlitre or more. ^{[2] [3]} The count must be corrected when the sample is bloodstained: subtract one polymorphonuclear leucocyte for every 250 red blood cells per microlitre. ^[2] Blood and ascitic fluid cultures should be obtained before antibiotics, but treatment must not wait for the result.

Presentation is variable: fever, abdominal pain or tenderness, new or worsening hepatic encephalopathy, renal failure, or ileus. Some patients have no symptoms at all, which is why diagnostic paracentesis is part of routine care. Infection is the most common trigger of acute kidney injury in this setting. ^[3]

Empirical treatment is a third-generation cephalosporin: cefotaxime 2 g intravenously every 6 to 8 hours, or ceftriaxone 1 g every 12 hours or 2 g once daily, for 5 to 7 days, adjusted to culture results and local resistance. ^[2] When suspicion of multidrug-resistant organisms is high, such as nosocomial infection or prior broad-spectrum antibiotic use, piperacillin-tazobactam or a carbapenem may be used instead, following local antibiograms. ^[3]

Intravenous albumin reduces renal failure and mortality in SBP. In high-risk patients (total bilirubin above 4 mg/dL or serum creatinine above 1 mg/dL) give 1.5 g/kg on the day of diagnosis and 1 g/kg on day 3. ^[2] Even outside that subgroup, the survival benefit of high-dose albumin combined with antibiotics is well documented. ^[3]

Secondary prophylaxis after a first episode is standard: norfloxacin 400 mg daily reduces recurrence substantially, from about 68 percent to about 20 percent in classic trials, and ciprofloxacin or trimethoprim-sulfamethoxazole are alternatives; rifaximin may also help. ^{[2] [3]}

Primary prophylaxis is reserved for selected patients: those with an ascitic protein concentration of 1.5 g/dL or less, especially with renal impairment, hyponatraemia or advanced liver failure, where norfloxacin 400 mg daily has shown benefit. ^{[2] [3]} Rifaximin and trimethoprim-sulfamethoxazole also have some efficacy. ^[2]

The prognosis after SBP is poor: in-hospital mortality is now around 20 percent, and patients who survive need transplant evaluation. ^[3]

Both are infections of ascites, but the difference matters because the treatment is completely different.

• SBP is a monomicrobial infection, usually an Enterobacterales or Streptococcus, with no intra-abdominal source. The ascitic fluid neutrophil count is 250 per microlitre or more, and peritoneal signs are often absent. Response is expected with antibiotics alone.
• Secondary bacterial peritonitis arises from a perforated viscus or intra-abdominal infection. The fluid tends to be polymicrobial, protein and lactate dehydrogenase are higher, glucose is low, and cytology or imaging may show an abdominal source. It does not respond to antibiotics alone and usually needs surgical or radiological source control, plus broad-spectrum antibiotics.

Clues to secondary peritonitis include multiple organisms on culture, very high neutrophil counts, failure to improve on cephalosporins, and focal peritonitis or free air on imaging. ^{[2] [3]}

The 2021 AASLD practice guidance brings together the diagnosis, evaluation and management of ascites, SBP and hepatorenal syndrome into one document. ^[4] It underpins the approach used above: diagnostic paracentesis at presentation, SAAG-led classification, salt restriction with diuretics, albumin with large-volume paracentesis, cephalosporin-first empirical SBP therapy with albumin in higher-risk patients, and targeted primary and secondary prophylaxis. Wording and thresholds differ between the AASLD, EASL and KASL documents (for example on which SBP patients receive albumin), and local practice should follow the guideline in force in your setting. ^{[2] [3] [4]}

Where TIPS, albumin or full culture facilities are unavailable:

• Diagnosis still rests on careful history and examination, plain imaging and a paracentesis that sends a cell count. Tuberculous peritonitis should be suspected when ascites occurs with a low SAAG, lymphocytes rather than neutrophils, high protein and high adenosine deaminase; it is treated with standard anti-tuberculous therapy. ^[2]
• Portal hypertension in many tropical regions is driven by schistosomiasis (presinusoidal, so surgical or endoscopic services may be as important as transplants) and by chronic viral hepatitis. Treat the cause where possible; propranolol or carvedilol remain cheap and effective for reducing portal pressure. ^[1]
• Ascites responds to sodium restriction and spironolactone; furosemide can be added carefully. Repeated inpatient LVP without albumin is still much better than no care, and oral midodrine is inexpensive where albumin is not.
• SBP can be treated with generic third-generation cephalosporins; ceftriaxone is stable and affordable. Primary prophylaxis with norfloxacin may be unavailable, so ciprofloxacin or trimethoprim-sulfamethoxazole are pragmatic substitutes. ^[2]
• Referral pathways should be agreed in advance for variceal bleeding, refractory ascites and hepatorenal syndrome.

Bedside and laboratory assessment. Look for jaundice, spider naevi, Dupuytren contracture, gynaecomastia and testicular atrophy in men, and palmar erythema; these point to chronic liver disease rather than a vascular cause in isolation. The full blood count often shows anaemia, leucopenia and thrombocytopenia from hypersplenism. Liver biochemistry, INR and albumin estimate synthetic function, while renal function and serum sodium are needed for prognostic scoring (Child-Pugh, MELD-Na).

Imaging. Ultrasound with Doppler is the first study. It shows an irregular liver, splenomegaly, ascites and the patency and flow direction in the portal vein (hepatopetal flow is normal; hepatofugal flow or reversed flow is a sign of established portal hypertension). Cross-sectional imaging (CT or MRI) maps collateral vessels, looks for hepatocellular carcinoma and confirms patency of the hepatic and portal veins. Transient elastography estimates liver stiffness, which correlates with the risk of clinically significant portal hypertension, and spleen stiffness is being studied as a non-invasive surrogate.

Endoscopy. Upper gastrointestinal endoscopy is the standard way to look for oesophageal and gastric varices and for portal hypertensive gastropathy. It is also therapeutic: band ligation and injection therapy. Patients with compensated cirrhosis and clinically significant portal hypertension or varices should be screened, and repeated after treatment; intervals follow local guidance and the Baveno criteria.

Hepatic venous pressure gradient measurement. HVPG is reserved for specialist centres, for clinical trials and for selected decisions such as pre-emptive TIPS. It is invasive but reproducible when performed with a balloon occlusion catheter, with triplicate readings after a stabilisation period, as outlined in the Baveno VII consensus. ^[1]

Follow-up. Patients with cirrhosis and portal hypertension are monitored for the onset of ascites, encephalopathy and variceal bleeding, with repeated imaging of the liver for hepatocellular carcinoma. Alcohol abstinence, control of the underlying cause (such as suppression of hepatitis B and C replication or sustained abstinence) and weight management are the long-term pillars.

Pregnancy. A portal decompressing procedure is rarely needed during pregnancy; acute variceal bleeding is managed with endoscopic band ligation and vasoactive drugs with obstetric support. Drugs used for portal hypertension (especially beta-blockers) and for ascites need individualised risk-benefit discussion in pregnancy, balancing maternal haemodynamics and fetal perfusion.

Children. Extrahepatic portal vein obstruction is the leading cause of portal hypertension in children in many regions, and schistosomiasis and congenital fibrosis are important in others. Surgery and endoscopic services, rather than liver transplantation, dominate care for many of these patients.

Older adults. Frailty, malnutrition and sarcopenia amplify risk; diuretic therapy needs closer renal monitoring, and falls and cognitive effects of drugs matter more than in younger adults.

A patient who fails to improve on antibiotics within 48 to 72 hours, or who has polymicrobial culture, should be re-evaluated urgently for a surgical abdomen.

• Portal hypertension is raised pressure in the portal system; HVPG above 5 mmHg confirms sinusoidal portal hypertension and HVPG of 10 mmHg or more defines clinically significant portal hypertension. ^[1]
• Collaterals form at characteristic sites: left gastric to azygos (oesophageal varices), paraumbilical to epigastrics (caput medusae), superior to middle and inferior rectal (anorectal varices) and retroperitoneal. A TIPS shunts portal blood to a hepatic vein.
• Causes are best classified by site: prehepatic (portal or splenic vein thrombosis), intrahepatic presinusoidal (schistosomiasis, PSVD), sinusoidal (cirrhosis), postsinusoidal and posthepatic (Budd-Chiari, right heart failure, constrictive pericarditis).
• Consequences include varices, ascites, splenomegaly with hypersplenism, portal hypertensive gastropathy and hepatic encephalopathy.
• New-onset ascites needs diagnostic paracentesis with cell count, albumin, total protein and culture in blood culture bottles.
• SAAG of 1.1 g/dL or more identifies portal hypertensive ascites; the cause list is split by high versus low SAAG. Add the ascitic protein level when the SAAG is high.
• Cirrhotic ascites: sodium restriction around 2 g daily; spironolactone 50 to 100 mg daily with furosemide 20 to 40 mg daily, rising together to a ceiling of 400 mg and 160 mg, with electrolyte and renal monitoring; avoid NSAIDs and ACE inhibitors; large-volume paracentesis needs albumin 6 to 8 g per litre removed. ^{[2] [3]}
• SBP: polymorphonuclear leucocytes 250 per microlitre or more in ascitic fluid; usual organisms are E. coli, Klebsiella and Streptococcus; treat with cefotaxime or ceftriaxone, plus albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 in high-risk patients; use secondary and, when selected, primary prophylaxis. ^[2]
• Secondary bacterial peritonitis is polymicrobial, with an intra-abdominal source and more severe peritonitis; it needs source control, not antibiotics alone.
• Poor prognosis after SBP means transplant evaluation should be considered. Low-resource care centres on sodium and diuretics, cephalosporins and antituberculous therapy. ^{[2] [3]}

Portal hypertension connects to cirrhosis and its complications, variceal haemorrhage and band ligation, hepatic encephalopathy, hepatorenal syndrome, liver transplantation, and to schistosomiasis and tuberculosis in endemic regions. Related MedGrasp topics on these will be linked when verified.