Compare conditions

Put any two — or three — conditions side by side, adult or pediatric, to spot the look-alike differences fast, row by row.

Ascites and Spontaneous Bacterial Peritonitis

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In one line

·Spontaneous bacterial peritonitis (SBP) is a bacterial infection of belly fluid (ascites) that happens when gut bacteria slip into the fluid—no hole in the bowel or other source you can fix with surgery.

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Normal physiology

·The peritoneum is a smooth, two-layer membrane that lines your belly and wraps your organs. It makes less than 50 milliliters (about three tablespoons) of clear, sterile fluid every day to let organs glide without rubbing. Your gut wall is a tight fence of cells glued together by proteins called tight junctions; these keep the trillions of bacteria living inside your intestines from leaking into your blood or belly. Your liver makes albumin (a protein that holds water inside blood vessels like a sponge), clotting factors, and immune proteins (complement, antibodies) that tag and kill any bacteria that slip through.

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What goes wrong

·Cirrhosis scars and stiffens the liver, so blood backs up in the portal vein (the big vein from your gut to your liver). That high pressure pushes water and protein out of blood vessels into your belly, forming fluid buildup in the belly (ascites). At the same time, cirrhosis means your liver cannot make enough albumin or infection-fighting proteins, so the fluid buildup in the belly fluid is weak and cannot kill bacteria. Cirrhosis also makes your gut wall leaky—swelling and low bile flow loosen the tight junctions between gut cells, letting bacteria sneak through into the belly fluid. Once bacteria land in fluid buildup in the belly, they multiply fast because there are not enough white blood cells or antibodies in the fluid to stop them. That runaway infection is spontaneous bacterial peritonitis.

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Hallmark signs

·Fever (temperature ≥38.0 °C / 100.4 °F)
·Belly pain or tenderness
·Worsening confusion or altered mental status (hepatic encephalopathy)
·Low blood pressure (systolic <90 mmHg or a drop of ≥40 mmHg from your usual)
·Sudden kidney injury (creatinine rises ≥0.3 mg/dL or urine drops to <0.5 mL per kilogram per hour)
·Very low body temperature (hypothermia <36.0 °C / 96.8 °F)
·Few or no symptoms at all (happens in up to 30 % of people)
·A stalled gut (Ileus) (belly bloating, no bowel sounds, nausea, vomiting)

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Red flags · escalate now

·Low blood pressure (systolic <90 mmHg) or signs of septic shock: cold arms and legs, blotchy skin, blood lactate >4 mmol/L (waste acid building up because organs aren't getting enough oxygen)
·Sudden kidney injury: creatinine rises ≥0.3 mg/dL in 48 hours, or urine output drops below 0.5 mL per kilogram per hour for 6 hours straight
·Severe confusion or unresponsiveness (hepatic encephalopathy grade III–IV): very sleepy, can't be woken easily, or in a coma
·High kidney waste or liver breakdown markers at diagnosis—creatinine ≥1 mg/dL, blood urea nitrogen (BUN) ≥30 mg/dL, or total bilirubin ≥4 mg/dL—all predict high risk of death and mean you need IV albumin (a protein infusion) to support blood pressure and kidneys
·Seeing lots of bacteria on a Gram stain of the belly fluid, or free air on a CT scan—this suggests the infection is NOT spontaneous bacterial peritonitis but secondary peritonitis from a hole in the bowel or an abscess, and you need emergency surgery

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Workup

·Diagnostic paracentesis with ascitic fluid analysis: cell count with differential, Gram stain, bacterial culture (inoculate blood culture bottles at bedside), total protein, and albumin
·Serum creatinine, blood urea nitrogen (BUN), and electrolytes (sodium, potassium) to assess kidney function and volume status
·Complete blood count (CBC) with differential, prothrombin time/INR (international normalized ratio), and liver function tests (total and direct bilirubin, AST, ALT, alkaline phosphatase, albumin)
·Blood cultures (two sets, aerobic and anaerobic bottles) drawn before starting antibiotics
·Ascitic fluid lactate dehydrogenase (LDH), glucose, total protein, albumin, carcinoembryonic antigen (CEA), and alkaline phosphatase if secondary bacterial peritonitis is suspected
·Abdominal ultrasound or CT (computed tomography) scan only if secondary bacterial peritonitis is suspected based on focal tenderness, peritoneal signs, or atypical fluid chemistry
·Repeat paracentesis 48 hours after starting antibiotics if clinical improvement is absent or if initial PMN count was very high (above 1,000 per cubic millimeter)

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Treatment

·Perform diagnostic paracentesis immediately, send fluid for cell count with differential, Gram stain, culture (inoculate blood culture bottles at bedside for highest yield), total protein, and albumin. Start empiric intravenous ceftriaxone 2 grams every 24 hours (or cefotaxime 2 grams every 8 hours) without waiting for culture results.
·Administer intravenous albumin 1.5 grams per kilogram of body weight within 6 hours of diagnosis (day 1), then 1.0 gram per kilogram on day 3. Use 25 percent albumin solution.
·Discontinue nephrotoxic medications: non-steroidal anti-inflammatory drugs (NSAIDs like ibuprofen, which block renal prostaglandins and reduce glomerular filtration), ACE inhibitors and angiotensin receptor blockers (ARBs, which dilate the efferent renal arteriole and drop filtration pressure), and aminoglycosides (antibiotics toxic to renal tubules). Temporarily hold diuretics (furosemide, spironolactone) until infection clears and blood pressure stabilizes.
·After infection resolves (repeat paracentesis showing PMN count below 250 per cubic millimeter and negative culture, or clinical resolution of fever and abdominal pain), start secondary prevention (prophylaxis) with oral norfloxacin 400 milligrams once daily (or ciprofloxacin 750 milligrams once weekly, or trimethoprim-sulfamethoxazole one double-strength tablet daily). Continue indefinitely or until liver transplantation.
·If performing large-volume paracentesis (removing 5 liters or more of ascitic fluid to relieve tense fluid buildup in the belly (ascites) and respiratory distress), administer intravenous albumin 6 to 8 grams per liter of fluid removed immediately after the procedure.
·If fluid buildup in the belly (ascites) becomes refractory (does not respond to maximum-dose diuretics: spironolactone 400 milligrams and furosemide 160 milligrams daily, with sodium restriction below 2 grams per day) and the patient has recurrent SBP or requires frequent large-volume paracentesis (3 or more times per month), refer for transjugular intrahepatic portosystemic shunt (TIPS, a radiologic procedure placing a stent between the portal vein and hepatic vein to bypass the cirrhotic liver and lower portal pressure).
·Evaluate for liver transplantation in all patients with SBP, especially those with MELD score above 15, refractory fluid buildup in the belly (ascites), hepatorenal syndrome, or recurrent SBP despite prevention (prophylaxis).

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NCLEX trap

·Do a paracentesis first—that means using a needle to pull out belly fluid and test it. Most of the time, the real problem is spontaneous bacterial peritonitis, or SBP. That means bacteria got into the belly fluid on their own, without any hole. A hole is rare and shows different clues: the belly is board-hard, it hurts when you press and let go quickly (rebound pain), and the fluid test shows very high bacterial counts with more than one kind of bacteria. Surgery is only needed if those clues are there.
·Albumin is not just fluid—it is a special protein that pulls water into blood vessels and keeps your kidneys working. Without it, the kidneys shut down suddenly (acute kidney injury, or AKI) even if the infection clears. Current guidelines from the American Association for the Study of Liver Diseases (AASLD) and the European Association for the Study of the Liver (EASL) say you must give ceftriaxone (an antibiotic) AND albumin 1.5 grams per kilogram of body weight on day 1, then 1 gram per kilogram on day 3, or the kidneys will fail.
·Up to one out of every three patients with spontaneous bacterial peritonitis has no fever at all. The diagnosis is made by doing a paracentesis and checking the belly fluid for neutrophils—a type of white blood cell that fights bacteria. If the fluid has 250 or more neutrophils per cubic millimeter, the patient has SBP. Never skip the paracentesis just because there is no fever or the patient seems only a little sick.
·ACE inhibitors make kidney blood flow worse and cause acute kidney injury in spontaneous bacterial peritonitis. They lower blood pressure and cut down the kidney's ability to filter blood, so kidney failure gets worse, not better. Do not use them. Instead, use albumin and normal saline (salt water given through an IV) to support blood pressure and protect the kidneys.
·NSAIDs (nonsteroidal anti-inflammatory drugs) block chemicals called prostaglandins that keep kidney blood vessels open. This causes acute kidney injury in patients with spontaneous bacterial peritonitis and cirrhosis (liver scarring). The kidneys are already at high risk. Use acetaminophen (Tylenol) for mild pain, or opioids (stronger pain medicines like morphine or oxycodone) if needed—never NSAIDs.
·Spontaneous bacterial peritonitis comes back in 50 to 70 out of every 100 patients within one year if you do not give prevention antibiotics after the first infection (called secondary prevention (prophylaxis)). Current guidelines from AASLD and EASL say patients need lifelong daily norfloxacin 400 milligrams or ciprofloxacin 500 milligrams to stop recurrence and help them live longer.

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