Ascites

Read the SAAG before you plan - The serum-ascites albumin gradient sorts the cause. A SAAG of 1.1 g/dL or greater means portal hypertension — cirrhosis, hepatic vein occlusion (Budd-Chiari), portal vein thrombosis, right heart failure. Under 1.1 g/dL points to peritoneal carcinomatosis, TB peritonitis, pancreatitis, serositis, or nephrotic syndrome. A cirrhotic belly and a malignant belly are different anesthetics.

Respiratory mechanics - Fluid load and raised intra-abdominal pressure produce shortness of breath and dyspnea, and the chest x-ray shows an elevated diaphragm. Preoxygenate deliberately and expect desaturation to come quickly once they are supine and apneic. For an elective case, ask whether tense ascites can be drained first.

Treat as a full stomach - A tense abdomen with raised intra-abdominal pressure and early satiety is not an empty stomach. RSI unless you have a good reason not to.

Diuretics leave them intravascularly dry - Standard therapy for high-albumin-gradient ascites is alcohol abstinence, sodium restriction to 88 mEq (2000 mg) per day, and spironolactone plus furosemide in a 100:40 mg/day ratio. The stated goal is to shrink the ascites without causing intravascular volume depletion, and that target gets missed often. Get a basic metabolic panel for sodium, potassium, and creatinine, and expect a soft pressure on induction.

Large-volume paracentesis - Therapeutic paracentesis is done for symptom relief or tense ascites, and albumin is given at the same time to prevent hypotension; terlipressin is recommended instead of albumin where it is available. If a paracentesis is happening around your case, find out when it was and how much came off.

Paracentesis contraindications - Coagulopathy in the setting of DIC, and massive ileus with bowel distension unless the procedure is image-guided so that bowel is not entered.

Spontaneous bacterial peritonitis - Fever, abdominal tenderness, and confusion in a patient with ascites. SBP and hepatorenal syndrome are the complications that drive the mortality here, so a septic-looking cirrhotic gets a septic workup and a septic anesthetic.

Renal function - Hepatorenal syndrome is the other lethal complication. Follow creatinine and urine output and protect renal perfusion rather than letting the pressure ride low.

Complications that touch your plan - Cellulitis, pleural effusion, and abdominal wall hernias. The hernias matter for positioning and for anything that further raises intra-abdominal pressure.

Definitive options - Transjugular intrahepatic portosystemic shunt is effective for patients who do not respond to diuretics. Peritoneovenous (Denver) shunts exist for chronic refractory ascites but are prone to obstruction, mechanical failure, and leaks. Once ascites is established, many of these patients are better transplant candidates than medical-therapy candidates — which is worth knowing before you commit to a big elective operation.

Ascites is pathologic accumulation of fluid in the peritoneal cavity. Cirrhosis causes roughly 80% of cases in the United States; the remainder are cancer (10%), heart failure (3%), tuberculosis (2%), dialysis (1%), and pancreatic disease (1%). In cirrhosis the first abnormality is portal hypertension — as the vasodilated state worsens, sodium-retentive vasoconstrictor hormones rise, renal function declines, and ascitic fluid forms. In heart failure and nephrotic syndrome the driver is a fall in effective arterial blood volume, which activates vasopressin, the renin-aldosterone axis, and the sympathetic nervous system to retain sodium and water.

The appearance of ascites marks the transition from compensated to decompensated cirrhosis. Three-year mortality in cirrhotic ascites is about 50%, and once ascites is refractory one-year survival is under 50%.