A 53-year-old male with past medical history significant for alcoholic cirrhosis complicated by esophageal varices presents to the intensive care unit (ICU) with hypoxia. He has noticed dyspnea on exertion that has been worsening over the last several months and complains of platypnea (shortness of breath relieved by lying down). Breath sounds are clear. Chest radiography is normal and contrast chest CT is negative for pulmonary embolus.
Which of the following is the MOST definitive treatment option for his disease?
Correct Answer: D
The history of dyspnea on exertion over a period of months in a patient with cirrhosis with portal hypertension (as evidenced by history of esophageal varices) makes hepatopulmonary syndrome a possible diagnosis. Platypnea and orthodeoxia affect up to 66% and 88% of patients with hepatopulmonary syndrome, respectively. Hepatopulmonary syndrome is progressive, and the only definitive treatment of hepatopulmonary syndrome is liver transplantation.
Normal chest radiography and absence of symptoms such as fever, cough, or sputum production make infection less likely as the etiology of hypoxia in this case and thus antibiotics are not indicated. Although this patient may have ascites, increased abdominal pressure from ascites causing dyspnea should improve with upright positioning and worsen with supine positioning. This makes tense ascites a less likely etiology of hypoxia in this case. A normal chest radiograph and CT make a process of bronchial obstruction that could be cleared with bronchoscopy less likely.
A patient presents with elevated aminotransferases approximately 15 times the upper limit of normal. Other laboratory values include:
The systemic arterial blood pressure is 90/50 mm Hg and the central venous pressure is 6 mm Hg.
Which of the following is LEAST likely to be the etiology of the liver dysfunction?
Correct Answer: B
Although markedly elevated aminotransferases are often from ischemic or hypoxic hepatitis, other causes for marked elevations include acute viral hepatitis, hepatic toxins or drug reaction, autoimmune hepatitis, focal arterial or venous obstruction, or HELLP syndrome. Ischemic or hypoxic hepatitis is generally associated with global hypoperfusion or hypoxia. The normal creatinine and lactate in this case do not support global hypoperfusion or hypoxia. Hypotension from nonhepatic trauma (and hypovolemia) rarely causes ischemic hepatitis, but cardiogenic shock with elevated cardiac filling pressures (high CVP, leading to hepatic venous congestion) has been shown to promote development of ischemic hepatitis. Thus, despite the borderline low systemic blood pressure, normal central venous pressure makes ischemic hepatitis less likely. When ischemic hepatitis is suspected other etiologies should be investigated by testing for acetaminophen levels, acute viral hepatitis serologies, autoimmune markers, and right upper quadrant ultrasound with doppler.
A 63-year-old female with history of cirrhosis complicated by ascites requiring previous paracentesis presents with fever, abdominal pain, and hypotension. Diagnostic paracentesis shows gramnegative bacteria on Gram stain and neutrophil count of 400 cells/mm3 .
Which of the following is the BEST next step in management?
This presentation of fever, abdominal pain, and ascitic fluid neutrophils >250 cells/mm3 in a patient with history of cirrhosis and ascites is highly suggestive of spontaneous bacterial peritonitis (SBP). Depending on other aspects of the patient’s history and presentation other workup could be warranted for secondary peritonitis, but this presentation is suspicious enough for SBP that treatment should be initiated regardless of additional ongoing workup. Empiric treatment is generally a third-generation cephalosporin, but cefotaxime has especially good penetration into the ascitic fluid so is preferred except when high rates of local resistance is present. A large volume paracentesis could put the patient at increased risk of hypotension in the setting of a current infection.
A 63-year-old male is in the ICU waiting to be listed for liver transplantation. He has become increasingly agitated and combative. His :
Head CT reveals mild cerebral edema with no bleed or focal abnormality. He is receiving lactulose and having bowel movements three times daily.
Which of the following is MOST LIKELY to improve his agitation?
Correct Answer: E
This patient has HE. Around 30% to 40% of patients with cirrhosis will at some point have HE. HE can be precipitated by a number of factors including infection, constipation, GI bleeding, and electrolyte disorders among others. Identifying and treating precipitating factors is an important component of treatment. Hypokalemia increases the production of ammonia within the kidney through an effect mediated by changes in pH within the renal tubule cells. Midazolam can precipitate and worsen delirium in general and may worsen HE specifically. Soft restraints may be useful in maintaining safety but will not improve the agitation. Broad spectrum antibiotics could be useful if there was a precipitating infection, but this patient has a normal white blood cell count and no other indication of infection. Lactulose is one of the most often used treatments and this patient is already stooling regularly, so the addition of a suppository is unlikely to be helpful.
A 62-year-old male with a history of hepatic cirrhosis complicated by ascites and esophageal varices presents with decreased urine output. His creatinine is elevated at 1.4 mg/dL. Investigation of the urine reveals fractional excretion of sodium <1%, no casts or blood cells, no protein, and renal ultrasound was normal. No improvement in urine output or creatinine is achieved after several doses of albumin. His white blood cell count is 7600 cells/µL, diagnostic paracentesis was not suggestive of infection, and his blood pressure is 98/62 mm Hg.
Which of the following is the MOST effective next treatment?
Correct Answer: A
This patient likely has hepatorenal syndrome (HRS). This is a diagnosis of exclusion that appears clinically very similar to prerenal acute kidney injury but fails to improve with administration of volume, such as albumin. Infection in patients with portal hypertension can increase the risk of HRS, but this patient has no signs of infection so would likely not be helpful in this case. Increasing the mean arterial pressure by 10 mm Hg in patients with HRS has been shown to increase urine output and decrease creatinine even if the patient is not initially hypotensive.
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