Rosen & Barkin's 5-Minute Emergency Medicine Consult (338 page)

DIAGNOSIS

Signs of acute or chronic liver disease:

• Signs of portal hypertension
  
• Ascites, often tense
  
• Progressive oliguria
  
• Jaundice or hepatic encephalopathy
  
• Coagulopathy
  
• Tachycardia
  
• Hypotension
  
• Dyspnea, tachypnea due to tense ascites
  

Acute or chronic hepatic disease with advanced hepatic failure and portal hypertension:

• Worsening liver function often predates acute renal dysfunction
  

• Consistent with severe hepatic disease
  
• Vital signs may show:
  
  • Fever in signs of sepsis
    
  • Hypotension in sepsis, intestinal bleeding, or even a low baseline intrinsic to liver disease
    

• CBC:
  
  • Anemia due to GI bleed
    
• Electrolytes:
  
  • Hyperkalemia
    
  • Acidosis
    
• Glucose
  
• Elevated BUN, creatinine (Cr):
  
  • Normal Cr found with low GFR) in association with muscle wasting, poor nutrition, and ascites.
    
  • Cr increased by some medications (cimetidine, trimethoprim, and spironolactone) due to inhibition of tubular secretion of Cr.
    
  • Hyperbilirubinemia can create a falsely lower serum Cr.
    
• PT, PTT
  
• Urinalysis:
  
  • Absence of casts distinguishes HRS from acute tubular necrosis (ATN).
    
  • Check for UTI.
    
• Spot urine sodium and Cr, and serum and urine osmolality:
  
  • Spot urine Na
    ⁺
    <10 mEq/L
    
  • Fractional excretion of Na
    ⁺
    <1%
    
  • Urine/plasma Cr >30:1
    
  • Hyperosmolar urine > plasma osmolarity
    
• 24 hr urine output (low in the absence of diuretics)
  
• 24 hr urine CrCl:
  
  • Accurately assess GFR
    
• Blood, ascitic fluid, and urine culture as indicated
  
• Urinary excretion of β
  ₂
  -microglobulin—useful marker of acute tubular damage
  

• CXR for signs of CHF or fluid overload
  
• Renal US: Rule out obstructive uropathy:
  
  • Duplex Doppler US can be used to assess degree of renal vasoconstriction.
    

• ECG for dysrhythmia or signs of hyperkalemia
  
• Foley catheter placement to assess for urine output and exclude urinary retention as cause of RF
  
• Central venous pressure (CVP) measurements may help assess volume status:
  
  • Differentiates prerenal (low) from HRS (elevated)
    

• HRS is diagnosis of exclusion
  
• Glomerulopathy:
  
  • Hepatitis B can lead to glomerulonephritis
    
  • Hepatitis C can cause intrinsic renal damage due to cryoglobulinemia
    
• ATN:
  
  • Urine sodium >30 mEq/L
    
  • Urine osmolality equals plasma osmolality
    
  • Urine casts and cellular debris
    
• Prerenal azotemia:
  
  • Over diuresis
    
  • GI bleeding
    
  • Urine output improves following correction of hypovolemia
    
• Obstructive uropathy
  
• Infections or sepsis
  
• Medications—NSAIDs
  
• Interstitial nephritis
  
• Post liver transplant renal dysfunction due to:
  
  • HRS due to failure of transplanted liver
    
  • Medications (e.g., cyclosporine)
    
  • Pre-existing renal disease
    
  • Perioperative hypovolemia
    

TREATMENT

Attention to ABCs:

• Airway control may be a concern in severe encephalopathy.
  
• Respiratory failure seen with tense ascites as well as volume overload
  
• Correction of hypotension and ensure adequate IV access
  

• ABCs
  
• Aggressive correction of hypovolemia with:
  
  • 0.9% NS IV fluid
    
  • Colloid volume expanders: 100 g albumin in 500 mL of NS
    
  • Closely monitor clinical status including use of CVP
    
  • Urine output should improve with correction of prerenal azotemia
    
• Manage life-threatening emergencies of RF:
  
  • Hyperkalemia
    
  • Severe acidosis
    
  • Hypoxemia
    
  • Uremic pericarditis
    

• Exclude reversible or treatable causes of HRS.
  
• Supportive care until hepatic function recovers
  
• Do no harm
  —discontinue potentially nephrotoxic agents:
  
  • NSAIDs
    
  • Aminoglycosides
    
  • Demeclocycline
    
• Treat primary disease
  
• Search for and treat coexisting renal disease
  
• Correct electrolyte imbalances
  
• Treat any associated cardiopulmonary disorder and hypoxia
  
• Initiate broad-spectrum antibiotics if sepsis suspected
  
• Correct liver-associated complications:
  
  • Obstructive jaundice
    
  • Hepatic encephalopathy
    
  • Hypoglycemia
    
  • Peritonitis
    
• Consider large-volume paracentesis with IV albumin replacement (to relieve tense ascites):
  
  • Increases renal blood flow
    
  • May briefly improve HRS
    
• Transhepatic intrahepatic portosystemic shunt (TIPS):
  
  • Promising results, but small studies
    
  • Those who survived the procedure had 40% survival at 12 mo compared to 90% at 3 mo.
    
• Dialysis:
  
  • Useful in correcting fluid, electrolytes, acid–base imbalances, pulmonary edema
    
  • Indicated for patients who have likelihood of hepatic regeneration, hepatic recovery, or liver transplantation
    
• Liver transplant:
  
  • Is currently the only definitive therapy
    

• No medications are first line and should only be considered after other causes of renal dysfunction excluded
  
• Dopamine (renal dose): 2–5 μg/kg/min:
  
  • May improve renal function
    
  • Not curative
    
• Midodrine (7.5–12.5 mg PO TID) and octreotide (100–200 μg SC TID):
  
  • Octreotide is the analog of somatostatin
    
  • Midodrine is a sympathomimetic drug
    
• Misoprostol: 0.4 mg PO QID:
  
  • Synthetic analog of prostaglandin E
    ₁
    
• Ornipressin:
  
  • Vasopressin analog
    
  • Increases renal perfusion pressure and function
    
  • Not available in US
    
• Terlipressin: 2 mg/d for 2 days:
  
  • Synthetic analog of vasopressin
    
  • Intrinsic vasoconstrictor activity
    
  • Not available in US
    

FOLLOW-UP

• All suspected HRS with GI and nephrology consults
  
• ICU admission for associated cardiopulmonary disease, hepatic encephalopathy, marked electrolyte imbalances
  

None

Any degree of renal dysfunction needs to be evaluated very seriously in patients with liver disease.

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• Nadim MK, Kellum JA, Davenport A, et al.
  Crit Care.
  2012;16(1):R23.
  
• Roberts LR, Kamath PS. Ascites and hepatorenal syndrome: Pathophysiology and management.
  Mayo Clin Proc
  . 1996;71:874–881.
  
• Senzolo M, Cholangitas E, Tibballs J, et al. Transjugular intrahepatic portosystemic shunt in the management of ascites and hepatorenal syndrome.
  Eur J Gastroenterol Hepatol
  . 2006;18:1143–1150.
  
• Verna EC, Wagener G.
  Curr Opin Crit Care.
  2013;19(2):133–141.
  
• Wong F, Blendis L. New challenge of hepatorenal syndrome: Prevention and treatment.
  Hepatology
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See Also (Topic, Algorithm, Electronic Media Element)

• Hepatic Encephalopathy
  
• Hepatitis
  

CODES