Table 5.

Management of cerebral edema

Prevention of cerebral edema
Allow spontaneous hyperventilation
Allow spontaneous hypothermia; generally, do not warm a patient with spontaneous low core temperatures
Initiate renal replacement therapy early, particularly in patients with risk factors for developing cerebral edema (serum ammonia > 100–150 μM, high-grade encephalopathy, presence of SIRS, oliguria, AKI)
Maintain serum sodium at high-normal levels (145–155 mM)
Management of established cerebral edema
Mannitol (0.5–1.0 g/kg body weight IV) bolus(es)
Hypertonic saline bolus(es)
Remove more volume and ammonia (CVVH)
Maintain cerebral perfusion pressure with norepinephrine (CPP > 60 mm Hg)
Consider therapeutic plasma exchange
Consider deeper sedation (propofol)
Consider ammonia scavenging agent (sodium phenylacetate, sodium benzoate; Ammonul)
Consider therapeutic hypothermia (core temperature 32–34°C)

Abbreviations: AKI, acute kidney injury; ALF, acute liver failure; CPP, cerebral perfusion pressure; CRRT, continuous renal replacement therapy; CVVH, continuous venovenous hemofiltration; HTS, hypertonic saline; ICP, intracranial pressure; IV, intravenous; MAP, mean arterial pressure;

OPA, L-ornithine phenylacetate; SIRS, systemic inflammatory response syndrome.

Note: The optimal management plan for cerebral edema in patients with ALF is undoubtedly prevention. In addition to the usual positional maneuvers (elevation of the head-of-bed; neutral neck rotation), patients should be allowed to hyperventilate such that their PCO₂ decreases to 30–40 mm Hg and allowed to be hypothermic (usual in patients on CVVH). CRRT should be initiated early in patients with risk factors for developing cerebral edema. Serum sodium should be raised to high-normal.

In patients with established cerebral edema, mannitol or HTS boluses should be administered promptly, and CVVH continued. If an ICP monitor is placed, the CPP should be maintained > 60 mm Hg by increasing the MAP with norepinephrine. Therapeutic plasma exchange should be considered, as this will not only improve the MAP, but will remove ammonia from the circulation. As desperate measures, deeper sedation with propofol and/or therapeutic hypothermia may be considered. Although not studied in patients with ALF, sodium phenylacetate/sodium benzoate (Ammonul) might be considered as an ammonia scavenging agent. The compound has been studied in children with urea cycle defects and acute hyperammonemic crises and is commercially available; OPA is not.