Management of cerebral edema

Cerebral edema should be presumed to be incipient or already present in all patients with advanced encephalopathy. Management generally involves the principles used in treating cerebral edema of any etiology. The airway should be secured if necessary (if compromised or to prevent aspiration), and mechanical ventilation instituted if there are abnormalities of respiratory drive or pulmonary gas exchange. Patients should be nursed with the head elevated to 20°; higher elevations may lead to a fall in cerebral perfusion pressure, probably because this maneuver results in a fall in mean arterial pressure due to peripheral vasodilatation. Venous return from the head should be unimpeded by malpositioning or tapes. Episodic agitation is common and may be associated with increased intracranial pressure ( MuDoZ. 1993). Although sedative drugs will obscure progression of neurological signs, judicious doses must be given in this situation to ensure patient safety. The most effective treatment of elevated intracranial pressure in ALF is mannitol infusion. In a controlled trial, infusion of 20 per cent mannitol (1 g/kg) reversed clinical signs of cerebral edema, reduced intracranial pressure by a mean of 22 mmHg, and increased survival. Subsequent studies have shown benefits with lower doses (0.5 g/kg), and have further demonstrated that mannitol infusion is associated with an increase in the cerebral metabolic rate for oxygen, and a decrease in cerebral lactate production (Wendon etaL 1994). Mannitol should be infused rapidly using a burette, but maximum reduction in intracranial pressure may not occur for 20 to 60 min.

The dose can be repeated to control further episodes of intracranial hypertension, provided that the serum osmolality remains below 320 mOsmol/kg. Complications of mannitol therapy include dehydration and hyperosmolality if renal function is normal. In patients with renal failure, mannitol should only be used in conjunction with hemodialysis or hemofiltration, since fluid overload may exacerbate cerebral edema. Furosemide (frusemide) may be a useful adjunctive therapy to maintain the initial osmotic gradient established by mannitol.

Hyperventilation may be useful to decrease intracranial pressure during an acute elevation, but does not reduce the incidence or severity of cerebral edema in the longer term. This may be due to establishment of a new equilibrium between PaCO2 and cerebral blood flow; alternatively, it may suggest that hyperventilation, with the consequent decrease in cerebral blood flow, may have adverse effects in ALF. In the study by Wendon et al. (1994), hyperventilation was associated with an expected decrease in cerebral blood flow but also a decrease in the cerebral metabolic rate for oxygen. However, mannitol and ^-acetylcysteine infusion were associated with the potentially beneficial effect of an increase in cerebral metabolic rate for oxygen but also an increase in cerebral blood flow. These findings raise the possibility that cerebral ischemia may be a trigger to cerebral edema formation in ALF. This issue is speculative; nevertheless, current recommendations are that extreme hyperventilation should be avoided in patients with ALF and that PaCO2 should be maintained in the range of 4.7 to 5.3 kPa (35-40 mmHg). Because of these findings, ^-acetylcysteine requires further evaluation as a means of preventing cerebral edema in ALF. Barbiturate therapy (specifically thiopentone by infusion) has been used to control intracranial pressure in patients with ALF, but has not been subjected to a randomized controlled trial. Although reductions in intracranial pressure occur, the concomitant decrease in mean arterial pressure resulting from cardiovascular depression can result in no change or a decrease in cerebral perfusion pressure. This treatment may have a place in treating cerebral edema refractory to mannitol therapy when liver transplantation is imminent, but only when intracranial pressure and therefore cerebral perfusion pressure is monitored. There is no evidence that lactulose administration will delay or ameliorate the progression of encephalopathy or cerebral edema in ALF. Nevertheless, it is widely used in a dose of 30 ml thrice daily by gastric tube or enema, although bowel distension associated with its use may complicate liver transplantation. Use of neomycin is not recommended because of its nephrotoxicity and ototoxicity. Corticosteroids do not influence the incidence and severity of cerebral edema. The usefulness of benzodiazepine antagonists has not been established.

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