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818 PART 6: Neurologic Disorders

and loss of cerebral autoregulation, which disrupts the blood-brain bar- shown to have an impact on controlling ICP in Reye syndrome. In
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rier and contributes to cerebral hyperemia. 187-190 FHF, it is best considered in patients with either refractory intracra-
The potential for the development of brain swelling should be nial hypertension and/or those with oliguria or anuria. In one study
anticipated in all FHF patients. Early detection of cerebral edema of 13 FHF patients with acute renal failure and refractory intracranial
is imperative in order to mitigate its progression and proactively hypertension, thiopental was infused slowly to a maximum of 500 mg
manage its complications. Since encephalopathy limits neurological to achieve an ICP <20 mm Hg, CPP >50 mm Hg, or until hypotension
examination, accurate detection of ICP elevations is frequently not developed. In each case, the ICP was reduced with the administration
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possible. Additionally, the symptoms of encephalopathy can mimic of 185 to 500 mg (median = 250 mg) of thiopental over a 15-minute
those of cerebral edema, making the selection of appropriate therapy period. In eight patients, a constant infusion was required (50-250 mg/h)
difficult. For example, stage IV encephalopathy patients frequently to maintain adequate ICP and CPP. Given the small number of patients
demonstrate diffuse hyperreflexia and increased motor tone with and unclearly defined end points, it is difficult to assess the true benefit
decerebrate posturing in the absence of cerebral edema. A fluctuating of the ICP-lowering effects of this agent in the setting of liver failure.
mental status can also mask underlying seizures, making this diagnosis However, unique to FHF, impaired barbiturate metabolism and clear-
difficult. It is therefore prudent to rule out seizures with EEG in FHF ance often precludes the need for a maintenance infusion.
patients demonstrating a fluctuating sensorium. Class I therapies for decreasing intracranial hypertension in FHF
Cerebral edema most often occurs in those with higher-stage enceph- include mannitol and hypertonic saline. Hyperventilation, hypo-
alopathy, and imaging should be performed in all patients with FHF to thermia, and bioartificial liver are supported by Class II evidence,
rule out intracerebral hemorrhage and to delineate the presence and indomethacin, thiopental, and propofol by Class III evidence. Liver
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severity of cerebral edema. Early stage cerebral edema may be misinter- transplantation is the ultimate treatment for liver failure and hepatic
preted as a normal imaging study in the hands of inexperienced physi- encephalopathy. Patients with high-grade hepatic encephalopathy
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cians. Furthermore, intracranial hypertension has been reported in FHF and significant cerebral edema are poorer candidates for transplant. In
patients with normal CT scans. 188,191 our experience, brain injury can be avoided with aggressive, proactive
Once a patient develops higher stages of FHF encephalopathy, cere- normalizing therapy.
bral edema and hypoperfusion occur and can be missed in the absence
of ICP monitoring. At present, the use of ICP monitoring in FHF is not ■ GLOBAL CEREBRAL HYPOPERFUSION
currently supported by Class I evidence but it is indicated as an adjunct Intracranial hypertension can be seen after global cerebral hypoperfu-
therapy. In our experience, bedside parenchymal monitors can be sion, cardiac arrest, prolonged hypotension, or severe hypoxia. It is a
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inserted without significant complications even in those with coagu- reflection of diffuse ischemic injury, which shares some pathophysi-
lopathy. We prefer to place a parenchymal monitor in the nondominant ologic mechanisms with other causes of global cerebral injury. Rapid
hemisphere with the administration of 2 units of fresh frozen plasma depletion of cerebral oxygen and ATP leads to loss of ionic gradients
(FFP) before, 1 unit during, and 2 units after the procedure. ICP monitor that normally consume three-fourths of total cell energy. Subsequently,
placement can be timed so that invasive line insertions can be coordi- potassium efflux and sodium influx result in neuronal and interstitial
nated with FFP infusions. swelling with extracellular accumulation of glutamate. Once spontane-
Some neuroclinicians prefer to insert EVDs in FHF patients with
potential intracranial hypertension to allow for CSF drainage to treat ous circulation is restored, different mechanisms contribute to reper-
fusion injury, among them impaired cerebral microcirculation and
plateaus in ICP. This modality of ICP monitoring carries a higher risk autoregulation plus the formation of damaging oxygen-free radicals.
of hemorrhagic complications in those with coagulopathy. Furthermore, Specific areas of the brain are especially vulnerable to ischemia, includ-
once the ventricles collapse, there is loss of hydrostatic CSF column and ing hippocampal CA1 neurons, pyramidal neurons in the cerebral
ICP measurements become unreliable. cortex, and cerebellar Purkinje cells. Frequently, brain regions between
Mannitol can be useful in some patients with FHF. Its use should pri-
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marily be considered in nonoliguric patients without significant hyper- major cerebral vascular territories (watershed zone) become ischemic as
well. Brain imaging (Fig. 86-21) demonstrates diffuse cerebral edema,
natremia. We generally use 0.25 to 0.5 g/kg aliquots of mannitol infused that is, global swelling and lack of delineation of gray and white matter
over a 20- to 30-minute period. FHF patients are frequently in a hyper- resulting loss of visible sulci.
osmolar state. Therefore, we do not titrate mannitol to a specific serum Rapid and early induction of cooling (eg, in the ambulance, emer-
osmolality. Rather, mannitol is administered intermittently to achieve gency room, or ICU) is employed in many cases. Figure 86-17
the desired effect on ICP. Mannitol may lose its effectiveness after several illustrates the different cooling methods to induce therapeutic, short-
doses, and other therapeutic strategies should therefore be considered term hypothermia. Seizures and various patterns of myoclonic jerks
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concurrently. As is typical with the use of an osmotic diuretic, volume are common following cardiac arrest and continuous video EEG
depletion can be an important complication with resultant hypotension. helps categorize the clinical findings. Management of these patients
Most patients with FHF will develop spontaneous hyperventilation,
which is thought to be related to an increase in circulating free fatty acids focuses on general brain-oriented therapeutic modalities; unfortu-
nately, “neuroprotective” pharmacologic interventions (eg, antioxidant
and ammonia. While the institution of hyperventilation can be beneficial medications, corticosteroids, calcium channel blockers, glutamate
in lowering ICP acutely, it has no prolonged benefit in FHF as is true with antagonists, etc) have no proven benefit.
most etiologies of cerebral edema and intracranial hypertension. 194,195
Induced hypothermia can be a favorable strategy for both neuropro- ■
to low normocapnic ranges is recommended.
Strict titration of the P CO 2 SEPTIC ENCEPHALOPATHY
tection and deterring the development of cerebral edema in FHF. In Impaired consciousness in some patients with prior focal deficits or
one study, FHF patients with intracranial hypertension refractory to seizures can be the early clinical signs of sepsis and sepsis- associated
osmotherapy and ultrafiltration were studied. Moderate hypothermia to delirium in up to 70% of patients. 198,199 Septic shock can lead to global
32°C to 33°C was achieved with cooling blankets. The mean ICP before hypoperfusion and eventually produce regional or global brain ischemia.
and after cooling was 45 and 16 mm Hg, respectively. The mean CPP In addition, other mechanisms (eg, hypoxemia, hypercapnia, glucose
rose from 45 to 70 mm Hg. Proactive strategies to allow early detection abnormalities, electrolyte imbalance, inflammatory reactions, and sys-
and treatment of fever (identified by increased cooling demands) are an temic organ dysfunction) can concomitantly affect cerebral blood flow,
important part of the management plan (Fig. 86-17). and autoregulation. Direct cerebral insults sustained in the setting of
Like most other therapeutic strategies for ICP lowering, in FHF there ongoing sepsis, such as ischemia, cerebral micro- and macro-hemor-
have been few reliable studies to guide barbiturate therapy. It has been rhage, microthrombi, microabscesses, and multifocal necrotizing

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