Hepatic Failure/GI/Endocrine Emergencies
iii.
Osmotic agents are used first line for control of ICP.
| (a) | Mannitol has been used effectively in acutely reducing ICP in patients with ALF, though |
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the effect is usually transient.
| (1) | Mannitol is given as 0.5–1 g/kg intravenously once, which may be repeated to effect |
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as long as the serum osmolality is less than 320 mOsm/L; however, mannitol is
typically ineffective if the baseline ICP is greater than 60 mm Hg.
| (A) | Serum osmolality is estimated based on serum sodium, glucose, and blood urea |
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nitrogen based on the following formula: (Na x 2) + (glucose/18) + (blood urea
nitrogen/2.8).
| (2) | Adverse effects to consider for mannitol administration include fluid overload, |
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particularly in patients with renal impairment, hyperosmolarity, hypotension, and
hypernatremia.
| (3) | Hypertonic saline bolus (23.4% 30-mL bolus or 3% 200- to 300-mL bolus) is |
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an alternative to mannitol for acute reductions in ICP. Adverse effects include
hypernatremia and hyperchloremia.
| (b) | In patients with grade III or grade IV encephalopathy, multiorgan failure, or hemodynamic |
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instability, prophylactic hypertonic saline (to goal 145–155 mEq/L) may be used to reduce
the risk of cerebral edema.
| (1) | In a small, randomized controlled trial, 30 patients with ALF and grade III or grade |
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IV encephalopathy were randomized to receive prophylactic hypertonic saline to
maintain a serum sodium of 145–155 mEq/L compared with patients maintained at
near-normal serum sodium levels (137–142 mEq/L). The primary outcome, incidence
of ICP defined as elevations greater than 25 mm Hg, was significantly decreased in
the hypertonic saline group (20% hypertonic saline vs. 46.7% control, p=0.04).
| (2) | Hypertonic saline in this study was administered as a 30% sodium chloride infusion |
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by a syringe at 5–20 mL/hour; however, many preparation and dosing strategies have
been used (e.g., 23.4% 30-mL bolus, 7.5% 2-mL/kg bolus, 3% 200- to 300-mL bolus,
or continuous infusion), and the goal should be to target a serum sodium of 145–155
mEq/L.
iv.
When severe ICP elevations do not respond to other measures, barbiturates such as pentobarbital
may be used to control ICP.
| (a) | Profound hypotension may limit barbiturate use in ALF when patients have hemodynamic |
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instability at baseline. Patients may require vasopressors to maintain adequate MAP (and
CPP) while receiving barbiturates.
| (b) | Barbiturate clearance is significantly decreased in patients with ALF, which may limit |
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clinicians’ ability to perform neurological assessments for extended periods.
Hyperventilation to a Paco2 of 25–30 mm Hg can restore cerebral autoregulation, which results
in vasoconstriction and decreased ICP.
| (a) | The effects of hyperventilation on ICP appear to be short-lived. A randomized controlled |
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trial of prophylactic hyperventilation showed no benefit on cerebral edema and survival.
In addition, there is concern that cerebral vasoconstriction with hyperventilation may
worsen cerebral hypoxia.
| (b) | Thus, hyperventilation currently plays no role in prevention of ICP and should only be |
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considered for refractory treatment of acute ICP.
vi.
Hypothermia (33°C–34°C) may control ICP in patients with ALF by lowering the production
of ammonia and by decreasing the cerebral uptake of ammonia and cerebral blood flow.
However, hypothermia for patients with ALF has not been compared with normothermia in
controlled trials, and a recent retrospective cohort study showed no difference in overall and
transplant-free survival when compared with normothermia. In addition, there are concerns
about coagulation disturbances and increased risk of infection with hypothermia.