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518 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

that ‘hyperacute’, ‘acute’ and ‘sub-acute’ liver failure
251
should be used instead. In this classification, hyper- TABLE 19.9 West Haven grading of hepatic
acute refers to patients who develop encephalopathy encephalopathy 258,261
within 7 days of the onset of jaundice, acute liver failure
should be used in patients between 8–28 days from jaun- Grade Characteristics
dice to encephalopathy and sub-acute liver failure when
encephalopathy occurs within 5–12 weeks of the onset I Trivial lack of awareness
Euphoria or anxiety
251
of jaundice. This has not received universal acceptance Shortened attention span
with the terms fulminant and sub-fulminant hepatic Impaired performance of simple tests e.g. addition
failure still used in clinical practice. II Lethargy or apathy
ALF without preexisting liver disease can result from Subtle personality changes
drug reactions, toxins or viral infection, or from the Inappropriate behaviour
effect on inflammatory mediators released in response III Somnolence to semi-stupor, but unresponsive to
to tissue injury. Liver failure can also occur as an acute verbal stimuli
decompensation of chronic liver disease (acute-on- Confusion
Gross disorientation
chronic liver failure: AoCLF) or as an end-stage decom-
pensation in chronic liver failure. AoCLF can be IV Coma: unresponsive to verbal or painful stimuli
precipitated by bacterial or viral infection, bleeding or
intoxication, and results in the same clinical syndrome
as seen in ALF. 234
End-stage decompensation of chronic liver failure repre-
sents irreversible deterioration with inadequate residual which leads to the development of cerebral oedema.
function to maintain homeostasis, and liver transplanta- Ammonia levels also seem to be related to the disruption
tion is the only viable treatment (see later in the chapter). of neurotransmission, resulting in decreased cerebral
234,236,256
However, in AoCLF, the function of the residual liver cell function. In addition, reactive oxidative species
mass may be adequate to maintain hepatic homeostasis causing oxidative stress and inflammatory cytokine
if the precipitating event can be treated. 234,236 release have been suggested, and the exact pathophysio-
257
logy is yet to be fully elucidated.
Liver dysfunction is also a common consequence of criti-
cal illness, 252,253 and may be caused by inadequate perfu- Previously, hepatic encephalopathy has been classified
258
sion leading to ischaemic injury or as a result of the using the West Haven criteria, a four-stage scale accord-
inflammatory response in sepsis. Given the number of ing to the severity of clinical signs and symptoms (Table
234
drugs that critically ill patients receive, the possibility of 19.9). However, the West Haven system has poor sensitiv-
liver injury as a result of drug reactions and toxicity ity and no inherent metric component. For instance, for
should always be considered. patients with grades III–IV encephalopathy, the Glasgow
Coma Scale (GCS) is probably a more sensitive tool for
CONSEQUENCES OF LIVER FAILURE neurological assessment. 256 Accordingly, other grading
259,260
criteria have been proposed
but are yet to be vali-
The consequences of liver failure manifest as a syn- dated in large clinical trials.
drome of hepatic encephalopathy (HE), hepatorenal
syndrome (HRS), oesophageal and gastric varices, ascites, Hepatorenal Syndrome
respiratory compromise, haemodynamic instability, sus- Hepatorenal syndrome (HRS) is the development of
ceptibility to infection, coagulopathy and metabolic renal failure in patients with severe liver disease (acute or
derangement. 234,236,237,254
chronic), in the absence of any other identifiable cause
of renal dysfunction. 262 HRS that develops rapidly in the
Hepatic Encephalopathy setting of ALF or AoCLF is classified as type 1 HRS, while
Hepatic encephalopathy is a reversible neuropsychiatric type 2 HRS is slowly progressing and is usually associated
complication due to metabolic dysfunction associated with diuretic-resistant ascites. 262,263
with liver disease. 255 The cerebral effects of liver failure
may manifest as an altered sleep–wake cycle, mild The pathophysiological features of HRS appear to be
confusion/disorientation, asterixis (i.e. abnormal tremor, caused by an inflammatory response from the injured
especially in the hands) and coma. Patients with liver, resulting in upregulation of nitric oxide production
234,236,262,263
AoCLF may develop a mild degree of cerebral oedema, (a vasodilator) and splanchnic vasodilation.
while a differential feature of ALF is the risk of Splanchnic vasodilation results in redistribution of circu-
death from cerebral oedema and raised intracranial lating blood volume and a lowered mean arterial pres-
pressure. 256 sure. The reduction in perfusion pressure results in an
enhanced sympathetic nervous system response and local
The exact mechanisms responsible for the development renal autoregulatory responses. The net result of these
of hepatic encephalopathy are unknown, although raised effects is a reduction in renal blood flow and increased
ammonia levels resulting from the failure of the liver urea activity of the renin–angiotensin–aldosterone system,
cycle are thought to be central to the pathogenesis. The resulting in sodium (aldosterone) and water retention
raised ammonia levels disrupt the blood–brain barrier, (arginine vasopressin; see Chapter 18).