BOX 1 Differential diagnosis of encephalopathy Subdural haematoma Sepsis Metabolic derangements Hypoxia Acidosis Electrolyte abnormalities Hypoglycaemia Uraemia
Toxins Psychoactive drugs Heavy metals
Prior alcohol abuse Delirium tremens Wernicke-Korsakoff syndrome
Precipitating factors Infection Sepsis
Electrolyte abnormalities Diarrhoea Vomiting Dehydration
Iatrogenic interventions Drugs – diuretics, benzodiazepines
Radiological stent insertion - TIPSS
GI haemorrhage Constipation Excess dietary protein
BOX 2 West Haven Criteria Grade 0 No abnormality detected
Grade 1 Trivial lack of awareness Euphoria or anxiety Shortened attention span Impaired performance of addition and subtraction
Grade 2 Lethargy or apathy Minimal disorientation in time or place
Subtle personality change Inappropriate behaviour
Grade 3 Somnolence to semi- stupor
Confusion Gross disorientation – responds to verbal stimuli
Grade 4 Coma – does not respond to verbal or noxious stimuli
activity is seen in patients with HE, and typical EEG findings demonstrate ‘triphasic waves’. Although this is not a finding specific to HE, EEG is useful where there is diagnostic uncertainty, or in situations where a diagnosis of HE must be excluded, for instance prior to procedures such as transjugular portosystemic stent shunts. The critical flicker frequency (CFF) was developed as a psychophysical assessment, which does not require psychological expertise. It assesses the frequency threshold at which a flickering light is still observed as flickering, and not continuous, and reflects functional efficacy of the cortex. However, CFF cannot reliably distinguish patients with MHE from patients without HE. Neuroimaging is only used as an adjunct in the diagnosis of HE. MRI can detect cerebral oedema, even at a low-grade. This is especially important in acute liver failure, where oedema may complicate encephalopathy but whether this exists in MHE is debated. Hyperintensity in the basal ganglia, attributed by some to manganese deposition in the globus pallidum, has been reported on T1
-weighted MRI
images from patients with cirrhosis. Although it is seen in the majority of patients, this observation is not pathognomonic of HE as impaired biliary secretion can give the same observation. A CT scan of the head may also be useful in excluding alternative pathology such as a subdural haematoma. Other forms of brain imaging including SPECT and PET scans, and MRS are more suited to research purposes at the current time. Although ammonia has been implicated in the pathogenesis of HE, there
is debate as to the utility of measuring its blood levels. While it is useful to do so in ALF, there is a limited role for it in CLD. Routine assessment of ammonia levels is not advised, as it does not influence management, and a single measurement does not correlate well with the severity of HE.
TREATMENT OF HE The aims and outcome of treatment depend on the severity and grade of encephalopathy. At the current time, there is a paucity of data to support treatment of MHE. By contrast, the management of OHE is better defined and can be discussed in terms of both
acute and long- term therapy. In the short-term, the goals of treatment comprise supportive measures, identification and elimination
ammonia, inhibiting central GABAA false neurotransmitters.
of precipitating factors, and assessment of need for liver transplantation. Long-term treatment aims to control precipitating factors, prevent recurrent episodes, and improve daily functioning. The specific therapies for HE target aspects of its pathogenesis, including reducing production and absorption of receptors, and decreasing generation of
Pharmacological therapies Non-absorbable disaccharides Lactulose is an example of a non-absorbable disaccharide, and is considered to be first-line therapy in patients with HE. These drugs have a laxative effect, which reduces the nitrogenous load from the gut. In addition, lactulose is able to lower the colonic pH, which produces an
054 ARAB HEALTH MAGAZINE ISSUE 2 2012
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