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In-depth information regarding diagnostic and treatment information within AlcoPath and its terms of use.

Pabrinex® prescribing

Chlordiazepoxide prescribing

What is Wernicke Encephalopathy-Korsakoff’s Psychosis?

Classic Triad (Confusion, Ataxia, Opthalmoplegia)

WEKP Cognitive assessment tool

What is Alcohol withdrawal syndrome?

Withdrawal Assessment tool




Pabrinex® prescribing

In the NICE Clinical Guideline 115 Pabrinex® is the recommended treatment choice for diagnosed or suspected Wernicke’s Encephalopathy-Korsakoff’s Psychosis (WEKP).

It is recommended that patients are prescribed and administer intravenously Pabrinex® two pairs (i.e. four ampoules), three times daily. This should be diluted in 100ml 0.9% sodium chloride or 5% glucose and infused over 30 minutes. Review using AlcoPath WEKP Cognitive Assessment on day three and consider continuation doses of Pabrinex® totalling at least 5 days duration (Joint formulary Committee, 2016).


Chlordiazepoxide prescribing

The British National Formulary states that a maximum dose per 24 hours is 250mg for Chlordiazepoxide. If side effects (for example: sedation) or co-morbidities are present (for example significant liver disease) then withholding or reduction of any prescribed doses could be considered. If there are no side effects or co-morbidities of concern then it is not recommended to reduce any prescribed doses within the first 24 hours of treatment. If doses are indicated due to ongoing alcohol withdrawal symptoms and maximum dose has been reached - it is recommended that a consultant (in the inpatient setting) or appropriate clinical lead is contacted to direct treatment.


What is Wernicke Encephalopathy-Korsakoff’s Psychosis?

Wernicke’s Encephalopathy is a disease that exists on a continuum where impairment progresses if un-treated to Korsakoff’s Psychosis (hence it is sometimes referred to as Wernicke-Korsakoff Syndrome). It is caused by persistent poor nutrition and uptake of Vitamin B1 (Thiamine) resulting in impaired neurological functioning.

Wernicke’s encephalopathy is reversible in the early stages with rapid restoration of CNS B-vitamins (in particular Thiamine) and treatment must be initiated immediately once a diagnosis is suspected.  The diagnosis should be based on the presence of any one or more of the following signs in the absence of another more probable explanation of these features (Chick, 2000; Cook, Hallwood & Thomson, 1998; Cook 2000; Morgan, 1998; Thomson & Marshall, 2005):

• Acute confusion

• Decreased consciousness level including unconsciousness or coma

• Memory disturbance

• Ataxia/unsteadiness

• Ophthalmoplegia (eye muscle paralysis causing squint or double vision)

• Nystagmus (involuntary rhythmic oscillation of one or both eyes)

• Unexplained hypotension with hypothermia

The risks of not treating with Pabrinex® are that there is no recovery of cognitive function, that the disease progresses to Korsakoff’s in 84% of cases and the risk of death is 1 in 5 (Victor et al, 1989).

These specific symptoms are often difficult to detect when alcohol misuse is also present - and sometimes a significant thiamine deficiency may be present requiring treatment without any of these symptoms noted. That is why Alcopath uses a list of risk factors adapted from Svanberg, Withall, Draper and Bowden (2014), these are:

• Poor nutrition (poor appetite)

• Significant weight loss

• Recent nausea/vomiting

• Poor or broken sleep

• Feeling weak or tired

• Double vision

• Alcohol abuse (drinking regularly above the binge limits)


Classic Triad

Though not always present - Wernicke’s Encephalopathy is sometimes described as having three specific symptoms that are used to diagnose the disorder – Alcopath guides the assessment for these symptoms, which are:


Confusion and poor memory are noted in the absence of intoxication and are a symptom of WEKP. Testing using a validated test with a clear threshold for impairment. Such tests focus on orientation to time and short-term recall (amongst other factors), which can then be re-tested to test response to Pabrinex® treatment.


Observed usually as a patient walking with an unsteady gait, ataxia can be assessed for by undertaking an observation of gait whilst walking a short distance. In WEKP the presence of this symptom is indicative of cerebellar dysfunction. Other tests of neurological functioning are able to be considered however these require more rigorous training to attain proficiency.


This refers to paralysis of one of or more of the motor nerves of the eye. One way opthalmoplegia can be assessed is by undertaking an observation of eye movements as they track an object (usually a finger or pen). The patient will display saccadic (jerking) movements by the eyes, which is not consistent bi-laterally during this test.  These abnormal movements are called Nystagmus, and if observed during testing is a positive symptom WEKP

Confusion, ataxia and opthalmoplegia are considered the triad, however they are only all present in 10% of cases (Cook, 2000), and in many cases – none are present yet a Thiamine deficiency exists (Harper et al, 1986).


WEKP Cognitive assessment tool

AlcoPath’s WEKP Cognitive assessment tool is made up of 10 questions, but chiefly among them are the elements of 6-CIT. 6-CIT is a validated (Brooke & Bullock, 1999) cognitive assessment ideally suited to those suspected of having confusion/memory problems thought to be attributed to WEKP. It gives a score which if 8 or above is considered positive for an impairment. The Kingshill Research Centre, Swindon, UK owns the copyright to The Kingshill Version 2000 of the 6-CIT but allows free usage to healthcare professionals. Alcopath supports use within the copyright conditions by users.


What is Alcohol withdrawal syndrome?

Alcohol withdrawal syndrome is a selection of symptoms that arise when a patient has been drinking alcohol at high levels (typically exceeding 15 units a day) for a period of time (usually several weeks, months or even years) and then stops or significantly reduces their alcohol intake. Alcohol withdrawal is the name given to a cluster of symptoms resulting from the rebound stimulatory effect on the central nervous system (CNS) the removal of alcohol causes in the patient. Gamma-aminobutryric acid (GABA) and glutamate neurotransmitters are affected by alcohol use. After significant regular heavy alcohol use it is thought that neuro-adaptation of the brain with respect to GABA production and the sensitivity of GABA receptors takes place. This means that when alcohol is withdrawn the GABA levels are below normal and without alcohol present there are less agents to facilitate inhibitory function – causing central nervous system (CNS) excitation (Petty et al, 1993). The CIWA-Ar (Clinical Institute Withdrawal Assessment – Alcohol Revised) is a validated tool for assessing 10 of these CNS excitation symptoms (Sullivan, Sykora, Schneiderman, Naranjo & Sellers, 1989). CIWA-Ar covers:

• Nausea & Vomiting

• Tremor

• Paroxysmal sweats

• Anxiety

• Agitation

• Tactile Disturbances (including hallucinations)

• Auditory Disturbances (including hallucinations)

• Visual Disturbances (including hallucinations)

• Headache

• Disorientation

CIWA-Ar is a newer version of a longer 15-item alcohol withdrawal syndrome test (CIWA-A) and has high inter-rater reliability when used different (trained) staff.


Withdrawal Assessment tool

AlcoPath incorporates CIWA-Ar with some key factors to consider, putting the withdrawal assessment into context. These factors were developed from clinical experience and can assist in decision-making in various clinical contexts.

Alcohol unit consumption and frequency of drinking is a chief concern as higher unit consumption prior to triggering a withdrawal state by stopping drinking is associated with more severe withdrawals. Time since last drink is important if the patient is being first assessed – as a high score and a long duration since last drink may mean immediate action is required (especially if no medication is charted). Similarly a short time since last drink and a low-score on CIWA-Ar may mean that re-assessment later is recommended. Breathalyser or blood alcohol content readings are useful to indicate if the patient still might be intoxicated, however some patients (usually with severe alcohol dependency) can show withdrawals even with a blood alcohol content of some significance. Differential diagnoses should be considered, particularly upon starting alcohol withdrawal monitoring as the symptoms registered on CIWA-Ar can be caused by co-morbid mental and physical health conditions as well as other substance use and withdrawal. An alcohol screen score (AUDIT, FAST or other tools for example) can be instructive about the wider history of the patient’s relationship with alcohol and puts the CIWA-Ar score in context. A low respiration rate should be considered as a patient who has compromised respiratory function and has a CIWA-Ar score that is 12 for example may require clinical judgment around withholding medication and this detail might be indicated in some local policies or protocols.


Reference list:

Brooke, P. & Bullock R. (1999). Validation of a 6 item cognitive impairment test with a view to primary care usage. International Journal of Geriatric Psychiatry, 14(11), 936-940.

Chick, J. (2000). Psychiatric disorders associated with alcohol misuse. Hospital Pharmacist, 7, 251–254.

Cook C. C., Hallwood, P. M. & Thomson, A. D. (1998). B Vitamin deficiency and neuropsychiatric syndromes in alcohol misuse. Alcohol & Alcoholism, 33(4), 317–336.

Cook, C. C. (2000). "Prevention and treatment of Wernicke-Korsakoff syndrome". Alcohol and Alcoholism Supplement, 35(1), 19–20.

Harper, C. G., Giles, M., Finlay-Jones, R. (1986). Clinical signs in the Wernicke-Korsakoff complex: a retrospective analysis of 131 cases diagnosed at necropsy. Journal of neurology, neurosurgery, and psychiatry, 49(4), 341–345.

Joint Formulary Committee. (2016). British National Formulary. (72nd ed.). London: British Medical Association and Royal Pharmaceutical Society of Great Britain.

Morgan, M. Y. & Ritson, B. (1998). Alcohol and Health. London: Medical Council on Alcoholism.

NICE. (2011). Alcohol-use disorders: diagnosis, assessment and management of harmful drinking and alcohol dependence. Available: Last accessed 18/11/2016.

Petty, F., Fulton, M., Moeller, F. G., Kramer, G., Wilson, L., Fraser, K. & Isbell, P. (1993). Plasma gamma-aminobutyric acid (GABA) is low in alcoholics. Psychopharmacology Bulletin, 29, 277–281.

Saitz, R., Mayo-Smith, M. F. & Roberts, M. S. (1994). Individualized Treatment for Alcohol Withdrawal: A randomized double-blind controlled trial. Journal of the American Medical Association, 272(7), 519-523.

Sullivan, J.T., Sykora, K., Schneiderman, J., Naranjo C. A., & Sellers, E. M. (1989). Assessment of alcohol withdrawal: The revised Clinical Institute Withdrawal Assessment for Alcohol scale (CIWA – Ar). British Journal of Addiction, 84, 1353-1357.

Svanberg, J., Withall, A., Draper, B. & Bowden, S. (Eds). (2014). Alcohol and the Adult Brain. Hove: Psychology Press.

Thomson, A. D. & Marshall, E. J. (2005). The Treatment of patients at risk of developing Wernicke's Encephalopathy in the Community. Alcohol and Alcoholism, 41(2), 159-167.

Victor, M. V., Adams, R. C. & Collins, G. H. (1989). The Wernicke-Korsakoff Syndrome and Related Neurologic Disorders Due to Alcoholism and Malnutrition. Philadephia: F. A. Davis.


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