Download Case - Wernicke

 56 yo male presenting with memory loss and poor
balance
 Memory Loss – 4/7 hx short term memory loss e.g.
unable to recall if ate a meal + recollection of past
events in present time e.g. though mother still alive
even though past away 5yrs ago
 Altered balance – unsteady gait, had x2 falls the night
before, recalls events, nil LOC. Stated legs felt weak
 Poor oral intake – 1/52
 Increased sleep patterns - 4/7, sleeps 15hrs/day,
denies daytime fatigue
 Previously well
 Nil cough, CP, abdo pain, diarrhoea/vomiting,
fevers, sweats or urinary symptoms
 Nil visual/hearing disturbances, dizziness,
paraesthesia, headache, neck pain or photophobia
 PMHx
 STEMI 2011
 Prostate adenocarcinoma 2012 – underwent
prostatectomy, PSA 19/1/12 <0.01
 Appendiceal adenocarcinoma 2009
 Dyslipidaemia
 Depression
 PSHx
 Prostatectomy Aug 2012
 Appendectomy 2009
 Stent 2011
 FHx
 Mother – x2 MIs 55yrs
 Father – MI in 60s
 Medications
 Aspirin 100mg
 Perindopril 5mg
 Metoprolol 25mg
 Clopidogrel 75mg
 Atrovastatin 80mg
 Fluoxetine 20mg (commenced 6/7 ago)
 Social Hx
 Lives with wife + 2 children
 Ex-truck driver – ceased work since prostectomy
 Smokes ½ - 1 pack/day
 Alcohol – varriable, 6-12/day. Since onset of symptoms
has reduced to 2/day
 Denies recreational drug use
 Denies recent travel or exposures
 Afebrile, BP 129/74, HR 62, RR 18, Sats 100% RA
 Alert, nil distress
 ECG NAD
 CVS
 Warm and well perfused
 HSDN, nil murmurs or added
 JVPNE
 Nil peripheral oedema
 Resp
 Chest clear, EA
 Nil wheezes or creps
 GIT
 Abdo soft, non-tender
 Nil jaundice, nil asterixis
 Nil organomegally
 CNS









Normal speech – comprehendable but vague
Alert and compliant
Nil neck stiffness
Disoriented to time and place (refers to previous
hospital admission)
Knows name, DoB & address but not age
19/30 on MMSE
Able to name objects
Impaired memory – unable to retain new information,
able to recall past events but gaps in long term memory
Nil confabulation
 CN II-XII intact
 Left lateral nystagmus
 Nil diplopia
 Power 5/5 globally, L=R upper & lower limbs
 Normal sensation and proprioception
 Past pointing on finger-nose test
 Nil dysdiadochokinesis
 Wide based gait
 Truncal ataxia
 CT Head Normal
 Chronic deep white matter ischaemia
 The degree of ventricular dilatation and prominence of
the subarachnoid spaces is most likely related to
involutional change. However, the differential of
normal pressure hydrocephalus needs to be considered
clinically, particularly given the degree of
periventricular white matter hyperintensity
 AWS
 Neuro Obs
 IV Thiamine 500mg TDS
 Feeling better
 Gait much improved
 Still not oriented to time and place
 Still ongoing short term memory impairment
 Continued IV thiamine
 Continued Physio/OT rv
 Wernicke’s Encephalopathy
 ?Menengitis/Encephalitis
 ?Other drug/medication related
 Patient transferred to Wynnum Hospital for ongoing
rehabilitation
 Continue course of thiamine and switching to oral
dose
 Will review in clinic with repeat MRI in 2 weeks
 Wernicke's encephalopathy (WE) is a common, acute
neurologic disorder caused by thiamine deficiency.
Clinical triad of encephalopathy, oculomotor
dysfunction, and gait ataxia
 Korsakoff's syndrome (KS) is a late, neuropsychiatric
manifestation of Wernicke's encephalopathy (WE) in
which there is a striking disorder of selective
anterograde and retrograde amnesia
 Described in 1881 after Carl Wernicke (Polish
Physician), also named Wernicke’s area & Sergei
Korsakoff (Russian psychiatrist)
 inadequate intake or absorption of thiamine (Vitamin
B1)
 Thiamine plays a vital role in the metabolism of
carbohydrates. Thiamine is a cofactor for several
essential enzymes in the Krebs cycle and the pentose
phosphate pathway
 The male-to-female ratio 1.7:1, likely owing to
alcoholism being 3-4 times more frequent in men than
in women.
 Average age at onset is 50 years
 Conditions associated with WE include:










Chronic alcoholism
Anorexia nervosa or dieting
Hyperemesis of pregnancy
Prolonged intravenous feeding without proper
supplementation
Prolonged fasting or starvation, or unbalanced nutrition,
especially with refeeding
Gastrointestinal surgery (including bariatric surgery)
Systemic malignancy
Transplantation
Hemodialysis or peritoneal dialysis
Acquired immunodeficiency syndrome
 Different stages of the disease
 Wernicke's encephalopathy (WE) is an acute
syndrome
 Korsakoff's syndrome (KS) refers to a chronic
neurologic condition that usually occurs as a
consequence of WE
 Clinical triad = ophthalmoplegia, ataxia, and global




confusion
Only 1/3 present this way
Confusion most common presentation
Most Patients profoundly disoriented, indifferent, and
inattentive, although rarely they have an agitated
delirium related to ethanol withdrawal
Stupor, coma, and death may ensue if left untreated
 Psychosis
 Normal pressure hydrocephalus
 Cerebrovascular accident
 Chronic hypoxia
 Closed-head injury
 Hepatic encephalopathy
 Postictal state
 Other substance abuse
 Alcohol withdrawl
 Delerium/Dementia
 Stroke/Ischemia
 Clinical Diagnosis
 FBC – exclude anemias and leukemias as causes of altered mental status
 Serum glucose levels - Exclude hypoglycemia and hyperglycemia
 ABG
 Toxic drug screening
 Consider lumbar puncture (LP) - Consider LP to exclude CNS infections
 Erythrocyte transketolase levels – but not necessary for diagnosis
Wernicke's disease. MRI reveals abnormal enhancement of
the mammillary bodies (atrophy), typical of acute Wernicke's
encephalopathy
 Require immediate administration of thiamine
 Usually 500mg IV tds for 2-3 days than reduce dose
 Administration of glucose without thiamine can
precipitate or worsen WE
 Thiamine should be administered before glucose
 Oral thiamine absorption often unreliable initially
 Significantly disabling but can be prevented or
reversed if treated early
 Persistent neurologic dysfunction is common
 Significant morbidity and mortality rate, especially if
no early signs of neurologic improvement are present
after repletion of thiamine
 A worse outcome may be expected in late-stage
Wernicke encephalopathy