WE

CASE PRESENTATION

DR.SULTAN MAHJA ALANAZI MEDICAL RESIDENT R424/01/2023

HISTORY

A 19 YEARS OLD SAUDI MALE PT , GASTRIC SLEEV 5 MONTHS AGO AND DIAGNOSED AS CHOLECYSTITS 1 MONTH AGOPT WAS COMPLETE COURSE OF IM VIT B12 AND THEN HE DOESN'T COMPLIANT ON HIS MEDICATION BUT PT CAN NOT REMEBER WHEN?PT C/O ALL LIMBS NUMBNESS SINCE 3 WEEKS (PT CAN NOT REMUBER WHICH ONE BECOME FIRST) LOWER LIMB WEAKNESS BILATERAL, BLURRED VISION, HEADACH AND NAUSEA

H.P.I

ALL SYMPTOMS STARTED GRADUALY PROGRESS , NUMBNESS THEN BLURRED VESION THEN PATIENT CAN'T WALK , HEADACHE AROUND ALL HEAD , WITHOUT AURANO HIX OF COUGH, VOMITING, DIARRHEA OR DYSUREA LAST COVID19 VACCINE DOSE BEFORE 3 MONTHS NO HIX OF CONTACT WHIH SICK PEOPLENO RECENT HIX OF TRAUMA

HX

FAMILY HX : NO HX OF SAME SOCIAL HX: ENGNERRING STUDENT NOT SMOKER NOR ALCHOLIC TRAVEL HX: TO RIYADH 1 MONTH AGO FOR 3DAYS HX OF RTA 1.5 YEARS AGO NOT ADMITTED LOST MUCH WAIGHT NOT DICUMANTED

O/E

PT IS CONSCIOUSE, ORIENTED BUT DIFFICULT CONCENTRATE WITH ME V/S:T:36.8 BP 120/70 HR 89/MIN SPO2 100%-CNS: CRAINAL NERVE: PIUPLE REACT EQUAL TO LIGHTRESTRECT MOVEMENT EYE BILATERAL TO ALL POSITION POWER 4/5 IN UPPER AND 3/5 LOWER LIMBLL> SENSATION DECREASED UNTIL UMBILICAL UL> SENSATION INTAKT JOINT POSITION VIBRATION INTAKT , -VE BABNESKI SIGN , CEREBELLAR SIGN: DIFICULT TO ASSESSREFLEX: HYPER-REFLEXIA IN UPPER LIMB AND HYPOREFLXIA IN LOWE LIMB , NORMAL TONE -CHEST: EBAE , CVS:S1+S2+0 , ABDOMEN: SOFT AND LAX FUNDOS EX: BILATERA DISC SWELLING

HYPERREFLEXIA

OPHTHALMOPLASIAPAPILOEDMA

DECREASED SENSATION

DIFFICULT CONCENTRATION

FINDING

HYPOREFLEXIA , WEAKNESS

• LAB:
• WBC 7.8 HB 18.2 HEMATOCRIT 55.2 PLT 290
• INR 1.0
• UREA 3.8 NA 141.4 K 4.5
• VIT-B12 IN OTHER HOSPITAL AROUND 742

DONE BEFORE 2 DAYS VIT B1 : PENDING

• CT-BRAIN: UNREMARKABLE

• DDx ??

MRI BRAIN: Symmetrical ABNORMALLY increased T2/FLAIR signal involving the mammillary bodies , dorsomedial thalami tectal plate , periaqueductal area and to a lesser extent around the third ventricle .

MRI BRAIN: Symmetrical ABNORMALLY increased T2/FLAIR signal involving the mammillary bodies , dorsomedial thalami tectal plate , periaqueductal area and to a lesser extent around the third ventricle .

Wernicke encephalopathy (WE) is an acute syndrome requiring emergent treatment to prevent death and neurologic morbidity. Korsakoff syndrome (KS) refers to a chronic neurologic condition that usually occurs as a consequence of WE.

Wernicke encephalopathy

Encephalopathy

Gait ataxia

Oculomotor dysfunction

CLINICAL MANIFESTATIONS The classic triad of WE

WE is diagnosed in patients with two of the following four Caine criteria:1- Oculomotor abnormalities 2- Cerebellar dysfunction 3- Either altered mental status or mild memory impairment4- Dietary deficiency

• Associated conditions — While most often associated with chronic alcoholism, WE occurs also in the setting of poor nutrition caused by malabsorption, poor dietary intake, increased metabolic requirement (eg, during systemic illnesses), or increased loss of the water-soluble vitamin thiamine (eg, in renal dialysis). In one autopsy series, non-alcohol abusers accounted for 12 of 52 cases (23 percent) of WE ]. Conditions associated with WE include:

●Chronic alcoholism ●Anorexia nervosa or other psychiatric illness leading to poor intake . ●Hyperemesis of pregnancy . ●Prolonged intravenous (IV) feeding without proper supplementation. ●Prolonged fasting or starvation, or unbalanced nutrition, especially with refeeding .●Gastrointestinal disease or surgery (especially bariatric surgery) .●Systemic malignancy . ●Transplantation . Hemodialysis or peritoneal dialysis .●Acquired immunodeficiency syndrome

and 250 mg IV or IM once daily for an additional five days, in combination with other B vitamins

A recommended regimen is 500 mg of thiamine IV infused over 30 minutes three times daily for two consecutive days

TREATMENT

Although dietary requirements for thiamine are only 1 to 2 mg daily

PATIENT HOSPITAL COURSE

Timeline

15/01/2022MEMORY IMPROVED OCULAR MOVMENT IMPROVED

13/01/2022MRI BRAIN DONE THIAMINE STARTED

16/01/2022CONSENTRATION IMPROVED OCULAR MOVMENT NOTED BY FAIMILY

14/01/2022OCULAR MOVMENT SOME IMPROVMENT NYSTAGMUS APPEAR

24/12/2021SYMPTOMS STARTED

ABOUT SENSORY

Peripheral neuropathy is common and typically involves just the lower extremities, Patients complain of the gradual onset of weakness, paresthesias, and pain affecting the distal lower extremities.

Recovery of vestibular function began during the second week after thiamine treatment; improvement in gait ataxia coincided with recovery of vestibular function . Confusion subsides over days and weeks.

CLINICAL COURSE

Prompt administration of thiamine leads to improvement in ocular signs within hours to days

In the largest cohort of patients reported on, residual deficits were the rule . While gaze palsies recovered completely in most cases, 60 percent had permanent horizontal nystagmus. Only approximately 40 percent recovered from ataxia; remaining deficits ranged from inability to walk at all to a wide-based, slow, shuffling gait. As the acute encephalopathy and confusion receded, deficits in learning and memory became more obvious; the latter recovered completely or substantively in only approximately 20 percent; the remainder had a permanent amnestic syndrome.

Prognosis

1- youngest patient 19 years old vs 20 - 31 - 36- 40 2-extensive thiamine was gaiven in our case and other 2 3-first case 2007 was reported last case our case 2022 4- many cases reported post Roux-en-Y gastric bypass

our case compared to other cases

PATIENT RETURNED TO UNIVERSITY AFTAR FAiled IN ENGiNERING COLLEGE NOW IN TECHINICAL COLLEGE 3RD SIMESTER

CLINICAL COURSE LAST VISIT 2 WEEKS AGO

ocular movment and concentration improved , very mild ataxia and prephreal neuropathy

Thank you!

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