PRE FINAL PRACTICAL (45 year old male with giddiness) LONG CASE

Presenting complaints45 year old male who is a resident of Narketpalli driver by occupation , came to the casuality who studied till degree came with complaints of :

Giddiness since yesterday afternoon  

vomiting’s 4 episodes  since afternoon 

shivering since afternoon which lasted till he was brought to the hospital subsided on medication . 



HOPI & PAST HISTORY : 


He’s the last child in his family .

Mother and father expired at 20 years  , mother expired because of paralysis . Father expired because of ? Renal issues . 

Marriage : consanguinity ( first degree ) at 20 years survived with 2 kids (2sons ) one son is intern completed and other is working in hyd in a laboratory. 


20 years back he worked in an pharmacy for 3-4 years , then he owned his own auto and drove for 3-4 years , later he brought his car gave it for trips ,and he worked  a private driver , and also used to drive hens to chicken shop , He’s an night driver , he used to leave home at 7:30 pm and come back next day 9:30 am 

After drinking alcohol and used to sleep till evening without eating food . 


Patient was apparently asymptomatic 4 months back, then he had shortness of breath grade 2-3  , which was associated with fever and chills , associated with dry cough for 4 days was brought to our hospital and was diagnosed with Community acquired pneumonia and was treated accordingly and got discharged after 4 days . 


Chronic alcoholic since 18 years and Chronic smoker since 18 years   (1pack/day ) non diabetic and non hypertensive .


His drinking increased since 2 months after his sons suicide due to betrayal by his close friends , was admitted in our hospital and got discharged . 


Now , presenting with complaints of giddiness which is postural and associated with vertigo and not associated with tinnitus and shivering since afternoon which was subsided after coming to hospital , lasted for 1 hour approx.

Vomitings 3 epiosdes non bilious, non projectile , butter milk as content , non foul smelling and non blood tinged . 


On examination : 

Patient is drowsy but arousable . 

Afebrile to touch  (Temp : 98.5F) 

Bp : 130/80mmhg

Pulse : 84bpm regular , normal volume 

CVS : s1s2 + no murmur 

P/A : soft , no organomegaly

Spo2: 98% RA

GRBS :(105mg/dl)


Personal history : mixed diet, appetite reduced

Regukar bowel and bladder movements

Smoker since 18 years ( daily one pack / day )


Family history : mother is hypertensive, expired due to cva after bedridden for 6 months .


Drug history : NONE 


CNS : patient is oriented to time , place and person  drowsy but arousable 

Right handed person , speech : normal  , no deviation of mouth , no sluuring of speech .

MMSE : couldn't be elicited as patient was drowsy 

GCS: 15/15


Cranial nerves : I) Sense of smell : couldn't be elicited

II) Visual acuity : NORMAL


a.Field of visison  NORMAL


b.Colour vision: couldn't be elicited as patient was drowsy 


c. Fundus: couldn't be elicited as patient was drowsy 













III)   EOM:


Pupil size: 2-3mm (Right)      2-3mm (left)


No Ptosis 


Nytagmus present + bilateral ( horizontal nystagmus + horizontal ) R>L

 NO DEVIATION OF MOUTH , FROWNING NORMAL 

Rinnes : air conduction >bone conduction 

webers : no laterisation



 IX , X: No deviation of uvula 

XII: SHRUGGING OF SHOULDERS NORMAL

XII: MOVEMENT OF TONGUE NORMAL

NO WASTING OF TONGUE /FASICULATIONS




MOTOR :

BULK : NORMAL


 Tone :                 Right             Left 

 Upper limb           N                   

 Lower limb           N                   


 Power : 

 Upper limb :         N                 

 Lower limb :         N                  

Motor : 

Biceps :               2+                  2+ 

Triceps :              2+                  2+ 

Supinator :           2+                  2+ 

Knee jerk :           2+                  2+ 

Ankle :                          mute 

Plantar :             Flexion          Flexion























   
SENSORY : COULDNT ELICIT PROPERLY AS PATIENT  WAS DROWSY 
HAS TAKEN TAB. LORAZAPEAM


Sensory examination :            

Spinothalamic:                                           right                              left 

crude touch :                                                 +                                   +

pain         :                                                     +                                   +
 

Posterior coulumn :
 
Fine touch :                                                     +                                   +

Vibration reduced


CORTICAL:                     STERIOGNOSIS +


CEREBELLUM :             NYSTAGMUS ++ 

Both vertical and horizontal in both eyes fast beating on right side 

Rombergs swaying to right back with open eyes 


Meninges : kernigs and brudzinskis negative 

Cvs: apex beat 5th ics , mid clavicular line 
no thrill or heave

RS: Inspection : chest elliptical, bilateral  symmetrical
 
no trachea deviation

movements appear normal 
 

inspection : inspectory findings present

percussion: resonant note heard in all areas 

auscultation: normal breath sounds heard in all areas 

P/A: no organomegaly , breath sounds +



DIAGNOSIS:  WERNICKES ENCEPHALOPATHY  (SECONDARY TO  THIAMINE DEFICIENCY )




Investigation:  






Hemogram:

Hb:11.8gm/dl
TLC:3000cells/cumm
Platelets 1.0Lakhs
PCV:35

RFT:
Urea:28mg/dl
Creatinine:0.6mg/dl
Sodium:139meq/lit
Potassium:3.6meq/lit
Chloride:99meq/lit

PT:17sec
INR:1.2
APTT:33sec

CUE :
Albumin nil
Sugar nil
Pus cells 3-4/hpf

LFT:
Total bilirubin:2.13
Direct bilirubin:1.09
AST:218
ALT:80
ALP:163
TP:6.2
Alb:3.8
A/G:1.64


TREATMENT GIVEN:

INJ. THIAMINE 400mg IV STAT
Followed by 200mg IV TID
Tab Lorazepam 2mg PO BD 
IVF NS @70ml/hr



DISCUSSION:  HOW THIAMINE CAUSES WERNICKES ?

Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism. This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation. Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death. Neuronal death in the mammillary bodies and thalamus were implicated in multiple cases of Wernicke encephalopathy studied. Studies involving computed tomography (CT) and magnetic resonance imaging (MRI) of patients with Wernicke encephalopathy revealed lesions in the thalamus with dilated ventricles and volume loss in the mammillary bodies. The lesions are usually symmetrical in the midbrain, hypothalamus, and cerebellum.

INFERENCE :

https://www.ncbi.nlm.nih.gov/books/NBK470344/#:~:text=Wernicke%20encephalopathy%20is%20an%20acute,peripheral%20and%20central%20nervous%20systems.





ROLE OF THIAMINE IN VARIOUS ENZYMATIC PATHWAY :







DIAGNOSIS: 

WERNICKES ENCEPHALOPATHY  (SECONDARY TO  THIAMINE DEFICIENCY )

ALCOHOLIC LIVER DISEASE

BICYTOPENIA SECONDARY TO ANEMIA 








 

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