Case Presentation Conferance

Shariati HospitalSurgery rotation

F. Seyedalipour

92/5/6CC

ارجاع جت بزرسی یپز کلسوی اختالل شیاری ها قبل دچارتع ، استفزاغ، بی اشتایی ضعف 5سال ای است ک اس 58بیوار خان

.کیلگزم شذ است 10 بی حالی کاش سى حذد ها در بیوارستاى سیای تبزیش بستزی بد با تشخیص پاکزاتیت تحت 2بیوار هذت

رس است ک استفزاغ کزد اشتای 2در حال حاضز هذت . درهاى قزار گزفت استرس قبل اس بستزی آتاکسی، ذیاى گیی، ضعف اذام 5اس حذد . بیوار بتز شذ است

. ا یستاگوس داشت تشخیص دلیزیم بزای ی هطزح بد است در آسهایشات یپزکلسوی(Ca=13.3) ،PTH 25 ( 12.5)سزکب(OH)vitD زهال

.داشت ک تحت درهاى با آهپل کلسی تیي قزار گزفت استجت بزرسی ای بیشتز ب بیوارستاى شزیعتی تزاى ارجاع شذ.

PMH

o ها پیش 2سابق تعیض یپ چپo ها قبل 2پاکزاتیت حادoیپزتاسیى

HH

DH

PhEبیوار خانن هسنی بودند که سطح هوشیاری کاهش یافته داشته ، ارتباط چشوی کوی

بزقزار هی کزدند، قادر به پاسخ گویی به سواالت نبوده هذیاى هی گفتند و .آگاهی اس سهاى و هکاى نداشتند

. تهوع و استفزاغ نداشتند.نیستاگووس افقی دو طزفه داشتند

Vital Signs:

BP:110/75 - PR:75/min - RR:18/min - T=37.7

سوع ریه ها: clear

نزهال: سوع قلب نزم و بدوى تندرنس، گاردینگ و ارگانوهگالی: شکن.

Lab data

o WBC=4800

o Hb=8.6

o Fe=68

o TIBC=224

o Plt=127000

LDH=

ESR=21

CRP=24

Amilase=133

BS=96

Ca=9.6- 7.5- 8.1

P=2.3

Na=135

K=3.9

Urea=22

Cr=1.4-1.1-0.9-0.7

AST=15

ALT=11

Alp=339

PTT=

PT=

INR=1

T.Pr=5.3

Alb=3.4

، اسالج غلیظ درکیسه prominantدر بررسی های انجام شده پانکراس •

.و هلیکوباکتر پیلوری مثبت داشته است erosive duodenitisصفراوی ،

•Brain CT :بدون ضایعه فضاگیر، هموراژی و شیفت میدالین

EF=55%: اکوکاردیوگرافی•

92/5/9

92/5/12

اختالل هوشیاری بیمار تشدید شده در پاسخ به محرک دردناک چشم خود را باز •

.می کرد

•Defecation نداشته و به علت عدم تحملPO الکتولوز دریافت نکرده بود.

+(2)ادم پاها افزایش یافته بود •

•T=39 ،PR=95،RR=20 ،BP=150/100

با توجه به سفتی گردن اندک ، تب و کاهش سطح هوشیاری شک به مننژیت • LPو درخواست شروع empiricآنتی بیوتیک درمانی . برای وی مطرح شد

.داده شد

92/5/13

mammillary، تاالموس، CTZبیمار ضایعات نکروزه در MRIدر • bodies

.وجود دارد که می تواند مطرح کننده انسفالوپاتی ورنیکه باشد

92/5/14

Vitمشاوره فارماکوتراپی از بابت شروع تغذیه وریدی، تامین • B1 فسفر و ،

.سایر المنت ها

92/5/15

Lab data(92/5/14)

o WBC=7200

o Hb=7.3

o Plt=164000

BS=169

Ca=8.1

Mg=1.5

P=1.3

Na=145

K=2.5

Urea=12

Cr=0.8

Alb=2.5

Procalcitonin=0.195 (N<0.5)

Drugs

• Amp Pantoprazole 40mg/IV/BD

• Amp Heparin 5000 IU/SC/BD

• Amp Ceftriaxone 2g/IV/BD

• Amp Vancomycin 1g/IV/BD

• Amp Ampicillin 2g Q 4hr

• Amp metoclopramide 10mg/IV/BD

• Tab Metoral 25mg/PO/BD

• Tab Losartan 25mg/PO/BD

• Serum H/S 1000ml + KCl 15% 20ml TDS

Wernicke-Korsakoff syndrome

• The best known neurologic complication of thiamine (vitamin B1) deficiency

• Wernicke's encephalopathy (WE) is an acute syndrome requiring emergent treatment to prevent death and neurologic morbidity.

• Korsakoff's syndrome (KS) refers to a chronic neurologic condition that usually occurs as a consequence of we.

EPIDEMIOLOGY

• 0.8 to 2.8 percent of the general population

• 12.5 percent of alcohol abusers

• While cases of WE in men outnumber those in women, women appear to be more susceptible to developing WE than men.

Associated conditions• 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

PATHOPHYSIOLOGY

• Thiamine is a cofactor for several key enzymes important in energy metabolism, including:

• Transketolase

• Alpha-ketoglutarate dehydrogenase

• Pyruvate dehydrogenase

• Thiamine requirements depend on metabolic rate, with the greatest need during periods of high metabolic demand and high glucose intake.

PATHOPHYSIOLOGY(con.)

• Low levels of magnesium, an essential cofactor of thiamine into its active diphosphate and triphosphate forms, have been implicated with thiamine deficiency in WE.

• Its deficiency initiates neuronal injury by inhibiting metabolism in brain regions with high metabolic requirements and high thiamine turnover.

• Events such as blood-brain barrier breakdown, N-methyl-D-aspartic acid (NMDA) receptor-mediated excitotoxicity, and increased reactive oxygen species have been implicated in thiamine deficiency-induced neurotoxicity.

PATHOPHYSIOLOGY(con.)

• Thiamine deficiency in alcohol abusers results from a combination of inadequate dietary intake, reduced gastrointestinal absorption, decreased hepatic storage, and impaired utilization.

Pathology

• Acute WE lesions are characterized by vascular congestion, microglial proliferation, and petechial hemorrhages.

• In chronic cases, there is demyelination, gliosis, and loss of neuropil with relative preservation of neurons. Neuronal loss is most prominent in the relatively unmyelinated medial thalamus.

• Atrophy of the mamillary bodies is a highly specific finding in chronic WE and Korsakoff syndrome and is present in up to 80 percent of cases.

Classic signs — The classic triad of Wernicke's encephalopathy (WE) includes:

› Encephalopathy

› Oculomotor dysfunction

› Gait ataxia

CLINICAL MANIFESTATIONS

› The encephalopathy is characterized by:

o Profound disorientation

o Indifference

o Inattentiveness

o Impaired memory and learning

oAgitation , delirium

oDepressed level of consciousness

oComa and death

Encephalopathy

› Nystagmus is the most common finding and is typically evoked by horizontal gaze to both sides.

› Vertical nystagmus can also occur, usually evoked by upward, rather than downward, gaze.

Oculomotor dysfunction

› Ataxia primarily involves stance and gait and is likely due to a combination of polyneuropathy, cerebellar involvement, and vestibular dysfunction.

› When severe, walking is impossible. Less affected patients walk with a wide-based gait and slow, short-spaced steps.

Gait ataxia

› Other signs — In addition to the classic triad, stupor or coma, hypotension, and hypothermia were prominent findings in unsuspected cases

› While overt beriberi heart disease is rare in WE, other cardiovascular signs and symptoms are common and include tachycardia, exertionaldyspnea, elevated cardiac output, and EKG abnormalities

› Clinical diagnosis

› Laboratory studies

› NeuroimagingDIAGNOSIS

› Intravenous administration of thiamine is safe, simple, inexpensive, and effective

TREATMENT

› antiberiberi factor

› soluble in water and partly soluble in alcohol

› larger quantities in food products such as yeast, legumes, pork, rice, and cereals.

› Milk products, fruits, and vegetables are poor sources

› high pH and high temperatures

Thiamine (Vitamin B1)

• The maximal absorption of thiamine is in the jejunum and ileum.

• The highest concentrations are found in the skeletal muscles, the liver, the heart, the kidneys, and the brain.

• Biologic half-life is approximately 10 to 20 days.

• Thiamine and all of its metabolites are excreted in the urine. Biliary excretion is a minor route of its homeostasis.

Metabolism

• No real syndrome of excess thiamine exists since the kidneys can rapidly clear almost all excess thiamine

Toxicity

• Recommended daily intake:• ≥19 years: Females: 1.1 mg; Males: 1.2 mg• Pregnancy, lactation: 1.4 mg• Adequate Intake:• 0-6 months: 0.2 mg/day• 7-12 months: 0.3 mg/day• Recommended daily intake:• 1-3 years: 0.5 mg• 4-8 years: 0.6 mg• 9-13 years: 0.9 mg• 14-18 years: Females: 1 mg; Males: 1.2 mg

The RDA is the level of dietary intake that is sufficient to meet the daily nutrient requirements of 97 percent of the individuals in a specific life stage group.

Recommended daily allowance (RDA)

• Treatment (manufacturer labeling): Initial: 100 mg I.V., then 50-100 mg/day I.M. or I.V. until consuming a regular, balanced diet.

• Alternate dosage: The Royal College of Physicians (U.K.) has recommended the use of higher doses of thiamine:

• Prophylaxis: 250 mg I.V. once daily for 3-5 days

• Treatment: Initial: 500 mg I.V. 3 times/day for 3 days. If response to thiamine after 2 days, continue with 250 mg I.M. or I.V. once daily for an additional 5 days or until clinical improvement

Wernicke's encephalopathy

• Daily oral administration of 100 mg of thiamine

• Pancreatic encephalopathy (PE) is an uncommon complication of acute pancreatitis (AP). PE, which is one of multiple organ dysfunction syndrome (MODS), generally occurs in early stage of severe acute pancreatitis (SAP) and has a high mortality of 57%.

• But in the last or restoration stage of AP, neurological complications are mostly Wernicke encephalopathy (WE) which results from long fasting, hyperemesis and total parenteral nutrition (TPN) without thiamine (vitamin B1).

• Ocular abnormalities are the hallmarks of WE, and horizontal nystagmus is common.

• In case differential diagnosis of PE and WE is baffled, Vit B1 diagnostic treatment may be useful:

• Patients’ condition of WE is supposed to improve after injected Vit B1 (100 mg/d) therapy for 1-3 d.

• If a patient, in the course of pancreatitis, has suspicious or unusual neurological symptoms and signs, a possible diagnosis of encephalopathy should be made, and the patient should be given intravenous thiamine without delay to avoid the potential morbidity and mortality associated with undiagnosed WE.

CASE REPORT

CASE REPORT

تبدار نبوده . حال عمومی بیمار خوب و هوشیاری وی بهتر شده بود•

.است Ca=9.2

Mg=2.3

P=4

Na=145

K=4.1

Alb=3

92/5/21

Thanks for your attention