اتى مريض مع مرافقيه وهو بحالة ماقبل الاغماء
precoma , the doctor ask him about his name , his answer slurred or monotonous
يسأله الطبيب عن اسمه فيجيب ببطئ ويتكلم كلام غير مفهوم
doctor ask him , where when who , his answer wrong
يسأله الطبيب في اي مكان انت وهل الان عصر ام مغرب ويسأله عن المرافقين فلايجيب او يجيب بشكل خاطئ
disorientation for time and place and person
وكذلك يذكر الطبيب خلال اسألته له كان يجيب يتصرف تصرفات غريبه
childish attitude , phasic excitation and depression
وهنا يشك الطبيب بأحدى الحالتين
*what are the differential diagnosis of disturbed level of consciousness ?
1-hepatic encephalopathy
2- hypoglycemia
and also
3-hypoxia
4-delirium tremens(alcohol withdrawal)
5-drunkenness
6-subdural hematoma
7-psychatric disorder
3h2dsp
if .....
subdural hematoma = hx of head trauma
delirium tremens = pt daily alcohol drinker with sudden withdrawal
drunkenness = pt with alcohol كان في سهره سكر
hypoxia = oximeter show the result
hypoglycemia = tachycardia , sweating
الاهم يجب ان نفرق بين
hypoglycemia and hepatic encephalopathy
بعد ان قمنا بوضع احتمالات لاختلال الوعي
يبدأ الطبيب بالفحص ليشم رائحة
fetor hepaticus
هنا يشك الطبيب بمرض
hepatic encephalopathy , doctor ask the relative
هل مريضكم عنده مشاكل في الكبد
فيجيبون بنعم وان المريض لديه تليف بالكبد منذ عدة سنوات
on history , the patient have liver cirrhosis many years ago
هنا يشك الطبيب بنسبة 90% ان الخلل في الكبد
فيتأكد اكثر بنسبة 100% ويقوم بفحص
asterixis (flapping tremor ) = positive
(it is lapse in posture due to impaired inflow of joint and other afferent information to the brain stem reticular formation)
also , he searching for other hepatic cell failure sign
1-fever 2- jaundice 3-ascites 4-palmar erythema , spider naevi 5-gynecomastia 6-cyanosis and clubbing
liver failure signs not necessarily all present , because hepatic encephalopathy not always due to hepatic cell failure , the cause may be acute fulminant hepatitis , or spontaneous shunting in patient with portal hypertension = chronic portosystemic encephalopathy
so , the diagnosis now hepatic encephalopathy , if doubt
1-EEG : diffuse slow triphasic waves 2-ammonia level : increase but not specific or sensitive
there are many stages to hepatic encephalopathy , the last one is the coma , other one respond to pain stimuli , but late no response
there are two test can be done to reveal early stage of hepatic encephalopathy :
1-constructional apraxia is an early sign (patient unable to draw five pointed star)
2-reitan number connection test (patient unable to join numbers)
before management , we must know the precipitating factor to hepatic encephalopathy ?
1-git bleeding 2-increase protein intake 3-old blood transfusion 4-aspiration of ascites 5-diuretics like lasix 6-others : drug-morphine , sbp-spontaneous bacterial peritonitis , surgery-porto-systemic shunt
the most common is git bleeding so in management :
1- hospitalization in ICU , endoscope should be done to localize the site of bleeding
2-diet -restrict protein intake , increase carbohydrate intake lead to decrease protein breakdown as source of eneregy , fats in small amount which lead to mild diarrhea which is good to wash intestine , excess k intake with found in fruit juice
3-enema/4h : wash the colon
4-antibiotics :to prevent the action of intestinal bacteria on protein
5-lactulose : 30-120 ml 3 times daily oral or rectal , osmotic diarrhea wash the colon and production of lactic acid which promote conversion of luminal ammonia NH3 to ammonium NH4
6-sedative should avoided , if necessary , small dose of diazepam
7- morphine is absolutely contraindicated
*what is the management of hepatic encephalopathy precipitated by git bleeding ?
1-addmission to ICU , ednoscopy
2-enema /4h to wash colon
3-antibiotics(neomycin-rifaximin) to prevent action of intestinal bacterial that convert protein
4-lactulose 30-120 ml 3 times daily
*what is the diet for hepatic encephalopathy or liver failure patient ?
protein restriction , high carbohydrate , small amount of fat , excess potassium
*what is the rule of lactulose in hepatic encephalopathy ?
lactulose convert to lactic acid-acetic acid in intestine , this will turn the intestine to acidic environment , and there the ammonia NH3 (which is the cause of encephalopathy due to neurotoxic effect) will convert to ammonium NH4and this will reduce the amount of ammonia that reach the brain
what are the rule of antibiotics in hepatic encephalopathy(neomycin-rifaximin) ?
it is not confirmed rule , but the mechanism is killing the bacterial in the intestine which convert protein to ammonia
what is the cause of hepatic encephalopathy in patient with liver git bleeding ?
or what is the relation between hepatic encephalopathy and git bleeding ?
in this case above , we consumed that our patient have git bleeding , like massive variceal bleeding from esophagus , then he develop DLOC and coma , so the relation between git bleeding and hepatic encephalopathy is the patient swallow large amount of blood , rbc converted to hemoglobin in intestine , and hemoglobin is protein , this protein digested and its final product is ammonia which lead to encephalopathy , also urea increased in those patient because ammonia converted to urea in liver