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Ensefalopati Uremikum Bu Yanti
Ensefalopati Uremikum Bu Yanti
Teaching Course 17
Email: Weissenborn.Karin@mh-hannover.de
Conflict of interest: The author has no conflict of interest in relation to
this manuscript
and hepatic encephalopathy (Brouns & De Deyn 2004; Seifter & Samuels
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2011, Jones & Weissenborn 1997). The diagnosis “metabolic encephalo-
pathy” can be made only after exclusion of other possible causes of brain
(EEG). Again, there are no specific findings for one or the other type
case. But even in patients with severe alterations of blood glucose levels
resonance imaging (MRI) is done for the exclusion of other than metabolic
pathies presents with specific CCT or MRI alterations. But, again there are
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patient presents with psychomotor slowing and Parkinsonism this MRI
finding suggests liver cirrhosis as cause of the symptoms and gives reason
this MRI finding does not prove uremic encephalopathy but has been
well as in other conditions with metabolic acidosis (Kumar & Goyal 2010).
also bilateral spike wave compexes may occur (Brouns & De Deyn 2004).
changes in the clinical status, and thus may announce a bout of hepatic
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Hepatic encephalopathy (HE)
grade III and IV HE, but can be present also in the other stages, on
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progressive HE – in a prospective study of 214 patients with liver cirrhosis
with liver cirrhosis and leads to severe spastic paraparesis without any
These patients are considered to suffer from the so called minimal hepatic
however, explains why mHE affects the working ability of blue collar
quality of life and working ability and it interferes with the patients
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be treated with 100 mg thiamine i.v. in every suspected case, before
Several tools have been used for the diagnosis of minimal HE. Currently
the most frequently used and recommended tools are the PSE-Syndrom-
using lactulose and rifaximin for six months after a HE episode has been
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et al. 2014; Bass et al. 2010). A further drug that can be used for the
brain edema in patients with ALF: 1) head of the bed greater than 30°; (2)
ventilation; (4) treat fever ; (5) treat seizures (prophylaxis has unclear
more effective ammonia clearance; (8) aim for a serum sodium of 145 to
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patients with grade III-IV HE; (9) consider using mannitol (0.5-1 g/kg
herniation.
Drugs which are used for the reduction of plasma ammonia levels in
nor with regard to survival (Lee et al. 2011, Acharya et al. 2009)
acute liver failure. Since part of the patients has a good prognosis even
without transplantation one of the most difficult tasks in the care of ALF
the most often used are the King's College criteria (O’Grady et al. 1989).
Uremic encephalopathy
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Knowledge about the pathophysiology of uremic encephalopathy,
in clinical practice since very often older people are referred to the
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Addressing these accompanying disorders is mandatory to improve the
Hypoglycemia
hemichorea, for example, but of course focal and generalized seizures and
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Hyperglycemia
dominantly affects patients with type I diabetes, and may even be the
need 7-10 l fluid replacement over the first 24 h of therapy, starting with
about 1 l/h over the first 3 hours. Insulin substitution includes a bolus of
monitored during the therapy and should not decrease more than 50
ness, seizures and focal neurological deficits are more frequent in patients
with HHS than in DKA. Of note, stroke might accompany HHS, either as a
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administered subcutaneously for prophylaxis of thrombosis. A protocol for
contralateral striatum, and may persist for several days after the
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References
13
14. Kircheis G, Nilius R, Held C et al. (1997) Therapeutic efficacy of
L-ornithine-L-aspartate infusions in patients with cirrhosis and
hepatic encephalopathy: Results of a placebo-controlled, double-
blind study. Hepatology 25: 1351–1360
15. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN (2009) Hyper-
glycemic crises in adult patients with diabetes. Diabetes Care
32(7): 1335–1343
16. Kumar G, Goyal MK. (2010) Lentiform Fork sign: a unique MRI
picture. Is metabolic acidosis responsible? Clin Neurol
Neurosurg;112(9):805-12
17. Lee WM, Larson AM, Stravitz RT. AASLD Position Paper:
The management of acute liver failure: Update 2011.
www.aasld.org, 2011
18. Morgan MY (1998); Cerebral magnetic resonance imaging in
patients with chronic liver disease. Met Brain Dis 13(4): 273-290
19. O'Grady JG, Alexander GJ, Hayllar KM, Williams R. (1989) Early
indicators of prognosis in fulminant hepatic failure.
Gastroenterology;97(2):439-45
20. Penin H (1967) Über den diagnostischen Wert des Hirnstrombildes
bei der hepato-portalen Encephalopathie. Fortschr Neurol Psychiatr
Grenzgeb 35: 174–234
21. Plum F, Posner JB (1982); The diagnosis of stupor and coma,
3rd edn. Davis, Philadelphia, pp 1–86
22. Rose C, Butterworth RF, Zayed J et al. (1999) Manganese
deposition in basal ganglia structures results from both portal-
systemic shunting and liver dysfunction. Gastroenterology
117(3): 640–644
23. Schomerus H, Hamster W (2001) Quality of life in cirrhotics with
minimal hepatic encephalopathy. Metab Brain Dis 16: 13–19
24. Seifter JL, Samuels MA (2011); Uremic encephalopathy and other
brain disorders associated with renal failure. Semin Neurol
31(2):139-143
25. Sherlock S, Summerskill WH, White LP, Phear EA. (1954) Portal-
systemic encephalopathy; neurological complications of liver
disease. Lancet; 267(6836):454-7.
26. Summerskill WH, Davidson EA, Sherlock S, Steiner RE. (1956) The
neuropsychiatric syndrome associated with hepatic cirrhosis and an
extensive portal collateral circulation. Q J Med.;25(98):245-66
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27. Vilstrup H, Amodio P, Bajaj J, Cordoba J, Ferenci P, Mullen KD,
Weissenborn K, Wong P. (2014) Hepatic encephalopathy in chronic
liver disease: 2014 Practice Guideline by the American Association
for the Study of Liver Diseases and the European Association for the
Study of the Liver. Hepatology ;60(2):715-35
28. Weissenborn K. (2014) Hepatic and pancreatic encephalopathy. In:
Aminoff’s Neurology and General Medicine, 5th edition (Eds.
Aminoff MJ, Josephson SA); Academic Press, pp223-236
29. Weissenborn K, Lockwood AH. (2015) Metabolic and toxic
encephalopathies. In: Bradley's Neurology in Clinical Practice, 7th
edition (Eds. Daroff R, Jankovic J, Mazziotta J, Pomeroy S);
Elsevier, chapter 84
30. Weissenborn K. (2015) The Clinical Relevance of Minimal Hepatic
Encephalopathy--A Critical Look. Dig Dis. 2015;33(4):555-61.
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