This lecture was conducted during the Nephrology Unit Grand Ground by Medical Student under Nephrology Division, Department of Medicine in King Saud University.

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Presentation transcript:

This lecture was conducted during the Nephrology Unit Grand Ground by Medical Student under Nephrology Division, Department of Medicine in King Saud University. Nephrology Division is not responsible for the content of the presentation for it is intended for learning and /or education purpose only.

Hepatic Encephalopathy Done by : Ghofran Sabri

Hepatic Encephalopathy reflects a spectrum of neuropsychiatric abnormalities seen in patients with liver dysfunction after exclusion of other known brain diseases

A classification of hepatic encephalopathy was introduced at the World Congress of Gastroenterology 1998 in Vienna Type A hepatic encephalopathy associated with Acute liver failure Type B portal-systemic shunting without associated intrinsic liver disease Type C liver c irrhosis

West Haven Criteria Grade 1 Trivial lack of awareness euphoria or anxiety shortened attention span impaired performance of addition or subtraction sleep disturbance Grade 2 Lethargy or apathy minimal disorientation for time or place subtle personality change inappropriate behavior Grade 3 Somnolence to semistupor responsive to verbal stimuli confusion gross disorientation Grade 4 Coma unresponsive to verbal or noxious stimuli

pathogenesis The hepatocytes are incapable of metabolizing the waste products or because portal venous blood bypasses the liver through collateral circulation or a medically constructed shunt. Nitrogenous waste products accumulate in the systemic circulation.

pathogenesis The most important waste product is ammonia (NH 3 ). This small molecule crosses the blood-brain barrier and is absorbed and metabolised by the astrocytes, a population of cells in the brain that constitutes 30% of the cerebral cortex

hepatic encephalopathy is caused or aggravated by an additional cause, and identifying these causes can be important to treat the episode effectively.

4] Excessive nitrogen load Consumption of large amounts of protein, gastrointestinal bleeding e.g. from esophageal varices, renal failure and constipation Electrolyte or metabolic disturbance Hyponatraemia and hypokalaemia - these are both common in those taking diuretics, alkalosis, hypoxia, dehydration Drugs and medications Sedatives such as benzodiazepines, narcotics and sedative antipsychotics, alcohol intoxication Infection Pneumonia, urinary tract infection, spontaneous bacterial peritonitis, other infections Others Surgery, progression of the liver disease, additional cause for liver damage (e.g. alcoholic hepatitis, hepatitis A) Unknown In 20–30% of cases, no clear cause for an attack can be found

The diagnosis of hepatic encephalopathy can only be made in the presence of confirmed liver disease (types A and C) or a portosystemic shunt (type B). liver function test Ultrasound Liver biopsy

Treatment Lactulose/lactitol Disaccharides that are not absorbed from the digestive tract render the ammonia inabsorbable by converting it to ammonium (NH 4 ) Doses of ml are administered three times a day Antibiotics Rifaximin Metronidazole

Thank you