Hepatic coma - Copy.pptx

MEDICINE

1. Hepatic coma Group three (3)

2. Presentation outline Brief anatomy and physiology Definition of hepatic coma Pathophysiology Causes Clinical manifestation Diagnosis Nursing and medical management complication

3. ANATOMY AND PHYSIOLOGY OF THE LIVER Picture of the liver with some part of the small intestines and the pancreas The liver is said to be the second largest organ of the body. It is located just below the diaphragm at the upper right quadrant of the abdomen and extent to the left. It has a larger right lobe and smaller left lobe divided by falciform ligament. Functions of the liver The functional unit of the liver is the hepatocyte responsible for several functions; Maintains blood glucose level Lipid metabolism for ATP Protein synthesizes and conversion of it toxic into less harmful for excretion Synthesis of plasma proteins albumin alpha and beta globulins, albumin, prothrombin, and fibrinogen. Activation of drugs into active and inactive form Stores vitamins (A, B12, D, E & K) Excretion of bilirubin Secretes bile which aids in dietary fats absorption

4. DEFINITION OF HEPATIC COMA Hepatic coma is advanced complication of liver failure characterized by a reversible decrease in neurologic function, loss of consciousness and other neuropsychiatric disorders as a resulting from failure of the liver to detoxify toxic agents due to hepatic insufficiency and porto –systemic shunt (abnormal connection between the portal vascular system and systemic circulation).

5. PATHOPHYSIOLOGY A failure in the several functions of the liver especially in the detoxification of the body due to endogenous cause e.g autoimmune or exogenous cause e.g. toxins leads to accumulation, which may bypass liver’s vascular system ( portal vein and artery) and enters straight into circulation through porto -systemic shunt ( PSS ), some PSS may be primary -congenital whiles others are secondary – acquired. Physiologically blood exits the intestines, spleen and pancreas, and enters the liver via the portal vein for metabolism and detoxification hence if a shunt is present, the liver is deprived of factors which aid in it development resulting in hepatic atrophy and insufficiency which then combine with toxins and nutrient which intend crosses the BBB and resulting in inflammation in the brain cells with it presenting clinical manifestation.

6. CAUSES ENDOTOXINS Ammonia Mercaptans (degradation of methionine in the gut) Phenios Free fatty acids Gamma amino butyric acid (GABA) Octopamine

7. CAUSES CHRONIC PARENCHYMAL LIVER DISEASE Chronic hepatitis Cirrhosis FULMINATING HEPATIC FAILURE Acute viral hepatitis Drugs Toxins SURGICAL Portal-systemic anastomoses, portacaval shunts, or transjugular intrahepatic portal systemic shunting (TIPS)

8. RISK FACTORS INCREASE NITROGEN LOAD Constipation GIT bleeding Excess dietary intake of protein and fatty acids Azotemia INFECTIONS AND TRAUMA

9. RISK FACTORS ELECTROLYTE AND METABOLIC IMBALANCE Hypokalemia Alkalosis Hypoxia Hyponatremia DRUG Diuretic Narcotics, tranquilizers, sedatives

10. CLINICAL MANIFESTATION 1) Disturbance in consciousness Insomnia Mental confusion Impaired memory Drowsiness Changes in personality Aggression Euphoria Foetor hepaticus- foul smelling breath associated with liver disease due to mercaptans

11. CLINICAL MANIFESTATION Neurological signs Flapping tremor Exaggerated tendon reflex Extensor plantar

12. DIAGNOSTIC INVESTIGATION Liver biopsy Liver ultrasound CBC, LFT, Electrolytes, urea, creatinine, prothrombin time EEG CSF & CT SCAN GCS

13. MANAGEMENT Treatment goals Treat underlying cause Supportive measures Decreasing ammonia production in the colon Controlling of risk factors

14. Nursing management Such patient require ICU care due possible airway obstruction and serious complications from the condition. Assess the airway and intubate Assess patient level of consciousness in order to aid in the treatment, evaluation and prognosis Place a nasogastric tube for safe administration of nutrients and medications. With the presence of infection antibiotics are often administered empirically (without knowledge of the exact source and nature of the infection).

15. Nursing management A diet with adequate protein and energy is therefore recommended. Some studies have shown benefit of administration of probiotics ("healthy bacteria").

16. Medical Management Lactulose/lactitol administration Doses of 15-30 ml are typically administered three times a day; the result is aimed to be 3–5 soft stools a day. There is decrease generation of ammonia by bacteria, render the ammonia in absorbable by converting it to ammonium (NH4+) ions, and increase transit of bowel content through the gut. Also, studies show constipation to be a cause for hepatic encephalopathy which leads to hepatic coma.

17. Medical Management Rifaximin The antibiotic rifaximin may be recommended in addition to lactulose for those with recurrent disease. It is a nonabsorbable antibiotic from the rifamycin class. This is thought to work in a similar way to other antibiotics but without the complications attached to neomycin or metronidazole. NB. Neomycin, metronidazole and other antibiotic may be used in the treatment but due their complication it is not recommended.

18. Medical Management L-ornithine and L-aspartate (LOLA) The combination of L-ornithine and L-aspartate (LOLA) lowers the level of ammonia in a person's blood. LOLA lowers ammonia levels by increasing the generation of urea through the urea cycle, a metabolic pathway that removes ammonia by turning it into the neutral substance urea.

19. COMPLICATIONS OF HEPATIC COMA Brain herniation Organ failure Brain edema and intracranial hypertension resulting in death

20. REFERENCES Wijdicks , EF (2016). "Hepatic Encephalopathy". The New England Journal of Medicine. 375 (17): 1660–1670. doi:10.1056/NEJMra1600561. PMID 27783916. "Hepatic encephalopathy". GARD. 2016. Archived from the original on 5 July 2017. Retrieved 24 July 2021. Cash WJ, McConville P, McDermott E, McCormick PA, Callender ME, McDougall NI (2010). "Current concepts in the assessment and treatment of hepatic encephalopathy". QJM. 103 (1): 9–16. doi:10.1093/ qjmed /hcp152. PMID 19903725. Starr, SP; Raines, D (2011). "Cirrhosis: diagnosis, management, and prevention". American Family Physician. 84 (12): 1353–9. PMID 22230269. "Portosystemic Encephalopathy - Hepatic and Biliary Disorders". Merck Manuals Professional Edition. Retrieved 23 July 2021. G. Tortora, B. Derrickson (2012) Principles of anatomy and physiology 13 th Ed. USA: Biological Science Textbook Inc. Davidson’s principles and practice of medicine 21 st Ed. Current Medical Diagnosis & Treatment 2014 Ed.