Hepatic coma is an advanced complication of liver failure characterized by reversible decreased neurologic function and loss of consciousness due to the liver's failure to detoxify toxic substances. It is caused by chronic liver disease, fulminant hepatic failure, or portosystemic shunts. Patients experience disturbances in consciousness, neurological signs, and mental changes. Treatment focuses on treating the underlying cause, decreasing ammonia production, and controlling risk factors through supportive care, lactulose, rifaximin, and L-ornithine/L-aspartate supplementation. Complications can include brain herniation, organ failure, and brain edema.

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;
1. Maintains blood glucose level
2. Lipid metabolism for ATP
3. Protein synthesizes and conversion of it toxic into less harmful for
excretion
4. Synthesis of plasma proteins albuminalpha and beta globulins,
albumin, prothrombin, and fibrinogen.
5. Activation of drugs into active and inactive form
6. Stores vitamins (A, B12, D, E & K)
7. Excretion of bilirubin
8. 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
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• "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 13th Ed. USA: Biological Science
Textbook Inc.
• Davidson’s principles and practice of medicine 21st Ed.
• Current Medical Diagnosis & Treatment 2014 Ed.