Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver failure and characterized by changes in cognition, behavior, and personality. It ranges from minor alterations in brain function to deep coma. The main causes are thought to be increased levels of ammonia and other toxins in the blood due to the liver's inability to remove them. Treatment focuses on reducing ammonia production in the gut through dietary changes, antibiotics, and lactulose. Managing precipitating factors and providing supportive care are also important. For severe or recurrent cases, procedures to bypass the liver such as TIPSS or liver transplantation may be considered.
This is a lecture note for 5th semester MBBS students. Lecture notes on hepatology, liver disease, alcoholic liver disease, alcohol-related liver disease, portal hypertension, and hepatic encephalopathy. Introduction to hepatic encephalopathy, causes, differentials, approach, and management of hepatic encephalopathy .
This is a lecture note for 5th semester MBBS students. Lecture notes on hepatology, liver disease, alcoholic liver disease, alcohol-related liver disease, portal hypertension, and hepatic encephalopathy. Introduction to hepatic encephalopathy, causes, differentials, approach, and management of hepatic encephalopathy .
Cirrhosis is a diffuse process characterized by liver necrosis & fibrosis and conversion of normal liver architecture into structurally abnormal nodules that lack normal lobular organization
basics about chronic liver disease for a pediatrician. fast and easy guide to common causes of chronic liver diseases in children
Please leave a comment if you like it..
Cirrhosis is a diffuse process characterized by liver necrosis & fibrosis and conversion of normal liver architecture into structurally abnormal nodules that lack normal lobular organization
basics about chronic liver disease for a pediatrician. fast and easy guide to common causes of chronic liver diseases in children
Please leave a comment if you like it..
dr Mohammed Hussien ( assistant Lecturer of Gastroenterologist and Hepatology at Kaferelsheik University Egypy) illusterating one of Major complication of Cirrhosis --H.E
Definitions of GI bleeding
GI Bleeding include Upper and Lower of GIB
Causes of GI bleeding
Pathogenesis of GI bleeding
Diagnosis of GI bleeding
Clinical of GI bleeding
Management of GI bleeding
Recommendation of GI bleeding
Clinical guideline of GI bleeding
INTRODUCTION
Cancer is a general term used to refer to a condition where the body’s cells begin to grow and reproduce in an uncontrollable way. Lung cancers are the fourth most common cancer reported in the Indian males.
DEFINITION
Lung carcinoma is a malignant lung tumor characterized by uncontrolled cell growth in tissues of the lung. If left untreated, this growth can spread beyond the lung by the process of metastasis into nearby tissue or other parts of the body.
CAUSES
The most common causes of fracture include,
I. Tobacco smoke
Tobacco use is responsible for more than one of every six deaths. The younger a person is when he or she starts smoking, the greater the risk of developing lung cancer.
II. Secondhand smoke
Passive smoking has been identified as a possible cause of lung cancer in nonsmokers. People who are involuntarily exposed to tobacco smoke in a closed environment (house, automobile, and building) have an increased risk of lung cancer when compared with unexposed nonsmokers.
III. Environmental and occupational exposure
Various carcinogens have been identified in the atmosphere, including motor vehicle emissions and pollutants fromrefineries and manufacturing plants. High levels of radon have been associated with the development of lung cancer, especially when combined with cigarette smoking. Chronic exposure to industrial carcinogens, such as arsenic, asbestos, mustard gas, chromates, coke oven fumes, nickel, oil, and radiation has been associated with the development of lung cancer.
IV. Genetics
Some familial predisposition to lung cancer seems apparent, because the incidence of lung cancer in close relatives of patients with lung cancer appears to be two to three times that in the general population regardless of smoking status.
TYPES OF LUNG CANCER:
1. Small cell lung carcinoma
• Accounts for 15%-25% of lung cancers
• It is most malignant form
• Tends to spread early via lymphatic and bloodstream
• Is frequently associated with endocrine disturbances
• Predominantly central and can cause bronchial obstruction and pneumonia.
2. Non-small cell lung carcinoma
Is further classified by cell type,
Adenocarcinoma
• Most common type
• Accounts for approximately 30%-40% of lung cancers
• More common in women
• Often gas no clinical manifestations until widespread metastasis is present
• Usually begins in mucous glandular tissue, is most commonly located in peripheral portions of lungs.
Squamous cell carcinoma
• Second most common type of lung cancer
• Accounts for 30%-35% of lung cancers
• Is more common in men
• Arises from the bronchial epithelium of the lungs or bronchus, slow-growing cancer that usually begins in the bronchial tubes.
Large cell carcinoma
• The least common form
• Accounts for 5%-15% of lung cancers
• Composed of large sized cells that are anaplastic and often arise in the bronchi, commonly causes cavitation
• Is highly metastatic via lymphatic and blood.
STAGING OF NON-SMALL CELL LUNG C
What is Hepatic Encephalopathy.
What is the Grading of Hepatic Encephalopathy.
How to Diagnose Hepatic Encephalopathy .
How to Treat Hepatic Encephalopathy.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Best Ayurvedic medicine for Gas and IndigestionSwastikAyurveda
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
2. • Hippocrates (460-370 BC) described a patient
with hepatitis who ‘barked like a dog, could
not be held and said things which could not be
comprehended’.
3. • Hepatic encephalopathy (HE) is a
potentially reversible , neuropsychiatric
syndrome characterized by changes in
cognitive function, behaviour, and
personality, as well as by transient
neurological symptoms and characteristic
EEG patterns associated with acute and
chronic liver failure.
4. • Clinical spectrum ranges from minor signs of
altered brain function to deep coma.
• The concordance of neuropsychiatric
manifestation in pt of liver dis should be
treated as HE unless proved otherwise.
5. Classification of HE
• Type A: HE associated with Acute liver failure
• Type B: HE associated with portal-systemic
Bypass, no intrinsic hepatocellular disease
• Type C: HE associated with Cirrhosis and portal
hypertension or portal-systemic shunts:
– Episodic HE: precipitated, spontaneous, recurrent
– Persistent HE: mild, severe, treatment-dependent
– Minimal HE
6. Pathogenesis
Ammonia intoxication hypothesis
Amino acid imbalance hypothesis(BCAA/AAA↓)
The gamma-aminobutyric acid hypothesis
Neurosteroids hypothesis
False neurotransmitters
Trace elements like zinc
Role of associated inflammation
7. Clinical features of HE
• For descriptive purposes, features of
encephalopathy can be separated into
changes in
– Consciousness
– Personality
– Intellect
– Speech
8. Disturbed consciousness
• Hypersomnia appears early and progresses to
reversal of the normal sleep pattern. Reduction of
spontaneous movement, a fixed stare, apathy, and
slowness and brevity of response are early signs.
• Further deterioration results in reaction only to
intense or noxious stimuli.
• Coma at first resembles normal sleep, but progresses
to complete unresponsiveness.
9. Personality changes
• These include childishness, irritability and loss
of concern for family.
• Even in remission the patient may present
similar personality features suggesting frontal
lobe involvement.
10. Intellectual deterioration
Varies from slight impairment of organic
mental function to gross confusion.
Speech
• Slow and slurred and the voice is
monotonous. In deep stupor, dysphasia
becomes marked.
11. Fetor hepaticus
• This is a sour, fecal smell in the breath, due to volatile
substances normally formed in the stool by bacteria.
• These mercaptans if not removed by the liver are
excreted through the lungs and appear in the breath.
• Fetor hepaticus does not correlate with the degree
or duration of encephalopathy and its absence does
not exclude HE.
12. Flapping tremor (asterixis)
• This is due to impaired inflow of joint and other afferent
information to the brainstem reticular formation resulting in
lapses in posture.
• It is demonstrated with the patient’s arms outstretched and
fingers separated or by hyperextending the wrists with the
forearm fixed.
• The rapid flexion-extension movements at the
metacarpophalangeal and wrist joints are often accompanied
by lateral movements of the digits.
• Absent at rest, less marked on movement and maximum on
sustained posture, the tremor is usually bilateral, although not
bilaterally synchronous, and one side may be affected more
than the other. In coma the tremor disappears.
• A ‘flapping’ tremor is not specific for hepatic precoma.
13. • Deep tendon reflexes are usually exaggerated.
Increased muscle tone is present at some stage and
sustained ankle clonus is often associated with
rigidity. During coma patients become flaccid and
lose their reflexes.
• The plantar responses are usually flexor becoming
extensor in deep stupor or coma.
• The clinical course fluctuates, and frequent
observation of the patient is necessary.
14. Clinical grading of HE
Flapping tremorClinical signsClinical grade
Infrequent at this
stage
Alert, euphoric, occasionally
depression. Poor
concentration, slow mentation
and affect, reversed sleep
rhythm.
Grade 1
(prodrome)
Easily elicitedDrowsiness, lethargic,
inappropriate behavior,
disorientation.
Grade 2
(impending coma)
Usually presentStuporose but easily rousable,
marked confusion, incoherent
speech
Grade 3
(early coma)
Usually absentComa, unresponsive but may
respond to painful stimulus
Grade 4
(deep coma)
15. Minimal hepatic encephalopathy
(MHE)
• Alternative terms were proposed to avoid medical
errors induced by a name that could implicate
that the condition is below the threshold of
significance.
• The current consensus is to use the term
‘MHE’, as proposed by the Working Party
commissioned by the 11th World Congress of
Gastroenterology in 1998.
• Prevalence is as high as 84% in patients with
hepatic cirrhosis.
16. Predisposing factors for HE development
OthersDrugsMetabolic
alteration
Nitrogen products
InfectionsOpiatesHypokalemiaGI bleeding
SurgeryBenzodiazepinesAlkalosisHyperazotemia
Renal failureDiureticsHypoxiaConstipation
Short fatty acidsSedativesHyponatremiaHigh-protein diet
Superimposed
hepatic injury
PhenolHyperkalemiaH. Pylori
AlcoholDehydrationUraemia
Rarely,hepatoma
and/or vascular
occlusion
HypoglycemiaPorto-systemic
shunt creation
(including TIPPS)
17. Investigations
• Electroencephalogram
– Bilateral synchronous slowing of the waves frequency
(with an increase in wave amplitude) from the normal
-rhythm down to the range
– Useful for diagnosis and to assess treatment
– Occur early
– Non-specific. However, in a conscious patient with liver
disease are virtually diagnostic.
• CSF
– Usually clear and under normal pressure
– Maybe increased protein conc. but cell count is
normal
– Glutamic acid and glutamine may be increased
18. • Neuropsychological tests:
– Especially used in clinical research
– Psychometric Hepatic Encephalopathy Score (PHES):
• A standardized test battery including 5 different tests
• Its use is restricted to the study of mild and minimal HE.
19. Other causes of encephalopathy or disturbed
consciousness in cirrhotic patients
• Severe hyponatremia
• Respiratory failure
• Severe sepsis
• Intracranial bleed
• Acute alcoholism
• Wernicke’s encephalopathy
• Status epilepticus
• Zinc deficiency
• Drug overdose
• Hypoglycemia
• Post ictal
• CNS sepsis
• Delirium tremens
• Hepato-lenticular
degeneration (Wilson’s
disease)
• Functional psychoses
21. Management of precipitating factors
ManagementPrecipitating factor
Endoscopic intervention,
vasoconstrictors,
prophylaxis for stress ulcers
GI bleed
AntibioticsSepsis
Correct abnormality, avoid
diuretics, fluid restriction
Electrolyte abnormalities
Flumazenil, naloxone
challenge
Exogenous sedatives
Avoid NSAIDs, control
sepsis, correct circulating
volume abnormalities
Azotemia
22. Diet
• It is important in cirrhotic patients to avoid protein
restriction any longer than is necessary.
• In the acute case, a short period of protein
deprivation may not be harmful but prolonged
restriction of protein in the cirrhotic patient
without encephalopathy is inappropriate.
• If animal protein is not well tolerated, vegetable
protein may be used.
23. • In the acute attack of HE dietary protein is
reduced to 20 g/day.
• During recovery, protein is added in 10g
increments on alternate days.
• Any relapse is treated by a return to the
previous level.
24. Protein restriction in HE:
necessary or illogical ?
• Evidence suggests that protein intake plays only a
limited role in precipitating encephalopathy.
• In fact, measures taken to suppress endogenous
protein breakdown are more effective than dietary
restrictions in reducing the load of amino acids on
the decompensated liver.
25. Non-absorbable disaccharides
(lactulose and lactilol)
• Since the 1980s, non-absorbable disaccharides have been
considered as the standard treatment for HE.
• Recent guidelines state that lactulose ( -galactosido-fructose) is
the first line pharmacological treatment for HE.
• When given by mouth lactulose reaches the cecum where it is
broken down by bacteria predominantly to lactic acid. The
osmotic volume of the colon is increased. The fecal pH drops.
• The growth of lactose-fermenting organisms is favored and
organisms such as bacteroides, which are ammonia formers, are
suppressed.
26. • Lactulose more than doubles the colonic output of
bacterial mass and ‘soluble’ nitrogen which is no
longer available for absorption as ammonia.
• The aim of treatment is to produce acid stools
without diarrhea.
• The dose is 10-30 ml, 3 times a day and is adjusted
to produce 2 semi-soft stools daily.
• Side-effects include flatulence, diarrhea and
intestinal pain.
27. • Lactilol ( -galactoside sorbitol) is a second-
generation disaccharide easily produced in
chemically pure crystalline form, which can be
dispensed as a powder.
• It is not broken down or absorbed in the small
intestine, but is metabolized by colonic bacteria.
• It seemed to be as effective as lactulose in chronic
and acute portal-systemic encephalopathy.
Patients responded more quickly to lactilol than
lactulose, and there was less diarrhea and
flatulence.
28. • The value of enemas in patients with hepatic
coma must be emphasized.
• Lactulose or lactose enemas may be used and
are superior to water.
• All enemas must be neutral or acid to reduce
ammonium absorption.
29. Antibiotics
• Neomycin given orally, is very effective in decreasing
gastrointestinal ammonium formation.
• Little neomycin is absorbed from the gut although blood
levels have been detected and impaired hearing or deafness
may follow its long-term use.
• Thus it should only be used for the acute case for 5-7 days
(4-6 g/day in divided doses).
• It should be used with particular caution in patients with
renal insufficiency.
• In acute hepatic coma, lactulose is given, and neomycin
added if the response is slow or partial.
30. • Metronidazole (200 mg 4 times per day orally)
seems to be as effective as neomycin.
• Because of dose-related CNS toxicity, it should not be
used long term.
31. Rifaximin
• A synthetic antibiotic structurally related to rifamycin.
• Displays a wide spectrum of antibacterial activity against
Gram-negative and Gram-positive bacteria, both aerobic and
anaerobic
• A very low rate of systemic absorption.
• This will minimize both antimicrobial resistance and systemic
adverse events.
• Safe in all patient populations and also in the long term.
32. Sodium benzoate and L-ornithine-L-aspartate
• Sodium benzoate promotes urinary excretion of
ammonia and is as effective as lactulose and is less
expensive.
• L-ornithine-L-aspartate treatment promotes hepatic
removal of ammonia by stimulating residual hepatic
urea cycle activity and promoting glutamine synthesis,
particularly in skeletal muscle.
33. Dopaminergic agonists
• The use of bromocriptine or L-dopa is restricted to
cases of chronic HE with important extrapyramidal
signs.
34. Benzodiazepine-receptor
antagonists
• Flumazenil had a significant beneficial effect
on short-term improvement of HE in patients
with cirrhosis and a highly favorable
prognosis.
• Flumazenil had no significant effect on
recovery or survival.
• At the moment, flumazenil may be
considered for patients with chronic liver
disease and HE, but cannot be
recommended for routine clinical use..
35. Branched-chain amino acids (BCAA)
• Infusions of solutions containing a high concentration of
BCAA have been used to treat acute and chronic HE.
• Results have been extremely conflicting, perhaps related
to differences in the nature of amino acid solutions, the
ways of administration and the patients studied.
36. Acarbose
• Inhibits the upper gastrointestinal enzymes (alpha-
glucosidases) that convert carbohydrates into
monosaccharides.
• It also promotes the proliferation of intestinal
saccharolytic bacterial flora that produce
mercaptans, benzodiazepine-like substances, and
ammonia. Their reduction could improve hepatic
encephalopathy.
37. Shunt occlusion
• In cases of chronic HE the reduction or obliteration of
large spontaneous porto-systemic anastomoses, or
shunts previously done by surgery or TIPSS, can be a
therapeutic option.
• A surgical shunt occlusion or the shunt may be
occluded by invasive radiology with the insertion of a
balloon or a steel coil.
• Risk of bleeding.
38. Artificial Extracorporeal Liver Support ‘Liver
dialysis'
• Patients frequently die while on the transplantation
waiting list because of organ scarcity.
• Systems supporting liver function may be useful to:
– Avoid further complications due to the typical toxic state.
– ‘Bridging' the patients to the transplantation.
– In the event of an acute decompensation of a chronic liver
disease, sustain liver function long enough to permit the
organ's regeneration and functional recovery.
39. • Novel treatments introduced to improve
detoxification, mainly of the protein-bound substances:
– Molecular adsorbent recirculation system (MARS): albumin
dialysis
– Prometheus systems: novel device for fractionated plasma
separation via an albumin-permeable filter that was developed to
improve removal of albumin-bound toxins.
• Different experiences have proved the efficacy of MARS
mainly in the treatment of HE, while data on survival are
still limited to small case series.
• Initial studies have proven clinical use of Prometheus to be
feasible and safe.
40. Liver transplantation
• This may be the ultimate answer to the
problem of chronic HE.
• Any patient who has presented an episode of
HE should be evaluated for this procedure.
• Proceed with early liver transplantation before
the development of important organic brain
lesions on sustained HE.
41. To conclude
• Identification and treatment of the precipitating
cause.
• Intervention to reduce the production and absorption
of gut-derived ammonia and other toxins.
• Prescription of agents to modify neurotransmitter
balance directly or indirectly. These are of limited
clinical value at present.