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Presented by:K. Prathyusha12352D.1009Pharm.D V yr.

Under the Guidance of

Dr. J. Sandeep Reddy

MD,DNB Gastroenterology

MGM HOSPITAL

Department of Pharmacy Practice CARE COLLEGE OF PHARMACY OGLAPUR, ATMAKUR, Warangal – 506311, (T.G) India.

CLERK SHIP-IIDEPARTMENT OF

GASTROENTEROLOGY

Academic year 2015-2016

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CASE PRESENTATIONA 35 year old male was admitted in the acute medical ward on 06/04/2016. Patient came with the complaints of fever since 3 months, swellings of both feet since 10days gradually progressed to knee, loss of appetite and sleep since 1wk. Patient was apparently asymptomatic 3months ago then he developed high grade fever with chills, intermittent subsides with medications and relapses. He is a Chronic alcoholic – gudumba 1lit/day since 6yrs, non-smoker having a habit of tobacco chewing since 15 yrs. Bowel and bladder movements are regular.

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SUBJECTIVEName: MS Age/sex: 35y/M IP#:12335Ward: AMW/M2 DOA: 6/4/16 DOD: 11/4/16Reasons for admission: Patient came with the complaints of fever since 3 months, swellings of both feet since 10days gradually progressed to knee, loss of appetite and sleep since 1wk.History of present illness: Apparently asymptomatic 3months ago then he developed high grade fever with chills, intermittent subsides with medications and relapses.Past medical history: Insignificant Family history: Insignificant. Personal history and habits: Chronic alcoholic – gudumba 1lit/day since 6yrs, non-smoker having a habit of tobacco chewing since 15 yrs. Bowel and bladder movements regular

OBJECTIVE

Physical examination Systemic examination

Blood Pressure: 100/60mmHg

CVS: S1+S2+

Temperature: 360 CNS:PULSE: 94bpm RS: clearRespiratory Rate: P/A: Distended & Tender

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General examination: Pallor, B/L Pedal edema [Pitting type], Icterus

Radiological examination: ----

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LABORATORY DATAParameter Report Normal value

RBS 60 70 – 130mg / DlUrea 52 10 – 40Sodium 135 135 – 145 mmol/lPotassium 4.1 3.5 – 5.5 mmol/lS.Cr 2mg/dl 0.9-1.6SGPT 185.5 0 – 35 U / LSGOT 61 36 – 141 KA UnitsBilirubin: Total

Direct:2.41.11

0.2 – 1 mgs %0 – 0.2

Cl 119 98 – 99 mmol/l

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HEPATIC ENCEPHALOPATHY WITH ALD:Alcohol’s harmful effects on liver cells not only interfere

with the normal functioning of the liver but also impact distant organs, including the brain. Prolonged liver dysfunction resulting from excessive alcohol consumption can lead to the development of a serious and potentially fatal brain disorder known as hepatic encephalopathy (HE).

It is a brain dysfunction caused by liver insufficiency and/or PSS; it manifests as a wide spectrum of neurological or psychiatric abnormalities ranging from subclinical alterations to coma.The most commonly used staging scale of HE is called the West Haven Grading system: Grade 0: Minimal HE-Asymptomatic, coordination impairment,

poor thinking ability. Grade 1: Mild HE-Mood changes like depression/ irritability and

have sleep problems Grade 2: Moderate HE- Inappropriate behavior, slurred speech,

impairment in mental status, difficult writing. Grade 3: Severe HE- Drowsiness, unable to perform mental

tasks, strange behavior, extremely anxious. Grade 4: Coma-Unconscious and slips into coma.

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SYMPTOMS Symptoms of hepatic encephalopathy differ depending on the underlyingcause of the liver damage.

Moderate Severe Difficulty thinkingPersonality changesPoor concentrationProblems with handwriting or loss of other small-hand movementsConfusionForgetfulnessPoor judgmentA musty or sweet breath odor

ConfusionDrowsiness or lethargyAnxietySeizuresSevere personality changesFatigueConfused speechShaky handsSlow movements

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CAUSES: Infections Kidney problems Dehydration Low oxygen levels (hypoxia) Recent surgery or trauma Use of medications to suppress the immune system Eating too much protein Use of medications (such as barbiturates or benzodiazepine

tranquilizers) that suppress the central nervous system Electrolyte imbalance, especially a decrease in potassium

after vomiting or taking diuretics Alcohol

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PATHOPHYSIOLOGY:

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DIAGNOSIS: 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), as its symptoms are similar to those encountered in other encephalopathies.

To make the distinction, sodium, potassium, ammonia, abnormal liver function tests and/or ultrasound suggesting liver disease are required, and ideally liver biopsy.

The symptoms of hepatic encephalopathy may also arise from other conditions, such as cerebral haemorrhage and seizures (both of which are more common in chronic liver disease).

A CT scan of the brain may be required to exclude haemorrhage, and if seizure activity is suspected an electroencephalograph (EEG) study may be performed.

Rarer mimics of encephalopathy are meningitis, encephalitis, Wilson's disease; these may be suspected on clinical grounds and confirmed with investigations

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TREATMENT: The treatment of hepatic encephalopathy depends on the suspected

underlying cause (types A, B or C) and the presence or absence of underlying causes.

If encephalopathy develops in acute liver failure (type A), even in a mild form (grade 1–2), it indicates that a liver transplant may be required.

Hepatic encephalopathy type B may arise in those who have undergone a TIPSS procedure; in most cases this resolves spontaneously or with the medical treatments, but in a small proportion of about 5%, occlusion of the shunt is required to address the symptoms.

In hepatic encephalopathy type C, the identification and treatment of alternative or underlying causes is central to the initial management.

Given the frequency of infection as the underlying cause, antibiotics are often administered empirically (without knowledge of the exact source and nature of the infection). Once an episode of encephalopathy has been effectively treated, a decision may need to be made on whether to prepare for a liver transplantation or not.

Medications mainly used are lactulose, l-ornithine and l-aspartate, flumazenil.

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PRESCRIPTION DRUGSDrug Category Use Toxicity

monitoring parameters

Dose

Lactulose

Laxative helps in elimination of ammonia

Hypernatremia,GI upset, excessive sweet taste

10g/15ml

Lactitol Laxative Prevents thrombosis

Hypernatremia

Neomycin

Macrolide Prevents bacterial growth

Nephro-ototoxicity 500mg

Rifaximin

Antitubercular agent

Bacterial growth inhibition

Neurotoxicity 200mgNeomycin-2-4g/d, Paromomycin-1-2g/d, vancomycin-1-2g/d,

metronidazole-500mg/d, aminopenicillins-2-4g/d are alternative medications.

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ASSESSMENT  Based on the subjective and objective evidence the patient was diagnosed as suffering from ‘GRADE-II ALCOHOLIC LIVER DISEADE WITH HEPATIC ENCEPHALOPATHY’Symptoms: Patient came with the complaints of fever since 3 months, swellings of both feet since 10days gradually progressed to knee, loss of appetite and sleep since 1wk.Apparently asymptomatic 3months ago then he developed high grade fever with chills, intermittent subsides with medications and relapses.Risk factors: Chronic alcoholic – gudumba 1lit/day since 6yrs, non-smoker having a habit of tobacco chewing since 15 yrs. Bowel and bladder movements regular.Diagnostic tests: S.BUN, LFT’s, S.Cr.Which are as per text book.

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Day wise assessment:

VITALS D1 D2 D3 D4 D5 D6

D7 D8 D9

D10

TEMP  38  38  37  36  -  -  -  - 36.7 

37 

BP[mmHg]

110/70

110/70

120/80

120/70

110/70

120/70

120/80

110/70

120/70

120/80

PULSE[bpm]

88 90 88 92 86 80 80 86 80 80

H/L NAD NAD NAD NAD NAD NAD NAD NAD NAD NAD

P/A Soft Soft Soft Soft soft

soft Soft soft soft Soft

Fresh complaints & OTHERS

No fresh c/o

- - - - - - - - -

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PLAN:S.NO

DRUGS DOSE[mg]

ROA FREQ DURATIONDay of

admissionDay of

stopping1 Lasix 20 IV BD D1 D102 Ceftriaxone 1000 IV BD D1 D103 PCM 500 PO TID D1 D104 PANTOP 40 IV OD D1 D105 UDILIV 300 PO BD D1 D106 MVT 500 PO BD D1 D107 ALBUMIN 25% IV OD q3rd

altr. day D1 D10

8 ALDACTONE 100 PO OD D3 D109 ULTRACET   PO OD D3 D10

Medication

Dose ROA Frequency

Duration of usage

Lactulose 1tsp PO BD 10dPCM 500mg PO BD 10d

Discharge medication:

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DRUGS DOSE[mg]

Category Use Monitoring parameters

Lasix 10-80 Diuretic pedal edema Electrolyte levelsCeftriaxone

1000 Cephalosporin

Reduce ammonia

Dizziness, diaphoresis

PCM 500 Antipyretic Reduce fever Hepatotoxicity, disorientation,hyperammonia

PANTOP 40 PPI Reduce HCL secretion

GI disturbances

UDILIV 300 Decrease cholesterol produced by liver

Dizziness, back pain, abdominal pain

MVT 500 Nutrition supplement

Neuropathy, metabolic functions

Constipation, dark stools

ALBUMIN 25g/25%

Protein [volume expander]

Replaces plasma protein

Edema, HTN

ALDACTONE

100 Diuretic Aldosterone antagonist

Drowsiness, confusion

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PHARMACIST INTERVENTIONS Checked for drug interactions, medication errors. Monitored signs and symptoms. Obtained patient history, including drug history and any known

allergies, and allergy to any of the drugs given. Monitored Blood pressure, Serum glucose, Serum urea levels, liver

function tests; incidence of seizures; renal function carefully during treatment.

Monitor if the condition is progressing. No need for paracetamol. Monitor LFTS, CT-Scan, MRI, endoscopy every 6-12 months.

Diagnosis and management Guidelines are according to the American Association for the Study of Liver Diseases (AASLD)

Practice Guidelines

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PATIENT COUNSELINGAbout disease:

Hepatic encephalopathy is a brain dysfunction caused by liver insufficiency and/or PSS; it manifests as a wide spectrum of neurological or psychiatric abnormalities ranging from subclinical alterations to coma. Symptoms include change in the behavior, confusion. drowsiness etc.About medication’’]ns: Lactulose/lactitol: Lactulose and lactitol are disaccharides that are

not absorbed from the digestive tract. They are thought to decrease the generation of ammonia by bacteria, render the ammonia inabsorbable by converting it to ammonium (NH4+) ions, and increase transit of bowel content through the gut.

Doses of 15-30 ml are administered three times a day; the result is aimed to be 3–5 soft stools a day, or (in some settings) a stool pH of <6.0. LOLA: A preparation of L-ornithine and L-aspartate (LOLA) is used to

increase the generation of urea through the urea cycle, a metabolic pathway that removes ammonia by turning it into the neutral substance urea. It may be combined with lactulose and/or rifaximin if these alone are ineffective at controlling symptoms

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About life style modifications: Avoid greasy, spicy, caffeine containing food. Have more liquids; easily digested and; low carbohydrate food. Don’t use or stop any medications without doctors order. Follow healthy life style. Avoid alcohol and tobacco. Adhere to the medication regimen. High-protein foods to avoid include poultry, red meat, eggs, and

fish. Consult physician if you observe any changes in your routine

behavior. Eat well balanced diet with less protein and rich carbohydrate.

[protein required-0.8-1.2g/kg] Assess urinary status. If patient develops frequency, dysuria,

edema or reduced urinary output, notify physician. Assess for any changes in hepatic status. If patient appears

jaundiced and mentally confused, notify physician. If nausea, vomiting, distention, diarrhea or anorexia occur, pedal

edema, ascities, black stools notify physician. Limit your intake of food. Avoid sea foods. Consult physician if experience constipation.

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Thank you