kpr ald+he
TRANSCRIPT
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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