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8/14/2019 hepatic encepahlopathy.docx
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IDENTIFICATION DATA: -
Name :Deepak
Age : 3 yrs
Sex :Male
C.R no :952583
Admission No. :07054
Bed no/ Ward :12/PGE
Religion :Hindu
Nationality :Indian
Date of admission :21/02/10
Diagnosis :Hepatic Encephalopathy
Consultant : Dr. Thapa
Fathers education : 5th
Fathers occupation :Daily basis
Mothers education :illiterate
Mothers occupation :House wife
Address :Vill.- Norampur, Th. Rampuar, Dist. Sharanpur
Informant :Mother
CHIEF COMPLAINTS:-
Child is having fever since admission, he has the headache 2days. Jaundice X 7days.
Altered sensorium.
HISTORY OF PRESENT ILLNESS: -
Deepak was app. Well before 14.02.10. He got fever X 7days, Jaundice, headache,
Constipation, altered sensorium, altered speech and didnt recognize parents. Child was
taken in local Hospital where the child received treatment Inj. PCM, Syr. Lactulose .
Then child was referred for further treatment in PGIMER Chandigarh. Parents Brought
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in Emergency where he was diagnosed as a case of Hepatic Encephalopahty and is
undergoing treatment
HISTORY OF PAST ILLNESS
No h/o any significant illness in the past
PERSONAL HISTORY
Antenatal History
The mother had undergone regular antenatal check-up
Birth History
Full Term Normal Vaginal Delivery. According to the mother, child cried immediately after birth.
PERSONAL HISTORY
Developmental History:
appropriate for age. No delay in any milestone.
Immunization History:
Child is immunized appropriate to age. He has received BCG at birth, three doses of Hep B, DPT and OPV and one
MMR, measles and DT.
FAMILY HISTORY:
He living in Nuclear Family. No evidence of any communicable disease, Genetic
disorder in his family.
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FAMILY TREE:
.
SOCIO-ECONOMIC STATUS: A Middle class family with adequate sanitation
facilities. Theirs is a concrete house with three rooms- including a separate kitchen and
bathroom. They have access for safe drinking.
GENERAL PHYSICAL EXAMINATIONBody built :Normally nourished
Gait :Normal
Height : 140 cm
Weight :32 kg
Pulse :140/min
RR :24/min
GCS :E4V4M5
Congenital malformations: absent
HEAD TO FOOT ASSESSMENT:
Head shape :Normal head size and shape, no hydrocephalus.
Eyes :Pupils normal size, reacting to light, normal eye color.
FATHER, 38
YEAR
MOTHER,
35 YEAR.
7 Yr. 4 Yr. 2 Yr. 5 Mo.
DEEPAK,
10 YEAR
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Lips :Pink, no cracked lips.
Nose :Normal, no abnormal discharge, no DNS
Ear :Normal hearing, no discharge, wax or pus formation.
Tongue :White coated
Teeth : Normal
Neck :Normal length, no palpable lymph nodes.
Chest :Normal chest movements, no wheezing, nipples are normal and
there is no discharge from the nipple.
Abdomen :Bowel sounds present, abdominal distension.
Back :Normal curvature of spine.
Extremities :Upper and lower extremities normal movement, No significant of
any defect
Genitalia :Bilateral testis normal, urinary meatus normal, on follys
catheterization
SYSTEMIC EXAMINATION:
Respiratory system:-
RR:26/min
Normal respiration
Bilateral chest clear, air entry equal.
Cardiovascular system:-
HR: 140bpm
S1, S2 normal
CFT:2 sec.
All peripheral pulses are palpable.
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Central Nervous system:-
No History of seizures, LOC,
Normal Reflexes
Both pupils are normal size and reacting to light.
Altered speech, altered sensorium, Disoriented.
GCS is E4V4M5
GI SYSTEM:
No Nausea/vomiting, bad odour from mouth, Abdominal distension, Constipation.
Bowel sound are poor.
NBM
Musculoskeletal system: -
All joints are normal, no inflammation in upper and lower extremities.
Genitourinary system:-
Bilateral testis normal.
Folys cathetrization, No hematuria, urinary tract infection
Integumentary system:-
Hydration Poor, normal colour and texture.
LAB INVESTIGATION
Lab 21.2.10 22.2.10 23.2.10 24.2.10
Na 125 140 142
K 4.9 4.9 4 4
Cl 90 106 105
Urea/creat 34/0.3 18/0.6130 134 120
Ammonia 130 134 120 100
P 4 4
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Ca 7.2 9 8 10
Protein 5 5 4.3 4
Albumin 2.1 2.5 3 3
Hb 5 7.2 8 9
TLC 4000 3400 3500
PT/PTT N N
ABG: PH. 7.34, Po2.90, PCo2. 40, HCo3. 24.
TREATMENT:
Inj. Vit. K 5mg X 3day Syr. Lactulose 30ml Q6H T. Actbile 150mg BD T. Metrogyl 400mgTDS Inj. Clox 1gm Inj. Cefotaxim 1.5 gm Q8h Inj. Amikacin 500mg OD IVF DNS 600ml Q6h.
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HEPATIC ENCEPHALOPATHY
Definition I
It represents a reversible decrease in neurologic function, based upon the disorder of
metabolism which are caused by severe decompensate liver disease.
Definition II
Portal-systemic encephalopathy patients with portal hypertension abnormal shunting of
blood.
Subclinical or latent HE diagnosed only by using precise mental tests or EEG, no
obvious clinical and biochemical abnormalities
Incidence/prevalence
Universal feature of acute liver failure 50%~70% in chronic hepatic failure Difficult to estimate
PATHOPHYSIOLGY:
Toxic materials derived from nitrogeneous substrate in the gut and bypass theliver.
Caused by several factors act synergistically. Several putative gut-derived toxins identified.
Postulated factors/mechanisms:
Ammonnia neurotoxicity Synergistic neurotoxins Excitatory inhibitory neurotransmitters and plasma amino acid imbalance hypothesis -Aminobutyric acid hypothesis
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Ammonia neurotoxicity
Resulting from the degradation of urea or protein primary site: gut Other site: kidney and skeletal muscles Gut-generating ammonia: 4g/day
Equilibrium of ammonia and ammonium:
Over production and/or hypocrisies:
Poor hepato-cellular function: incomplete metabolism Portal-systemic encephalopathy: bypass Ammonia intoxication Interfere with cerebral metabolism: Depletion of glutamic
acid, aspartic acid and ATP Depression cerebral blood flow and oxygen
consumption
Absolute concentration of ammonia, ammonia metabolites in blood orcerebrospinal fluids, correlates only roughly with the presence or severity of HE
ETIOLOGY
Fulminant hepatic failure
acute severe viral hepatitis, drug/toxin acute fatty liver of pregnancy Due to acute hepatocellular necrosis
Chronic liver disease
cirrhosis of all types (70%), primary liver cancer surgically induced portal-cava shunts Due to one or more potentially reversible precipitating factors
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common precipitating factors
NitrogenousEncephalopathy :
Uremia/azotemia Gastrointestinal bleeding Dehydration Metabolic alkalosis Hypokalemia Constipation Excessive dietary protein Infection
Non-NitrogenousEncephalopathy :
Sedative Benzodiazepines Hypoxia Hypoglycemia Hypothyroidism Anemia
CLINICAL STAGES OF HEPATIC ENCEPHALITIS
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CLINICAL SPECTRUM:-
Stage I:
sleep disturbance, general restless, mood fluctuation, impaired attention
Stage II:
Flapping tremor Asterixis: inability to sustain muscle tone Ataxiadysarthria
Stage III:
Somnolence, disorientation Increased reflex, clonic spasm Pyramidal symptoms
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Stage IV:
Coma With/without response to pain
DIFFERENTIAL DIAGNOSIS:
Laboratory and other tests
Serum ammonia:Elevation of serum ammonia: 60%~80%particularly in chronicHE (with portosystemic shunting)
Electroencephalogram (EEG):Severe slowing with frequencies in the theta anddelta
Imaging Techniques: CT scan, MRI, PET etcTREATMENT
Identify and correct the precipitating cause(s) Initiate ammonia-lowering therapy Correction of fluid, electrolyte, glucose, acid- alkaline abnormalities
Management of cerebral edema, bacteremia
Decreasing nitrogen load Decreasing ammonia production Decreasing absorption of enteric toxins Bowel cleaning: Laxative (e.g., magnesium citrate), Cleaning enema Antibiotics:Neomycin, Metronidozol. Lactulose : Synthetic disaccharide Drug of choice Release lactic and acetic acids by bacteria
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Decreasing stool pH to about 5.5 Reduce portion of ammonia and its absorption Effective in 80% of patients Cause 2~4 soft stool/d Given by retention enema 30ml lactulose + 70ml water
SURGERY MANAGEMENT:
Ultimate answer to the problem of chronic HENURSING MANAGEMENT:
The patient receiving lactulose is monitored closely for the development of waterydiarrheal stools, because they indicate a medication overdose
Neurologic status is assessed frequently. A daily record is kept of handwriting andperformance in arithmetic to monitor mental status.
Fluid intake and output and body weight are recorded each day. Vital signs are measured and recorded every 4 hours. Serum ammonia level is monitored dailyElectrolyte status is monitored and
corrected if abnormal
Maintaining a safe environment to prevent injury, bleeding, and infection. If the patient recovers from hepatic encephalopathy and coma, rehabilitation is
likely to be prolonged.
TEACHING PATIENTS SELF-CARE:
If the patient has recovered from hepatic encephalopathy and is to be dischargedhome, the nurse instructs the family to watch for subtle signs of recurrent
encephalopathy.
In the acute phase of hepatic encephalopathy, dietary protein may be reduced to0.8 to 1.0 g/kg per day. Instruct the patient in maintenance of a low-protein, high-calorie diet
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REFERENCES:-
Kliengman and et al; Nelson Textbook of Pediatrics; 17th edition; 1808-1896.
Isselbacher et al; Harrisons Principles of Internal Medicine7th Edition;274-254.
OP Ghai and et al; Ghai Essential Pediatrics; 7thEdition; Pages:287-288. Donna L Wong; Essentials of Pediatric Nursing; 5thedition; Pages;930-931. Hockenberry et al. Wongs NursingCare of Infants and Children. 7th
Edition; Pages: 1485-1487.
Lipponcot Mannual of nursing Practice 8thedition1530-1569. www.google.com www.wikipedia.com
http://www.google/http://www.google/http://www.wikipedia.com/http://www.wikipedia.com/http://www.wikipedia.com/http://www.google/