IDENTIFICATION DATA: Name Age Sex C.R no Admission No.

Bed no/ Ward Religion Nationality Date of admission Diagnosis Consultant Fathers education Fathers occupation Mothers education Mothers occupation Address Informant :Deepak : 3 yrs :Male :952583 :07054 : 12/PGE :Hindu :Indian :21/02/10 :Hepatic Encephalopathy : Dr. Thapa : 5th :Daily basis :illiterate :House wife : Vill.- Norampur, Th. Rampuar, Dist. Sharanpur :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

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.

FAMILY TREE:

FATHER, 38 YEAR

MOTHER, 35 YEAR.

DEEPAK, 10 YEAR

7 Yr.

4 Yr.

2 Yr.

5 Mo.

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 EXAMINATION

Body built Gait Height Weight Pulse RR GCS :Normally nourished :Normal : 140 cm :32 kg :140/min :24/min :E4V4M5

Congenital malformations: absent

HEAD TO FOOT ASSESSMENT:

Head shape Eyes :Normal head size and shape, no hydrocephalus. :Pupils normal size, reacting to light, normal eye color.

Lips Nose Ear Tongue Teeth Neck Chest

:Pink, no cracked lips. :Normal, no abnormal discharge, no DNS :Normal hearing, no discharge, wax or pus formation. :White coated : Normal :Normal length, no palpable lymph nodes. :Normal chest movements, no wheezing, nipples are normal and there is no discharge from the nipple. :Bowel sounds present, abdominal distension. :Normal curvature of spine. :Upper and lower extremities normal movement, No significant of any defect :Bilateral testis normal, urinary meatus normal, on follys catheterization

Abdomen Back Extremities

Genitalia

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.

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 Na K Cl Urea/creat Ammonia P

21.2.10 125 4.9 90 34/0.3 130

22.2.10 140 4.9 106 18/0.6130 134 4

23.2.10 142 4 105 134 120

24.2.10

4 120 100 4

Ca Protein Albumin Hb TLC PT/PTT

7.2 5 2.1 5 4000 N

9 5 2.5 7.2 3400 N PCo2. 40, HCo3. 24.

8 4.3 3 8 3500

10 4 3 9

ABG: PH. 7.34, Po2.90,

TREATMENT:
Inj. Vit. K Syr. Lactulose T. Actbile T. Metrogyl Inj. Clox Inj. Cefotaxim Inj. Amikacin IVF DNS 5mg X 3day 30ml Q6H 150mg BD 400mgTDS 1gm 1.5 gm Q8h 500mg OD 600ml Q6h.

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 the liver. 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

Ammonia neurotoxicity Resulting from the degradation of urea or protein primary site: Other site: kidney and skeletal muscles Gut-generating ammonia: 4g/day Equilibrium of ammonia and ammonium: gut

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 or cerebrospinal 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

common precipitating factors

Nitrogenous Encephalopathy : Uremia/azotemia Gastrointestinal bleeding Dehydration Metabolic alkalosis Hypokalemia Constipation Excessive dietary protein Infection

Non-Nitrogenous Encephalopathy : Sedative Benzodiazepines Hypoxia Hypoglycemia Hypothyroidism Anemia

CLINICAL STAGES OF HEPATIC ENCEPHALITIS

CLINICAL SPECTRUM:Stage I:
sleep disturbance, general restless, mood fluctuation, impaired attention

Stage II:
Flapping tremor Asterixis: inability to sustain muscle tone Ataxia

dysarthria Stage III:

Somnolence, disorientation Increased reflex, clonic spasm Pyramidal symptoms

Stage IV:
Coma With/without response to pain

DIFFERENTIAL DIAGNOSIS: Laboratory and other tests

Serum ammonia:Elevation of serum ammonia: 60%~80%particularly in chronic HE (with portosystemic shunting) Electroencephalogram (EEG): Severe slowing with frequencies in the theta and delta Imaging Techniques: CT scan, MRI, PET etc

TREATMENT
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

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 HE

NURSING MANAGEMENT:
The patient receiving lactulose is monitored closely for the development of watery diarrheal stools, because they indicate a medication overdose Neurologic status is assessed frequently. A daily record is kept of handwriting and performance 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 discharged home, 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 to 0.8 to 1.0 g/kg per day. Instruct the patient in maintenance of a low-protein, highcalorie diet

REFERENCES:

Kliengman and et al; Nelson Textbook of Pediatrics; 17th edition; 18081896. Isselbacher et al; Harrisons Principles of Internal Medicine7th Edition;274254. OP Ghai and et al; Ghai Essential Pediatrics; 7th Edition; Pages:287-288. Donna L Wong; Essentials of Pediatric Nursing; 5th edition; Pages;930-931. Hockenberry et al. Wongs Nursing Care of Infants and Children. 7th Edition; Pages: 1485-1487. Lipponcot Mannual of nursing Practice 8th edition1530-1569.
www.google .com www.wikipedia.com