hepatic encepahlopathy.docx

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/

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hepatic encepahlopathy.docx