Case Report Enchephalopathy Presentators: Dewi Putri Rejekinta Berutu Azmeilia Syafitri Lubis Supervisor: Prof. dr. H. Munar Lubis, Sp.A (K) DEPARTMENT OF PEDIATRIC HAJI ADAM MALIK GENERAL HOSPITAL FACULTY OF MEDICINE UNIVERSITY OF NORTH SUMATERA 2012 1
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Case ReportEnchephalopathy
Presentators: Dewi Putri Rejekinta Berutu
Azmeilia Syafitri Lubis
Supervisor:Prof. dr. H. Munar Lubis, Sp.A (K)
DEPARTMENT OF PEDIATRIC HAJI ADAM MALIK GENERAL HOSPITAL
FACULTY OF MEDICINEUNIVERSITY OF NORTH SUMATERA
2012
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Chapter 1
• Introduction• Objective
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. Introductionis a general term for a disease that alters a person’s brain function and mental state.
Enchephalopathy
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Introduction
• There are many possible precipitants of encephalopathy.• Symptomps of enchephalopathy can generalized causing
decreased level of conciousness from minimal lethargy to coma.
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Objective
• The aim of this study is to explore more about the theoritical aspects on metabolic enchephalopathy, and to integrate the theory and application of hepatic enchephalopathy case in daily life.
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Chapter 2
• Literature Review: Enchepalophathy
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Defenition
•Encephalopathy is an acute confusional state that is accompanied by an alterations in cortical function and disturbances of consciousness may range from mild confusional states to coma
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Some types of enchephalopathy :
• Glycine enchephalopathy : caused by a metabolic disorder• Hepatic enchephalopathy : caused by disorders that affect the liver• Hypoxic enchephalopathy : caused by reduce oxygen to brain• Static enchephalopathy : permanent brain damage• Uremic enchephalopathy : caused by toxins remaining in the body• Wernicke’s enchephalopathy : caused by a thiamine deficiency, usually due to alcoholism.• Hashimoto’s enchephalopathy : an autoimmune disorder • Hypertensive enchehalophaty : caused by very high blood pressure• Toxic-metabolic enchephalopathy : general term to describe enchephalopathies caused by
•Over 5.5 million people in the United States have been diagnosed with cirrhosis. One of this population, 30–45 % of patients develop overt encephalopathy during the course of their disease. This debilitating condition can negatively impact quality of life for patients and their families.•The frequency of hospitalization for enchephalopathy has nearly doubled over the last decade, with lengths of stay between 5 and 7 days.
• Glycine enchephalopathy : caused by a metabolic disorder• Hepatic enchephalopathy : caused by disorders that affect the liver• Hypoxic enchephalopathy : caused by reduce oxygen to brain• Static enchephalopathy : permanent brain damage• Uremic enchephalopathy : caused by toxins remaining in the body• Wernicke’s enchephalopathy : caused by a thiamine deficiency, usually due to alcoholism.• Hashimoto’s enchephalopathy : an autoimmune disorder • Hypertensive enchehalophaty : caused by very high blood pressure• Toxic-metabolic enchephalopathy : general term to describe enchephalopathies caused by
infections, toxins or organ failure.• Metabolic enchephalopathy : broad category that describes abnormalities of the water, electrolytes,
vitamins and other chemicals that adversely affect brain function
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Pathophysiology
The pathogenesis of encephalopathy is incompletely understood, and the discussion that follows represents a collection of ideas and concepts that have emerged from recent research.
There is probably no single pathophysiology. Rather, many different perturbations of brain function may produce the same clinical syndrome. Potential mechanisms include a deficiency of substrates for oxidative metabolism, impaired synaptic transmission, and gross alterations in the water and electrolyte composition of the internal milieu. These mechanisms may be interrelated.
For example, Hyponatraemia is defined as a serum sodium <135 mEq/l. Under normal circumstances, the human body is able to maintain the plasma sodium within the normal range (135–145 mEq/l) despite wide fluctuations in fluid intake. The body’s primary defence against developing hyponatraemia is the kidney’s ability to generate a dilute urine and excrete free water. Hyponatraemia usually develops when there are underlying conditions that impair the kidney’s ability to excrete free water. There are a few clinical settings where patients most often develop hyponatraemic encephalopathy.
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DIAGNOSIS
Mild•Change in sleep patterns•Changes in thinking•Confusion that is mild•Forgetfulness•Mental fogginess•Personality or mood changes•Poor concentration•Poor judgment•Worsening of handwriting or loss of other small hand movements
Severe•Abnormal movements or shaking of hands or arms•Agitation, excitement, or seizures (occur rarely)•Disorientation•Drowsiness or confusion•Inappropriate behavior or severe personality changes•Slurred speech•Slowed or sluggish movement
Symptoms many begin slowly and gradually worsen, or they may begin suddenly and be severe from the start. Patients with hepatic encephalopathy can become unconscious, unresponsive,
and possibly enter a coma.
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•Jaundice, petechial hemorrhages, gastrointestinal bleeding, ascites, or hypothermia may indicate hepatic dysfunction.• A coarse facies, dry hair, or bradycardia suggests hypothyroidism.• Acne, obesity, and hypertension are common in Cushing syndrome.• Needle tracks in the skin raise the possibility of a toxic encephalopathy.• Hypertension suggests that the encephalopathy is caused by a metabolic disorder (e.g., a renal or endocrinologic disorder) or an ischemic disorder (e.g., a cerebrovascularor cardiovascular condition), and•Hepar enlargement, lead to cirrhosis hepatic.• Hypothermia suggests a metabolic or toxic cause.•Neurologic examination
PHYSICAL EXAMINATION
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Blood testCT Scan of the head or MRIEEGLumbar PunctureArterial blood gasesElectrolyteChest radiograph
Tests may include:
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Management & Treatment
•Dehydration : diuretics, intravenous infusion of physiologic saline, and therapy for the underlying cause of increased fluid and electrolyte losses. • Gastrointestinal bleeding is identified and treated appropriately. •Hypokalemia : vigorously corrected with parenteral potassium in enchephalopathy. •Severe hyponatremia : Limited infusions of hypertonic saline (3% NaCl, 150 mL intravenous) may be needed for very severe hyponatremia.
Correction
Precipating Factor
s
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Management & Treatment
•Dietary protein : Restriction of dietary protein to 40 g/day or less used to be advocated for patients with enchephalopathy because of excessive dietary protein. The current recommended protein diet for patients is 0.8 to 1.5 g/kg/d.•Tranplantation•Adjuvant (antibiotics & dissacharides)•Symptomatic
Correction
Precipating Factor
s
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Brain herniationBrain swellingIncreased risk of: Cardiovascular collapseKidney failureRespiratory failureSepsisPermanent nervous system damage (to movement, sensation, or mental state)Progressive, irreversible comaSide effects of medications
Complication
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Acute encephalopathy may be treatable. Chronic forms of the disorder often keep getting worse or continue to come back.
Prognosis
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Chapter 3
• Case Report
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Case Report
Name : AIPAge : 4 monthsSex : Female Date of Admission:
May, 7th 2012
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Main Complain
Seizure
3 days ago
Tonic clonic
Frek 10 times/day;
5’
Precipated by fever
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Diarrhoea (+)◦ 3 days before fever◦ Frequency >10 times /day especially after having milk◦ Volume = 10-20 cc/ diarrhoea◦ Watery
Impairment of consciousness (+)◦ weak cry with moan impression (+) 2 days ago after
seizure.
Urine output(+) ◦ Colour : yellow (+)◦ Volume : less◦ Vomit (-)◦ history of melena (+) since 2 days ago◦ dyspnoe (-).
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• Spontaneous and cried immediately• Help by midwives in clinic.• BW =3 Kg and BBL =48 cm• Injection of vitamin K (+)
History of Birth
• hypertension , DM, using herbal medicine (-).
• Early fetal membrane broken (+)
Historyof Pregnancy
• From birth to 3 months : Breast milk• From 3 months to now : Breast milk
+ formula milk
Feeding History
• Patient has been able to face downward
History of Growth and
Development
• Hep B, BCG, Polio, DPTHistory of Immunisation
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Sensorium
Consciousness: ◦Alert (GCS 12: E:4, C=3, M=5)◦Temperature: 38oC.◦Body length: 63 cm. Head circumferences: 38 cm.
Upper Arm Circumferences: 9,5 cm.Anemic (-). Icteric (-). Cyanosis (-).
P Management:•Head elevation 30°•O2 ½ - l L/i nasal canule•Rehydration RL 99 gtt/I since 19.30 pm - 23.30 pm•Injection of Ampicillin 250 mg/6 hr/iv (Skin Test)•Injection of Cefotaxim 350 mg/8 hr/iv (Skin Test)•Injection of dexamethasone 1mg/8 hr/iv•Paracetamol 3 x 100 mg (if needed)•Diet breast milk/ PASI 60 cc/2 hr/NGT•10.00 pm Injection Phenytoin 100 mg in 20 cc NaCl 0,9 % out in 20 minutes, after 12 hours 25 mg/12 hr in 20 cc NaCl 0.9 %.
- Meningoenchephalitis + Mild to moderate dehydration
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P Management:•Head elevation 30°•O2 ½ - l L/i nasal canule•IVFD D5 restriction 25 % 16 gtt/i•Phenytoin 25 mg/12 hr/iv in 20 cc NaCl 0,9 % out in 20 minutes•Injection of Ampicillin 250 mg/6 hr/iv (H1)•Injection of Cefotaxim 350 mg/8 hr/iv (H1)•Injection of dexamethasone 1mg/8 hr/iv (H1)•Paracetamol 3 x 100 mg (if needed)•Diet breast milk/ PASI 70 cc/3 hr/NGT.•(10.30 am) : Phenytoin 10 mg/kgBW in 6cc NaCl 0,9% out in 20 minutes•(05.00 pm): Correction of hipocalsemy (Ca= 6,6 mg/dl) 0,5 mg/kg BB= 0,5 x 5,3= 2,65 mg in 3 cc out in 20 minutes
R •Consult to neurology•Consult to respirology•Mantoux test•Lumbal punction•Electroenchepalograph•Head CT-Scan•Electrolyte test: LFT, RFT, blood culture, urine culture, AGDA, CRP, procalcitonin, lactate acid, LED
Result of Consult to Radiology: - The heart, sinus & diaphragma are normal. - The lung: consolidation upper right lung field. There is triangle opaque shadow at lower right lung field.-Impression: a. Pneumoniab. Atelectasis segmental at posterior right lung
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Laboratory finding on 8th May 2012
Parameters Value Normal Value
Complete Blood Count
Hemoglobin 10,3 gr% 10,7 – 17,1 gr%
Erithrocyte 3,72 x 106 /mm3 3,75 – 4,95 x 106 /mm3
• Change in sleep patterns• Changes in thinking• Confussion impairment• Mental fogginess• Personality or mood changes• Poor concentration• Abnormal movements or shaking of hands or arms• Agitation, excitement, or seizures (occur rarely)• Disorientation• Drowsiness or confusion• Inappropriate behavior or severe personality changes• Slurred speech• Slowed or sluggish movement
In this patient, seizure and conciousness impairment was found
Supporting Examination
Blood testCT Scan of the head or MRIEEGLumbar PunctureArterial blood gasesElectrolyteChest radiograph
In this patient, supporting examinations are:-Complete blood count-Chest radiograph-Arterial blood gases-Electrolyte
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THEORY PATIENT
Management
Correction by Precipating Factors, adjuvant therapy (antibiotics and dissacharides), transplantation and symptomatic.
Treatment of this patients are:- RL 99 gtt/i micro (rehydration from 19.30 to 23.30)•Head elevation 30°•O2 ½ - l L/i nasal canule•IVFD D5 Nacl 25 % 16 gtt/i•Phenytoin 25 mg/12 hr/iv in 20 cc NaCl 0,9 % out in 20 minutes•Injection of Ampicillin 250 mg/6 hr/iv (H1)•Injection of Cefotaxim 350 mg/8 hr/iv (H1)•Injection of dexamethasone 1mg/8 hr/iv (H1)•Paracetamol 3 x 100 mg (if needed)•Diet breast milk/ PASI 70 cc/3 hr/NGT.•(10.30 am) : Phenytoin 10 mg/kgBW in 6cc NaCl 0,9% out in 20 minutes•(05.00 pm): Correction of hipocalsemy (Ca= 6,6 mg/dl) 0,5 mg/kg BB= 0,5 x 5,3= 2,65 mg in 3 cc out in 20 minutes
Prognosis Acute encephalopathy may be treatable. Chronic forms of the disorder often keep getting worse or continue to come back.
In this patient, enchephalopathy was treatable.,
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THANK YOU
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References
Camara-Chua, Pia Teresa A, MD., Enchephalopathies. 2010. Available from: NEJM.org\
Garcia-Tsao G. Cirrhosis and its sequelae. In: Goldman L, Ausiello D, eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 156.
K. Lin , Chou-Ching. EEG Manifestations in Metabolic Encephalopathy.2005. Acta Neurologica Taiwanica Vol 14 No 3 September 2005
Kaplan PW, Fisher RS, Pathophysiology of Encephalopathy. 2005. New York: Demos Medical Publishing.
Munos, J.S., Hepatic Enchephalopathy. Available from: http://www.med.upenn.edu/gastro/documents/MedClinNAencephalopathy2008.pdf
Myer, Edwin, MD., Acute toxic-metabolic encephalopathy in children.2010. Available from: file:///E:/Print/acute-toxic-metabolic-encephalopathy-in-children.htm
Riordhan, M.S., Treatment of hepatic enchepalophaty. 2012. Available from: http://www.nejm.org/action/showImage?doi=10.1056%2FNEJM199708143370707&iid=t01