Nursing Process in Client with Hepar

Disorder

Oleh : Dina Dewi SLI

 Hepar Disorder

• Hepatitis :
• Viral (A, B , C, D, E, and G)
• Nonviral (Toxic Hepatitis, Drug Induced Hepatitis)
• Fulminant Hepatic Failure
• Hepatic Chirrosis
• Abcess Hepatic
• Hepatic Carcinoma
 Hepatitis A
• Nonenveloped SS-RNA picovirus
• Benign and self limited disease, Travelers &
children at high risk
• Reservoir : Contaminated food, water, fecal-
oral spread of virus
• 15 – 50 days incubation
• Sytmptom : without symptom (flulike illness,
anicteric); Preicteric phase (Headache,
malaise, fatigue, anorexia, low grade fever);
Icteric Phase (dark urine, jaundice sklera &
skin, tender liver)
 Hepatitis B
• Enveloped DS-DNA hepadvirus
• Present in all body fluid excp. Stool, spread by
blood or body fluid contact Transmited through
mucous membrane & break in the skin
• Parenteral/ intimate contact with carrier or people
with acute hepatitis
• 28 – 160 days incubation
• Symptom : similar to hepatitis A, may develop
arthralgias, rash
• Increase risk of hepatocelluler carcinoma
• May coexist with hepatitis D
• Treatment : Interferon, Bed rest, adequat nutrision,
 Hepatitis C
• Enveloped SS-RNA flavivirus
• Transmitted in blood product & tranfussion,
sexual contact (e.g : drug user, sexually active
with multiple partner)
• 15 – 160 days incubation
• Symptom : similar to HBV, less severe &
anicteric
• Treatment : combination interferon & ribavirin,
two antiviral agent,
 Hepatitis D

• Delta agent
• Occurs as a coinfection with HBV or as a
superinfection of those with /or carriers of HBV
Transmissions same with HBV
• Can convert mild HBV into severe fulminant
hepatitis
• 21 – 140 days incubation
• Symptom like HBV
• Can cause acute hepatitis in asymptomatic carrier
• Can increase tendency for progression to chronic
hepatitis & chirrosis
 Hepatitis E
• Acute Hepatitis
• Manifestations same with hepatitis A
• Fecal – oral Transmissions
• 15 – 65 days incubations
• High mortality rate in pregnant women in
developing countries.
 Hepatitis G
• Risk factor same with hepatitis C
• Transmitted by transfusion
• 14 – 145 days incubation (too long for hepatitis
B or C)
• In the U.S about 5 % of chronic liver disease
remains cryptogenic (non-A, non-B, non-C)
half of patient have been transfused
 Toxic Hepatitis

• The chemical most induced hepatitis : carbon

tetrachloride, phosphorus, chloroform, and
gold compounds.
• Symptom : Anorexia, nausea, vomiting, fever,
jaundice, hepathomegaly
• There are no effective antidotes
• Treatment : Liver transplantation, Fluid &
electrolyte balance.
 Drug-induced Hepatitis

• Medications that leads hepatitis are isoniazid,

halothane, acetaminophen, certain antibiotic,
antimetabolites, and anesthetic agent
• Symptom : chills, fever, rash, pruritus,
arthralgia, pruritus, anorexia, nausea
• Treatment : short course of high dose
corticosteroids, Liver transplantation,
 Fulminant Hepatic Failure
• Etiology : Viral hepatitis, Toxic medication,
chemical, metabolic disturbances, structural
change
• Symptom : progression from jaundice to
encephalohepathy, accompenied by
coagulation defect, renal failure, electrolite
disturbance,infection, hypoglicemia,
ancelophathy, crebral edema
• Three categories :hyperacute (0-7 days), acute
(8 – 28 days), subacute (28 -72 days)
• Treatment : plasma exchanges or charcoal
hemoperfision
 ABCESS HEPAR
Two type:
1. Pyrogenic (Bacteria)
Infenting bacteria : E. coli,
Klebsiella, Enterobacter, Salmonella,
Staphylococcus, Enterococcus
2. Protozoan (Protozoa) :
Entamoeba Histolotica
Clinical Manifestation

 Pain on right upper  Fever & Chills

abdominal quadrant  Nausea
with palpable
 Tender liver
 Anorexia
 Weight loss
 Vomiting
 Hepatic Cancer
Three type of Primary Liver Tumor :

 Hepatocelluler carcinoma (HCC)

 Cholangiocelluler carcinoma
 Combined HCC &
Cholangiocellulercarcinoma
Risk Factor
 Hepatitis B &C
 Chirrosis Hepatic
 Chronic Infection
 Exposure to certain chemical toxins (e.g
Vinylchloride, Arsenic)
 Cigarrette & alcohol
 Aflatoxin
Liver Metastasis

 Metastasis from other primary site

 50 % cancer cases
 Limfogen, hematogen (Potal system),
direct extention
Clinical manifestation
 Continous dull ache in the right upper
quadrant, epigastrium, or back
 Weight loss
 Loss of strenght
 Liver enlarged & irregular on palpable
 Jaundice present only if the larger bile
duct are occluded
 Anorexia
 Anemia
Assement & diagnostic finding
 Clinical sign & symptom
 History examination
 Physical examination
 X-ray
 SGOT, SGPT, GGT
 Leucocytosis, Erythrocytosis, Hypercalcemia,
Hypoglikemia, Hypocholesterolemia
 Special finding : Fetoprotein alevated 30-
40%, Carcinomaembryonic
Medical Management
Non Surgical : Surgical :

• Radiotherapy
• Chemotherapy • Lobectomy
• Percutaneous Billiary • Cryosurgery
drainage • Liver Transplantstion
• Laser Hyperthermia
• Immunotherapy
• Transcateter arterial
embolization
Komplikasi Post Operatif pada Transplantasi Hati :
 Perdarahan
 Hipertensi Portal
 Hipotensi
Manajemen Klien Post Operatif

 Lingkungan bersih dari fungi, bakteri dan

virus
 Monitor Fungsi Vital : jantung, paru, renal,
 neurologi, metabolik
 Monitor fungsi Hepar : Protein, Faktor
Pembekuan, Glikogen
Manajemen Keperawatan
 Membantu Keluarga dan Klien untuk
memutuskan treatmen yang akan
diambil, sumber daya yang akan
digunakan
 Membantu Klg & Klien untuk
menghadapi kondisi sakit kronik
 Mempersiapkan psikologi Klg & Klien
selama menunggu organ Donor
 Rujukan ke perawat jiwa, psikolog,
atau psikiater
 Anatomic of Liver

•The biggest Endocrine, it weight about 1500gr

is divided in two Major Lobus Right & Left
•Approximately 75 % the Blood supply comes
from the portal vein, which is rich in
Nutrition
•Central vein join to form hepatic vein and empties
into the vena cava
•Belonging Phagocyte cell (Kuffers cell)
 Function of the Liver
• Glucose Metabolism
• Ammonia Conversion
• Protein Metabolism
• Fat Metabolism
• Vitamin & Iron Storage
• Drug Metabolism
• Bile Formation
• Billirubin Excretion
 Clinical manifestation of chirrosis
(continued)
• Infection and peritonitis
• GI varises
• Edema
• Vitamin deficiency
• Mental deterioraton
 Diagnostic test (continued)
• Percutaneus needle biosy
• Ultrasonograaphy
• CT scan
• Magnetic resonance imaging
• Laparoscopy/ Endoscopy
 ABDOMINAL ASSESSMENT
• CONTOUR-ascites Inspect
• SYMMETRY-umbilicus
• SKIN-jaundice, cutaneous
angiomas (spider nevi),
caput medusae
• POSITION-knee chest or
fetal
• BOWEL SOUNDS
(Bruits = vascular sounds)
• PERCUSS FOR TYMPANY
(dullness with fluid )
• LIGHT PALPATION
(guarding/rigidity )
• DEEP PALPATION
(rebound tenderness, fluid
wave, Fluid Wave, ascites)
 Cirrhosis Complication
• Ascites
• Varises Esophageal
• Ensepalopathy Hepatic
• Syndroma Hepatorenal
 Development of collateral
vessels
• Large collateral channels develop in rectum
(hemoroids), asophagus (varices), around
umbilicus (caput medusa)
• Blood flow reverses between portal vein &
other veins
• Thin-walled varicosities & impaired
synthesis of clotting factor & low platelet
count bleeding esophageal varicosities
Medical management for Esophageal varices

• Non- Surgical :
• Pharmacology Therapy
• Ballon Tamponade
• Endoscopic Sclerotherapy
• Esophageal banding therapy Transjunggular
• Intrahepatic Portosystemic Shunting
• Surgical :
• Bypass procedur
• Devascularization and Transection
 Ascites management
• Dietary Modification : Low sodium diet
• Diuretic (spironolakton)
• Paracentesis
• Peritoneovenous Shunt
Hepatic Encelophathy & Coma

 Result from the accumulation ammonia & other

toxic metabolite in the blood
 Liver failed to detoxify & convert the ammonia to
urea
 Ammonia enters to blood stream, increased
ammonia concentration in the blood causes
brain dysfunction & damage
Assessment and Diagnostig Finding in
Encepalophathy hepatic :
 Asterixis
 Constructional apraxia

Management in Encephalopathy hepatic :

 Lactulose
 Monitor for Hypokalemia, dehydration
 Glucose IV
 Monitor mental status, serum ammonia level
Fluid intake – out put
Restriction protein intake
Sindrom Hepatorenal
 Kumpulan gejala penurunan fungsi ginjal
karena penurunan volume plasma sirkulasi
ginjal akibat penyakit hati.
 Merupakan akibat lanjut dari asites &
Hipertensi portal yang menyebabkan
penurunan filtrasi ginjal dan vasokonstriksi
perifer sehingga perfusi diginjal menurun
yang mengakibatkan penurunan fungsi ginjal
Masalah Keperawatan yang mungkin Muncul
 Gangguan Pola Nafas
 Gangguan Keseimbangan Cairan : Berlebih
 Gangguan Kebutuhan Makanan : Kurang dari
Kebutuhan tubuh
 Intoleransi aktifitas
 Gangguan integritas kulit
 Risiko tinggi injury
 Gangguan citra diri
Diagnosa Keperawatan :
1. Gangguan pola nafas b.d ekspansi paru tidak maksimal,
adanya asites
Tujuan :
Tidak terjadi gangguan pola nafas
Intervensi :
 Berikan posisi fowler atau semifowler (30 °)
 Pertahankan kekuatan klien dengan membatasi
aktivitas, latihan pada klien
 Rubah posisi setiap 2 jam
 Diagnosa Keperawatan :
2. Gangguan keseimbangan cairan : berlebih
b.d gangguan mekanisme regulasi
Tujuan :
Gangguan keseimbangan cairan dapat
teratasi
Intervensi :
 Pantau intake-output cairan
 Monitor status TTV, jantung, paru,
 Ukur lingkar perut setiap hari
 Ukur Berat badan setiap hari
 Kolaborasikan : Diuretik (Aldakton)
3. Gangguan kebutuhan nutrisi : kurang dari kebutuhan
tubuh b.d gangguan absorbsi dan metabolisme Pencernaan
makanan
Tujuan :
 Kebutuhan nutrisi dapat terpenuhi
Intervensi :
 Batasi masukan Na
 Berikan makanan sedikit dan sering
 Batasi masukan alkohol
 Berikan makanan tinggi karbohidrat dan rendah
protein
Kolaborasikan :
 antinausea, antivomiting atau diare
 Glukosa dan Protein IV sesuai indikasi