RTRMF – BSN LEVEL III BATCH TOPAZ

NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: DEAN CORA GASCO

MALABSORPTION AND HEPATIC  Direct infusion of vasopressin into the superior mesenteric
artery is most effective Vasopressin
DISORDERS PT. 2  Given in junction with nitroglycerin to minimize vasoconstrictive
side effects
TOPIC OUTLINE

SIDE EFFECTS OF VASOPRESSIN

1. Esophageal Varices a. Hypothermia
2. Drug-induced Hepatitis
b. Myocardial and gastrointestinal tract ischemia
3. Hepatic Encephalopathy
c. Acute renal failure
4. Hepatitis G
5. Toxic Hepatitis 2. Beta-adrenergic Blocking Agents
6. Liver Metastases  For management of acute variceal bleeding
7. Liver Transplantation
EXAMPLES OF BETA-ADRENERGIC BLOCKING AGENTS
a. Propranolol (Inderal)
ESOPHAGEAL VARICES
b. Metaprolol (Lopressor)
 Esophageal varices develop in the majority of patients with
c. Nadolol (Cogard)
cirrhosis
 Varices are varicosities that develop from elevated pressure
NURSING MANAGEMENT
in the veins that drain into the portal system
1. Monitoring the patient's physical condition and evaluating
CLINICAL MANIFESTIONS emotional responses and cognitive status
 Hematemesis 2. Monitor vital signs
 Melena 3. Assess the patient's nutritional and neurologic status
 General deterioration 4. Frequent oral hygiene and moist sponges to the lips
 In mental or physical status 5. Provides support and explanations about medical and nursing
 Cool, clammy skin management
 Hypotension See to it that the drugs are correct and correctly given.
 Tachycardia
ASSESSMENT AND DIAGNOSTIC FINDINGS DRUG-INDUCED HEPATITIS
a. X-ray studies  Due to so many drugs that a person takes
b. Barium swallow  Most common cause of acute liver failure
c. Ultrasonography  Accounts for more than 50% of all cases in the US
d. CT Scan  Manifestations of sensitivity to a medication may occur on the first
e. Angiography day of its use or not until several months later
 Hepatotoxic Drugs – drugs that are toxic to the liver
MEDICAL MANAGEMENT
 Balloon Tamponade
SIGNS AND SYMPTOMS
o To control hemorrhage
1. Usually the onset is abrupt, with:
o In this procedure, pressure is exerted on the cardia
● Chills
(upper orifice of the stomach) and against the bleeding varices by
● Fever
a double-balloon tamponade (Sengstaken-Blakemore tube)
● Rash
 Sclerotherapy
● Pruritus
o Also referred to as injection sclerotherapy, sclerosing
● Arthralgia
agent is injected through a fiber optic endoscope into the
● Anorexia
bleeding esophageal through varices to promote thrombosis and
● Nausea
eventual sclerosis
Pruritus occurs because of bile salts that are produced in the liver. Rash
 Transjugular Intrahepatic Portosystemic Shunting
occurs from the pruritus. Fever is due to inflammation.
o Is indicated for the treatment of an acute episode of
2. Later, there may be:
variceal bleeding refractory to pharmacologic or endoscopic
● Jaundice
therapy
● Dark urine
 Esophageal Banding Therapy (Variceal Band Ligation)
● Enlarged and tender liver
o Also referred to as esophageal variceal ligation (EVL)
If there is dark urine, the stool's color is gray. The liver becomes cirrhotic
o A modified endoscope loaded with an elastic rubber
and inflamed which makes it enlarged (hepatomegaly).
band is passed through an overtube directly into the varix (or
3. If fever, rash or pruritus occurs from any medication, its use should
varices) to be banded
be stopped immediately.
o After the bleeding varix suctioned into the tip of the
endoscope, the rubber band is slipped over the tissue, causing
NURSING MANAGEMENT
necrosis, ulceration, and eventually sloughing the varix.
1. After the offending medications are withdrawn, symptoms
 Surgical Bypass Procedure
may gradually subside. However, reactions can be severe or
o Surgical decompression of the portal circulation can prevent
fatal even if the medication is stopped.
variceal bleeding if the shunt remains patent
o One of the various surgical shunting procedures is the distal
CAUSES OF DRUG-INDUCED HEPATITIS
splenorenal shunt, which is made between the splenic vein and the left 1. Acetaminophen
renal vein after splenectomy. ● Although any medication can affect liver function, its use
has been identified as the leading cause of acute liver
PHARMACOLOGIC THERAPY failure
1. Vasopressin ● Found in many OTC medications used to treat fever and
 IV vasopressin is administered to stop variceal bleeding pain
 Achieves temporary lowering of portal pressure 2. Other causes commonly associated with liver injury include:
 These agents reduce portal venous blood flow by ● Many anesthetic agents
constricting afferent arterioles

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● Medications used to treat rheumatic and CLINICAL SYMPTOMS

musculoskeletal disease - Stuporous
● Antidepressants - Difficult to rouse
- Sleeps most of the time
● Psychotropic medications
- Marked confusion
● Anticonvulsants
- Incoherent speech
● Antituberculosis agents CLINICAL SIGNS
o A short course of high dose corticosteroids may be used in - Increase deep tendon reflexes
patients with severe hypersensitivity reactions, although its - Rigidity of the extremities
efficacy is uncertain. - EEG changes
o Liver transplantation is an option for drug induced hepatitis, - EEG markedly abnormal
Stage 4
but outcomes may not be as successful as with other causes
CLINICAL SYMPTOMS
of liver failure.
- Comatose
o If a person has rheumatic disease, the doctor will prescribe - May not respond to painful stimuli
Arcoxia only once. The danger of this drug is renal and liver CLINICAL SIGNS
failure. This is not used in the US because this causes cerebral - Absence of asterixis
hemorrhage. Antidepressant drugs also cause renal and liver - Absence of deep tendon reflexes
failure. - Flaccidity of extremities
- EEG changes
HEPATIC ENCEPHALOPATHY
CLINICAL MANIFESTATIONS
 Hepatic encephalopathy or post systemic encephalopathy
1. The earliest symptoms of hepatic encephalopathy are MENTAL
(PSE) is a life-threatening complications of liver disease that
CHANGES AND DISTURBANCES.
occurs with profound liver failure.
2. The patient appears:
 Have no avert signs of the illness but do have abnormalities
o Slightly CONFUSED
on neuropsychologic testing.
o UNKEMPT
 Hepatic encephalopathy is the neuropsychiatric
o HAS ALTERATIONS IN MOOD AND SLEEP
manifestations of hepatic failure associated with portal
PATTERNS
hypertension and the shunting of blood from the portal
o The patient tends to sleep during the DAY
venous system into the systemic circulation.
o Has RESTLESSNESS and INSOMNIA at NIGHT
 The reversible metabolic form of encephalopathy can
o Difficult to awaken
improve with recovery of liver function
o Completely disoriented with respect to time and
place
o The patient lapses into frank coma and may have
seizures.
o Asterixis (flopping tremor of the hands) may be
seen in Stage II encephalopathy
o Handwriting becomes difficult
o Constructional Apraxia- inability to produce simple
figure
o Deep tendon reflexes are hyperactive
o Fetor hepaticus – a sweet slightly fecal odor to the breath
Stage 1 that is presumed to be of intestinal origin, may be noted.
CLINICAL SYMPTOMS ASSESSMENT AND DIAGNOSTIC FINDINGS
- Normal level of consciousness with periods of lethargy and  The electroencephalogram (EEG) shows generalized slowing
euphoria  Increase in the amplitude of brain waves
- Reversal of day-night-patterns
 Characteristic triphasic waves
CLINICAL SIGNS
MEDICAL MANAGEMENT
- Asterixis
- Impaired writing and ability to draw line figures  Focuses on identifying and eliminating the precipitating cause
- EEG changes if possible
- Normal EEG  Initiating ammonia-lowering therapy
Asterixis  Minimizing the potential medical complications of cirrhosis
- Is a flapping tremor and depressed consciousness
CAUSE
 Reversing the underlying liver disease if possible
- Imbalance between the agonist and antagonist muscle due
Correction of the possible reasons for the deterioration is essential such
to disturbed dencephalic motor centers
DETECTION AREAS as:
- Tongue and the upper and lower extremities  Bleeding
- Not specific to the liver  Electrolyte abnormalities
- Carbon dioxide intoxications, uremia, organ failure and  Sedation or azotemia
stroke of basal ganglia  Lactulose (Cephulac)
- Not seen in advanced cases and coma
Stage 2
LACTULOSE (Cephulac)
CLINICAL SYMPTOMS
- Increased drowsiness It acts several mechanisms promoting the excretion of ammonia in the
- Disorientation stool
- Inappropriate behavior 1. Ammonia is kept ionized state
- Mood swings o Resulting in a decrease in colon pH
- Agitation o Reversing the normal passage of ammonia from the
CLINICAL SIGNS
colon to the blood
- Asterix
2. Evacuation of bowel takes place
- Fetor hepaticus EEG changes
- Abnormal EEG with generalized slowing o Decrease the ammonia absorbed from the colon
Stage 3 3. The fecal flora is changed to organisms

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NCM 116 (MEDICAL-SURGICAL NURSING II)
o That do not produce ammonia from urea
o Two to three soft stool per day are desirable- this
indicates that lactulose is performing as intended.
NURSING ALERT
 The patient receiving lactulose is monitored closely for
the development closely for the development of watery
diarrheal stools, because they indicate a medication
overdose.
CONSIDERATION
 The patient is closely monitored for HYPOKALEMIA and
DEHYDRATION
 Other laxatives are not prescribed during lactulose
administrations because their effects disturb dosage
regulation.
 Lactulose may be administered by nasogastric tube for
enema for patients who are COMATOSE or for those in
whom oral administration is contraindicated
impossible.
OTHER ASPECTS OF MANAGEMENT
 IV administration of glucose – to minimize protein
breakdown
 Administration of vitamins – to correct deficiencies
 Correction electrolyte imbalances (especially potassium)
 ANTIBIOTICS – Antibiotics may also be added to the
treatment regimen such as:
o Neomycin
o Metronidazole (Flagyl)
o Rifaximin (Xifaxan)
NURSING RESPONSIBILITIES
 Neurologic status is asses frequently
 Mental status is monitored by keeping a daily record
of handwriting and arithmetic performance
 Fluid intake and output and body weight are recorded
each day
 Vital signs are measured are recorded every 4 hours.
 Potential sites of infection (peritoneum, lungs) are
assessed frequently, abnormal findings are reported
promptly and
 Serum ammonia level is monitored daily.
 Protein intake is moderately restricted in patients who
are comatose or who have encephalopathy that is
refractory to lactulose and antibiotic therapy.
 Long term restrictions if dietary protein to less than
1g/kg daily should be avoided.
 If animal protein precipitates encephalopathy,
vegetable or dairy proteins may be used as most
patients can tolerate a diet of vegetable proteins up to
120/day.
 Patients and families are advised about foods that are
high in protein (eg, meat) which may be eliminated from
the diet for the short term to reproduce production of
ammonia.
 Enteral feeding is provided for patients
encephalopathic state persists.
 Reduction in the absorption of ammonia from the GI
tract is accomplished by the use of gastric suction,
enemas or oral antibiotics,
 Electrolyte status is monitored and corrected if
abnormal
 Sedatives, tranquilizers, and analgesic medications are
discontinued.
 Administrations of Benzodiazepine
(Romazico) to improve encephalopathy.
NURSING MANAGEMENT
 Maintaining a safe environment- to prevent injury,
bleeding and infections
 Administers the prescribed treatments and monitors or
the numerous potential complications
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LECTURER: DEAN CORA GASCO
 Encourages deep breathing and position changes-prevent the
development of atelectasis, pneumonia, and other respiratory
complications.
 Informing the patients family about patients’ status and
supports by explaining the procedures and treatments that
are part of the patients care.
PROMOTING HOME AND COMMUNITY BASED CARE
 Teaching patients’ self-care
 Instruct patient in maintenance of a moderate-protein, high
calorie diet.
 Assesses the patient's physical and mental status and
collaborates closely with the physicians.
NUTRITIONAL MANAGEMENT OF HEPATIC ENCEPHALOPATHY
 Prevent the formation and absorption of toxins principally
ammonia, from the intestine
 Keep daily protein intake between 1.0 and decompensation.
or
HEPATITIS G
 HEPATITIS G (the latest form) is a posttransfusion hepatitis with an
incubation period of 14 to 145 days too long for hepatitis B or C.
 Autoantibodies are absent
RISK FACTORS
 Recipient of blood products or organ transplant before 1992
or clotting factor concentrates before 1987.
 Healthcare and public safety workers after a needlestick
injuries or mucosal exposure to blood. Ito na aksidente kala na prick,
kinahanglan naka double gloving kun na BT.
 Children born to women infected with hepatitis virus.
 Past/current illicit IV / injection drug use.
 Past treatment with chronic hemodialysis.
 Multiple sex partners, history of sexually transmitted disease,
unprotected sex.
 Patients undergone blood transfusion.
HISTORY
 In 1967, Dienhardt et al initiated human viral hepatitis
transmission studies in marmoset monkeys.
 They identified an unknown (possibly infectious agent called
GB in a blood of a 34-year old surgeon, with the initials GB) tungod kan
GB asya nagkamayda Hepatitis GB who had developed acute hepatitis
from an unknown source.
 In 1995, Simons et al identified 2 flavi-virus genomes in
tamarin marmosets after passage with the GB agent. They called him
GBV-A and GBV-B. GBV-C was identified in a patient with unknown
hepatitis shortly thereafter.
 In the United States, about 5% of chronic liver disease remains
cryptogenic (does not appear to be autoimmune or viral in origin), and
50% of these patients have received blood transfusions before
developing disease.
 Therefore, another form of hepatitis, called Hepatitis G virus
(HGV) or GB virus-C (GBV-C) has been described; these are thought to
whose be two different isolates of the same virus. Antibodies are absent.
 There is no clear relationship between HGV/GBV-C infection
and progressive liver disease. Persistent infection does not occur but
does not affect the clinical source.
CONFIRMATORY TEST
 A GBV-C RNA by a polymerase chain reaction (PCR) is
available for detection of viremia. It is unclear when it might be
indicated, as GBV-C is not strongly implicated in human disease.
SIGNS AND SYMPTOMS
flumazenil  Patients are mostly asymptomatic.
LONG TERM EFFECTS:
1. HGV can cause chronic infection and viremia; however,
there is no conclusive evidence to indicate that HGV
causes fulminant or chronic liver disease.
2. Co-infection with Hepatitis B virus (HBV) or HCV does not
seem to worsen the course or severity of disease.
TRANSMISSION
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1. Blood and sexual contact

2. Transplacental, rarely
COMMUNICABILITY:
 Unknown

PREVENTIONS AND MANAGEMENT

 No specific measures have been identified.
 No treatments have been found and are indicated.
 Post-exposure management is not known.

TOXIC HEPATITIS
TOXIC HEPATITIS
 The Kupffer cells (liver cells) are destroyed by alcohol,
chemicals, street drugs, and some nutritional supplements. Majority LIVER METASTASES
of the cause is intake of alcohol.  Metastases from other primary sites, particularly the digestive
 At the onset of the disease, toxic hepatitis resembles system, breast, and lung, are found in the liver 2.5 times more
viral hepatitis. frequently than tumors due to primary liver cancers (Rodes, et al.
 Obtaining a history exposure to: 2007)
 Hepatotoxic chemicals  Malignant tumors are likely to reach the liver eventually, by way of
 Medications the portal system or lymphatic channels, or by direct extension
 Botanical agents from an abdominal tumor.
 Other toxic agents assist in early treatment and  Often the first evidence of cancer is an abdominal organ is the
removal of the causative agent appearance of liver metastases; unless exploratory surgery or an
PHYSICAL ASSESSMENT autopsy is performed, the primary tumor may never be identified.
 Jaundice MANIFESTATION
The early manifestations of malignancy of the liver include:
 Pain- a continuous dull ache in the right upper quadrant,
epigastrium, or back.
 Weight loss
 Loss of strength
 Anorexia
 Anemia may also occur
 Jaundice is present only if the larger bile ducts are occluded by the
pressure of malignant nodules in the hilum of the liver
 Ascites develops if such nodules obstruct the portal veins or if
tumor tissue is seeded in the peritoneal cavity
  Hepatomegaly DIAGNOSTIC TESTS
MANAGEMENT ● Based on clinical signs and symptoms, the history and physical
 Recovery from acute toxic hepatitis is rapid if the examination, and laboratory and x-ray studies results.
hepatotoxins identified early and removed or if ● Increased:
exposure to the agent has been limited. ○ serum levels of bilirubin
 Recovery is unlikely if there is a prolonged period ○ Alkaline Phosphatase
between exposure and onset of symptoms ○ AST
 There is no effective antidote ○ GGT
SYMPTOMS ○ Lactic Dehydrogenase
Severe Symptoms: ● Leukocytosis (increased WBC)
 Fever rises; the patient becomes toxic and prostrated ● Erythrocytosis (increased RBC)
 Vomiting may be persistent, with the emesis containing ● Hypercalcemia
blood ● Hypoglycemia
 Clotting abnormalities may be severe, and ● Hypocholesterolemia
hemorrhages may appear under the skin ● The serum level of alpha-fetoprotein (AFP), which serves as a
Symptoms may lead to vascular collapse: tumor marker, is elevated in 30% - 40% of patients with primary
 Delirium, coma, and seizures develop liver cancer.
 Within a few days the patient may die of fulminant ● The level of carcinoembryonic antigen (CEA), a marker of advanced
hepatic failure unless he or she receives a liver digestive tract cancer, may be elevated.
transplant ● Many patients have metastases from the primary liver tumor to
other sites by the time the diagnosis is made; metastases occur
MANAGEMENT: primarily to the lung but may also occur to:
Therapy is directed toward restoring and maintaining: ○ Regional lymph nodes
 Fluid and electrolyte balance ○ Adrenals
 Blood replacement ○ Bone
 Comfort and supportive measures ○ Kidneys
 A few patients recover from acute toxic hepatitis only to ○ Heart
develop chronic liver disease ○ Pancreas
 If the liver heals, there may be scarring followed by post ○ Stomach
necrotic cirrhosis ● Positive emission tomography (PET) Scan are used to evaluate a
wide range of liver metastatic tumors.
● Confirmation of tumor histology can be made by biopsy under
imaging guidance (CT scan or ultrasound) or laparoscopy.

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● Local or systemic dissemination of the tumor by needle  It is another treatment modality under investigation.
biopsy or fine-needle biopsy can occur, but it is rare.  In this therapy, lymphocytes with antitumor reactivity are
MEDICAL MANAGEMENT: administered to the patient with hepatic cancer.
● Although surgical resection of the liver tumor is possible in  Tumor regression has been demonstrated in patients with
some patients. The underlying cirrhosis is so prevalent in metastatic cancer for whom standard treatment has failed.
liver cancer that it increases the risk associated with surgery.
RADIATION THERAPY LIVER TRANSPLANTATION
● The use of external beam radiation for treating liver tumors  A surgery to remove a diseased liver and replace it with a healthy
has been limited by the radiosensitivity of normal  A liver with cirrhosis, with a tumor, and is sclerotic
hepatocytes and the risk of destruction of the normal liver  A patient's entire liver is removed, and replaced by either a
parenchyma. completely new liver of a portion of a healthy liver.
● More effective methods of delivering radiation to tumors of  A lot are in line for a liver transplant waiting for a donor that signed or
the liver include: that consented to donate his/her body part to others.
○ IV or intra-arterial injection of antibodies tagged  The wait is so long that some patients couldn't wait any longer and just
with radioactive isotopes that specifically attack die before receiving the transplant
tumor-associated antigens. INDICATIONS
○ Percutaneous placement of a high-intensity source ● Liver Failure
for interstitial radiation therapy (delivering - Cirrhosis, that is caused by Hepatitis C, is the most
radiation directly to the tumor cells). common reason for liver transplants
CHEMOTHERAPY ● Diseases of the Bile Ducts
● Typically, studies of patients with advanced cases of liver - Biliary Atresia (this is genetic or hereditary, where the child
cancer have shown that the use of systemic is born without a bile duct that the newborn would instantly
chemotherapeutic agents leads to poor outcomes. die in just 3 days)
● There is no evidence to support standard systemic ● Wilson Disease
chemotherapy; in the United States, there is no approved ● Hemochromatosis
systemic treatment. ● Liver Cancer
● Systemic chemotherapy may be used to treat metastatic CONTRAINDICATIONS
liver lesions. Embolization of tumor vessels with  Brain Death
chemotherapy (a process known as trans arterial  Extrahepatic Malignancy (cancer outside the liver) 
chemoembolization (TACE) produces anoxic necrosis with
 Active uncontrolled infection
high concentrations of trapped chemotherapeutic agents.
 Active alcoholism and substance abuse
● An implantable pump has been used to deliver a high
concentration of chemotherapy by a constant infusion to the  AIDS

liver through the hepatic artery in cases of metastatic  Severe cardiopulmonary disease - CAD 
disease.  Hypertension
PERCUTANEOUS BILIARY DRAINAGE  Uncontrolled sepsis
 Percutaneous biliary or transhepatic drainage is used to  Inability to comply with medical regimen
bypass biliary ducts obstructed by liver, pancreatic, or bile
 Lack of psychosocial support
duct tumors in patients who have inoperable tumors or are
 Anatomic abnormalities precluding liver transplantation 
considered poor surgical risks.
 Compensated cirrhosis without complications
 The removal of a tumor with no need of a surgical procedures
 is done under fluoroscopy, a catheter is inserted through the
 Cholangiocarcinoma (cancer of the gallbladder)

abdominal wall and past the obstruction into the duodenum.  Portal vein thrombosis
 Such procedures are used to reestablish biliary drainage,  Psychological instability
relieve pressure and pain from the buildup of bile behind COMPLICATIONS
the obstruction, and decrease pruritus and jaundice.  VASCULAR 
 For several days after its insertion, the catheter is opened to  Hepatic artery
external drainage. o Stenosis, thrombosis, PA
 The bile is observed closely for:  Portal vein
● Amount o Stenosis, thrombosis
● Color
 IVC & HV
● Presence of blood and debris
o Stenosis, thrombosis
Complications
 Splenic artery
● Sepsis
o Splenic artery steal syndrome
● Leakage of bile
● Hemorrhage  BILIARY

● Re-obstruction of the biliary system by debris in the  Obstruction

catheter or by encroaching tumor. o Stenosis, stones, biliary cast
Management  OTHERS
● Patients are observed for:  Abscess Collections
1. Fever and chills o Hematoma, biloma
2. Bile drainage around the catheter  Neoplasms
3. Changes in vital signs, and o HCC-PTLPD
4. Evidence of biliary obstruction, including:
 Recurrent disease
- Increased pain or pressure,
o PSC
- Pruritus
 Cirrhosis & its complications
- Recurrence of jaundice.
IMMUNOTHERAPY
2 MAIN COMPLICATIONS 

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A. REJECTION   Has a charitable desire of donation without financial [interest]

 Immune system works to destroy foreign substances PROCEDURE (LIVER DONOR OPERATION)
that invade your body 1. Incision in the upper abdomen. If the recipient is a child, only a
 Immune system cannot distinguish between your portion of the left part of the liver is removed from the donor. -
transplanted liver and unwanted invaders such as 25% of the donor’s total liver.
bacteria and virus
2. If the recipient is an adult. A larger portion of the liver needs to be
 The patient is given steroids to avoid liver transplant
removed from the donor, usually the right portion of the liver.
rejection. The side effect of steroids is moon face. Your
3. Blood vessels supplying the portion of the liver to be removed are
immune system will go down making you more susceptible
to infections so stay away from people especially people separated out.
with respiratory disease, avoid concerts, market, or any 4. The liver itself is divided and the portion to be transplanted is
crowd of people.   removed.
B. INFECTION 5. The portion is brought to a separate operating room for the
 Anti-rejection drugs that suppress the immune system recipient. - Donor operation takes 6-8 hrs.
are needed to prevent the liver from being rejected LIVER TRANSPLANTATION SYMPTOMS
 Not all patients have problems with infections, most People who have liver disease may have many of the ff problems:
infections can be treated Successfully as they occur
1. Jaundice
2. Itching
1. Living Donor Transplantation 
3. Dark, tea-colored urine
 Blood type and body size are critical factors in
determining who is an appropriate donor 4. Gray or clay colored blood movements

 Recipients for the living donor transplantation must be 5. Ascites

active on the transplant waiting list. Their health must 6. Vomiting of blood
also be stable enough to undergo transplantation with 7. Tendency to bleed
chances of success POST-OPERATIVE CARE
2. Cadaver 1. Frequent assessment of cardiac and pulmonary function, serum
 Donor may be a victim of an accident or head injury. glucose and electrolytes, renal and liver functions, coagulation
 Donor’s heart is still beating, but the brain has stopped status and blood count are crucial.
functioning. 2. Adequate pain control, prevention of shivering and hypothermia to
 Heart continues to beat because the donor is attached avoid excessive sympathetic nervous.
to a respirator. Respirator delivers adequate supply of 3. The requirements of blood transfusion continue also in the post-
oxygen to all vital organs. operative.
 Donor is in the ICU. 4. If ongoing bleeding, despite correction of coagulopathy and
TEST REQUIRED PRIOR GETTING A LIVER TRANSPLANT rewarming of the pt especially if hemodynamic instability and
1. Previous Doctor Records: oliguria are present, the patient should undergo immediate
 X-Ray reoperation to identify and stop the ongoing.
 Liver Biopsy slides 5. Eating a healthy diet and taking medications are part of taking care
 Record of medications of the new liver.
2. Computer Tomography Scan (CT-Scan) which uses x-
rays and a computer to generate pictures of the liver,
showing its size and shape.
3. Doppler Ultrasound: detect if blood vessels in the liver
are open.
4. ECG: to evaluate your heart
5. Pulmonary function test: to determine your blood type,
biochemicals status of blood. To gauge liver function.
6. AIDS testing
7. Hepatitis screening
WHAT HAPPENS WHEN THEY FIND YOU A MATCH?
 When an organ has been identified for you, a transplant
coordinator will contact you by telephone or by pager. Make
sure that you do not eat or drink anything once you have
been called to the hospital. The transplant coordinator will
notify you of any additional instructions. When you arrive at
the hospital, additional blood tests, an Electrocardiogram
and a chest X-ray will generally be taken before the
operation. You may also meet with the anesthesiologist and
a surgical resident. If the donor liver is found to be
acceptable you will proceed with the transplant. If not, you
will be sent home to continue waiting.
TYPES OF LIVER TRANSPLANTATION
1. Living Donor Transplantation
2. Cadaveric Transplantation
 Not dead, tipatay pala. The heart is still beating.
LIVER DONOR REQUIREMENTS
 Must be in good health.
 Has a blood type that matches with or is compatible with the
recipients, although some centers now perform blood group
incompatible transplants with special immunosuppression
protocols

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