1. Nursing Care of Patients with Hepatobiliary Disorders
C. Cummings RN, EdD.

2. Anatomy Diaphragm Liver Hepatic Duct Cystic Duct Pancreas Gall Bladder
Sphincter of Oddi
Common Bile Duct
Duodenum

3. Pancreas Exocrine- 80% of organ, acinar cells with digestive enzymes:
What are they?
Endocrine- islets of langerhans
Alpha cells- ?
Beta cells- ?

4. Acute Pancreatitis Cause:
Pancreatic enzymes destroy ductal tissue and cancreatic cells autodigestion and fibrosis
Can be life threatening
NHP- necrotizing hemorrhagic pancreatitis
20%, diffuse bleeding
Enzymes are activated before they reach the duodenum
Toxic injury to pancreatic cells

5. Four major physiologic processes
Lipolysis
Caused by lipase, release fatty acids and combine with I Ca  causes?
Proteolysis
Caused by trypsin, splits proteins into smaller polypeptides  what??

6. Four major physiologic processes
Necrosis of the Blood Vessels
Caused by elastase, elastic fibers of the blood vessels and ducts dissolve  what?
Kallikrein releases vasoactive peptides, bradykinin and kinin what? and increased ?
Inflammation
Leukocytes form around hemorrhagic and necrotic areas  pus, abcess formation and if walled off pancreatic what??

7. Why does enzyme activation occur?
Bile Reflux- obstruction of CBD
Hypersecretion-obstruction theory- pancreatic duct ruptures
Alcohol induced changes- stimulates hydrochloric acid and secretin production exocrine functions, also causes edema of the duodenum and ampulla of Vater, this obstructs flow, may also decrease tone at sphincter of Oddi and cause duodenal reflux

8. Other causes
Besides alcohol ingestion and biliary disorders, can also be caused by:
Trauma- blunt or surgical (whipple/ ERCP)
Pancreatic obstruction- such as?
Metabolic disturbances- hyperlipidemia, hyperparathyroid
Renal failure or transplant
Ulcers that lead to peritonitis
Coxsackievirus B infections
Drug toxicities- such as?

9. Complications Pancreatic infection Peritonitis Hypovolemia Hemorrhage
ARF
Paralytic ileus
Septic Shock
What are other complications??

10. Symptoms of Acute Pancreatitis
What is predominant symptom?
Where is it?
When is it worse?
Jaundice
Cullen’s sign- what is that?
Turner’s sign- and that?
Bowel sounds may be decreased or absent
Abdominal tenderness
Watch for signs of shock
Respiratory effusions/ SOB
Assess for excessive alcohol intake

11. Turner’s sign

12. Laboratory Diagnoses Elevated Serum What are major enzymes? Trypsin
Elastase
Also, increased serum
Glucose
Bilirubin
Alanine aminotransferase
Leukocyte count
Decreased
Calcium and magnesium

13. Diagnoses for Acute Pancreatitis
What are two primary nursing diagnoses?
Nausea
Risk for fluid volume deficit
Risk for infection
Risk for ineffective breathing pattern
Risk for activity and sleep disturbances

14. Collaborative Diagnoses
What are two potential nursing diagnoses?
Potential for Hypovolemic or Septic Shock
Potential for ARDS
Potential for Paralytic Ileus
Potential for MOSF

15. Nursing Interventions
Acute Pain
What is primary method to relieve pain, other than medication?
IV fluids for hydration
Replacement of Ca and Mg
NG drainage and suction
Assess for return of bowel sounds and pain control

16. Pain Control Opiods, IV and PCA
Demerol for relief of spasms at the sphincter of Oddi, but it has problems with breakdown and is rarely used now
Fentanyl patch
Epidural morphine with bipivacaine
Pain may last how long?

17. Other management of pain
Anticholinergics, atropine, glucagon, calcitonin, histamine receptor antagonists (Zantac), protease inhibitors are used for what?
Antibiotics
Ceftazidime, cefuroxime, imipenem (Primaxin)

18. Other Management of Pain
Surgery
ERCP (endoscopic retrograde cholangiopancreatography)
- used to open sphincter
Pseudocystojejunostomy or
Pseudocystogastrotomy to drain abcess or pseudocyst
JP drains or sump tubes may be used for excessive drainage

19. ERCP

20. ERCP

21. Imbalanced nutrition: less than body requirements
Maintain on NPO, may have NGT
May not eat for 7-10 days
Receive nutritional support through what?
Begin back on what kind of diet? What should they not take in?
Diet teaching and teaching on signs of chronic progression should be stressed with the patient

22. Chronic Pancreatitis
Usually develops after repeated episodes of acute pancreatitis
What is the most common cause?
Types:
Chronic Calcifying Pancreatitis- alcohol induced, proteins plug the ducts 
lead to atrophy and dilation 
ulceration and inflammation 
fibrosis, intraductal calification and cystic sacs develop
Hard, firm organ with pancreatic insufficiency

23. Chronic Pancreatitis Type Chronic Obstructive Pancreatitis
Inflammation, spasm and obstruction of the sphincter of Oddi
Inflammation and sclerotic lesions occur at the head of the pancreas obstruction and backflow of secretion

24. Chronic Pancreatitis with pseudocysts

25. Results Loss of exocrine function:
Aqueous bicarbonate- neutralizes duodenal contents
Pancreatic enzymes- what do they do?
Enzyme secretion is reduced by 80%  steatorrhea, what do the stools look like?
Fat malabsorption  wt loss and muscle wasting and edema r/t loss of albumin

26. Results Pancreatic endocrine dysfunction causes what disease?
May also have pulmonary complications from edema and pancreatic ascites
ARDS may develop
Chronic pancreatitis is a major risk factor for pancreatic cancer

27. Symptoms of Chronic Pancreatitis
Intense abdominal pain and tenderness
Ascites
What type of stools?
Respiratory compromise
Wt loss or gain?
Jaundice
What does the urine look like? Why?
Signs of diabetes
Elevated lipase and amylase
Elevated bilirubin, alkaline phosphatase and glucose
Definitive dx- by biopsy to look for calcification

28. Nursing Management Manage pain- how?
Enzyme replacement- dietary supplements, pancrease, viokase, cotazyme, donnazyme- take before or during meals, take according to number of stools/day and wipe lips after
Insulin therapy
NPO or TPN for days, then what kind of diet?
Histamine receptor blockers to decrease acid
Octreotide (Sandostatin) like somatostatin may be used for diarrhea to slow motility

29. Health teaching
Surgery is not an option, unless there is a cyst, obstruction or possible transplant for diabetes
Diet and alcohol avoidance is stressed
Medication compliance with insulin, pancreatic enzymes
Skin care for irritation r/t steatorrhea
What should the patient monitor?

30. Case Study
44 year old female admitted with abdominal pain, nausea and vomiting. She states that she has a lot of gas pain that wakes her up in the night.
What do you suspect?

31. Case Study What are the symptoms of GB disease?
What can precipitate it?
What is the treatment?
How can you prepare her for surgery? How do you decide between laparoscopic and open?
What needs to be done postop?

32. Case Study What structures are located in the RUQ of the abdomen?
Which of the above organs are palpable in the RUQ?
Given the patient’s diagnosis, what lab values would be important to evaluate?
List 4 preop preparations that to be done.

33. Case Study
The patient undergoes a laproscopic cholecystectomy, why is a T-tube inserted?
What type of postoperative care would be required?
The patient is sent home with the T-tube, what care would be appropriate?
What type of diet should they be on?

34. Case Study
The patient is medicated with Morphine and the pain has decreased from 10-4 in 1 hour, what else could be done for his pain?
What data charted in the assessment is consistent with common bile duct obstruction?
The patient spikes a temp of 38.6, a CXR is ordered and the patient is started on an antibiotic, imipenem. What should be done before the antibiotic is started?

35. Case Study She is ready for discharge What type of teaching is needed?
What should be avoided, what about care of the T-tube?

36. Cholecystectomy Removal of the Gallbladder
Can be done open or laproscopic
Signs are nausea, vomiting, abdominal pain
Risk Factors:
Fat, Female, Forty and Fertile
lap cholecystectomy

37. Lap Cholecystectomy

38. T-tube

39. Post-operative Care Pain control- demerol or PCA
NPO until bowel sounds return, then clear liquids to DAT
Diet depends on what patient can tolerate
T-tube may remain in for 1-6 weeks
Monitor drainage, should be bile colored
Less than 1000ml/day
Never irrigate, aspirate or clamp a T-tube without an MD order

40. Disorders of the Liver
Largest organ in the body and is located in the RUQ
Large right lobe and smaller left lobe
Made up of lobules
Bile is made in hepatocytes, secreted into bile canaliculi
Receives 1500 ml of blood/min

41. Liver Functions 400 functions Storage: Protective: Metabolism:
What types of vitamins and minerals?
Protective:
Kupfer cells, phagocytic, destroy bacteria, anemic RBC’s
Detoxifies what?
Metabolism:
Makes proteins, for what?
Breaks down amino acids to remove ammonia, converted to what?
Synthesizes plasma proteins, albumin, prothrombin and fibrinogen
Stores and releases glycogen
Breaks down and stores fatty acids and triglycerides
Forms and secretes what substance?

42. Liver Disorders
Cirrhosis/ Liver Failure
Hepatitis

43. Case Study
53 year old male admitted to the ED with abdominal pain, nausea and vomiting, weight loss. His abdomen is large and tender. His skin is light yellow. He has a fruity odor to his breath.
What do you suspect?

44. Case Study What lab work should be done?
What interventions would you perform and why?
Your patient becomes belligerent after a few hours and wants to leave, what would you do?
What radiology studies may be done?

45. Case Study
His liver enzymes are extremely elevated and he is becoming confused. He is admitted to the floor.
What symptoms are you likely to see in this patient?
He starts to vomit blood, what does this mean and what may be done?
What medications may be given to this patient?

46. Case Study He has improved and is now ready for discharge.
What kind of teaching would this patient need?
What should be done about rehab?

47. Cirrhosis
Scarring of the liver, caused by a chronic, irreversible reaction to hepatic inflammation and necrosis
Causes:
#1 cause?
#2 cause?
Destruction of hepatocytes, tissue becomes nodular, block bile ducts and blood flow from fibrous connective tissue
Liver begins enlarged and then shrinks

48. Cirrhosis

49. Complications Compensated and Decompensated Cirrhosis Liver failure 
Portal hypertension, what is this?
Ascites, why?
Bleeding esophageal varices
Coagulation defects, why?
Jaundice, what causes this?
Portal systemic encephalopathy and coma
Hepatorenal syndrome
Bacterial peritonitis

50. Liver Dysfunction PSE Esophageal Varices Jaundice Bleeding
Hepatorenal Syndrome
Bacterial Peritonitis
Ascites

51. Portal Hypertension Increase in pressure within the portal vein
Increased resistance or blockage in the flow of blood through the portal vein
Seeks collateral circulation
Blood flows back into the spleen, causing splenomegaly
What veins become dilated?
Can lead to esphageal varices, caput medusa (what is that??) and hemorroids

52. Ascites Accumulation of free fluid within the peritoneal cavity
Increased hydrostatic pressure from the portal hypertension causes fluid to leak into cavity
Albumin accumulates in peritoneal fluid and this reduces the circulating proteins, this decreases serum colloid osmotic pressure and can lead to a decrease in what?
Decrease in intravascular circulation causes renal vasoconstriction, triggers the renin-angiotensin system. This causes Na and water retention, which does what to fluid hydrostatic pressure and fluid volume?, where does the fluid accumulate?

53. Ascites

54. Bleeding esophageal varices
Blood backs up from liver into esophageal and gastric vessels
Increased pressure, causes esophageal vessels to become fragile and distended
Life threatening emergency, significant blood loss and this can lead to what?
Bleeding is manifested as hematemesis and melena, what does that mean?
Any activity that increases abdominal pressure can lead to bleeding, such as what?
Also, then to have portal hypertensive gastropathy, this leads to slow GI bleeds and cause chronic anemia

55. Coagulation defects
Decrease in the synthesis of bile, this prevents the absorption of fat-soluble vitamins and clotting factors are not produced
What fat soluble vitamin is predominant in clotting?
What lab values would be abnormal?
Splenomegaly results from the backup of blood, this destroys platelets and leads to thrombocytopenia, one of earliest signs of liver dysfunction

56. Jaundice
Hepatocellular disease and intrahepatic obstruction are the cause
Liver cells can not excrete bilirubin, what are the liver cells called?
Excessive circulating bilirubin
Obstruction jaundice is from edema, fibrosis and scarring that block bile ducts
Excess bilirubin causes the skin to become yellow gold, sclera are yellow and skin is pruritic and “frosty”

57. Portal system encephalopathy
PSE or hepatic coma in later stages
Altered level of consciousness, impaired thinking and neuromuscular disorders
Can reverse the encephalopathy with early intervention
Liver is unable to detoxify substances and ammonia is most common cause
Some encephalopathy may occur without elevated ammonia, may be other toxins

58. Portal systemic encephalopathy
Factors that may precipitate:
High-protein diet
Infections
Hypovolemia
Hypokalemia
Constipation
GI bleeding, large protein load in intestines
Drugs, such as hypnotics, opioids, sedatives, analgesics and diuretics
Paracentesis or shunting of veins may also cause
Why does protein increase encephalopathy??

59. Stages of encephalopathy
Prodromal
Personality changes, agitation, emotional lability, impaired thinking, fatigue, slurred speech, inability to concentrate
Impending
Mental confusion, disoriented to person, place and time, asterixis (liver flap) how do you test for this?
Stuporous
Drowsy, but arousable, muscle twitching, hyperreflexia, abnormal EEG
Comatose
Unresponsive, 85% lead to death, obtunded, response to pain, no asterixis, positive babinski, muscle rigidity, fetor hepaticus, seizures, why seizures?

60. Hepatorenal syndrome Often cause of death
Sudden decrease in urinary flow
Elevated BUN and Creatinine levels and decreased urine sodium excretion
Increased urine osmolarity, what is that?
Why is there a decrease in fluid volume to the kidneys?

61. Bacterial Peritonitis
Occurs spontaneously
Low concentrations of what type of proteins, that protect against bacteria, cause this?
Bacteria are from the bowel and reach the ascitic fluid when they are pulled through the bowel wall, what type of pressure would cause this?
Symptoms are: fever, chills, abdominal pain and tenderness
Diagnosis is made by culture of ascitic fluid and leukocyte count

62. Causes of Cirrhosis
Alcoholic hepatitis- if alcohol intake is stopped, liver damage will reverse, if not, cellular necrosis continues. It may take years to develop
Viral Hepatitis- C is most common, but B may also affect. It causes inflammation and cell damage
Autoimmune hepatitis- autoantibodies
Steatohepatitis- “fatty liver” fat and cholesterol deposits occur over time, cause is obesity and elevated lipids
Drugs and toxins- medications, such as illegal drug use, chemotherapy, tylenol !
Biliary disease- primary biliary cirrhosis and primary sclerosing cholangitis
Metabolic- hematochromatosis, what is that?, Alpha-antitrypsin deficiency and cystic fibrosis, why?

63. Cirrhosis Patient

64. Physical Manifestations
Fatigue
Change in wt
GI symptoms
Abdominal pain and tenderness
Pruritis
Jaundice and icterus (what’s that?)
Dry skin and rashes
Petechiae and ecchymosis, why?
Vascular lesions, “spider angiomas” on nose, checks, shoulders
Dependent edema

65. Physical manifestations
Ascites, can lead to disruption in what major function?
Tested by fluid wave, what is that?
How do you test for hepatomegaly?
Why would you measure abdominal girth?
Melena and fetor hepaticus may also be present, what does this mean?
Amenorrhea, testicular atrophy and gynecomastia may also occur because of inactive hormones that are normally made in the liver

66. Fluid Wave

67. Lab tests Decreased values are: Elevated values are: AST
ALT
LDH
Alkaline phosphatase
Bilirubin in serum and urine
Total protein
Serum globulin (immune response to liver disease)
Ammonia
Prothrombin time
Decreased values are:
Fecal urobilinogen
Total protein (in chronic disease)
Serum albumin

68. Other assessments CT scan, Ultrasound of liver
Liver Biopsy, how is this done and what precautions should be taken?
EGD- what does this mean and why would this be done, what are they looking for?

69. Liver Biopsy

70. Nursing Diagnoses
#1 is related to fluid volume, would it be excess or deficit fluid volume, what is it related to?
What are two potential problems?
What collaborative problems are these patients at risk for? (there are at least 7 or 8)

71. Nursing Management of Excess Fluid Volume
Diet Therapy
Low Na diet, 500 to 2 gm/day
IV and oral fluid is restricted to L/day
Vitamin supplements, thiamine, folate may be needed
Drug Therapy
Diuretics, what are some?
What should you monitor for?
What electrolyte is affected by diuretics?
Antibiotics to prevent bacterial peritonitis

72. Management of Excess Fluid Volume
Paracentesis
MD inserts a catheter into the abdomen to remove and drain ascitic fluid
Should void first, HOB is elevated
Should monitor vital signs and drain slowly, why?
Cultures may be sent
What blood product may be given prior to removing ascites fluid?

73. Paracentesis

74. Other measures Comfort: Keep HOB elevated, use creams for pruritis
Monitor lung sounds and give O2 if needed
Monitor fluid and electrolyte levels
Surgical:
Peritoneovenous shunt- catheter and one way valve to let fluid flow from abdomen to superior vena cava, can have clots and infection
Portacaval shunt- diverts blood from the liver to the kidney or inferior vena cava
TIPS- transjugular intrahepatic portal-systemic shunt, track is made between the portal vein, hepatic veins and systemic circulation. The shunts are kept open with stents that are inserted and this increases the systemic circulation and decreases the portal hypertension

75. Peritoneal-venous Shunt

76. TIPS

77. Nursing Outcomes for Excess Fluid Volume
Name 8 desired nursing outcomes for a patient with excess fluid volume 1. 2. 3. 4. 5. 6. 7. 8.

78. Potential for Hemorrhage
Goal is to prevent bleeding
Drug therapy is to control HR and BP, this decreases the hepatic venous pressure gradient, may use a Beta Blocker to do both and keep the HR about 55/min
Gastric Intubation- NGT with iced saline or water lavage to vasoconstrict ulcerations
device.

79. Potential for Hemorrhage
Balloon Tamponade- esophagogastric- Blakemore tube- it has 2 balloons, an esophageal and gastric, one balloon in esophagus to compress varices, one larger in stomach to anchor tube, and another lumen for suctioning. Inserted through the mouth, once in place, balloons are inflated and clamped. Traction may be performed by anchoring it to a helmet

80. Potential for Hemorrhage
Complications of the Blakemore tube are aspiration, the balloons may decompress and become lodged in the back of the pharynx. Blood and gastric contents may also be aspirated. The stomach balloon should always be deflated first and then the esophageal.
Blood transfusions may be needed and emergently, PRBC’s and FFP

81. Potential for Hemorrhage
Endoscopic- Band Ligation- small “O” bands are placed around the base of the varices, octreotide may be given at the time to decrease bleeding and secretions. Injection sclerotherapy may also be done to stop bleeding, a sclerosing agent is injected via endoscopy
TIPS procedure or portal-systemic shunts may be needed
What lab work should be monitored for these patients?

82. Banded esophageal Varices

83. Blakemore Tube

84. Portal Systemic Encephalopathy
Ammonia is the probably cause, toxic to the brain
Drug Therapy- Lactulose- high molecular wt disaccharide, it is thick and sticky with a sweet taste. It cleanses the GI tract and decreases the bacterial content, also creates and acid environment in the bowel and decreases the acid from 7-5, this keeps ammonia as an ion and pulls it into the colon. It may be given po or enema. Po is 20-30g q 4 hour. Monitor the number of stools and ammonia levels. It may cause cramping and often patients do not want to take it.

85. Portal-Systemic Encephalopathy
Drug Therapy- Neomycin may also be used to cleanse the bowel and decrease protein breakdown, it can be given po or enema. Metronidazole (Flagyl) is also a bowel antibiotic with less renal side-effects
Monitor the patient for neurologic changes, look for stupor, asterixis and fetor hepaticus
Maintain patient safety

86. Patient Education
Patient teaching should revolve around three main areas, what should be discussed under each?
1. Diet Therapy
2. Drug Therapy
3. Alcohol Abstinence
Goal is to have a decrease in ascites, electrolytes WNL and no bleeding or PSE

87. Hepatitis
Viral infection, can be acute or chronic, caused by one of five viruses, A-E, hepatitis F and G have been identified too
Leads to inflammation of the liver cells
Can also be caused by exposure to chemicals, toxins and medications
Can be secondary to infections from Epstein-Barr, herpes, varicella and cytomegalovirus

88. Hepatitis

90. Types of Hepatitis Hepatitis A HAV is an RNA virus
Spread fecal-oral, contaminated water, shellfish and food contaminated by food handlers
Incubation is days
Often the disease is mild and people don’t know that they have it
Can lead to more severe liver disease in compromised people

91. Types of Hepatitis Hepatitis B
HBV, it is a particle of DNA that is surrounded by a core and surface antigen
Spread by:
Unprotected sex
Sharing needles or needle sticks
Blood transfusions, hemodialysis
Maternal-fetal route
Symptoms occur in days. They are:
Anorexia, nausea, vomiting, fever, fatigue, RUQ pain, dark urine and light stool, joint pain and jaundice
Can lead to cirrhosis and liver failure
Often develop immunity and can become carriers

92. Hepatitis C HCV is a single strand RNA virus
Transmitted blood to blood
Spread by:
IV drug needle sharing
Blood, blood products or transplants
Needle stick injury with contaminated blood
Tattoos and intranasal cocaine
Not transmitted by casual contact
Should not share razors, toothbrushes or pierced earrings
Incubation is days, average 7 weeks
Most don’t know they are infected until it becomes chronic
Scarring leads to cirrhosis, can lead to liver cancer
Many receive liver transplants

93. Hepatitis D
HDV is a defective RNA virus that needs helper function of HBV
Coinfects and needs HBV for replication
Can be a superinfection and lead to a chronic infection
Incubation is days
Spread is mostly IV blood transmission

94. Hepatitis E HEV, single strand RNA virus
Transmitted by fecal-oral route, similar to HAV
Waterborne epidemic in India, now in Asia, Africa, Middle East, Mexico and Central & South America
Incubation of days

95. Incidence 250,000 people in the US develop HAV
200 million worldwide have HCV
3.9 million have HCV in the US and 3 million have chronic liver disease
Chronic hepatitis is through to be inflammation of the liver for > 6 months
Usually the result of HCV or HBV
Can lead to fulminant liver failure, which is life-threatening, due to total failure of the organ

96. Prevention
What things can you tell a client to prevent the spread of hepatitis? (for both HAV and HBV/HCV)
Which viruses have vaccines?
If exposed to the virus, is there anything that can be taken?

97. Patient assessment Assess for: Liver Biopsy- confirmatory Labs:
Abdominal pain
Jaundice
Arthralgia
Myalgia, why?
Diarrhea
Changes in stool and urine color
Fever, lethargy
Nausea/vomiting
History of contamination
Liver Biopsy- confirmatory
Labs:
Liver enzymes- AST, ALT, alk phos, bilirubin all elevated
Enzyme assays- antibodies to virus, anti-HAV, HBsAG (HBV surface antigen), anti HBcIgM (core antigen)
Elisa for HCV and antiHCV
Anti-HDV and HEV
Usually present within 6 months

98. Nursing Diagnoses
What do you think are the most common nursing diagnoses for Hepatitis? 1. 2. 3.
What interventions would be appropriate?

99. Nursing Interventions
Drug Therapy
Use medications sparingly to rest liver
Antivirals, such as lamivudine (epivir-HBV) or Hepsera
Interferon for HCV and HBV, SQ with ribavirin, take the combination for weeks until negative HCV RNA level

100. Home Care Education
What type of home care education would be appropriate?
Discuss disease with family, especially spread
Discuss community resources, chronic, long term disease
Good handwashing, prevent spread of blood
Measures to prevent the spread of infection to the patient
Avoid alcohol
Allow for rest periods

101. Liver Transplantation
Assess patient both physically and psychologically prior to transplantation
Contraindicated if:
Severe cardiovascular or respiratory disease
Active alcohol or drug use
Metastatic disease
Inability to follow treatment or lack of appropriate caregiver
Most transplants are cadaver livers, but some are donors of single lobes. Usually done with children
Livers are obtained through the UNOS, United Network of Organ Sharing in cooperation with OPO, organ procurement organizations. In Jacksonville, we use Lifequest. There are presently 2300 people waiting for organ transplants within our area.

102. Liver Transplantation
Most common complications are graft rejection and infection
Rejection can occur quickly or years out.
Medications to prevent rejection are:
Cell-cept, Prograf, Imuran, Sirolimus, prednisone and FK-506
Signs of rejection are RUQ pain, fever, tachycardia, decreased bile production and increased jaundice, elevated liver enzymes

103. Liver Transplantation
Infection
Immunosuppressive therapy can cause rejection, plus they are very debilitated, immobile and have multiple lines
Cytomegalovirus, mycobacterial and parasitic infections are most common
Usually on many antibiotics
Other complications:
Hemorrhage, hepatic artery thrombosis, pulmonary atelectasis, electrolyte imbalances- usually Ca, Mg and K, ARF

104. Nursing Care
Usually these patients are very ill, they may be in the ICU for many days, some are “fast-tracked”
Return intubated, with a Swan line, arterial line and have continuous cardiac outputs and SvO2 readings.
Some are on CVVH (continuous veno-venous hemofiltration) for renal perfusion
Need a lot of psychological support

105. Liver transplantation

106. UNOS

107. Liver transplant video
transplant surgery