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DIABETES MELLITUS

A chronic multisystem disease related to abnormal insulin production,


impaired insulin utilization, or both.
Leading cause of:
o End-stage renal disease
o Adult blindness
o Nontraumatic lower limb amputation
Major contributing factor
o Heart disease
o Stroke
Etiology/Pathophysiology
o Theories link causes to single/combination of these factors:
Genetic, autoimmune, viral, environmental
o Two most common types: Type 1 & Type 2
Other types: gestational, prediabetes, secondary diabetes
o Regardless of its cause, diabetes is primarily a disorder of glucose
metabolism related to absent or insufficient insulin supply and/or
poor utilization of available insulin.
Normal insulin metabolism:
Produced by beta cells (Islets of Langerhans)
The insulin is continuously released into the
bloodstream in small increments with larger amounts
released after food.
Stabilizes glucose range to 70-120 mg/dL
Insulin
Promotes glucose transport from the bloodstream
across cell membrane to the cytoplasm of a cell.
o Decreases glucose in the bloodstream.
Insulin increases in the body after a meal
o Stimulates storage of glucose as glycogen in
liver and muscle.
o Inhibits gluconeogenesis
o Enhances fat deposition
o Increases protein synthesis
The fall in insulin level during normal overnight fasting
facilitates the release of stored glucose from the liver,
protein from muscle, and fat from adipose tissue.


o Counterregulatory Hormones
Oppose effects of insulin
Increases blood glucose levels
Provide regulated release of glucose for energy
Help maintain normal blood glucose levels
Ex. Glucagon, epinephrine, growth hormone, cortisol
Abnormal production of any or all of these hormones
may be present in diabetes
o Skeletal muscle and adipose tissue- insulin-dependent tissues
o Other tissues (brain, liver, blood cells)- do not directly depend on
insulin for glucose transport.
Although liver cells are not considered insulin-dependent
tissue, insulin receptor sites of the liver facilitate the hepatic
uptake of glucose and its conversion to glycogen.

ALTERED
MECHANISMS
IN TYPE I & II
DIABETES


Formerly known as juvenile-onset or insulin-dependent diabetes.
Most often occurs in people younger than 40 years of age.
o Occurs more frequently in younger children.
o 40% of those with Type I-onset before age of 20.
Incidence has increased by 3% to 5% over recent decades.
o As a person grows older the Beta Cells take longer to respond; and
this is why the incidence has become increased, as a person gets
older.
Accounts for 5-10% of all people with diabetes.
Etiology and Pathophysiology-
o End result of long-standing process
Progressive destruction of pancreatic beta cells by the
bodys own T cells.
Auto antibodies cause a reduction of 80-90% in normal beta
cell functioning before manifestations occur.
o Causes:
Genetic predisposition
Related to human leukocyte antigens (HLAs)
Exposure to a virus
Idiopathic diabetes is a form of type 1 diabetes that is not
related to autoimmunity but is strongly inherited. This occurs
only in a small number of people with type 1 diabetes, and is
most often in those of African or Asian ancestry.
















RENAL FAILURE
Chronic Kidney Disease (CKD)
o Involves progressive, irreversible loss of kidney function
o Definition: The presence of:
Kidney damage
Pathologic abnormalities
Markers of damage (blood, urine,
imaging tests)
Glomerular filtration rate (GFR)
<60 mL/min for 3 months or longer
Disease staging based on decreased
in GFR
o Normal GFR 125 mL/min, which
is reflected by urine creatinine clearance
o Last stage of kidney failure
End-stage renal disease (ESRD)
occurs when GFR <15mL/min
o Up to 80% of GFR may be lost with few changes in
functioning of body.
o Remaining nephrons hypertrophy to compensate.
o End result is a systemic disease involving every organ.
o Because the kidneys are highly adaptive, kidney diseases
often are not recognized until considerable loss of
nephrons has occurred.
Because patients with CKD are frequently
asymptomatic, it has been estimated that about
70% of people with CKD are unaware that they
have the disease
o Each year, 70,000 people die from causes related to renal
failure.
o More than 26 million Americans have CKD.
o Mortality rates are 19% to 24% for those with stage 5
CKD on dialysis.
o Leading causes of ESRD: Diabetes & Hypertension
Diabetes about of cases and hypertension about
1/3 of cases.


Lewis Ch 47
1172-1197
Grodner Ch 21
Ch 47 study
guide
ATI ch 68




Clinical Manifestations
o Result of retained substances
Urea
Creatinine
Phenois
Hormones
Electrolytes
Water
Other substances
o Uremia
Syndrome that incorporates all signs and symptoms
seen in various systems throughout the body






o Urinary System
Polyuria
Results from inability of kidneys to
concentrate urine
Occurs most often at night
Specific gravity fixed around 1.0.10
Oliguria
Occurs as CKD worsens
Anuria
Urine output <40 mL per 24 hours
o Metabolic Disturbances
Waste product accumulation
As GFR , BUN and serum creatinine levels

o BUN
Not only by kidney failure but by
protein intake, fever,
corticosteroids, and catabolism
N/V, lethargy, fatigue, impaired
thought processes, and headache
may occur
Altered carbohydrate metabolism
Caused by impaired glucose use
o From cellular insensitivity to the normal
action of insulin
Defective carbohydrate metabolism
Pts with diabetes who become uremic may
require less insulin than before the onset of
CKD.
Insulin dependent on kidneys for excretion
Serum creatinine and creatinine clearance
determinations (calculated glomerular filtration rate)
are considered more accurate indicators of kidney
function than BUN or creatinine.
Efforts are made to initiate renal replacement
therapy before a patient becomes severely
symptomatic.
Elevated Triglycerides
Hyperinsulinemia stimulates hepatic
production of triglycerides.
o Elevated glucose levels lead to
increased insulin levels, and insulin
stimulates hepatic production of
triglycerides.
Altered lipid metabolism
o levels of enzyme lipoprotein lipase
Important in breakdown of
lipoproteins
Almost all patients with uremia develop
dyslipidemia, with elevated very-low-density
lipoproteins (VLDLs), normal or decreased low-
density lipoproteins (LDLs), and decreased high-
density lipoproteins (HDLs).
Most pts with CKD die from cardiovascular disease.
o Electrolyte/Acid-Base Imbalances
Potassium
Hyperkalemia
o Most serious electrolyte disorder in
kidney disease
o Fatal dysrhythmias
Fatal dysrhythmias can occur
when the serum potassium level
reaches 7 to 8 mEq/L (7 to 8
mmol/L).
Hyperkalemia results from
decreased excretion of potassium
by the kidneys, breakdown of
cellular protein, bleeding, and
metabolic acidosis.
Potassium may come from the
food consumed, dietary
supplements, drugs, and IV
infusions.
Sodium
May be normal or low
Because of impaired excretion, sodium
retained
o Water is retained
Edema
Hypertension
CHF
Calcium and Phosphate alterations
Magnesium alterations
Hypermagnesemia generally is not a problem
unless the patient is ingesting magnesium
(e.g., milk of magnesia, magnesium citrate,
antacids containing magnesium).
Clinical manifestations of hypermagnesemia:
o can include absence of reflexes,
decreased mentalstatus, cardiac
dysrhythmias, hypotension, and
respiratory failure.
Metabolic acidosis
Results from:
o Inability of kidneys to excrete acid load
(primary ammonia)
o Defective reabsorption/regeneration of
bicarbonate
o Hematologic System
Anemia
Due to production of erythropoietin
o From in functioning renal tubular cells
Other factors contributing to anemia:
o nutritional deficiencies, decreased RBC
life span, increased hemolysis of RBCs,
frequent blood samplings, and bleeding
from the GI tract.
Bleeding tendencies
Defect in platelet function
Defects in platelet function are caused by
impaired platelet aggregation and impaired
release of platelet factor III.
Infection
Changes in leukocyte function
Altered immune response and function
Diminished inflammatory response
o Cardiovascular System
Hypertension
Heart failure
Left ventricular hypertrophy
Peripheral edema
Dysrhythmias
Uremic pericarditis
The most common cause of death in patients with
CKD is cardiovascular disease. Even a slight
reduction in GFR has been associated with a
greater risk for development of coronary artery
disease.
Traditional CV risk factors such as hypertension and
elevated lipids are common in patients with CKD.
However, much of the CV disease may be related to
nontraditional CV risk factors such as vascular
calcification and arterial stiffness.
o Respiratory System
Kussmaul respiration
Dyspnea
Pulmonary edema
Uremic pleuritis
Pleural effusion
Predisposition to respiratory infection
o Gastrointestinal System
Every part of the GI is affected
Due to excessive urea
o Mucosal ulcerations
o Stomatitis
Found with exudates and
ulcerations
A metallic taste in the mouth
o Uremic fetor (urinous odor of breath)
o GI bleeding
o Anorexia, nausea, vomiting
May develop if CKD progresses to
ESRD and is not treated with
dialysis.

o Neurologic System
Expected as renal failure progresses.
Attributed to:
nitrogenous waste products
Electrolyte imbalance
Metabolic acidosis
Axonal atrophy
Demyelination of nerve fibers
Restless leg syndrome
Muscle twitching
Irritability
Decreased ability to concentrate
Peripheral neuropathy
Altered mental ability
Seizures
Coma
Dialysis encephalopathy
The treatment for neurologic problems is dialysis or
transplantation. Altered mental status is often the
signal that dialysis must be initiated.
Dialysis should improve general CNS symptoms
and may slow or halt the progression of
neuropathies.
o Musculoskeletal System
CKD mineral and bone disorder
Systemic disorder of mineral and bone
metabolism
Results in skeletal complications
o (osteomalacia, ostetis fibrosa) and
extraskeletal (vascular) calcifications
o Integumentary System
Pruritus
Cause is multifactorial
Includes dry skin, calcium-phosphate
deposition in skin, and sensory neuropathy
The itching may be so intense that it can lead
to bleeding or infection secondary to
scratching
Uremic frost
Rare
o Reproductive System
Infertility
Both sexes
Decreased libido
Low Sperm Counts
Sexual dysfunction
o Psychologic Changes
Personality and behavioral changes
Emotional ability
Withdrawal
Depression
Changes in body image caused by edema,
integumentary disturbances, and access devices
(e.g., fistulae, catheters) may contribute to the
development of anxiety and depression.
Diagnostic Studies
o History and physical examination
o Dipstick evaluation
o Albumin-creatinine ratio (first morning void)
o GFR
o Renal ultrasound
o Renal scan
o CT scan
o Renal biopsy
o A person with persistent proteinuria (1+ protein on
standard dipstick testing two or more times over a 3-
month period) should have further assessment of risk
factors and a diagnostic workup with blood and urine
tests.
o The two equations used most frequently to estimate GFR
are the Cockcroft-Gault formula and the Modification of
Diet in Renal Disease (MDRD) Study equation (see Table
47-8).
Collaborative Therapy
Correction of extracellular fluid volume overload or
deficit
Nutritional therapy
Erythropoietin therapy
Calcium supplementation, phosphate binders
Antihypertensive therapy
Measures to lower potassium
Adjustment of drug dosages to degree of renal
function.
o Drug Therapy
Hyperkalemia
IV insulin
o IV glucose to manage hypoglycemia
IV 10% calcium gluconate
Sodium polystyrene sulfonate (Kayexalate)
o Cation-exchange resin
o Resin in bowel exchanges potassium for
sodium.
Hypertension
Weight loss
Lifestyle changes
Diet recommendations
Sodium and fluid restrictions
Antihypertensive drugs
o Diuretics
o Calcium channel blockers
o ACE inhibitors
o ARB agents
It is recommended that the target BP should
be <130/80 mm Hg for patients with CKD and
125/75 for patients with significant proteinuria.
The BP should be measured periodically in
supine, sitting, and standing positions to
effectively monitor the effects of
antihypertensive drugs.
CKD-MBD
Phosphate intake restricted to <1000 mg/day
Phosphate binders
o Should be administered with each meal
o Side effect: constipation
o Calcium carbonate (caltrate)
Binds phosphate in bowel and
excretes
o Sevelamer hydrochloride (Renagel)
Lowers cholesterol and LDLs
Interventions for CKD mineral and bone
disorder include limiting dietary phosphorus,
administering phosphate binders,
supplementing vitamin D, and controlling
hyperparathyroidism.
Supplementing Vitamin D
o Calcitriol (Rocaltrol)
o Serum phosphate level must be lowered
before calcium or vitamin D is
administered.
Controlling secondary hyperparathyroidism
o Calcimimetic agents
Cinacalcet (Sensipar)
sensitivity of calcium
receptors in parathyroid
glands
o Subtotal parathyroidectomy
Anemia
o Erythropoietin
Epoetin alfa (Epogen, Procrit)
Administered IV or
subcutaneously
Increased hemoglobin and
hematocrit in 2 to 3 weeks
Side effect: Hypertension
o Iron Supplements
If plasma ferritin <100 ng/mL
Side effects: gastric irritation,
constipation
May make stool look dark in color
Another side effect of EPO
therapy is the development of iron
deficiency resulting from increased
demand for iron to support
erythropoiesis.
Orally administered iron should
not be taken at the same time as
phosphate binders because
calcium binds the iron, preventing
its absorption.
o Folic Acid Supplements
Needed for RBC formation
Removed by dialysis
o *Avoid blood transfusions
Dyslipidemia
Goal:
o Lowering LDL below 100 mg/dL
o Triglyceride level below 200 mg/dL
Statins
o MHG-CoA reductase inhibitors
Most effective for lowering LDL
Evidence supports the use of statins in patients with
CKD (especially diabetics) not yet on dialysis. The
effectiveness of statins in patients on dialysis is still
being studied.
Fibrates (fibric acid derivatives)
such as gemfibrozil (Lopid)
are used to lower triglyceride levels and can
also increase HDLs.
o Complications of Drug Therapy
Drug toxicity
Digitalis
Antibiotics
Pain medications (Demerol, NSAIDS)
o Nutritional Therapy
Protein restriction (benefits are being studied)
Water restriction (intake depends on daily urine
output)
Calorie-protein malnutrition
A potential and serious problem that results
from altered metabolism, anemia, proteinuria,
anorexia, and nausea.
Additional factors leading to malnutrition
include depression and complex diets that
restrict protein, phosphorus, potassium, and
sodium.
For the patient who is undergoing dialysis, protein is
not routinely restricted.
Although some evidence suggests that protein
restriction has benefits, many patients find these
diets difficult to adhere to.
For CKD stages 1 through 4, many clinicians just
encourage a diet with normal protein intake.
Generally, 600 mL (from insensible loss) plus an
amount equal to the previous days urine output is
allowed for a patient receiving hemodialysis.
Sodium restriction
Diets vary from 2 to 4 g, depending on the
degree of edema and hypertension
Sodium and salt should not be equated.
Salt substitutes should not be used because
they contain potassium chloride.
Instruct the patient to avoid high-sodium foods
such as cured meats, pickled foods, canned
soups and stews, frankfurters, cold cuts, soy
sauce, and salad dressings.
Potassium restriction
2 to 3 g
High potassium foods should be avoided.
o Foods with high potassium content that
should be avoided include oranges,
bananas, melons, tomatoes, prunes,
raisins, deep green and yellow
vegetables, beans, and legumes.
Phosphate therapy
1000 mg/day
Foods high in phosphate (dairy products)
Most foods high in phosphate are also high in
protein.
Nursing Management:
o Nursing Assessment/Diagnosis
o Complete hx or any existing renal disease, family history
o Long-term health problems
o Dietary habits
o Excess fluid volume
o Risk for injury
o Imbalanced nutrition: Less than body requirements
o Grieving
o Risk for infection
o Because many drugs are potentially nephrotoxic, the
nurse should ask the patient about both current and past
use of prescription and over-the-counter drugs and herbal
preparations.
o Medications of concern:
Antacids, NSAIDs, decongestants, and
antihistamines.
o Planning/Implementation
o Overall goals:
Demonstrate knowledge and ability to comply wth
therapeutic regimen.
Participate in decision making
Demonstrate effective coping strategies
Continue with ADLs within psychologic limitations
o Health Promotion
ID individuals at risk for CKD
History of renal disease
Hypertension
Diabetes Mellitus
Repeated UTI
Regular checkups and changes in urinary
appearance, frequency, and volume should be
reported
o Nursing Implementation
o Acute Intervention
Daily weight
Daily BPs
ID s/s of fluid overload
ID s/s of hyperkalemia
Strict dietary adherence
Medication education
Motivate patients in management of their diseases
o Ambulatory & Home Care
When conservative therapy is no longer effective,
HD, PD, and transplantation are treatment options
Patient/family need clear expectation of dialysis and
transplantation.
o Evaluation
Maintenance of ideal body weight
Acceptance of chronic disease
No infection
No edema
Hematocrit, hemoglobin, and serum albumin levels
in acceptable range
Dialysis
o Half of patients with CRF eventually will require dialysis
o Diffuse harmful waste out of body
o Controls BP
o Keeps safe levels of chemicals in the body
o Two types:
Hemodialysis
3-4 times a week
Takes 2-4 hours
Machine filters blood and returns it to the
body.
Types of Access:
o Temporary site: Perm cath- THIS IS
THEIR LIFELINE..DO NOT ACCESS IT!

o AV fistula
Surgeon constructs by combining
an artery and a vein
3-6 months to mature
o AV graft
Man-made tube inserted by a
surgeon to connect artery and vein
2-6 weeks to mature


What this means for ME as a NURSE
Cannot take BP on the same arm as the
fistula
Protect the arm from injury
Control obvious hemorrhage
o Bleeding will be arterial
o Maintain direct pressure
No IV on same arm as fistula
A thrill will be felt-this is normal
Check for bruit every shift
Access Problems:
o AV graft thrombosis
o AV fistula or graft bleeding
o AV graft infection
o Steal phenomenon
Early post-op
Ischemic distally
Apply a small amount of pressure
to reverse symptoms
Peritoneal dialysis


Abdominal lining filters the blood
3 Types:
o Continuous ambulatory
o Continous cyclical
o Intermittent
Considerations:
o Make sure the dressing remains intact
o Do not push or pull on the catheter
o Do not disconnect any of the catheters
o Always transport the patient and
bags/catheters as one piece
o Never inject anything into the catheter






LIVER FAILURE

Functions of the liver:
1. Bile Formation
2. Drug and Hormone Metabolism
3. Carb metabolism
4. Protein synthesis (includes proteins important for blood coagulation)
5. Detoxification of Noxious Substances
6. Phagocytosis by means of Kupfer Cells

Medications
Lactulose
o Acidifies intestine so ammonia can be converted into a form that
can be eliminated via bowel movements.
Rifaximin
o Antibiotic therapy that reduces bacterial action on the protein in
the gut
Decreases ammonia production
Vitamin K
o Given parenterally to lower Prothrombin time (PT)
Hepato-toxic Drugs
Monitor Acetaminophen use
o Total daily dose: 4 gm/day is normal
o Individuals with liver impairment- 2 gm/day
OTC drugs
o Many have Tylenol especially cold medications
Narcotic pain medications
o Percocet or Roxicet: Oxycodone with Tylenol (350-500 mg)
o Vicodin or Lortab or Lorcet: Hydrocodone with Tylenol (500-750
mg)
Drugs for Agitation
Oxazepam (Serax)
o Benzodiazepine/antianxiety
o Not metabolized by liver
o Maybe used to treat acute agitation and alcohol withdrawal
o Dose: 15-30 mg tid-qid
o Watch for hypotension
Forces Causing Ascites
1. Portal HTN
a. Increases hydrostatic pressure (Forces that push fluid out of the
blood vessels)
2. Congested lymph channels leak protein abdomen
a. Decreases colloidal osmotic pressure (Pressure that keeps fluid in
the veins)
3. Damaged liver cant make albumin (60-70% COP)
a. Decreases colloidal osmotic pressure
Kidneys Response to Fluid Shifts
As ascites continues, decreased vascular volume causes kidneys to secrete
more aldosterone
o Retention of sodium and water
Damaged liver cant inactivate aldosterone (Hyperaldosteronism)
Paracentesis
Nursing care pre-procedure
o Weight patient
o Take VS
o Measure abdominal girth
o Have pt empty bladder
o Place sitting in upright position
o Assemble needed equipment
During Procedure
o Monitor VS especially RR & effort
o Reassure pt throughout procedure
Post Procedure
o Monitor VS, especially BP & Respiratory effort
o Monitor for bleeding or excessive drainage from the puncture site
o Send specimens to the lab (if ordered)
o Change dressing as needed
o Monitor for infection
Diet Therapy
1. Protein restriction
a. 20-40 gm/day
b. Increase by 10 gm/day when appropriate
2. Sodium restriction
a. 2 gm/day
3. Possible fluid restriction
Skin care for Jaundice
Can cause pruritis
o Comfort measures such as:
Keeping the air temp cool (68-70 degrees F)
Humidity of air at 30-40 percent
Avoid hot showers
Use emollient lotion
Neuro Impairments
Alcoholic polyneuropathy
Asterixis
Wernike-Korsakoff syndrome
o Wernike component: physical changes
o Korsakoff: mental changes
Nursing Care:
o Safety measures at all times
o ABCs especially with ascities and
possible GI bleeding
o Aspiration precautions
HOB up 30 degrees
o Dont give sedatives for agitated or
delirious behavior
o Monitor closely for minor changes in
orientation to avoid hepatic coma
Role of Aldosterone
Spironolactone
o K+ sparing diuretic
o Antagonizes aldosterone- body holds onto K+ and gets rid of
Na+
Portal Hypertension
Anything that interferes or obstructs portal circulation
Collateral circulation forms to go around obstruction
Other blood vessels dilate
Variceal Hemorrhage
Emergent care:
1. Protect airway

a. Prevent aspiration
b. Turn patient to one side
c. High Fowlers position
d. Yankauer suction catheter readily available
2. Provide hemodynamic support
a. Blood transfusions to maintain Hgb 8g/dl or Hct 24-
30%
3. Treat coagulopathy
a. Fresh frozen plasma
b. Possible parenteral vitamin K (necessary for
coagulation)
4. Reduce portal pressure
a. Octreotide (Sandostatin)
i. Given IV
ii. Indirecty causes vaconstriction of the viscera
iii. Decreases hepatic blood flow
iv. Decreases portal vein pressure
b. Vasopressin (Pitressin)
i. Given IV
ii. *Extremely potent
iii. Constricts mesenteric arterioles
iv. Decreases portal flow
1. Lowers portal pressure
2. Vasconstrictive effect on heart and
intestines
Endoscopic Treatment
Once hemostasis has been achieved
Endoscopic Variceal Ligation (EVL)
o Preferred therapy
o Use elastic band to tie off varices
o Causes vessel thrombosis, necrosis, and fibrosis
Eliminates varices
Endoscopic Injection Sclerotherapy (EIS)
o Inject a sclerosing agent (sodium morrhuate) directly into the
varices.
TIPS Procedure
Shunts blood between the portal vein and hepatic vein












Surgical Decompression



Sengstaken Blakemore Tube




I. Bleeding
A. Due to:
1. Decreased in formation of plasma proteins-fibrinogen,
prothrombin.
2. Portal hypertension can cause bleeding esophageal varices or
varices in upper part of the stomach and bleeding
hemorrhoids.
3. Splenomegaly from portal hypertension can cause increase in
platelet destruction.
4. Conditions causing biliary obstruction cause lack of absorption of
Vit.K.
Thus the liver cannot synthesize prothrombin from Vit. K.

B. Possible Nursing Diagnosis:
1. Potential for bleeding
2. Altered tissue perfusion; systemic related to hemorrhagic shock.
3. Activity intolerance; fatigue-weakness related to anemia from
blood loss

C. Nursing Care
1. Goals: Prevent trauma and detect early bleeding.

2. Small gauge needles used for injections; prolonged pressure
needed at injection sites and venipuncture sites.
3. Soft bristled toothbrush and gentle mouth care.
4. Check stool for occult blood (guaiac)
5. Observe for bleeding from nose, urine, mouth, skin, emesis, gums.
6. Move and handle extremities at joints-not muscle belly.
7. Check on stool consistency. If hard, get order for stool softener.
Hard stools increase chance of bleeding from hemorrhoids.
8. Dont blows nose hard or manipulate nose excessively.
9. If O2 is given, be sure it is well humidified.
10. Check V.S. for increased pulse, decreased BP. Do orthostatic BP
and pulse if bleeding is suspected or to monitor blood loss.
11. If varices are present, no coarse foods given (mechanical soft diet),
avoid straining, vomiting, lifting, coughing, retching
anything that would increase intra-abdominal pressure.
12. Vit. K is sometimes given parenterally.
a. If bleeding is due to decreased absorption of Vit. K, the
prothrombin time should return to normal.
b. If liver is badly damaged, Vit. K will not help and little or
no change in pro time because liver cannot synthesize
prothrombin from Vit. K.
13. Check lab values of prothrombin tinme and INR
a. Pro time: the greater in seconds from normal, the greater
the chance for bleeding.
b. INR: the larger the number from 1.0, the greater the chance
for bleeding.

II. Problem of Edema

A. Can be due to:
1. Decreased plasma proteins decreased colloid osmotic pressure.
2. Portal hypertensionincreased hydrostatic pressure in portal
system and destruction of lymphaticsascites. Fluid high in
protein. Increased oncotic pressure of peritoneal fluid pulls
fluid out from vascular compartment.
3. Decreased renal perfusion due to decreased circulating blood
volumerenin-angiotensin-aldersterone mechanism
activatedincreased Na and water to restore blood volume.

B. Possible Nursing Diagnosis:
1. Alteration in fluid volume: excess
2. Alteration in body image or self-concept.
3. Ineffective breathing pattern.
4. Alteration in nutrition: less than body needs.
5. Alteration in skin integrity: decubiti
6. Alteration in tissue perfusion: peripheral & DVT
7. Alteration in comfort: abdominal pain.
8. Potential for injury: falls
9. Potential alteration in electrolyte balance.

C. Nursing Care
1. Edema usually generalized: ascities and hydrothorax often present
2. Review care for patients with CHF.
3. Skin care essential-total serum proteins also reduced, building and
repairing of tissue potentially decreased
4. I/O, daily weights
5. Know fluid goal: fluids restricted in some cases, esp. if Na+ is low.
6. If ascities is present:
a. self image altered
b. may be unsteady-center of gravity is off, safety factors;
need help with foot care and parts that are difficult to
reach.
c. abdomen can be very taut, tense and painful.
d. may need to measure abd. girth daily. Do so at umbilicus
e. increased abdominal pressure may decrease volume return
from lower extremities. Thrombo-embolic events
possible.
1) dorsiflexion exercises; avoid dependent position of
legs
2) no pressure on veins; prevent injury to legs.
f. breathing difficulties-impingement on diaphragm; semi-
Fowlers position most comfortable usually. Keep
fluid in lower part of peritoneal space; decreased
activity and need for oxygen.
g. anorexia and difficulty eating due to congestion of
abdominal viscera and liver disease per se.
1) frequent small feedings
2) feed patients when they are hungry.
3) calorie count kept on these patients, if necessary.
4) must encourage patients to eat; diet is their medicine
5) usually salt restricted diet-not too appealing.
h. administer diuretics as ordered
1) watch I/O & daily weights. 1-2 lb.weight loss per day is
good
2) observe for fluid and electrolyte imbalances esp.
decreased K. Remember decreased K can precipitate
hepatic coma.
3) spironalactone is a diuretic frequently given. Causes
K+ to be spared. Check K+ levels frequently and urine
output to be sure K+ levels will not increase dangerously
due to lack of urine output.
7. Note blood chemistry teststotal serum protein and serum albumin.
8. Shunt surgery to decrease ascites.

III. Encephalopathy or Hepatic Coma

A. Mechanism involved which causes cerebral symptoms is: NH3 ties up
glutamic acid needed for brain tissue activity and functioning. NH3
interferes with oxidation of glucose which brain needs for energy.
B. Signs and symptomscharacterized by progressive failure of all aspects
of liver function and associated with neurological manifestations.
Symptoms include:
1. Mild apathy, lethargy, drowsiness, mental dullness (obtunded), loss of
memory, loss of neatness, sloppy in eating, distant stare.
2. Confusion, disorientation, irritability abusiveness, slurred speech.
3. Lethargy progresses to stupor and coma.
4. Fetor hepaticusbad taste in mouth, sweet, musty odor of breath
characteristic of diffuse liver necrosis; may be early sign of
impending coma.
5. Increased temperature.
6. Flapping tremor or liver flap called ASTERIXIS. Check for this daily.
7. Muscular twitching and poor muscle coordination. Unable to
construct a simple design, e.g. O or +, worsening or change in
handwriting from day to day (check this daily)
8. Unable to think clearly, e.g. subtract serial &s, translate parables.
9. Increased blood NH3

C. Possible Nursing Diagnosis:
1. Potential for injury (falls and other injuries)
2. Alteration in communication: confusion, forgetfulness
3. Self care deficit: ADLs
4. All of the diagnoses that deal with immobility if the person is
comatose.
5. Alteration in mental status and thought processes
6. Alteration in respiratory function: potential airway obstruction (if
comatose)

D. Treatment and Nursing Care:
1. Patient safety-patient is stuporous, lethargic or even comatose; does
not use good judgment and may have difficulty with muscular
coordination.
2. Good oral hygiene (fetor hepaticus)
3. Dont give sedatives for delirious or agitated behavior.
4. Do a mental test on patients daily-simple math, orientationtime,
place, person, who is the president of the US etc.
5. Patients can be difficult to deal with due to personality changes.
Simple directions, dont argue with patients. Try to keep them
oriented and safe.
6. If in a comakeep airway open, safety factors, problems of
immobility, never leave unconscious patients on their backs
unattended-may aspirate fluid into the lung. Elevate HOB 23-30
degrees.
7. Observe patients frequently for even minor changes so that a coma can
be aborted by early treatment. Very important nursing function.
8. Carry out medical plan of care
a. Reduction of dietary protein20 Gm/day
b. Enemas or laxatives to purge GI tract of any blood and by-
products of protein breakdown (blood is good source of
protein on which gut bacteria can act)
c. Administration of antibiotics to sterilize the bowel may be
ordered
1) Neomycin may be ordered. Poorly absorbed and less
toxic
2) Causes inhibition of bacterial action on protein
substances in the bowel. Destroys normal bacterial
flora of gut so they are no longer present to break
down protein with resultant production of NH3
3) With Neomycin therapy, dietary protein can often be
increased
d. Lactulose syrup (Cephulac or Duphaluc)
1) Dose 30-40 cc tid or qid po, NG or rectally.
2) Mechanism: acidifies colon contents. Colon retains
NH3 as NH4; blood NH3 migrates to colon. It also
forms NH4 and is trapped in bowel; laxative action
of lactulose expels NH4 out of colon in stool.
3) Side effects: flatulence, belching, abd. cramps, diarrhea
(watch for > 6 stools/day)
9. Avoid conditions that can precipitate coma.
a. Excessive protein intake.
b. Massive bleeding in GI tract
c. Certain diuretics: thiazides
d. K+ depletion (check K+ levelsif on diuretics, extremely
important)
e. Paracentesisprobable mechanism in increased NH3
formation by kidneys or acid-base imbalance.
f. Acute infections and surgical procedures; increased demands
on already failing liver due to increased metabolic needs.
g. morphine (mechanism unknown)
h. AZOTEMIA (increased nitrogenous products in blood)
10. Know blood ammonia level and plan care accordingly. (The higher it
is, the greater the potential for coma or coma present). Patients do
vary in terms of NH3 levels and presence of S&S. Some tolerate
high levels without symptoms, others may be in a coma with
lower levels.

IV. Problem of Drug Toxicity
1. Observe for S&S of drug toxicity or intensified action of drugs
2. Dont give MSO4, barbiturates or Tylenol to these patients or only in very
small dosages.
3. Patients should take no medications unless ordered by doctor. Drugs that are
metabolized or detoxified by the liver are the greatest danger.
4. Further liver damage can result from effects of some drugs: Compazine
family, birth control pills, anesthetics such as Halothane and Tylenol,
certain antibiotics such as sulfa drugs.














COPD