The liver is the largest internal organ in the body.

It consists of
rows of hepatocytes or liver cells arranged in cords that radiate
out from a central vein. Capillaries called sinusoids lie between
the rows of hepatocytes. Sinusoids are lined with Kupffer cells
which carry out phagocytotic activity by removing bacteria and
toxins from the blood. Hepatic cells secrete bile into tiny canals
called canaliculi. These merge with other canals to form larger,
interlobular bile ducts, which unite them into the 2 main left and
right hepatic ducts. Remember, the liver has a rich blood supply
and can also be frequently injured with blunt/ penetrating
abdominal injuries.
The liver has many functions:
• Inactivates drugs and harmful substances
o It is also involved in the first-pass effect with
administration of PO drugs where about 70% of a drug
is metabolized and deactivated before reaching
circulation
• Synthesizes and secretes bile
o Bile consists of water, cholesterol, bile salts,
electrolytes, fatty acids, and bilirubin
o Bile deficiency results in steatorrhea
• Controls bilirubin, which is the product of hemoglobin
breakdown
o Bilirubin binds to albumin in the bloodstream. This is
known as unconjugated bilirubin which is not water
soluble
o When transported to the liver, bilirubin becomes
conjugated or water soluble. This facilitates its
excretion in the urine. It then travels to the intestines
where it is converted to urobilinogen. A small amount
 of urobilinogen is reabsorbed into the blood and then
transported back into the liver through portal
circulation. There it is excreted again in the bile or
entered circulation later to be excreted by the kidneys
• Stores vitamins [A, D, E, K as well as B vitamins] and
minerals like iron and copper
o Inability to store vitamins results in malnutrition,
anemia, and steatorrhea
Vitamin K deficiency affects blood coagulation
• Makes prothrombin
o Liver disease can prolong PT meaning that the blood
will take too long to form a clot
• Stores glycogen so after long periods of not eating and is
released when needed
• Makes albumin which maintains oncotic pressure and fluid
within the vascular space
o Lack of albumin will lead to fluid shifting and ascites
• Metabolizes protein we consume and converts ammonia to
urea so it may be excreted in the urine
• Synthesizes lipoproteins, breaks down triglycerides into
fatty acids and forms ketone bodies
• Synthesizes 75% cholesterol and breaks it down
• Breaks down excess steroids
o Too many steroids can lead to reproductive and
integumentary changes
In the early stage of any liver disease, the liver may become
tender, inflamed [hepatitis], and enlarged [hepatomegaly]. If the
inflammation persists, it can damage the liver permanently and
the liver will start to scar. As excess scar tissue grows, it
replaces healthy liver tissue. This process is called fibrosis.
Inflammation can be triggered by many things including high-fat
diets, hepatitis viruses, and alcohol use. When the liver is
 compromised, all these functions mentioned above are affected.
Liver cells will regenerate but once the damage is permanent,
there is no turning back.
Liver failure may occur acutely when certain drugs are ingested
in large amounts, usually acetaminophen. A thorough history,
physical examination, and blood work to determine the

:*
underlying cause and disease severity. A CT scan or ultrasound
"of the liver may also be conducted. Acetaminophen toxicity

¥ requires clearing of the GI tract of any remaining drug. N-

acetylcysteine aka Mucomyst is a mainstay of therapy for
reversing the toxic effects. Gastric lavage and charcoal are other
alternatives. The provider decides. It occurs less commonly in
viral hepatitis, usually B. This type of hepatitis is also known as
fulminant hepatitis. Liver failure may also occur due to
hemodynamic shock due to lack of perfusion to the liver. It is
sudden and progresses quickly causing irreversible damage to
liver cells thus decreasing the liver’s ability to function and meet
the body’s needs. Sometimes only a liver transplant may be the
only way to treat this condition. The client must meet the
transplant criteria to be eligible. Clients who have severe cardiac
and respiratory disease, metastatic malignant liver cancer, or
alcohol/substance use disorder are usually not candidates for
liver transplantation. Remember, immunosuppressant agents are
prescribed for life to prevent rejection. Tachycardia, fever, right
upper quadrant pain, change in bile color [T tube may be in
place] or increased jaundice, increased ALT and AST levels are
manifestations of organ rejection. The kidneys can begin to fail
as well. This is also known as hepatorenal syndrome. This
occurs secondary to systemic hypotension and renal
vasoconstriction. Monitor for acute kidney injury such as change
in urine output, increased BUN and creatinine levels, and
electrolyte imbalances.
Hepatic encephalopathy [HE] is a syndrome observed in
patients with advanced liver dysfunction. It occurs when
ammonia builds up and crosses the BBB. Symptoms typically
include changes in memory, concentration, and personality to
lack of coordination, abnormal reflexes, and asterixis. Loss of
consciousness, abnormal posturing, and coma can result. Fetor
hepaticus, musty breath smell, may occur. Ammonia levels will
need to be decreased with the laxative lactulose [oral, NGT, or
enema form]. Lactulose is typically given in syrup form at a
dose of 15 to 30 mL two to four times a day to aim for multiple
semisoft stools per day and prevent constipation. Monitor
electrolyte levels. Rifaximin and neomycin may be ordered to
reduce bacteria in the gut. Limiting protein intake will be
important as the liver cannot metabolize protein. Protein
restriction is only of use in patients with acute flare-ups. There
are many triggers that can increase risk for encephalopathy.

CT or MRI of the brain and

EEG help diagnose
encephalopathy. Those at
risk for aspiration or
respiratory compromise due
tipp
to altered LOC should be
prophylactically intubated
and monitored in the ICU

Hepatitis viruses include A, B, C, D, and E

S/S of liver dysfunction including hepatitis infection include:
• Fatigue
• Low-grade fever
• Anorexia lack of appetite
Meals
• N/V entourage small Mla .

• Weight loss
 • Headache
• Jaundice 9 Bilirubin
• Pruritis
o Pruritus sometimes accompanies jaundice and occurs
due to accumulation of bile salts beneath the skin
• Right upper quadrant abdominal pain
• Joint pain
• Muscle soreness
• Dark colored urine
o The urine may appear darker because of excess
bilirubin being excreted by the kidneys
• Clay colored stools
• Inflammation of the bile ducts prevents bile from entering
the intestines thus the stools will be light or clay colored
• Hepatomegaly enlarged liver
• Splenomegaly enlarged spleen *

Lab alterations in liver dysfunction include:

Remember,
]Pancreas amylase and
lipase are altered
with pancreatic
involvement
• Hepatitis A is transmitted through fecal-oral routes. Risk day cares
*

factors include ingestion of contaminated food or water, * poor

especially shellfish, and contact with infected stool [may hygiene
occur with anal sex]. Once infected, antibodies will be
present in serology. It will also be present with vaccination.
The vaccine can be administered prophylactically before
travel or if a person who has not previously received
hepatitis A vaccine and has direct contact with someone
with hepatitis A, that person should get hepatitis A vaccine
 within 2 weeks after exposure with or without
immunoglobulins
• Hepatitis B is transmitted through blood but primarily
through body fluids including saliva. Risk factors include
unprotected sex, maternal-fetal transmission, IV drug use,
and contact with infected blood. Hospital workers and
hemodialysis patients are at risk because of exposure to
blood. It is very infectious and live on surfaces for up to 7
days. Once infected, antigens and antibodies will be present
in serology. Carriers are infectious for life, and which can
lead to the development of cirrhosis. A liver biopsy can be
performed to provide more information. It is invasive. →
Fasting is started at midnight on the day of the procedure. ooag
Bleeding is certainly a risk because the liver is highly 19B$
vascular. Void prior to procedure. The client should be in
the supine position with the upper right quadrant of the
abdomen exposed. The patient should hold their breath
upon needle insertion and should hold breath for 10
seconds until after the needle is removed. Always monitor
respiratory function. After the procedure, the patient should
be in a right side-lying position and maintain for several
hours to prevent bleeding. Watch for the flank region and
abdomen for any signs of bleeding or peritonitis to BP 1- achy
,

o The Hep B vaccine is administered in a series of three

doses. The first at birth, the second a month later, and
the third six months from the first one. It can be
declined at birth if the mother chooses to do so. It is
safe to administer during pregnancy. Make sure to
review signs and symptoms, lab alterations, and
treatment. Although abstinence from sexual activity is
ideal, condoms should always be used with sexual
partners. Immunoglobins can be administered as part
of acute treatment. If hepatitis B becomes chronic,
treatment will involve antiviral PO medications such
 as nucleoside analogs [entecavir, lamivudine,
telbivudine] and/ or nucleotide analogs [adefovir or
tenofovir]. Administration of interferons via SubQ
injections may also be part of therapy. These
immunostimulant drugs will produce flu-like symptom
and prolonged use may cause them to lose their
non efficacy. The goal of antivirals is normalization of

¥1s liver enzymes and undetectable hepatitis B viral DNA.

Surgical intervention for hepatitis B is only indicated
for fulminant liver disease requiring transplantation
• Hepatitis C is transmitted primarily through blood but also
body fluids. Risk factors include IV drug use, blood
transfusions, organ transplants, sexual contact, and
exposure to contaminated needles used for piercing or
tattoos. There is no vaccine for hepatitis C. It takes years
before advanced liver damage occurs. With highly active
direct-acting antivirals, duration of treatment has been
reduced from 48 weeks to 12 weeks, improving the adverse
effects, increasing cure rates to 90% to 97%, and
eliminating the need for injectable agents. It may or may
not include the use of ribavirin
• Hepatitis D is only contracted when the person has hepatitis
B and can develop into chronic liver disease vaccine
"
B"
• Hepatitis E is similar to hepatitis A and is also transmitted
through fecal-oral routes. Risk factors include ingestion of
contaminated food or water specifically in Mexico or Asia
and Africa
Viral hepatitis infections [B or C usually] resulting in fulminant
hepatic failure require immediate transfer to a liver transplant
center for evaluation of liver transplantation. Care after hepatitis
infection includes bed rest and limiting physical activity. A
high-carbohydrate, high-calorie, moderate fat, and moderate-
protein diet after nausea and anorexia subsides is recommended.
Treat N/V with antiemetics. If vomiting is severe, hospitalization
for administration of IV fluids or supplemental enteral nutrition
therapy may be necessary. Encourage small, frequent meals to
promote nutrition and healing. Vitamin supplements, particularly
B-complex and vitamin K, may be prescribed. Avoid alcohol
and medications harmful to the liver. Cholestyramine or control the*
hydroxyzine may be ordered along with lotions containing Itching
calamine or moisturizing bath oils like Alpha Keri. Use soft
linens, control environmental temperature, keep nails short and
clean, and teach those affected to rub with the knuckles rather
than scratch with the nails. Avoid sexual intercourse until
hepatitis antibody testing is negative
HEALTH PROMOTION
● Follow vaccination recommendations according to the CDC
● Follow infection control precautions according to the CDC
● Reinforce and use safe injection practices
● Use proper hand hygiene before preparing and eating food, after using the toilet or changing a diaper
● When traveling to underdeveloped countries, drink purified water, and avoid sharing eating utensils and bed
linens

Cirrhosis involves extensive scarring of the liver over a

prolonged period. Damage is permanent. Make sure to review
how all body systems are affected by cirrhosis.

lack Of
21 Alk B12
of ammonia

-
lack of appetite

improper
steroid .

metabolism

Portal HTN occurs from the scarring which leads to obstruction

 of blood flow and pressure. Splenomegaly occurs due to
increased blood return to the spleen. Enlargement of the spleen
results in pancytopenia and impaired coagulation which can lead
to disseminated intravascular coagulation [DIC]. Unfiltered
blood is returned into the bloodstream. It can worsen ascites.
The ascites causes proteins to shift from the blood vessels to
lymph space and leak into the peritoneum. Furthermore, the
production of albumin decreases due to cirrhosis, which worsens
the ascites. Although fluid retention occurs in the peritoneum,
the person may become dehydrated due to massive fluid shift.
Sodium may also shift from the blood into the peritoneum as it
follows water. Intake should be restricted to 2 g per day but may
vary with serum sodium levels and severity of ascites.
Potassium-sparing diuretics may be used if needed as they retain
potassium which is lost due to excess circulating aldosterone.
Furosemide may be prescribed but can decrease potassium
levels requiring replacement. As fluid builds up in the
peritoneum, breathing may become difficult. Paracentesis may
be attempted. Keep the HOB elevated 30 to 45 degrees. Witness
consent signature and have person void prior. A local anesthetic
will be administered to the site prior to needle aspiration. Weigh
Ñmm client before and after the procedure. Send fluid for pathology
and document it as output. Monitor vital signs and promote bed
kidney rest. Albumin infusions may be administered prior to or after the
function procedure depending on levels. Monitor for signs and symptoms
of hypovolemia and shock. Perforation of the bladder and bowel hematuria
after paracentesis can lead to shock and peritonitis. The
abdomen may become tender, distended, and rigid/ board-like.
aBdpaÑ
Monitor for sudden spike in fever, hypotension, and tachycardia.
Routine upper esophagogastroduodenoscopy [EGD] can be
performed to screen for varices and monitor them. This requires
NPO status 6 to 8 hours prior, moderate sedation via IV access,
and left side-lying positioning with HOB elevated.
Complications include infection, bleeding, and perforation.
Reaction to the sedative may occur in certain clients. Symptoms
of perforation include radiating, upper back pain, chest pain,
difficulty swallowing, fever, tachypnea, tachycardia, and
hypotension. There may be internal bleeding. Surgery will
depend on the location and size of the perforation. If surgery is
needed, it is best done within 24 hours. After EGD, always
assess for respiratory distress and return of gag reflex.
Prevention of variceal rupture also involves long-term
management with nonselective beta blockers like naldolol or contra .

propranolol will be ordered to reduce risk for rupture and *

hemorrhage. PPIs like omeprazole can be administered to asthma
minimize production of gastric acid. NSAIDs and alcohol
should be avoided. Stool softeners may be prescribed to avoid
straining. Heavy lifting, coughing, and sneezing should be 4 FLUID
avoided. Signs and symptoms of bleeding include hematemesis,
hypotension, tachycardia, dizziness, pallor, cold/ clammy skin, TABER
and altered mental status.
If acute bleeding occurs from varices, manage airway and
ventilation. Keep NPO! Obtain 2 large bore IVs and begin
infusion of 0.9% sodium chloride. Type and crossmatch may be
obtained for blood transfusions. PRBCs, FFP, vitamin K, and
PPIs can be administered. Lactulose and rifaximin may be given
to prevent hepatic encephalopathy from breakdown of blood and
the release ammonia. Prepare for immediate EGD ligation/
sclerotherapy or balloon tamponade. The provider decides. Drug
therapy with octreotide and vasopressin in combination with
sclerotherapy or band ligation may be performed to control
acute bleeding. Epinephrine can also be directly injected to the
veins to produce constriction and minimize bleeding. Monitor
glucose with octreotide therapy, it may elevate. Vasopressin will
increase BP and HR.
Balloon tamponade is another option to control acute
hemorrhage; however, it should not be used for more than 12
hours as the tube can cause necrosis of tissue if left in place for
an extended period of time. It involves placement of a special
tube, sometimes referred to as a Sengstaken-Blakemore tube,
that has 2 balloons [gastric and esophageal] with three lumens:
one lumen for the gastric balloon, one for the esophageal
balloon, and one for gastric aspiration. Both seal the stomach
and esophagus. Check balloons for leaks prior to insertion. The
gastric should be inflated first. It is important to label the lumens
to avoid confusion. The person should be monitored at all times
as this tube is an airway risk. NPO status should be initiated as
the tube will prevent the patient from swallowing. Clients are
often intubated to protect the airway. Frequent oral and nasal
care, including encouraging the patient to spit saliva into a tissue
or basin and suctioning to remove secretions. Keep HOB
elevated. Suction as needed. Monitor the client who has
decreased mentation or confusion and who might pull on the
tube. X-ray verifies placement. Balloon is inflated with 250 mL
of air with a desired pressure of 20 to 40 mm Hg. Deflate
balloons for 5 minutes every 8 to 12 hours to prevent tissue
necrosis. Scissors should be kept by the bedside in case
respiratory distress occurs and the tube needs to cut rapidly. The
patient must remain on bed rest while the tube is in place to
prevent accidental dislodgement of the tube which can cause
asphyxia.
TIPS procedure or transjugular intrahepatic portosystemic
shunt TIPS is used to treat an acute episode of bleeding when
EVL and pharmacological measures are not controlling the
variceal bleeding. It rapidly lowers the portal pressure. The
procedure is costly, and therefore is only used when other
measures do not work. While the client is under sedation or
general anesthesia, a catheter is passed into the liver via the
jugular vein in the neck. A stent is then placed between the
portal and hepatic veins bypassing the liver. Portal hypertension
is subsequently relieved. It helps control varices and ascites.
Post-procedural complications include stent occlusion, sepsis,
shock, and hepatic encephalopathy. Lactulose is usually
prescribed. Monitor laboratory findings, including potassium
because clients can become hypokalemic with increase stools
from the lactulose therapy. Assess for changes in LOC. Report
asterixis and fetor hepaticus immediately to the provider. These
are clinical indications that encephalopathy is worsening.
HEALTH PROMOTION
While lifestyle changes cannot cure cirrhosis, behavioral modifications can prevent or at least delay disease
progression and provide symptomatic relief. Modifiable lifestyle factors include:
• Eliminating ethanol [alcohol] consumption
• Dietary interventions
o High-calorie, moderate-fat diet
o Low-protein [if encephalopathy, elevated ammonia]
o Small, frequent, well-balanced nutritional meals
o Nutritional supplement drinks or shakes and a daily multivitamin as well as replacement and
administration of vitamins A D E K B 12
,

o Low-sodium diet to reduce water retention

r%¥a→t•
• Vaccinations for pneumonia, influenza, and hepatitis *

The pancreas has both exocrine and endocrine functions. The

exocrine function contributes to digestion through the
break down
production and release of digestive enzymes. → enzymes
barbs fat Protein .

Acute pancreatitis involves inflammation of the pancreas. The

, .

major causes include chronic alcoholism and cholelithiasis or

presence of gallstones. It may also be triggered by a variety of
drugs like tetracycline, thiazides, acetaminophen, and oral
contraceptives. Other risk factors include increased age,
genetics, cigarette smoking, biliary sludge, > 500 triglycerides
hypertriglyceridemia, trauma, metabolic disorders, and vascular
diseases. Early correction is key! Inflammation can block the
pancreatic duct thus interfering with the release of pancreatic
enzymes. This results in autodigestion of the pancreas by
pancreatic enzymes that activate prematurely before reaching
the intestines and are stuck in the pancreas. The enzymes are
literally eating away at the pancreases activating the
inflammatory response producing inflammation. Clients present weight
with N/V, fever, and severe, mid-epigastric pain that is boring or loss
slowly dissipating in nature. Pain is worse when lying down and
 may be relieved by fetal position or sitting down. Abdominal
distension and rebound tenderness may be present as well. •
Bowel sounds may be decreased or absent. Lab alterations ¥m%%I÷ .

include elevated WBC, amylase, lipase, glucose, triglycerides,

and ESR. Amylase elevates first within 24 hr and remains
increased for 2 to 3 days [continued elevation can indicate
pancreatic abscess or pseudocyst]. Blood lipase increases slowly
and can remain increased for days longer than amylase. Urine
amylase remains increased for up to 1 week. Calcium and
magnesium levels may be decreased due to fatty necrosis and
elevated lipase levels. Hypocalcemia occurs in part because

÷¥¥→ calcium combines with fatty acids released during fat necrosis of
the pancreas. The nurse should observe for symptoms of tetany,
such as jerking, irritability, muscular twitching, and positive
A Biti Chvostek’s and Trousseau’s signs. Numbness or tingling around
the lips and in the fingers is an early indicator of hypocalcemia.
Ca and Mg will need to be replaced. Abdominal ultrasound and
CT scan are usually ordered and will aid in diagnosis. Since
presence of gallstones can also cause pancreatitis,
cholecystectomy may be performed. ERCP to create an opening
in the sphincter of Oddi if pancreatitis is caused by gallstones.
Just FYI, ERCP can worsen pancreatitis.
Pancreaticojejunostomy [Roux-en-Y] reroutes drainage of
pancreatic secretions into jejunum. The provider makes
decisions on what procedures will be performed. Inflammation
of pancreatic tissue leads increased pressure and duct
obstruction which can lead to rupture, necrosis, and hemorrhage.
Seepage of blood-stained exudates into the tissue producing
ecchymoses on the flanks and/ or bluish-grey periumbilical
discoloration. These are known as Grey-Turner and Cullen
signs.
ICU admission is required when secondary complications occur
such as infection, shock, and ARDS. In its severe form, SIRS/
MODS may result. Infection risk is increased as pancreatic cysts
and abscess can develop. Vasodilation and fluid shifting can lead
hypovolemia, hemorrhage, shock, sepsis, DIC, and respiratory
symptoms including development of ARDS. Damage to the
pulmonary vasculature caused by activated trypsin leads to
increased endothelial permeability while the main culprit for
pulmonary insufficiency and ARDS in patients of acute
pancreatitis. Pancreatic abscess or pancreatic pseudocysts may
develop. Pseudocysts occur outside pancreas and abscesses
inside the pancreas. Monitor for fever, epigastric mass, N/V, and
jaundice. Some resolve with observation alone with periodic
follow-up using CT, however, in some cases, drainage may be
 required. Rupture is a medical emergency and lead to peritonitis
and sepsis. The provider will decide how to best manage cysts
and abscesses. If infection is suspected, the preferred antibiotic
regimen includes a carbapenem alone, or combination of a
quinolone, ceftazidime, or cefepime with metronidazole.
Management of pseudocysts and abscesses may involve
laparotomy. Emergent laparotomy followed by ICU admission
where an external drainage and lavage system may be placed
and maintained over the next few weeks. NPO status and TPN
will be prescribed to avoid stimulation of the pancreas.
Carbapenems, quinolones, or metronidazole antibiotics may be
prescribed.
Systemic support during an episode of acute pancreatitis
involves managing ABCs, initiating NPO status, NGT insertion,
fluid resuscitation with normal saline or Lactated Ringer's, no tonio
analgesia administration [morphine, hydromorphone or FIUI D8
ketolorac], and antiemetics like metoclopramide, ondansetron,
or promethazine for N/V. PPIs like omeprazole will be ordered
to decrease gastric acid secretion. NGT suctioning will prevent antispasmodic
gastric contents from entering the duodenum and stimulating OXBUtinyin
pancreatic secretion. Electrolyte imbalances are corrected, andGilieusontro
glucose controlled. When abdominal pain, N/V, appetite, and
lipase→ileus improve, feedings may be attempted. For severe
decrease pancreatitis, expect enteral or parenteral nutrition to be ordered.
When diet is resumed, it should be limited to bland, high
protein, and low-fat foods with no stimulants such as caffeine.
Encourage small, frequent meals.
HEALTH PROMOTION
For pancreatitis induced by alcohol use disorder, abstain from further alcohol intake as well as
smoking cessation

Alcohol use/ smoking cessation support groups can be helpful

Avoid high-fat foods or heavy meals to prevent episodes of acute pancreatitis

avtfpdoy foods
Dietary and lifestyle modifications including weight reduction, low-fat diet, and regular exercise
q protein
 Home health services can be indicated for clients regarding nutritional needs, possible wound
care, and
assistance with ADLs

Chronic pancreatitis is continuous, prolonged inflammatory

and fibrosing process of the pancreas. It is the “cirrhosis of the cystic
pancreas”. It can result in permanent damage to the organ as Fibrosis
well as dysfunction of endocrine and exocrine functions. Type 1
DM may develop from destruction of pancreatic beta cells due
to scarring and will require long-term diabetes management. It
most often occurs with alcohol abuse and chronic obstructive
pancreatitis due to gallstones. Chronic pancreatitis can present
with abdominal pain, nausea, and vomiting. However, it can also
be painless, and patients can present with steatorrhea and weight

r.at/0ilP-YehuY :Yo e*panorea1ipaseaK oren

→
loss. Amylase/lipase levels can be elevated or normal. The
treatment for chronic pancreatitis involves pain control, and
counseling regarding smoking and alcohol cessation, and
pancreatic enzyme replacement. Most importantly, diet should
be adjusted to eat a low-fat diet in small meals. Pain relief can
be achieved with combined medications using nonopioids, mild
opioids, and strong opioids. Many with chronic pancreatitis
receive antioxidants with their pain medicine, which has been
shown to help with pain relief. There are other options for pain
relief, such as a celiac plexus block, which may provide another
option for significant pain relief. The celiac plexus block is
achieved via injection and prevents the nerves that travel from
the pancreas from reporting pain signals back to the brain. If
there is a narrowing of the pancreatic duct, placement of a stent
into the duct can be helpful in alleviating pain symptoms.
Surgical interventions include pancreaticojejunostomy or
modified Puestow procedure where drainage of pancreatic
secretions is rerouted into the jejunum.

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Enteral nutrition [EN] is nutrition delivered using the gut. This

can refer to oral, gastric, or postpyloric feeds. Standard NGTs
are used for tube feedings for short-term feeding problems
because prolonged therapy can result in irritation and erosion of
the mucosa of the upper GI tract. Gastric reflux and the potential
for aspiration can occur with both tubes that deliver fluids into
the stomach. Both NGT and gastrostomy tubes can become
displaced and deprive the client of the sensations associated with
eating. There are many indications requiring a feeding tube to
deliver nutrition or hydration. This is known as tube feeding,
enteral feeding, or gavage. It can be in addition to an oral diet, or
it can be the only source of nutrition. Advantages of EN over
parenteral nutrition include better safety, more effective,
decreased risk of infection, decreased cost, prevents gut atrophy,
and preserving the barrier function of the gut [less risk for ulcer
formation]
Just FYI, don’t memorize…
▪ Approximately 25 kcal/kg per day is the usual energy
requirement
▪ Carbohydrate intake should be approximately 4 gm/kg per
day with a target glucose level below 180 mg/dL
▪ Lipid intake should be between 0.7 to 1.5 gm/kg per day
 ▪ Amino acid should be adjusted to 1 to 1.8 g/kg per day with
an adequate supply of micronutrients
There are special formulas for those with diabetes and liver,
kidney, or lung disease. Most are lactose free. Formulas are
available in standard/ whole molecule or hydrolyzed/ smallest
molecule to promote easy absorption for those who have IBD,
pulmonary impairment, or pancreatic disease. The more
calorically dense a formula is, the less water it contains. The
more hydrolyzed or broken down the nutrients, the greater the
osmolality. Monitor weight and albumin levels as both should
increase with EN. Formulas should be discarded after 24 hours
to prevent bacterial growth
Parenteral nutrition [PN] is used when the enteral route is
contraindicated. There are two types. Partial parenteral nutrition
or peripheral parenteral nutrition [PPN] is less hypertonic,
intended for short-term use, and administered in a large
peripheral vein. Risk for phlebitis is increased due to osmolalilty
of the solution. Total parenteral nutrition [TPN] is more
hypertonic containing more than 10% dextrose [usually 20 to
50%] with an even higher osmolality than PPN and is indicated
when long-term support is necessary or when the client requires
high protein and caloric requirements. TPN requires a central
line such as a PICC line as risk for irritation and
thrombophlebitis is greater. Chest x-ray needed before use. PN
is prepared by pharmacy and requires a provider prescription to
be renewed every 24 hours. The solution contains sodium,
potassium, magnesium, calcium and phosphate. It also contains
vitamins, and trace elements [zinc, copper, chromium, and
manganese]. Those with renal and liver impairments will have
special adjustments. Medications like insulin, heparin, and
albumin can be added by the pharmacy in the solution. It may
even contain PPIs or H2 receptor antagonists. PN must be
refrigerated until 30 minutes before use. Calories in PN are
supplied by carbohydrates in the form of dextrose and by fat in
lipid emulsions. Up to 100 to 150 g of dextrose can be
administered daily
Lipid emulsions are available in 10%, 20%, and 30% and
 SAFFLOWER
contain eggs. Assess for allergies to egg or soy. The maximum
daily dose is 2.5 g/kg/day and should be infused over 8 to 12
hours. Serum triglyceride levels will be monitored during
therapy. If lipids are infused too quickly, N/V and hyperthermia
may occur. Other complications include headaches, jaundice,
hepatosplenomegaly, respiratory difficulty, fluid overload, and
spontaneous hemorrhage → Bright yellow
What to do before infusing PN/ lipids? → looks like milk
▪ Check label and ingredients in the PN to make sure they
match the order form
▪ The PN form needs to be renewed every 24 hours
▪ In most facilities, it requires second witnessing with another
nurse
▪ Examine the solution for leaks, color changes, and clarity
▪ Check for cracking in fat emulsions, label tubing and filter
with date and time
Never increase the rate to “catch up” or stop abruptly. The
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solution should be replaced every 24 hours. If the PN empties 14018
before the new bag is delivered from pharmacy, hang dextrose
solution in water based on the amount of dextrose in the PN or
highest amount available to avoid hypoglycemia. Glucose range
should be maintained between 110 to 150 mg/dL but may be as
high as 180 mg/dL. Change IV tubing for both TPN and lipid
emulsions with new bag. Observe the catheter site for signs of
inflammation and infection. Monitor vital signs every 4 to 8
hours, weigh daily, and check glucose, electrolytes, and BUN
every 4 to 6 hours. CBC and LFTs should be obtained 3x per
week then weekly
Metabolic complications
◦ Refeeding syndrome then Petlodofstarration
F1Uid1MBAlA→
◦ Hyper or hypoglycemia you
. feed
hypokalemia
◦ Altered renal/liver function a phosphorus
◦ Hyperlipidemia trmaonlslum
Catheter-related problems
 ◦ Monitor for air embolism [sudden onset of dyspnea,
chest pain, or anxiety]
◦ Clamp the catheter immediately and place the
client on their left side in Trendelenburg position
to trap air
◦ Maintain strict aseptic technique when hanging
solution and change solution and tubing every 24
hours
◦ Observe the insertion site for local infection and
change dressing every 48 to 72 hours or when visibly
soiled
Fluid imbalance
◦ TPN is a hyperosmotic solution [three to six times the
osmolarity of blood], which poses a risk for fluid
shifts, placing client at increased risk of fluid volume
excess
◦ Assess for fluid overload and monitor for respiratory
distress