Disorders of the Small and Large Intestines and

their Management

1. Crohn's Disease or/Regional enteritis

• This is a chronic inflammatory disease that can affect any segment of the GI tract. It
may occur at any age and being chronic, it is marked by exacerbations and remissions.
• The cause is unknown, but is thought to be as a result of:
 Hereditary factors
 Immunological reactions that may affect the GIT
 Environmental factors: bacteria, virus or any environmental factor that may
trigger the immune system

1
Intestines
Clinical manifestations include:
• Crohn's disease manifests with intermittent diarrhoea, pain,
weight loss, malaise and sometimes fever
• Depending upon the area of intestine involved, the stool
may contain
occult blood
• Where there is involvement of the upper GIT, symptoms
similar to those of peptic ulcer disease may be experienced
• Malnutrition may be present when the distal small intestine
is involved due to inadequate absorption of nutrients
Management
• Treatment is aimed at reducing inflammation and infection and
alleviating symptoms.
• This is achieved by use of antimicrobial drugs and steroids.
• The patient needs a high calorie, high vitamin, high protein, low
residue and milk free diet.
complications

Perforation,
 Fistula Formation
Haemorrhage,
 Toxic Megacolon,
 Obstruction,
 Malabsorption
Susceptibility To Neoplasia
 2. Ulcerative Colitis

• Ulcerative colitis is a recurrent ulcerative and inflammatory disease

affecting the colon and the rectum.
• The inflammation is usually limited to the mucosal and sub mucosal
layers of the intestinal wall.

• Accompanied systemic complications and a high mortality rate

• 5% of patients with ulcerative colitis develop colon cancer.

Causes /contributing factors
• The cause is unknown, but the contributing factors are the same as for
Crohns disease is thought to be as a result of:
Hereditary factors
Immunological reactions that may affect the GIT
Environmental factors: bacteria, virus or any environmental factor
that may trigger the immune system
 Clinical manifestation

These include
 Diarrhoea,(sterile)
Passage Of Mucus And Pus
 Other symptoms include lower abdominal pain and abdominal tenderness,
intermittent tenesmus and rectal bleeding
 The patient may also present with fever, anorexia, weight loss, nausea and
vomiting and dehydration
Edematous and inflamed mucosa , and abscsess formation
 hypocalcemia , anemia and fatigue frequently develop
Rebound tenderness right lower quantrant
Extra intestinal manifestations: skin lesions e.g. erythemanodosum, eye lesion
e.g. uveitis, joint abnormalities e.g athritis ,and liver disease
Eventually bowel narrows , shortens and thickens because of muscular
hypertrophy and fat deposits
Diagnosis:
• Sigmoidoscopy or colonoscopy -show inflamed mucosa with
ulceration , to define extend and severity of disease
• Barium enema – show mucosal irregularities
• CT scan ,MRI, and ultrasound –identify abscess
• Stool examination to rule out dysentery
Complications
Perforation
toxic mega colon-affects muscles, inhibiting contraction,
causing its distention ,with fever , abdominal pain , vomiting
and fatigue and shock.
Bleeding
cancer
 Management
• The patient with mild disease requires:
 a low roughage diet,

 no milk or milk products.

They receive anti-microbial drugs,
corticosteroid to decrease inflammation,
anti-cholinergics and anti-diarrhoea drugs.
In severe ulcerative colitis
Those with severe disease may be given:
Nil per oral
 IV fluids with electrolytes,
blood transfusion,
NG tube for low suction in addition to the measures that have
been mentioned for mild disease.
If there is no improvement, these patients may be operated on
and have a colostomy (fecal diversion).
Appendicitis
• Appendicitis is inflammation of the appendix. This is a common
disorder in the 5 to 30 years age group.
cause :
Cause is not clear but is related
• to obstruction by FB ,
• worms,
• Fecalith
• lympadenitis,
• twisting of the appendix.
Appendicitis
Clinical Manifestations
• At the onset, the patient may have low grade fever. Abdominal pain is
initially peri-umbilical but gradually localises to the right lower
quadrant. Other features include rebound tenderness,
nausea ,malaise ,vomiting and an elevated white blood cell count.
• Rebound tenderness, constipation or diarheal
• Rovsing’s sign – palpating left lower quadrant ,causes pain to be felt
in right lower quadrant
• Diffuse pain if appendix ruptured ,abdominal distension develops as a
result of paralytic ileus and patient condition worsens
Management
• This involves surgical removal of the appendicitis (appendectomy) as
soon as possible to decrease the risk of perforation .
• laparatomy or laprascopy operation is done.
• General Pre operative care and post operative care
• Antibiotics and iv fluids are administered until operation is done –to
prevent dehydration , and sepsis.
• Nursing care should aim at pain relief, maintaining vital signs within
normal limits, preventing infections and ensuring that the patient
returns to routine dietary intake, activity level and normal bowel
function.
• Complications---perforation ,abscess, portal pylephlebitis (septic
thrombosis of portal vein)
 Colorectal cancer
• Tumours of the colon and rectum are relatively common and their
incidence increases with age.
• It is a disease of western cultures. In most cases, the patients are
asymptomatic for long periods and only seek medical help when they
notice a change in bowel habits or rectal bleeding.
The Risk Factors of Colorectal Cancer

• Age (40 years+) i.e. increasing age

• High consumption of alcohol.
• History (previous) of colon cancer or adenomatous polyps
• Family history of colon cancer or polyps
• Cigarette smoking
• Obesity
• History of gastrectomy
• History of inflammatory bowel disease
• High fat ,high protein , low fibre diet
• Genital cancer, or breast cancer in women
Clinical manifestation
Relate to tumour size and location.
Symptoms of cancer of the colon include changes in bowel habits,
 Passage of blood in stool,
Rectal/abdominal pain,
Anaemia,
Weight loss,
 Obstruction and perforation.
Tumours of the right colon usually present with vague symptoms of
abdominal pain and mild anaemia.
The stool is usually positive for occult blood.
On examination: most patients have a palpable mass on the right
lower quadrant. Obstruction resulting from right colon tumours is
uncommon.
• Patients with tumours affecting the left colon present with symptoms
of obstruction.
• The pain which is usually due to gradual progressive obstruction is
often relieved with defaecation on or the passage of flatus. Overt
bleeding and change in the stool are common with left sided tumours.
• In rectal carcinoma, rectal bleeding is the main complaint.
• The bleeding may be evidenced as blood mixed with faeces, blood on
the sides of the faeces, or rectal bleeding if the patient strains when
passing stool.
• Changes in bowel habits are common in rectal carcinoma and there is
usually alternating constipation and diarrhoea, tenesmus, and a
feeling of incomplete rectal evacuation.
• Rectal carcinoma is often palpable on careful rectal examination.
Diagnosis Of Colon Cancer:
• Patients who are suspected of colon cancer should undergo
proctosigmoidoscopy.
• A Barium enema is useful in delineating the extent of the pathology
and in ruling out other colonic lesions.
• Colonoscopy can also be done to visualise the entire colonic mucosa.
Management
• The tumour site and extent determine the surgical approach to be used in
treatment of the carcinoma.
• When the tumour is removed, the involved colon is excised for some distance on
each side of the growth to remove the tumour and the area of its lymphatic
spread.
• The intestine is then re-united by an end-to-end anastomosis of the colon.
• If the tumour is located low in the sigmoid or rectum, the colon is cut above the
growth and brought out through the abdominal wall. This abdominal anus is
called a colostomy.
• Radiation is recommended for lesions that may not be operable. A combination
of radiation and chemotherapy has been shown to result in longer survival rates.
Care of a Patient with a
Colostomy
• Before the procedure, the patient requires psychosocial support in order to
accept a colostomy and adjust to a new life style.
• This support is necessary given that the patient and their family are dealing
with two issues; diagnosis of cancer and the shock of a colostomy.
• Prior to the surgery, intestinal antibiotics may be given to reduce the
bacterial content of the colon. Mechanical cleansing may be done by use of
laxatives, enemas or colonic irrigation.
• Preoperative nasogastric intubation facilitates performance of intestinal
surgery and minimises post operative distension.
• An indwelling catheter is inserted to ensure that the bladder is empty
during surgery.
• After surgery, the patient should be monitored for signs of complications
which include prolapse of the stoma, perforation, leakage from an
anastomotic site, stoma retraction, faecal impaction, skin irritation and
pulmonary complications.
• The colostomy is opened on the second or third post operative day. Since the
stoma on the abdomen doesn't have voluntary muscular control, emptying
may occur at irregular intervals.
• This can be regulated by irrigation or by training the bowel to evacuate
naturally without irrigation.
• This usually depends on an individual and on the nature of the colostomy.
Irrigating a colostomy aids in emptying the colon of gas, mucus and faeces.
When this is done regularly, there is less retention of gas and irritating fluids.
• Irrigation is best done after a meal as ingestion of food usually stimulates
defecation.
• The peri-stomal skin should be washed frequently to avoid irritation.
Ascending Colostomy Descending Colostomy
Sigmoid Colostomy Single Barrelled Transverse Colostomy Double
Barrelled
Ileostomy
 Acute Abdomen
Acute abdomen the term refers to a group of abdominal conditions for which
prompt surgical treatment must be considered to treat perforation,
peritonitis, vascular and other intra-abdominal catastrophes.
Causes of acute abdomen include:
1. Bowel - Acute appendicitis, perforated peptic ulcer, diverticular disease,
intestinal obstruction and strangulation
2. Vascular - Acute vascular insufficiency, ruptured aortic aneurysm
3. Gynaecological - Ruptured ectopic pregnancy, ruptured ovarian cyst,
acute salpingitis
4. Others - Cholecystitis, pancreatitis, penetrating injury
Clinical Features
• Abdominal pain is the most prominent symptom with the pain being
localised to the area of abdomen affected. Other features depend on
the
underlying cause.
Management
• The emergency management of the patient with acute abdomen
involves monitoring:
the airway,
administering oxygen,
 establishing intravenous access
monitoring vital signs.
 An indwelling catheter should be inserted.
Pain management preferably with an opioid analgesics
intake and output should be monitored while observing for
vomiting.
The specific nursing interventions will depend on the
medical or surgical management of the client.
mnx
• Acute abdomen as a result of gynaecological problems would require the
management to focus on the cause.
The gynaecological causes include
a ruptured ectopic pregnancy,
 pelvic inflammatory disease
 torsion of ovary.
 You will cover these conditions in Reproductive Health.
Mnx cont’
• The patient with abdominal trauma should receive the same
management as indicated for acute abdomen.
• In addition they may undergo exploratory laparotomy and any other
operations that are necessary.
• You should, therefore, provide these patients with pre and post-
operative care.
Mnx cont’
• Adults with peritonitis and inflammatory bowel diseases receive;
• fluid replacement,
• antibiotic therapy,
• NG suction, analgesics and preparation for surgery.
• They may also require total parenteral nutrition in addition.
• Post operatively, the patient receives nil per oral and low intermittent suction.
Always nurse the patient in Semi-Fowler’s position. The patient should be on fluid
replacement, antibiotics and sedations.
Anal Rectal Problems and
Haemorrhoids
• These include anorectal abscess, fistula in ano, fissure in ano and
haemorrhoids.
Anorectal Abscess:
This is an infection localised in the anorectal region.
The abscess is often painful and contains foul smelling pus.
 For superficial abscesses, swelling, tenderness and redness are observed.
 Deeper abscesses result in toxic symptoms, lower abdominal pains and fever.
Fistulas may result from the abscesses.
 The abscess can be incised and drained surgically.
 Palliative therapy consists of sitz baths and analgesics.
Fissure in Ano
• This refers to a longitudinal ulcer in the anal canal. They are caused by
diarrhoeal stools and persistent tightening of the anal canal. They can also
occur during child birth, trauma to after cathartic abuse. There is usually pain
and bleeding during defaecation. These usually heal on their own though
minor surgery for repair may be necessary in others. Stool softeners and
increased intake of water helps in easing the defaecation process. A
suppository combining an anaesthetic with steroid may be comforting.

Fistula in Ano
• This is a tiny tubular tract that extends into the anal canal from an opening
located outside the anus. Fistulectomy is the recommended surgical
procedure for repair of the fistula.
Haemorrhoids
• These are varicose veins in the anal canal. Those occurring above the
internal sphincter are referred to as internal haemorrhoids and those
appearing outside the external sphincter are called external haemorrhoids.

Clinical Features and Management

• Haemorrhoids cause itching, bleeding during bowel movements and pain.
Internal haemorrhoids are usually not painful until they prolapse or bleed
due to enlargement.
• Symptoms of discomfort are relieved by personal hygiene and avoiding
excessive straining during defaecation. Straining can be reduced through
intake of a diet that contains roughage and increased fluid intake.
Clinical Features and Management – cont’d
• Ice packs alternated with warm packs are useful for thrombosed
haemorrhoids. Internal haemorrhoids can be legated in addition to anal
dilatation. A patient whose
problem persists may have to have surgical excisions of the
haemorrhoids.
• Nursing care must include pain management, teaching the patient to
avoid prolonged standing or sitting, use of sitz baths and stool softeners.
• Causes/risk factors
• HT, Obesity, pregnancy, alcohol overindulgence, vit E deficiency,
prolonged periods of sitting or standing ,family tendency
Intestinal Obstruction
 Intestinal Obstruction
• Exists when blockage prevents the normal flow of intestinal
contents through the intestinal tract
• Intestinal obstruction is a condition that can be considered as part of
acute abdomen.
• Intestinal obstruction can either be caused by:
1. mechanical obstruction due to hernia, twisting of intestines
(volvulus ,intussusception) faecal impaction, tumours or adhesions,
worms ,
2. functional obstruction e.g. paralytic ileus, which sometimes follows
abdominal surgery or peritonitis neurologic disorders e.g. parkinson’s
disease. (intestinal musculature cannot propel the contents along the
bowel.
Intestinal Obstruction
• When there is obstruction, the blockage leads to strangulation and formation of
gangrenous tissue.
• There follows pain, constipation, bloating, abdominal distension and vomiting
and shock .
• At first, the intestines try to remove the obstruction by hyper-peristalsis.
Obstruction may be partial or complete
• Abdominal sounds can be heard at this time as rumbles. Later the rumbling
disappears with strangulation and necrosis. (blood supply is disturbed) The pain
also changes character.
• There is abdominal rigidity; the patient is weak, anxious and restless.
This condition requires urgent attention before the gut becomes perforated and
gangrenous .
Clinical manifestations-small bowel
obstruction
• Pt may pass blood and mucus
• nausea and Vomiting
• Complete obstruction peristaltic waves increase initially , eventually assume a reverse
direction
• Fecal vomiting for obstruction at the ileum
• Constipation
• Dehydration , intense thirst ,drowsiness generalised malaise , parched tongue,
tarchycardia
• Distended abdomen
• Colicky abdominal pain
• Hypotention, Hypovolemic shock and loss of plasma volume
Large Bowel Obstruction
• Symptoms develop and progress slowly
• Colon and rectum obstruction ,constipation may be the only symptom for
months
• Altered stool
• Blood in stool may lead to-iron deficiency anemia
• Weakness ,weight loss, anorexia,
• Abdominal distension
• loops of large bowel become visibly outlined in the abdominal wall
• Crampy lower abdominal pain,
• Fecal vomiting , shock may occur
Management of Intestinal
Obstruction
• In the patient with intestinal obstruction, treatment and care is
directed towards decompression of the intestines by removal of gas
and fluid, nasogastric aspiration (by NG tube ) , Correction and
maintenance of fluids and electrolyte balance and removal of the
obstruction is also necessary. colonoscopy may be performed to to
untwist and decompress the bowel.
• A cecostomy ( operation to provide out let for gas and small amounts
of drainage) into the cecum may be urgently performed to relieve
obstruction in patients who are poor surgical risk. (patients who can
not withstand surgery)
Management of Intestinal
Obstruction
• A rectal tube is used to decompress an area that is lower in the
bowel. In most mechanical obstructions, necrosis is present. The
usual treatment is surgical resection to remove the obstruction.
• A temporary or permanent colostomy may be necessary . An
ileoanal anastomosis may be performed if removal of the entire large
bowel is nacessary
• Whenever you perform such procedures as gastric lavage, NG tube
fixing, giving enema, irrigation and care of colostomies and
ileostomies you must remember to obtain informed consent from
the patient.
Management – cont’d
• On the other hand, you yourself must understand the preparation,
necessary steps of the procedure and complications to be anticipated
before you get started.
• The post-operative care of a patient who has gastric surgery should
focus on assessing the wound or stoma, protecting the skin, and
assisting the patient to adapt physiologically and psychologically to
their wounds. The patient’s nutrition is also an important aspect. You
must ensure that the patient receives all the necessary nutrients.
Disorders of the Liver
• Normal function of the liver is disrupted when regeneration of
hepatocytes does not keep up with damage resulting in
hepatocellular failure and also when there is gradual replacement of
damaged cells with fibrous tissue
• . Diseases that lead to hepatocellular dysfunction may be caused by
bacteria and viruses , anoxia , metabolic disorders, toxins and drugs
and nutritional deficiencies and hypersensitivity states
and ,obstruction of bile flow.
• Once the liver cells have been destroyed, cell regeneration can occur
only if the disease process is not too toxic for the cells. The end result
of chronic damage is a shrunken fibrotic liver.
Clinical Manifestation

• Manifestations of liver disease are mainly due to an alteration of

metabolic and excretory functions of the liver. Jaundice is present due
to an increase in serum bilirubin levels. Abnormal protein metabolism
results in decreased serum albumin concentration and oedema.
Serum ammonia levels increase leading to signs of central nervous
impairment. Ascites and varices ,occurs due to increased portal vein
blood pressure ( portal hypertension) which results in leakage of
fluid into the peritoneal cavity. The patient may also have easy
bleeding due to lack of production of blood clotting factors
(nutritional deficiencies) and hepatic encephalopathy and coma
Management of Liver Disease
• Viral hepatitis is treated with a low protein, high carbohydrate and low-fat
diet. Vitamin supplements and rest will help the patient recover faster. No
drugs are given to these patients because the liver may be unable to
metabolise them. However, supportive therapy can be included. General
infection prevention measures are necessary to avoid the spread of viral
hepatitis. Immunisation and use of immune globulin may also be useful.

Toxic and drug induced hepatitis are largely managed with support to the
patient in terms of nutrition, rest, fluids and electrolyte monitoring. The
patient with liver cirrhosis needs at least 300 calories in the diet per day.
High carbohydrate intake, low proteins (depending on the stage), low fat
diet, low sodium (for the patient with ascitis) is all indicated.
Clinical Manifestation
• Acute liver damage may be completely reversible or may progress to
cirrhosis whereby the parenchymal cells are replaced with fibrotic
tissue. When the ability of the liver to carry out its excretory and
metabolic function falls below the needs of the body, the patient is
said to be in Liver failure. Hepatic coma results when liver
dysfunction is so severe that the liver is unable to remove end
products of metabolism from the blood stream.
Acute Hepatitis
• This may be a result of viral infection or ingestion of toxic substances.

Viral Infections
• Hepatitis A, ( formally infectious hepatitis ) caused by the Hepatitis A
virus and is transmitted through the fecal oral route. The incubation
period is 15 to 40 days and the viruses are excreted in feaces. More
prevalent in countries with overcrowding and poor sanitation It is
commonly transmitted sexually in homosexual men.
• With infection no carrier states exists ,no chronic hepatitis associated
with HAV and confers immunity against itself.
Acute Hepatitis
• Hepatitis B ( formerly serum hepatitis) is the more serious of the viral
hepatitis. The incubation period is 50 to 180 days. It is spread by blood and
blood products, thus making it common among persons whose occupation
involves contact with blood and blood products and also among
intravenous drug addicts and male homosexuals .HBV is transmitted
through mucous membranes and breaks in the skin. The virus is also
spread by body fluids e.g. saliva, semen, vaginal secretions and from the
mother to the foetus not via the umbilical vein but from mother at time of
birth and contact there after .
• 90% of HBV patients recover in 6/12 .10% progress carrier state or develop
chronic hepatitis with persistent HBV infection and hepatocellular injury
and inflammation.
Acute Hepatitis
• Infection usually leads to severe illness lasting 2 to 6 weeks. On
infection, antibodies are formed and immunity persists after recovery.
Type B virus may cause massive liver necrosis and death. This
condition can result in hepatocellular carcinoma and liver cirrhosis.
• Hepatitis C virus (formerly non A , non B hepatitis) is also spread by
blood and blood products and is therefore prevalent in IV drug
abusers. The infection can be asymptomatic but when hepatitis
develops, it is often recurrent and may result in chronic liver disease.
Other viruses are hepatitis D,E, and G
Acute Hepatitis
non viral hepatitis
• Toxic hepatitis . Certain chemicals have toxic effects on the liver and
produce acute liver cell necrosis ,or toxic hepatitis when
inhaled ,injected parenterally or taken by mouth ie carbon
tetrachloride, phosphorus ,chloroform,and gold compounds .The
extent of the damage usually depends on the dose and duration of
exposure.
• . Alcohol toxicity also causes hepatitis. This occurs after chronic abuse
of alcohol and the symptoms include jaundice, hepatomegally ,
anorexia and malaise.
Acute Hepatitis
non viral hepatitis

• Drug induced hepatitis

• Due to sensitivity to medications ,with abrupt onset of chills ,fever
rash, pruritus ,arthralgia, anorexia and nausea .drugs include
isoniazid ,halothane, acetaminophen ,methyldopa ,some
antibiotics ,antimetabolites and anesthetic agents .later jaundice ,dark
urine ,enlarged and tender liver. If fever ,rash ,or pruritus occurs from
any medication its use should be stopped immediately
• High doses of corticosteroids is used to treat severe hypersensitivity
reactions.
Chronic Hepatitis
• This is where hepatitis persists for more than 6 months.

Diagnosis of Liver Disease

• Liver function is measured using liver function tests. However, these
tests are not sensitive indicators as many other disorders can influence
the results.
• On physical examination, the liver of a patient with cirrhosis is small and
hard, while the liver of a patient with acute hepatitis is quite soft.
Tenderness of the liver is a sign of recent acute enlargement with
consequent stretching of the liver capsule. The absence of tenderness
may imply that the enlargement is longstanding.
DX of liver disease
• The liver of a patient with viral hepatitis is tender, while that of a
patient with alcoholic hepatitis is not.
• Liver enlargement is an abnormal finding that requires further
evaluation.
• Liver biopsy facilitates sampling of the liver tissue by needle aspiration
and this aids in diagnosis of hepatic disorders.
Management of Liver Disease
• Viral hepatitis is treated with a low protein, high carbohydrate and low-fat
diet. Vitamin supplements and rest will help the patient recover faster. No
drugs are given to these patients because the liver may be unable to
metabolise them. However, supportive therapy can be included. General
infection prevention measures are necessary to avoid the spread of viral
hepatitis. Immunisation and use of immune globulin may also be useful.

Toxic and drug induced hepatitis are largely managed with support to the
patient in terms of nutrition, rest, fluids and electrolyte monitoring. The
patient with liver cirrhosis needs at least 300 calories in the diet per day.
High carbohydrate intake, low proteins (depending on the stage), low fat
diet, low sodium (for the patient with ascites) is all indicated.
Management of Liver Disease -
cont’d
• Should the condition get worse, proteins should be limited to avoid
accumulation of ammonia in the body leading to hepatic
encephalopathy. This particular patient should receive complete bed
rest, diuretics and B-complex vitamins. They should abstain from alcohol
totally.

The complications of cirrhosis that should be managed at the same time

are portal hypertension and oesophageal varices, peripheral oedema,
ascitis, hepatic encephalopathy and the hepatorenal syndrome. No
doubt you have nursed patients with these complications. Hypertension
is managed with antihypertensive medication. Anaemia should be
treated with transfusion if it is severe or with haematinic drugs.
Portal Hypertension
• This is a condition characterised by an elevation of portal venous pressure. Portal
venous pressure is determined by the portal blood flow and the portal vascular
resistance. In many instances, increased vascular resistance is usually the main factor
in the aetiology of portal hypertension. In childhood, extrahepatic portal vein
obstruction is frequently the cause of portal hypertension while in adults, cirrhosis is
the main cause. Schistosomiasis also causes portal hypertension in endemic areas.
• Increased portal vascular resistance results in a gradual reduction in the flow of
portal blood to the liver and simultaneously to the development of collateral vessels
which allow portal blood to bypass the liver and enter the systemic circulation
directly. Collateral vessel formation is widespread but occurs predominantly in the
GIT, mainly in the oesophagus, stomach, rectum, anterior abdominal wall and in the
renal, ovarian and testicular vasculature.
Portal Hypertension
• Clinical features result from portal venous congestion and from
collateral vessel formation. These include splenomegally and
hypersplenism. Collateral vessels may be visible on the anterior
abdominal wall and occasionally radiate from the umbilicus to from a
caput medusae. Collateral vessels in the stomach, oesophagus and
rectum cause bleeding. This condition can lead to ascites, renal failure
and hepatic encephalopathy. Diagnosis of portal hypertension is via
ultrasonography and portal venography.
Liver Cirrhosis
• This is a disease characterised by fibrosis and formation of abnormal nodules of
liver tissue. The disorder is commonly associated with alcoholism, but it can also
follow such other conditions as hepatitis, toxic reactions, and iron and copper
deposition. Cirrhosis can be post necrotic, that is, following an infection like viral
hepatitis or it can be biliary which is preceded by obstruction to bile flow.
• Patients present with pruritus, hepatomegally, pain, ascitis and easy bleeding
because of decreased production of clotting factors. Toxic substances of
metabolism will also accumulate and patients can have many other symptoms.
Anaemia, peripheral oedema, oliguria, malabsorption, drug toxicities and hepatic
encephalopathy develop. These manifestations affect the endocrine system, skin
and haematological functions. It therefore, requires serious consideration during
management.
Hepatic Encephalopathy
• This is a neuropsychiatric syndrome caused by liver disease that is thought to result from
accumulation of toxic substances such as ammonia within the brain. This occurs when these
substances are not metabolised in the liver as occurs in cirrhosis.

Clinical features include changes of intellect, personality, emotions and consciousness, with or
without neurological signs. In early stages, features are mild but as the condition becomes more
severe, the patient has inability to concentrate, confusion, disorientation, drowsiness, slurring of
speech and sometimes convulsions. Overt psychosis and convulsions may also occur.
• Episodes of encephalopathy are usually reversible until terminal stages of cirrhosis. In managing
this condition, the aim is to reduce or eliminate protein intake, and to suppress production of
neurotoxins by bacteria in the bowel. Lactulose is also given and it produces an osmotic laxative
effect, reduces the pH of the colonic content thereby limiting colonic ammonia absorption and
promotes the incorporation of nitrogen into the bacteria. Neomycin is also used as it acts by
reducing the bowel flora.
• You should read further on hepatic coma and the hepatorenal syndrome.
Diseases of the Gall Bladder
• The gall bladder is most commonly affected by gallstones
(cholelithiasis) and inflammation (cholecystitis). Gallstones are
formed through precipitation of constituents of bile.
• Abnormal composition of bile, stasis of bile and inflammation of the
gallbladder contribute to the process of precipitation. Gallstones start
manifesting symptoms when they block the ducts. Pain is common.
Factors that predispose to gallstones include:
• Changes in bile composition
• High levels of blood and dietary cholesterol
• Cholecystitis
• Diabetes Mellitus when associated with high blood cholesterol levels
• Haemolytic disease
• Female gender
• Obesity
• Long term use of oral contraceptives
Gallstones – cont’d
• Diagnosis of gallstones is by
ultrasonography, cholecystography
and percutaneous Transhepatic
Cholangiography.
• Complications of cholelithiasis
include biliary colic, inflammation
and inpaction.
• Cholelithiasis commonly occurs
together with cholecystitis. The
manifestations of cholecystitis
include:
Gallstones – signs and symptons
• Intolerance of fatty foods
• Belching
• Vomiting
• Jaundice
• Fever
• Cholecystitis can be acute or
chronic. If chronic, it can
contribute to cancer of the gall
bladder.
Care of the Patient with Gall
Bladder Disease
• The management of an adult with gall bladder disease should start
with a primary assessment. The data will be obtained by finding out
about the clinical presentation of the disease, which has already been
mentioned. In those patients with gall bladder disease, it is advisable
to concentrate on certain goals to be able to achieve desired results.
These goals include:
• Relief of pain and discomfort
• Prevention of complications after surgery
• Prevention of recurrent attacks and maintenance of desired lifestyle
Care of the Patient with Gall
Bladder Disease
• The patient with cholelithiasis (gall stones) may be put either on
conservative or surgical treatment. Conservatively IV fluids, nil per
oral, NG tube feeding, low fat diet, antiemetics, analgesics and fat
soluble vitamins (ADE and K) are used. Anticholinergics, bile salts,
antibiotics and bile acid therapy will benefit the patient. The
Anticholinergics will affect the contraction of the bile duct.
• The surgical management involves cholecystectomy. When one has
cholecystitis, treatment is mainly supportive and symptomatic. For
instance, if nausea and vomiting are severe, gastric decompression is
done to prevent gall bladder stimulation. Anticholinergic and
analgesics may be given to these patients to decrease the pain.
Pancreatitis
• Pancreatitis is an inflammation of the pancreas. Acute pancreatitis is
when the structure and function of the pancreas usually return to
normal after the acute attack.
• Chronic pancreatitis results in permanent abnormalities of pancreatic
function. Acute pancreatitis occurs after digestion of this organ by the
very enzymes it produces, especially trypsin. Other associated causes
of pancreatitis include bacterial or viral infections, blunt abdominal
trauma, ischemic vascular disease and use of drugs such
corticosteroids, oral contraceptives, narcotics and thiazide diuretics.
Management of Pancreatitis
• The patient should therefore minimise physical activity through bed rest, receive a
strong analgesic, nil per oral with NG tube suction, and IV fluids. The use of anti-
cholonergic drugs can decrease pain.
• The patient with chronic pancreatitis requires prevention of attacks and frequent doses
of analgesics. Pancreatic exocrine and endocrine insufficiency should be assessed and
modes of management considered. Diet, pancreatic enzyme replacement and control of
the diabetes are measures used to control the insufficiency. The patient may not
tolerate fatty, rich and stimulating foods and, these must be avoided. You should stress
that the patients avoid alcohol totally. Antacids and anti-cholinergic drugs are given to
decrease hydrochloric acid secretion. Surgery may be used to treat chronic pancreatitis.
Patients who have surgery should have replacement of the hormones.
• Always remember to manage this patient for the potential of development of diabetes
mellitus.
JAUNDICE
• When the bilirubin concentration in the blood is abnormally
• elevated, all the body tissues, including the sclerae and the skin,
• become yellow-tinged or greenish-yellow, a condition called jaundice
Management of Pancreatitis
• The objectives of therapeutic management of acute pancreatitis
include:
• Relief of pain
• Prevention or treatment of shock
• Reduction of pancreatic secretions
• Control of fluids and electrolyte balance
• Prevention and treatment of infection
• Removal of the precipitating cause
• jaundice.
• Jaundice becomes clinically evident when the serum bilirubin
• level exceeds 2.5 mg/dL (43 fmol/L). Increased serum bilirubin levels
• and jaundice may result from impairment of hepatic uptake,
• conjugation of bilirubin, or excretion of bilirubin into the biliary
• system. There are several types of jaundice: hemolytic, hepatocellular,
• obstructive, or jaundice due to hereditary hyperbilirubinemia.
• Hepatocellular and obstructive jaundice are the two types commonly
associated with liver disease
Hemolytic Jaundice
• Hemolytic jaundice is the result of an increased destruction of the
• red blood cells, the effect of which is to flood the plasma with
• bilirubin so rapidly that the liver, although functioning normally,
• cannot excrete the bilirubin as quickly as it is formed. This type
• of jaundice is encountered in patients with hemolytic transfusion
• reactions and other hemolytic disorders. The bilirubin in the blood
• of these patients is predominantly of the unconjugated, or free,
• type. Fecal and urine urobilinogen levels are increased, but the
• urine is free of bilirubin. Patients with this type of jaundice, unless
• their hyperbilirubinemia is extreme, do not experience symptoms
• or complications as a result of the jaundice per se. Prolonged
• jaundice, however, even if mild, predisposes to the formation of
• pigment stones in the gallbladder, and extremely severe jaundice
• (levels of free bilirubin exceeding 20 to 25 mg/dL) poses a risk for brain stem damage
Obstructive Jaundice
• Obstructive jaundice of the extrahepatic type may be caused by
• occlusion of the bile duct by a gallstone, an inflammatory process,
• a tumor, or pressure from an enlarged organ. The obstruction may
• also involve the small bile ducts within the liver (ie, intrahepatic
• obstruction), caused, for example, by pressure on these channels
• from inflammatory swelling of the liver or by an inflammatory
• exudate within the ducts themselves. Intrahepatic obstruction resulting
• from stasis and inspissation (thickening) of bile within the
• canaliculi may occur after the ingestion of certain medications,
Assessment-bulging flanks in supine position
percussion /fluid wave
• Medical Management
• DIETARY MODIFICATION
• The goal of treatment for the patient with ascites is a negative
• sodium balance to reduce fluid retention. Table salt, salty foods,
• salted butter and margarine, and all ordinary canned and frozen
• foods (foods that are not specifically prepared for low-sodium diets)
• should be avoided. It may take 2 to 3 months for the patient’s taste
• buds to adjust to unsalted foods. In the meantime, the taste of unsalted
• foods can be improved by using salt substitutes such as lemon
• juice, oregano, and thyme. Commercial salt substitutes need to be
• approved by the physician because those containing ammonia
• could precipitate hepatic coma. Most salt substitutes contain potassium
Hepatocellular Jaundice
• Hepatocellular jaundice is caused by the inability of damaged
• liver cells to clear normal amounts of bilirubin from the blood.
• The cellular damage may be from infection, such as in viral hepatitis
• (eg, hepatitis A, B, C, D, or E) or other viruses that affect
• the liver (eg, yellow fever virus, Epstein-Barr virus), from medication
• or chemical toxicity (eg, carbon tetrachloride, chloroform,
• phosphorus, arsenicals, certain medications), or from alcohol.
• Cirrhosis of the liver is a form of hepatocellular disease that may
• produce jaundice. It is usually associated with excessive alcohol
• intake, but it may also be a late result of liver cell necrosis caused
• by viral infection. In prolonged obstructive jaundice, cell damage
• eventually develops, so that both types appear together.
• Patients with hepatocellular jaundice may be mildly or severely
• ill, with lack of appetite, nausea, malaise, fatigue, weakness,
• and possible weight loss. In some cases of hepatocellular disease,
• jaundice may not be obvious. The serum bilirubin concentration
• and urine urobilinogen level may be elevated. In addition, AST
• and ALT levels may be increased, indicating cellular necrosis. The
• patient may report headache, chills, and fever if the cause is infectious.
• Depending on the cause and extent of the liver cell
• damage, hepatocellular jaundice may or may not be completely reversible
Hereditary Hyperbilirubinemia
• Increased serum bilirubin levels (hyperbilirubinemia) resulting from
• several inherited disorders can also produce jaundice. Gilbert’s
syndrome
• is a familial disorder characterized by an increased level of
unconjugated
• bilirubin that causes jaundice. Although serum bilirubin
• levels are increased, liver histology and liver function test results are
• normal, and there is no hemolysis. This syndrome affects 2% to 5
PORTAL HYPERTENSION
• Obstructed blood flow through the damaged liver results in increased
• blood pressure (portal hypertension) throughout the
• portal venous system. Although portal hypertension is commonly
• associated with hepatic cirrhosis, it can also occur with noncirrhotic
• liver disease. While splenomegaly (enlarged spleen) with
• possible hypersplenism is a common manifestation of portal hypertension,
• two major consequences of portal hypertension are
• ascites and varices.
• In ascites, fluid accumulates in the abdominal cavity. Although
• ascites is often a result of liver damage, it may also occur
• with disorders such as cancer, kidney disease, and heart failure.
• Varices are varicosities that develop from elevated pressures transmitted
• to all of the veins that drain into the portal system. They
• are prone to rupture and often are the source of massive hemorrhages
• from the upper GI tract and the rectum. In addition,
• blood clotting abnormalities, often seen in patients with severe
• liver disease, increase the likelihood of bleeding
ASCITES
• Clinical Manifestations
• Increased abdominal girth and rapid weight gain are common
• presenting symptoms of ascites. The patient may be short of
• breath and uncomfortable from the enlarged abdomen, and striae
• and distended veins may be visible over the abdominal wall. Fluid
• and electrolyte imbalances are common.
Assessment-bulging flanks in supine position
percussion /fluid wave
• Medical Management
• DIETARY MODIFICATION
• The goal of treatment for the patient with ascites is a negative
• sodium balance to reduce fluid retention. Table salt, salty foods,
• salted butter and margarine, and all ordinary canned and frozen
• foods (foods that are not specifically prepared for low-sodium diets)
• should be avoided. It may take 2 to 3 months for the patient’s taste
• buds to adjust to unsalted foods. In the meantime, the taste of unsalted
• foods can be improved by using salt substitutes such as lemon
• juice, oregano, and thyme. Commercial salt substitutes need to be
• approved by the physician because those containing ammonia
• could precipitate hepatic coma. Most salt substitutes contain potassium
BED REST
In patients with ascites, an upright posture is associated with
activation
of the renin-angiotensin-aldosterone system and sympathetic
nervous system (Porth, 2002). This results in reduced renal
glomerular filtration and sodium excretion and a decreased
response
to loop diuretics. Bed rest may be a useful therapy, especially
for patients whose condition is refractory to diuretics.
PARACENTESIS
Paracentesis is the removal of fluid (ascites) from the peritoneal
cavity through a small surgical incision or puncture made
through
the abdominal wall under sterile conditions. Ultrasound
guidance
may be indicated in some patients at high risk for bleeding
because of an abnormal coagulation profile or in those who
have
had previous abdominal surgery and who may have adhesions.
Paracentesis was once considered a routine form of treatment
for
ascites but is now performed primarily for diagnostic
examination
of ascitic fluid, for treatment of massive ascites that is resistant
to
nutritional and diuretic therapy and that is causing severe
problems
to the patient, and as a prelude to diagnostic imaging studies,
peritoneal dialysis, or surgery. A sample of the ascitic fluid may
be
sent to the laboratory for analysis. Cell count, albumin and total
protein levels, culture, and occasionally other tests are perform
ESOPHAGEAL VARICES
• Pathophysiology
• Esophageal varices are dilated, tortuous veins usually found in the
• submucosa of the lower esophagus, but they may develop higher in
• the esophagus or extend into the stomach. This condition nearly
• always is caused by portal hypertension, which in turn is due to obstruction
• of the portal venous circulation within the damaged liver.
• Because of increased obstruction of the portal vein, venous
• blood from the intestinal tract and spleen seeks an outlet through
• collateral circulation (new pathways of return to the right atrium).
• The effect is increased pressure, particularly in the vessels in the
• Clinical Manifestations
• The patient with bleeding esophageal varices may present with
• hematemesis, melena, or general deterioration in mental or physical
• status and often has a history of alcohol abuse. Signs and symptoms
of shock
Medical Management
• Bleeding from esophageal varices can quickly lead to hemorrhagic
• shock and is an emergency. This patient is critically ill,
• requiring aggressive medical care and expert nursing care, and
• is usually transferred to the intensive care unit for close monitoring
• and management
• IV fluids to replace fluid volume and electrolytes
• Blood transfusion may be required
• Catheterize to monitor urine output
PHARMACOLOGIC THERAPY
• Vasopressin (Pitressin) may be
• the initial mode of therapy because it produces constriction of the
• splanchnic arterial bed and a resulting decrease in portal pressure.
• It may be administered intravenously or by intra-arterial infusion
• Close monitoring of vital signs and intake output –vasopressin may cause
hyponatremia and have antidiuretic effect
• Vasopressin with nitroglcerine
• Somatostatin
• Propranolol –beta blocking agents decresase portal pressure
• Nitrates –lower portal pressure by decreas
BALLOON TAMPONADE
• To control hemorrhage in certain patients, balloon tamponade
• may be used. In this procedure, pressure is exerted on the cardia
• (upper orifice of the stomach) and against the bleeding varices
• by a double-balloon tamponade (Sengstaken-Blakemore tube)
• (Fig. 39-7). The tube has four openings, each with a specific purpose:
• gastric aspiration, esophageal aspiration, inflation of the
• gastric balloon, and inflation of the esophageal balloon
HEPATIC CIRRHOSIS
• Cirrhosis is a chronic disease characterized by replacement of normal
• liver tissue with diffuse fibrosis that disrupts the structure and
• function of the liver. There are three types of cirrhosis or scarring
• of the liver:
• • Alcoholic cirrhosis, in which the scar tissue characteristically
• surrounds the portal areas. This is most frequently
• due to chronic alcoholism and is the most common type
• of cirrhosis
• • Postnecrotic cirrhosis, in which there are broad bands of
• scar tissue as a late result of a previous bout of acute viral
• hepatitis.
• • Biliary cirrhosis, in which scarring occurs in the liver around
• the bile ducts. This type usually is the result of chronic biliary
• obstruction and infection (cholangitis); it is much less
• common than the other two types.
Clinical Manifestations
• Compensated (less severe)
• Intermittent mild fever
• Vascular spiders
• Palmar erythema (reddened palms)
• Unexplained epistaxis
• Ankle edema
• Vague morning indigestion
• Flatulent dyspepsia
• Abdominal pain
• Firm, enlarged liver
• Splenomegaly
Clinical manifestations
(hepatic dysfunction)
• Decompensated
• Ascites hypotension
• Jaundice sparse body hair
• Weakness
• Muscle wasting white nails
• Weight loss
• Continuous mild fever gonadal atrophy
• Clubbing of fingers
• Purpura (due to decreased platelet count)
• Spontaneous bruising
• Epistaxis
Medical Management
• The management of the patient with cirrhosis is usually based on
• the presenting symptoms. For example, antacids are prescribed to
• decrease gastric distress and minimize the possibility of GI bleeding.
• Vitamins and nutritional supplements promote healing of
• damaged liver cells and improve the general nutritional status.
• Potassium-sparing diuretics (spironolactone [Aldactone], triamterene
• [Dyrenium]) may be indicated to decrease ascites, if
• present; these diuretics are preferable to other diuretic agents because
• they minimize the fluid and electrolyte changes common
• with other agents. An adequate diet and avoidance of alcohol are
• essential. Although the fibrosis of the cirrhotic liver cannot be reversed,
• its progression may be halted or slowed by such measures.
NURSING PROCESS:
THE PATIENT WITH HEPATIC CIRRHOSIS
• Assessment
• Nursing assessment focuses on the onset of symptoms and the history
• of precipitating factors, particularly long-term alcohol abuse,
• as well as dietary intake and changes in the patient’s physical and
• mental status. The patient’s past and current patterns of alcohol
• use (duration and amount) are assessed and documented. It is also
• important to document any exposure to toxic agents encountered
• in the workplace or during recreational activities. The nurse documents
• and reports exposure to potentially hepatotoxic substances
• (medications, illicit IV/injection drugs, inhalants) or general anesthetic
• agents
NURSING DIAGNOSES
• • Activity intolerance related to fatigue, general debility, muscle
• wasting, and discomfort
• • Imbalanced nutrition, less than body requirements, related
• to chronic gastritis, decreased GI motility, and anorexia
• • Impaired skin integrity related to compromised immunologic
• status, edema, and poor nutrition
Liver Abscesses
• Two categories of liver abscess have been identified: amebic and
• pyogenic. Amebic liver abscesses are most commonly caused by
• Entamoeba histolytica. Most amebic liver abscesses occur in the
• developing countries of the tropics and subtropics because of
• poor sanitation and hygiene. Pyogenic liver abscesses are much
• less common but are more common in developed countries than
• the amebic type.
Pathophysiology
• Whenever an infection develops anywhere along the biliary or GI
tract, infecting organisms may reach the liver through the biliary
System, portal venous system, or hepatic arterial or lymphatic
system ,Most bacteria are destroyed .bacteria toxins destroy liver cells .
leucocytes migrate to the affected area .the result is an abscess cavity
full of liquid containing bacteria , dead and live leucocytes and
liquefied liver cells
Clinical Manifestations
• The clinical picture is one of sepsis with few or no localizing
• signs. Fever with chills and diaphoresis, malaise, anorexia, nausea,
• vomiting, and weight loss may occur. The patient may
• complain of dull abdominal pain and tenderness in the right
• upper quadrant of the abdomen. Hepatomegaly, jaundice, anemia,
• and pleural effusion may develop. Sepsis and shock may be
• severe and life-threatening.
Assessment and Diagnostic
Findings
• Blood cultures are obtained but may not identify the organism.
• Aspiration of the liver abscess, guided by ultrasound, CT, or MRI,
• may be performed to assist in diagnosis and to obtain cultures of
• the organism. Percutaneous drainage of pyogenic abscesses is carried
out to evacuate abscess and promote healing
• catheter may be left in place for continuous drainage; the patient
• must be instructed about its management.s material and promote
healing
Medical Management
• Treatment includes IV antibiotic therapy; the specific antibiotic
• used in treatment depends on the organism identified. Continuous
• supportive care is indicated because of the serious condition of the
• patient. Open surgical drainage may be required if antibiotic therapy
• and percutaneous drainage are ineffective.
 Nursing Management
• For patients who undergo evacuation and drainage of
• the abscess, monitoring of the drainage and skin care are imperative.
• Strategies must be implemented to contain the drainage and
• to protect the patient from other sources of infection. Vital signs
• are monitored to detect changes in the patient’s physical status.
• Deterioration in vital signs or the onset of new symptoms such as
• increasing pain, which may indicate rupture or extension of the
• abscess, is reported promptly. The nurse administers IV antibiotic
• therapy as prescribed. The white blood cell count and other laboratory
• test results are monitored closely for changes consistent with
• worsening infection. The nurse prepares the patient for discharge
• by providing instruction about symptom management, signs and
• symptoms that should be reported to the physician, management
• of drainage, and the importance of taking antibiotics as prescribed.