Transcript Pancreatitis Definition and Etiology

Ahmad Hormati
Assistant Professor of Gastroenterology
Qom University of Medical Sciences.
Email: [email protected]
http://hormatigi.ir/
Pancreatitis
Definition and Etiology
An acute inflammation process of the pancreas
with associated escape of the pancreatic
enzyme into surrounding tissue.
The primary etiologic factors are alcoholism &
biliary tract disease.
May be a complication of viral or bacterial
disease, peptic ulcer, trauma.
Demographic features
 Clinical, biochemical, and radiologic features need to
be considered together since none of them alone is
diagnostic of acute pancreatitis
 the two most common causes of acute pancreatitis in
adults are gallstones and alcoholism
 Acute gallstone pancreatitis occurs more often in
women
 while alcoholic pancreatitis occurs more often in men
Symptoms
 Pain:
Unlike biliary colic, which may last for six to eight hours, the pain of
pancreatitis can last for days.
Its onset is rapid, but not as abrupt as that with a perforated viscus,
reaching maximum intensity in many cases within 10 to 20 minutes.
One characteristic of the pain that is present in about one-half of
patients, and that suggests a pancreatic origin, is band-like radiation to
the back.
The abdominal pain is typically accompanied (in approximately 90
percent of patients) by nausea and vomiting, which may persist for
many hours.
Restlessness, agitation, and relief on bending forward are other notable
symptoms.
Painless disease is uncommon (5 to 10
percent) and may be seen in:
 the postoperative setting (especially renal
transplantation)
 in patients receiving peritoneal dialysis
 those with Legionnaire's disease
Physical examination
 Systemic features include fever, tachycardia, and, in
severe cases, shock and coma.
 In mild disease, the epigastrium may be minimally
tender. However, severe episodes are often associated
with abdominal distention, especially in the
epigastrium, and tenderness and guarding, which are
less than expected from the intensity of the patient's
discomfort.
 Respirations may be shallow due to diaphragmatic
irritation from inflammatory exudate, and dyspnea may
occur if there is an associated pleural effusion.
Physical examination
 Ecchymotic discoloration in the flank (Grey-
Turner's sign) or the periumbilical region (Cullen's
sign) occurs in 1 percent of cases but is not
diagnostic.
 These signs reflect intraabdominal hemorrhage and
are associated with a poor prognosis.
 Obstruction of the common bile duct, due to
choledocholithiasis or edema of the head of the
pancreas, can lead to jaundice.
Pancreatitis
Incidence & Risk Factors
Major- Biliary stones, Alcohol use/abuse
Minor- Age: 55 to 65 yrs. for biliary pancreatitis
45- 55 yrs. For alcohol-related
Female for biliary tract pancreatitis; Male-for
alcohol-related pancreatitis.
Trauma, Infectious disease, drug toxicities,
chronic diseases( inflammatory diseases).
Pancreatitis
Assessment
Pain:
Steady & severe in nature; located in the
epigastric or umbilical region; may radiate to
the back. Worsened by lying supine; may be
lessened by flexed knee, curved-back position.
Vomiting
Varies in severity, but is usually protracted,
worsened by ingestion of food or fluid. Does not
relieve the pain. Usually accompanied by
nausea.
Pancreatitis
Assessment con’t……
Fever:
Rarely exceeds 39 C.
Abdominal Finding:
Rigidity, tenderness, guarding, distended, decreased
or absent peristalsis and paralytic ileus.Fatty stools(steatorrhea)
Laboratory Finding:
Elevation of white count- 20,000-50,000.
Elevated serum lipase and amylase(5 to 40 times);
glucose, bilirubin, alkaline phosphatase. Urine amylase
elevated.Abnormal low serum CA, Na & Mg.-due to
dehydration. Binding of Ca in areas of fat necrosis.
Pancreatitis
Ranson’s criteria
Admission criteria
Age: 55 yrs. Or older
Criteria during initial 48
hours
Hct: decrease or more than
10%
WBC: 16,000/mm3 or
higher
BUN:increase greater than 5
mg/dl.
LDH: 350 IU/L or higher
Glucose > 200 mg/dl.
CA: falls to less than 8
mg/dl.
PaO2 < 60 mm Hg
Fluid sequestration; greater
than 6 liter.
AST: 250 U/L or higher
Background
Mild AP (no necrosis) – 0%

Sterile necrosis – 10%

Infected necrosis – 25%
Diagnosis
Laboratory
Amylase
 Lipase

Radiological
US
 CT scan

Blood tests
Amylase and lipase
Plasma level peak within 24 hours
t1/2 of amylase << lipase
Amylase
Lipase
Sensitivity
67-100
82-100
Specificity
85-98
86-100
Gut 1997,41:431-35; Br J Surg 1998,84:1665-69.
LABORATORY TESTS
 Serum amylase rises within 6 to 12 hours of onset, and is
cleared fairly rapidly from the blood (half-life approximately
10 hours).
 In uncomplicated attacks, serum amylase is usually elevated
for three to five days
 The serum amylase concentration in acute pancreatitis is
usually more than three times the upper limit of normal
 Substantial elevations in serum amylase (more than two
times the upper limit of normal) may, for reasons that are not
well understood, be less common in patients with
hypertriglyceridemia-associated pancreatitis
hyperamylasemia in nonpancreatic disease
 Disease can occur in other organs (eg, salivary glands
and fallopian tubes) that produce amylase
 Transmural absorption in intestinal infarction and
transperitoneal absorption with a perforated viscus
and peritonitis probably explain the hyperamylasemia
in these conditions
 There is decreased renal clearance of amylase in
patients with renal failure
 Increased serum amylase in cholecystitis is probably
due to subclinical or undiagnosed coexistent
pancreatitis
 Urine amylase: normal 3 percent amylase-to-
creatinine clearance ratio (ACCR), increases to
approximately 10 percent
Renal insufficiency interferes with accuracy and
specificity of the ACCR
Urinary amylase excretion is not increased in
macroamylasemia
other than to diagnose macroamylasemia, urinary
amylase and the ACCR offer no advantage over routine
serum amylase
 Serum lipase :difficult to perform and lacked precision
nonspecific elevations of lipase have been reported in
almost as many diseases as amylase
we and others have found that the combination of
enzymes does not improve diagnostic accuracy
daily measurement of enzymes has no value in
assessing the clinical progress or prognosis
The level of pancreatic enzyme elevation does not
correlate with severity of disease.
 Nonenzymatic pancreatic secretory
products
Pancreatitis-associated protein (PAP) no better
than conventional tests
 trypsinogen activation peptide (TAP) :TAP may
be useful in detection of early acute pancreatitis

 Markers of immune activation: Levels of
C-reactive protein above 150 mg/dL at 48
hours discriminate severe from mild disease
RADIOLOGIC FEATURES
 Abdominal plain film
unremarkable in mild disease
localized ileus of a segment of small intestine
("sentinel loop") or the "colon cutoff sign" in more
severe disease
 Chest film — Approximately one-third have
abnormalities such as elevation of a hemidiaphragm,
pleural effusions, basal atelectasis, pulmonary
infiltrates, or acute respiratory distress syndrome
 Abdominal ultrasound — A diffusely enlarged,
hypoechoic pancreas is the classic ultrasonographic
image of acute pancreatitis; it can also detect gallstones
in the gallbladder
colon cutoff sign
 CT scan — CT scan is the most important imaging test
pancreatic necrosis :which are seen as unenhanced areas
(less than 50 Hounsfield units after IV contrast) greater
than 3 cm in size.
there is little evidence in humans to support that contrast
media increase necrosis
Grade A – Normal pancreas
Grade B – Focal or diffuse enlargement of the gland
Grade C – grade B plus peripancreatic inflammation
Grade D – Grade C plus associated single fluid collection
Grade E – Grade C plus two or more peripancreatic fluid
collections or gas in the pancreas or retroperitoneum
Lipase has slightly higher sensitivity and
specificity and greater overall accuracy
than amylase
(Evidence category A)
US findings should be examined in all
patients with possible acute pancreatitis
on admission
(Evidence category B)
CT scan
Not necessary for the diagnosis
Diagnostic doubt
Atypical presentations
 Asymptomatic hyperamylasaemia or
hyperlipasemia

Gastroenterol Clin N Am 1990;19:811-42
Routine use of CT scan within 24-48 hours
of admission
(Evidence category C)
Initial Management
Monitoring – temp., pulse, blood pressure,
and urine output
Treatment –
Cardiopulmonary care
 Sufficient fluid resuscitation
 Pain control

Severity Stratification
Rationale
• Differentiate mild from severe acute
pancreatitis
Desirable features of Markers of
Severity
Accuracy - High sensitivity & PPV
Predictability within 24 hours of
admission
Easy to use
Clinical Features
Clinical examination
Age > 70 years
 Abdominal findings

increased tenderness
 rebound
 distension
 hypoactive bowel sounds

In first 24 hours of admission - unreliable
After 48 hours- as accurate as Ranson score
Multiple Factors Scoring
System
Ranson
Separate for alcohol and gallstone etiology
 Score > 3 = severe acute pancreatitis

Glasgow

valid in all types of pancreatitis
Both of these systems require 48 hours from
the admission for full assessment
Can J Gastroent 2003 325-328
APACHE II
Acute Physiology and Chronic Health Evaluation
as good as the Ranson or Glasgow at 24 and
48 hours of the admission
APACHE II score > 8 = Severe acute pancreatitis
Cumbersome to use if one does not use a pc or
palm - where the formula is easily downloaded
Br J Surg 1997,84:1665-69
If a multiple factor scoring system is to
be used, the best choice at present
appears to be APACHE II calculated at
24 hours Evidence category A
Tests
Trypsinogen
Trypsinogen activation peptide (TAP)
I
Trypsin
Inflammatory cascade (IL6, IL-8, TNF-)
II
C - reactive protein
Pancreatic injury
III
Amylase, Lipase, Trypsinogen
IV
Markers for Leakage of
Pancreatic Enzymes
Amylase/ Lipase
Degree of elevation shows little correlation with
disease severity and prognosis
 May have an inverse relationship with severity

Trypsinogen 2
Excreted into the urine
 Used as a screening test for acute
pancreatitis

Trypsinogen activation peptide
(TAP)

Small peptide
Advantage

Appear very early during the disease
Disadvantage

Limited "diagnostic window".


decrease very quickly irrespective of the course of
the disease
Not suitable for rapid simple analysis
Markers of Inflammation
TNF-alpha
Major role in mediating inflammatory response
 Conflicting reports as a predictor of severity

Interleukin-6 and 8.
Principal cytokine mediator
 Measured in serum and urine
 Discriminate severe from mild cases on day 1

C-reactive protein (CRP)
Acute phase reactant
Synthesized by the hepatocytes
Synthesis is induced by the release of
interleukin 1 and 6
Peak in serum is three days after the onset
of pain
Most popular single test severity marker
used today
Isenmann et al Pancreas 1993;8:358-61
C-reactive protein (CRP)
Gold standard for the prediction of the
necrotizing course of the disease
Accuracy of 86%
Readily available
C-reactive protein (CRP)
Advantage
• Used to monitor the clinical course of the
disease
Disadvantage
• Not always present on admission
• Lack specificity
Recommendation
A dynamic CT scan should be performed
in all (predicted) severe cases between 3
and 10 days after admission
(Evidence grade B)
Management of the Biliary
Pancreatitis
Passage or impaction of a
stone
Women (age of 50-70)
Mortality 6%
Endoscopic Retrograde
Cholangiopancreatography
(ERCP)
ERCP


Gold standard
Potential serious
complications
Abdominal Ultrasound
• GB stone
• CBD stone
Sensitivity
60-80%
30-60%
Infected Necrosis
June 10, 323 BC
The End
Pancreatitis
Nursing Interventions
Alleviate pain & anxiety. Anxiety increases pancreatic
secretions. Demerol-then morphine.
Reduce pancreatic stimulus- NPO, NGT to remove
gastric secretions. Drugs to reduce pancreatic secretionsanticholinergics-suppress vagal stimulation, NaHcoreverse metabolic acidosis.Regular insulin to treat
hyperglycemia.
Prevent or treat infection-with abx.
Aggressive respiratory care- monitor ABG.
Reduce body metabolism- bedrest, cool quiet environment.
Provide client and family instruction-avoid alcohol,
coffee,heavy meals and spicy food.
Pancreatitis
Major complications
Cardiovascular- hypotension/shock from hypovolemia.
Hematologic-Anemia from blood loss, DIC,
leukocytosis from gen.inflammation or secondary
infections.
Respiratory-atelectasis, pneumonia, pleural effusion,
ARDS
GI- bleeding
Renal- oliguria, acute tubular necrosis
Metabolic-hyperglycemia, hypocalcemia.
Complications:
Pancreatic Pseudocyst or Abscess
Cavity continuous with, surrounding or within the
pancreas fills with necrotic products and liquid
secretions
Leakage of enzymes inflame adjacent tissues
Sx: abdominal pain, N&V, palpable epigastric mass,
anorexia, persistently amylase levels, Leukocytosis,
Fever
May be visible on abdominal CT scan
May resolve or rupture causing peritonitis
Rx: prompt surgical drainage to prevent sepsis
©Altmiller
Systemic Complications:
Pulmonary: pleural effusion, atelectasis, pneumonia
which are all caused by enzyme induced inflammation
from the passage through transdiaphragmatic lymph
channels. Pt can develop ARDS
CV: Hypotension & shock due to hemorrhages into
pancreas or activated enzymes forming kinins which
cause vasodilation, capillary permeability,&
vascular tone
Neuro: Tetany due to hypocalcemia
©Altmiller
Goals
Relief of pain
Prevention or alleviation of shock
Reduction of pancreatic secretions
Normal fluid & electrolyte balance
Removal of the precipitating causes
Prevention of complications
Prevention of recurrent attacks
©Altmiller
Collaborative Care
Aggressive hydration with LR or volume expanders
(dextran, albumin)
CVP readings to guide fluid replacement
Dopamine to systemic vascular resistance (SVR)
for ongoing hypotension
Pain Management: may use MSO4 with an antispasmotic
Management of metabolic complications
©Altmiller
algorithm 1
CA of the Pancreas
Postoperative Care
Monitor vital parameters. Check vital signs, ABG,
intake and output. Be alert to signs of bleeding or
shock. Maintain urine output at 30 to 50 ml/hr.
Initiate pulmonary hygiene.
Establish effective pain management.
Monitor dressing and drainage tubes.
Maintain nutritional support with enteral and
parenteral support. Monitor BS and insulin.
Administer pancreatic enzyme replacement. Assess for
signs of dumping syndrome ( rapid shift of fluid from
vascular into the intestinal lumen with a resultant
decrease in blood volume).
Clinical Manifestations of
Chronic Pancreatitis
Heavy, gnawing feeling,
burning and cramp-like in
LUQ or mid-epigastic area
Malabsorption & weight
loss
Constipation
Steatorrhea
Mild jaundice with dark
urine
Diabetes mellitius
Increased serum amylase
Increased serum bilirubin
Increased alkaline phosphatase
Mild leukocytosis
Elevated sedimentation rate
Hyperglycemia
Arteriography or X-ray shows
fibrosis and calcification
ERCP indicates biliary disease
(chronic obstructive or chronic
calcifying pancreatitis)
©Altmiller
Collaborative Care for Chronic Pancreatitis
Prevention of attacks
Relief of pain with analgesics
Control of pancreatic exocrine and endocrine insufficiency
Bland, low-fat, high-carb, high-protein diet
Pancreatic enzyme replacement
 Pancreatin or pancrelipase
Bile salts to absorption of fat soluble vits (A, D, E, K)
Control of Diabetes if it develops
Total elimination of alcohol
Acid-neutralizing and acid-inhibiting drugs
Surgery indicated when biliary disease is present or if
obstruction or pseudocyst develops
©Altmiller
CHRONIC
PANCREATITIS
A 49-year-old man was admitted with a ninemonth history of intermittent attacks of epigastric
pain, jaundice and fever.
These attacks usually last up to several days
associated with nausea and vomiting.
He was well in between attacks and had no loss of
weight
What is your next step?
Lab Results
AP =1017
GGT= 269
AST =103
ALT =186
TB =2 (DB= 1.1)
Alb= 3.2
Lipase =33 (up to 244
during attacks)
Amylase= 44
Hb =12
WBC= 5.7
Plts= 223
Na =141
K =4.2
Ur =15
Cr =0.9
Ca =8.9
FBS:178
What are arrows?
Pancreatic calcification
Transabdominal US: No gallstones or
mass in head of pancreas
CT scan: The extrahepatic bile duct was
mildly dilated and "generous pancreas" was
noted but there was no mass.
Endoscopic Ultrasound
Diffuse hypoechoic enlargement of pancreas. Fine needle
aspirate of the pancreas was negative for tumor.
ERCP
There was a long segment of extrahepatic biliary stricture. The
pancreatic duct was normal in size but irregular. Brushings,
biopsies and bile aspirate were negative for tumor
The patient underwent Whipple's
operation
Histology of the pancreas showed
chronic pancreatitis, no
malignancy
Two presentation:
Episodes of acute inflammation in a previously
injured pancreas
 Chronic damage with persistent pain or
malabsorption

Etiology :

same as acute pancreatitis “pancreatitis associated
with gallstones predaminantly acute or relapsingacute”

More idiopathic types
Most common cause :
In adults: alcohol intake
 In children: cystic fibrosis

Idiopathic chronic pancreatitis is the leading
cause of nonalcoholic chronic pancreatitis
PATHOPHYSIOLOGY
The events that initiate an inflamatory process are
still not well understood
In the alcohol-induced : suggested that the primary
defect may be the precipitation of
protein(inspissated enzyme )
In fact ,shown that alcohol has direct toxic effect on
the pancreas
Clinical features
abdominal pain:


may be continuous, intermittent or absent
Pattern is often atypical




RUQ or LUQ of the back
Diffuse throughout upper abdomen
May be referred to the anterior chest or flank
Typical form:




Persistent , deep-seated,
Unresponsive to antacids
Worsened by alcohol intake or a heavy meal (especially fatty
foods)
Often need narcotics
Pancreatic insufficiency
Weight loss
 Fat malabsorption:



Pancreatic diabetes:


Steatorrhea: 15% of patients present with steatorrhea
and no pain
Like DM1 needs insulin , but risk of hypoglycemia
is more than it (because alfa cells is also affected
Fat-soluble vitamin deficiency rare
Lab data
Amylase and lipase : usually normal
CBC ,electrolytes, and liver function tests are typically
normal
Bilrubin and ALP may be increased
Impaired glucose intolerance and elevated fasting blood
glucose
Sudan staining of feces or quantitative test for steatorrhea
fecal elastase (Among pancreatic function tests, fecal
elastase measurement is the most sensitive and specific,
especially in the early phases of pancreatic insufficiency)
Cont,
Classic triad “ pancreatic calcification , steatorrhea , and
diabetes mellitus “usually establishes chronic
pancreatitis
Classic triad : found in fewer than one-third
It is often necessary to perform secretin stimulation test
(abnormal when 60% or more of pancreatic exocrine
function has been lost)
A decreased serum trypsinogen (<20ng/ml) or a fecal
elastase level of <100ug/mg of stool strongly suggests
severe pancreatic insufficiency
Imaging studies
Plain films :
Pancreatic calcifications : % 30
 most common with alcoholic pancreatitis, but is
also seen in the hereditary and tropical forms of
the disorder; it is rare in idiopathic pancreatitis.

CT, MRI, US
calcifications
ductal dilatation
enlargement of the pancreas
fluid collections (eg, pseudocysts)
ERCP
Choice when calcifications are not present
and there is no evidence of steatorrhea.
a normal study should not rule out the
diagnosis of chronic pancreatitis
ERCP
May provide useful information on the status of
the pancreatic ductal system
Abnormalities include :
1)luminal narowing
2)irregularitis in the ductal system with stenosis,
dilation,saculation,and ectasia
3)blockage of the duct by calcium deposits
Endoscopic ultrasonography
The most predictive endosonographic feature is the
presence of stone
Other suggestive features include:







visible side branches
cysts
lobularity
irregular main pancreatic duct,
hyperechoic foci and strands
dilation of the main pancreatic duct
hyperechoic margins of the main pancreatic duct.
Complications
pseudocyst formation
bile duct or duodenal obstruction
pancreatic ascites or pleural effusion
splenic vein thrombosis
Pseudoaneurysms
pancreatic cancer
acute attacks of pancreatitis( particularly
alcoholics who continue drinking)
DIFFERENTIAL DIAGNOSIS
Pancreatic cancer (most important)







older age
absence of a history of alcohol use
weight loss
a protracted flare of symptoms
onset of significant constitutional symptoms
pancreatic duct stricture greater than 10 mm in length on ERCP
Markers such as CA 19-9 and CEA
peptic ulcer disease
gallstones
irritable bowel syndrome
Acute pancreatitis
TREATMENT
PAIN MANAGEMENT
stepwise approach :
general recommendations
 pancreatic enzyme supplementation
 Analgesics
 invasive options

General recommendations
Establish a secure diagnosis
Cessation of alcohol intake
Small meals
Pancreatic enzyme supplements
not very effective
response may be better in young women with small duct disease.
MECHANISM:

suppression of feedback loops in the duodenum that regulate the release of
cholecystokinin (CCK), the hormone that stimulates digestive enzyme
secretion from the exocrine pancreas
six tablets of Viokase® which contains:



16,000 units of lipase
30,000 units of protease
30,000 units of amylase.
Patients should also be treated with acid
suppression (either with an H2 receptor
blocker or a proton pump inhibitor) to
reduce inactivation of the enzymes from
gastric acid.
Analgesics
if pancreatic enzyme therapy fails to control pain.
short course of narcotics coupled with low dose amitriptyline and a
nonsteroidal antiinflammatory
Simultaneous short-term hospitalization, with the patient kept NPO to
minimize pancreatic stimulation, may also be of benefit in breaking the
pain cycle.
Chronic narcotic analgesia may be required in patients with persistent
significant pain. Long-acting agents such as MS Contin or Fentanyl
patches are generally more effective than short acting medications,
which last only three or four hours.
Other medical therapies
octreotide :cannot be recommended for
general use.
Antioxidant therapy :vitamin C, E,
methionine and selenium
Specialized approaches
Celiac nerve blocks
Endoscopic stenting of the pancreatic duct or
pancreatic sphincterotomy
Extracorporeal shock wave lithotripsy
Surgery
Maldigestion management
Pancreatic enzymes:

Steatorrhea could be abolished if 10% of the normal
amount of lipase could be delivered to the duodenum at
the proper time

Poor therapeutic results because of :



Lipase is inactivated by gastric acid
Food empties from the stomach faster than do the pancreatic
enzymes
Batches of commercially available pancreatic extracts vary in
enzyme activity
Adjuants:
H2 blockers
 Sodium bicarbonate
 PPIs

Pancres
CA of the Pancreas
Etiology
Etiology-unknown. Malignant disease of the
exocrine pancreas & more than 85% of the cases
are ductal adenocarcinomas. 2/3 develop in the
head; remainder occur in the body or tail of the
gland. It occurs more commonly in male.
The tumor is usually deeply encased in normal
tissue & poorly demarcated. The common duct is
often obstructed and distended by the presence of
the tumor. Metastasis has almost always occurred
before the tumor produces the first symptoms.
CA of the Pancreas
Signs and Symptoms
Jaundice (lesions of pancreatic head only)
Clay-colored stool
Dark urine
Abdominal pain: usually vague, dull, non-specific
Weight loss
Anorexia
Nausea and vomiting
Glucose intolerance
GI bleeding
Spleenomegaly
ascites
CA of the Pancreas
Interventions
Non-surgical- High doses of opioid analgesics.
Chemotherapy, radiation therapy-intensive external
beam radiation therapy by shrinking the tumor
cells.
Surgical management: Whipple procedures: the
procedure entails the removal of the head of the
pancreas, duodenum, a portion of the jejunum, the
stomach and the gallbladder, with the anastomosis
of the pancreatic duct, the common bile duct, and
the stomach to the jejunum.
Pancreas:



head
body
tail
Investigations:







transabdominal ultrasound
contrast-enhanced spiral CT scan
laparoscopy
ERCP
percutaneous needle biopsy
MRI scanning and endoscopic ultrasound
several tumour markers (CA19-9)
Stages of pancreatic cancer:
I
II
III
IV
Treatment:

surgery
Whipple`s procedure
 total pancreatectomy
 distal pancreatectomy

radiation therapy
 chemotherapy

Whipple`s procedure:
WHO Pain relief ladder
Freedom from cancer pain
Prognosis:

dismal
Mean survival: < 6 months
5yr survival: < 2 %
After Whipple`s procedure: 5-14%
Better if: tumour < 3 cm
no nodes involved
negative resection margins at surgery
ampullary or islet cell tumors
Cholelithiasis
Definition, Incidence, Predisposing Factors
Also known as stones in the gallbladder
It is the most common disorder of the biliary
system and it has been estimated that 8-10% of
all adults in the U.S. have this condition.
Predisposing factors includes: gender, age,
estrogen RX or BCP’s, sedentary lifestyle, family
history and obesity.
Cholecystitis- inflammation of the gallbladder.
Cholelithiasis
Clinical Manifestations
Sudden-onset pain in the right upper quadrant (RUQ)
of the abdomen. Severe and steady in quality.
Frequently radiates to the right scapula or shoulder.
Persists for abt. 1 to 3 hours. May awaken the patient
at night. May be associated with consumption of a
large fatty meals.
Anorexia, nausea and vomiting.
Mild to moderate fever
Decreased or absent bowel sounds
Acute abdominal tenderness
Elevated WBC, slightly elevated bilirubin, and alkaline
phosphatase.
Cholelithiasis
Diagnostic Test
Ultrasound-best way to dx; 90-95% effective.
Serum studies- liver function test and serum
amylase
Cholangiogram
Gallbladder x-ray test.
Cholelithiasis
Interventions
Provide relief from vomiting. NGT-reduces distention
& eliminates gastric juices that stimulate
cholecystokinin.
Maintain fluid and electrolyte balance.
Monitor drug therapy. Administer broad spectrum
Abx. Chenodeoxycholic acid- bile acid dissolves
cholesterol calculi (60% of the stone).
NTG & papaverine to reduce spasms of duct.
Synthetic narcotics (Demerol, methadone) MSO4 may
cause spasms of Oddi and increase spasms.
Cholelithiasis
Interventions con’t…..
Provide low-fat diet to decrease gallbladder
stimulation; avoid alcohol and gas forming foods.
Maintain bedrest
Extracorporeal shock wave lithotripsy- shock wave
that disintegrates stones in the biliary system.
Ultrasound is used for stone localization before the
lithotriptor send waves through a water bag upon
which the patient is lying. Analgesics and sedatives to
reduce pain during procedures.
Cholecystitis
Assessment
Epigastric pain- after eating
Pain- localized in RUQ because of somatic sensory
nerves. Murphy’s sign- can’t take a deep inspiration
when assessor’s fingers are pressed below hepatic
margin. Pain begins 2 to 4 hours after eating fried or
fatty foods and persist more than 4 to 6 hours.
Nausea, vomiting, anorexia
Low-grade fever
Jaundice
Weight loss
Cholecystitis
Surgical Management
Cholecystectomy- removal of gallbladder after
ligation of the cystic duct and vessels.
Choledochostomy-opening into the common bile
duct for removal of stones. T-tube inserted into
duct and connected to drainage bottle. Purposeto decompress biliary tree and allow for
postoperative cholangiogram.
Endoscopic cholecystectomy-removal of
gallbladder through small puncture hole in the
abdomen. Laser dissects gallbladder.
Cholecystitis
Implementation
Position in low-to semi fowler’s position to facilitate
bile drainage.
Maintain skin integrity.
Prevent respiratory complications: TCDB, use of IS.
IF NGT is inserted-to relieve distention and increase
peristalsis.
If t-tube inserted-measure amt. & color. Clamp tube
before eating. As t-tube clamp-observe for abdominal
discomfort and distention. Unclamp if any N/V.
Provide low-fat high carb. and high protein.
Maintain for at least 2 to 3 months postoperatively.
Ultrasound images of a gallbladder
adenomatous polyp (left panel
arrowhead) compared to a gallstone
(right panel arrowhead). Note the
shadow cast by the stone (red