Transcript Slide 1

PANCREATITIS
By;
Col. Abrar Hussain Zaidi
INTRODUCTION
Pancreatitis is
an inflammatory process
in which pancreatic enzymes
auto digest the gland.
INTRODUCTION
Inflammation of Pancreas
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Acute
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Chronic
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Recurrent acute
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Acute on chronic
INTRODUCTION
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Acute pancreatitis - May heal without any loss of
function or morphologic changes.
Recurrent pancreatitis - recurs intermittently,
contributing to the functional and morphologic loss
of the gland.
Chronic pancreatitis-persistent low grade
inflammations.
INTRODUCTION
Clinical importance
-?
INTRODUCTION
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One of the commonest conditions that
a physician or a surgeon comes
across
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Associated morbidity is high
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The cost of treatment is high
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In severe cases the mortality
may be 20-30%
INTRODUCTION
Prevention of disease is possible
If
we are aware of etiological factors
and pathogenesis
ANATOMY
ANATOMY
PHYSIOLOGY
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EXOCRINE FUNCTION
ENDOCRNE FUNCTION
Acute pancreatitis
EPIDEMIOLOGY
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3% of all cases of abdominal pain admitted to hospital.
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40 cases per year per 100,000 adults.[International]
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Ranges between 5 and 80 per 100,000 population
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The highest incidence recorded in the United States and
Finland
In 80% of cases: mild and resolves without serious prob.
Sex No predilection exists.
Age- 35-64 years
PATHOPHYSIOLOGY
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located in the retroperitoneal space
No capsule,
inflammation can spread easily.
Local effects
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Acute edematous pancreatitis : When Parenchyma
edema and peripancreatic fat necrosis occur first
Haemorrhagic or narcotizing pancreatitis: When
necrosis involves the parenchyma, accompanied by
hemorrhage and dysfunction of the gland
PATHOPHYSIOLOGY
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pancreatic abscesses and Pseudocysts
due to necrotizing pancreatitis because
enzymes can be walled off by
granulation tissue
PATHOPHYSIOLOGY
systemic effects ;
Due to cytokines: bradykinins and phospholipase A.
Cytokines cause
Vasodilatation, increase in vascular permeability, pain,
and leukocyte accumulation in the vessel walls.
Fat necrosis may cause hypocalcaemia. Pancreatic B-cell
injury may lead to hyperglycemia.
PATHOPHYSIOLOGY
systemic effects ;
in its most severe form.
 Acute respiratory distress syndrome (ARDS),
 acute renal failure,
 cardiac depression,
 hemorrhage, and hypotensive shock
CAUSES
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Alcohol abuse - 44% of patients
At cellular level - ethanol leads to intracellular
accumulation of digestive enzymes and their
premature activation and release.
At ductal level - increases the permeability of
ductules, enzymes reach the parenchyma, resulting in
pancreatic damage.
Formation of protein plugs due to increases the
protein content of the pancreatic juice and decreases
bicarbonate levels and trypsin inhibitor concentrations.
This leads to the that block the pancreatic outflow and
obstruction.
OTHER MAJOR CAUSES
Biliary calculi
cholelithiasis, choledocholithiasis
calculi lodge in the pancreatic duct or ampulla of Vater
and obstruct the pancreatic duct, leading to
extravasation of enzymes into the parenchyma.
 Medications, including azathioprine, corticosteroids,
sulfonamides, thiazides, furosemides, NSAID”S
 Viral infections
 Trauma
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OTHER CAUSES
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ERCP
Hypertriglyceridemia (When the triglyceride level exceeds 1000 mg/U
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Peptic ulcer disease
Abdominal or cardiopulmonary bypass surgery, -by ischemia
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Trauma –blunt+penetrating
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Carcinoma of the pancreas, - outflow obstruction
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Viral infections, including mumps, coxsackievirus, cytomegalovirus (CMV),
hepatitis virus, Epstein-Barr virus (EBV), and rubella
Bacterial infections, such as mycoplasma ,Tuberculosis
Intestinal parasites, such as Ascaris, which can block the pancreatic outflow
Pancreas divisum
Scorpion and snake bites
ischemia or vasculitis
Autoimmune pancreatitis
CLINICAL PRESENTATION
History
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The main presentation - Epigastric pain or right
upper quadrant pain radiating through, rather than
around, to the back.
Nausea and/or vomiting
Fever
History of previous biliary colic Physical
Palpitations
Muscular spasm –in extremities may be noted
secondary to hypocalcemia.
CLINICAL PRESENTATION
Ask the patient about ;
 Recent surgery or invasive procedure e.g. ERCP
 Family history of hypertriglyceridemia.
 Alcohol consumption
CLINICAL PRESENTATION
EXAMINATION
Patients are acutely ill
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Tachypnea
Hypotension
Fever
Abdominal tenderness, distension, guarding, and
rigidity
Mild jaundice
Diminished or absent bowel sounds
CLINICAL PRESENTATION
EXAMINATION
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Basilar rales, especially in the left lung.
Pleural effusion
Because of contiguous spread of inflammation
from the pancreas
Severe cases may have;
Grey Turner sign (ie, bluish discoloration of the
flanks)
Cullen sign (ie, bluish discoloration of the
periumbilical
area)
caused by the retroperitoneal leak of blood from the
pancreas in hemorrhagic pancreatitis.
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Differential Diagnoses
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Abdominal Aneurysm
Hepatitis
Cholangitis
Mesenteric Ischemia
Cholecystitis and Biliary Colic
Intestinal Obstruction
Cholelithiasis
Choledocholithiasis
Gastroenteritis
Perforated viscus/du-perforation
Pancreatic cancer
Malabsorption syndromes
Ectopic pregnancy
DIAGNOSTIC WORK-UP
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HISTORY AND CLINICAL EXAMINATION
LABORATORY TESTS
IMMAGING STUDIES
DIAGNOSTIC WORK-UP
Laboratory Studies
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leukocytosis (WBC >12,000) -> polymorphs.
Hyperglycemia.
Disturbed in the electrolyte balance:Urea/creatinin
Na, K, Cl, CO2, P, Mg---secondary to third spacing
of fluids.
Acid base disturbances
Amylase levels, preferably the amylase P.> 3 times
-suggest the diagnosis .[ serum/peritoneal]
Lipase - elevated / remain high for 12 days.
Anemia
DIAGNOSTIC WORK-UP
Laboratory Studies
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liver function tests particularly in biliary calculi.
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Misc. Done in some hospitals in addition to the above,
especially to identify pancreatitis post ERCP .
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Urinary trypsinogen activation peptide
Increased serum trypsinogen2
Trypsin 2-alpha 1 antitrypsin complex values
DIAGNOSTIC WORK-UP
Imaging Studies
Plain X-rays
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kidneys, ureters, bladder (KUB)
Exclude viscus perforation (ie, air under the
diaphragm).
In patients with a recurrent episode of chronic
pancreatitis, peripancreatic calcifications may be
noted.
DIAGNOSTIC WORK-UP
Ultrasonography
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A screening test. poorly visualised in 25-50% of cases /
overlying gas shadows
Can show swollen pancreas, dilated common bile duct, and
free peritoneal fluid.
Useful to detect presence of gallstones.
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CT –scan is the most reliable imaging modality in the diagnosis of
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acute pancreatitis. The criteria for diagnosis are divided by Balthazar
and colleagues into 5 grades:
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Grade A - Normal pancreas
Grade B - Focal or diffuse gland enlargement
Grade C - Intrinsic gland abnormality recognized by haziness on the
scan
Grade D - Single ill-defined collection or phlegmon
Grade E - Two or more ill-defined collections or the presence of gas
in or nearby the pancreas
DIAGNOSTIC WORK-UP
Misc. Tests
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Urine para-aminobenzoic acid test (ie, bentiromide [Chymex] test) is
used for chronic pancreatitis to assess for the reserve function of the
pancreas. In patients with severe pancreatic insufficiency and
malabsorption, the sensitivity is 80–90%. In those with mild-tomoderate functional impairment, the sensitivity is as low as 37–46%.
Serum trypsinogen assay or the serum trypsin test can also be used
to assess the function of the pancreas in chronic pancreatitis. Only a
very low level of serum trypsinogen (<20 ng/mL) is reasonably
specific (90%) for chronic pancreatitis, and these are seen in
advanced chronic pancreatitis with steatorhea.7
Both of these tests are available to test for the pancreatic reserve in
chronic pancreatitis, and their specificity is similar in the advanced
versus the moderate chronic pancreatitis. Ordering them is
according to availability.
Value in acute on chronic pancreatitis
DIAGNOSTIC WORK-UP
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Peritoneal aspiration - free fluid without bacterial
contamination +>amylase+>TLC.
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ERCP with a sphincterotomy is warranted within the
first 72 hours. where a dilated obstructed common
bile duct is diagnosed by CT or USG with elevated
plasma bilirubin (>5 mg/dL)
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Laparoscopy or laparotomy: where suspicion is
high but tests are inconclusive.
Severity and prognostic assessment
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Prediction is difficult and unreliable.
Clinically apparent organ failure indicates a severe
attack.
Scoring systems: do increase accuracy.
Initially assessing the severity of an attack into mild
or severe has important implications for
management - and may prevent deaths.
Severity and prognostic assessment
Scoring systems:
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Glasgow
Ranson
Apache II scores
can indicate prognosis particularly
Glasgow prognostic score
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Age >55 years
WBC >15 x109/l
Urea >16mmol/l
Glucose >10mmol/l
pO2 <8kPa (60mmhg)
Albumin <32g/l
Calcium <2mmol/l
LDH >600 units/l
AST/ALT >200 units
Ranson's criteria
Present on admission:
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Age >55 years
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WBC >15 x109/l
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Glucose >10mmol/l
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LDH >600 units/l
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SGOT >250 units/l
Developing during first 48 hours:
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Haematocrit fall 10%
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Urea increase >8mg/dl
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Serum Ca <8mg/dl
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Arterial O2 saturation <60mmHg
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Base deficit >4meq/l
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Estimated fluid sequestration >600ml
Any 3 factors means severe in both systems.
scoring.
 A Ranson score of 0-2 has a minimal mortality rate,
and the patient is admitted to the regular ward for
medical therapy and support.
 A Ranson score of 3-5 has a 10-20% mortality rate,
and the patient should be admitted to the intensive
care unit.
 A Ranson score after 48 hours higher than 5 has a
mortality rate of more than 50% and is associated
with more systemic complications.
Treatment
According to severity
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Mild cases in wards
Severe cases to be Treat in ITU or high dependency
unit.
Majority - treated conservatively
Emergency surgery in small proportion of cases
Elective surgery in biliary calculi
Treatment
Emergency Department Care
Most of the cases are treated conservatively, and
approximately 80% respond to such treatment.
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Fluid resuscitation
Monitor accurate intake/output and electrolyte
balance of the patient.
Crystalloids / packed red blood cells –[ in the case
of hemorrhagic pancreatitis]
CVP line with monitoring-- severe fluid loss and
very low blood pressure.
TREATMENT
In Wards/ICU
The goal -to relieve pain and minimize complications.
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Analgesics .
Meperidine is preferred over morphine because of the
greater spastic effect of the latter on the sphincter of Oddi.
Parenteral NSAID”S
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Anti ulcer drugs
Prevention of gastric/duodenal stress ulcers
Antibiotics
Empiric- enteric anaerobic and aerobic gramAdjust as per c/s reports.Ceftriaxone
Aminoglycosides/ Metronidazole
TREATMENT
Rationale for antibiotics
 Other conditions, such as biliary pancreatitis
associated with cholangitis, also need antibiotic
coverage. The preferred antibiotics are the ones
secreted by the biliary system, such as ampicillin
and third-generation cephalosporins.
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Continuous oxygen saturation should be monitored
by pulse oximetry, and acidosis should be
corrected. When tachypnea and pending respiratory
failure develops, intubation should be performed.
TREATMENT
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NG intubation if the patient is vomiting
[for symptomatic relief and to avoid aspiration]
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Guided aspiration of necrotic areas, if necessary.
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An ERCP may be indicated for common duct stone
removal
Surgery in Acute pancreatitis
Diagnostic/Therapeutic
for complications
Bleeding
Pseudocysts
Abscess
drain, repair, or remove the affected tissues
where there is fulminent infection and necrosis.
open surgical debridement.
Postoperative lavage or abdominal packing
closure of abdomen - partial or non
Establish a feeding jejunostomy.
Surgery in Acute pancreatitis
For phlegmon of the pancreas,
surgery can achieve drainage of any abscess or
scooping of necrotic pancreatic tissue. It should be
followed by postoperative lavage of the pancreatic
bed.
 In patients with hemorrhagic pancreatitis, surgery
is indicated to achieve hemostasis, particularly
because major vessels may be eroded in acute
pancreatitis.
 Patients who fail to improve despite optimal
medical treatment or patients who push the Ranson
score even further are taken to the operating room.
Surgery in these cases may lead to a better
outcome or confirm a different diagnosis.
Surgery in Acute pancreatitis
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Sphincterotomy - In biliary pancreatitis, a (ie,
surgical emptying of the common bile duct) can
relieve the obstruction.
A cholecystectomy may be performed to clear the
system from any source of biliary stones.
Hyperbaric oxygen therapy - administration of 100%
oxygen at a pressure of 2.5 atmospheres for 90
min twice daily for 5 days has been shown to
improve
Complications in Acute pancreatitis
Local complications
 Pancreatic necrosis -Infected necrosis is almost
always fatal without intervention.
 Acute Fluid Collections are common in patients
with severe pancreatitis (occurring in 30%-50%).
 Pancreatic abscess is a collection of pus adjacent to
pancreas presenting several months after attack.
 Acute pseudocyst
rupture or haemorrhage in pseudocyst.
 Pancreatic ascites occurs when a pseudo-cyst
collapses into peritoneal cavity or major pancreatic
duct breaks down and releases pancreatic juices
into peritoneal cavity.
Complications in Acute pancreatitis
Systemic complications
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Respiratory:Pulmonary oedema/Pleural effusions
Consolidation/ARDS
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Cardiovascular:Hypovolaemia/Shock/arrhythmias
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Disseminated intravascular coagulopathy (DIC)
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Renal dysfunction due to hypovolaemia, intra-vascular
coagulation. Usually avoided by adequate fluid replacement
plus/minus low-dose dopamine but acute tubular or cortical
necrosis can follow.
GIT: Haemorrhage/Ileus
Complications in Acute pancreatitis
Metabolic:
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Hypocalcaemia
Hypomagnesaemia
Hyperglycaemia
Complications in Acute pancreatitis
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Weber Christian disease:
Subcutaneous fat necrosis - relapsing febrile
nodular nonsuppurative panniculitis. Recurring
crops of tender nodules in skin and subcutaneous
fat of trunk, thighs and buttocks, which is more
common in middle-aged women.
Often ulcerate and scar on healing.
Difficult to treat - prednisolone or
immunosuppressives.
Splenic vein thrombosis
Prognosis-acute Pancreatitis
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Mild edematous pancreatitis occurs in about 80%
cases, and the mortality rate is below 1%.
Severe acute pancreatitis occurs in about 20% of
presentations, with a mortality rate reaching 30%. .
Follow-up acute Pancreatitis
further Outpatient Care
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The patient should be monitored routinely with physical examination
and amylase and lipase assays.
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Transfer
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Transfer patients with Ranson scores of 0-2 to a hospital floor.
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Transfer patients with Ranson scores 3-5 to an intensive care unit.
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Transfer patients with Ranson scores higher than 3 to an intensive
care unit with emergency surgery as a possibility, depending on the
patient's progress and findings on abdominal CT scanning.
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Patient Education
Educate patients about the disease and advise them to avoid alcohol
in binge amounts and to discontinue any risk factor, such as fatty
meals and abdominal trauma.
Summary –acute pancreatitis
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Begins with: the digestive enzymes becoming active
inside the pancreas and autodigestion
Could be : acute/acute recurrent /acuteon chronic
Common causes: are gallstones and alcohol abuse.
Sometimes no cause for pancreatitis can be found.
Symptoms of acute pancreatitis include pain in the
abdomen, nausea, vomiting, fever, and a rapid
pulse.
Treatment include: intravenous fluids, analgesics
oxygen, antibiotics, anti ulcer and surgery.
May becomes chronic- when pancreatic tissue is
destroyed and scarring develops
Questions-acute Pancreatitis ?