PANCREATITIS

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PANCREATITIS

• By
• Col. Abrar Hussain Zaidi

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INTRODUCTION

• Pancreatitis is
• an inflammatory process
• in which pancreatic enzymes
• auto digest the gland.

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INTRODUCTION

• Inflammation of Pancreas
• Acute
• Chronic
• Recurrent acute
• Acute on chronic

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INTRODUCTION

• 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.

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INTRODUCTION

• Clinical importance -?

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INTRODUCTION

• One of the commonest conditions that a physician
  or a surgeon comes across
• Associated morbidity is high
• The cost of treatment is high
• In severe cases the mortality
• may be 20-30

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INTRODUCTION

• Prevention of disease is possible
• If
• we are aware of etiological factors and
  pathogenesis

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ANATOMY
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ANATOMY
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PHYSIOLOGY

• EXOCRINE FUNCTION
• ENDOCRNE FUNCTION

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• Acute pancreatitis

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EPIDEMIOLOGY

• 3 of all cases of abdominal pain admitted to
  hospital.
• 40 cases per year per 100,000 adults.Internationa
  l
• Ranges between 5 and 80 per 100,000 population
• 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

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PATHOPHYSIOLOGY

• located in the retroperitoneal space
• No capsule,
• inflammation can spread easily.
• Local effects
• 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

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PATHOPHYSIOLOGY

• pancreatic abscesses and Pseudocysts
• due to necrotizing pancreatitis
  because
• enzymes can be walled off
  by
• granulation tissue

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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.

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PATHOPHYSIOLOGY

• systemic effects
• in its most severe form.
• Acute respiratory distress syndrome (ARDS),
• acute renal failure,
• cardiac depression,
• hemorrhage, and hypotensive shock

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CAUSES

• 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.

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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, NSAIDS
• Viral infections
• Trauma

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OTHER CAUSES

• ERCP
• Hypertriglyceridemia (When the triglyceride
  level exceeds 1000 mg/U
• Peptic ulcer disease
• Abdominal or cardiopulmonary bypass surgery, -by
  ischemia
• Trauma bluntpenetrating
• Carcinoma of the pancreas, - outflow obstruction
• 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

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CLINICAL PRESENTATION

• History
• 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.

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CLINICAL PRESENTATION

• Ask the patient about
• Recent surgery or invasive procedure e.g. ERCP
• Family history of hypertriglyceridemia.
• Alcohol consumption

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CLINICAL PRESENTATION

• EXAMINATION
• Patients are acutely ill
• Tachypnea
• Hypotension
• Fever
• Abdominal tenderness, distension, guarding, and
  rigidity
• Mild jaundice
• Diminished or absent bowel sounds

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CLINICAL PRESENTATION

• EXAMINATION
• 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

• 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

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DIAGNOSTIC WORK-UP

• HISTORY AND CLINICAL EXAMINATION
• LABORATORY TESTS
• IMMAGING STUDIES

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DIAGNOSTIC WORK-UP

• Laboratory Studies
• leukocytosis (WBC gt12,000) -gt polymorphs.
• Hyperglycemia.
• Disturbed in the electrolyte balanceUrea/creatini
  n Na, K, Cl, CO2, P, Mg---secondary to third
  spacing of fluids.
• Acid base disturbances
• Amylase levels, preferably the amylase P.gt 3
  times -suggest the diagnosis . serum/peritoneal
• Lipase - elevated / remain high for 12 days.
• Anemia

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DIAGNOSTIC WORK-UP

• Laboratory Studies
• liver function tests particularly in biliary
  calculi.
• Misc. Done in some hospitals in addition to the
  above, especially to identify pancreatitis post
  ERCP .
• Urinary trypsinogen activation peptide
• Increased serum trypsinogen2
• Trypsin 2-alpha 1 antitrypsin complex values

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DIAGNOSTIC WORK-UP

• Imaging Studies
• Plain X-rays
• 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.

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DIAGNOSTIC WORK-UP

• Ultrasonography
• 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.
• CT scan is the most reliable imaging modality in
  the diagnosis of acute pancreatitis. The criteria
  for diagnosis are divided by Balthazar and
  colleagues into 5 grades
• 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

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DIAGNOSTIC WORK-UP

• Misc.
  Tests
• 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 8090. In those with
  mild-to-moderate functional impairment, the
  sensitivity is as low as 3746.
• 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 (lt20 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
  

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DIAGNOSTIC WORK-UP

• Peritoneal aspiration - free fluid without
  bacterial contamination gtamylasegtTLC.
• 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 (gt5 mg/dL)
• Laparoscopy or laparotomy where suspicion is
  high but tests are inconclusive.

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Severity and prognostic assessment

• 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.

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Severity and prognostic assessment

• Scoring systems
• Glasgow
• Ranson
• Apache II scores
• can indicate prognosis particularly

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Glasgow prognostic score

• Age gt55 years
• WBC gt15 x109/l
• Urea gt16mmol/l
• Glucose gt10mmol/l
• pO2 lt8kPa (60mmhg)
• Albumin lt32g/l
• Calcium lt2mmol/l
• LDH gt600 units/l
• AST/ALT gt200 units

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Ranson's criteria

• Present on admission
• Age gt55 years
• WBC gt15 x109/l
• Glucose gt10mmol/l
• LDH gt600 units/l
• SGOT gt250 units/l
• Developing during first 48 hours
• Haematocrit fall 10
• Urea increase gt8mg/dl
• Serum Ca lt8mg/dl
• Arterial O2 saturation lt60mmHg
• Base deficit gt4meq/l
• Estimated fluid sequestration gt600ml
• Any 3 factors means severe in both systems.

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• 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.

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Treatment

• According to severity
• 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

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Treatment

• Emergency Department Care
• Most of the cases are treated conservatively, and
  approximately 80 respond to such treatment.
• 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.

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TREATMENT

• In Wards/ICU
• The goal -to relieve pain and minimize
  complications.
• Analgesics .
• Meperidine is preferred over morphine
  because of the
• greater spastic effect of the latter on the
  sphincter of Oddi.
• Parenteral NSAIDS
• Anti ulcer drugs
• Prevention of gastric/duodenal stress ulcers
• Antibiotics
• Empiric- enteric anaerobic and aerobic gram-
• Adjust as per c/s reports.Ceftriaxone
• Aminoglycosides/ Metronidazole

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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.
• 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.

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TREATMENT

• NG intubation if the patient is vomiting
• for symptomatic relief and to avoid
  aspiration
• Guided aspiration of necrotic areas, if
  necessary.
• An ERCP may be indicated for common duct stone
  removal

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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.

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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.

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Surgery in Acute pancreatitis

• 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.

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• 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

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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.

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Complications in Acute pancreatitis

• Systemic complications
• RespiratoryPulmonary oedema/Pleural effusions
• Consolidation/ARDS
• CardiovascularHypovolaemia/Shock/arrhythmias
• Disseminated intravascular coagulopathy (DIC)
• 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

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Complications in Acute pancreatitis

• Metabolic
• Hypocalcaemia
• Hypomagnesaemia
• Hyperglycaemia

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Complications in Acute pancreatitis

• 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

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Prognosis-acute Pancreatitis

• 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. .

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Follow-up acute Pancreatitis

• further Outpatient Care
• The patient should be monitored routinely with
  physical examination and amylase and lipase
  assays.
• Transfer
• Transfer patients with Ranson scores of 0-2 to a
  hospital floor.
• Transfer patients with Ranson scores 3-5 to an
  intensive care unit.
• 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.
• 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.

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Summary acute pancreatitis

• 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

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• Questions-acute Pancreatitis ?

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Thank you