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Acute Pancreatitis

This document discusses acute pancreatitis including its anatomy, causes, pathophysiology, clinical presentation, diagnosis, assessment of severity, management, and complications. It provides details on the history, physical exam, laboratory and imaging findings used to diagnose and monitor acute pancreatitis. It also outlines scoring systems to determine severity and treatments based on mild or severe disease.

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Mustafa Husain
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280 views40 pages

Acute Pancreatitis

This document discusses acute pancreatitis including its anatomy, causes, pathophysiology, clinical presentation, diagnosis, assessment of severity, management, and complications. It provides details on the history, physical exam, laboratory and imaging findings used to diagnose and monitor acute pancreatitis. It also outlines scoring systems to determine severity and treatments based on mild or severe disease.

Uploaded by

Mustafa Husain
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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ACUTE

PANCREATITIS
Sujata Chawla 17/155
Nida Tahir 17/117
Ali Iftikhar 17/139
Outline:
• Anatomy of Pancreas
• Aetiology
• Pathophysiology
• Clinical Approach – History and Physical Examination
• Differential Diagnosis
• Investigation
• Assessment of Severity
• Management of Acute Pancreatitis
• Complications
Anatomy of Pancreas:
• Retroperitoneal organ
• In adults- 15cm long & 70-
100 weighs
• 3 portions- head, body and
tail
• Relations:
1. Head
2. Neck
3. Uncinate
4. Body
5. Tail
Vasculature of Pancreas:
• ARTERIAL SUPPLY:
The pancreas is supplied by
the pancreatic branches of
the splenic artery. The head
is additionally supplied by
the superior and inferior
pancreaticoduodenal
arteries which are branches
of the gastroduodenal
(from coeliac trunk) and
superior mesenteric
arteries, respectively.
• VENOUS DRAINAGE:
Venous drainage of the head of the pancreas is into the superior
mesenteric branches of the hepatic portal vein. The pancreatic
veins draining the rest of the pancreas do so via the splenic vein.
• LYMPHATICS:
The pancreas is drained by lymphatic vessels that follow the
arterial supply. They empty into the pancreaticosplenal nodes
and the pyloric nodes, which in turn drain into the superior
mesenteric and coeliac lymph nodes.
• DUCT SYSTEM:
Pancreatitis:
ACUTE CHRONIC
• presenting with abdominal • long-standing inflammation
pain and is usually of the pancreas that alters
associated with raised the organ's normal
pancreatic enzyme levels in structure and functions. It
the blood or urine as a can present as episodes of
result of pancreatic acute inflammation in a
inflammation. previously injured
pancreas, or as chronic
damage with persistent
pain or malabsorption.
Incidence:
• 3 % of all cases of abdominal pain
• Hospital admission rate for is 9.8 per 100 000 population
anually
• Worldwide, 50 per 100 000 cases anually.
• The disease may occur at any age, with a peak in young men
and older women.
Aetiology:
Two major causes are :
• biliary calculi (50–70%)
• alcohol abuse (25%)

The remaining cases may be due to rare causes or be idiopathic.


Causes of Acute Pancreatitis:
• Gallstones
• Alcoholism
• Post-ERCP
• Abdominal trauma
• Ampullary tumor
• Hyperparathyroidism
• Hypercalcaemia
• Autoimmune Pancreatitis
• Viral infections (mumps)
• Malnutrition
• Drugs (corticosteriods, azathioprine, thiazides, oestrogens)
Types of Acute Pancreatitis:
GALLSTONE PANCREATITIS ALCOHOL PANCREATITIS
• Transient blockage of • High risk in:
common bile duct reflux 1. Long standing alcohol intake
of bile into pancreatic duct for at least 2 years or single
and impair flow of normal session of heavy drinking
pancreatic juice 2. Consumption >80g/day
premature activation of
pancreatic enzymes within • Cause:
duct system. 1. Direct toxic effect of alcohol
in genetically predisposed
individuals
2. Viscid secretion of pancreatic
juice  formation of protein
plugs and impairment of flow
Pathophysiology:
• Premature activation of pancreatic enzymes within the
pancreas, leading to a process of autodigestion.
• Anything that injures the acinar cell and impairs the secretion
of zymogen granules, or damages the duct epithelium and
thus delays enzymatic secretion, can trigger acute pancreatitis.
• Once cellular injury has been initiated, the inflammatory
process can lead to pancreatic oedema, haemorrhage and,
eventually, necrosis.
• As inflammatory mediators are released into the circulation,
systemic complications can arise.
Detailed History:
PURPOSE OF HISTORY TAKING:
• Pain
• Causes
• Complications
History Taking:
1) Abdominal Pain: Remember SOCRATES!

• Site: Diffuse, upper abdominal pain


• Onset: Sudden
• Character: Boring Pain
• Radiation: Radiates to the back
• Associated factor: Nausea, vomiting, dyspnea
• Timing: Pain escalates in intensity and peaks within 10-20
minutes of onset.
• Aggravating and relieving factor: Aggravated by breathing with
increased chest expansion and relieved by leaning forward.
• Severity: Depending on severity, patient may present in shock
2) History of underlying causes :

‘I GET SMASHED’

• Idiopathic (10%)
• Gallstone (45%)
• Ethanol (35%)
• Trauma (10%)
• Steroids
• Mumps
• Autoimmune
• Scorpion / Snake
• Hyperlipidemia
• ERCP
• Drugs (10%)
3) History of complications:

SYSTEMIC: LOCAL:

• ARDS • Mostly develop silently


• Renal Failure • Pancreatic abscess – high
• Shock, arrythmias grade fever
• Metabolic: hypocalcemia, • Pseudocyst
hyperglycemia • Pancreatic effusion
• Encephalopathy
Physical Examination:
• ABDOMINAL EXAMINATION:

1. Inspection: abdominal distension

2. Palpation:
• Hepatomegaly
• Tenderness
• Cullen sign
• Gray turner sign
• Peritoneal signs
Because of hemoperitoneum
• Rigidity
• Guarding
3. Percussion : Dullness suggesting ascites

4. Auscultation: auscultate the abdomen for hypoactive or an


absent bowel sounds or an abdominal bruit. Ileus is common in
pancreatitis.

• Ausculation of lungs: 10-20% of patients have pulmonary


findings, commonly left sided findings.
1. Basilar rales
2. Atelectasis
3. Pleural effusion
Differential Diagnosis:
Investigations:
• The diagnosis if made on basis of clinical presentation, an
elevated serum Amylase level and characteristic Imaging
features.

• Biological :
1. Serum Amylase increase 3x than normal or more than
1000IU/mL (Peak within the first 24hours after onset of
Symptom)
2. Serum Lipase has longer half life thus more useful in delayed
cases.
3. Serum Lipase: more sensitive & specific for Pancreatitis than
Amylase
Imaging: Ultrasound
• Trans-abdominal USG: Does not establish a diagnosis.
•
• USG should be performed within 24 hours in ALL patients
1. To detect gallstones
2. To rule out Acute Cholecystitis
3. To determine whether the common bile duct is dilated

• To evaluate change on pancreas i.e. edema, mass in Pancreas


• Transverse Transbadominal
Ultrasound shows a
swollen pancreatic body
with ill-defined
heterogeneous hypoechoic
pattern.
ERCP:
• Diagnostic and therapeutic
• To look for Gallstones, CBD stones or CBD dilatation
• In patient with severe acute gallstone pancreatitis & signs of on
going biliary obstruction and cholangitis – an urgent ERCP
should be sought.
X-RAY:
• Plain erect chest & abdominal X-ray are not diagnostic of
Acute Pancreatitis but are useful in differential diagnosis.
• Non specific findings in Pancreatitis : Generalized or local ileus
(Sentinel Loop), a colon cut off sign, and calcified gallstones.
• Erect CXR: Look for pleural effusion.
• In severe cases, a diffuse alveolar shadowing (Acute
Respiratory Distress Syndrome)
CT SCAN:
• Not necessary for all patients.
• May reveal pseudo cyst or abscess (complication of acute
pancreatitis)

• A contrast-enhanced CT is indicated in following :


1. If there is diagnostic uncertainty
2. In Pt. with severe acute Pancreatitis to distinguish
interstitial from necrotizing pancreatitis.
3. In Pt. with organ failure, signs of sepsis or progressive
clinical deterioration
4. When a localized complication is suspected I.e. fluid
collection, pseudo cyst.
Complications:
Assessment of Severity:
• Ranson Score
• Glasgow Scale
• APACHE II Score
Ranson Score: 3 or more factors present
- SEVERE

To predict severity of acute pancreatitis.


On Admission (LEGAL)
• L – Leucocytes >16000
• E – Enzyme AST > 250
• G – Glucose > 200
• A – Age > 55
• L – LDH > 350
During Next 48 Hours (C.HOBBS)
• C – Calcium 8mg/dl
• H – Hematocrit fall of >10%
• O2– Pa02 < 60mmHG
• B – Base deficit > 4mmol/L
• B – BUN rise > 5
• S – Sequestration (Fluid) > 6 litres
Glasgow Scale: 3 or more factors present -
SEVERE
APACHE II Score: 8 or more factors present -
SEVERE
Management:

• MILD ACUTE PANCREATITIS:

1. Nil by mouth
2. Fluid resuscitation : 4 pints
3. Analgesia : IM Tramal 50mg TDS
4. Treat underlying cause
5. No role for antibiotics
• SEVERE ACUTE PANCREATITIS:
Admission to intensive care or high dependency unit

1. Oxygen supplementation
2. Analgesia
3. Aggressive fluid rehydration
4. Monitor vital signs
5. Monitor haematological & biochemical parameters
6. Nasogastric drainage
7. Antibiotic prophylaxis –imipenem, cefuroxime
8. CT scan
9. ERCP within 72 hours
10. Supportive therapy for organ failure
11. Nutritional support
Complications:
SYSTEMIC: LOCAL:
• Cardiovascular - shock - • Acute fluid collection
arrhythmia • Sterile pancreatic necrosis
• Pulmonary - ARDS • Infected pancreatic necrosis
• Renal failure • Pacreatic abscess
• Haematological - DIC • Pseudocyst
• Gastrointestinal - Ileus • Pancreatic ascites
• Pleural effusion
• Portal or systemic vein
thrombosis
• Pseudocyst
Complications and their
management:
ACUTE FLUID COLLECTION:
• No intervention unless pressure effect
• Aspirate under US or CT guidance

PANCREATIC NECROSIS
• No intervention

INFECTED PANCREATIC NECROSIS:


• Aspirate under CT guidance
• Percutaneous drainage
• Prophylactic antibiotic
PSEUDOCYST:

• Percutaneous transgastric cystogastrotomy and place double-


pigtail drain
• Endoscopic under EUS guidance and place tube drain
• Surgical drainage – internal drainage into gastric or jejunum
lumen
Cystogastrotomy:
References:
• BAILEY, H., LOVE, R. J. M., MANN, C. V., & RUSSELL, R. C. G.
(1992). Bailey and Love's short practice of surgery. London,
Chapman & Hall Medical.
• COLLEDGE, N. R., WALKER, B. R., RALSTON, S., & DAVIDSON, S.
(2010). Davidson's principles and practice of medicine.
Edinburgh, Churchill Livingstone/Elsevier.
THANKYOU

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