09 pancreatitis

AnatomyLocation and relationDucts Blood supply

AnatomyLocation:

- Retroperitoneal (posterior to stomach, transverse mesocolon and lesser omentum)

- At the level of the body of L2

Divided into:

1. Head: includes uncinate process and abuts the second part of the duodenum.

2. Neck: portion anterior to superior mesenteric vein.

3. Body: lies to the left of the neck, forms posterior floor of lesser sac.

4. Tail: enters splenorenal ligament, adjacent to splenic hilum* *susceptible to injury during splenectomy.

AnatomyDucts:

1. Wirsung duct:

The main duct; runs entire length of pancreas. It joins the

common bile duct and empties into the second part of the

duodenum at the ampulla of Vater.

1. Santorini duct:

(Small duct) is an accessory duct often joining the

duodenum more proximally than the ampulla of Vater

AnatomyBlood supply:

Head:

Anterior and posterior superior pancreaticoduodenal

arteries—branches of the gastroduodenal artery.

Anterior and posterior inferior pancreaticoduodenal

arteries— branches of the superior mesenteric artery.

Neck, body and tail:

Splenic artery and branches (dorsal pancreatic artery).

Anatomy

Nerve supply:

Sympathetics: Pain sensation is provided by the celiac

plexus (via the splanchnic nerves).

Parasympathetics: Islets, acini, and ducts are innervated

by branches of the vagus.

*Clinical note: Celiac plexus block can be done for pain control

in pancreatic disease.

PhysiologyExocrine vs. Endocrine

PhysiologyExocrine:

1. Acinar cells: secrete enzymes (e.g. chymotrypsin, trypsin, carboxypeptidase, amylase, lipase).

2. Centroacinar & ductal cells: secrete water & electrolytes (e.g. Na+, K+, HCO3−, Cl−).

Endocrine:

1. Insulin: From beta cells in islets of Langerhans.2. Glucagon: From alpha cells in islets of Langerhans.3. Somatostatin: From delta cells in islets of

Langerhans.

Control of the exocrine function of the pancreas is via the

hormones gastrin, cholecystokinin & secretin which are secreted

by cells in the stomach and duodenum, in response to distension

and/or food and which cause secretion of pancreatic juices.

The precursor enzymes (termed zymogens or proenzymes) are

inactive variants of the enzymes; thus autodegradation, which

can lead to pancreatitis, is avoided.

Once released in the intestine, the enzyme enteropeptidase

present in the intestinal mucosa activates trypsinogen by

cleaving it to form trypsin. The free trypsin then cleaves the rest

of the trypsinogen, as well as chymotrypsinogen to its active

form chymotrypsin.

Acute pancreatitis Inflammation (NOT infection) of the pancreas due

to parenchymal autodigestion by proteolytic

enzymes

Has a significant mortality and morbidity rates.

Acute pancreatitis (causes)1. Gallstones.2. Alcohol.3. Iatrogenic.4. Metabolic.5. Infection.6. Drugs.7. Tumors.8. Ischemia.9. Congenital anomalies.

Pathophysiology

Gallstone:when a migrating gallstone obstructs the ampulla of Vater.

Alcohol:- At the cellular level, ethanol leads to intracellular accumulation

of digestive enzymes and their premature activation and release.

- At the ductal level, it increases the permeability of ductules, allowing enzymes to reach the parenchyma and cause pancreatic damage.

PathophysiologyThe underlying mechanism of injury in pancreatitis is thought

to be 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 (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

Severity Mild acute pancreatitis

Characterized by interstitial edema & minimal organ dysfunction.

80% of patients will have a mild attack of pancreatitis, the

mortality from which is around 1%.

Severe acute pancreatitis

Characterized by pancreatic necrosis, a severe systemic

inflammatory response and often multi-organ failure.

Acute pancreatitis (approach)

Case study

A 50-year-old man, presents to the ER complaining of severe epigastric pain for 3 hours duration.

Acute pancreatitis

(approach) History: History of present illness:

The pain was sudden, constant, epigastric, radiates to the back, deep

dull in nature, he gave it 8.5/10. It improves when leaning forward,

worsens with deep inspiration and movement. The patient vomited a

large amount of undigested food but the pain is not relieved.

Systemic review: free

Past medical history: recurrent attacks of colicky RUQ pain.

Past surgical history: clear

Family history: DM and HTN and PUD (mother)

Social history: smoker (1pack/day), drink alcohol only in the weekends!

Acute pancreatitis (approach)

Physical Examination:

General:

Patient is in pain, looks ill and jaundiced Vital signs: T= 38.8, BP= 110/60, HR= 110, RR= 28

Abdominal exam:

The abdomen was rigid and tender in the epigastric and periumbilibal area.

Mild abdominal distension was noticed.

Signs of acute pancreatitis

GENERAL SIGNS:

Fever (76%) tachycardia (65%) & hypotensionAbdominal tenderness(68%) & distention (65%)Jaundice (28%)Dyspnea (10%); tachypneaIn severe cases, hemodynamic instability (10%) and

hematemesis or melena (5%).

1- These signs are not specific for acute pancreatitis; they can occur in any retroperitoneal bleeding

2- These are uncommon physical findings and they are associated with severe necrotizing pancreatitis

Local Late Signs:

Acute pancreatitis (approach)

Diagnosis is clinical, but laboratory tests are usually obtained:

To confirm the diagnosisTo define an etiology, look for complications & determine the

prognosis

Investigations (labs)CBC: For leukocytosis and anemia is severe cases

Serum amylase and lipase

• Typically elevated in patients with acute pancreatitis• Lipase level remains high for 12 day • Increase 3 times in amylase suggests Acute pancreatitis.• The elevated amylase is less specific for pancreas than lipase*

*Lipase Only found in gastric, intestinal mucosa and liver. While Amylase apart from intestine found also in salivary glands, ovaries, testes, and skeletal muscle.

*High amylase levels are seen in intestinal disease, perforated ulcer, ruptured ectopic pregnancy, salpingitis, salivary gland disorders, renal failure & DKA.

Investigations (labs)Liver enzymes:

Alkaline phosphatase, total bilirubin, AST and ALT levels to search for

evidence of gallstone pancreatitis.

Serum electrolytes, BUN, creatinine, glucose,

cholesterol and triglycerides.

C-reactive protein (CRP).

LDH and bicarbonate.

Investigations (imaging)

I. X-ray

Sentinel loop sign Colon cut-off sign

Gaseous distension of the right and transverse colon with ↓ or absent air beyond the splenic flexure

localized ileus from nearby inflammation

Investigations (imaging)

II. Ultrasonography: It is the most useful initial test in determining the etiology of

pancreatitis.

pseudocysts, phlegmon, abscesses or cholelithiasis.

III. ERCP Should be used with extreme caution in patients with acute

pancreatitis and should never be used as a first-line diagnostic

tool in this disease.

Diagnostic and therapeutic (in biliary pancreatitis)

IV. Abdominal CT:

Diagnostic test of choice (90% sensitive and 100% specific)

Can differentiate between mild and severe pancreatitis.

Demonstrates pseudocysts, phlegmon, abscesses or pancreatic

necrosis

What are the indications to use the CT scan ?

1. If diagnosis is uncertain,

2. To distinguish INTERSTITIAL from NECROTISING pancreatitis,

3. If there are organ failure & clinical worsening,

4. When a localized complication is suspected.

Lab results:

CBC: WBC= 19.000, Hb= 17 g/dl, Hct= 47 %

LFT:Bilirubin= 3.2 mg/dl, AST= 435 U/l, LDH= 300U/L , Amylase=

6800 IU/L

Back to our case

CT Abdomen

Management:

In acute pancreatitis always stabilization of the patient is the most important step.

Then classify your patient according to:

Glasgow Ranson’s Criteria APACHE II score CT severity index CRP level

Glasgow criteriaOne form of the Glasgow criteria suggests that a case be

considered severe if at least three of the following are true:

Age > 55 yearsBlood levels:

P02 Oxygen < 60mmHgWhite blood cells > 15Calcium < 2 mmol/LUrea > 16 mmol/LLactate dehydrogenase (LDH) > 600iu/LAspartate transaminase (AST) > 100iu/LAlbumin < 32g/LGlucose > 10 mmol/L in the absence of diabetes

Ranson’s criteria

Evaluation of severity of pancreatitis

Severe pancreatitis is suspected if: Ranson >= 3 (or) Glasgow >=3

Mortality in mild pancreatitis is less than 1%, while in severe pancreatitis is 10-30%.

R-Regimen (except pancreatic necrosis)

1. Rest the pain by pethidine NOT morphine (?)

2. Rest the bowel NPO, nasogastric tube

3. Resuscitation IVF & electrolytes

4. Resist infection Antibiotics (controversial)

5. Repeated examination (every 2 hrs)

6. Repeated serum tests (WBC, Ca, albumin…)

7. Respiratory support (O2, assisted ventilation if needed)

Nutrition

TPN in early period of disease

Post-pyloric enteral feeding (in which a feeding tube is endoscopically or

radiographically introduced to the third portion of the duodenum)

The advantage of enteral feeding is that it is more physiological, prevents

gut mucosal atrophy, and is free of the side effects of TPN (such as

fungemia).

The additional advantages of post-pyloric feeding are the inverse

relationship of pancreatic exocrine secretions and distance of nutrient

delivery from the pylorus, as well as reduced risk of aspiration.

Endoscopic (ERCP)

If gall stone is strongly suspected as the cause of pancreatitis, the stones should be removed through endoscopic sphincterotomy.

If there is severe pancreatitis, or cholangitis, both sphinterotomy and ERCP is done

Surgery – indicated in:

i) Infected pancreatic necrosis.ii) Diagnostic uncertainty.iii) Complications.

What are the complications of acute pancreatitis?

Acute pseudocyst

Is a collection of pancreatic fluid that is walled off by

granulation tissue after an episode of acute pancreatitis,

It requires 4 or more weeks to develop

If after 6 weeks they have not resolved and are > 6 cm in

size, internal drainage of the mature cyst is indicated via

cyst gastrostomy or Roux-en-Y cyst jejunostomy.

Intra-abdominal infection It is common.

Within the first 1-3 weeks, fluid collection or

pancreatic necrosis can become infected and

jeopardize clinical outcome.

From 3 to 6 weeks, pseudocysts may become

infected or a pancreatic abscess may develop.

Pancreatic necrosis It is a nonviable area of pancreatic parenchyma that

is often associated with peripancreatic fat necrosis

and is principally diagnosed with the aid of dynamic

spiral CT scan.

No enhancement of pancreas with IV contrast

Pancreatic fat necrosis

Fat necrosis is a consequence of enzyme damage to the membranes of the adipocytes near the affected pancreatic tissue.

The term "saponification" has been used to describe this lesion in fat, due to the "soap-like" alteration of the triglycerides released from the adipocytes.

Treatment

Minimally invasive management: necrosectomy through small incision in skin (left flank) or stomach

Conventional management: necrosectomy with simple drainage

Closed management: necrosectomy with closed continuous postoperative lavage

Open management: necrosectomy with planned staged reoperations at definite intervals (up to 20+ reoperations in some cases)

Definition:

Chronic inflammation or recurrent acute pancreatitis

that causes irreversible parenchymal fibrosis,

destruction and calcification, leading to loss of

endocrine and exocrine function.

Etiology

Alcohol abuse (70%).Idiopathic (20%).Other (10%): Hyperparathyroidism,

hypertriglyceridemia, congenitalPancreatic anomalies, hereditary, obstruction.

Typical Hx of chronic pancereatitis

A 41-year-old alcoholic patient, has a 6-year

history of recurrent attacks of pancreatitis

characterized by epigastric pain radiating to the

back. Recently developed evidence of diabetes

and steatorrhoea. CT imaging shows pancreatic

calcifications but no cystic or mass lesions.

Clinically Recurrent or constant epigastric and/or

back pain. Malabsorption/malnutrition (exocrine

dysfunction). Steatorrhea (exocrine dysfunction), fat-

soluble vitamin deficiency.DM (endocrine dysfunction).

Diagnosis

Serum amylase and lipase levels may be slightly

elevated

Fecal fat analysis.

Abdominal X-ray

CT scan

ERCP

X-ray (kidneys, ureters & bladder): Pancreatic calcifications

CT: Pseudocysts, Gland enlargement/ atrophy, calcifications, masses

ERCP: Chain-of-lakes pattern—ductal irregularities with dilation and stenosis.

TreatmentNonoperative: Includes control of abdominal pain, endocrine and

exocrine insufficiency (insulin and pancreatic enzymes therapy).

Operative:(must do preop. ERCP to evaluate the anatomy)

Persistent pain Gastrointestinal or biliary obstruction Pseudocyst infection, hemorrhage, rupture or enlarging

Surgical methods Pain relief: Celiac plexus block.

Ampullary procedures: ERCP with endoscopic sphincterotomy

Ductal decompression procedures:

Puestow procedure (longitudinal pancreaticojejunostomy) for segmental ductal dilation.

Duval procedure (retrograde drainage with distal resection and end-to-end pancreaticojejunostomy).

Ablative procedures (resection of portions of pancreas):

Frey procedure (longitudinal pancreaticojejunostomy with partial

resection of the pancreatic head).

Whipple procedure (pancreaticoduodenectomy with

choledochojejunostomy, pancreaticojejunostomy and

gastrojejunostomy).

Near-total pancreatectomy.

Thank you :)Mai Mazin & Hanan Al-Fayyomi