09 pancreatitis
DESCRIPTION
surgery lectures slidesTRANSCRIPT
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