Acute pancreatitis

Objectives • Anatomy and Physiology of the pancreas

• Definition and pathophysiology of acute pancreatitis

• Clinical presentation

• Investigation and Diagnosis

•Complications

•Management

Embryology During the 4th week of gestation, the pancreas begins to develop from the duodenal endoderm.

Two buds form (which then rotate and fuse by the 8th week): VENTRAL BUD (from the convex part of the duodenum)Uncinate process and part of the head DORSAL BUD (from the concave part of the duodenum) Remaining part of the head, neck, body and tail.

The ventral bud rotates with the duodenum and then migrates posteriorly to fuse with the dorsal part.

The pancreas has two ducts: the main pancreatic duct, called the Duct of Wirsung( ventral duct ), which arises in the tail and traverses the length of the pancreas to terminate at the papilla of Vater within the wall of the duodenum; and the Duct of Santorini(dorsal duct), which is much smaller and arises from the lower part of the head, terminating separately at the lesser papilla.

Anatomy of the pancreas

• Retroperitoneal organ ,behind the stomach at level of L1-L2. weighs 75- 100g and measures about 10 cm in length.

• Four parts?

The head of the pancreas abuts the C loop of the duodenum and extends obliquely to the neck, anterior to the mesenteric ves- sels and portal vein.(Uncinate process Small portion of it lies posteriorly to the superior mesenteric vein.)

neck..Lies over the SMV

Body which is generally accepted to begin at the left border of the superior mesenteric vein (SMV), lying pos- terior to the stomach and anterior to the splenic vessels.

tail …has a close relation with the splenic hilum (Tickles the spleen)

Blood and Neve supplyThe pancreas receives its blood supply from both the celiac trunk and the superior mesenteric artery (SMA).

The arterial supply of the pancreatic head is provided by the inferior pancreaticoduodenal arteries (from the SMA) and the superior pan- creaticoduodenal arteries (from the gastroduodenal artery).

The tail receives its arte- rial supply from branches of the splenic artery.

Venous drainage is primarily by the pancreaticoduodenal veins, which drain into the portal vein.

Nerve supply :

• Sympathatic : inhibits secretion by splanchnic nerves.

• Parasympathatic: for the glands (ducts) by the celiac branch of the vagus nerve.

Acute PANCREATITIS

Pancreatitis is reversible inflammation of the pancreas as a result of autodigestion by its own enzymes (unregulated activation of trypsin within pancreatic acinar cells).

• Prolonged and frequently lifelong disorder resulting

from development of fibrosis within

pancreas(irreversable morphological changes)

• Abdominal emergency• If sever :Mortality rate 20%

• revisable

Acute pancreatitis

chronic pancreatitis

Pathophysiology

Pancreatic duct obstruction Defective

intracellular transport Premature

activation of the pancreatic enzymes

Acinar cell injury

continued release of activated proteolytic enzymes is responsible for increased capillary permeability and

rapture, protein exudation ,then retropertineal edema andexuadation (Formation of pseudocyst)

Due to exuadation and hemorrage there may behypovolemia and shock

Lipases destroying peripancreatic to leading fat necrosis and liquefactive hemorrhagic necrosis can also develop

Release of cytokines into systemic circulation may initiates SIRS ,With ,subsequent multiorgan failure ,ARDS.DIC,.....

HOW does the patientpresent

Associated symptoms -Nausea and vomting for

several times (may contribute to hypovolemia)

-Retching and pt may have anorexia-Fever -Juandice

PAIN-Cardinal

Symptom -Sudden onsetsever progressive epigastric

pain radiating to the back, reaching maximum

intensity within minutes, continuous persisting for hours or days, increases when lying supine and decreases when leaning forward refractory to

analgesia.-

PE:Vitals?? 1. Tachycardia

2. Tachypnea

3. Fever

4. Pt may be in shock

• Abdominal exam?? Epigastric tenderness/diffuse abd tenderness

Cullen’s sign [Umbilical hemoperitoneum]

Grey-Turner sign [Flank hemoperitoneum]

Fox’s sign [bluish discoloration of the inguinal ligament]

Abdominal mass (inflammatory pancreatic mass ,or pancreatic abscess, or pseudocyst)

Abdominal distension (due to paralytic ileus or ascites)

Juandice

Due to necrosis induced

hemorrhaging spread to ST of of these body areas

Diagnosis of Acute

Pancreatitis• Clinical

presentation(HX and P.E)

• Lab Studies:

LFT

1. IfAlkaline phosphatase was high → think of biliary stones.

2. If AST > ALT → Think of alcohol.3. Hyperbilirubinemia

CBC

• LEUKOCYTOSIS• HB my be elevated initially due to

hemoconcentration , but can drop if hemorrhagic pancreatitis

Serum pancreatic enzymes

• 1-Serum amylase concentrations increase in 2 to 12 hrs After the onset of pancreatitis.

• 2-levels of amylase will peak 24 to 72 hrs• 3-Remain elevated for 3-5 days before returning to

normal• 4-levels are usually 3 times normal (value required for

diagnosis is1000U/L• 5-serum Lipase is more sensitive and specific as it

remains elevated for longer period

• Other lab test:

Serum electrolyte : pt may have hypocalcemia??

Fat necrosis consumes calcium KFT??

Hypovolemia may lead to AKI and elevated creatinine level

Peritoneal fluid analysis???

if the patient has ascites, you take a sample from the fluid >> send it for amylase test if amylase > 100,000/cm3 (+) for pancreas so the cause of ascitis is acute pancreatitis.

RADIOLOGICAL STUDIES

CHEST AND ABDOMINAL X-RAY: to look for

Pleural effusion(left) and Atelactasis :

1.One of the mechanisms is the transdiaphragmatic lymphatic blockage.

2. formation of a pancreaticopleural fistula.

3. Exudation of fluid into the pleural cavity from the subpleural diaphragmatic vessels may also cause pleural effusion.

4.Sentinal loop and colon cut off sign.

Gallstones on AXR if

radiopaque

Air-filled small bowel in LUQm.c sign on X-ray.

Abrupt ending of transversecolon.

Ultrasound (U/S):

• Swollen pancreas with peripancreatic collection of pus and fluid may be seen.

• Gallstones or dilated biliary duct may be detected.

• specificity 95%, yet its sensitivity ranges between 62% and 95%

CT scan with intravenous contrast remains the gold standard for diagnosing AP and its complications(sensitivity and specificity of CT are 90% and 100%, respectively)

• Enlarged, oedematous pancreas

• Fuzzy pancreas borders

• Fluid around pancreas

• ‘Fat stranding’ in retroperitoneum (fluid density due to oedema in fat)

• Pseudocyst

• Areas of non-enhancement indicate necrosis

ERCP: Indications:

• Preoperative evaluation of patients with suspected traumatic pancreatitis to determine whether the pancreatic duct is disrupted

• Patients with jaundice, suspected biliary pancreatitis, and possible cholangitis who are not clinically improving by 24 hours after admission should undergo endoscopic sphincterotomy and stone extraction.

• Patients older than age 40 years with no identifiable cause to rule out occult common bile duct stones, pancreatic, or ampullary carcinoma or other causes of obstruction.

Assessment of severity• Acute pancreatitis was divided into two groups as

1. Interstitial edematous pancreatitis

which is characterized by acute inflammation of the pancreatic parenchyma and peripancreatic tissues, but without recognizable tissue necrosis.

2. Necrotizing pancreatitis

Necrotizing acute pancreatitis, which is characterized by inflammation associated with pancreatic parenchymal necrosis and/or peripancreatic necrosis can be complicated by systemic inflammatory response syndrome (SIRS) and multiorgan dysfunction syndrome (MODS)

This classification identifies two phases of the disease—early and late—

• and severity of the disease has been classified as mild, moderate, or severe depending on the absence or presence of organ failure, fluid collections, and comorbid conditions.

If you have a patient with 3 points or more, you should immediately admit him to the ICU.

CT severity index (CTSI):

(A)Normal.

(B) Enlargement.

(C) Peripancreatic inflammation.

(D)Single peripancreatic fluid collection.

(E)Multiple peripancreatic fluid collection.

early LateAcute fluid collection Pancreatic Abscess

Shock and acute Renal failure

ARDS ,SIRS and multi organ failure Pancreatic Pseudocyst

Superior mesenteric/Splenic/Portal vein thrombosis Pancreatic necrosis and fat necrosis

pancreatic ascites and pleural effusion

Hyperglycemia and Hypocalcemia

Complications of acute pancreatitis

1.Acute fluid collection

Occurs early in course of acute pancreatitis less than 4 wks ,adjacent to pancreas with no fully defined wall , appear as homogenous fluid density, sterile and mostly resolve spontanously

2. Pancreatic pseudocysts

1. Defined as fluid collection over 4 weeks old that is surrounded by a defined wall made up of fibrous tissue and surrounding organs. It consists mostly of pancreatic secretions and inflammatory exudate .

2. More than half of all pseudocysts are small and resolve within 4 to 6 weeks.

3. After 6 weeks, spontaneous resolution is less likely and surgical intervention is indicated, usually in the form of a cystogastrostomy , cystodudonostomy or cystojejunostomy, and aims to avoid infection, hemorrhage and rapture.

4. Suspected it in a patient with acute pancreatitis with unresolved pain+Palpable epigastric mass.

Complications : Rupture +hemorrhage +infection +gastric outlet, duodenal or biliary obstruction

CT scan is the diagnostic imaging of scan (wall thickness, calcifications and number of pseudocysts).

Tx…Endoscopic drainage(if the pseudocyst doesn’t resolve spontaneously within 6 weeks)

3. Pancreatic Abscess.

1.Pancreatic abscesses are defined as a circumscribed, intra-abdominal collection of pus in proximity to the pancreas, containing little or no pancreatic necrosis.

2.Contains enteric bacteria

3.For pancreatic abscess, the treatment consists of adequate drainage and antibiotic coverage .

4.Drainage can be achieved either by image-guided placement of percutaneous drains or a formal surgical debridement.

4. Pancreatic necrosis

1. Pancreatic necrosis is defined as diffuse or focal area(s) of nonviable pancreatic parenchyma, often associated with peripancreatic fat necrosis.

2. . CT is diagnostic in more than 90% of the cases. Focal or diffuse well circumscribed areas of nonenhanced pancreatic parenchyma larger than 3 cm, or involving more than 30% of the gland, are required for CT diagnosis .

3. Infected pancreatic necrosis is an indication for surgical debridement(pancreatic necrostomy). Therefore, the clinical differentiation between sterile and infected pancreatic necrosis is essential.

4. Because clinical and laboratory findings in these two groups can be identical, the distinction is best made by cultures and Gram stains from percutaneously attained needle aspirates.

5. Sterile necrotic pancreatitis can be managed conservatively

How do we manage acute pancreatitis• Patients with Interstitial edematous pancreatitis(80 % cases) are treated conservatively

((90% of cases will resolve) incluiding

1- Early aggressive fluid and electrolyte resuscitation(in the first 12-24hrs)

• 250-500cc/hr

• Isotonic crystalloids are the preferred fluid(lactated ringer is the prefered crystalloids)

• Adjust fluid therapy at frequent interval withn 6 hrs of admission and for the next 24-48 hrs(vital signs , urine output, BUN ,Creatinine ,hematocrit).

2. NPO , NGT, parenteral antiemetics (such as promethazine and ondansetron) (in pt with ,nausea and vomiting)

3. Oxygen supply and serial monitoring of po2 and ABG

4- Analgesia :opiates

5-nutritional support :

• IN mild AP ,oral feeding can be started immediately if there is no nausea and vomiting ,abd pain is resolving .starting with low fat solid diet is as save as clear liquid diet

• IN sever AP enteral feeding (feeding through NGT )is recommended to prevent gut failure and infectious complications(Enteral feeds have the advantage of maintaining the integrity of the intestinal mucosa and decreasing bacterial translocation)

6.Inhibit pancreatic enzymatic secretions : Somatostatin analogue : octerotide, H2-blockers

7.Antibiotics???

Pancreatitis is a sterile inflammation unless complicated by infection, The use and efficacy of prophylactic antibiotic therapy in acute pancreatitis has long been a point of controversy

8- Role of ERCP and cholycystectomy

• In pt with gallstone pancreatitis and Juandice /cholangitis , urgent ERCP (within first 72 hrs of symptoms onset) is recommended .

• In patients with mild gallstone pancreatitis, cholecystectomy should be performed during the index hospitalization.

References

• Bailey___loves_short_practice_of_surgery_27th_edition

• https://journals.lww.com/ajg/Fulltext/2013/09000/American_College_of_Gastroenterology_Guideline_.6.aspx

• https://wjes.biomedcentral.com/articles/10.1186/s13017-019-0247-0

https://wjes.biomedcentral.com/articles/10.1186/s13017-019-0247-0https://wjes.biomedcentral.com/articles/10.1186/s13017-019-0247-0https://wjes.biomedcentral.com/articles/10.1186/s13017-019-0247-0

–Almaza albakri

Thank you 😊