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ACUTE PANCREATITIS

What we will talk about

• Anatomy and Physiology of the pancreas

• Definition and pathphysiology of acute pancreatitis

• Clinical presentation

• Investigation and Diagnosis

• Management

• Complications

Anatomy of the pancreas • Retroperitoneal organ ,behind lesser sac and stomach at level of L1-L2. weighs 75-

100g and measures about 10 cm in length • Four parts? 1-Head in c-shaped concavity of duodenum(Uncinate process) 2-Neck (ant to SM Vessels) 3-BODY 4- Tail (btw layers of splenorenal ligment) • Blood and Neve supply 1. Celiac Trunk → gastroduodenal → Sup pancreaticduodenal Artery(Ant and Post branches) 2. SMA → Inf. Pancreaticduodenal artery (ANT and Post branches) 3. Splenic artery→ Dorsal and caudal pancreatic arteries. Venous drainage is by SM VEIN and splenic vein NERVE SUPPLY PSNS:VAGUS NERVE (stimulate endocrine and exocrine

secretion) SNS :Splanchenic nerves (inhibits secretion )

These supply the HEAD

These branches supply the neck ,body .tail

PANCREATITIS

• Abdominal emergency

• If sever :Mortality rate 20%

• revisable

Acute pancreatitis

• Prolonged and frequently lifelong disorder resulting from development of fibrosis within pancreas(irreversable morphological changes)

Chronic pancreatitis

Pancreatitis is an inflammation of the gland parenchyma pancreas as a result of autodigestion by its own enzymes ( when they are in the active form).

Etiology of Acute Pancreatitis 40%

35%

4%

1.5%

2%

Pathophysiology of Acute pancreatitis

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 and

exuadation (Formation of pseudocyst)

Due to exuadation and hemorrage there may be and shock hypovolemia

liquefactiveand fat necrosis to leading peripancreaticLipases destroying

can also develop necrosishemorrhagic

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

HOW does the patient present?

PAIN -Cardinal

Symptom -Sudden onset

and sever And progressive

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.-

Associated symptoms

-Nausea and vomting for several

times (may contribute to hypovolemia)

-Retching and pt

may have anorexia -Fever

-Juandice

• ON physical Exam: Vitals?? 1. Tachycardia 2. Tachypnea 3. Fever 4. Pt may be in shock • Abdominal exam?? 1. Epigastric tenderness/diffuse abd tenderness 2. Cullen’s sign [Umbilical hemoperitoneum] 3. Grey-Turner sign [Flank hemoperitoneum] 4. Fox’s sign [bluish discoloration of the inguinal ligament] 5. Abdominal mass (inflammatory pancreatic mass ,or

pancreatic abscess, or pseudocyst) 6. Abdominal distension (due to paralytic ileus or ascites) 7. Juandice

Diagnosis of Acute Pancreatitis • Clinical presentation(HX and P.E)

• Lab Studies

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 LFT

1. If Alkaline phosphatase was high → think of biliary stones.

2. If AST > ALT → Think of alcohol.

3. Hyperbilirubinemia

• 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

1. 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

• Sentinal loop and colon cutoff sign

2. Ultrasound (U/S):

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

• Gallstones or dilated biliary duct may be detected.

3. CT scan with intravenous contrast remains the gold standard for diagnosing AP and its complications

• Enlarged, oedematous pancreas

• Fuzzy pancreas borders

• Fluid around pancreas

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

• Areas of non-enhancement indicate necrosis

4. ERCP:

Is not routinely indicated for the evaluation of patients during an

attack of acute pancreatitis but in Patients with jaundice, suspected biliary pancreatitis. Its both diagnostic and therapeutic

CECT coronal image showed

congested and enlarged pancrease heterogenous partially non enhancing

pancreatic parenchyma with misty fat planes and

surrounding fluid suggestive of acute pancreatitis

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.

1. and “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

100%

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 12-24 hrs)

• 1.250-500cc/hr

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

• 3.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.

What about complications of acute pancreatitis

Early

Acute fluid collection

Shock and acute Renal failure

ARDS ,SIRS and multi organ failure

Superior mesenteric/

Splenic/Portal vein thrombosis

EARLY

Pancreatic ascites and pleural

effusion

Hyperglycemia and Hypocalcemia

Late

Pancreatic necrosis and fat

necrosis

Pancreatic Abscess

Pancreatic Pseudocyst

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.

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 . Without it, virtually all patients die. 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

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