Pancreatitis

Nkechi Nweke
Oceania University of Medicine
September 2022
 Anatomy
The pancreas with the exception of the tail is a retroperitoneal organ located in the epigastric and left hypochondrium regions. The pancreas has
exocrine (digestive) and endocrine (hormonal) functions. It is divided into the head, uncinate process, neck, body and tail. Intralobular ducts drain
into main pancreatic duct which joins the CBD forming the ampulla of Vater. This opens into the 2nd part of duodenum via major duodenal papilla
(controlled by a muscular valve - sphincter of Oddi).

Relations

- The head is the widest portion, which lies within the C-shaped curve of the duodenum.
- Stomach and pylorus are anterior to pancreas. SMA is posterior to neck and anterior to uncinate process.
- CBD descends posterior to head of pancreas before opening into 2nd part of duodenum along with major pancreatic duct via major
duodenal papilla. Aorta and IVC lie posterior to head of pancreas. Splenic vein and SMV unite to form portal vein posterior to neck.
- Spleen is posterolateral. The lienorenal ligament connects spleen to tail of pancreas. Splenic artery traverses superior border of pancreas.

Vascular supply: Pancreatic branches of splenic artery

- Additional supply to the head from superior and inferior pancreaticoduodenal arteries ( branches of gastroduodenal from celiac trunk and
SMA respectively)
- Venous drainage of head via SM branches of portal vein; rest of pancreas via splenic vein

Lymphatics: Lymphatic vessels follow supplying arteries. They empty into pyloric and pancreaticosplenic nodes which drain into SM and celiac
nodes.

Innervation: Vagus nerve (parasympathetic), greater and lesser splanchnic nerves T5-T12 (sympathetic).
Epidemiology
Annual incidence of pancreatitis is 5 to 80 per 100 000 (acute) and 5 to 12 per 100 000 (chronic). The average age of onset depends on etiology for
example, alcohol related -39 years, drug induced - 42 years, biliary tract related - 69 years, trauma related- 66 years.

Acute pancreatitis affects more males than female. There is no clear gender predilection for idiopathic pancreatitis.

A higher frequency of acute pancreatitis has been noted among blacks followed by hispanics, asians and then american indians.

Etiology
The major causes of acute pancreatitis are alcohol abuse, gallstones and idiopathic. Others include:
- Certain medications
- ERCP
- Trauma
- Hypertriglyceridemia
- Abdominal surgery
- Hypercalcemia which may be caused by hyperparathyroidism
- Pancreatic cancer
- Genetic disorders (hereditary pancreatitis, cystic fibrosis, alpha 1-antitrypsin deficiency)
- Infection
Pathophysiology
Pancreatic duct and acinar injury are the mechanisms of acute pancreatitis. Digestive enzymes which are improperly
secreted by the pancreas cause autodigestion and pancreatic inflammation. The inciting event is activation of
trypsinogen to trypsin within the acinar cells and not the lumen of the duct.
Obstruction of pancreatic duct from gallstones, ERCP and other etiologies result in temporary obstruction of the
duct. Alcohol can cause pancreatitis from direct toxicity and immunologic response.
Repeated attacks of acute pancreatitis will lead to inflammatory infiltrates and fibrosis in the pancreas over time,
resulting in chronic pancreatitis. This can lead to pancreatic insufficiency.

Presentation
- Severe sharp epigastric pain radiating to the back and often associated with nausea and vomiting.
- Chronic pancreatitis can present with abdo pain, vomiting and nausea or can be painless. Patients can present
with weight loss and steatorrhea.
- Dyspnea from diaphragm irritation, pleural effusion, ARDS.
- Pale appearance, diaphoresis in severe acute pancreatitis.
- Muscle spasm in extremities secondary to hypocalcemia.
Physical exam
- Take a history including social history.
- Vitals : pulse, BP, RR, temp.
- Do an abdo exam. Jaundice may indicate biliary tree obstruction. Tenderness, guarding, decreased bowel sounds if ileus is present.
Ecchymosis in flanks (Grey-Turner sign) or around umbilicus (Cullen’s sign) may signify blood in the abdomen from pancreatic
necrosis.
- Severe pancreatitis can alter mental status.

Differentials
Acute Pancreatitis Chronic Pancreatitis

Cholecystitis Acute recurrent pancreatitis

Peptic ulcer Chronic mesenteric ischemia

Perforated viscus Pancreatic cancer

Choledocholithiasis
Acute mesenteric ischemia
Investigations
- Diagnosis of acute pancreatitis require 2 of the following: abdo pain characteristic of pancreatitis, lipase or amylase level greater
than 3 times of upper limit and findings of acute pancreatitis on imaging.
- In chronic pancreatitis, lipase can be normal. Pancreatic calcifications on imaging can point towards chronic pancreatitis.

- Bloods: metabolic panel, CBC, serum lipase, lactate, serum triglycerides, CRP , LFTs . The best assessment of acute pancreatitis
progression can be made with rising BUN or hematocrit.
- Abdo USS for choledocholithiasis and bile duct dilatation.
- CXR to evaluate pleural effusion in moderate to severe cases
- CT contrast in cases where diagnosis is equivocal or in cases where patient has failed to improve inspite of IV fluids over 48
hours.
- ERCP for recurrent acute pancreatitis.
- MRCP or endoscopic ultrasound in consultation with a gastroenterologist when no cause for pancreatitis is found with other
evaluation.
- Other tests: alpha-1-antitrypsin, IgG4/ANA, genetic testing (CFTR, SPINK1, PRSS1) especially if patient is young or there is a
positive family history.
Treatment
- In acute pancreatitis, patient is commonly NPO until nausea, vomiting, abdo pain, ileus, appetite improve. Oral feedings should
commence as soon as patient can tolerate them.
- Aggressive fluid resuscitation is the most important step in management of acute pancreatitis. IV Lactated Ringer preferably at
15 to 20 ml/kg bolus then 3 ml/kg/hr for the first 24 hours. BUN, hematocrit and urine output are monitored every 4 to 6 hours in
the first 24 hours to adjust fluid resuscitation rate especially if there is cardiovascular or renal comorbidities.
- Give empiric antibiotics if infection is suspected until culture results are available.
- Analgesic for pain including IV opioids.
- Gastroenterology consult and urgent ERCP for patients with acute pancreatitis and acute cholangitis.
- Cholecystectomy for gallstones. Delay surgery if there is concern for necrotizing acute pancreatitis, until surrounding
inflammation has settled.
- In acute pancreatitis caused by hypertriglyceridemia, place patient on insulin drip to activate lipoprotein lipase.

- For chronic pancreatitis, control pain, counsel patient on lifestyle modification and pancreatic enzyme replacement.

- Where medical therapy fails, surgery, celiac plexus block, ESWL for duct stones.
Complications
Complications of acute pancreatitis can be local or systemic:

Local complications Systemic Complications

Pancreatic pseudocyst ARDS

Walled-off necrosis Compartment syndrome

Peri-pancreatic fluid collection Acute kidney injury

Acute necrotic collection Disseminated intravascular coagulation (DIC)

Complications of chronic pancreatitis include:

- Pseudocyst formation
- Diabetes
- Splenic vein thrombosis
- Pseudoaneurysm
- Recurrent acute pancreatitis
- Chances of progression to pancreatic cancer
Prognosis
Mortality rate from acute pancreatitis is about 2%. Endocrine and exocrine insufficiency can manifest in 20 to 30%
of patients, following an episode of acute pancreatitis. Risk for recurrence includes the same etiology of the initial
attack, the severity of the attack and the degree of structural damage.
References
1. Acute Pancreatitis: Practice Essentials, Background, Pathophysiology. (2019, November 10). Medscape.com.
https://emedicine.medscape.com/article/181364-overview
2. Chatila, A. T., Bilal, M., & Guturu, P. (2019). Evaluation and management of acute pancreatitis. World Journal of
Clinical Cases, 7(9), 1006–1020. https://doi.org/10.12998/wjcc.v7.i9.1006
3. Gapp, J., & Chandra, S. (2020). Acute Pancreatitis. PubMed; StatPearls Publishing.
https://www.ncbi.nlm.nih.gov/books/NBK482468/
4. Nabeeha Mohy-ud-din, & Morrissey, S. (2019, February 19). Pancreatitis. Nih.gov; StatPearls Publishing.
https://www.ncbi.nlm.nih.gov/books/NBK538337/
5. Shah, A., Mourad, M., & Bramhall, S. (2018). Acute pancreatitis: current perspectives on diagnosis and
management. Journal of Inflammation Research, Volume 11, 77–85. https://doi.org/10.2147/jir.s135751