11. Acute Pancreatitis
• CLINICAL DEFINITION
- An acute condition presenting with abdominal pain-usually
associated with raised blood/urine pancreatic enzymes as a
result of pancreatic inflammation
• PATHOLOGICAL DEFINITION
- Reversible* pancreatic parenchymal injury characterized by
• Interstitial oedema
• Infiltration by acute inflammatory cells
• Necrosis, apoptosis, and haemorrhage
25. Aetiology
Causes are; GET SMASHED
• G – gallstones
• E – ethanol
• T – trauma
• S – steroid
• M – mumps
• A – autoimmune diseases
• S – scorpion sting
• H – hypercalcaemia, hyperlipidaemia
• E – ERCP
• D – drugs e.g. NSAIDS, sulphonamides, azathioprine, diuretics.
• Others include-idiopathic, Ca head of pancreas, pregnancy, cystic fibrosis,
ascariasis, pancreas divisum.
33. Alcohol-induced Pancreatitis
• Manifests as a spectrum, ranging from discrete episodes of AP to chronic
irreversible silent changes.
• Diagnosis should not be entertained unless a person has a history of
over 5-(10) years of heavy (>50 g per day, types less significant) alcohol
consumption.
• Clinically evident AP occurs in <5 % of heavy drinkers; thus, there are
likely other factors that sensitize individuals to the effects of alcohol, such
as genetic factors and tobacco use.
• 1st attack is considered alcohol induced AP
– Although it may be 1st manifestation of (acute on) chronic pancreatitis
34. Idiopathic Acute Pancreatitis
• Defined as pancreatitis with no aetiology established after initial
laboratory (including lipid and calcium level, autoimmune markers,
viral titres) and imaging tests (USG and CT in the appropriate
patient)
– In some patients an aetiology may eventually be found (70 % of
IAP due to microlithiasis), yet in others no definite cause is ever
established.
• Patients with IAP should be evaluated at centres of excellence
focusing on pancreatic disease, providing advanced endoscopy
services and a combined multidisciplinary approach.
35. Hyperlipidemia induced AP
• In the absence of gallstones and/or significant history of alcohol use, a serum
triglyceride should be obtained and considered the aetiology if > 1,000 mg/dl
• Lactescent (milky) serum has been observed in as many as 20 % of patients
with AP
-Therefore a fasting triglyceride level should be re-evaluated 1 month
after discharge when hypertriglyceridemia is suspected
• MOA: Lipase liberate large amounts of toxic fatty acids into pancreatic
microcirculation
- Leading to endothelial injury, sludging of blood cells, and consequent
ischemic states
109. Prognosis
• Overall mortality – 10 to 15%
• Better with underlying gall bladder disease than with alcohol
• Hemorrhagic disease as opposed to oedematous pancreatitis
carries a poorer prognosis
• Operation is considered detrimental to the outcome of
disease
111. References:
• BAJA, 5th Edition
• ACG 2013 Guideline
• Greenfield’s surgery : scientific principles and practice, 6th Edition
• Cope’s Early Diagnosis of the Acute Abdomen, 2nd Edition
• WHO
• h
Editor's Notes
PANCREAS Greek word with literal meaning ‘pan’ (all/whole), ‘creas’ (flesh): sweatbread
Stroma – connective tissue, functionally supportive framework
Parenchyma – functional cellular tissue
The pancreas begins developing during the fifth week of gestation at the junction of the foregut and midgut as two endodermal pancreatic buds, the dorsal bud and the ventral bud comprising endoderm covered in splanchnic mesoderm.
Both the acinar and islet cells differentiate from the endodermal cells found in the embryonic buds while the splanchnic mesoderm eventually develops into the dorsal and ventral mesentery.
The dorsal bud forms first, is larger and forms much of the head, body, and tail of the pancreas.
As the duodenum grows and rotates, the ventral bud rotates clockwise and fuses with the dorsal bud forming the uncinate process and inferior head of the pancreas.
The acinar cells, containing zymogen granules, are pyramidal cells with an apex that faces the pancreatic ductal network.
Twenty to 40 acinar cells that cluster together to form the functional unit called an acinus.
The centroacinar cell, also present within the acinus, functions to secrete fluid and electrolytes of the correct pH into the pancreatic ductal system.
The acinus drains into small intercalated ducts, which join to form interlobular ducts that also secrete fluid and electrolytes.
The pancreatic ductal system. These interlobular ducts form secondary ducts that drain into the main pancreatic duct.
The pancreatic gland lies transversely in the retroperitoneal tissues in close relationship with the celiac plexus and ganglia.
The head is surrounded by and slightly overlaps the duodenum; the body lies in front of the first lumbar vertebra; the tail reaches the left loin and lies against the hilum of the spleen.
2012 global consensus clinical classification
*if underlying cause of pancreatitis is removed, heal without any impairment of function or morphologic loss of gland
*Recurrent attacks with irreversible parenchymal injury leading to impairment of function and morphologic loss is chronic pancreatitis
Pressure-adjusted heart rate (PAR) is calculated by heart rate (HR) multiplied by the ratio of the central venous pressure (CVP) to the mean arterial pressure (MAP).
The total score, ranging from 0 to 24, arises from the sum of all single organ scores using the first measured value of the day.
Overall mortality – 5%-10%
Workers in some populations have reported an increased incidence among AIDS patients.
Trend in Africa is not clear, AIDS-related cases are being recorded.
The pathogenesis of acute pancreatitis relates to inappropriate activation of trypsinogen to trypsin (the key enzyme in the activation of pancreatic zymogens) and a lack of prompt elimination of active trypsin inside the pancreas.
Autodigestion of the pancreas by these proteolytic enzymes is prevented by packaging of proteases in an inactive precursor form and by the synthesis of protease inhibitors including pancreatic secretory trypsin inhibitor (PSTI), serine protease inhibitor, kazal type 1 (SPINK1), and protease serine 1 (PRSS1).
Activation of proteolytic enzymes, possibly through colocalization of zymogen granules and lysosomes, and subsequent rupture of zymogen granules releasing the activated enzymes into the cytoplasm of the pancreatic acinar cell.
Activation of digestive enzymes causes pancreatic injury and results in an inflammatory response that is out of proportion to the response of other organs to a similar insult. The acute inflammatory response itself causes substantial tissue damage and may progress beyond the pancreas to a systemic inflammatory response syndrome, multiorgan failure, or death.
None of these duplicates the actual human situation.
Pancreatic duct obstruction causes ductal hypertension, activated enzyme reflux and acinar cell injury
The common channel theory suggests that bile reflux, through a common biliopancreatic channel, triggers acute pancreatitis.
Duodenal reflux - ? ERCP complications (ampullary injury/disruption)
-Effects of diet
-Malnutrition
-Direct toxicity of alcohol
-Concomitant tobacco smoking
-Hypersecretion of gastric and pancreatic juices(rich in protein, low in bicarbonate/trypsin inhibitor) - Protein plugs - Duct obstruction/reflux
-Hyperlipidemia
-Increased ductal permeability - Enzymes extrusion - damage
-Release of free radicals; superoxide, hydroxyl
-Spasm of sphincter of Oddi
Characteristic abdominal pain
Signs of shock caused by marked outpouring of plasma volume and extracellular fluid
Cyanosis - ? ARDS from atelectasis/pulmonary failure by lipase destruction of pulmonary surfactant; partial inhibition of diaphragmatic movements;
Neither of these is pathognomonic of acute pancreatitis
Also ? Effect of circulating pancreatic lipase on surfactants; limited diaphragmatic movements due to inflammation
Purtscher retinopathy is a hemorrhagic and vasoocclusive vasculopathy, which, in 1912, was first described as a syndrome of sudden blindness associated with severe head trauma. These patients had findings of multiple white retinal patches and retinal hemorrhages that were associated with severe vision loss.
180 mg/dl ~10 mmol/L
Three enzymes derived from pancreatic acinar cells—amylase, lipase, and the proenzyme trypsinogen—have been tested as biochemical markers of acute pancreatitis; serum amylase is the most commonly used of these in clinical practice.
Not diagnostic of Acute Pancreatitis; useful in differential diagnosis
Remarkably shown on the CT scan
Transabdominal ultrasonography is more sensitive than either CT or MRI for identifying gallstones and sludge and for detecting bile-duct dilatation, but it is insensitive for detecting stones in the distal bile duct.
Endoscopic ultrasonography may be the most accurate test for diagnosing or ruling out biliary causes of acute pancreatitis and may guide the emergency use of endoscopic retrograde cholangiopancreatography (ERCP).
Endoscopic ultrasonography may be the most accurate test for diagnosing or ruling out biliary causes of acute pancreatitis and may guide the emergency use of endoscopic retrograde cholangiopancreatography (ERCP).
Each system has merits and demerits, and none is currently recognized as a criterion standard
Although amylase/lipase are used in diagnosing pancreatitis, they are NOT used for predicting severity of disease – i.e. patient with normal amylase (raised in 90 % cases) levels may still have severe acute pancreatitis
American College of Gastroenterologists
Probiotics are live bacteria and yeasts promoted as having various health benefits. They're usually added to yoghurts or taken as food supplements, and are often described as 'good' or 'friendly' bacteria.
Probiotics are thought to help restore the natural balance of bacteria in your gut (including your stomach and intestines) when it's been disrupted by an illness or treatment.
