Definition
Acute inflammatory process of the pancreas with variable involvement of regional or remote tissues
Epidemiology
1–5/10,000
Predominant age:
- Acute pancreatitis: None
- Chronic pancreatitis: 35–45 years (usually related to alcohol)
Male = Female
Aetiology
I - idiopathic.(10%) Thought to be hypertensive sphincter or microlithiasis.
G - gallstone. (40%)
E - ethanol (alcohol) (35%)
T – trauma (usually in children), tumour
S - steroids
M - mumps (paramyxovirus) and other viruses (Epstein-Barr virus, CMV)
A - autoimmune disease (Polyarteritis nodosa, Systemic lupus erythematosus)-in pt <40
S - scorpion sting , snake bites
H - hypercalcemia, hyperlipidemia/hypertriglyceridemia and hypothermia
E - ERCP (4%) , emboli
D - drugs (SAND - steroids & sulfonamides, azathioprine, NSAIDS, diuretics such as furosemide and thiazides, & didanosine) and duodenal ulcers
Pathophysiology
epigastric/central abdomen dull, boring and steady pain, sudden onset, increasing severity. may radiate to back, relieved by sitting forward
nausea, vomiting
fever, tachycardia, shock
jaundice (28%)
ileus, rigid abdomen, tenderness
periumbilical discoloration (Cullen’s sign) or in the flanks (Grey Turner’s sign) – due to methaemalbumin formed from digested blood tracks around the abdomen
Less common sign
Differential Diagnosis
Acute cholecystitis, organ rupture, AAA, PUD, any acute abdomen
Investigation
Criteria for Severity
Several examples of scoring system:
Dx for severe pancreatitis : Ranson score >3, APACHE score >8, modified Glasgow score >3. Balthazar score – proven to be more accurate
Management
Complications
Prognosis
80% improve rapidly
20% have at leat one complication from which 1/3 die
Ranson scoring:
Acute inflammatory process of the pancreas with variable involvement of regional or remote tissues
Epidemiology
1–5/10,000
Predominant age:
- Acute pancreatitis: None
- Chronic pancreatitis: 35–45 years (usually related to alcohol)
Male = Female
Aetiology
I - idiopathic.(10%) Thought to be hypertensive sphincter or microlithiasis.
G - gallstone. (40%)
E - ethanol (alcohol) (35%)
T – trauma (usually in children), tumour
S - steroids
M - mumps (paramyxovirus) and other viruses (Epstein-Barr virus, CMV)
A - autoimmune disease (Polyarteritis nodosa, Systemic lupus erythematosus)-in pt <40
S - scorpion sting , snake bites
H - hypercalcemia, hyperlipidemia/hypertriglyceridemia and hypothermia
E - ERCP (4%) , emboli
D - drugs (SAND - steroids & sulfonamides, azathioprine, NSAIDS, diuretics such as furosemide and thiazides, & didanosine) and duodenal ulcers
Pathophysiology
- begins with injuries to acinar cells or impairment of zymogen granules secretion.
- lysosomal and zymogen granule fuse, enabling trypsin production
- trypsin triggers auto-digestion by zymogen activation cascade
- secretory vesicles extrude into the interstitium, attracting inflammatory cells
- Activated neutrophills release superoxide, proteolytic enzyme
- Macrophages release cytokines (tumour necrosis factor alpha, IL-6, IL-8)
- Mediators cause increased pancreatic vascular permeabilityà haemorrhage, edema, necrosis.
epigastric/central abdomen dull, boring and steady pain, sudden onset, increasing severity. may radiate to back, relieved by sitting forward
nausea, vomiting
fever, tachycardia, shock
jaundice (28%)
ileus, rigid abdomen, tenderness
periumbilical discoloration (Cullen’s sign) or in the flanks (Grey Turner’s sign) – due to methaemalbumin formed from digested blood tracks around the abdomen
* Cullen’s sign | * Grey Turner’s sign |
- Körte's sign (pain or resistance in the zone where the head of pancreas is located (in epigastrium, 6–7 cm above the umbilicus)
- Kamenchik's sign (pain with pressure under the xiphoid process)
- Mayo-Robson's sign (pain while pressing at the top of the angle lateral to the Erector spinae muscles and below the left 12th rib (left costovertebral angle(CVA))
Differential Diagnosis
Acute cholecystitis, organ rupture, AAA, PUD, any acute abdomen
Investigation
FBC | an admission hematocrit > 47% may inidicate more severe disease Leukocytosis may represent inflammation or infection | ||
ABG | if pt is dyspnoeic, monitor oxygenation, acid base status | ||
CRP | 24-48 hours after presentation | ||
Calcium, magnesium, cholesterol, and triglycerides | search for an etiology of pancreatitis (hypercalcemia or hyperlipidemia) or complications of pancreatitis (hypocalcemia resulting from saponification of fats in the retroperitoneum). | ||
Amylase | ↑ amylase (>1000u/ml, falls after 2d) may be normal (in 10% of cases) | ||
Lipase | rises 4 to 8 hours from the onset lipase more sensitive & specific (falls after 7-14d) | ||
LFT | ALT >150 U/L suggests gallstone pancreatitis and a more fulminant disease course. | ||
Serum electrolytes, BUN, creatinine, glucose | electrolyte imbalances, renal insufficiency, and pancreatic endocrine dysfunction | ||
LDH, BUN, and bicarbonate | Measured at admission and at 48h to determine Ranson Criteria | ||
IgG4 | evaluate for autoimmune pancreatitis | ||
Abdomen U/S | if suspect gallstone + AST↑, FNA- for bacterial infection | ||
Endoscopic U/S | evaluating the cause of severe pancreatitis, particularly microlithiasis and biliary sludge, and can help identify periampullary lesion | ||
Abdominal CT scanning | Indicated for severe pancreatitis scan within the first 72h Acute pancreatitis. Pancreatic necrosis. Note the nonenhancing pancreatic body anterior to the splenic vein. Also present is peripancreatic fluid extending anteriorly from the pancreatic head. | ||
MRI | alternative for CT, in pt with contrast allergy or renal insufficiency. Image: Focal pancreatitis involving pancreatic head. Pancreatic head is enlarged with adjacent ill-defined peripancreatic inflammation and fluid collections | ||
ERCP | Indication: severe acute gallstone pancreatitis that is not responding to supportive therapy or with ascending cholangitis with worsening signs and symptoms of obstruction,
| ||
AXR | Limited role in acute pancreatitis detect free air in the abdomen, ‘sentinel loop’ of proximal jejunum (solitary air-filled dilatation) | ||
erect CXR | exlude other causes, eg perforation. |
Criteria for Severity
Several examples of scoring system:
Scoring System | Criteria | ||||||||||||||||||
Modified Glasgow Criteria | Pa O2 <8kPa Age >55 Neutrophils WCC> 15x 109/L Calcium < 2mmol/L Raised urea >16mmol/L Enzymes: LDH>600iu/L, AST >200iu/L Albumin<32g/L Sugar : blood glucose >10 mmol/L | ||||||||||||||||||
Ranson's Criteria | Present on Admission - GA LAW Glucose (blood) greater than 200 mg/dl Age >55 years LDH (serum) > 350 I.U./L AST >250 I.U./L WBC > 16,000/ul Developing During the First 48 Hours: - C HOBBS Calcium (serum) < 8 mg/dl Hematocrit fall > 10% Oxygen (arterial) saturation l< 60 mm Hg BUN increase> 8 mg/dl. Base deficit > 4 meq/L Sequestration of fluid > 600 ml | ||||||||||||||||||
Computed Tomography Severity Index (CTSI)/ Balthazar score |
|
Dx for severe pancreatitis : Ranson score >3, APACHE score >8, modified Glasgow score >3. Balthazar score – proven to be more accurate
Management
Fluids | (large 0.9% saline) to stabilize vital signs, urine flow >30mL/h, urinary catheter & consider CVP monitoring | ||||||||||||||||
Nutrition | Early initiation of enteral nutritional supplementation TPN (2nd line)has been shown to reduce mortality rate | ||||||||||||||||
Antibiotics | imipenem. (Controversial) | ||||||||||||||||
Analgesia | pethidine or morphine(may cause sphincter of oddi to contract more but it is a better analgesic, no CI) | ||||||||||||||||
Monitor | Hourly pulse, BP, urine output, daily FBC, U&E, Ca, glucose, amylase, ABG | ||||||||||||||||
If worsening | take to ICU. O2 if PaO2 ↓. Suspected abscess/necrosis(CT) à PTN +laparotomy & debridement. Antibiotic controversial (imipenem) | ||||||||||||||||
ERCP | if suspected CBD stone or clinical deterioration. Not in acute condition | ||||||||||||||||
Follow up | Ensure alcohol incontinence Within weeks to months after onset: check for signs of intra-abdominal infection, pancreatic pseudocyst, intra-abdominal hemorrhage, colon perforation, obstruction or fistulization, and multiorgan system failure. CT-guide needle aspiration in the setting of necrotizing pancreatitis Repeat CT/US to monitor complication (eg. pseudocyst) | ||||||||||||||||
Surgery for infected pancreatic necrosis | indication: infected pancreatic necrosis, diagnostic uncertainty, complications.
| ||||||||||||||||
Management for pancreatic pseudocyst |
| ||||||||||||||||
Pancreatitic abscess | Pancreatic abscesses generally occur late in the course of pancreatitis. Many of these respond to percutaneous catheter drainage and antibiotics. Those that do not respond require surgical debridement and drainage. |
Complications
Early | Shock, ARDS, renal failure, Disseminated intravascular coagulation (DIC), sepsis, SIRS, Ca2+↓ |
Late(>1wk) | pseudocyst (most common) Pancreatic necrosis Infection (Within the first 1-3 weeks) abscess bleeding (eg: splenic artery), thrombosis fistula, recurrent oedematous pancreatitis. |
Prognosis
80% improve rapidly
20% have at leat one complication from which 1/3 die
Ranson scoring:
- Ranson score of 0–2: Minimal mortality
- Ranson score of 3–5: 10–20% mortality
- Ranson score of >5: >50% mortality
3 comments:
Very well written and informative article, thank you :-)
Toshiba PVT-375BT
Too much informative , thank you.
If you time please make an article that includes all the clinical sign of the body and tag to me.
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Took Onglyza off and on for a year. I have an enlarged adrenal gland. Still I await the outcome of that CT, but I know that much. Will find out more.
I had the CT because of chronic pancreatic pain that started out as "attacks" from a couple of times a month to finally after 3 months of use without interruption, "attacks" 2-3 times a week. My PA put Onglyza on my allergies list.
In the meantime, I lost almost 50 lbs in 5 months due to illness. Loss of appetite, pancreatic pain, chronic diarrhea, then eventually, inability to move my bowels. Severe back pain from the pancreas, and severe chest pain sent me to the ER where I was worked up for cardiac pain. I was cardiac cleared, but told my amylase was very low.
Still seeking a diagnosis, but I lay the blame squarely on Onglyza. I'd had pancreatic issues in the past, and argued with the PA that prescribed it, she was calling me non-compliant, and I feared repercussion from my insurance company.
I even took an article about the dangers of Onglyza, particularly in patients with a history, and she made me feel foolish.
I wish I had listened to my instincts, I fear not only damage to my pancreas that is irreversible, but also severe damage to my left kidney, though I have bilateral kidney pain.
I was off all diabetes meds, and control sugars strictly low to no carb. I can barely eat anymore, I have severe anorexia.
I would warn anyone taking Onglyza to consider a change and try Dr Itua Herbal Medicine, and anyone considering taking it, to select a different avenue. I have been suffering severely for about 9 months, but the past 7 months have been good with the help of Dr Itua herbal medicine which I took for 4 weeks.
I have been off Onglyza now, for 7 months, and simply 100% improvement with the help of Dr Itua. I had none of these issues except a history of pancreatitis in my distant past.
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