Wednesday, February 23, 2011

Acute Pancreatitis

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
  • 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.
Presentation
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
Less common 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
FBCan admission hematocrit > 47% may inidicate more severe disease
Leukocytosis may represent inflammation or infection
ABGif pt is dyspnoeic, monitor oxygenation, acid base status
CRP24-48 hours after presentation
Calcium, magnesium, cholesterol, and triglyceridessearch 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)
Lipaserises 4 to 8 hours from the onset
lipase more sensitive & specific (falls after 7-14d)
LFTALT >150 U/L suggests gallstone pancreatitis and a more fulminant disease course.
Serum electrolytes, BUN, creatinine, glucoseelectrolyte imbalances, renal insufficiency, and pancreatic endocrine dysfunction
LDH, BUN, and bicarbonateMeasured at admission and at 48h to determine Ranson Criteria
IgG4 evaluate for autoimmune pancreatitis
Abdomen U/Sif suspect gallstone + AST↑,
FNA- for bacterial infection
Endoscopic U/Sevaluating the cause of severe pancreatitis, particularly microlithiasis and biliary sludge, and can help identify periampullary lesion
Abdominal CT scanningIndicated 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
ERCPIndication: severe acute gallstone pancreatitis that is not responding to supportive therapy or with ascending cholangitis with worsening signs and symptoms of obstruction,

This patient with acute gallstone pancreatitis underwent endoscopic retrograde cholangiopancreatography. The cholangiogram shows no stones in the common bile duct and multiple small stones in the gallbladder. The pancreatogram shows narrowing of the pancreatic duct in the area of the genu, the result of extrinsic compression of the ductal system by inflammatory changes in the pancreas.

AXRLimited role in acute pancreatitis
detect free air in the abdomen, ‘sentinel loop’ of proximal jejunum (solitary air-filled dilatation)
erect CXRexlude other causes, eg perforation.


Criteria for Severity
Several examples of scoring system:
Scoring System
Criteria
Modified Glasgow CriteriaPa 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 CriteriaPresent 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

Balthazar Grade
Appearance on CT
CT Grade Points
Grade A
Normal CT
0 points
Grade B
Focal or diffuse enlargement of the pancreas
1 point
Grade C
Pancreatic gland abnormalities and peripancreatic inflammation
2 points
Grade D
Fluid collection in a single location
3 points
Grade E
Two or more fluid collections and / or gas bubbles in or adjacent to pancreas
4 points


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
NutritionEarly initiation of enteral nutritional supplementation
TPN (2nd line)has been shown to reduce mortality rate
Antibioticsimipenem. (Controversial)
Analgesiapethidine or morphine(may cause sphincter of oddi to contract more but it is a better analgesic, no CI)
MonitorHourly pulse, BP, urine output, daily FBC, U&E, Ca, glucose, amylase, ABG
If worseningtake to ICU. O2 if PaO2 ↓. Suspected abscess/necrosis(CT) à PTN +laparotomy & debridement. Antibiotic controversial (imipenem)
ERCPif suspected CBD stone or clinical deterioration. Not in acute condition
Follow upEnsure 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 necrosisindication: infected pancreatic necrosis, diagnostic uncertainty, complications.
  • Closed management - necrosectomy with closed continuous postoperative lavage
  • Open management - necrosectomy with planned staged reoperations at definite intervals (up to 20+ reoperations in some cases)

Management for pancreatic pseudocyst
DefinitionPseudocyst-peripancreatic fluid collections persisting for more than 4 weeks are termed acute pseudocysts. Pseudocysts lack an epithelial layer and, thus, are not considered true cyst.
Imaging*
CT scan of a large symptomatic pancreatic pseudocyst abutting the posterior wall of the stomach.
Investigationfluid in lesser sac, T↑, a mass + persistent ↑
amylase/LFT: 40% resolve spontaneously 6-12wk, supportive mgt until thick wall has formed,drainage externally or into stomach , biopsy to rule out malignancy.
Indication for interventionsymptomatic (pain, bleeding, or infection)
larger than 7 cm and are rapidly expanding
Percutaneous aspirationfor pt with very large fluid collection
Endoscopic techniqueby transpapillary or transmural techniques
The proximal end of the stent is placed into the cyst cavity
Success rate= 83%, complication rate = 12%
Transmural enterocystostomyfor noncommunicating pseudocysts
Success rate= 85%, complication rate = 17%
Surgical cyst-enterostomyInternal pseudocyst enteric anastomosis
operative mortality rate of 3-5%

Pancreatitic abscessPancreatic 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

EarlyShock, 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:

Unknown said...

Very well written and informative article, thank you :-)

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Unknown said...

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.

Anonymous said...

Hi,
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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