What is Acute Pancreatitis?

Question

My Neighbor got this Acute Pancreatitis and she expired because of improper treatment, Hence what is the Acute Pancreatitis all about and the treatment method?

Answer 1

If your neighbors have doubts about the adequacy treatment method they should ask for an autopsy.

But maybe your neighbor died from complications. Among others, acute pancreatitis can cause breathing problems. Many people develop hypoxia, which means that cells and tissues are not receiving enough oxygen.

Sometimes a person cannot stop vomiting and needs to have a tube placed in the stomach to remove fluid and air. In mild cases, a person may not eat for 3 or 4 days and instead may receive fluids and pain relievers through an intravenous line.

If an infection develops, the doctor may prescribe antibiotics. Surgery may be needed for extensive infections. Surgery may also be necessary to find the source of bleeding, to rule out problems that resemble pancreatitis, or to remove severely damaged pancreatic tissue.

Acute pancreatitis can also cause kidney failure.

The treatment depends on the severity of the attack. If no kidney or lung complications occur, acute pancreatitis usually improves on its own. Treatment, in general, is designed to support vital bodily functions and prevent complications.

Answer 2

pancreas is an organ that can secrete enzyme, a chemical that can digest things.
in acute pancreatitis, there is some inflammation going on in it, can either be blockage by gallstones, reflux of alcohol, infection, and many other causes. the inflammation causes the pancreas to "burst" and all the enzymes pour out into the abdomen. this causes sudden onset severe abdominal pain. the enzyme then can "digest" the abdominal organs, and finally causing death.
due to many other diseases that can present the same way e.g. appendicitis, ectopic pregnancy, the diagnosis of acute pancreatitis can be delayed.
the treatment is surgery.

Answer 3

Acute pancreatitis is an inflammation of the pancreas. It is treated with IV therapy, sometimes antibiotics and nothing by mouth to give the pancreas a rest. Pain management is also a factor.

Answer 4

Acute Pancreatitis is the sudden onset of an inflammation of the pancreas.

Answer 5

olive leaf extract will help
eat 2-3 baby beets 1- 2 times per day
use natural / herbal / organic toiletries & dish detergent
avoid alcohol, beer, yeast bread, pig meat and processed foods and any chemical product

Answer 6

inflammation of the pancrease occuring over a short period of time
disease with generaly bad prognosis
causes multi-system faliure
treatment is usually supportive + try to treat complications

Answer 7

Acute pancreatitis is a rapidly-onset inflammation of the pancreas. Depending on its severity, it can have severe complications and high mortality despite treatment. While mild cases are often successfully treated with conservative measures or laparoscopy, severe cases require invasive surgery (often more than one intervention) to contain the disease process

Symptoms and signs:
Common symptoms include:

Severe abdominal pain often radiating through to the back.
Nausea, vomiting, diarrhea and loss of appetite.
Fever
Shock, hemodynamic instability
Common signs include

Grey Turner sign (hemorrhagic discoloration of the flanks), Cullen sign (hemorrhagic discoloration of the umbilicus)
Recovery may be followed by development of pancreatic pseudocyst, pancreatic dysfunction (malabsorption due to exocrine failure) or diabetes mellitus.

Most common causes
A common mnemonic for the causes of pancreatitis is:

I - idiopathic
G - gallstone. Gallstones that travel down the common bile duct and which subsequently get stuck in the Ampulla of Vater can cause obstruction in the outflow of pancreatic juices from the pancreas into the duodenum. The backflow of these digestive juices causes lysis (dissolving) of pancreatic cells and subsequent pancreatitis.
E - ethanol (alcohol)
T - trauma
S - steroids
M - mumps (paramyxovirus) and other viruses (Epstein-Barr virus, Cytomegalovirus)
A - autoimmune disease (Polyarteritis nodosa, Systemic lupus erythematosus)
S - scorpion sting - Tityus Trinitatis - Trinidad/ snake bite
H - hypercalcemia, hyperlipidemia/hypertriglyceridemia and hypothermia
E - ERCP (Endoscopic Retrograde Cholangio-Pancreatography - a form of endoscopy)
D - drugs (SAND - steroids & sulphonamides, azathioprine, NSAIDS, diuretics such as furosemide and thiazides, & didanosine) and duodenal ulcers

Less common causes

pancreas divisum
long common duct
carcinoma of the head of pancreas, and other cancer
ascaris blocking pancreatic outflow
ischemia from bypass surgery
fatty necrosis
pregnancy
infections other than mumps, including varicella zoster
repeated marathon running.

Causes by demographic
The most common causes of pancreatitis, are as follows :

Western countries - chronic alcoholism and gallstones accounting for more than 85% of all cases
Eastern countries - gallstones
Children - trauma
Adolescents and young adults - mumps

Pathogenesis

The exocrine pancreas produces a variety of enzymes, such as proteases, lipases and saccharidases. These enzymes contribute to food digestion by breaking down food tissues. In acute pancreatitis, the worst offender among these enzymes may well be the protease trypsinogen which converts to the active trypsin which is most responsible for auto-digestion of the pancreas which causes the pain and complications of pancreatitis.

Histopathology The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas parenchyma, focal enzymic necrosis of pancreatic fat and vessels necrosis - hemorrhage. These are produced by intrapancreatic activation of pancreatic enzymes. Lipase activation produces the necrosis of fat tissue in pancreatic interstitium and peripancreatic spaces. Necrotic fat cells appear as shadows, contours of cells, lacking the nucleus, pink, finely granular cytoplasm. It is possible to find calcium precipitates (hematoxylinophilic). Digestion of vascular walls results in thrombosis and hemorrhage. Inflammatory infiltrate is rich in neutrophils. Photos at: Atlas of Pathology

Investigations
Blood Investigations - Full blood count, Renal function tests, Liver Function, serum calcium, serum amylase and lipase, Arterial blood gas
Imaging - Chest Xray (for exclusion of perforated viscus), Abdominal Xrays (for detection of "sentinel loop" dilated duodenum sign, and gallstones which are radioopaque in 10%) and CT abdomen

Amylase and lipase

Serum amylase rises 2 to 12 hours from the onset of symptoms, and normalises within 1 week
Serum lipase rises 4 to 8 hours from the onset of symptoms and normalises within 8 to 14 days.
Serum amylase may be normal (in 10% of cases) for cases of acute on chronic pancreatitis (depleted acinar cell mass) and hypertriglyceridemia
Reasons for false positive elevated serum amylase include salivary gland disease (elevated salivary amylase) and macroamylasemia
If Lipase level is about 2.5 to 3 times that of Amylase, it is an indication of pancreatitis due to Alcohol[1].

CT abdomen
CT abdomen should not be performed before the 1st 48 hours of onset of symptoms as early CT (<48 h) may result in equivocal or normal findings.

CT Findings can be classified into the following categories for easy recall :

Intrapancreatic - diffuse or segmental enlargement, edema, gas bubbles, pancreatic pseudocysts and phlegmons/abscesses (which present 4 to 6 wks after initial onset)
Peripancreatic / extrapancreatic - irregular pancreatic outline, obliterated peripancreatic fat, retroperitoneal edema, fluid in the lessar sac, fluid in the left anterior pararenal space
Locoregional - Gerota's fascia sign (thickening of inflamed Gerota's fascia, which becomes visible), pancreatic ascites, pleural effusion (seen on basal cuts of the pleural cavity), adynamic ileus,

Balthazar scoring
Balthazar Scoring for the Grading of Acute Pancreatitis

Grade A - normal CT
Grade B - focal or diffuse enlargement of the pancreas
Grade C - pancreatic gland abnormalities and peripancreatic inflammation
Grade D - fluid collection in a single location
Grade E - two or more collections and/or gas bubbles in or adjacent to pancreas

Classification by severity
Progression of pathophysiology
Acute pancreatitis can be further divided in mild and severe pancreatitis. Mostly the Atlanta classification (1992) is used. In severe pancreatitis serious amount of necrosis determine the further clinical outcome. About 20% of the acute pancreatitis are severe with a mortality of about 20%. This is an important classification as severe pancreatitis will need intensive care therapy whereas mild pancreatitis can be treated on the common ward.

Necrosis will be followed by a systemic inflammation response syndrom (SIRS) and will determine the immediate clinical course. The further clinical course is then determined by bacterial infection. SIRS is the cause bacterial translocation from the patients colon.

There are several ways to help distinguish between these two forms. One is the above mentioned Ranson Score.


Prognostic indices
Important biochemical markers for pancreatitis are serum amylase and lipase levels. Amylase and lipase levels can rise to more than a hundred times normal levels in cases of acute pancreatitis.

In addition, in predicting the prognosis, there are several scoring indices that have been used as predictors of survival. Two such scoring systems are the Ranson and APACHE (Acute Physiology, Age and Chronic Health Evaluation) II indices.


Ranson
Ranson's Criteria on Admission :

age greater than 55 years
a white blood cell count of > 16,000/µL
blood glucose > 11 mmol/L (>200 mg/dL)
serum LDH > 350 IU/L
serum AST >250 IU/L
Ranson's Criteria after 48 hours of admission :

fall in hematocrit by more than 10 percent
fluid sequestration of > 6 L
hypocalcemia (serum calcium < 2.0 mmol/L (<8.0 mg/dL))
hypoxemia (PO2 < 60 mmHg)
increase in BUN to >1.98 mmol/L (>5 mg/dL) after IV fluid hydration
base deficit of >4 mmol/L
The prognostic implications of Ranson's criteria are as follows :

Score 0 to 2 : 2% mortality
Score 3 to 4 : 15% mortality
Score 5 to 6 : 40% mortality
Score 7 to 8 : 100% mortality

APACHE
"Acute Physiology And Chronic Health Evaluation" (APACHE II) score > 12 points

Hemorrhagic peritoneal fluid
Obesity
Indicators of organ failure
Hypotension (SBP <90 mmHG) or tachycardia > 130 beat/min
PO2 <60 mmHg
Oliguria (<50 mL/h) or increasing BUN and creatinine
Serum calcium < 1.90 mmol/L (<8.0 mg/dL) or serum albumin <33 g/L (<3.2.g/dL)>

Treatment

General measures
Antibiotics for infected necrosis and severe pancreatitis improves outcome. The drug of choice is imipenem.
Supportive for shock.
Pain relief
The following have no role in the management of acute pancreatitis

Enzyme inhibitors are not proven to work.
The use of octreotide has not been shown to improve outcome.
In the management of acute pancreatitis, the treatment is to stop feeding the patient, giving him or her nothing by mouth, giving intravenous fluids to prevent dehydration, and sufficient pain control. As the pancreas is stimulated to secrete enzymes by the presence of food in the stomach, having no food pass through the system allows the pancreas to rest.

Recently, there has been a shift in the management paradigm from TPN (total parenteral nutrition) to early, post-pyloric enteral feeding (in which a feeding tube is endoscopically or radiographically introduced to the third portion of the duodenum). The advantage of enteral feeding is that it is more physiological, prevents gut mucosal atrophy, and is free from the side effects of TPN (such as fungemia). The additional advantages of post-pyloric feeding are the inverse relationship of pancreatic exocrine secretions and distance of nutrient delivery from the pylorus, as well as reduced risk of aspiration. Disadvantages of a naso-enteric feeding tube include increased risk of sinusitis (especially if the tube remains in place greater than two weeks) and a still-present risk of accidentally intubating the bronchus even in intubated patients (contrary to popular belief, the endotracheal tube cuff alone is not always sufficient to prevent NG tube entry into the trachea).


ERCP
Early ERCP (endoscopic retrograde cholangiopancreatography), performed within 24 hours of presentation, is known to reduce morbidity and mortality. The indications for early ERCP are as follows :

Clinical deterioration or lack of improvement after 24 hours
Detection of common bile duct stones or dilated intrahepatic or extrahepatic ducts on CT abdomen
The disadvantages of ERCP are as follows :

ERCP precipitates pancreatitis, and can introduce infection to sterile pancreatitis
The inherent risks of ERCP i.e. bleeding
It is worth noting that ERCP itself can be a cause of pancreatitis.


Surgery
Surgery is indicated for (i) infected pancreatic necrosis and (ii) diagnostic uncertainty and (iii)complications. The most common cause of death in acute pancreatitis is secondary infection. Infection is diagnosed based on 2 criteria

Gas bubbles on CT scan (present in 20 to 50% of infected necrosis)
Positive bacterial culture on FNA (fine needle aspiration, usually CT or US guided) of the pancreas.
Surgical options for infected necrosis include:

Conventional management - necrosectomy with simple drainage
Closed management - necrosectomy with closed continuous lavage
Open management - necrosectomy with planned staged reoperations at definite intervals (up to 7 reoperations in some cases)

Complications
Complications can be systemic or locoregional.

Systemic complications include ARDS, multiple organ dysfunction syndrome, DIC, hypocalcemia (from fat saponification), hyperglycemia and insulin dependent diabetes mellitus (from pancreatic insulin producing beta cell damage)
Locoregional complications include pancreatic pseudocyst and phlegmon / abscess formation, splenic artery pseudoaneurysms, hemorrhage from erosions into splenic artery and vein, thrombosis of the splenic vein, superior mesenteric vein and portal veins (in descending order of frequency), duodenal obstruction, common bile duct obstruction, progression to chronic pancreatitis