CRITERIOS DE ATLANTA PARA PANCREATITIS AGUDA PDF

revision of the Atlanta classification and definitions by international consensus sification system for acute pancreatitis.1 Although the Atlanta. Las definiciones Atlanta’92 de la gravedad de la pancreatitis aguda están muy . la puntuación APACHE II o los criterios de Ranson) para predecir la gravedad. Por ello las guías actuales de tratamiento de la pancreatitis aguda grave Se utilizó el sistema APACHE II y los criterios de Atlanta para evaluar la gravedad.

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Temporallytwo phases of acute pancreatitis are identified in the Revised Atlanta Classification:. The s everity is classified into three categories based on clinical and morphologic findings:. The diagnosis is usually established when there is a combination of abdominal pain and elevated pancreatic enzymes and CECT is not required, unless there is uncertainty about the diagnosis.

These images are of a patient who presented with acute severe epigastric pain very suggestive of acute pancreatitis. Early severity stratification of acute pancreatitis is important to identify patients with the highest morbidity. These patients may benefit from timely transfer to the intensive care unit or tertiary referral centre.

Mild pancreatitis These patients have no organ failure.

Most of them have no fluid collections and no necrosis. These patients usually recover by the end of the first week.

Moderate severe and severe pancreatitis The clinical condition of the patient is determined by the host response to the pancreatitis. Cytokine cascades result in a systemic inflammatory response syndrome SIRSwhich increases the risk of organ failure.

The extent of morphologic changes like necrosis and fluid collections is not directly proportional to the severity of organ failure. Many of these patients however will have necrotizing pancreatitis and the mortality increases when the necrosis becomes infected.

The Revised Atlanta Classification discerns 4 types of peripancreatic fluid collections in acute pancreatitis depending on the content, degree of encapsulation and time. All these collections may remain sterile or become infected. Infection is rare during the first week. The table summarizes the CT criteria for gauda and peripancreatic fluid collections in acute pancreatitis. The CT severity index CTSI combines the Balthazar grade points with the extent of pancreatic necrosis points on a point severity scale.

On the day of admission, scoring systems based on imaging do not outperform scoring systems based on clinical and biochemical parameters with regard to predicting clinical outcome. Therefore, performing CT on day of admission solely for prediction purposes is not recommended.

CT is the imaging modality of choice for the diagnosis and staging of acute pancreatitis and its complications. Since the diagnosis of acute pancreatitis is usually made on clinical and laboratory findings, an early CT is only recommended when the diagnosis is uncertain, or in case of suspected early complications such as bowel perforation or ischemia.

An early CT may be misleading regarding the morphologic severity of the pancreatitis, because it may underestimate the presence and amount of necrosis. The images show a normally enhancing pancreas on day 1.

As the patient’s condition worsened, a second CT was performed on day 3. Notice how the greater part of the pancreatic body and tail no longer enhances indicating necrotizing pancreatitis arrows. The first CT underestimated the severity of the pancreatitis.

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This patient died on day 5 due to severe SIRS and panceratitis organ failure. Morphologically there are 2 types of acute pancreatitis criiterios interstitial or oedematous pancreatitis and necrotizing pancreatitis. Here an example of interstitial pancreatitis. There is normal enhancement of the entire pancreatic gland with only mild surrounding fatty infiltration. There are no fluid pancrwatitis and there is no necrosis of the pancreatic parenchyma.

The pancreas is swollen and there is peripancreatic inflammation 2 points. It is characterized by a protracted clinical course, a high incidence of local complications, and a high mortality rate. Necrosis of peripancreatic tissue can be vary difficult to diagnose, but is suspected when the collection is inhomogeneous, i. The CT shows an acute necrotizing pancreatitis.

The body and tail of the pancreas do not enhance. There is normal enhancement of the pancreatic head arrow. These collections also show homogeneous high signal intensity on a fat-suppressed T2-weighted MRI image, are fully encapsulated and contain clear fluid i.

pancreatitis aguda experiencia: Topics by

This patient had an acute necrotizing pancreatitis with onset 2 months earlier. The CT-image shows a homogeneous peripancreatic collection in the transverse mesocolon arrow. A T2-weighted MRI sequence shows that the collection has a low signal intensity arrow. Most likely this is necrotic fat tissue i. This patient had no fever or signs of sepsis. Endoscopic or percutaneous drainage would have little or no effect on its size, but increases the risk of infection.

Intraabdominal fluid collections and collections of necrotic tissue are common in acute pancreatitis. These collections develop early in the course of acute pancreatitis. In the early stage, such a collection does not have a wall or capsule.

Preferred locations of fluid collections are:. These collections are the result of the release of activated pancreatic enzymes which also cause necrosis of the surrounding tissues.

Pancreas – Acute Pancreatitis 2.0

This explains why many of these collections harbor solid necrotic debris. They may remain sterile or develop infection. On day 5 this collection can be diagnosed as probable acute necrotic collection. On day 18 an incomplete wall is present, but we can assume that in a couple of days this will be a walled-of-necrosis with a complete wall.

When peripancreatic collections persist or increase, it is usually due to the pnacreatitis of fat necrosis. Because fat does not enhance on CT, the diagnosis of fat necrosis can be difficult. Necrosis can be diagnosed with MRI, which of course should only be performed if auda has direct clinical implications. This patient presented with a gastric outlet obstruction 2 criterioss after an agda of acute pancreatitis.

There is a criteruos well-demarcated peripancreatic collection in the lesser sac, which abuts the stomach and the pancreas. The patient did not have fever. The collection underwent successful percutaneous drainage, which showed clear fluid with high amylase and subsequently resolved criteriox with the patient’s symptoms.

Therefore, this collection proved to be a true pancreatic pseudocyst. A Pseudocyst is a collection of pancreatic juice or fluid enclosed by a complete wall of fibrous atlana It occurs in interstitial pancreatitis and the absence of necrotic tissue is imperative for its diagnosis.

Communication with the pancreatic duct may be present. A pseudocyst requires dw or more weeks to develop. The differential diagnosis includes walled-off necrosis and sometimes a pseudoaneurysm or even a cystic tumor. Most often, they occur in the lesser sac. Most collections that persist after 4 weeks are walled-of-necrosis. True pseudocysts are uncommon, since critterios acute peripancreatic fluid collections resolve within 4 weeks.

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Based on CT alone it is sometimes impossible gauda determine whether a collection contains fluid only or a mixture of fluid and necrotic tissue. Consequently it is sometimes better to describe these as ‘indeterminate peripancreatic collections’. The images are of a patient with atlantw pancreatitis. On xtlanta upper image is a collection in the area of the pancreatic head in the right anterior pararenal space.

At this stage, it is not possible to distinguish between an acute peripancreatic fluid collection and acute necrotic collection. On a follow-up scan the collection in the right anterior pararenal space increased in size. It has fluid density and a thin enhancing wall. This can be a pseudocyst or walled-off-necrosis and it may or may not be infected. The patient became septic and a percutaneous drainage was performed. After drainage the collection barely diminished in size.

The patient underwent surgery and the collection was found to consist of necrotic debris, which was not appreciated on CT, hence this was a walled-off-necrosis and not a pseudocyst. These CT-images are of a patient on day This patient had central gland necrosis and now developed fever. The CT shows a similar collection of fluid density to that of the patient with the pseudocyst, except for its pancreatic location.

During endoscopic debridement this collection contained fluid and necrotic tissue, which was removed from critfrios area of the pancreas. Although the imaging characteristics in this case are similar to the patient with the pseudocyst, this proved to be infected walled-off-necrosis. Here we see a homogeneous pancreatic and peripancreatic collection, well demarcated with an enhancing wall, on day 25 of an episode of acute necrotizing pancreatitis.

This patient had fever and multiple organ failure. Therefore, this collection was suspected to be infected WON and not a pseudocyst. At surgery, the collection contained much necrotic debris, which was not depicted on CT. These cases illustrate that at times CT cannot reliably differentiate between collections psncreatitis consist of fluid only and those that contain fluid and solid necrotic debris with or without infection. The term pancreatic abcess is no longer used, since a collection of pus without necrotic tissue is extremely uncommon in acute pancreatitis.

In this patient there is normal enhancement of the pancreas with surrounding septated heterogeneous acute necrotic collections with fluid- and fat densities. This is probably necrosis of the peripancreatic tissues. Two weeks later there are gas bubbles in the peripancreatic collection consistent with an infected acute necrotic collection. This patient underwent surgery. This indicates that during surgery the differentiation between pancreatic necrosis and necrosis of the peripancreatic tissues is sometimes impossible.

Central gland necrosis is a specific form of necrotizing pancreatitis, representing full thickness necrosis between the pancreatic head and tail and is nearly always associated with disruption of the pancreatic duct.

This leads to persistent collections as the viable pancreatic tail continues to secrete pancreatic juices. These collections mayreact poorly to endoscopic or percutaneous drainage.