Acute pancreatitis can be a severe and deadly disease. The leading cause of acute pancreatitis is gallstones. The incidence of acute pancreatitis is increasing, probably because of the increasing incidence of metabolic syndrome and obesity, associated with gallstone formation. A publication on Medscape by John Watson (June 2024) talks about acute pancreatitis and new things we should know that can help us identify the etiology, predict severity and progression, and improve treatment outcomes.
Diagnosis of acute pancreatitis is made when two of the following three criteria are met:
Abdominal pain consistent with acute pancreatitis
Serum amylase and lipase at least three times the upper limit of the normal range (patients with normal renal function)
CT scan with features of acute pancreatitis
Etiology can be complicated to diagnose. It is easy to establish the etiology when image findings show gallstones. This accounts for about 40% of cases, affects more women than men, and is associated with elevated liver parameters (ALT has 95% specificity for gallstone etiology when it is elevated threefold). Alcohol use is responsible for 30% of cases. It affects more men, and it is associated with a history of heavy consumption vs social drinking. Alcohol can also exacerbate a genetic pancreatic injury. Hypertriglyceridemia is responsible for 2-7% of acute pancreatitis, associated with triglyceride levels > 1000 ng/mL. Medications are the fourth cause (<5%) of acute pancreatitis. It is hard to establish medications as a cause. It is usually necessary to stop the suspected medication and observe if symptoms reoccur upon reintroducing the same medication with no other possible etiologies. In my opinion, having certainties about the etiology is not easy. Several different factors can be present in the same patient. How can we know which one is the real responsible? How can we know if there is more than one etiology? The idea is to deliver support treatment to the patient and treat all possible causes.
It is difficult to predict severity. Acute pancreatitis can be mild (no organ failure or complications), moderately severe (transient organ failure, local complications), or severe (persistent organ failure > 48h). Around 80% of pancreatitis are mild, and patients improve in 48h. Severe or necrotizing pancreatitis has a mortality rate of 20-50%. According to Medscape, it is not easy to predict which patients will develop severe forms of pancreatitis and severe complications. Laboratory markers only assess the inflammation degree rather than predicting severity, and imaging findings only diagnose severe pancreatitis after it has already arisen. No scoring system accurately predicts severity. In this Medscape text, the systemic inflammatory response system is presented as a marker of progression, highlighting the measure of five cytokines (angiopoietin 2, hepatocyte growth factor, interleukin 8, resistin, soluble tumor necrosis factor receptor 1A). This panel was superior to existing laboratory and clinical scores.
It is paramount to know that several patients develop diabetes after one episode of acute pancreatitis. This is usually misdiagnosed as type 2 diabetes, but it is secondary diabetes known as post-pancreatitis diabetes mellitus (PPDM), also known as type 3c diabetes. The risk of developing this form of diabetes is not influenced by severity, etiology, age, or gender. These patients have worse glycemic control and have a higher risk of hospitalization and mortality from cancer, infectious diseases, and gastrointestinal disease than type 2 diabetes. PPDM may be a sign of pancreatic malignancy. Some studies suggest statins may protect against PPDM.
A fourth idea presented by John Watson in this Medscape work is that procalcitonin may help reduce antibiotic usage. Acute pancreatitis can cause infectious complications such as infected necrosis. However, doctors face the difficulty of distinguishing between infection and inflammation. Prophylactic antibiotics are not advised in acute pancreatitis. Additionally, and contrary to many doctors’ ideas, necrosis should only be treated with antibiotics if an infection arises (CT scan with gas within the necrosis), and necrosectomy is only indicated in infected necrosis and only after 28 days (no infection, no necrosectomy). A procalcitonin-based decision introduced in the UK reduced antibiotic usage from 63% to 45%. They initiated or continued antibiotics only if the patient had a procalcitonin level ≥ 1.0 ng/mL.
Finally, John Watson states that the “new standard of care” is moderate fluid resuscitation. This is a different idea from the recent past medical care when the objective was an aggressive fluid resuscitation. The WATERFALL trial showed that moderate resuscitation (bolus of 10mL/kg in patients with hypovolemia – no hypovolemia no bolus; followed by 1.5mL/kg/h) had better results that aggressive fluid resuscitation (bolus of 20mL/kg followed by 3mL/kg/h). Fluid overload was significantly higher in aggressive resuscitation, and there was no difference in the incidence of moderate or severe pancreatitis between both approaches. It was so evident for the investigators that they concluded aggressive resuscitation "should be abandoned”.
In my point of view, this means an accurate and constant patient evaluation is necessary, and these patients should be treated in an Intensive Care Unit (ICU) environment. However, ICUs usually do not accept these patients until they need invasive ventilation. This approach is inadequate, I think.
Acute pancreatitis is a disease without a specific treatment to change its course. The first part of the treatment is to deliver support treatment and improve the patient's condition. The second part is to decide when to treat the etiology (e.g. gallstones). Acute pancreatitis continues to be difficult to treat and we never know what will be the course of the disease. Many will survive, but others will succumb. The future is unpredictable when dealing with acute pancreatitis...
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Dr. Carlos Eduardo Costa lmeida
General Surgeon
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