ACUTE PANCREATITIS

ACUTE PANCREATITIS

SAMIR EL ANSARY

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2Acute pancreatitis

AP is an inflammatory condition of the pancreas that has a broad spectrum of severity ranging from mild and self-limited to severe and associated with multiorgan failure.

Clinically it is associated with the acute onset of abdominal pain and elevation of serum biochemical markers. The underlying pathophysiology is early and inappropriate activation of digestive enzymes within acinar cells.Different degrees of AP, and how are they defined?

Mild APPancreatic inflammation (of any cause) without persistent organ failure or local complications.

Severe acute pancreatitis (SAP)Associated with systemic complications, including multiple-organ failure, and local complications, such as necrosis, abscess, and/or pseudocyst. This degree of pancreatitis requires aggressive therapy in an intensive care setting to prevent significant morbidity or mortality.Causes of AP?

Gallstone-related disease and excessive alcohol intake comprising 70% of all cases.

hypertriglyceridemia (serum triglyceride level above 1500 mg/dL), trauma, and hypercalcemia. Smoking is a risk factor for AP in a time- and dose-dependent manner. Causes of AP?

A large number of medications have been implicated in causing AP, including angiotensin-converting enzyme inhibitors, furosemide, tetracycline, aminosalicylic acid, corticosteroids, procainamide, thiazides, metronidazole, and ranitidine.

Because of the varied duration between exposure and development of symptoms, and the usual lack of a clear mechanism, it is often difficult to identify a drug as the sole cause of AP. Causes of AP?

True idiopathic cases of AP are diminishing as more genetic causes of the disease are discovered. Endoscopic retrograde cholangiopancreatography (ERCP) causes pancreatitis in approximately 5% of individuals who undergo this procedure.The presenting signs and symptoms of AP?

AP is characterized by the sudden onset of abdominal pain, classically located in the epigastrium and usually associated with nausea and/or vomiting. Radiation of pain from the epigastrium through to the back that is alleviated with the patient leaning forward is a typical but not a necessary feature. Tachycardia related to pain or volume depletion and low-grade fever may be present.

The presenting signs and symptoms of AP?Two additional findings associated with severe pancreatitis may be presentthe Grey Turner and Cullen signs. The Grey Turner sign is an ecchymosis of the flank due to retroperitoneal hemorrhage. When present, it usually occurs 3 to 7 days after the onset of pain and is indicative of severe pancreatitis. The Cullen sign is periumbilical ecchymosis associated with both severe necrotizing pancreatitis and retroperitoneal hemorrhage of various causes.Are amylase and/or lipase measurements helpful in the diagnosis?

The most commonly used diagnostic markers are serum amylase and lipase. Although serum amylase levels have a high sensitivity in the first 24 hours the specificity is very low. In addition to pancreatitis, elevated amylase levels are seen with many other conditions including bowel infarction, renal failure, perforated peptic ulcer, trauma to the salivary glands, and macroamylasemia. Are amylase and/or lipase measurements helpful in the diagnosis?

In contrast, serum lipase levels are both more specific and more sensitive than amylase measurements.

Of note, no correlation exists between the absolute levels of amylase and lipase and the severity of pancreatitis.Role of imaging in the diagnosis of AP

Abdominal plain radiographs may be nonspecific or reveal an ileus if the pancreatitis is severe. Ultrasound evaluation of the pancreas itself is often limited by overlying bowel gas and/or patient discomfort. This test may, however, detect signs of biliary abnormalities in cases where this cause is suspected.

Role of imaging in the diagnosis of AP

Computed tomography (CT) with oral and intravenous (IV) contrast Can offer information regarding severity of disease and development of complications. Features that may be identified on CT include evidence of inflammation (pancreatic parenchymal edema or peripancreatic fat stranding), peripancreatic or intrapancreatic fluid collections, pancreas perfusion, and presence and extent of pancreatic necrosis.Should all patients have imaging studies done at the time of presentation?

The timing of performing CT in the evaluation of AP has been frequently debated and studied. Obtaining CT early in the course of illness has not been shown to establish alternative diagnoses or change clinical management. The need for cross-sectional imaging should be evaluated on a case-by-case basis and reserved for those who do not improve clinically after several days of supportive therapy and/or in whom worrisome symptoms such as fever orleukocytosis develop. Should all patients have imaging studies done at the time of presentation?

Advanced imaging should be considered early in a patient's course of illness if the diagnosis itself is uncertain or if suspicion exists of a complication from AP that, if identified, would significantly alter management, or if alternative diagnoses requiring surgical management are considered.

What if the patient cannot receive contrast for imaging?

Magnetic resonance imaging (MRI) has a growing role in the diagnosis and management of AP and is a reasonable option in patients who cannot receive iodinated contrast for CT.

Enhanced MRl requires the administration of gadolinium, which has been implicated in severe toxic side effects (nephrogenic systemic fibrosis) in patients with compromised renal function. What if the patient cannot receive contrast for imaging?

Good correlation has been noted, however, when comparing magnetic resonance cholangiopancreatography (MRCP), with or without gadolinium contrast, with CT in the evaluation AP.

MRCP also has the added benefit of being able to better define the pancreatic and biliary ductal system in cases where this cause is suspected but the pretest probability is too low to proceed directly to ERCP.Determination of the severity and prognosis of AP

Recognizing and differentiating mild AP from Severe AP is important so that patients can be triaged to the appropriate setting and treatment plan.

Over decades, several clinical predictors have emerged. Although all are imperfect, they are considered superior to clinical judgment alone. Ranson criteriaWere one of the earliest and widely used scoring systems. Their major disadvantage was that they required 48 hours to complete. The Acute Physiology and Chronic Health Evaluation (APACHE) II system, developed to evaluate critically ill patients, has also been used to differentiate mild AP from SAP { Severe AP }.

The major disadvantage of this system is that many find it cumbersome as it requires 12 physiologic measures to calculate.

A CT severity index (Balthazar score )Has been developed and often used to predict severity of pancreatitis on the basis of radiographic features.

The bedside index of severity in AP (BISAP) score integrates the systemic inflammatory response syndrome (SIRS) criteria and can be calculated relatively quickly on admission.RANSON PROGNOSTIC SIGNSETIOLOGY OF PANCREATITIS { GALL STONES AND NON GALL STONES }At initial presentation :70White blood cell count (k/mm3)Lactate dehydrogenase (U/L)During first 48 hoursDecrease in hematocritElevation in blood urea nitrogen (mg/dl )Base deficit (mmol/L)Fluid sequestration (L) The treatment for AP

The mainstay of treatment in AP is aggressive supportive and symptomatic therapy that includes volume repletion, pain control, nutritional support, correction of electrolyte abnormalities, treatment of infection (if present), and treatment of associated or causative conditions.Adequate volume repletion and restoration of perfusion to pancreatic microcirculation is imperative to stave off progression of disease and development of local complications.

Inadequate volume repletion is associated with higher rates of pancreatic necrosis. No randomized trials exist to guide rate or volume of fluid administration. Most experts recommend isotonic crystalloid infusion rates of 250 to 300 Ml/hr or greater for the first 48 hours or enough to maintain urine output at 0.5 ml/kg/hr. Narcotics are usually necessary to establish pain control. IV morphine or hydromorphone at 2- to 4-hour intervals should be considered.Occasionally, continuous infusion with additional patient-administered boluses is necessary.Antisecretory agents have been considered for use in pancreatitis. The inhibitory effect of octreotide, a pharmaceutical analog of somatostatin, on pancreatic enzyme secretion has led to its study in the treatment of AP. The largest randomized trial comparing placebo with octreotide in the treatment of moderate or severe pancreatitis found no significant difference

With regard to mortality, rate of new complications, rate of surgical intervention, duration of pain, or length of hospital stay.

BALTHAZAR CT GRADING OF AP AND CT SEVERITY INDEXA Normal pancreasB Enlarged pancreasC Inflammation of pancreas orD One peripancreatic fluid collectionE More than one peripancreatic fluid collection and /or air in retroperitoneumNECROSIS FACTOR :Percentage of necrosis . *CT grade points + necrosis points.How should patients with pancreatitis be fed?

Enteral feeding

Is the preferred method of nutritional support for all patients who are seen with pancreatitis. It is thought to help maintain the intestinal mucosal barrier, thereby preventing translocation, which is thought to be a major source of infection. Enteral feeding

No strong evidence exists that nasojejunal feeding is advantageous over nasogastric feeding.

Still, many experts recommend fluoroscopic or endoscopic placement of a jejunal, or postpyloric, feeding tube if possible.Parenteral nutritionshould be initiated in patients unable to tolerate oral feeding because of pain, ileus, and/or nausea.

Opinion with regard to the timing of initiation of parenteral nutrition ranges from 2 to 5 days after presentation.Should all patients with AP receive antibiotics?

No. The use of prophylactic antibiotics to prevent infection of pancreatic necrosis has been controversial but is not currently recommended. No significant benefit has been found with regard to mortality, rates of infected necrosis,need for operative treatment, or overall infections when administering prophylactic antibiotics.Broad-spectrum antibiotics should be administered if objective evidence exists of infected necrosis on the basis of clinical status (i.e., fever) or cultured aspirate. Some experts believe antibiotics are warranted when evidence is seen on CT of necrosis in > 30% of the pancreas.In such cases, the use of antibiotics should be limited to 7 to 14 days because of the risk of fungal superinfection.

If the patient's condition continues to deteriorate, he or she should be evaluated for minimally invasive and/or surgical debridement or necrosectomy .The bedside index of severity in AP BlSAP SCORE :1 point for each of the following if present. 0 ooints if absenlBUN >25 mg/dL (8.9 mmol/L)Impaired mental state statusSIRS (two or more of the following) :Pulse > 90 beats/minRespiratory rate >20/min or PaC02 < 32 mm HgTemperature >38" C or