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Epidural analgesia is an effective method of pain management in patients with AP. Furthermore, it has additional beneficial effects in AP. There is growing evidence that the microcirculation plays a crucial role in the development of pancreatic necrosis in AP. Pancreatic tissue has been shown to be very sensitive to hypoxemia and ischemia, with rapid progression to necrosis if the local circulation is compromised. The bowel mucosa is also very vulnerable to hypoperfusion and hypoxia, requiring extensive amounts of oxygen to maintain functional integrity. In severe AP, decompensated microvascular perfusion compromises the intestinal mucosal barrier leading to translocation of bacteria and secondary pancreatic infection. Animal and human studies have suggested that thoracic epidural analgesia may improve splanchnic blood flow and pancreatic perfusion. These effects have been attributed to sympathetic nerve blockade that redistributes blood flow to nonperfused regions. Furthermore, epidural analgesia increases ileal and renal perfusion, preserves gut barrier function, decreases liver damage and inflammatory response, and reduces the extent of pancreatic necrosis and mortality during AP in animal studies. In addition, epidural analgesia improves gastrointestinal motility in comparison to intravenous morphine. All these factors are crucial in the development of AP complications [14].

Table 9.2 Epidural administration of local anesthetics and opioids.

Drug	Concentration	Infusion rate	Bolus/hour
Ropivacaine	2 mg/ml	5–15 ml/h	5–10 ml/h
Bupivacaine	1 mg/ml	5–15 ml/h	5–10 ml/h
Ropivacaine + fentanyl	2 mg/ml + 2 μg/ml	5–15 ml/h	5–10 ml/h
Bupivacaine + fentanyl	1 mg/ml + 2 μg/ml	5–15 ml/h	5–10 ml/h
Ropivacaine + sufentanil	2 mg/ml + 0.5 μg/ml	5–15 ml/h	5–10 ml/h

Epidural analgesia (continuous infusion containing a mix of bupivacaine 0.1% and fentanyl 2 μg/ml at 6–15 ml/hour) has been demonstrated to reduce pain and improve perfusion of the pancreas compared with patients receiving controlled intravenous analgesia (fentanyl 10 μg/ml at a rate of 10–20 μg/hour) [15]. The increased pancreatic blood flow suggests that the use of epidural analgesia may decrease progression from edematous to severe necrotizing pancreatitis caused by early ischemia of the gland and thus could reduce severity of the disease. Epidural analgesia reduced the development of acute mesenteric ischemia and 30‐day mortality in critically ill patients with AP [16]. These findings support the use of epidural analgesia as a therapeutic intervention in AP.

Epidural analgesia‐related complications are rare, but may be potentially severe and include hypotension, infection, nerve damage, or epidural hematoma. Hypotension is one of the awaited side effects of the sympathetic blockade from epidural analgesia, with an incidence of 8%. It responds adequately to intravenous fluid administration and vasopressor therapy.

The pancreas sympathetic afferent innervations originate in T6–L2. The catecholamine release, one of the main factors contributing to maintenance of blood pressure, occurs by stimulation of the adrenal medulla, innervated by T5–L1. Therefore, a low thoracic block (T8–T10) should be used to minimize the block extension and lower the risk of hypotension.

Catheter dislocation can occur in 20% of patients, but the catheter can be safely replaced in patients showing no signs of local infection.

The optimal length of epidural analgesia is not well defined. Good clinical tolerance was observed with a duration of 11 days. Replacement of the catheter should be discussed if it stays in place for a longer period in order to avoid infection risks. A close follow‐up searching for local and systemic signs of untreated infection is required, and the catheter should be removed as soon as serious infectious risks are detected.

Epidural analgesia with local anesthetic can provide adequate pain relief. However, combined epidural analgesia using a major analgesic and local anesthetic resulted in better analgesia with smaller doses and a reduced hypotension rate in prospective randomized trials. Combined epidural analgesia is therefore recommended.

Epidural analgesia can be provided using a patient‐controlled epidural analgesia device, with a continuous infusion rate of 5–15 ml/hour. A bolus of 5–10 ml every 30–60 minutes could be added upon request (Table 9.2).

Use of epidural analgesia is currently limited in AP. Therefore, the clinical application and management of epidural analgesia, for example the precise thoracic level at which the epidural catheter is inserted, the duration the catheter stays in place, the type and dose of local anesthetics, and the type of opiate to be used, should be standardized. A multicenter randomized controlled trial of epidural analgesia in AP is ongoing, which will further contribute to assessing efficacy of this procedure [17]. Until then, epidural analgesia is a feasible, safe and effective procedure in patients with severe AP when managed by expert anesthesiologists in the intensive care unit and favor its clinical use in this setting. It has a promising effect on the microcirculation and organ dysfunction in AP. Epidural analgesia should be introduced as early as possible, when conventional analgesic therapy is insufficient to prevent the potential side effects of major analgesics. Furthermore, it can be supplemented by intravenous administration of NSAIDs.