Acute pancreatitis (AP) is a very complex entity, and a global perspective of the patient is crucial for improving outcomes. While interstitial AP is usually associated with few or no systemic manifestations, local complications frequently induce a systemic inflammatory response syndrome (SIRS) that may evolve to organ failure [1]. There are two peaks in the incidence of organ failure, the first within the first week after disease onset, most frequently due to the aseptic pancreatic inflammation itself (the clinician should rule out coexisting acute cholangitis and cholecystitis in patients with gallstone AP in this scenario); and the second, after the first week, is usually caused by infections [2]. The most frequent infections in AP are bacteremia, followed by infection of necrosis and pneumonia [2]. Other relatively frequent sources of organ failure are pulmonary thromboembolism, intestinal ischemia (colon necrosis is a complication of AP), exacerbation of preexisting comorbidity, or iatrogenic perforation of the digestive tract. Organ failure is linked to increased risk of death, so early detection by monitoring the patient and efficient treatment are of extreme importance. In this context, a complete multidisciplinary protocol for the management of AP, adapted to the characteristics of each center, can help us in clinical practice. In a recent experience, the application of such a protocol in a series of patients with AP in an intensive care unit (ICU) setting was associated with improved outcomes [3].
Acute Pancreatitis and Systemic Complications: Definitions, Importance, and Incidence
The revision of the Atlanta classification [4] provides definitions for systemic complications and organ failure (see Chapter 3). Organ failure is defined as a score of 2 or more on the modified Marshall score, in at least one of three organ systems (respiratory, renal, and cardiovascular) (Table 8.1) [4]. Organ failure lasting for 48 hours or less is called transient organ failure. Persistent organ failure is defined as organ failure lasting for more than 48 hours. While transient organ failure is associated with increased morbidity, persistent organ failure is characterized by maximum morbidity and a very high risk of death, 50% according to a nationwide prospective study [5]. For this reason, persistent organ failure is a marker for severe disease (the core of its definition in the revision of the Atlanta classification). “Systemic complications” refers to exacerbation of preexisting comorbidity precipitated by the episode of AP, for example coronary artery disease or chronic lung disease. Systemic complications following this definition are associated with worse outcomes [5]. When exacerbation of preexisting comorbidity leads to persistent organ failure, it is considered as persistent organ failure [4].
The overall incidence of organ failure depends on the type of hospital. Tertiary care hospitals receiving transferrals from other centers will have a falsely high proportion of patients with organ failure (up to 40%) [1]. In contrast, according to population‐based studies, between 8 and 20% of patients develop organ failure [1]. In the previously mentioned nationwide prospective study, 14% of the patients had organ failure, comprising 7% transient and 7% persistent organ failure, and 8.5% single and 5.6% multiple organ involvement [5]; mortality was 7% for patients with transient and 52% for patients with persistent organ failure. Multiple organ failure was also associated with a 54% risk of death, higher than with single organ failure (13%). According to a post‐hoc analysis of a prospective database, 38% of patients with necrotising AP develop organ failure; 92% of them had respiratory failure with 37% mortality, 82% cardiovascular failure with 40% mortality, and 44% renal failure with 47% mortality [6].
Table 8.1 Modified Marshall scoring system for organ dysfunction.
Source: Banks et al. [4]. © 2013 BMJ. Reproduced with permission of BMJ Publishing Group.
| Organ system | Score | ||||
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | |
| Respiratory (PaO 2/FiO 2) | >400 | 301–400 | 201–300 | 101–200 | ≤101 |
| Renal (serum creatinine, μmol/l) | ≤134 | 134–169 | 170–310 | 311–439 | >439 |
| Renal (serum creatinine, mg/dl) | <1.4 | 1.4–1.8 | 1.9–3.6 | 3.6–4.9 | >4.9 |
| Cardiovascular (systolic blood pressure, mmHg) | >90 | <90, fluid responsive | <90, not fluid responsive | <90, pH <7.3 | <90, pH <7.2 |
Monitoring Respiratory Function and Management of Respiratory Failure
Respiratory failure is probably the most common organ failure in patients with AP [6]. Pleural effusion, atelectasis, and pulmonary infiltrates are common radiological findings in patients with moderate‐to‐severe AP, but these are not directly correlated with the presence of hypoxemia [7,8]. In addition, there are cases with hypoxemia without these findings, so other mechanisms of lung injury have been proposed [4]. Several mediators and pathophysiological pathways are involved during the different phases of acute lung injury and acute respiratory distress syndrome. The initial exudative phase is characterized by diffuse alveolar damage, microvascular injury, and influx of inflammatory cells [4,7]. This phase is followed by a fibro‐proliferative phase with lung repair, type II pneumocyte hypoplasia, and proliferation of fibroblasts [4,7]. Proteases derived from polymorphonuclear neutrophils and various proinflammatory mediators and phospholipases seem to be involved, among others [4,7]. Contributing factors that promote pancreatitis‐associated acute lung injury may be found in the gut and mesenteric lymphatics [4,7].
Another important factor in the development of respiratory failure could be increased intra‐abdominal pressure (IAP), with subsequent abdominal compartment syndrome, mainly due to the restrictive effect on respiratory mechanics [9,10].
All patients admitted to hospital due to AP should be carefully observed, especially in the first 48 hours [11]. Hypoxemia may be an early event during the first 48 hours after presentation [12], but it may present later in the course of disease [7]. Older patients, smokers, or patients with preexisting pulmonary diseases have an increased risk of developing respiratory failure [8]. A direct relationship between necrosis extension on abdominal computed tomography (CT) and respiratory complications has been described [7]. If a patient develops respiratory failure, a complete evaluation should be performed, including arterial gasometry, chest imaging, and measurement of IAP. An abdominal CT scan may be useful as respiratory failure could be a consequence of local and systemic complications, such as intestinal ischemia, infected necrosis, or intestinal perforation,
The management of a patient with respiratory failure and hypoxemia includes adequate analgesia and medical or surgical treatment of intra‐abdominal hypertension [13]. Respiratory mechanics and oxygen saturation should be periodically monitored, and if there is no improvement the patient should be managed in an ICU setting [14]. Oxygen delivery is important, initially using noninvasive devices [15]. High‐flow nasal cannula therapy may offer relief to patients suffering from high work of breathing [16]. Noninvasive ventilation could be an option for treating acute respiratory