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Ischemia is an established cause of acute pancreatitis; however, acute pancreatitis has never been reported after cardiac arrest.
We report a case of acute pancreatitis following cardiac arrest with prolonged cardiopulmonary resuscitation in a 58-year-old man, the mechanism of which is likely to be ischemic. The patient developed severe ischemic en...
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... abdominal examination did not improve, and there was no sign of awakening despite the cessation of sedation. An abdominal CT scan confirmed the diagnosis of acute pancreatitis with a CT severity index of 4 (Figure 2), and a cerebral CT scan revealed diffuse hypodensity with severe ischemic brain edema. After eight days in the ICU, in the absence of awakening, a therapeutic limitation was decided, leading to death. ...
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... 3 Another reported case cites the development of pancreatitis after prolonged CPR, believed to be due to ischemia in the setting of cardiac arrest. 4 In our case, the patient presented without signs of pancreatitis before her cardiac arrest. She was later diagnosed by computed tomography (CT), which confirmed necrotizing pancreatitis, subsequently found to be infected. ...
Acute pancreatitis has been reported as a complication of cardiac arrest and cardiopulmonary resuscitation. However, necrotizing pancreatitis as a subsequent complication has not. Because pancreatic necrosis develops 7–10 days after the initial episode of pancreatitis, it may be difficult to identify and, therefore, diagnose. This case details the course of a patient who developed infected necrotizing pancreatitis after receiving cardiopulmonary resuscitation after cardiac arrest.
... Another possibility is that myocardial infarction affects the blood supply of the pancreas, resulting in impaired function and increased serum amylase level. Previous cases have reported that cardiac arrest or hemorrhagic shock can cause pancreatitis and elevated serum amylase level [6,9] . However, in this patient, the heart function was not impaired, and CT did not reveal abnormalities in the pancreas. ...
Serum amylase predominantly comprises pancreatic and salivary amylases and its elevation is commonly associated with pancreatitis and other physical diseases. This case report presents a 63-year-old male with first-episode depression who exhibited abnormally elevated serum amylase. Shortly after admission, the patient entered a sub-stupor state. The patient developed symptoms such as high fever and excessive sweating on the second night. In addition, myocardial damage was observed. The serum amylase was found to be elevated in the morning on the 3rd day. Following symptomatic and supportive treatments, the patient’s serum amylase level gradually dropped to drop to normal over approximately 2 weeks. On careful analysis of the patient’s medical condition, we suspect the increased serum amylase level may be linked to his psychiatric symptoms. Based on this case, we speculate that besides physical illness, the stupor symptoms observed in patients with depression may also lead to elevated serum amylase. Therefore, clinicians must prioritize addressing psychiatric symptoms when encountering such situations.
... The role of ischemia in pancreatitis has been well reported in both clinical and laboratory studies [27][28][29]. However, we believe that there is only one case report about hypoxic pancreatitis following cardiac arrest, and in this case, the patient survived but developed ischemic encephalopathy [30]. In the present study, increase in pancreatic enzyme levels was a frequent complication and was related to an unfavorable neurologic prognosis and mortality in patients treated with TTM after OHCA. ...
This study investigated the patient outcomes, incidence, and predisposing factors of elevated pancreatic enzyme levels after OHCA. We conducted a retrospective cohort study of patients treated with targeted temperature management (TTM) after out-of-hospital cardiac arrest (OHCA). Elevation of pancreatic enzyme levels was defined as serum amylase or lipase levels that were at least three times the upper limit of normal. The factors associated with elevated pancreatic enzyme levels and their association with neurologic outcomes and mortality 28 days after OHCA were analyzed. Among the 355 patients, 166 (46.8%) patients developed elevated pancreatic enzyme levels. In the multivariable analysis (odds ratio, 95% confidence interval), initial shockable rhythm (0.62, 0.39–0.98, p = 0.04), time from collapse to return of spontaneous circulation (1.02, 1.01–1.04, p < 0.001), and history of coronary artery disease (1.7, 1.01–2.87, p = 0.046) were associated with elevated pancreatic enzyme levels. After adjusting for confounding factors, elevated pancreatic enzyme levels were associated with neurologic outcomes (5.44, 3.35–8.83, p < 0.001) and mortality (3.74, 2.39–5.86, p < 0.001). Increased pancreatic enzyme levels are common in patients treated with TTM after OHCA and are associated with unfavorable neurologic outcomes and mortality at 28 days after OHCA.
... Increased lactate production as a result of anaerobic glucose breakdown under hypoxia/anoxia causes intracellular acidosis, which is one of the main inducers of premature intracellular trypsinogen autoactivation and subsequent triggering of the enzyme cascade in acinar cells [18]. Since 90% of proteins synthesized by acinar cells are digestive enzymes, the inevitable ischemia periods provide "ideal" conditions for triggering autolytic processes in the pancreas [19]. The negative effect of endogenous pancreatic proteases on functional ability of islets was noted, in particular, in ischemia/ reperfusion-induced pancreatitis developing during preservation of donor pancreas [20]. ...
The success of pancreatic islet allotransplantation in the treatment of patients with a difficult-to-manage type 1 diabetes depends mainly on the quantity and quality of islets isolated from the pancreas of deceased donors using enzyme preparations, primarily collagenase. Numerous studies on improvement and standardization of islet isolation techniques have reached their limits in the last decade. This has made it impossible to further boost the number and quality of clinical transplants. Taking into account the negative impact of collagenase technique on the morphofunctional properties of isolated islets, this work has studied the possibility of enzyme-free isolation of islet tissue purified of exocrine ballast. Experiments using the pancreas of newborn and young rabbits showed that developing methodological approaches to obtaining islet-like cultures without the use of exogenous enzymes is feasible.
... The controversy of anomalies in general pancreatic condition report 15% of prevalence at normal finding that simply disturb the microcirculation of anatomical structure of intimating pancreas which reduces the perfusion of established capillaries compromising the components of acidosis and homeostasis in cellular mechanism propagating the maturity of autodigestive responses aggravating the initiation of primary severity in post-operative cases. [63][64][65][66][67][68][69][70][71][72] On understanding interstitial neoplasm in pancreatitis appear notorious in majority of pit fall presentation on visualizing the diagnostic processes of vascular appearances solidifying the peri-ampullary cystic tumors adding the adenocarcinoma challenges attacking the recurrent estimation on inflammatory malignancy resection the therapeutic severe attacks. [73][74][75][76][77][78] The regional lymphocytic nodes in structural metastases suspicious to liver organ [78] explain the major surgeries involvement distantly to compare gastrectomy and sphincteroplasty manipulating the normal thyroid functioning causing the parathyroid hernia repair. ...
Abstract:
In the guidelines of acute pancreatitis risk factors dominance of several biomarkers play its role differently to validate its extremity in cellular studies biologically for defining multi-organ dysfunctions. Moreover, we concentrate basically on known etiological conditions characterizing the appropriate diagnostic ways to ascertain both acute and chronic phase of pancreatitis that remain relative to history of disease and non-invasive techniques in age grouped studies.
... Although uncommon, this can lead to severe graft pancreatitis after pancreas transplantation. [7][8][9][10][11][12] Therefore, many centers are hesitant to accept pancreas grafts from donors with a history of cardiac arrest and CPR (CACPR). 6,13 In other SOT, studies indicate that CACPR in organ donors does not negatively impact posttransplant outcomes. ...
It has been hypothesized that transplanting simultaneous pancreas kidney (SPK) grafts from donors with a history of cardiac arrest and cardiopulmonary resuscitation (CACPR) leads to inferior post‐transplant outcomes due to organ hypoperfusion during cardiac arrest and mechanical trauma during resuscitation. Using SRTR data, we identified 13,095 SPK transplants from 2000‐2018, of which 810 (6.2%) were from donors with a history of CACPR. After inverse probability of treatment weighting on donor and recipient characteristics, we found that 1‐, 5‐ and 10‐year patient (CACPR: 96.4%, 89.9% and 78.9%; non‐CACPR: 96.3%, 88.9% and 76.0%; p=0.3), death‐censored pancreas graft survival (CACPR: 89.3%, 82.7%, 75.0%; non‐CACPR: 89.9%, 82.7%, 76.3%; p=0.7), and death‐censored kidney graft survival (CACPR: 97.0%, 89.5%, 78.2%; non‐CACPR: 96.9.9%, 88.7%, 80.0%; p=0.4) were comparable between the two groups. There were no differences in the risk of pancreatitis (CACPR: 2.9%, non‐CACPR: 2.4%; weighted OR=0.74 1.22 2.02; p=0.4), anastomotic leak (CACPR: 1.6%, non‐CACPR: 2.0%; weighted OR=0.54 1.02 1.93; p>0.9), or median length of hospital stay (CACPR: 8 days, non‐CACPR: 9 days; p=0.6) for recipients of CACPR vs. non‐CACPR donors. Our findings suggest that CACPR donors could be used to expand the SPK donor pool without compromising short or long‐term outcomes.
... In one instance the patient was resuscitated using LUCAS™ Chest Compression System, however, the patient suffered further complications including pancreatic pseudocyst, pancreatic fistula and ultimately hemorrhagic pancreas leading to death [2]. In another case, a 58-year-old gentleman suffered pancreatitis following cardiac arrest for 80 minutes during which he got continuous CPR but ultimately the patient passed away [3]. There has been one other occurrence where an 8-year-old child received intra-abdominal compressions as part of CPR protocol in pediatric population. ...
An elderly gentleman was successfully revived after undergoing cardiopulmonary resuscitation(CPR) for cardiac arrest. Post CPR, the patient developed acute pancreatitis which was likelycomplication of inappropriately delivered chest compressions which caused furthercomplications and resulted in the death of the patient. This case underlines the importance ofquality chest compressions that includes correct placement of hands by the operator givingchest compressions to avoid lethal injuries to the receiver.
... The increased production of lactate by anaerobic glucose breakdown during hypoxia/anoxia causes intracellular acidosis, which is one of the main inducers of premature intracellular auto-activation of trypsinogen and subsequent activation of the enzyme cascade in acinar cells [89]. Since 90% of the proteins synthesized by acinar cells are digestive enzymes, short periods of ischemia provide 'ideal' conditions to trigger autolytic processes within the pancreas [90][91][92]. The relevance of endogenous pancreatic proteases for islet function has also been extensively assessed in ischemia/reperfusion-induced pancreatitis after organ preservation [93][94][95]. ...
In comparison to procedures used for the separation of individual cell types from other organs, the process of human pancreatic islet isolation aims to digest the pancreatic exocrine matrix completely without dispersing the individual cells within the endocrine cell cluster. This objective is unique within the field of tissue separation, and outlines the challenge of islet isolation to balance two opposing priorities. Although significant progress has been made in the characterization and production of enzyme blends for islet isolation, there are still numerous areas which require improvement. The ultimate goal of enzyme production, namely the routine production of a consistent and standardized enzyme blend, has still not been realized. This seems to be mainly the result of a lack of detailed knowledge regarding the structure of the pancreatic extracellular matrix and the synergistic interplay between collagenase and different supplementary proteases during the degradation of the extracellular matrix. Furthermore, the activation of intrinsic proteolytic enzymes produced by the pancreatic acinar cells, also impacts on the chance of a successful outcome of human islet isolation. This overview discusses the challenges of pancreatic enzymatic digestion during human islet isolation, and outlines the developments in this field over the past 5 decades.
... The increased production of lactate by anaerobic glucose breakdown during hypoxia/anoxia causes intracellular acidosis, which is one of the main inducers of premature intracellular auto-activation of trypsinogen and subsequent activation of the enzyme cascade in acinar cells [89]. Since 90% of the proteins synthesized by acinar cells are digestive enzymes, short periods of ischemia provide 'ideal' conditions to trigger autolytic processes within the pancreas [90][91][92]. The relevance of endogenous pancreatic proteases for islet function has also been extensively assessed in ischemia/reperfusion-induced pancreatitis after organ preservation [93][94][95]. ...
In comparison to procedures used for the separation of individual cell types from other organs, the process of human pancreatic islet isolation aims to digest the pancreatic exocrine matrix completely without dispersing the individual cells within the endocrine cell cluster. This objective is unique within the field of tissue separation, and outlines the challenge of islet isolation to balance two opposing priorities. Although significant progress has been made in the characterization and production of enzyme blends for islet isolation, there are still numerous areas which require improvement. The ultimate goal of enzyme production, namely the routine production of a consistent and standardized enzyme blend, has still not been realized. This seems to be mainly the result of a lack of detailed knowledge regarding the structure of the pancreatic extracellular matrix and the synergistic interplay between collagenase and different supplementary proteases during the degradation of the extracellular matrix. Furthermore, the activation of intrinsic proteolytic enzymes produced by the pancreatic acinar cells, also impacts on the chance of a successful outcome of human islet isolation. This overview discusses the challenges of pancreatic enzymatic digestion during human islet isolation, and outlines the developments in this field over the past 5 decades.
... However, multivariate regression analysis by manjuck et al. 33 indicated that hyperlipidemia was related to hypotension, anemia, mechanical ventilation and hyperbilirubinemia, and our previous study suggested that shock, sepsis, diabetes, cardiac arrest, hyperlactacidemia, invasive mechanical ventilation and hemodialysis were risk factors of PEI in ICU patients. 3 it has been demonstrated that splanchnic hypoperfusion was able to induce severe damage to the pancreas, [52][53][54] which may contribute to the occurrence of Pei in patients with shock, sepsis, lactic acidosis and cardiac arrest. Similarly, the incidence of Pei in patients with anemia, mechanical ventilation and hyperlactacidemia may attribute to hypoxia-induced pancreatic damage. ...
Pancreatic exocrine insufficiency is usually present in patients with pancreatic diseases. Surprisingly, recent studies indicated that patients with critical illness often suffer from pancreatic injury due to non-specific reasons other than pancreatic diseases, and pancreatic exocrine insufficiency is also commonly observed in critically ill adult patients without preexisting pancreatic diseases. It is well known that malnutrition is the main clinical consequence of pancreatic exocrine insufficiency, thus, the high incidence of pancreatic exocrine insufficiency is most likely to be an important contributor of malnutrition which is a frequent problem associated with detrimental clinical outcomes in critically ill patients admitted into intensive care unit. In order to prevent pancreatic exocrine insufficiency due to primary pancreatic diseases, pancreatic enzyme replacement therapy is indispensable to treat indigestion, malabsorption and nutritional deficiency. Similarly, pancreatic enzyme supplementation has the potential to be an adjuvant therapy in critically ill patients with enteral nutrition therapy, which may be helpful to improve the nutritional status and the prognosis of critically ill patients by reducing the occurrence of malnutrition. Here, we reviewed the diagnostic methods of pancreatic exocrine function, the epidemiology and risk factors of pancreatic exocrine insufficiency, and potential treatment strategies for pancreatic exocrine insufficiency in critically ill adult patients.
