Severe Hemorrhagic Pancreatitis Research Articles

English

BACKGROUND Acute pancreatitis (AP) is a dormant deadly illness. The range of seriousness of the ailment goes from mellow self-restricting disease to an exceptionally lethal severe necrotizing pancreatitis. The disease has such a variable course that it may manifest as a simple pain in the abdomen to severe haemorrhagic pancreatitis with septicaemic shock, multi-organ dysfunction syndrome and ultimately leading to death. A cost-effective better prognosticative index is needed for the assessment of the severity of AP. Here in this study, we wanted to assess the role of BISAP scoring systems and CRP for analysis and comparing their values to determine the severity of AP and the prognosis of the disease. METHODS A prospective observational study was done on 83 patients diagnosed with AP after fulfilment of inclusion criteria. Patients were subjected to severity index, bedside index for severity in acute pancreatitis (BISAP) score and CRP calculation and statistical analysis was done with SPSS software. RESULTS In our study, AP was more prevalent in males 87.95 % than females 12.05 %. AP was found to be more common in cases ≤ 40 years of age, however, the mean age of presentation was 38.14 ± 12.59 years. We calculated the sensitivity and specificity of the BISAP score and C-reactive protein (CRP) by co-relating it with CT severity index as gold standard according to which the sensitivity was found to be 64 % and specificity was found to be 85 % for BISAP. The sensitivity and specificity of CRP was 64 % and 85 % respectively. CONCLUSIONS BISAP is an easy way to anticipate the severity of AP within 24 hours. It also helps to prognosticate AP. CRP can also be used to aid BISAP in the assessment of severe acute pancreatitis (SAP). KEY WORDS Acute Pancreatitis, BISAP, CRP.

Acute pancreatitis with Cullen's sign presentation in a case of mixed type I and II choledochal cyst

A 3 year old girl presented initially with acute severe hemorrhagic pancreatitis diagnosed by clinical features including a positive Cullen's sign and raised serum amylase. A contrast enhanced computed tomography (CECT) scan corroborated the same and also reported a type I choledochal cyst. Magnetic resonance cholangiopancreatography (MRCP) 2 months later reported a type II choledochal cyst and a persistent pseudo pancreatic cyst. Intraoperative features and close perusal of the CECT and MRCP films showed the presence of mixed type I and II choledochal cyst. The case is reported for the presence of Cullen's sign, CECT and MRCP features of a mixed type I and II choledochal cyst and successful surgical outcome. It appears to be only the fifth case of mixed type I and II choledochal cyst in world literature in the pediatric age group, following the 4 previous cases in children reported from Japan.

A devastating case of severe hemorrhagic pancreatitis in adolescent

A devastating case of severe hemorrhagic pancreatitis in adolescent

Severe acute hemorrhagic pancreatitis secondary to cholelithiasis as a rare cause of sudden unexpected death in medico-legal case

Introduction:Acute pancreatitis (AP) is an uncommon disease with a wide clinical course varying from mild and self-limiting to severe with eventual death. However, death caused by AP is rare. Most cases of AP reported in the English-language literature are based on clinical data; few are medico-legal studies.Case presentation:The author recently experienced a case of sudden unexpected death in a young man caused by extensive severe hemorrhagic AP secondary to cholelithiasis, not chronic alcoholism, which is a much more prominent etiology of AP in medico-legal perspectives. The deceased had complained of dizziness, nausea, and fatigue without significant abdominal pain for about 1 week and received some home medications for symptomatic treatment including an antibiotic drug from a clinic just 2 days prior to his death. He had complained of lower extremity weakness, intense thirst, and subsequently collapsed and was brought to a nearby hospital where he was pronounced dead shortly after his admission following unsuccessful advanced cardiopulmonary resuscitation attempts.Conclusion:This case is herein reported with an extensive review of the pertinent literature to highlight the findings of the case and raise awareness within the medico-legal profession and also the medical profession.

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Introduction: Hypertriglyceridemia-induced pancreatitis (HTGP) is associated with a higher severity of illness and more complications than acute pancreatitis (AP) without hypertriglyceridemia (HTG). Diabetic ketoacidosis (DKA) may be a risk factor for AP, but it is uncertain if AP triggers DKA or vice-versa. We describe a patient with DKA and AP managed with continuous IV insulin and apheresis. A 30 year-old male with type 1 diabetes, familial HTG, and AP presented with a 10 day history of worsening epigastric pain. Laboratory and imaging studies were consistent with HTGP and DKA. He was started on IV insulin and intubated for respiratory distress. On day 2 ketosis resolved, but he was continued on IV insulin for HTGP. Renal replacement therapy was started for acute kidney injury. Due to severity of illness and lack of adequate response to insulin, apheresis was initiated. After 2 sessions, TG decreased from 3362 mg/dl to 192 mg/dl. On day 9 he was transitioned from IV to subcutaneous insulin and TG remained <500 mg/dl. The remainder of his hospitalization was complicated by severe hemorrhagic pancreatitis, candidemia, and pneumonia. On day 11 he was extubated and on day 17 he left the ICU. On day 38 he was discharged on insulin detemir and omega-3 fish oil. The relationship between AP, DKA, and HTG is complicated, making identification of the primary cause difficult. AP can exacerbate DKA and moderate HTG in DKA is common. Optimal management of these patients is unknown since there are no large trials or consensus statements to guide treatment. Common strategies include apheresis and insulin. As seen in our patient, use of apheresis results in immediate reduction in TG levels, but large well-conducted trials are necessary to support this practice. Use of IV insulin to control DKA and HTGP appears safe and effective. However, once ketosis resolves and blood glucose normalizes, the insulin infusion may be inappropriately stopped while TG are still critically elevated. Thus, communication of clear goals of therapy is paramount. Although the most appropriate length of time to provide IV insulin is uncertain, it is reasonable to continue therapy until TG <1000 mg/dl.

Highly variable pharmacokinetics of dexmedetomidine during intensive care: a case report

IntroductionDexmedetomidine is a selective and potent alpha2-adrenoceptor agonist licensed for use in the sedation of patients initially ventilated in intensive care units at a maximum dose rate of 0.7 μg/kg/h administered for up to 24 hours. Higher dose rates and longer infusion periods are sometimes required to achieve sufficient sedation. There are some previous reports on the use of long-term moderate to high-dose infusions of dexmedetomidine in patients in intensive care units, but none of these accounts have cited dexmedetomidine plasma concentrations.Case presentationWe describe the case of a 42-year-old Caucasian woman with severe hemorrhagic pancreatitis following laparoscopic cholecystectomy who received dexmedetomidine for 24 consecutive days at a maximum dose rate of 1.9 μg/kg/h. Samples for the measurement of dexmedetomidine concentrations in her plasma were drawn at intervals of eight hours. On average, the observed plasma concentrations were well in accordance with previous knowledge on the pharmacokinetics of dexmedetomidine. There was, however, marked variability in the concentration of dexmedetomidine in her plasma despite a stable infusion rate.ConclusionThe pharmacokinetics of dexmedetomidine appears to be highly variable during intensive care.

Qinghai-like H5N1 from Domestic Cats, Northern Iraq

Qinghai-like H5N1 from Domestic Cats, Northern Iraq

Treatment of Bleeding in Severe Hemorrhagic Pancreatitis with Recombinant Factor VIIa

Recombinant factor VIIa (rFVIIa) has been used to treat bleeding complications in patients with hemophilia. It acts at the site of vessel injury, forming a complex with tissue factor to activate the clotting cascade. Recent reports have shown rFVIIa may be a useful hemostatic agent in patients after obstetrical, urologic, trauma, or transplant procedures. We report the first documented case of bleeding from hemorrhage pancreatitis treated with rFVIIa.

54-Year-Old Man With Dyspnea and Abdominal Wall Bruising

54-Year-Old Man With Dyspnea and Abdominal Wall Bruising

Antibiotics in Severe Pancreatitis

Therapeutic antibiotics for acute pancreatitis has been a controversial issue; most data indicate no benefit over supportive care. Antibiotic prophylaxis has, however, yielded some benefit in severe necrotizing or hemorrhagic pancreatitis. These authors conducted a prospective, multisite, controlled study comparing imipenem, a …

The effect of sennosides on bacterial translocation and survival in a model of acute hemorrhagic pancreatitis.

Bacterial translocation leading to subsequent infectious complications is a significant determinant of outcome in acute hemorrhagic pancreatitis (AHP). The colonic ileus and impaired intestinal barrier function that often accompany AHP may predispose to translocation. Sennoside is a naturally occurring cathartic and choleretic agent that stimulates intestinal mucous secretion and has potent promotility effects. The impact of sennoside-induced intestinal motility and secretory function on bacterial translocation and survival was studied in a rat model of AHP. Severe acute pancreatitis was induced in rats by the intraductal infusion of 2% sodium deoxycholate (DCA, 0.4 ml/kg). A group of sham-operated rats (group A) received intraductal saline, whereas experimental animals were subsequently administered distilled water (group B) or sennoside solution (group C) by gavage every 8 h. After 48 h, intestinal transit of fluorescein isothiocyanate-labeled dextran, serum endotoxin, and amylase levels, and bacterial translocation to mesenteric lymph nodes (MLNs) and pancreatic tissue were determined. The pancreas and intestine were sampled for histologic study. All group A animals survived and did not develop pancreatitis or endotoxemia, whereas groups B and C all demonstrated severe hemorrhagic pancreatitis with evidence of necrosis. Mortality at 48 h was 55% in group B versus 12.5% in group C. Inhibition of intestinal motility was noted in 40% versus 20%, and endotoxin levels were 61.36+/-28.26 pg/L versus 5.41+/-3.58 pg/L in group B versus group C rats, respectively (p<0.001). Pancreatic tissue and MLN cultures were positive in 100% of group B survivors versus 14% of group C survivors (p<0.05). Histologic examination of the intestine in group C animals showed increased mucous secretion, proliferation of goblet cells, and evidence of rapid turnover/renewal of enterocytes. Treatment with the cathartic agent, sennoside, reduced translocation of endotoxin and bacteria, restored intestinal motility, increased mucous secretion, and reduced mortality in a model of acute hemorrhagic pancreatitis in the rat. Other cathartics may have similar properties and may be useful in preventing infectious complications in acute pancreatitis.

Effect of a specific synthetic inhibitor of neutrophil elastase (ONO-5046) on the course of acute hemorrhagic pancreatitis in dogs.

In acute pancreatitis, particularly in severe cases, polymorphonuclear neutrophil (PMN) elastase induces tissue damage in remote organs such as the lung, as well in the pancreas itself. Therefore, we examined the therapeutic effect of a specific synthetic inhibitor of PMN elastase (ONO-5046: Ono Pharmaceuticals, Osaka, Japan) on the lung, liver, and kidney, as well as pancreas, in severe hemorrhagic pancreatitis in dogs. Acute hemorrhagic pancreatitis was induced by the injection of a mixture of autologous bile and porcine trypsin into the main pancreatic duct. Lipopolysaccharide (LPS) was administered intravenously as a septic challenge. Two animal groups were used. In one group, continuous infusion of ONO-5046 was started prior to the injection of LPS (ONO group). In the other group (control), saline was infused instead. At the end of the experiment (330 min after the injection of bile and trypsin), the pancreas revealed severe hemorrhagic pancreatitis, and a large amount of bloody ascites had accumulated in the peritoneal cavity. The white blood cell count was markedly reduced in response to the induction of pancreatitis, and was decreased further by the septic attack, irrespective of the administration of ONO-5046, although the count increased again in the ONO group. Serum levels of amylase and alpha2-macroglobulin-trypsin complex increased similarly in both groups following administration of bile and trypsin. Serum Ca levels decreased in both groups. At the end of the experiment, the wet weight of the lung was slightly higher in the control group (without ONO-5046). Microscopically, the pancreas showed severe hemorrhage accompanied by extensive interstitial edema in both groups. The lung and liver demonstrated mild infiltration of inflammatory cells in the interstitium in both groups, although the inflammatory change in the liver was slightly milder in the ONO group. These findings indicate that severe hemorrhagic pancreatitis cannot be alleviated by the administration of a specific inhibitor of PMN elastase alone, although this may lessen damage to remote organs such as the liver and lung. The white blood cell count decreased markedly after the induction of acute pancreatitis, and much more after a septic challenge. This seems to be closely related to the accumulation of bloody ascites in the peritoneal cavity.

Combined treatment with C1 esterase inhibitor and antithrombin III improves survival in severe acute experimental pancreatitis.

Patients with severe acute pancreatitis die of complications closely related to the systemic activation of protease cascades. To examine the effects of human C1 esterase inhibitor (C1 INH) and antithrombin III (AT III) on two experimental models of acute pancreatitis. Oedematous pancreatitis was induced by continuous intravenous infusion of caerulein and haemorrhagic pancreatitis by retrograde injection of sodium taurocholate into the biliopancreatic duct. C1 INH and AT III were given intravenously, either before or after the induction of pancreatitis. Treatment with C1 INH and AT III had no beneficial effect on oedematous pancreatitis. On the other hand, combined C1 INH and AT III therapy improved the survival in haemorrhagic pancreatitis compared with treatment with human serum albumin. This reduction in mortality was found regardless of whether the treatment was given prophylactically or therapeutically. Treatment with C1 INH and AT III represents a promising therapeutic concept for patients with severe haemorrhagic pancreatitis.

Severity and Mortality of Experimental Pancreatitis Are Dependent on Interleukin-1 Converting Enzyme (ICE)

Interleukin-1 beta (IL-1 beta) is produced in large amounts during acute pancreatitis and is believed to play a role in disease progression. Because secretion of IL-1 beta is dependent on intracellular processing of pro-IL-1 beta by IL-1 converting enzyme (ICE), we aimed to determine the efficacy of a novel ICE inactivator (VE-13045) in inhibiting secretion of active IL-1 beta in vivo and if the loss of ICE activity would affect the severity and mortality of experimental pancreatitis. Severe hemorrhagic pancreatitis was induced in adult rats by infusion of bile acid into the pancreatic duct. Animals were randomized to receive VE-13045 or vehicle before induction of pancreatitis. To confirm our findings and to ensure that the results were not model dependent, a second series of experiments was conducted using mice possessing a homozygous knockout of the ICE gene in which lethal pancreatitis was induced by feeding a choline-deficient, ethionine-supplemented diet. The severity of pancreatitis was assessed for both experiments by standard surrogate markers, blind histologic grading, and serum IL-1 beta and tumor necrosis factor-alpha (TNF-alpha) levels. Pancreatic IL-1 beta mRNA induction was assessed by differential RT-PCR. Acute pancreatitis was associated with a 120-fold increase in IL-1 beta mRNA, which was not affected by ICE inhibition or gene deletion. Cytokine processing and secretion were affected, as evidenced by decreased serum levels of IL-1 beta and TNF-alpha (p < 0.001) in all animals with an inactive ICE enzyme. This lack of cytokine production increased survival from 32% to 78% following bile salt pancreatitis (p < 0.01) and from 24% to 80% following diet-induced pancreatitis (p < 0.005). Both ICE-defective groups demonstrated decreased pancreatic necrosis, edema, inflammation, wet weight (all p < 0.05), and amylase and lipase (p < 0.01). In vivo blockade or genetic deletion of ICE inhibits pancreatitis-induced secretion of proinflammatory cytokines without altering IL-1 mRNA production and is associated with decreased pancreatitis severity and dramatic survival benefits.

“Human Pancreas-Specific Protein” (Procarboxypeptidase B)

Human pancreas-specific protein (PASP) has been characterized previously as a serum marker for pancreatitis. It was then identified as pancreatic procarboxypeptidase B (PCB). The aim of the present study was to verify the usefulness of PASP (PCB) as a serum marker in patients with acute (n = 20) and chronic (n = 12) pancreatitis and in those following endoscopic retrograde cholangiopancreaticography (ERCP) (n = 44). Serum PASP values were analyzed by radioimmunoassay, with a range of normal values between 15 and 111 ng/ml. Between April 1992 and September 1992, 20 subjects (19-86 years of age) with acute pancreatitis (alcoholic, 8; biliary, 8; other, 4) were studied. We found edematous pancreatitis in 17 cases and severe hemorrhagic pancreatitis in three cases. At admission, peak levels of PASP (average value, 1,976 +/- 329 ng/ml), pancreatic isoamylase (942 +/- 151 U/L) and lipase (2,946 +/- 534 U/L) were detected in 15 of 20, 16 of 20, and 12 of 20 cases, respectively. The etiology of the pancreatitis had no influence on the PASP values. Furthermore, 10 patients with alcoholic and two patients with nonalcoholic chronic pancreatitis (29-67 years of age) were studied. The average peak level of PASP was 1,229 +/- 434 ng/ml. In this group, PASP paralleled the time course of amylase and lipase. Maximal PASP, amylase, and lipase levels were found in 11 of 12, nine of 12, and five of 12 patients, respectively, on the day of admission. ERCP was performed in 44 patients (36-87 years of age), demonstrating common bile duct stones in 16 and bile or pancreatic ductal tumors in 15 cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Dynamic Liver Scintigraphy: A New Way of Measuring the Function of the Reticulo-endothelial System of the Liver

The phagocytic function and biokinetics of the hepatic reticuloendothelial system (RES) were evaluated using a 25-nm diameter colloid (Nanocoll) and a scintillation camera technique in opossums with obstruction of the pancreatic duct (group I) and additional obstruction of the common bile duct (group II). The liver net uptake curve was analysed using natural log regression. The regression curves proved to fit very well (r > 0.93) and a parameter R was calculated to describe the curves. In group I there was a slight but significant decrease in the RES function and no morphological change in the pancreas. In group II, RES function was significantly more suppressed than in group I. The opossums developed severe haemorrhagic pancreatitis. The results show that the regression parameter R is well suited to described liver RES function, and suggest that a suppressed liver RES after biliary obstruction could be an important factor in the pathogenesis of biliary pancreatitis.

Microcirculatory distrubances aggravate cerulein-induced edematous pancreatitis into severe hemorrhagic pancreatitis in rats

Microcirculatory distrubances aggravate cerulein-induced edematous pancreatitis into severe hemorrhagic pancreatitis in rats

Pancreatic exocrine secretion in acute experimental pancreatitis

Little is known about exocrine pancreatic secretory function in patients with acute pancreatitis, in particular during the early phase of the disease. Therefore, this study evaluates basal and stimulated pancreatic secretion in vivo and in vitro in four different models of acute pancreatitis which reflect its clinical spectrum of severity: (a) edematous pancreatitis induced in the rat by seven IP injections of 50 μg/kg cerulein at hourly intervals; (b) edematous pancreatitis with cellular necrosis induced in the mouse by seven IP injections of 50 μg/kg cerulein at hourly intervals; (c) hemorrhagic pancreatitis induced in the mouse by feeding an ethionine-supplemented, choline-deficient diet for 66 hours; and (d) hemorrhagic pancreatitis induced in the rat by retrograde infusion of 0.6 mL 5% sodium taurocholate into the pancreatic duct. Secretory studies were performed in vivo and in vitro at various times after onset of pancreatitis. The results show that the exocrine pancreas gradually became resistant to cholecystokinin stimulation after the onset of acute pancreatitis in all four animal models. Cholecystokinin-stimulated secretion was almost abolished in vivo and in vitro at the time of maximal histological damage. In vivo basal secretion was also reduced. In vitro there was an increase in basal release of amylase from isolated acini that was not caused by an increase in luminal secretion but by enzyme release from damaged cells. The time course of improvement of secretory function after acute experimental pancreatitis depended on the severity of the pancreatitis. Recovery of secretory capacity took longer after severe necrotizing pancreatitis than after edematous pancreatitis. However, the ultimate resolution of secretory function was remarkable, in particular after severe hemorrhagic pancreatitis. In all four models, secretory capacity became indistinguishable from normal before the morphological alterations had completely resolved. The present experimental data suggest that pancreatic secretion, and particularly pancreatic secretory response to cholecystokinin, may also be reduced in patients early after the onset of acute pancreatitis.

Pentamidine-Associated Fatal Acute Pancreatitis

Severe hemorrhagic pancreatitis developed in a patient with the acquired immunodeficiency syndrome (AIDS) during pentamidine isethionate treatment for Pneumocystis carinii pneumonia. Despite prompt withdrawal of administration of the drug, the patient died of complications of pancreatitis. Pentamidine is known to be toxic to pancreatic islet cells, causing both hypoglycemia and hyperglycemia in clinical use. However, it rarely causes symptomatic pancreatitis. A review of the literature indicates that this is the second report of fatal pancreatitis associated with pentamidine therapy.

A Randomized Double-Blind Study Using CaNa2EDTA, a Phospholipase A2Inhibitor, in the Management of Human Acute Pancreatitis

In a randomized double-blind study the effect of CaNa2EDTA, a phospholipase A2 inhibitor, was tested as a treatment for acute pancreatitis. CaNa2EDTA was infused intravenously during the first 2 days after admission to hospital, in addition to normal conservative treatment. CaNa2EDTA decreased the serum phospholipase A2 activity and appeared to promote recovery from the illness. To what extent the inhibition of serum phospholipase activity may prevent the progress of severe haemorrhagic pancreatitis or diminish mortality and morbidity in acute pancreatitis should be investigated in further studies.