Retrograde Infection Research Articles

JPN Guidelines for the management of acute pancreatitis: epidemiology, etiology, natural history, and outcome predictors in acute pancreatitis

Acute pancreatitis is a common disease with an annual incidence of between 5 and 80 people per 100 000 of the population. The two major etiological factors responsible for acute pancreatitis are alcohol and cholelithiasis (gallstones). The proportion of patients with pancreatitis caused by alcohol or gallstones varies markedly in different countries and regions. The incidence of acute alcoholic pancreatitis is considered to be associated with high alcohol consumption. Although the incidence of alcoholic pancreatitis is much higher in men than in women, there is no difference in sexes in the risk involved after adjusting for alcohol intake. Other risk factors include endoscopic retrograde cholangiopancreatography, surgery, therapeutic drugs, HIV infection, hyperlipidemia, and biliary tract anomalies. Idiopathic acute pancreatitis is defined as acute pancreatitis in which the etiological factor cannot be specified. However, several studies have suggested that this entity includes cases caused by other specific disorders such as microlithiasis. Acute pancreatitis is a potentially fatal disease with an overall mortality of 2.1%–7.8%. The outcome of acute pancreatitis is determined by two factors that reflect the severity of the illness: organ failure and pancreatic necrosis. About half of the deaths in patients with acute pancreatitis occur within the first 1–2 weeks and are mainly attributable to multiple organ dysfunction syndrome (MODS). Depending on patient selection, necrotizing pancreatitis develops in approximately 10%–20% of patients and the mortality is high, ranging from 14% to 25% of these patients. Infected pancreatic necrosis develops in 30%–40% of patients with necrotizing pancreatitis and the incidence of MODS in such patients is high. The recurrence rate of acute pancreatitis is relatively high: almost half the patients with acute alcoholic pancreatitis experience a recurrence. When the gallstones are not treated, the risk of recurrence in gallstone pancreatitis ranges from 32% to 61%. After recovering from acute pancreatitis, about one-third to one-half of acute pancreatitis patients develop functional disorders, such as diabetes mellitus and fatty stool; the incidence of chronic pancreatitis after acute pancreatitis ranges from 3% to 13%. Nevertheless, many reports have shown that most patients who recover from acute pancreatitis regain good general health and return to their usual daily routine. Some authors have emphasized that endocrine function disorders are a common complication after severe acute pancreatitis has been treated by pancreatic resection.

Ventriculoperitoneal shunt catheter masquerading as ascariasis

We describe extrusion of a ventriculoperitoneal shunt catheter through the anus occurring in an eight month child with hydrocephalus. This is a rare complication of ventriculoperitoneal shunt. Perforation of the bowel by the peritoneal catheter of the shunt occurred without peritonitis or retrograde infection of the shunt system. Pathogenesis and the literature is reviewed.

Timing of surgical treatment for pancreatic pseudocyst secondary to severe acute pancreatitis

目的 探讨重症急性胰腺炎后假性胰腺囊肿的手术时机.方法 27例胰腺炎后4～8周出现的假性胰腺囊肿,行囊肿内引流术(早期手术组),其中10例采用吻合器行囊肿空肠吻合术.与30例病人囊肿形成后,等待24周再施行手术的 (晚期手术组)进行比较.结果两组病例相比,早期手术组的术后吻合口漏发生率、平均住院时间、平均住院费用明显低于晚期手术组,差异有显著性意义(P 0.05),晚期手术组有5例在等待手术的过程中出现并发症而急诊手术(1例囊肿内出血,2例囊肿内感染,2例囊肿破裂).结论术前明确诊断,严格掌握手术指征,早期行假性胰腺囊肿内引流术是安全可行的,且避免了等待过程中囊肿内感染、出血和破裂的发生。

Vector Competence of <I>Culicoides sonorensis</I> (Diptera: Ceratopogonidae) for Vesicular Stomatitis Virus

To determine the vector competence of Culicoides sonorensis Wirth & Jones midges for vesicular stomatitis virus (VSV)-New Jersey, insects were experimentally infected per os and sampled over time. Viral replication, as determined by in situ hybridization, was seen in epithelial, neural, and hemolymph cell types throughout the insect. Spatial and temporal distribution of virus was determined by immunohistochemical examination of sequentially sampled insects. Tissues of the alimentary canal were infected in a temporal pattern that paralleled the route of digestion/absorption: foregut and midgut by day 1, surrounding hemolymph and Malpighian tubules by day 3, and finally the midgut/ hindgut junction, hindgut, and rectal region by day 5. The circulation of virus in the hemolymph by day 3 coincided with infection of the dermis and fat bodies, the salivary glands, eyes, cerebral and subthoracic ganglia, and the ovaries. Oviduct epithelium and ovarial sheaths were infected by day 3, followed by infection of the developing oocytes by day 5. Interestingly, neural infections were seen in the subabdominal ganglia innervating the midgut in 33% of insects by 1 d postfeeding in the absence of positive staining in the hemolymph or surrounding tissues. A retrograde axonal transport infection route for these ganglia is discussed. The disseminated, productive, noncytolytic infection in Culicoides is consistent with that of an efficient biological vector for VSV. Virus readily replicated throughout the insect, passing both midgut and salivary gland infection barriers and reaching transmission-related organs in 3 d. Establishing the competence of this insect vector for VSV provides the foundation for animal transmission studies in the future. The possibility of horizontal, transovarial, and mechanical transmission is discussed.

Polysynaptic pathways from the vestibular nuclei to the lateral mammillary nucleus of the rat: substrates for vestibular input to head direction cells

The activity of some neurons in the lateral mammillary nucleus (LMN) of the rat corresponds with the animal's current head direction (HD). HD cells have been studied extensively but the circuitry responsible for the generation and maintenance of the HD signal has not been established. The present study tested the hypothesis that a polysynaptic pathway connects the vestibular nuclei with the LMN via one or more relay nuclei. This circuitry could provide a substrate for the integration of sensory input necessary for HD cell activity. This hypothesis is based upon the prior demonstration that labyrinthectomy abolishes HD selectivity in thalamic neurons. Viral transneuronal tracing with pseudorabies virus (PRV) was used to test this hypothesis. We injected recombinants of PRV into the LMN and surrounding nuclei of adult male rats and defined the patterns of retrograde transneuronal infection at survival intervals of 60 and 72 h. Infected medial vestibular neurons (MVN) were only observed at the longest postinoculation interval in animals in which the injection site was localized largely to the LMN. Robust infection of the dorsal tegmental nucleus (DTN) and nucleus prepositus hypoglossi (PH) in these cases, but not in controls, at both survival intervals identified these nuclei as potential relays of vestibular input to the LMN. These data are consistent with the conclusion that vestibular information that contributes to the LMN HD cell activity is relayed to this caudal hypothalamic cell group via a polysynaptic brainstem circuit.

Management and Prevention of Retrograde Peri-Implant Infection from Retained Root Tips: Two Case Reports

Fracture of root tips in the maxillary premolar region is not an uncommon finding because of the high incidence of bifid and root dilacerations. Therefore, a retained root tip may serve as a nidus of infection when a dental implant is placed. The likely result is the development of an implant periapical lesion. This case report shows the successful management of a rapidly developing implant periapical lesion caused by an undetected retained root tip. Initially, systemic antibiotics failed to subdue the infection. A retained root fragment was retrieved surgically, together with the implant, and a new wide-body implant was engaged with DFDBA mixed with tetracycline. A 5-month follow-up showed increased radiographic density, and clinical reentry revealed the formation of bone with a hard consistency. The second case demonstrates the management of a retained root tip via a guided bone regeneration technique when it is detected prior to or during implant placement. Finally, a systematic therapeutic approach is proposed based on 17 case reports on implant periapical lesion management.

Up-regulation of cathelicidin in chronic sialadenitis

Problem: Salivary secretions play a critical role in maintaining oral health via innate host defense mechanisms and secretion of secretory IgA. One of the antimicrobial peptides, LL-37 is the only cathelicidin protein so far identified in human beings. Cathelicidins are a family of peptides thought to provide an innate defensive barrier against a variety of potential microbial pathogens. The purpose of this study was to examine the expression of cathelicidin in human salivary glands and to investigate up-regulation of cathelicidin in inflammatory conditions. Methods: Reverse transcriptase polymerase chain reaction (RT-PCR) and immunohistochemical staining were performed on 20 salivary gland tissues, 10 from normal and 10 from chronic sialadenitis. Results: Cathelicidin mRNA transcripts were detected in the normal salivary gland and chronic sialadenitis. The level of cathelicidin mRNA in chronic sialadenitis was significantly increased compared with that in the normal salivary gland. cathelicidin protein was expressed in the glandular epithelium of the normal salivary gland and chronic sialadenitis. Conclusion: The results indicate that cathelicidin might play an important role in the innate host defense of human salivary glands. Significance: In the present study, we showed the localizing expression of the human cathelicidin in salivary glands and up-regulation in the inflammatory conditions. This finding suggested the physiologic importance of cathelicidin in the defense of retrograde infection. Other functions for this broadly expressed peptide and possible expression of cathelicidin in saliva need to be evaluated. Support: None reported.

Anterograde Transneuronal Viral Tracing of Central Viscerosensory Pathways in Rats

Previous studies demonstrated that strain H129 of herpes simplex virus-1 undergoes anterograde transneuronal transport in mice and primates after peripheral or central injection. In this study, H129 was used in rats to identify CNS regions that receive relayed viscero-sensory inputs from the stomach wall. We also examined whether transneuronal viral transport in this model is exclusively anterograde. H129 or an established retrograde transneuronal viral tracer, pseudorabies virus (PRV), was injected into the ventral stomach wall in intact rats or in rats with previous subdiaphragmatic vagal sensory deafferentation. Rats were perfused with fixative 3-5 d later, and tissues were processed for immunocytochemical detection of transported virus. In intact rats, H129 was transported transneuronally via vagal and spinal viscerosensory neurons to postsynaptic target cells in the medullary dorsal vagal complex and thoracic dorsal horn, respectively, with subsequent transport to discrete regions of the medullary and pontine reticular formation, cerebellum, parabrachial nucleus, periaqueductal gray, thalamus, hypothalamus, amygdala, bed nucleus of the stria terminalis, and other central sites. Comparison of labeling patterns in intact and vagal deafferented rats indicated that H129 also produced first-order retrograde infection of autonomic neurons that project directly to virus injection sites, similar to PRV. Unlike PRV, however, H129 was not transported transneuronally in the retrograde direction from infected neurons to central sources of presynaptic input. We conclude that transneuronal transport of H129 occurs exclusively in the anterograde direction to reveal CNS regions that receive direct and relayed viscerosensory signals.

Epididymitis after prostate brachytherapy

Objectives To analyze the incidence, time-course, and potential predisposing factors for what was clinically diagnosed as postimplant epididymitis. Methods Of 517 patients randomized and treated on two treatment protocols, with a planned total accrual of 1200, 5 patients were identified who developed clinically diagnosed epididymitis after iodine-125 or pallidium-103 prostate brachytherapy. Implants were performed by standard techniques, using a modified peripheral loading pattern. Perioperative antibiotics (cefazolin and ciprofloxacin) were given to 258 patients, according to physician preference. Treatment-related morbidity was monitored by mailed questionnaires, using standard American Urological Association (AUA) and Radiation Therapy Oncology Group criteria at 1, 3, 6, 12, and 24 months. Patients who did not respond to the mailed questionnaires were interviewed by telephone. Although the patients were not queried specifically regarding epididymitis, its occurrence was noted when discovered in the course of follow-up examinations. Results Postimplant epididymitis occurred in 5 (1%) of 517 consecutive brachytherapy patients. None of the 5 patients had had a prior history of orchitis, epididymitis, vasectomy, or preimplant catheterization. The symptoms of epididymitis first appeared at 4, 7, 10, 150, and 300 days after implantation. Patients with epididymitis had prostate volumes, preimplant AUA scores, and ages typical of other implant patients. No association was apparent between postimplant epididymitis and the degree of implant-related prostate swelling or the number of seeds implanted. Only the preimplant AUA score predicted for epididymitis, but 2 of the 5 patients had low scores. Only 1 (0.4%) of the 258 patients who received perioperative antibiotics developed epididymitis, and 4 (1.5%) of the 259 patients with prophylactic antibiotics developed epididymitis. Conclusions Epididymitis is an uncommon postimplant complication occurring in 1% of a large patient cohort. That epididymitis patients had greater preimplant AUA scores is consistent with a retrograde infection route, at least in some cases.

Surgical Pearl: Use of the Vacutainer as a closed, active, surgical drain

J Am Acad Dermatol 2003;48:933-4.

Organization of the circadian system in the subterranean mole rat, Cryptomys hottentotus (Bathyergidae)

The mole rat, Cryptomys hottentotus (Bathyergidae) is a gregarious subterranean rodent, which shows no entrainment to ambient light–dark cycles. The locomotor activity of individuals or of a whole colony, which shows no circadian rhythmicity. Since the lack of both synchronization to light–dark cycle and an endogenous rhythm of locomotor activity could be related to the organization of the circadian system, we have investigated the neuropeptidergic features of the SCN and IGL, and have used pseudorabies viral tracing methods to identify the visual and circadian pathways in this species. The precise topographic distribution of certain neuropeptide populations in the SCN differs from typical rodent pattern of organization and may be correlated with the apparent absence of light entrainment of activity and lack of endogenous rhythmicity. The IGL is highly reduced in size. This structure can nevertheless be identified by the presence of NPY and CALB positive neurons, as well as by a dense network of SP fibers. Viral tracing using intraocular injection of the PRV-Becker and PRV-Bartha strains, leads to differential infection of neurons in circadian and visual structures. With the Bartha strain, infected neurons are principally observed in the SCN, whereas the Becker strain leads primarily to infection of the dLGN and shows an anatomical regression of visual structures. Transsynaptic retrograde infection of the retina contralateral to the injected eye reveals a morphologically homogeneous population, which resemble to retinohypothalamic ganglion cells described in other mammals.

Retrograde labeling of mouse spinal descending tracts by a recombinant adenovirus.

The present study tested whether a gene-transfer based upon the retrograde axonal transport of the lacZ adenovirus is effective in the spinal descending tracts of the adult mouse. A small volume of a replication-defective recombinant adenovirus encoding E. coli beta-galactosidase was injected into the upper lumbar cord, and, seven days later, the mice were transcardially perfused by a fixative solution. X-gal staining of coronal or sagittal sections of the spinal cord and the brain revealed that many sites of origin for rubrospinal, vestibulospinal, and reticulospinal tracts were retrogradely labeled, whereas few of the corticospinal tract neurons were retrogradely labeled. Ependymal cells surrounding the central canal of the spinal cord, which were located far from the injection site, showed a high expression of beta-galactosidase activity. Motoneurons around the injection site were strongly stained by X-gal staining, and their axons in the ventral root were anterogradely labeled. Afferent fibers in the dorsal root were labeled by the transganglionic transport of beta-galactosidase. To examine the efficacy of the uptake and retrograde transport of HRP and adenovirus, we injected a mixed solution of 10% HRP and recombinant adenovirus. The number of HRP-labeled corticospinal neurons overwhelmed the number of X-gal stained ones, while the numbers of HRP-labeled rubrospinal and subcoeruleus-spinal neurons were smaller in comparison with the numbers of beta-galactosidase-positive counterparts. The present study revealed that the origins for the spinal descending tracts except for corticospinal neurons could be efficiently gene-transferred by the retrograde infection of a recombinant adenovirus. Such a difference in efficacy of retrograde infection among the spinal descending tracts is practically important when an adenovirus-mediated gene transfer is designed to treat certain neurological diseases affecting the spinal descending tracts.

Transmission of Human Cytomegalovirus from Infected Uterine Microvascular Endothelial Cells to Differentiating/Invasive Placental Cytotrophoblasts

Analysis of placentas infected with human cytomegalovirus (CMV) suggested that viral transmission could involve differentiating/invasive cytotrophoblasts in villi that attach the placenta to the uterine wall. To parse the cellular components in this process, we developed a coculture system of polarized uterine microvascular endothelial cell (UtMVEC) infection with an endothelial cell–tropic pathogenic strain of CMV. Then we evaluated the potential role of neutrophils and endothelial cells in the spread of infection to differentiating cytotrophoblasts. As shown by immunocytochemistry and analysis of viral replication, CMV preferentially infected endothelial cells via apical membranes and disrupted cell junction proteins, thereby altering paracellular permeability and cell polarity. Neutralizing antibodies to CMV glycoprotein B, an envelope component that facilitates virion penetration, blocked plaque formation in polarized UtMVEC. Neutrophils transmitted CMV infection to UtMVEC, which in turn infected cytotrophoblasts. However, neutrophils did not directly infect cytotrophoblasts. These findings implicate endothelial cells from the uterine microvasculature as a potential source for CMV infection of endovascular cytotrophoblasts of the anchoring villi. Possibly the cytokine/chemokine milieu in the pregnant uterus could attract immune cells that infect endothelial cells in hybrid fetal–maternal vessels. In turn, these cells could infect endovascular cytotrophoblasts, one possible initiation point of a cascade that results in retrograde placental CMV infection.

Intravitreal injection of the attenuated pseudorabies virus PRV Bartha results in infection of the hamster suprachiasmatic nucleus only by retrograde transsynaptic transport via autonomic circuits.

Intravitreal injection of the attenuated strain of pseudorabies virus (PRV Bartha) results in transneuronal spread of virus to a restricted set of central nuclei in the rat and mouse. We examined the pattern of central infection in the golden hamster after intravitreal inoculation with a recombinant strain of PRV Bartha constructed to express enhanced green fluorescent protein (PRV 152). Neurons in a subset of retinorecipient nuclei [i.e., suprachiasmatic nucleus (SCN), intergeniculate leaflet, olivary pretectal nucleus (OPN), and lateral terminal nucleus] and autonomic nuclei [i.e., paraventricular hypothalamic nucleus and Edinger-Westphal nucleus (EW)] are labeled by late stages of infection. Infection of the EW precedes infection in retinorecipient structures, raising the possibility that the SCN becomes infected by retrograde transsynaptic infection via autonomic (i.e., EW) circuits. We tested this hypothesis in two ways: (1) by removing the infected eye 24 hr after PRV 152 inoculation, well before viral infection first appears in the SCN; and (2) by examining central infection after intravitreal PRV 152 injection in animals with ablation of the EW. The pattern and time course of central infection were unchanged after enucleation, whereas EW ablation before intravitreal inoculation eliminated viral infection in the SCN. The results of EW lesions along with known connections between EW, OPN, and SCN indicate that intravitreal injection of PRV Bartha produces a retrograde infection of the autonomic innervation of the eye, which subsequently labels a restricted set of retinorecipient nuclei via retrograde trans-synaptic infection. These results, taken together with other genetic data, indicate that the mutations in PRV Bartha render the virus incapable of anterograde transport. PRV Bartha is thus a retrograde transsynaptic marker in the CNS.

Intravitreal Injection of the Attenuated Pseudorabies Virus PRV Bartha Results in Infection of the Hamster Suprachiasmatic Nucleus Only by Retrograde Transsynaptic Transport via Autonomic Circuits

Intravitreal injection of the attenuated strain of pseudorabies virus (PRV Bartha) results in transneuronal spread of virus to a restricted set of central nuclei in the rat and mouse. We examined the pattern of central infection in the golden hamster after intravitreal inoculation with a recombinant strain of PRV Bartha constructed to express enhanced green fluorescent protein (PRV 152). Neurons in a subset of retinorecipient nuclei [i.e., suprachiasmatic nucleus (SCN), intergeniculate leaflet, olivary pretectal nucleus (OPN), and lateral terminal nucleus] and autonomic nuclei [i.e., paraventricular hypothalamic nucleus and Edinger–Westphal nucleus (EW)] are labeled by late stages of infection. Infection of the EW precedes infection in retinorecipient structures, raising the possibility that the SCN becomes infected by retrograde transsynaptic infection via autonomic (i.e., EW) circuits. We tested this hypothesis in two ways: (1) by removing the infected eye 24 hr after PRV 152 inoculation, well before viral infection first appears in the SCN; and (2) by examining central infection after intravitreal PRV 152 injection in animals with ablation of the EW. The pattern and time course of central infection were unchanged after enucleation, whereas EW ablation before intravitreal inoculation eliminated viral infection in the SCN. The results of EW lesions along with known connections between EW, OPN, and SCN indicate that intravitreal injection of PRV Bartha produces a retrograde infection of the autonomic innervation of the eye, which subsequently labels a restricted set of retinorecipient nuclei via retrograde trans-synaptic infection. These results, taken together with other genetic data, indicate that the mutations in PRV Bartha render the virus incapable of anterograde transport. PRV Bartha is thus a retrograde transsynaptic marker in the CNS.

Cholangiojejunal fistula caused by bile duct stricture after intraoperative injury to the common hepatic artery

A 68-year-old man, admitted for the treatment of recurrent cholangitis after a pancreatoduodenectomy (PD) performed 3 years previously was diagnosed as having multiple hepaticolithiasis. On laparotomy, the hepatic artery was not recognized. The anastomosed common hepatic duct was obstructed, and a fistula had been formed between the right hepatic duct and the Roux limb of the jejunum. Lithotripsy was performed from this fistula and it was reanastomosed. Angiography was performed postoperatively and it revealed common hepatic artery injury, most likely to have occurred during the previous PD. The patient's postoperative course was uneventful and he has been asymptomatic for 8 months after the operation, indicating that reanastomosis of the fistula can be an effective method. The stricture of the anastomosis was suspected to be mainly due to cholangial ischemia, because no episode of anastomotic leak or retrograde biliary infection had occurred during the PD perioperative period. There are several reports of late stricture of anastomosis 5 or more years after cholangiojejunostomy. This patient, therefore, requires further long-term follow up.

Targeted Retrograde Gene Delivery for Neuronal Protection

The cellular heterogeneity and complex circuitry of the central nervous system make it difficult to achieve precise delivery of experimental and therapeutic agents. We report here an in vivo retrograde gene delivery strategy to target mature projection neurons using adeno-associated virus, a vector with low toxicity and the capacity for long-term gene expression. Viral delivery to axon terminal fields in the hippocampus and striatum resulted in viral internalization, retrograde transport, and transgene expression in specific projection neurons in entorhinal cortex and substantia nigra. Retrograde delivery of the anti-apoptotic gene Bcl2l (also known as Bcl-xL) protected entorhinal projection neurons from subsequent damage-induced cell death. Given the broad distribution of neurons affected by neurodegenerative diseases, gene delivery to both the terminal fields and the projection neurons through retrograde infection provides for strategic therapeutic intervention at both levels of the neural circuit. This approach may also facilitate experimental studies of defined neural circuits.

Transneuronal retrograde transport of attenuated pseudorabies viruses within central visual pathways.

Pseudorabies virus (PRV) has been shown to be an effective transneuronal tracer within both the peripheral and the central nervous system. The only investigations of this virus in the visual system have examined anterograde transport of PRV from injection sites in the retina. In the present study, we injected attenuated forms of PRV into the primary visual cortex of both rats and cats to determine whether transneuronal retrograde infection would occur back to the retina. In rats, we made small injections into visual cortex of a strain of PRV (Bartha Blu) that contained a beta-galactosidase promoter insert. In cats, we injected PRV-M201 into area V1 of visual cortex. After a 2- to 4-day incubation period, we examined tissue from these animals for the presence of the beta-galactosidase marker (rats) or the virus itself (cats). Cortical PRV injections resulted in transneuronal retrograde infection of the lateral geniculate nucleus (LGN), thalamic reticular nucleus (TRN), and retina. PRV was retinotopically distributed in the pathway. In addition, double-labeling experiments in cats using an antibody against gamma-aminobutyric acid (GABA) were conducted to reveal PRV-labeled interneurons within the LGN and TRN. All TRN neurons were GABA+, as was a subset of LGN neurons. Only the subset of TRN neurons adjacent to the PRV-labeled sector of LGN was labeled with PRV. In addition, a subset of GABA+ interneurons in LGN was also labeled with PRV. We processed some tissue for electron microscopy to examine the morphology of the virus at various replication stages. No mature virions were detected in terminals from efferent pathways, although forms consistent with retrograde infection were encountered. We conclude that the PRV strains we have used produce a local infection that progresses primarily in the retrograde direction in the central visual pathways. The infection is transneuronal and viral replication maintains the intensity of the label throughout the chain of connected neurons, providing a means of examining detailed circuitry within the visual pathway.

Computed tomography evaluation of acute pancreatitis.

In the United States, approximately 250,000 cases of acute pancreatitis occur each year, resulting in greater than 4,000 deaths, a Approximately 90% of cases result from biliary tract disease (cholelithiasis with choledocholithiasis) and alcoholism, although multiple other causes exist including hyperlipidemia, hypercalcemia, genetic conditions, drugs, trauma, mechanical obstruction, endoscopic retrograde cholangiopancreatography (ERCP), infection, and hypoperfusion. Patients may present with a variety of clinical, pathologic, and radiologic findings, depending on the amount of pancreatic inflammation, autodigestion, and necrosis that results. Although the actual cellular events leading to the development of AP have been elusive and poorly understood, recent research suggests that its progression is dependent on the production of inflammatory mediators.: Of these, the cytokines interleukin 1 and tumor necrosis factor, and the biologically active phospholipid platelet-activating factor (PAF) are most important. These inflammatory mediators stimulate production of each other and also mediate distant organ dysfunction, including the development of fever, hypotension, shock, adult respiratory distress syndrome, hepatic dysfunction, acute tubular necrosis, and disseminated intravascular coagulation. 2 Most patients with AP seek medical attention within 12 to 18 hours after the onset of abdominal pain. It has been shown that cytokine production peaks approximately 30 hours

Diagnosis and treatment of congenital choledochal cyst: 20 years' experience in China.

To summarize the experience of diagnosis and treatment of congenital choledochal cyst in the past 20 years (1980-2000). The clinical data of 108 patients admitted from 1980 to 2000 were analyzed retrospectively. Abdominal pain,jaundice and abdominal mass were presented in most child cases. Clinical symptoms in adult cases were non-specific, resulting in delayed diagnosis frequently. Fifty-seven patients (52.7%) had coexistent pancreatiobiliary disease. Carcinoma of the biliary duct occurred in 18 patients (16.6%). Ultrasonic examination was undertaken in 94 cases, ERCP performed in 46 cases and CT in 71 cases. All of the cases were correctly diagnosed before operation. Abnormal pancreatobiliary duct junction was found in 39 patients. Before 1985 the diagnosis and classification of congenital choledochal cyst were established by ultrasonography preoperatively and confirmed during operation, the main procedures were internal drainage by cyst enterostomy. After 1985, the diagnosis was established by ERCP and CT, and cystectomy with Roux-en-Y hepaticojejunostomy was the conventional procedures.In 1994, we reported a new and simplified operative procedure in order to reduce the risk of choledochal cyst malignancy. Postoperative complication was mainly retrograde infection of biliary tract, which could be controlled by the administration of antibiotics, there was no perioperative mortality. The concept in diagnosis and treatment of congenital choledochal cyst has obviously been changed greatly.CT and ERCP were of great help in the classification of the disease.Currently, cystectomy with Roux-en-Y hepaticojejunostomy is strongly recommended as the choice for patients with type I and type IV cysts. Piggyback orthotopic liver transplantation is indicated in type V cysts (Caroli's disease) with frequently recurrent cholangitis.