Cerebral venous thrombosis as a complication of leptospirosis

Leptospirosis is an acute infectious disease caused by a spirochete of the leptospira gender and it is characterized by severe vasculitis. It is not common for leptospirosis to present as a primary neurological disease. On the other hand, no study has been reported on the progression of cerebral venous thrombosis (CVT) in patients with leptospirosis so far. This is the first case reported which shows CVT as a complication after the leptospirosis infection. An acutely developed leptospirosis and post-infectious CVT in a 21-year-old soldier is described here.     

Severe pulmonary manifestation of leptospirosis

Based on increasing incidence and the occurrence of worldwide outbreaks, leptospirosis is recognised as an emerging zoonosis. Severe manifestations are associated with high morbidity and mortality rates and may therefore pose an important risk to public health, especially in certain high prevalence areas. A considerable number of infections progress to a severe form, which can present as the well-known triad of jaundice, impaired renal function and haemorrhage, known as Weil's disease. The severe pulmonary form of leptospirosis (SPFL) is a less known entity and is characterised by intra-alveolar haemorrhage and can lead to acute respiratory failure and death when adequate treatment fails. Prognostic factors correlating with severity and survival of leptospirosis include indicators of renal failure, pulmonary involvement and electrolyte imbalances. We report an imported case of SPFL in a returning traveller, and review the literature discussing epidemiology, clinical manifestations, prognostic factors and treatment of this resurgent disease.     

Overlapping clinical features of lupus and leptospirosis

Systemic manifestations of infectious disease may be confused with systemic lupus erythematosus (SLE), leading to potential patient morbidity and mortality. We report the case of a patient with severe renal failure and liver involvement who was initially diagnosed and treated for leptospirosis infection. It was later determined that his organ involvement was related to active SLE. We review the clinical and laboratory features common to both SLE and leptospirosis infection to highlight not only the importance of maintaining a high index of suspicion for infectious organisms in a patient with a suspect travel history but also the recognition of atypical features of a systemic autoimmune disease.     

Overlapping clinical features of lupus and leptospirosis

Systemic manifestations of infectious disease may be confused with systemic lupus erythematosus (SLE), leading to potential patient morbidity and mortality. We report the case of a patient with severe renal failure and liver involvement who was initially diagnosed and treated for leptospirosis infection. It was later determined that his organ involvement was related to active SLE. We review the clinical and laboratory features common to both SLE and leptospirosis infection to highlight not only the importance of maintaining a high index of suspicion for infectious organisms in a patient with a suspect travel history but also the recognition of atypical features of a systemic autoimmune disease.     

Fulminant course of leptospirosis complicated by multiple organ failure

We describe a case of a 39-year-old male, who initially presented with severe muscle pain, fever, shortness of breath and tachycardia. He was admitted to hospital with suspected myocarditis. The next days he developed a generalized icterus and acute renal failure. Suspecting leptospirosis an intravenous therapy with penicillin was started. Due to pulmonary and circulatory insufficiency intensive care was necessary. In course the patient developed all known manifestations of leptospirosis including, cardiac arrhythmia and asystolia due to AV-block III degrees, recurrent atelectases of the lungs, hyperbilirubinemia, thrombocytopenia, hepatitis, pancreatitis, very severe rhabdomyolysis and polyradiculitis with areflexia and tetraplegia. Additionally, the patient had a transient hyperthyreosis, which has not been described in the literature so far. After 33 days the patient left the intensive care unit and was discharged out of hospital a fortnight later. 4 weeks later he was able to return to work. The only residuum of this illness is a partial paresis of his right quadriceps muscle.     

High serum nitric oxide levels in patients with severe leptospirosis

Leptospirosis is a globally distributed zoonosis of major public health importance and is associated with severe disease manifestations such as acute renal failure and pulmonary haemorrhage syndrome. However, the extent to which the pathogenesis of leptospirosis mimics sepsis caused by Gram-negative bacteria remains unknown. The aim of this study was to evaluate serum levels of nitric oxide (NO) in patients diagnosed with severe leptospirosis. Sera from 35 confirmed cases of severe leptospirosis and 13 healthy subjects were analysed. Patients with severe leptospirosis had significantly higher NO levels compared to healthy individuals (30.82 ± 10.90 μM versus 3.86 ± 1.34 μM, P < 0.001), indicating that this immune mediator plays a role in the underlying systemic inflammatory response.     

Management of acute severe hyperlipidemic pancreatitis

BACKGROUND/AIM: Hypertriglyceridemia is rare and can provoke acute severe hyperlipidemic pancreatitis when triglyceride levels exceed 11.3 mmol/l. In 10 patients we evaluated the therapeutic guidelines for severe hyperlipidemic pancreatitis. METHODS: Ten patients (8 men and 2 women) were admitted to the intensive care unit with a diagnosis of acute severe hyperlipidemic pancreatitis. They underwent standard treatment. Heparin, insulin and antihyperlipidemic drugs were used to lower the triglyceride levels. The patients underwent plasmapheresis within 48 h of admission, and fat-free parenteral nutrition was used. Two of the patients underwent surgery because of infection of necrotic segments. RESULTS: Standard treatment was essential for all the patients but plasmapheresis was the procedure that lowered the triglyceride and lipid levels in all cases. It improved abdominal pain, clinical state, and signs and symptoms of the disease. Two patients underwent surgery due to infection of the necrotic segments and one of them died. Follow-up lasted 4-54 months with no recurrences of pancreatitis. CONCLUSION: Our study shows that standard treatment is essential, but plasmapheresis successfully lowered lipid levels with no complications and relieved the patients from the symptoms in the acute phase of the disease. Hyperlipidemic pancreatitis should initially be treated conservatively. Plasmapheresis is a method that has lately been used successfully for hyperlipidemic pancreatitis. It seems that all therapeutic measures should be applied as early as possible, within the first 48 h.     

Leptospirosis and pancytopenia: two case reports and review of the literature

Besides the classical manifestations, leptospirosis may rarely occur with erythroid hypoplasia and/or pancytopenia. In this study, we reported two cases of leptospirosis presented with pancytopenia as the prevailing manifestation. In addition, the presence of pancytopenia in leptospirosis is reviewed. In both patients, the outcome was favourable as the bone marrow aplasia reversed completely after treatment with intravenous penicillin. In conclusion, this case study suggests that Leptospira infection should be included in the differential diagnosis of febrile pancytopenia, even in the absence of classical signs of severe disease as jaundice, meningitis, renal failure and pulmonary infiltrates.     

Histology and bacteriology of closed duodenal loop models of experimental acute pancreatitis in the rat

Three variants of closed duodenal loop models of experimental acute pancreatitis in the rat have been analysed histologically and bacteriologically. Histological studies showed that the resulting pancreatitis was usually mild to moderate, being severe only in association with sepsis. Furthermore the duodenal wall became necrotic in most animals. Bacteriological studies revealed gross infection as a major complication. Peritoneal fluid and blood cultures taken at the time of animal sacrifice consistently demonstrated large numbers of bacteria. It is concluded that although these models undoubtedly cause acute pancreatitis, other more severe pathological events occur. Deductions regarding acute pancreatitis drawn from this type of model are therefore not relevant to the human disease.     

Mild, self-resolving acute leptospirosis in an HIV-infected patient in the Peruvian Amazon

We report a case of acute, self-resolving leptospirosis presenting in a HIV-positive patient from the Peruvian Amazon. The patient presented with an undifferentiated acute febrile illness that resolved without treatment, diagnosed retrospectively as leptospirosis by serology and real-time polymerase chain reaction. Five months later, he was admitted because of a febrile illness with jaundice, hepatosplenomegaly, peripheral edema, and oral candidiasis. Because of the clinical suspicion of AIDS, stored sera of the previous admission were tested, and HIV seropositivity was confirmed, proving that the condition was present at the first admission. Acute leptospirosis in HIV coinfection is not inevitably severe, and there is probably a wide variation in clinical manifestations similar to what occurs in immuno-competent hosts.     

Lessons from acute pancreatitis-induced thrombotic thrombocytopenic purpura

Acute pancreatitis is an inflammatory disease characterized by local tissue injury which can trigger a systemic inflammatory response. There is increasing evidence that endothelial dysfunction is one of the critical pathophysiologic manifestations in patients with severe form of acute pancreatitis. In keeping with this, there have been recent reports of a haematological disorder, thrombotic thrombocytopenic purpura (TTP), as being precipitated by acute pancreatitis. However, the patients who develop TTP, secondary to acute pancreatitis, do not always have the characteristic low levels of VonWillebrand multimer cleaving enzyme, ADAMTS-13 suggesting the involvement of other pathophysiological factors. On the contrary, the occurrence of acute pancreatitis in haemolytic diseases may suggest TTP as being a precipitating factor for the pancreatic inflammatory state. This review focuses on the association of these two conditions which have given insights into the role players and the pathogenic mechanisms leading to the development of either of these conditions.     

Significance of apoptotic cell death in systemic complications with severe acute pancreatitis

In severe acute pancreatitis, multiple organ failure in the early stage after onset, and sepsis in the late stage, due to infection of pancreatic or peripancreatic devitalized tissue, contribute to its high mortality. In analogy with sepsis, evidence has accumulated of the significance of apoptotic cell death in the systemic manifestations associated with acute pancreatitis. Since we identified apoptosis-inducing activity in pancreatitis-associated ascitic fluid in 1995, a number of investigators, including our group, have reported, through animal experiments, that apoptosis occurred in the parenchymal cells constituting organs, such as alveolar epithelial cells in the lung, renal tubular cells in the kidney, and hepatocytes in the liver, and this apoptosis was involved in organ dysfunction with severe acute pancreatitis. Moreover, through clinical and experimental investigations, apoptosis has been revealed to be involved in the mechanism of infectious complications in acute pancreatitis. Namely, apoptosis in lymphatic tissues and peripherally circulating lymphocytes is involved in the impairment of cellular immunity, and apoptosis in gut epithelial cells is implicated in bacterial translocation. These results suggest that apoptotic cell death may play a considerable role in affecting mortality and morbidity in severe acute pancreatitis. Control of apoptosis could be a potent strategy for improvement of the clinical outcome in severe acute pancreatitis.     

Urinary trypsinogen activation peptide is more accurate than hematocrit in determining severity in patients with acute pancreatitis: a prospective study

OBJECTIVE: The management of patients with acute pancreatitis is complicated by the inability to distinguish mild from severe disease during the early stages. It has been previously shown that urinary trypsinogen activation peptide (TAP) and hematocrit (Hct) may serve as early predictors of severity in patients with acute pancreatitis. To establish which marker is more accurate in the determination of severity in patients with acute pancreatitis, a prospective study was performed. METHODS: A consecutive series of patients admitted with pain consistent with acute pancreatitis and an amylase of three times the upper limit of normal were included. The admission and 24-h Hct was obtained. A urine sample was obtained within 12 h of admission. Urinary TAP was determined using a modified solid phase ELISA. Severity was defined by the Atlanta Symposium, as the presence of organ failure and/or pancreatic necrosis. RESULTS: Fifty-eight consecutive patients with acute pancreatitis participated. There were 33 men and 25 women with a mean age of 60 +/- 19. Thirty-nine patients had mild disease; 19 had severe disease. Urinary TAP was elevated in 26 patients. All patients with severe pancreatitis were correctly identified as having severe disease by an elevated urinary TAP (sensitivity 100%, specificity 77%). The admission Hct was higher than 47 in only three patients, all with mild disease. Of the patients with a rise in Hct, eight had mild disease, and only one had severe disease. Using a Hct of 44 as a cutoff did not affect the accuracy. There was no association between a rise in Hct and failure of Hct to decrease in the determination of severity. CONCLUSIONS: In comparison to admission Hct, urinary TAP was more accurate in determining severity in patients with acute pancreatitis by Atlanta, APACHE II, and Ranson criteria. We conclude that urinary TAP is a more accurate predictor of severity in patients with acute pancreatitis compared with Hct. Urinary TAP should be used to determine severity in patients early in the course of acute pancreatitis.     

Natural history of acute pancreatitis and the role of infection.

Bacterial infection of pancreatic necrotic tissue is a frequent complication of severe acute pancreatitis. Infected pancreatic necrotic tissue is observed in 30-70% of all patients suffering from necrotizing pancreatitis. It is the leading cause of deaths in severe acute pancreatitis, with mortality rates ranging from 15 to 30%. The incidence of infection increases with the extent of the necrotic areas and with the time after onset of pancreatitis. Compared to patients with sterile necrosis, those with infection of the necrotic areas have an increased mortality, and systemic complications occur more frequently. Standard treatment for infected pancreatic necrotic tissue is surgical debridement, whereas conservative management is feasible in approximately 30% of the patients with sterile necrosis. As bacterial infection of pancreatic necrotic tissue has a tremendous impact on the prognosis of the disease and on the patient's clinical course, efforts have been made to prevent it. Although clinical and experimental data provide evidence that prophylactic antibiotics have beneficial effects on the outcome and course of patients with severe acute pancreatitis, this topic has to be investigated further. General recommendations concerning the early use of antibiotics have to await the results of larger, double-blind studies.     

Review of experimental animal models of acute pancreatitis

The underlying mechanisms involved in the pathogenesis of acute pancreatitis are ill understood. The mortality rate of this disease has not significantly improved over the past few decades. Current treatment options are limited, and predominantly aimed at supportive therapy. A key feature of severe acute pancreatitis is the presence of extensive tissue necrosis with both local and systemic manifestations of inflammatory response syndromes. A better understanding of the underlying pathophysiology of severe acute pancreatitis may lead to more targeted therapeutic options, potentially leading to improved survival. Animal models of acute pancreatitis are therefore an essential investigative tool for these aims to be achieved. This review discusses the suitability of recent non-invasive models of acute pancreatitis such as hormone-induced, alcohol-induced, immune-mediated, diet-induced, gene knockout and L-arginine; and invasive models including closed duodenal loop, antegrade pancreatic duct perfusion, biliopancreatic duct injection, combination of secretory hyperstimulation with minimal intraductal bile acid exposure, vascular-induced, ischaemia/reperfusion and duct ligation.     

Acute pancreatitis: treatment strategies

Acute pancreatitis is an acute painful abdominal disease of sudden onset that ranges from a mild and self-limited illness to a severe and severe life-threatening condition. In spite of decades of intensive research, there are no causal therapeutic options. Treatment relies on supportive treatment principles based on adequate volume replacement to compensate for fluid loss in the intraperitoneal space and analgesics for pain relief. In cases with acute pancreatitis predicted to have a severe course of the disease, antibiotic therapy is recommended to avoid infection of pancreatic necrosis. Despite a substantial set of clinical trials in favor of antibiotic treatment to reduce morbidity, there is no general consensus on the prophylactic antibiotic treatment. Adequate nutritional support is required for patients with severe acute pancreatitis and a protracted course of the disease. Enteral nutrition appears to be superior to enteral nutrition.     

Prevention of severe change in acute pancreatitis: prediction and prevention

Bacterial infection of pancreatic necrosis is the most frequent local complication of severe acute pancreatitis and is responsible for the majority of deaths in this disease. The development of systemic complications of severe acute pancreatitis such as septic multiple organ failure is closely related to infected necrosis. In this review, the factors predisposing to a severe course of acute pancreatitis are discussed as are clinical and laboratory markers which allow identification of patients at risk. Prevention of complications of acute pancreatitis is difficult. A variety of drugs including antiproteases and antiinflammatory agents have been shown to be of no benefit with regard to the reduction of severe complications. At present, based on the results of controlled trials, there is the widespread belief that prophylactic antibiotics are capable of reducing the incidence of infected pancreatic necrosis. New approaches for the prevention of systemic complications of severe acute pancreatitis are total enteral nutrition and local arterial infusion of antibiotics and antiproteases into the celiac trunk.     

Irreversible sequels of leptospirosis

Leptospirosis is a zoonotic feral nidal disease (synonyms: Weil-Vasilyev disease, waterborne fever) running as an acute febrile disease with evident intoxication, renal, hepatic, and central nervous system involvements, evolving hemorrhagic syndrome mainly with its severe complicated course and high mortality rates. The clinical features of leptospirosis have been little studied in patients with comorbidities. Its poor outcomes are generally due to the development of serious complications, such as infection-toxic shock, acute renal and hepatic failure, massive hemorrhagic syndrome, infectious myocarditis, etc. This communication describes a case of the disease with developed irreversible complications: involvement of the kidney and heart in 1 case and that of the kidney with a fatal outcome. Leptospirosis mortality is frequently associated with delayed diagnosis due to the misunderstanding of the clinical picture of this disease (particularly in its similarity to hemorrhagic fever with renal syndrome). The severer acute course of the infectious process in leptospirosis is burdened with the activation of the infection foci existing in the body or the exacerbation of somatic comorbidity, which substantiates the necessity of goal-oriented early individual, background pathology-depended correction of diagnostic, etiotropic, and pathogenetic therapy, rehabilitative measures. Comorbidities in patients with leptospirosis exert a significant impact on the development of its clinical form and the course of the infectious process manifesting itself as its worsening, the more frequent and more prolonged signs ofendogenous intoxication and multiple organ dysfunction, and a larger number of nonspecific complications in the structure of causes of deaths.     

Use of antibiotics in acute pancreatitis: ten major concerns

Abstract

Acute pancreatitis is one of the most common gastrointestinal causes for hospitalization. In 15–20% it evolves into severe necrotizing pancreatitis. Recent studies have shown no association between the initiation of antibiotic therapy in acute pancreatitis and severe outcomes such as organ failure, infection of pancreatic necrosis, extrapancreatic infections or mortality. Specific subgroups with predicted severe acute pancreatitis or both extensive sterile necrosis and persistent organ failure may benefit from prophylactic antibiotics. Local infection develops in 30% of patients with pancreatic necrosis and results in morbidity and mortality. Contrast enhanced computed tomography should be performed in all patients with acute pancreatitis who develop sepsis, organ failure or fail to improve. C-reactive protein is an independent predictor of severe acute pancreatitis. Procalcitonin is the most sensitive laboratory test for detection of pancreatic infection. Antibiotics do however play a large role in patients with suspected or confirmed infected pancreatic necrosis and extrapancreatic infections. In clinical practice most clinicians prescribe antibiotics in the first 3?days of acute pancreatitis which in turns lead to excessive, unjustified use of antibiotics. Deep knowledge of the recent guidelines combined with an individualized management based on right clinical judgment is a rationale approach of patients with acute pancreatitis.     

Coronavirus Disease-19 (COVID-19) associated with severe acute pancreatitis: Case report on three family members

Background/ObjectivesAbdominal pain is one of the known symptoms associated with coronavirus disease 2019. Little is known about the development of acute pancreatitis as a complication of severe acute respiratory syndrome coronavirus 2 infection. This case report describes the presentation of acute pancreatitis in two of three family members with severe COVID-19 infection.MethodsData were collected from three family members admitted with COVID-19 to the intensive care unit in March 2020. This study was reviewed and approved by the local data and ethics committee (31-1521-253).ResultsTwo of the three family members were diagnosed with acute pancreatitis associated with SARS-CoV-2. Other causes of acute pancreatitis were excluded for both patients (including alcohol, biliary obstruction/gall stones, drugs, trauma, hypertriglyceridemia, hypercalcemia, and hypotension).ConclusionsThese cases highlight acute pancreatitis as a complication associated with COVID-19 and underlines the importance of measuring pancreas-specific plasma amylase in patients with COVID-19 and abdominal pain.