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ABSTRACT: Background:
Treatment of blunt splenic trauma has undergone dramatic changes over the last few decades. Nonoperative management (NOM)
is now the preferred treatment of choice, when possible. The outcome of NOM has been evaluated. This study evaluates the results
following the management of blunt splenic injury in adults in a Swedish university hospital with a low blunt abdominal trauma
incidence.
Method:
Fifty patients with blunt splenic trauma were treated at the Department of Surgery, Lund University Hospital from January
1994 to December 2003. One patient was excluded due to a diagnostic delay of > 24 h. Charts were reviewed retrospectively
to examine demographics, injury severity score (ISS), splenic injury grade, diagnostics, treatment and outcome measures.
Results:
Thirty-nine patients (80%) were initially treated nonoperatively (NOM), and ten (20%) patients underwent immediate surgery
(operative management, OM). Only one (3%) patient failed NOM and required surgery nine days after admission (failure of NOM,
FNOM). The patients in the OM group had higher ISS (p < 0.001), higher grade of splenic injury (p < 0.001), and were hemodynamically
unstable to a greater extent (p < 0.001). This was accompanied by increased transfusion requirements (p < 0.001), longer stay
in the ICU unit (p < 0.001) and higher costs (p = 0.001). Twenty-seven patients were successfully treated without surgery.
No serious complication was found on routine radiological follow-up.
Conclusion:
Most patients in this study were managed conservatively with a low failure rate of NOM. NOM of blunt splenic trauma could
thus be performed in a seemingly safe and effective manner, even in the presence of established risk factors. Routine follow-up
with CT scan did not appear to add clinically relevant information affecting patient management.
European Journal of Trauma and Emergency Surgery 04/2012; 35(2):102-107. · 0.33 Impact Factor
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ABSTRACT: Gut barrier function is essential in critical illness and contributes to the systemic inflammatory response. Failure of the gut barrier includes both changes in microbial ecology, permeability and potential translocation, as well as local gut inflammatory response. The present review summarizes experiences made from acute pancreatitis, including pathophysiological mechanisms and ways of intervention.
07/2009; 2(2):93-100.
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ABSTRACT: Non-operative management (NOM) of blunt liver trauma is currently, if possible, the preferred treatment of choice. The present study evaluates the experience of blunt liver injury in adults in a Swedish university hospital.
Forty-six patients with blunt liver trauma were treated from January 1994 through to December 2004. Patient charts were reviewed retrospectively to examine injury severity score (ISS), liver injury grade, diagnostics, treatment and outcome.
Thirty-five patients (76%) were initially treated non-operatively and 11 (24%) patients had immediate surgery. In four (11%) patients, NOM failed and the patients required surgery 8-72 h after admission. Patients failing non-operative care had a significantly lower systolic blood pressure on admission as compared with patients with successful NOM (P = 0.001). Patients immediately operated upon had higher ISS (P < 0.001) and were haemodynamically unstable to a greater extent (P < 0.001) as compared with patients initially considered for NOM. Operated patients had increased transfusion requirements (P < 0.001), longer total hospital stay (P = 0.011) and stay in the intensive care unit (ICU) unit (P < 0.001) as compared with NOM. One immediately operated and one failed NOM died (total mortality 4%). Seventeen patients in the NOM group were successfully treated without surgery despite the presence of at least one described risk factor.
Most patients with blunt liver trauma can be treated without surgery, and non-operative management may be performed even in the presence of established risk factors.
HPB 01/2009; 11(1):50-6. · 1.60 Impact Factor
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ABSTRACT: The initiating events in the onset of pancreatitis are poorly understood. Possible candidates may be endogenous ligands, acting on receptors within ductal, acinar or stellate cells, which have previously been shown to cause a systemic inflammatory response syndrome. The aim of this study was to investigate whether acute pancreatitis could be induced by heparan sulphate (HS)infused into the pancreatic ducts in the rat.
Retrograde biliary-pancreatic infusion of heparan sulphate of different structures, taurodeoxycholate (TDC) or phosphate buffered saline (PBS) was performed. Local pancreatic inflammation was evaluated after 6 h by means of morphological evaluation, neutrophil and macrophage infiltration and levels of plasma amylase. Systemic inflammation was evaluated by measuring plasma IL-6, MCP-1 and CINC-1 concentrations.
Heparan sulphate induced a local inflammatory response visualized as a rapid infiltration of neutrophils and macrophages into the pancreas. Heparan sulphate induced inflammation and oedema without causing damage to acinar cells, as measured by morphological changes and plasma amylase concentrations. Furthermore, an increase in serum concentrations of CINC-1 and IL-6 was seen. The positive control (TDC) had increased levels of all variables analysed and the negative control (heparan sulphate administered intraperitoneally) was without effects.
Our findings suggest a receptor-mediated innate immune response of the pancreatic cells induced by heparan sulphate. This finding may be helpful in elucidating some of the mechanisms involved during the initiation of pancreatitis, as well as in the search for a potential future therapeutic application.
Scandinavian journal of gastroenterology 02/2008; 43(4):480-9. · 2.08 Impact Factor
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ABSTRACT: nificant differences compared to challenge, except for N-acetyl cysteine, which significantly increased permeability. Conclusion: Pre-treatment with cellulose derivatives was more efficient against disturbances in intestinal permea-bility and microbial populations than the antioxidant N-acetyl cysteine. INTRODUCTION Acute pancreatitis (AP) is a rather common disease associated with high morbidity and in its severe form, also a high mortality. 1 The disease progresses from a lo-cal auto-digestive reaction confined to the pancreas to a systemic inflammation (systemic inflammatory response syndrome, SIRS). The inflammatory reaction is believed to be elevated by the immunological activity of the gut. The gut barrier consists of several different systems that prevent bacteria and bacterial products to enter the cir-culation. These barriers include both physical barriers such as the mucosal layer and other mechanisms such as the immunological status and gut flora. Normally, the microbial ecological system is kept in balance but may be altered during disease. Under these circumstances both pathogenic and opportunistic bacteria might in-crease in number. Overgrowth of Escherichia coli (E. coli) has experimentally been demonstrated in rats 2,3 and over-growth of potentially pathogenic bacteria has been sug-gested to be one of the causes underlying the multiple organ dysfunction syndrome. 4,5 Prevention of these changes in intestinal microbial ecology is of obvious im-Editorial on page 225 SUMMARY Background: An increase in intestinal permeability and sub-sequent bacterial translocation has been demonstrated in critical illness. Cellulose derivatives have in the past been shown to reduce gut leakage following liver resection.
