Pre-operative inspiratory muscle training preserves postoperative inspiratory muscle strength following major abdominal surgery �C a randomised pilot study

INTRODUCTION

The aim of this pilot study was to assess the effect of pre-operative inspiratory muscle training (IMT) on respiratory variables in patients undergoing major abdominal surgery.

PATIENTS AND METHODS

Respiratory muscle strength (maximum inspiratory [MIP] and expiratory [MEP] mouth pressure) and pulmonary functions were measured at least 2 weeks before surgery in 80 patients awaiting major abdominal surgery. Patients were then allocated randomly to one of four groups (Group A, control; Group B, deep breathing exercises; Group C, incentive spirometry; Group D, specific IMT). Patients in groups B, C and D were asked to train twice daily, each session lasting 15 min, for at least 2 weeks up to the day before surgery. Outcome measurements were made immediately pre-operatively and postop-eratively.

RESULTS

In groups A, B and C, MIP did not increase from baseline to pre-operative assessments. In group D, MIP increased from 51.5 cmH₂O (median) pre-training to 68.5 cmH₂O (median) post-training pre-operatively (P < 0.01). Postoperatively, groups A, B and C showed a fall in MIP from baseline (P < 0.01, P < 0.01) and P = 0.06, respectively). No such significant reduction in postoperative MIP was seen in group D (P = 0.36).

CONCLUSIONS

Pre-operative specific IMT improves MIP pre-operatively and preserves it postoperatively. Further studies are required to establish if this is associated with reduced pulmonary complications.     

A Mouse Model of Lethal Synergism Between Influenza Virus and Haemophilus influenzae

Secondary bacterial infections that follow infection with influenza virus result in considerable morbidity and mortality in young children, the elderly, and immunocompromised individuals and may also significantly increase mortality in normal healthy adults during influenza pandemics. We herein describe a mouse model for investigating the interaction between influenza virus and the bacterium Haemophilus influenzae. Sequential infection with sublethal doses of influenza and H. influenzae resulted in synergy between the two pathogens and caused mortality in immunocompetent adult wild-type mice. Lethality was dependent on the interval between administration of the bacteria and virus, and bacterial growth was prolonged in the lungs of dual-infected mice, although influenza virus titers were unaffected. Dual infection induced severe damage to the airway epithelium and confluent pneumonia, similar to that observed in victims of the 1918 global influenza pandemic. Increased bronchial epithelial cell death was observed as early as 1 day after bacterial inoculation in the dual-infected mice. Studies using knockout mice indicated that lethality occurs via a mechanism that is not dependent on Fas, CCR2, CXCR3, interleukin-6, tumor necrosis factor, or Toll-like receptor-4 and does not require T or B cells. This model suggests that infection with virulent strains of influenza may predispose even immunocompetent individuals to severe illness on secondary infection with H. influenzae by a mechanism that involves innate immunity, but does not require tumor necrosis factor, interleukin-6, or signaling via Toll-like receptor-4.Infections with influenza virus cause mild to severe respiratory illness and may result in death in vulnerable human populations.^1,2,3,4 On average, influenza causes three to five million cases of severe illness per year worldwide and over 200,000 hospitalizations and 36,000 deaths in the United States alone.¹ 5 to 20% of the US population are infected annually. While healthy adults typically experience only acute uncomplicated infection, influenza virus predisposes the lungs to bacterial co-infections,^5,6,7 which cause significant additional morbidity, particularly in young children, elderly and immunocompromised individuals.^8,9,10,11,12 Secondary bacterial infections may also significantly increase mortality in the population as a whole during influenza pandemics.^13,14,15,16 For example, in the 1918 influenza pandemic, which killed approximately 50 million people worldwide, while infection with the virus alone could be lethal, the majority of deaths appeared to result from secondary bacterial pneumonia.^16,17,18,19 The most common bacterial agents mediating such secondary infections in the U.S. are Streptococcus pneumoniae, Staphylococcus aureus, and Haemophilus influenzae.^20,21,22,23H. influenzae is a small Gram-negative coccobacillus that exists in capsulated or non-capsulated forms. H. influenzae is a common cause of otitis media, acute sinusitis, bronchitis, pneumonia and exacerbations of chronic obstructive pulmonary disease.^{24,25,26,27,28,29} A vaccine against H. influenzae type b (Hib) has greatly reduced the incidence of invasive disease, such as meningitis, caused by this organism in children under 5 years of age.^30,31,32,33 However, Hib invasive disease in children remains a problem in countries where the vaccine is not widely available.^32,34,35 Furthermore, other encapsulated and non-typable (NTHi) forms are increasing in frequency as causes of illness in young children.^28,29,36 During the 1918 influenza pandemic, H. influenzae was often isolated from the autopsied lungs of young adults, a subpopulation who do not usually die from influenza infection.¹⁶Early studies by Shope³⁷ showed that infection of pigs with both influenza virus and H. influenzae suis resulted in severe disease or death, whereas the individual agents induced only mild infection. Similarly, Orticoni et al³⁸ reported that administration of both filtrates of nasal secretions from 1918 influenza patients and H. influenzae caused a lethal disease in guinea pigs, but there was no effect if either agent was administered alone. Influenza also increases the susceptibility of new-born rats to H. influenzae-induced meningitis³⁹ and synergizes with the bacteria in the development of otitis media in the chinchilla.⁴⁰ A single study conducted in 1945 showed that infection with both influenza virus and H. influenzae killed mice at doses that were sublethal when either agent was administered alone.⁴¹ However, this study pre-dated modern immunological techniques, precluding assessment of the underlying mechanism.To investigate the pathobiological mechanisms further, we established a model of influenza and H. influenzae co-infection in mice. Herein, we report that H. influenzae synergizes with influenza virus to cause more severe disease in immunocompetent adult mice, leading to 100% lethality at doses that cause no mortality when the agents are give individually. The mechanism leading to disease exacerbation does not involve T or B cells, and thus appears to be mediated by innate immunity. However, tumor necrosis factor (TNF), interleukin-6 (IL-6), and Toll-like receptor (TLR)-4 are not essential for synergistic lethality in this model.     

Hepatitis C virus infection and lichen planus: a short review

OBJECTIVE: To review the current literature regarding the association of lichen planus (LP) and liver disease, with particular attention to the association of the oral variant of the disease with hepatitis C virus (HCV) infection.
MATERIALS AND METHODS: Available literature of the possible association of LP with systemic disorders, in particular chronic hepatic disease, has been reviewed. RESULTS: LP is sometimes associated with infectious or autoimmune disease and/or neoplasia, however an aetio-logical association between LP and these disorders seems unlikely. A more consistent association exists between LP and chronic hepatic disease. The precise cause of this association is not known. However, in the last 6 years a notable association between HCV infection and LP has been observed, particularly in patients in Spain, Italy and Japan. The pathogenesis of this possible HCV-associated LP is not known, but it may involve a cell mediated response to an altered epithelial antigen.
CONCLUSION: There is now evidence to suggest a significant association between HCV infection and LP in some groups of patients.     

Angioedema and swellings of the orofacial region

OBJECTIVE: Patients may have various forms of angioedema and require dental treatment which can cause or contribute to the onset of an episode of angioedema. This paper seeks to highlight the causes and the management of this serious condition.
DESIGN: An outline of the different types of angioedema is given here, along with three case reports which illustrate treatment and management.
SUBJECTS AND METHODS: Three patients who presented to an Oral Medicine clinic with angioedema are presented to illustrate various types of angioedema and the different contributing factors that precipitated episodes of the condition.
MAIN OUTCOME MEASURES: The three patients were all investigated for biochemical and allergic factors which may have caused their disease.
RESULTS: Both drugs and dental materials were shown to be involved in the pathogenesis of angioedema in this short series of patients.
CONCLUSIONS: Dental treatment or the use of some materials may promote or contribute to the disorder. Referral to hospital for specialist care is indicated for certain groups of patients who require invasive dental treatment. The multi-disciplinary team approach in the investigation and management of patients with angioedema is emphasised.