A study exploring the role of intercostal nerve damage in chronic pain after thoracic surgery.

OBJECTIVE: Our aim was to investigate the prevalence of intra-operative nerve damage and its association with chronic pain. METHODS: Our prospective study of 33 patients used nerve conduction studies to assess intercostal nerve function during elective thoracic surgical procedures. We used two methods to study nerve conduction: pre-operative magnetic stimulation (in 10 patients) and intra-operative nerve conduction studies (in all patients) We correlated these findings with specific intra-operative parameters, pain and psychological questionnaires pre-op and 3 month post-op and altered cutaneous sensation. RESULTS: Magstim (magnetic stimulation) assessments were not reliable and were therefore abandoned. Intraoperative intercostal nerve studies revealed two distinct patterns of nerve injury and also that nerve injury was less in those cases where a rib was not resected. However, intercostal nerve damage detected at the time of operation is not associated with chronic pain or altered cutaneous sensation at 3 months post-op. CONCLUSIONS: The study findings suggest that either the amount of intra-operative intercostal nerve damage is not indicative of long-term nerve damage or that there is a more significant cause for chronic pain other than intercostal nerve injury.

A questionnaire study investigating the prevalence of the neuropathic component of chronic pain after thoracic surgery.

OBJECTIVE: Our questionnaire study set out to assess the prevalence of chronic pain after thoracic surgery, the contribution of the neuropathic component of chronic pain and the impact of chronic pain on patients' lives. METHODS: A questionnaire was sent to 1152 patients who had undergone thoracic surgery in our department between 7 months and 7 years ago. The questionnaire was designed specifically for the study and included questions on neuropathic symptoms. Responses were correlated with data from our prospectively entered database for analysis. RESULTS: Nine hundred and forty-eight people were included in the study, of which 600 responded (63%). Prevalence of chronic pain is 57% at 7-12 months, 36% at 4-5 years and 21% at 6-7 years. Patient age, consultant and time since the operation all have significant effects. Surgical approach (video-assisted thoracoscopic surgery, thoracotomy) and diagnosis are not significant. Thirty-nine percent of those with pain take analgesia, 46% felt their pain is their worst medical problem and 40% reported it limits their daily activities. The prevalence of each neuropathic symptom is between 35 and 83%. The presence of a neuropathic symptom is associated with significantly more severe pain, more analgesia use and pain more likely to limit daily activity. CONCLUSIONS: Chronic pain has a significant prevalence and impact on patients' lives for several years after thoracic surgery. Nerve dysfunction is associated with more severe pain, a greater impact and tends to persist. The reason for the individual consultant being an important factor in post-thoracotomy pain needs further investigation.

Catastrophic haemoptysis during rigid bronchoscopy: a discussion of treatment options to salvage patients during catastrophic haemoptysis at rigid bronchoscopy.

OBJECTIVE: We report a negative experience of fatal haemorrhage during rigid bronchoscopy when an intrabronchial lesion was biopsied. Despite being prepared for and carrying out emergency sternotomy and clamping the lung hilum, the patient died. METHODS: We reviewed mainly non-surgical literature for recommendations for the management of catastrophic bleeding at bronchoscopy. RESULTS: The literature does provide advice for management of 'massive haemoptysis' defined as more than 600 ml in 24 h and 'exsanguinating haemoptysis' which is at least 1000 ml blood loss at a rate more than 150 ml/h. However there is little in the current surgical literature on the immediate treatment of 'catastrophic haemoptysis' which we define as major bleeding from the airway causing an immediate threat to life requiring immediate surgery. Gathering treatment options from various authors we present a suggested protocol for the management of this thoracic surgical emergency. CONCLUSIONS: We recommend the initial salvage treatment to be: (1) wedge the rigid bronchoscope into the haemorrhaging bronchus, (2) tamponade the bleeding site with a balloon-tipped vascular catheter, (3) remove the bronchoscope and intubate with a double-lumen tube, (4) undertake emergency definitive surgery. We strongly recommend that a suitable catheter be kept immediately available for this very rare but dangerous complication.

Lung volume reduction surgery in a ventilator-dependent patient.

In recent years lung volume reduction surgery (LVRS) has been advocated in a selected group of severe chronic obstructive pulmonary disease (COPD) patients. There are few reports of successful surgical intervention on ventilator-dependent patients. We present our own experience with a 53-year-old male who suffered an acute exacerbation of COPD and who could not be weaned off ventilation after 22 days. He underwent bilateral LVRS after which he was successfully weaned from ventilation. He is alive 4 years later with a satisfactory quality of life.

Changes in human immunodeficiency virus type 1 Gag at positions L449 and P453 are linked to I50V protease mutants in vivo and cause reduction of sensitivity to amprenavir and improved viral fitness in vitro.

Human immunodeficiency virus type 1 (HIV-1) Gag protease cleavage sites (CS) undergo sequence changes during the development of resistance to several protease inhibitors (PIs). We have analyzed the association of sequence variation at the p7/p1 and p1/p6 CS in conjunction with amprenavir (APV)-specific protease mutations following PI combination therapy with APV. Querying a central resistance data repository resulted in the detection of significant associations (P < 0.001) between the presence of APV protease signature mutations and Gag L449F (p1/p6 LP1'F) and P453L (p1/p6 PP5'L) CS changes. In population-based sequence analyses the I50V mutant was invariably linked to either L449F or P453L. Clonal analysis revealed that both CS mutations were never present in the same genome. Sequential plasma samples from one patient revealed a transition from I50V M46L P453L viruses at early time points to I50V M46I L449F viruses in later samples. Various combinations of the protease and Gag mutations were introduced into the HXB2 laboratory strain of HIV-1. In both single- and multiple-cycle assay systems and in the context of I50V, the L449F and P453L changes consistently increased the 50% inhibitory concentration of APV, while the CS changes alone had no measurable effect on inhibitor sensitivity. The decreased in vitro fitness of the I50V mutant was only partially improved by addition of either CS change (I50V M46I L449F mutant replicative capacity approximately 16% of that of wild-type virus). Western blot analysis of Pr55 Gag precursor cleavage products from infected-cell cultures indicated accumulation of uncleaved Gag p1-p6 in all I50V viruses without coexisting CS changes. Purified I50V protease catalyzed cleavage of decapeptides incorporating the L449F or P453L change 10-fold and 22-fold more efficiently than cleavage of the wild-type substrate, respectively. HIV-1 protease CS changes are selected during PI therapy and can have effects on both viral fitness and phenotypic resistance to PIs.