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Background: Understanding the risk of conversion from video-assisted thoracic surgery (VATS) to thoracotomy is important when considering patient selection and preoperative surgical risk assessment. This review aims to estimate the rate of intraoperative conversions to thoracotomy, predictive factors, and associated outcomes for VATS anatomic lung resections. Methods: PubMed/MEDLINE and EMBASE were searched systematically in May of 2020. Observational studies examining conversions of VATS anatomic resections to thoracotomy were included. Conversion rates, causes, risk factors, and post-operative outcomes were reviewed and analyzed in aggregate. Results: Twenty retrospective studies were reviewed, with a total of 72,932 patients undergoing VATS anatomic lung resection. The median conversion rate was 9.6% (95% CI: 6.6-13.9%). Nine studies reported a total of 114 emergency conversions, with a median incidence rate of 1.3% (95% CI: 0.6-2.8%). The most common reasons for thoracotomy were vascular injury/bleeding, difficulty lymph node dissection, and adhesions, accounting for 27.9%, 26.2% and 19% of conversions, respectively. Risk factors for conversion varied, but frequently included nodal disease, large tumors, and induction therapy. The risk of complications (OR 2.06; 95% CI: 1.77-2.40) and mortality (OR 4.11; 95% CI: 1.59-10.61) were significantly increased following conversions. There was also a significant increase in chest tube duration and length of stay following conversion. Conclusions: The risk of conversion to thoracotomy may be as high as one in ten patients undergoing VATS anatomic lung resections, but may vary significantly based on patient selection. Although emergent conversions are rare, the need for thoracotomy may significantly increase postoperative morbidity and mortality.

Previous studies have suggested that increased norepinephrine plays an important role in recovery of function after brain injury; however, the majority of these studies used drugs that are known to also affect other monoamines to increase or decrease norepinephrine. The purpose of the present study was to determine if norepinephrine is required to promote recovery after ischemia. A form of enriched rehabilitation was used to rehabilitate animals after ischemia and the neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine was used to selectively destroy norepinephrine projections from the locus coeruleus. Three sensorimotor tests were used to evaluate the recovery of the animals. Depletion of norepinephrine improved sensorimotor recovery in standard-housed animals and did not impede recovery in the rehabilitation groups. Dopamine beta hydroxylase staining was used to confirm N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine-depleted terminal norepinephrine levels. The amount of norepinephrine terminal staining negatively correlated with recovery of function in the staircase test after ischemia. In addition, enriched rehabilitation increased, but depletion of norepinephrine had no effect on, brain-derived neurotrophic factor protein levels, which have also been linked to improved recovery of function. Together the above findings question the previously postulated role of norepinephrine in recovery of function after stroke.

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