High vs mid thoracic epidural analgesia – A comparative study on the ease of insertion and effects on pain, hemodynamics, and oxygenation in patients undergoing thoracotomies

Background: Thoracic epidural analgesia offers effective perioperative pain relief in patients undergoing thoracotomies apart from attenuating stress responses. It helps in fast tracking by facilitating early mobilization and improving respiratory function. Literature on high (T1–T2 level) thoracic segmental analgesia for thoracotomy is less. Aim: The aim of present study was to compare the ease of insertion, effect on pain relief in high (T1–T2 level) vs mid (T5–T6) approach of thoracic epidural. Setting and Design: The present study was a randomized control trial conducted at our institute. Materials and Methods: About 52 patients aged between 18–65 years scheduled for elective thoracotomies under general and thoracic epidural anesthesia were randomized into two groups. Intraoperatively ease of epidural insertion, extent of blockade, and postoperatively pain relief were assessed. Ropivacaine with fentanyl was used for epidural analgesia. Statistical Analysis: Data were presented as mean ± standard deviation and analyzed by the Student's t test, Chi-square test, and non-parametric test whereever applicable. A P value <0.05 was considered statistically significant. Results: We observed that high thoracic epidural anesthesia was easier to place (time taken 123.42 vs 303.08 s) P < 0.05, with less number of attempts (1.27 vs 1.92) P < 0.05. Extent of blockade, postoperative pain scores, rescue analgesia requirement, hemodynamics, and oxygenation were comparable. Conclusion: We conclude that high thoracic epidural is easier to insert, provides adequate pain relief, and stable hemodynamics with the advantage of patient comfort and safety.

Neurogenic stress cardiomyopathy: What do we need to know

The interaction between the heart and brain is complex and integral to the maintenance of normal cardiovascular function. Even in the absence of coronary disease, acute neuronal injury can induce a variety of cardiac changes. Recent neuroimaging data revealed a network including the insular cortex, anterior cingulate gyrus, and amygdala playing a crucial role in the regulation of central autonomic nervous system. Damage in these areas has been associated with arrhythmia, myocardial injury, higher plasma levels of brain natriuretic peptide, catecholamines, and glucose. Some patients after brain injury may die due to occult cardiac damage and functional impairment in the acute phase. Heart failure adversely influences acute stroke mortality. Troponin and NT-proBNP are elevated in acute brain injury patients, in response to the activated renin–angiotensin–aldosterone system and other neurohumoral changes, as a protective mechanism for sympathoinhibitory activity. Such patients have been shown to be associated with higher short- and long-term mortality. While thrombolysis, neuroprotection, and other measures, alone or in combination, may limit the cerebral damage, attention should also be directed toward the myocardial protection. Early administration of cardioprotective medication aimed at reducing increased sympathetic tone may have a role in myocardial protection in stroke patients. For a full understanding of the brain–heart control, the consequences of disruption of this control, the true incidence of cardiac effects of stroke, and the evidence-based treatment options further research are needed.