Anesthesia in older patients is challenging and requires a range of skills in various techniques, both during surgery and in the post-operative period. Post-operative delirium is one of the most common cognitive dysfunctions after surgery, and elderly patients are at the highest risk. The pathophysiology of post-operative delirium remains incompletely understood. Several mechanisms (vascular, neurodegenerative, neuroimmune, neuroinflammation, drug-induced, stress-induced, and monoaminergic) have been considered to play a role. The type of anesthesia—general (gas, total intravenous), regional, or combined—was identified as a predictive factor. However, numerous prospective and retrospective studies have failed to determine which anesthetic technique is the best for preventing post-operative delirium. The type of surgery appears to be more critical than the type of anesthesia. However, the development of post-operative cognitive dysfunction could be linked to the depth of anesthesia. Dexmedetomidine displayed promising therapeutic potential for the efficient prevention or treatment of hyperactive post-operative delirium. The management of hypoactive post-operative delirium still requires further investigations, particularly in elderly patients.

Background/Objectives: Lactic acidosis is one of the most common causes of metabolic acidosis in hospitalized patients. It happens when lactic acid production exceeds lactic acid clearance. The elevation of lactate was commonly improved after the restoration of tissue perfusion. However, there are rare cases of severe lactate elevation (greater than 8 mmol/L) in the intraoperative period of thoracoscopic surgery. A poor prognosis with high morbidity and mortality characterizes these cases. Case Description: A 72-year-old man was admitted to the Soroka University Medical Center for thoracoscopic robotic left upper lobe lobectomy due to squamous cell carcinoma. At the end of surgery (overall, 8.5 h), the lactate level reached 10.2 mmol/L with the development of severe lactic metabolic acidosis. Thiamine was successfully given to patients to stimulate lactate clearance towards the cycle of tricarboxylic acids via pyruvate. Conclusions: Though the pathogenesis of this state in our case is not fully clear, it may have been induced by chemotherapy and during tumor manipulation by a surgeon. The successful recovery of blood lactic levels after thiamine treatment is suggestive of thiamine deficiency as a possible cause of lactic acidosis in our patient. Although we do not have data on the plasma thiamine level, we suggest that its determination in the perioperative period would be beneficial for excluding a probable thiamine deficiency in the case of severe lactic acidosis.