Background:The goal of awake craniotomy is to maintain adequate sedation, analgesia, respiratory, and hemodynamic stability and also to provide a cooperative patient for neurologic testing. An observational study carried out to evaluate the efficacy of dexmedetomidine sedation for awake craniotomy.Materials and Methods:Adult patients with age >18 year who underwent awake craniotomy for intracranial tumor surgery were enrolled. Those who were uncooperative and had difficult airway were excluded from the study. In the operating room, the patients received a bolus dose of dexmedetomidine 1 μg/kg followed by an infusion of 0.2–0.7 μg/kg/h (bispectral index target 60–80). Once the patients were sedated, scalp block was given with bupivacaine 0.25%. The data on hemodynamics at various stages of the procedure, intraoperative complications, total amount of fentanyl used, intravenous fluids required, blood loss and transfusion, duration of surgery, Intensive Care Unit (ICU), and hospital stay were collected. The patients were assessed for Glasgow outcome scale (GOS) score and patient satisfaction score (PSS).Results:A total of 27 patients underwent awake craniotomy during a period of 2 years. Most common intraoperative complication was seizures; observed in five patients (18.5%). None of these patients experienced any episode of desaturation. Two patients had tight brain for which propofol boluses were administered. The average fentanyl consumption was 161.5 ± 85.0 μg. The duration of surgery, ICU, and hospital stays were 231.5 ± 90.5 min, 14.5 ± 3.5 h, and 4.7 ± 1.5 days, respectively. The overall PSS was 8 and GOS was good in all the patients.Conclusion:The use of dexmedetomidine infusion with regional scalp block in patients undergoing awake craniotomy is safe and efficacious. The absence of major complications and higher PSS makes it close to an ideal agent for craniotomy in awake state.

Background: Preclinical studies have reported significant changes in the gut microbiome after traumatic brain injury (TBI). We hypothesized that TBI induces the growth of Proteobacteria in the human gut. Our primary outcome was to study the profile of the human fecal microbiome after TBI and the secondary outcome was to identify colonization with colistin-resistant and multidrug-resistant pathogens.Methods: Consecutive patients with moderate-severe TBI admitted to the neurotrauma-intensive care unit within 48 hours of injury were enrolled into this observational study. Samples from rectal swabs obtained on days 0, 3, and 7 after admission were assessed for microbial growth and antibiotic resistance. Demographic data and variables such as hypotension, blood transfusion, surgery, start of nasogastric feeding, use of antibiotics, length of hospital stay and mortality were noted.Results: One hundred one patients were enrolled into this study; 57 (56.4%) underwent surgery, 80 (79.2%) required blood transfusion, 15 (14.9%) had an episode of hypotension, 37 (36.6%) received enteral feed within the first 3 days, and 79 (78.2%) received antibiotics. Rectal microbiological samples were collected from 101, 95, and 85 patients on days 0, 3, and 7, respectively. All organisms isolated at the 3 time-points belonged to the Proteobacteria phylum, with Enterobacteriaceae forming the largest group. Colistin-resistant organisms were found in 17 (16.8%) of 101 patients and multidrug-resistant organisms in 25 (64.1%) of the 39 patients in whom isolates were tested against the entire panel of antimicrobials.Conclusion: TBI is associated with widespread colonization with Proteobacteria as early as 48 hours after injury. Colonization with colistin and multidrug-resistant organisms highlights the importance of the judicious use of antibiotics.

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A 50-year-old male weighing 70 kg was scheduled for awake craniotomy and excision of left temporal glioma under monitored anesthesia care. During the preoperative period, the heart rate (HR) was 67 beats/min (bpm) and blood pressure (BP) 132/68 mm Hg. Airway examination showed Mallampati Grade II. All the preoperative investigations including electrocardiogram (ECG) and chest X-ray were within normal limits. On the day of surgery, standard monitors such as ECG, non-invasive BP, pulse oximeter and oxygen nasal cannula with end-tidal CO 2 monitoring were connected. An arterial cannula was inserted in the left radial artery under local anesthesia. Loading dose of dexmedetomidine infusion 1 μg/kg over 10 min was started. Three minutes later, the BP started increasing along with simultaneous decrease in HR; the maximum effect occurred at 7 min (BP up to 211/96 mm Hg, mean BP 134 mm Hg, and HR up to 37 bpm). However, it was not associated with changes in ST-T wave in ECG. The patient was conscious without any complaints of chest pain or headache; respiratory rate and SpO 2 were 16 breaths/min and 98%, respectively. The loading dose of dexmedetomidine was stopped at 5 min and a maintenance infusion 0.5 ug/kg/h was continued. The hemodynamic parameters came back close to normal baseline values within 4 min and remained stable at 124/66-140/74 mm Hg and 50-55 bpm. Regional scalp block was given with 0.25% bupivacaine bilaterally, and surgery was carried out uneventfully. The hemodynamic parameters remained stable during the postoperative period.Here, we present a case of severe hypertension during dexmedetomidine loading infusion in a patient undergoing awake craniotomy. The anesthesia technique for awake craniotomy should provide adequate sedation, analgesia and ensure respiratory and hemodynamic stability. A safe and acceptable analgesic/amnesic state for these procedures can be provided by the use of dexmedetomidine, with or without the addition of an opioid. 1 Dexmedetomidine is a highly selective α 2 -agonist which has dose-dependent sedative, anxiolytic and analgesic effects without respiratory depression. In addition, sympatholytic and antinociceptive properties allow for hemodynamic stability at critical moments of neurosurgical stimulation. 2 The common side effects include hypotension, bradycardia, worsening of heart block and nausea. Dexmedetomidine may evoke a biphasic response to BP; a short hypertensive phase followed by subsequent hypotension. An initial transient rise with a reflex fall in HR is brought about by stimulation of α 2 B subtypes of receptors present in vascular smooth muscles. This is followed by fall in BP and HR due to inhibition of central sympathetic outflow and stimulation of presynaptic α 2 A receptors. Hypertension associated with dexmedetomidine is usually mild and transient. 3 In this patient, 7 min after initiation of the loading dose, the systolic BP increased to more than 200 mm Hg. The BP was normalized, after reduction of the infusion dose. The hypertensive response is a normal ...