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A 29-year-old male admitted with severe traumatic brain injury following a road traffic accident was sedated and ventilated uneventfully for 72 h. On the fourth posttrauma day, after stopping sedation to assess readiness for extubation, he developed sudden onset desaturation; arterial blood gas showed severe diffusion defect with very low PaO2/FiO2 ratio following an episode of generalized tonic-clonic seizure. The differential diagnoses and further management are discussed.

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Title Utility of transcranial Doppler (TCD) in estimating cerebral perfusion pressure (eCPP) in traumatic brain injury—a prospective observational trial. Aim To validate the utility of a noninvasive technique of eCPP estimation using transcranial Doppler (TCD). Materials and Methods Eighteen patients with severe traumatic brain injury (TBI) requiring intracranial pressure (ICP) monitoring as per the Brain Trauma Foundation guidelines were prospectively recruited for the study. ICP was measured in all patients using an intraventricular catheter. Mean arterial pressure (MAP) was recorded from an intra-arterial catheter. Cerebral perfusion pressure (CPP) was calculated as the difference between MAP and ICP. Middle cerebral blood flow velocities were recorded using TCD, and CPP was estimated from the middle cerebral artery (MCA) flow velocities (eCPP) using the formula eCPP = (MAP × end diastolic velocity [EDV]/mean velocity [MV]) + 14. Total 185 simultaneous readings of CPP and eCPP were available for analysis. Reliability statistics between CPP and eCPP were computed to calculate the intraclass correlation (ICC). Results The average CPP measured using intraventricular catheter was 73.2 (+/−12.4), and the mean estimated eCPP was 76.7 (+/−10.9). We found a very good Pearson's correlation between CPP and eCPP (r = 0.743) with a Cronbach's α of 0.843. In 86.2% of examinations, the estimation error of measuring CPP was within 10 mm Hg, and in 93.1% examinations, it was within 15 mm Hg. Conclusion eCPP estimated using TCD can serve as reliable noninvasive alternative in situations in which ICP monitoring is not available, even in moderate or mild head injury.

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Two different regimes propofol-normal saline vs propofol -ephedrine in prevention of hypotension during induction of anaesthesia, significant decrease in Systolic blood pressure (P<0.001) in both groups (both fluid and non-fluid groups) after induction of anaesthesia with propofol was observed. The incidence of hypo-tension was significant in control and crystalloid group when compared with ephedrine group. Systolic blood pressure decreased in all three groups and decrease in Systolic blood pressure at 2min, 3min and 5min with P values. 0.010, 0.00, 0.000 respectively. Also decrease in Mean Arterial pressure in P group when compared with E-group at 1, 2, 3, 4, and 5min with P values 0.038, 0.02, 0.012 and 0.029 respectively.

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A 46-year-old female with intraventricular space occupying lesion was posted for craniotomy and excision of the same. Immediately following routine induction of general anaesthesia and a bougie-guided intubation, she developed increased airway pressures and desaturation associated with a decreased air entry on the right side of the chest suggestive of a right-sided pneumothorax which was confirmed with radio imaging and following the placement of chest drain the saturation improved and airway pressures decreased. To be faced with a pneumothorax following an intubation could be surprising for a non-suspecting anaesthesiologist and it can have important implications especially in neurosurgical cases where a tight control of intracranial pressure is warranted. Hence, this case report emphasises the need for a high index of clinical suspicion for proper management and safe patient outcome.