Preparation of the patient and the airway for awake intubation

Awake intubation is usually performed electively in the presence of a difficult airway. A detailed airway examination is time-consuming and often not feasible in an emergency. A simple 1-2-3 rule for airway examination allows one to identify potential airway difficulty within a minute. A more detailed airway examination can give a better idea about the exact nature of difficulty and the course of action to be taken to overcome it. When faced with an anticipated difficult airway, the anaesthesiologist needs to consider securing the airway in an awake state without the use of anaesthetic agents or muscle relaxants. As this can be highly discomforting to the patient, time and effort must be spent to prepare such patients both psychologically and pharmacologically for awake intubation. Psychological preparation is best initiated by an anaesthesiologist who explains the procedure in simple language. Sedative medications can be titrated to achieve patient comfort without compromising airway patency. Additional pharmacological preparation includes anaesthetising the airway through topical application of local anaesthetics and appropriate nerve blocks. When faced with a difficult airway, one should call for the difficult airway cart as well as for help from colleagues who have interest and expertise in airway management. Preoxygenation and monitoring during awake intubation is important. Anxious patients with a difficult airway may need to be intubated under general anaesthesia without muscle relaxants. Proper psychological and pharmacological preparation of the patient by an empathetic anaesthesiologist can go a long way in making awake intubation acceptable for all concerned

Effect of positive airway pressure during pre-oxygenation and induction of anaesthesia upon safe duration of apnoea

Background and Aims: Induction of general anaesthesia per se as also the use of 100% oxygen during induction of anaesthesia, results in the development of atelectasis in dependent lung regions within minutes of anaesthetic induction. We aimed to assess the effect of application of a continuous positive airway pressure (CPAP) of 5 cm H 2 O during pre-oxygenation and induction of anaesthesia on the period of apnoea before the occurrence of clinically significant desaturation. Methods: In this prospective, randomised, and double-blind study, 40 patients posted for elective surgery were enrolled. Duration of apnoea was measured as the time from the administration of succinylcholine hydrochloride to the time when oxygen saturation fell to 93%. Student′s t-test was used for comparing the duration of apnoea. Results: The safe duration of apnoea was found to be significantly longer in patients receiving CPAP of 5 cm H 2 O (Group P; n = 16) compared to the group receiving no CPAP (Group Z; n = 20), that is, 496.56 ± 71.68 s versus 273.00 ± 69.31 s (P < 0.001). Conclusion: The application of CPAP of 5 cm H 2 O using a Mapleson "A" circuit with a fixed positive end-expiratory pressure device during 5 min of pre-oxygenation with 100% oxygen prior to the induction of anaesthesia provides a clearly longer duration of apnoea before clinically significant arterial desaturation occurs

Effect of intravenous dexmedetomidine administered as bolus or as bolus-plus-infusion on subarachnoid anesthesia with hyperbaric bupivacaine

Background: Subarachnoid anesthesia is a widely practiced regional anesthetic for infraumbilical surgeries. Intravenous dexmedetomidine is known to prolong both sensory and motor blockade when administered along with subarachnoid anesthesia. Material and Methods: Seventy-five patients scheduled to undergo elective infraumbilical surgeries under subarachnoid anesthesia were randomly allocated to one of the three groups. Group B received intravenous saline over 10 min followed by 12.5 mg intrathecal bupivacaine and then intravenous saline over 60 min. Group bupivacaine + dexmedetomidine bolus (BDexB) received intravenous dexmedetomidine (1 μg/kg) over 10 min followed by 12.5 mg intrathecal bupivacaine and then intravenous saline over 60 min. Group bupivacaine + dexmedetomidine bolus-plus-infusion (BDexBI) received intravenous dexmedetomidine (0.5 μg/kg) over 10 min followed by 12.5 mg intrathecal bupivacaine and then intravenous dexmedetomidine (0.5 μg/kg) over 60 min. Onset of analgesia (at T10), complete motor block (Bromage score 3), and highest level of analgesia were noted. Sensory and motor levels were checked periodically till sensory recovery (at S2–S4) and complete motor recovery (Bromage score 0). Ramsay sedation score and incidence of bradycardia/hypotension were noted. Results: Sensory recovery was significantly longer in Group BDexB (303 min) and Group BdexBI (288 min) as compared to Group B (219.6 min). Motor recovery was also significantly prolonged in Group BDexB (321.6 min) and Group BDexBI (302.4 min) as compared to Group B (233.4 min). Patients receiving dexmedetomidine were sedated but were easily arousable. Conclusion: Intravenous dexmedetomidine given as bolus or bolus-plus-infusion with intrathecal hyperbaric bupivacaine prolongs both sensory and motor blockade

Diabetes and Risk of Sudden Death in Coronary Artery Disease Patients Without Severe Systolic Dysfunction

ObjectivesThis study sought to determine the absolute and relative associations of diabetes mellitus (DM) and hemoglobin A1c (HbA1c) with sudden and/or arrhythmic death (SAD) versus other modes of death in patients with coronary artery disease (CAD) who do not qualify for implantable cardioverter-defibrillators.BackgroundPatients with CAD and DM are at elevated risk for SAD; however, it is unclear whether these patients would benefit from implantable cardioverter-defibrillators given competing causes of death and/or whether HbA1c might augment SAD risk stratification.MethodsIn the PRE-DETERMINE study of 5,764 patients with CAD with left ventricular ejection fraction (LVEF) of &gt;30% to 35%, competing risk analyses were used to compare the absolute and relative risks of SAD versus non-SAD by DM status and HbA1c level and to identify risk factors for SAD among 1,782 patients with DM.ResultsOver a median follow-up of 6.8 years, DM and HbA1c were significantly associated with SAD and non-SAD (P&nbsp;&lt;&nbsp;0.05 for all comparisons); however, the cumulative incidence of non-SAD (19.2%; 95%&nbsp;CI: 17.3%-21.2%) was almost 4 times higher than SAD (4.8%; 95%&nbsp;CI: 3.8%-5.9%) in DM patients. A similar pattern of absolute risk was observed across categories of HbA1c. In analyses limited to patients with DM, HbA1c was not associated with SAD, whereas low LVEF, atrial fibrillation, and electrocardiogram measurements were associated with higher SAD risk.ConclusionsIn patients with CAD and LVEF of &gt;30% to 35%, patients with DM and/or elevated HbA1c are at much higher absolute risk of dying from non-SAD than SAD. Clinical risk markers, and not HbA1c, were associated with SAD risk in patients with DM. (PRE-DETERMINE: Biologic Markers and MRI SCD Cohort Study; NCT01114269)