Delayed awakening from anesthesia following electrolyte and acid-base disorders, two cases

Delayed awakening from anesthesia remains one of the biggest challenges that involve anesthesiologists. Most commonly, delayed awakening is due to drugs effects persistence. Metabolic [like hypo- hyperglycemia], electrolyte, acid-base disorders and hypothermia may cause delayed emergence from anesthesia. Structural disorders of cerebral nervous system [like increase in intracranial pressure, brain ischemia] and psychological disorders can be regarded as other uncommon causes of this condition. Hypokalemia is induced by low potassium intake, excessive excretion from gastrointestinal [GI] and kidneys [like using diuretics] or a shift from extracellular space into intracellular space. In these two reported cases, although proper measures had been taken to reverse the effects of anesthetic drugs, the patients did not regain their consciousness as fast as expected. The only significant finding in postoperative tests, along with respiratory alkalosis, was low serum potassium level [K=2.5 and K=2.9 in the first and the second patients, respectively]. Correction of serum potassium [to K=3.3 and K=3.2 in the first and the second, respectively] improved patients level of consciousness, and they were discharged from intensive care unit [ICU] with good general condition. During surgery; pain, stress, sympathetic increase, catecholamine release and the consequent beta-stimulation, certain drugs, and respiratory alkalosis due to hyperventilation may cause acute shift of potassium into the cells, which will be intensified in the patients with preoperative hypokalemia. Hypokalemia induces consciousness impairment and increases muscle relaxation, both of which affect patient awakening. Serum potassium evaluation is recommended in cases of delayed emergence from anesthesia.

[ incidence of hypotension, nausea and vomiting after spinal anesthesia for elective caesarean section: a comparison between bupivacaine 0.5% and lidocaine 5%]

Hypotension and nausea are common side effects during spinal anesthesia. This study compared the incidence of hypotension and nausea-vomiting induced by bupivacaine and lidocaine in parturients undergoing caesarean section under spinal anaesthesia. In this clinical trial, 120 parturients undergoing caesarean section were randomly allocated into two groups. 60 patients received subarachnoid lidocaine 5% [75-100 mg] and the other group of patients received bupivacaine 0.5% [12-15 mg]. If systolic blood pressure decreased to 80 mm Hg or less than 70% of the pre-anesthesia value, 5mg ephedrine was injected. We evaluated Blood pressure each 3 minutes up to 15 min and every 5 min thereafter till the end of the recovery stay. There was no statistically significant difference in the incidence of nausea -vomiting between the two groups after spinal anesthesia. On the other hand, there was significant difference in systolic blood pressure 12 minutes after the procedure and also a significant difference was noted in diastolic blood pressure 3, 9, 15, and 40 minutes after performing spinal anesthesia [P < 0.05]. The amount of ephedrine used in both groups did not show either any significant difference. Intrathecal bupivacaine may yield more hemodynamic stability than intrathecal lidocaine in elective cesarean section