Prophylactic esmolol infusion for the control of cardiovascular responses to extubation after intracranial surgery.

INTRODUCTION: Emergence from general anaesthesia and extubation are often accompanied by significant surges in heart rate and blood pressure. To document these changes and the efficacy of low-dose beta-blocker infusions in ameliorating these rises, we undertook a descriptive dose-ranging study comparing the use of esmolol to placebo in patients emerging from neuro-anaesthesia. MATERIALS AND METHODS: Thirty-six patients undergoing intracranial surgery were randomised to receive saline, esmolol 100 micrograms/kg/min or 200 micrograms/kg/min infusions. The number of patients developing severe hypertension or tachycardia in each group was compared using Fisher's exact test. RESULTS: Systolic blood pressure (SBP) and heart rate (HR) increased in all 3 groups during emergence and peaked at extubation. The proportion of patients with severe tachycardia or hypertension was reduced from 92% in the placebo group to 40% (P = 0.02) and 8% (P = 0.001) in the low and intermediate dose esmolol groups, respectively. Results were better in the intermediate dose group but the difference was not statistically significant. Two patients from the esmolol infusion groups required supplemental medication for bradycardia. CONCLUSION: Severe hypertension or tachycardia occurs in 92% of patients during extubation following neuro-anaesthesia and warrants the consideration of routine prophylaxis. Prophylactic esmolol infusion for the control of haemodynamic disturbances during extubation is feasible and safe. A modest level of obtundation is evident at 100 micrograms/kg/min but a rate of 200 micrograms/kg/min may prove to be more effective.

Diabetes insipidus in neurosurgical patients.

Diabetes insipidus (DI) is an uncommon but important complication in the neurosurgical population. This retrospective study aimed to determine the incidence, profile and outcome of patients admitted to an 18-bedded neurosurgical intensive care unit who developed DI. The overall incidence was 3.7% (29/792 admissions). Aetiologies included subarachnoid haemorrhage (12/29), severe head injury (11/29), post-surgical excision of craniopharyngioma or pituitary adenoma (5/29) and acute haemorrhagic stroke (1/29). All patients were treated with a regime of fluid replacement, electrolyte correction, parenteral or intranasal desmopressin (DDAVP), or parenteral pitressin. Overall mortality was 72.4%. There were no deaths in the patients who underwent excision of tumours. Complications included acute pulmonary oedema, hypernatremia and hypokalaemia. The development of DI was found to be associated with impending brain death and mortality in the majority of patients with subarachnoid haemorrhage and severe head injury. However, careful diagnosis and management of DI after hypothalamo-neurohypophyseal surgery did not result in any permanent neurological sequelae.

A case of pseudohyperkalaemia and thrombocytosis.

An unusual cause of "hyperkalaemia" was observed in a neurosurgical patient admitted to our intensive care unit. The cause of the hyperkalaemia was not known initially and treatment with cation ion exchange resin was initiated to lower the elevated serum potassium level. The concurrent occurrence of thrombocytosis and hyperkalaemia raised the possibility of psuedohyperkalaemia associated with thrombocytosis. Simultaneous measurement of plasma and serum potassium with the Hitachi 917 Analyzer (indirect ion selective electrode, coefficient of variation = 1% to 2%) confirmed the diagnosis. Correlation between thrombocytosis and pseudohyperkalaemia was found to be highly significant (r = 0.54; P = 0.014). It is estimated that for for every 100 x 10(9)/L of platelets, an increase of 0.07 to 0.15 mmol/L of potassium is expected. In thrombocytosis, plasma rather than serum potassium should be measured.

Severe laryngospasm without intravenous access--a case report and literature review of the non-intravenous routes of administration of suxamethonium.

Severe laryngospasm may occur during inhalational induction of paediatric patients. Effective and rapid treatment of this complication is extremely important to prevent severe hypoxia. The treatment of choice is intravenous suxamethonium if muscle relaxation is desired. However, in the absence of intravenous access, alternate routes of administration have to be considered. The rapidity and the effectiveness in treating laryngospasm by these non-intravenous routes are important to the outcome of the patient. Though the intramuscular route may be relatively slower in onset time (time taken to reach maximum effect of paralysis) compared with the intravenous route, clinical experience so far indicates satisfactory result in the treatment of laryngospasm. Current evidences indicate that the intraosseous route is probably superior to the intramuscular route and comparable to the intravenous route in terms of onset time.

Tracheostomy in a neuro-intensive care setting: indications and timing.

A retrospective review was made of 49 survivors who were mechanically ventilated for more than 48 hours in the neurosurgical ICU. Thirty-two patients (Gp I) were successfully extubated, 9 patients (Gp II) underwent tracheostomy after one or more failed extubations, and 8 patients (Gp III) underwent elective tracheostomy. Glasgow Coma Scale (GCS) scores at extubation were 11.3 +/- 2.8 (mean (SD) for Gp I vs 7.8 +/- 2.7 for Gp II (P = n.s.) and at elective tracheostomy (Gp III) was 5.4 +/- 2.3. Incidence of ventilator-associated pneumonia were 35% in Gp I vs 100% of patients in Gp II and III (P < 0.05). Reasons for reintubation in 7 of 9 patients (Gp II) were upper airway obstruction and tenacious tracheal secretions while 14 of 17 patients were weaned off the ventilator within 48 hours of tracheostomy. The length of stay in ICU was 16.8 +/- 7.1 days in Gp II vs 11.7 +/- 2.9 days in Gp III (P < 0.05). In our study, elective tracheostomy for selected patients with poor GCS scores and nosocomial pneumonia has resulted in shortened ICU length of stay and rapid weaning from ventilatory support.

Spread of spinal anaesthesia with 0.5% bupivacaine: influence of the vertebral interspace and speed of injection.

Three millilitres of plain 0.5% bupivacaine were injected intrathecally at two different spinal interspaces (L2/3 and L4/5) and at two different speeds (15 and 30 sec) in four groups of ten patients. Injection at L2/3 over 15 sec produced a significantly higher mean maximum spread of analgesia (T6.4) when compared to injection at L4-5 over 15 sec (T10.3) (P < 0.05). Over the same interspace L2/3, injection over 15 sec also produced a higher level of spread as compared to the 30 sec group (p < 0.05). At 15 min there was a greater fall in blood pressure in the L2/3 15 sec group when compared to the other groups (p < 0.01). There was a further decrease in the blood pressure in L2/3 15 sec and L4/5 30 sec groups after 30 minutes of blockade (p < 0.01). Therefore close monitoring of cardiovascular parameters must be continued for at least 30 min in spinal anaesthesia with bupivacaine.

Intravenous sedation for upper gastrointestinal endoscopy: Midazolam versus propofol.

Propofol was compared with Midazolam for sedation during upper gastrointestinal endoscopy in a randomised, double blind study. Both drugs were equally acceptable to endoscopists and patients. There was significant oxygen desaturation after sedation and during endoscopy (p < 10(-6)). Significantly more patients in the propofol group could remember the diagnosis which was revealed to them immediately after the gastroscopy (p < 0.001).