Joseph A. Stirt

Increases in intracranial pressure from succinylcholine: prevention by prior nondepolarizing blockade

Whether succinylcholine causes an increase in intracranial pressure (ICP) in patients with brain lesions is uncertain and, if increased ICP does occur, its pathophysiology remains unknown. The authors investigated both the effect of succinylcholine on ICP and its modification with prior neuromuscular blockade by measuring ICP (subarachnoid bolt) in 13 consecutive patients with brain tumors who received succinylcholine both before and after complete neuromuscular blockade with vecuronium. Anesthesia was induced with thiopental, 6 mg · kg−1 iv, and nitrous oxide, 70% in oxygen, while ventilation was controlled (Paco2 = 37.2 mmHg ± 1.7 SE). Succinylcholine, 1 mg · kg−1 iv, was administered and ICP, heart rate (HR), and blood pressure (BP) were recorded until normal twitch tension was restored. Complete neuromuscular blockade was then established with vecuronium, 0.14 mg · kg−1 iv; 3 min later, succinylcholine, 1 mg · kg−1 iv, was repeated. The resulting changes in ICP, HR, and BP were recorded for 3 min. Following the first dose of succinylcholine, mean ICP increased from 15.2 mmHg ± 1.3 SE to 20.1 mmHg ± 2.0 SE (P < 0.05), with five of the patients sustaining increases in ICP of 9 mmHg or greater. In contrast, when succinylcholine was given after vecuronium-induced paralysis, no patient developed an increase in ICP greater than 3 mmHg (P < 0.05 compared with the incidence of ICP ≥ 9 mmHg observed after the first dose of succinylcholine). A second group of six patients received two doses of succinylcholine according to the same protocol but without an intervening dose of vecuronium. These patients sustained increased ICP after both doses of succinylcholine. The authors conclude that increases in ICP may be induced by succinylcholine in patients with compromised intracranial compliance and the possibility of such an increase should be considered in their anesthetic management. While the exact mechanism of this phenomenon remains unknown, the results indicate that complete neuromuscular blockade with vecuronium prevents succinylcholine-induced increases in ICP.

Defasciculation with metocurine prevents succinylcholine-induced increases in intracranial pressure

In order to determine whether a small, “defasciculating” dose of metocurine could prevent increases in intracranial pressure (ICP) induced by succinylcholine (Sch), the authors studied 12 patients (ages 25–79 yr) undergoing craniotomy for excision of malignant supratentorial gliomas. After insertion of a subarachnoid bolt for ICP monitoring and a radial arterial cannula for determination of blood pressure and blood gas tensions, six patients (group I) were randomly allocated to receive MTC 0.03 mg/kg 3 min before induction of general anesthesia with thiopental 4 mg/kg and nitrous oxide 70% in O2. Six other patients (group II) received saline 0.015 ml/kg instead of MTC, followed by the same induction sequence. After induction of anesthesia, ventilation was controlled by mask (Paco2, = 40 mmHg ± 2 SE), and arterial and intracranial pressures were allowed to stabilize. Four minutes after thiopental administration (7 min after MTC), after a 1-min period of relatively stable arterial pressure and ICP, Sch 1 mg/kg was administered as a bolus. ICP and blood pressure were recorded continuously until normal twitch tension was restored. In group I (MTC pretreatment), ICP did not change significantly from the mean value observed before Sch, 14 mmHg ± 2 SE. In group II (saline pretreatment), ICP increased from 11 mmHg ± 2 SE to 23 mmHg ± 4 SE (P < .05). This study not only confirms previous work showing that Sch may induce marked ICP increases in lightly anesthetized patients with intracranial mass lesions, but also indicates that pretreatment with a “defasciculating” dose of MTC can prevent these potentially deleterious ICP increases in patients known to be at risk.

Neuromuscular effects of atracurium in man.

The neuromuscular effects of atracurium were studied in 25 A. S. A. class I or II patients anesthetized by a N2O-O2narcotic technique. In five patients incremental doses of 0.05 to 0.1 mg/kg of atracurium were given intravenously every 3 minutes until approximately 95% depression of the evoked electromyographic (EMG) response of the adductor policus muscle was produced. This required 0.25 to 0.35 mg/kg of atracurium. The duration of block (return to 95% of control) was 25 to 50 minutes. In addition, four groups of five patients each received 0.15, 0.25, 0.375, or 0.6 mg/ kg of atracurium. The block produced by 0.15 mg/kg was 10% to 92% and lasted 8 to 55 minutes. The block produced by 0.25, 0.375, and 0.6 mg/kg was 95% or greater with a duration of action of 30 to 68 minutes, 52 to 70 minutes, and 65 to 95 minutes, respectively. Tracheal intubation was easily carried out in all patients in whom there was a block of 90% or greater. The block could be antagonized by the common clinical combination of atropine and neostigmine. Changes in heart rate and blood pressure following atracurium were less than 5%.

Aminophylline is a diazepam antagonist.

A 69-year-old, 56-kg, A.S.A. class 11, white man with urinary retention, was scheduled for cystoscopy and transurethral bladder neck resection. The patient had a history of heavy cigarette smoking and chronic bronchitis; he used no medications. Preoperative serum electrolyte levels were: sodium, 141 meq/L; potassium, 4.4 meq/L; chloride, 105 meq/L; and bicarbonate, 27.9 meq/L; glucose was 110 mg/ 100 ml. Prothrombin and partial thromboplastin times were within normal limits, and urinalysis and electrocardiogram findings were normal. A chest roentgenogram showed no acute disease. The patient was not premedicated. Immediately before induction of anesthesia, blood pressure (BP) was 120/80 torr, heart rate (HR) was 90 beats per minute, and respiratory rate (RR) was 16 breaths per minute. Anesthesia was induced with diazepam administered into a rapidly flowing intravenous line containing 5% dextrose and Ringer’s lactate solution. After 10 mg of diazepam at 11:24 a.m., the patient’s eyes slowly closed at 11:25 a.m., and the eyelid reflex disappeared after another 10 mg, a total of 20 mg at 11:26 a.m. A mixture of 60% NzO and 40% 0 2 via mask and a semiclosed circle system was begun at 11:26 am., and at 11:27 a.m. another 10 mg of diazepam was administered. At this time BP was 105/70 torr, HR was 90 beats per minute, and RR was 20 breaths per minute. At 11:28 a.m. surgical preparation was begun, with no response from the spontaneously breathing patient. An additional 10 mg of diazepam was administered at 11:29 a.m., again at 11:32 a.m., and again at 11:34 a.m., to a total of 60 mg. Vital signs remained unchanged. At 11:35 a.m. succinylcholine, 60 mg IV, was administered without subsequent fasciculations, and cystoscopy was begun at 11:

Lidocaine pharmacokinetics in children during general anesthesia.

In spite of the increasing use of intravenous lidocaine in the operating room, no pharmacokinetic data exist for intravenous lidocaine in children. We studied ten children, ages 0.5–3 yr, and eight adults to determine lidocaine pharmacokinetics during anesthesia with halothane, nitrous oxide, and oxygen. After induction of anesthesia, tracheal intubation, and insertion of venous and arterial catheters, lidocaine, 1 mg/kg, was infused intravenously over 30 sec. Arterial samples were drawn at 0.5, 1, 2, 4, 5, 10, 15, 30, 60, 90, and 120 min. Plasma was separated and analyzed for lidocaine, using gas chromatography. Plasma concentration vs time data were fitted to a two-compartment model.Using standard formulas, we derived the following data: Children: distribution half-life (t1/2α) 3.2 min, elimination half-life (t1/2β) 58 min, volume of the central compartment (V1) 0.22 L/kg, volume of distribution (Vd area) 1.1 L/kg, and total plasma clearance (Cl) 11.1 ml·kg−1·min−1. Adults: t1/2α 3.6 min, t1/243 min, V1 0.16 L/kg, Vd area 0.71 L/kg, and Cl 9.8 ml·kg−1·min−1. No significant differences were found between children and adults for all parameters analyzed. We conclude that children older than 6 months of age distribute and eliminate intravenous lidocaine in the same manner as adults.

Anesthetic problems in Rubinstein-Taybi syndrome.

Rubinstein-Taybi syndrome is a congenital anomaly characterized b y broad thumbs and first toes, facial abnormalities, and mental retardation (1, 2). There are no published reports of anesthetic-related problems in patients with this syndrome. I describe here the rather eventful course of three separate anesthetics administered over a period of 12 years to a single patient with Rubinstein-Taybi syndrome.

Anisocoria after anaesthesia

Unequal pupil size following anaesthesia is an unsettling finding, suggestive of acute, perioperative intracranial pathology. We report here an unusual cause of anisocoria after anaesthesia: unintended entrance of phenyle-phrine nasal vasoconstrictor solution into the eye.RésuméDes pupilles de diamètre inégal après l’ anesthésie restent un problème non résolu suggérant une pathologie algue intracrânienne péri-opératoire. On rapporte le cas d’ une cause inhabituelle d’nisocorie après anesthésie: l’entrée involontaire dans l’ œil d’ une solution de phénylephrine administrée pour vasoconstriction nasale.

Intracranial pressure after atracurium in neurosurgical patients.

In order to investigate the usefulness of atracurium for neurosurgical anesthesia, we studied its impact on intracranial pressure (subarachnoid bolt) mean arterial pressure (radial artery catheter) and cerebral perfusion pressure (mean arterial pressure-intracranial pressure) in 20 patients undergoing elective craniotomy for brain tumor excision. General anesthesia was induced with thiopental, 4 mg/kg intravenously, and maintained with 70 percent nitrous oxide in oxygen. Ventilation was controlled by face mask, with end-tidal CO2 held constant. Once intracranial pressure and mean arterial pressure had stabilized, the response to atracurium, 0.5 nig/kg intravenously, was continuously recorded for 5 min in 10 patients. An additional 10 patients received no atracurium and served as matched controls. Thiopental caused reductions in ICP in both groups of patients. Comparing the responses of the patients who received atracurium with those who did not, we found that atracurium had no significant effect on intracranial pressure, mean arterial pressure or cerebral perfusion pressure. Based on these data we conclude that atracurium appears to be preferable to the other available neuromuscular blocking agents that have been evaluated for neurosurgical anesthesia.

Atracurium, vecuronium, and intraocular pressure in humans

: We studied 60 nonophthalmologic patients, allocated to six treatment groups, to assess the effects of atracurium and vecuronium on intraocular pressure (IOP). All patients had IOP measured while awake, using pneumotonometry. In group 1, anesthesia was induced with thiopental, 5 mg/kg, and maintained with N2O, 70% in O2, using controlled mask ventilation, for 5 min. These patients then received atracurium, 0.5 mg/kg. After 5 additional minutes of ventilation, the trachea was intubated. From 1 min after thiopental administration until 1 min after intubation, IOP was recorded every minute. Patients in groups 2, 3, and 4 were treated identically to those in group 1, except the muscle relaxant given was atracurium, 1.0 mg/kg, vecuronium, 0.1 mg/kg, or vecuronium, 0.2 mg/kg, respectively. Patients in groups 5 and 6 underwent rapid sequence induction with thiopental, 5 mg/kg, and atracurium, 1.0 mg/kg, or vecuronium, 0.2 mg/kg, respectively. IOP was measured 1 min later, followed by intubation and IOP measurements for the next 3 min. Intraocular pressure decreased significantly in groups 1, 2, 4, and 6 after thiopental and remained stable in all groups during ventilation with N2O. Neither atracurium nor vecuronium affected IOP, nor was there any correlation between IOP and degree of neuromuscular blockade. However, IOP increased significantly after intubation in all six groups. We conclude that atracurium or vecuronium alone has no adverse effects on IOP.

Lack of arrhythmogenicity of isoflurane following administration of aminophylline in dogs.

Induction of halothane anesthesia after aminophylline administration may cause ventricular arrhythmias. Isoflurane may be as effective a bronchodilator as halothane. This study was designed to determine whether induction of isoflurane anesthesia after intravenous aminophylline is arrhythmogenic in dogs. One group of six dogs was anesthetized with 1.5% isoflurane in the absence of aminophylline. Three additional groups of six dogs were given intravenous aminophylline 10, 25, or 50 mg/kg, respectively, followed 3 min later by 1.5% isoflurane. No arrhythmias occurred after aminophylline and isoflurane at any time in any animal. In contrast to halothane, induction of isoflurane anesthesia after aminophylline is safe and does not cause cardiac arrhythmias.