Diagnosis and management of transient neurologic symptoms following subarachnoid block with single-shot isobaric 2% lidocaine.

Hyperbaric 5% lidocaine has been used extensively for spinal anesthesia for the last 50 yr. The implication of lidocaine as specifically etiologic for transient neurologic symptoms (TNS) has led to increasing focus on lidocaine spinal anesthesia and reports of TNS with single-shot, hyperbaric lidocaine. We report the details of a case of TNS associated with single-shot, isobaric 2% lidocaine in a 69-year-old female, scheduled for outpatient hysteroscopy, dilatation and curettage, and endometrial biopsy while placed in the lithotomy position.

Perioperative cardiovascular morbidity in patients with coronary artery disease undergoing vascular surgery after percutaneous transluminal coronary angioplasty.

OBJECTIVE: Patients with coronary artery disease (CAD) who undergo noncardiac surgery are at increased risk for perioperative myocardial infarction (PMI). Undergoing successful coronary artery bypass grafting (CABG) before such surgery has been shown to decrease perioperative cardiac morbidity and mortality. Percutaneous transluminal coronary angioplasty (PTCA) is an alternative treatment for these patients. Perioperative cardiac morbidity in patients with CAD who underwent PTCA before their vascular surgery was reviewed. SETTING: A tertiary care referral center for patients with cardiovascular heart disease. PARTICIPANTS: Review of vascular surgery database for patients who underwent vascular surgery preceded by PTCA between 1984 and 1995. Patients were excluded if they had a history of CABG within 2 years of surgery, had PTCA more than 18 months before surgery, or had incomplete data. MEASUREMENTS: Data were collected concerning cardiac history, left ventricular (LV) function, perioperative cardiac morbidity (angina, MI, congestive heart failure [CHF], and arrhythmias). MAIN RESULTS: Of 194 patients who underwent aortic abdominal surgery, carotid endarterectomy (CEA), or peripheral vascular surgery preceded by PTCA, 104 (54%) had a previous MI. Twenty-six patients (13.4%) had perioperative cardiac morbidity. Only one patient had an MI (0.5%; 95% confidence interval [CI], 0.0 to 2.8), whereas one patient died of CHF followed by multisystem organ failure (0.5%). The median interval between PTCA and surgery was 11 days (interquartile range, [IQR] 3 to 49 days). Patients who developed perioperative cardiac morbidity were older than those who did not (p = 0.02). Patients who had a history of CABG (before PTCA) had a higher incidence of postoperative angina (p = 0.04). The degree of preoperative LV dysfunction was linearly related to the incidence of new postoperative CHF (p = 0.01). Arrhythmias were more common in patients undergoing abdominal vascular surgery (17.9%) than in those undergoing CEA (2.5%; p = 0.03) or peripheral vascular surgery (5.2%; p = 0.02). CONCLUSION: High-risk cardiac patients undergoing vascular surgery who have had PTCA performed up to 18 months preoperatively have a low incidence of perioperative cardiac morbidity. Prophylactic PTCA may be beneficial in patients with CAD who are at high risk for perioperative cardiac complications.

Bilobar atelectasis after difficult tracheal intubation.

Acute intra-operative collapse of a lobe without apparent cause is rare. We report a case of transient bilobar atelectasis that developed without any apparent cause after a difficult tracheal intubation in a healthy young patient. Intrabronchial obstruction was ruled out by bronchoscopy. The bilobar atelectasis developed acutely and resolved quickly with mechanical ventilation. The characteristics of the lung collapse were atypical, suggesting either its reflex nature or acute reduction of lung volume owing to intubation-induced coughing. We present a review of the mechanisms of atelectasis.

A pharmacokinetic-pharmacodynamic model for a muscle relaxant: atracurium.

Our goal was to develop a pharmacokinetic-pharmacodynamic model that describes the fate of atracurium and its metabolite laudanosine as well as the time course of the neuromuscular block. The model was based on the consideration of mass balance of atracurium and was constructed by postulating an effect compartment linked to the central compartment in the previously described open mammillary model for atracurium. The entry and exit rate constants, kCE and kEC, were adjusted to satisfy the requirement that the peak amount in the effect compartment coincides with the peak submaximal block. We used previously published clinical data to arrive at the times to 50% neuromuscular block either during the onset of the block following an ED50 dose or during the recovery following larger doses of atracurium. Laplace transforms were used to define the model, and the solution was obtained by iterative numeric adjustments of the rate constants. The model provides an excellent fit of the observed plasma concentrations of atracurium and laudanosine and simulates well the development and waning of the neuromuscular block. The model projects that the peak amount of atracurium in the effect compartment amounts to 14% of the injected dose and is reached at 7.6 min after the injection.

Onset of the nondepolarizing neuromuscular block in humans: quantitative aspects.

The purpose of our study was a unified description of the time course for the onset of the neuromuscular block produced by different muscle relaxants after bolus intravenous injections. The environment of the receptors on the motor end plate was assumed to be a part of the interstitial space of the muscle. A unified consideration of four muscle relaxants was accomplished by expressing the concentrations of each relaxant in the interstitial space as multiples of the relaxant's dissociation constant. A flow-limited model was developed to describe the time course of the relaxant's concentration in the interstitial space as a function of its plasma concentration, the plasma flow to the muscle, and the volume of the interstitial space. The results show that those relaxants whose plasma concentrations decrease rapidly achieve an earlier (4-8 min), but relatively lower, peak concentration in the interstitial space. The relaxants with more sustained plasma concentrations reach the peak concentration later, 9-16 min after the bolus intravenous injection. The model allows the interpretation of several observations encountered with the clinical use of the muscle relaxants.

Pharmacokinetic modelling of a parent drug and its metabolite. Atracurium and laudanosine.

A pharmacokinetic model was designed to describe simultaneously the plasma concentrations of atracurium and its metabolite laudanosine. The proposed model satisfactorily fits the observations and is based on the assumptions that the parent drug spontaneously degrades to laudanosine at the rate comparable with that observed in vitro at pH 7.4 and 37 degrees C; that 2 molecules of laudanosine are formed from 1 molecule of atracurium; that an initial very rapid decay of a fraction of the atracurium dose is responsible for the initially high plasma laudanosine concentrations; that the rapid disappearance of atracurium from plasma is accounted for by its spontaneous degradation and by the sequestration of atracurium in a deep compartment; and that laudanosine formed from atracurium is added to its central compartment, with its disposition described by a simple 2-compartment model with elimination from the central compartment. The model projects that about 43% of the atracurium dose is rapidly converted to laudanosine and that nearly the whole injected amount of atracurium is degraded to laudanosine.