Risk factors for pulmonary complications in the postoperative head and neck surgery patient.

BACKGROUND: Pulmonary complications are a primary source of increased cost and morbidity in surgically treated head and neck cancer patients. This study investigates potential risk factors related to postoperative pulmonary complications (pneumonia, adult respiratory distress syndrome (ARDS), and prolonged mechanical ventilation) in head and neck cancer patients. METHODS: Data from 144 major head and neck procedures performed at the University of Washington between 1985 and 1991 were retrospectively reviewed. Univariate and multivariate analysis were used to evaluate preoperative and perioperative variables identified as potential risk factors for postoperative pulmonary complications. RESULTS: Fifteen percent of patients had a postoperative pulmonary complication, (n = 21: 18 postoperative pneumonia; 2 ARDS; and 4 prolonged ventilation). The most common pneumonia pathogen was Staphylococcus aureus (62%). Univariate analysis identified smoking and weight loss as significant factors associated with pulmonary complications. The variables preoperative blood urea nitrogen, white blood cell count, and operative chest flap closure all approached but did not reach significance. Multivariate analysis of a subgroup of patients identified smoking history and perioperative antibiotic choice as the only independently significant variables. CONCLUSIONS: Patient smoking history was the primary variable related to postoperative pulmonary problems, with evidence of increasing risk with increased exposure. Other variables added only limited additional risk association information after multivariate analysis.

Vasopressin levels in major head and neck surgery.

In an effort to further understand the perioperative intravascular volume status of major head and neck surgery patients, serum antidiuretic hormone (ADH) and osmolality levels were assessed at four perioperative junctures. Thirty-five major head and neck surgical patients were randomly selected for examination with placement of a central venous pressure monitor. Serum osmolality and serum vasopressin levels were obtained at four junctures perioperatively. ADH levels were lower both after patients were anesthetized and five hours into the procedure than at either baseline or 24 hours after the end of the procedure. ADH levels after patients were anesthetized did not differ from those at five hours into the procedure, nor did ADH levels at baseline differ from those 24 hours after the end of the procedure. In addition, osmolality levels did not change over time. Additional analyses examining relationships between preoperative, intraoperative, and postoperative characteristics and ADH levels after patients were anesthetized and five hours into the procedure, as well as changes from baseline at these times and the baseline levels themselves, detected no significant relationships. This study provides information about the perioperative intravascular volume status of major head and neck surgery patients which may be important to intraoperative care, especially to decisions regarding invasive intraoperative fluid monitoring. Specifically, the data provide additional evidence against the need for the routine placement of central venous catheters to guide fluid administration during major head and neck surgery.

Defining the concentration-effect relationship of volatile anesthetics in vessels using an in vitro nonsteady-state technique.

We compared traditional steady-state experiments with nonsteady-state experiments in defining the vasodilating potency of isoflurane in isolated cerebral vessels. The effects of volatile anesthetics on isolated arterial vessel wall tension are typically examined by means of steady-state methodology. This requires the prolonged administration of the agent under study until a stable wall tension is achieved. An alternative, non-steady-state approach to such experiments is proposed as an adjunct technique to help simplify and in some cases evaluate more fully vascular response. Cylindrical segments of the rabbit basilar artery were placed into a perfused tissue bath, stretched to a resting tension of approximately 2000 dynes and then constricted with 30 nM K+. Thirty minutes later, 2.0 MAC of isoflurane was introduced into the fluid reservoir supplying the chamber. This administration was continued for 10 min, at which time isoflurane was discontinued and vessel tension was monitored for another 10 min. During this 20-min washin-washout period, samples of bath fluid were obtained q 1 min and isoflurane concentrations were subsequently determined by gas chromatography. After completion of these "nonsteady-state" measurements, another 30-min waiting period was allowed, after which vessels were exposed to stable concentrations of 0.5, 1.0, 1.5 and 2.0 MAC of isoflurane in varied order. Each exposure was for 15 min, with a 30-min agent-free rest period between exposures. An effect compartment model was selected for analysis of the nonsteady-state data. Ke0, a first order rate constant linking the concentrations in the bath to a theoretical effect compartment, was estimated by using a hysteresis minimization technique.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetic considerations in porphyrias.

Four hereditary types of porphyria are now classified as acute porphyrias. Enzymatic defects result in accumulation of porphyrin precursors (usually ALA and PGB). The quantity of these precursors may be normal or slightly increased in latent periods but increase to toxic levels during a porphyric crisis. Iatrogenic induction of ALA synthetase by administration of certain triggers (classically barbiturates) is only one of several factors which contribute to porphyric crisis. Signs and symptoms of acute porphyric attack consist primarily of neurologic dysfunction, which occurs secondary to neurotoxicity of ALA or diminished intraneuronal heme levels. Appropriate anesthetic management of porphyria requires knowledge of the type of porphyria (acute vs non-acute), assessment of latent versus active (crisis) phase, awareness of clinical features of porphyric attack, and knowledge of safe pharmacologic intervention.

The efficacy of routine central venous monitoring in major head and neck surgery: a retrospective review.

STUDY OBJECTIVE: To further define the efficacy of routine central venous catheter placement for major head and neck surgery from the standpoint of fluid and blood administration, and various other parameters of perioperative management. DESIGN: Randomized, retrospective chart review. SETTING: University-affiliated medical center. PATIENTS: 104 patients who had undergone major head and neck surgery (defined as surgery lasting longer than 4 hours with a predicted blood loss of 500 ml or greater) at the University of Iowa Hospitals and Clinics between 1985 and 1992. MEASUREMENTS AND MAIN RESULTS: Central venous monitoring was used in 51 of the 104 (49%) procedures. Patients with and without central monitors did not differ in age, weight, preoperative laboratory values [i.e., hemoglobin (Hb), blood urea nitrogen (BUN), creatinine), incidence of significant cardiac or renal disease, or a smoking history exceeding 30 pack years. In addition, these patients did not differ with respect to the following intraoperative characteristics: general type of anesthetic; duration of surgery; estimate of blood loss; Hb values; lowest urine output per hour; development of oliguria; total urine output; amount of replacement of blood, colloid, or crystalloid; development of systolic blood pressure less than 70 mmHg; or use of a myocutaneous flap. Patients also did not differ with respect to the following postoperative characteristics: duration of stay in the surgical intensive care unit or hospital, BUN or creatinine values on days 1 and 2, total urine output or the development of oliguria on days 1 through 3, incidence of reintubation, fever on days 1 through 5, wound dehiscence, death, myocardial infarction, or the development of pneumonia, pulmonary edema, or sepsis. Patients with central monitors had a greater incidence of having a tracheostomy performed and a slightly lower Hb level on the first postoperative day than those without central monitors. CONCLUSIONS: The study raises doubt about the efficacy of routine central venous catheter placement as a necessary guide for fluid and blood administration for these procedures, or as a necessary adjunct for several other parameters of perioperative management. It suggests the need for a randomized, prospective evaluation.

Quality in anesthesia care: lessons from industry and a proposal for valid measurement and improvement.

Quality anesthetic care is a goal fundamental to our tradition and our training, but defining and measuring quality in anesthesia presents special challenges. Industrial models of quality, especially those so fundamental to the re-emergence of post-war Japan, deserve careful study and are discussed at some length, but they clearly have limitations in understanding quality in anesthesiology. We suggest that most current quality efforts are inherently flawed. Whether or not they rigorously attempt to define quality, they are hampered by lack of data concerning outcomes and alternatives, as well as lack of distinction between quality and efficacy. Quality efforts in American medicine and anesthesiology seem mired in a "criterion of potential benefit," which is still central to many of our prescriptions for individual medical care. Current quality improvement efforts do not seem well suited to correct these flaws. Anesthetic care, and that of American medicine in general, is fragmented, enormously costly, and sometimes inappropriate or poor. Anesthesiologists are suspicious of current quality efforts to improve this care. The system often seems more geared to eliminate bad apples than to improve patient care. Because anesthesia is a specialty that facilitates care but seldom "cures," we face greater challenges in studying and defining quality than do other specialties. Because of this, it is imperative that several principles govern future quality improvement efforts in anesthesiology. First, a reasonable balance must be attained between study of outcomes and processes of anesthesia care. Second, anesthesia-specific severity of illness indexing must be developed. Third, and perhaps most important, anesthetic processes and outcomes must be reported on a national level. Fundamental to future quality efforts in our specialty, we believe, is the establishment of a protected National Anesthesia Outcome Registry. This article reviews the industrial and medical history of quality, its measurement and improvement, and attempts to apply principles learned over many decades to anesthesiology.

A comparison of the vasodilating effects of halothane and isoflurane on the isolated rabbit basilar artery with and without intact endothelium.

Although volatile anesthetics result in cerebral arterial dilation, the precise mechanisms underlying this effect are not known. In vitro tension recordings were used to study the vasodilating potencies of halothane and isoflurane in isolated cerebral vessels and to examine the possible role of the endothelium in modulating any effects observed. Cylindrical segments of the rabbit basilar artery and midline ear artery from the same animal were placed in a flow-through bath of 37 degrees C oxygenated (95% O2/5% CO2) physiologic salt solution and stretched to a resting tension of approximately 2,000 dynes. They were then constricted with 3.0 x 10(-2) M K+, 1.0 x 10(-3) M norepinephrine, or 5.0 x 10(-6) M serotonin and exposed to either halothane or isoflurane at concentrations of approximately 0.5, 1.0, 1.5, and 2.0 MAC in varied order for 15 min at each concentration. A 30-min period of perfusion with anesthetic-free, vasoconstrictor-containing perfusate separated successive exposures to an anesthetic. Vessels prepared in this fashion retained their responsiveness to both vasoconstrictors and volatile anesthetics for as long as 4 h. They also relaxed appropriately to acetylcholine, indicating that the endothelium was intact. Concentrations of volatile anesthetic in the tissue perfusate were directly measured using gas chromatography, and the relationship between bath concentrations (expressed as MAC fractions) and the degree of relaxation were determined. The data were analyzed by parallel line regression. Halothane was found to be a significantly more potent vasodilator of the isolated basilar artery than was isoflurane. For example, in K(+)-constricted vessels, the concentration of halothane needed to produce a 50% reduction in tension was 1.32 MAC, compared with 1.66 MAC for isoflurane. Comparable differences were found in the basilar artery in the presence of other constrictors. However, there was no significant difference between the two agents in their effects upon the ear artery. In a separate series of experiments, the endothelium of basilar artery segments was removed by drying. Removal was confirmed by observing a diminished dilator response to acetylcholine. These vessels were subsequently constricted with K+, and relaxation dose-response curves were obtained for both halothane and isoflurane. There were no differences in the dose-response curves for deendothelialized versus intact vessels, with halothane still the more potent relaxant after endothelial removal. These data demonstrate that halothane and isoflurane cause a dose-dependent relaxation of rabbit cerebral vessels, regardless of the vasoconstrictor used. Halothane was a more potent relaxant of the basilar artery when expressed on a MAC-fraction basis.(ABSTRACT TRUNCATED AT 400 WORDS)

The influence of inhalational anesthetics on in vivo and in vitro benzodiazepine receptor binding in the rat cerebral cortex.

The effect of volatile anesthetics on benzodiazepine receptor binding was examined autoradiographically in the rat brain both in vivo and in vitro with the use of [3H]-Ro-15-1788, a benzodiazepine antagonist. For in vitro studies, slide-mounted brain sections were incubated at 37 degrees C in Tris buffer (50 mM, pH 7.4) with [3H]-Ro-15-1788 (flumazenil, 0.5-12.0 nM) in the presence of air (control) or 1 MAC concentrations of halothane or isoflurane. Brain sections were exposed to x-ray film and their images digitized, and specific cortical [3H]-Ro-15-1788 binding was determined. A Scatchard plot of specific cortical binding was constructed, and the dissociation constant (KD) and maximum bound ligand per milligram tissue (Bmax) were determined for each experimental group. In the in vivo trials, rats were anesthetized with 1 MAC halothane or isoflurane; 0.5 microCi/g [3H]-Ro-15-1788 was given intravenously, and the animals were killed 15 min later. Seven standardized sagittal brain sections were examined from autoradiographs. Mean specific cortical binding was determined for each group and was compared with binding in unanesthetized control rats. A third experimental trial analyzed the timed arterial blood history of [3H]-Ro-15-1788 in animals prepared exactly as in the in vivo study. The [3H]-Ro-15-1788 blood clearance over 20 min and plasma [3H]-Ro-15-1788 levels at 15 min after injection of isotope were evaluated. In vitro Scatchard analysis showed no difference in experimental groups in KD or Bmax at 37 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Omeprazole and cimetidine versus pentagastrin in canine ex vivo gastric chamber.

The effects of acid inhibitory doses of omeprazole were compared with equieffective doses of cimetidine in the canine ex vivo stomach model (n = 30). Systemic blood pressure, temperature, stomach fluid and ion fluxes, potential difference, blood flow rates, and arterial and venous blood gases were monitored during each of nine 30-min periods. Two resting periods preceded seven periods of pentagastrin stimulation. During the last four of these, the drug effect was recorded (cimetidine 1.2 or 4.8 mumol.kg-1.h-1; omeprazole 0.3, 0.6, or 1.2 mumol/kg). Omeprazole (1.2 mumol/kg) produced 100% inhibition of stimulated acid efflux, no significant decrease in total gastric blood flow (venous outflow), 90% return of potential difference (PD) toward resting values, and a 55% reduction in stimulated oxygen consumption. Omeprazole also showed a dose-dependent K+ efflux at the two lower doses. Cimetidine (4.8 mumol.kg-1.h-1) given during pentagastrin stimulation showed a 70% decrease in total gastric blood flow, a 40% return of PD toward resting, and a 77% reduction in stimulated oxygen consumption. Neither drug showed significant changes in mucosal blood flow from resting values, thus supporting the principle that changes in gastric acid secretion and changes in blood flow are not necessarily correlated.

A system for trochanteric osteotomy and reattachment for total hip arthroplasty with a ninety-nine percent union rate.

In certain circumstances osteotomy of the greater trochanter in total hip arthroplasty is of benefit. To attack the problem of nonunion following trochanteric osteotomy, the authors apply several different wiring techniques. To quantify the efficacy of these approaches, they have reviewed 804 consecutive total hip arthroplasties in which the greater trochanter was osteotomized, including 725 primary total hip arthroplasties. Ninety-nine percent of the trochanters united. Among the 79 revision cases, the trochanter united in every case. The use of two independent vertical wires with one transverse wire was the preferred technique.

The cytoprotective effects of (+/-)-15-deoxy-16-alpha, beta-hydroxy-16-methyl PGE1 methyl ester (sc-29333) versus aspirin-shock gastric ulcerogenesis in the dog.

SC-29333 (SC) has been reported to protect the gastric mucosa from the effects of topical aspirin. We compared SC and 16,16-dimethyl PGE2 (16-dm) in 20 chambered canine stomachs (6 controls and 7 of each PG). Prostaglandin was added to an acid solution (100 mM HCl; 54 mM NaCl) at 0, .001, .01, 0.1, and 1.0 microgram/ml (two periods each). Then aspirin (20 mM) and PG (1.0 microgram/ml) (two periods) were followed by hemorrhagic shock (near 60 mm Hg mean arterial pressure). 16-dm caused a significant efflux of fluid (-6.5 +/- 5.3 to 17.3 +/- 6.7 microliters/min), Na+ (2.1 +/- 0.5 to 6.8 +/- 1.6 muEq/min), and Cl- (-0.9 +/- 2.4 to 5.3 +/- 1.3 muEq/min), but did not affect K+ or H+. 16-dm also caused a slight drop in potential difference (PD) (67.6 +/- 1.7 to 60.3 +/- 2.0 mV). 16-dm did not significantly affect total blood flow. Percent lesion formation was more severe than controls (20.2 +/- 3.5 vs 11.6 +/- 1.7 percent) but not statistically significant. SC had no significant effect on fluid, H+, Na+, K+, or Cl-. It caused an increase in blood flow (6.85 +/- 1.46 to 26.20 +/- 2.74 ml/min, p less than .001). SC significantly reduced percent lesion formation (1.9 +/- 0.9% p less than .001). We conclude: 1) SC causes an increase in mucosal blood flow and protects from aspirin-shock ulcerogenesis. 2) 16-dm stimulates an efflux of non-parietal extracellular fluid and fails to protect against aspirin injury during mucosal ischemia. 3) SC cytoprotection may be mediated by increased mucosal blood flow. 4) The mechanism of cytoprotection with 16-dm may require sufficient mucosal blood flow for filtration of non-acid fluid from blood to gastric lumen.

Limits to growth in world food production.

The dramatic increases in wheat yields that began in the mid-1930's in the United States will soon begin to level off. The favorable mix of genetics and technology that has characterized this era must build upon an ever higher yield base for the future. At the same time the residue of factors that can lower wheat yields includes a larger proportion of forces not easily shaped or controlled by man. An example is weather. The result is a natural yield ceiling that is already visible and that will impose a limit on future productivity growth.