A model for occupational stress amongst paediatric and adult critical care staff during COVID-19 pandemic.

PURPOSE: The coronavirus 2019 pandemic has placed all intensive care unit (ICU) staff at increased risk of psychological distress. To date, measurement of this distress has largely been by means of validated assessment tools. We believe that qualitative data may provide a richer view of staff experiences during this pandemic. METHODS: We conducted a cross-sectional, observational study using online and written questionnaires to all ICU staff which consisted of validated tools to measure psychological distress (quantitative findings) and open-ended questions with free-text boxes (qualitative findings). Here, we report our qualitative findings. We asked four questions to explore causes of stress, need for supports and barriers to accessing supports. A conventional content analysis was undertaken. RESULTS: In total, 269 of the 408 respondents (65.9%) gave at least one response to a free-text question. Seven overarching themes were found, which contribute to our proposed model for occupational stress amongst critical care staff. The work environment played an important role in influencing the perceived psychological impact on healthcare workers. Extra-organisational factors, which we termed the "home-work interface" and uncertainty about the future, manifested as anticipatory anxiety, had a proportionally larger influence on worker well-being than would be expected in non-pandemic conditions. CONCLUSION: Our findings have important implications for appropriate allocation of resources and ensuring well-being of the ICU multidisciplinary team for this and future pandemics.

Increased thrombin generation potential in symptomatic versus asymptomatic moderate or severe carotid stenosis and relationship with cerebral microemboli.

INTRODUCTION: The importance of thrombin generation in the pathogenesis of TIA or stroke and its relationship with cerebral microembolic signals (MES) in asymptomatic and symptomatic carotid stenosis has not been comprehensively assessed. METHODS: Plasma thrombin generation parameters from patients with moderate or severe (≥ 50%) asymptomatic carotid stenosis were compared with those from patients with symptomatic carotid stenosis in the early (≤ 4 weeks) and late phases (≥ 3 months) after TIA or stroke in this prospective, pilot observational study. Thrombin generation profile was longitudinally assessed in symptomatic patients with data at each time point. Bilateral transcranial Doppler ultrasound monitoring of the middle cerebral arteries was performed whenever possible to classify patients as MES-positive or MES-negative. RESULTS: Data from 31 asymptomatic, 46 'early symptomatic' and 35 'late symptomatic' patients were analysed. Peak thrombin (344.2 nM vs 305.3 nM; p = 0.01) and endogenous thrombin potential (1772.4 vs 1589.7; p = 0.047) were higher in early symptomatic than asymptomatic patients. Peak thrombin production decreased in symptomatic patients followed up from the early to late phase after TIA or stroke (339.7 nM vs 308.6 nM; p = 0.02). Transcranial Doppler ultrasound data were available in 25 asymptomatic, 31 early symptomatic and 27 late symptomatic patients. Early symptomatic MES-positive patients had a shorter 'time-to-peak thrombin' than asymptomatic MES-positive patients (p=0.04), suggesting a more procoagulant state in this early symptomatic subgroup. DISCUSSION: Thrombin generation potential is greater in patients with recently symptomatic than asymptomatic carotid stenosis, and decreases over time following TIA or stroke associated with carotid stenosis. These data improve our understanding of the haemostatic/thrombotic biomarker profile in moderate-severe carotid stenosis.

Increased endothelial activation in recently symptomatic versus asymptomatic carotid artery stenosis and in cerebral microembolic-signal-negative patient subgroups.

BACKGROUND AND PURPOSE: von Willebrand factor propeptide (VWF:Ag II) is potentially a more sensitive marker of acute endothelial activation than von Willebrand factor antigen (VWF:Ag). These biomarkers have not been simultaneously assessed in asymptomatic versus symptomatic carotid stenosis patients. The relationship between endothelial activation and cerebral microembolic signals (MESs) detected on transcranial Doppler ultrasound is unknown. METHODS: In this multicentre observational analytical study, plasma VWF:Ag and VWF:Ag II levels in patients with ≥50% asymptomatic carotid stenosis were compared with those from patients with ≥50% symptomatic carotid stenosis in the 'early' (≤4 weeks) and 'late' (≥3 months) phases after transient ischaemic attack or ischaemic stroke. Endothelial activation was also longitudinally assessed in symptomatic patients during follow-up. Transcranial Doppler ultrasound monitoring classified patients as MES-positive or MES-negative. RESULTS: Data from 31 asymptomatic patients were compared with those from 46 early symptomatic and 35 late phase symptomatic carotid stenosis patients, 23 of whom had undergone carotid intervention. VWF:Ag II levels were higher in early (12.8 µg/ml; P < 0.001), late (10.6 µg/ml; P = 0.01) and late post-intervention (10.6 µg/ml; P = 0.038) symptomatic patients than asymptomatic patients (8.9 µg/ml). VWF:Ag levels decreased in symptomatic patients followed up from the early to late phase after symptom onset (P = 0.048). Early symptomatic MES-negative patients had higher VWF: Ag II levels (13.3 vs. 9.0 µg/ml; P < 0.001) than asymptomatic MES-negative patients. CONCLUSIONS: Endothelial activation is enhanced in symptomatic versus asymptomatic carotid stenosis patients, in early symptomatic versus asymptomatic MES-negative patients, and decreases over time in symptomatic patients. VWF:Ag II levels are a more sensitive marker of endothelial activation than VWF:Ag levels in carotid stenosis. The potential value of endothelial biomarkers and concurrent cerebral MES detection at predicting stroke risk in carotid stenosis warrants further study.

High on-treatment platelet reactivity on commonly prescribed antiplatelet agents following transient ischaemic attack or ischaemic stroke: results from the Trinity Antiplatelet Responsiveness (TRAP) study.

BACKGROUND AND PURPOSE: The prevalence of ex vivo 'high on-treatment platelet reactivity' (HTPR) to antiplatelet regimens in patients with ischaemic cerebrovascular disease (CVD) is uncertain. METHODS: HTPR was assessed with PFA-100 collagen-epinephrine (C-EPI) and collagen-ADP (C-ADP) cartridges. Platelet activation (CD62P, CD63 and leucocyte-platelet complex formation) was assessed with whole-blood flow cytometry. Patients were assessed at baseline [≤ 4 weeks of transient ischaemic attack (TIA) or ischaemic stroke], and at 14 days and ≥ 90 days after changing treatment from (i) no medication to aspirin monotherapy (N = 26) or (ii) aspirin to clopidogrel monotherapy (N = 22). HTPR was defined in a novel, 'longitudinal fashion' as failure to prolong relevant closure times compared with the patient's 'baseline value' before he/she underwent an antiplatelet change by more than twice the coefficient of variation of the assay. RESULTS: (i) C-EPI closure times increased at 14 days and 90 days after commencing aspirin (P = 0.002); 24% at 14 days and 18% at 90 days demonstrated HTPR on aspirin. (ii) C-ADP closure times increased at 14 days (P = 0.001) but not 90 days (P = 0.09) after changing from aspirin to clopidogrel; 41% at 14 days, and 35% at 90 days demonstrated HTPR on clopidogrel. Platelet activation was unaffected by aspirin (P = 0.09). The percentage neutrophil-platelet complexes decreased at 14 days (P = 0.02), but this reduction was not maintained 90 days after changing to clopidogrel (P = 0.3). No patient had a recurrent vascular event during prospective follow-up. CONCLUSIONS: Longitudinal definitions of HTPR in patients with ischaemic CVD who are undergoing a change in antiplatelet therapy have the potential to provide more clinically meaningful information than traditional 'cross-sectional definitions' of HTPR which are usually based on the comparison of patients' values with those in healthy controls. Using our novel, longitudinal definition of HTPR, the PFA-100 could be used to monitor ex vivo responsiveness to aspirin, and larger, prospective studies are warranted to assess the clinical predictive value of this and other platelet function tests in patients with ischaemic CVD.

von Willebrand Factor Antigen, von Willebrand Factor Propeptide, and ADAMTS13 in Carotid Stenosis and Their Relationship with Cerebral Microemboli.

BACKGROUND: The relationship between von Willebrand factor antigen (VWF:Ag), VWF propeptide (VWFpp), VWFpp/VWF:Ag ratio, ADAMTS13 activity, and microembolic signal (MES) status in carotid stenosis is unknown. METHODS: This prospective, multicenter study simultaneously assessed plasma VWF:Ag levels, VWFpp levels and ADAMTS13 activity, and their relationship with MES in asymptomatic versus symptomatic moderate-to-severe (≥50-99%) carotid stenosis patients. One-hour transcranial Doppler ultrasound of the middle cerebral arteries classified patients as MES+ve or MES-ve. RESULTS: Data from 34 asymptomatic patients were compared with 43 symptomatic patients in the "early phase" (≤4 weeks) and 37 patients in the "late phase" (≥3 months) after transient ischemic attack (TIA)/ischemic stroke. VWF:Ag levels were higher (p = 0.049) and VWFpp/VWF:Ag ratios lower (p = 0.006) in early symptomatic than in asymptomatic patients overall, and in early symptomatic versus asymptomatic MES-ve subgroups (p ≤0.02). There were no intergroup differences in VWFpp expression or ADAMTS13 activity (p ≥0.05). VWF:Ag levels and ADAMTS13 activity decreased (p ≤ 0.048) and VWFpp/VWF:Ag ratios increased (p = 0.03) in symptomatic patients followed up from the early to late phases after TIA/stroke. Although there were no differences in the proportions of symptomatic and asymptomatic patients with blood group O, a combined analysis of early symptomatic and asymptomatic patients revealed lower median VWF:Ag levels in patients with blood group O versus those without blood group O (9.59 vs. 12.32 µg/mL, p = 0.035). DISCUSSION: VWF:Ag expression, a marker of endothelial ± platelet activation, is enhanced in recently symptomatic versus asymptomatic carotid stenosis patients, including in MES-ve patients, and decreases with ADAMTS13 activity over time following atherosclerotic TIA/ischemic stroke.

Relationship between 'on-treatment platelet reactivity', shear stress, and micro-embolic signals in asymptomatic and symptomatic carotid stenosis.

BACKGROUND: Assessment of 'high on-treatment platelet reactivity (HTPR)' could enhance understanding of the pathophysiology of first or recurrent vascular events in carotid stenosis patients on antiplatelet therapy. METHODS: This prospective, multi-centre study assessed antiplatelet-HTPR status and its relationship with micro-emboli signals (MES) in asymptomatic vs. symptomatic ≥ 50-99% carotid stenosis. Platelet function/reactivity was assessed under 'moderately high shear stress' with the PFA-100® and 'low shear stress' with VerifyNow® and Multiplate® analysers. Bilateral 1-h transcranial Doppler ultrasound of the middle cerebral arteries classified patients as MES + ve or MES - ve. RESULTS: Data from 34 asymptomatic patients were compared with 43 symptomatic patients in the 'early phase' (≤ 4 weeks) and 37 patients in the 'late phase' (≥ 3 months) after TIA/ischaemic stroke. Median daily aspirin doses were higher in early symptomatic (225 mg; P < 0.001), but not late symptomatic (75 mg; P = 0.62) vs. asymptomatic patients (75 mg). There was a lower prevalence of aspirin-HTPR in early (28.6%; P = 0.028), but not late symptomatic (38.9%; P = 0.22) compared with asymptomatic patients (56.7%) on the PFA-100®, but not on the VerifyNow® or Multiplate® (P ≤ 0.53). Early symptomatic patients had a higher prevalence of aspirin-HTPR on the PFA-100® (28.6%) vs. VerifyNow® (9.5%; P = 0.049), but not Multiplate® assays (11.9%, P = 0.10). There was no difference in aspirin-HTPR prevalence between any symptomatic vs. asymptomatic MES + ve or MES - ve subgroup. DISCUSSION: Recently symptomatic moderate-severe carotid stenosis patients had a lower prevalence of aspirin-HTPR than their asymptomatic counterparts on the PFA-100®, likely related to higher aspirin doses. The prevalence of antiplatelet-HTPR was positively influenced by higher shear stress levels, but not MES status.

Increased Leucocyte-Platelet Complex Formation in Recently Symptomatic versus Asymptomatic Carotid Stenosis Patients and in Micro-emboli Negative Subgroups.

INTRODUCTION: Cerebral micro-embolic signals (MES) predict risk of stroke in carotid stenosis patients. However, MES-negative 'recently symptomatic patients' also have a higher stroke risk than 'asymptomatic patients'. Differences in platelet activation status may contribute to this disparity in risk. METHODS: This prospective, observational study assessed platelet biomarkers and their relationship with MES in asymptomatic versus symptomatic moderate (≥50-69%) or severe (≥70-99%) carotid stenosis patients. Full blood count parameters were measured and whole-blood flow cytometry was used to quantify platelet surface CD62P and CD63 expression and leucocyte-platelet complex formation. Bilateral simultaneous transcranial Doppler ultrasound of the middle cerebral arteries classified patients as 'MES positive' or 'MES negative'. RESULTS: Data from 34 asymptomatic patients were compared with those from 43 symptomatic patients in the 'early phase' (≤ 4 weeks) and 37 of these symptomatic patients in the 'late phase' (≥ 3 months) after transient ischaemic attack/ischaemic stroke. There were no differences in %CD62P or %CD63 expression between early or late symptomatic and asymptomatic patients overall (p > 0.05). The percentage of lymphocyte-platelet complexes was higher in early symptomatic than in asymptomatic patients (2.8 vs. 2.16%; p < 0.001). MES were more commonly observed in early symptomatic (31.4%; p = 0.027) but not in late symptomatic (6.7%; p = 0.996) versus asymptomatic patients (7.1%). The percentage of lymphocyte-platelet complexes was higher in early symptomatic than in asymptomatic MES-negative patients (2.7 vs. 2.17%; p = 0.02). CONCLUSION: These data add to the evidence that leucocyte-platelet complex formation/platelet activation is increased in recently symptomatic versus asymptomatic patients, and may contribute to the pathogenesis of first and subsequent strokes in carotid stenosis patients, including those who are MES negative.

Profile of von Willebrand factor antigen and von Willebrand factor propeptide in an overall TIA and ischaemic stroke population and amongst subtypes.

INTRODUCTION: Von Willebrand factor propeptide (VWF:Ag II) is proposed to be a more sensitive marker of acute endothelial activation than von Willebrand factor antigen (VWF:Ag). Simultaneous data on VWF:Ag and VWF:Ag II profiles are very limited following TIA and ischaemic stroke. METHODS: In this prospective, observational, case-control study, plasma VWF:Ag and VWF:Ag II levels were quantified in 164 patients≤4weeks of TIA or ischaemic stroke (baseline), and then ≥14days (14d) and ≥90days (90d) later, and compared with those from 27 healthy controls. TIA and stroke subtyping was performed according to the TOAST classification. The relationship between VWF:Ag and VWF:Ag II levels and platelet activation status was assessed. RESULTS: 'Unadjusted' VWF:Ag and VWF:Ag II levels were higher in patients at baseline, 14d and 90d than in controls (p≤0.03). VWF:Ag levels remained higher in patients than controls at baseline (p≤0.03), but not at 14d or 90d after controlling for differences in age or hypertension, and were higher in patients at baseline and 90d after controlling for smoking status (p≤0.04). 'Adjusted' VWF:Ag II levels were not higher in patients than controls after controlling for age, hypertension or smoking (p≥0.1). Patients with symptomatic carotid stenosis (N=46) had higher VWF:Ag and VWF:Ag II levels than controls at all time-points (p≤0.002). There was no significant correlation between platelet activation status and VWF:Ag or VWF:Ag II levels. CONCLUSIONS: VWF:Ag and VWF:Ag II levels are increased in an overall TIA and ischaemic stroke population, especially in patients with recently symptomatic carotid stenosis. VWF:Ag II was not superior to VWF:Ag at detecting acute endothelial activation in this cohort and might reflect timing of blood sampling in our study.

Impact of the informed consent process on patients' understanding of varicose veins and their treatment.

AIM: It is particularly important that patients have reasonable understanding of the risks, benefits and nature of elective surgery. This study sought to analyse this level of understanding in patients undergoing varicose vein surgery METHODS: Eighty two patients completed a questionnaire in the vascular outpatient clinic and were asked to complete a telephone questionnaire following the clinic. RESULTS: Pain (n = 46) was the primary reason patients considered varicose vein surgery followed by appearance (n = 32). Most patients felt that varicose veins placed them at high risk of leg ulcers (n = 46) and DVT (n = 41). A high level of expectation that surgery would significantly affect pain and flares was recorded. While the outpatient visit did not materially change these misconceptions, an educational leaflet significantly enhanced the recall of complications (p = 0.028) in patients who remembered receiving a leaflet. CONCLUSION: Patients attending varicose vein clinics have an unrealistic expectation of the benefits of surgery and fail to understand the benign nature of their condition. The outpatient process has little effect on patient-held beliefs.

Contractility of human gallbladder muscle in vitro.

This study examined the effects of transmural nerve stimulation, acetylcholine, adrenoceptor agonists and several peptides on the contractility of strips of human gallbladder in vitro. Acetylcholine caused concentration-related contractions of the tissues and the sensitivity to acetylcholine was similar in gallbladders with mild and severe chronic cholecystitis. Noradrenaline and adrenaline relaxed gallbladder strips, probably via beta 2-adrenoceptor stimulation. Transmural nerve stimulation always caused contractions, but in the presence of atropine inhibitory responses were demonstrable and these were antagonized by propranolol. There was no evidence of non-adrenergic inhibitory neural responses. Of the peptides tested, only cholecystokinin octapeptide (CCK-OP), gastrin, pentagastrin, substance P and caerulein caused contractions. Responses to CCK-OP, gastrin and pentagastrin were antagonized by dibutyryl cyclic GMP. Hormones which had no effect upon human gallbladder strips included motilin, secretin, bombesin, neurotensin, glucagon, vasopressin, VIP and somatostatin. Considerable differences therefore exist between human tissues and those from experimental animals with respect to the direct actions of neural and hormonal stimuli on gallbladder contractility.

The lack of effect of variable blood withdrawal rates on the measurement of mixed venous oxygen saturation.

In a study of 12 critically ill patients, values for mixed venous oxygen saturation (SVO2) were measured from samples of pulmonary arterial blood drawn at five rates of withdrawal (1, 3, 10, 20, and 30 ml/min). Samples were drawn from properly placed pulmonary arterial catheters with the balloon deflated. Physiologic stability was documented at the beginning and end of the sampling period in all but one patient. Results in each patient demonstrated a close grouping of values for SVO2 obtained at the five rates of withdrawal (largest standard deviation, 1.9 percent). Evaluations by paired t-test comparing all rates of withdrawal with the slowest rate (1 ml/min) showed no significant differences. The rate of withdrawal of the sample is not associated with significant errors in SVO2 when samples are drawn from a properly positioned pulmonary arterial catheter.

Evaluation of the portable chest roentgenogram for quantitating extravascular lung water in critically ill adults.

The diagnosis of pulmonary edema is frequently made from characteristic findings on the chest roentgenogram that suggest an increase in lung water. Optimal radiographic technique depends on a cooperative upright patient, which is not possible with most critically ill patients. These patients may also have multiple radiographic abnormalities that make interpretation of the chest roentgenogram difficult. The ability of portable chest roentgenograms to accurately identify the presence of excess lung water and monitor changes in lung water has not previously been evaluated in critically ill adults who are intubated and ventilated and in the supine position when the films are exposed. In 12 patients the pulmonary edema seen on portable chest roentgenograms was given a score (0 to 390 points), which was then compared with a determination of extravascular lung water using the thermal-dye indicator dilution technique. A linear correlation was observed (r = 0.51; p less than 0.05; n = 73). Evaluation of a change in radiographic score vs a change in lung water showed no linear correlation (r = 0.1; p greater than 0.05). While portable chest roentgenograms exposed under the conditions described were a useful technique for demonstrating pulmonary edema, they were not accurate in monitoring modest changes in lung water in critically ill patients.

The effect of hypothermic preservation of the heart and lungs on cardiorespiratory function following canine heart-lung transplantation.

The effect of hypothermic preservation of the heart and lungs with a crystalloid solution was evaluated in 12 mongrel dogs receiving heart-lung allografts. Six animals served as controls and received an immediate heart-lung transplant. Six animals were in the experimental group and received a heart-lung transplant after 5 hours of preservation at 4 degrees C following perfusion of both organs with a crystalloid solution. Physiological function of the heart and lungs was studied for 20 hours after transplantation. While cardiac function was minimally depressed following preservation, pulmonary function testing demonstrated significantly greater increases in extravascular lung water in experimental animals, suggesting that an ischemic lung injury occurred with this preservation technique. The model allows for future evaluation of other methods of combined preservation of both the heart and lungs for transplantation.

Hypothermic preservation of the heart and lungs with Collins solution: effect on cardiorespiratory function following heart-lung allotransplantation in dogs.

The effect of preserving the heart and lungs with hypothermia and Collins solution was studied in 13 mongrel dogs undergoing combined heart-lung transplantation. The five control animals who underwent an immediate transplant following Collins solution perfusion had small increases in extravascular lung water when measured 2.5 hours posttransplant as seen in a previous study. The eight animals who had hypothermic preservation following Collins solution perfusion had significantly higher extravascular lung water than controls (16.3 +/- 1.8 ml/kg in preserved animals; 11.2 +/- 1.7 ml/kg in controls p less than 0.05). The level of lung water reached at 2.5 hours postoperatively was similar to that reached with a previously reported, unacceptable preservation technique. Survival beyond this point was poor due to severe pulmonary edema. We conclude that the use of this solution, given under the experimental conditions which we describe, is not acceptable for hypothermic preservation of the heart and lungs for combined transplantation.

Acute physiological changes following heart-lung allotransplantation in dogs.

The feasibility of clinical heart-lung transplantation requires a better understanding of the physiological consequences of the operation, heart-lung denervation, and the quality of graft preservation. An acute canine model was used to evaluate heart-lung function during the first 24 hours after transplantation. Measurements of cardiopulmonary dynamics were performed in 5 donor animals and compared sequentially after transplantation in the respective recipients. Orthotopic allotransplantation was performed on cardiopulmonary bypass with moderate hypothermia after perfusion of both the heart and lung with a clinical cardioplegic solution (4 degrees C; potassium chloride, 30 mEq/L; mannitol, 20 gm/L). Postoperatively, the animals were ventilated continuously and anesthetized. Hemodynamic variables were monitored, and measurements were made of arterial and venous oxygen, carbon dioxide, saturation, and pulmonary mechanics. Cardiac output and a derived measurement of lung water were determined. Pulmonary vascular resistance, arteriovenous shunt, resistance, and compliance were calculated. At the termination of the experiment, significant differences were observed between donor and recipient lung-water levels (7.7 +/- 0.9 ml/kg versus 12.0 +/- 3.1 ml/kg, respectively; p less than 0.05); 100% arterial oxygen tension (509 +/- 37 mm/Hg versus 227 +/- 114 mm/Hg, respectively; p less than 0.01); and pulmonary compliance (38 +/- 18 ml/cm H2O versus 11 +/- 4 ml/cm H2O, respectively; p less than 0.05). Arteriovenous shunt increased from 12.2 +/- 4 to 16.5 +/- 5% (p = 0.2). This model evaluates the technique currently employed clinically and will be used in the future to compare methods of heart-lung preservation with the goal of allowing distant heart-lung procurement.

Pulmonary management of the urologic patient.

Morbidity and mortality from pulmonary complications following urinary tract operations can be reduced by preoperative identification of the high risk patient. Pulmonary function tests and arterial blood gases are necessary to identify these patients and to delineate the severity of their pulmonary disease. Respiratory complications can be prevented in many patients with the proper use of pre- and postoperative chest physical therapy and oxygen therapy. Despite the most careful pulmonary management, some patients develop acute respiratory failure following urologic operations. Respiratory failure results from a combination of physiologic abnormalities which impair alveolar ventilation and oxygenation. Utilizing controlled ventilation, supplemental oxygen, and a physiologic approach to treating the underlying cause of respiratory failure, three fourths of urologic patients in respiratory failure may be expected to survive.

Current treatments for axillary hyperhidrosis.

Primary hyperhidrosis affects up to 1% of the population and has a significant negative impact on quality of life. It affects the axillae in approximately 80% of cases. Hyperhidrosis results from excessive sympathetic stimulation of the eccrine sweat glands: the various treatment modalities available target points along the pathway between the central nervous system and the peripheral gland. The first line of treatment is topical aluminium chloride, which is effective in the majority of cases. Alternative treatments such as systemic anti-cholinergics and iontophoresis have significant disadvantages, while surgical sympathectomy has been regarded as the gold-standard in treatment of this condition. Recently, attention has focused on the use of intradermal botulinum toxin for the treatment of axillary hyperhidrosis. This is a highly effective, minimally-invasive treatment with few side effects, and is now recommended as the treatment of choice in isolated axillary hyperhidrosis

Staged resection or primary anastomosis for obstructing lesions to the left colon.

The management of obstructing left-sided colonic and rectal lesions has traditionally been by a staged procedure. The introduction of 'on-table lavage', has made primary resection and anastomosis of the large bowel feasible for patients presenting as emergencies. We have studied the perioperative course of 28 patients who presented with left colonic obstruction to determine whether primary anastomosis conferred additional morbidity. The patients ranged in age from 29 to 89 years (mean 66 years) at presentation. The ASA status of patients was comparable in both groups (Table 1). Fourteen patients underwent resection, on-table lavage, and primary anastomosis (PA) and 14 a Hartmann's procedure (HP). The mean operative time for the PA procedure was 200 minutes compared to 110 minutes for the HP group. There was no significant difference in the postoperative complication rate nor mean hospital stay rate for the primary procedures between the two groups. There was no clinical anastomotic leak in patients undergoing primary anastomosis. However secondary surgery for patients undergoing colorectal reconnection conferred added morbidity for patients who had a HP. We conclude that resection, on-table lavage, and primary anastomosis is safe in the management of left-sided colonic obstruction and in most cases is the treatment of choice.

Management of perioperative dysrhythmias.

This paper reviews cardiac dysrhythmias occurring in the perioperative period. Electrocardiography was the first application of electronic monitoring to anesthesia care. The detection of dysrhythmias remains the most important use of this technology today. While the description of dysrhythmias dates back to the early 1900's, the first large series was reported in 1936. Early descriptions of the kinds seen and the predisposing factors have changed little in the past 50 years. Several factors tend to emerge when one evaluates perioperative dysrhythmias. These are the anesthetic given, the site of surgery, abnormalities of blood gases or electrolytes, tracheal intubation, reflexes such as vagal slowing and the oculocardiac reflex, stimulation of the central nervous system the presence of pre-existing heart disease, and the use of intracardiac devices. In the evaluation of cardiac dysrhythmias several facts need to be determined. The most important is to determine if there is an underlying complication of anesthesia and surgery which may explain the dysrhythmia. In addition, one needs to evaluate the heart rate, the regularity, the number of P waves per QRS, and the configurations of the QRS. The anesthesiologist needs to determine whether the rhythm is dangerous to the patient and whether it requires treatment. The two major abnormalities of sinus rhythm are sinus bradycardia and the sinus tachycardia. Sinus bradycardia can be due to hypoxia, vagal stimulation, drug effects, a high sympathetic block or an acute myocardial infarction. Sinus tachycardia can be due pain, light anesthesia, hypovolemia, sepsis, hypoxia, hypercapnia and drug effects. The major atrial dysrhythmias are paroxysmal atrial tachycardia, atrial fibrillation and atrial flutter. Each require treatment if perfusion is impaired or if the heart rate is persistently elevated. The new agents esmolol and adenosine are particularly useful in managing atrial dysrhythmias. The major ventricular dysrhythmias are ventricular premature contractions, ventricular tachycardia and ventricular fibrillation. The later two demand emergency management with DC cardioversion when perfusion is impaired. The major abnormality of conduction is complete heart block which usually requires emergency treatment in the perioperative period. Prompt evaluation and management of perioperative dysrhythmias reduce anesthetic morbidity and mortality.