Anesthetics and Automaticity of Dominant and Latent Pacemakers in Chronically Instrumented Dogs: IV. Dysrhythmias after Sinoatrial Node Excision

Background: Subsidiary atrial pacemakers assume control after sinoatrial (SA) node excision, and anesthetic-catecholamine interactions can produce severe bradycardia during isoflurane anesthesia. We hypothesized that epinephrine enhances atrial, atrioventricular junctional, and ventricular dysrhythmias after SA node excisions in dogs and that inhalation anesthetics would facilitate such dysrhythmias.

Methods: In eight dogs, SA nodes were excised and epicardial electrodes implanted at the atrial appendages, at the His bundle, and along the sulcus terminalis. Site of the earliest atrial activation and incidences of nonatrial beats were determined in the conscious state, with methylatropine, with epinephrine, and during halothane, isoflurane, or enflurane anesthesia.

Results: After SA node excision, a stable, regular subsidiary atrial pacemaker rhythm resulted. Epinephrine and halothane shifted the site of earliest activation to more remote atrial sites. Epinephrine-induced ventricular escape was increased by all anesthetics tested, but atropine prevented ventricular escape. Epinephrine-induced His bundle (atrioventricular junctional) and premature ventricular beats were increased by halothane and enflurane. After SA node excision, ventricular escape occurred as a result of epinephrine-anesthetic interactions, especially during anesthesia with isoflurane.     

Pulmonary Vascular Effects of Isoflurane Anesthesia after Left Lung Autotransplantation in Chronically Instrumented Dogs

Background: Single lung transplantation has become a viable therapy for treatment of end-stage pulmonary disease. We previously observed that left lung autotransplantation (LLA) results in a chronic increase in pulmonary vascular resistance and enhanced pulmonary vascular reactivity to sympathetic alpha adrenoreceptor activation. The effects of inhalational anesthetics on the pulmonary circulation after lung transplantation have not been investigated. In the current study, the authors tested the hypothesis that isoflurane anesthesia, known to cause systemic vasodilation, would exert a vasodilator influence on the baseline pulmonary circulation after LLA. In addition, they tested the hypothesis that isoflurane anesthesia, known to attenuate the systemic vasoconstrictor response to sympathetic alpha adrenoreceptor agonists, would reduce the magnitude of the pulmonary vasoconstrictor response to sympathetic alpha adrenoreceptor activation after LLA.

Methods: Left pulmonary vascular pressure-flow (LPQ) plots were generated in chronically instrumented dogs by measuring the pulmonary vascular pressure gradient (pulmonary arterial pressure-left atrial pressure) and left pulmonary blood flow during inflation of a hydraulic occluder implanted around the right main pulmonary artery. Left pulmonary vascular pressure-flow plots were generated in 8 dogs 2-5 weeks after LLA in the conscious and isoflurane-anesthetized states at baseline, after beta adrenoreceptor block with propranolol, and during the cumulative administration of the alpha agonist, phenylephrine. Left pulmonary vascular pressure-flow plots also were generated in eight conscious, sham-operated control dogs at baseline, after beta block, and during phenylephrine administration.

Results: Compared with conscious control dogs, LLA resulted in a leftward shift (P < 0.01) in the baseline left pulmonary vascular pressure-flow relation, indicating chronic pulmonary vasoconstriction. Despite the enhanced level of pulmonary vasomotor tone after LLA, isoflurane did not exert a vasodilator influence on the baseline left pulmonary vascular pressure-flow relation. The pulmonary vasoconstrictor response to phenylephrine was enhanced (P < 0.01) after LLA compared with the response measured in conscious control dogs. The magnitude of the pulmonary vasoconstrictor response to phenylephrine after LLA was not attenuated during isoflurane anesthesia.     

Ketamine Preserves and Propofol Potentiates Hypoxic Pulmonary Vasoconstriction Compared with the Conscious State in Chronically Instrumented Dogs

Background: The authors tested the hypothesis that ketamine and propofol anesthesia would alter the magnitude of hypoxic pulmonary vasoconstriction compared with the conscious state. In addition, they assessed the extent to which cyclooxygenase pathway inhibition and adenosine triphosphate-sensitive potassium channel inhibition modulate hypoxic pulmonary vasoconstriction in the conscious state, and whether these pathways are altered during propofol anesthesia.

Methods: Twenty conditioned, male mongrel dogs were chronically instrumented to measure the left pulmonary vascular pressure-flow relationship. Pressure-flow plots were measured during normoxia and hypoxia (systemic arterial PO2 reduced to about 60 and about 50 mmHg) on separate days in the conscious state, during ketamine anesthesia, and during propofol anesthesia. The effects of indomethacin and glibenclamide on the magnitude of hypoxic pulmonary vasoconstriction were also assessed in the conscious and propofol-anesthetized states.

Results: Neither ketamine nor propofol had an effect on the baseline pressure-flow relationship during normoxia compared with the conscious state. Hypoxia resulted in stimulus-dependent pulmonary vasoconstriction (P < 0.01) in the conscious state. Compared with the conscious state, the magnitude of hypoxic pulmonary vasoconstriction was preserved during ketamine but was potentiated (P < 0.01) during propofol anesthesia. Indomethacin enhanced (P < 0.01) hypoxic pulmonary vasoconstriction in both the conscious and propofol-anesthetized states. In contrast, glibenclamide only enhanced (P < 0.01) hypoxic pulmonary vasoconstriction in the conscious state and had no effect during propofol anesthesia.     

Role of Heparin and Nitric Oxide in the Cardiac and Regional Hemodynamic Properties of Protamine in Conscious Chronically Instrumented Dogs

Background: Because protamine is administered to reverse heparin, a drug that might itself affect the pharmacologic properties of protamine, this study was designed to assess the properties of protamine alone and in the presence of heparin in conscious dogs.

Methods: Twelve dogs were instrumented to continuously record cardiac and regional hemodynamics. On separate occasions, a dose of protamine (0.5, 1, 3, 5, and 8 mg/kg) was randomly administered either alone or in the presence of heparin (ratio 100 IU/mg). Heparin (300 IU/kg) and protamine (3 mg/kg) were administered in the presence of N-methyl-l-arginine, a specific nitric oxide synthase inhibitor. Identical experiments were performed with protamine (8 mg/kg) in the absence of heparin on a separate occasion.

Results: Protamine alone produced limited cardiac and regional changes. In the presence of heparin, protamine produced hypotension at 3, 5, and 8 mg/kg, vasodilatation at 3 and 5 mg/kg, and a more pronounced dose-dependent increase in pulmonary pressure at 3, 5, and 8 mg/kg. Simultaneously, transient carotid vasodilatation at 3 and 5 mg/kg, coronary and hepatic vasodilatation at 3, 5, and 8 mg/kg, as well as a decrease in vertebral vascular resistance were recorded at 1, 3, and 8 mg/kg. Protamine produced an immediate increase followed by a secondary decrease in renal vascular resistance. Protamine-induced secondary pulmonary pressor effects were attenuated. In the presence of heparin, nitric oxide synthase blockade selectively attenuated protamine-induced immediate hypotension, systemic vasodilatation, and coronary, mesenteric, and hepatic vasodilations as well as the decrease in portal blood flow and accentuated the renal vasoconstriction.     

Preservation of Hypoxic Pulmonary Vasoconstriction during Sevoflurane and Desflurane Anesthesia Compared to the Conscious State in Chronically Instrumented Dogs

Background: The authors' objective was to assess the extent to which sevoflurane and desflurane anesthesia alter the magnitude of hypoxic pulmonary vasoconstriction compared with the response measured in the same animal in the conscious state.

Methods: Left pulmonary vascular pressure-flow plots were generated in seven chronically instrumented dogs by continuously measuring the pulmonary vascular pressure gradient (pulmonary arterial pressure-left atrial pressure) and left pulmonary blood flow during gradual ([tilde operator] 1 min) inflation of a hydraulic occluder implanted around the right main pulmonary artery. Pressure-flow plots were generated during normoxia and hypoxia on separate days in the conscious state, during sevoflurane ([tilde operator] 3.5% end-tidal), and during desflurane ([tilde operator] 10.5% end-tidal) anesthesia. Values are mean +/- SEM.

Results: In the conscious state, administration of the hypoxic gas mixture by conical face mask decreased (P < 0.01) systemic arterial PO2 from 94 +/- 2 mmHg to 50 +/- 1 mmHg and caused a leftward shift (P < 0.01) in the pressure-flow relationship, indicating pulmonary vasoconstriction. The magnitude of hypoxic pulmonary vasoconstriction in the conscious state was flow-dependent (P < 0.01). Neither anesthetic had an effect on the baseline pressure-flow relationship during normoxia. The magnitude of hypoxic pulmonary vasoconstriction during sevoflurane and desflurane was also flow-dependent (P < 0.01). Moreover, at any given value of flow the magnitude of hypoxic pulmonary vasoconstriction was similar during sevoflurane and desflurane compared with the conscious state.     

Isoflurane and the Pulmonary Vascular Pressure-Flow Relation at Baseline and during Sympathetic alpha- and beta-Adrenoreceptor Activation in Chronically Instrumented Dogs

Background: The extent to which isoflurane anesthesia alters systemic vascular regulation has received considerable attention. In contrast, the pulmonary vascular effects of isoflurane have not been elucidated. Our initial objective was to investigate the net effect of isoflurane on the baseline left pulmonary vascular pressure-flow (LPQ with dot with dot) relation compared with values measured in the conscious state. In addition, we assessed the extent to which isoflurane alters the pulmonary vascular responses to sympathetic alpha- and beta-adrenoreceptor activation.

Methods: Twelve conditioned mongrel dogs were chronically instrumented to measure the LPQ with dot relation. LPQ with dot plots were generated by continuously measuring the pulmonary vascular pressure gradient (pulmonary arterial pressure left atrial pressure) and left pulmonary blood flow during gradual ([nearly equal] 1 min) inflation of a hydraulic occluder implanted around the right main pulmonary artery. LPQ with dot plots were generated at baseline in the conscious and isoflurane-anesthetized states (n 12). The pulmonary vascular dose-response relation to the sympathetic alpha-adrenoreceptor agonist phenylephrine also was investigated in conscious and isoflurane-anesthetized dogs (n 6). Finally, after preconstriction with the thromboxane analogue U46619, the dose-response relation to the sympathetic beta-adrenoreceptor agonist isoproterenol was assessed in the conscious and isoflurane-anesthetized states (n 8).

Results: Compared with values measured in the conscious state, isoflurane anesthesia had no net effect on the baseline LPQ with dot relation. The magnitude of the pulmonary vasoconstrictor response to phenylephrine observed in conscious dogs was not altered during isoflurane anesthesia. In contrast, the pulmonary vasodilator response to isoproterenol was markedly potentiated (P < 0.01) during isoflurane anesthesia compared with that in the conscious state.     

Effects of Halothane and Enflurane Anesthesia on Sympathetic β-adrenoreceptor-mediated Pulmonary Vasodilation in Chronically Instrumented Dogs

Background: The authors previously reported that the pulmonary vasodilator response to the sympathetic [beta]-adrenoreceptor agonist isoproterenol is potentiated during isoflurane anesthesia compared with the conscious state. In the present in vivo study, the authors tested the hypothesis that halothane and enflurane anesthesia also enhance sympathetic [beta] adrenoreceptor-mediated pulmonary vasodilation. The authors also used the membrane-permeable analog of cyclic adenosine monophosphate (cAMP), dibutyryl cAMP, to help delineate the site in the signaling pathway for an anesthesia-induced effect on [beta] adrenoreceptor-mediated pulmonary vasodilation.

Methods: Mongrel dogs were chronically instrumented to measure the left pulmonary vascular pressure-flow (LPQ) relationship. LPQ plots were measured on separate days in the conscious, halothane-, and enflurane-anesthetized states at baseline, after preconstriction with the thromboxane analog U46619, and during the cumulative intravenous administration of isoproterenol. LPQ plots were also measured in conscious, halothane-, and isoflurane-anesthetized dogs after U46619 preconstriction and during the cumulative intravenous administration of dibutyryl cAMP.

Results: Compared with the conscious state, neither halothane nor enflurane had an effect on the baseline LPQ relationship. The magnitude of the pulmonary vasodilator response to isoproterenol was potentiated during halothane anesthesia but unchanged during enflurane anesthesia. The pulmonary vasodilator response to dibutyryl cAMP was not altered during either halothane or isoflurane anesthesia compared with the conscious state.     

Gastric Mucosal Perfusion in Dogs: Effects of Halogenated Anesthetics and of Hemorrhage

The gastrointestinal tract is one of the first organs affected by hypoperfusion during hemorrhagic shock. The hemodynamics and oxygen transport variables during hemorrhagic shock and resuscitation can be affected by the anesthetics used. In a model of pressure-guided hemorrhagic shock in dogs, we studied the effects of three halogenated anesthetics—halothane, sevoflurane, and isoflurane—at equipotent concentrations on gastric oxygenation. Thirty dogs were anesthetized with 1.0 minimum alveolar anesthetic concentration (MAC) of either halothane, sevoflurane, or isoflurane. A gastric tonometer was placed in the stomach to determine mucosal gastric CO₂ (PgCO₂) and for the calculation of gastric-arterial PCO₂ gradient (PCO₂ gap). The dogs were splenectomized and hemorrhaged to hold mean arterial pressure at 40–50 mm Hg over 45 min and then resuscitated with the shed blood volume. Hemodynamics, systemic oxygenation, and PCO₂ gap were measured at baseline, after 45 min of hemorrhage, and at 15 and 60 min after blood resuscitation. Hemorrhage induced reductions of mean arterial pressure and cardiac index, while systemic oxygen extraction increased (p <. 05), without significant differences among groups (p >. 05). Halothane group showed significant lower PCO₂ gap values than the other groups (p <. 05). After 60 min of shed blood replacement, all groups restored hemodynamics, systemic oxygenation, and PCO₂ gap to the prehemorrhage levels (p >. 05), without significant differences among groups (p >. 05). We conclude that halothane is superior to preserve the gastric mucosal perfusion in comparison to isoflurane and sevoflurane, in dogs submitted to pressure-guided hemorrhagic shock at equipotent doses of halogenated anesthetics.     

Primary Management of Cutaneous Melanoma: Excision and Sentinel Node Biopsy

During the last decade, the treatment of primary cutaneous melanoma has considerably changed. The aggressive behaviour of this disease stimulated surgeons to perform extensive resections and manage the regional nodes in a radical way. However, numerous studies indicate that a less aggressive treatment with lesser cosmetic and functional injury is associated with a similar outcome. There is no doubt that the quality of life will be significantly improved by using narrower excision margins and by further refinements of the sentinel node technique.     

Effects of Volatile Anesthetics on Atrial and AV Nodal Electrophysiological Properties in Guinea Pig Isolated Perfused Heart

Background: Knowledge of the anesthetic effects on atrial and atrioventricular (AV) nodal electrophysiologic properties is fundamental to understand the modulatory role of anesthetics on the pathogenesis of supraventricular tachycardias, and to individualize the perioperative management of patients with supraventricular tachycardias or AV nodal conduction disturbances. Therefore the authors studied the effects of three commonly used volatile anesthetics on the electrophysiologic properties of the atrium and AV node.

Methods: The concentration-dependent electrophysiologic effects of halothane, isoflurane, and desflurane (0 - 2 minimum alveolar concentration [MAC]) were studied in guinea pig Langendorff-perfused hearts fit with instruments to simultaneously measure atrial and AV nodal conduction times and atrial monophasic action potential duration. Atrial and AV nodal effective refractory periods were measured simultaneously using a computer-assisted premature stimulation protocol. The concentrations of anesthetics in the gas phase were monitor by an infrared gas analyzer.

Results: Volatile anesthetics caused markedly different concentration-dependent effects on atrial conduction, repolarization, and refractoriness, and on AV nodal function. At equianesthetic concentrations, halothane depressed atrial conduction the most, whereas desflurane caused the greatest shortening of atrial monophasic action potential duration. Halothane had no significant effect on atrial refractoriness, whereas at 2 MAC desflurane significantly shortened and isoflurane significantly prolonged atrial effective refractory periods by 18.1 +/- 13.5% and 13.2 +/- 14.7%, respectively. On an equi-MAC basis, the rank order of potency for the anesthetics to prolong AV nodal conduction time and AV nodal ERP was halothane > desflurane > isoflurane.     

Impact of Autonomic Nerve Preservation and Lateral Node Dissection on Male Urogenital Function after Total Mesorectal Excision for Lower Rectal Cancer

Introduction Urogenital dysfunction is a well recognized complication of rectal cancer surgery. The aim of this study was to assess the impact of autonomic nerve preservation (ANP) and lateral node dissection (LND) on male urogenital function after total mesorectal excision for lower rectal cancer. Methods We studied, using a questionnaire, preoperative and current urogenital function in 47 male patients who underwent total mesorectal excision with the ANP technique for lower rectal cancer. Patients with and without LND were analyzed separately. Results A total of 37 patients (78.7%) (22 patients without LND, 15 with LND) returned the questionnaire. Among the 15 patients with LND, 2 underwent unilateral ANP. One patient without LND had urinary dysfunction preoperatively, and among the other 21 patients only 2 (9.5%) reported minor urinary complications postoperatively. After LND, 5 patients (33%) reported minor complications; there were no severe complications. Among patients who were sexually active prior to the operation, 90% and 70% of patients without LND and 50% and 10% of those with LND maintained sexual activity and ejaculation, respectively. However, 50% of patients who underwent low anterior resection or Hartmann resection without LND and all patients with abdominoperineal resection or LND reported reduced overall sexual satisfaction. Conclusions The ANP technique offers the great advantage of maintaining urogenital function after rectal cancer surgery. After LND, although the ANP technique minimized urinary dysfunction, sexual function, particularly ejaculation, was often damaged. Careful follow-up is important even after ANP to improve postoperative sexual satisfaction.     

Effects of Intravenous Anesthetics on Atrial Wavelength and Atrioventricular Nodal Conduction in Guinea Pig Heart: Potential Antidysrhythmic Properties and Clinical Implications

Background: Supraventricular tachydysrhythmias such as atrial fibrillation frequently complicate the perioperative period. Two electrophysiologic factors critical to the pathogenesis of supraventricular tachydysrhythmias are: 1) atrial wavelength, the product of atrial conduction velocity (CV) and effective refractory period (ERP), and 2) atrioventricular nodal conduction. Modulation of these factors by drugs has important clinical ramifications. The authors studied the effects of propofol, thiopental, and ketamine on atrial wavelength and atrioventricular nodal function in guinea pig isolated atrial trabeculae and hearts, respectively.

Methods: Electrocardiogram recordings in superfused atrial tissue were obtained using hanging microelectrodes. A stimulating and two recording electrodes were placed on a single atrial trabecula, and the interelectrode distance was measured. Atrial ERP determinations were made using a premature stimulus protocol. The time (t) required for a propagated impulse to traverse the interelectrode distance (d) was measured. Conduction velocity was calculated as d/t. Langendorff-perfused guinea pig hearts were instrumented for low atrial pacing (cycle length = 300 ms) and for measurements of stimulus-to-His bundle interval, an index of atrioventricular nodal conduction. To investigate the frequency-dependent behavior of the atrioventricular node, computer-based measurements were made of Wenckebach cycle length (WCL) and atrioventricular nodal ERP.

Results: Thiopental significantly prolonged atrial ERP in a concentration-dependent manner, whereas propofol and ketamine had no significant effect on atrial refractoriness. In contrast, ketamine caused a dose-dependent decrease in atrial CV, but propofol and thiopental had no significant effect on CV. Therefore, thiopental, ketamine, and propofol caused an increase, a decrease, and no change, respectively, in atrial wavelength. All anesthetics caused a concentration-dependent prolongation of the stimulus-to-His bundle interval, atrioventricular nodal ERP, and WCL. However, on an equimolar basis, significant differences in potencies were found. The concentrations of drug that caused a 20% increase in ERP (ERP20) and WCL (WCL20) for propofol, thiopental, and ketamine were 14+/-2 micro Meter, 26+/-3 micro Meter, and 62 +/-11 micro Meter, and 17+/-2 micro Meter, 50+/- 1 micro Meter, and 123+/-19 micro Meter (mean+/-SEM), respectively. Therefore, the rank order of potency for frequency-dependent atrioventricular nodal effects is propofol > thiopental > ketamine.     

Effects of Isoflurane Anesthesia on Pulmonary Vascular Response to K (ATP)+ Channel Activation and Circulatory Hypotension in Chronically Instrumented Dogs

Background: The objective of this study was to evaluate the effects of isoflurane anesthesia on the pulmonary vascular responses to exogenous adenosine triphosphate-sensitive potassium (KATP+) channel activation and circulatory hypotension compared with responses measured in the conscious state. In addition, the extent to which KATP+ channel inhibition modulates the pulmonary vascular response to circulatory hypotension in conscious and isoflurane-anesthetized dogs was assessed.

Methods: Fifteen conditioned, male mongrel dogs were fitted with instruments for long-term monitoring to measure the left pulmonary vascular pressure-flow relation. The dose-response relation to the KATP+ channel agonist, lemakalim, and the pulmonary vascular response to circulatory hypotension were assessed in conscious and isoflurane-anesthetized (approximately 1.2 minimum alveolar concentration) dogs. The effect of the selective KATP+ channel antagonist, glibenclamide, on the pulmonary vascular response to hypotension was also assessed in conscious and isoflurane-anesthetized dogs.

Results: Isoflurane had no effect on the baseline pulmonary circulation, but it attenuated (P < 0.05) the pulmonary vasodilator response to lemakalim. Reducing the mean systemic arterial pressure to approximately 50 mmHg resulted in pulmonary vasoconstriction (P < 0.05) in the conscious state, and this response was attenuated (P < 0.05) during isoflurane. Glibenclamide had no effect on the baseline pulmonary circulation, but it potentiated (P < 0.05) the pulmonary vasoconstrictor response to hypotension in conscious and isoflurane-anesthetized dogs.     

Atrial fibrillation after non-cardiac surgery: P-wave characteristics and Holter monitoring in risk assessment.

BACKGROUND: We investigated the role of 12-lead ECG P-wave duration and dispersion and of Holter monitoring as predictors of post-thoracic surgery atrial fibrillation. METHODS: One hundred and five consecutive patients (88 males-17 females; age 60+/-9), undergoing thoracic surgery at National Cancer Institute between 2001 and 2003, were enrolled and both standard ECG and Holter monitoring were obtained from each patient. P-wave study was made on a magnified ECG paper copy. Holter monitoring was performed 1-3 days before surgery; patients were divided into three classes according to number and complexity of premature supra ventricular complexes (0: <30/h and no repetitive forms; 1: >30/h or couplets; 2: run of supraventricular tachycardia or atrial fibrillation). RESULTS: Atrial fibrillation was detected in 12 patients (11%) within 96 h from surgery. In univariable logistic model, P-wave duration was not associated with postoperative atrial fibrillation while P-wave dispersion and Holter monitoring demonstrated a statistically significant association with the occurrence of atrial fibrillation (OR of 30 vs 20 ms=2.06; CI: 1.17-3.64; p=0.012, OR of class 1-2 vs class 0=8.16; CI: 2.04-35.59; p=0.003, respectively). In the multivariable model, both P-wave dispersion and Holter were shown to be significantly associated with the end-point. Holter monitoring enhanced the predictive ability of P-wave dispersion (area under the ROC curve increased from 0.64 to 0.80). CONCLUSIONS: P-wave dispersion, but not duration, was associated with atrial fibrillation after thoracic surgery. Preoperative Holter monitoring adds further information and could be used to enhance the P-wave predictive power.     

Ectopic bone after hip replacement. Excision and free fat transplants in four cases

In four patients ectopic bone formed after total hip replacement was replaced with free fat transplants. One year later the patients were free from pain, and hip flexion had increased by 60 degrees on average. Ectopic bone was completely absent in one patient, and markedly reduced in the remaining three patients. Bone scintigraphy was found to be a sensitive technique to reveal early ectopic bone formation. Fat transplantation seems to be a satisfactory complement in the treatment of ectopic bone.     

Extopic bone after hip replacement: Excision and free fat transplants in four cases

In four patients ectopic bone formed after total hip replacement was replaced with free fat transplants. One year later the patients were free from pain, and hip flexion had increased by 60 degrees on average. Ectopic bone was completely absent in one patient, and markedly reduced in the remaining three patients. Bone scintigraphy was found to be a sensitive technique to reveal early ectopic bone formation. Fat transplantation seems to be a satisfactory complement in the treatment of ectopic bone.     

Excision of the lunate in Kienb?ck's disease. Results after long-term follow-up

Excision of the lunate was performed for 18 patients with Kienb?ck's disease; 14 were followed up for an average of almost 12 years. Carpal collapse progressed with time, but rearrangement of the remaining carpal bones preserved a satisfactory range of movement and grip strength. Degenerative changes were not severe. All the patients had relief of pain, were able to carry out their normal activities, and all but two could perform strenuous activities.     

Local Recurrence after Intended Curative Excision of Presacral Lesions: Causes and Preventions

Objective  

This study was designed to explore causes for local recurrence of presacral lesions after intended curative surgery and discuss prevention strategies.