FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2076674772> ?p ?o ?g. }

• W2076674772 endingPage "815" @default.
• W2076674772 startingPage "812" @default.
• W2076674772 abstract "Patients with pulmonary hypertension have markedly increased morbidity and mortality with anesthesia and surgery [1,2]. For patients with Eisenmenger's syndrome undergoing cesarean section, mortality is 46%-70% [3]. The risks associated with primary pulmonary hypertension (PPH) seem to be even more frequent than those related to secondary pulmonary hypertension [4]. Reports of successful outcomes of surgery in patients with primary pulmonary hypertension include curative procedures such as lung or heart-lung transplantation, cesarean section [2,3], and relatively brief procedures with minor blood loss and fluid shifts (lung biopsy, cholecystectomy, femoral artery repair, and laparoscopic tubal ligation) [5-9]. The following case report describes a patient with PPH who successfully underwent combined abdominal aortic aneurysmectomy and hysterectomy. This case report emphasizes the value of preoperative pulmonary vasodilator testing to determine the risks of anesthesia and surgery and to provide a therapeutic option in the perioperative period. In this case report, we also discuss an approach to postoperative management of these patients. Case Report A 72-yr-old, 160-cm, 83-kg woman with pulmonary hypertension presented for repair of an abdominal aortic aneurysm and supracervical hysterectomy with bilateral salpingo-oophorectomy. Her medical history was significant for borderline hypertension (150/90 mm Hg), hypercholesterolemia, localized scleroderma (skin involvement only), and obesity. Because of a 2-yr history of progressive dyspnea on exertion, she underwent an echocardiogram, which showed normal left ventricular size and contractility, left ventricular hypertrophy, right atrial enlargement, a dilated hypokinetic right ventricle, a D-shaped septum (consistent with right ventricular pressure overload), moderate tricuspid regurgitation, and an estimated pulmonary artery (PA) systolic pressure of 74 mm Hg. Pulmonary evaluation included a chest radiograph remarkable only for increased prominence of the central pulmonary vessels; normal lung perfusion scan; analysis of blood gases: fraction of inspired oxygen 0.21, PaO2 49 mm Hg, PaCO (2) 48 mm Hg, and pHa 7.43; and pulmonary function tests: forced expiratory volume in 1 s 1.00 L, forced vital capacity 1.05 L, total lung capacity 2.56 L, and carbon monoxide diffusing capacity 64%. Immunologic studies revealed a positive antinuclear antibody at 1:160 with a speckled pattern, but negative anti-centromere, anti-DNA, anti-ENA, anti-SCL-70, and Sjogren's antibodies. Her oral medications included furosemide 120 mg qd, KCl 20 mEq qd, digoxin 0.25 mg qd, cimetidine 800 mg qd, and apresoline 20 mg qid. A large pelvic mass was noted on physical examination, and an ultrasound demonstrated a markedly enlarged fibroid uterus (approximately 20-wk size) with an area suspicious for neoplasm. An incidental finding on ultrasound was an 8- to 9-cm infrarenal abdominal aortic aneurysm (AAA). An abdominal aortogram confirmed a 9-cm AAA. To determine the patient's suitability for surgery, she was admitted to the intensive care unit for preoperative trials of pulmonary vasodilator therapy. A PA catheter was inserted. Baseline PA pressure (PAP) was 69/25 mm Hg with a mean of 42 mm Hg and a pulmonary artery occlusion pressure (PAOP) of 10 mm Hg (Table 1). The pulmonary vasodilator responses to oxygen, inhaled nitric oxide (via a nonrebreathing mask), IV nitroglycerin, and oral nifedipine were assessed (Table 1). Significant decreases in pulmonary hypertension and pulmonary vascular resistance occurred with oxygen and nitroglycerin but not with inhaled nitric oxide (5 and 20 ppm) or nifedipine (80 mg over 6 h). The responses to nitroglycerin and oxygen were additive, and inhaled nitric oxide did not increase the response to oxygen. Because pulmonary hypertension during combined oxygen and nitroglycerin therapy was only moderate, the patient was considered a candidate for the planned major surgery.Table 1: Pulmonary Artery Pressure (PAP) and Cardiac Output (CO) in Response to Pulmonary VasodilatorsBefore the induction of anesthesia 2 wk later, radial artery and PA catheters were inserted. PAP was 80/27 mm Hg with a mean of 52 mm Hg. General endotracheal anesthesia was induced with oxygen, sufentanil, pancuronium, and midazolam IV, and an infusion of nitroglycerin was begun. Anesthesia was maintained with sufentanil and midazolam. PAP decreased to 51/27 mm Hg with a mean of 39 mm Hg before incision. The patient underwent supracervical hysterectomy with bilateral salpingo-oophorectomy, followed by resection of a 10-cm infrarenal AAA and reconstruction with an aortobiiliac graft. Surgery duration was 5 h 45 min. Estimated blood loss was 3800 mL. IV fluid administration included 8 U of packed red blood cells, 1000 mL of cell-saver blood, and 1100 mL of crystalloid. Aortic cross-clamp time was 1 h 22 min. A nitroglycerin infusion was titrated throughout surgery to maintain a mean PAP of 25-35 mm Hg. With the exception of a brief period of hypotension requiring small-dose epinephrine (25 ng kg-1 min-1) after removal of the aortic cross-clamp, the patient's systemic and pulmonary hemodynamic variables were stable throughout surgery. The patient was transferred to the intensive care unit after surgery. On admission to the intensive care unit, hemodynamics included PAP 38/21 mm Hg with a mean of 27 mm Hg, PAOP 10 mm Hg, and cardiac output 3.5 L/min. Based on the high risk of severe perioperative exacerbation of the patient's pulmonary hypertension, it was decided to continue deep sedation (patient unresponsive to verbal stimuli) and mechanical ventilation for the next 48 h. Sedation was achieved with a fentanyl infusion and intermittent doses of midazolam. Fluid balance for the first 2 days was positive by 4 L. Mean PAP increased to 35-40 mm Hg, but PAOP never exceed 10 mm Hg. On Postoperative Day (POD) 3, PAOP increased to 14 mm Hg, and active diuresis with a furosemide infusion (2-4 mg/h) was initiated. Fluid balance was negative by 1.5 L on that day and by an additional 5 L on the following day. Decreased sedation and weaning from mechanical ventilation were attempted on POD 5 but resulted in marked increases in the PAP (80/38 mm Hg) and an episode of pulseless bradycardia (mean arterial pressure 35 mm Hg) that spontaneously resolved over 2-3 min. Sedation was increased, and full mechanical ventilation was continued. Further attempts at weaning on PODs 6 and 7 resulted in less severe increases of PAP, which were successfully treated with nitroglycerin (0.3-0.5 [micro sign]g kg-1 min-1) to maintain mean PAP <35 mm Hg; fluid balance was negative by approximately 1.5 L on each of these days. The patient's trachea was extubated on POD 7. The remainder of her hospital course was unremarkable. She was discharged home with medications that included nitroglycerin ointment. Pathologic results from her uterus revealed papillary serous adenocarcinoma, and the patient was referred to an oncologist for follow-up. Discussion This patient successfully underwent anesthesia and surgery for combined abdominal aortic resection and supracervical hysterectomy. This is the first report of a patient with pulmonary hypertension surviving a noncardiac procedure of this magnitude other than liver transplantation [10,11]. This patient seems to have primary pulmonary hypertension, possibly in association with an as yet undiagnosed connective tissue disease. Pulmonary hypertension caused by left ventricular failure, valvular heart disease, cardiac shunts, and pulmonary thromboembolism were excluded by the diagnostic studies. The significant abnormalities on pulmonary function tests were not severe enough to produce pulmonary hypertension; the restrictive pattern and mild hypoxemia seen in this patient are not uncommon in patients with PPH [12]. The operative and perioperative anesthetic treatment of patients with pulmonary hypertension undergoing noncardiac surgery has received little attention in the literature. Most discussion has been limited to obstetrical anesthesia case reports in adults and case series of repair of congenital heart defects in pediatric patients [1,2,13]. Two anesthetic techniques used during open lung biopsies have also been reported: Armstrong [6] described the use of a combination of general anesthesia and epidural analgesia, whereas Cheng and Edelist [5] used general anesthesia with isoflurane to decrease PAP. Davies and Beavis [8] used epidural anesthesia for femoral artery repair, and Mallampatti [7] used epidural anesthesia for cholecystectomy. Similarly, we have used thoracic epidural anesthesia for cholecystectomy, general anesthesia for placement of a peritoneal catheter for daily drainage of chronic ascites, and either general anesthesia or epidural anesthesia for cesarean section and therapeutic abortion in patients with pulmonary hypertension. However, a successful outcome with an operation of the magnitude of this case seems to be unprecedented, except those in which the operation is itself directed toward the etiology of pulmonary hypertension (repair of congenital heart disease, lung transplantation). Progressive or acute increases in PAP leading to acute right heart failure are the major complications of anesthesia and surgery in patients with pulmonary hypertension. At the time of initial evaluation, this patient's pulmonary hypertension seemed to be severe enough to preclude major surgery. Given the extreme risk of rupture of a 9-cm AAA, we decided to determine whether pulmonary vasodilators would decrease her pulmonary hypertension to a level compatible with an acceptable operative risk. This approach is used in the evaluation of patients with pulmonary hypertension for heart transplantation [14-16] and has been advocated in selected patients with pulmonary hypertension undergoing noncardiac surgery [17,18]. The results of our patient were unexpected, with a response to nitroglycerin and oxygen but with no response to inhaled nitric oxide or calcium channel blockers. Nitroglycerin produces vasodilation in both the pulmonary and systemic vasculature by releasing nitric oxide (endothelium-derived relaxing factor), which binds to guanylyl cyclase and increases intracellular levels of cyclic GMP. Inhaled nitric oxide produces pulmonary vasodilation without producing systemic vasodilation because it is inactivated by hemoglobin when absorbed into the blood from the lung [19-21]. The pulmonary vasodilator effects of inhaled nitric oxide are at least as large as those of IV vasodilators [14-16,21-23]. On the basis of its rapid onset, brief duration of action, and selective pulmonary vasodilator effects, inhaled nitric oxide has been used as a screening drug to assess pulmonary vascular reactivity. Most of those studies have compared inhaled nitric oxide with calcium channel blockers or acute IV prostacyclin. The current case report demonstrates that patients may respond to nitroglycerin despite a lack of response to inhaled nitric oxide. Nitroglycerin is an effective vasodilator in patients with chronic pulmonary hypertension [24] and for acute postoperative pulmonary hypertension [25,26]. Presumably, nitroglycerin released nitric oxide in portions of the pulmonary circulation in which inhaled nitric oxide was not effective. Although nitric oxide diffuses readily across cell membranes, it may not have reached vessels upstream (arterioles) or vessels downstream (venules) from the alveoli, which were perfused by blood and responded to IV nitroglycerin. Additionally, nitric oxide would not have reached alveolar vessels that were perfused but not ventilated; such vessels would respond to IV nitroglycerin but not to inhaled nitric oxide, a situation that occurs in patients with the acute respiratory distress syndrome but is not usually considered to occur in patients with PPH. The ability of inhaled oxygen but not inhaled nitric oxide to decrease pulmonary hypertension is more difficult to explain, because both molecules should reach similar vessels in the lung, and inhaled nitric oxide effectively reverses hypoxic pulmonary vasoconstriction. Deaths of patients with pulmonary hypertension undergoing surgery often occur during the first several postoperative days and may occur suddenly [1,3,17]. Neonates who develop paroxysms of severe pulmonary hypertension after the repair of congenital heart defects likewise have a high mortality [27]. Possible etiologies include a progressive increase in pulmonary vascular tone, acute pulmonary vasospasm, pulmonary thromboembolism, increased sympathetic tone, and fluid shifts. To minimize these risks, we decided to treat this patient's first 48 h postoperatively as an extended operative period, i.e., the patient was kept fully sedated and mechanically ventilated. This strategy was initially successful because she had stable pulmonary and systemic hemodynamics during this time period. After 48 h, during weaning from mechanical ventilation, she had paroxysms of severe pulmonary hypertension, one of which may have precipitated her brief episode of pulseless electrical activity. Weaning was then delayed until POD 5, allowing further recovery from surgery and diuresis. Increased PAPs during subsequent weaning attempts were successfully treated with nitroglycerin. In summary, a woman with severe pulmonary hypertension successfully underwent major surgery with extensive blood loss. A preoperative trial of pulmonary vasodilator therapy was used to demonstrate reduction in pulmonary hypertension to a level compatible with an acceptable operative risk. Despite a lack of response to inhaled nitric oxide and nifedipine, pulmonary hypertension markedly decreased with IV nitroglycerin. After surgery, sedation and mechanical ventilation were used to prevent reactive pulmonary hypertension, followed by nitroglycerin to control pulmonary hypertension during weaning. This approach may be useful for patients with pulmonary hypertension who require major surgery." @default.
• W2076674772 created "2016-06-24" @default.
• W2076674772 creator A5042596253 @default.
• W2076674772 creator A5048492805 @default.
• W2076674772 date "1998-10-01" @default.
• W2076674772 modified "2023-09-30" @default.
• W2076674772 title "Pulmonary Hypertension and Major Surgery" @default.
• W2076674772 cites W1900412604 @default.
• W2076674772 cites W1927797304 @default.
• W2076674772 cites W1978633994 @default.
• W2076674772 cites W1984917769 @default.
• W2076674772 cites W2004513382 @default.
• W2076674772 cites W2009344627 @default.
• W2076674772 cites W2031480665 @default.
• W2076674772 cites W2039926254 @default.
• W2076674772 cites W2042322531 @default.
• W2076674772 cites W2047189953 @default.
• W2076674772 cites W2055212431 @default.
• W2076674772 cites W2062256657 @default.
• W2076674772 cites W2064537677 @default.
• W2076674772 cites W2069058817 @default.
• W2076674772 cites W2070272817 @default.
• W2076674772 cites W2080591848 @default.
• W2076674772 cites W2140148084 @default.
• W2076674772 cites W2162769174 @default.
• W2076674772 cites W2399243884 @default.
• W2076674772 cites W2412024152 @default.
• W2076674772 cites W2462912424 @default.
• W2076674772 cites W316293548 @default.
• W2076674772 cites W4240624833 @default.
• W2076674772 cites W4249385634 @default.
• W2076674772 doi "https://doi.org/10.1097/00000539-199810000-00013" @default.
• W2076674772 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9768775" @default.
• W2076674772 hasPublicationYear "1998" @default.
• W2076674772 type Work @default.
• W2076674772 sameAs 2076674772 @default.
• W2076674772 citedByCount "13" @default.
• W2076674772 countsByYear W20766747722012 @default.
• W2076674772 countsByYear W20766747722013 @default.
• W2076674772 countsByYear W20766747722014 @default.
• W2076674772 countsByYear W20766747722015 @default.
• W2076674772 countsByYear W20766747722018 @default.
• W2076674772 countsByYear W20766747722019 @default.
• W2076674772 countsByYear W20766747722023 @default.
• W2076674772 crossrefType "journal-article" @default.
• W2076674772 hasAuthorship W2076674772A5042596253 @default.
• W2076674772 hasAuthorship W2076674772A5048492805 @default.
• W2076674772 hasBestOaLocation W20766747721 @default.
• W2076674772 hasConcept C164705383 @default.
• W2076674772 hasConcept C177713679 @default.
• W2076674772 hasConcept C2780930700 @default.
• W2076674772 hasConcept C71924100 @default.
• W2076674772 hasConceptScore W2076674772C164705383 @default.
• W2076674772 hasConceptScore W2076674772C177713679 @default.
• W2076674772 hasConceptScore W2076674772C2780930700 @default.
• W2076674772 hasConceptScore W2076674772C71924100 @default.
• W2076674772 hasIssue "4" @default.
• W2076674772 hasLocation W20766747721 @default.
• W2076674772 hasLocation W20766747722 @default.
• W2076674772 hasLocation W20766747723 @default.
• W2076674772 hasOpenAccess W2076674772 @default.
• W2076674772 hasPrimaryLocation W20766747721 @default.
• W2076674772 hasRelatedWork W2046069863 @default.
• W2076674772 hasRelatedWork W2048862592 @default.
• W2076674772 hasRelatedWork W2333145688 @default.
• W2076674772 hasRelatedWork W2410314862 @default.
• W2076674772 hasRelatedWork W2412645198 @default.
• W2076674772 hasRelatedWork W2595673966 @default.
• W2076674772 hasRelatedWork W2790232384 @default.
• W2076674772 hasRelatedWork W2990595088 @default.
• W2076674772 hasRelatedWork W2999964781 @default.
• W2076674772 hasRelatedWork W584255262 @default.
• W2076674772 hasVolume "87" @default.
• W2076674772 isParatext "false" @default.
• W2076674772 isRetracted "false" @default.
• W2076674772 magId "2076674772" @default.
• W2076674772 workType "article" @default.