Intractable hypotension caused by acute superior vena cava obstruction after lung cancer surgery: a case report

Intractable hypotension caused by acute superior vena cava obstruction after lung cancer surgery: a case report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Intractable hypotension caused by acute superior vena cava obstruction after lung cancer surgery: a case report Qing Li, Xianqiang Ding, Jungang Luo, Peng Guo, Xianglin Wang This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-4299863/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract The purpose of this case report is to inform other anesthesiologists about the identification, judgment, and management of sudden severe refractory hypotension in resuscitation after right pneumonectomy. We present a patient who underwent right lung and mediastinal lymph node resection. When the patient recovered from anesthesia, due to the change of position, the mediastinal free tissue entered the space and pressed on the superior vena cava (SVC), resulting in complete obstruction of the SVC and causing severe intractable hypotension. A 48-year-old man with bronchial lung cancer developed severe hypotension while preparing to recover from open-chest surgery under general anesthesia combined with intraspinal anesthesia. There was no response to rapid dilatation, fluid replacement, or treatment with drugs that could raise blood pressure (such as ephedrine, norepinephrine, and deoxyadrenalin). Since early symptoms of acute SVC syndrome in general combined epidural anesthesia were similar to those of severe anaphylaxis, general spinal anesthesia, hemorrhagic shock, pulmonary embolism, and pericardial tamponade, it was difficult to make judgments. A second thoracic operation was performed to remove the remaining tissue that caused the compression, ultimately making a successful recovery. Severe hypotension induced by acute SVC obstruction may trigger and aggravate brain edema and other complications if we cannot quickly identify the patient or administer traditional treatment (upper limb or internal jugular vein dilation and fluid replacement). Given the risk of disease deterioration, immediate identification of the cause of intractable hypotension is crucial. Hypotension Intraspinal anesthesia Anaphylactic reaction Hemorrhagic shock Cardiogenic shock Acute SVC syndrome Figures Figure 1 Figure 2 Introduction Intraoperative hypotension is one of the most common complications after the induction of general anesthesia[1]. Quick identification of hypotension causes is instrumental for treating low blood pressure. The likelihood of acute SVC resulting from thoracic surgery is increased due to the anatomical proximity of the mediastinum and superior vena cava (SVC)[2]. For patients with no prior history of SVC stenosis, acute SVC obstruction due to sudden accidents may induce severe hemodynamic disturbances and cerebral edema because there is no collateral circulation to return[3]. Given that perioperative acute SVC is extremely rare and early signs of low blood pressure are hard to recognize, we analyzed the differentiation of total spinal anesthesia, anaphylactic shock, hemorrhagic shock, cardiogenic shock, pericardial tamponade, and SVC obstruction, as well as corresponding treatment measures. Case A 48-year-old male patient weighing 68 kg was diagnosed with lung cancer. After chemotherapy failed, the right thoracotomy was performed under general anesthesia combined with intraspinal anesthesia. A chest CT scan revealed right upper lobe central lung cancer complicated with upper lobe obstructive atelectasis and enlarged mediastinal lymph nodes (Figure 1). Other relevant tests such as electrocardiogram, heart color ultrasound, blood gas, and other tests demonstrated normal results. When the right lung was removed, intraoperative blood loss increased, accompanied by a gradual decrease in blood pressure. Rapid fluid rehydration and multiple intravenous ephedrine injections maintained blood pressure at 80-100 mmHg /50-60 mmHg. After hemostasis, blood pressure gradually increased to 120-140 mmHg/70-80 mmHg. The heart rate was maintained at approximately 100 beats/min, and the infusion speed decreased. Blood gas was rechecked at the end of the operation, showing no further decrease in hemoglobin and showing 800 mL of total blood loss, 1400 mL of urine volume, 2000 mL of crystal, and 500 mL of colloidal.The operation lasted a total of six hours. After the operation, the patient was maintained in a supine position to prepare for recovery. With gradually decreased blood pressure and increased heart rate but no changes in oxygen saturation and end-expiratory carbon dioxide observed, we performed immediate intravenous fluid replacement and administrated pressor medication. The blood pressure gradually decreased to 60-70/30-40 mmHg, and the heart rate exceeded 120 beats per minute. Increasing doses of intravenous blood pressure-raising drugs remained ineffective (blood pressure-raising drugs include ephedrine, norepinephrine, deoxyadrenalin etc). Considering the patient’s unexplained severe hypotension, we immediately contacted another anesthesiologist for help. Subsequently, we continued to increase the dose of intravenous blood pressure-raising medications. We found eyelid edema, jugular vein swelling, facial cyanosis. Central venous pressure was monitored again, showing central venous pressure at 40 cmH2O. Therefore, we immediately stop fluid replenishment. Over time, the patient’s upper chest started to turn purple. Considering that the patient had no special history, this may be caused by surgical factors. We therefore prepared to conduct chest exploration again. The right-side incision was performed again for chest exploration. It was found that after mediastinal lymph node resection, the free mediastinal tissue entered the space formed by lymph node dissection, thus compressing the SVC and causing acute SVC obstruction. After the rapid removal of the remaining tissue, blood pressure immediately returned to the normal range and the heart rate gradually decreased. As the surgeon removed the remaining mediastinal tissue, internal jugular vein irritation was observed and the patient’s skin color gradually returned to normal. The thoracic surgeon observed no other abnormalities, thus continuing the suture. This case presented a patient who underwent an operation for lung cancer to resect mediastinal lymph nodes, with acute obstruction of the SVC occurring due to the nearby residual tissue filling the space left after lymph node removal. The induced acute and refractory hypotension lasted for nearly 30 minutes, exhibiting no response to any vasopressor drug including norepinephrine and ephedrine. At the end of the operation, all symptoms of the patient were eliminated, and the patient’s blood pressure and heart rate returned to a stable state. The patient was sent to ICU for further treatment and observation. Fortunately, the next day after surgery, no abnormalities were found on chest CT examination after the tracheal catheter was removed (Figure 2). Therefore, the patient was returned to a general ward and discharged after 3 weeks. Discussion In recent years, the incidence of adverse cardiovascular events increased after perioperative surgery, attracting people’s wide attention to perioperative hypotension[1]. Current common definitions of intraoperative hypotension include a systolic blood pressure <80 mmHg, a systolic blood pressure drop below 20% of the patient’s baseline blood pressure, or a reduction of 30% greater than the patient’s baseline blood pressure despite a systolic blood pressure <100 mmHg[4].Low blood pressure that is not corrected in time can lead to insufficient perfusion of tissues and organs, thereby resulting in a series of complications[1].Severe hypotension during the perioperative period requires to be identified quickly and dealt with in time, thus reducing the incidence of complications. Unexpected intraspinal anesthesia can induce severe hypotension and even cardiac arrest, mainly sympathetic nerve block, causing vasodilation and severe blood volume insufficiency[5]. However, most hypotension can be corrected with rapid replenishment of blood volume and the application of vasopressor drugs[5]. However, epidural administration of small doses of opioids or local anesthetics can reduce postoperative pain stimulation, enabling patients to get out of bed as early as possible, thus promoting patients’ recovery and shortening the length of hospital stay[6]. For selective thoracic and abdominal open major surgery, if there is no contraindication, general anesthesia combined with epidural intraspinal anesthesia is more conducive to postoperative recovery[7]. Therefore, in this case, we used general combined intraspinal anesthesia. It is necessary to be alert to the possibility of total spinal anesthesia. Nonetheless, low blood volume was not indicated by the expansion of fluid, no response of hypotension to large doses of vasopressor drugs, tachycardia, or further increases in central venous pressure. As a result, hypotension caused by PSM was less likely. Anaphylaxis is a severe systemic hypersensitivity reaction with a rapid onset that features life-threatening airway, respiratory, and circulatory problems, associated with skin and mucosal changes[8]. Perioperative use of general anesthesia, local anesthesia, antibacterials, and other drugs can trigger severe allergic reactions.In this case, since we did not find any significant change in airway pressure, wheezing sound in lung auscultation, or presence of urticaria, skin flushing, and erythema during the treatment of hypotension, the anaphylactic shock was less likely. Traumatic hemorrhagic shock is a leading cause of death in emergencies. If left untreated, hemorrhagic shock will result in death. As an important means to monitor the adequacy of circulating blood volume in shock patients, CVP alone does not accurately reflect changes in effective blood volume because CVP is vulnerable to its own and external influences such as mechanical ventilation, severe cough, cardiac function, and other effects [9]. The continuous monitoring of the dynamic changes of CVP before and after the perioperative period is necessary to determine whether the fluid volume needs to be supplemented. Permissive hypotension and restricted fluid therapy are recommended for acute blood loss after using a combination of crystalline and colloidal solutions in the initial treatment. If the bleeding is not controlled, immediate blood product administration is recommended[10]. After treatment with rapid fluid rehydration and antihypertensive drugs, the patient’s blood pressure did not considerably improve. Thoracic drainage did not considerably increase. Blood gas report revealed no notable decrease in hemoglobin. Central venous pressure increased. Therefore, we believed that blood loss did not cause hypotension. Since echocardiography can quickly assess the underlying condition of the heart, patients suspected of cardiogenic shock are required to perform an immediate ultrasound, which helps analyze the cause of cardiogenic shock and determine if it is caused by pericardial tamponade[11]. In this case, when the patient had tachycardia, severe hypotension, high central venous pressure, and no response to medication, a cardiac ultrasound could be performed to quickly aid diagnosis. Acute pulmonary embolism is also a crucial risk factor for hemodynamic instability.In this case, the patient’s blood pressure was too low to perform CTPA. However, the patient did not undergo lower extremity surgery. He had no abnormal coagulation function before surgery, and did not undergo SVC clamping during surgery. The existing extremely high central venous pressure and cyanosis of the upper body skin indicated that pulmonary embolism was less likely. Severe intractable hypotension caused by intraoperative acute SVC syndrome is rare. SVC syndrome, including a range of symptoms and signs caused by SVC obstruction, is reported to occur in approximately 15,000 people in the United States each year[12]. Most of the SVC syndrome is induced by tumor compression in the mediastinum and is commonly present in primary small-cell bronchial carcinoma, non-Hodgkin lymphoma, and metastatic tumors[12]. Iatrogenic thrombosis or SVC stenosis leads to an increase in SVC, the main cause of which is the pacemaker’s lead after installation and the long-term deep venous catheter used for hemodialysis or chemotherapy[12]. Furthermore, such as acute SVC syndrome caused by chest surgery (such as heart surgery or lung surgery) have also been reported[2]. SVC walls are relatively thin. When they are located in the mediastinal plane and within the mediastinal space, they are susceptible to compression by tumors, enlarged lymph nodes, or other masses[12]. In patients with no history of SVC stenosis, accidental complete obstruction of SVC without collateral circulation return can cause severe hemodynamic disturbances and cerebral edema[3]. Acute obstruction often leads to a rapid increase in venous pressure, resulting in severe jugular vein irritation, eyelid edema, upper body cyanosis, and even severe hypotension[12]. If the obstruction is not alleviated in time, it will further lead to brain edema, which may be life-threatening. Intraoperative management of acute SVC obstruction indicates that if hypotension is strongly suspected to be caused by SVC obstruction, the lower limb vein should be opened immediately and fluid rehydration through the lower limb vein or pressor medication should be administered[2]. Since the blood flow to the SVC cannot return to the heart, the drug injection through the SVC is ineffective, and the lower limb venous access needs to be opened immediately. A certain average blood pressure is maintained, with cerebral perfusion ensured and brain tissue damage caused by ischemia and hypoxia reduced[2]. For the existing SVC syndrome before surgery, the head position should be properly elevated during the operation to avoid the compression of the neck vein, promoting the cerebral venous return through the SVC-specific collateral circulation vein and reducing the brain pressure as well as the risk of cerebral edema[2]; Hyperventilation through a ventilator can reduce PCO2, cerebrovascular contraction, and craniocerebral pressure as well as relieve brain edema[13]; Preventive use of hormone drugs can reduce cell permeability, improve the tolerance of brain cells, and prevent the occurrence of brain edema[2]; The application of mannitol and diuretics can also reduce intracranial pressure and hinder the further progression of brain edema[14]; The ice pack can cool the brain in vitro , reduce the metabolism of brain tissue, and relieve the damage of brain tissue caused by edema[15]; If acute SVC obstruction due to surgical reasons is suspected, it is critical to communicate with the surgeon immediately to remove the obstruction in time. Cardiopulmonary bypass support should be applied if necessary[2]; Finally, attention should be paid to the risk of pulmonary embolism in the case of cross-clamping SVC in thoracic surgery for the reason that the prolonged occlusion of the SVC can cause blood clots[2]. In this case, after mediastinal lymph node resection, because of the change in position, the remaining mediastinal tissue entered the space after lymph node resection. Since acute SVC obstruction is rare and not recognized in time due to relative inexperience, methods that lead to early dilation and fluid replacement for hypotension may aggravate the progression of the condition. Fortunately, an abnormal increase in central venous pressure was detected over time. Fluid replenishment was stopped in a timely manner to avoid further aggravating cerebral edema. The surgeon removed the obstruction in a timely manner, preventing further injury to the patient. Acute SVC obstruction is an acute and life-threatening complication. In the case of general epidural anesthesia, anaphylactic shock, general spinal anesthesia, pericardial tamponade, and pulmonary embolism may also present with hypotension as the first symptom. Sometimes it is difficult to identify in a short period, which is an intangible challenge for anesthesiologists. At present, with the development of minimally invasive surgical techniques, blood loss during minimally invasive surgery in the chest and abdomen is decreasing. Moreover, since there are too many factors affecting CVP, CVP monitoring is sometimes ignored. Conclusion In conclusion, severe hypotension induced by acute SVC obstruction may trigger and aggravate brain edema and other complications if we cannot quickly identify the patient or administer traditional treatment (upper limb or internal jugular vein dilation and fluid replacement). Severe perioperative hypotension must be treated immediately, despite all the difficulties. Given the risk of disease deterioration, immediate identification of the cause of intractable hypotension is crucial. Abbreviations SVC Superior vena cava CT Computed Tomography Declarations Availability of data and materials No datasets were generated or analysed during the current study. Ethics approval and consent to participate Since this is a case report, no ethical review board approval is required. Consent for publication Written informed consent was obtained from the patient for publication of this case report. Competing interests No potential conflict of interest relevant to this article was reported. Funding None. Author Contributions DXQ and LJG analysed and interpreted the patient data, and was a major contributor in the writing of the manuscript. DXQ，GP and WXL was the anesthesiologist in the operating room during the surgery. DXQ，LJG，GP，WXL and LQ reviewed the manuscript and made appropriate changes. All authors read and approved the final manuscript. References Wesselink EM, Kappen TH, Torn HM, Slooter AJC, van Klei WA. Intraoperative hypotension and the risk of postoperative adverse outcomes: a systematic review. Br J Anaesth, 2018. 121(4): 706-721.doi: 10.1016/j.bja.2018.04.036. Goh MS, Chellappa V. Acute, unanticipated, and prolonged superior vena cava occlusion during pneumonectomy. J Clin Anesth, 2016. 35: 78-84.doi: 10.1016/j.jclinane.2016.07.015. Straka C, Ying J, Kong FM, Willey CD, Kaminski J, Kim DW. Review of evolving etiologies, implications and treatment strategies for the superior vena cava syndrome. Springerplus, 2016. 5: 229.doi: 10.1186/s40064-016-1900-7. Monk TG, Saini V, Weldon BC, Sigl JC. Anesthetic management and one-year mortality after noncardiac surgery. Anesth Analg, 2005.100(1):4-10.doi:10.1213/01.ANE.0000147519.82841.5E. Veroli P. [Prevention and treatment of hypotension during spinal anesthesia]. Cah Anesthesiol, 1993. 41(6): 603-5. Guay J, Nishimori M, Kopp S. Epidural local anaesthetics versus opioid-based analgesic regimens for postoperative gastrointestinal paralysis, vomiting and pain after abdominal surgery. Cochrane Database Syst Rev, 2016. 7(7): CD001893.doi: 10.1002/14651858.CD001893.pub2. Ju H, Feng Y, Yang BX, Wang J. Comparison of epidural analgesia and intercostal nerve cryoanalgesia for post-thoracotomy pain control. Eur J Pain, 2008. 12(3): 378-84.doi： 10.1016/j.ejpain.2007.07.011. Reber LL, Hernandez JD, Galli SJ. The pathophysiology of anaphylaxis. J Allergy Clin Immunol, 2017. 140(2): 335-348.doi： 10.1016/j.jaci.2017.06.003. De Backer D, Vincent JL. Should we measure the central venous pressure to guide fluid management? Ten answers to 10 questions. Crit Care, 2018. 22(1): 43.doi：10.1186/s13054-018-1959-3 Chee YE, Liu SE, Irwin MG. Management of bleeding in vascular surgery. Br J Anaesth, 2016. 117 Suppl 2: ii85-ii94. Chioncel O, Parissis J, Mebazaa A, Thiele H, Desch S, Bauersachs J, et al. Epidemiology, pathophysiology and contemporary management of cardiogenic shock - a position statement from the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail, 2020. 22(8): 1315-1341.doi: 10.1002/ejhf.1922. Wilson LD, Detterbeck FC, Yahalom J. Clinical practice. Superior vena cava syndrome with malignant causes. N Engl J Med, 2007. 356(18): 1862-9.doi: 10.1056/NEJMcp067190. Doron O, Zadka Y, Barnea O, Rosenthal G. Interactions of brain, blood, and CSF: a novel mathematical model of cerebral edema. Fluids Barriers CNS, 2021. 18(1): 42.doi: 10.1186/s12987-021-00274-z. JA, Garcia-Yuste M, Florez S, Ramos G, Alvarez T, Coca JM. Hemodynamic and cerebral repercussions arising from surgical interruption of the superior vena cava. Experimental model. J Thorac Cardiovasc Surg, 1994. 107(4): p. 1044-9. Sandroni C, Natalini D, Nolan JP. Temperature control after cardiac arrest. Crit Care, 2022. 26(1): p. 361.doi: 10.1186/s13054-022-04238-z. 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Quick identification of hypotension causes is instrumental for treating low blood pressure. The likelihood of acute SVC resulting from thoracic surgery is increased due to the anatomical proximity of the mediastinum and superior vena cava (SVC)[2]. For patients with no prior history of SVC stenosis, acute SVC obstruction due to sudden accidents may induce severe hemodynamic disturbances and cerebral edema because there is no collateral circulation to return[3]. Given that perioperative acute SVC is extremely rare and early signs of low blood pressure are hard to recognize, we analyzed the differentiation of total spinal anesthesia, anaphylactic shock, hemorrhagic shock, cardiogenic shock, pericardial tamponade, and SVC obstruction, as well as corresponding treatment measures.\u003c/p\u003e"},{"header":"Case","content":"\u003cp\u003eA 48-year-old male patient weighing 68 kg was diagnosed with lung cancer. After chemotherapy failed, the right thoracotomy was performed under general anesthesia combined with intraspinal anesthesia. A chest CT scan revealed right upper lobe central lung cancer complicated with upper lobe obstructive atelectasis and enlarged mediastinal lymph nodes (Figure 1). Other relevant tests such as electrocardiogram, heart color ultrasound, blood gas, and other tests demonstrated normal results.\u003c/p\u003e\n\u003cp\u003eWhen the right lung was removed, intraoperative blood loss increased, accompanied by a gradual decrease in blood pressure. Rapid fluid rehydration and multiple intravenous ephedrine injections maintained blood pressure at 80-100 mmHg /50-60 mmHg. After hemostasis, blood pressure gradually increased to 120-140 mmHg/70-80 mmHg. The heart rate was maintained at approximately 100 beats/min, and the infusion speed decreased. Blood gas was rechecked at the end of the operation, showing no further decrease in hemoglobin and showing 800 mL of total blood loss, 1400 mL of urine volume, 2000 mL of crystal, and 500 mL of colloidal.The operation lasted a total of six hours.\u003c/p\u003e\n\u003cp\u003eAfter the operation, the patient was maintained in a supine position to prepare for recovery. With gradually decreased blood pressure and increased heart rate but no changes in oxygen saturation and end-expiratory carbon dioxide observed, we performed immediate intravenous fluid replacement and administrated pressor medication. The blood pressure gradually decreased to 60-70/30-40 mmHg, and the heart rate exceeded 120 beats per minute. Increasing doses of intravenous blood pressure-raising drugs remained ineffective (blood pressure-raising drugs include ephedrine, norepinephrine, deoxyadrenalin etc). Considering the patient\u0026rsquo;s unexplained severe hypotension, we immediately contacted another anesthesiologist for help. Subsequently, we continued to increase the dose of intravenous blood pressure-raising medications. We found eyelid edema, jugular vein swelling, facial cyanosis. Central venous pressure was monitored again, showing central venous pressure at 40 cmH2O. Therefore, we immediately stop fluid replenishment. Over time, the patient\u0026rsquo;s upper chest started to turn purple. Considering that the patient had no special history, this may be caused by surgical factors. We therefore prepared to conduct chest exploration again. The right-side incision was performed again for chest exploration. It was found that after mediastinal lymph node resection, the free mediastinal tissue entered the space formed by lymph node dissection, thus compressing the SVC and causing acute SVC obstruction. After the rapid removal of the remaining tissue, blood pressure immediately returned to the normal range and the heart rate gradually decreased. As the surgeon removed the remaining mediastinal tissue, internal jugular vein irritation was observed and the patient\u0026rsquo;s skin color gradually returned to normal. The thoracic surgeon observed no other abnormalities, thus continuing the suture. This case presented a patient who underwent an operation for lung cancer to resect mediastinal lymph nodes, with acute obstruction of the SVC occurring due to the nearby residual tissue filling the space left after lymph node removal. The induced acute and refractory hypotension lasted for nearly 30 minutes, exhibiting no response to any vasopressor drug including norepinephrine and ephedrine.\u003c/p\u003e\n\u003cp\u003eAt the end of the operation, all symptoms of the patient were eliminated, and the patient\u0026rsquo;s blood pressure and heart rate returned to a stable state. The patient was sent to ICU for further treatment and observation. Fortunately, the next day after surgery, no abnormalities were found on chest CT examination after the tracheal catheter was removed (Figure 2). Therefore, the patient was returned to a general ward and discharged after 3 weeks.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eIn recent years, the incidence of adverse cardiovascular events increased after perioperative surgery, attracting people\u0026rsquo;s wide attention to perioperative hypotension[1]. Current common definitions of intraoperative hypotension include a systolic blood pressure \u0026lt;80 mmHg, a systolic blood pressure drop below 20% of the patient\u0026rsquo;s baseline blood pressure, or a reduction of 30% greater than the patient\u0026rsquo;s baseline blood pressure despite a systolic blood pressure \u0026lt;100 mmHg[4].Low blood pressure that is not corrected in time can lead to insufficient perfusion of tissues and organs, thereby resulting in a series of complications[1].Severe hypotension during the perioperative period requires to be identified quickly and dealt with in time, thus reducing the incidence of complications.\u003c/p\u003e\n\u003cp\u003eUnexpected intraspinal anesthesia can induce severe hypotension and even cardiac arrest, mainly sympathetic nerve block, causing vasodilation and severe blood volume insufficiency[5]. However, most hypotension can be corrected with rapid replenishment of blood volume and the application of vasopressor drugs[5]. However, epidural administration of small doses of opioids or local anesthetics can reduce postoperative pain stimulation, enabling patients to get out of bed as early as possible, thus promoting patients\u0026rsquo; recovery and shortening the length of hospital stay[6]. For selective thoracic and abdominal open major surgery, if there is no contraindication, general anesthesia combined with epidural intraspinal anesthesia is more conducive to postoperative recovery[7]. Therefore, in this case, we used general combined intraspinal anesthesia. It is necessary to be alert to the possibility of total spinal anesthesia. Nonetheless, low blood volume was not indicated by the expansion of fluid, no response of hypotension to large doses of vasopressor drugs, tachycardia, or further increases in central venous pressure. As a result, hypotension caused by PSM was less likely.\u003c/p\u003e\n\u003cp\u003eAnaphylaxis is a severe systemic hypersensitivity reaction with a rapid onset that features life-threatening airway, respiratory, and circulatory problems, associated with skin and mucosal changes[8]. Perioperative use of general anesthesia, local anesthesia, antibacterials, and other drugs can trigger severe allergic reactions.In this case, since we did not find any significant change in airway pressure, wheezing sound in lung auscultation, or presence of urticaria, skin flushing, and erythema during the treatment of hypotension, the anaphylactic shock was less likely.\u003c/p\u003e\n\u003cp\u003eTraumatic hemorrhagic shock is a leading cause of death in emergencies. If left untreated, hemorrhagic shock will result in death.\u0026nbsp;As an important means to monitor the adequacy of circulating blood volume in shock patients, CVP alone does not accurately reflect changes in effective blood volume because CVP is vulnerable to its own and external influences such as mechanical ventilation, severe cough, cardiac function, and other effects\u0026nbsp;[9]. The continuous monitoring of the dynamic changes of CVP before and after the perioperative period is necessary to determine whether the fluid volume needs to be supplemented. Permissive hypotension and restricted fluid therapy are recommended for acute blood loss after using a combination of crystalline and colloidal solutions in the initial treatment. If the bleeding is not controlled, immediate blood product administration is recommended[10]. After treatment with rapid fluid rehydration and antihypertensive drugs, the patient\u0026rsquo;s blood pressure did not considerably improve. Thoracic drainage did not considerably increase. Blood gas report revealed no notable decrease in hemoglobin. Central venous pressure increased. Therefore, we believed that blood loss did not cause hypotension.\u003c/p\u003e\n\u003cp\u003eSince echocardiography can quickly assess the underlying condition of the heart, patients suspected of cardiogenic shock are required to perform an immediate ultrasound, which helps analyze the cause of cardiogenic shock and determine if it is caused by pericardial tamponade[11]. In this case, when the patient had tachycardia, severe hypotension, high central venous pressure, and no response to medication, a cardiac ultrasound could be performed to quickly aid diagnosis. Acute pulmonary embolism is also a crucial risk factor for hemodynamic instability.In this case, the patient\u0026rsquo;s blood pressure was too low to perform CTPA. However, the patient did not undergo lower extremity surgery. He had no abnormal coagulation function before surgery, and did not undergo SVC clamping during surgery. The existing extremely high central venous pressure and cyanosis of the upper body skin indicated that pulmonary embolism was less likely.\u003c/p\u003e\n\u003cp\u003eSevere intractable hypotension caused by intraoperative acute SVC syndrome is rare. SVC syndrome, including a range of symptoms and signs caused by SVC obstruction, is reported to occur in approximately 15,000 people in the United States each year[12]. Most of the SVC syndrome is induced by tumor compression in the mediastinum and is commonly present in primary small-cell bronchial carcinoma, non-Hodgkin lymphoma, and metastatic tumors[12]. Iatrogenic thrombosis or SVC stenosis leads to an increase in SVC, the main cause of which is the pacemaker\u0026rsquo;s lead after installation and the long-term deep venous catheter used for hemodialysis or chemotherapy[12]. Furthermore, such as acute SVC syndrome caused by chest surgery (such as heart surgery or lung surgery) have also been reported[2]. SVC walls are relatively thin. When they are located in the mediastinal plane and within the mediastinal space, they are susceptible to compression by tumors, enlarged lymph nodes, or other masses[12]. In patients with no history of SVC stenosis, accidental complete obstruction of SVC without collateral circulation return can cause severe hemodynamic disturbances and cerebral edema[3]. Acute obstruction often leads to a rapid increase in venous pressure, resulting in severe jugular vein irritation, eyelid edema, upper body cyanosis, and even severe hypotension[12]. If the obstruction is not alleviated in time, it will further lead to brain edema, which may be life-threatening.\u003c/p\u003e\n\u003cp\u003eIntraoperative management of acute SVC obstruction indicates that if hypotension is strongly suspected to be caused by SVC obstruction, the lower limb vein should be opened immediately and fluid rehydration through the lower limb vein or pressor medication should be administered[2]. Since the blood flow to the SVC cannot return to the heart, the drug injection through the SVC is ineffective, and the lower limb venous access needs to be opened immediately. A certain average blood pressure is maintained, with cerebral perfusion ensured and brain tissue damage caused by ischemia and hypoxia reduced[2]. For the existing SVC syndrome before surgery, the head position should be properly elevated during the operation to avoid the compression of the neck vein, promoting the cerebral venous return through the SVC-specific collateral circulation vein and reducing the brain pressure as well as the risk of cerebral edema[2]; Hyperventilation through a ventilator can reduce PCO2, cerebrovascular contraction, and craniocerebral pressure as well as relieve brain edema[13]; Preventive use of hormone drugs can reduce cell permeability, improve the tolerance of brain cells, and prevent the occurrence of brain edema[2]; The application of mannitol and diuretics can also reduce intracranial pressure and hinder the further progression of brain edema[14]; The ice pack can cool the brain \u003cem\u003ein vitro\u003c/em\u003e, reduce the metabolism of brain tissue, and relieve the damage of brain tissue caused by edema[15]; If acute SVC obstruction due to surgical reasons is suspected, it is critical to communicate with the surgeon immediately to remove the obstruction in time. Cardiopulmonary bypass support should be applied if necessary[2]; Finally, attention should be paid to the risk of pulmonary embolism in the case of cross-clamping SVC in thoracic surgery for the reason that the prolonged occlusion of the SVC can cause blood clots[2].\u003c/p\u003e\n\u003cp\u003eIn this case, after mediastinal lymph node resection, because of the change in position, the remaining mediastinal tissue entered the space after lymph node resection. Since acute SVC obstruction is rare and not recognized in time due to relative inexperience, methods that lead to early dilation and fluid replacement for hypotension may aggravate the progression of the condition. Fortunately, an abnormal increase in central venous pressure was detected over time. Fluid replenishment was stopped in a timely manner to avoid further aggravating cerebral edema. The surgeon removed the obstruction in a timely manner, preventing further injury to the patient. Acute SVC obstruction is an acute and life-threatening complication. In the case of general epidural anesthesia, anaphylactic shock, general spinal anesthesia, pericardial tamponade, and pulmonary embolism may also present with hypotension as the first symptom. Sometimes it is difficult to identify in a short period, which is an intangible challenge for anesthesiologists. At present, with the development of minimally invasive surgical techniques, blood loss during minimally invasive surgery in the chest and abdomen is decreasing. Moreover, since there are too many factors affecting CVP, CVP monitoring is sometimes ignored.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eIn conclusion, severe hypotension induced by acute SVC obstruction may trigger and aggravate brain edema and other complications if we cannot quickly identify the patient or administer traditional treatment (upper limb or internal jugular vein dilation and fluid replacement). Severe perioperative hypotension must be treated immediately, despite all the difficulties. Given the risk of disease deterioration, immediate identification of the cause of intractable hypotension is crucial.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eSVC Superior vena cava\u003c/p\u003e\n\u003cp\u003eCT Computed Tomography\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNo datasets were generated or analysed during the current study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eSince this is a case report, no ethical review board approval is required.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the patient for publication of this case report.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNo potential conflict of interest relevant to this article was reported.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor Contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eDXQ and LJG analysed and interpreted the patient data, and was a major contributor in the writing of the manuscript. DXQ，GP and WXL was the anesthesiologist in the operating room during the surgery. DXQ，LJG，GP，WXL and LQ reviewed the manuscript and made appropriate changes. All authors read and approved the final manuscript.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eWesselink EM, Kappen TH, Torn HM, Slooter AJC, van Klei WA. Intraoperative hypotension and the risk of postoperative adverse outcomes: a systematic review. Br J Anaesth, 2018. 121(4): 706-721.doi: 10.1016/j.bja.2018.04.036.\u003c/li\u003e\n\u003cli\u003eGoh MS, Chellappa V. Acute, unanticipated, and prolonged superior vena cava occlusion during pneumonectomy. J Clin Anesth, 2016. 35: 78-84.doi: 10.1016/j.jclinane.2016.07.015.\u003c/li\u003e\n\u003cli\u003eStraka C, Ying J, Kong FM, Willey CD, Kaminski J, Kim DW. Review of evolving etiologies, implications and treatment strategies for the superior vena cava syndrome. Springerplus, 2016. 5: 229.doi: 10.1186/s40064-016-1900-7.\u003c/li\u003e\n\u003cli\u003eMonk TG, Saini V, Weldon BC, Sigl JC. Anesthetic management and one-year mortality after noncardiac surgery. Anesth Analg, 2005.100(1):4-10.doi:10.1213/01.ANE.0000147519.82841.5E. \u003c/li\u003e\n\u003cli\u003eVeroli P. [Prevention and treatment of hypotension during spinal anesthesia]. Cah Anesthesiol, 1993. 41(6): 603-5. \u003c/li\u003e\n\u003cli\u003eGuay J, Nishimori M, Kopp S. Epidural local anaesthetics versus opioid-based analgesic regimens for postoperative gastrointestinal paralysis, vomiting and pain after abdominal surgery. Cochrane Database Syst Rev, 2016. 7(7): CD001893.doi: 10.1002/14651858.CD001893.pub2.\u003c/li\u003e\n\u003cli\u003eJu H, Feng Y, Yang BX, Wang J. Comparison of epidural analgesia and intercostal nerve cryoanalgesia for post-thoracotomy pain control. Eur J Pain, 2008. 12(3): 378-84.doi： 10.1016/j.ejpain.2007.07.011. \u003c/li\u003e\n\u003cli\u003eReber LL, Hernandez JD, Galli SJ. The pathophysiology of anaphylaxis. J Allergy Clin Immunol, 2017. 140(2): 335-348.doi： 10.1016/j.jaci.2017.06.003. \u003c/li\u003e\n\u003cli\u003eDe Backer D, Vincent JL. Should we measure the central venous pressure to guide fluid management? Ten answers to 10 questions. Crit Care, 2018. 22(1): 43.doi：10.1186/s13054-018-1959-3 \u003c/li\u003e\n\u003cli\u003eChee YE, Liu SE, Irwin MG. Management of bleeding in vascular surgery. Br J Anaesth, 2016. 117 Suppl 2: ii85-ii94.\u003c/li\u003e\n\u003cli\u003eChioncel O, Parissis J, Mebazaa A, Thiele H, Desch S, Bauersachs J, et al. Epidemiology, pathophysiology and contemporary management of cardiogenic shock - a position statement from the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail, 2020. 22(8): 1315-1341.doi: 10.1002/ejhf.1922.\u003c/li\u003e\n\u003cli\u003eWilson LD, Detterbeck FC, Yahalom J. Clinical practice. Superior vena cava syndrome with malignant causes. N Engl J Med, 2007. 356(18): 1862-9.doi: 10.1056/NEJMcp067190.\u003c/li\u003e\n\u003cli\u003eDoron O, Zadka Y, Barnea O, Rosenthal G. Interactions of brain, blood, and CSF: a novel mathematical model of cerebral edema. Fluids Barriers CNS, 2021. 18(1): 42.doi: 10.1186/s12987-021-00274-z. \u003c/li\u003e\n\u003cli\u003eJA, Garcia-Yuste M, Florez S, Ramos G, Alvarez T, Coca JM. Hemodynamic and cerebral repercussions arising from surgical interruption of the superior vena cava. Experimental model. J Thorac Cardiovasc Surg, 1994. 107(4): p. 1044-9.\u003c/li\u003e\n\u003cli\u003eSandroni C, Natalini D, Nolan JP. Temperature control after cardiac arrest. Crit Care, 2022. 26(1): p. 361.doi: 10.1186/s13054-022-04238-z.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Hypotension, Intraspinal anesthesia, Anaphylactic reaction, Hemorrhagic shock, Cardiogenic shock, Acute SVC syndrome","lastPublishedDoi":"10.21203/rs.3.rs-4299863/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-4299863/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"The purpose of this case report is to inform other anesthesiologists about the identification, judgment, and management of sudden severe refractory hypotension in resuscitation after right pneumonectomy. We present a patient who underwent right lung and mediastinal lymph node resection. When the patient recovered from anesthesia, due to the change of position, the mediastinal free tissue entered the space and pressed on the superior vena cava (SVC), resulting in complete obstruction of the SVC and causing severe intractable hypotension. A 48-year-old man with bronchial lung cancer developed severe hypotension while preparing to recover from open-chest surgery under general anesthesia combined with intraspinal anesthesia. There was no response to rapid dilatation, fluid replacement, or treatment with drugs that could raise blood pressure (such as ephedrine, norepinephrine, and deoxyadrenalin). Since early symptoms of acute SVC syndrome in general combined epidural anesthesia were similar to those of severe anaphylaxis, general spinal anesthesia, hemorrhagic shock, pulmonary embolism, and pericardial tamponade, it was difficult to make judgments. A second thoracic operation was performed to remove the remaining tissue that caused the compression, ultimately making a successful recovery. Severe hypotension induced by acute SVC obstruction may trigger and aggravate brain edema and other complications if we cannot quickly identify the patient or administer traditional treatment (upper limb or internal jugular vein dilation and fluid replacement). Given the risk of disease deterioration, immediate identification of the cause of intractable hypotension is crucial.","manuscriptTitle":"Intractable hypotension caused by acute superior vena cava obstruction after lung cancer surgery: a case report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2024-04-30 19:38:19","doi":"10.21203/rs.3.rs-4299863/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"ee7a8276-05ff-45a3-9a51-809cf547bd5b","owner":[],"postedDate":"April 30th, 2024","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2024-04-30T19:38:21+00:00","versionOfRecord":[],"versionCreatedAt":"2024-04-30 19:38:19","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-4299863","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-4299863","identity":"rs-4299863","version":["v1"]},"buildId":"ehx78VzkSd0WSzXnipQa-","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}