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.