Overview: Definition: Tearing of the intima and middle layer of the aortic wall forms an intimal tear, which exposes the middle layer directly to the lumen. Blood in the aorta, driven by pulse pressure, penetrates directly through the diseased middle layer via the intimal tear, separating the middle layer to form a sandwich. After a tear in the middle layer of the aorta occurs, blood flows in the torn layer (false lumen) and the original aortic lumen is called the true lumen. The true and false lumens are separated by the intima and part of the middle layer, and are connected by one or several ruptures. Yang Zaizhen, Department of Cardiac and Macrovascular Surgery, Zhengzhou People’s Hospital Etiology: endogenous: degeneration of the aortic wall or lesions of the middle elastic fibers and smooth muscle. Exogenous causes: intra-aortic luminal hemodynamic changes (e.g., hypertension). Etiology and risk factors: congenital aortic disease: aortic duplex malformation, connective tissue disease, aortic constriction, Ehlers-Danlos syndrome, familial arterial ring developmental anomalies, familial arterial entrapment, and Marfon syndrome. Acquired aortic disease: atherosclerosis, diabetes mellitus, abnormal lipid metabolism, hypertension, renal disease. Medical factors: cardiac catheterization, aortic or valve surgery. Vascular disease: Behcet’s disease, giant cell arteritis, syphilitic aortitis, multiple aortitis. Other factors: drug use or cocaine drugs, long-term smoking, pregnancy. Aortic coarctation staging: by site of lesion: DeBakey staging: according to the site of initiation of the primary intimal rupture and the extent of coarctation involvement. stanford staging: according to the extent of coarctation involvement. By time: acute within 2 weeks; chronic beyond 2 weeks. The risk of mortality and progression decreases gradually over time. Domestic Sun’s staging. Pathophysiology, clinical manifestations, signs: 1. pain; 2. aortic dissection; 3. aortic valve closure insufficiency; 4. impaired blood supply to vital organs; signs: blood pressure; heart, thorax and abdomen, nervous system, etc. Ninety percent of the rupture (endothelial tear) is located in the ascending aorta, which is subject to the greatest blood flow impact. The pulsatile force of the left ventricular ejection separates the aortic wall longitudinally, progressing proximally and distally along the middle layer. Proximal detachment may enter the aortic root, distorting the aortic valve leaflets and causing incomplete aortic valve closure; or compress the coronary artery opening causing acute myocardial ischemia and infarction; and infiltrate into the pericardial cavity forming pericardial tamponade. Distally, it may reach different ranges along the descending and abdominal aorta and involve its branches. Continuous dilatation of the false lumen and narrowing or collapse of the true lumen are the most important and basic pathophysiological changes of aortic coarctation. The pathophysiological changes, clinical manifestations and signs vary according to the impact of the entrapment on the aortic valve, the aortic wall or the corresponding branches of the aorta. Pain: persistent and severe chest pain. The observation of physical signs emphasizes the observation of blood pressure and pulse in the extremities, as they are related to the location and degree of involvement of the entrapment rupture. Ancillary investigations: electrocardiogram, X-ray chest film, blood tests, ultrasound, enhanced CT: 64-row volumetric CT, magnetic resonance imaging (MRI), digital subtraction angiography (DSA).CTA is the gold standard for the diagnosis of aortic coarctation and can provide important information about the rupture, the extent of the coarctation tear and the true or false lumen. On the other hand, the peak age of patients with entrapment is 50-70 years old, and it is obviously inappropriate to go back for coronary angiography before emergency surgery, thus the application of 64-row volumetric CT through 3D reconstruction enables us to have a general understanding of the major branches of the coronary arteries before emergency surgery and thus decide whether to perform coronary artery bypass grafting at the same time. There are also some patients who complain of “chest pain” and suspect “heart attack”, and aortic coarctation is found in coronary angiography and aortogram. Natural course: Type A: Mortality: 1-3d, 1-2%/h. 1W, 50%. 1M, 75%. 1Y, 90%. Type B: Mortality: 14d, 10%. 5Y, 20-40%. 10Y, 55-60%. Preoperative monitoring setup and disposition pathway: Patients were admitted to the intensive care unit immediately after admission for a full set of continuous monitoring of vital signs: blood pressure, urine output, central venous pressure, mental status, extremity blood pressure, pulse and activity status. The main goal of pharmacological treatment was to lower systolic blood pressure and reduce left ventricular contractility. Treatment is given with morphine for sedation and pain relief, application of sodium nitroprusside for blood pressure control, and here the application of beta-blockers or calcium antagonists is emphasized, capable of producing a negative inotropic effect and reducing the contractility of the heart, thus reducing cardiac ejection for the tearing of the entrainment. Control goals: systolic blood pressure of 100-120 mmHg and heart rate of 60-80 beats/min, or the lowest level that can maintain perfusion of vital organs. A rapid examination and preoperative preparation is performed after the patient is slightly stabilized to understand the cumulative extent and degree of entrapment. Depending on the condition, a decision is made for surgical or interventional treatment. This is the time to say: time is life! Treatment principles: aggressive surgery for acute type A aortic coarctation. Main objectives: to prevent and avoid patient death due to acute pericardial tamponade, bleeding from ruptured entrapment and severe organ ischemia; to perform pseudolumpectomy, endothelial tear repair or artificial vessel replacement for aortic entrapment that has ruptured or is about to rupture to maximize restoration of blood flow to the aorta and its major branch vessels. The main objective is to deal with proximal aortic lesions. Another aim is to correct aortic valve closure insufficiency due to type A coarctation. type A coarctation, once diagnosed, should be operated on urgently, and in our country, due to geographical, treatment technology and economic conditions, many patients have difficulty in getting access to emergency surgery. One important piece of information is the diameter of the aortic root, which is greater than 5 cm and usually requires urgent treatment. Sun’s refined staging also helps the timing of surgery and the choice of surgical approach. type B aortic coarctation: simple type B aortic coarctation: endoluminal repair (usually 1-2 weeks), composite surgery (cephalobrachial artery diversion + endoluminal repair). Complex type B aortic coarctation: thoracic descending aortic replacement or partial thoracic descending aortic replacement + stent elephant trunk, total thoracoabdominal aortic artery replacement. intraoperative management of type A aortic coarctation: procedure: ascending aortic replacement/David’s procedure/Bentanll’s procedure, half/whole arch replacement, stent elephant trunk (Sun’s procedure), three-branch aortic arch overlay stent; extracorporeal circulation: deep hypothermic stop circulation , selective cerebral protection: 5-10 ml/kg・min, albumin and ultrafiltration application. The management of the aortic root is determined by the extent of the entrapment, either by simple replacement of the ascending aorta or by David’s operation. Most of the treatment of the arch and the distal end is done by the technique of total arch replacement + stenting of the elephant trunk. Special emphasis should be placed on the three-branch aortic arch overlay stent that is currently being successfully used in China, which greatly simplifies the treatment of the arch, shortens the time to stop circulation, and facilitates anastomosis and hemostasis. This is another technical innovation after the traditional elephant trunk surgery. The incidence of postoperative bleeding, neurological and other systemic complications has been reduced accordingly. The surgery is a systematic project, and the cooperation of anesthesia and extracorporeal circulation is very important during the surgery. Because the operation needs to be done under deep hypothermia and circulation suspension, the axillary artery and cephalic artery should be perfused in parallel to perform selective cerebral protection, with a perfusion flow rate of 5-10 ml/kg/min, a perfusion pressure of about 60 mmHg, and a venous oxygen saturation of more than 60% to reduce the damage to brain cells by ischemia and hypoxia, and in addition, albumin and ultrafiltration techniques are routinely applied intraoperatively to improve colloid osmolarity, which also has a very obvious effect on the removal of inflammatory mediators, thus can reduce the incidence of postoperative neurological complications. The general duration of intraoperative circulatory arrest is about 20 min, and patients can be awake on the same day or the next day after surgery when this method is applied. Postoperative management: intensive care, postoperative treatment, prevention and treatment of common complications. Special pathophysiological changes in the perioperative period of aortic coarctation: often combined with poor perfusion syndrome, less common in chronic. Systemic inflammatory response syndrome and coagulation system activation, these pathophysiological changes will invade all systems of the body in severe cases and even lead to multi-organ failure. Selective cerebral perfusion with deep hypothermic withdrawal of circulation: ischemia, hypoxia, platelet and coagulation disorders, and peripheral vascular paralysis. High surgical trauma. Critical care: vital signs: blood pressure, heart rate and rhythm, central venous pressure, oxygen saturation, urine output, neurological symptoms and signs, bowel sounds, extremity blood pressure, pulse and temperature, etc.; pleural fluid volume; ancillary tests: routine blood, electrolytes, liver and kidney function, bedside chest X-ray, etc.; four coagulation items and cardiac enzyme profile (if necessary). Postoperative treatment: ventilator assisted breathing; drug application: circulatory system: sodium nitroprusside or nitroglycerin, diltiazem, dobutamine, etc.; respiratory system: antibiotics; mucosolvan; digestive system: loxacarb; glucose + fatty milk + amino acids + vitamins; neurological system: treatment of cerebral edema: mannitol, glycerol fructose; furosemide; for patients with entrapment, their cardiac function is generally not poor, and most are hypertensive. At least normal (mafan patients) and thus we often have to lower the blood pressure treatment. The same emphasis here is placed on the application of beta-blockers or calcium antagonists, which can produce a negative inotropic effect, reducing the contractility of the heart, as well as reducing the effects of myocardial remodeling, etc., which can be of great benefit for the control of perioperative blood pressure and the prevention of complications such as bleeding. Other: sedation: propofol, fentanyl + midazolam, valium; anticoagulation: warfarin (for valve replacement patients); heparin; anti-inflammatory: methylprednisolone; ustekin; for patients with prosthetic vessels we generally do not advocate heparin anticoagulation unless there are symptoms of thrombosis or corresponding high-risk factors, because the blood flow in the aorta is very fast. For patients undergoing Bentall’s valve replacement, anticoagulation is the same as that required for valve replacement patients, with warfarin being started the day after surgery and PT being adjusted to an appropriate level. Prevention and treatment of common complications: 1. bleeding: etiology: surgical causes; coagulation abnormalities: preoperative consumption of large amounts of coagulation factors and platelets; intraoperative deep hypothermic arrest of circulation for blood destruction and the impact of coagulation; perioperative hypertension, etc. Prevention and treatment: ① good timing of surgery; ② intraoperative blood protection; ③ intraoperative hemostatic techniques: establishment of aortic-right auricular “tunnel” anastomosis, three-branch intracavitary stent; ④ adequate postoperative drainage, transfusion of platelets, fresh frozen plasma, whole blood or red blood cell suspension; ⑤ open-heart hemostasis; ⑥ control of blood pressure and body temperature. Therefore, for the prevention of bleeding, first of all, we should choose a good timing of surgery, and we can wait to do the best after the acute period, which can escape this dangerous period: large consumption of coagulation factors, release of large amount of inflammatory mediators, etc. Intraoperatively, it is important to protect the blood, to stop bleeding thoroughly, to wrap the outer wall of the aortic aneurysm around the artificial vessel, and to create an aortic-right auricular “tunnel” anastomosis. It is also important to emphasize here that the use of a three-branch endoluminal stent can reduce the incidence of complications such as bleeding because the intraoperative anastomosis is easy, precise, and easily hemostatic. Postoperatively, adequate drainage and transfusion of platelets, fresh frozen plasma, whole blood or red blood cell suspension, if necessary, are used to supplement coagulation factors and improve coagulation function. Open chest to stop bleeding if necessary: bleeding 200ml/h for 4-6h; 1500ml/12h; sudden increase of 300-500ml; large and bright red bleeding. 2. Cardiac insufficiency: Etiology: aortic regurgitation; poor myocardial protection and ischemic reperfusion; perioperative myocardial ischemia or infarction. Prevention and treatment: ① early surgery: especially massive regurgitation of the main valve or pericardial compression; ② preoperative cardiopulmonary function adjustment; ③ intraoperative myocardial protection; ④ adjustment of anterior and posterior loads; ⑤ pharmacotherapy; ⑥ load-reducing therapy and assisted circulation. Clinically, preload is adjusted by rehydration, application of vasodilators and diuretics. Correct arrhythmias and apply temporary pacemakers if necessary. Application of positive inotropic force. Application of vasodilators to reduce afterload. Decompression therapy and assisted circulation: ventilator-assisted breathing; renal replacement therapy. 3. Respiratory insufficiency: clinical manifestations: hypoxemia; hypercapnia; acute and chronic respiratory insufficiency; difficulty in deconditioning. Etiology: ① pulmonary lesions: preoperative pre-existing high risk factors for respiratory complications; pulmonary infection; fluid pneumothorax; cardiogenic and non-cardiogenic pulmonary edema; pulmonary atelectasis; bronchospasm; ② inflammatory response to deep hypothermic arrest circulation and extracorporeal circulation; pulmonary edema due to increased pulmonary circulation pressure caused by poor left heart drainage; surgical stimulation of the lung and pleura; ③ pulmonary inflammatory response caused by massive reservoir blood input and fluid transfusion, edema, pulmonary capillary microembolism; surgical incision pain; systemic inflammatory response syndrome; low cardiac output or anemia; central nervous system complications, etc. Prevention and treatment: ① intraoperative ultrafiltration; ② mechanical ventilation (tracheotomy): PEEP application; ③ comprehensive treatment: anti-infection, release of bronchospasm, etc.; diuresis; nutritional support; dehydration, sedation. Ustatin inhibits inflammatory response to prevent lung injury. 4. Neurological complications: including brain and spinal cord complications and peripheral nerve injury. Etiology: ischemia-hypoxia; ischemia-reperfusion; hydrostatic pressure elevation leading to cerebral edema. History of cerebral infarction, cerebral hemorrhage, deep hypothermic stop circulation, low perfusion pressure, improper intraoperative neurological protection, air thrombosis, poor perioperative blood pressure control. Improper stent elephant trunk position, timing and level of aortic block, variation in spinal cord blood supply. Brain complications: ① Classification: temporary neurological dysfunction: delayed awakening, delirium; permanent neurological dysfunction – cerebral infarction; severe whole brain dysfunction: massive cerebral infarction, cerebral hemorrhage and brain herniation. ② Prevention and treatment: hypothermic cerebral protection; ensure safe time limit for stopping circulation: 20 degrees, 35-40 minutes. Application of three-branch type intraluminal overlay stent. Intraoperative extracorporeal circulation management: mean arterial pressure > 60 mmHg; selective cerebral perfusion techniques; application of albumin and ultrafiltration techniques; treatment of cerebral edema: mannitol, albumin + diuretics, adrenocorticotropic hormone; postoperative control of hypertension, hypoxia, hyperglycemia, and secondary causative injury from hyperthermia. Mechanical ventilation and tracheotomy; nutrition of cerebral nerves, hyperbaric oxygen therapy. Apply albumin and ultrafiltration techniques to increase colloid osmotic pressure and prevent cerebral edema and neurological complications. Blood pressure control: maintain steady blood pressure and control it to the lowest level with urine. Tracheotomy may be considered for patients with neurological complications who are temporarily unable to come off the ventilator. Apply diuretics and other treatments for cerebral edema. Spinal cord complications: ① Classification: paraplegia and mild paralysis of the lower extremities: ischemic injury of the spinal cord, including immediate and delayed forms. ②Prevention and treatment: hypothermia: 30 degrees for 60 minutes. Distal perfusion: left heart diversion. Intercostal artery and lumbar artery reconstruction. Cerebrospinal fluid drainage: Keep cerebrospinal fluid pressure below 10 mm Hg. Avoid taking the end of the elephant trunk above the T8 level. Protecting the root aorta is the key to avoid paraplegia. 75% of the root aorta originates from the 6th to 12th intercostal artery, and the chance of originating from the intercostal artery above T6 is extremely small, so the end of the elephant trunk should be avoided above the T8 level.5. Renal insufficiency/failure: etiology: pre-operative pre-existing renal insufficiency (entrapment involvement); contrast; heart failure, shock hypotension, and perioperative application of high-dose vasoconstrictive drugs caused by inadequate renal perfusion; systemic inflammatory response syndrome; certain nephrotoxic drugs (antibiotics), etc. Definition of renal failure: blood creatinine is 50% higher than preoperative or 44umol/L. Prevention and treatment: ① reduce the amount of contrast agent used for preoperative examination; ② maintain intraoperative perfusion pressure > 60mmHg; ③ improve renal perfusion after surgery: dobutamine 3-5ug/kg.min; ④ diuretics and diuretic combination application; ⑤ continuous renal replacement therapy CRRT. ⑥ serious malformation without obvious reasons Renal failure with anuria should be highly suspected of renal artery reconstruction failure and early reoperation. Reduce the amount of contrast agent used for preoperative examination, maintain perfusion pressure > 60 mmHg intraoperatively, improve renal perfusion postoperatively: dopamine 3-5ug/kg.min, apply diuretics and diuretic combination to try to maintain negative balance, if the diuretic dosage is large (60-80 mg/d) and urine volume is also small (less than 1000-1500 ml/d), and creatinine progressively rises to 200 umol/L or more, continuous renal replacement therapy CRRT can be applied as early as possible, and it is better to use it early than late.6. Gastrointestinal complications: gastrointestinal bleeding, ischemic gastrointestinal insufficiency and hepatic insufficiency. Etiology: old age; previous history of ulcer disease; hormone application, stress; low cardiac output and hypoperfusion; constrictive drug application; impaired abdominal arterial supply. Autonomic dysfunction; ischemia; inflammatory response. Prevention and treatment: ① omeprazole, thioglycollate, growth inhibitors; endoscopic hemostasis; surgery. (ii) gastrointestinal nutrition; (iii) correction of cardiac insufficiency and increase of perfusion pressure; hepatoprotective therapy; symptomatic treatment; CRRT, artificial liver. Special cases: Gastrointestinal haemorrhage: history of duodenal ulcer, recurrent gastrointestinal haemorrhage → ineffective after application of ice saline + norepinephrine + prothrombin complex nasal feeding → gastroscopic discovery of duodenal ulcer erosion and small vessels of gastroduodenal artery, ineffective hemostasis by chemical method → successful super-selective gastroduodenal artery embolization. 7. Multi-organ failure: systemic inflammatory response. Multiple organ ischemia and ischemia-reperfusion in patients with aortic coarctation, extracorporeal circulation and aortic surgery induced oxidative stress, and severe damage to an organ induced systemic inflammatory response syndrome or multiple organ failure. Prevention and treatment: Improving surgical techniques, shortening the duration of extracorporeal circulation, applying hormones and anti-inflammatory agents, actively managing low cardiac output and hypoxemia, strengthening gastrointestinal management, and preventing infection are the guarantee of successful prevention and treatment. 8. Other: Wound infection and sternal doffing: main causes: obesity; poor fixation of the sternum; incomplete hemostasis; hormone application; inability to tightly close the vocal cords resulting in weak coughing up sputum; pre-existing respiratory system disorders or postoperative complications; malnutrition. Prevention and treatment: For patients with obesity and other high-risk factors, special attention should be paid to secure sternal wire fixation and complete hemostasis; postoperative chest band fixation; anti-infection and nutritional support; secondary debridement and suturing. Postoperative review: CTA or ultrasound examination: once in 3 months in the first year after surgery; once in the next 6 months; once a year after 1 year. The review interval is decided according to the aortic thickening: CTA once a year for 4-4.5cm or less, and once a year for 5cm or more in the first half of the year.