Difference between abdominal aortic aneurysm and aortic coarctation
An abdominal aortic aneurysm is a localized weakness of the abdominal aorta due to various reasons, and then the abdominal aortic aneurysm is formed when the internal pressure of the abdominal aorta bulges outward.
In the case of abdominal aortic coarctation aneurysm, the middle layer of the abdominal aortic vessel wall is damaged, either by cystic necrosis or degeneration, and when the intima is damaged, the blood flow in the abdominal aorta enters the abdominal aortic vessel wall under the pressure of blood pressure, and because the middle layer is damaged, the blood flow enters and further tears the middle layer apart. The blood flow enters to form a false lumen, which is called abdominal aortic coarctation aneurysm.
Aortic coarctation.
Also known as aortic coarctation separation, aortic coarctation aneurysm, and aortic coarctation hematoma. Aortic coarctation refers to a hematoma formed when blood in the aortic lumen enters the middle layer of the aortic wall through a breach in the endothelium, and is not an expansion of the aortic wall, as opposed to an aortic aneurysm, which used to be called an aortic coarctation aneurysm, but is now mostly referred to as an aortic coarctation hematoma, or aortic coarctation separation, or aortic coarctation for short.
Prognosis of aortic coarctation
Most cases die within a few hours to a few days after onset, with a mortality rate of 1% to 2% per hour within the first 24 hours, depending on the location, extent and degree of the lesion.
Causes of aortic coarctation
1, hypertension: about 50% or more of patients with aortic coarctation have hypertension. Especially long-term and severe hypertension can increase the impact of hemodynamic forces on the aortic wall and put the aortic nutrient vessels in a state of spasm and pressure, causing ischemia, degeneration, necrosis and elastic fiber fracture, fibrosis and endothelial rupture of the middle layer smooth muscle, and finally forming an intercalated hematoma.
2, connective tissue genetic defects: such as Marfan syndrome, Ehlers-Danlos syndrome, congenital aortic constriction, bilobed aortic valve and mitral valve prolapse, etc. Patients often have genetic defects in the connective tissue of the aortic wall, manifesting as degeneration of collagen and fibrous tissue in the middle layer of the aorta, followed by cystic necrosis and lack of endothelial support, which can easily lead to endothelial rupture and formation of intercalated hematoma.
3.Atherosclerosis: It often occurs in patients with hypertension, hyperlipidemia, hyperglycemia and advanced age. Atherosclerotic plaque ruptures from the inner lumen and can form a sandwich hematoma.
4.Other: Severe aortic trauma, inflammation (syphilitic aortitis, systemic lupus erythematosus, etc.), end of pregnancy and during interventional cardiovascular treatment operations can cause aortic coarctation hematoma.
Pathological changes of aortic coarctation
The basic lesion is cystic mesangial necrosis. There is localized fracture or necrosis of the elastic fibers of the middle layer of the artery, and the stroma has mucinous and cystic formation. Splits often occur in the ascending aorta, which experiences the greatest blood flow impact, while the distal part of the aortic arch has fewer and less severe lesions. The aortic wall splits into two layers with accumulation of blood and clots between them, where the aorta is significantly enlarged and pyknotic or cystic in shape. If the lesion involves the aortic annulus, the annulus enlarges and causes aortic valve insufficiency. The lesion may extend distally from the aortic root as far as the iliac and femoral arteries, and may also involve branches of the aorta, such as the innominate artery, common carotid artery, subclavian artery, and renal artery.
The coronary arteries are generally unaffected, but the clot in the aortic root may have a compressive effect on the coronary artery opening. Most of the origins of the clots have transverse fissures of the intima, often located above the aortic valve, and the fissures can also be in two places, with the clot communicating with the aortic lumen. In a few cases, the endothelium is intact without fissures. In some cases, the outer membrane ruptures and causes hemorrhage. The rupture is all in the ascending aorta, and the bleeding can easily enter the pericardial cavity, or the mediastinum or the thoracic cavity if the rupture site is lower, or the mediastinum, thoracic cavity or retroperitoneal space if the rupture site is lower. Chronic dehiscence of the interstitial layer can form a double-lumen aorta, with one duct being placed inside the other.
Clinical manifestations of aortic coarctation
Depending on the site of the lesion, the main manifestations are as follows.
(i) Pain
Most patients experience sudden pain in the chest, radiating to the chest and back, which may extend to the abdomen, lower extremities and neck depending on the extent of the entrapment. The pain is severe and unbearable, reaching a peak immediately after the onset of the disease, with a slashing or tearing pattern. In a few cases with slow onset, the pain may not be significant.
(ii) Hypertension
Patients have the appearance of shock due to severe pain, anxiety, profuse sweating, pallor, and accelerated heart rate, but blood pressure is often not low or increased, or decreased if the episclera ruptures and bleeds. Many patients with pre-existing hypertension have increased blood pressure due to severe pain after the onset of the disease.
(C) Cardiovascular symptoms
(1) Aortic valve closure insufficiency. It occurs when the clotted hematoma involves the aortic annulus or affects the support of the heart valve-lobe, so a diastolic blowing murmur may suddenly appear in the aortic valve area, and the pulse pressure is widened, and acute aortic regurgitation may cause heart failure.
(②Pulse changes, usually seen in the carotid, brachial or femoral arteries, with a weakened or absent pulse on one side, reflecting compression of branches of the aorta or blockage of its origin by endothelial lobes.
③Pulsation at the sternoclavicular joint or a pulsatile mass may be palpable in the suprasternal fossa.
④There may be a pericardial friction sound, and the rupture of the entrapment into the pericardial cavity may cause pericardial blockage.
(⑤) Pleural effusion, caused by rupture of the entrapment into the pleural cavity.
(iv) Neurological symptoms
Aortic entrapment extending to the carotid artery or intercostal artery of the aortic branch may cause cerebral or spinal cord ischemia, resulting in hemiparesis, coma, confusion, paraplegia, limb numbness, abnormal reflexes, visual and bowel disorders.
(E) Compression symptoms
Compression of abdominal cavernous artery and mesenteric artery by aortic entrapment may cause nausea, vomiting, abdominal distension, diarrhea, black stool and other symptoms; compression of cervical sympathetic ganglion may cause Horner syndrome; compression of the recurrent laryngeal nerve may cause hoarseness; compression of superior vena cava may cause superior vena cava syndrome; involvement of renal artery may cause hematuria, urinary shutdown and increased blood pressure after renal ischemia.
Abdominal aortic aneurysm
It is a dilated bulge in the wall of the abdominal aorta. Abdominal aortic aneurysms can gradually increase in size and eventually rupture and bleed, leading to the patient’s death. Abdominal aortic aneurysms occur mainly in older people over 60 years of age, with a male to female ratio of 10:3. They are often associated with hypertension and heart disease, but are also occasionally seen in younger people. They are more common in men than in women. Other rare causes are congenital dysplasia of the aorta, syphilis, trauma, infection, aortitis, and Marfan syndrome.
Disease etiology
The common causes are atherosclerosis, cystic degeneration of the middle layer of the artery, syphilis, congenital, traumatic and infectious.
Among them, atherosclerosis is the most common cause. When atherosclerosis occurs in the artery, the middle elastic fibers break down and the wall becomes weak, so it cannot withstand the pressure of blood flow in the aorta and becomes locally enlarged, forming an aortic aneurysm. Due to the high pressure of blood flow in the aneurysm, the aneurysm gradually expands and can compress the adjacent organs, even erode the sternum, ribs or bulge out to the body surface to become a pulsating mass. In the enlarged aneurysm, blood flow is slowed down and vortexes are formed, which can produce attached wall thrombus. Patients may die due to severe compression of vital organs or rupture of the aneurysm on its own. Cystic aneurysms are more likely to rupture than pyknotic ones.
Clinical symptoms
They are rare before the age of 50 and most commonly seen in men between the ages of 60 and 80.
1. Most patients are asymptomatic and are often found incidentally on physical examination for other reasons. The typical abdominal aortic aneurysm is a distended abdominal aortic aneurysmal mass that pulsates laterally and anteriorly and anteriorly, with a vascular murmur in about 50% of patients.
2. Pain: It is a common symptom before rupture, mostly located around the umbilicus and in the middle and upper abdomen. If the aneurysm invades the lumbar spine, there may be lumbosacral pain. If there is severe pain in the abdomen or lumbar region recently, it often indicates that the aneurysm is on the verge of rupture. Abdominal mass: The most important sign is a distending, pulsating mass around the umbilicus or in the upper and middle abdomen, which is usually palpable unless the patient is obese. The femoral artery or dorsalis pedis artery pulsation is weakened or absent.
Rupture: It can be the first symptom of fatal complications, most commonly rupture of the tumor, blood from the tumor into the peritoneal cavity, fortunately more commonly into the retroperitoneal cavity, the bleeding from this part is slow. Abdominal pain and shock from blood loss can last for hours or days, and the patient may seek medical attention. Occasionally, the bleeding is limited, and the patient may have abdominal pain, fever, mild to moderate blood loss, and often rupture again. It may also rupture into the inferior vena cava, producing an aorto-venous fistula with a continuous murmur, high cardiac output, and heart failure. Occasionally, it may enter the duodenum and cause gastrointestinal bleeding.
4.Other serious complications: Acute thrombosis may occasionally be formed in the aneurysm. Abdominal aortic aneurysm thrombosis or atherosclerotic debris can cause lower limb embolism. Intestinal obstruction may occur due to duodenal compression, and peripheral edema may be caused by inferior vena cava obstruction. Secondary bacterial infections are rare.