A review of postoperative syncope control in anorectal disease

  Syncope, also known as fainting, is a transient state of loss of consciousness due to momentary widespread cerebral hypoperfusion, in which the patient falls to the ground due to loss of muscle tone and inability to maintain normal posture. The attack is usually sudden, with rapid recovery and few after-effects.
  Syncope is a symptom of a transient, self-limiting loss of consciousness that often leads to fainting. The mechanism of syncope is transient cerebral ischemia, which occurs relatively quickly and is followed by a complete and automatic recovery. Some syncope has aura symptoms, but more often the loss of consciousness occurs suddenly and without aura symptoms. Usually, with the recovery of syncope, behavior and orientation are immediately restored. Retrograde amnesia may sometimes occur, mostly in older patients.
  Sometimes recovery from syncope may be followed by significant weakness. Typical syncopal episodes are brief, and the time to complete loss of consciousness in vasovagal syncope is usually less than 20 seconds. Individual syncopal episodes can last longer than several minutes and should be distinguished from other causes of loss of consciousness.
  1, the etiology of syncope
  The causes of syncope are broadly divided into four categories.
  (1) vasodilatory disorders: seen in simple syncope, postural hypotension, carotid sinus syndrome, urinary syncope, cough syncope and pain syncope, etc. Postoperative syncope after anorectal disease is often of this type.
  (2) Cardiogenic syncope: It is seen in severe arrhythmias, obstructed cardiac blood displacement and myocardial ischemic diseases, such as paroxysmal tachycardia, paroxysmal atrial fibrillation, pathological sinus node syndrome, high atrioventricular block, aortic stenosis, certain types of congenital heart disease, angina pectoris and acute myocardial infarction, primary hypertrophic cardiomyopathy, etc. The most serious one is Adams-Stokes ) syndrome.
  (3) Cerebral syncope: seen in cerebral atherosclerosis, transient ischemic attack, migraine, pulselessness, chronic lead poisoning encephalopathy, etc.
  (4) Blood component abnormalities: seen in hypoglycemia, hyperventilation syndrome, severe anemia and plateau syncope, etc.
  2.Occurrence mechanism and clinical manifestations
  Vasodilation disorders
  (1) Simple syncope (vasodepressive syncope): mostly seen in young and frail women, attacks often have obvious triggers (such as pain, emotional stress, fear, minor bleeding, various punctures and minor surgery, etc.), and are more likely to occur in hot weather, dirty air, fatigue, fasting, insomnia and pregnancy. The syncope is preceded by dizziness, vertigo, nausea, epigastric discomfort, pallor, limb tenderness, fidgeting and anxiety, and lasts for several minutes followed by a sudden loss of consciousness, often accompanied by a drop in blood pressure and a weak pulse, which can wake up spontaneously after a few seconds or minutes without sequelae.
  The mechanism of occurrence is due to various stimuli through the vagal reflex, causing transient vascular bed dilation, reduced return blood volume, reduced cardiac transfusion bleeding, and decreased blood pressure resulting in insufficient cerebral blood supply.
  (2) Postural hypotension (upright hypotension): manifests as syncope when there is an abrupt change in position, mainly when standing up suddenly from a lying or squatting position. It can be seen in.
  ①Some long-term standing in a fixed position and long-term bed-ridden people;
  ②Taking certain drugs, such as chlorpromazine, guanethidine, nitrites, etc. or post-sympathectomy patients;
  ③Some systemic diseases, such as spinal cord cavitation, polyneuritis, cerebral atherosclerosis, recovery from acute infectious diseases, chronic malnutrition, etc. The mechanism of occurrence may be due to low venous tone in the lower extremities, blood accumulation in the lower extremities (postural), peripheral vasodilatation stasis (taking nitrite drugs) or impaired reflex regulation of blood circulation, resulting in reduced return blood volume, reduced cardiac output and decreased blood pressure leading to insufficient cerebral blood supply.
  (3) Carotid sinus syndrome: Due to lesions near the carotid sinus, such as local arteriosclerosis, arteritis, lymphadenitis or lymph node enlargement around the carotid sinus, tumor and scar compression or stimulation of the carotid sinus, resulting in vagal nerve excitation, slowing of heart rate, reduced cardiac output, and decreased blood pressure, resulting in insufficient cerebral blood supply. It may manifest as episodic syncope or with convulsions. The common triggers are hand pressure on the carotid sinus, sudden head turning, and tight collar.
  (4) Urinary syncope: Most often seen in young men, the attack occurs during or at the end of urination and lasts about 1 to 2 min, with self-awakening and no sequelae. The mechanism may be a combination of autonomic instability, sudden change of position (getting up at night), reduced cardiac output during urination or through vagal reflexes, decreased blood pressure, and cerebral ischemia.
  (5) Cough syncope: seen in people with chronic lung disease and occurs after a violent cough. The mechanism may be due to an increase in intrathoracic pressure during a violent cough, obstruction of venous blood return, decreased cardiac output, decreased blood pressure, and cerebral ischemia; it is also believed that the rapid increase in cerebrospinal fluid pressure during a violent cough is caused by a shocking effect on the brain.
  (6) Other factors: such as severe pain, inferior vena cava syndrome (late pregnancy and compression of large abdominal masses), esophageal and mediastinal diseases, thoracic diseases, biliary colic, bronchoscopy due to vasodilatory dysfunction or vagal excitation, resulting in episodes of syncope.
  Cardiogenic syncope occurs due to a sudden decrease in cardiac output or cardiac arrest, resulting in a lack of oxygen to the brain tissue. The most severe form is Adams-Stokes syndrome, which is characterized by syncope in 5 to 10 s of cardiac arrest and convulsions in more than 15 s of arrest, with occasional incontinence.
  Cerebral syncope is caused by circulatory disorders in the blood vessels of the brain or blood vessels supplying blood to the brain, resulting in a momentary widespread cerebral blood supply deficiency. For example, cerebral arteriosclerosis causes narrowing of the vascular lumen, hypertension causes cerebral artery spasm, migraine and basilar artery diastolic disorder in cervical spondylosis, and various causes of cerebral artery microembolism, arteritis and other lesions can cause syncope. Among them, transient ischemic attacks can manifest as a variety of neurological dysfunction symptoms. The manifestations are diverse depending on the damaged blood vessels, such as migraine, numbness of the limbs, and speech impairment.
  Blood component abnormalities
  (1) Hypoglycemic syndrome: It is caused by low blood glucose which affects the energy supply of the brain, manifested as dizziness, weakness, hunger, nausea, sweating, tremor, confusion, fainting and even coma.
  (2) Hyperventilation syndrome: It is due to emotional stress or hysteria attack, shortness of breath, hyperventilation, increased carbon dioxide emission, resulting in respiratory alkalosis, brain capillary constriction, brain hypoxia, manifested as dizziness, weakness, pins and needles sensation in the face and extremities, and hand and foot convulsions because it can be accompanied by reduced blood calcium.
  (3) Severe anemia: syncope occurs during exertion due to low blood oxygen.
  (4) Plateau syncope: It is caused by transient hypoxia.
  Concomitant symptoms.
  1, accompanied by obvious autonomic dysfunction (such as pallor, cold sweat, nausea, weakness, etc.), mostly seen in vasopressor syncope or hypoglycemic syncope.
  2, accompanied by pallor, cyanosis, dyspnea, seen in acute left heart failure.
  3, accompanied by significant changes in heart rate and rhythm, seen in cardiogenic syncope.
  4. With convulsions, see central nervous system disease, cardiogenic syncope.
  5.With headache, vomiting, visual and hearing impairment suggest central nervous system disease.
  6.With fever, edema, pestle finger suggest cardiopulmonary disease.
  7. Deep and rapid breathing, tingling of the hands and feet, and convulsions are seen in hyperventilation syndrome, hysteria, etc.
  Differential diagnosis
  Differentiation of postoperative syncope in analgia should be noted from epilepsy, hysteria and vertigo. In epileptic seizures, there are no obvious prodromal symptoms, loss of consciousness during seizures, incontinence, limb convulsions, biting of the tongue, etc. There are abnormal findings in EEG and brain CT or MRI. Hysteria attack mostly has obvious mental stimulation factors, the attack lasts for a long time, there is no loss of consciousness during the attack, and there is reaction to the surrounding people and objects. Vertigo is a kind of motion hallucination or motion illusion. Patients feel that the external environment or themselves are rotating, moving or shaking, which is caused by the lesion of vestibular nervous system.
  Management of the occurrence of syncope
  Postoperative syncope is prone to occur after anorectal disease, preferably within 24 h after surgery, and is often simple syncope, also known as vasovagal syncope and vascular decompression syncope.
  Clinically more common, syncope is preceded by obvious triggers, such as pain, high temperature, nervousness, fear, emotional excitement, poor ventilation, foul air, fatigue, continuous standing, hunger, pregnancy, and the later stages of various chronic diseases. The pre-syncope period lasts for a short period of time, usually 15-30s. If you lie down quickly and immediately during this period, the prodromal symptoms disappear, and the prodromal symptoms are mostly dizziness, nausea, pallor, and sweating.
  The performance of the syncope period is also temporary, lasting generally 30s to 2-3min, manifested by loss of consciousness, pale face, weakness of limbs, decreased blood pressure, slowed and weak heart rate, dilated pupils, loss of response to light, and attention should be paid to the presence of urinary incontinence, twitching of limbs, biting of the tongue, etc. Late symptoms of syncope may include transient weakness or dizziness, etc. Recovery is usually quicker and there are no obvious sequelae symptoms.