Postoperative circulatory disorder (PCD) refers to a series of pathophysiological changes and clinical manifestations in surgical patients after surgery due to various reasons resulting in a decrease in the body’s systemic or local effective circulating blood volume, inadequate tissue perfusion, and disturbances in cellular metabolism, which cause impaired function of important organs of the body. The effective circulating blood volume refers to the amount of blood circulating through the cardiovascular system per unit time, excluding the amount of blood stored in the blood sinuses of the liver and spleen or retained in the capillaries. The effective circulating blood volume of the body depends on factors such as adequate blood volume, effective cardiac output, perfect peripheral vascular tone and vascular patency. When any one of these factors changes beyond the compensatory capacity of the body, it can lead to a sharp decrease in the effective circulating blood volume, resulting in insufficient perfusion of oxygenated blood to organs and tissues of the body, severe cellular hypoxia, metabolic disorders and impaired cellular function. Inadequate perfusion of tissues caused by postoperative circulatory disorders can eventually develop into multiple organ dysfunction syndrome (MODS) or multiple organ failure (MOF).
I. Classification of postoperative circulatory disorders
(a) Classification by etiology: postoperative circulatory disorders can be classified according to their causes: hypovolemic, infectious toxic, traumatic, cardiogenic, neurogenic, allergic and other types.
(B) Classification by site: postoperative circulatory disorders can be divided into two major types according to the site of occurrence: postoperative systemic circulatory disorders and postoperative regional (local) circulatory disorders.
Second, the etiology of postoperative circulatory disorders
(A) the etiology of postoperative systemic circulatory disorders: there are more etiologies causing postoperative systemic circulatory disorders, and the common ones are as follows.
1.Severe blood volume deficiency: Surgical patients are highly susceptible to blood volume deficiency in the perioperative period, the causes of which are.
① Preoperative dehydration is not corrected in time: such as acute intestinal obstruction, acute diffuse peritonitis, severe acute pancreatitis and other patients with a large amount of preoperative fluid loss, if not corrected in time before or during surgery, postoperative hypovolemia is bound to occur.
② Preoperative history of massive blood loss: such as various trauma patients, patients with gastrointestinal haemorrhage or biliary haemorrhage, etc., who need emergency surgery and fail to correct blood volume thoroughly in time before surgery.
③ large intraoperative bleeding, long operation time, and large evaporation of water: in major abdominal surgery, such as pancreatic head duodenectomy, patients often have deep jaundice, coagulation dysfunction, and the intraoperative trauma surface is prone to blood leakage. Because of the large surgical trauma and rich retroperitoneal lymphatic circulation, the amount of exudation from the surgical field is very high. If the postoperative fluid input is insufficient, acute hypovolemia can occur.
④Acute postoperative massive bleeding: such as postoperative trauma hemorrhage, intra-abdominal hemorrhage or gastrointestinal hemorrhage, etc.
⑤ Postoperative abdominal drainage or gastrointestinal decompression etc. cause additional loss of body fluid, and the infusion fails to replenish this part of fluid in time. In addition, in addition to bleeding, large amount of body fluid exudation after tissue damage, bacterial contamination or neurological factors, etc., are all factors for the occurrence of blood volume deficiency in major surgery.
2, postoperative infection or poisoning: postoperative infection can be caused by a variety of pathogens and their toxins, such as bacteria, viruses, fungi, parasites, spirochetes or rickettsiae, etc., of which Gram-negative bacteria are common, such as meningococci, large intestine, deformation, green pus, Klebsiella, dysentery bacilli, etc.. Can also be seen in gram-positive bacteria, such as pneumococcus, Staphylococcus aureus and Pneumocystis aeruginosa. In recent years, a disease related to the production of toxins by S. aureus has been discovered. These S. aureus are non-invasive and form colonies on the mucosal surface, and the toxins produced by them can be absorbed into the body to cause toxic shock syndrome (TSS), which is clinically highlighted by inadequate perfusion of the microcirculation. In addition, after surgery such as strangulated intestinal obstruction or diffuse peritonitis, a large amount of toxins are absorbed into the blood, which can also cause serious toxic reactions in the body.
3, postoperative cardiac insufficiency: elderly surgical patients, especially those with preoperative heart disease, due to surgical trauma, anesthesia and other effects, can induce acute myocardial infarction, or even cause acute cardiac insufficiency. Such as suffering from severe arrhythmia, pericardial tamponade, pulmonary artery embolism, etc., which make the left ventricle systolic function diminished or diastolic filling insufficient, resulting in a sharp decrease in cardiac output. In addition, perioperative infusion too fast or too much infusion can also cause acute pulmonary edema.
4, neurogenic factors: due to the influence of surgical trauma, anesthesia and other stimuli or continuous epidural analgesic pump left after surgery, strong neuroreflex vasodilatation can be caused, and the peripheral vascular tone is sharply reduced, resulting in a relative shortage of effective circulation.
5, allergic factors: the perioperative use of certain drugs, allogeneic proteins or plasma, etc., can sometimes cause the body to have an allergic reaction, resulting in a sudden expansion of the systemic blood vessels, causing postoperative circulatory disorders.
6, other factors: such as the patient’s extreme fear of surgery, excessive fatigue, preoperative hunger, hypoglycemia, dehydration, heatstroke or cold and other factors can also affect the patient, causing postoperative circulatory disorders.
(B) Etiology of postoperative regional circulatory disorders: In addition to the etiology of systemic circulatory disorders, postoperative regional circulatory disorders are often related to the reduction of blood flow to local organs and local organ tissue hypoxia. For example, the complication of abdominal compartment syndrome (ACS) after severe trauma or major abdominal surgery can cause circulatory disorders in the thoracic and abdominal organs; postoperative portal vein system thrombosis can cause circulatory disorders in the liver or intestines; acute pulmonary embolism caused by postoperative venous thrombosis can lead to pulmonary circulatory disorders; postoperative deep vein thrombosis in the lower extremities caused by long-term bedridden patients can lead to postoperative lower extremity circulatory obstruction; portal vein cancer thrombosis in primary hepatocellular carcinoma patients after surgery can also cause circulatory obstruction in the liver.
Organ damage of postoperative circulatory disorders
In addition to postoperative systemic circulatory disorders, postoperative regional circulatory disorders can also be caused or aggravated by the latter. In severe cases of postoperative circulatory disorders, multiple visceral organ insufficiencies can occur, called multi-organ dysfunction syndrome (MODS), and can further develop into multi-organ failure (MOF). The occurrence of organ damage is closely related to the cause and duration of postoperative circulatory impairment. Short-term postoperative hypovolemic circulatory disorders are generally less likely to cause organ damage, but if the circulatory disorder lasts longer than a certain time frame, it is likely to trigger functional damage to organs.
(A) Lung: postoperative systemic circulatory disorders can cause reduced pulmonary blood perfusion, and when circulatory disorders are complicated by diffuse intravascular coagulation, it can cause pulmonary microcirculatory embolism, and at this time, if a large amount of reservoir blood is input, because it contains more microaggregates, it can also aggravate pulmonary microcirculatory embolism. Postoperative regional circulatory disorders such as venous thrombosis of the lower extremities can also cause pulmonary embolism, and pulmonary ischemia and hypoxia can damage capillary endothelial cells and alveolar epithelial cells, reduce the production of alveolar surface active substances, increase the surface tension of the liquid-gas interface in the alveoli, prompting alveolar atrophy and causing pulmonary atelectasis, at which time the blood in the pulmonary capillaries cannot carry out effective gas exchange, and the amount of alveolar ventilation and pulmonary capillary blood perfusion The normal ratio of alveolar ventilation to pulmonary capillary blood perfusion (ventilation/perfusion) is 0.8. When the pulmonary circulation is impaired, the atrophied alveoli cannot be ventilated normally, while some of the still good alveoli do not get good blood perfusion, so that the ventilation/perfusion ratio is out of balance, the ineffective cavity ventilation and venous mixed blood increase, the right and left intrapulmonary shunt increases, making hypoxemia more serious, and a series of symptoms of progressive dyspnea can appear clinically, which can be caused by Acute lung injury (ALI) quickly developed into acute respiratory distress syndrome (ARDS), manifested as severe postoperative circulatory disorders after active resuscitation, the circulation tends to stabilize and improve, but the patient appeared gradually aggravated dyspnea, ARDS is one of the main causes of death in patients with postoperative circulatory disorders.
(B) Heart: 80% of coronary perfusion in the heart occurs in diastole. The smooth muscle of coronary artery is dominated by β receptors. During the compensatory period of postoperative systemic circulatory disorder, although there is a large amount of catecholamine secretion in the body, the contraction of coronary artery is not obvious, so the blood supply to the heart is not significantly reduced. Entering the postoperative systemic circulatory disorder decompensation period, the cardiac output and aortic pressure decrease, and the diastolic blood pressure also decreases, which can cause a significant decrease in coronary artery perfusion and impaired myocardial hypoxia, resulting in cardiac insufficiency. In addition, hypoxemia, metabolic acidosis and hyperkalemia can also cause myocardial damage, and thrombus formation within the cardiac microcirculation can cause focal myocardial necrosis, and severe coronary infarction can further develop into acute heart failure.
(C) Brain: postoperative systemic circulatory disorders in patients with low arterial pressure reduce cerebral blood flow. The smooth muscle contraction of small arteries in the brain is influenced by the partial pressure of carbon dioxide and changes in acidity of the blood, and cerebral blood flow can increase when the partial pressure of carbon dioxide is elevated or acidosis is present. However, this regulatory mechanism requires the body to maintain a certain level of cardiac output and mean arterial pressure in order to function. Therefore, persistent hypotension can cause insufficient blood perfusion to the brain, resulting in swelling of the cerebral glial cells around the capillaries, as well as extravasation of plasma into the interstitial brain cells due to increased capillary permeability, causing acute cerebral edema and increased intracranial pressure, which can lead to brain herniation or coma in severe cases. Postoperative regional cerebral circulation disorders such as cerebral infarction can have transient ischemic attacks, such as dizziness, vertigo, and weakness of one limb, which start slowly and often occur during sleep or quiet time. In contrast, those caused by emboli mostly have no prodromal symptoms and an acute onset. Cerebral infarction generally rarely presents with symptoms such as severe disorders of consciousness and intracranial hypertension.
(iv) Kidney: early postoperative systemic circulatory disorders can cause insufficient renal blood flow, when the body’s antidiuretic hormone and aldosterone secretion increases, which can cause prerenal oliguria. If the circulatory disorder is short, the renal function can be restored after the blood pressure is restored by timely and active infusion treatment. If the postoperative circulatory disorder lasts for a long time and renal ischemia lasts for more than 3 hours, renal parenchymal damage can occur, which can be complicated by acute renal failure in severe cases. When postoperative complications such as severe acute pancreatitis or intestinal obstruction, such as abdominal compartment syndrome, cause postoperative regional circulatory disorders in the abdominal cavity, the circulatory disorders in the kidney can also be aggravated. Acute renal failure complicated by postoperative circulatory disorders is mainly due to inadequate tissue blood perfusion, but also related to the deposition of certain substances such as hemoglobin and myoglobin in the renal tubules to form mechanical blockage of the tubular pattern and damage to the tubular epithelium by toxic substances.
(E) Liver: The total blood flow of the liver accounts for about 1/4 of the cardiac output and can reach 1500 m1/min in normal individuals. when the circulation is impaired after surgery, the visceral blood vessels become spasmodic and the blood flow to the liver is significantly reduced. Patients with portal hypertension can often be complicated by thrombosis of the portal venous system after surgery, and blood stagnation in the portal vein can aggravate circulatory disorders in the liver and cause ischemia and hypoxia in the liver. At this time, there can be microthrombosis in the hepatic sinusoids and central veins, resulting in central necrosis of the liver lobules and even large areas of hepatic necrosis, causing serious impairment of liver function and hepatic metabolic insufficiency, leading to acute liver failure.
(vi) Gastrointestinal: Because the density of angiotensin II receptors in mesenteric vessels is higher than other parts of the body, the sensitivity to vasopressure substances is high, and the blood flow in the superior mesenteric artery can be reduced by 70% in severe postoperative circulatory impairment. Gastrointestinal ischemia and hypoxia can cause gastrointestinal mucosal erosion and bleeding, and impaired intestinal mucosal barrier function can easily occur in the intestinal bacteria or its toxins through the lymphatic or portal pathway to infringe on the body, which causes intestinal bacteria or endotoxin displacement, leading to enterogenic infection, which is one of the important causes of postoperative MODS.
Fourth, the clinical manifestations of postoperative circulatory disorders
(A) postoperative systemic circulatory disorder clinical manifestations: that is, the performance of shock, early consciousness, increased excitability of the central nervous system, sympathetic-adrenal axis excitation, manifested as mental tension, excitement. Subsequently, there may be indifferent expression or irritability due to brain hypoxia, and in severe cases, the consciousness is gradually blurred and even coma. The patient has pale and moist skin and mucous membranes, rapid heart rate, rapid breathing, cyanosis, and decreased urine output. The peripheral blood vessels are poorly filled, the peripheral veins are atrophied, and the extremities are syncopal cold. Due to myocardial hypoxia and weak contraction, the pulse is weak and peripheral arterial pulsations such as the radial and dorsalis pedis arteries are not palpable. Due to hypoxia and acidosis, the patient’s breathing accelerates and deepens, and respiratory alkalosis may occur. In severe cases, consciousness is blurred or coma, the whole body skin and mucous membranes are obviously cyanotic, blood pressure is undetectable, and there is little or no urine. The decrease in urine output is mostly prerenal in the early stage due to insufficient blood volume and poor renal blood perfusion, and may be due to renal damage in the later stage. Further development of diffuse intravascular coagulation may result in skin mucosal petechiae or gastrointestinal bleeding. If the patient develops progressive dyspnea, which cannot be improved by oxygenation, the possibility of complicated ARDS should be considered.
(B) Clinical manifestations of postoperative regional circulatory disorders: The main manifestation is the abnormal function of regional organs. If postoperative pulmonary embolism causes pulmonary circulatory disorder, the clinical manifestation is sudden dyspnea, chest pain and hemoptysis, which is called pulmonary infarction triad. There may also be panic, cough, syncope, excessive sweating, cyanosis, near-death feeling, hypotensive shock, right heart failure, and hypothermia. Physical examination reveals an upward shift of the affected diaphragm, a shift of the trachea to the affected side, turbid percussion, rales and dry and wet rales, pleural friction sounds, and a hyperactive second pulmonary artery sound. The most meaningful sign is the increased filling and pulsation of the jugular vein reflecting the increased right heart load, which is an important manifestation of right heart insufficiency.
Postoperative myocardial infarction is manifested by sudden onset of angina pectoris, accompanied by nausea, vomiting, profuse sweating, bradycardia, acute cardiac insufficiency, severe arrhythmia or large fluctuations in blood pressure, such as relief of angina pectoris while systolic blood pressure is still lower than 80 mmHg, the patient is irritable, pale, wet and cold skin, thin and rapid pulse, profuse sweating, reduced urine output, or even fainting, suggesting cardiogenic shock, or acute Heart failure and other manifestations. The electrocardiogram shows momentary significant ST-segment elevation or depression, and T-wave inversion or elevation. Postoperative cerebral infarction mainly shows signs of focal cerebral deficits, such as ipsilateral monocular blindness or Horner’s syndrome and contralateral hemiparesis in internal carotid artery infarction; complete contralateral hemiparesis, sensory impairment and ipsilateral hemianopia in middle cerebral artery infarction; vertigo, nausea, vomiting, hoarseness, dysphagia, ipsilateral Horner’s syndrome, ataxia, ipsilateral superficial sensory loss and contralateral hemianopia in posterior inferior cerebellar artery infarction. superficial hyperalgesia and superficial sensory loss in the contralateral limb or mild hemiparesis.
In patients with postoperative hepatic circulation disorders, there may be anorexia, nausea, fatigue, abdominal distention, yellowing of the whites of the eyes and skin, and in severe cases, ascites or hepatic encephalopathy, etc. Laboratory tests may include elevated liver enzymes and serum bilirubin, decreased serum albumin, and prolonged prothrombin time. Patients with postoperative gastrointestinal circulation disorders may have abdominal distension, abdominal pain, nausea, vomiting, and in severe cases, vomiting blood, black stool or peritonitis. Postoperative lower limb circulation disorders mainly manifest as swelling, pressure pain, stiffness, pigmentation or superficial varicose veins in the affected limbs, and easy fatigue or increased swelling of the affected limbs after walking. Patients with postoperative ventricular compartment syndrome may have clinical manifestations of organ dysfunction such as heart, lung, liver, kidney and gastrointestinal tract at the same time.
V. Diagnosis and monitoring of postoperative circulatory disorders
Surgical patients with early postoperative symptoms such as sweating, excitement, accelerated heart rate, reduced pulse pressure difference or decreased urine output should be considered as having the possibility of postoperative circulatory disorders. The early diagnosis of postoperative circulatory disorders is based on.
①Increased blood pressure and decreased pulse pressure difference;
②Significant increase in heart rate;
③Thirst;
④Moist skin, white mucous membrane and cold extremities;
⑤ Skin vein atrophy;
⑥Decrease in urine output (25-30ml/h). The diagnosis of shock is confirmed if the following signs are present.
①Systolic blood pressure <10.7kpa (80mmHg) and pulse pressure <2.7kpa (20mmHg);
② Clinical signs of poor tissue perfusion, such as apathy, irritability, cold and wet limbs, pale or cyanotic skin, etc;
However, clinicians should pay more attention to strengthen the postoperative monitoring of surgical patients in order to detect the postoperative circulatory disorders early, remove the causes and improve the circulatory disorders in time.
(A) General monitoring
1, the state of consciousness: can reflect the perfusion of brain tissue and systemic circulatory status. If the patient is clearly conscious, responsive to external stimuli and in good mental state, it means that the circulating blood volume is sufficient; on the contrary, if the patient has indifferent expression, restlessness, delirium, drowsiness or coma, it mostly indicates that brain cell dysfunction occurs due to insufficient circulating blood volume in brain tissue.
2, limb temperature and color: can reflect the perfusion of the body surface. Pale, wet and cold skin of the extremities, pale color when lightly pressing the nails or lips of the mouth, and slow recovery of redness after loosening the pressure, indicate the existence of obvious poor perfusion of the limb tissues.
3, blood pressure: gradual decline in blood pressure after surgery, systolic blood pressure lower than 12kPa (90mmHg), pulse pressure difference less than 2.67kPa (20mmHg) is evidence of postoperative circulatory disorders; such as blood pressure rebound, pulse pressure difference increases, indicating the body’s good circulatory status. It should be noted, however, that blood pressure is not the most sensitive indicator of circulatory impairment, and it should not be determined by the value of a single measurement, but should emphasize regular measurement and dynamic comparison. Although postoperative blood pressure changes have an important reference value, it should not be used as the only criterion to diagnose postoperative circulatory disorders. This is because blood pressure only reflects cardiac output and peripheral vascular resistance, and does not represent the actual perfusion of the tissues. Early in the compensatory phase of postoperative circulatory disorders, there may also be a transient increase in blood pressure due to increased peripheral vascular resistance, but the increase in diastolic blood pressure is more pronounced, thus leading to a narrowing of pulse pressure. It is only when decompensation occurs that the patient experiences a decrease in blood pressure. Due to the lack of blood volume, the return blood volume decreases and the heart rate increases compensatively to maintain tissue perfusion, but the volume of each heart beat out is very small.
4. Pulse rate: Changes in pulse rate mostly occur before changes in blood pressure. When the blood pressure is still low, but the pulse rate has recovered and the limbs are warm, it often indicates that the circulation has improved. Shock index [pulse rate / systolic blood pressure (calculated in mmHg)] can help determine the presence or absence of shock and the degree of shock. Shock index below 0.5 indicates no shock; more than 1.0 to 1.5 indicates the presence of shock; above 2.0 indicates severe shock.
5.Urine volume: It can reflect the renal blood perfusion. Urine volume less than 25ml/h, urine specific gravity increases, indicating the existence of renal vasoconstriction or blood volume deficiency; blood pressure is normal, but the urine volume is still low, urine specific gravity decreases, then acute renal failure may have occurred; urine volume stable in more than 30ml/h, indicating good circulatory status. However, when judging this index, attention should be paid to the presence or absence of osmotic diuretics, the presence or absence of post-cranial trauma urinary collapse phenomenon, and the presence or absence of oliguria and anuria caused by urinary tract injury.
(II) Special monitoring
1, central venous pressure (CVP): represents the change of pressure in the right atrium or the vena cava of the thoracic segment, which can reflect the relationship between systemic blood volume and right heart function. the normal value of CVP is 0.49-0.98kPa (5-10cmH2O). In hypotension, when CVP is lower than 0.49kPa (5cmH20), it indicates insufficient blood volume; when CVP is higher than 1.47kPa (15cmH20), it indicates cardiac insufficiency, excessive constriction of venous vascular bed or increased resistance of pulmonary circulation; when CVP is higher than 1.96kPa (20cmH20), it indicates congestive heart failure. Clinically, continuous measurement is usually performed to dynamically observe the trend of changes.
2, pulmonary capillary wedge pressure (PCWP): the normal value of pulmonary capillary wedge pressure is 0.8-2.0kPa (6-15mmHg), and the normal value of pulmonary artery pressure (PAP) is 1.3-2.9kPa (10-22mmHg). PCWP is more sensitive than CVP because it can reflect the resistance of pulmonary circulation, while central venous pressure cannot directly reflect the pressure of pulmonary veins, left atrium and left ventricle. 30 mmHg) in pulmonary edema. When the PCWP is increased, but the central venous pressure is not increased, that is, too much infusion should be avoided to prevent acute pulmonary edema, and consideration should be given to reduce the pulmonary circulatory resistance.
3. Cardiac output (CO) and cardiac index (CI): Cardiac output is the amount of blood output per minute from the ventricles. Cardiac output = output per beat x heart rate. It is 5-6 L/min in a normal person at rest, and is an important indicator of the heart’s pumping function. The right heart float catheter “thermodilution method” is recognized as the “gold standard” for measuring cardiac output. However, this method is invasive and is now being replaced by noninvasive hemodynamic monitoring. In postoperative circulatory disorders, cardiac output is generally reduced, but can be increased in high-drain, low-resistance shock. If the cardiac output is calculated per unit body surface area (square meter), it is called cardiac index. The body surface area of a medium-sized adult is about 1.6~1.7 square meters, and the cardiac output is about 5~6L/min under quiet and fasting conditions, so the cardiac index is about 3.0~3.5L/(min.m2).
4.Arterial blood gas analysis: It can reflect the pulmonary ventilation and acid-base balance to understand the severity of postoperative circulatory disorders.
5.Arterial blood lactate measurement: the normal value is 1~1.5 mmol/L. Generally speaking, the longer the duration of shock, the more serious the blood perfusion disorder, the higher the arterial blood lactate concentration. Lactate concentration continues to rise, indicating a serious condition and poor prognosis. In critically ill patients, it can reach 2mmol/L. It has been reported that if the arterial blood lactate concentration exceeds 8mmol/L, the morbidity and mortality rate is almost 100%.
6.Intramucosal pH (pHi) measurement: It can reflect the blood perfusion and pathological damage of gastrointestinal tissues, as well as the oxygenation status of systemic tissues, which is valuable for assessing the metabolic situation in the gastrointestinal mucosa and evaluating the resuscitation effect. pHi’s normal range is 7.35~7.45.
7. Laboratory tests for disseminated intravascular coagulation (DIC).
① Platelet count below 80×109/L;
② Plasma fibrinogen less than 1.5g/L or progressive decrease;
③Prothrombin time is more than 3 seconds longer than normal;
④3P test (plasma fisetin coagulation test) is positive;
(⑤) More than 2% of broken red blood cells in the blood smear. Three or more abnormalities in the above five examination indexes, combined with clinical symptoms of shock and microvascular embolism or bleeding tendency can be diagnosed as diffuse intravascular coagulation.
(C) Organ function monitoring of postoperative regional circulatory disorders
1.Liver function determination: For postoperative complications of portal vein thrombosis or portal vein cancer embolism causing liver circulation disorder, liver function changes should be detected, such as determination of serum bilirubin, albumin, prothrombin time, transaminases and other indicators, and further imaging examinations such as B ultrasound, CT, MRI or CTA, MRA, etc. to observe liver function and liver circulation status.
2.Renal function determination: For patients with postoperative abdominal compartment syndrome, in addition to monitoring heart, lung, liver, gastrointestinal and other functions, it is more important to detect changes in renal function, such as determination of blood urea nitrogen, creatinine, determination of serum electrolytes, such as blood potassium, blood phosphorus, blood calcium and other measurements. And routine arterial blood gas analysis and urine routine examination.
3. Gastrointestinal function measurement: In addition to the above-mentioned measurement of pH within the gastrointestinal mucosa (pHi), there is no uniform monitoring standard due to the diversity and complexity of gastrointestinal tract functions, mainly observing whether there is absorption and peristaltic disorders in the gastrointestinal tract, whether there is gastrointestinal mucosal erosion or bleeding on endoscopy, and whether there is damage to mucosal barrier function. At the same time, imaging and other methods should be used to exclude the presence of necrotizing small bowel colitis, mechanical intestinal obstruction, intestinal perforation and other surgical acute abdominal conditions. Apply color Doppler, CT-enhanced scan or MRA to observe whether there is thromboembolism in the mesenteric arteries.
4.Respiratory function measurement: In addition to understanding the respiratory rate and the presence of dry and wet rales, arterial blood gas analysis can reflect the pulmonary ventilation and acid-base balance to understand the severity of pulmonary circulation disorders. Chest X-ray or CT examination can observe the texture changes of both lungs and whether there is edema in the interstitial lung and whether there are solid shadows in the lungs. Pulmonary arteriography is currently recognized as the gold standard for the diagnosis of pulmonary embolism, with high sensitivity and specificity.
①Filling defect in the lumen of the vessel;
②Pulmonary artery truncation phenomenon;
The important signs of pulmonary arteriography include: (1) intravascular filling defects; (2) pulmonary artery truncation; (3) decreased blood flow in a certain lung region. However, this method is an invasive monitoring method, and non-invasive examination methods such as CT-enhanced scan or MRA should be used first.
5.Other monitoring: cranial CT and MRI can be done for postoperative cerebral infarction patients; electrocardiogram and coronary angiography can be done for postoperative myocardial infarction patients; color Doppler examination, CT-enhanced scan and lower limb venography can be done for postoperative lower limb venous thrombosis patients. In addition, blood D-dimer determination can be done. D-dimer is a soluble degradation product produced by cross-linked fibrin under the action of fibrinolytic enzymes, which is a specific marker of fibrinolysis process, and the concentration of D-dimer in blood is obviously increased due to thromboembolic fibrinolysis in thromboembolic diseases.