[Crisis Management] Sudden acute pulmonary edema during perianesthesia

Sudden acute pulmonary edema in the peri-anesthesia period 1.
Occurrence and harm of sudden acute pulmonary edema in the peri-anesthesia period Edema, and then enter the alveoli, causing bloody secretions to appear in the respiratory tract, leading to serious physiological disorders
.

Peri-anesthesia acute pulmonary edema is pulmonary edema induced by various factors during the peri-anesthesia period, including anesthesia factors, primary disease factors, surgical factors, etc.
Acute pulmonary edema caused by anesthesia factors alone is rare
.

In the early stage of awake patients, there may be anxiety, irritability, shortness of breath or even dyspnea, cyanosis and hypoxemia, as well as rough dry rales, large, medium and small wet rales and crepitus on auscultation
.

Early chest radiographs of pulmonary edema show vasodilation and congestion in the upper part of the lung, especially in the apex, and marked increased lung markings
.

Intraoperative blood oxygen saturation decreased, end-tidal carbon dioxide partial pressure first decreased and then increased
.

Blood gas analysis showed that when interstitial pulmonary edema, PaCO2 decreased, pH increased, showing respiratory alkalosis; when alveolar edema, PaCO2 increased and (or) PaO2 decreased, pH decreased, manifested as hypoxemia and respiratory acidosis
.

Respiratory symptoms in patients with general anesthesia are often masked, but the breathing resistance of either manual or mechanical ventilation will increase significantly, and SpO2 may also decrease.
At this time, pulmonary edema should be vigilant
.

The characteristic pink foamy sputum gushing out of the respiratory tract during anesthesia is a basic but advanced diagnosis
.

Pulmonary edema with obvious clinical manifestations in the peri-anesthesia period is relatively rare, with an incidence of 0.
2% to 7.
6%.
Once acute pulmonary edema occurs during the peri-anesthesia period, the main impact on patients is as follows
.

1.
Pulmonary function affects the accumulation of fluid in the pulmonary interstitium and alveoli, which reduces the gas volume in the lungs and the lung capacity; reduces the elasticity of the lung tissue and reduces the compliance; even affects the effect of alveolar surfactants, further reducing the lung capacity.
Compliance and lung capacity
.

The proportion of ventilation and blood flow is imbalanced, and the alveoli with fluid accumulation is poorly ventilated, but the blood perfusion is basically normal, V/Q decreases, arteriovenous shunt, and PaO2 decreases
.

In patients with pulmonary edema, pulmonary interstitial pressure increases, capillary resistance increases, and there is also hypoxic pulmonary arteriole constriction, which increases pulmonary arterial pressure and increases right heart afterload
.

The small airways of patients with pulmonary edema are prone to stenosis, blockage or even premature closure due to increased interstitial pressure
.

2.
Effects on systemic organs The effects of pulmonary edema on systemic organs are related to the hypoxia of tissue cells caused by hypoxemia, as well as the effects of acid-base imbalance and electrolyte changes in the body's internal environment
.

2.
Analysis of the causes of sudden acute pulmonary edema in the peri-anesthesia period (1) The formation mechanism of acute pulmonary edema 1.
Increased pulmonary capillary hydrostatic pressure (1) Cardiogenic: such as mitral valve stenosis, left ventricular failure, left ventricular Atrial myxoma, three-chambered heart, cardiomyopathy,
etc.

(2) Non-cardiac origin: such as pulmonary vein stenosis caused by congenital pulmonary vein root stenosis, mediastinal granuloma, and mediastinal tumor
.

(3) Excessive infusion: Including excessive liquid input and too fast infusion per unit time
.

2.
Increased vascular wall permeability (1) Infectious pulmonary edema
.

(2) Toxin inhalation pulmonary edema
.

(3) Vasoactive substances
.

(4) Diffuse capillary leak syndrome
.

(5) Disseminated intravascular coagulation (DIC)
.

(6) Uremia
.

(7) Other causes
.

3.
Lymphatic drainage disorders such as lung transplantation, silicosis, etc.
make lymphatic drainage disorders, which will inevitably increase the volume of fluid and protein content in the lung tissue space
.

4.
Decreased colloidal osmotic pressure, such as hypoalbuminemia, nutrient deficiency and intestinal protein loss caused by liver and kidney disease, lead to decreased colloidal osmotic pressure
.

5.
Increased negative pulmonary interstitial pressure (1) Pulmonary edema after upper airway obstruction ①Acute: laryngospasm, epiglottitis, laryngotracheal bronchitis, spastic croup, airway foreign body, laryngeal edema, tumor, upper airway trauma, An abscess in the back of the pharynx or around the tonsils
.

② Chronic: Obstructive sleep apnea syndrome, hyperplasia or tonsil hypertrophy, nasopharyngeal mass, goiter, neck tumor, maxillofacial tumor, acromegaly
.

③Laryngeal spasm is common in the induction period of anesthesia.
It is often caused by the difficulty of endotracheal intubation due to adverse drug reactions, strong stimulation of surgical anesthesia, and anatomical abnormalities.
It is common in adults
.

Epiglottitis, spastic croup and laryngotracheobronchitis are more common in infants and children (2) Recruitment pulmonary edema: clinically seen in atelectasis caused by pneumothorax or pleural effusion (blood), the course of the disease can be several However, it is more common to perform rapid lung recruitment after 3 days, and the clinical symptoms of pulmonary edema can appear within 1 hour
.

Features: It is more common in the use of negative pressure suction for lung recruitment, and can also occur in patients undergoing closed drainage
.

Suction a large amount of pleural effusion in a short time, the effusion volume is more than 2000ml
.

50% occur in patients over the age of 50
.

The ratio of edema fluid protein content to plasma protein content is >0.
6
.

6.
Unexplained pulmonary edema Causes of pulmonary edema such as post-pneumonectomy, high altitude pulmonary edema, pulmonary embolism, pulmonary parenchyma, cardioversion, cardiopulmonary bypass,
etc.

7.
Neurogenic pulmonary edema, traumatic brain injury, brain abscess, cerebrovascular accident, meninges and brain inflammation, brain tumor, grand mal seizures
.

(2) Analysis of the causes of acute pulmonary edema in the peri-anesthesia period 1.
Primary disease factors (1) In the perioperative period of patients with mitral valve stenosis, once the blood volume returned to the heart increases and the left ventricular output is blocked again, the left atrial pressure and pulmonary artery pressure will further increase.
It is easy to induce pulmonary edema, and the triggering factors mainly include mental stress and tachycardia
.

(2) Pulmonary edema caused by heart failure may occur after intracardiac surgery to correct the lesion or deformity, such as severe pulmonary valve stenosis, huge atrial defect in adults, ventricular defect,
etc.

(3) In patients with pheocytoma, a large amount of catecholamines are released during the operation, the peripheral blood vessels are strongly constricted, and a large amount of blood enters the pulmonary vascular bed, causing pulmonary hypertension and pulmonary edema; in addition, when such patients have catecholamine myocarditis, they cannot tolerate the tumor after resection Pulmonary edema occurs due to blood pressure drop and fluid infusion
.

(4) Neurogenic pulmonary edema is easily caused by craniocerebral injury and cerebrovascular accident
.

(5) Sepsis can cause permeability pulmonary edema
.

(6) Obstruction of the upper airway caused by various reasons, causing severe hypoxia and forced breathing, which can lead to pulmonary edema
.

2.
Surgical factors (1) Too long cardiopulmonary bypass time can change pulmonary capillary permeability, reduce colloid osmotic pressure, and may induce the occurrence of pulmonary edema
.

During cardiopulmonary bypass, a large amount of bronchial blood supply is returned to the left atrium or the left atrium is poorly drained, resulting in pulmonary vasodilation, pulmonary hypertension, and pulmonary edema
.

(2) Pneumonectomy makes patients very sensitive to the amount of fluid infusion, and pulmonary edema easily occurs during or after surgery
.

Extensive dissection of lymph nodes in esophageal surgery will hinder lymphatic return, and it is also sensitive to infusion, which is easy to induce pulmonary edema
.

(3) Prostate resection, hysteroscopy and other operations take a long time, and too much fluid enters the patient's body, which is prone to pulmonary edema
.

3.
Pulmonary edema caused by anesthesia-related factors is rare, and it is often the case that patients have potential pulmonary edema factors, plus anesthesia factors
.

(1) Factors of pulmonary edema during induction of anesthesia: During the induction of anesthesia, the following factors may induce pulmonary edema in patients with cardiac insufficiency: ① The patient is anxious and restless; ② Posture changes (such as changing from sitting to supine); ③ Improper medication , such as the application of atropine, pancuronium bromide, ketamine to induce tachycardia; ④ the use of anesthetics with myocardial depression or a receptor agonists; ⑤ cardiac insufficiency, lack of adequate preparation before surgery; Cardiovascular stress response
.

(2) Dosage of anesthetics: Pulmonary edema caused by overdose during anesthesia can be seen in morphine, methadone, acute barbiturate and diacetamorphine poisoning, and the pathogenesis is still unclear
.

It may be related to the following factors: (1) Inhibition of the respiratory center, causing severe hypoxia, increased pulmonary capillary permeability, accompanied by pulmonary hypertension, resulting in acute pulmonary edema; (2) Hypoxia stimulates the hypothalamus to cause peripheral vasoconstriction and blood redistribution And cause increased blood volume; ③ pulmonary edema caused by heroin may be related to neurogenic pathogenesis; ④ susceptibility or allergy of individual patients
.

(3) Oxygen toxicity pulmonary edema: refers to pulmonary edema caused by lung tissue damage caused by prolonged inhalation of high concentrations (>60%) of oxygen
.

Generally, inhalation of pure oxygen under normal pressure for 12 to 24 hours, under high pressure for 3 to 4 hours, can cause damage to mucosal cells and the formation of alveolar hyaline membranes, thereby causing pulmonary edema, and oxygen poisoning can occur
.

The damage of oxygen toxicity is mainly in lung tissue, which is manifested as epithelial cell damage, reduction of alveolar surfactant, formation of alveolar hyaline membrane, causing alveolar and interstitial edema, and atelectasis
.

Its toxic effect is due to the intermediate product free radicals (such as superoxide anion, hydrogen peroxide, hydroxyl radical and singlet oxygen) generated when oxygen molecules are reduced to water
.

Normally, oxygen free radicals are scavenged by antioxidant systems in tissues such as superoxide dismutase (SOD), catalase, and glutathione oxidase
.

Inhalation of high concentrations of oxygen accelerates the formation of oxygen free radicals.
When the amount exceeds the scavenging ability of the tissue antioxidant system, lung tissue damage can be caused, resulting in lung damage
.

(4) Obstruction of airway: perioperative laryngospasm is commonly seen in strong stimulation of intubation during anesthesia induction, and also in intraoperative nerve traction reaction, as well as airway stimulation due to incomplete nerve block in thyroid surgery
.

When the airway is unobstructed, the intrathoracic pressure has little effect on the interstitial pressure in the lung tissue, but in the case of acute upper airway obstruction, the negative pressure in the pleural cavity increases due to forced inhalation, and almost all of it is transmitted to the perivascular space, which promotes the entry of intravascular fluid into the lung tissue.
gap
.

When the upper airway is obstructed, the patient is in a state of struggle, and hypoxia and sympathetic nerve activity are extremely hyperactive, which can lead to spastic constriction of pulmonary arterioles, constriction of pulmonary venules, and increased pulmonary capillary permeability
.

And acidosis can increase the inhibition of cardiac work.
Unless the airway obstruction is relieved, a vicious circle will be formed and the development of pulmonary edema will be accelerated
.

(5) Aspiration: perioperative vomiting or reflux of gastric contents can cause aspiration pneumonia and bronchospasm, inactivation of pulmonary surfactant and damage to pulmonary capillary endothelial cells, resulting in fluid leakage into the lung tissue space Inside, pulmonary edema occurs
.

The patient presented with cyanosis, tachycardia, bronchospasm, and dyspnea
.

The degree of lung tissue damage is directly related to the pH of gastric contents.
The damage caused by gastric juice with pH>2.
5 is much less than that with pH<2.
5
.

(6) Lung over-inflation: One-sided lung atelectasis with one-lung ventilation, all the tidal volume enters one side of the lung, resulting in over-expansion of the lung, followed by pulmonary edema, the mechanism may be related to the increase in lung capacity
.

(7) Factors of postoperative pulmonary edema: the occurrence of postoperative pulmonary edema mostly occurs 30 minutes after stopping anesthesia, which may be related to the following factors: ① withdrawal of positive pressure ventilation; ② increased cardiac output; ③ increased PaCO2; ④ decreased PaO2; ⑤ airway obstruction; ⑥ hypertension
.

3.
Coping strategies for sudden acute pulmonary edema in the peri-anesthesia period Early diagnosis and proper management of acute pulmonary edema in the peri-anesthesia period are the keys to improving the prognosis, and its reduction requires anesthesiologists to be more vigilant in the perioperative period, especially for those with high-risk potential Primary disease factors and certain surgeries with a high incidence of pulmonary edema
.

In addition to treating the cause, effective methods should be used to reduce pulmonary vascular hydrostatic pressure, increase plasma colloid osmotic pressure, improve pulmonary capillary permeability, improve pulmonary gas exchange, and correct hypoxemia.
In addition, active prevention should be used.
infection
.

Specifically, the following measures are included
.

1.
Sufficient oxygen supply through nasal cannula and simple face mask is often insufficient to improve hypoxia in patients with severe hypoxemia.
Pressurized oxygen supply, including intermittent positive pressure oxygen supply ventilation, increases alveolar pressure and lung tissue interstitial pressure, reduces Pulmonary capillary fluid leakage, reducing venous blood return, lowering the filling pressure of the right atrium, and cutting off the vicious circle of pulmonary edema and hypoxia
.

Use a de-foaming agent to reduce the surface tension of the foam and eliminate the foamy phlegm of the respiratory tract.
Usually, 50% ethanol is placed in a humidifier and inhaled together with oxygen, but long-term application should be avoided
.

2.
Diuresis Rapid diuresis is an effective method to reduce excess fluid in the pulmonary interstitium and alveoli.
It can also dilate veins, reduce venous return and reduce pulmonary edema
.

However, when a large amount of diuresis should be used, the internal environment and electrolytes should be monitored more intensively
.

3.
Vasodilator drugs reduce the preload and afterload of the heart.
Nitroglycerin or sodium nitroprusside directly act on vascular smooth muscle, reduce peripheral vascular resistance, increase cardiac output, transfer blood from pulmonary circulation to systemic circulation, and reduce pulmonary edema
.

Morphine is also a conventional drug for the treatment of acute pulmonary edema.
It not only has a central sedative effect and reduces oxygen consumption, but also dilates small arteries, reduces systemic venous tone, and reduces right heart filling pressure and left atrial pressure
.

4.
The use of cardiotonic drugs, especially when acute pulmonary edema is combined with hypotension, the use of positive inotropic drugs such as Maohuaxi C and dopamine drugs can enhance myocardial contractility and increase cardiac output , to improve tissue perfusion, correct tissue ischemia, hypoxia, is conducive to the recovery of pulmonary edema
.

5.
Aminophylline Aminophylline can not only enhance myocardial contractility, reduce afterload, but also relax bronchial smooth muscle, increase renal blood flow and sodium excretion
.

However, attention should be paid to the injection speed to prevent adverse effects on the heart
.

6.
There are still differences in the therapeutic value of high-dose corticosteroids for pulmonary edema.
It is generally believed that it can prevent the increase of capillary permeability, stabilize the lysosomal membrane, and inhibit the inflammatory response, which is especially beneficial to permeability.
Recovery of pulmonary edema, but it is inconclusive whether it can restore damaged capillaries
.

7.
Albumin The use of albumin is not beneficial for all patients with pulmonary edema and should be determined on a case-by-case basis
.

In high-pressure pulmonary edema, the pulmonary capillary hydrostatic pressure is greater than the colloid osmotic pressure, and a large amount of low-protein fluid is transferred to the pulmonary interstitium, alveoli, and even hypovolemic shock; albumin infusion can rapidly increase the colloid osmotic pressure and promote the development of pulmonary edema.
restore
.

However, for patients with permeability pulmonary edema, the vascular permeability is increased, and albumin infusion may be harmful.
After albumin leaks into the pulmonary interstitium, more fluid can accumulate in the interstitial space and aggravate pulmonary edema
.

However, if there is hypoalbuminemia, supplementation of albumin and the application of diuretics can facilitate the negative production of fluid and improve hypoxia
.

8.
The application of sedatives such as midazolam, diazepam, propofol, etc.
has a strong sedative effect and reduces the nervousness of patients, reduces the negative pressure caused by shortness of breath, stabilizes breathing, reduces work of breathing, and is more conducive to The patient cooperated with respiratory therapy
.

9.
Prevention of infection: Pulmonary edema caused by various reasons should be intravenously infused with sensitive and effective high-dose antibiotics to prevent pulmonary infection.
It can be used in combination with adrenal cortex hormones, which is more beneficial to promote the regression of pulmonary edema
.

4.
Thoughts on sudden acute pulmonary edema during peri-anesthesia period We believe that the effective preventive measures for acute pulmonary edema during peri-anesthesia period are as follows
.

1.
Control the infusion speed and infusion gods (1) Excessive infusion speed and excessive crystalloid input are the most common causes of pulmonary edema during anesthesia, especially for the elderly, infants and patients with poor cardiac function
.

(2) Intraoperative application of central venous pressure monitoring to guide blood transfusion
.

2.
Unobstructed airway and respiratory support (1) Keep the airway unobstructed, prevent excessive secretion of respiratory tract, vomiting, reflux and aspiration to avoid airway blockage, laryngospasm and bronchospasm
.

(2) During the process of single-lung anesthesia, pay attention to slowly recruit the collapsed lung to prevent the occurrence of atelectasis and recruited pulmonary edema
.

(3) Avoid excessive suction negative pressure and long suction time during the suction process
.

(4) Ensure adequate alveolar ventilation and avoid hypoxia and carbon dioxide accumulation
.

(5) When the positive pressure ventilation is withdrawn, it should be gradually transitioned, such as reducing the ventilation frequency and pressure, to avoid stopping the positive pressure ventilation too quickly
.

3.
Avoid overdose of anesthetics Avoid overdose of anesthetics during surgery, such as morphine, methadone, sodium thiopental and other drugs should not be overdose
.

4.
To prevent oxygen poisoning.
It is not advisable to inhale pure oxygen for a long time during the operation and after the operation.
The pure oxygen inhalation time should be less than 6 hours under normal pressure and less than 1 hour under high pressure
.

The oxygen concentration of the mask is controlled below 40% for long-term oxygen inhalation
.

The alveolar FiO2 value monitored during anesthesia is generally above 90%, and there is a CO2 absorption circuit
.

5.
Maintain hemodynamic stability (1) Maintain hemodynamic stability during the perioperative and postoperative period, and avoid blood pressure fluctuations, such as hypertension, hypotension, especially shock and heart failure
.

(2) For patients with preoperative infection, infection should be strictly controlled before and during the perioperative period to prevent the occurrence of toxic shock
.

V.
Typical cases of sudden acute pulmonary edema during peri-anesthesia.
Case 1.
Acute pulmonary edema after high ligation of varicocele under laparoscopy
.

The patient is a male, 18 years old, 183cm tall and 55kg in weight
.

The patient was admitted to the hospital due to swelling and discomfort of the left scrotum for 4 years.
He was supine, and the symptoms were relieved after rest.
The left varicocele was diagnosed preoperatively
.

Laparoscopic high ligation of the left varicocele was planned
.

The electrocardiogram, chest X-ray, biochemistry, coagulation, etc.
were normal, ASAI grade, and no cardiopulmonary disease
.

After entering the operating room, venous access was opened, and vital signs were monitored: blood pressure 110/70 mmHg, heart rate 70 beats/min, SpO2 99%, and respiration 20 beats/min
.

Intravenous injection of "Changtuoning" 0.
6g 10 minutes before anesthesia
.

General anesthesia with endotracheal intubation, general anesthesia induction drugs were followed by midazolam 0.
06mg/kg, propofol 1mg/kg, fentanyl 3ug/kg, vecuronium 0.
15mg/kg
.

Quickly insert the No.
4 laryngeal mask through the mouth, auscultate the two lungs with clear breath sounds, connect to an anesthesia machine to control breathing, tidal volume 8ml/kg, frequency 13 times/min, airway pressure 14~16cm H2O, inhaled sevoflurane 1.
5% during surgery ~2.
5MAC, remifentanil 0.
6mg/h was pumped, BIS monitoring was continued to maintain an appropriate depth of anesthesia, and cisatracurium 5mg/h was continuously pumped to maintain muscle relaxation
.

After the anesthesia was satisfied, the head was lowered to a height of about 30°, and the artificial pneumoperitoneum was established.
The carbon dioxide pressure of the abdominal pneumoperitoneum was below 1.
9kPa
.

The operation began to establish artificial pneumoperitoneum, adjust the concentration of sevoflurane in the vaporizer to 2.
5MAC, and inject fentanyl 0.
15mg to deepen anesthesia.
The surgeon complained that the patient was not satisfied with the pneumoperitoneum.
Please check the carbon dioxide inflation tube and adjust the pneumoperitoneum needle.
Direction and depth until the effect is satisfactory
.

At this time, the blood pressure suddenly dropped to 78/48mmHg, the heart rate increased to 98 beats/min, the PETCO2 dropped from 42mmHg to 28mmHg, and the SpO2 dropped to 90%.
To 43 beats/min, after administration of atropine 0.
5mg, the heart rate returned to 70 beats/min, and the blood pressure also returned to 100/58mmHg
.

Laparoscopy found a small amount of blood in the abdominal cavity, the cause was not identified, and the operation continued
.

After 10 minutes, PETCO2 began to rise to 55~60mmHg, increase the tidal volume to 500ml, increase the respiratory rate to 15 times/min, drop to 45mmHg after 5 minutes, and continue at this level
.

After laparoscopic exploration, a 6cmX3cm hematoma was found in the retroperitoneum.
Consultation with general surgery and vascular surgery was required.
No damage to the bowel was found, but a hole in the mesentery was found.
Observation first, no laparotomy for the time being, no obvious enlargement after 30 minutes, close the suture, the operation is over, and the patient is sent to PACU with a tube
.

The operation lasted for 1 hour and 40 minutes, and 800ml of Ringer's solution, 500ml of "Tianli" and 200ml of urine were input
.

15 minutes after entering the recovery room, the patient woke up, the swallowing reflex, cough reflex recovered, and spontaneous breathing recovered, atropine 0.
5mg, neostigmine 2mg were antagonized, and then the laryngeal mask was pulled out.
After 5 minutes, it was found that SpO2 dropped to 78%, and oxygen was given with pressure mask immediately, and SpO2 rose to 96%.
However, the patient had severe cough and sputum, pink foamy sputum appeared in the oral and nasal cavity, and diffuse rales in both lungs were auscultated
.

After rapid suction, continue to give oxygen by mask, blood gas analysis: pH7.
2, PCO2 67mmHg, PaO2 86mmHg, Na+138mmol/L, K4.
0mmol/L, Ca2+1.
18mmol/L, glucose 8.
6mmol/L, serum lactate (Lac) 1.
5mmol/L> hematocrit 62%, hemoglobin 10.
2g/L, BE-4.
1mmol/L, furosemide 20mg, morphine 5mg, dexamethasone 10mg
.

After 30 minutes, the urine output was 800ml, and both lungs were auscultated.
The breath sounds of the left lung were clear, and no crackles were heard.
The breath sounds of the right lung were still relatively weak, and there were diffuse crackles
.

SpO2 can reach 90% under oxygen inhalation.
Bedside chest X-ray shows: patchy high-density shadows in the right lung and left middle lung, increased lung markings, unclear trachea, and exudative lesions in both lungs
.

Continue high-concentration oxygen inhalation, take a semi-recumbent position, and give furosemide 15mg again.
After 1 hour, the urine output reaches 1300ml.
The patient's consciousness is clear and easy to answer questions.
After 1 hour of observation, he was sent back to the ward, where he continued to inhale high-concentration oxygen therapy and monitored ECG, and his vital signs were stable
.

On the second day of follow-up, the patient had stable blood circulation, good spontaneous breathing, clear consciousness, no abnormal limb muscle strength, and other general conditions of the body.
The chest X-ray was repeated, and both lungs were normal
.

Discharged on the 4th day after surgery
.

The discussion analysis is as follows
.

The patient had no previous underlying diseases, normal vital signs, and preoperative examinations: ECG, chest X-ray, biochemistry, coagulation, etc.
were all normal, no drug was taken, no hypoxia and carbon dioxide accumulation, and electrolytes before and during surgery were normal, etc.
, can rule out the patient's primary disease factors
.

During anesthesia, the operation time is 1 hour and 40 minutes, the infusion rate is slow, and the total amount of fluid is 1200ml, which can rule out the excessive and fast infusion
.

Intraoperative continuous pumping of 5 mg/ml cis-atracurium to maintain muscle relaxation, continuous BIS monitoring to maintain the corresponding depth of anesthesia, can rule out mechanical lung injury caused by human-machine confrontation
.

Laparoscopic surgery patients are inserted into a laryngeal mask, and the possibility of reflux and aspiration cannot be ruled out during the operation and extubation process.
The acid gastric juice refluxes into the respiratory tract and alveoli, damages the capillary endothelium and alveolar epithelium, increases its permeability and causes pulmonary edema
.

This case is extremely rare.
The surgeon inserted the needle into the inferior vena cava during the establishment of pneumoperitoneum and was not found in time.
A large amount of carbon dioxide gas filled the inferior vena cava and entered the right heart, and entered the pulmonary circulation through the right ventricle and pulmonary artery, causing the right ventricular outflow tract.
and pulmonary arterial carbon dioxide gas embolism, the early manifestations are a sharp decrease in cardiac output, a significant drop in blood pressure, myocardial perfusion, myocardial ischemia, and slow heart rate; Gas exchange dysfunction and pulmonary edema
.

When carbon dioxide gas rapidly diffuses into the pulmonary arterioles and pulmonary capillary network, the capillaries of the pulmonary bronchioles, bronchioles and alveoli will be ischemia and hypoxia due to embolism, PetCO2 will decrease, and the pulmonary capillary endothelium and alveolar epithelium will be damaged.
Permeability increases, and neutrophils are stimulated to mediate inflammatory responses, superoxide dismutase and oxygen free radicals to induce pulmonary edema
.

Due to the high level of carbon dioxide dispersion, it is easily soluble in blood and tissue fluid, and can be quickly exhaled through alveolar exchange.
The patient is young and has no cardiopulmonary disease.
When blood pressure, heart rate and hypoxemia occur, vasopressors should be used quickly.
And the sinus node agonist gradually recovered without serious consequences such as arrhythmia, circulatory failure and cardiac arrest
.

However, the pulmonary capillary endothelium and alveolar epithelium have been greatly damaged, the permeability is increased, the production of alveolar surfactant is reduced, the protein reflection coefficient of the alveolar epithelium is reduced, the fluid continues to extravasate, the pneumoperitoneum is relieved after the operation, and the raised diaphragm Return to the original position, suddenly increase the negative pressure in the thoracic cavity, reduce the venous water pressure around the microvascular, and increase the filtration pressure difference
.

At the same time, due to the effect of excessive negative pleural pressure, the number of open pulmonary capillaries and the inflow of blood flow increase, which increases the filtration area and filtration coefficient, thereby causing pulmonary edema
.

The treatment experience of this case: pulmonary edema was found to be properly handled after extubation, and the mask was immediately pressurized to give high-concentration oxygen, and the built-in 75% alcohol in the humidifier helped to eliminate foam
.

Pulmonary edema was confirmed by auscultation of both lungs and bedside chest radiography
.

Taking the semi-recumbent position increases the volume of the thoracic cavity, increases the tidal volume, and improves ventilation; at the same time, it reduces the venous blood return, reduces the burden of pulmonary circulation, and relieves pulmonary edema
.

Stop or slow down the infusion rate, intravenous injection of the secret to quickly diuretic, reduce circulating blood volume and increase plasma colloid osmotic pressure, reduce the amount of fluid filtered by microvessels; in addition, it can dilate veins and reduce venous return, even before the diuretic effect is exerted.
Can produce the effect of reducing pulmonary edema
.

The use of morphine can reduce anxiety, reduce myocardial oxygen consumption, and reduce peripheral vascular resistance through central sympathetic inhibition, transfer blood from pulmonary circulation to systemic circulation, and relax airway smooth muscles and improve ventilation
.

Intravenous glucocorticoids can reduce inflammation, reduce microvascular permeability, promote surfactant synthesis, enhance myocardial contractility, reduce peripheral vascular resistance and stabilize lysosomal membranes
.

However, the disadvantage is that the observation during the operation is not careful enough.
During the establishment of pneumoperitoneum, unexplained blood appears, and when blood pressure, heart rate, and end-expiratory carbon dioxide are abnormal, the cause is not carefully analyzed, and the possibility of carbon dioxide gas embolism is suspected.
Take the right interventions to block its further development into pulmonary edema
.

Case 2, acute pulmonary edema after cesarean section with gestational hypertension
.

The patient, a female, 28 years old, weighing 85kg, was admitted to the hospital because of 38+5 weeks of intrauterine pregnancy in the first child, headache and edema of both lower extremities, unable to lie supine for 1 month, and irregular uterine contractions for 1 hour
.

Physical examination: body temperature 36.
8°, heart rate 110 beats/min, respiration 20 beats/min, blood pressure 180/110mmHg, shortness of breath, cardiac color Doppler ultrasound: left ventricular enlargement, mitral valve insufficiency; urine protein (++ )
.

Platelet 90X109/L: Liver function: increased alanine aminotransferase, decreased total protein; fundus examination showed: retinal edema with flocculent oozing
.

Diagnosis: gestational hypertension (severe)
.

The patient received no formal treatment before surgery
.

The emergency department pushed the patient into the operating room, opened the fluid path, and performed combined lumbar-epidural anesthesia in the L2-3 space in the right lateral position.
After seeing the outflow of cerebrospinal fluid, slowly give 0.
75% bupivacaine 2.
0ml + 10% glucose solution 0.
5ml, A 3.
0 cm epidural catheter was placed in the head, and the patient was instructed to lie supine, inhaling oxygen, with the head high and the feet low, and the right medulla was elevated by 20°.
Zolam 2mg into the pot
.

10 minutes after the fetus was delivered, the maternal heart rate reached 130 beats/min, and 0.
2 mg of Maohuaxi C and 20 mg of furosemide were given intravenously.
The vital signs gradually stabilized.
The operation ended 40 minutes later.
The bleeding was about 300 ml, the fluid replacement was 500 ml, and the urine output was 200 ml.
, return the mother to the ward safely
.

20 minutes after returning to the ward, the patient suddenly experienced palpitation, shortness of breath, cyanotic lips, and coughed up a lot of pink foamy sputum.
Blood pressure was measured at 160/110 mmHg, heart rate was 130 beats/min, breath was 30 beats/min, and small dampness could be heard at the bottom of both lungs.
Rales, immediately in a semi-sitting position, inhaling oxygen through a mask, 0.
4 mg of Maohuaxi C, 20 mg of furosemide, and 20 mg of dexamethasone intravenously, 5 minutes later, the patient was irritable, dyspnea worsened, and unconsciousness appeared, SpO2 70%, Emergency tracheal intubation connected to ventilator for positive pressure ventilation, morphine 5mg into the pot, phentolamine 20mg + 5% glucose solution 250ml slow intravenous drip, appropriate adjustment of the drip rate according to blood pressure changes, 5% sodium bicarbonate 200ml intravenous drip , Aminophylline 0.
25g+10% glucose solution 20ml diluted slowly intravenously, furosemide 20mg intravenously
.

After 40 minutes, the patient's consciousness gradually became clear, and there was only a small amount of pink foamy sputum.
The blood pressure was measured at 120/75 mmHg, the heart rate was 110 beats/min, and the SpO2 was 92%.
A few moist rales could be heard at the bottom of both lungs
.

After 2 hours, the patient had obvious cough and could not tolerate the endotracheal tube.
After suctioning, the endotracheal tube was pulled out
.

After 2 days, the patient exhausted gas, began to eat liquid food, and could lie down and move on the ground.
After 8 days, the patient recovered and was discharged from the hospital
.

There was no abnormality at follow-up after half a month
.

The discussion analysis is as follows
.

Severe gestational hypertension may present with cerebral vasospasm, cerebral edema, headache, coma, or even brain herniation in individual patients; glomerular dilation, plasma protein leakage from glomeruli to form proteinuria, and increased plasma musculature.
Oliguria and renal failure occur in severe cases; systemic arteriolar spasm, increased vascular permeability, hemoconcentration, increased hematocrit, thrombocytopenia, and even microangiopathic hemolysis; impaired liver function, elevated various transaminases; liver Periarterial resistance increases, and in severe cases, necrosis around the portal vein; vasospasm, blood pressure increases, peripheral resistance increases, myocardial contractility and ejection resistance increase, cardiac output decreases significantly, the heart is in a state of low output and high resistance, and ventricular function is high In the dynamic state, vascular permeability increases due to endothelial cell activation, resulting in myocardial ischemia, necrosis, and in severe cases, heart failure and acute pulmonary edema
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This case belongs to a patient with severe pregnancy-induced hypertension.
No formal treatment was given before the operation, which seriously damaged the functions of the mother's heart, lungs, and kidneys.
Sufficient sedation, control of infusion volume, high head and low foot position, timely detection of early symptoms of heart failure during the operation, and correct treatment, relieved the development of the disease to a certain extent, but after arriving in the ward, due to the stable condition of the patient, The mother was placed in a supine position, resulting in a sharp increase in the return of blood to the heart, and symptoms such as acute left-sided heart failure and pulmonary edema
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This case reminds that for patients with severe pregnancy-induced hypertension, it is necessary to control blood pressure in time before, during and after surgery, reduce the pre- and after-load of the heart, keep the patient's vital signs stable, and prevent possible complications in advance
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Article: Hangbo Typesetting: Rou Rou END