[Challenge] How should you deal with sudden extensive bleeding in the surgical field in patients with perianesthesia shock?

Click the blue word to pay attention to our patients with perianaesthesia shock patients with sudden surgical field extensive bleeding 1.
Occurrence and harm of sudden surgical field extensive bleeding in patients with perianaesthetic shock Extensive blood oozing in the operative field in patients with shock during peri-anesthesia refers to the presence of coagulation dysfunction in patients with shock caused by various reasons during the peri-anesthesia period.
, was "sweaty"-like bleeding, and the commonly used hemostatic methods and hemostatic effects are not good
.

2.
Occurrence and harm of sudden surgical field extensive oozing in patients with perianaesthesia shock.
Studies have shown that 25% to 35% of patients already have acute coagulation dysfunction before arriving at the emergency room
.

About 10% of deaths worldwide are caused by trauma every year.
Deaths caused by blood loss account for 30% to 40% of the early mortality of trauma patients, and blood loss factors account for more than 50% of patients who die within 24 hours after trauma
.

If there is coagulopathy at the same time, the incidence of traumatic bleeding is significantly increased, and the mortality rate will increase fourfold
.

The incidence of abnormal bleeding in surgery is 0.
05% to 4%, and it is 12% in cardiopulmonary surgery
.

Mild coagulation disorders may have no obvious clinical symptoms, and extensive persistent bleeding can cause large hematomas, blur the surgical field, increase the difficulty or risk of surgery, lead to massive blood volume loss, induce disseminated intravascular coagulation and multiple organ failure.
, The persistent extensive oozing that cannot be effectively controlled endangers the patient's life
.

2.
Analysis of the causes of sudden and extensive oozing of blood in the surgical field in patients with shock during the peri-anesthesia period Deficiency of plasma coagulation factors, congenital diseases such as hemophilia and acquired diseases such as disseminated intravascular coagulation; ③ abnormal platelets, abnormal platelet number, morphology and function; ④ hyperfibrinolysis
.

(2) Patients with abnormal liver function: The liver is an important protein synthesis site in the human body, synthesizing coagulation factors involved in coagulation, anticoagulant proteins and proteins of the fibrinolytic system
.

It also removes and metabolizes activated coagulation factors and plasmin and their activators from the circulation
.

Patients with liver disease are characterized by thrombocytopenia, decreased fibrinogen levels, deficiency of various coagulation factors, and enhanced coagulation activation and fibrinolytic activity
.

In addition to severe disturbance of coagulation function in the late stage of acute liver failure or chronic liver disease, decompensation of coagulation function will also increase in the case of a sharp increase in liver function load such as shock, and severe bleeding will affect the operation and postoperative recovery.
even endanger the patient's life
.

(3) Patients taking anticoagulants: due to the need for treatment or prevention, the elderly and patients with chronic diseases need to take a variety of anticoagulants for a long time, or some have no anticoagulant effect but can inhibit the bone marrow and affect anticoagulation.
Blood drug metabolism affects the body's coagulation function
.

2.
Surgical factors cardiopulmonary bypass, heparinization, protamine antagonism, liver transplantation, local vascular disease
.

2.
Anesthesia factors Anesthesia can increase or decrease arterial pressure and venous pressure, and vasodilation during deep anesthesia can lead to increased oozing
.

3.
Patients with dilutional coagulopathy need volume expansion therapy due to insufficient effective circulating blood volume, and massive infusion, red blood cell suspension and plasma replacement can lead to hemodilution and coagulation disorders
.

①Crystalline solution can aggravate tissue edema and affect microcirculation blood flow.
Although hypertonic solution can stabilize circulation and reduce tissue edema, it can inhibit platelet function at the same time; ②Large infusion of normal saline can lead to dilutional acidosis, which affects the Thrombin generation and fibrin aggregation; (3) Gelatin can inhibit fibrin aggregation, and hydroxyethyl starch blocks fibrinogen receptors by coating platelets, causing fibrin aggregation disorders and aggravating bleeding tendency
.

5.
Consuming coagulopathy (1) Exogenous procoagulant substances: ① Amniotic fluid embolism; ② Venomous snake bite; ③ Early placental abruption and intrauterine stillbirth; ④ Malignant tumor; ⑤ Infusion of autologous ascites; ⑥ Fat embolism; ⑦ Excessive Infusion of vitamin K-dependent coagulation factor concentrate,
etc.

(2) Intravascular procoagulant substances: ① acute hemolysis caused by wrong blood transfusion matching; ② cardiopulmonary bypass; ③ liver transplantation; ④ freshwater drowning,
etc.

(3) Vascular injury: ① bacterial sepsis, septic shock; ② persistent tissue hypoperfusion and severe tissue damage caused by shock are considered to be important drivers of coagulation disorders; ③ trauma, burns, craniocerebral injury and In major surgical operations, tissue factor released from damaged tissue can activate the local coagulation system, and massive consumption of platelets and coagulation factors can induce disseminated intravascular coagulation; ④ heat stroke; ⑤ cardiac arrest; ⑥ high altitude hypoxia,
etc.

(4) Other reasons: ① hydatidiform mole: ② allergic reaction; ③ hypothermia; ④ malignant hyperthermia
.

6.
Hypothermia Hypothermia is the most common and easily overlooked cause of coagulation dysfunction.
A large number of hypothermic fluid resuscitation, exposure to low temperature environments, and slowing of shock energy metabolism lead to heat loss and insufficient heat production
.

Even if the levels of coagulation factors and platelets are normal, when the core temperature of the body is lower than 33~34°C, it will reduce the production of thrombin, the formation of platelet thrombus and fibrin clot, and promote the dissolution of thrombus, thereby causing coagulation dysfunction, manifested as Decreased thrombin production, thrombocytopenia, platelet dysfunction, hyperfibrinolysis, and easy disintegration of blood clots
.

7.
Insufficient tissue perfusion of acidosis The body's anaerobic glycolysis is enhanced, and the body's anaerobic metabolism produces a large amount of acidic substances, and the infusion of a large amount of crystalloid solution can also lead to chlorine-containing acidosis
.

Acidosis leads to coagulation dysfunction by inhibiting coagulation factor activity and inhibiting thrombin production, and this inhibition is more pronounced at hypothermia
.

Hypothermia, acidosis and coagulation disorders are known as the "death triangle".
Low temperature can aggravate acidosis, and acidosis can easily lead to coagulation disorders.
The three promote each other to form a vicious circle
.

3.
Coping strategies for sudden and extensive bleeding in the surgical field in patients with shock during the peri-anesthesia period ②In order to make a timely judgment on the bleeding in the surgical field caused by active bleeding or coagulation dysfunction at an early stage, it is necessary to keep close observation on the scope, speed and blood clot formation on the wound surface; 4.
Diagnosis of acute coagulation dysfunction in patients with shock: prothrombin time (PT)>18s, activated partial prothrombin time (APTT)>60s , Thrombin time (TT)>15s
.

2.
Monitoring plasma routine coagulation function tests including PT, APTT, TT, fibrinogen, platelet count, D-dimer, fibrin degradation products (FDP), etc.
The examination usually takes 30-60 minutes and cannot reflect active bleeding in time.
The coagulation status of the patient
.

Moreover, these indicators can only reflect the function of the initial stage of coagulation, and cannot provide information such as platelet function, thrombus strength, and fibrinolytic activity
.

Immediate bedside thromboelastography (TEG) is a method for evaluating the viscoelastic characteristics of whole blood during coagulation, which has certain advantages in judging coagulation function and guiding blood transfusion therapy
.

Thromboelastography is the first choice, followed by laboratory tests such as APTT, PT, INR (International Normalized Ratio), Fib, TT, and PLT
.

Repeat examinations at 4-hour intervals, after blood transfusion, or when the blood replacement volume reaches 1/3 of the total blood volume
.

When APTT and PT are 1.
5 times of the normal value, when Fib is less than 1g/L, be alert to coagulation dysfunction and perform disseminated intravascular coagulation related tests; for patients suspected of coagulation dysfunction, coagulation factor activity and content determination, Platelet count and function testing, vascular disease-related factors testing, etc.
; monitoring of body temperature and arterial blood gas to understand the situation of hypothermia and acidosis
.

3.
Treatment (1) Comprehensive surgical treatment measures: ① Active anti-shock therapy before surgery to maintain effective tissue oxygen supply and hemodynamic stability, and avoid massive intraoperative bleeding; ② Angiography and other methods can accurately find large blood vessel damage bleeding site; ③ topical or intravenous application of hemostatic drugs (thrombin, vitamin K, phenethylamine, etc.
); ④ large gauze pad with warm saline to compress to stop bleeding; Adhesive, etc.
, plus dry gauze compression to stop bleeding; ⑥ large gauze pad packing
.

(2) Transfusion of red blood cells: supplement effective circulating blood volume, improve oxygen transport capacity, and improve tissue oxygen supply
.

The 2010 European guidelines for the management of severe traumatic bleeding recommend maintaining hemoglobin at 70 to 90 g/L
.

For patients with traumatic brain injury (TBI), it is recommended to maintain about 100g/L in order to improve the oxygen supply to the patient's brain
.

(3) Transfusion of platelets: involved in hemostasis, platelet thrombus formation and thrombus retraction
.

The platelet count can be increased by (7.
5~10.
0)X109/L per unit of platelet concentrate transfusion
.

European guidelines recommend that the goal of platelet transfusion and maintenance is ≥50X109/L, and for patients with disseminated intravascular coagulation or hyperfibrinolysis resulting in increased fibrin degradation products, it is recommended to maintain the target at 75X109/L
.

(4) Infusion of fresh frozen plasma (FFP): supplementation of coagulation factors
.

European guidelines recommend that patients with traumatic hemorrhage should be treated with fresh frozen plasma early, with an initial dose of 10-15ml/kg; when PT or APTT is greater than 1.
5 times the normal value, fresh frozen plasma (10-15ml/kg) should be transfused to correct coagulation disorders ; When the red blood cell input is less than 6U, it is not necessary to supplement fresh frozen plasma; when it is greater than 6U, supplement fresh frozen plasma 2U, and then supplement 2U fresh frozen plasma for every 5 units of red blood cells
.

(5) Supplementing fibrinogen: Fibrin is a key link in the coagulation process.
When fresh frozen plasma alone is not enough to provide the required fibrinogen, cryoprecipitate should be infused at the same time
.

European guidelines recommend that patients with active bleeding such as fibrinogen less than 1.
5~2.
0g/L or functional fibrinogen deficiency by TEG should be infused with concentrated fibrinogen 3-4g or cryoprecipitate 50mg/kg, and according to the experiment Laboratory test or TEG results guide the dosage again
.

(6) Prevention and treatment of "death triangle": in the state of low temperature and acidosis, commonly used hemostasis methods such as electrocoagulation, ligation and drugs are often ineffective.
During shock resuscitation, warm measures should be taken to restore the patient's body temperature as soon as possible, and try to infuse normal temperature liquid, take measures such as heating blankets and thermal blankets if necessary
.

Correct acidosis and electrolyte disturbances based on the results of arterial blood gas monitoring to prevent the vicious circle of the "triangle of death"
.

4.
Thoughts on sudden and extensive bleeding in the surgical field in patients with shock during the peri-anesthesia period 1.
Preoperative coagulation function assessment Laboratory coagulation function tests cannot replace detailed medical history review and careful physical examination
.

① Careful inquiries about the medical history and careful physical examination before surgery to know whether the patient has a history of spontaneous bleeding, skin bruising and ecchymosis, history of anemia, history of epistaxis, menstrual cycle and the amount of bleeding each time; ② Check whether the limbs and trunk have any Skin bleeding spots or ecchymosis and hepatosplenomegaly; ③ The history of bleeding after trauma, surgery or tooth extraction can accurately reflect the coagulation function of the patient; ④ Patients with severe congenital blood diseases often have a history of bleeding since childhood: ⑤ Some congenital blood diseases Patients with acquired hematological and acquired hematological diseases may have no previous history of bleeding, and it is necessary to inquire about the medical history in detail and perform corresponding examinations to confirm the diagnosis; ⑥Some patients are found to have abnormal coagulation function even after chronic bleeding after surgery
.

2.
Preoperative doctor-patient communication Chronic diseases can lead to abnormal coagulation function.
Such patients may not have bleeding tendency before surgery, but factors such as surgical trauma, peri-anesthesia stress and medication are likely to cause the patient's blood volume to exceed its compensation.
Therefore, the risks of surgery and anesthesia should be carefully evaluated, and patients and their families should be fully communicated to actively take effective measures to reduce risks or postpone surgery
.

V.
Sharing of typical cases of sudden surgical field extensive bleeding in patients with shock during the peri-anesthesia period He was hospitalized for mid-segment cancer, and underwent subtotal gastrectomy and gastrojejunostomy in 1986 for gastric ulcer
.

After investigation: white blood cells 3.
73X109/L, hemoglobin 90.
8g/L, platelets 223X109/L, PT 11.
5 seconds, PTT 28.
3 seconds, FIB 9.
2g/L, all five indicators of hepatitis B were negative, and liver and kidney functions were normal
.

After fluid rehydration, blood transfusion, albumin transfusion support and preoperative preparation, total esophagectomy was performed, and colon was replaced by esophagus neck anastomosis
.

During the operation, laparotomy was performed to dissociate the colon, and there was little blood oozing from the wound surface; after thoracotomy, due to extensive separation of the pleural cavity adhesion, the wound surface oozes more blood, and blood clots can be seen; Difficulty, once in shock
.

After comprehensive treatment such as wound compression hemostasis, rapid blood transfusion, and blood pressure boosting, the operation was completed.
Intraoperative fluid replacement was 11000ml, plasma 200ml and blood bank 4800ml, and blood loss was about 6000ml
.

Postoperative examination PT 32.
2 seconds, APTT 71.
0 seconds, 3P negative
.

After anti-inflammatory and hormone therapy, blood transfusion was continued, and at the same time, hemostasis was treated with phensulfame, aminotoluic acid, batroxobin, fresh plasma 1500ml, cryoprecipitate 8U, fibrinogen, calcium and fresh whole blood 600ml.
Bleeding stopped in 2 days
.

Review PT 13.
5 seconds, APTT 29.
0 seconds, FIB 7.
9g/L
.

2.
During the peri-anesthesia period of placenta implantation, there was extensive blood oozing and shock in the surgical field, and the rescue failed.
One patient was a female, 26 years old, 27 weeks pregnant
.

She was admitted to the hospital due to 3 days of painless vaginal bleeding due to menopause for more than 6 months
.

Married at the age of 23, 5 pregnancies in 3 years after marriage were spontaneously aborted at 3+ months of pregnancy and underwent uterine evacuation
.

In this pregnancy, a small amount of vaginal bleeding occurred again in the 3+ months of pregnancy, and the bleeding stopped after taking traditional Chinese medicine in a private clinic
.

No obstetric examination was performed during pregnancy
.

Physical examination on admission: body temperature 36.
5 ℃, pulse 84 beats/min, respiration 12 beats/min, blood pressure 14/9kPa
.

The general condition is good, and the heart and lungs are normal
.

Palace height 21cm, abdominal circumference 82cm, right sacral anterior position, fetal heart rate 148 beats/min
.

Blood routine hemoglobin 113g/L, white blood cells 10.
4X109/L, red blood cells 3.
45X1012/L, neutrophils 88%, lymphocytes 12%
.

BT2 minutes, CT3 minutes
.

B-ultrasound showed: central placenta previa, single breech presentation, normal fetal heart rate and amniotic fluid
.

Clinical diagnosis: central placenta previa, precious child
.

Considering that the patient has less vaginal bleeding and the fetus is immature, at the same time, at the strong request of the patient and his family, expectant therapy is given under close monitoring, and treatment such as uterotonic drugs and hemostatic drugs is given
.

On the 2nd day of admission, a large amount of vaginal bleeding suddenly occurred, the amount was about 1000ml, and emergency cesarean section was performed while anti-shock.
During the operation, it was found that the placenta was attached to the anterior wall of the uterus, the anterior wall of the lower uterine segment and the entire internal cervical orifice, and the placenta was removed.
The bleeding continued, and the placenta was taken by hand immediately after injecting ergometrine 0.
2mg and oxytocin 10U into the uterus, and the placenta accreta was found in the anterior wall of the lower uterine segment and the internal cervical orifice during stripping
.

The bleeding was extensive and rapid, and the effect of suture hemostasis and ligation of the ascending branches of the bilateral uterine arteries was ineffective.
A total hysterectomy was performed, with extensive oozing of blood, which was clear and non-coagulated.
The patient quickly developed a deep coma, and laboratory tests showed rapid disseminated intravascular coagulation.
Coagulation dysfunction, although actively rescued by blood transfusion, died 6 hours after the operation
.

Pathological examination: partial placenta accreta, partially penetrated through the muscularis to the serosa
.

END Recommended reading [Challenge] Sudden refractory hypotension under general anesthesia during peri-anesthesia, how should you deal with it? [Challenge] How to deal with sudden anaphylactic shock of general anesthesia during peri-anesthesia? [Challenge] How do you deal with sudden stress ulcers during peri-anesthesia? [Challenge] How to deal with sudden esophageal foreign body during peri-anesthesia? [Challenge] · How should you deal with sudden intraoperative awareness in peri-anesthesia patients? [Tuesday] "Challenges of peri-anesthesia emergencies" · Sudden agitation during peri-anesthesia period in patients with awakening [Tuesday] "Challenges of peri-anesthesia emergencies" · Peri-anesthesia application of propofol for sudden hallucinations of the spinal canal Complications of internal anesthesia [Tuesday] "Challenges of emergencies in the peri-anesthesia period" · Consensus study of guidelines for acute poisoning of local anesthetics in the peri-anesthesia period day26 Expert consensus on the prevention and treatment of complications of spinal canal block [Tuesday] "Sudden emergencies in the peri-anesthesia period" "Challenge of Incidents" · Sudden intracranial gas accumulation in the peri-anesthesia period [Tuesday] "Challenges of sudden incidents in the peri-anesthesia period" · Sudden acute brain swelling in the peri-anesthesia period [Tuesday] "The challenge of sudden incidents in the peri-anesthesia period" ·Expert Consensus on Prevention and Treatment of Complications of Sudden Cerebrovascular Accident Peripheral Nerve Block in Peri-anesthesia