Obstetric shock

Introduction to obstetric shock Obstetric shock refers only to shock that is unique to maternal, and refers to shock that is directly related to pregnancy and childbirth. Obstetric shock is mainly caused by hemorrhagic shock, followed by shock caused by septic shock and other special causes. Therefore, obstetric shock is divided into two types: hemorrhagic and non-hemorrhagic shock. basic knowledge The proportion of illness: 0.001% Susceptible people: good for postpartum women Mode of infection: non-infectious Complications: obstetric shock

Obstetric shock cause

(1) Causes of the disease

Hemorrhagic shock

(1) Pregnancy:

1 ectopic pregnancy: abortion or uterine rupture.

2 intrauterine pregnancy: incomplete abortion, expired abortion, placenta previa, placental abruption, cervical pregnancy, coagulation mechanism disorders.

(2) Childbirth: vulva, vaginal varices bleeding, vagina, cervix, uterine injury or rupture, uterine venous plexus rupture, broad ligament hematoma, sail-like placenta and other bleeding.

(3) After the delivery of the fetus: postpartum hemorrhage: poor uterine contraction, retention or residual placenta, partial implantation of the placenta, soft birth canal laceration, coagulation mechanism disorder, wound rupture after cesarean section.

2. Non-hemorrhagic shock

(1) Anesthetic reaction: anesthesia allergy, excessive anesthesia, spinal anesthesia or epidural anesthesia into the spinal cavity.

(2) Surgical operation: placenta retention repeatedly squeezed the uterus to cause uterine varus, hand stripped placenta, curettage, mid-term induction of intrauterine injection, traumatic shock.

(3) supine hypotension syndrome: pregnancy full-term supine position delivery, uterus compression of the aorta to reduce the amount of blood return, can occur shock, foreign literature reported that cesarean delivery bed is inclined 30o surgery is appropriate.

(4) Low-sodium syndrome: long-term consumption of low-salt or salt-free diet, diuretic or heatstroke dehydration, sodium loss.

(5) Abortion or puerperal infection sepsis: especially illegal abortion and old method delivery, prone to Gram-negative bacterial infection endotoxin infection symptoms are sinister, septic shock is a serious complication of obstetric infection, common pathogens are:

1 Anaerobic bacteria: common are anaerobic lactobacilli, bacillus, digestive cocci, digestive streptococci, Escherichia coli, aerogens, Pseudomonas aeruginosa, fragile bacilli, and tetanus.

2 Streptococcus: Gram-positive cocci, divided into A, B, C 3, of which type B hemolytic streptococcus is the most pathogenic, producing hemolysin and a variety of enzymes, easy to cause infection spread and sepsis, for obstetrics Important strains of infection, in recent years, the study of Streptococcus mutans (GBS) in the reproductive system of women is quite high, can cause maternal infections, including chorioamnion, amnion, sepsis, urinary tract infection, and Caused by late abortion, stillbirth, fetal dysplasia (IUGR), premature delivery and premature rupture of membranes, and proved that type Ia and III are the main pathogenic serotypes, accounting for about 2/3 of type III in developed countries.

3 Staphylococcus: Gram-positive cocci, divided into three categories: golden, white, and lemon. Among them, Staphylococcus aureus has the strongest curative effect, easily causes multiple metastatic abscesses, and is prone to drug resistance. It is important for obstetrics and gynecology surgery. Bacteria, although antibiotics control infection, bacterial resistance and flora variation should be taken seriously.

(6) embolization: amniotic fluid embolism, thromboembolism, air embolism more than uterine sinus caused by venous thrombosis, pulmonary hypertension, if the embolus is small, cerebral embolism can occur through the pulmonary capillaries to the pulmonary veins, diffuse intravascular coagulation.

(7) Microvascular hemolysis: Hellstein syndrome (1982) first reported gestational hypertension disease hemolytic anemia, elevated enzyme, low platelet, referred to as Hellp syndrome, The syndrome relies on laboratory screening to confirm the diagnosis (Table 1), delay diagnosis, treatment is not timely, can lead to liver, brain, kidney bleeding, shock, activation of intravascular coagulation.

(two) pathogenesis

The pathophysiological changes of effective circulating blood loss have the following three aspects:

1. Hemodynamic changes When the effective blood volume is reduced, the carotid sinus and aortic baroreceptors are stimulated, through the glossopharyngeal nerve and the vagus nerve, the medullary heartbeat center, the vasomotor center and the sympathetic nerves are excited. The heart, small blood vessels and adrenal glands accelerate the heart rate and increase cardiac output. The adrenal medulla and sympathetic ganglia fibers release a large amount of catecholamines. The catecholamines strongly contract the small blood vessels of the skin, limbs, intestines, kidneys, etc., including microvessels and The contraction resistance of the anterior capillaries increases, and the amount of blood entering the true capillaries is reduced. The direct passage of the microcirculation, or even the opening of the arteriovenous stenosis, allows the blood volume of the vein to be maintained, so that the blood pressure can not be maintained, and the heart can still be maintained. And cerebral vasoconstriction is not obvious, thus ensuring vital vital organs, heart, brain perfusion, this period is vasoconstriction, is the shock compensation period of microcirculation compensation (Figure 1).

If the treatment of supplemental blood volume is not obtained during the compensation period, the blood volume of the microcirculation will be progressively reduced, the arterioles will be contracted for a long time, and the blood will not flow through the capillary bed, and the true capillary network and tissue cells cannot be performed. Nutrients and metabolites, as well as the exchange of O2 and CO2, the blood directly enters the open arteriovenous short circuit, and the arteries directly flow into the vein. Although the heart and brain circulation are preferentially supplied, the blood of the capillary network continues to decrease, the tissue perfusion is insufficient, and nutrition Substance and O2 can not meet the needs of the organization, tissue ischemia, hypoxia, metabolic disorders, metabolic waste and acidic substances produced by hypoxia metabolism, lactic acid and pyruvic acid can not be ruled out, long-term microcirculation blood flow is insufficient or stagnant Cell metabolism of acid accumulation, local acidosis is aggravated, the anterior capillaries of the capillaries are still in a contracted state, a large amount of blood stagnate in the capillaries, hydrostatic pressure rises, and vascular endothelial cells are damaged by hypoxia and capillary permeability. Increased sex, so that a large amount of fluid and protein in the blood vessels ooze out to the interstitial fluid, blood concentration; blood viscosity increased , Decreased venous return, cardiac output is more reduced, blood pressure, the diastolic period of microcirculation, inhibition of entering shock shown.

Due to blood concentration, endothelial cells are damaged, red blood cells and platelets are easily attached to the damaged vascular endothelium, or even form microthrombus, diffuse intravascular coagulation occurs, blood perfusion stops, cell hypoxia is more serious, resulting in intracellular The lysosomal membrane ruptures, releasing a variety of acidic hydrolases, directly digesting tissue proteins, and catalyzing the formation of various kinins in various proteins, causing autolysis and damage of various cells. If capillary obstruction exceeds 1 h, the damaged cells are metabolized. Stop, the cells will die, so shock develops into diffuse intravascular coagulation, indicating microcirculatory failure, and shock enters decompensation (Figure 2).

The following is a brief description of the changes in microcirculatory blood flow and the staging of shock:

2. Before the change of body fluid, the secretion of catecholamine in shock has been mentioned, which not only affects hemodynamics, but also inhibits the secretion of insulin, promotes the secretion of glucagon (glucagon), accelerates the decomposition of muscle, glycogen and glucoside The role of health, blood sugar, blood volume reduction, renal blood flow reduction, renin secretion, renin promotes angiotensin secretion, angiotensin increases adrenaline production of aldosterone, aldosterone action sodium storage potassium The role of pressurization and blood volume is increased. As the blood pressure drops, the left atrial perfusion pressure decreases, and the hyperbaric receptor is stimulated, which promotes the secretion of antidiuretic hormone in the posterior pituitary gland, which is conducive to the recovery of plasma volume, cellular ischemia and hypoxia. Intracellular glucose anaerobic metabolism can only produce a small amount of high-energy adenosine monophosphate (ATP), while lactate production increases, liver ischemia, lactic acid can not complete metabolic decomposition in the liver, lactic acid accumulation acidosis, protein Increased catabolism, blood urea, inosine, uric acid content increased, adenosine triphosphate reduced energy, cell membrane sodium pump function decreased, so that intracellular cation Potassium moves to the outside of the cell, sodium ions enter the cell, and even edema or even death in the cell, can also affect the cell membrane, mitochondrial membrane and lysosomal membrane, lysosome membrane rupture and release tissue protein acid, but tissue protein decomposition, A variety of active polypeptides such as kinins, myocardial inhibitors, prostaglandins and the like are produced.

3. Multiple organ damage, long-term shock, visceral tissue ischemia, long time of hypoxia, tissue cell degeneration, necrosis and hemorrhage, causing organ failure, several organs are simultaneously or sequentially damaged, resulting in multiple system organs Multiple system organ failure (MSOF) is the main cause of death in shock patients. It is the cause of so-called irreversible shock in the past. MSOF syndrome is the key issue of shock research in the past 10 years.

Obstetric shock prevention

Prevention of postpartum hemorrhagic infection is the focus of prevention of shock. Special attention should be paid to the observation of vaginal bleeding during childbirth and after childbirth. If necessary, uterine contractions should be used to strengthen uterine contractions to prevent postpartum hemorrhage, and actively induce the factors inducing obstetric infection. Early DIC findings were found and DIC was actively treated.

1. Active prevention of postpartum hemorrhage

(1) Timely detection of soft birth canal injury or uterine rupture, and active treatment.

(2) Accurately estimate the amount of bleeding in time, especially for small amounts of persistent bleeding. The amount of bleeding can be objectively estimated by monitoring changes in hemoglobin and hematocrit.

(3) Replenish blood volume in time, conditionally transfuse as much as possible, and avoid excessive supplementation of crystalloid.

(4) promptly and decisively remove the cause of bleeding, including hysterectomy or open exploration.

(5) Terminate pregnancy at the right time, especially placental abruption.

Obstetric shock complications Complications obstetric shock

The main complications of obstetric shock are found in DIC, multiple organ dysfunction syndrome.

Obstetric shock symptoms common symptoms nausea reaction slow liver cell necrosis hyperthermia toxic cold sweat blood injury trauma liver failure hairpin

According to the cause of shock and the tolerance of personal physique, the degree of shock varies, but the performance is common according to the stage of microcirculatory pathological changes.

1. Shock compensation period is also known as pre-shock, this symptom is often ignored if not carefully observed, because in hemorrhagic shock, the blood loss has not exceeded the body's blood volume [body weight (kg) × 7% ~ 8%] 20 %, the patient's blood flow and the compensatory role of the nervous system, maintain normal or slightly higher blood pressure, increased excitability of the central nervous system and sympathetic nervous system, manifested as pale, nervous, irritated and nausea, accelerated heart rate, small pulse compression The urine volume is normal or reduced. In this period, if the intravenous solution is added intravenously, the shock can be corrected quickly. If it is not treated or treated improperly to the vasoconstrictor, the disease develops and enters the inhibition phase.

2. In the shock inhibition period, the patient's expression is indifferent, the reaction is slow, the lips and limbs are cyanotic, cold sweat, pulse speed, pulse pressure difference is lower, serious unconsciousness or coma, the skin mucous membrane is obviously hypoxic and cyanosis, and the limbs are cool. The pulse is weak and even can not be clearly touched, blood pressure drops even 0, oliguria or no urine, CO2 binding reduces acidosis, skin, mucous membrane bleeding point or gastrointestinal bleeding, indicating that the disease has progressed to the disseminated intravascular coagulation stage, if active There is still no improvement in treatment, and it may be difficult to breathe. If the arterial blood pressure drops below 8 kPa (60 mmHg), although the symptoms of pressurized oxygen can not be improved, the oxygen partial pressure cannot be improved, suggesting that dyspnea syndrome and other organ damage will enter. Depletion period.

Obstetric shock is similar to the shock history of each subject, but it has its own particularity. Shock caused by any cause is easy to induce DIC because it has the following special factors:

1 late pregnancy uterus compression of the inferior vena cava, return to the heart of the blood decreased, inferior vena cava congestion, slow blood flow is easy to induce thrombosis.

2 uterine venous system dilatation, sinus opening is prone to amniotic fluid embolism and air embolism.

3 uterine compression ureter during pregnancy, ureteral dilatation, urinary retention, prone to urinary tract infection, postpartum or abortion placenta stripping surface, because blood is the best medium for bacteria susceptible to endometritis, intrauterine infection.

4 fetus and its appendages, due to pathological conditions, necrotic degeneration, can produce exogenous thromboplastin, activate the coagulation system.

5 normal pregnant women to adapt to the bleeding during childbirth, physiological needs, I, VII, VIII, IX, X blood coagulation factors increased, blood coagulation.

Obstetric shock examination

1. Peripheral blood, elevated white blood cells, increased neutrophils, hemoglobin, red blood cell reduction, thrombocytopenia, etc.

2. Freeze-dried human fibrinogen (fibrinogen), prothrombin assay, euglobulin lysis test, protamine paracoagulation test, fibrin degradation products and clot test, abnormal fiber dissolution test can confirm the occurrence of DCI .

3. Biochemical, electrolyte, liver and kidney function tests.

According to clinical manifestations, symptoms, signs, B-ultrasound, X-ray, electrocardiogram, etc.

Obstetric shock diagnosis

Diagnostic criteria

Hemorrhagic shock and septic shock, general diagnosis is not difficult, there is a history of bleeding and infection, it is important to diagnose early. In the past, the diagnosis of shock was mainly based on the blood pressure reduction index, the actual blood pressure was reduced, and the treatment was lost. Shock has been a manifestation of decompensation, entering the inhibition period, because blood pressure = cardiac output × total peripheral resistance, blood loss and high heat loss, although early cardiac output decreased, but small arterial contraction strengthened, total The peripheral resistance increases and the blood pressure does not decrease. Therefore, the blood perfusion decreases before the blood pressure drops. Therefore, a large amount of blood loss, fluid loss, trauma and persistent high fever in the short term should be considered, and the possibility of shock should be considered.

1. Early diagnosis of life indicators Blood pressure, pulse observation is important, but the clinical comprehensive observation of tissue perfusion is helpful for the early diagnosis of shock compensation.

2. During the shock inhibition period, the blood pressure drops below 90mmHg (12kPa), the pulse is weak, the mouth is thirsty, the mind is indifferent, the reaction is slow, the cold sweat, the limbs are cold, and the urine is less (less than 30ml per hour), you should be aware Shock has been transferred from the aforementioned compensation period to the decompensation period.

3. Common hypoxemia, hemorrhagic shock and septic shock in obstetric failure, no proper and timely treatment, there are systemic damage factors: systemic tissue ischemia and hypoxia can be caused when the effective circulation is too low , cardiac output decreased, coronary ischemia, blood pressure decreased, acute heart failure, renal ischemia, can lead to decreased glomerular filtration rate and even tubular necrosis, acute renal failure, serum creatinine 178.6mol / L, urine output 24h<400ml or more urine, liver ischemia, can reduce the liver's metabolic function, and even cause acute liver failure, blood bilirubin> 34.2mol / L (2mg / dl), lasting 5 days, GOT higher than normal 2 times, even liver cell necrosis, gastrointestinal ischemia, intestinal mucosal damage, gastrointestinal bleeding, perforation, blood in the stool, stress ulcer, various sepsis infections, bacterial toxins, immune complexes, inflammatory mediators, etc. With the blood flowing around the body, damage to tissues and organs, damage to the vascular endothelium, increase the permeability of blood vessels, rough endothelium, platelets adhere to form micro-plugs, such as dyspnea syndrome, or even diffuse blood Internal coagulation, central nervous system ischemia, impaired hypoxia, manifested as sluggish and even unconscious coma, so shock can not only cause an organ failure, but also affect other organ dysfunction, interact to form a chain reaction, organ disorder order Permeation occurs, but before and after the occurrence of clinical organ failure, there are differences in weight and weight. Hemorrhagic shock with hypovolemia is often preceded by renal dysfunction. Infection causes sepsis. In sepsis, heart, lung, and brain dysfunction often appear first. In general, when an organ has dysfunction, it begins to be mild, such as renal dysfunction. The first manifestation is oliguria. The blood biochemical examination may not be abnormal. Without careful treatment, the function continues to decline and worse. If acute tubular necrosis occurs, There will be blood urea nitrogen, elevated creatinine levels, water and electrolytes, acid-base imbalance and affect heart, lung, brain, liver and other organs dysfunction, followed by multiple system organ failure (MSOF), MSOF concept is 20th century 70 In the era, it mainly refers to various organ dysfunctions that occur in acute and severe diseases, emphasizing the sequentiality of the disease, and strive for accumulation. Extremely stop its development from deteriorating to save the lives of patients, but when the disease develops extremely severely, multiple organs can fail at the same time, and some patients have not yet clarified because of poor physical condition, or chronic liver and kidney disease. Which organ first fails to develop rapidly into acute MSOF, resulting in irreversible shock. According to the literature, the mortality rate of three organ failure patients is 80%, and four organ failure patients have not survived.

Differential diagnosis

1. Syncope refers to a transient loss of consciousness caused by insufficient supply of cerebral blood flow, mainly due to vagal excitability leading to slow heart rate, vasodilatation, and decreased blood pressure caused by temporary cerebral ischemia, usually in the supine or taking the head low foot high You can recover.

2. Supine hypotension shock and spinal anesthesia neurogenic shock These two kinds of conditions, some people think that can not be called shock, can only be called hypotension, because microcirculation perfusion has no significant changes, this article will be listed in two cases For non-hemorrhagic shock, it is because the uterus affects the posture and the curvature of the spine has its particularity. If it is not treated in time, it will lead to circulatory disturbance.

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