Abdominal compartment syndrome

Introduction to abdominal compartment syndrome Compartment syndrome (compartmentyndrome) refers to the performance of tissue function and circulatory disturbance caused by elevated pressure in a confined gap. Septal syndrome occurs mostly in the compartment of the limb fascia, called the compartment syndrome. If it occurs in the eyeball called glaucoma, it is called intracranial hypertension syndrome in the cranial cavity, and the ventricular septal syndrome occurs in the abdominal cavity. It is called abdominal compartment syndrome (ACS). Abdominal compartment syndrome refers to organ failure or organ dysfunction caused by progressively elevated intra-abdominal pressure, also known as acute intraperitoal hypertension (AIH) or intra-abdominal hypertension syndrome and abdominal subcutaneous syndrome. Under physiological conditions, the intra-abdominal pressure is on average zero (equivalent to atmospheric pressure) or close to zero. Any increase in the amount of abdominal cavity can cause an increase in intra-abdominal pressure. However, in chronic conditions such as ascites, pregnancy, and large abdominal tumors, the amount of abdominal cavity slowly increases, the abdominal wall is gradually stretched, and the intra-abdominal pressure does not rise sharply. Acute abdominal hypertension occurs and ACS does not occur. Therefore, ACS is a syndrome that occurs when acute intra-abdominal hypertension occurs to a certain extent. basic knowledge The proportion of illness: 0.003%--0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: acute renal insufficiency, renal insufficiency, acute cardiac insufficiency

The cause of abdominal compartment syndrome

(1) Causes of the disease

Surgical clinical acute intra-abdominal pressure is common in acute peritonitis, acute pancreatitis, acute intestinal obstruction and other severe intra-abdominal infection with septic shock, severe abdominal trauma, abdominal aortic aneurysm rupture, intra-abdominal acute hemorrhage or retroperitoneal hematoma, Abdominal tamponade for hemorrhagic shock or hepatic dorsal hemorrhage after abdominal hemorrhage, acute visceral edema after adequate fluid resuscitation, pneumoperitoneum laparoscopic surgery, aerated anti-shock.

Application, liver transplantation, complicated abdominal vascular surgery and postoperative positive pressure mechanical ventilation.

1. Hemorrhagic shock after liquid expansion

(1) Abdominal trauma: Foreign reports of severe abdominal trauma for the most common causes, Behrman (1998) reported hemorrhagic shock, intra-abdominal hemorrhage, pancreatic injury in 222 cases, fluid volume 5800 ~ 12000ml, blood transfusion 800 ~ 5000ml, ACS 3 occurred example.

(2) No abdominal trauma: Ivy (1999) reported that the burn area was >70%, followed by ACS in 3 cases, and the fluid volume was >20000ml. Therefore, it is considered that large-area burns with high fluid input cases complicated with airway pressure, oliguria or anuria Should be alert to ACS, Maxwell (1999) reported 1216 cases of hemorrhagic shock, of which 6 cases had no history of abdominal trauma, about 2/6 secondary ACS, the group entered a liquid volume of 19000 ± 5000ml, the author cautioned: input crystal liquid more than 10000ml Be alert to the ACS.

Severe abdominal trauma hemorrhagic shock or traumatic hypovolemic shock through systemic capillary expansion of systemic capillary permeability, peritoneal and visceral progressive edema, high abdominal edema, increased volume, intestinal curvature If the bulge is above the plane of the incision, it can not be reconciled. Considering the ACS first, the above situation occurs. For example, if the abdominal wall incision is forcibly closed, the intra-abdominal pressure will rise rapidly, and the breathing will occur after leaving the operating room.

In many cases, he died within 10 hours after surgery. He is often misdiagnosed as multiple organ dysfunction syndrome (MODS).

2. After septic shock fluid expansion: Most reports abroad are severe abdominal trauma and hemorrhagic shock leads to ACS after adequate fluid resuscitation. The difference is that severe pancreatitis and acute suppurative cholangitis are rare in Western Europe, North America. In China, it is a common disease of ACS. Because of the presence of infectious systemic inflammatory response (ISIR), such cases are difficult to treat, and the mortality rate is much higher than that of hemorrhagic shock.

Abdominal compartment syndrome often occurs due to a combination of a variety of intra-abdominal pressure rise factors. A typical clinical example is severe abdominal infection or trauma itself, which causes edema of the abdominal organs, which is often accompanied by hypovolemia. This is the implementation of adequate fluid resuscitation caused by progressive edema of the peritoneum and viscera; and due to hypoperfusion, edema caused by reperfusion injury after visceral ischemic resuscitation; also due to dressing stuffing hemostasis, mesenteric vein occlusion or temporary portal vein When the blockage is aggravated, trauma, shock, severe pancreatitis, severe peritonitis or major surgery, the body has severe ISIR. As a result, a large amount of extracellular fluid enters the cell or interstitial space, and a third interstitial effect or fluid seizure occurs. Significant positive balance, that is, the input amount far exceeds the discharge amount. At this time, only enough input balance liquid can offset the positive balance, maintain effective circulating blood volume, avoid blood concentration, otherwise there will be a decrease in blood flow, and the heart rate will increase. Decreased discharge, HCT rises, hypotension, and peritoneal and visceral edema and ascites have been inevitable in the above cases. From the perspective of effective circulation of blood, the amount of fluid infusion is not too much, and the high degree of edema is only the result of ISIR. It is not necessary to negate the necessity of fluid resuscitation. The fluid extravasation in this cycle is temporary, when ISIR is alleviated. When the capillary permeability is restored, the extracellular fluid that is excessively sequestered is absorbed back, the positive balance of the liquid is turned into a negative balance, and the edema rapidly subsides.

(two) pathogenesis

Peritoneal and visceral edema, abdomen effusion caused by a rapid increase in intra-abdominal pressure caused by abdominal compartment syndrome, can impair the physiological functions of the abdomen and systemic organs, leading to organ dysfunction and circulatory failure.

1. Increased abdominal wall tension: When the intra-abdominal pressure is increased, the wall tension increases, and when it is severe, it can cause abdominal distension and abdominal wall tension. At this time, Doppler ultrasonography reveals that the blood flow of the rectus abdominis is weakened, such as forced operation after open surgery. In the abdomen, the incidence of wound infection and incision rupture is high. The dV/dP (capacity/pressure) curve of the abdominal cavity is not linear, and rises abruptly like the oxygen dissociation curve. Even after a certain limit, the amount of abdominal cavity content increases evenly. It is enough to increase the intra-abdominal pressure; on the contrary, partial decompression can significantly reduce the abdominal high pressure.

2. tachycardia, decreased cardiac output: after the increase of intra-abdominal pressure, the stroke volume is significantly reduced, and the cardiac output is also decreased. During laparoscopic surgery, the belly is as low as 1.33 to 2.00 kPa (10 to 15 mmHg). Endogenous pressure can produce adverse reactions, cardiac output (and stroke volume) decreased due to decreased venous return, increased left ventricular filling pressure and decreased myocardial compliance due to increased chest pressure, increased systemic vascular resistance, venous return The decrease was mainly caused by the decrease of posterior capillary venule pressure and central venous pressure gradient, the reduction of inferior vena cava blood return, the inferior vena cava functional stenosis or mechanical compression after thoracic hemorrhage Increased by the increase, etc., at this time, the femoral venous pressure, central venous pressure, pulmonary capillary wedge pressure and right atrial pressure are proportional to the intra-abdominal pressure.

Tachycardia is the first cardiovascular response to increase intraluminal pressure in an attempt to compensate for a decrease in stroke output while maintaining cardiac output. Obviously, tachycardia, if not sufficient to compensate for reduced stroke volume, The cardiac output drops sharply and circulatory failure will follow.

3. Increased thoracic pressure and decreased lung compliance: abdominal high pressure causes bilateral diaphragmatic muscle elevation and movement amplitude to decrease, chest volume and compliance decrease, chest pressure increases, and chest pressure increases to limit lung expansion and lung compliance Sexual decline, the results showed increased peak airway pressure during mechanical ventilation, decreased alveolar ventilation and functional residual capacity, on the other hand, increased pulmonary vascular resistance, abnormal ventilation/blood flow ratio, hypoxemia, hypercapnia Hemorrhage and acidosis. When using a ventilator to support ventilation, high pressure is required to input sufficient tidal volume; if the abdominal high pressure is not relieved in time, mechanical ventilation will continue to increase the chest pressure, and the above changes will be further deteriorated.

4. Renal blood flow reduction: The most common manifestation of elevated intra-abdominal pressure is oliguria, Doty (1999) reported: intra-abdominal pressure increased to 1.33 kPa (10 mmHg), urine output began to decrease, and average urine output at 2.00 kPa (15 mmHg) Can be reduced by 50%, 2.67 ~ 3.33kPa (20 ~ 25mmHg) significantly oliguria, 5.33kPa (40mmHg) without urine, decompression lh urine volume is restored, decreased intra-abdominal pressure is also caused by multiple factors Including the reduction of renal superficial cortical area, renal blood flow reduction, renal vascular effusion caused by renal vein compression, renal vascular resistance increased, glomerular filtration rate decreased, renin activity and aldosterone levels increased, all of the above factors Due to direct compression of abdominal high pressure, but the ureter is compressed and may cause post-renal obstruction.

Experimental studies have shown that after the intra-abdominal pressure is increased at least after the urine, the abdominal high pressure is not relieved immediately, but the oliguria begins to reversal after about 60 minutes, indicating that the mechanical compression of the abdominal hypertension is not the only cause of oliguria. Urinary and gastrointestinal effects are related to the effects of aldosterone and ADH.

5. Intra-abdominal blood perfusion reduction: When the intra-abdominal pressure is increased, the hepatic artery, portal vein and hepatic microcirculation blood flow is progressively reduced, and the hepatic arterial blood flow changes earlier and more severely than the portal vein blood flow; mesenteric arterial blood Flow and intestinal mucosal blood flow, as well as gastroduodenal, pancreatic and splenic arterial perfusion are reduced. In short, all intra-abdominal blood perfusion is reduced except for the adrenal gland. The above changes may be more than the decrease in cardiac output. When the intra-abdominal pressure is increased and the cardiac output and systemic vascular resistance are still normal.

Abdominal hypertension in patients with cirrhosis and ascites can cause elevation of hepatic venous pressure, hepatic venous wedge pressure and azygous venous blood flow (gastric esophageal collateral blood flow index) are further increased; intra-abdominal pressure is decreased, but intra-abdominal pressure is increased There is still controversy that causes esophageal varices bleeding.

Prevention of abdominal compartment syndrome

Close observation of abdominal signs and systemic changes is the key to the discovery of abdominal compartment syndrome. If abdominal distension and abdominal wall tension occur, organ dysfunction occurs, and timely decompression can also reduce the mortality rate of abdominal compartment syndrome.

Complications of abdominal compartment syndrome Complications acute renal insufficiency renal insufficiency acute cardiac insufficiency

Cardiac, lung, kidney and other important organ dysfunction are the main complications of this disease.

1. Renal insufficiency: It is characterized by reduced urine output or even no urine, supplementation with liquid or administration of dopamine and furosemide (furosemide).

2. Respiratory insufficiency: early manifestations of shortness of breath, Pa02 decreased, late PaC02 increased and peak airway pressure increased.

3. Incomplete circulatory function: The earliest tachycardia can compensate for the decrease in stroke output and maintain the cardiac output; after that, decompensation, due to insufficient blood volume, the cardiac output decreases, blood pressure drops, but CVP and PCWP Raise.

Symptoms of abdominal compartment syndrome Common symptoms Hypercapnia No urine pressure drop edema shock Increased urinary abdominal pressure

Clinical features of the abdominal compartment syndrome include:

1. Abdominal expansion and abdominal wall tension: It is the most direct manifestation of abdominal cavity hypertension caused by the increase of abdominal cavity content. Open ventral decompression can show high degree of edema of the intestine, and the intestine can not be returned.

2. The increase in the peak value of the inspiratory pressure is >8.34 kPa (85 cmH2O), which is the result of the elevation of the diaphragm, the increase of the chest pressure, and the decrease of the lung compliance.

3. oliguria: caused by insufficient renal blood perfusion, increased aldosterone and ADH, at this time for fluid resuscitation, the use of dopamine and myelin diuretics [furosemide (furosemide)] will not increase urine output.

4. Refractory hypoxemia and hypercapnia: due to mechanical ventilation can not provide sufficient alveolar ventilation, and the arterial oxygen partial pressure is reduced, CO2 retention.

After the ventral decompression, the above changes can be quickly reversed.

Examination of abdominal compartment syndrome

1. Renal function test

(1) Urine volume <0.5ml / (kg · h), suggesting renal insufficiency.

(2) Decreased glomerular filtration rate, increased renin activity and aldosterone levels.

2. Blood gas analysis: Early shows that PaO2 decreased, late PaCO2 increased, and CO2-CP increased.

Intra-abdominal pressure measurement is an important basis for the diagnosis of this disease.

3. Direct pressure measurement method: directly connect the intra-abdominal catheter to the pressure transducer to measure the abdominal pressure. The clinical can also be directly inserted into the abdominal cavity with a metal cannula or a thick needle to connect with the water column tube for pressure measurement. In laparoscopic surgery, the electronic inflator used. It is equipped with a pressure measuring device for continuous pressure measurement. The above methods are all invasive operations. When the intra-abdominal pressure increases the abdominal expansion, the intestinal tube is easily damaged, so it is rarely used clinically.

4. Indirect pressure measurement method: Animal experiments show that the pressure of the inferior vena cava is directly related to the intra-abdominal pressure. Therefore, the inferior vena cava pressure can be measured by the femoral vein cannula to indirectly reflect the intra-abdominal pressure, but there is no clinical application report yet. Clinically, the indirect method is most commonly used for transurethral intravesical balloon catheter pressure measurement. In addition, there is a transnasal tube or gastrostomy tube pressure measurement, a ureteral tube pressure measurement, a transrectal pressure measurement method, and a transurethral bladder balloon catheter test. When the patient is pressed, the patient is supine, the water is injected through the catheter 50-100ml, the pubic symphysis is zero, the water column height represents the intra-abdominal pressure; the nasal pressure tube or the gastrostomy tube is the same, and the mid-line level is zero.

Although the indirect method is invasive, it is difficult to accurately reflect the level of intra-abdominal pressure due to factors such as receptor position. However, in the above method, the intravesical pressure is measured by the transurethral balloon catheter in the supine position, which is closest to the actual intra-abdominal pressure.

Diagnosis and diagnosis of abdominal compartment syndrome

Diagnostic criteria

1. According to the criteria for diagnosis of intra-abdominal pressure: there is no consensus on the extent to which intra-abdominal pressure rises. There is no consensus on the ACS due to the acute increase of intra-abdominal pressure. According to the available data, the intra-abdominal pressure can be increased. The classification is as follows: mild increase of 1.33 ~ 2.67kPa (10 ~ 20mmHg), when the time is short, the body condition is good, can compensate, no obvious clinical symptoms; moderate increase of 2.67 ~ 5.33kPa (20 ~ 40mmHg), the body Decompensated; severely increased 5.33kPa (40mmHg), the body has developed serious physiological disorders.

In 1999, Mayberry enquired 292 trauma surgeons, 7l% of doctors made diagnosis based on clinical features, and 14% of doctors determined surgery based on bladder pressure measurement. Therefore, most surgeons currently diagnose and diagnose abdominal cavity based on clinical manifestations. Septal syndrome.

2. According to the criteria for clinical characteristics diagnosis

(1) History: Hemorrhagic, septic shock, sufficient fluid input (>12000ml).

(2) Abdominal signs: high abdominal abdomen, high abdominal wall tension; high intestinal edema after surgery, swelling can not be repaid, forced return to cause heart, lung, renal insufficiency; open decompression can be seen high intestinal edema, gushing out of the incision Outside, heart, lung, and kidney dysfunction are reversed.

(3) Organ function: heart rate increased and/or blood pressure decreased; respiratory rate increased, peak inspiratory pressure increased > 8.34 kPa (85 cm H20), hypoxemia; oliguria or no urine, with diuretic drug ineffective.

The medical history is necessary, the abdominal signs are the first one, and the organ dysfunction is complete, and the diagnosis can be diagnosed as ACS.

Differential diagnosis

Clinically, due to insufficient understanding of ACS, it is easy to be misdiagnosed as early model MODF. The difference between the two is that ACS is secondary to abdominal hypertension, heart, lung, renal insufficiency, abdominal distension and abdominal wall tension, and organ dysfunction. The pulmonary dysfunction of ACS is different from ARDS. The former is insufficient for pulmonary dilatation, causing PaO2 to decrease and PaCO2 to increase. Acute respiratory distress syndrome (ARDS) is characterized by alveolar dispersal disorder, and its PaO2 and PaCO2. Both are falling.

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