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Increased intra-abdominal pressure

Introduction
Cause
Examine
Diagnosis

Introduction

Introduction 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.

Cause

Cause

(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 abdomen Vascular surgery and postoperative positive pressure mechanical ventilation.

1. Hemorrhagic shock after liquid expansion

(1) Abdominal trauma: The most common cause of severe abdominal trauma in foreign countries. Behrman (1998) reported 222 cases of hemorrhagic shock, intra-abdominal hemorrhage, and pancreatic injury. The fluid volume was 5800-12000ml, blood transfusion was 800-5000ml, and ACS occurred in 3 cases.

(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 believed that large-area burns should be alert to ACS when a large number of fluid-input cases are associated with high airway pressure, oliguria or anuria. Maxwell (1999) reported 1216 cases of hemorrhagic shock, 6 of which had no history of abdominal trauma, and about 2/6 of secondary ACS. The volume of fluid input in this group was 19,000±5000 ml. The authors cautioned that the input of crystalloid fluid was more than 10,000 ml.

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, volume increase, intestinal curvature If the bulge is above the plane of the incision and cannot be reimbursed, consider ACS first. In the above situation, if the abdominal wall incision is forcibly closed, the intra-abdominal pressure will increase rapidly. After leaving the operating room, respiratory and circulatory deterioration will occur, and oliguria will be urinated. Most cases will die within 10 hours after surgery. 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 with acute suppurative cholangitis is rare in Western Europe and North America, but it is a common disease of ACS in China. Such cases are difficult to treat because of the presence of an infectious systemic inflammatory response (ISIR), and the mortality rate is much higher than that of hemorrhagic shock.

Abdominal compartment syndrome often occurs due to a combination of multiple factors of sharp increase in intra-abdominal pressure. A typical clinical example is a severe infection of the abdominal cavity or trauma itself, which causes edema of the abdominal organs and a sharp increase in volume. At this time, it is often accompanied by hypovolemia. For this reason, adequate fluid resuscitation causes peritoneal and visceral progressive edema; and due to hypoperfusion, edema is caused by reperfusion injury after visceral ischemia and resuscitation; Stuffing with hemostasis, mesenteric venous obstruction, or temporary portal vein blockage. In trauma, shock, severe pancreatitis, severe peritonitis or major surgery, severe ISIR occurs in the body. As a result, a large amount of extracellular fluid enters the cell or interstitial space, and a third gap effect or liquid seizure occurs. The liquid treatment shows a significant positive balance. That is, the input amount far exceeds the discharge amount. At this time, only a sufficient amount of input balance liquid can offset the positive balance, maintain effective circulating blood volume, and avoid blood concentration. Otherwise, there will be a decrease in blood flow, a rapid increase in heart rate, a decrease in cardiac output, an increase in HCT, and a decrease in hypotension. In the above cases, peritoneal and visceral edema and ascites have been inevitable. From the perspective of maintaining effective circulating blood volume, the amount of infusion is not too much, and high edema is only the result of ISIR, which cannot negate the liquid resuscitation. necessity. The fluid extravasation in this cycle is temporary. When the ISIR is relieved and the capillary permeability is restored, the extracellular fluid that is excessively sequestered is absorbed back, the positive balance of the liquid is converted to a negative balance, and the edema rapidly subsides.

(two) pathogenesis

Peritoneal and visceral edema, abdomen effusion caused by a sharp 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 raised, the tension of the lumen wall increases, and in severe cases, the abdominal distension and abdominal wall tension may occur. At this time, Doppler ultrasonography showed that the blood flow of the rectus abdominis sheath was weakened. For example, the abdominal incision was forced to close the abdomen, and the incidence of wound infection and incision splitting was high. The dV/dP (capacity/pressure) curve of the abdominal cavity is not linear, and rises abruptly like the oxygen dissociation curve. Even if there is a small increase in the amount of the abdominal cavity, the intra-abdominal pressure is increased greatly; Decompression can significantly reduce abdominal high pressure.

2. tachycardia, reduced cardiac output

After the increase of intra-abdominal pressure, the stroke volume was significantly reduced, and the cardiac output was also decreased. In laparoscopic surgery, an intra-abdominal pressure as low as 1.33 to 2.00 kPa (10 to 15 mmHg) can cause an adverse reaction. The decrease in cardiac output (and stroke volume) was caused by a decrease in venous return, an increase in left ventricular filling pressure due to an increase in pleural pressure, a decrease in myocardial compliance, and an increase in systemic vascular resistance. The decrease of venous return is mainly caused by the decrease of posterior capillary venule pressure and central venous pressure gradient, the reduction of inferior vena cava blood return, and the inferior vena cava functional stenosis or mechanical compression of the diaphragm after hemostasis. Increased chest pressure and so on. 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 volume while maintaining cardiac output. Obviously, if the tachycardia is not enough to compensate for the reduced stroke volume, the cardiac output will drop sharply, and circulatory failure will follow.

3. Increased pleural pressure and decreased lung compliance. The abdominal high pressure caused bilateral diaphragmatic muscle elevation and movement amplitude to decrease, chest volume and compliance decreased, and chest pressure increased. On the one hand, the increase in chest pressure limits lung expansion and decreases lung compliance. The result is an increase in the peak airway pressure during mechanical ventilation, and a decrease in alveolar ventilation and functional residual capacity. On the other hand, pulmonary vascular resistance is increased, causing abnormal ventilation/blood flow ratio, hypoxemia, hypercapnia, and acidosis. When using a ventilator to support ventilation, a higher pressure is required to input sufficient tidal volume; if the abdominal high pressure is not relieved in time, mechanical ventilation causes the chest pressure to continue to rise, and the above changes will be further deteriorated.

4. Renal blood flow is reduced

The most common manifestation of elevated intra-abdominal pressure is oliguria. Doty (1999) reported that the intra-abdominal pressure rose to 1.33 kPa (10 mmHg) and the urine volume began to decrease. At 2.00 kPa (15 mmHg), the urine volume decreased by 50% on average, and from 2.67 to 3.33 kPa (20 to 25 mmHg), significant oliguria, 5.33 There is no urine when kPa (40mmHg), and the urine volume is restored after decompression lh. Decreased urine output is also caused by multiple factors including increased perfusion of the superficial renal cortex, decreased renal blood flow, partial obstruction of renal vascular effusion due to renal vein compression, increased renal vascular resistance, and glomerular filtration. The rate decreased, renin activity and aldosterone levels increased. All of the above factors are caused by direct compression of abdominal high pressure, but the ureter may be affected by post-renal obstruction.

Experimental studies have shown that after the increase of intra-abdominal pressure is at least urine, the release of abdominal high pressure does not immediately appear polyuria, but after about 60 minutes, oliguria begins to reverse, indicating that mechanical compression of abdominal hypertension is not the only cause of oliguria. The effect of aldosterone and ADH is related to oliguria and elevated intra-abdominal pressure.

5. Reduced blood perfusion of abdominal organs

When the intra-abdominal pressure is increased, the hepatic artery, portal vein and hepatic microcirculation blood flow are progressively reduced, and the hepatic arterial blood flow changes earlier and more severely than the portal vein blood flow; mesenteric artery blood flow and intestinal mucosal blood flow, and stomach ten The perfusion of the digestive, pancreatic and splenic arteries was reduced. In all, all intra-abdominal blood perfusion was reduced except for the adrenal gland. The above change exceeds the result of a decrease in cardiac output, and may also occur 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.

Examine

an examination

Related inspection

Abdominal vascular ultrasound examination of abdominal plain film

Clinical features of the abdominal compartment syndrome include:

1. Abdominal expansion and abdominal wall tension

It is the most direct manifestation of increased abdominal volume resulting in abdominal high pressure. Open decompression can be seen in the high degree of edema of the intestine, out of the incision, the intestine can not be returned.

2. Increase in suction pressure peak > 8.34kPa (85cmH2O)

It is the result of the squatting uplift, the increase in chest pressure, and the decline in lung compliance.

3. Lack of urine

Insufficient perfusion of renal blood flow, caused by increased aldosterone and ADH. At this time, for fluid resuscitation, the use of dopamine and myelin diuretics [furosemide (furosemide)] will not increase the amount of urine.

4. refractory hypoxemia and hypercapnia

Because mechanical ventilation can not provide enough alveolar ventilation, and the arterial oxygen partial pressure is reduced, CO2 retention.

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

1. According to the criteria for diagnosis of intra-abdominal pressure

There is no consensus on the extent to which intra-abdominal pressure rises to ACS, and the compliance individuals are different due to the acute increase in intra-abdominal pressure. According to the available data, the intra-abdominal pressure can be graded as follows: mild increase of 1.33 ~ 2.67 kPa (10 ~ 20 mmHg), when the time is short, the systemic condition is good, can compensate, no obvious clinical symptoms; moderate rise The height is 2.67 ~ 5.33kPa (20 ~ 40mmHg), the body has been decompensated; severely increased 5.33kPa (40mmHg), the body has developed serious physiological disorders.

At present, most surgeons comprehensively analyze the diagnosis of abdominal compartment syndrome based on clinical manifestations.

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 edema of the intestines, expansion can not be repaid, forced return to lead to heart, lung, kidney dysfunction; open decompression can be seen in the high degree of edema of the intestine, gushing out of the incision In addition, 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.

Diagnosis

Differential diagnosis

Clinically, due to insufficient understanding of ACS, it is easily misdiagnosed as early model MODF. The difference between the two is: ACS is secondary to abdominal hypertension, heart, lung, renal insufficiency, abdominal distension and abdominal wall tension in the front, organ dysfunction in the posterior; and ACS pulmonary insufficiency is different from ARDS, the former is lung expansion Insufficient ventilation caused PaO2 to decrease and PaCO2 to increase. Acute respiratory distress syndrome (ARDS) was characterized by alveolar dispersal disorder, and both PaO2 and PaCO2 decreased.