Abdominal compartment syndrome

　　1. Etiology

　　In surgical practice, acute intraperitoneal hypertension is commonly seen in severe intra-abdominal infections accompanied by septic shock, such as acute peritonitis, acute pancreatitis, and acute intestinal obstruction, severe abdominal trauma, rupture of abdominal aortic aneurysm, acute intra-abdominal hemorrhage or retroperitoneal hematoma, and postoperative hemorrhagic shock or massive bleeding in the hepatic retroperitoneal area after packing for hemostasis. After sufficient fluid resuscitation, there is acute progressive visceral edema, laparoscopic surgery under pneumoperitoneum, and inflation to counteract shock.

　　Application, after liver transplantation, complex abdominal vascular surgery, and postoperative positive pressure mechanical ventilation, etc.

　　1. Hemorrhagic shock:

　　(1) Abdominal trauma: Overseas reports indicate that severe abdominal trauma is the most common cause of this disease. Behrman (1998) reported 222 cases of hemorrhagic shock, massive intra-abdominal hemorrhage, and pancreatic injury, with fluid resuscitation ranging from 5,800 to 12,000 ml, blood transfusion of 800 to 5,000 ml, and 3 cases developed ACS.

　　(2) No abdominal trauma: Ivy (1999) reported 3 cases of acute respiratory distress syndrome (ARDS) secondary to extensive burns (>70%) with fluid intake exceeding 20,000 ml. Therefore, it is believed that in cases of extensive burns with massive fluid input, hypertension in the airways, oliguria, or anuria should raise suspicion for ACS. Maxwell (1999) reported 1216 cases of hemorrhagic shock, including 6 without a history of abdominal trauma, approximately 2/6 developed ACS, and the fluid intake was 19,000 ± 5,000 ml. The author warned to be vigilant about ACS with fluid intake exceeding 10,000 ml.

　　Severe abdominal trauma with hemorrhagic shock or traumatic hypovolemic shock presenting with systemic capillary permeability changes after fluid expansion, progressive peritoneal and visceral edema, and marked intestinal edema, increased volume, and significant intussusception above the incision plane, which cannot be retracted, should be initially considered as abdominal compartment syndrome (ACS). In such cases, if the abdominal wall incision is forcibly closed, it will lead to a rapid increase in intraperitoneal pressure, followed by deterioration of respiration and circulation after leaving the operating room, oliguria, and eventually anuria. Most patients die within 10 or more hours after surgery, and this condition is often misdiagnosed as multiple organ failure syndrome.

　　2. Infection shock:After fluid expansion, most of the reported cases abroad are severe abdominal trauma with hemorrhagic shock leading 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 causing ACS in China. In such cases, because there is an existing infectious systemic inflammatory response, treatment is difficult, and the mortality rate is much higher than that of hemorrhagic shock.

　　Abdominal compartment syndrome often occurs due to the combined effects of various factors causing a sharp increase in intra-abdominal pressure. A typical clinical example is severe abdominal infection or trauma itself causing edema and a significant increase in volume of abdominal visceral organs. At this time, it is often accompanied by hypovolemia, and the implementation of adequate fluid resuscitation leads to progressive edema of the peritoneum and visceral organs; and due to low blood perfusion, visceral ischemia-reperfusion injury after resuscitation can further worsen edema; it can also be exacerbated by dressing packing for hemostasis, mesenteric vein obstruction, or temporary portal vein occlusion. During trauma, shock, severe pancreatitis, severe peritonitis, or major surgery, the body may develop severe ISIR, resulting in a large amount of extracellular fluid entering the intracellular space or tissue spaces, causing a third space effect or fluid retention, with fluid therapy showing a significant positive balance, that is, the input volume far exceeds the output volume. At this time, only adequate input of balanced fluid can offset the positive balance, maintain effective circulating blood volume, and avoid blood concentration, otherwise, there will be a decrease in return blood volume, an increase in heart rate, a decrease in cardiac output, an increase in HCT, and hypotension. In the above situations, peritoneal and visceral edema and abdominal effusion have become inevitable. From the perspective of maintaining effective circulating blood volume, the fluid volume at this time is not too much, and the severe edema is only the adverse effect of ISIR, and it cannot be used to negate the necessity of fluid resuscitation. This fluid leakage in the circulation is temporary. When ISIR is reduced and capillary permeability returns, the excessive retained extracellular fluid is reabsorbed, the fluid positive balance turns into a negative balance, and edema quickly subsides.

　　2. Pathogenesis

　　When the peritoneum and visceral edema, and abdominal effusion cause acute abdominal compartment syndrome due to a sharp increase in intra-abdominal pressure, it can damage the physiological function of abdominal and systemic organs, leading to organ dysfunction and circulatory failure.

　　1. Increase in abdominal wall tension:When the intra-abdominal pressure increases, the tension of the abdominal wall increases, which can lead to abdominal distension and abdominal wall tension in severe cases. At this time, Doppler ultrasound examination may find a decrease in blood flow in the rectus sheath muscle, and if the abdominal cavity is closed forcibly after laparotomy, the incidence of incisional infection and incisional dehiscence is high. The dV/dP (volume/pressure) curve of the abdominal cavity is not linear, but rises abruptly like the oxygen dissociation curve, and after reaching a certain limit, even a small increase in the abdominal content is enough to cause a significant increase in intra-abdominal pressure; conversely, partial decompression can significantly reduce abdominal hypertension.

　　2. Tachycardia, decreased cardiac output:Increased intraperitoneal pressure significantly reduces stroke output, and cardiac output also decreases accordingly. During laparoscopic surgery, an intraperitoneal pressure as low as 1.33-2.00 kPa (10-15 mmHg) can produce adverse reactions. The reasons for the decrease in cardiac output (and stroke output) include reduced venous return, increased left ventricular filling pressure due to increased thoracic pressure, decreased myocardial compliance, and increased systemic vascular resistance. The reduction in venous return is mainly caused by a decrease in the pressure gradient between the postcapillary venous pressure and the central venous pressure, reduced blood return to the inferior vena cava, functional stenosis or mechanical compression of the inferior vena cava at the diaphragmatic location after filling and止血 due to severe lateral injury of the great vein of the liver, and increased thoracic pressure, etc. At this time, the pressures such as femoral venous pressure, central venous pressure, pulmonary capillary wedge pressure, and right atrial pressure all increase proportionally with the intraperitoneal pressure.

　　Tachycardia is the first cardiovascular response to increased intracavitary pressure, attempting to compensate for the decrease in stroke output to maintain cardiac output. Clearly, if tachycardia is not sufficient to compensate for the decreased stroke output, cardiac output will drop sharply, and circulatory failure will follow.

　　3. Increased thoracic pressure and decreased lung compliance:Increased intraperitoneal pressure raises and reduces the amplitude of movement of both diaphragmatic muscles, leading to a decrease in thoracic cavity volume and compliance, and an increase in thoracic pressure. On one hand, the increase in thoracic pressure restricts lung expansion, reduces lung compliance, resulting in increased peak airway pressure during mechanical ventilation, reduced alveolar ventilation volume, and reduced functional residual capacity. On the other hand, it increases pulmonary vascular resistance, causing an abnormal ventilation/perfusion ratio, leading to hypoxemia, hypercapnia, and acidosis. When supporting ventilation with a respirator, a higher pressure is needed to input sufficient tidal volume; if the increased intraperitoneal pressure is not relieved in time, mechanical ventilation will continue to increase thoracic pressure, and the above changes will further worsen.

　　4. Decreased renal blood flow:The most common manifestation of increased intraperitoneal pressure is oliguria. Doty (1999) reported that when the intraperitoneal pressure reaches 1.33 kPa (10 mmHg), the urine volume begins to decrease; at 2.00 kPa (15 mmHg), the average urine volume can decrease by 50%; at 2.67-3.33 kPa (20-25 mmHg), significant oliguria occurs; at 5.33 kPa (40 mmHg), anuria occurs, and the urine volume recovers after 1 hour of decompression. The decrease in urine volume during increased intraperitoneal pressure is caused by multiple factors, including reduced perfusion in the superficial cortex of the kidney, reduced renal blood flow, obstruction of renal vascular outflow due to compression of the renal veins, increased renal vascular resistance, decreased glomerular filtration rate, increased renin activity, and increased aldosterone levels. These factors are all caused by direct compression of abdominal hypertension, but the possibility of post-renal obstruction due to compression of the ureters does not exist.

　　Experimental studies have proven that after the increase of intraperitoneal pressure, the relief of abdominal hypertension does not immediately lead to polyuria, but rather the decrease in urine volume begins to reverse after about 60 minutes, indicating that the mechanical compression of abdominal hypertension is not the only cause of oliguria. Oliguria is related to the action of aldosterone and ADH after the increase of intraperitoneal pressure.

　　5. Decreased blood perfusion of abdominal organs:When intraperitoneal pressure increases, the blood flow of the hepatic artery, portal vein, and hepatic microcirculation decreases progressively. The changes in hepatic artery blood flow are earlier and more severe than those in portal vein blood flow; the blood flow of mesenteric artery and intestinal mucosal blood flow, as well as the perfusion of the gastroduodenal, pancreatic, and splenic arteries, all decrease. In summary, the blood perfusion of all abdominal organs except the adrenal gland decreases. These changes can exceed the result of decreased cardiac output and can also appear when intraperitoneal pressure increases while cardiac output and systemic vascular resistance remain normal.

　　Abdominal hypertension in patients with liver cirrhosis and ascites can cause increased hepatic venous pressure, further increased hepatic venous wedge pressure and paraaortic blood flow (gastroesophageal collateral blood flow index); conversely, when intraperitoneal pressure decreases. However, whether increased intraperitoneal pressure can cause esophageal variceal rupture and bleeding is still controversial.

　　Cardiovascular, pulmonary, renal, and other important organ dysfunction are the main complications of the disease.

　　1. Renal dysfunction:It is characterized by reduced urine output, even anuria, and supplementation with fluid or administration of dopamine and furosemide (Lasix) is ineffective.

　　2. Respiratory dysfunction:Early manifestations include tachypnea and decreased PaO2, and later PaCO2 increases and the peak airway pressure increases.

　　3. Circulatory dysfunction:The earliest manifestation is tachycardia, which can compensate for the decrease in stroke volume to maintain cardiac output; thereafter, it becomes decompensated, and due to insufficient return blood volume, the cardiac output decreases accordingly, blood pressure decreases, but CVP and PCWP increase.

　　The clinical features of abdominal compartment syndrome include:

　　1. Abdominal distension and abdominal wall tension:It is the most direct manifestation of increased abdominal content and abdominal hypertension. Laparotomy decompression can see that the intestines are highly edematous, extruding beyond the incision, and the intestines cannot be returned after the operation.

　　2. Increased peak inspiratory pressure:>8.34kPa (85cmH2O) is the result of diaphragmatic elevation, increased chest pressure, and decreased lung compliance.

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

　　4. Refractory hypoxemia and hypercapnia:Due to the insufficient alveolar ventilation provided by mechanical ventilation, the partial pressure of oxygen in arterial blood decreases, and carbon dioxide is retained.

　　After laparotomy decompression, the above changes can be rapidly reversed.

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

　　1. Develop good living habits, quit smoking and limit alcohol consumption. Smoking, according to the World Health Organization's prediction, if people stop smoking, the world's cancer will decrease by 1/3 after 5 years; secondly, do not overindulge in alcohol. Cigarettes and alcohol are extremely acidic substances, and people who smoke and drink for a long time are prone to acidic constitution.

　　2. Do not eat too much salty and spicy food, do not eat overheated, cold, expired, and deteriorated food; for the elderly, the weak, or those with certain genetic predispositions to diseases, eat some anti-cancer foods and alkaline foods with high alkaline content appropriately, and maintain a good mental state.

　　1. Renal function tests

　　1. Urine volume

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

　　2. Blood gas analysis:Early in the disease, PaO2 decreases, while PaCO2 increases in the later stage, and CO2-CP increases. The measurement of intra-abdominal pressure is an important basis for the diagnosis of this disease.

　　3. Direct pressure measurement method:Directly connect the abdominal catheter to the pressure transducer to measure abdominal pressure. In clinical practice, it is also possible to measure pressure by directly inserting a metal sleeve or a thick needle into the abdomen and connecting it to the water column tube. In laparoscopic surgery, the electronic inflator used has a pressure measurement device that can perform continuous pressure measurement. All of the aforementioned methods are invasive operations, and it is easy to damage the intestinal tract when the intra-abdominal pressure increases and the abdomen swells, so they are rarely used in clinical practice.

　　4. Indirect pressure measurement method:Animal experiments show that the level of inferior vena cava pressure is directly related to intra-abdominal pressure, so the pressure of the inferior vena cava can be measured through femoral vein catheterization to indirectly reflect intra-abdominal pressure. However, there are no clinical application reports at present. Clinically, the most commonly used indirect method is to measure pressure through a urethral bladder balloon catheter. In addition, there are other methods such as measuring pressure through a nasogastric tube or gastrostomy tube, measuring pressure through an indwelling ureteral catheter, and measuring pressure through the rectum. When measuring pressure through a urethral bladder balloon catheter, the patient is in a supine position, 50-100 ml of water is injected through the catheter, and the symphysis pubis is taken as the zero point, with the height of the water column representing the intra-abdominal pressure; the method of measuring pressure through a nasogastric tube or gastrostomy tube is the same, with the level of the axillary midline as the zero point.

　　5. Indirect methods:Although minimally invasive, the results are affected by factors such as body position, making it difficult to accurately reflect the level of intra-abdominal pressure. However, among the aforementioned methods, measuring bladder pressure through a urethral balloon catheter in the supine position is closest to the actual intra-abdominal pressure.

　　According to different symptoms, there are different dietary requirements. It is necessary to consult a doctor specifically and formulate different dietary standards for specific diseases. The patient's diet should be light and easy to digest, with an emphasis on eating more vegetables and fruits, and a reasonable dietary combination, paying attention to adequate nutrition. In addition, patients should also pay attention to avoiding spicy, greasy, cold, and deteriorated foods.

　　1. Treatment

　　1. Abdominal decompression:The fundamental cause of organ dysfunction caused by acute cholangitis is the increase in intra-abdominal pressure, therefore, decompression of the abdomen is the only effective treatment. It is also the basis for further confirming the diagnosis of acute cholangitis. Maxwell (1999) reported that all cases with an average decompression time of 3 hours after the occurrence of acute cholangitis survived, while those with an average of 25 hours all died. Therefore, early recognition and early decompression can significantly improve the prognosis. In surgery, the highly edematous and bulging intestinal tract cannot be forced to close the abdomen, and the incision must be extended for decompression. Although some authors suggest that decompressive laparotomy should be performed when the intra-abdominal pressure is 2.67-3.33 kPa (20-25 mmHg), most surgeons recommend performing decompressive laparotomy as soon as the clinical features of abdominal compartment syndrome are found.

　　To prevent hemodynamic disorders after decompression, under the condition of perfect continuous monitoring, first fluid resuscitation is used to replenish effective blood volume, so that the reduction in venous return can be compensated for, to maintain cardiac output. At the same time, oxygen is fully supplied. The rapid drop in intraperitoneal pressure after laparotomy can lead to lethal reperfusion syndrome, and even severe hypotension and cardiac arrest, which may be the consequence of anaerobic metabolic by-products entering the circulation after reperfusion washing. Morris et al. reported that the application of 2 liters of 0.45% sodium chloride solution plus 100g mannitol and 100mmol sodium bicarbonate given intravenously before laparotomy decompression can prevent reperfusion injury or reduce it to a lesser degree.

　　After abdominal decompression, leaving the skin and fascia open without suturing can maximize the reduction of intraperitoneal pressure, but it can lead to visceral prolapse and bowel fistula. At this time, it should be avoided to force a regular closure of the abdomen and choose one of the following temporary 'abdominal closure' methods.

　　2. Temporary 'abdominal closure' technique

　　To date, there is no comparative study on the temporary 'abdominal closure' technique, so clinical reports are all based on individual experience. Although many studies have reported that after expanding the midline incision as much as possible, using 20-30 gauze clamps or monofilament nylon thread to suture the skin continuously while not suturing the fascia can prevent abdominal hypertension, this method is not sufficient to decompress in some cases and can still cause the intraperitoneal pressure to reach 6.66 kPa (50 mmHg) or higher.

　　The second case of acute necrotizing pancreatitis complicated with suppurative cholangitis seen in the Department of General Surgery of Wuhan Workers' Medical College Affiliated Hospital was treated with 3 liters of intravenous nutrition infusion bag as temporary abdominal closure material after spontaneous decompression of the abdomen. This case underwent an abdominal incision at the xiphoid process to 3 cm below the umbilicus under tracheal intubation and general anesthesia, and underwent cholecystectomy, exploration and T-tube drainage of the common bile duct, incision of the serosal surface of the pancreas to remove necrotic tissue, and gastrostomy surgery. After the operation, a 3-liter intravenous nutrition infusion bag was cut open on both sides and sutured temporarily to the fascial margin with silk thread, and returned to the ward with a tracheal tube for SIMV assisted breathing. Postoperative urine output recovered, peak airway pressure ≤ 2.94 kPa (30 cmH2O), SpO2 98%; the small intestine protruding under the plastic bag covering was significantly higher than the abdominal wall and fluctuated with respiration. The color of the small intestine was normal through the plastic bag, with peristalsis but no signs of bowel obstruction such as dilatation of the bowel. 2 hours later, the protruding small intestine stopped fluctuating, the abdominal wall became tense again, there was no urine, the peak airway pressure was 7.85-9.81 kPa (80-100 cmH2O), SpO2 85%, and ultimately died of organ dysfunction due to abdominal compartment syndrome. The lesson from this case of death was that the patient's diagnosis and treatment were delayed and the surgical decompression was not timely, and the incision was not large enough to completely decompress. The other four cases of ACS encountered by the Department of General Surgery of Wuhan Workers' Medical College Affiliated Hospital were all early surgery, with an incision from the xiphoid process to the midline of the pubic symphysis for abdominal decompression. The result was that 3 cases survived, and only 1 case died of aspiration asphyxia after surgery. The use of a 3-liter plastic bag for temporary 'abdominal closure' not only has the advantages of being sterile and reliable, smooth surface, large capacity, and transparency to observe the abdominal organs and the presence or absence of bleeding, but also is inexpensive, easy to obtain, and convenient to use. In comparison, other prosthetic materials are expensive and difficult to obtain, so they are difficult to use.

　　3. Regular abdominal closure:In cases with good resuscitation, if polyuria, negative fluid balance, reduction of abdominal circumference, descent of visceral organs into the abdominal cavity, and regression of abdominal wall edema occur, the abdominal decompression cover prosthesis can be removed, the foreign bodies in the incision can be cleared, and the abdomen can be closed by tension-free suture with钢丝 outside the peritoneum, and the skin can be sutured separately. There is no need to suture the subcutaneous tissue and fascia, and this is the technique of mass closure (mass closure) of the abdominal wall.

　　II. Prognosis

　　Although the incidence of abdominal compartment syndrome is low, its mortality rate can reach as high as 62.5% to 75%. The reason lies in the insufficient understanding of the disease. However, early diagnosis of abdominal compartment syndrome and timely laparotomy decompression can quickly reverse all lesions after decompression.