Chen Xukai, Li Wenxiong, SICU, Beijing Chaoyang Hospital, Capital Medical University
Acute kidney injury (AKI) is one of the common complications of abdominal hypertension. Normal intra-abdominal pressure (IAP) in adults is <8 mm Hg (1 mm Hg = 0.133 kPa), the World Association for Abdominal Septal Syndrome defines intra-abdominal pressure above 12 ,FOIH 119 as abdominal intra-abdominal hypertension (IAIt), and abdominal septal compartment syndrome (ACS) is defined as persistent IAP >20 mm Hg with associated new-onset organ dysfunction or failure The incidence of IAH and ACS in the ICU is 30% to 54% and 5% to 12%, respectively… The morbidity and mortality rate of patients with IAH in the ICU is approximately 37.9%, and the higher the IAP, the higher the morbidity and mortality.’21 In critically ill patients, IAP >12 mm Hg is an independent risk factor for predicting the development of AKI. When patients develop AKI, the morbidity and mortality rate and medical costs will be significantly increased. Therefore, it is of great clinical significance to explore the pathogenesis and treatment principles of AKI complicated by abdominal hypertension. Qiu Zhanjun, Department of Emergency Medicine, Affiliated Hospital of Shandong University of Traditional Chinese Medicine
The pathogenesis of acute kidney injury complicated by abdominal hypertension: IAH induces AKI by decreasing renal artery blood flow. increased IAP causes the diaphragm to shift cephalad, and 20% to 80% of IAP is transferred to the thoracic cavity, resulting in increased intrathoracic pressure, which directly compresses the heart and reduces the end-diastolic volume of the left and right ventricles; IAH decreases the venous return flow from the abdomen or lower extremities, resulting in IAH decreases venous return flow from the abdomen or lower extremities, leading to decreased right ventricular preload; increased intra-abdominal and thoracic pressure directly compresses the vascular bed, leading to increased left ventricular afterload. The combined effect of the above significantly decreases cardiac output and renal arterial blood flow in patients with IAH; IAH also increases renal venous pressure and decreases renal venous blood flow, leading to decreased renal arterial perfusion and renal cortical perfusion, which decreases glomerular filtration rate and induces acute kidney injury. Clinical manifestations include increased serum urea nitrogen and creatinine, oliguria or anuria, imbalance of acid-base balance and electrolyte disturbance. iAH induces acute kidney injury by decreasing the abdominal perfusion pressure (APP), which is the difference between mean arterial pressure (MAP) and IAP, approximating renal perfusion pressure, and is the effective pressure to maintain renal arterial blood flow. In general, glomerular filtration pressure (GFP) is close to APP or renal perfusion pressure. The glomerular filtration gradient (FG) is the difference between GFP and glomerular intracapsular pressure.FG is the net glomerular filtration pressure and the effective pressure for producing primary urine, reflecting the balance between glomerular capillary hydrostatic pressure (which promotes the entry of filtrate into the glomerular capsule) and colloid osmotic pressure (which promotes the entry of filtrate from the glomerular capsule into the glomerular capillaries). The intra-glomerular capsule hydrostatic pressure is approximately equal to the proximal tubular pressure (PTP), so FG=GFP a scapular P. In the IAH state, both intra-glomerular capsule pressure and PTP are close to IlAP, and under the assumption that the mechanism of glomerular perfusion autoregulation (contraction and diastole of the small inlet and outlet arteries) does not exist, FG=GFP a scapular P=(MAP -IAP)iIAP=MAP i(2×IAP). It can be seen from the equation that as IAP increases, FG decreases more significantly. It was found that L32, when IAP was 8-12 mm Hg, the kidneys showed significant hypoperfusion; when IAP exceeded 15 mm Hg, the organism showed oliguria, and anuria usually appeared after IAP exceeded 25-30 Inn Hg. In critically ill patients, the incidence of AKI was 33% at IAP ≥ 18 mm Hg, whereas the incidence of AKI was only 14% at IAP < 18 mm ttg, indicating that the incidence of AKI correlates with the level of IAP. Renal venous pressure, as the afterload of the kidney, is another important factor affecting renal perfusion pressure. When IAP is increased, both central venous pressure (CVP) and renal venous pressure increase, which leads to a decrease in renal perfusion pressure. In our previous study of acute kidney injury complicated by infectious shock, we found that H1, high CVP with the same volume load resulted in increased morbidity and mortality of AKI and aggravation of AKI. Therefore, the effect of renal venous pressure on renal perfusion pressure should also be considered in the mechanism of AKI complicated by abdominal hypertension.IAH induces acute kidney injury through activation of the renin-angiotensin-aldosterone system and systemic inflammatory response.IAH leads to a decrease in cardiac output and blood pressure, reflex activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system, and increased release of antidiuretic hormone, resulting in widespread When IAH progresses to a certain level, cytokines are released from ischemic tissues, especially from the ischemic intestine, leading to an increase in circulating cytokines such as TNF-ol, IL-1 and IL_6. This in turn damages distant organs such as kidney, liver and lung, inducing multi-organ dysfunction (MODS). The presence of IAH at the time of admission to the ICU is closely related to the subsequent onset of MODS, and almost all patients with IAH-induced MODS have AKI, which is usually an early clinical manifestation of IAH. AKI can occur after IAH, so there is a lag effect, suggesting that the impairment of renal function by IAH can be a gradual process.
2. Monitoring and treatment of acute kidney injury complicated by abdominal hypertension: Abdominal hypertension induces AKI mainly by reducing renal blood flow and perfusion pressure. Therefore, eliminating the cause, monitoring and controlling intra-abdominal pressure, increasing renal perfusion pressure and improving renal perfusion are the core elements of monitoring and treatment of patients with acute kidney injury complicated by abdominal hypertension. First, proper blood volume should be maintained to ensure effective renal perfusion; IAH itself can lead to reduced venous return and inadequate organ perfusion, and further increased intrathoracic pressure exacerbates the cardiovascular manifestations in patients with IAH while they are receiving positive pressure ventilation. The goals of volumetric resuscitation are to increase intravascular preload and cardiac output, correct hypovolemia and anaerobic metabolism, and restore organ perfusion. Studies have found that proper fluid resuscitation improves survival in patients with IAH/ACS. However, excessive fluid resuscitation leads to excessive fluid collection in the intestine, mesenteric, free peritoneal gap, retroperitoneal, intestinal wall, and abdominal wall edema, further increasing IAP and making the patient’s prognosis worse. Therefore, how to optimize fluid resuscitation has been the most complex issue in the management of patients with IAH/ACS. Hemodynamic monitoring is necessary when the patient’s blood volume status is difficult to determine. The sepsis guidelines emphasize “early targeted therapy”, which defines the endpoint of volume resuscitation in the early stages of severe sepsis, with the goal of correcting hypovolemia and achieving a central venous pressure of 8-12 mm Hg for fluid resuscitation. The concept of “early target therapy” is also applicable to the critically ill patient with IAH/ACS, but the fluid resuscitation goals are different; the interaction between abdominal, thoracic, and intravascular pressures in the IAH state results in a significant increase in CVP, and therefore, higher CVP goals should be considered when performing fluid resuscitation in the IAH state. Clinicians should be careful to identify the impact of elevated intra-abdominal and intrathoracic pressures on the accuracy of the hemodynamic pressure parameters CVP and pulmonary artery obstruction pressure (PAOP). Transmural PAOP and CVP measurements provide a more reliable estimate of intravascular volume in patients with IAH/ACS and are calculated as follows: transmural CVP = CVP – 0.5 x IAP and transPAOP = PAOP – 0.5 X IAP. It should be emphasized that a higher CVP will increase renal venous pressure, when a combination of measures should be considered to lower intrathoracic pressure to reduce CVP (adjusting ventilator parameters, controlling intra-abdominal pressure to lower intrathoracic pressure, etc.) and improve renal perfusion. Functional hemodynamic parameters such as beat-to-beat volume variability and pulse pressure variability are commonly used to evaluate volume responsiveness in critically ill patients, and the predictive value of beat-to-beat volume variability and pulse pressure variability for volume responsiveness decreases in the IAH state. Volumetric parameters such as right ventricular end-diastolic volume index, whole heart end-diastolic volume index, and cardiac ultrasound parameters improve the ability of clinicians to interpret vascular filling. It should be noted that decreased cardiac output may not be the primary cause of IAH-induced AKI. Animal studies have shown that increasing cardiac output by volume expansion does not prevent the development of IAH-induced AKI, and the benefit of volume expansion on renal function may only occur in cases of extreme volume depletion. These findings indirectly suggest that intra-abdominal pressure has a more important effect on renal function than volume factors. When increased oxygen delivery through volume expansion does not continue to improve systemic tissue metabolism and organ function, continued volume expansion is not beneficial. At this time, restrictive fluid resuscitation should be implemented to minimize positive fluid balance and avoid excessive fluid resuscitation. Limiting the use of crystalloids and combining colloid and diuretics can relieve swelling of the intestinal wall, reduce the collection of third interstitial fluid, more quickly facilitate the patient’s transition from positive fluid balance to negative fluid balance, reduce lAP, shorten the duration of mechanical ventilation, and possibly improve the prognosis. It is even more important to control intra-abdominal pressure and maintain appropriate peritoneal perfusion pressure. In patients with acute disease in IAH/ACS, effective reduction of IAP is the most effective way to improve AKI, and renal function improves in most patients immediately after IAP is controlled.Mullens et al’6 o In a study of patients with congestive heart failure complicated by AKI, it was found that reducing IAP by hemofiltration dehydration and/or perforated drainage of ascites to treat AKI was more effective than optimizing hemodynamic parameters. Appropriate removal of excess third interstitial fluid collection usually reduces IAP, increases APP, and improves renal perfusion and function. However, excessive colloid osmotic pressure will reduce glomerular filtration gradient and glomerular filtration rate; therefore, when combining colloid and diuretics, it is important to find the optimal balance between IAP-lowering effect and filtration gradient-lowering effect. Oda et al. “found that hemofiltration reduced circulating cytokine levels and their effect on IAP in patients with acute severe pancreatitis and reduced excess interstitial fluid. incidence of ACS and improve the prognosis. When acute tubular necrosis or tubular apoptosis has already occurred in the kidney, even controlling IAP to restore renal blood flow and glomerular filtration gradient does not result in rapid recovery of AKI; therefore, the timing of surgical intervention for IAH/ACS is important. The World Association for Abdominal Intercompartmental Syndrome recommends that open decompression should be considered for patients with IAP > 25 mmHg and APP < 50 mmHg, with new organ dysfunction or failure, when conservative medical treatment has failed. In patients with controlled IAH and continued deterioration of AKI, the timing, modality and dose of renal replacement therapy should be decided based on the biochemical parameters associated with AKI, fluid load, disease severity and other systemic conditions of the patient. Because abdominal tissue blood flow is directly related to APP, patients with IAH/ACS need to maintain appropriate APP, which is a more accurate indicator of actual abdominal tissue oxygen delivery and predictor of patient prognosis than IAP, and the morbidity and mortality rate is significantly higher in those who fail to maintain APP ≥60 mm Hg on day 3 of IAH, and maintaining APP >60 mm Hg is one of the important resuscitation endpoints for patients with IAH. Patients with IAH/ACS whose APP remains below 60 mm Hg after appropriate fluid resuscitation should be treated with vasoactive drugs to increase mean arterial pressure to an APP > 60 mm Hg. Norepinephrine is the most commonly used vasoconstrictor in clinical practice, especially in patients with low afterload (e.g., distributive shock). Cardiac output remains below the normal range after appropriate fluid resuscitation, and cardiac positive inotropic drugs should be used to increase cardiac output and improve systemic tissue perfusion. As mentioned previously, maintaining appropriate APP actually also maintains effective renal perfusion pressure and glomerular filtration pressure, thus playing an important renoprotective role.
In summary, decreased abdominal perfusion pressure and cardiac output are the most important causes of acute kidney injury complicated by abdominal hypertension. Elevated intra-abdominal pressure directly leads to poor renal perfusion and decreased glomerular filtration rate, and decreases effective circulating blood volume and cardiac output, and decreased cardiac output further worsens renal perfusion. pressure (intra-abdominal pressure) is always the driving force behind the development and progression of acute kidney injury, and volume ( too much or too little effective blood volume) is its aggravating factor, therefore, the role of pressure over volume. Targeted volume management should be implemented in critically ill patients with abdominal hypertension by combined monitoring of cardiac parameters, oxygen delivery parameters, urine output, and intra-abdominal pressure; appropriate application of cardiac positive inotropic and vasoactive drugs to maintain appropriate abdominal perfusion pressure and improve renal perfusion and filtration, while preventing the adverse effects of increased intra-abdominal pressure by excessive fluid resuscitation; high intra-abdominal pressure state by volume expansion as well as In high intra-abdominal pressure, surgical decompression to control intra-abdominal pressure is the only option when renal function cannot be improved by volume expansion and other medical measures.
From: Chinese Medical Journal, Vol. 92, No. 15, April 17, 2012, Expert Forum