Advances in Medical Ethics
Open Access

Enhanced Intra-Abdominal Pressure in Acute Kidney Injury

Jaafar Ismail^{1* *}Correspondence: Jaafar Ismail, Department of Pharmaceutical Analysis, International University of Africa, Khartoum, Sudan, Email:

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Description

The detrimental effects of increased Intra-Abdominal Pressure (IAP) on kidneys and other intra-abdominal organs have been known for a long time, particularly in postoperative conditions. In recent decades, the significance of Intra-Abdominal Hypertension (IAH) has been increasingly recognized because it is much more prevalent than expected and is associated with increased morbidity and mortality in critically ill patients. Studies of mixed populations in medical and surgical Intensive Care Units (ICUs) demonstrated a prevalence of IAH of up to 64%. The prevalence is higher in patients with septic shock, especially those who received massive volume resuscitation. The development of IAH is associated with a worse clinical outcome.

IAP is typically 5-7 mmHg in critically ill patients, and it rises in conditions with greater abdominal contents or impaired abdominal wall compliance. An increase in IAP of at least 12 mmHg that is prolonged or recurrent is referred to as IAH. Abdominal compartment syndrome is characterized by a persistent IAP of 20 mmHg along with new organ failure. An innovative metric that represents both IAH and circulatory impairment is the Abdominal Perfusion Pressure (APP). The difference between the IAP and the mean arterial pressure, or APP, is calculated. APP may be more effective than IAP at predicting patient outcomes, according to some research. Maintaining an APP of less than 50 mmHg appears to be necessary for healthy intra-abdominal circulation. Trans vesicular measurement is the method most frequently used for determining IAP.

It is possible for an elevated IAP level to have both direct and indirect impacts on the kidneys' ability to function. IAH's impact on the cardiovascular system can be attributed to a number of reasons. The diaphragm is displaced cranially as a result of IAH's increased intrathoracic pressure, which also causes the heart to be compressed. In addition, there is a decline in venous return and cardiac preload. Last but not least, direct compression of the arterial beds raises systemic afterload. IAP elevation ultimately results in a reduction in cardiac output. Humans with experimentally generated IAP have clearly visible reductions in urine production and glomerular filtration rate. When the IAP was raised by external compression, the directly measured renal vein pressure increased from 5.8 mmHg to 18.3 mmHg and the urine flow was reduced by half. Venous congestion is the primary hemodynamic mechanism causing the impairment of renal function in decompensated heart failure, and that AKI in heart failure-the so-called cardio renal syndrome-and hepatorenal syndrome with ascites are other conditions in which this may occur. In patients with cardio renal syndrome, it is a frequently observed occurrence that successful volume reduction, even in minor amounts, is followed by the restoration of kidney function. Moreover, despite worries about hypovolemia, some patients with hepatorenal syndrome have diuresis and an improvement in their azotemia after paracentesis. Future research should clarify the precise function of IAH in the hepatorenal syndrome.

Conclusion

IAH should be checked for in patients who develop AKI, especially in ICU settings, given its high prevalence (79%), along with other well-known nephrotoxic insults. In actual practice, nephrologists frequently fail to recognize how IAH contributes to AKI. Second, contrary to earlier research indicating that prior IAH predisposed critically ill patients to the development of AKI, this paper explained the link between AKI and IAH in a different way. IAH was not linked in this study to renal or patient outcomes in patients with preexisting AKI. This shows that volume retention over IAH in the wake of AKI. IAP would lose its predictive value.