Renal- and Pulmonary Function in Relation to Abdominal Hypertension After Abdominal Reconstruction: The REPARE-study

Introduction Incisional hernia is the most common long-term complication following abdominal surgery with an estimated incidence of 10.3% within 24 months. Large incisional hernias are associated with patient discomfort, reduced quality of life and are surgically challenging with increased risks of postoperative complications. Constant contraction of the lateral abdominal wall muscles may cause displacement of a greater proportion of the abdominal contents through the hernia defect, thereby reducing volume in the abdominal cavity (loss of domain).

Abdominal wall reconstruction in patients with loss of domain may lead to increased abdominal pressure with pressures persistently being measured above 12 mm Hg. Abdominal hypertension results in direct compression on intraabdominal vessels, which can result in oedema, reduced cardiac output and hypoxia due to hypoperfusion and reduced venous return. If intraabdominal pressures exceeds 20 mm Hg abdominal compartment syndrome occurs, leading to multiorgan failure.

Intraabdominal hypertension is additionally a known risk factor in development of acute kidney injury (AKI). A pooled incidence of AKI is estimated to 13.4% after major abdominal surgery. Development of AKI is independently recognized to be associated to increased mortality, length of stay and costs in hospitalized patients. Patients with AKI are at increased risk of developing acute coronary syndrome, heart failure and infection. Additionally, patients developing AKI after general surgery are estimated to have an eight-fold increased risk of 30-day mortality. Thus, treatment of AKI is vital, complex and time-consuming.

Intraabdominal pressures above 16 mm Hg lead to pulmonary parenchymal compression, resulting in alveolar atelectasis, pulmonary infection, decreased oxygen transport across the pulmonary capillary and decreased carbon dioxide excretion. Furthermore, elevated intraabdominal pressure to the diaphragmatic pleura may hamper diaphragmatic movement, resulting in restricted respiratory compliance with reduced forced vital capacity (FVC) but retained ratio of the forced expiratory volume within 1 second above FVC (FEV1/FVC). This condition is comparable with restrictive lung disorders.

It is possible to limit postoperative acute kidney injury and respiratory complications following intermittent intraabdominal hypertension using decompressive treatment and fluid therapy. Elevated intraabdominal pressure may ideally be limited with additional surgical procedures. However, there are few reports the relationship between abdominal wall reconstruction, intraabdominal hypertension, renal- and pulmonary function. In addition, predictive factors regarding patient characteristics, hernia dimensions and surgical procedures are still unclear. In the preoperative evaluation prior to abdominal wall reconstruction, it is important to know risks and consequences of elevated abdominal pressure. Furthermore, it is important to identify patients needing close monitoring, additional decompressing management or prophylactic surgical procedures in order to decrease costs, morbidity and mortality.