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  • Foto do escritorCarlos E Costa Almeida

Quaternary Abdominal Compartment Syndrome. What can we do better?

All surgeons must be able to treat abdominal wall hernias. Ventral hernias complicate 11-23% of all laparotomies (incisional hernias). The objective of a hernia repair is to regain a functional abdominal wall while avoiding recurrence. Most of the time restoring the rectus abdominal muscles to their normal position by closing the fascial plane and placing a prosthesis is possible without tension and without raising intra-abdominal pressure. However, sometimes this is not possible, and a quaternary abdominal compartment syndrome arises. Who are the patients with risk for a postoperative QACS?


 

QACS is usually transitory with medical treatment.

 

A recent paper published in “International Journal of Abdominal Wall and Hernia Surgery” by Catarina Quintela et al. (group of my colleague and friend Dr. Fernando Ferreira) from the Surgery Department of Matosinhos, Portugal, retrospectively analyses a group of 115 patients with complex ventral hernias to give us the incidence and risk factors for QACS following an abdominal wall reconstruction (AWR). According to these authors, the complex hernia is defined by several factors, namely size > 10 cm, enterocutaneous fistulae, multiple defects, history of mesh infection, and loss of domain (>20%). This last factor is especially important since it is associated with an abdominal compartment syndrome (ACS) following hernia repair and failure to reconstruct the abdominal wall. In this setting, according to Sabbagh et al. hernia sac volume (HSC)/ abdominal cavity volume (ACV) < 20% is an independent factor for a tension-free repair. ACS is an intra-abdominal pressure (IAP) > 20 mmHg associated with organ failure. If untreated it is fatal. Quaternary Abdominal Compartment Syndrome (QACS) is an ACS in the setting of an abdominal wall repair, with less inflammatory response and usually transitory with medical treatment. QACS can occur in up to 16% of patients, but in most cases, the pressure decreases to baseline levels within 24h or till postoperative day 2.


The authors treated 115 patients with complex abdominal hernias with different techniques. Of those 115 patients, 5 developed a QACS (4,3%) and all of them had a LOD>20%. However, 14 patients with a LOD>20% did not develop a QACS. Why was that so? The authors conducted a comparison between the group of patients with LOD>20% that developed ACS and the group with LOD>20% but without ACS. It would have been interesting to have a comparison between all patients including those without LOD>20%. It could probably give us some other factors implicated in the postoperative QACS. Probably this group of surgeons will do this analysis in a future publication.


 

PRP variation is a risk factor for QACS. These variations may change medical practice and surgeon decisions.

 

The two groups studied were identical according to demographics and treatment characteristics. Even the ASA scores, the hernia volume, and HSV/ACV were similar and without statistical significance. What the authors found was a statistical significance in the variation in the Peak Respiratory Pressure (PRP) before skin incision and after fascial closure between both groups (7,4 mmHg in the group with ACS vs 3,7 mmHg in the group without ACS). Catarina Quintela et al present this variation in PRP as a risk factor.


This group of Portuguese surgeons with great experience in complex hernia treatment proposes us a guideline based on PRP variations during abdominal closure:

  • PRP variation of 1-3 mmHg – the patient may go to the surgery ward.

  • PRP variation of 4-5 mmHg – Intermediate Care Unit surveillance.

  • PRP variation > 6 mmHg – Intensive Care Unit surveillance.

  • PRP variation > 10 mmHg – do not completely close fascial plane (bridging).


Four of the five patients who developed ACS had a QACS that was solved with medical treatment. However, one patient had progressive organ dysfunctions despite medical treatment and was submitted to a decompression laparotomy on day 3. Bowel ischemia was found, and the patient died. The authors made an honest and direct evaluation of this case. They raised the question of whether the laparotomy was too late since the patient had a sustained ACS for more than 48h. In that setting, the authors tell us that sustained intra-abdominal hypertension for at least 48h should raise the suspicion for severe organ dysfunction or an ACS resulting from postoperative complications. They conclude with the following idea: “In the absence of reversed IAP and maintained organ dysfunction, 24-48h after AWR surgery, our group strongly recommends reviewing the abdomen in the operating theatre.” This is paramount for clinical practice.


 

Sustained intra-abdominal hypertension for at least 48h should raise the suspicion for severe organ dysfunction.

 

Although taken from a small number of patients, I believe there are three important take-home messages from this paper:

  1. PRP variation 6 – 10 mmHg is a risk factor for ACS.

  2. PRP variation > 10 mmHg prevents fascial plane closure.

  3. Sustained ACS for 24-48 h indicates a decompressive laparotomy.


This paper comes from one of the most experienced surgery departments in the treatment of complex hernias. This group of surgeons uses different surgical techniques tailored to the patient. Additionally, they use a combination of preoperative techniques to increase abdominal compliance in patients with a high risk for QACS. This center treats the most complex cases, receives complex cases from hospitals around the country, and does not deny a challenge in hernia repair. They are a reference in abdominal wall reconstruction and all surgeons recognize their great work in this field.


Although this paper could have done a deeper analysis, the take-home messages are paramount for clinical practice. From now on I will always be looking for PRP variations in a complex hernia repair. I will support my practice in their recommendations, and I strongly recommend you do the same…


Link to article:


Dr. Carlos Eduardo Costa Almeida

General Surgeon


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