Compartment Syndrome in Extramusculoskeletal Sites

**33**

**Chapter 3**

**Abstract**

**1. Introduction**

Syndrome

*Abdulaziz Shaher*

Thoracoabdominal Compartment

As we advance our knowledge in understanding abdominal compartment syndrome, it is worth going back to revisit our basic embryologic development of the main determinant of the abdominal and thoracic cavities, i.e., the diaphragm. The abdominal and thoracic cavities used to be one cavity at some stage of the embryonic life — "intraembryonic coelom" — before the "septum transversum" diaphragmatic origin — divided it into two cavities. Therefore, if a condition develops that will impair the diaphragm from separating the cavities, leading to the possibility of pressures to transmit from one cavity to another, this becomes relevant as abdominal compartment syndrome. Diaphragmatic eventration is a congenital developmental defect in the muscular portion of the diaphragm with preserved attachments to the sternum, ribs, and dorsolumbar spine, leading to a semi-membranous diaphragm that anatomically separates the two cavities, but not physiologically. In the case of high abdominal pressure, the pressure will transmit to the thoracic cavity, causing derangement in both the anatomy and physiology. This

was reported and named "Thoracoabdominal Compartment Syndrome".

The diaphragm is formed from a number of composite origins in the embryo. The most important is the "septum transversum", which is a thick mass of cranial mesenchyme that gives rise to parts of the thoracic diaphragm. Without dwelling into more details, the septum transversum merges with mesoderm surrounding the esophagus, the growing pleura and peritoneum ('pleuroperitoneal folds') and the growing muscles of the abdominal wall. The septum transversum gives rise to the central tendon, while the pleuroperitoneal fold and abdominal wall

**Figures 1** and **2** show a brief introduction on the embryogenic development of

The incidence of fetal breathing increases at up to about 30 weeks of gestation.

After birth, the movement of the diaphragm accounts for the majority of the change in intrathoracic volume during quiet inspiration until it reaches 75% in adulthood. The diaphragmatic fibers attach around the inferior aspect of the

Once the fetal breathing movements are characterized by a fluent downward movement of the diaphragm, outward displacement of the abdomen and inward

**Keywords:** Thoracoabdominal Compartment Syndrome, eventration,

diaphragmatic paralysis, abdominal compartment syndrome

muscles give rise to the muscular posterolateral parts.

the diaphragm and the truncal cavities.

displacement of the thorax occur [1].

#### **Chapter 3**

## Thoracoabdominal Compartment Syndrome

*Abdulaziz Shaher*

#### **Abstract**

As we advance our knowledge in understanding abdominal compartment syndrome, it is worth going back to revisit our basic embryologic development of the main determinant of the abdominal and thoracic cavities, i.e., the diaphragm. The abdominal and thoracic cavities used to be one cavity at some stage of the embryonic life — "intraembryonic coelom" — before the "septum transversum" diaphragmatic origin — divided it into two cavities. Therefore, if a condition develops that will impair the diaphragm from separating the cavities, leading to the possibility of pressures to transmit from one cavity to another, this becomes relevant as abdominal compartment syndrome. Diaphragmatic eventration is a congenital developmental defect in the muscular portion of the diaphragm with preserved attachments to the sternum, ribs, and dorsolumbar spine, leading to a semi-membranous diaphragm that anatomically separates the two cavities, but not physiologically. In the case of high abdominal pressure, the pressure will transmit to the thoracic cavity, causing derangement in both the anatomy and physiology. This was reported and named "Thoracoabdominal Compartment Syndrome".

**Keywords:** Thoracoabdominal Compartment Syndrome, eventration, diaphragmatic paralysis, abdominal compartment syndrome

#### **1. Introduction**

The diaphragm is formed from a number of composite origins in the embryo. The most important is the "septum transversum", which is a thick mass of cranial mesenchyme that gives rise to parts of the thoracic diaphragm. Without dwelling into more details, the septum transversum merges with mesoderm surrounding the esophagus, the growing pleura and peritoneum ('pleuroperitoneal folds') and the growing muscles of the abdominal wall. The septum transversum gives rise to the central tendon, while the pleuroperitoneal fold and abdominal wall muscles give rise to the muscular posterolateral parts.

**Figures 1** and **2** show a brief introduction on the embryogenic development of the diaphragm and the truncal cavities.

The incidence of fetal breathing increases at up to about 30 weeks of gestation. Once the fetal breathing movements are characterized by a fluent downward movement of the diaphragm, outward displacement of the abdomen and inward displacement of the thorax occur [1].

After birth, the movement of the diaphragm accounts for the majority of the change in intrathoracic volume during quiet inspiration until it reaches 75% in adulthood. The diaphragmatic fibers attach around the inferior aspect of the

#### **Figure 1.**

*Sagittal View of the embryo at 8 weeks, showing the early development of septum transversum.*

**Figure 2.**

*Cross sectional view at the level of the septum transversum (Drawn by the author).*

thoracic cage, arching over the liver and contracting downward (inspiration) and relaxing upwards (expiration), exactly like a piston. The movement distance can be up to 7 cm with deep inspiration, and as a result, it is the main determinant of abdominal pressure, along with the abdominal wall muscles and fat [2].

For example, during vomiting and eructation, intra-abdominal pressure is increased by contraction of the costal fibers, but the crural fibers remain relaxed, allowing material to pass from the stomach into the esophagus [2].

The maximum transdiaphragmatic pressure (Pdimax) reflects the diaphragmatic function and force. To measure Pdimax (the difference between intra-abdominal and intrathoracic pressures), pressure transducers are placed through the external nares to the stomach (to approximate intra-abdominal pressure) and in the esophagus (to approximate intrathoracic pressure). However, this technique is not commonly utilized.

Measuring pleural pressure is essential in ventilated patients in the Intensive Care Unit who have Acute Respiratory Distress Syndrome (ARDS). Accurate measurement of the ventilator parameters is required to assure safe and effective ventilation for already injured lungs.

**35**

*Thoracoabdominal Compartment Syndrome DOI: http://dx.doi.org/10.5772/intechopen.97307*

The diaphragm behaves very much like the plunger of a syringe; inspiration contracts the diaphragmatic fibers, pulling the diaphragm downwards and decreasing the pressure (negative value below atmospheric pressure) in the thoracic cavity.

*Creating the negative pressure by syringe plunger simulating the action of the diaphragm.*

Diaphragmatic eventration is an uncommon condition that is usually incidentally discovered. The classical patient presentation is an incidental elevation hemidiaphragm on chest X-ray. The most important and common imitator of eventration is diaphragmatic paralysis, which has a different etiology and histopathological picture; however, the clinical presentation in adults is similar and these two condi-

True diaphragmatic eventration is a congenital developmental defect in the muscular portion of the diaphragm with preserved attachments to the sternum, ribs, and dorsolumbar spine, maintaining the anatomical separation of the two cavities. It is rare, with an incidence of <0.05%, more common in males, and more

In contrast to true diaphragmatic eventration, diaphragmatic paralysis is a more common, acquired condition that generally results from traumatic or iatrogenic

There have been multiple descriptions of associations of diaphragmatic eventration with other congenital abnormalities like dextrocardia, intestinal malrotation

Patients who have diaphragmatic eventration may not have the normal caudal movement of the diaphragm necessary for appropriate inspiration. As a result, diaphragmatic movement can be diminished, absent, or even paradoxic.

An imaging study required to diagnose eventration besides chest X-ray is fluoroscopy. Specifically, a fluoroscopic sniff test is indicated. During this test, the diaphragm normally moves downward during sniffing; however, in paralysis or

Diaphragmatic eventration can be bilateral, unilateral, or localized to a certain anatomical zone of the diaphragm (anterior, posterolateral, or medial) [3]. Microscopically, the eventrated portion has disseminated fibroelastic tissues at the expense of myocytes [4]. Patients with diaphragmatic paralysis have a normal

This activity allows air to flow to the chest (**Figure 3**).

tions are sometimes very difficult to distinguish from each other.

injury to the phrenic nerve or as a result of tumor invasion.

amount of muscle fibers, but the main issue is their atrophy.

**2. Diaphragmatic eventration**

**Figure 3.**

often affects the left hemidiaphragm [3].

and renal agenesis [5].

eventration, it moves upwards.

*Thoracoabdominal Compartment Syndrome DOI: http://dx.doi.org/10.5772/intechopen.97307*

*A Comprehensive Review of Compartment Syndrome*

thoracic cage, arching over the liver and contracting downward (inspiration) and relaxing upwards (expiration), exactly like a piston. The movement distance can be up to 7 cm with deep inspiration, and as a result, it is the main determinant of

For example, during vomiting and eructation, intra-abdominal pressure is increased by contraction of the costal fibers, but the crural fibers remain relaxed,

The maximum transdiaphragmatic pressure (Pdimax) reflects the diaphragmatic function and force. To measure Pdimax (the difference between intra-abdominal and intrathoracic pressures), pressure transducers are placed through the external nares to the stomach (to approximate intra-abdominal pressure) and in the esophagus (to approximate intrathoracic pressure). However, this technique is not commonly utilized. Measuring pleural pressure is essential in ventilated patients in the Intensive Care Unit who have Acute Respiratory Distress Syndrome (ARDS). Accurate measurement of the ventilator parameters is required to assure safe and effective

abdominal pressure, along with the abdominal wall muscles and fat [2].

*Sagittal View of the embryo at 8 weeks, showing the early development of septum transversum.*

allowing material to pass from the stomach into the esophagus [2].

*Cross sectional view at the level of the septum transversum (Drawn by the author).*

**34**

**Figure 1.**

**Figure 2.**

ventilation for already injured lungs.

**Figure 3.** *Creating the negative pressure by syringe plunger simulating the action of the diaphragm.*

The diaphragm behaves very much like the plunger of a syringe; inspiration contracts the diaphragmatic fibers, pulling the diaphragm downwards and decreasing the pressure (negative value below atmospheric pressure) in the thoracic cavity. This activity allows air to flow to the chest (**Figure 3**).

#### **2. Diaphragmatic eventration**

Diaphragmatic eventration is an uncommon condition that is usually incidentally discovered. The classical patient presentation is an incidental elevation hemidiaphragm on chest X-ray. The most important and common imitator of eventration is diaphragmatic paralysis, which has a different etiology and histopathological picture; however, the clinical presentation in adults is similar and these two conditions are sometimes very difficult to distinguish from each other.

True diaphragmatic eventration is a congenital developmental defect in the muscular portion of the diaphragm with preserved attachments to the sternum, ribs, and dorsolumbar spine, maintaining the anatomical separation of the two cavities. It is rare, with an incidence of <0.05%, more common in males, and more often affects the left hemidiaphragm [3].

In contrast to true diaphragmatic eventration, diaphragmatic paralysis is a more common, acquired condition that generally results from traumatic or iatrogenic injury to the phrenic nerve or as a result of tumor invasion.

Diaphragmatic eventration can be bilateral, unilateral, or localized to a certain anatomical zone of the diaphragm (anterior, posterolateral, or medial) [3]. Microscopically, the eventrated portion has disseminated fibroelastic tissues at the expense of myocytes [4]. Patients with diaphragmatic paralysis have a normal amount of muscle fibers, but the main issue is their atrophy.

There have been multiple descriptions of associations of diaphragmatic eventration with other congenital abnormalities like dextrocardia, intestinal malrotation and renal agenesis [5].

Patients who have diaphragmatic eventration may not have the normal caudal movement of the diaphragm necessary for appropriate inspiration. As a result, diaphragmatic movement can be diminished, absent, or even paradoxic.

An imaging study required to diagnose eventration besides chest X-ray is fluoroscopy. Specifically, a fluoroscopic sniff test is indicated. During this test, the diaphragm normally moves downward during sniffing; however, in paralysis or eventration, it moves upwards.

The main treatment for eventrated diaphragm is diaphragmatic plication through various either open or minimally invasive. While diaphragmatic pacing is mainly quadriplegics with diaphragmatic paralysis.

#### **3. Syndromes with increased truncal compartmental pressures**

#### **3.1 Tension pneumothorax**

Tension pneumothorax is a well-known pathophysiological state in which the thoracic cavity develops very high pressure as a result of accumulated air in the pleural cavity, displacing the mediastinum and preventing the preload from draining back to the right side of the heart. This can affect left-sided heart afterload and ultimately lead to hemodynamic compromise.

The most common mechanism is traumatic lung injury, or iatrogenic injury due central venous cannulation. According to the American Trauma Life Support manual [6], the management of such a life-threatening injury is immediate pleural decompression. This can be done in many ways depending on the physician's experience; either by using a needle, finger, or intercostal pleural drainage tube, as long it is done promptly and safely, to not cause any further injuries. Once the drainage is done, the tension pneumothorax will turn into a simple pneumothorax and the management of a simple pneumothorax is beyond the scope of this book.

#### **3.2 Tension pneumoperitoneum and ascites (Hydroperitoneum)**

Tension pneumoperitoneum is a much less known pathology compared to tension pneumothorax [7]. In this condition, air or fluid accumulates in the peritoneal cavity, leading to respiratory and hemodynamic compromise. The most common cause of pneumoperitoneum is pathological perforated viscus (e.g., perforated duodenal ulcers, perforated colonic mass). Peritoneal fluid can increase in the abdomen in large amounts, reaching 10–15 L (ascites or hydroperitoneum) due to advanced liver cirrhosis, or it can be malignant ascites secondary to advanced metastatic abdominal malignancy. Both of these conditions can lead to increases in abdominal pressure and compromise of respiratory function.

As a result of increasing cases of liver cirrhosis worldwide, the incidence of cirrhosis-induced ascites is common, and the effect of massive ascites on respiratory function and thoracoabdominal movement (cirtometry) have been studied before and after paracentesis [8]. After paracentesis, minute ventilation, tidal volume, and dyspnea scale were better and a significant p-value, compared to before the procedure, indicated that abdominal pressure will still transmit to the pleural pressure, even in the presence of a normal diaphragm.

The term "tension" has been linked to hemodynamic compromise and shock. Therefore, for ascites to cause respiratory embarrassment without shock would not make it "tension hydroperitoneum" in the conventional wisdom. Most of the cases of hydroperitoneum and respiratory compromise reported in the literature occurred in the pediatric age group, and due to delayed perforated viscus, respiratory compromise can be explained due to the septic inflammatory response, rather than the mere machinal displacement of the diaphragm and pressure transmission [9].

The pathophysiological cascade in tension pneumoperitoneum happens at the beginning, when abdominal pressure exceeds venous pressure and the lower venous return cannot be drained back to the right side of the heart. While the upper body venous return is not enough to sustain the preload due to severe hypovolemia, this results in hemodynamic compromise, a condition termed "tension

**37**

described it [11].

**Figure 4.**

phragmatic eventration.

**4. Conclusion**

*Thoracoabdominal Compartment Syndrome DOI: http://dx.doi.org/10.5772/intechopen.97307*

thoracoabdominal compartment syndrome.

able diaphragm, as depicted in **Figure 4**.

**3.3 Thoracoabdominal compartment syndrome**

*Thoracoabdominal Compartment syndrome chest radiograph [11].*

and there are a few existing case reports that describe it.

pneumoperitoneum". It is imperative to keep in mind that the thoracic cavity pressure should be normal because the barrier (diaphragm) should be functioning well. What would happen if the abdominal pressure gets very high while the diaphragm is diseased and cannot prevent the pressure from transmitting to the thoracic cavity, as in diaphragmatic eventration? This condition is known as

Thoracoabdominal compartment syndrome is a recently described syndrome,

The first possible description of such a pathophysiological phenomenon was given by Haldane et al. [10], who reported a case of tension pneumoperitoneum causing hemodynamic compromise. These authors described the reason as tension pneumothorax despite the lack of air in the pleural cavity. Therefore, the exact pathophysiological association of the hemodynamic compromise, as a result of transmitted pressure from the abdominal cavity to the pleural cavity through the intact (but pliable) diaphragm, was not coined as a syndrome until Shaher et al.

In the former report, the case was of a perforated gastric ulcer that caused tension pneumoperitoneum. The association of diaphragmatic eventration allowed an

The reasons for elevated abdominal pressure in this case was a significantly dilated megacolon with compromise of the thoracic cavity pressure due to the pli-

A postmortem case report was recently published [12], reporting a thoracoabdominal compartment syndrome in a 65-year-old male, with the colon in right hemithorax with near total lung collapse, mediastinal shift and associated dia-

Thoracoabdominal Syndrome is a rare complication of diaphragmatic eventration, usually present with hemodynamic compromise as a result of transmitted pressure from the abdominal cavity to the pleural space. Moreover, it is usually

increase in abdominal pressure to be transmitted to the thoracic cavity.

*Thoracoabdominal Compartment Syndrome DOI: http://dx.doi.org/10.5772/intechopen.97307*

*A Comprehensive Review of Compartment Syndrome*

**3.1 Tension pneumothorax**

mainly quadriplegics with diaphragmatic paralysis.

ultimately lead to hemodynamic compromise.

pressure and compromise of respiratory function.

pressure, even in the presence of a normal diaphragm.

The main treatment for eventrated diaphragm is diaphragmatic plication through various either open or minimally invasive. While diaphragmatic pacing is

Tension pneumothorax is a well-known pathophysiological state in which the thoracic cavity develops very high pressure as a result of accumulated air in the pleural cavity, displacing the mediastinum and preventing the preload from draining back to the right side of the heart. This can affect left-sided heart afterload and

The most common mechanism is traumatic lung injury, or iatrogenic injury due central venous cannulation. According to the American Trauma Life Support manual [6], the management of such a life-threatening injury is immediate pleural decompression. This can be done in many ways depending on the physician's experience; either by using a needle, finger, or intercostal pleural drainage tube, as long it is done promptly and safely, to not cause any further injuries. Once the drainage is done, the tension pneumothorax will turn into a simple pneumothorax and the

Tension pneumoperitoneum is a much less known pathology compared to tension pneumothorax [7]. In this condition, air or fluid accumulates in the peritoneal cavity, leading to respiratory and hemodynamic compromise. The most common cause of pneumoperitoneum is pathological perforated viscus (e.g., perforated duodenal ulcers, perforated colonic mass). Peritoneal fluid can increase in the abdomen in large amounts, reaching 10–15 L (ascites or hydroperitoneum) due to advanced liver cirrhosis, or it can be malignant ascites secondary to advanced metastatic abdominal malignancy. Both of these conditions can lead to increases in abdominal

As a result of increasing cases of liver cirrhosis worldwide, the incidence of cirrhosis-induced ascites is common, and the effect of massive ascites on respiratory function and thoracoabdominal movement (cirtometry) have been studied before and after paracentesis [8]. After paracentesis, minute ventilation, tidal volume, and dyspnea scale were better and a significant p-value, compared to before the procedure, indicated that abdominal pressure will still transmit to the pleural

The term "tension" has been linked to hemodynamic compromise and shock. Therefore, for ascites to cause respiratory embarrassment without shock would not make it "tension hydroperitoneum" in the conventional wisdom. Most of the cases of hydroperitoneum and respiratory compromise reported in the literature occurred in the pediatric age group, and due to delayed perforated viscus, respiratory compromise can be explained due to the septic inflammatory response, rather than the mere machinal displacement of the diaphragm and pressure transmission [9]. The pathophysiological cascade in tension pneumoperitoneum happens at the beginning, when abdominal pressure exceeds venous pressure and the lower venous return cannot be drained back to the right side of the heart. While the upper body venous return is not enough to sustain the preload due to severe hypovolemia, this results in hemodynamic compromise, a condition termed "tension

management of a simple pneumothorax is beyond the scope of this book.

**3.2 Tension pneumoperitoneum and ascites (Hydroperitoneum)**

**3. Syndromes with increased truncal compartmental pressures**

**36**

**Figure 4.** *Thoracoabdominal Compartment syndrome chest radiograph [11].*

pneumoperitoneum". It is imperative to keep in mind that the thoracic cavity pressure should be normal because the barrier (diaphragm) should be functioning well.

What would happen if the abdominal pressure gets very high while the diaphragm is diseased and cannot prevent the pressure from transmitting to the thoracic cavity, as in diaphragmatic eventration? This condition is known as thoracoabdominal compartment syndrome.

#### **3.3 Thoracoabdominal compartment syndrome**

Thoracoabdominal compartment syndrome is a recently described syndrome, and there are a few existing case reports that describe it.

The first possible description of such a pathophysiological phenomenon was given by Haldane et al. [10], who reported a case of tension pneumoperitoneum causing hemodynamic compromise. These authors described the reason as tension pneumothorax despite the lack of air in the pleural cavity. Therefore, the exact pathophysiological association of the hemodynamic compromise, as a result of transmitted pressure from the abdominal cavity to the pleural cavity through the intact (but pliable) diaphragm, was not coined as a syndrome until Shaher et al. described it [11].

In the former report, the case was of a perforated gastric ulcer that caused tension pneumoperitoneum. The association of diaphragmatic eventration allowed an increase in abdominal pressure to be transmitted to the thoracic cavity.

The reasons for elevated abdominal pressure in this case was a significantly dilated megacolon with compromise of the thoracic cavity pressure due to the pliable diaphragm, as depicted in **Figure 4**.

A postmortem case report was recently published [12], reporting a thoracoabdominal compartment syndrome in a 65-year-old male, with the colon in right hemithorax with near total lung collapse, mediastinal shift and associated diaphragmatic eventration.

#### **4. Conclusion**

Thoracoabdominal Syndrome is a rare complication of diaphragmatic eventration, usually present with hemodynamic compromise as a result of transmitted pressure from the abdominal cavity to the pleural space. Moreover, it is usually

associated with multiple congenital abnormalities. Most of the cases reported presented late due to the inability to diagnose early, leading to a very high mortality rate. Diaphragmatic eventration should be surgically repaired through plication as soon as feasible to maintain the physiological function of the diaphragm and to prevent such a syndrome from developing.

### **Conflict of interest**

The author declares no conflicts of interest.

### **Author details**

Abdulaziz Shaher Armed Forces Hospital – Southern Region, Abha, Kingdom of Saudi Arabia

\*Address all correspondence to: dr.shaher@gmail.com

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

**39**

*Thoracoabdominal Compartment Syndrome DOI: http://dx.doi.org/10.5772/intechopen.97307*

[1] Dewbury K. Ultrasound in obstetrics and gynaecology. London: Churchill

Reports. 2012;2012(apr04 1): bcr0120125512-bcr0120125512.

[11] Shaher A, Alqahtani AM, Sinnah KN, Al Bakheet SM.

Rep. 2019;12(6):e229475.

2020;10(2):e2020155.

Diaphragmatic eventration unusual presentation: A novel thoracoabdominal compartment syndrome case. BMJ Case

[12] Omenai SA, Adebowale EO, Nwanji ID. Thoracoabdominal compartment syndrome complicating right-sided diaphragmatic eventration with co-existent unilateral renal agenesis. Autops Case Rep [Internet].

medical physiology. New York: McGraw-

[3] Groth S, Andrade R. Diaphragmatic Eventration. Thoracic Surgery Clinics.

[4] Shah-Mirany J. Eventration of the Diaphragm. Archives of Surgery.

[5] Sharma S, Debnath P, Tripathi R. Bilateral eventration of the diaphragm with malrotation and unilateral renal agenesis. The Indian Journal of Pediatrics. 2007;74(5):503-504.

[6] Advanced Trauma Life Support. München: Elsevier, Urban et

[7] De Smet R, De Paepe P, Buylaert W, Hachimi Idrissi S. Spontaneous tension pneumoperitoneum presenting as an out of hospital cardiac arrest: A case report and review of the literature. Acta Clinica Belgica. 2016;71(4):258-262.

[8] Witter V, Lima R, Maia M, Duarte H, Paro F. Respiratory and symptomatic impact of ascites relief by paracentesis in patients with hepatic cirrhosis. Arquivos de Gastroenterologia.

[9] Im S, Lim G, Hahn S. Spontaneous gastric perforation in a neonate presenting with massive

hydroperitoneum. Pediatric Radiology.

[10] Akoglu H, Coban E, Guneysel O.

Tension pneumoperitoneum complicated with tension pneumothorax in a patient with diaphragmatic eventration. Case

[2] Barrett K. Ganong's review of

**References**

Livingstone; 2001.

Hill Education; 2019.

2009;19(4):511-519.

1968;96(5):844.

Fischer; 2015.

2020;57(1):64-68.

2005;35(12):1212-1214.

*Thoracoabdominal Compartment Syndrome DOI: http://dx.doi.org/10.5772/intechopen.97307*

#### **References**

*A Comprehensive Review of Compartment Syndrome*

prevent such a syndrome from developing.

The author declares no conflicts of interest.

**Conflict of interest**

associated with multiple congenital abnormalities. Most of the cases reported presented late due to the inability to diagnose early, leading to a very high mortality rate. Diaphragmatic eventration should be surgically repaired through plication as soon as feasible to maintain the physiological function of the diaphragm and to

**38**

**Author details**

Abdulaziz Shaher

Armed Forces Hospital – Southern Region, Abha, Kingdom of Saudi Arabia

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

\*Address all correspondence to: dr.shaher@gmail.com

provided the original work is properly cited.

[1] Dewbury K. Ultrasound in obstetrics and gynaecology. London: Churchill Livingstone; 2001.

[2] Barrett K. Ganong's review of medical physiology. New York: McGraw-Hill Education; 2019.

[3] Groth S, Andrade R. Diaphragmatic Eventration. Thoracic Surgery Clinics. 2009;19(4):511-519.

[4] Shah-Mirany J. Eventration of the Diaphragm. Archives of Surgery. 1968;96(5):844.

[5] Sharma S, Debnath P, Tripathi R. Bilateral eventration of the diaphragm with malrotation and unilateral renal agenesis. The Indian Journal of Pediatrics. 2007;74(5):503-504.

[6] Advanced Trauma Life Support. München: Elsevier, Urban et Fischer; 2015.

[7] De Smet R, De Paepe P, Buylaert W, Hachimi Idrissi S. Spontaneous tension pneumoperitoneum presenting as an out of hospital cardiac arrest: A case report and review of the literature. Acta Clinica Belgica. 2016;71(4):258-262.

[8] Witter V, Lima R, Maia M, Duarte H, Paro F. Respiratory and symptomatic impact of ascites relief by paracentesis in patients with hepatic cirrhosis. Arquivos de Gastroenterologia. 2020;57(1):64-68.

[9] Im S, Lim G, Hahn S. Spontaneous gastric perforation in a neonate presenting with massive hydroperitoneum. Pediatric Radiology. 2005;35(12):1212-1214.

[10] Akoglu H, Coban E, Guneysel O. Tension pneumoperitoneum complicated with tension pneumothorax in a patient with diaphragmatic eventration. Case

Reports. 2012;2012(apr04 1): bcr0120125512-bcr0120125512.

[11] Shaher A, Alqahtani AM, Sinnah KN, Al Bakheet SM. Diaphragmatic eventration unusual presentation: A novel thoracoabdominal compartment syndrome case. BMJ Case Rep. 2019;12(6):e229475.

[12] Omenai SA, Adebowale EO, Nwanji ID. Thoracoabdominal compartment syndrome complicating right-sided diaphragmatic eventration with co-existent unilateral renal agenesis. Autops Case Rep [Internet]. 2020;10(2):e2020155.

**41**

**Chapter 4**

**Abstract**

**1. Introduction**

Syndrome

Abdominal Compartment

between physicians, intensivists, and surgeons.

intensive care unit, open abdomen, multiple organ failure

1.02–1.04) are risk factors for IAH or ACS occurrence [5].

*Kuo-Ching Yuan, Chih-Yuan Fu and Hung-Chang Huang*

Abdominal compartment syndrome (ACS) is a progressively increasing intraabdominal pressure of more than 20 mm Hg with new-onset thoracoabdominal organ dysfunction. Primary abdominal compartment syndrome means increased pressure due to injury or disease in the abdominopelvic region. Secondary abdominal compartment syndrome means disease originating from outside the abdomen, such as significant burns or sepsis. As the pressure inside the abdomen increases, organ failure occurs, and the kidneys and lungs are the most frequently affected. Managements of ACS are multidisciplinary. Conservative treatment with adequate volume supple and with aggressive hemodynamic support is the first step. Decompressive laparotomy with open abdomen is indicated when ACS is refractory to conservative treatment and complicated with multiple organ failure. ACS can result in a high mortality rate, and successful treatment requires cooperation

**Keywords:** abdominal compartment syndrome, intraabdominal pressure,

A compartment syndrome happened when the pressure in a closed anatomic space increases to a level that compromises surrounding tissue viability. In the abdominal space with elevated pressure, the impact to the end-organ function within and outside the abdominal cavity can be lethal. The abdominal compartment syndrome (ACS) is not a solo disease; it can have many causes and develop many disease processes. ACS is a highly under-recognized but very lethal entity [1–3]. If inadequately treated, the patient may rapidly proceed into multiple organ failure, and patient mortality. In a systemic review, the reported prevalence of Intra-Abdominal Hypertension (IAH) and ACS is about 30% to 49% [4]. The prevalence is exceptionally high in pancreatitis (57%), orthotopic liver transplantation (7%), and abdominal aorta surgery (5%) [5]. It is reported that Body mass index (odds ratio 1.08, 95% confidence interval 1.03–1.13), mechanical ventilation (OR 3.52, 95% CI 2.08–5.96), and APACHE IV score at ICU admission (OR 1.03, 95% CI

ACS has received heightened attention in critical care medicine, and the prevention of IAH and ACS are of tremendous importance in the care of critically ill, surgical, and trauma patients. The etiology of ACS is various and can be complicated. Diagnosis is made by clinical presentations and intraabdominal pressure (IAP) measurements. Serial or continuous IAP measurements are essential to the timely

**Chapter 4**

## Abdominal Compartment Syndrome

*Kuo-Ching Yuan, Chih-Yuan Fu and Hung-Chang Huang*

#### **Abstract**

Abdominal compartment syndrome (ACS) is a progressively increasing intraabdominal pressure of more than 20 mm Hg with new-onset thoracoabdominal organ dysfunction. Primary abdominal compartment syndrome means increased pressure due to injury or disease in the abdominopelvic region. Secondary abdominal compartment syndrome means disease originating from outside the abdomen, such as significant burns or sepsis. As the pressure inside the abdomen increases, organ failure occurs, and the kidneys and lungs are the most frequently affected. Managements of ACS are multidisciplinary. Conservative treatment with adequate volume supple and with aggressive hemodynamic support is the first step. Decompressive laparotomy with open abdomen is indicated when ACS is refractory to conservative treatment and complicated with multiple organ failure. ACS can result in a high mortality rate, and successful treatment requires cooperation between physicians, intensivists, and surgeons.

**Keywords:** abdominal compartment syndrome, intraabdominal pressure, intensive care unit, open abdomen, multiple organ failure

#### **1. Introduction**

A compartment syndrome happened when the pressure in a closed anatomic space increases to a level that compromises surrounding tissue viability. In the abdominal space with elevated pressure, the impact to the end-organ function within and outside the abdominal cavity can be lethal. The abdominal compartment syndrome (ACS) is not a solo disease; it can have many causes and develop many disease processes. ACS is a highly under-recognized but very lethal entity [1–3]. If inadequately treated, the patient may rapidly proceed into multiple organ failure, and patient mortality. In a systemic review, the reported prevalence of Intra-Abdominal Hypertension (IAH) and ACS is about 30% to 49% [4]. The prevalence is exceptionally high in pancreatitis (57%), orthotopic liver transplantation (7%), and abdominal aorta surgery (5%) [5]. It is reported that Body mass index (odds ratio 1.08, 95% confidence interval 1.03–1.13), mechanical ventilation (OR 3.52, 95% CI 2.08–5.96), and APACHE IV score at ICU admission (OR 1.03, 95% CI 1.02–1.04) are risk factors for IAH or ACS occurrence [5].

ACS has received heightened attention in critical care medicine, and the prevention of IAH and ACS are of tremendous importance in the care of critically ill, surgical, and trauma patients. The etiology of ACS is various and can be complicated. Diagnosis is made by clinical presentations and intraabdominal pressure (IAP) measurements. Serial or continuous IAP measurements are essential to the timely

diagnosis, proper management, and good recovery in these patients. Urinary bladder pressure measurement is an excellent method to estimate for IAP as it is easily performed in all patients at risk for significant elevations in IAP [6–8]. A pressure more than 12 mmHg is considered IAH, and if the IAP is higher than 20 mmHg with new-onset organ failure, it is ACS. Medical treatment is usually adopted first, and decompressive laparotomy is indicated if medical treatment failed. The development of ACS can profoundly impact patient recovery and outcome. The rate of renal replacement therapy was much higher in ACS (38.9%) than in patients with normal intra-abdominal pressure (1.2%). Both intensive care and 90-day mortality were also significantly higher in ACS (16.7% and 38.9%) than regular IAP patients (1.2% and 7.1%) [5].

#### **2. Pathophysiology**

The abdomen is in anatomy a closed space with surrounding structures either rigid (costal arch, spine, and pelvis) or elastic (the muscular wall and diaphragm). The elasticity of the walls and the parenchymal character of abdominal contents determine the pressure inside the abdomen. Most of the abdomen contents are essentially non-compressive and behavior as fluid by Pascal's law; the pressure detected at any point can represent the pressure within the whole abdomen [9]. IAP is literally a status with steady pressure within a conceal cavity, and the reference range is approximately 5–7 mmHg and is increasing to 12–15 mmHg postoperatively. Diseases associated with a chronic elevated IAP include ascites after liver cirrhosis, ovarian tumors, chronic ambulatory peritoneal dialysis (CAPD), and obesity.

IAP that is more than 12 mm Hg is intra-abdominal hypertension (IAH) and has four grades [1]:


The WSACS proposed the following classification for IAH [1]: Primary IAH results from injury or disease from the abdominal-pelvis requiring surgical or other intervention. Secondary IAH is the result due to disease not associated with the abdominopelvic disease. Recurrent IAH is the condition redeveloped following previous management of primary or secondary IAH/ACS.

Abdominal compartment syndrome is defined as a sustained IAP of at least 20 mm Hg associated with new organ dysfunction/failure. It should be noted that the IAP ranges associated with these grades have been revised downward in recent years as the detrimental impact of elevated IAP on end-organ function has been recognized. Physiologically, IAP increases with inspiration (diaphragmatic contraction) and decreases with expiration (diaphragmatic relaxation). Pathophysiology of ACS is multifactorial. With the increasing of pressures inside abdomen, compression of the arterial inflow at first and then compression of the venous outflow of the visceral organs can lead to organ hypoperfusion. Compression of the blood vessels also damage heart function. Besides, the diaphragm's upward displacement can lead to hypoventilation, respiratory rate changes, and eventually hypoxia [10]. This complex physiological

**43**

*Abdominal Compartment Syndrome*

**Figure 1.**

*DOI: http://dx.doi.org/10.5772/intechopen.96972*

*Vicious cycle of elevated intraabdominal pressure.*

change regarding the organ system mentioned above can be applied to all body systems concerning impact caused by ACS. Elevated IAP can lead to a vicious cycle and result in multiple organ failure (**Figure 1**). Elevated intra-abdominal pressured causes IVC compression and reduced venous return as venous return reduced, so as cardiac output reduced. Therefore, many organs suffered from low perfusion and presented with organ dysfunction as clinical signs. Aggressive fluid resuscitation may be prescribed, which leads to progressive tissue edema with increasing intraabdominal pressure. Abdominal perfusion pressure (APP), calculated as MAP minus IAP, has been proposed as a predictor of visceral perfusion and a potential endpoint for resuscitation [11, 12]. By considering both arterial inflow (MAP) and restrictions to venous outflow (IAP), APP has been demonstrated as a parameter predicting patient survival from IAH and ACS. Studies have also identified that APP is also superior to other standard resuscitation endpoints, including arterial pH, base deficit, arterial lactate, and hourly urinary output [11]. A target APP of more than 60 mmHg is

Increased respiration rate is usually the first detected clinical sign at the initial development of ACS, even with ventilator and sedation. Although tachypnea may have resulted from hypovolemia or hemorrhage, the whole clinical presentation is not compatible with low volume status since CVP is usually high or positive fluid balance. Application of bedside echo and thorough physical exam can often detect massive ascites or hemoperitoneum. ACS is usually the consequence or complication of a particular medical disease or medical treatment. The most common cause of ACS is major abdominal trauma, abdominal sepsis, and pancreatitis. The medical treatments that can cause ACS are massive transfusion, intraperitoneal packing, and intra-aorta stent for ruptured abdominal aorta aneurysm. Primary symptoms of ACS include abdominal pain and distention. Secondary signs of ACS include respiratory depression, decreased cardiac output, visceral ischemia due to decreased perfusion, and renal failure. This condition can be fatal if not properly treated. It becomes increasingly more critical for the overall prognosis that ACS is recognized and treated timely. Detection of ACS can be interfered with by other clinical conditions. A blunt abdominal trauma patient may have active upper gastrointestinal bleeding due to stress ulcers and unstable vital signs. Hypovolemia and inadequate fluid resuscitation may be the first impression as the cause of shock. However, CT may also reveal massive hemoperitoneum compressing intra-abdominal contents leading to ACS. This kind of patient may present with hemodynamic

positively correlated with better survival from IAH and ACS [11].

• Definition: APP = MAP – IAP.

instability as the first clinical indicator of ACS.

**3. Clinical manifestation**

#### *Abdominal Compartment Syndrome DOI: http://dx.doi.org/10.5772/intechopen.96972*

#### **Figure 1.**

*A Comprehensive Review of Compartment Syndrome*

(1.2% and 7.1%) [5].

**2. Pathophysiology**

obesity.

four grades [1]:

• grade I: 12–15 mmHg

• grade II: 16–20 mmHg

• grade III: 21–25 mmHg

• grade IV: > 25 mm Hg

diagnosis, proper management, and good recovery in these patients. Urinary bladder pressure measurement is an excellent method to estimate for IAP as it is easily performed in all patients at risk for significant elevations in IAP [6–8]. A pressure more than 12 mmHg is considered IAH, and if the IAP is higher than 20 mmHg with new-onset organ failure, it is ACS. Medical treatment is usually adopted first, and decompressive laparotomy is indicated if medical treatment failed. The development of ACS can profoundly impact patient recovery and outcome. The rate of renal replacement therapy was much higher in ACS (38.9%) than in patients with normal intra-abdominal pressure (1.2%). Both intensive care and 90-day mortality were also significantly higher in ACS (16.7% and 38.9%) than regular IAP patients

The abdomen is in anatomy a closed space with surrounding structures either rigid (costal arch, spine, and pelvis) or elastic (the muscular wall and diaphragm). The elasticity of the walls and the parenchymal character of abdominal contents determine the pressure inside the abdomen. Most of the abdomen contents are essentially non-compressive and behavior as fluid by Pascal's law; the pressure detected at any point can represent the pressure within the whole abdomen [9]. IAP is literally a status with steady pressure within a conceal cavity, and the reference range is approximately 5–7 mmHg and is increasing to 12–15 mmHg postoperatively. Diseases associated with a chronic elevated IAP include ascites after liver cirrhosis, ovarian tumors, chronic ambulatory peritoneal dialysis (CAPD), and

IAP that is more than 12 mm Hg is intra-abdominal hypertension (IAH) and has

The WSACS proposed the following classification for IAH [1]: Primary IAH results from injury or disease from the abdominal-pelvis requiring surgical or other intervention. Secondary IAH is the result due to disease not associated with the abdominopelvic disease. Recurrent IAH is the condition redeveloped following

Abdominal compartment syndrome is defined as a sustained IAP of at least 20 mm

Hg associated with new organ dysfunction/failure. It should be noted that the IAP ranges associated with these grades have been revised downward in recent years as the detrimental impact of elevated IAP on end-organ function has been recognized. Physiologically, IAP increases with inspiration (diaphragmatic contraction) and decreases with expiration (diaphragmatic relaxation). Pathophysiology of ACS is multifactorial. With the increasing of pressures inside abdomen, compression of the arterial inflow at first and then compression of the venous outflow of the visceral organs can lead to organ hypoperfusion. Compression of the blood vessels also damage heart function. Besides, the diaphragm's upward displacement can lead to hypoventilation, respiratory rate changes, and eventually hypoxia [10]. This complex physiological

previous management of primary or secondary IAH/ACS.

**42**

*Vicious cycle of elevated intraabdominal pressure.*

change regarding the organ system mentioned above can be applied to all body systems concerning impact caused by ACS. Elevated IAP can lead to a vicious cycle and result in multiple organ failure (**Figure 1**). Elevated intra-abdominal pressured causes IVC compression and reduced venous return as venous return reduced, so as cardiac output reduced. Therefore, many organs suffered from low perfusion and presented with organ dysfunction as clinical signs. Aggressive fluid resuscitation may be prescribed, which leads to progressive tissue edema with increasing intraabdominal pressure.

Abdominal perfusion pressure (APP), calculated as MAP minus IAP, has been proposed as a predictor of visceral perfusion and a potential endpoint for resuscitation [11, 12]. By considering both arterial inflow (MAP) and restrictions to venous outflow (IAP), APP has been demonstrated as a parameter predicting patient survival from IAH and ACS. Studies have also identified that APP is also superior to other standard resuscitation endpoints, including arterial pH, base deficit, arterial lactate, and hourly urinary output [11]. A target APP of more than 60 mmHg is positively correlated with better survival from IAH and ACS [11].

• Definition: APP = MAP – IAP.

#### **3. Clinical manifestation**

Increased respiration rate is usually the first detected clinical sign at the initial development of ACS, even with ventilator and sedation. Although tachypnea may have resulted from hypovolemia or hemorrhage, the whole clinical presentation is not compatible with low volume status since CVP is usually high or positive fluid balance. Application of bedside echo and thorough physical exam can often detect massive ascites or hemoperitoneum. ACS is usually the consequence or complication of a particular medical disease or medical treatment. The most common cause of ACS is major abdominal trauma, abdominal sepsis, and pancreatitis. The medical treatments that can cause ACS are massive transfusion, intraperitoneal packing, and intra-aorta stent for ruptured abdominal aorta aneurysm. Primary symptoms of ACS include abdominal pain and distention. Secondary signs of ACS include respiratory depression, decreased cardiac output, visceral ischemia due to decreased perfusion, and renal failure. This condition can be fatal if not properly treated. It becomes increasingly more critical for the overall prognosis that ACS is recognized and treated timely. Detection of ACS can be interfered with by other clinical conditions. A blunt abdominal trauma patient may have active upper gastrointestinal bleeding due to stress ulcers and unstable vital signs. Hypovolemia and inadequate fluid resuscitation may be the first impression as the cause of shock. However, CT may also reveal massive hemoperitoneum compressing intra-abdominal contents leading to ACS. This kind of patient may present with hemodynamic instability as the first clinical indicator of ACS.

#### **4. Radiographic features**

Computed tomography is the most used method for etiology evaluation in patients with a distended abdomen. CT findings suggestive of ACS include a tense infiltration of the retroperitoneum exceeding primary peritoneal disease, narrowing the inferior vena cava due to external compression, and an increased ratio of anteroposterior-to-transverse abdominal diameter. Besides, compression or displacement of the kidney, extensive bowel wall thickening with enhancement, and simultaneously bilateral inguinal herniation are also potentially indicative of ACS [13].

The ratio of maximal anteroposterior to the transverse abdominal diameter and peritoneal-to-abdomen height ratio are reported statistically associated with elevated IAP [14]. There are several other signs in CT and echo that may support the diagnosis of ACS. Still, most of these are considered nonspecific or insensitive for ACS [15]. Suppose CT findings suggestive of increased intraabdominal pressure are noticed. In that case, the radiologist should swiftly communicate with physicians to treat the patient because the abdominal compartment syndrome may require urgent intervention.

#### **5. Measuring IAP**

IAP monitoring and IAH/ACS management are increasing importance as critical for the patient outcome; various pressure measurement methods using either direct (abdominal pressure measurement with a catheter) and indirect (use pressure inside the urinary bladder, stomach, colon, or uterine) techniques have been suggested [16–18]. Among these methods, the bladder technique is the most widespread adoption due to its simplicity and low cost [9, 16, 19]. Some methods providing continuous IAP measurement via the stomach, peritoneal cavity, and bladder have been validated [20–22]. The trans-bladder device can be connected with the ICU bedside monitor to provide an integrated patient monitor with other vital signs. The trans-bladder device also provides a closed system to avoid contamination and reduce urinary tract infection (**Figure 2**). Although these techniques seem promising, more clinical validation is required before general use can be recommended.

One of the questions for IAP measurement is the reference point. Many studies had suggested using the symphysis pubis is widely used in many studies as the reference point, but this can cause different IAP results within the same patient in some clinical conditions. For example, changes in different body positions (supine,

**45**

*Abdominal Compartment Syndrome*

accuracy of IAP measurements [9].

patients with IAH.

**6.1 ACS in post-cardiac surgery**

harmful result of IAH [26].

resuscitation failure [29].

**6.2 ACS after acute pancreatitis**

*DOI: http://dx.doi.org/10.5772/intechopen.96972*

prone, the elevation of head), abdominal contracture during a seizure, and abnormal bladder detrusor muscle contractions have been demonstrated to impact the

**6. Acute compartment syndrome in specific situations**

Another disparity among IAP measurement techniques is the priming-volume instilled into the bladder to ensure a conductive fluid column between the bladder wall and transducer [23, 24]. Several studies have shown that too many volumes may increase bladder pressure and poorly reflect true abdominal pressure [19]. The reference standard for intermittent IAP measurement is via the bladder with a maximal installation volume of 25 ml sterile saline. Point-of-care ultrasound (POCUS) as a bedside modality in ACS patients is not well studied. A prospective observational study for patients who met the criteria of IAH was assigned to undergo POCUS and small bowel ultrasound as adjuvant tools in their IAH management [25]. POCUS can detect gastric content (fluid vs. concrete) and diagnoses of gastric paresis. POCUS can find small bowel obstruction and even mesenteric vessel occlusion or transmesenteric internal hernia. POCUS can help the nonoperative management of IAH, especially in diagnosing and treating

The incidence of IAH after cardiac surgery is between 26.9% and 83.3%. There is limited evidence regarding IAH after cardiac surgery and is interpreted with caution. Obesity is a strong predictor of postoperative IAH, although not confined to a central pattern or body mass index. Prolonged cardiopulmonary bypass and aortic cross-clamp time are predisposed to IAH in some reports. IAH in cardiac surgery patients is associated with hepatic and renal failure, and corresponding biochemical markers may help screen but lack specificity. In contrast to the development of IAH in other settings, the evidence for the role of fluid balance is insufficient. Precise prediction of IAH remains challenging. Based on the present evidence, regular IAP measurement is indicated postoperatively in patients who are obese, those with preoperative renal or hepatic impairment, prolonged cardiopulmonary bypass or operative time, requiring vasopressor support, to prevent the

Acute pancreatitis can lead to severe systemic complications. ACS is one of the lethal complications of acute pancreatitis. Mortality rate in acute pancreatitis complicated with ACS can result in a 49% mortality rate, but it is only about 11% without ACS [27]. Severe form pancreatitis patients are incredibly high risk for ACS due to tissue edema after initial aggressive fluid resuscitation, profound peripancreatic inflammation, massive ascites, and ileus due to intraperitoneal inflammation. Frequent measurement of the intra-abdominal pressure is indicated for severe pancreatitis patients to obtain prompt diagnosis and treatment of ACS [28]. A high index of suspicion is needed for patient care of acute pancreatitis. Management of ACS after pancreatitis consists of supportive care and abdominal decompression if indicated. The highest mortality rate reported in patients with necrotizing pancreatitis and decompression laparotomy reduces it by 8.7%. Decompressive laparotomy should be used as soon as possible if medical

**Figure 2.** *Wound stage of open abdomen.*

#### *Abdominal Compartment Syndrome DOI: http://dx.doi.org/10.5772/intechopen.96972*

*A Comprehensive Review of Compartment Syndrome*

Computed tomography is the most used method for etiology evaluation in patients with a distended abdomen. CT findings suggestive of ACS include a tense infiltration of the retroperitoneum exceeding primary peritoneal disease, narrowing the inferior vena cava due to external compression, and an increased ratio of anteroposterior-to-transverse abdominal diameter. Besides, compression or displacement of the kidney, extensive bowel wall thickening with enhancement, and simultaneously bilateral inguinal herniation are also potentially indicative of

The ratio of maximal anteroposterior to the transverse abdominal diameter and peritoneal-to-abdomen height ratio are reported statistically associated with elevated IAP [14]. There are several other signs in CT and echo that may support the diagnosis of ACS. Still, most of these are considered nonspecific or insensitive for ACS [15]. Suppose CT findings suggestive of increased intraabdominal pressure are noticed. In that case, the radiologist should swiftly communicate with physicians to treat the patient because the abdominal compartment syndrome may require urgent

IAP monitoring and IAH/ACS management are increasing importance as critical for the patient outcome; various pressure measurement methods using either direct (abdominal pressure measurement with a catheter) and indirect (use pressure inside the urinary bladder, stomach, colon, or uterine) techniques have been suggested [16–18]. Among these methods, the bladder technique is the most widespread adoption due to its simplicity and low cost [9, 16, 19]. Some methods providing continuous IAP measurement via the stomach, peritoneal cavity, and bladder have been validated [20–22]. The trans-bladder device can be connected with the ICU bedside monitor to provide an integrated patient monitor with other vital signs. The trans-bladder device also provides a closed system to avoid contamination and reduce urinary tract infection (**Figure 2**). Although these techniques seem promising, more clinical validation is required before general use can be

One of the questions for IAP measurement is the reference point. Many studies had suggested using the symphysis pubis is widely used in many studies as the reference point, but this can cause different IAP results within the same patient in some clinical conditions. For example, changes in different body positions (supine,

**4. Radiographic features**

ACS [13].

intervention.

**5. Measuring IAP**

recommended.

**44**

**Figure 2.**

*Wound stage of open abdomen.*

prone, the elevation of head), abdominal contracture during a seizure, and abnormal bladder detrusor muscle contractions have been demonstrated to impact the accuracy of IAP measurements [9].

Another disparity among IAP measurement techniques is the priming-volume instilled into the bladder to ensure a conductive fluid column between the bladder wall and transducer [23, 24]. Several studies have shown that too many volumes may increase bladder pressure and poorly reflect true abdominal pressure [19]. The reference standard for intermittent IAP measurement is via the bladder with a maximal installation volume of 25 ml sterile saline. Point-of-care ultrasound (POCUS) as a bedside modality in ACS patients is not well studied. A prospective observational study for patients who met the criteria of IAH was assigned to undergo POCUS and small bowel ultrasound as adjuvant tools in their IAH management [25]. POCUS can detect gastric content (fluid vs. concrete) and diagnoses of gastric paresis. POCUS can find small bowel obstruction and even mesenteric vessel occlusion or transmesenteric internal hernia. POCUS can help the nonoperative management of IAH, especially in diagnosing and treating patients with IAH.

#### **6. Acute compartment syndrome in specific situations**

#### **6.1 ACS in post-cardiac surgery**

The incidence of IAH after cardiac surgery is between 26.9% and 83.3%. There is limited evidence regarding IAH after cardiac surgery and is interpreted with caution. Obesity is a strong predictor of postoperative IAH, although not confined to a central pattern or body mass index. Prolonged cardiopulmonary bypass and aortic cross-clamp time are predisposed to IAH in some reports. IAH in cardiac surgery patients is associated with hepatic and renal failure, and corresponding biochemical markers may help screen but lack specificity. In contrast to the development of IAH in other settings, the evidence for the role of fluid balance is insufficient. Precise prediction of IAH remains challenging. Based on the present evidence, regular IAP measurement is indicated postoperatively in patients who are obese, those with preoperative renal or hepatic impairment, prolonged cardiopulmonary bypass or operative time, requiring vasopressor support, to prevent the harmful result of IAH [26].

#### **6.2 ACS after acute pancreatitis**

Acute pancreatitis can lead to severe systemic complications. ACS is one of the lethal complications of acute pancreatitis. Mortality rate in acute pancreatitis complicated with ACS can result in a 49% mortality rate, but it is only about 11% without ACS [27]. Severe form pancreatitis patients are incredibly high risk for ACS due to tissue edema after initial aggressive fluid resuscitation, profound peripancreatic inflammation, massive ascites, and ileus due to intraperitoneal inflammation. Frequent measurement of the intra-abdominal pressure is indicated for severe pancreatitis patients to obtain prompt diagnosis and treatment of ACS [28]. A high index of suspicion is needed for patient care of acute pancreatitis. Management of ACS after pancreatitis consists of supportive care and abdominal decompression if indicated. The highest mortality rate reported in patients with necrotizing pancreatitis and decompression laparotomy reduces it by 8.7%. Decompressive laparotomy should be used as soon as possible if medical resuscitation failure [29].

#### **6.3 ACS after hip arthroplasty**

A relatively rare condition is ACS after hip arthroplasty. There some case reports regarding this unusual condition [30, 31]. A patient suffered from an acetabulum fracture and received open reduction and internal fixation with hip arthroscopy. Hypothermia, increased airway pressure and oliguria happened during the operation. Desaturation and metabolic acidosis were noted. A postoperative CT revealed a large volume of irrigation fluid in the peritoneal cavity and retroperitoneum, and ACS was confirmed. The patient was treated by percutaneous peritoneal drainage and was discharged eight weeks after the operation smoothly. Intraperitoneal extravasation of irrigation fluid may occur during hip arthroscopic surgery and causes ACS later [32].

Some authors had proposed an algorithm to prevent and treat this possible lethal complication following hip arthroscopy [33].

#### **6.4 ACS in severely burned patients**

An observational study that included 56 mechanical ventilated burn patients between April 2007 and December 2009 with IAP measurement every day showed that 78.6% of patients developed IAH and 28.6% progressed into ACS [34]. Patients with ACS had larger TBSAs of burn injury (35.8 ± 30% vs. 20.6 ± 21.4%, P = 0.04) and more cumulative fluid balances after 48 hours treatment (13.6 ± 16 L vs. 7.6 ± 4.1 L, P = 0.03). The TBSA of burn injury was closely correlated with the mean IAP (R = 0.34, P = 0.01). Mortality was also significantly higher in patients with IAH (34.1% vs. 26.8%, P = 0.014) and ACS (62.5% vs. 26.8%, P < 0.0001). The author concluded that IAH/ACS incidence is high in ventilated burn patients compared to other groups of critically ill patients. The TBSA of burn injury correlates with the IAP. The combination of positive fluid balance, high IAP, elevated lung water is suggestive of an unfavorable outcome. Non-surgical interventions usually adopted for burn patient with ACS, and it appears to improve end-organ function. Since decompressive laparotomy is difficult to perform in major burn patients, the persistence of IAH is highly related to a worse outcome.

#### **7. Treatment in ACS**

As proposed by the World Society of ACS (WSACS), the standard of care is divided into two algorithms: the medical management and surgical management pathway based on clinical presentation [1]. Medical management of ACS initiated upon recognition of elevated intra-abdominal pressures (Grade I C recommendation). This includes sedation, neuromuscular blockade, evacuating intraluminal contents, paracentesis of ascites or hemoperitoneum, percutaneous drainage, cautious fluid resuscitation, and adequate organ support. The ultimate goal is an alleviation of pressures and definitive management with surgery. A protocol with serial monitoring of intra-abdominal pressures every 2–4 hours or using continuous monitoring to maintain pressures less than 15 mmHg is recommended. Percutaneous drainage is indicated in the presence of space-occupying fluid inside the peritoneal cavity. However, using catheter-directed decompression as definitive management instead of decompressive laparotomy has yet well studied.

The patient's respiratory rate, oxygenation, heart rate, and blood pressure usually rapidly improved after placing intra-abdominal catheters to alleviate the pressure. This displays the advantage of having the interventional radiology team available for definitive ACS management secondary to abdominal cavity

**47**

**Table 1**.

*Abdominal Compartment Syndrome*

settings [36].

*DOI: http://dx.doi.org/10.5772/intechopen.96972*

**8. Open abdomen treatment in ACS**

adopted to provide exemplary patient recovery.

cells transfusion, or > 6 L of crystalloids within 24 hours.

space-occupying lesions/fluid collections. Catheter-directed drainage of ACS is indicated due to its less invasive nature and rapid availability [35]. Decompressive laparotomy may leave patients with an open abdomen with morbidities such as increased fluid losses, infection, fluid collections, fistula formation, hernias, or cosmetic concerns. Interventional radiologists are uniquely positioned to provide drainage guided management for abdominal compartment syndrome in emergent

After decompressive laparotomy, ACS patients are usually in an open abdomen status and represent patient care difficulty. Open abdomen (OA) is a surgical technique that the abdominal fascial edges are intentionally left open after laparotomy. OA shortens the operation time and allows the patient to return to the Intensive Care Unit earlier under the unstable condition, and facilitates further treatment. OA's advantages include a concise operation time, fewer postoperative complications, and the prevention of early multiple-organ failure [37]. Besides adopted for abdominal trauma, OA is now part of the Damage-Control Surgical (DCS) for various complicated abdominal conditions, including ACS [38]. ACS usually happens in a trauma patient who received massive fluid resuscitation and blood transfusion in the primary survey and is now considered crucial to patient mortality. With the advancement in treatment regarding multiple-organ failure after trauma and ACS, decompressive laparotomy and OA patient care is now part of the essential strategy

Although the precise percentage of OA in trauma patients is not exact, this approach is now generally applied [38]. Ogilvie first reported the OA technique about 80 years ago with the design to provide adequate drainage and source control for intra-abdominal sepsis [39]. In December 2014, the first international conference for consensus about OA was held. The guidelines were proposed to clarify OA's indications, the technique for temporary abdominal closure (TAC), and the abdomen's closure. According to the Eastern Association for the Surgery of Trauma (EAST) practice management committee guidelines [40], OA is indicated when patient presented with severe metabolic acidosis (pH < 7.2), hypothermia (temperature < 35 °C), and coagulopathy, or when patient received >10 units of red blood

Although an open abdomen can reduce ACS mortality, it also created new problems, such as severe fluid and protein loss, nutritional problems, enter atmospheric fistulas, fascial retraction with loss of abdominal domain, and the development of massive incisional hernias [41]. A multidisciplinary approach with active interaction between the surgical team and intensive care unit team is required to manage a critically ill patient with ACS and OA, which should be done with a specific staged process with protocol [38]. A list of outlines for OA patient care is provided in

Patient care challenges regarding prolonged OA include delay in extubation, the risk for repeated infections, and possible enter atmospheric fistulae. Therefore, optimizing the patient condition for the early abdomen closure is the primary goal in OA patient care. The physiological derangement of hypothermia, acidosis, and coagulopathy needs to be aggressively reversed with resuscitation in ICU. ACS patients usually have poor pulmonary compliance, and mechanical ventilation with high ventilatory pressure is necessary. We often need to cautiously distend the alveoli with high ventilatory pressure since the transpulmonary pressure is high. However, if the tidal volume is inadequate, it will cause hypoxia and respiratory

*A Comprehensive Review of Compartment Syndrome*

complication following hip arthroscopy [33].

persistence of IAH is highly related to a worse outcome.

**6.4 ACS in severely burned patients**

A relatively rare condition is ACS after hip arthroplasty. There some case reports regarding this unusual condition [30, 31]. A patient suffered from an acetabulum fracture and received open reduction and internal fixation with hip arthroscopy. Hypothermia, increased airway pressure and oliguria happened during the operation. Desaturation and metabolic acidosis were noted. A postoperative CT revealed a large volume of irrigation fluid in the peritoneal cavity and retroperitoneum, and ACS was confirmed. The patient was treated by percutaneous peritoneal drainage and was discharged eight weeks after the operation smoothly. Intraperitoneal extravasation of irrigation fluid may occur during hip arthroscopic surgery and

Some authors had proposed an algorithm to prevent and treat this possible lethal

An observational study that included 56 mechanical ventilated burn patients between April 2007 and December 2009 with IAP measurement every day showed that 78.6% of patients developed IAH and 28.6% progressed into ACS [34]. Patients with ACS had larger TBSAs of burn injury (35.8 ± 30% vs. 20.6 ± 21.4%, P = 0.04) and more cumulative fluid balances after 48 hours treatment (13.6 ± 16 L vs. 7.6 ± 4.1 L, P = 0.03). The TBSA of burn injury was closely correlated with the mean IAP (R = 0.34, P = 0.01). Mortality was also significantly higher in patients with IAH (34.1% vs. 26.8%, P = 0.014) and ACS (62.5% vs. 26.8%, P < 0.0001). The author concluded that IAH/ACS incidence is high in ventilated burn patients compared to other groups of critically ill patients. The TBSA of burn injury correlates with the IAP. The combination of positive fluid balance, high IAP, elevated lung water is suggestive of an unfavorable outcome. Non-surgical interventions usually adopted for burn patient with ACS, and it appears to improve end-organ function. Since decompressive laparotomy is difficult to perform in major burn patients, the

As proposed by the World Society of ACS (WSACS), the standard of care is divided into two algorithms: the medical management and surgical management pathway based on clinical presentation [1]. Medical management of ACS initiated upon recognition of elevated intra-abdominal pressures (Grade I C recommendation). This includes sedation, neuromuscular blockade, evacuating intraluminal contents, paracentesis of ascites or hemoperitoneum, percutaneous drainage, cautious fluid resuscitation, and adequate organ support. The ultimate goal is an alleviation of pressures and definitive management with surgery. A protocol with serial monitoring of intra-abdominal pressures every 2–4 hours or using continuous monitoring to maintain pressures less than 15 mmHg is recommended. Percutaneous drainage is indicated in the presence of space-occupying fluid inside the peritoneal cavity. However, using catheter-directed decompression as definitive

management instead of decompressive laparotomy has yet well studied.

The patient's respiratory rate, oxygenation, heart rate, and blood pressure usually rapidly improved after placing intra-abdominal catheters to alleviate the pressure. This displays the advantage of having the interventional radiology team available for definitive ACS management secondary to abdominal cavity

**6.3 ACS after hip arthroplasty**

causes ACS later [32].

**7. Treatment in ACS**

**46**

space-occupying lesions/fluid collections. Catheter-directed drainage of ACS is indicated due to its less invasive nature and rapid availability [35]. Decompressive laparotomy may leave patients with an open abdomen with morbidities such as increased fluid losses, infection, fluid collections, fistula formation, hernias, or cosmetic concerns. Interventional radiologists are uniquely positioned to provide drainage guided management for abdominal compartment syndrome in emergent settings [36].

#### **8. Open abdomen treatment in ACS**

After decompressive laparotomy, ACS patients are usually in an open abdomen status and represent patient care difficulty. Open abdomen (OA) is a surgical technique that the abdominal fascial edges are intentionally left open after laparotomy. OA shortens the operation time and allows the patient to return to the Intensive Care Unit earlier under the unstable condition, and facilitates further treatment. OA's advantages include a concise operation time, fewer postoperative complications, and the prevention of early multiple-organ failure [37]. Besides adopted for abdominal trauma, OA is now part of the Damage-Control Surgical (DCS) for various complicated abdominal conditions, including ACS [38]. ACS usually happens in a trauma patient who received massive fluid resuscitation and blood transfusion in the primary survey and is now considered crucial to patient mortality. With the advancement in treatment regarding multiple-organ failure after trauma and ACS, decompressive laparotomy and OA patient care is now part of the essential strategy adopted to provide exemplary patient recovery.

Although the precise percentage of OA in trauma patients is not exact, this approach is now generally applied [38]. Ogilvie first reported the OA technique about 80 years ago with the design to provide adequate drainage and source control for intra-abdominal sepsis [39]. In December 2014, the first international conference for consensus about OA was held. The guidelines were proposed to clarify OA's indications, the technique for temporary abdominal closure (TAC), and the abdomen's closure. According to the Eastern Association for the Surgery of Trauma (EAST) practice management committee guidelines [40], OA is indicated when patient presented with severe metabolic acidosis (pH < 7.2), hypothermia (temperature < 35 °C), and coagulopathy, or when patient received >10 units of red blood cells transfusion, or > 6 L of crystalloids within 24 hours.

Although an open abdomen can reduce ACS mortality, it also created new problems, such as severe fluid and protein loss, nutritional problems, enter atmospheric fistulas, fascial retraction with loss of abdominal domain, and the development of massive incisional hernias [41]. A multidisciplinary approach with active interaction between the surgical team and intensive care unit team is required to manage a critically ill patient with ACS and OA, which should be done with a specific staged process with protocol [38]. A list of outlines for OA patient care is provided in **Table 1**.

Patient care challenges regarding prolonged OA include delay in extubation, the risk for repeated infections, and possible enter atmospheric fistulae. Therefore, optimizing the patient condition for the early abdomen closure is the primary goal in OA patient care. The physiological derangement of hypothermia, acidosis, and coagulopathy needs to be aggressively reversed with resuscitation in ICU. ACS patients usually have poor pulmonary compliance, and mechanical ventilation with high ventilatory pressure is necessary. We often need to cautiously distend the alveoli with high ventilatory pressure since the transpulmonary pressure is high. However, if the tidal volume is inadequate, it will cause hypoxia and respiratory


#### **Table 1.**

*Principles for OA patient care.*

acidosis, which can be fatal in an ACS patient with a tense abdomen. Once the abdomen is opened, the ventilator settings must be changed to maintain appropriate tidal volume without overexpansion of the alveoli. After OA, the increase in venous return can cause right ventricular overload if there is preexisting pulmonary hypertension due to hypercarbia or preexisting cardiomyopathy, which can be treated with dobutamine or milrinone. Significant pleural effusion may occur after OA due to increased venous load with high hydrostatic pressure, and pleural effusion drainage is indicated.

ACS patients usually have marked bowel edema, and the cause is multifactorial. The gut's perfusion is compromised during unstable blood pressure, and the mesenteric venous return is impaired when the IAP is elevated, which leads to progressive congestion in the already ischemic gut. The ischemia gut is reperfused after volume resuscitation and OA, but there is also the production of free-radical and increased mucosa permeability that can cause further bowel edema. Since a more than 10% increase in fluid-related weight gain is considered a significant negative factor for primary closure in OA [38], the goal in ICU care is to prevent fluid overload and alleviate gut edema so that a primary fascial closure can be achieved as early as possible. The OA patient can receive enteral feeding, and the only contraindication is intestinal discontinuity. Viscera exposure does not necessarily cause paralytic ileus, and feeding in OA does not cause gut edema. Early full enteral feeding should be initiated when the patient is no need to use an inotropic agent or vasopressor. Enteral feeding can maintain gut integrity, modulate the systemic inflammatory response, decrease infection rate, decrease the rate of ventilator-associated pneumonia, facilitate early closure of OA, and decrease fistulas formation. High nitrogen loss is expected in OA with ascites loss, and it is necessary to calculate the caloric demand and nitrogen balance carefully to avoid underfeeding.

Early definitive closure is the basis of preventing or reducing the risk of these complications. The key to optimizing outcome is early abdominal closure within seven days because failure to do so will increase morbidity, mortality, and fistulae formation [41, 42]. However, early fascia closure is not always feasible.

If delayed fascia closure is inevitable, proper wound care and a thorough understanding of the open abdomen is necessary. For a prolonged open abdomen, the OA wound would go through three stages (**Figure 2**). The first stage is the serosa stage, where the exposed small bowel is grossly visible, and their integrity is easily differentiated with the eyeball. In the second stage, the granulation stage, diffuse granulation tissue development over the bowel serosa happened after bowel adhesion. The outline of the small bowel is very different from the typical appearance. The third stage is the confluence stage, where the whole small bowel is in a confluent status and undifferentiable. In the third stage, the skin wound will have ingrowth into the bowel surface, and the wound will also start to contract. Therefore, the wound will become smaller and more comfortable to care for. After 3–6 months of wound care, we suggest using CT to determine the fascia

**49**

**Author details**

Kuo-Ching Yuan1

\*, Chih-Yuan Fu2

a protocolized care plan is essential for this OA patient care.

Taipei Medical University Hospital, Taipei, Taiwan

Chang-Gung Memorial Hospital, Linkou, Taiwan

provided the original work is properly cited.

\*Address all correspondence to: traumayuan@gmail.com

1 Division of Acute Care Surgery and Trauma, Department of Surgery,

2 Division of Trauma and Emergency Surgery, Department of Surgery,

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

and Hung-Chang Huang1

*Abdominal Compartment Syndrome*

fascia gap is less than 8 cm.

**9. Conclusion**

*DOI: http://dx.doi.org/10.5772/intechopen.96972*

gap between the open abdomen's two edges. Abdominal closure is indicated if the

ACS is a challenging condition in ICU patient care with a high prevalence in acute pancreatitis, orthotopic liver transplantation, and abdominal aorta surgery. Massive resuscitation and swelling of the abdominal viscera are the primary cause of ACS. ACS can cause rapid deterioration of hemodynamic status and progresses into multiple organ failure eventually. IAP monitoring with frequent clinical evaluation is crucial for early diagnosis, and early diagnosis with prompt management is key to good patient recovery. Medical treatment is usually adopted first, but decompressive laparotomy is indicated if organ failure progresses after medical treatment. After decompressive laparotomy, the patient is in OA status, and gap between the open abdomen's two edges. Abdominal closure is indicated if the fascia gap is less than 8 cm.

### **9. Conclusion**

*A Comprehensive Review of Compartment Syndrome*

• Fluid: Maintain adequate volume status by urine amount

• Ventilation: Weaning and extubation after hemodynamic stable • Sedation: A short duration of sedation just after operation

• Infection: Antibiotic use by culture result

• Wound care: Clear gauze cover on IV bag

• Nutrition: early enteral feeding

sion drainage is indicated.

*Principles for OA patient care.*

**Table 1.**

acidosis, which can be fatal in an ACS patient with a tense abdomen. Once the abdomen is opened, the ventilator settings must be changed to maintain appropriate tidal volume without overexpansion of the alveoli. After OA, the increase in venous return can cause right ventricular overload if there is preexisting pulmonary hypertension due to hypercarbia or preexisting cardiomyopathy, which can be treated with dobutamine or milrinone. Significant pleural effusion may occur after OA due to increased venous load with high hydrostatic pressure, and pleural effu-

ACS patients usually have marked bowel edema, and the cause is multifactorial. The gut's perfusion is compromised during unstable blood pressure, and the mesenteric venous return is impaired when the IAP is elevated, which leads to progressive congestion in the already ischemic gut. The ischemia gut is reperfused after volume resuscitation and OA, but there is also the production of free-radical and increased mucosa permeability that can cause further bowel edema. Since a more than 10% increase in fluid-related weight gain is considered a significant negative factor for primary closure in OA [38], the goal in ICU care is to prevent fluid overload and alleviate gut edema so that a primary fascial closure can be achieved as early as possible. The OA patient can receive enteral feeding, and the only contraindication is intestinal discontinuity. Viscera exposure does not necessarily cause paralytic ileus, and feeding in OA does not cause gut edema. Early full enteral feeding should be initiated when the patient is no need to use an inotropic agent or vasopressor. Enteral feeding can maintain gut integrity, modulate the systemic inflammatory response, decrease infection rate, decrease the rate of ventilator-associated pneumonia, facilitate early closure of OA, and decrease fistulas formation. High nitrogen loss is expected in OA with ascites loss, and it is necessary to calculate the caloric

Early definitive closure is the basis of preventing or reducing the risk of these complications. The key to optimizing outcome is early abdominal closure within seven days because failure to do so will increase morbidity, mortality, and fistulae

If delayed fascia closure is inevitable, proper wound care and a thorough understanding of the open abdomen is necessary. For a prolonged open abdomen, the OA wound would go through three stages (**Figure 2**). The first stage is the serosa stage, where the exposed small bowel is grossly visible, and their integrity is easily differentiated with the eyeball. In the second stage, the granulation stage, diffuse granulation tissue development over the bowel serosa happened after bowel adhesion. The outline of the small bowel is very different from the typical appearance. The third stage is the confluence stage, where the whole small bowel is in a confluent status and undifferentiable. In the third stage, the skin wound will have ingrowth into the bowel surface, and the wound will also start to contract. Therefore, the wound will become smaller and more comfortable to care for. After 3–6 months of wound care, we suggest using CT to determine the fascia

demand and nitrogen balance carefully to avoid underfeeding.

formation [41, 42]. However, early fascia closure is not always feasible.

**48**

ACS is a challenging condition in ICU patient care with a high prevalence in acute pancreatitis, orthotopic liver transplantation, and abdominal aorta surgery.

Massive resuscitation and swelling of the abdominal viscera are the primary cause of ACS. ACS can cause rapid deterioration of hemodynamic status and progresses into multiple organ failure eventually. IAP monitoring with frequent clinical evaluation is crucial for early diagnosis, and early diagnosis with prompt management is key to good patient recovery. Medical treatment is usually adopted first, but decompressive laparotomy is indicated if organ failure progresses after medical treatment. After decompressive laparotomy, the patient is in OA status, and a protocolized care plan is essential for this OA patient care.

### **Author details**

Kuo-Ching Yuan1 \*, Chih-Yuan Fu2 and Hung-Chang Huang1

1 Division of Acute Care Surgery and Trauma, Department of Surgery, Taipei Medical University Hospital, Taipei, Taiwan

2 Division of Trauma and Emergency Surgery, Department of Surgery, Chang-Gung Memorial Hospital, Linkou, Taiwan

\*Address all correspondence to: traumayuan@gmail.com

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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**51**

enough is enough.

*Abdominal Compartment Syndrome*

compartment syndrome.

method for measurement.

in children.

monitoring.

pressure.

*DOI: http://dx.doi.org/10.5772/intechopen.96972*

for semicontinuous intra-abdominal pressure measurements using a

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[24] De Waele Jj Fau - Billiet, E. A. I., Billiet Ea Fau - Hoste, E., Hoste E Fau - Blot, S. I., Blot Si Fau - Colardyn, F. A. & Colardyn, F. A. Fluid vs. air

measurement technique.

K. & Sandrasegaran, K. Abdominal compartment syndrome.

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[17] Davis, P. J., Koottayi S Fau - Taylor, A., Taylor A Fau - Butt, W. W. & Butt, W. W. Comparison of indirect methods of measuring intra-abdominal pressure in children.

[18] De Potter, T. J., Dits H Fau - Malbrain, M. L. N. G. & Malbrain, M. L. Intra- and interobserver variability during in vitro validation of two novel methods for intra-abdominal pressure monitoring.

[19] Gudmundsson, F. F., Viste A Fau - Gislason, H., Gislason H Fau - Svanes, K. & Svanes, K. Comparison of different methods for measuring intra-abdominal pressure.

[20] Balogh, Z., Jones F Fau - D'Amours, S., D'Amours S Fau - Parr, M., Parr M Fau - Sugrue, M. & Sugrue, M. Continuous intra-abdominal pressure measurement technique.

[21] Schachtrupp, A. et al. Evaluation of a modified piezoresistive technique and a water-capsule technique for direct and continuous measurement of intraabdominal pressure in a porcine model.

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[23] De Waele, J., Pletinckx P Fau - Blot, S., Blot S Fau - Hoste, E. & Hoste, E. Saline volume in transvesical intraabdominal pressure measurement: enough is enough.

[24] De Waele Jj Fau - Billiet, E. A. I., Billiet Ea Fau - Hoste, E., Hoste E Fau - Blot, S. I., Blot Si Fau - Colardyn, F. A. & Colardyn, F. A. Fluid vs. air

for semicontinuous intra-abdominal pressure measurements using a compliance catheter.

[25] Bitar, Z. A.-O. et al. The use of point-of-care ultrasound to guide clinical management in intra-abdominal hypertension. LID - 10.1007/s40477- 020-00546-8 [doi].

[26] Tyson, N. & Efthymiou, C. Predictive risk factors for intraabdominal hypertension after cardiac surgery. LID - ivaa336 [pii] LID - 10.1093/icvts/ivaa336 [doi].

[27] van Brunschot, S. et al. Abdominal compartment syndrome in acute pancreatitis: a systematic review.

[28] Singh, B. et al. Hypertriglyceridemia induced pancreatitis complicated by compartment syndrome and managed by surgical decompression and plasmapheresis.

[29] Muresan, M. et al. How much does decompressive laparotomy reduce the mortality rate in primary abdominal compartment syndrome?: A singlecenter prospective study on 66 patients.

[30] Schwenter, A., Schuepfer, G., Beck, M. & Mauch, J. Abdominal compartment syndrome after hip arthroscopy.

[31] Sharma, A., Sachdev H Fau - Gomillion, M. & Gomillion, M. Abdominal compartment syndrome during hip arthroscopy.

[32] Shakuo, T., Bito, K., Yasuda, S. & Asagi, C. Abdominal compartment syndrome during hip arthroscopy for an acetabular fracture: a case report.

[33] Ciemniewska-Gorzela, K., Piontek T Fau - Szulc, A. & Szulc, A. Abdominal compartment syndrome--the prevention and treatment of possible lethal complications following hip arthroscopy: a case report.

**50**

*A Comprehensive Review of Compartment Syndrome*

[8] Malbrain, M. L. N. G., De laet, I. & Cheatham, M. CONSENSUS CONFERENCE DEFINITIONS AND RECOMMENDATIONS ON INTRA-ABDOMINAL HYPERTENSION (IAH) AND THE ABDOMINAL COMPARTMENT SYNDROME (ACS) - THE LONG ROAD TO THE FINAL PUBLICATIONS, HOW DID WE GET THERE? Acta Clinica Belgica 62, 44-59, doi:10.1179/acb.2007.62.s1.007 (2007).

[9] Malbrain, M. L. Different techniques to measure intra-abdominal pressure (IAP): time for a critical re-appraisal.

[10] Cheatham, M. L. Abdominal Compartment Syndrome: pathophysiology and definitions. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine 17, 10, doi:10.1186/1757-7241-17-

[11] Cheatham, M. L., White Mw Fau - Sagraves, S. G., Sagraves Sg Fau - Johnson, J. L., Johnson Jl Fau - Block, E. F. & Block, E. F. Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal

[12] Deeren, D. H., Dits H Fau - Malbrain, M. L. N. G. & Malbrain, M. L. Correlation between intraabdominal and intracranial pressure in

[13] Pickhardt, P. J., Shimony Js Fau - Heiken, J. P., Heiken Jp Fau - Buchman, T. G., Buchman Tg Fau - Fisher, A. J. & Fisher, A. J. The abdominal compartment syndrome: CT findings.

[14] Bouveresse, S. et al. Abdominal compartment syndrome and intraabdominal hypertension in critically ill patients: diagnostic value of computed

[15] Patel, A., Lall Cg Fau - Jennings, S. G., Jennings Sg Fau - Sandrasegaran,

nontraumatic brain injury.

10 (2009).

hypertension.

tomography.

[1] Kirkpatrick, A. W. et al. Intraabdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal

**References**

s00134-013-2906-z (2013).

[2] Pereira, B. M. Abdominal compartment syndrome and intraabdominal hypertension. Current Opinion in Critical Care 25 (2019).

[3] Sosa, G., Gandham, N., Landeras, V., Calimag, A. P. & Lerma, E. Abdominal compartment syndrome. Disease-a-Month 65, 5-19, doi:https://doi.org/10.1016/j. disamonth.2018.04.003 (2019).

A Systematic Review.

00746-9 (2020).

0016-7 (2015).

0349-5 (2006).

[4] Khot, Z. A.-O. et al. Incidence of Intra-Abdominal Hypertension and Abdominal Compartment Syndrome:

[5] Smit, M. et al. Intra-abdominal hypertension and abdominal compartment syndrome in patients admitted to the ICU. Annals of Intensive Care 10, 130, doi:10.1186/s13613-020-

[6] Kyoung, K.-H. & Hong, S.-K. The duration of intra-abdominal hypertension strongly predicts outcomes for the critically ill surgical patients: a prospective observational study. World Journal of Emergency Surgery 10, 22, doi:10.1186/s13017-015-

[7] Malbrain, M. L. N. G. et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I.

Definitions. Intensive Care Medicine 32, 1722-1732, doi:10.1007/s00134-006-

Compartment Syndrome. Intensive Care Medicine 39, 1190-1206, doi:10.1007/

[34] Wise R Fau - Jacobs, J. et al. Incidence and prognosis of intraabdominal hypertension and abdominal compartment syndrome in severely burned patients: Pilot study and review of the literature.

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Section 4

Diagnosis of Compartment

Syndrome

**53**

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[41] Demetriades, D. & Salim, A. Management of the open abdomen.

[42] Sugrue, M. Abdominal compartment syndrome and the open abdomen: any unresolved issues?

### Section 4
