Compartment Syndrome in Special Situations

experimental in vitro study. Patient Saf

*A Comprehensive Review of Compartment Syndrome*

Weber CD, Jeromin S, Zimmermann F, Turner J, Hildebrand F, Pape HC. Assessment of elevated compartment

[50] Bloch A, Tomaschett C, Jakob SM,

[51] Sellei RM, Wollnitz J, Reinhardt N, de la Fuente M, Radermacher K, Weber CD, Kobbe P, Hildebrand F. Non-invasive measurement of muscle compartment elasticity in lower limbs to

syndrome: Clinical results with pressure related ultrasound. Injury. 2020; 51:

[52] Marmor MT, Charlu J, Knox R, Curtis W, Hoogervorst P, Herfat S. Use of standard musculoskeletal ultrasound to determine the need for fasciotomy in an elevated muscle compartment pressure cadaver leg model. Injury.

[53] Marmor MT, Barker JP, Matz J, Donohoe E, Herring MJ. A dual-sensor ultrasound based method for detecting elevated muscle compartment pressure: A prospective clinical pilot study. Injury. 2021; doi: 10.1016/j.injury. 2021.02.054.Online ahead of print

[54] Sellei RM, Warkotsch U, Kobbe P, Weber CD, Reinhard N, de la Fuente M, Radermacher K, Hildebrand F. Noninvasive and reliable assessment of compartment elasticity by pressure related ultrasound: An in-vitro study. Injury. 2020; doi: 10.1016/j.injury. 2020.10.069. Online ahead of print

Surgery. 2015; 9:4-10

[49] Sellei RM, Hingmann SJ,

pressures by pressure-related ultrasound: A cadaveric model. Eur J Trauma Emerg Surg. 2015; 41:639.645

Schwinghammer A, Schmid T. Compression sonography for noninvasive measurement of lower leg compartment pressure in an animal model. Injury. 2018; 49:532-537

determine acute compartment

301-306

**68**

2019; 50: 627-632

**71**

**Chapter 6**

**Abstract**

patients.

**1. Introduction**

Patients

Abdominal Compartment

Syndrome among Medical

*Dweep Barbhaya and Salim Surani*

*Kejal Gandhi, Pahnwat Taweesedt, Munish Sharma,* 

Abdominal compartment syndrome and intra-abdominal hypertension (IAH) has been widely studied in surgical and trauma patients, even though the incidence of IAH in medical intensive care unit (MICU) remains high. Studies have shown that the time to decision making regarding diagnosis and management of IAH is twice in MICU compared to the corresponding surgical side. MICU patients often require large volume resuscitation such as in sepsis, hemorrhage, or an inflammatory condition such as acute pancreatitis, which increases the risk of development of IAH. It is often underdiagnosed and undertreated in MICU due to a lack of awareness of the consequences and mortality associated with it. Elevated intraabdominal pressure has systemic effects causing atelectatic lungs, decreased cardiac output, and renal insufficiency. IAH, if not recognized early, can quickly progress to compartment syndrome causing multiorgan failure and death. Approach to ACS management between medical and surgical intensivists varies largely because of lack of experience with surgical decompression. This article provides an overview of definitions, incidence, pathophysiology, clinical presentation, diagnosis, and management of IAH and abdominal compartment syndrome in critically in medical

**Keywords:** abdominal compartment syndrome, intra-abdominal hypertension,

A progressive increase in intra-abdominal pressure initially results in intraabdominal hypertension and later, affects end-organ perfusion resulting in abdominal compartment syndrome. It is often under-diagnosed as the end-organ perfusion caused by intra-abdominal hypertension in this patient population can also be explained by their overall critical condition. Thus, clinicians must have a high suspicion for intra-abdominal hypertension to prevent it from progressing to

intra-abdominal pressure, medical intensive care unit, bladder pressure,

multiorgan failure, decompression laparotomy

compartment syndrome and death.

#### **Chapter 6**

## Abdominal Compartment Syndrome among Medical Patients

*Kejal Gandhi, Pahnwat Taweesedt, Munish Sharma, Dweep Barbhaya and Salim Surani*

#### **Abstract**

Abdominal compartment syndrome and intra-abdominal hypertension (IAH) has been widely studied in surgical and trauma patients, even though the incidence of IAH in medical intensive care unit (MICU) remains high. Studies have shown that the time to decision making regarding diagnosis and management of IAH is twice in MICU compared to the corresponding surgical side. MICU patients often require large volume resuscitation such as in sepsis, hemorrhage, or an inflammatory condition such as acute pancreatitis, which increases the risk of development of IAH. It is often underdiagnosed and undertreated in MICU due to a lack of awareness of the consequences and mortality associated with it. Elevated intraabdominal pressure has systemic effects causing atelectatic lungs, decreased cardiac output, and renal insufficiency. IAH, if not recognized early, can quickly progress to compartment syndrome causing multiorgan failure and death. Approach to ACS management between medical and surgical intensivists varies largely because of lack of experience with surgical decompression. This article provides an overview of definitions, incidence, pathophysiology, clinical presentation, diagnosis, and management of IAH and abdominal compartment syndrome in critically in medical patients.

**Keywords:** abdominal compartment syndrome, intra-abdominal hypertension, intra-abdominal pressure, medical intensive care unit, bladder pressure, multiorgan failure, decompression laparotomy

#### **1. Introduction**

A progressive increase in intra-abdominal pressure initially results in intraabdominal hypertension and later, affects end-organ perfusion resulting in abdominal compartment syndrome. It is often under-diagnosed as the end-organ perfusion caused by intra-abdominal hypertension in this patient population can also be explained by their overall critical condition. Thus, clinicians must have a high suspicion for intra-abdominal hypertension to prevent it from progressing to compartment syndrome and death.

### **2. Definitions**

#### **2.1 Intra-abdominal pressure**

The abdomen is a closed cavity with a steady state pressure within it. This pressure is called Intra-abdominal pressure (IAP). Intra-abdominal pressure depends on the abdominal wall compliance and volume of the organs within the abdominal cavity. Thus, it is affected by the conditions that decreases the compliance of the wall (burn eschars or third spacing) or by additional volume of organs (such as fecal matter, presence of ascites, or space-occupying lesions such as tumors) [1].

Normal IAP varies between 5–7 mmHg [2]. Body Mass Index positively affects IAP with pressure being high in pregnant and morbidly obese individuals. Similarly, recent abdominal surgery can also affect the IAP.

#### **2.2 Abdominal perfusion pressure (APP)**

Abdominal perfusion pressure (APP) is measured by subtraction of intraabdominal pressure from the mean arterial pressure (MAP) [3].

$$\text{APP} = \text{MAP} - \text{IAP} \tag{1}$$

**73**

failure.

**3. Incidence**

resuscitation, sepsis, burns.

*Abdominal Compartment Syndrome among Medical Patients*

superimposed acute or subacute IAH [6].

and urine production than changes in MAP [7].

**2.5 Abdominal compartment syndrome (ACS)**

surgical or interventional radiology intervention [8].

It is associated with significant morbidity and mortality [9].

• Chronic IAH refers to the elevation of IAP over months to years such as in patients with increased abdominal wall compliance (pregnant or morbidly obese). These patients are at high risk for development of ACS if they have

Oliguria is most often the first sign of IAH. FG is measured as glomerular filtration pressure (GFP) – PTP (proximal tubular pressure) and is a measure of pressure

Since, PTP = IAP (3)

Therefore, FG = GFP - PTP = (MAP - IAP) - IAP (4)

Thus, FG = MAP - 2xIAP (5)

This equation shows that changes in IAP have a higher effect on renal function

Abdominal compartment syndrome (ACS) is defined as sustained IAP above 20 mmHg with evidence of end-organ dysfunction. ACS is further classified into primary, secondary, and recurrent based on the etiology and duration of end-organ

Primary: ACS occurring due to etiology primarily within the abdominopelvic cavity is termed as primary; for example, abdominal trauma, pancreatitis, abdominal surgery, hemoperitoneum, liver transplantation. It frequently requires early

Secondary: ACS occurring due to extra-abdominal etiology; example: fluid

Recurrent: Development of ACS again after the early resolution of the previous either primary or secondary ACS. It can occur despite the presence of an open abdomen or after abdominal closure following the resolution of the first episode.

Abdominal compartment syndrome has been studied widely in surgical and trauma patients. However, very few studies are available on the MICU patients. Many patients in MICU undergo large-volume resuscitation common conditions such as sepsis, hemorrhage, systemic inflammatory response syndrome, and are at high risk for the development of IAH. An incidence study done on MICU patients receiving large-volume resuscitation showed that 85% of patients enrolled

GFP MAP – IAP APP = = (2)

*DOI: http://dx.doi.org/10.5772/intechopen.96174*

**2.4 Filtration gradient (FG)**

across the glomerulus.

With the increase in IAP, APP decreases, and thereby, causing decreased perfusion to the abdominal viscera. APP is a better maker than arterial pH, base deficit, arterial lactate and hourly urine output, as an endpoint for resuscitation.

#### **2.3 Intra-abdominal hypertension (IAH)**

The World Society of Abdominal Compartment Syndrome (WSACS) established the definition of IAH and ACS in 2004 [4].Intra-abdominal hypertension (IAH) is defined as intra-abdominal pressure (IAP) greater than or equal to 12 mmHg.

IAH is further graded based on the IAP as shown in **Table 1**. IAH can also be divided as follows based on duration:



**Table 1.** *IAH classification based on IAP value [5].* • Chronic IAH refers to the elevation of IAP over months to years such as in patients with increased abdominal wall compliance (pregnant or morbidly obese). These patients are at high risk for development of ACS if they have superimposed acute or subacute IAH [6].

#### **2.4 Filtration gradient (FG)**

*A Comprehensive Review of Compartment Syndrome*

recent abdominal surgery can also affect the IAP.

**2.2 Abdominal perfusion pressure (APP)**

**2.3 Intra-abdominal hypertension (IAH)**

progress to ACS.

*IAH classification based on IAP value [5].*

The abdomen is a closed cavity with a steady state pressure within it. This pressure is called Intra-abdominal pressure (IAP). Intra-abdominal pressure depends on the abdominal wall compliance and volume of the organs within the abdominal cavity. Thus, it is affected by the conditions that decreases the compliance of the wall (burn eschars or third spacing) or by additional volume of organs (such as fecal matter, presence of ascites, or space-occupying lesions such as tumors) [1]. Normal IAP varies between 5–7 mmHg [2]. Body Mass Index positively affects IAP with pressure being high in pregnant and morbidly obese individuals. Similarly,

Abdominal perfusion pressure (APP) is measured by subtraction of intra-

With the increase in IAP, APP decreases, and thereby, causing decreased perfusion to the abdominal viscera. APP is a better maker than arterial pH, base deficit,

The World Society of Abdominal Compartment Syndrome (WSACS) established the definition of IAH and ACS in 2004 [4].Intra-abdominal hypertension (IAH) is defined as intra-abdominal pressure (IAP) greater than or equal to 12 mmHg.

• Hyperacute IAH refers to the transient elevation of the intra-abdominal pressure lasting for seconds such as while laughing, sneezing, straining, coughing.

• Acute IAH refers to the sustained elevation of IAP over hours such as in intraabdominal trauma or hemorrhage and has the potential to progress to ACS.

• Subacute IAH refers to the elevation of IAP over days and is mostly seen in the MICU patients receiving large volume resuscitation and also has potential to

arterial lactate and hourly urine output, as an endpoint for resuscitation.

IAH is further graded based on the IAP as shown in **Table 1**. IAH can also be divided as follows based on duration:

**Grades IAP** Grade I 12–15 mmHg Grade II 16–20 mmHg Grade III 21–25 mmHg Grade IV >25 mmHg

APP MAP IAP = − (1)

abdominal pressure from the mean arterial pressure (MAP) [3].

**2. Definitions**

**2.1 Intra-abdominal pressure**

**72**

**Table 1.**

Oliguria is most often the first sign of IAH. FG is measured as glomerular filtration pressure (GFP) – PTP (proximal tubular pressure) and is a measure of pressure across the glomerulus.

$$\text{GFP} = \text{MAP} - \text{IAP} = \text{APP} \tag{2}$$

$$\begin{aligned} \text{Since,} \\\\ \text{Therefore,} \\\\ \text{Therefore,} \end{aligned} \qquad \text{PTP-IAP} \tag{3}$$

$$\text{Therefore,} \qquad \text{FG} \equiv \text{GFP - PTP} \equiv \text{(MAP - IAP) - IAP} \tag{4}$$

$$\text{Thus,}\tag{5}\\
\text{Thus,}\\
\text{FG}=\text{MAP}-2\text{xIAP}\tag{5}$$

This equation shows that changes in IAP have a higher effect on renal function and urine production than changes in MAP [7].

#### **2.5 Abdominal compartment syndrome (ACS)**

Abdominal compartment syndrome (ACS) is defined as sustained IAP above 20 mmHg with evidence of end-organ dysfunction. ACS is further classified into primary, secondary, and recurrent based on the etiology and duration of end-organ failure.

Primary: ACS occurring due to etiology primarily within the abdominopelvic cavity is termed as primary; for example, abdominal trauma, pancreatitis, abdominal surgery, hemoperitoneum, liver transplantation. It frequently requires early surgical or interventional radiology intervention [8].

Secondary: ACS occurring due to extra-abdominal etiology; example: fluid resuscitation, sepsis, burns.

Recurrent: Development of ACS again after the early resolution of the previous either primary or secondary ACS. It can occur despite the presence of an open abdomen or after abdominal closure following the resolution of the first episode. It is associated with significant morbidity and mortality [9].

#### **3. Incidence**

Abdominal compartment syndrome has been studied widely in surgical and trauma patients. However, very few studies are available on the MICU patients. Many patients in MICU undergo large-volume resuscitation common conditions such as sepsis, hemorrhage, systemic inflammatory response syndrome, and are at high risk for the development of IAH. An incidence study done on MICU patients receiving large-volume resuscitation showed that 85% of patients enrolled developed IAH with IAP > 12 mmHg, 33% developed IAP > 20 mmHg and 25% met the criteria for ACS. These patients had median fluid balance of +6.9 L and Acute Physiology and Chronic Health Evaluation II (APACHE II) score of 23. Thus, data emphasized the high incidence of IAH in MICU patients receiving large-volume resuscitation [10]. In another prospective multi-institutional study done in 15 ICUs, of 491 patients enrolled, IAH occurred in almost half of all the patients and was twice as common in mechanically ventilated patients compared to those who were breathing spontaneously The study revealed that intra-abdominal hypertension proportionally increased the 28 and 90-day mortality [11]. Given the prevalence of IAH/ACS and associated mortality, it is important to be vigilant regarding the ACS development in MICU, especially in patients receiving the large-volume resuscitation.

#### **4. Etiology**

The abdomen is a closed cavity surrounded by rigid (pelvic bones, rib cage, spine) and flexible borders (Visceral organs, abdominal wall, diaphragm). There is an extent to which abdominal girth can increase and after an extent, the girth does not increase and results in intra-abdominal hypertension and thus, progressing to abdominal compartment syndrome.

Risk factors for IAH and ACS development can be divided as follows **Table 2**:


**75**

**5.3 Renal**

*Abdominal Compartment Syndrome among Medical Patients*

pulmonary diseases are at high risk of decompensation [13].

Like any other compartment syndrome, an increase in IAH, causes the decrease in perfusion of the contents within the abdominal cavity due to increased venous resistance, causing decreased capillary perfusion. However, IAH is an area of particular significance given the multi-systemic effect involving cardiac, pulmonary, and renal systems. Patients with underlying cardiomyopathy, renal insufficiency,

Increase in IAP causes cephalad movement of the diaphragm leading to increased intrathoracic pressure. This phenomenon results in the following:

Decrease venous return: Increase in IAP, increases the pressure in the IVC and with the cephalad motion of the diaphragm, the thoracic inlet of the IVC constricts; thus, decreasing the venous return and the preload, thereby, affecting a component of cardiac output. Decreased venous return increases the hydrostatic pressure in lower extremities resulting in peripheral edema and increased risk for development

Increase SVR: Increase in IAP causes increased pressure in systemic and aortic vasculature and also, increase pulmonary vascular resistance secondary to increased intrathoracic pressure. These factors thus increase SVR and thereby, decreasing the

Impaired cardiac function: Elevation of the diaphragm and increased intrathoracic pressure caused by IAH also causes cardiac compression, thus, decreasing

In conclusion, the MAP is affected by both SVR and Cardiac output. In absence

An increase in the IAP compresses the lung parenchyma by direct transmission of IAP and cephalad deviation of the diaphragm. Compression of lung parenchyma thus results in atelectasis, which results in increasing shunting of the blood and causes ventilation-perfusion mismatch. The atelectatic lung is also at higher risk for infection. In mechanically ventilated patients, increased IAP causes the peak inspiratory pressure and mean airway pressure to increase, thus causing the alveolar barotrauma. These patients also have decreased chest wall compliance and spontaneous tidal volume, causing hypoxemia and hypercarbia, which are the clinical features of ACS [16].

IAH significantly decreases the renal function and thus urine output by significantly affecting the renal blood flow. In comparison with superior mesenteric and celiac blood flow, studies have shown preferential decrease in renal blood flow with elevated IAP [17]. IAH results in renal arterial constriction and an increase in renal

of severe IAH, SVR increases, and cardiac output decreases (due to decreased preload). Thus, MAP remains stable despite a decrease in both preload and cardiac output. However, in patients with decreased intravascular volume or with poor cardiac function, even a mild to moderate increase in IAP can result in decreasing MAP. Therefore, preload augmentation with volume resuscitation appears to be beneficial to compensate for the increasing systemic vascular resistance. In ventilated patients, high PEEP or auto-PEEP can further decrease the venous return and

thus, are also at risk of decompensation at the lower elevation of IAP.

*DOI: http://dx.doi.org/10.5772/intechopen.96174*

**5. Pathophysiology**

**5.1 Cardiovascular**

of deep vein thrombosis [14].

ventricular compliance and contractility.

cardiac output [15].

**5.2 Pulmonary**

#### **Table 2.** *Risk factors predisposing to IAH and ACS [12].*

#### **5. Pathophysiology**

*A Comprehensive Review of Compartment Syndrome*

large-volume resuscitation.

abdominal compartment syndrome.

1. Decrease in abdominal wall compliance

Mechanical ventilation with high PEEP

Large volume resuscitation (> 5 L fluids in 24 hours) Hypothermia (core temperature less than 33 degree Celsius)

Massive blood transfusion (>10 PRBC in 24 hrs)

*Risk factors predisposing to IAH and ACS [12].*

2. Increase in intra-abdominal volume *2.1 Increase in intra-luminal volume* Fecal matter/air/fluid within the organs

Damage control laparotomy *2.2 Increase in extra-luminal content* Retroperitoneal tumor or hemorrhage

**Risk factors for IAH and ACS**

Rectus sheath hematoma Obesity (BMI > 30 kg/m2)

Abdominal surgery

Prone positioning

Pancreatitis Abdominal abscess Hemo/Pneumoperitoneum Liver transplantation Peritoneal dialysis Peritonitis 3. Secondary ACS

Acidosis (pH < 7.2)

Sepsis Major burns

Burn Eschars

Ascites

**4. Etiology**

developed IAH with IAP > 12 mmHg, 33% developed IAP > 20 mmHg and 25% met the criteria for ACS. These patients had median fluid balance of +6.9 L and Acute Physiology and Chronic Health Evaluation II (APACHE II) score of 23. Thus, data emphasized the high incidence of IAH in MICU patients receiving large-volume resuscitation [10]. In another prospective multi-institutional study done in 15 ICUs, of 491 patients enrolled, IAH occurred in almost half of all the patients and was twice as common in mechanically ventilated patients compared to those who were breathing spontaneously The study revealed that intra-abdominal hypertension proportionally increased the 28 and 90-day mortality [11]. Given the prevalence of IAH/ACS and associated mortality, it is important to be vigilant regarding the ACS development in MICU, especially in patients receiving the

The abdomen is a closed cavity surrounded by rigid (pelvic bones, rib cage, spine) and flexible borders (Visceral organs, abdominal wall, diaphragm). There is an extent to which abdominal girth can increase and after an extent, the girth does not increase and results in intra-abdominal hypertension and thus, progressing to

Risk factors for IAH and ACS development can be divided as follows **Table 2**:

Intestinal/Gastric distention such as colonic pseudo-obstruction, ileus, gastroparesis

Coagulopathy (platelets <55,000 or prothrombin time > 15 secs or INR >1.5)

**74**

**Table 2.**

Like any other compartment syndrome, an increase in IAH, causes the decrease in perfusion of the contents within the abdominal cavity due to increased venous resistance, causing decreased capillary perfusion. However, IAH is an area of particular significance given the multi-systemic effect involving cardiac, pulmonary, and renal systems. Patients with underlying cardiomyopathy, renal insufficiency, pulmonary diseases are at high risk of decompensation [13].

#### **5.1 Cardiovascular**

Increase in IAP causes cephalad movement of the diaphragm leading to increased intrathoracic pressure. This phenomenon results in the following:

Decrease venous return: Increase in IAP, increases the pressure in the IVC and with the cephalad motion of the diaphragm, the thoracic inlet of the IVC constricts; thus, decreasing the venous return and the preload, thereby, affecting a component of cardiac output. Decreased venous return increases the hydrostatic pressure in lower extremities resulting in peripheral edema and increased risk for development of deep vein thrombosis [14].

Increase SVR: Increase in IAP causes increased pressure in systemic and aortic vasculature and also, increase pulmonary vascular resistance secondary to increased intrathoracic pressure. These factors thus increase SVR and thereby, decreasing the cardiac output [15].

Impaired cardiac function: Elevation of the diaphragm and increased intrathoracic pressure caused by IAH also causes cardiac compression, thus, decreasing ventricular compliance and contractility.

In conclusion, the MAP is affected by both SVR and Cardiac output. In absence of severe IAH, SVR increases, and cardiac output decreases (due to decreased preload). Thus, MAP remains stable despite a decrease in both preload and cardiac output. However, in patients with decreased intravascular volume or with poor cardiac function, even a mild to moderate increase in IAP can result in decreasing MAP. Therefore, preload augmentation with volume resuscitation appears to be beneficial to compensate for the increasing systemic vascular resistance. In ventilated patients, high PEEP or auto-PEEP can further decrease the venous return and thus, are also at risk of decompensation at the lower elevation of IAP.

#### **5.2 Pulmonary**

An increase in the IAP compresses the lung parenchyma by direct transmission of IAP and cephalad deviation of the diaphragm. Compression of lung parenchyma thus results in atelectasis, which results in increasing shunting of the blood and causes ventilation-perfusion mismatch. The atelectatic lung is also at higher risk for infection. In mechanically ventilated patients, increased IAP causes the peak inspiratory pressure and mean airway pressure to increase, thus causing the alveolar barotrauma. These patients also have decreased chest wall compliance and spontaneous tidal volume, causing hypoxemia and hypercarbia, which are the clinical features of ACS [16].

#### **5.3 Renal**

IAH significantly decreases the renal function and thus urine output by significantly affecting the renal blood flow. In comparison with superior mesenteric and celiac blood flow, studies have shown preferential decrease in renal blood flow with elevated IAP [17]. IAH results in renal arterial constriction and an increase in renal

venous resistance, thus causing decrease in the venous drainage from the kidney. Secondarily, a decrease in cardiac output also results in activation of the reninangiotensin-aldosterone system, thus causing renal arterial vasoconstriction. As mentioned above an increase in IAP affects the filtration gradient and thus, resulting in a net decrease in urine output. A study has shown development of oliguria at IAP of approximately 15 mmHg, whereas elevation of IAP to 30 mmHg results in anuria [18].

#### **5.4 Gastrointestinal system**

The gut is most sensitive to increased IAP. It affects the gut in the following ways: Decreasing mesenteric blood flow: Mesenteric blood flow is decreased at IAP as low as 10 mmHg. A study showed 43% decrease in the celiac artery blood flow and 69% decrease in superior mesenteric artery blood flow when IAP is elevated to 40 mmHg. This is accentuated by shock and hypotension [17].

Compressing mesenteric veins: IAH compresses mesenteric veins in the intestinal wall causing impaired venous flow from the intestine and thus, causing intestinal edema. This edema in turn causes an elevation in the IAP, thus initiating a vicious cycle. This results in worsened hypoperfusion leading to elevation of lactic acid and intestinal ischemia.

Loss of intestinal mucosa: Gut hypoperfusion results in the loss of protective intestinal mucosal barrier, leading to gut bacterial translocation and results, in sepsis with multi-organ failure [19].

#### **5.5 Hepatic**

Elevation in IAP causes decreased hepatic arterial flow and increases the portal venous and hepatic venous resistance, thus, resulting in decreased microcirculatory blood flow in the liver. This results in decreased mitochondrial function and production of ATPs. Overall, the liver's capacity to clear lactic acid decreases. This has been seen at IAP elevation to as low as 10 mmHg in presence of normal cardiac output and MAP [20].

#### **5.6 Central nervous system**

Elevation in IAP causes increase in intracranial pressure (ICP) by decreasing the lumbar venous plexus blood flow and decreasing the cerebral venous outflow. Overall increase in partial pressure of carbon dioxide results in cerebral venous constriction resulting in increased ICP This, in turn, decreases the cerebral perfusion pressure and function [21].

#### **5.7 Abdominal wall**

Increased IAP can cause a decrease in blood flow to the abdominal wall, leading to wall ischemia and edema. Rectus sheath blood flow decreases in proportion to increase in the intra-abdominal pressure. It decreases by approximately 58% from baseline with IAP as low as 10 mmHg. This further reduces the abdominal wall compliance and exacerbates the IAH [22].

#### **6. Clinical presentation**

Early identification of IAH is imperative to prevent further progression to ACS. Most patients with ACS are critically ill and unable to express the symptoms, therefore, identifying the signs of IAH or developing ACS is very important.

**77**

*Abdominal Compartment Syndrome among Medical Patients*

**6.1 Signs of abdominal compartment syndrome**

**6.2 Imaging findings**

**7. IAP measurement**

**7.1 Intravesical pressure**

port is accessed.

used is as follows:

measure IAP at early stage and have high suspicion for ACS.

pression of IVC or renal displacement, bowel wall thickening [24].

Intraabdominal hypertension through its delirious effect on multi-organ system

These are not diagnostic for ACS, however, can be used as signs for early identification for developing abdominal compartment syndrome. Chest X-ray significant for elevated hemidiaphragm, pulmonary atelectasis and decreased lung volumes. CT scan findings are consistent with abdominal distention, tense infiltration of retroperitoneum out of proportion to the retroperitoneal disease, extrinsic com-

In multiple prospective studies, the sensitivity of clinical examination in the diagnosis of IAH is only 40–60% [25, 26]. Abdomen being a hollow cavity filled with viscera, IAP can be measured by measuring the pressure within various viscera. However, IAP is typically measured via trans-bladder pressure measurement as recommended by the World Society of Abdominal Compartment Syndrome (WSACS) in 2006 due to ease of measurement [27]. Other ways to measure IAP include manometry from the abdominal drain, measuring pressure from central venous catheter inserted into inferior vena cava, measuring pressure via nasogastric tube, measuring rectal/uterine pressure [28]. Advanced modalities such as measuring abdominal wall thickness via ultrasound are also currently being investigated.

Measurement of intravesical pressure has evolved over the years to decrease complications including the need for repeat measurements, urinary tract infection, and to decrease the incidence of needlestick injuries. The most common technique

• A three-way stopcock is used to decrease the number of times an aspiration

including kidney, lungs and cardiovascular system results in following clinical entities as mentioned in **Table 3** [23]. These clinical signs are seen commonly in critically ill patients having multiple comorbidities. Thus, it is very important to

*DOI: http://dx.doi.org/10.5772/intechopen.96174*

• Increased peak inspiratory pressure and PEEP

*Clinical signs of abdominal compartment syndrome [23].*

• Refractory metabolic acidosis

• Abdominal distention and elevated IAP • Oliguria refractory to volume resuscitation

**Signs of ACS**

• Hypoxia • Hypercarbia

• Elevated ICP

**Table 3.**

*Abdominal Compartment Syndrome among Medical Patients DOI: http://dx.doi.org/10.5772/intechopen.96174*

#### **Signs of ACS**

*A Comprehensive Review of Compartment Syndrome*

**5.4 Gastrointestinal system**

acid and intestinal ischemia.

**5.6 Central nervous system**

sion pressure and function [21].

compliance and exacerbates the IAH [22].

**5.7 Abdominal wall**

**6. Clinical presentation**

**5.5 Hepatic**

sepsis with multi-organ failure [19].

venous resistance, thus causing decrease in the venous drainage from the kidney. Secondarily, a decrease in cardiac output also results in activation of the reninangiotensin-aldosterone system, thus causing renal arterial vasoconstriction. As mentioned above an increase in IAP affects the filtration gradient and thus, resulting in a net decrease in urine output. A study has shown development of oliguria at IAP of approximately 15 mmHg, whereas elevation of IAP to 30 mmHg results in anuria [18].

The gut is most sensitive to increased IAP. It affects the gut in the following ways: Decreasing mesenteric blood flow: Mesenteric blood flow is decreased at IAP as low as 10 mmHg. A study showed 43% decrease in the celiac artery blood flow and 69% decrease in superior mesenteric artery blood flow when IAP is elevated to

Compressing mesenteric veins: IAH compresses mesenteric veins in the intestinal wall causing impaired venous flow from the intestine and thus, causing intestinal edema. This edema in turn causes an elevation in the IAP, thus initiating a vicious cycle. This results in worsened hypoperfusion leading to elevation of lactic

Loss of intestinal mucosa: Gut hypoperfusion results in the loss of protective intestinal mucosal barrier, leading to gut bacterial translocation and results, in

Elevation in IAP causes decreased hepatic arterial flow and increases the portal venous and hepatic venous resistance, thus, resulting in decreased microcirculatory blood flow in the liver. This results in decreased mitochondrial function and production of ATPs. Overall, the liver's capacity to clear lactic acid decreases. This has been seen at IAP elevation to as low as 10 mmHg in presence of normal cardiac output and MAP [20].

Elevation in IAP causes increase in intracranial pressure (ICP) by decreasing the lumbar venous plexus blood flow and decreasing the cerebral venous outflow. Overall increase in partial pressure of carbon dioxide results in cerebral venous constriction resulting in increased ICP This, in turn, decreases the cerebral perfu-

Increased IAP can cause a decrease in blood flow to the abdominal wall, leading to wall ischemia and edema. Rectus sheath blood flow decreases in proportion to increase in the intra-abdominal pressure. It decreases by approximately 58% from baseline with IAP as low as 10 mmHg. This further reduces the abdominal wall

Early identification of IAH is imperative to prevent further progression to ACS. Most patients with ACS are critically ill and unable to express the symptoms, therefore, identifying the signs of IAH or developing ACS is very important.

40 mmHg. This is accentuated by shock and hypotension [17].

**76**


**Table 3.**

*Clinical signs of abdominal compartment syndrome [23].*

#### **6.1 Signs of abdominal compartment syndrome**

Intraabdominal hypertension through its delirious effect on multi-organ system including kidney, lungs and cardiovascular system results in following clinical entities as mentioned in **Table 3** [23]. These clinical signs are seen commonly in critically ill patients having multiple comorbidities. Thus, it is very important to measure IAP at early stage and have high suspicion for ACS.

#### **6.2 Imaging findings**

These are not diagnostic for ACS, however, can be used as signs for early identification for developing abdominal compartment syndrome. Chest X-ray significant for elevated hemidiaphragm, pulmonary atelectasis and decreased lung volumes. CT scan findings are consistent with abdominal distention, tense infiltration of retroperitoneum out of proportion to the retroperitoneal disease, extrinsic compression of IVC or renal displacement, bowel wall thickening [24].

#### **7. IAP measurement**

In multiple prospective studies, the sensitivity of clinical examination in the diagnosis of IAH is only 40–60% [25, 26]. Abdomen being a hollow cavity filled with viscera, IAP can be measured by measuring the pressure within various viscera. However, IAP is typically measured via trans-bladder pressure measurement as recommended by the World Society of Abdominal Compartment Syndrome (WSACS) in 2006 due to ease of measurement [27]. Other ways to measure IAP include manometry from the abdominal drain, measuring pressure from central venous catheter inserted into inferior vena cava, measuring pressure via nasogastric tube, measuring rectal/uterine pressure [28]. Advanced modalities such as measuring abdominal wall thickness via ultrasound are also currently being investigated.

#### **7.1 Intravesical pressure**

Measurement of intravesical pressure has evolved over the years to decrease complications including the need for repeat measurements, urinary tract infection, and to decrease the incidence of needlestick injuries. The most common technique used is as follows:

• A three-way stopcock is used to decrease the number of times an aspiration port is accessed.


Although, intravesical pressure measurement is the gold standard to measure the intra-abdominal pressure, it has many technical difficulties. Though the evolution of technique has decreased the risk of needlestick injuries, this technique still is cumbersome, intermittent and carries potential risk of urinary tract infection. Most of the ventilated patients in MICU have head of bed elevated to prevent aspiration risk and studies have shown that the intravesical pressure increases significantly even with mild head of bed elevation [29].

#### **7.2 Intra-gastric pressure**

This method involves measurement of the pressure within the stomach using the nasogastric tube. It can be used when the patient does not have a foley catheter or intravesical pressure measurement is not possible due to bladder trauma, pelvic hematoma, peritoneal adhesions or neurogenic bladder. The use of tonometer to measure the intragastric pressure has been validated and showed good correlation with the IAP [30]. However, the IAP measured via nasogastric tube is affected by the migrating motor complex and the effects of enteral tube feeding on the IAP measurement are still unknown. The intra-gastric pressure measurement can also be used to monitor continuous intra-abdominal pressure. The most advanced method involves the air-pouch system where the tip of the nasogastric tube contains a pressure transducer which can automatically calibrate every hour and provides continuous intra-abdominal pressure measurement, however, this method is not validated in humans yet.

#### **7.3 Inferior vena cava pressure**

IVC catheter placed via femoral cannulation can be connected to the pressure transducer to provide IVC pressure measurement. A study validating the indirect methods of IAP measurement in rabbits showed good correlation of IVC and transvesical pressure with direct intraperitoneal pressure measurements. However, IVC catheter are associated with increased risk of infection and sepsis. A multicenter observational study showed that femoral vein pressure has good correlation with the IAP when intra-abdominal pressure is >20 mmHg and can be used as a surrogate to bladder pressure, thus, allowing continuous measurement of IAP [31].

**79**

**Figure 1.**

*Medical management for intra-abdominal hypertension [27].*

*Abdominal Compartment Syndrome among Medical Patients*

techniques have not been validated in the ICU setting [32].

Management can be divided into medical and surgical interventions.

Rectal and transvaginal pressure measurement is less practical given the pressure can be affected by the residual fecal mass or gynecological bleeding. Both these

Management of ACS involves early recognition of IAH and/or end-organ failure and prompt interventions. It has been outlined by WSACS as shown in **Figures 1** and **2**.

Non-surgical measures include decreasing the IAP by decreasing the content within the visceral organs that might be causing the IAH. Ileus is a common postabdominal surgical complication and is also common amongst patients receiving large volume resuscitation, in patients with peritonitis, electrolyte imbalance and those receiving narcotic medications. These factors are independently associated to increase risk for IAH/ACS. Thus, treating ileus by nasogastric suction and rectal suction, use of prokinetic agents, colonoscopic decompression, and frequent enemas helps to decrease IAP by decreasing the volume of intra-luminal contents. In patients where extra-luminal factors are leading to elevated IAH, alleviating the cause is most advisable to improve the abdominal wall compliance. If any space-occupying lesion is contributing to the IAH, thorough investigation including Ultrasound and CT scan should be done to identify the nature of space occupying lesion (SOL) and if indicated, either percutaneous drainage or surgical removal of the SOL can help with reducing the IAP. If ascites is contributing to the IAH, then

*DOI: http://dx.doi.org/10.5772/intechopen.96174*

**7.4 Rectal and uterine pressure**

**8.1 Non-surgical management**

**8. Management**

#### **7.4 Rectal and uterine pressure**

Rectal and transvaginal pressure measurement is less practical given the pressure can be affected by the residual fecal mass or gynecological bleeding. Both these techniques have not been validated in the ICU setting [32].

#### **8. Management**

*A Comprehensive Review of Compartment Syndrome*

• A 50 ml syringe is attached to the 2nd stopcock.

• The urine drainage port of the foley is clamped.

the stopcocks to the pressure transducer is opened.

even with mild head of bed elevation [29].

**7.2 Intra-gastric pressure**

validated in humans yet.

**7.3 Inferior vena cava pressure**

point where the mid-axillary line crosses the iliac crest.

stopcock.

• A saline infusion set with 1000 ml normal saline bag is inserted in the first

• The third stopcock is attached to the pressure transducer and it is zeroed at a

• Instill 25 ml normal saline at room temperature into the bladder. Given that this normal saline can also result in detrusor muscle contraction and falsely increased the measured IAP, it is advisable to wait 30–60 seconds after saline administration to measure the pressure. Also, the patient should be in the complete supine position with a measurement done at end-expiration to ensure no abdominal muscle contraction is present. The measurement is done after

Although, intravesical pressure measurement is the gold standard to measure the intra-abdominal pressure, it has many technical difficulties. Though the evolution of technique has decreased the risk of needlestick injuries, this technique still is cumbersome, intermittent and carries potential risk of urinary tract infection. Most of the ventilated patients in MICU have head of bed elevated to prevent aspiration risk and studies have shown that the intravesical pressure increases significantly

This method involves measurement of the pressure within the stomach using the nasogastric tube. It can be used when the patient does not have a foley catheter or intravesical pressure measurement is not possible due to bladder trauma, pelvic hematoma, peritoneal adhesions or neurogenic bladder. The use of tonometer to measure the intragastric pressure has been validated and showed good correlation with the IAP [30]. However, the IAP measured via nasogastric tube is affected by the migrating motor complex and the effects of enteral tube feeding on the IAP measurement are still unknown. The intra-gastric pressure measurement can also be used to monitor continuous intra-abdominal pressure. The most advanced method involves the air-pouch system where the tip of the nasogastric tube contains a pressure transducer which can automatically calibrate every hour and provides continuous intra-abdominal pressure measurement, however, this method is not

IVC catheter placed via femoral cannulation can be connected to the pressure transducer to provide IVC pressure measurement. A study validating the indirect methods of IAP measurement in rabbits showed good correlation of IVC and transvesical pressure with direct intraperitoneal pressure measurements. However, IVC catheter are associated with increased risk of infection and sepsis. A multicenter observational study showed that femoral vein pressure has good correlation with the IAP when intra-abdominal pressure is >20 mmHg and can be used as a surrogate to bladder pressure, thus, allowing continuous measurement

**78**

of IAP [31].

Management of ACS involves early recognition of IAH and/or end-organ failure and prompt interventions. It has been outlined by WSACS as shown in **Figures 1** and **2**. Management can be divided into medical and surgical interventions.

#### **8.1 Non-surgical management**

Non-surgical measures include decreasing the IAP by decreasing the content within the visceral organs that might be causing the IAH. Ileus is a common postabdominal surgical complication and is also common amongst patients receiving large volume resuscitation, in patients with peritonitis, electrolyte imbalance and those receiving narcotic medications. These factors are independently associated to increase risk for IAH/ACS. Thus, treating ileus by nasogastric suction and rectal suction, use of prokinetic agents, colonoscopic decompression, and frequent enemas helps to decrease IAP by decreasing the volume of intra-luminal contents.

In patients where extra-luminal factors are leading to elevated IAH, alleviating the cause is most advisable to improve the abdominal wall compliance. If any space-occupying lesion is contributing to the IAH, thorough investigation including Ultrasound and CT scan should be done to identify the nature of space occupying lesion (SOL) and if indicated, either percutaneous drainage or surgical removal of the SOL can help with reducing the IAP. If ascites is contributing to the IAH, then

**Figure 1.** *Medical management for intra-abdominal hypertension [27].*

#### **Figure 2.**

*Evaluation and management of abdominal compartment syndrome [4].*

therapeutic paracentesis can help. However, in patients with progressive IAH or not responding to therapeutic paracentesis, continuous percutaneous drainage guided by Ultrasound or CT scan should be considered. Studies have shown that continuous percutaneous drainage decreases the rate of open abdominal decompression in 81% of the patients treated. However, if percutaneous drain fails to drain at least 1 L of fluid and decrease the intra-abdominal pressure by at least 9 mmHg in first four hours, the likelihood for requirement of surgical decompression increases [33].

Abdominal compliance can also be improved by adequate sedation and analgesia, removal of constrictive dressing, and eschars. Supine positioning or reverse Trendelenburg position also helps alleviate the abdominal muscle contracture. Low evidence is available but neuromuscular blockade should be considered per WSACS guidelines [27].

Managing the volume status of the patient is equally important, as hypovolemia can further exacerbate the effects of IAH and the large volume resuscitation can also similarly be shown as a predictive factor for progression to ACS. Thus, it's important to judge the volume status of the patient and maintain euvolemia. Hemodynamic monitoring is advisable for judicious administration of fluids. Recent study in burn patients receiving large volume resuscitation has shown that hypertonic saline or colloid solution effectively decreases the risk for developing IAH/ACS [34].

Despite adequate fluid resuscitation, some patients with IAH/ACS develop total body fluid overload secondary to capillary leakage and excessive third spacing with significant elevation in IAP [35]. Diuretics are generally contraindicated as

**81**

**9. Prognosis**

**10. Conclusion**

sepsis and multi-organ failure.

*Abdominal Compartment Syndrome among Medical Patients*

ment of IAP even after abdominal closure is necessary.

these patients are intravascularly volume depleted. However, once these patients become hemodynamically stable with resolution of shock, diuretics along with colloid administration helps to the fluid from the third space. Continuous renal replacement therapy to remove excess fluid judiciously and increase abdominal wall compliance can also help decrease the IAP However, it's important to ensure that intra-vascular volume is adequately maintained for appropriate organ perfusion and avoidance of multi-organ failure development secondary to inadequate

When the non-surgical methods fail to consistently decrease the IAP, surgical abdominal decompression via laparotomy is the treatment of choice. Decompressive laparotomy results in a decrease in intra-abdominal volume and thus decreases the IAP. Delay in surgical depression in surgical and non-surgical patients is associated with increased mortality [36]. There is also an increased risk of ischemia–reperfusion syndrome especially in patients with significantly high IAP for a prolonged period. Abdominal laparotomy with negative peritoneal pressure therapy is preferred given that it improves visceral perfusion and also decreases bacterial translocation. In multiple studies, surgical decompression has been shown to decrease IAP and improve respiratory, cardiac, and renal function [37]. However, studies on the mortality related to ACS requiring decompressive laparotomy are inconclusive as there is a significant difference in when the decision to do decompression is made by the intensivist based on their specialty. Studies have shown that medical intensivists prefer diuresis and dialysis more and take double the time than surgical intensivists to decide on decompressive laparotomy. Surgical decompression, though a life-saving procedure, has significant morbidity and mortality associated with it. In a study, three out of four patients of severe acute pancreatitis who underwent surgical decompression died and two of them from uncontrollable retroperitoneal hemorrhage [38]. Decompressive laparotomy can result in excess loss of fluids from the exposed tissue resulting in exsanguination or can result in a large ventral hernia or fistula [39]. The open abdomen also increases risk for bacterial translocation and sepsis. Thus, steps should be taken to close the abdomen as soon as possible with most surgeons planning staged closure every 48 hours. Continued manometric measure-

ACS is associated with high mortality and hence, it's imperative to identify the early signs of intra-abdominal hypertension. Presence of IAH on day 1 of ICU is not an independent risk factor for mortality, however, occurrence and persistence of IAH during the ICU stay has significant associated with mortality [40]. Studies have shown that mortality increases proportionally with abdominal hypertension. A study showed 45.1% mortality in ACS patients compared to 21% mortality in patients with increased IAP [41]. Most common cause leading to death includes

Intra-abdominal hypertension and abdominal compartment syndrome are prevalent amongst critically ill medical patients and associated with high mortality.

*DOI: http://dx.doi.org/10.5772/intechopen.96174*

perfusion.

**8.2 Surgical management**

these patients are intravascularly volume depleted. However, once these patients become hemodynamically stable with resolution of shock, diuretics along with colloid administration helps to the fluid from the third space. Continuous renal replacement therapy to remove excess fluid judiciously and increase abdominal wall compliance can also help decrease the IAP However, it's important to ensure that intra-vascular volume is adequately maintained for appropriate organ perfusion and avoidance of multi-organ failure development secondary to inadequate perfusion.

#### **8.2 Surgical management**

*A Comprehensive Review of Compartment Syndrome*

therapeutic paracentesis can help. However, in patients with progressive IAH or not responding to therapeutic paracentesis, continuous percutaneous drainage guided by Ultrasound or CT scan should be considered. Studies have shown that continuous percutaneous drainage decreases the rate of open abdominal decompression in 81% of the patients treated. However, if percutaneous drain fails to drain at least 1 L of fluid and decrease the intra-abdominal pressure by at least 9 mmHg in first four hours, the likelihood for requirement of surgical decompression increases [33]. Abdominal compliance can also be improved by adequate sedation and analgesia, removal of constrictive dressing, and eschars. Supine positioning or reverse Trendelenburg position also helps alleviate the abdominal muscle contracture. Low evidence is available but neuromuscular blockade should be considered per WSACS

*Evaluation and management of abdominal compartment syndrome [4].*

Managing the volume status of the patient is equally important, as hypovolemia can further exacerbate the effects of IAH and the large volume resuscitation can also similarly be shown as a predictive factor for progression to ACS. Thus, it's important to judge the volume status of the patient and maintain euvolemia. Hemodynamic monitoring is advisable for judicious administration of fluids. Recent study in burn patients receiving large volume resuscitation has shown that hypertonic saline or colloid solution effectively decreases the risk for developing

Despite adequate fluid resuscitation, some patients with IAH/ACS develop total

body fluid overload secondary to capillary leakage and excessive third spacing with significant elevation in IAP [35]. Diuretics are generally contraindicated as

**80**

guidelines [27].

**Figure 2.**

IAH/ACS [34].

When the non-surgical methods fail to consistently decrease the IAP, surgical abdominal decompression via laparotomy is the treatment of choice. Decompressive laparotomy results in a decrease in intra-abdominal volume and thus decreases the IAP. Delay in surgical depression in surgical and non-surgical patients is associated with increased mortality [36]. There is also an increased risk of ischemia–reperfusion syndrome especially in patients with significantly high IAP for a prolonged period. Abdominal laparotomy with negative peritoneal pressure therapy is preferred given that it improves visceral perfusion and also decreases bacterial translocation. In multiple studies, surgical decompression has been shown to decrease IAP and improve respiratory, cardiac, and renal function [37]. However, studies on the mortality related to ACS requiring decompressive laparotomy are inconclusive as there is a significant difference in when the decision to do decompression is made by the intensivist based on their specialty. Studies have shown that medical intensivists prefer diuresis and dialysis more and take double the time than surgical intensivists to decide on decompressive laparotomy. Surgical decompression, though a life-saving procedure, has significant morbidity and mortality associated with it. In a study, three out of four patients of severe acute pancreatitis who underwent surgical decompression died and two of them from uncontrollable retroperitoneal hemorrhage [38].

Decompressive laparotomy can result in excess loss of fluids from the exposed tissue resulting in exsanguination or can result in a large ventral hernia or fistula [39]. The open abdomen also increases risk for bacterial translocation and sepsis. Thus, steps should be taken to close the abdomen as soon as possible with most surgeons planning staged closure every 48 hours. Continued manometric measurement of IAP even after abdominal closure is necessary.

#### **9. Prognosis**

ACS is associated with high mortality and hence, it's imperative to identify the early signs of intra-abdominal hypertension. Presence of IAH on day 1 of ICU is not an independent risk factor for mortality, however, occurrence and persistence of IAH during the ICU stay has significant associated with mortality [40]. Studies have shown that mortality increases proportionally with abdominal hypertension. A study showed 45.1% mortality in ACS patients compared to 21% mortality in patients with increased IAP [41]. Most common cause leading to death includes sepsis and multi-organ failure.

#### **10. Conclusion**

Intra-abdominal hypertension and abdominal compartment syndrome are prevalent amongst critically ill medical patients and associated with high mortality. Thus, medical staff should have a high suspicion of ACS in critically ill patients. Large volume resuscitation should be rationalized, and early surgical decompression must be considered if indicated.

### **Conflict of interest**

The authors declare no conflict of interest.

### **Author details**

Kejal Gandhi1 , Pahnwat Taweesedt2 , Munish Sharma2 , Dweep Barbhaya1 and Salim Surani3 \*

1 Georgetown University/Medstar Washington Hospital Center, Washington, DC, USA

2 Corpus Christi Medical Center, Texas, USA

3 Christus Spohn Hospital Corpus Christi – Memorial, Corpus Christi, Texas, USA

\*Address all correspondence to: srsurani@hotmail.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.

**83**

*Abdominal Compartment Syndrome among Medical Patients*

obesity, pregnancy, and general medicine. Anaesthesiol Intensive Ther.

[7] Dalfino L, Tullo L, Donadio I, Malcangi V, Brienza N. Intra-abdominal hypertensionand acute renal failurein critically ill patients. Intensive Care Med [Internet]. 2008;34(4):707-13. Available from: https://doi.org/10.1007/

[8] Tons C, Schachtrupp A, Rau M, Mumme T, Schumpelick V. Abdominal compartment syndrome: avoidance and treatment. Der Chir. 2000;71(8):918-926.

[9] Rajasurya V, Surani S. Abdominal compartment syndrome: Often overlooked conditions in medical intensive care units. World J Gastroenterol. 2020;26(3):266.

[10] Daugherty EL, Liang H, Taichman D, Hansen-Flaschen J, Fuchs BD. Abdominal Compartment Syndrome Is Common in Medical Intensive Care Unit Patients Receiving Large-Volume Resuscitation. J Intensive

Care Med [Internet]. 2007 Sep 1;22(5):294-9. Available from: https:// doi.org/10.1177/0885066607305247

[11] Reintam Blaser A, Regli A, De Keulenaer B, Kimball EJ, Starkopf L, Davis WA, et al. Incidence, Risk Factors, and Outcomes of Intra-Abdominal Hypertension in Critically Ill Patients-A

Prospective Multicenter Study (IROI Study). Crit Care Med. 2019

article/pii/S0272523108000919

[13] Papavramidis TS, Marinis AD, Pliakos I, Kesisoglou I, Papavramidou N.

[12] Malbrain MLNG, De laet IE. Intra-Abdominal Hypertension: Evolving Concepts. Clin Chest Med [Internet]. 2009;30(1):45-70. Available from: http://www.sciencedirect.com/science/

Apr;47(4):535-542.

2015;47(3):228-240.

s00134-007-0969-4

*DOI: http://dx.doi.org/10.5772/intechopen.96174*

[1] Bailey J, Shapiro MJ. Abdominal compartment syndrome. Crit Care [Internet]. 2000;4(1):23. Available from: https://doi.org/10.1186/cc646

[2] De Keulenaer BL, De Waele JJ, Powell B, Malbrain M. What is normal intra-abdominal pressure and how is it affected by positioning, body mass and positive end-expiratory pressure? Intensive Care Med.

[3] Cheatham ML, White MW, Sagraves SG, Johnson JL, Block EFJ. Abdominal Perfusion Pressure: A Superior Parameter in the Assessment of Intra-abdominal Hypertension. J Trauma Acute Care Surg [Internet].

2000;49(4). Available from: https://journals.lww.com/jtrauma/ Fulltext/2000/10000/Abdominal\_ Perfusion\_Pressure\_\_A\_Superior\_

[4] Cheatham ML, Malbrain MLNG, Kirkpatrick A, Sugrue M, Parr M, De Waele J, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations. Intensive Care Med [Internet]. 2007;33(6):951-62. Available from: https://doi.org/10.1007/

[5] Malbrain MLNG, De laet IE, De Waele JJ, Kirkpatrick AW. Intraabdominal hypertension: Definitions, monitoring, interpretation and management. Best Pract Res Clin Anaesthesiol [Internet]. 2013;27(2):249- 270. Available from: http://www. sciencedirect.com/science/article/pii/

[6] Malbrain MLNG, De Keulenaer BL,

Kirkpatrick AW, et al. Intra-abdominal

Oda J, De Waele J, Roberts DJ,

hypertension and abdominal compartment syndrome in burns,

Parameter.8.aspx

s00134-007-0592-4

S152168961300044X

2009;35(6):969-976.

**References**

*Abdominal Compartment Syndrome among Medical Patients DOI: http://dx.doi.org/10.5772/intechopen.96174*

#### **References**

*A Comprehensive Review of Compartment Syndrome*

The authors declare no conflict of interest.

must be considered if indicated.

**Conflict of interest**

Thus, medical staff should have a high suspicion of ACS in critically ill patients. Large volume resuscitation should be rationalized, and early surgical decompression

**82**

**Author details**

and Salim Surani3

, Pahnwat Taweesedt2

2 Corpus Christi Medical Center, Texas, USA

provided the original work is properly cited.

\*Address all correspondence to: srsurani@hotmail.com

\*

, Munish Sharma2

1 Georgetown University/Medstar Washington Hospital Center, Washington, DC,

3 Christus Spohn Hospital Corpus Christi – Memorial, Corpus Christi, Texas, USA

© 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,

, Dweep Barbhaya1

Kejal Gandhi1

USA

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[3] Cheatham ML, White MW, Sagraves SG, Johnson JL, Block EFJ. Abdominal Perfusion Pressure: A Superior Parameter in the Assessment of Intra-abdominal Hypertension. J Trauma Acute Care Surg [Internet]. 2000;49(4). Available from: https://journals.lww.com/jtrauma/ Fulltext/2000/10000/Abdominal\_ Perfusion\_Pressure\_\_A\_Superior\_ Parameter.8.aspx

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[11] Reintam Blaser A, Regli A, De Keulenaer B, Kimball EJ, Starkopf L, Davis WA, et al. Incidence, Risk Factors, and Outcomes of Intra-Abdominal Hypertension in Critically Ill Patients-A Prospective Multicenter Study (IROI Study). Crit Care Med. 2019 Apr;47(4):535-542.

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*DOI: http://dx.doi.org/10.5772/intechopen.96174*

[26] Blaser AR, Sarapuu S, Tamme K, Starkopf J. Expanded Measurements of Intra-Abdominal Pressure Do Not Increase the Detection Rate of Intra-Abdominal Hypertension: A Single-Center Observational Study\*. Crit Care Med [Internet]. 2014;42(2). Available from: https://journals.lww. com/ccmjournal/Fulltext/2014/02000/ Expanded\_Measurements\_of\_Intra\_ Abdominal\_Pressure.18.aspx

[27] Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain MLNG, De Keulenaer B, et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment

Syndrome. Intensive Care Med [Internet]. 2013;39(7):1190-206. Available from: https://doi.org/10.1007/

[28] Malbrain MLNG. Different

techniques to measure intra-abdominal pressure (IAP): time for a critical re-appraisal. Appl Physiol intensive care

[29] Cheatham ML, De Waele JJ, De Laet I, De Keulenaer B, Widder S, Kirkpatrick AW, et al. The impact of body position on intra-abdominal pressure measurement: A multicenter analysis\*. Crit Care Med [Internet]. 2009;37(7). Available from: https:// journals.lww.com/ccmjournal/ Fulltext/2009/07000/The\_impact\_ of\_body\_position\_on\_intra\_

[30] Sugrue M, Buist MD, Lee A, Sanchez DJ, Hillman KM. Intra-

abdominal pressure measurement using a modified nasogastric tube: description and validation of a new technique. Intensive Care Med [Internet]. 1994;20(8):588-590. Available from: http://europepmc.org/abstract/

s00134-013-2906-z

Med. 2006;105-119.

abdominal.8.aspx

MED/7706574

*Abdominal Compartment Syndrome among Medical Patients DOI: http://dx.doi.org/10.5772/intechopen.96174*

[26] Blaser AR, Sarapuu S, Tamme K, Starkopf J. Expanded Measurements of Intra-Abdominal Pressure Do Not Increase the Detection Rate of Intra-Abdominal Hypertension: A Single-Center Observational Study\*. Crit Care Med [Internet]. 2014;42(2). Available from: https://journals.lww. com/ccmjournal/Fulltext/2014/02000/ Expanded\_Measurements\_of\_Intra\_ Abdominal\_Pressure.18.aspx

*A Comprehensive Review of Compartment Syndrome*

and hepatic microcirculatory blood flow. J Trauma [Internet]. 1992 Aug;33(2):279—82; discussion 282—3. Available from: https:// doi.org/10.1097/00005373-

[21] Bloomfield GL, Ridings PC, Blocher CR, Marmarou A,

Sugerman HJ. Effects of Increased Intraabdominal Pressure upon Intracranial and Cerebral Perfusion Pressure before and after Volume Expansion. J Trauma Acute Care Surg [Internet]. 1996;40(6). Available from: https://journals.lww. com/jtrauma/Fulltext/1996/06000/ Effects\_of\_Increased\_Intra\_abdominal\_

199208000-00019

Pressure\_upon.12.aspx

S0039610905705843

Sep;173(3):575-579.

gov/10851415

[24] Pickhardt PJ, Shimony JS,

Heiken JP, Buchman TG, Fisher AJ. The abdominal compartment syndrome: CT findings. AJR Am J Roentgenol. 1999

[25] Kirkpatrick AW, Brenneman FD, McLean RF, Rapanos T, Boulanger BR. Is clinical examination an accurate indicator of raised intra-abdominal pressure in critically injured patients? Can J Surg [Internet]. 2000 Jun;43(3):207-211. Available from: https://pubmed.ncbi.nlm.nih.

surg/134

[22] Diebel, L., Saxe, J. M., & Dulchavsky S. Effects of Intra-Abdominal Pressure on Abdominal Wall Blood Flow. Am Surg [Internet]. 1992;58(9):573-576. Available from: https://corescholar.libraries.wright.edu/

[23] Ivatury RR, Diebel L, Porter JM, Simon RJ. INTRA-ABDOMINAL HYPERTENSION AND THE ABDOMINAL COMPARTMENT SYNDROME. Surg Clin North Am [Internet]. 1997;77(4):783- 800. Available from: http://www. sciencedirect.com/science/article/pii/

Abdominal compartment syndrome– Intra-abdominal hypertension: Defining, diagnosing, and managing. J Emergencies, Trauma Shock.

[14] Kashtan J, Green JF, Parsons EQ, Holcroft JW. Hemodynamic effects of increased abdominal pressure. J Surg Res [Internet]. 1981;30(3):249- 255. Available from: http://www. sciencedirect.com/science/article/

[15] Luca A, Cirera I, García-Pagán JC, Feu F, Pizcueta P, Bosch J, et al.

Hemodynamic effects of acute changes in intra-abdominal pressure in patients with cirrhosis. Gastroenterology. 1993

2011;4(2):279.

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Jan;104(1):222-227.

Suppl 1:78-88.

[16] Pelosi P, Quintel M,

Malbrain MLNG. Effect of intraabdominal pressure on respiratory mechanics. Acta Clin Belg. 2007;62

[17] Barnes GE, Laine GA, Giam PY, Smith EE, Granger HJ. Cardiovascular

responses to elevation of intraabdominal hydrostatic pressure. Am J Physiol Integr Comp Physiol [Internet]. 1985 Feb 1;248(2):R208-13. Available from: https://doi.org/10.1152/

ajpregu.1985.248.2.R208

Feb;197(2):183-187.

2007;31(2):88-99.

[18] Richards WO, Scovill W, Shin B, Reed W. Acute renal failure associated with increased intraabdominal pressure. Ann Surg. 1983

[19] De Laet IE, Malbrain M.

[20] Diebel LN, Wilson RF, Dulchavsky SA, Saxe J. Effect of increased intra-abdominal pressure on hepatic arterial, portal venous,

Current insights in intra-abdominal hypertension and abdominal

compartment syndrome. Med intensiva.

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[27] Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain MLNG, De Keulenaer B, et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med [Internet]. 2013;39(7):1190-206. Available from: https://doi.org/10.1007/ s00134-013-2906-z

[28] Malbrain MLNG. Different techniques to measure intra-abdominal pressure (IAP): time for a critical re-appraisal. Appl Physiol intensive care Med. 2006;105-119.

[29] Cheatham ML, De Waele JJ, De Laet I, De Keulenaer B, Widder S, Kirkpatrick AW, et al. The impact of body position on intra-abdominal pressure measurement: A multicenter analysis\*. Crit Care Med [Internet]. 2009;37(7). Available from: https:// journals.lww.com/ccmjournal/ Fulltext/2009/07000/The\_impact\_ of\_body\_position\_on\_intra\_ abdominal.8.aspx

[30] Sugrue M, Buist MD, Lee A, Sanchez DJ, Hillman KM. Intraabdominal pressure measurement using a modified nasogastric tube: description and validation of a new technique. Intensive Care Med [Internet]. 1994;20(8):588-590. Available from: http://europepmc.org/abstract/ MED/7706574

[31] Howard AE, Regli A, Litton E, Malbrain MM, Palermo A-M, De Keulenaer BL. Can Femoral Venous Pressure be Used as an Estimate for Standard Vesical Intra-Abdominal Pressure Measurement? Anaesth Intensive Care [Internet]. 2016 Nov 1;44(6):704-11. Available from: https:// doi.org/10.1177/0310057X1604400604

[32] Sugrue M, De Waele J, De Keulenaer BL, Roberts DJ, Malbrain MLNG. A user's guide to intra-abdominal pressure measurement. Anaesthesiol Intensive Ther. 2015;47(3):241-251.

[33] Cheatham ML, Safcsak K. Percutaneous catheter decompression in the treatment of elevated intraabdominal pressure. Chest. 2011 Dec;140(6):1428-1435.

[34] O'Mara MS, Slater H, Goldfarb IW, Caushaj PF. A prospective, randomized evaluation of intra-abdominal pressures with crystalloid and colloid resuscitation in burn patients. J Trauma. 2005 May;58(5):1011-1018.

[35] Cordemans C, De laet I, Van Regenmortel N, Schoonheydt K, Dits H, Huber W, et al. Fluid management in critically ill patients: the role of extravascular lung water, abdominal hypertension, capillary leak, and fluid balance. Ann Intensive Care [Internet]. 2012;2(1):S1. Available from: https://doi. org/10.1186/2110-5820-2-S1-S1

[36] Mentula P, Hienonen P, Kemppainen E, Puolakkainen P, Leppäniemi A. Surgical Decompression for Abdominal Compartment Syndrome in Severe Acute Pancreatitis. Arch Surg [Internet]. 2010 Aug 1;145(8):764-9. Available from: https://doi.org/10.1001/ archsurg.2010.132

[37] Rogers WK, Garcia L. Intraabdominal Hypertension, Abdominal Compartment Syndrome, and the Open Abdomen. Chest [Internet]. 2018;153(1):238-250. Available from: http://www. sciencedirect.com/science/article/pii/ S0012369217313193

[38] De Waele JJ, Hoste E, Blot SI, Decruyenaere J, Colardyn F. Intraabdominal hypertension in patients with severe acute pancreatitis. Crit Care [Internet]. 2005;9(4):R452. Available from: https://doi.org/10.1186/cc3754

[39] De Waele JJ, Kimball E, Malbrain M, Nesbitt I, Cohen J, Kaloiani V, et al. Decompressive laparotomy for abdominal compartment syndrome. Br J Surg. 2016;103(6):709.

[40] Malbrain MLNG, Chiumello D, Pelosi P, Bihari D, Innes R, Ranieri VM, et al. Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study. Crit Care Med. 2005;33(2):315-322.

[41] Parsak CK, Seydaoglu G, Sakman G, Acarturk TO, Karakoc E, Hanta I, et al. Abdominal Compartment Syndrome: Current Problems and New Strategies. World J Surg [Internet]. 2008;32(1): 13-9. Available from: https://doi. org/10.1007/s00268-007-9286-x

**87**

**Chapter 7**

**Abstract**

Compartment Syndrome Related

Surgical Treatment of Urolithiasis

The incidence of urolithiasis is progressively increasing worldwide, as is the surgical treatment of urinary stones. The most frequent surgery for urolithiasis is ureterorenoscopy, which is performed in the lithotomy position. This position is also used in the endoscopic approach to bladder stones. Lateral decubitus is rarely used in the treatment of urinary stones. In the case of complex kidney stones, the gold standard treatment is percutaneous nephrolithotomy. This surgery has traditionally been performed in the prone position. However, the use of the supine (Valdivia) position is increasing in recent times. Furthermore, the Galdakaomodified supine Valdivia position has been widely used for percutaneous nephrolithotomy since it was described by Ibarluzea et al. in 2007. Treatment of kidney and ureteral stones simultaneously is allowed in both supine positions. In addition, they allow the removal of encrusted stents and the easy placement of double J stents and, in the case of the Galdakao-modified supine Valdivia position, percutaneous nephrostomies. Compartment syndrome is a rare complication in the lithotomy position, but scarcely described in the supine position. This especially applies to the Galdakao-modified supine Valdivia position, in which the lower limbs are in moderate flexion, with the ipsilateral lower limb in a slightly lower position relative to the other. This complication can lead to skin necrosis, myoglobinuric renal failure, amputation, permanent neuromuscular dysfunction, and even death. Risk factors include Body Mass Index, male gender, obesity, increased muscle mass, peripheral vascular disease (advanced age, hypertension, hyperlipidemia and diabetes mellitus), height, lack of operative experience, significant bleeding during surgery, hypothermia, acidemia, combination general-spinal anesthesia, prolonged surgical time, systemic hypotension, ASA (American Society of Anesthesiologists) class or vasoconstrictor drugs. Therefore, compartment syndrome of the leg is a potentially devastating complication that must be suspected and treated through early decompression of the compartment by four compartment fasciotomy. Preventive

to Patient Positioning in the

*Alberto Artiles-Medina and Javier Burgos-Revilla*

*Inés Laso-García, Fernando Arias-Fúnez,* 

*Gemma Duque-Ruiz, David Díaz-Pérez,* 

measures reduce the incidence of this condition.

valdivia position, complications, compartment syndrome

**Keywords:** lithiasis, percutaneous nephrolithotomy, Galdakao-modified supine

#### **Chapter 7**

*A Comprehensive Review of Compartment Syndrome*

and the Open Abdomen. Chest [Internet]. 2018;153(1):238-250. Available from: http://www.

S0012369217313193

Surg. 2016;103(6):709.

sciencedirect.com/science/article/pii/

[39] De Waele JJ, Kimball E, Malbrain M, Nesbitt I, Cohen J, Kaloiani V, et al. Decompressive laparotomy for

abdominal compartment syndrome. Br J

intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study. Crit Care Med. 2005;33(2):315-322.

[41] Parsak CK, Seydaoglu G, Sakman G, Acarturk TO, Karakoc E, Hanta I, et al. Abdominal Compartment Syndrome: Current Problems and New Strategies. World J Surg [Internet]. 2008;32(1): 13-9. Available from: https://doi. org/10.1007/s00268-007-9286-x

[40] Malbrain MLNG, Chiumello D, Pelosi P, Bihari D, Innes R, Ranieri VM, et al. Incidence and prognosis of

[38] De Waele JJ, Hoste E, Blot SI, Decruyenaere J, Colardyn F. Intraabdominal hypertension in patients with severe acute pancreatitis. Crit Care [Internet]. 2005;9(4):R452. Available from: https://doi.org/10.1186/cc3754

**86**

## Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis

*Inés Laso-García, Fernando Arias-Fúnez, Gemma Duque-Ruiz, David Díaz-Pérez, Alberto Artiles-Medina and Javier Burgos-Revilla*

#### **Abstract**

The incidence of urolithiasis is progressively increasing worldwide, as is the surgical treatment of urinary stones. The most frequent surgery for urolithiasis is ureterorenoscopy, which is performed in the lithotomy position. This position is also used in the endoscopic approach to bladder stones. Lateral decubitus is rarely used in the treatment of urinary stones. In the case of complex kidney stones, the gold standard treatment is percutaneous nephrolithotomy. This surgery has traditionally been performed in the prone position. However, the use of the supine (Valdivia) position is increasing in recent times. Furthermore, the Galdakaomodified supine Valdivia position has been widely used for percutaneous nephrolithotomy since it was described by Ibarluzea et al. in 2007. Treatment of kidney and ureteral stones simultaneously is allowed in both supine positions. In addition, they allow the removal of encrusted stents and the easy placement of double J stents and, in the case of the Galdakao-modified supine Valdivia position, percutaneous nephrostomies. Compartment syndrome is a rare complication in the lithotomy position, but scarcely described in the supine position. This especially applies to the Galdakao-modified supine Valdivia position, in which the lower limbs are in moderate flexion, with the ipsilateral lower limb in a slightly lower position relative to the other. This complication can lead to skin necrosis, myoglobinuric renal failure, amputation, permanent neuromuscular dysfunction, and even death. Risk factors include Body Mass Index, male gender, obesity, increased muscle mass, peripheral vascular disease (advanced age, hypertension, hyperlipidemia and diabetes mellitus), height, lack of operative experience, significant bleeding during surgery, hypothermia, acidemia, combination general-spinal anesthesia, prolonged surgical time, systemic hypotension, ASA (American Society of Anesthesiologists) class or vasoconstrictor drugs. Therefore, compartment syndrome of the leg is a potentially devastating complication that must be suspected and treated through early decompression of the compartment by four compartment fasciotomy. Preventive measures reduce the incidence of this condition.

**Keywords:** lithiasis, percutaneous nephrolithotomy, Galdakao-modified supine valdivia position, complications, compartment syndrome

#### **1. Introduction**

#### **1.1 Urolithiasis**

Urinary lithiasis is a disease known since ancient times, characterized by the formation of urinary stones (**Figure 1**). The prevalence of lithiasis in the population in 1913 has been estimated to be 1–2%, and a progressive increase has been found to 2.7% in 1985. [1] An article studying the evolution of the prevalence in a 25-yearperiod, showed an annual increase in stone formation. The prevalence of lithiasis in population has grown even more in recent years. [2] The incidence of lithiasis in the United States doubled in a 4 year-period. [3]

Furthermore, Scales et al. described a prevalence of almost 9% of the population. [4] Nevertheless, it has been observed a variation according to the country studied: 1–5% in Asia, 5–9% in Europe, 13% in North America and 20% in Saudi Arabia. [5]

In recent years, in the United Kingdom, a 63% increase in hospitalization episodes associated with urolithiasis has been observed. [6] The number of extracorporeal shock wave lithotripsy has increased from 14,491 in 2000 to 822,402 in 2010. There has been an increase of 127% in the number of ureteroscopies. The acts aimed at treating urinary lithiasis have increased compared to other urological activities. In 2010, shock wave lithotripsy was performed with the same frequency as transurethral resection of the prostate or transurethral resection of the bladder. More ureteroscopies were performed than nephrectomies, prostatectomies, and cystectomies combined; and more percutaneous nephrolithectomies than cystectomies. [7] Therefore, the surgical treatment of urolithiasis is of great clinical relevance.

#### **1.2 Surgical positions in urological surgery and urolithiasis**

The most frequent surgery for urolithiasis is ureterorenoscopy, which is performed in the lithotomy (Lloyd-Davies) position. This position is also used in the endoscopic approach to bladder stones.

**89**

**Figure 2.**

*Right kidney staghorn lithiasis.*

*Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis*

renal and renoureteral stones (for example, staghorn lithiasis, **Figure 2**). This surgery has traditionally been performed in the prone position, but in recent years the number of urologists who perform it in the supine position (Valdivia Position)

In addition, it allows two surgeons to operate simultaneously.

**1.3 The Galdakao-modified supine valdivia position for percutaneous** 

passage of a nephroscope, reaching the upper urinary tract lumen.

be lengthy, or even ineffective, in treating the entire stone.

**1.4 Compartment syndrome related to patient positioning**

procedure is called Endoscope Combined IntraRenal Surgery (ECIRS).

Occasionally, lower extremities are bandaged to prevent venous thrombosis. Once the patient is placed, retrograde pyelography is performed. The upper urinary tract is accessed through an X-ray and ultrasound guided puncture of the lower calyx. After Alken telescopic dilatation, an Amplatz sheath is placed to allow the

Using the nephroscope and a retrograde flexible ureteroscope, the whole upper urinary tract can be managed, as decribed by Ibarluzea and Scoffone. [10, 11] This

Sources of lithiasis fragmentation, such as Holmium laser, as well as nitinol baskets, are used to remove the lithiasis. If the stone is too complex, this process can

The position in which a patient is placed, and the duration for which it is maintained, are key factors in the development of well-leg compartment syndrome. Acute compartment syndrome of the extremities rarely develops in the supine position, commonly used in urologic open surgeries, such as cystolithotomy. Lateral decubitus position is rarely used in the treatment of urolithiasis. Laparoscopic

Ibarluzea et al. described the Galdakao-modified supine Valdivia position in 2007, and it has been widely used for percutaneous nephrolithotomy since then. [11] Treatment of kidney and ureteral stones simultaneously is allowed in both supine positions. In addition, they allow the removal of encrusted stents and the easy placement of double J stents and, in the case of the Galdakao-modified supine Valdivia position, percutaneous nephrostomies. Unlike the prone position, the patient does not need to be relocated during surgery, shortening the operating time.

Percutaneous nephrolithectomy is currently the treatment of choice for complex

*DOI: http://dx.doi.org/10.5772/intechopen.96971*

has increased. [8–11]

**nephrolithotomy**

*Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis DOI: http://dx.doi.org/10.5772/intechopen.96971*

Percutaneous nephrolithectomy is currently the treatment of choice for complex renal and renoureteral stones (for example, staghorn lithiasis, **Figure 2**). This surgery has traditionally been performed in the prone position, but in recent years the number of urologists who perform it in the supine position (Valdivia Position) has increased. [8–11]

Ibarluzea et al. described the Galdakao-modified supine Valdivia position in 2007, and it has been widely used for percutaneous nephrolithotomy since then. [11] Treatment of kidney and ureteral stones simultaneously is allowed in both supine positions. In addition, they allow the removal of encrusted stents and the easy placement of double J stents and, in the case of the Galdakao-modified supine Valdivia position, percutaneous nephrostomies. Unlike the prone position, the patient does not need to be relocated during surgery, shortening the operating time. In addition, it allows two surgeons to operate simultaneously.

#### **1.3 The Galdakao-modified supine valdivia position for percutaneous nephrolithotomy**

Occasionally, lower extremities are bandaged to prevent venous thrombosis. Once the patient is placed, retrograde pyelography is performed. The upper urinary tract is accessed through an X-ray and ultrasound guided puncture of the lower calyx. After Alken telescopic dilatation, an Amplatz sheath is placed to allow the passage of a nephroscope, reaching the upper urinary tract lumen.

Using the nephroscope and a retrograde flexible ureteroscope, the whole upper urinary tract can be managed, as decribed by Ibarluzea and Scoffone. [10, 11] This procedure is called Endoscope Combined IntraRenal Surgery (ECIRS).

Sources of lithiasis fragmentation, such as Holmium laser, as well as nitinol baskets, are used to remove the lithiasis. If the stone is too complex, this process can be lengthy, or even ineffective, in treating the entire stone.

#### **1.4 Compartment syndrome related to patient positioning**

The position in which a patient is placed, and the duration for which it is maintained, are key factors in the development of well-leg compartment syndrome.

Acute compartment syndrome of the extremities rarely develops in the supine position, commonly used in urologic open surgeries, such as cystolithotomy. Lateral decubitus position is rarely used in the treatment of urolithiasis. Laparoscopic

**Figure 2.** *Right kidney staghorn lithiasis.*

*A Comprehensive Review of Compartment Syndrome*

United States doubled in a 4 year-period. [3]

endoscopic approach to bladder stones.

**1.2 Surgical positions in urological surgery and urolithiasis**

*Calcium oxalate lithiasis: conventional microscope and scanning electron microscope.*

Urinary lithiasis is a disease known since ancient times, characterized by the formation of urinary stones (**Figure 1**). The prevalence of lithiasis in the population in 1913 has been estimated to be 1–2%, and a progressive increase has been found to 2.7% in 1985. [1] An article studying the evolution of the prevalence in a 25-yearperiod, showed an annual increase in stone formation. The prevalence of lithiasis in population has grown even more in recent years. [2] The incidence of lithiasis in the

Furthermore, Scales et al. described a prevalence of almost 9% of the population. [4] Nevertheless, it has been observed a variation according to the country studied: 1–5% in Asia, 5–9% in Europe, 13% in North America and 20% in Saudi Arabia. [5] In recent years, in the United Kingdom, a 63% increase in hospitalization episodes associated with urolithiasis has been observed. [6] The number of extracorporeal shock wave lithotripsy has increased from 14,491 in 2000 to 822,402 in 2010. There has been an increase of 127% in the number of ureteroscopies. The acts aimed at treating urinary lithiasis have increased compared to other urological activities. In 2010, shock wave lithotripsy was performed with the same frequency as transurethral resection of the prostate or transurethral resection of the bladder. More ureteroscopies were performed than nephrectomies, prostatectomies, and cystectomies combined; and more percutaneous nephrolithectomies than cystectomies. [7] Therefore, the surgical treatment of urolithiasis is of great clinical relevance.

The most frequent surgery for urolithiasis is ureterorenoscopy, which is performed in the lithotomy (Lloyd-Davies) position. This position is also used in the

**1. Introduction**

**1.1 Urolithiasis**

**88**

**Figure 1.**

#### *A Comprehensive Review of Compartment Syndrome*

pyelolithectomy would be one of the examples. General complications of lateral decubitus positioning are similar to those found with the supine position.

It has been described that lithotomy position, in general surgical, urological and orthopedic patients, is associated with changes in intracompartmental pressure that may eventually develop a compartment syndrome, especially in prolonged surgeries. [12–15]

Well-leg compartment syndrome has also been described in patients placed in the hemilithotomy position. The majority of cases described in the literature have been lengthy procedures with surgical time greater than 5 h. [13]

Prolonged positioning in a steep Trendelenburg position during, for example, a laparoscopic prostatectomy, may cause hypoperfusion of the lower extremities, pressure marks, tissue injury, and even rhabdomyolysis. After long surgical procedures involving extreme positions, rhabdomyolysis from muscle ischemia has been observed. [16]

Acute compartment syndrome of the leg occurs following a rise in the pressure inside the muscle compartment. [16] A significant decrease in deep muscle mixed tissue oxygen saturation of calf muscles is observed, due to the combined effect of perfusion related factors, such as hydrostatic forces, blood and intra-abdominal pressure, which lead to tissue underperfusion. [17, 18]

A delay in the diagnosis and treatment of a compartment syndrome may lead to devastating outcomes for the patient. [19] It may lead to admission to an Intensive Care Unit and necessity of renal replacement therapy, multiple organ dysfunction syndrome, and even death.

Therefore, the suspicion of this syndrome in a patient who presents symptoms compatible with this adverse outcome, is essential to avoid further complications.

#### **2. Epidemiology**

Prolonged urological surgeries performed in the lithotomy or extreme Trendelemburg positions for the treatment of urolithiasis may rarely lead to wellleg compartment syndrome. [20] It is thought to be underreported in the literature, especially those with less severe clinical features. Moreover, it is generally misdiagnosed as other possible surgical complications, such as deep vein thrombosis or neuropraxia. [21, 22] In the lithotomy position, the estimated total rate is approximately 1: 3500. [17]

However, studies reporting on the compartment syndrome associated with the lithotomy position in the fields of general and gynecological surgeries are somewhat frequent [23] This complication has also been described in the literature regarding urological surgeries. [21] In some cases, the complication occurs in both extremities simultaneously. [24–26] This circumstance is often described in relation to the performance of a radical prostatectomy, either laparoscopic or robotic, in the extreme Trendelenburg position. [19, 27]

Nonetheless, the appearance of this complication is not frequent during a percutaneous nephrolithotomy. It has hardly been reported in both supine positions, in which the lower limbs present a more moderate flexion than in other endourological procedures. In the Galdakao-Modified Supine Valdivia Position, the patient is placed in a slightly different position from the classic lithotomy, with the lower limbs in moderate flexion, and with the ipsilateral lower limb in a slightly inferior position with respect to the other (**Figure 3**). [28] On the other hand, the appearance of acute abdominal compartment syndrome has already been described during the performance of a percutaneous nephrolithotomy. [29]

**91**

**Table 1.**

**3. Etiology**

**Figure 3.**

*Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis*

Risk factors (**Table 1**) associated with the development of compartment syndrome reported include Body Mass Index (BMI), male gender, obesity, height, peripheral vascular disease (advanced age, hypertension, hyperlipidemia and

ASA (American Society of Anesthesiologists) class

Advanced age Hypertension Hyperlipidemia Diabetes Mellitus

Height BMI Male sex

Related to the surgery Prolonged surgery time

*Risk factors associated to the development of compartment syndrome.*

Increased muscle bulk

Systemic hypotension

Lack of operative experience Combined general-spinal anesthesia

The use of vasoconstricting drugs Important bleeding during the surgery

Wrapping elevated legs

Acidemia

Hypothermia

*DOI: http://dx.doi.org/10.5772/intechopen.96971*

*The Galdakao-modified supine Valdivia position.*

Related to the patient Obesity

*Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis DOI: http://dx.doi.org/10.5772/intechopen.96971*

**Figure 3.** *The Galdakao-modified supine Valdivia position.*

#### **3. Etiology**

*A Comprehensive Review of Compartment Syndrome*

surgeries. [12–15]

observed. [16]

complications.

**2. Epidemiology**

mately 1: 3500. [17]

Trendelenburg position. [19, 27]

the performance of a percutaneous nephrolithotomy. [29]

syndrome, and even death.

pyelolithectomy would be one of the examples. General complications of lateral decubitus positioning are similar to those found with the supine position.

It has been described that lithotomy position, in general surgical, urological and orthopedic patients, is associated with changes in intracompartmental pressure that may eventually develop a compartment syndrome, especially in prolonged

Well-leg compartment syndrome has also been described in patients placed in the hemilithotomy position. The majority of cases described in the literature have

Prolonged positioning in a steep Trendelenburg position during, for example, a laparoscopic prostatectomy, may cause hypoperfusion of the lower extremities, pressure marks, tissue injury, and even rhabdomyolysis. After long surgical procedures involving extreme positions, rhabdomyolysis from muscle ischemia has been

Acute compartment syndrome of the leg occurs following a rise in the pressure inside the muscle compartment. [16] A significant decrease in deep muscle mixed tissue oxygen saturation of calf muscles is observed, due to the combined effect of perfusion related factors, such as hydrostatic forces, blood and intra-abdominal

A delay in the diagnosis and treatment of a compartment syndrome may lead to devastating outcomes for the patient. [19] It may lead to admission to an Intensive Care Unit and necessity of renal replacement therapy, multiple organ dysfunction

Therefore, the suspicion of this syndrome in a patient who presents symp-

toms compatible with this adverse outcome, is essential to avoid further

Prolonged urological surgeries performed in the lithotomy or extreme Trendelemburg positions for the treatment of urolithiasis may rarely lead to wellleg compartment syndrome. [20] It is thought to be underreported in the literature, especially those with less severe clinical features. Moreover, it is generally misdiagnosed as other possible surgical complications, such as deep vein thrombosis or neuropraxia. [21, 22] In the lithotomy position, the estimated total rate is approxi-

However, studies reporting on the compartment syndrome associated with the lithotomy position in the fields of general and gynecological surgeries are somewhat frequent [23] This complication has also been described in the literature regarding urological surgeries. [21] In some cases, the complication occurs in both extremities simultaneously. [24–26] This circumstance is often described in relation to the performance of a radical prostatectomy, either laparoscopic or robotic, in the extreme

Nonetheless, the appearance of this complication is not frequent during a percutaneous nephrolithotomy. It has hardly been reported in both supine positions, in which the lower limbs present a more moderate flexion than in other endourological procedures. In the Galdakao-Modified Supine Valdivia Position, the patient is placed in a slightly different position from the classic lithotomy, with the lower limbs in moderate flexion, and with the ipsilateral lower limb in a slightly inferior position with respect to the other (**Figure 3**). [28] On the other hand, the appearance of acute abdominal compartment syndrome has already been described during

been lengthy procedures with surgical time greater than 5 h. [13]

pressure, which lead to tissue underperfusion. [17, 18]

**90**

Risk factors (**Table 1**) associated with the development of compartment syndrome reported include Body Mass Index (BMI), male gender, obesity, height, peripheral vascular disease (advanced age, hypertension, hyperlipidemia and


**Table 1.** *Risk factors associated to the development of compartment syndrome.* diabetes mellitus), lack of operative experience, significant bleeding during surgery, hypothermia, acidemia, combination general-spinal anesthesia, prolonged surgical time, systemic hypotension, ASA (American Society of Anesthesiologists) class or vasoconstrictor drugs. Increased muscle bulk is associated with a tighter and less compliant compartment, and also with greater accumulation of toxic metabolites and free radicals. [17, 18, 21–23, 29–31]

The use of compressive leg wraps has been associated with well-leg compartment syndrome in some studies, [12] while in others a reduction in intracompartment pressure of the lower leg was observed with the use of external intermittent compression. [14]

#### **4. Pathophysiology**

Compartment syndromes can arise in any area of the body that has little or no capacity for tissue expansion, such as the abdomen, buttocks and hands.

The lower extremity has four main compartments, which are superficial posterior, deep posterior, anterior and lateral. Bone and inelastic fascial layers border the muscles and neurovascular structures. The following nerves traverse these compartments: the tibial and sural nerves, and the superficial and deep branches of the peroneal nerve. The compartment can be accommodated to a limited extent by the sheath. [16] Most commonly involved compartment is the anterior one. [21] As soon as legs are placed in the lithotomy position, the compartmental pressures begin to increase. [17] The height above the level of the heart at which the legs rise is crucial. [17, 18]

An increase in intracompartment pressure in the lithotomy position, with the use of support behind the calf or knee, has been described from 10.7 (SD 5.8) mmHg to 16.5 (SD 3.4) mmHg. [14] Circulation compromise occurs with increased tissue pressure within a closed osteofascial compartment. Compression of the calf produces local ischaemia through two mechanisms: by direct occlusion of the arterial blood flow and by indirect obstruction of the venous drainage. The weight of the limb itself, as well as the use of devices such as braces and cushions, produces greater compression. It should also be noted that operating personnel can cause more compression. [17]

The difference between capillary perfusion pressure and the interstitial fluid pressure determines tissue perfusion. When interstitial fluid pressure exceeds capillary perfusion pressure, capillary collapse and consequent ischemia of the muscles and nerves occurs. [32] It has two main implications: a decrease in the rates of both delivery of oxygenated arterial blood and drainage of deoxygenated venous blood. [17]

The integrity of the vascular endothelium is impaired by initial ischemia. Its capacity as a barrier to the movement of solute and serum disappears. Thus, a self-perpetuating cycle of ischaemia and tissue oedema begins. When the patient returns to the initial position, the compartment pressure may increase even further, producing a reperfusion injury. [16, 17] After 1 h of ischaemia, on restoring blood flow, through the release of prostaglandins and thromboxane, platelets are activated. This may predispose to deep vein thrombosis, which may increase venous pressure and therefore, compromise local blood flow. [18]

In addition, once reperfusion occurs, large amounts of toxic intracellular content are released into the bloodstream. They are the markers of rhabdomyolysis. [18] After surgery, serum creatine phosphokinase increases significantly, peaking at 18 hours. [19] The main pathophysiologic mechanisms involved in renal insufficiency from rhabdomyolysis are renal vasoconstriction, intraluminal cast formation, and direct myoglobin toxicity. [16]

**93**

*Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis*

Once the patient is in the recovery room, in the immediate postoperative period,

despite analgesic infusion, significant pain is reported in the lower extremity (a pain out of proportion). The limb appears oedematous and cyanotic, although the pedis pulses may be preserved. General inflammation of the leg and dorsal ankle flexion and toe mobility deficit is observed. In a more advanced stage, we may

Once the compartment fasciotomy has been performed, we can observe that only the deep compartments may be affected by ischemia. In this case, the muscle mass of the anterolateral compartment and the deep posteromedial compartment shows evidence of necrosis. Muscles show pale pink edema. Stimulation with an electric scapel shows absence of contractility. Correct tonality and contractility can be seen in the muscle mass of both superficial compartments if this occurs. When diagnosis and treatment are delayed, both deep and superficial masses are affected

After lengthy surgeries, we must be aware of the possibility of the development of a compartment syndrome. Prompt diagnosis and treatment should be performed using a four-compartment fasciotomy to avoid serious and irreversible complications. [23] The appearance of the following signs and symptoms must warn us: pink skin, presence of pulse, paresis of muscles, paraesthesia and a disproportionate pain, generally described by the patient as burning and deep. It is reproduced by passive stretching of the muscles of the compartment. The diagnosis is more difficult in

On analysis, serum creatinine kinase activity is increased. We must bear in mind that the first signs are subtle and more often neurological. This is due to the fact that nonmyelinated type C sensory fibers are the tissues most sensitive to hypoxia. [21, 32] Therefore, a delay in the diagnosis should be considered with the use of

However, the definitive diagnosis is made by direct measurement of the compartmental pressure. Compartment pressure can be measured with different pressure catheters. These catheters have fine bore and their use is associated with minimal morbidity. [24] It can be measured by using a simple needle manometer, continuous infusion, wick catheter, slit catheter, or solid-state transducer method. [30] The indication for a fasciotomy is a value greater than 20–30 mmHg, although it may vary depending on the perfusion pressure and the clinical setting. [32] We can use various non-invasive imaging techniques to determine intracompartment pressure, including laser Doppler flowmetry, ultrasonic devices, or near infrared spectroscopy. [16] These techniques might be particularly useful in pediatric patients, in whom invasive monitoring is not ideal. Near-infrared spectroscopy has proven useful in one-month-old infants. Nevertheless, both laser Doppler flowmetry and near-infrared spectroscopy may be more useful in chronic compartment syndrome, as they measure variations in muscle oxygenation. In acute compartment syndrome, changes may have already occurred at the time of

*DOI: http://dx.doi.org/10.5772/intechopen.96971*

observe the absence of peripheral pulses. [24]

**5. Clinical features**

**5.1 Clinical findings**

**5.2 Intraoperative findings**

unconscious and sedated patients.

epidural anesthesia, due to a masking effect. [21]

by ischemia.

**6. Diagnosis**

*Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis DOI: http://dx.doi.org/10.5772/intechopen.96971*

#### **5. Clinical features**

*A Comprehensive Review of Compartment Syndrome*

metabolites and free radicals. [17, 18, 21–23, 29–31]

compression. [14]

**4. Pathophysiology**

more compression. [17]

blood. [17]

diabetes mellitus), lack of operative experience, significant bleeding during

surgery, hypothermia, acidemia, combination general-spinal anesthesia, prolonged surgical time, systemic hypotension, ASA (American Society of Anesthesiologists) class or vasoconstrictor drugs. Increased muscle bulk is associated with a tighter and less compliant compartment, and also with greater accumulation of toxic

The use of compressive leg wraps has been associated with well-leg compartment syndrome in some studies, [12] while in others a reduction in intracompartment pressure of the lower leg was observed with the use of external intermittent

Compartment syndromes can arise in any area of the body that has little or no

The lower extremity has four main compartments, which are superficial posterior, deep posterior, anterior and lateral. Bone and inelastic fascial layers border the muscles and neurovascular structures. The following nerves traverse these compartments: the tibial and sural nerves, and the superficial and deep branches of the peroneal nerve. The compartment can be accommodated to a limited extent by the sheath. [16] Most commonly involved compartment is the anterior one. [21] As soon as legs are placed in the lithotomy position, the compartmental pressures begin to increase. [17] The height above the level of the heart at which the legs rise is crucial. [17, 18] An increase in intracompartment pressure in the lithotomy position, with the use of support behind the calf or knee, has been described from 10.7 (SD 5.8) mmHg to 16.5 (SD 3.4) mmHg. [14] Circulation compromise occurs with increased tissue pressure within a closed osteofascial compartment. Compression of the calf produces local ischaemia through two mechanisms: by direct occlusion of the arterial blood flow and by indirect obstruction of the venous drainage. The weight of the limb itself, as well as the use of devices such as braces and cushions, produces greater compression. It should also be noted that operating personnel can cause

The difference between capillary perfusion pressure and the interstitial fluid pressure determines tissue perfusion. When interstitial fluid pressure exceeds capillary perfusion pressure, capillary collapse and consequent ischemia of the muscles and nerves occurs. [32] It has two main implications: a decrease in the rates of both delivery of oxygenated arterial blood and drainage of deoxygenated venous

The integrity of the vascular endothelium is impaired by initial ischemia. Its capacity as a barrier to the movement of solute and serum disappears. Thus, a self-perpetuating cycle of ischaemia and tissue oedema begins. When the patient returns to the initial position, the compartment pressure may increase even further, producing a reperfusion injury. [16, 17] After 1 h of ischaemia, on restoring blood flow, through the release of prostaglandins and thromboxane, platelets are activated. This may predispose to deep vein thrombosis, which may increase venous

In addition, once reperfusion occurs, large amounts of toxic intracellular content

are released into the bloodstream. They are the markers of rhabdomyolysis. [18] After surgery, serum creatine phosphokinase increases significantly, peaking at 18 hours. [19] The main pathophysiologic mechanisms involved in renal insufficiency from rhabdomyolysis are renal vasoconstriction, intraluminal cast forma-

pressure and therefore, compromise local blood flow. [18]

tion, and direct myoglobin toxicity. [16]

capacity for tissue expansion, such as the abdomen, buttocks and hands.

**92**

#### **5.1 Clinical findings**

Once the patient is in the recovery room, in the immediate postoperative period, despite analgesic infusion, significant pain is reported in the lower extremity (a pain out of proportion). The limb appears oedematous and cyanotic, although the pedis pulses may be preserved. General inflammation of the leg and dorsal ankle flexion and toe mobility deficit is observed. In a more advanced stage, we may observe the absence of peripheral pulses. [24]

#### **5.2 Intraoperative findings**

Once the compartment fasciotomy has been performed, we can observe that only the deep compartments may be affected by ischemia. In this case, the muscle mass of the anterolateral compartment and the deep posteromedial compartment shows evidence of necrosis. Muscles show pale pink edema. Stimulation with an electric scapel shows absence of contractility. Correct tonality and contractility can be seen in the muscle mass of both superficial compartments if this occurs. When diagnosis and treatment are delayed, both deep and superficial masses are affected by ischemia.

#### **6. Diagnosis**

After lengthy surgeries, we must be aware of the possibility of the development of a compartment syndrome. Prompt diagnosis and treatment should be performed using a four-compartment fasciotomy to avoid serious and irreversible complications. [23]

The appearance of the following signs and symptoms must warn us: pink skin, presence of pulse, paresis of muscles, paraesthesia and a disproportionate pain, generally described by the patient as burning and deep. It is reproduced by passive stretching of the muscles of the compartment. The diagnosis is more difficult in unconscious and sedated patients.

On analysis, serum creatinine kinase activity is increased. We must bear in mind that the first signs are subtle and more often neurological. This is due to the fact that nonmyelinated type C sensory fibers are the tissues most sensitive to hypoxia. [21, 32] Therefore, a delay in the diagnosis should be considered with the use of epidural anesthesia, due to a masking effect. [21]

However, the definitive diagnosis is made by direct measurement of the compartmental pressure. Compartment pressure can be measured with different pressure catheters. These catheters have fine bore and their use is associated with minimal morbidity. [24] It can be measured by using a simple needle manometer, continuous infusion, wick catheter, slit catheter, or solid-state transducer method. [30] The indication for a fasciotomy is a value greater than 20–30 mmHg, although it may vary depending on the perfusion pressure and the clinical setting. [32]

We can use various non-invasive imaging techniques to determine intracompartment pressure, including laser Doppler flowmetry, ultrasonic devices, or near infrared spectroscopy. [16] These techniques might be particularly useful in pediatric patients, in whom invasive monitoring is not ideal. Near-infrared spectroscopy has proven useful in one-month-old infants. Nevertheless, both laser Doppler flowmetry and near-infrared spectroscopy may be more useful in chronic compartment syndrome, as they measure variations in muscle oxygenation. In acute compartment syndrome, changes may have already occurred at the time of

measurement. Magnetic resonance imaging has limited utility in the diagnosis of acute compartment syndrome, as it can detect oedema and swelling, but only when the syndrome is well established, delaying the diagnosis.

In rhabdomyolysis, we can observe the presence of myoglobinuria in the absence of urinary erythrocytes. An increase in serum creatine phosphokinase activity is observed. Increased levels of other markers, such as phosphate, potassium, lactate dehydrogenase, aspartate, and alanine aminotransferase, may be seen in rhabdomyolysis. [17]

Venous thrombosis should be ruled out through Doppler ultrasound. Differential diagnoses include venous thrombosis and peripheral nerve or arterial injury.

It has to be taken into account that the limb may be capable of being saved up to 10–12 hours after the complication sets in.

#### **7. Treatment**

#### **7.1 Surgical treatment**

Regarding treatment (**Table 2**), early decompression of the compartment must be performed by an orthopedic surgeon, to avoid the self-perpetuating cycle of ischaemia and oedema.

Long incisions (20–25 cm) are made along the length of the leg. After that adequate and extensile incision, complete released of all involved compartment and preservation of vital structures is performed. All necrotic tissue is removed. Care should be taken to avoid the superficial peroneal nerve damage. The relief of pressure minimizes functional impairment, structural damage, and breaks the cycle of ischemia and edema, preventing additional devitalization of tissue and infection risk. [12]

If necessary, the four compartments are open, and if the muscles are under tension, the skin is left open, and approximated with vessel-loop temporarily. Only around 15% can be primarily closed without high compartment pressure.


**95**

*Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis*

Moist dressings are used the following days, and the skin incisions are usually closed after a few days or weeks with a non-absorbable (polypropylene) suture. There may be need for repeat irrigation and debridement before final wound closure. [17, 32] Other options for the closure of fasciotomy wounds include split-thickness skin graft. It has been recommended the use of meshed split-thickness skin graft secured

with foam vacuum suction dressing after excising all devitalized tissues. [24]

Pain is a major feature of compartment syndrome and adequate analgesia should

Creatine phosphokinase may reach values over 80,000 IU / L. In rhabdomyolysis, myoglobinuric renal failure develops, followed by multisystemic organ failure and possible death. Renal failure should be treated with early and aggressive fluid replacement, central venous monitoring and transfer to high dependency unit/

Mean Arterial Pressure should be maintained over 65 mmHg. Patients should be adequately hydrated to achieve a target urinary output of at least 0.5 mL/Kg. [16] Mannitol may be used as it has a renal vasodilator effect. It also expands intravascular volume and decreases oxygen radicals. Urinary pH should be maintained as neutral as possible to avoid urate and myoglobin precipitation by alkalizing urine

Wound infection is a potential complication, which has to be considered and

Rehabilitation Service to improve leg recovery and normal mobility.

Through intensive therapy with serum and diuretics, a progressive and complete recovery of kidney function is usually achieved. Rhabdomyolysis is also controlled, observing a decrease in its markers during admission to the Intensive Care Unit. Before the patient is discharged from hospital, it is advisable to request the

The damage is thought to be reversible if the ischemic time is less than 2 hours. When cell death occurs it results in permanent disability (in this order: sensitive

Prognosis depends on various factors: injury severity, duration of ischaemia, pre-injury status and comorbidities and, most importantly, time to fasciotomy. [32] A delay in decompression may lead to 20% of the patients requiring amputation.

Muscle necrosis and nerve ischemia lead to permanent neuromuscular dysfunction after the first 12 hours. [16] Other possible sequela is a Volkmann contracture. Exposure of the necrotic muscle after a delayed surgery is associated with loss of the

In case the diagnosis has been missed or delayed, definitive reconstructive surgery should be postponed. Meanwhile, the patient should be treated through

From the four compartments of the legs, the loss of one or two can be tolerated. If the patient attends aggressive physical therapy, and also uses ankle-foot braces or splints, he or she can return to normal ambulation eventually. However, if more than two compartments are affected, amputation is sometimes required. The following sequelae are the consequence of nerve injuries: claw or hammer toes, cavus foot, quinovarus, ankle equines, foot drop. All this causes difficulties in the use of footwear, pressure zones as a result of the deformity and impairment of gait. [21]

supportive renal therapy until the morbidity has been removed. [32]

*DOI: http://dx.doi.org/10.5772/intechopen.96971*

be prescribed. [16]

**7.2 Medical treatment**

intensive care therapy unit.

controlled.

**8. Prognosis**

extremity. [17]

with sodium bicarbonate or acetazolamide. [21]

nerves, motor nerves, muscle and bone). [17]

#### **Table 2.** *Surgical and medical treatment of well-leg compartment syndrome.*

#### *Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis DOI: http://dx.doi.org/10.5772/intechopen.96971*

Moist dressings are used the following days, and the skin incisions are usually closed after a few days or weeks with a non-absorbable (polypropylene) suture. There may be need for repeat irrigation and debridement before final wound closure. [17, 32]

Other options for the closure of fasciotomy wounds include split-thickness skin graft. It has been recommended the use of meshed split-thickness skin graft secured with foam vacuum suction dressing after excising all devitalized tissues. [24]

Pain is a major feature of compartment syndrome and adequate analgesia should be prescribed. [16]

#### **7.2 Medical treatment**

*A Comprehensive Review of Compartment Syndrome*

10–12 hours after the complication sets in.

olysis. [17]

rial injury.

**7. Treatment**

risk. [12]

**Surgical treatment**

**Medical treatment**

**7.1 Surgical treatment**

ischaemia and oedema.

the syndrome is well established, delaying the diagnosis.

measurement. Magnetic resonance imaging has limited utility in the diagnosis of acute compartment syndrome, as it can detect oedema and swelling, but only when

Venous thrombosis should be ruled out through Doppler ultrasound. Differential diagnoses include venous thrombosis and peripheral nerve or arte-

In rhabdomyolysis, we can observe the presence of myoglobinuria in the absence of urinary erythrocytes. An increase in serum creatine phosphokinase activity is observed. Increased levels of other markers, such as phosphate, potassium, lactate dehydrogenase, aspartate, and alanine aminotransferase, may be seen in rhabdomy-

It has to be taken into account that the limb may be capable of being saved up to

Regarding treatment (**Table 2**), early decompression of the compartment must be performed by an orthopedic surgeon, to avoid the self-perpetuating cycle of

Long incisions (20–25 cm) are made along the length of the leg. After that adequate and extensile incision, complete released of all involved compartment and preservation of vital structures is performed. All necrotic tissue is removed. Care should be taken to avoid the superficial peroneal nerve damage. The relief of pressure minimizes functional impairment, structural damage, and breaks the cycle of ischemia and edema, preventing additional devitalization of tissue and infection

If necessary, the four compartments are open, and if the muscles are under tension, the skin is left open, and approximated with vessel-loop temporarily. Only

> Long incisions (20–25 cm) along the length of the leg Complete release of all involved compartments

Avoidance of superficial peroneal nerve damage In muscles under tension: skin left open

Skin incisions closing after a few days (for repeat irrigation and debridement)

Use of mannitol (renal vasodilator effect, expands intravascular volume and decreases

Urinary pH maintained as neutral as possible (avoidance urate and myoglobin

Transferring to high dependency unit/intensive care therapy unit Adequately hydration (target urinary output of at least 0.5 ml/kg.)

precipitation): sodium bicarbonate or acetazolamide

around 15% can be primarily closed without high compartment pressure.

If necessary, four compartments opening

Early and aggressive fluid replacement

Preservation of vital structures Necrotic tissue removal

Use of moist dressings

Adequate analgesia

oxygen radicals)

*Surgical and medical treatment of well-leg compartment syndrome.*

Central venous monitoring

**94**

**Table 2.**

Creatine phosphokinase may reach values over 80,000 IU / L. In rhabdomyolysis, myoglobinuric renal failure develops, followed by multisystemic organ failure and possible death. Renal failure should be treated with early and aggressive fluid replacement, central venous monitoring and transfer to high dependency unit/ intensive care therapy unit.

Mean Arterial Pressure should be maintained over 65 mmHg. Patients should be adequately hydrated to achieve a target urinary output of at least 0.5 mL/Kg. [16] Mannitol may be used as it has a renal vasodilator effect. It also expands intravascular volume and decreases oxygen radicals. Urinary pH should be maintained as neutral as possible to avoid urate and myoglobin precipitation by alkalizing urine with sodium bicarbonate or acetazolamide. [21]

Wound infection is a potential complication, which has to be considered and controlled.

Through intensive therapy with serum and diuretics, a progressive and complete recovery of kidney function is usually achieved. Rhabdomyolysis is also controlled, observing a decrease in its markers during admission to the Intensive Care Unit.

Before the patient is discharged from hospital, it is advisable to request the Rehabilitation Service to improve leg recovery and normal mobility.

#### **8. Prognosis**

The damage is thought to be reversible if the ischemic time is less than 2 hours. When cell death occurs it results in permanent disability (in this order: sensitive nerves, motor nerves, muscle and bone). [17]

Prognosis depends on various factors: injury severity, duration of ischaemia, pre-injury status and comorbidities and, most importantly, time to fasciotomy. [32]

A delay in decompression may lead to 20% of the patients requiring amputation. Muscle necrosis and nerve ischemia lead to permanent neuromuscular dysfunction after the first 12 hours. [16] Other possible sequela is a Volkmann contracture. Exposure of the necrotic muscle after a delayed surgery is associated with loss of the extremity. [17]

In case the diagnosis has been missed or delayed, definitive reconstructive surgery should be postponed. Meanwhile, the patient should be treated through supportive renal therapy until the morbidity has been removed. [32]

From the four compartments of the legs, the loss of one or two can be tolerated. If the patient attends aggressive physical therapy, and also uses ankle-foot braces or splints, he or she can return to normal ambulation eventually. However, if more than two compartments are affected, amputation is sometimes required. The following sequelae are the consequence of nerve injuries: claw or hammer toes, cavus foot, quinovarus, ankle equines, foot drop. All this causes difficulties in the use of footwear, pressure zones as a result of the deformity and impairment of gait. [21]

#### **Figure 4.**

*Magnetic resonance imaging showing sequelae of the compartment syndrome after 6 months: the presence of a certain degree of discrete muscular oedema in a trajectory of approximately 18 cm is observed, affecting the soleus muscles, with a chronic appearance. There is a certain degree of fat infiltration mainly in the proximal third of the muscle mass. Likewise, an apparent degree of scarring and / or fibrosis is also detected in the muscle. The fascia signal is preserved.*


#### **Table 3.**

*Fasciotomy complications.*

Although the majority of positioning injuries resolve in one month, they may persist beyond 6 months, and the patient may still be needing rehabilitation care. [31] Patient's MRI (Magnetic Resonance Imaging) still shows signs of damage 6 months after the surgery, even in the case of being attending rehabilitation care (**Figure 4**).

In the long-term, reported complication rates of early and late fasciotomies are 4.5% and 54%, respectively (**Table 3**). Pain and altered sensation around the fasciotomy wound occur in 10% and 77%, respectively. [18]

**97**

*Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis*

Fasciotomy wounds can cause dry scaly skin in 40% of cases, discolored wounds in 30%, tethered scars in 26%, muscle herniation in 13%, pruritus in 33%, swollen limbs in 25%, recurrent ulceration in 13% and tethered tendons in 7%. Chronic venous insufficiency due to impaired calf muscle pumps may also occur. [21, 32]

Well-leg compartment syndrome may lead to permanent disability and, therefore, has considerable medico-legal implications. This may apply to other rare and life-threatening syndromes during percutaneous nephrolithotomy, such as acute

Strategies have been developed to prevent the occurrence of this complication, including limitation of the patients' position, optimal medical management of

In terms of positional preventive measures, the most important thing is to reserve the positioning in extreme Trendelenburg, lithotomy, Trendelenburg or supine Valdivia modified by Galdakao only for when it is necessary. [34] Wrapping of raised legs should be avoided. Intermittent compression is still controversial. It increases the risk of compartment syndrome of the leg, but significantly reduces the occurrence of deep vein thrombosis. Complete passive plantar flexion should be avoided. [17] The use of stirrups has theoretical disadvantages over the use of a split leg table. [18] Positioning the patient's calves just below the level of the right atrium may be beneficial, as it minimizes the degree of elevation of the ankle. [21, 30] It has been advised to remove leg from support every 2 hours for short periods if

Overweight patients should be advised to lose weight before the procedure. Other diseases, such as peripheral vascular disease or diabetes, must be optimized. [35] Use of checklists has been shown to help avoid complications by directing

Regarding anesthetic issues, we must perform an epidural block with intensity appropriate to the potential pain of the patient. During surgery, the patient must be adequately hydrated, and we must maintain blood pressure in the standard

Intraoperative measurement of serum creatine phosphokinase in patients with risk factors who undergo prolonged surgery during ventilation and sedation may be helpful in anticipating an early diagnosis of compartment syndrome of the leg. [21] In addition, in these types of patients, intraoperative monitoring of compartment pressure could be an option. This monitoring can detect signs of compartment syndrome before the onset of clinical ones. Thus, it could reduce the treatment time for compartment syndrome (fasciotomy) and, therefore, the risk of subsequent complications. [32] If the patient exhibits small elevations, mannitol can be used to induce osmotic diuresis. Additionally, mannitol is as a free radical scavenger. In high risk patients or in prolonged surgeries, urinary pH monitoring allows us to avoid the precipitation of myoglobin and urates, through the infusion of acetazolamide or

Well-leg compartment syndrome is a rare, but potentially devastating complication that may occur during urological surgeries performed in the lithotomy

*DOI: http://dx.doi.org/10.5772/intechopen.96971*

abdominal syndrome. [33]

operating for more than 4 hours. [21]

**9. Prevention**

range. [17]

sodium bicarbonate. [17]

**10. Conclusions**

Appearance of the scars affects 23% of the patients. [17]

comorbidities before surgery, or even the use of checklists. [18]

attention to risk factors associated with the operation. [18]

*Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis DOI: http://dx.doi.org/10.5772/intechopen.96971*

Fasciotomy wounds can cause dry scaly skin in 40% of cases, discolored wounds in 30%, tethered scars in 26%, muscle herniation in 13%, pruritus in 33%, swollen limbs in 25%, recurrent ulceration in 13% and tethered tendons in 7%. Chronic venous insufficiency due to impaired calf muscle pumps may also occur. [21, 32] Appearance of the scars affects 23% of the patients. [17]

Well-leg compartment syndrome may lead to permanent disability and, therefore, has considerable medico-legal implications. This may apply to other rare and life-threatening syndromes during percutaneous nephrolithotomy, such as acute abdominal syndrome. [33]

#### **9. Prevention**

*A Comprehensive Review of Compartment Syndrome*

**96**

**Table 3.**

*Fasciotomy complications.*

**Figure 4.**

*muscle. The fascia signal is preserved.*

Although the majority of positioning injuries resolve in one month, they may persist beyond 6 months, and the patient may still be needing rehabilitation care. [31] Patient's MRI (Magnetic Resonance Imaging) still shows signs of damage 6 months after the surgery, even in the case of being attending rehabilitation care (**Figure 4**). In the long-term, reported complication rates of early and late fasciotomies are 4.5% and 54%, respectively (**Table 3**). Pain and altered sensation around the

*Magnetic resonance imaging showing sequelae of the compartment syndrome after 6 months: the presence of a certain degree of discrete muscular oedema in a trajectory of approximately 18 cm is observed, affecting the soleus muscles, with a chronic appearance. There is a certain degree of fat infiltration mainly in the proximal third of the muscle mass. Likewise, an apparent degree of scarring and / or fibrosis is also detected in the* 

**Complication Percentage** Dry scaly skin 40% Discolored wounds 30% Tethered scars 26% Muscle herniation 13% Pruritus 33% Swollen limbs 25% Recurrent ulceration 13% Tethered tendons 7% Appearance of scars causing discomfort 23% Chronic venous insufficiency —

fasciotomy wound occur in 10% and 77%, respectively. [18]

Strategies have been developed to prevent the occurrence of this complication, including limitation of the patients' position, optimal medical management of comorbidities before surgery, or even the use of checklists. [18]

In terms of positional preventive measures, the most important thing is to reserve the positioning in extreme Trendelenburg, lithotomy, Trendelenburg or supine Valdivia modified by Galdakao only for when it is necessary. [34] Wrapping of raised legs should be avoided. Intermittent compression is still controversial. It increases the risk of compartment syndrome of the leg, but significantly reduces the occurrence of deep vein thrombosis. Complete passive plantar flexion should be avoided. [17] The use of stirrups has theoretical disadvantages over the use of a split leg table. [18] Positioning the patient's calves just below the level of the right atrium may be beneficial, as it minimizes the degree of elevation of the ankle. [21, 30] It has been advised to remove leg from support every 2 hours for short periods if operating for more than 4 hours. [21]

Overweight patients should be advised to lose weight before the procedure. Other diseases, such as peripheral vascular disease or diabetes, must be optimized. [35] Use of checklists has been shown to help avoid complications by directing attention to risk factors associated with the operation. [18]

Regarding anesthetic issues, we must perform an epidural block with intensity appropriate to the potential pain of the patient. During surgery, the patient must be adequately hydrated, and we must maintain blood pressure in the standard range. [17]

Intraoperative measurement of serum creatine phosphokinase in patients with risk factors who undergo prolonged surgery during ventilation and sedation may be helpful in anticipating an early diagnosis of compartment syndrome of the leg. [21]

In addition, in these types of patients, intraoperative monitoring of compartment pressure could be an option. This monitoring can detect signs of compartment syndrome before the onset of clinical ones. Thus, it could reduce the treatment time for compartment syndrome (fasciotomy) and, therefore, the risk of subsequent complications. [32] If the patient exhibits small elevations, mannitol can be used to induce osmotic diuresis. Additionally, mannitol is as a free radical scavenger. In high risk patients or in prolonged surgeries, urinary pH monitoring allows us to avoid the precipitation of myoglobin and urates, through the infusion of acetazolamide or sodium bicarbonate. [17]

#### **10. Conclusions**

Well-leg compartment syndrome is a rare, but potentially devastating complication that may occur during urological surgeries performed in the lithotomy

#### *A Comprehensive Review of Compartment Syndrome*

position. It is also possible the development of a compartment syndrome during a percutaneous nephrolithotomy in the Galdakao-modified Supine Valdivia Position.

The factors associated with the development of this complication include: obesity, advanced age, hypertension, hyperlipidemia, diabetes mellitus, combined general-spinal anesthesia, prolonged surgery time and systemic hypotension.

In prolonged surgeries and in patients with risk factors, high levels of awareness of the possibility of this condition are advisable, leading possibly to early treatment. Definitive diagnosis is assessed by directly measuring compartmental pressure.

Early diagnosis and treatment by four compartment fasciotomy is the only way to prevent irreversible damage. Preventive measures reduce the incidence of this condition, which may lead to skin necrosis, permanent neuromuscular dysfunction, myoglobinuric renal failure, amputation and even death.

#### **Conflict of interest**

The authors declare no conflict of interest.

#### **Author details**

Inés Laso-García\*, Fernando Arias-Fúnez, Gemma Duque-Ruiz, David Díaz-Pérez, Alberto Artiles-Medina and Javier Burgos-Revilla Ramón y Cajal University Hospital, Alcalá University, IRYCIS, Madrid, Spain

\*Address all correspondence to: ines.laso.garcia@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.

**99**

*Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis*

stone disease. BJU Int [Internet]. 2012 Apr [cited 2017 Feb 13];109(7):1082-7. Available from: http://www.ncbi.nlm.

nih.gov/pubmed/21883851

[8] Zhao F, Li J, Tang L, Li C. A comparative study of endoscopic combined intrarenal surgery (ECIRS) in the galdakao-modified supine valdivia (GMSV) position and minimally invasive percutaneous nephrolithotomy

for complex nephrolithiasis: a retrospective single-center study. Urolithiasis [Internet]. Springer; 2020 [cited 2021 Feb 1];Aug 10. Available from: https://pubmed.ncbi.nlm.nih.

[9] Melo PA de S, Vicentini FC, Perrella R, Murta CB, Claro JF de A. Comparative study of percutaneous nephrolithotomy performed in the traditional prone position and in three different supine positions. Int Braz J Urol [Internet]. Brazilian Society of Urology; 2019 Jan 1 [cited 2021 Feb 1];45(1):108-17. Available from: https:// pubmed.ncbi.nlm.nih.gov/30521168/

[10] Scoffone CM, Cracco CM. Invited review: the tale of ECIRS (Endoscopic Combined IntraRenal Surgery) in the Galdakao-modified supine Valdivia position [Internet]. Urolithiasis. Springer Verlag; 2018 [cited 2021 Jan 31]. p. 115-23. Available from: https:// pubmed.ncbi.nlm.nih.gov/29189885/

[11] Ibarluzea G, Scoffone CM, Cracco CM, Poggio M, Porpiglia F, Terrone C, et al. Supine Valdivia and modified lithotomy position for simultaneous anterograde and retrograde endourological access. BJU Int [Internet]. 2007 Jul [cited 2019 Oct 15];100(1):233-6. Available from: http://doi.wiley.

com/10.1111/j.1464-410X.2007.06960.x

[12] Cohen SA, Hurt WG. Compartment syndrome associated with lithotomy

gov/32776245/

*DOI: http://dx.doi.org/10.5772/intechopen.96971*

[1] Ljunghall S. Incidence of upper urinary tract stones. Miner Electrolyte Metab [Internet]. 1987 Jan [cited 2015 Jun 1];13(4):220-7. Available from: http://www.ncbi.nlm.nih.gov/

[2] Johnson CM, Wilson DM,

[3] Boyce WH, Garvey FK,

O'Fallon WM, Malek RS, Kurland LT. Renal stone epidemiology: a 25-year study in Rochester, Minnesota. Kidney Int [Internet]. 1979 Nov [cited 2016 Oct 25];16(5):624-31. Available from: http://www.ncbi.nlm.nih.gov/

Strawcutter HE. Incidence of urinary calculi among patients in general hospitals, 1948 to 1952. J Am Med Assoc [Internet]. 1956 Aug 11 [cited 2016 Oct 25];161(15):1437-42. Available from: http://www.ncbi.nlm.nih.gov/

[4] Scales CD, Smith AC, Hanley JM, Saigal CS, Urologic Diseases in America Project. Prevalence of Kidney Stones in the United States. Eur Urol [Internet]. 2012 Jul [cited 2017 Feb 25];62(1):160-5. Available from: http://www.ncbi.nlm.

[5] Ramello A, Vitale C, Marangella M. Epidemiology of nephrolithiasis. J Nephrol [Internet]. 2000 [cited 2017 Mar 27];13 Suppl 3:S45-50. Available from: http://www.ncbi.nlm.nih.gov/

[6] Decoster M, Bigot JC, Carre JL, Morin JF, Mahé JL, Tanquerel T, et al. [Epidemiologic study of urinary calculi in Western France]. Presse Med [Internet]. 2002 Jan 26 [cited 2016 Oct 25];31(3):113-8. Available from: http://www.ncbi.nlm.nih.gov/

[7] Turney BW, Reynard JM, Noble JG, Keoghane SR. Trends in urological

nih.gov/pubmed/22498635

pubmed/11132032

pubmed/11859735

**References**

pubmed/3306313

pubmed/548606

pubmed/13345602

*Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis DOI: http://dx.doi.org/10.5772/intechopen.96971*

#### **References**

*A Comprehensive Review of Compartment Syndrome*

myoglobinuric renal failure, amputation and even death.

The authors declare no conflict of interest.

position. It is also possible the development of a compartment syndrome during a percutaneous nephrolithotomy in the Galdakao-modified Supine Valdivia Position. The factors associated with the development of this complication include: obesity, advanced age, hypertension, hyperlipidemia, diabetes mellitus, combined general-spinal anesthesia, prolonged surgery time and systemic hypotension.

In prolonged surgeries and in patients with risk factors, high levels of awareness of the possibility of this condition are advisable, leading possibly to early treatment. Definitive diagnosis is assessed by directly measuring compartmental pressure. Early diagnosis and treatment by four compartment fasciotomy is the only way to prevent irreversible damage. Preventive measures reduce the incidence of this condition, which may lead to skin necrosis, permanent neuromuscular dysfunction,

**98**

**Author details**

**Conflict of interest**

Inés Laso-García\*, Fernando Arias-Fúnez, Gemma Duque-Ruiz, David Díaz-Pérez,

© 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,

Ramón y Cajal University Hospital, Alcalá University, IRYCIS, Madrid, Spain

Alberto Artiles-Medina and Javier Burgos-Revilla

provided the original work is properly cited.

\*Address all correspondence to: ines.laso.garcia@gmail.com

[1] Ljunghall S. Incidence of upper urinary tract stones. Miner Electrolyte Metab [Internet]. 1987 Jan [cited 2015 Jun 1];13(4):220-7. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/3306313

[2] Johnson CM, Wilson DM, O'Fallon WM, Malek RS, Kurland LT. Renal stone epidemiology: a 25-year study in Rochester, Minnesota. Kidney Int [Internet]. 1979 Nov [cited 2016 Oct 25];16(5):624-31. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/548606

[3] Boyce WH, Garvey FK, Strawcutter HE. Incidence of urinary calculi among patients in general hospitals, 1948 to 1952. J Am Med Assoc [Internet]. 1956 Aug 11 [cited 2016 Oct 25];161(15):1437-42. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/13345602

[4] Scales CD, Smith AC, Hanley JM, Saigal CS, Urologic Diseases in America Project. Prevalence of Kidney Stones in the United States. Eur Urol [Internet]. 2012 Jul [cited 2017 Feb 25];62(1):160-5. Available from: http://www.ncbi.nlm. nih.gov/pubmed/22498635

[5] Ramello A, Vitale C, Marangella M. Epidemiology of nephrolithiasis. J Nephrol [Internet]. 2000 [cited 2017 Mar 27];13 Suppl 3:S45-50. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/11132032

[6] Decoster M, Bigot JC, Carre JL, Morin JF, Mahé JL, Tanquerel T, et al. [Epidemiologic study of urinary calculi in Western France]. Presse Med [Internet]. 2002 Jan 26 [cited 2016 Oct 25];31(3):113-8. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/11859735

[7] Turney BW, Reynard JM, Noble JG, Keoghane SR. Trends in urological

stone disease. BJU Int [Internet]. 2012 Apr [cited 2017 Feb 13];109(7):1082-7. Available from: http://www.ncbi.nlm. nih.gov/pubmed/21883851

[8] Zhao F, Li J, Tang L, Li C. A comparative study of endoscopic combined intrarenal surgery (ECIRS) in the galdakao-modified supine valdivia (GMSV) position and minimally invasive percutaneous nephrolithotomy for complex nephrolithiasis: a retrospective single-center study. Urolithiasis [Internet]. Springer; 2020 [cited 2021 Feb 1];Aug 10. Available from: https://pubmed.ncbi.nlm.nih. gov/32776245/

[9] Melo PA de S, Vicentini FC, Perrella R, Murta CB, Claro JF de A. Comparative study of percutaneous nephrolithotomy performed in the traditional prone position and in three different supine positions. Int Braz J Urol [Internet]. Brazilian Society of Urology; 2019 Jan 1 [cited 2021 Feb 1];45(1):108-17. Available from: https:// pubmed.ncbi.nlm.nih.gov/30521168/

[10] Scoffone CM, Cracco CM. Invited review: the tale of ECIRS (Endoscopic Combined IntraRenal Surgery) in the Galdakao-modified supine Valdivia position [Internet]. Urolithiasis. Springer Verlag; 2018 [cited 2021 Jan 31]. p. 115-23. Available from: https:// pubmed.ncbi.nlm.nih.gov/29189885/

[11] Ibarluzea G, Scoffone CM, Cracco CM, Poggio M, Porpiglia F, Terrone C, et al. Supine Valdivia and modified lithotomy position for simultaneous anterograde and retrograde endourological access. BJU Int [Internet]. 2007 Jul [cited 2019 Oct 15];100(1):233-6. Available from: http://doi.wiley. com/10.1111/j.1464-410X.2007.06960.x

[12] Cohen SA, Hurt WG. Compartment syndrome associated with lithotomy

position and intermittent compression stockings. Obstet Gynecol. 2001;97(5):832-3.

[13] Clarke D, Mullings S, Franklin S, Jones K. Well leg compartment syndrome. Trauma Case Reports. Elsevier Ltd; 2017 Oct 1;11:5-7.

[14] Pfeffer SD, Halliwill JR, Warner MA. Effects of lithotomy position and external compression on lower leg muscle compartment pressure. Anesthesiology [Internet]. 2001 Sep [cited 2019 Oct 15];95(3):632-6. Available from: https://insights.ovid.com/crossref ?an=00000542-200109000-00014

[15] Gill M, Fligelstone L, Keating J, Jayne DG, Renton S, Shearman CP, et al. Avoiding, diagnosing and treating well leg compartment syndrome after pelvic surgery. Br J Surg. John Wiley and Sons Ltd; 2019 Aug 1;106(9):1156-66.

[16] Mattei A, Di Pierro GB, Rafeld V, Konrad C, Beutler J, Danuser H. Positioning Injury, Rhabdomyolysis, and Serum Creatine Kinase-Concentration Course in Patients Undergoing Robot-Assisted Radical Prostatectomy and Extended Pelvic Lymph Node Dissection. J Endourol [Internet]. 2013 Jan [cited 2019 Oct 15];27(1):45-51. Available from: http://www.liebertpub. com/doi/10.1089/end.2012.0169

[17] Mabvuure NT, Malahias M, Hindocha S, Khan W, Juma A. Acute Compartment Syndrome of the Limbs: Current Concepts and Management. Open Orthop J [Internet]. 2012 Nov 30 [cited 2019 Oct 15];6(1):535-43. Available from: https://openorthopaedicsjournal.com/ VOLUME/6/PAGE/535/

[18] Mumtaz FH, Chew H, Gelister JS. Lower limb compartment syndrome associated with the lithotomy position: Concepts and perspectives for the urologist. BJU Int. 2002;90(8):792-9.

[19] Sukhu T, Krupski TL. Patient positioning and prevention of injuries in patients undergoing laparoscopic and robot-assisted urologic procedures. Curr Urol Rep [Internet]. 2014 Apr 27 [cited 2019 Oct 15];15(4):398. Available from: http://link.springer.com/10.1007/ s11934-014-0398-1

[20] Chung JH, Ahn KR, Park JH, Kim CS, Kang KS, Yoo SH, et al. Lower leg compartment syndrome following prolonged orthopedic surgery in the lithotomy position -A case report-. Korean J Anesthesiol [Internet]. 2010 Dec [cited 2020 Apr 21];59 Suppl(SUPPL.):S49-52. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/21286459

[21] RAZA A, BYRNE D, TOWNELL N. Lower Limb (Well Leg) Compartment Syndrome After Urological Pelvic Surgery. J Urol [Internet]. 2004 Jan [cited 2019 Oct 15];171(1):5-11. Available from: http://www.ncbi.nlm. nih.gov/pubmed/14665832

[22] Simms MS, Terry TR. Well leg compartment syndrome after pelvic and perineal surgery in the lithotomy position. Postgraduate Medical Journal. 2005. p. 534-6.

[23] Wassenaar EB, van den Brand JGH, van der Werken C. Compartment syndrome of the lower leg after surgery in the modified lithotomy position: report of seven cases. Dis *Colon rectum* [Internet]. 2006 Sep [cited 2019 Oct 15];49(9):1449-53. Available from: https://insights.ovid.com/crossref ?an=00003453-200649090-00025

[24] Chin KY, Hemington-Gorse SJ, Darcy CM. Bilateral well leg compartment syndrome associated with lithotomy (Lloyd Davies) position during gastrointestinal surgery: a case report and review of literature. Eplasty [Internet]. 2009 Oct 14 [cited 2020 Apr 21];9:e48. Available from: http://www. ncbi.nlm.nih.gov/pubmed/19915657

**101**

pubmed/26955278

*Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis*

[Combined risk factors leading to well-leg compartment syndrome after laparoscopic radical prostatectomy]. Actas Urol Esp [Internet]. 2009 Sep [cited 2019 Oct 15];33(8):920-4. Available from: http://www.ncbi.nlm.

nih.gov/pubmed/19900389

Aug;190(2):580-4.

Conaway MR, Schenkman NS, Krupski TL. Positioning injuries associated with robotic assisted urological surgery. J Urol. 2013

Ltd.; 2014 Jul 17;8(1):185-93.

nih.gov/pubmed/31373561

pubmed/30121089

[32] Mills JT, Burris MB, Warburton DJ,

[33] Donaldson J, Haddad B, Khan WS. The Pathophysiology, Diagnosis and Current Management of Acute Compartment Syndrome. Open Orthop J. Bentham Science Publishers

[34] Googe B, Lackey AE, Arnold PA, Vick LR. The Modified Lithotomy: A Surgical Position for Lower Extremity Wound Care Procedures in Super Morbidly Obese Patients. A Case Study. Wound Manag Prev [Internet]. 2019 Jul [cited 2020 Apr 21];65(7):30-4. Available from: http://www.ncbi.nlm.

[35] Takechi K, Kitamura S, Shimizu I, Yorozuya T. Lower limb perfusion during robotic-assisted laparoscopic radical prostatectomy evaluated by near-infrared spectroscopy: an observational prospective study. BMC Anesthesiol [Internet]. BioMed Central Ltd.; 2018 Aug 18 [cited 2020 Apr 21];18(1):114. Available from: http://www.ncbi.nlm.nih.gov/

*DOI: http://dx.doi.org/10.5772/intechopen.96971*

[25] Yamamoto T, Fujie A, Tanikawa H, Funayama A, Fukuda K. Bilateral Well Leg Compartment Syndrome Localized in the Anterior and Lateral Compartments following Urologic Surgery in Lithotomy Position. Case Rep Orthop [Internet]. 2018 Nov 14 [cited 2019 Oct 15];2018:1-4. Available from: http://www.ncbi.nlm.nih.

[26] Tison C, Périgaud C, Vrignaud S, Capelli M, Lehur PA. Syndrome bilatéral des loges de jambe après chirurgie colorectale en position à double équipe. Ann Chir. 2002

[27] Rosevear HM, Lightfoot AJ, Zahs M, Waxman SW, Winfield HN. Lessons learned from a case of calf compartment syndrome after robotassisted laparoscopic prostatectomy. J Endourol [Internet]. 2010 Oct [cited 2019 Oct 15];24(10):1597-601. Available from: http://www.liebertpub.com/ doi/10.1089/end.2009.0666

[28] Wollin DA, Preminger GM. Percutaneous nephrolithotomy: complications and how to deal with them. Urolithiasis. Springer Verlag;

Sun Z quan, Qian W qing. Acute Abdominal Compartment Syndrome as a Complication of Percutaneous Nephrolithotomy: Two Cases Reports and Literature Review. Urol Case Reports. Elsevier Inc; 2016 Sep 1;8:12-4.

[30] Mizuno J, Takahashi T. Male sex, height, weight, and body mass index can increase external pressure to calf region using knee-crutch-type leg holder system in lithotomy position. Ther Clin Risk Manag [Internet]. 2016 Feb [cited 2019 Oct 15];12:305. Available from: http://www.ncbi.nlm.nih.gov/

[31] Romero FR, Pilati R, Kulysz D, Canali FA V, Baggio P V, Brenny Filho T.

[29] Tao J, Sheng L, Zhang H jie, Chen R,

gov/pubmed/30538877

Sep;127(7):535-8.

2018. p. 87-97.

*Compartment Syndrome Related to Patient Positioning in the Surgical Treatment of Urolithiasis DOI: http://dx.doi.org/10.5772/intechopen.96971*

[25] Yamamoto T, Fujie A, Tanikawa H, Funayama A, Fukuda K. Bilateral Well Leg Compartment Syndrome Localized in the Anterior and Lateral Compartments following Urologic Surgery in Lithotomy Position. Case Rep Orthop [Internet]. 2018 Nov 14 [cited 2019 Oct 15];2018:1-4. Available from: http://www.ncbi.nlm.nih. gov/pubmed/30538877

*A Comprehensive Review of Compartment Syndrome*

[19] Sukhu T, Krupski TL. Patient positioning and prevention of injuries in patients undergoing laparoscopic and robot-assisted urologic procedures. Curr Urol Rep [Internet]. 2014 Apr 27 [cited 2019 Oct 15];15(4):398. Available from: http://link.springer.com/10.1007/

[20] Chung JH, Ahn KR, Park JH, Kim CS, Kang KS, Yoo SH, et al. Lower leg compartment syndrome following prolonged orthopedic surgery in the lithotomy position -A case report-. Korean J Anesthesiol [Internet]. 2010 Dec [cited 2020 Apr 21];59 Suppl(SUPPL.):S49-52. Available from: http://www.ncbi.nlm.nih.gov/

[21] RAZA A, BYRNE D, TOWNELL N. Lower Limb (Well Leg) Compartment Syndrome After Urological Pelvic Surgery. J Urol [Internet]. 2004 Jan [cited 2019 Oct 15];171(1):5-11. Available from: http://www.ncbi.nlm.

s11934-014-0398-1

pubmed/21286459

nih.gov/pubmed/14665832

2005. p. 534-6.

[22] Simms MS, Terry TR. Well leg compartment syndrome after pelvic and perineal surgery in the lithotomy position. Postgraduate Medical Journal.

[23] Wassenaar EB, van den Brand JGH, van der Werken C. Compartment syndrome of the lower leg after surgery in the modified lithotomy position: report of seven cases. Dis *Colon rectum* [Internet]. 2006 Sep [cited 2019 Oct 15];49(9):1449-53. Available from: https://insights.ovid.com/crossref ?an=00003453-200649090-00025

[24] Chin KY, Hemington-Gorse SJ, Darcy CM. Bilateral well leg compartment syndrome associated with lithotomy (Lloyd Davies) position during gastrointestinal surgery: a case report and review of literature. Eplasty [Internet]. 2009 Oct 14 [cited 2020 Apr 21];9:e48. Available from: http://www. ncbi.nlm.nih.gov/pubmed/19915657

position and intermittent compression

[13] Clarke D, Mullings S, Franklin S, Jones K. Well leg compartment syndrome. Trauma Case Reports. Elsevier Ltd; 2017 Oct 1;11:5-7.

[Internet]. 2001 Sep [cited 2019 Oct 15];95(3):632-6. Available from: https://insights.ovid.com/crossref ?an=00000542-200109000-00014

[15] Gill M, Fligelstone L, Keating J, Jayne DG, Renton S, Shearman CP, et al. Avoiding, diagnosing and treating well leg compartment syndrome after pelvic surgery. Br J Surg. John Wiley and Sons Ltd; 2019 Aug 1;106(9):1156-66.

[16] Mattei A, Di Pierro GB, Rafeld V, Konrad C, Beutler J, Danuser H.

Course in Patients Undergoing

[17] Mabvuure NT, Malahias M, Hindocha S, Khan W, Juma A. Acute Compartment Syndrome of the Limbs: Current Concepts and Management. Open Orthop J [Internet]. 2012 Nov 30 [cited 2019 Oct 15];6(1):535-43. Available from: https://openorthopaedicsjournal.com/

VOLUME/6/PAGE/535/

[18] Mumtaz FH, Chew H, Gelister JS. Lower limb compartment syndrome associated with the lithotomy position: Concepts and perspectives for the urologist. BJU Int. 2002;90(8):792-9.

Positioning Injury, Rhabdomyolysis, and Serum Creatine Kinase-Concentration

Robot-Assisted Radical Prostatectomy and Extended Pelvic Lymph Node Dissection. J Endourol [Internet]. 2013 Jan [cited 2019 Oct 15];27(1):45-51. Available from: http://www.liebertpub. com/doi/10.1089/end.2012.0169

stockings. Obstet Gynecol.

[14] Pfeffer SD, Halliwill JR, Warner MA. Effects of lithotomy position and external compression on lower leg muscle compartment

pressure. Anesthesiology

2001;97(5):832-3.

**100**

[26] Tison C, Périgaud C, Vrignaud S, Capelli M, Lehur PA. Syndrome bilatéral des loges de jambe après chirurgie colorectale en position à double équipe. Ann Chir. 2002 Sep;127(7):535-8.

[27] Rosevear HM, Lightfoot AJ, Zahs M, Waxman SW, Winfield HN. Lessons learned from a case of calf compartment syndrome after robotassisted laparoscopic prostatectomy. J Endourol [Internet]. 2010 Oct [cited 2019 Oct 15];24(10):1597-601. Available from: http://www.liebertpub.com/ doi/10.1089/end.2009.0666

[28] Wollin DA, Preminger GM. Percutaneous nephrolithotomy: complications and how to deal with them. Urolithiasis. Springer Verlag; 2018. p. 87-97.

[29] Tao J, Sheng L, Zhang H jie, Chen R, Sun Z quan, Qian W qing. Acute Abdominal Compartment Syndrome as a Complication of Percutaneous Nephrolithotomy: Two Cases Reports and Literature Review. Urol Case Reports. Elsevier Inc; 2016 Sep 1;8:12-4.

[30] Mizuno J, Takahashi T. Male sex, height, weight, and body mass index can increase external pressure to calf region using knee-crutch-type leg holder system in lithotomy position. Ther Clin Risk Manag [Internet]. 2016 Feb [cited 2019 Oct 15];12:305. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/26955278

[31] Romero FR, Pilati R, Kulysz D, Canali FA V, Baggio P V, Brenny Filho T. [Combined risk factors leading to well-leg compartment syndrome after laparoscopic radical prostatectomy]. Actas Urol Esp [Internet]. 2009 Sep [cited 2019 Oct 15];33(8):920-4. Available from: http://www.ncbi.nlm. nih.gov/pubmed/19900389

[32] Mills JT, Burris MB, Warburton DJ, Conaway MR, Schenkman NS, Krupski TL. Positioning injuries associated with robotic assisted urological surgery. J Urol. 2013 Aug;190(2):580-4.

[33] Donaldson J, Haddad B, Khan WS. The Pathophysiology, Diagnosis and Current Management of Acute Compartment Syndrome. Open Orthop J. Bentham Science Publishers Ltd.; 2014 Jul 17;8(1):185-93.

[34] Googe B, Lackey AE, Arnold PA, Vick LR. The Modified Lithotomy: A Surgical Position for Lower Extremity Wound Care Procedures in Super Morbidly Obese Patients. A Case Study. Wound Manag Prev [Internet]. 2019 Jul [cited 2020 Apr 21];65(7):30-4. Available from: http://www.ncbi.nlm. nih.gov/pubmed/31373561

[35] Takechi K, Kitamura S, Shimizu I, Yorozuya T. Lower limb perfusion during robotic-assisted laparoscopic radical prostatectomy evaluated by near-infrared spectroscopy: an observational prospective study. BMC Anesthesiol [Internet]. BioMed Central Ltd.; 2018 Aug 18 [cited 2020 Apr 21];18(1):114. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/30121089

### *Edited by Saqeb Beig Mirza and Khaled Elawady*

Compartment syndrome is a condition caused by an increase in pressure in a closed anatomical space. It can lead to irreversible damage and necrosis of the contents of that space with devastating consequences for the patient. It can affect the musculoskeletal system as well as sites outside the musculoskeletal system including the thorax and abdomen. This book describes the occurrence of compartment syndrome at all these sites, diagnosis and adjuncts to diagnosis, and the importance of timely management of this condition to prevent major morbidity and preserve function.

Published in London, UK © 2021 IntechOpen © grinvalds / iStock

A Comprehensive Review of Compartment Syndrome

A Comprehensive Review of

Compartment Syndrome

*Edited by Saqeb Beig Mirza and Khaled Elawady*