**Meet the editor**

Selcan Karakuş is currently working as an assistant professor at the Department of Chemistry, Istanbul University (IU), Turkey. She received her Master of Science degree in Physical Chemistry from IU in 2006. She received her Doctor of Philosophy degree in Physical Chemistry from IU in 2011. She worked as a visiting researcher at the Department of Polymer Science and Engineering,

University of Massachusetts. She has a research experience in drug carrier system, nanoparticles, nanocomposites, nanoemulsion self-assembled polymeric nanostructures, and copolymer blends. She has worked on different projects funded by the Istanbul University. She has published several research articles and a book chapter in this area.

Contents

**Preface VII**

**Analysis 9**

Chapter 1 **Introductory Chapter: The Perspective of**

Chapter 2 **Stresses and Strains Distribution of a Developed Cold**

Chapter 3 **Emulsifying Properties of Hemicelluloses 29**

**Bituminous Emulsion Mixture Using Finite Element**

Chapter 4 **Sol-Gel Microencapsulation Based on Pickering Emulsion 43** Fabien Salaün, Chloé Butstraen and Eric Devaux

Chapter 6 **Effects of Interfacial Tension Alteration on the Destabilization**

Aliyu Adebayo Sulaimon and Bamikole Joshua Adeyemi

Chapter 7 **An SVM-Based Classification and Stability Analysis of Synthetic Emulsions Co-Stabilized by a Nonionic Surfactant and**

Abubakar A. Umar, Ismail M. Saaid and Aliyu A. Sulaimon

Chapter 5 **Factors Affecting the Stability of Emulsions Stabilised by**

Yvonne Maphosa and Victoria A. Jideani

**of Water-Oil Emulsions 83**

Hayder Kamil Shanbara, Felicite Ruddock and William Atherton

Emmanuel O. Olorunsola, Ekaete I. Akpabio, Musiliu O. Adedokun

**Emulsion Systems 1** Selcan Karakuş

and Dorcas O. Ajibola

**Biopolymers 65**

**Laponite Clay 111**


**5. Conclusions**

An enzymatic method on an automated spectrophotometric system was used for the quantification of acetic acid in vinegar. The enzymatic method met many validation requirements (linearity, sensitivity, and uncertainties) but not accuracy. However, the method can be considered applicable as the precision and uncertainty are lower than those of the Community method (deviations are around 10%). The validation of instrumental analytical methods not yet used as conventional methods should find more space in the scientific literature. By transferring knowledge on operating methods, the repetition of long and laborious validation processes that involve high costs and waste of time will be avoided.

**Supplementary Materials:** The following are available online at http://www.mdpi.com/2304-8158/9/6/761/s1, Figure S1: Standard calibration curve, Figure S2: Normal residual probability, Figure S3: Shapiro-Wilk test (5% significance levels), Figure S4: Balsamic wine vinegar accuracy statistical analyses, Figure S5: Red wine vinegar accuracy statistical analyses, Figure S6: White wine vinegar accuracy statistical analyses, Table S1: Data considering calculating type A uncertainty, Table S2: Type B: Systematic uncertainty estimates, Table S3: Red wine vinegar data, Table S4: Withe wine vinegar data, Table S5: Balsamic wine vinegar data, Table S6: Upper and lower limit of repeatability.

**Author Contributions:** I.D., data curation and writing—review and editing; R.D.L., investigation; A.S., investigation; D.C., investigation.; S.L., investigation. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research received no external funding.

**Conflicts of Interest:** The authors declare no conflict of interest.

#### **References**

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).


**Abstract**

The musical practice is an extremely complex activity that involves a series of cognitive abilities and functions, among them are hearing, memory, motor coordination, attention, affection, mathematical calculation, and the association of all of these concomitantly, including situations of public exposure. Because of this, musical performance is particularly susceptive to anxiety symptoms. Musical performance anxiety (MPA) is defined as an experience of persistent and distressing apprehension and/or real prejudice of the performance abilities in a public context in an unjustifiable degree given the individual musical aptitude and preparation level. It prevails more commonly on the female gender in a 3:1 proportion and affects about 20% of the professional musicians. In the present chapter, its main etiologies and psychic mechanisms, evaluation instruments, as well as the current therapeutic strategies available will be presented.

**Keywords:** performance anxiety, musical performance anxiety, musicians, perceived causes, psychological intervention, drug therapies, optimal performance

### **1. Introduction**

The musical practice is an extremely complex activity that involves a series of cognitive abilities and functions, among them are hearing, memory, motor coordination, attention, affection, mathematical calculation, and the association of all of these concomitantly, including situations of public exposure [1]. Because of this, musical performance is particularly susceptive to anxiety symptoms.

Anxiety in itself is, up to a certain point, something favorable to the performance [2], since it helps the performer to perceive what favors him and disregard what could hinder his performance. After a certain point, anxiety starts to influence negatively the musical performance efficiency, according to the Yerkes-Dodson curve (**Figure 1**).

Musical performance anxiety (MPA) is a term that encompasses many dimensions and started being described in 1990. It is the experience of a persistent and distressing apprehension and/or real prejudice of the performance abilities in a public context in an unjustifiable degree given the individual musical aptitude and preparation level [3].

In the musical environment, MPA has been called as "stage fright" although MPA encompasses something much bigger than that [4]. The reason is that MPA has three axes that complement each other in terms of subjective manifestations of this picture.

**Figure 1.** *The Yerkes-Dodson curve.*

Performance anxiety affects equally music professional and students. There is a prevalence of around 18% [5]. The main reported symptoms are concentration decrease, tachycardia, tremor, sweating, and xerostomia, which are severe enough to negatively impact on the performance level [5, 6].

In the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, or DSM-5, social anxiety disorder (SAD) is highlighted, in which the subject feels fear or anxiety in social interaction situations when he worries about the possibility of coming to be evaluated by the public [4].

In the present chapter, general aspects of MPA, its possible etiologies, its occurrence in the diverse age groups, the instruments of evaluation, and, at last, the therapeutic approaches will be approached.


*2.3.3 Process evaluation*

Often left out of the disaster cycle is the appreciation of the interpretation of actions during the disaster response and recovery periods. It is from this analysis, that the lessons learned from the response and recovery are adapted into the foundations of mitigation and preparedness. Without establishing an understanding of systemic successes and failure, mistakes will be repeated.


*Article* **Glycosylation States on Intact Proteins Determined by NMR Spectroscopy**

**Audra A. Hargett 1, Aaron M. Marcella 1, Huifeng Yu 1, Chao Li 2, Jared Orwenyo 2, Marcos D. Battistel 1, Lai-Xi Wang 2 and Darón I. Freedberg 1,\***

**Abstract:** Protein glycosylation is important in many organisms for proper protein folding, signaling, cell adhesion, protein-protein interactions, and immune responses. Thus, effectively determining the extent of glycosylation in glycoprotein therapeutics is crucial. Up to now, characterizing protein glycosylation has been carried out mostly by liquid chromatography mass spectrometry (LC-MS), which requires careful sample processing, e.g., glycan removal or protein digestion and glycopeptide enrichment. Herein, we introduce an NMR-based method to better characterize intact glycoproteins in natural abundance. This non-destructive method relies on exploiting differences in nuclear relaxation to suppress the NMR signals of the protein while maintaining glycan signals. Using RNase B Man5 and RNase B Man9, we establish reference spectra that can be used to determine the different glycoforms present in heterogeneously glycosylated commercial RNase B.

**Keywords:** glycosylated proteins; heteronuclear NMR; HSQC-TOCSY; natural abundance; T2 filter; glycoprotein


Preface

Compartment syndrome is a condition that can be both limb-threatening as well as life-threatening. It often develops in limbs that have been subjected to major trauma, including open injuries. It can develop in any closed osteofascial compartment and its consequences can be devastating to the individual affected.

This book provides a brief synopsis of this very important condition. The first chapter provides an overview of the musculoskeletal compartment syndrome. A section on the musculoskeletal system describes the etiology and pathogenesis of compartment syndrome in detail and looks at the vicious downward spiral that occurs if the condition goes unrecognized, leading to irreversible muscle damage and necrosis. In addition, it looks at the various anatomical sites in the musculoskeletal system in which this condition occurs, acknowledging the need for timely diagnosis. The section also illustrates the various anatomical approaches for decompression of compartments at each site, including the hand and foot.

Compartment syndrome can affect sites other than limbs, with equally devastating complications. The third section discusses these sites, including the thorax and abdomen. It describes the etiologies of the syndrome in these sites, which are many and varied, and provides suggestions for the diagnosis and management of abdominal compartment syndrome.

The fourth section covers the diagnosis of compartment syndrome, which can be challenging. If compartment syndrome is suspected, prompt decompression is generally advocated to save the structures involved from irreversible damage and consequences that may have a significantly negative impact on the patient's life. There are, however, certain situations where compartment pressure monitoring may be useful, for example, in unconscious or ventilated patients. This section describes various methods of compartment pressure monitoring along with their advantages and drawbacks. It also discusses newer methods of diagnosis. However, the current gold standard is still timely clinical examination, a high index of suspicion, and prompt surgical decompression.

The fifth section describes the occurrence of compartment syndrome in special situations. Some of these situations include compartment syndrome in medical patients, those related to patient positioning, and bleeding into compartments in bleeding disorders.

Compartment syndrome remains a condition that can have significant negative consequences for patients if not diagnosed on time. A high index of suspicion is necessary for its diagnosis and time-critical intervention may prevent significant morbidity associated with this condition.

**II**

**Chapter 7 87**

Compartment Syndrome Related to Patient Positioning in the Surgical

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

Treatment of Urolithiasis

We would like to thank all the authors that contributed to the book as well as IntechOpen Author Service Manager Maja Bozicevic.

#### **Saqeb Beig Mirza**

Consultant Trauma and Orthopedic Surgeon, University Hospital of Wales, United Kingdom

#### **Khaled Elawady**

**1**

Section 1

Introduction

Fellow, Trauma and Orthopaedic Surgery, Oxford University Hospitals, United Kingdom

Section 1 Introduction

**3**

**Table 1.**

*Compartment syndrome risk factors, adapted from [1].*

**Chapter 1**

**Abstract**

leg compartments

**1. Introduction**

Syndrome

Review of Compartment

and pathophysiology, as well as the management of this condition.

Males—average age 32 years 91% Females—average age 44 years 9% Tibial diaphyseal fracture 36.0% Soft-tissue injury 23.2% Distal radial fracture 9.8% Crush syndrome 7.9% Diaphyseal fracture of the radius/ulna 7.9% Femoral fracture 3.0% Tibial plateau fracture 3.0%

Compartment syndrome is a painful condition, caused by increased pressure in a closed muscular compartment. A compartment is a group of muscles enclosed in fascia and septa of connective tissue, which separates different muscle groups. The chambers created receive their blood supply through the arteries. As the pressure builds in the closed space, the blood supply to muscles enclosed decreases. Normal compartment pressure allows blood to flow in and then venous outflow to exit the compartment. However, with increased pressure in the compartment, the arterial flow is impaired. Subsequently, venous outflow stops, adding to the volume of the closed chamber, and hence, pressure builds to the point when the arterial flow stops as well. This chapter provides a general overview of the compartment syndrome in orthopaedic surgical practice. It includes definitions, causes, microscopic anatomy

**Keywords:** compartment, syndrome, osteofascial, contracture, fasciotomy, plastics,

Compartment syndrome is an acute surgical emergency; it can be limb threatening and potentially life threatening. It results from decreased tissue perfusion secondary to increased pressure within an osteofascial compartment, the consequences of which may result in tissue necrosis. Incidence is more in young men, commonly under 35 years old, and the mean age is different between males (30 years old) and

*Khaled Elawady and Saqeb Beig Mirza*

#### **Chapter 1**

## Review of Compartment Syndrome

*Khaled Elawady and Saqeb Beig Mirza*

#### **Abstract**

Compartment syndrome is a painful condition, caused by increased pressure in a closed muscular compartment. A compartment is a group of muscles enclosed in fascia and septa of connective tissue, which separates different muscle groups. The chambers created receive their blood supply through the arteries. As the pressure builds in the closed space, the blood supply to muscles enclosed decreases. Normal compartment pressure allows blood to flow in and then venous outflow to exit the compartment. However, with increased pressure in the compartment, the arterial flow is impaired. Subsequently, venous outflow stops, adding to the volume of the closed chamber, and hence, pressure builds to the point when the arterial flow stops as well. This chapter provides a general overview of the compartment syndrome in orthopaedic surgical practice. It includes definitions, causes, microscopic anatomy and pathophysiology, as well as the management of this condition.

**Keywords:** compartment, syndrome, osteofascial, contracture, fasciotomy, plastics, leg compartments

#### **1. Introduction**

Compartment syndrome is an acute surgical emergency; it can be limb threatening and potentially life threatening. It results from decreased tissue perfusion secondary to increased pressure within an osteofascial compartment, the consequences of which may result in tissue necrosis. Incidence is more in young men, commonly under 35 years old, and the mean age is different between males (30 years old) and

#### **Table 1.**

*Compartment syndrome risk factors, adapted from [1].*

females (44 years old). Sixty-four per cent are associated with fractures, with the annual incidence being 1–7.3 per 100,000 [1].

Acute compartment syndrome affects patients involved in trauma and those patients with associated neurologic and other injuries that can mask the diagnosis. A high degree of suspicion, as well as understanding the natural history and limited value of signs and symptoms, will increase the awareness of the possible diagnosis. The following risk factors can aid in making the diagnosis (**Table 1**) [2].

#### **2. Pathophysiology**

Acute compartment syndrome is caused by an increase in the contents of an enclosed space (e.g. bleeding) or a decrease in the volume of a space (e.g. tight cast), or a combination of the two factors. Intercompartmental pressure (ICP) is a function of and an interaction between interstitial pressure and perfusion pressure at the level of the capillary bed. When the interstitial pressure exceeds the perfusion pressure at capillary bed level, there is increased pressure at the venous end of the capillary bed. The resulting increased hydrostatic pressure and further increased intracompartmental pressure eventually limit arteriolar inflow within the system [3]. As a result, the perfusion pressure reduces and ultimately, the perfusion of the compartment stops, leading to anoxia and death of compartment contents (**Figure 1**).

At a cellular level, diminishing ATP levels correlate closely with worsening muscle necrosis, leading to complete muscle necrosis. In a canine study, after 6 h of ischaemia, only 20% of pre-ischaemic ATP remained, which led to complete muscle necrosis [4].

Histologically, there is central muscle necrosis with a surrounding zone of partial ischaemia and peripheral tissue oedema, often within areas of incomplete injury [1]. Adenosine triphosphate (ATP) breakdown occurs as a result of ischaemic injury to the muscle and the severity of this damage is directly related to the level of energy depletion [5].

**5**

syndrome [10].

*Review of Compartment Syndrome*

**3. Classification**

understood [9].

**4. Diagnosis**

(exertional) compartment syndrome.

*DOI: http://dx.doi.org/10.5772/intechopen.99996*

Skeletal muscles are affected by ischaemia more than other body tissues. With regard to susceptibility to muscle ischaemia, red muscle fibres, for example those located in the anterior compartment of the leg, are more vulnerable to the effects of ischaemia due to their predominant reliance on aerobic metabolic energy in contrast to white muscle fibres, for example the gastrosoleus complex that relies on anaerobically derived energy [6, 7]. Injury (the amount of muscle necrosis) is determined by duration of ischaemia, fibre type, the available residual blood flow and temperature at which ischaemia takes place. Increased collateral blood flow and decreased ischaemic temperature lead to less muscle necrosis [8]. Longer time to diagnose and definitive treatment result in progressive skeletal muscle death and the degree of skeletal muscle injury correlate directly with the severity and duration of ischaemia.

The two main types of compartment syndrome exist, acute and chronic

muscle bruises, tight casts or bandages, bleeding into compartments in patients

with coagulation disorders and heavy drinking or drug abuse.

limb closely for any signs of evolving compartment syndrome.

Acute compartment syndrome occurs following a fracture, crush injuries, severe

Chronic exertional compartment syndrome follows repetitive exercise motion and occurs most frequently in people under 40. However, it can develop at any age. Risk increases with exercises such as swimming, tennis or running, and intense or frequent workouts can also increase the risk. The link between exercise and its association with chronic (exertional) compartment syndrome is not fully

There are a few situations that put patients at significant risk of developing compartment syndrome and warrant routine observations for compartment syndrome. These include major limb injuries including open or segmental long-bone injuries caused by high-energy mechanisms, operative management of major limb injuries and prolonged surgical procedures that may compromise or affect limb perfusion adversely. In these cases, it should be routine procedure to monitor the

The BOAST guidelines recommend meticulous documentation of the clinical findings in suspected compartment syndrome. In addition, it is important to record the mechanism of injury and the time it occurred as well as the initial time of evaluation and ongoing clinical reviews. Pain levels and analgesic requirements should be recorded and whether or not any regional anaesthetics had been used thus far [10]. The most important and diagnostically significant signs include pain on passive stretch of the muscles in the individual compartments affected and pain out of proportion to the injury, and these should be acted upon in a timely manner [1, 2]. Documentation of neural function and vascular perfusion including capillary refill time and pulses need to be recorded and documented even though they have little role in the early and timely diagnosis of an evolving acute compartment

Classic features including pain, pallor, pulselessness, paraesthesia, poikilothermia and paralysis are more considered late signs of a limb that has been vascularly compromised and do not really play a part in early diagnosis of ACS [11]. Undiagnosed acute compartment syndrome will cause progressive muscle damage.

**Figure 1.** *Illustration of pathophysiologic sequence for the development of acute compartment syndrome.*

*Review of Compartment Syndrome DOI: http://dx.doi.org/10.5772/intechopen.99996*

Skeletal muscles are affected by ischaemia more than other body tissues. With regard to susceptibility to muscle ischaemia, red muscle fibres, for example those located in the anterior compartment of the leg, are more vulnerable to the effects of ischaemia due to their predominant reliance on aerobic metabolic energy in contrast to white muscle fibres, for example the gastrosoleus complex that relies on anaerobically derived energy [6, 7]. Injury (the amount of muscle necrosis) is determined by duration of ischaemia, fibre type, the available residual blood flow and temperature at which ischaemia takes place. Increased collateral blood flow and decreased ischaemic temperature lead to less muscle necrosis [8]. Longer time to diagnose and definitive treatment result in progressive skeletal muscle death and the degree of skeletal muscle injury correlate directly with the severity and duration of ischaemia.

#### **3. Classification**

*A Comprehensive Review of Compartment Syndrome*

annual incidence being 1–7.3 per 100,000 [1].

**2. Pathophysiology**

necrosis [4].

energy depletion [5].

females (44 years old). Sixty-four per cent are associated with fractures, with the

Acute compartment syndrome affects patients involved in trauma and those patients with associated neurologic and other injuries that can mask the diagnosis. A high degree of suspicion, as well as understanding the natural history and limited value of signs and symptoms, will increase the awareness of the possible diagnosis.

Acute compartment syndrome is caused by an increase in the contents of an enclosed space (e.g. bleeding) or a decrease in the volume of a space (e.g. tight cast), or a combination of the two factors. Intercompartmental pressure (ICP) is a function of and an interaction between interstitial pressure and perfusion pressure at the level of the capillary bed. When the interstitial pressure exceeds the perfusion pressure at capillary bed level, there is increased pressure at the venous end of the capillary bed. The resulting increased hydrostatic pressure and further increased intracompartmental pressure eventually limit arteriolar inflow within the system [3]. As a result, the perfusion pressure reduces and ultimately, the perfusion of the compartment

The following risk factors can aid in making the diagnosis (**Table 1**) [2].

stops, leading to anoxia and death of compartment contents (**Figure 1**).

At a cellular level, diminishing ATP levels correlate closely with worsening muscle necrosis, leading to complete muscle necrosis. In a canine study, after 6 h of ischaemia, only 20% of pre-ischaemic ATP remained, which led to complete muscle

Histologically, there is central muscle necrosis with a surrounding zone of partial ischaemia and peripheral tissue oedema, often within areas of incomplete injury [1]. Adenosine triphosphate (ATP) breakdown occurs as a result of ischaemic injury to the muscle and the severity of this damage is directly related to the level of

**4**

**Figure 1.**

*Illustration of pathophysiologic sequence for the development of acute compartment syndrome.*

The two main types of compartment syndrome exist, acute and chronic (exertional) compartment syndrome.

Acute compartment syndrome occurs following a fracture, crush injuries, severe muscle bruises, tight casts or bandages, bleeding into compartments in patients with coagulation disorders and heavy drinking or drug abuse.

Chronic exertional compartment syndrome follows repetitive exercise motion and occurs most frequently in people under 40. However, it can develop at any age.

Risk increases with exercises such as swimming, tennis or running, and intense or frequent workouts can also increase the risk. The link between exercise and its association with chronic (exertional) compartment syndrome is not fully understood [9].

#### **4. Diagnosis**

There are a few situations that put patients at significant risk of developing compartment syndrome and warrant routine observations for compartment syndrome. These include major limb injuries including open or segmental long-bone injuries caused by high-energy mechanisms, operative management of major limb injuries and prolonged surgical procedures that may compromise or affect limb perfusion adversely. In these cases, it should be routine procedure to monitor the limb closely for any signs of evolving compartment syndrome.

The BOAST guidelines recommend meticulous documentation of the clinical findings in suspected compartment syndrome. In addition, it is important to record the mechanism of injury and the time it occurred as well as the initial time of evaluation and ongoing clinical reviews. Pain levels and analgesic requirements should be recorded and whether or not any regional anaesthetics had been used thus far [10].

The most important and diagnostically significant signs include pain on passive stretch of the muscles in the individual compartments affected and pain out of proportion to the injury, and these should be acted upon in a timely manner [1, 2].

Documentation of neural function and vascular perfusion including capillary refill time and pulses need to be recorded and documented even though they have little role in the early and timely diagnosis of an evolving acute compartment syndrome [10].

Classic features including pain, pallor, pulselessness, paraesthesia, poikilothermia and paralysis are more considered late signs of a limb that has been vascularly compromised and do not really play a part in early diagnosis of ACS [11]. Undiagnosed acute compartment syndrome will cause progressive muscle damage. Therefore, it may be beneficial for one experienced assessor to serially examine the patient, so the evolution of the condition is noted rather than at one point in time and at the same time avoid interobserver error [11, 12].

The presence of all five features may indicate a late diagnosis and irreversible damage because some features such as paralysis occur very late in the pathogenesis of acute compartment syndrome. Frequent serial clinical assessment must be interpreted taking into consideration the patient's individual risk [11].

When compartment pressure measurements are indicated, for example in unconscious patients, the diastolic blood pressure is recorded. If the difference between diastolic blood pressure and compartment pressure is less than 30 mmHg, this suggests an increased risk of compartment syndrome and a decision should be made either to proceed to surgical decompression or to continue monitoring. This decision-making process should involve a senior clinician [10].

Bayes' theorem has been used to calculate the predictive values of some of the cardinal features of acute compartment syndrome. These included pain, paraesthesia, paresis and pain on passive movement of the muscles involved. The high specificity and negative predictive values for these factors suggested that their absence correlated with a less likelihood of the presence of an acute compartment syndrome, but they had a low-positive predictive value indicating that presence of these symptoms on their own had a low correlation with acute compartment syndrome [13].

#### **5. Management**

The initial management should involve splitting the plaster dressing to skin level. Studies have shown that removing dressings overlying the compartment suspected of raised ICP, splitting the cast reduced ICP by a mean of 65% [14]. Moreover, a 10–20% further reduction occurred after the padding cut to skin level. However, even after the removal of tight casts, continued monitoring for clinical features of ACS should occur and it is recommended that the limb should not be elevated excessively but rather be maintained at heart level to perfuse the compartment [14].

If acute compartment syndrome clinical features do not regress following this, a fasciotomy indicated and should be carried out as an emergency procedure [15]. In some special situations, fasciotomy may not be indicated, for example in patients who already have muscle death due to muscle crush syndrome suffered in situations such as natural disasters. In these cases, conservative management may be more appropriate in these patients. The decision to proceed with fasciotomy was based on a comprehensive clinical assessment [16].

In certain circumstances, some authors consider primary amputation a better option than decompressive fasciotomy, especially if there has been a duration of greater than 8 h following the onset of symptoms of acute compartment syndrome with absent muscle function [17].

Compartment pressure measurement can be used as an adjunct to clinical examination, especially if the clinical symptoms cannot be elicited, for example in unconscious or ventilated patients, or if clinical examination is equivocal, or unreliable [17].

Serial compartment pressure measurement, with the initial measure used as a reference point, detects a further rise in the compartment pressure [1].

Two standard techniques for compartment pressure measurement are the slit catheter and the side-port needle. The slit catheter is a low-volume infusion technique [18]. The catheter may be left within the compartment for repeated or continuous compartment pressure measurements for hours.

**7**

grafting.

(**Figure 2**).

**5.1 Forearm compartment syndrome**

**5.2 Hand compartment syndrome**

interosseous (three).

*Review of Compartment Syndrome*

*DOI: http://dx.doi.org/10.5772/intechopen.99996*

ments taken with a slit catheter or the side-port needle [19].

available for determining the intracompartmental pressures.

the highest pressure measurement at the fracture site [20].

fasciotomy of all compartments with elevated pressures is necessary.

dorsal compartment and mobile wad of Henry (lateral) compartments.

Side-port needles can be used to measure multiple compartments, and studies have shown no significant difference statistically when comparing the measure-

Using an18-gauge needle to measure intracompartmental pressure tends to overestimate the value of the intracompartmental pressure by 20 mmHg when compared with the slit catheter method or the side-port needle and may hence be less accurate. Several commercially available pressure measurement devices are

There is a relationship between compartmental tissue pressure and the distance from the site of the fracture. In one study, the highest pressure recorded was in the deep posterior or anterior compartments, or both, and 89% of compartments had

Once an impending or confirmed compartment syndrome diagnosis has been made, immediate measures necessary must be taken to reduce the chances of progression. These include splitting or taking any casts or occlusive dressings off. Cast padding or circumferential dressings have to be released around their entire circumference, and the limb has to be elevated to the level of the patient's heart to maximise perfusion while minimising swelling. If, in spite of these steps, the clinical signs of compartment syndrome do not resolve, emergent and complete

Patients should be counselled about the risks associated with fasciotomy such as wound healing problems, weakness, chronic venous insufficiency, non-union of the associated fractures and subsequent plastic surgical intervention, for example skin

There are several techniques of decompression for different parts of the body.

There are three compartments: the volar compartment (superficial and deep),

Decompression of all involved compartments is mandatory, involves a volar incision 1 cm proximal and 2 cm lateral to the medial epicondyle and obliquely crosses the antecubital fossa and over the volar aspect of the mobile wad, and then curves medially, reaching the midline at the junction of the middle and distal third of the forearm and continued just medial to the palmaris longus tendon to avoid the palmar cutaneous branch of the median nerve incision, crossing the wrist crease at an angle and extending into the mid-palm for a carpal tunnel release if necessary

The lacertus fibrosus and fascia overlying the flexor carpi ulnaris must be opened and flexor carpi ulnaris is retracted ulnarly, and the flexor digitorum superficialis is retracted radially to permit opening of the fascia of the deep volar compartment, avoiding the ulnar nerve and artery carefully during dissection.

Dorsal compartment release is through a longitudinal incision 2 cm distal to the lateral epicondyle towards the midline of the wrist, dissecting between the interval of extensor digitorum communis and extensor carpi radialis brevis. The muscles of the forearm should be palpated and if soft, no further procedure should be performed. If residual muscle tension is felt, then an epimysiotomy is performed.

In the hand, 10 compartments may be affected by rising compartment pressures. They are hypothenar, thenar, adductor pollicis, dorsal interosseous (four) and volar

#### *Review of Compartment Syndrome DOI: http://dx.doi.org/10.5772/intechopen.99996*

*A Comprehensive Review of Compartment Syndrome*

and at the same time avoid interobserver error [11, 12].

Therefore, it may be beneficial for one experienced assessor to serially examine the patient, so the evolution of the condition is noted rather than at one point in time

The presence of all five features may indicate a late diagnosis and irreversible damage because some features such as paralysis occur very late in the pathogenesis of acute compartment syndrome. Frequent serial clinical assessment must be

When compartment pressure measurements are indicated, for example in unconscious patients, the diastolic blood pressure is recorded. If the difference between diastolic blood pressure and compartment pressure is less than 30 mmHg, this suggests an increased risk of compartment syndrome and a decision should be made either to proceed to surgical decompression or to continue monitoring. This

Bayes' theorem has been used to calculate the predictive values of some of the cardinal features of acute compartment syndrome. These included pain, paraesthesia, paresis and pain on passive movement of the muscles involved. The high specificity and negative predictive values for these factors suggested that their absence correlated with a less likelihood of the presence of an acute compartment syndrome, but they had a low-positive predictive value indicating that presence of these symptoms on their own had a low correlation with acute compartment

The initial management should involve splitting the plaster dressing to skin level. Studies have shown that removing dressings overlying the compartment suspected of raised ICP, splitting the cast reduced ICP by a mean of 65% [14]. Moreover, a 10–20% further reduction occurred after the padding cut to skin level. However, even after the removal of tight casts, continued monitoring for clinical features of ACS should occur and it is recommended that the limb should not be elevated excessively but rather be maintained at heart level to perfuse the compartment [14]. If acute compartment syndrome clinical features do not regress following this, a fasciotomy indicated and should be carried out as an emergency procedure [15]. In some special situations, fasciotomy may not be indicated, for example in patients who already have muscle death due to muscle crush syndrome suffered in situations such as natural disasters. In these cases, conservative management may be more appropriate in these patients. The decision to proceed with fasciotomy was based on

In certain circumstances, some authors consider primary amputation a better option than decompressive fasciotomy, especially if there has been a duration of greater than 8 h following the onset of symptoms of acute compartment syndrome

Compartment pressure measurement can be used as an adjunct to clinical examination, especially if the clinical symptoms cannot be elicited, for example in unconscious or ventilated patients, or if clinical examination is equivocal, or

Serial compartment pressure measurement, with the initial measure used as a

Two standard techniques for compartment pressure measurement are the slit catheter and the side-port needle. The slit catheter is a low-volume infusion technique [18]. The catheter may be left within the compartment for repeated or

reference point, detects a further rise in the compartment pressure [1].

continuous compartment pressure measurements for hours.

interpreted taking into consideration the patient's individual risk [11].

decision-making process should involve a senior clinician [10].

**6**

syndrome [13].

**5. Management**

a comprehensive clinical assessment [16].

with absent muscle function [17].

unreliable [17].

Side-port needles can be used to measure multiple compartments, and studies have shown no significant difference statistically when comparing the measurements taken with a slit catheter or the side-port needle [19].

Using an18-gauge needle to measure intracompartmental pressure tends to overestimate the value of the intracompartmental pressure by 20 mmHg when compared with the slit catheter method or the side-port needle and may hence be less accurate. Several commercially available pressure measurement devices are available for determining the intracompartmental pressures.

There is a relationship between compartmental tissue pressure and the distance from the site of the fracture. In one study, the highest pressure recorded was in the deep posterior or anterior compartments, or both, and 89% of compartments had the highest pressure measurement at the fracture site [20].

Once an impending or confirmed compartment syndrome diagnosis has been made, immediate measures necessary must be taken to reduce the chances of progression. These include splitting or taking any casts or occlusive dressings off. Cast padding or circumferential dressings have to be released around their entire circumference, and the limb has to be elevated to the level of the patient's heart to maximise perfusion while minimising swelling. If, in spite of these steps, the clinical signs of compartment syndrome do not resolve, emergent and complete fasciotomy of all compartments with elevated pressures is necessary.

Patients should be counselled about the risks associated with fasciotomy such as wound healing problems, weakness, chronic venous insufficiency, non-union of the associated fractures and subsequent plastic surgical intervention, for example skin grafting.

There are several techniques of decompression for different parts of the body.

#### **5.1 Forearm compartment syndrome**

There are three compartments: the volar compartment (superficial and deep), dorsal compartment and mobile wad of Henry (lateral) compartments.

Decompression of all involved compartments is mandatory, involves a volar incision 1 cm proximal and 2 cm lateral to the medial epicondyle and obliquely crosses the antecubital fossa and over the volar aspect of the mobile wad, and then curves medially, reaching the midline at the junction of the middle and distal third of the forearm and continued just medial to the palmaris longus tendon to avoid the palmar cutaneous branch of the median nerve incision, crossing the wrist crease at an angle and extending into the mid-palm for a carpal tunnel release if necessary (**Figure 2**).

The lacertus fibrosus and fascia overlying the flexor carpi ulnaris must be opened and flexor carpi ulnaris is retracted ulnarly, and the flexor digitorum superficialis is retracted radially to permit opening of the fascia of the deep volar compartment, avoiding the ulnar nerve and artery carefully during dissection.

Dorsal compartment release is through a longitudinal incision 2 cm distal to the lateral epicondyle towards the midline of the wrist, dissecting between the interval of extensor digitorum communis and extensor carpi radialis brevis. The muscles of the forearm should be palpated and if soft, no further procedure should be performed. If residual muscle tension is felt, then an epimysiotomy is performed.

#### **5.2 Hand compartment syndrome**

In the hand, 10 compartments may be affected by rising compartment pressures. They are hypothenar, thenar, adductor pollicis, dorsal interosseous (four) and volar interosseous (three).

#### **Figure 2.**

*Illustration of the incisions used to decompress the volar forearm.*

Release of the volar and dorsal interosseous compartments and the adductor compartment to the thumb is done with two longitudinal incisions dorsally over the second and fourth metacarpals (**Figure 3**).

Incising the fascia over the dorsal interosseous muscles and blunt dissection is performed along the ulnar side of the second metacarpal to decompress the first volar interosseous through the more radial incision, and the radial aspect of the fourth and fifth metacarpals is dissected through an ulnar incision to release the second and third volar interosseous compartments. For releasing the thenar and hypothenar compartments, longitudinal incisions are made at the junctions of the glabrous and non-glabrous skin over the radial side of the first metacarpal and the ulnar side of the fifth metacarpal.

Ideally, hand fasciotomies should be done by a hand surgeon unless there is an immediate need with no access to a hand surgeon [21].

Various locations in the lower extremity can develop compartment syndromes, for example the gluteal musculature, the muscles of the thigh and lower leg, and foot.

Early recognition and decompression are the key to avoid long-term complications and even amputation of the limb.

**9**

**Figure 4.**

*Review of Compartment Syndrome*

**5.3 Gluteal musculature**

*DOI: http://dx.doi.org/10.5772/intechopen.99996*

**5.4 Thigh compartment syndrome**

**5.5 Leg compartment syndrome**

adequately [17].

ture used sufficiently to decompress the gluteal region.

decompression through the long lateral incision.

the skin from creating a tight compartment envelope [22].

compartments on either side of the septum are decompressed [23].

Posterior incision decompresses the gluteus maximus and the abductor muscula-

A long single lateral incision can sufficiently decompress the anterior and posterior compartments of the thigh. A medial adductor incision may be required if ongoing symptoms of increased compartment pressure are evident despite adequate

The length of the skin incision influences fascial decompression in the leg associated with an acute compartment syndrome, to normalise the compartment pressures and restore perfusion to the tissues. Some authors favour limited incisions, claiming low morbidity, while others recommend long incisions, emphasising that these are required to decompress the affected compartment

In a trauma situation, long incisions are recommended for adequate decompression. Hyperaemia post-decompression is avoided by using long incisions to prevent

Leg decompression can be done *via* a one-incision or a two-incision approach. The one-incision technique, although described, is difficult and not widely used. It involves a long single lateral incision over the anterolateral leg made 5 cm of distal to the head of the fibula and proximal to the lateral malleolus [22]. This is followed by identifying the septum between the anterior and lateral compartments and avoiding the injury to the superficial peroneal nerve distally, the anterior and lateral

*Two-incision fasciotomies; the medial incision alone is usually sufficient for debridement and preserves the perforators arising from the posterior tibial vessels, which form the basis of local fasciocutaneous flaps.*

**Figure 3.** *Drawing of the two incisions used for the hand compartment decompression.*

#### **5.3 Gluteal musculature**

*A Comprehensive Review of Compartment Syndrome*

A

B

second and fourth metacarpals (**Figure 3**).

*Illustration of the incisions used to decompress the volar forearm.*

immediate need with no access to a hand surgeon [21].

*Drawing of the two incisions used for the hand compartment decompression.*

ulnar side of the fifth metacarpal.

tions and even amputation of the limb.

and foot.

**Figure 2.**

Release of the volar and dorsal interosseous compartments and the adductor compartment to the thumb is done with two longitudinal incisions dorsally over the

Incising the fascia over the dorsal interosseous muscles and blunt dissection is performed along the ulnar side of the second metacarpal to decompress the first volar interosseous through the more radial incision, and the radial aspect of the fourth and fifth metacarpals is dissected through an ulnar incision to release the second and third volar interosseous compartments. For releasing the thenar and hypothenar compartments, longitudinal incisions are made at the junctions of the glabrous and non-glabrous skin over the radial side of the first metacarpal and the

Ideally, hand fasciotomies should be done by a hand surgeon unless there is an

Various locations in the lower extremity can develop compartment syndromes,

Early recognition and decompression are the key to avoid long-term complica-

for example the gluteal musculature, the muscles of the thigh and lower leg,

**8**

**Figure 3.**

Posterior incision decompresses the gluteus maximus and the abductor musculature used sufficiently to decompress the gluteal region.

#### **5.4 Thigh compartment syndrome**

A long single lateral incision can sufficiently decompress the anterior and posterior compartments of the thigh. A medial adductor incision may be required if ongoing symptoms of increased compartment pressure are evident despite adequate decompression through the long lateral incision.

#### **5.5 Leg compartment syndrome**

The length of the skin incision influences fascial decompression in the leg associated with an acute compartment syndrome, to normalise the compartment pressures and restore perfusion to the tissues. Some authors favour limited incisions, claiming low morbidity, while others recommend long incisions, emphasising that these are required to decompress the affected compartment adequately [17].

In a trauma situation, long incisions are recommended for adequate decompression. Hyperaemia post-decompression is avoided by using long incisions to prevent the skin from creating a tight compartment envelope [22].

Leg decompression can be done *via* a one-incision or a two-incision approach.

The one-incision technique, although described, is difficult and not widely used. It involves a long single lateral incision over the anterolateral leg made 5 cm of distal to the head of the fibula and proximal to the lateral malleolus [22]. This is followed by identifying the septum between the anterior and lateral compartments and avoiding the injury to the superficial peroneal nerve distally, the anterior and lateral compartments on either side of the septum are decompressed [23].

#### **Figure 4.**

*Two-incision fasciotomies; the medial incision alone is usually sufficient for debridement and preserves the perforators arising from the posterior tibial vessels, which form the basis of local fasciocutaneous flaps.*

Then, the lateral compartment musculature is lifted from the intramuscular septum and incising the intramuscular septum to access the lateral portion of the superficial posterior compartment, and through this incision, the deep posterior compartment can be decompressed by mobilising the superficial compartment posteriorly [17].

The more widely used and accepted approach is a two-incision technique (**Figure 4**), and this is the approach recommended in the UK BOAST/BAPRAS guidelines.

The location of the medial skin incision is crucial as muscles in the superficial posterior compartment are proximal and the incision needs to reach the proximal part of the deep posterior compartment to decompress these muscles adequately.

The leg deep posterior musculature is on the other hand in the distal half of the limb and decompressing them involves detaching the soleus origin from the medial aspect of the tibial shaft. Extra care is taken at this point as posterior tibial neurovascular bundle lies just deep to the investing fascia. A careful assessment of muscle viability is needed, and all non-viable muscles should be excised.

It should be noted that the lateral incision, if inadvertently placed over the fibula (too lateral), can expose the periosteum, and if placed too far distally, the incision can expose the peroneal tendons, exposing bone and/or tendons increase incidence of infection and delayed healing, and may end in amputation [20].

#### **5.6 Foot compartment syndrome**

Foot compartment syndrome is a controversial subject, as some foot and ankle specialists advocate not interfering surgically due to the associated morbidity with surgery.

In the foot, there are nine main compartments: medial, lateral, interosseous (four) and central (three), and dual dorsal incisions are recommended for decompression of the foot compartments (**Figure 5**).

A dorsal medial incision is made medial to second metatarsal, and this releases the first and second interosseous, medial and deep central compartment.

The dorsal lateral incision is made lateral to the fourth metatarsal and releases the third and fourth interosseous, lateral, superficial and middle central compartments.

To do this, the dorsal fascia of each interosseous compartment is opened longitudinally, muscles stripped from the medial fascia of the first interosseous compartment, split adductor compartment and a medial incision may be added

**11**

**Author details**

Khaled Elawady1

1 Oxford University Hospital, UK

2 University Hospital of Wales, UK

provided the original work is properly cited.

\* and Saqeb Beig Mirza2

\*Address all correspondence to<EMAIL_ADDRESS>
© 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,

*Review of Compartment Syndrome*

**6. Conclusion**

**Abbreviations**

*DOI: http://dx.doi.org/10.5772/intechopen.99996*

surgical intervention is the key to success.

ICP intracompartmental pressure ACS acute compartment syndrome

for decompression of calcaneal compartment with the release of the fascia of the

Acute compartment syndrome is an acute limb-threatening condition. Its diagnosis is mainly clinical and involves certain cardinal features. A high index of suspicion is needed to make the diagnosis. The condition is time critical and timely

intrinsic foot muscles at their metatarsal attachments [24, 25].

for decompression of calcaneal compartment with the release of the fascia of the intrinsic foot muscles at their metatarsal attachments [24, 25].

### **6. Conclusion**

*A Comprehensive Review of Compartment Syndrome*

posteriorly [17].

guidelines.

adequately.

compartments.

Then, the lateral compartment musculature is lifted from the intramuscular septum and incising the intramuscular septum to access the lateral portion of the superficial posterior compartment, and through this incision, the deep posterior compartment can be decompressed by mobilising the superficial compartment

The more widely used and accepted approach is a two-incision technique (**Figure 4**), and this is the approach recommended in the UK BOAST/BAPRAS

The location of the medial skin incision is crucial as muscles in the superficial posterior compartment are proximal and the incision needs to reach the proximal part of the deep posterior compartment to decompress these muscles

The leg deep posterior musculature is on the other hand in the distal half of the limb and decompressing them involves detaching the soleus origin from the medial aspect of the tibial shaft. Extra care is taken at this point as posterior tibial neurovascular bundle lies just deep to the investing fascia. A careful assessment of muscle

It should be noted that the lateral incision, if inadvertently placed over the fibula (too lateral), can expose the periosteum, and if placed too far distally, the incision can expose the peroneal tendons, exposing bone and/or tendons increase incidence

Foot compartment syndrome is a controversial subject, as some foot and ankle specialists advocate not interfering surgically due to the associated morbidity with surgery. In the foot, there are nine main compartments: medial, lateral, interosseous (four) and central (three), and dual dorsal incisions are recommended for decom-

A dorsal medial incision is made medial to second metatarsal, and this releases

MT

MM

the first and second interosseous, medial and deep central compartment. The dorsal lateral incision is made lateral to the fourth metatarsal and releases the third and fourth interosseous, lateral, superficial and middle central

*Drawing depicts the two dorsal and medial incisions used to decompress the foot compartments.*

To do this, the dorsal fascia of each interosseous compartment is opened longitudinally, muscles stripped from the medial fascia of the first interosseous compartment, split adductor compartment and a medial incision may be added

viability is needed, and all non-viable muscles should be excised.

of infection and delayed healing, and may end in amputation [20].

**5.6 Foot compartment syndrome**

pression of the foot compartments (**Figure 5**).

**10**

**Figure 5.**

Acute compartment syndrome is an acute limb-threatening condition. Its diagnosis is mainly clinical and involves certain cardinal features. A high index of suspicion is needed to make the diagnosis. The condition is time critical and timely surgical intervention is the key to success.

### **Abbreviations**

### **Author details**

Khaled Elawady1 \* and Saqeb Beig Mirza2

1 Oxford University Hospital, UK

2 University Hospital of Wales, UK

\*Address all correspondence to<EMAIL_ADDRESS>
© 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.

#### **References**

[1] McQueen MM, Gaston P, Court-Brown CM. A molecular interaction database. Acute compartment syndrome. Who is at risk? The Journal of Bone and Joint Surgery. British Volume. 2000;**82**(2):200-203

[2] McQueen MM, Christie J, Court-Brown CM. Compartment pressures after intramedullary nailing of the tibia. The Journal of Bone and Joint Surgery. British Volume. 1990;**72**: 395-397

[3] Tiwari A, Hag AI, Myint F, et al. Acute compartment syndromes. Journal of British Surgery. 2002;**89**:397-412. DOI: 10.1046/j.0007-1323.2002.02063. x

[4] Hayes G, Liauw S, Romaschin A, et al. Separation of reperfusion injury from ischemia-induced necrosis. Surgical Forum. 1988;**39**:306-308

[5] Lindsay T, Liauw F, Romaschin S, et al. The effect of ischemia/reperfusion on adenine nucleotide metabolism and xanthine oxidase production in skeletal muscle. Journal of Vascular Surgery. 1990;**12**:8-15

[6] Blaisdell FW. The pathophysiology of skeletal muscle ischemia and the reperfusion syndrome: A review. Cardiovascular Surgery. 2002;**10**:620- 630. DOI: 10.1016/S0967-2109 (02)00070-4

[7] Jennische E. Ischemia-induced injury in glycogen-depleted skeletal muscle: Selective vulnerability of the FG-fibres. Acta Physiologica Scandinavica. 1985;**125**:727-734. DOI: 10.1111/j.1748- 1716.1985.tb07776.x

[8] Petrasek PF, Homer-Vanniasinkam S, Walker PM. Determinants of ischemic injury to skeletal muscle. Journal of Vascular Surgery. 1994;**19**:623-631. DOI: 10.1016/ S0741-5214(94)70035-4

[9] Bae DS, Kadiyala RK, Waters PM. Acute compartment syndrome in children: Contemporary diagnosis, treatment, and outcomes. Journal of Pediatric Orthopaedics. 2001;**21**:680- 688. DOI: 10.1097/00004694- 200109000-00025

[10] BOAST British Orthopaedic Association Standards for Trauma. Review date: December 2016. For correspondence, contact: policy@ boa.ac.u

[11] Malik AA, Khan WS, Chaudhry A, et al. Acute compartment syndrome a life and limb-threatening surgical emergency. Journal of Perioperative Practice. 2009;**19**(5):137-142

[12] Shuler FD, Dietz MJ. Physicians' ability to manually detect isolated elevations in leg intracompartmental pressure. The Journal of Bone & Joint Surgery. 2010;**92**(2):361-367

[13] Ulmer T. The clinical diagnosis of compartment syndrome of the lower leg: Are clinical findings predictive of the disorder? Journal of Orthopaedic Trauma. 2002;**16**(8):572-577

[14] Köstler W, Strohm PC, Südkamp NP. Acute compartment syndrome of the limb. Injury. 2004;**35**(12):1221-1227

[15] Murphy JB. Myositis. JAMA: The Journal of the American Medical Association. 1914;**63**:1249

[16] Mubarak SJ, Hargens AR. Acute compartment syndromes. Surgical Clinics of North America. 1983;**63**(3):539-565

[17] Olson SA, Glasgow RR. Acute compartment syndrome in lower extremity musculoskeletal trauma. Journal of the American Academy of Orthopaedic Surgeons. 2005;**13**(7): 436-444

**13**

*Review of Compartment Syndrome*

[19] Moed BR, Thorderson PK. Measurement of intracompartmental pressure: A comparison of the slit catheter, side-ported needle, and simple needle. The Journal of Bone and Joint Surgery: American Volume. 1993;**75**:

231-235

*DOI: http://dx.doi.org/10.5772/intechopen.99996*

[18] Shakespeare DT, Henderson NJ, Clough G. The slit catheter: A

comparison with the wick catheter in the measurement of compartment pressure. Injury. 1982;**13**:404-408

[20] Heckman MM, Whitesides TE Jr, Grewe SR, et al. Compartment pressure

in association with closed tibial fractures: The relationship between tissue pressure, compartment, and the distance from the site of the fracture. The Journal of Bone and Joint Surgery. American Volume. 1994;**76**:1285-1292

[21] Ouellette EA. Compartment syndromes in obtunded patients. Hand

[22] Cohen MS, Garfin SR, Hargens AR, et al. Acute compartment syndrome: Effect of dermotomy on fascial

decompression in the leg. The Journal of Bone and Joint Surgery. British Volume.

[23] Purcell D, Terry BA, Sharp BR. Acute compartment syndrome. In: Purcell D, Chinai S, Allen B, Davenport M, editors. Emergency Orthopedics Handbook. Cham: Springer; 2019. DOI: 10.1007/978-

[24] Sigamoney K, Khincha P, Badge R,

[25] Prasarn ML, Ouellette EA. Acute compartment syndrome of the upper extremity. J Am Acad Orthop Surg. 2011 Jan;19(1):49-58. doi: 10.5435/00124635- 201101000-00006. Erratum in: J Am Acad Orthop Surg. 2011 May;19(5):50A.

et al. Compartment syndrome: Challenges and solutions. Orthopedic Research and Reviews. 2015;7:137-148.

DOI: 10.2147/ORR.S50776

Clinics. 1998;**14**(3):431-450

1991;**73**:287-290

3-030-00707-2\_3

PMID: 21205767.

*Review of Compartment Syndrome DOI: http://dx.doi.org/10.5772/intechopen.99996*

[18] Shakespeare DT, Henderson NJ, Clough G. The slit catheter: A comparison with the wick catheter in the measurement of compartment pressure. Injury. 1982;**13**:404-408

[19] Moed BR, Thorderson PK. Measurement of intracompartmental pressure: A comparison of the slit catheter, side-ported needle, and simple needle. The Journal of Bone and Joint Surgery: American Volume. 1993;**75**: 231-235

[20] Heckman MM, Whitesides TE Jr, Grewe SR, et al. Compartment pressure in association with closed tibial fractures: The relationship between tissue pressure, compartment, and the distance from the site of the fracture. The Journal of Bone and Joint Surgery. American Volume. 1994;**76**:1285-1292

[21] Ouellette EA. Compartment syndromes in obtunded patients. Hand Clinics. 1998;**14**(3):431-450

[22] Cohen MS, Garfin SR, Hargens AR, et al. Acute compartment syndrome: Effect of dermotomy on fascial decompression in the leg. The Journal of Bone and Joint Surgery. British Volume. 1991;**73**:287-290

[23] Purcell D, Terry BA, Sharp BR. Acute compartment syndrome. In: Purcell D, Chinai S, Allen B, Davenport M, editors. Emergency Orthopedics Handbook. Cham: Springer; 2019. DOI: 10.1007/978- 3-030-00707-2\_3

[24] Sigamoney K, Khincha P, Badge R, et al. Compartment syndrome: Challenges and solutions. Orthopedic Research and Reviews. 2015;7:137-148. DOI: 10.2147/ORR.S50776

[25] Prasarn ML, Ouellette EA. Acute compartment syndrome of the upper extremity. J Am Acad Orthop Surg. 2011 Jan;19(1):49-58. doi: 10.5435/00124635- 201101000-00006. Erratum in: J Am Acad Orthop Surg. 2011 May;19(5):50A. PMID: 21205767.

**12**

*A Comprehensive Review of Compartment Syndrome*

[9] Bae DS, Kadiyala RK, Waters PM. Acute compartment syndrome in children: Contemporary diagnosis, treatment, and outcomes. Journal of Pediatric Orthopaedics. 2001;**21**:680- 688. DOI: 10.1097/00004694-

[10] BOAST British Orthopaedic Association Standards for Trauma. Review date: December 2016. For correspondence, contact: policy@

[11] Malik AA, Khan WS, Chaudhry A, et al. Acute compartment syndrome a life and limb-threatening surgical emergency. Journal of Perioperative

[12] Shuler FD, Dietz MJ. Physicians' ability to manually detect isolated elevations in leg intracompartmental pressure. The Journal of Bone & Joint

[13] Ulmer T. The clinical diagnosis of compartment syndrome of the lower leg: Are clinical findings predictive of the disorder? Journal of Orthopaedic

[14] Köstler W, Strohm PC, Südkamp NP. Acute compartment syndrome of the limb. Injury. 2004;**35**(12):1221-1227

[15] Murphy JB. Myositis. JAMA: The Journal of the American Medical Association. 1914;**63**:1249

[16] Mubarak SJ, Hargens AR. Acute compartment syndromes. Surgical

[17] Olson SA, Glasgow RR. Acute compartment syndrome in lower extremity musculoskeletal trauma. Journal of the American Academy of Orthopaedic Surgeons. 2005;**13**(7):

Clinics of North America. 1983;**63**(3):539-565

436-444

Practice. 2009;**19**(5):137-142

Surgery. 2010;**92**(2):361-367

Trauma. 2002;**16**(8):572-577

200109000-00025

boa.ac.u

compartment syndrome. Who is at risk? The Journal of Bone and Joint Surgery. British Volume. 2000;**82**(2):200-203

pressures after intramedullary nailing of the tibia. The Journal of Bone and Joint Surgery. British Volume. 1990;**72**:

[3] Tiwari A, Hag AI, Myint F, et al. Acute compartment syndromes. Journal of British Surgery. 2002;**89**:397-412. DOI: 10.1046/j.0007-1323.2002.02063. x

[4] Hayes G, Liauw S, Romaschin A, et al. Separation of reperfusion injury from ischemia-induced necrosis. Surgical Forum. 1988;**39**:306-308

[5] Lindsay T, Liauw F, Romaschin S, et al. The effect of ischemia/reperfusion on adenine nucleotide metabolism and xanthine oxidase production in skeletal muscle. Journal of Vascular Surgery.

[6] Blaisdell FW. The pathophysiology of

[7] Jennische E. Ischemia-induced injury in glycogen-depleted skeletal muscle: Selective vulnerability of the FG-fibres.

[8] Petrasek PF, Homer-Vanniasinkam S,

skeletal muscle ischemia and the reperfusion syndrome: A review. Cardiovascular Surgery. 2002;**10**:620- 630. DOI: 10.1016/S0967-2109

Acta Physiologica Scandinavica. 1985;**125**:727-734. DOI: 10.1111/j.1748-

Walker PM. Determinants of ischemic injury to skeletal muscle. Journal of Vascular Surgery. 1994;**19**:623-631. DOI: 10.1016/ S0741-5214(94)70035-4

[1] McQueen MM, Gaston P, Court-Brown CM. A molecular interaction database. Acute

**References**

[2] McQueen MM, Christie J, Court-Brown CM. Compartment

395-397

1990;**12**:8-15

(02)00070-4

1716.1985.tb07776.x

**15**

Section 2

Compartment Syndrome

in Musculoskeletal Sites

### Section 2


*Edited by Alvaro G. Estévez*

Our understanding of the pathology of amyotrophic lateral sclerosis is a continuously changing field. New hypotheses are generated with each new discovery; they are abandoned to be reanalyzed after some time under the light of new observations. This book present a series of reviews from experts in different aspects of the disease focus on these hypotheses. There are also a few review chapters providing clear examples of these new observations that make the field to reanalyze previous conclusions.

ISBN 978-953-51-1195-5

Current Advances in Amyotrophic Lateral Sclerosis

Photo by Ralwel / iStock


*<IP_ADDRESS> Surface plasmon resonance (SPR)*

Because of its light guidance inside fiber based on the TIR effect, simple and flexible design, compactness, and remote sensing ability, optical fiber has proven to be a very useful instrument in the SPR sensing system. When light travels through the core of the fiber, some of it will pass through the cladding region. The plasmonic metal surface interacts with the evanescently leaked light, which stimulates the surface's free electrons. Surface plasmon is created when the evanescent field and free electron

**Figure 7.** *Fiber optic gas sensing set-up using evanescent wave absorption based on experiment [55].*

*Fiber Optic Sensors for Gas Detection: An Overview on Spin Frustrated Multiferroics DOI: http://dx.doi.org/10.5772/intechopen.106863*

surface frequencies are in resonance. This generated wave propagates along the metaldielectric interface and exhibits both charge motion in the metal (surface plasmon) and electromagnetic wave in the air or dielectric (polariton) [54].

#### *<IP_ADDRESS> Evanescent wave absorption type (EWA)*

The leakage/loss of electromagnetic energy at the interface of the core and the cladding medium during a total internal reflection (TIR) event determines the evanescent wave absorption based sensing phenomenon. If the diameters of a fiber are big in comparison to the wavelength of light, this method may be applied. When a propagating beam's incident angle (θi) is greater than the critical angle (θc), TIR causes the ray to reflect back from the core-cladding contact. A small fraction of the guided wave's energy enters the cladding medium at each TIR event, generating an electromagnetic field known as a "evanescent wave." The evanescent wave is greatly affected by variations in refractive index at the core-cladding contact, which provides a foundation for sensors based on evanescent wave absorption as shown in **Figure 7** [55, 56].

### **2. Materials used in gas sensing**

### **2.1 Spin frustrated Multiferroics: A novel frustrated ordering studied in gas sensors**

Spin frustration in ME multiferroics have received enormous attention ever since the concept was introduced in 1977 by Gerard Toulouse. It is an important feature in the field of magnetism and multiferroics, as it stems from the relative arrangement of spins. Interestingly, it is not the strength of ME coupling or the high polarization that makes these materials unique; in fact, such systems have weak coupling and low magnitude of polarization compared to other multiferroics [57–60]. Still, the reason for its long sought control of electric properties by magnetic fields, lies in the magnetic origin of their ferroelectricity, which is induced by the presence of complex spin structures, characteristic of frustrated magnets [61]. Basically, in most of the magnetic solids, the magnetic moments form a long range ordered ferromagnetic (**↑↑** moments) or antiferromagnetic (**↑↓** moments) structure when cooled below a certain temperature. However, in "frustrated" magnetic solids, there is no long range ordering at low temperature phase. Instead, they develop high degenerate states with short range spin correlations. Typical examples of geometrically frustrated structures are 2D triangular or tetrahedron non collinear magnetic structures, where the lattice consists of triangular or tetrahedral arrangements of anti-ferromagnetically (AFM) coupled

spins as shown in **Figure 8**. The spin on the third site can be in any one direction, either up (or) down, but then the interaction between this site and the other two sites will be different. As a consequence, the third site will move closer to one site and away from the other, which will break the symmetry and induce ferroelectricity. This kind of lattice geometry creates large degeneracy of ground states within which the system can fluctuate with almost no energy expenditure, even below few milli Kelvin temperatures. A one dimensional anti-ferromagnetic material has ground state in alternating series of spins: up, down, up, down, etc. But, in 2D equilateral triangular AFM lattice, multiple ground states can occur, with three spins, one on each vertex. If each spin can take on only two values (up or down), there are 23 = 8 possible states of the system, six of which are ground states. Two situations, which does not favor ground states are when all three spins are up or are all down. However, in other six states, there will be two favorable interactions and one unfavorable one. This illustrates spin frustration: the inability of the magnetic system to find a single ground state [58, 60].

*2.1.1 Factors to consider for sensor interrogation of spin frustrated multiferroic materials*

The main factors that are critical in gas detection, particularly when employing multiferroic materials as sensing materials are


*3.2.2. Quantitative analysis*

Visual analysis of **Figures 6** and **7** states a pressure distribution which is far from uniformity. In this section, this fact is demonstrated with a statistical analysis based on the median. Since the pressure films used for the experiments are ranged from 0.6 to 2.5 MPa, those parts that work with a pressure out of scale will not be appropriately represented. Thus, the median is the most significant parameter to analyze: half of the pixels work under that pressure while the other half works above it.

distribution in the modules, which is in turn related to the thermal contact resistance. If the module works under an uneven pressure distribution, the generation will be reduced, since

The Importance of the Assembly in Thermoelectric Generators

http://dx.doi.org/10.5772/intechopen.75697

133

The most appropriate configuration seems that in which each module has the biggest amount of screws as close as possible to it. Furthermore, as the torque of these screws increases, the clamping pressure will get bigger as well as better distributed, and therefore, the thermal contact resistance will be reduced, leading to a better generation unless bending is provoked.

Last section has concluded that it is recommended to have an individual tightening of the modules in order to ensure a uniform pressure distribution that leads to a good thermal contact. In order to achieve it, screws are necessary although they represent a type of

By definition, a thermal bridge is an area or component of an object which has higher thermal conductivity than the surrounding materials, creating a path of least resistance for heat transfer [45, 46]. In thermoelectric generators, there are two main sources for thermal bridges. On the one hand, the screws used to ensure a good contact and pressure distribution are normally metallic, and therefore, highly thermal conductive. In order to reduce the amount of heat lost through these screws, it is typical to use nylon washers. Nonetheless, even with this nylon

On the other hand, due to the small thickness of the thermoelectric modules (most commonly 3 mm), it can occur that part of the heat directly flows within the heat exchangers, instead of through the thermoelectric modules. Therefore, insulating materials are usually inserted

In the present section, assuming there is a good thermal contact, three different alternatives of insulating materials that are normally used in order to avoid thermal bridges will be studied:

rings, it is estimated that the thermal resistance of each screw is 52 K/W.

some parts of the module can even be not in contact with the heat exchangers.

**Figure 8.** Median of the pressure against the applied torque for the configuration of two modules.

**4. How to avoid thermal bridges**

thermal bridge.

between the heat exchangers.

On the one hand, for the heat exchanger with two modules, in the case in which there are only four screws, most of the module works under a pressure of 0.6 MPa or less. This value improves if the bending is restricted by means of an additional pair of screws located between the modules. As shown in **Figure 8**, and accordingly to the previous states, the median of the pressure increases with the torque in a proportion that seems linear.

On the other hand, in the heat exchanger with four modules, the lack of macroscopic contact is evident with the median value of 0.6 MPa, i.e. most parts of the modules have a clamping pressure of less than 0.6 MPa. Nonetheless, although the visual analysis evinces a slight improvement when the fifth screw is introduced and a more significant torque exerted, this fact is not appreciable in the median value since the range of pressures of both configurations is much lower than 0.6 MPa, the lower limit of the scale of the film.

Hence, despite not being considered a critical aspect, screw distribution and torque are aspects to definitely take into account. The assembly configuration determines the pressure

**Figure 7.** Pressure films for (a) four screws, 1 Nm (b) five screws, 2 Nm.

**Figure 8.** Median of the pressure against the applied torque for the configuration of two modules.

distribution in the modules, which is in turn related to the thermal contact resistance. If the module works under an uneven pressure distribution, the generation will be reduced, since some parts of the module can even be not in contact with the heat exchangers.

The most appropriate configuration seems that in which each module has the biggest amount of screws as close as possible to it. Furthermore, as the torque of these screws increases, the clamping pressure will get bigger as well as better distributed, and therefore, the thermal contact resistance will be reduced, leading to a better generation unless bending is provoked.