Sd. Compartimental y AR A CL 2022

A c u t e Ex t re m i t y
C o m p a r t m e n t S y n d ro m e a n d
(Regional)
Anesthesia: The Monster Under the Bed
José A. Aguirre, MD, MSca,c,*, Morné Wolmarans, MD

b
,
Alain Borgeat, MDc,d
KEYWORDS
Acute compartment syndrome Regional anesthesia Extremity Complication
Tissue pressure
KEY POINTS
Acute compartment syndrome (ACS) is a devastating posttrauma/surgery complication,
which can lead to permanent disability of upper and lower extremities
The clinical signs/symptoms for ACS are unreliable. The use of intracompartmental pres-
sure measurement is necessary to confirm the diagnosis of ACS.
Continuous peripheral regional anesthesia is an effective technique for postoperative
analgesia of upper and lower extremities.
The main factors for adverse outcome after ACS are delays in definitive diagnosis
(compartment pressure measurement) and surgical management (fasciotomy).
A review of the literature emphasizes breakthrough pain, present in most described cases,
as the most important clinical sign.
Continuous neuraxial anesthesia might produce dense motor and sensory blocks and has
the potential to delay the diagnosis of ACS. Caution is warranted.
The application of local anesthetics at low concentrations through peripheral regional
catheter, intra-articular analgesia, (continuous) fascial plane blocks, and sensory blocks
is considered effective and safe means to provide analgesia for trauma/postsurgical pa-
tients at risk for ACS.
a
Institute of Anaesthesiology, Triemli City Hospital Zurich, Birmensdorferstrasse 497, 8063
Zürich, Switzerland; b Department of Anesthesia, Norfolk and Norwich University Hospital NHS
Trust, Regional Anesthesia UK (RA-UK), Colney Lane, Norwich NR4 7UY, UK; c Balgrist Campus,
Lengghalde 5, 8008 Zürich, Switzerland; d Department of Surgery, University of Illinois at
Chicago, 402 CSB MC 958840 South Wood Street, Chicago, IL 60612, USA
* Corresponding author.
E-mail address: [email protected]
Anesthesiology Clin 40 (2022) 491–509

https://doi.org/10.1016/j.anclin.2022.06.001 anesthesiology.theclinics.com
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492 Aguirre et al
Abbreviations
CEDA continuous epidural anesthesia
EDA epidural anesthesia
ESP erector spinae block
PCEA patient controlled epidural analgesia
PECS pectoral nerve block
QLB quadratus lumborum block
TCI target controlled anesthesia
TAP transversus abdominis block
THE HISTORY OF COMPARTMENT SYNDROME
Volkmann1 described in 1881 myonecrosis and secondary contracture after pro-

longed muscle ischemia. He suspected that limb splints caused muscle cell death
due to diminished arterial blood flow, describing an untreated compartment syn-
drome. Bardenheuer2 reported in 1911 the first forearm compartment decompression
for impending compartment syndrome, and Griffiths3 published in 1940 patients
developing Volkmann’s contractures after embolectomy of the brachial artery. He
was the first to introduce the 5 P’s of compartment syndrome (pain, pallor, paresthe-
sias, paralysis, pulselessness) in clinical practice. Whitesides and colleagues4
described the effects of time on muscle survival in compartment pressure, demon-
strating that less than 5% of muscle cells were damaged after 4 hours of ischemia,
whereas nearly 100% were damaged after 8 hours of ischemia. In a cadaveric forearm
model, Havig and colleagues5 demonstrated that fasciotomy is the decisive interven-
tion to return the compartment pressures to normal values.
DEFINITION OF ACUTE COMPARTMENT SYNDROME
ACS is defined as an increase of pressure within a fixed osteofascial anatomic space,

leading to an impairment of cellular function due to decreased local tissue perfusion
and, when sustained, to irreversible damage to the contents of the compartment
(nerves, muscles).6 There are 3 variables (factors) affecting the outcome in the case
of elevated compartment pressure: (1) how high is the pressure, (2) how long is the
elevated pressure sustained, and (3) how severe are concomitant injuries? Classifica-
tion systems should consider the most important variables in this progressive tissue
injury: time and pressure, as described by Leversedge and colleagues.7 It is important
to note that the physiologic pressures vary between 8 mm Hg in adults and 10 to
15 mm Hg in children.8,9
Traditionally, an absolute pressure value of 30 mm of Hg was taken as a cutoff value,
above which intervention was required. However, the difference in the diastolic pres-
sure and intracompartmental pressure is used more reliably because compartment
pressure depends on perfusion or the systemic blood pressure. According to White-
sides and Heckman10 compartment syndrome occurs when the pressure increases up
to 20 mm Hg below the diastolic pressure. Some investigators recommend an inter-
vention when the delta pressure (DP 5 diastolic pressure intracompartmental
pressure) is less than 30 mm Hg considering this value (30 mm Hg) as diagnostic.11
CAUSE AND RISK FACTORS
Data from the Royal Infirmary of Edinburgh show an average annual incidence of 3.1
per 100,000 people (7.3 per 100,000 men and 0.7 per 100,000 women).12 ACS is more
Acute Extremity Compartment Syndrome is approved 493
Box 1
Causes of compartment syndrome
External compression
Constriction by casts, splint, pneumatic antishock garments
Excessive traction to fractures
Early surgical closure of fascial defects
Third-degree burns (thermal, electric)
Secondary increased compartment pressure
Iatrogenic injection
Infiltrated intravenous catheters/inadvertent intra-arterial drug injection
Intracompartmental hemorrhage
Bleeding after injury
Spontaneous bleeding due to hereditary bleeding disorders
Anticoagulant therapy
Trauma from fractures (open or closed), osteotomies, vessel laceration
Intramedullary nailing
Gunshot
Soft tissue trauma
Prolonged positioning during surgery (lithotomy position)
Crush injuries
Ergotamine ingestion
Drug overdose
Prolonged tetany
Intraosseous fluid administration in children
Use of pumps during arthroscopy
Postischemic
Ischemia reperfusion (after embolectomy, clamping of arteries, and so on)
Tourniquet
Arterial injury/arterial spasm
Tissue edema after snakebite
Thrombosis/embolization
Limb reimplantation
Modified from Tollens et al.97
common in males and in patients younger than 35 years.13 Forty percent of all cases of
ACS derive from tibial shaft fracture, 23% from soft tissue tibial trauma, and 18% from
forearm fractures.14 The Scottish series report that 36% of all tibial fractures and
23.2% of all blunt soft tissue injuries are associated with ACS.12
Children have a higher preexisting compartment pressure, but the ACS incidence
in children is lower.15 In the case of soft tissue damage, ACS can also occur in the
absence of fractures. Factors associated with an increased risk of ACS after trauma
are medical comorbidities associated with abnormal bleeding diatheses (clotting
disorders, the use of anticoagulants), volume resuscitation, altered mental status,
or neurologic compromise diminishing sensitivity and sensibility of the limbs12
(Box 1).
PATHOPHYSIOLOGY OF COMPARTMENT SYNDROME
The pathophysiology of the compartment syndrome is complex. In this syndrome fluid

shifts from the blood to the extracellular and intracellular space leading to an
increased tissue pressure within the compartment. This shift leads to a decrease of
capillary blood flow and a decrease in tissue PO2 and ends in a metabolic deficit result-
ing in muscle ischemia and necrosis. When tissue pressures reach the threshold of 30
to 40 mm Hg16 the extraluminal pressure causes progressive arteriole collapse and
494 Aguirre et al
Fig. 1. Pathophysiology and the vicious circle of the acute compartment syndrome. (Modi-
fied from Janzing HM.98)
local tissue hypoxia occurs with secondary shunting to areas with less vascular resis-
tance. Dahn and colleagues17 showed that local tissue perfusion stopped when the
interstitial tissue pressure equals the diastolic blood pressure. Cell hypoxia is thus
related to diminished arteriolar flow, venous obstruction, and a decreased arteriove-
nous gradient (Fig. 1).
There are 2 generally well-accepted pathophysiology theories:
The arteriovenous gradient theory18 and
The ischemia-reperfusion syndrome18,19
Both theories advocate the increasing tissue pressure, the resulting decreasing
capillary blood flow, and the decrease of tissue PO2 with the end result of a metabolic
deficit.
However, the latter hypothesis focuses on free radicals, calcium, and vasoactive
substrates released under ischemic conditions resulting in the increased vessel
permeability and subsequent increase in extravascular fluid and pressure. Both the-
ories agree that the excess compartment pressure can only be rectified by creating
the ability for the tissues to expand by fasciotomy.
DIAGNOSIS
The most important tool for diagnosis of an ACS is to keep a high index of clinical sus-
picion, especially in high-risk cases. However, signs and symptoms can be ambig-
uous leading to a late diagnosis of ACS.18 Diagnosis becomes even more difficult in
obtunded patients after a polytrauma, in the presence of equivocal clinical findings,
after head injury with unconsciousness, and under perioperative narcotics or regional
anesthesia (RA), where the clinical picture can be obscured.
Clinical Diagnosis of Acute Compartment Syndrome
The main clinical symptom of a developing ACS is considered to be pain. Palpable
tension, paresthesia, paresis, and pulselessness might also be associated with ACS
(Box 2). However, none of the commonly used signs in clinical practice is neither
Box 2
Symptoms and signs of acute compartment pressure
Symptoms:
Pain is greater than expected or increasing
Increase in pain and analgesic demand
No relief after splinting or removal of casts
Paresthesia in affected extremity
Signs:
Pain on palpation/passive stretching of the affected compartment
Tense and swollen compartment
Sensory deficit of the nerves enclosed in the compartment
Muscle weakness
Pallor
Pulselessness
CAVE:
Usually pulses are present in the early stage of compartment and absent in late stage.
Caution: Acute compartment syndrome can occur with palpable pulses.
Normal capillary refill present during early development of acute compartment syndrome.
Open fractures do not protect from acute compartment syndrome.
Clinical signs are of unclear value due to their low specificity and sensitivity
Suggested clinical signs (in the case of RA or opioid PCA):
Breakthrough pain despite well-working RA
Increase demand of analgesics
Abbreviation: PCA, patient-controlled analgesia.

Modified from Torrero et al.21
reliable nor sufficiently specific or sensitive.20 Pulselessness has to be considered a

late sign with bad prognosis indicating muscle death with consequent need for radical
surgery and severe disability.14,20–23 Pain is also unreliable.14,22 Moreover, Badhe and
colleagues24 described 4 cases of ACS of the lower extremity after trauma and surgery
without considerable pain reported from the patients. Even the clinical palpation of the
tense and swollen extremity as diagnostic criteria for detecting ACS has been shown
to be strongly assessor dependent and unreliable with sensitivity of 24% and speci-
ficity of 55%25 (Table 1).
Technical Diagnosis of Acute Compartment Syndrome

The most useful diagnostic method to decide if fasciotomy is indicated is the measure-
ment of interstitial tissue pressures.
Although previous studies have reported that resting interstitial tissue pressures in
the healthy vary between 0 and 8 mm Hg for the dorsal and volar forearm
Table 1
Accuracy of clinical signs for the diagnosis of acute compartment syndrome20
Sensitivity 13%–19%
Specificity 97%–98%
Positive predictive value 11%–15%
Negative predictive value 97%–98%
Probability of ACS if 1 clinical syndrome present 25%
Probability of ACS if 3 clinical syndromes present 93%
496 Aguirre et al
compartments and less than 15 mm Hg in the interosseous muscles of the hand,26,27

several investigators have reported the diagnostic accuracy of different methods of
pressure measurement if properly used. Interstitial tissue pressure measurements of
noninjured forearms showed statistically significant differences over distances of
only 4 cm.26 Measurements performed at varying distances from a fracture showed
statistically significant differences in pressure, with higher pressures within 5 cm of
the fracture.28 These findings illustrate the importance of proper placement of the nee-
dle for pressure monitoring.
In a case series of 116 consecutive patients, of whom 3 required fasciotomy, the use
of a DP of less than or equal to 30 mm Hg as a threshold for fasciotomy led to no missed
cases of ACS, no unnecessary fasciotomies, and no complications in any patients.29
The disadvantage to these measurements is that using both absolute and DP
thresholds can result in high false-positive rates of up to 82%.30
Several studies have analyzed the reliability of various techniques for measuring
compartment pressures. Boody and Wongworawat31 compared different measure-
ment equipment and concluded that side-port needles and slit catheters were more
accurate than straight needles and that the arterial line manometer was the most ac-
curate device. The Stryker device was also very accurate, but the Whitesides manom-
eter apparatus was not precise enough for clinical use.31
An interesting development in noninvasive measurement techniques was intro-
duced by the near-infrared spectroscopy (NIRS), which detects changes and trends
in relative oxygen saturation of hemoglobin.32,33 Using the Beer-Lambert law this tech-
nique profits from different light absorption properties to calculate concentrations of
oxygenated and deoxygenated hemoglobin.
Adding spatial configuration, this method can measure changes in local muscle ox-
ygen saturation and thus has the potential to detect and provide continuous moni-
toring of intracompartmental ischemia and hypoxia.34 For noninvasive continuous
monitoring NIRS has been labeled as safe and useful.35 However, more studies are
warranted to define how well NIRS correlates with critical pressure thresholds, consid-
ering limits to its penetration depth.
TREATMENT AND OUTCOME
When the suspicion of an incipient compartment syndrome is raised, often following

clinical assessment, sometimes followed by invasive compartment pressure measure-
ment, re-evaluation must be frequently performed and accurately documented.7
Casts and circumferential dressings must be removed and positioning with tension
or distortion must be avoided to not further compromise blood flow. Fluid therapy
must be carefully evaluated, and electrolytes, renal function, and coagulation param-
eters carefully monitored.
Once the diagnosis of ACS has been established, the only available treatment is a
surgical decompression of the affected osteofascial compartments.36 Adequate
decompression must be ascertained by direct visualization of the muscle groups while
passively moving. After fasciotomy and judicious excision of nonviable tissue has
been performed, a careful search for separate subcompartments should be
undertaken.37
The essential factors for the outcome after fasciotomy seem to be the timing and the
concomitant injuries.
Delaying fasciotomy for more than 12 hours has been shown to significantly worsen
outcome.28,38,39 According to Hayakawa and colleagues40 fasciotomy performed
within 6 hours after diagnosis of ACS led to a satisfactory outcome in 88% of the cases
with an amputation rate of 3.2% and mortality rate of 2%, whereas fasciotomy after
12 hours showed satisfactory outcome in only 15% of cases, with 14% amputations
and 4.3% deaths. There is sparse data about the time frame of greater than 6 hours
but less than 12 hours, because residual deficits also occur if fasciotomy time is
only 2 hours after ACS diagnosis.41
Considering medicolegal aspects, Bhattacharyya and Vrahas42 reported 19 claims be-
tween 1980 and 2003. Ten claims were resolved in favor of the physician. Increasing time
from the onset of symptoms to the fasciotomy was linearly associated with an increased
indemnity payment (P < .05). A fasciotomy performed within 8 hours after the first presen-
tation of symptoms was uniformly associated with a successful defense.42
ANESTHESIA AND COMPARTMENT SYNDROME

The Role of Regional Anesthesia
RA in patients with trauma or in patients at risk for development for ACS is a highly contro-
versial topic, and a point of eternal contention between anesthesiologists and orthopedic
and trauma surgeons.43–45 However, there is no randomized trial comparing the clinical
outcome of patients at risk of ACS who receive RA or do not. The actual clinical practice is
based on narrative and often biased reviews of case reports, retrospective case series,
recommendations, and reviews and differs from institution to institution.22 Widely held
beliefs suggest that the relief of postoperative pain and the sensory blockade from RA
can mask ACS,14,22,42–44 and therefore RA should be completely avoided.
However, the recently published guidelines from the Association of Anaesthetists of
Great Britain and Ireland (AAGBI) on lower leg trauma and the risk of ACS46 clearly
state that good analgesia is a basic human right. Further recommendations from
this guideline include early identification of patients at risk of developing ACS, multi-
disciplinary management protocols, and appropriate equipment for intercompartment
pressure monitoring, with appropriately trained staff and protocols to deal with
abnormal measurements. Single-shot spinal anesthesia, with the addition of an opioid,
and single-shot or continuous peripheral nerve blocks (PNBs) using lower concentra-
tions of local anesthetic drugs without adjuvants are not associated with delays in
diagnosis, as long as appropriate postinjury and postoperative surveillance is used,
including objective scoring charts.
In addition, both the European and the American Societies of Regional Anesthesia
clearly acknowledge the lack of evidence-based data supporting the notion that RA
increases the risk of delayed ACS diagnosis in children.47 Data from the American Col-
lege of Surgeons National Surgical Quality Improvement Project also show no differ-
ences in postoperative complications after lower extremity traumatic fractures
between patients who received regional and general anesthesia.48 Finally, large
case series in which regional blocks were used for analgesia during extremity trauma
surgery did not report cases of compartment syndrome.49
Few reviews concentrate on different techniques or types of RA and ACS,22,50,51 and
some present a collection of published literature for peripheral and central blocks.15,52,53
This review compiles all the information for the upper and lower extremities
including central blocks, discussing the role of different techniques of RA and their
impact on the diagnosis of ACS according to existing literature and offering accept-
able practical solutions for safe RA practice.
Intravenous Regional Anesthesia and Compartment Syndrome

Different reports have implicated intravenous RA (IVRA) in causing ACS.54–58 The most
debated theories on the pathogenesis center on the double tourniquet required for this
498 Aguirre et al
technique and cite ischemia-reperfusion injury with hyperemia, swelling, and the
administration of high volumes of local anesthetics and adjuvants into a “newly
created compartment.”55 The latter theory could not be confirmed in a volunteer study
that showed no compartment pressure increase after IVRA with 1.5 mL/kg saline.58
However, this study was not performed on fractured extremities, which limits its rele-
vance to trauma care. Moreover, inflation pressure and duration have also been impli-
cated as tourniquet-related factors of compartment syndrome.
Neuraxial Blocks and Lower Limb Compartment Syndrome

Anesthesia
There are no published case reports implicating single-shot epidural or single-shot
spinal anesthesia in ACS. Although many investigators state that epidural analgesia
does not contribute to delay the diagnosis of ACS,59–67 epidural anesthesia and anal-
gesia has still been implicated in masking symptoms of ACS leading to a delay in
diagnosis.22
In most of the published cases epidural anesthesia was considered to have masked
clinical symptoms of ACS such as pain.22,50,68 Mar and colleagues22 reviewed 23
cases in which epidural anesthesia (EDA) was supposed to have masked ACS and
showed that in 90% the classical symptoms of ACS were actually present but not
recognized soon enough. Breakthrough pain, which is a clear clinical indicator for
an ACS, was present in most cases. In 4 cases the diagnosis of ACS was masked
by a dense block caused by EDA, blunting the occurrence of breakthrough pain.
Peripheral Nerve Blocks and Compartment Syndrome

Anesthesia
No randomized study analyzing the effects of single shot or even continuous periph-
eral RA on ACS has been published. Only case reports or case series of varying qual-
ity22,69–71 that have been subject of case scenarios72 and of recent reviews are
available.
Moreover, to date there is no case report confirming a diagnosis delay of ACS after
RA of the upper extremity72–75; this is of importance because contrary to the lower
limb, the upper extremity can be completely blocked with a single nerve block. For
the lower extremities, 2 or 3 peripheral blocks are required for a complete limb block;
this could reduce the probability that PNB masks an ACS, for example, if a saphenous
nerve block is applied to provide analgesia to the tibia plateau, while the muscular
compartments below the knee are not affected, owing to their innervation by the
sciatic nerve. However, some of the published case reports have wrongly implicated
a PNB for an ACS in a territory that was blocked, demonstrating that PNB could not be
the cause for delaying ACS diagnosis.69
In other cases, breakthrough pain as a sign of an incipient ACS was simply ignored
for hours delaying the diagnosis and early therapy for ACS.76,77
Since the widespread use of adjuvants prolonging analgesia, single-shot perineural
blocks are becoming more popular for anesthesia or as combination to general anes-
thesia.78 Ganeshan and colleagues75 reported the case of a 75-year-old patient with a
complicated forearm fracture receiving an axillary brachial plexus block (without a
description of the type, volume, and concentration of the local anesthetic solution)
for ambulatory internal fixation of the radius. Subsequently, the patient was dis-
charged pain free and comfortable, but developed a compartment syndrome during
the next 24 hours with a loss of sensation in the fingers, multiple swelling over the fore-
arm and hand, and loss of motor function of the fingers. He was readmitted after
24 hours and a fasciotomy was performed.75 In this case the signs of ACS were obvi-
ously present after the block had worn off.
Local anesthetics and postoperative analgesia

The duration of motor and sensory block clearly depends on the local anesthetic, the
concentration, and the volume used. Motor block duration up to 20 hours for bupiva-
caine 0.5% has been described.79 Sensory blocks usually last from 12.5 hours for
ropivacaine 0.5% to 16 hours for levobupivacaine 0.33%.80 The introduction of ultra-
sound for peripheral RA has shown that the volumes for block performance can be
reduced leading to a shortening of the block time: 9.9 hours for ropivacaine
0.75%81 and 106 to 185 minutes for lidocaine 1.5% with or without epinephrine.82
Furthermore, shortening of motor and sensory block can be achieved by using
intermediate-acting agents like mepivacaine (up to 5 hours block duration) or even
short-acting agents like lidocaine with or without additives (up to 5.5 hours block dura-
tion with epinephrine).83 Chloroprocaine 3% has been shown to produce a sensory
blockade of 101 to 112 minutes depending on the block performed and is a valid
alternative.84
Continuous perineural blocks offer many advantages compared with single-shot RA
concerning better postoperative pain therapy and avoidance of rebound pain.85 More-
over, ACS can be confounded with rebound pain after a single-shot RA. Clinical eval-
uation of the patient is essential for a correct diagnosis.
Source of possible concern might be a prolonged loss of motor or sensory function
for hours with the risk of masking clinical symptoms of ACS. Even after stopping or
reducing an infusion of CPB, a sensory block may take 2 to 4 hours to recover. If
the time frame of 6 hours for intervention shall be the standard then this delay has
to be avoided. The idea of performing CPB with higher volumes and lower concentra-
tions has led to a higher incidence of insensate limbs in some studies, but these find-
ings have not been reproduced by all investigators. On the other hand, reducing the
volume and augmenting the concentration has been shown to influence the incidence
of pain.86 Unfortunately, reduction of the ropivacaine concentration to 0.1%, as used
for the walking epidural analgesia in obstetrics, has been shown to be inadequate for
knee arthroplasty and hand surgery.87 The catheter infusion should be started with a
low concentration bolus of 10 to 20 mL ropivacaine 0.1% to 0.2% to avoid initial motor
function loss, and continued with a continuous infusion (or patient controlled infusion)
using ropivacaine 0.2% (4–6 mL/h, bolus 3–4 mL, lock out 20–30 min). Ropivacaine
0.3% does not influence motor strength more than 0.2% for interscalene block while
offering improved opioid-sparing effects and could be used for continuous infusion af-
ter extremely painful surgery after an initial anesthetic bolus.88
Intra-articular and Single-Shot/Continuous Wound Infusion for Extremity Surgery

Continuous wound (articular) infusion (CWI) or periarticular infiltration (local infiltration
analgesia [LIA]) has no impact on motor or major sensory block because it does not
affect major nerves but improves postoperative analgesia.89,90 The best evidence
for LIA is in total knee arthroplasty, whereas other indications such as hip surgery
and upper extremity trauma are less clear.91
There is no case report blaming LIA or CWI of delaying diagnosis of ACS.
Compartment/Fascial Plane Blocks

Fascial plane blocks are a new way of providing RA, where high volumes of usually low
concentrated local anesthetics are applied to offer analgesia avoiding central blocks
or PNBs. Fascial plane block leads to minimal, if at all, motor block and offers an
500 Aguirre et al
interesting alternative for patients at risk for ACS. Subsartorial block of the saphenous
nerve for medial tibia plateau fractures, supraumbilical fascia iliaca block for femur
neck fractures, and quadratus lumborum blocks for hip fractures could become alter-
natives to classic PNBs in these patients.92
There is no case report blaming fascial plane blocks of delaying diagnosis of ACS.
DISCUSSION
To the best of our knowledge, case reports blaming single-shot or continuous PNB for
the upper limb, single-shot or continuous PNB for the lower limb, single-shot EDA or
spinal anesthesia, or continuous spinal anesthesia were rather missed diagnosis than
masking symptoms of ACS. The remaining reports concentrate on continuous EDA for
the lower limb.15,22,52,53
If well documented, almost all published cases showed that patient complained
about increasing pain despite RA,70 loss of motor function despite reduction of local
anesthetic concentration,68 or increasing analgesic demand.22 Only in 4 cases in liter-
ature, a dense motor block after EDA at the time of diagnosis was observed.93,94
Nerve blocks have been blamed for masking ACS in a territory the block did not
even theoretically cover.69 Some case reports did not give any details about docu-
mentation and/or patient management before start of symptoms/clinical signs.22
Therefore, RA can only be considered to be associated, but not the cause in diagnosis
delay.
Despite these considerations, the use of RA for patients at risk for ACS remains a
topic of dispute between anesthetists and surgeons.44 As reported by Cascio and col-
leagues95 a good, standardized documentation improves the awareness of this com-
plex diagnosis. The investigators found in a retrospective study of preoperative
medical records of 30 consecutive patients who underwent fasciotomies for ACS
that documentation was inadequate in 21 (70%) patient records.41
Proper documentation and a high level of suspicion coupled with postoperative
repeated clinical and, if needed, invasive monitoring are of utmost importance.37,41
Data must be recorded at least at 2-hour interval; in the case of new or pathologic find-
ings, the frequency of assessment must be adapted. The classical 5 P’s (see Box 2,
Table 1) is of unreliable value20 particularly in the presence of RA, and should therefore
be complemented by the clinical signs breakthrough pain and increasing analgesic
demand.50 As described by Bae and colleagues96 an increase in analgesic need pre-
ceded neurovascular changes by an average of 7.3 hours (range 0–30). A compart-
ment syndrome must be excluded at this point.96
SUGGESTED CLINICAL PRACTICE FOR THE USE OF REGIONAL ANESTHESIA IN

PATIENTS AT RISK FOR ACUTE COMPARTMENT SYNDROME
Based on the literature presented in this review and following the recommendations of
the latest guideline from the AAGBI,46 the use of RA is a safe option if surgeons, an-
esthesiologists, and nurses in the post anesthesia care unit (PACU) and wards keep
a high index of suspicion and have the knowledge how to document, diagnose, and
treat ACS. Multidisciplinary protocols, objective scoring charts, patient consent, and
senior surgical colleague consensus should be documented to provide every patient
with a satisfactory analgesia plan.
As previously done per case scenario, the authors present an updated version of
possible concepts for anesthesia and analgesia management of patients at risk for
ACS72 (Table 2).
Table 2
Recommendation for anesthesia and postoperative analgesia for patients at high risk for postoperative acute compartment syndrome
Anesthesia
Techniques Recommendation Drugs to Be Used Duration of Action Comments
GA Yes if not high-risk patient. Propofol/gas Remifentanil: 5 min
For analgesia combine Low-dose long-acting opioids after TCI is stopped Consider central blocks
preferably with Lc-CPNB (fentanyl); remifentanil additional to GA only
until Lc-CPNB postoperative pain is an
issue that cannot be controlled
with peripheral nerve blocks or
systemic drugs. If used, use
short- medium-acting local
anesthetics to allow motoric
Acute Extremity Compartment Syndrome is approved

recovery after surgery
SSPA Consider pharmacology of LA Bupivacaine 0.5% hyperbaric/ Bupivacaine: 3–4 h No case report related
relevant to duration isobaric low dose Mepivacaine: 2–3 h to ACS. Consider
to surgery time (7.5–max 10 mg) Chloroprocaine: 1–2 h unilateral SSPA for
If needed add: Prilocaine: 1.5–2.5 h shorter duration.
fentanyl/morphine/clonidine Avoid combination
Chloroprocaine 1% 50 mg with continuous EDA
Prilocaine 2%
hyperbaric/isobaric 30–60 mg
CSPA No if GA possible Surgery: Bupivacaine isobaric or Bupivacaine: 2–3.5 h, No case report related
No if SSPA possible hyperbaric 0.5% during surgery depending on the to ACS. Start the
Yes if GA contraindicated and 0.5–2 mL initial bolus, thereafter intraoperative titration analgesia with the
surgery longer as duration adaptation to surgery time lowest concentration
of SSPA (1additives) and sensory level and increase the sensory
Analgesia: Bupivacaine isobaric level just to cover the
0.125%–0.2% for 0.5–1 mL/h site of surgery. Close
documented monitoring
(every hour) during infusion
(continued on next page)
501
502
Table 2
Aguirre et al
(continued )
Anesthesia
Techniques Recommendation Drugs to Be Used Duration of Action Comments
Single-shot No if GA possible. Consider Ropivacaine 0.75%–1% Ropivacaine: 3–6h No case report related
epidural combination with SSPA (CSE) Lidocaine 1.5% Lidocaine: 3.5 h to ACS. Avoid combination
(EDA) Yes if GA contraindicated and Chloroprocaine 3% Chloroprocaine: 2.5 h with continuous EDA
drugs can be adapted
to surgical time
Continuous No if GA possible Ropivacaine 0.1% ( 0.2%) During infusion and Avoid EDA whenever
epidural No if postoperative analgesia Levobupivacaine 0.125% 2-4 h after infusion stop possible. Many case
(CEDA) is possible with CPNB If needed add sufentanil Wash out with 30 mL reports, although
Yes in rare exceptions Lc-CEDA 1 m/mL, fentanyl 1–3 m/mL) saline leads to block only 4 with dense
resolution within 60 min motor block associated
with ACS. Close
documented monitoring
(every hour) during
infusion. Consider
wash out. No PCEA
SPNB Only if postoperative Lidocaine 1.5% Lidocaine: 2.5–3 h Case reports for the lower
pain is minimal Mepivacaine 1% Mepivacaine: 2–4 h extremity (but ACS
and only if local anesthetics Chloroprocaine 2%–3% Chloroprocaine: 1–2 h signs ignored)
can be adapted to Ropivacaine 0.2%
surgery time
Lc-CPNB is the better choice
CPNB Yes if catheter Ropivacaine: bolus with During infusion and Case reports for the lower
placement possible 10–20 mL of 0.1%–0.2% 30–60 min after infusion extremity (but ACS signs
without previous block or PCRA: ropivacaine stop. Motor function ignored). If possible
short-duration PNB 0.1%–0.2% (0.3%) typically not impaired avoid initial bolus,
4-6 mL/h, bolus with these dosages or perform it with
3-4 mL, lock out 20–30 min the lowest concentration.
PCRA or CPNB possible.
0.3% only if pain problem
after exclusion of ACS
Continuous Yes Ropivacaine 0.2%–0.3% Covers pain only during For lower extremity
wound/ Bupivacaine 0.25% infusion; for single-shot not inferior to PNB,
intra-articular analgesia up to 24 h for upper extremity

infusion (LIA) unclear data, PNB
probably more effective
Fascia Yes Ropivacaine 0.2%–0.3% Depending on location, No association with missed
plane blocks Bupivacaine 0.25% volume, and concentration ACS. As no (reduced)
(FIB, ESP, TAP, resulting motor block,
QLB, PECS) good alternative for
pain treatment
Abbreviations: CPNB, continuous perineural block; CSPA, continuous spinal anesthesia; CSE, combined spinal and epidural anesthesia; GA, general anesthesia; LA,
local anesthetics; Lc, low concentration; LIA, local infiltration analgesia; max, maximum; PCRA, patient-controlled regional anesthesia; SPNB, single-shot PNB;
SSPA, single-shot spinal anesthesia.72
Acute Extremity Compartment Syndrome is approved

503
504 Aguirre et al
Anesthesia
General anesthesia should be avoided if there are clear advantages for RA but
limitation of block duration relative to surgery time should be considered to
avoid a dense and long-lasting sensory and motor block.
IVRA should be avoided in cases at risk for ACS.
Spinal anesthesia for surgery is a good option to avoid general anesthesia.
Long-acting drugs (bupivacaine 0.5%) should be used only for surgeries
greater than 90 minutes; otherwise advantage of prilocaine 2% or chloropro-
caine 1% should be taken for shorter surgeries. The addition of spinal opioids
may also be considered. Continuous spinal anesthesia or combinations with
EDA (combined spinal and epidural anesthesia) are indicated only for cases
in which general anesthesia is contraindicated.
Analgesia
Intraoperative LIA or CWI are good analgesia regimens for upper and lower ex-
tremities and have no implication regarding motor function.
Fascial plane blocks using dilute local anesthetics offer good analgesia, and
their effect can be extended using catheters. Similarly, here, there is almost
no impact on motor function.
Continuous central nerve blocks are only indicated when no PNB can be per-
formed; they can produce a dense sensory and motor block and are the only
blocks that have been shown to mask the diagnosis of ACS. If used, lowest
possible concentrations (ropivacaine 0.1%–0.2%) should be applied.
PNBs are the preferred method for analgesia but need thorough postoperative
documentation and follow-up by the pain team. Again, the lowest possible
concentrations with higher flow rates should be used to avoid dense motor
blocks. Even top-ups over the catheter should be performed with low concen-
tration (ropivacaine 0.2%–0.3%) and higher volumes (20 mL). Caution: A top-
up need can be a sign of ACS!
CLINICS CARE POINTS
In the clinical findings, paralysis and pulselessness are already late sings of an ACS
The only safe way to exclude or proof an ACS is the measurement of the compartment
pressure.
Breakthrough pain described as a pain that suddenly overcharges the ongoing pain therapy
(peripheral regional anesthesia or intravenous opioids) is a serious sign for an ACS.
DISCLOSURE
The authors have nothing to disclose.
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A c u t e Ex t re m i t y

José A. Aguirre, MD, MSca,c,*, Morné Wolmarans, MD

Anesthesiology Clin 40 (2022) 491–509

THE HISTORY OF COMPARTMENT SYNDROME

Volkmann1 described in 1881 myonecrosis and secondary contracture after pro-

DEFINITION OF ACUTE COMPARTMENT SYNDROME

ACS is defined as an increase of pressure within a fixed osteofascial anatomic space,

CAUSE AND RISK FACTORS

Modified from Tollens et al.97

PATHOPHYSIOLOGY OF COMPARTMENT SYNDROME

The pathophysiology of the compartment syndrome is complex. In this syndrome fluid

Abbreviation: PCA, patient-controlled analgesia.

reliable nor sufficiently specific or sensitive.20 Pulselessness has to be considered a

Technical Diagnosis of Acute Compartment Syndrome

compartments and less than 15 mm Hg in the interosseous muscles of the hand,26,27

TREATMENT AND OUTCOME

When the suspicion of an incipient compartment syndrome is raised, often following

ANESTHESIA AND COMPARTMENT SYNDROME

Intravenous Regional Anesthesia and Compartment Syndrome

Neuraxial Blocks and Lower Limb Compartment Syndrome

Peripheral Nerve Blocks and Compartment Syndrome

Local anesthetics and postoperative analgesia

Intra-articular and Single-Shot/Continuous Wound Infusion for Extremity Surgery

Compartment/Fascial Plane Blocks

SUGGESTED CLINICAL PRACTICE FOR THE USE OF REGIONAL ANESTHESIA IN

Acute Extremity Compartment Syndrome is approved

(continued on next page)

intra-articular analgesia up to 24 h for upper extremity

Acute Extremity Compartment Syndrome is approved

CLINICS CARE POINTS

The authors have nothing to disclose.

1. Volkmann R. Die ischaemischen Muskellaehmungen und Kontrakturen. Centralbl

4. Whitesides TE, Haney TC, Morimoto K, et al. Tissue pressure measurements as a

27. Ardolino A, Zeineh N, O’Connor D. Experimental study of forearm compartmental

67. Tuckey J. Bilateral compartment syndrome complicating prolonged lithotomy po-

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