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Introduction
Paraspinal compartment syndrome (PCS), initially identified by
Carr et al. in 1985, has garnered attention through a small
number of submitted case reports and case series over the years
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DOI: https://doi.org/10.13107/jocr.2024.v14.i12.5082
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229
Dr. Arash BadraghehDr. Mark LaGreca Dr. Nathan Jones
Original Article
Access this article online
Website:
www.jocr.co.in
DOI:
https://doi.org/10.13107/jocr.2024.v14.i12.5082
1Department of Orthopedic Surgery, Philadelphia College of Osteopathic Medicine, Philadelphia, United States of America,
2Department of Medicine, Philadelphia College of Osteopathic Medicine, Philadelphia, United States of America.
Address of Correspondence:
Dr. Mark LaGreca,
Department of Orthopedic Surgery, Philadelphia College of Osteopathic Medicine, Philadelphia, United States of America.
E-mail: ML194690@pcom.edu
© 2024 Journal of Orthopaedic Case Reports Published by Indian Orthopaedic Research Group |
Dr. Thomas Falconiero
Journal of Orthopaedic Case Repor ts 2024 December:14(12):Page 229-236
1 2 1 1 1
Mark LaGreca , Arash Badragheh , Nathan Jones , Thomas Falconiero , Brian Danshaw
Introduction: This review of case series and case reports explores conservative management strategies for paraspinal compartment syndrome
(PCS), a rare clinical condition. Extremity compartment syndrome has been shown to be managed most effectively with emergent surgical
release of the fascial compartment. Given the rarity of PCS and the paucity of research in the literature, some authors have suggested the
possibility of conservative treatment. There has been no study to date that has specifically investigated the cases of non-operative management of
PCS.
Materials and Methods: There are 16 case reports in the literature with 22 cases of PCS treated conservatively. The authors reviewed these
cases, specifically viewing the clinical courses, why the decision was made to manage conservatively, and the reported outcomes.
Results: The etiology of PCS varied, with weightlifting being the primary cause in 11 out of 22 cases, followed by strenuous sporting events and
postsurgical complications. All patients in this review were male, aged between 18 and 61 years old. Acute presentations exhibited severe back
pain, rigid paraspinal musculature, and subjective paraspinal paresthesias. Magnetic Resonance Imaging findings of the spine revealed profound
bilateral symmetric intramuscular edema. Among the cases, 8 explicitly reported a return to normal function, while 8 continued to experience
symptoms related to the initial injury. Nine cases chose conservative measures primarily because of delayed presentation, seven instances
reported successful outcomes with conservative measures; one case cited concerns about infection risk.
Discussion: The probability of underreporting related to PCS may result in a substantial number of cases being omitted from medical literature.
Pathologically, PCS is characterized by increased intra-compartmental pressure, triggering rhabdomyolysis due to significant soft tissue damage.
Emergent surgical intervention is the treatment of choice for any compartment syndrome; however, conservative management of these cases has
shown satisfactory clinical outcomes. Hyperbaric oxygen therapy emerges as a potential adjunctive treatment to enhance tissue viability, though
its efficacy and accessibility warrant further investigation in the context of PCS management.
Conclusion: Early recognition and treatment of PCS are critical in preventing chronic pain and permanent complications. Given the limitations
identified in non-operative management, further research is imperative to optimize treatment strategies.
Keywords: Paraspinal compartment syndrome, conservative management, back pain.
Abstract
Learning Point of the Article:
Compartment syndrome is typically treated with fasciotomies. There are case reports of paraspinal compartment syndrome treated
conservatively for a multitude of reasons. This case series reviews the cases of conservatively treated paraspinal compartment syndrome
case reports.
Conservative Management of a Rare Clinical Phenomenon: Paraspinal
Compartment Syndrome – A Review of Existing Literature
Submitted: 18/09/2024; Review: 30/10/2024; Accepted: November 2024; Published: December 2024
Dr. Brian Danshaw
www.jocr.co.in
[1]. This syndrome manifests due to edema within the
paravertebral myofascial compartment from a variety of causes,
including exertion and post-operative cases [2]. Elevated intra-
compartmental pressure (ICP) resulting from increased
compartment volume can compromise the blood supply to the
muscles, which may result in ischemia and subsequent muscle
necrosis. A spectrum of perspectives exists on the management
of this syndrome, leading to varied treatment modalities. The
primary objective of this study was to review the literature on
PCS, with the overarching goal of delineating conservative
management approaches for this uncommon clinical entity.
Materials and Methods
A comprehensive literature search was performed using
PubMed, MEDLINE, and Cochrane Librar y electronic
databases. The search term “PCS” was used and appeared in the
title, abstract, or keyword fields. The original search yielded 56
results. Articles were then examined for inclusion of non-
operative management. We reviewed the reference lists of
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LaGreca M, et al
Author Mechanism of Injury Lateralit
yCPK
Compartment
pressure (mm
Hg) (L)
Compartment
pressure (mm
Hg) (R)
Symptoms on Presentation Reason for Non-Op Outcome
Carr et. al. (1985) [2] Strenuous sport (skiing) BL
CPK on
day 6 =
5465
N/A N/A Severe and unrelenting LBP, referred
pain upon deep abdominal palpation Delayed presentation Pain with vigorous activity
Haig et alet. al. (2009) [13] Surgery (aortoiliac bypass
surgery) BL N/A N/A N/A Excruciating LBP Delayed presentation N/A
Haig et alet. al. (2009) [13] Surgery (gastric bypass) BL N/A N/A N/A Complete sensory loss from upper
sacrum to T11 bilaterally Delayed presentation N/A
Wik et alet. al. (2010) [14] Weightlifting (deadlifting) BL >82,000 20 mmHg 150 mmHgG Acute LBP with exertion, bilateral
throbbing sensation Delayed presentation Pain with vigorous activity
Ogoshi et alet. al. (2020) [16] Weightlifting BL 53084 64
mmHGmmHg 105 mmHGmmHg Persistent back pain at rest Non-surgical sufficiency Normal
Ferreira Ferreira et alet. al. (2003) [15] Surgery (AAA repair) BL 25000 N/A N/A Acute LBP with lumbar paravertebral
muscle tenderness and swelling Risk of infection, delayed presentation Pain with vigorous activity
Allerton et alet. al. (2012) [17] Weightlifting (deadlifting) UL 60800
4 days after
presentation:
7mmHg
20 mmHGmmHg
Severe LBP radiating to the right
groin, with altered sensation in the
right leg
Delayed presentation N/A
Karam et alet. al. (2010) [18] Weightlifting (squats) BL 77440 N/A N/A Rapidly increasing and unbearable
LBP Non-surgical sufficiency Normal
Saadat and Rezania et. al. (2020 2021) [21] Surgery (right ankle
surgery) UL 20000 N/A N/A
Paresthesia in the lower left flank,
leg, and lateral foot, with absent left
ankle reflex
Delayed presentation Pain with vigorous activity
DiFazio et alet. al. (1991) [22] Strenuous sport (skiing) BL 60000 80
mmHGmmHg 70 mmHGmmHg
Chronic and persistent LBP with
bilateral rigidity of paravertebral
musculature, exacerbated by straight
leg raising (SLR)
Non-surgical sufficiency Pain with vigorous activity
Kanaya et alet. al. (2017) [23] Strenuous sport (rowing) BL 46190 64 mmHgG 105 mmHgG
Severe back pain with paresthesias
on the right lumbar region and
weakness of paravertebral
musculature
Non-surgical sufficiency Normal
Hoyle et alet. al. (2014) [24] Weightlifting UL
CPK on
day 9 =
4949
N/A N/A Severe right loin and back pain
radiating to the abdomen Non-surgical sufficiency Pain with vigorous activity
Chavez and Gonzalez et. al. (2013) [25] Strenuous sport (Cross Fit) UL 42000 N/A N/A
Rapidly progressive stabbing LBP
with leg radiation and difficulty with
ambulation
Delayed presentation N/A
Calvert et alet. al. (2012) [26] Weightlifting UL 60800
Measured 3
days after
presentation -
20mmHg
7 mmHGmmHg
Worsening lumbar back pain
radiating to the right groin post-
activity
Delayed presentation N/A
Anaya et alet. al. (2013) [27] Idiopathic (woke up from
sleep with pain) UL 626 N/A N/A
Sharp constant midline LBP with
lower back numbness, exacerbated
by movement
Delayed presentation Pain with vigorous activity
Eichner et al.et. al (2016) [28]
Strenuous sport (Sprinting
first 1st time, basketball
second 2nd time)
BL 55400 N/A N/A
Severe LBP with lumbar
paravertebral muscle tenderness,
bilateral stiffness, and progressive
worsening
Did not specify Pain with vigorous activity
Eichner et al.et. al (2016) [28] Weightlifting (squats) UL 10648 N/A N/A Cramping sensation in legs and low
back with paravertebral tenderness Did not specify Normal
Eichner et al.et. al (2016) [28] Weightlifting (squats) UL 2136 N/A N/A Exertional pain with leg instability Did not specify Normal
Eichner et al.et. al (2016) [28] Weightlifting BL 10000 N/A N/A
Severe LBP without radicular pain but
discomfort in the right buttock and
thigh, paravertebral tenderness, and
limited ROM
Did not specify Normal
Eichner et al.et. al (2016) [28] Weightlifting UL 14797 N/A N/A Severe LBP with radiation to testicles Non-surgical sufficiency Normal
Eichner et al.et. al (2016) [28] Weightlifting and sprints BL 40000 N/A N/A
Acute LBP with mild limitation in
ROM, lumbar muscle spasm, and
negative straight leg raisingSLR
Did not specify Normal
Fitch et alet. al. (2014) [29] Surgery (AAA repair) BL N/A N/A N/A
Numbness post-surgery with diffuse
lumbar tenderness and weakness of
lumbar extensor musculature
Non-surgical sufficiency N/A
Table 1: Analysis of diagnosis, presentation, laboratory results, and outcome in paraspinal compartment syndrome
UL: Unilateral, BL: Bilateral, R: Right paraspinal muscle compartment, L: Left paraspinal muscle compartment, CPK: Creatinine phosphokinase, LBP: Lower back pain, AAA: Abdominal aortic aneurysm
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previously conducted systematic reviews to identify additional
pertinent literature. The references cited in the identified
studies were cross-checked to ensure the inclusion of any
relevant material overlooked in the initial search. The chosen
studies comprised original articles featuring one or more case
reports detailing non-operative treatments for lumbar PCS.
This systematic approach led to the identification of 22 non-
operative cases derived from 16 distinct studies, all of which
were incorporated into our comprehensive review (Fig. 1). The
authors recorded information such as patient demographics,
la boratory values, desc riptions of imaging findings,
compartment measurements, reasons for undergoing non-
operative treatment, and reported clinical outcomes.
Results
The causative etiology of the cases in our research varied, with
weightlifting identified as the explicit cause in 12/22 cases
(Table 1). Following this, incidents related to strenuous
sporting events constituted 5/22 cases. Within this category,
downhill skiing was a factor in 2/22 cases. These additional
sporting events included a range of activities: Rowing, CrossFit
exercises, and basketball-related activities. Postsurgical
situations contributed to 5/22 cases, with abdominal vascular
surgery contributing to 2/22 of instances, ankle surgery 1/22,
aortoiliac bypass surgery 1/22, and gastric bypass surgery 1/22.
The remaining and final case was from acute lower back pain
(LBP) that woke the patient up from sleep.
All of the patients in this review were male, with ages ranging
from 18 to 61 years old. Acute cases of PCS were most
commonly associated with vigorous exercise, including
weightlifting, specifically squatting or deadlifting (15/17 acute
cases). The time span from the initiating event to the onset of
acute lumbar compartment syndrome varied widely, ranging
from minutes to hours. A majority (16/22) sought medical
attention within the initial 36 h. However, notable outliers, such
as cases in Saadat and Rezania and Fitch et al. presented with 7
years of chronic LBP postoperatively. 4/5 chronic cases were
associated with surgery. The last chronic case was a patient with
2 years of LBP exacerbated by strenuous activity, namely
downhill skiing. Acute presentations presented some form or
combination of the following: unrelenting back pain, rigid
paraspinal musculature, and subjective paraspinal paresthesias
(14/17 acute cases).
All acute cases were associated with elevated levels of creatine
phosphokinase (average 35,333 U/L in those tested).
Myoglobinuria was also noted across the identified case studies.
Elevated liver enzymes, such as aspartate aminotransferase
(AST) averaging 619 U/L in two cases (normal range <40
U/L), alanine aminotransferase (ALT) averaging 208 U/L in
four cases (normal range <36 U/L), and lactate dehydrogenase
averaging 2260.5 U/L in two cases (normal range <225 U/L),
were observed. One case study noted the abuse of isotretinoin,
cocaine, and testosterone by the patient.
Acute presentations had magnetic resonance imaging (MRI)
ordered at some point during the patient’s hospital stay. Bilateral
symmetric intra-muscular edema affecting paraspinal muscles
from T12 down to the sacrum is a consistent finding in these
case reports (18/22). The MRI results in nearly every case were
described as “extensive edema” or “myonecrosis in the
paraspinal musculature”. Imaging also captured complications
post-surgery, including areas of scarring and abnormal signals
within paraspinal muscles. Patients with chronic lumbar PCS
presented with exaggerated low back pain during exertion but
were asymptomatic at rest, maintaining a normal range of spinal
motion. MRIs in the chronic cases revealed fluid and fat
infiltration of paraspinal musculature.
In the overall cli nic al pic ture of acute paraver tebral
compartment syndrome, patients frequently exhibited severe
back pain and rigid paraspinal musculature as the primary
symptoms and exam findings. Laboratory values exhibited
rhabdomyolysis of ten requiring inter ventions such as
crystalloid fluid infusions and analgesics. Among cases
specifying conservative approaches (22 in total), 9 cited
LaGreca M, et al
Figure 1: Study selection flow chart
Figure 2: Mechanisms of muscle damage during exertional rhabdomyolysis.
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232
delayed presentation and diagnosis as the rationale for
conservative management. Conservative treatments yielded
relief to a degree where surgical intervention was deemed
potentially detrimental. Other considerations for non-
operative management included elevated infection risk and low
measured compartment pressure due to delayed presentation.
In eight out of the 22 non-surgically treated cases, patients
explicitly reported a return to normal, while eight continued to
experience symptoms related to the initial insult. The
remaining six did not specify the patients’ return-to-normal
status. Most case reports noted a gradual improvement in pain,
allowing a resumption of physical activities, though limitations
persisted in more vigorous activities. Recovery times varied,
with patients achieving a sense of full recovery spanning from 1
to 2 weeks to 1 year.
Discussion
Paralumbar compartment syndrome was first reported as a
possible diagnosis by Peck et al. in 1981. It was not until 4 years
later that Carr et al. published a case report on the first
diagnosed paralumbar compartment syndrome in 1985. There
have been few case reports and case series written since; some
were treated with fasciotomies and some were treated
conservatively. However, the uncommon occurrence of PCS in
clinical practice may hinder consistent management. It is
essential to acknowledge the lack of consensus surrounding the
management of PCS, leaving case reports and case series as the
sole point of reference for comparison. Hence, clinicians face
the challenge of recognizing atypical manifestations of
uncommon conditions such as PCS. This necessitates a
thorough understanding of the anatomy, pathology, diagnostic
nuances, and treatment options specific to PCS, enabling
clinicians to promptly and accurately manage the condition.
Anatomical considerations
Understanding the function of the thoracolumbar fascia (TLF)
is pertinent in the context of PCS. Historically, the TLF was
thought to primarily serve as the origin for abdominal wall
muscles [3]. However, a study by Tesh et al. has shown that the
arrangement of the fibers in the fascia suggests that the internal
oblique and transversus abdominis muscles arise principally
from the middle layer of the TLF with only a restricted origin
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from the posterior layer. Their study highlights the TLF’s main
function as forming a compartment around the lower lumbar
and sacral paraspinal muscles, contributing to the rise of ICP
during erector spinae muscle contraction. Cadaver dissections
by Carr et al. and Willard et al. support these findings,
characterizing the TLF by well-defined fascial sheaths and
attachments to surrounding bony structures, underscoring its
critical function in isolating the paraspinal muscles [1, 4].
The irregular arrangement of collagen fibers in the TLF imparts
an unyielding and non-distensible quality, allowing it to
function as packing tissue and resist tensional forces universally
[4]. In instances of PCS, patients commonly exhibit back pain
following trauma, with the syndrome often manifesting in the
context of sporting events. This is particularly evident during
high-intensity exercises such as heavy back squats, downhill
skiing, sprints, and row ing, which impose substantial
compression and loading on the lumbar paraspinal muscles,
resulting in heightened compartment pressure. Recorded
pressures in all cases surpassed thresholds recommended by
Songcharoen et al. 5 mmHg for normal, healthy paravertebral
compartmental pressure. Resting ICP in healthy individuals
typically ranges from 3 to 7.95 mmHg, with transient increases
up to 25 mmHg during exercise, returning to preexisting ICP
within 1–6 min [5]. Typically, pulse pressure, also known as
delta pressure, is used as a quantitative indicator for diagnosing
compartment syndrome. This metric, calculated by subtracting
intramuscular pressure from diastolic blood pressure, offers a
threshold of 30 mm Hg or below to signify inadequate perfusion
to the extremity [6]. Delta pressure may be used in conjunction
with other clinical symptoms of compartment syndrome.
Pathology
Rhabdomyolysis, manifesting as a secondary consequence of
compartment syndrome, is marked by an increase in serum
creatine kinase. Better and Stein proposed that exertional and
metabolic rhabdomyolysis in humans result in impaired
sarcolemma sodium-potassium-adenosine triphosphatase
activity in damaged muscles [7]. This impairment contributes
to the disruption of myofibrils and muscle damage through the
activation of neutral proteases due to an increase in cytosolic-
free calcium [7]. In addition, in injured tissue, the breakdown of
crucial energy-dependent transcellular pump systems, such as
the Na/K-ATPase and Ca2+ATPase pumps, vital for myocyte
integrity, can result in muscle cell swelling [8]. This swelling
elevates intramuscular pressure within the injured muscle,
exceeding arteriolar-perfusion pressure and leading to
weakened contraction of the muscle fibers and myoneural
ischemic damage in some cases. Fig. 2 is a demonstration of this
pathway.
Furthermore, the increase in pressure within the compartment
may surpass capillary hydrostatic pressure, causing vascular
stasis and prompting a shift toward anaerobic metabolism. This,
in turn, induces oxygen debt within skeletal muscles, leading to
increased capillary permeability and initiating inflammatory
cascades [7]. Consequently, a significant rise in ICP ensues,
causing additional muscle damage, severe impairment of local
circulation, and neuromuscular function [2, 9]. Blood flow to
the paraspinal musculature is managed by the dorsal branches
of parietal arteries, known as intercostal and lumbar arteries.
These arteries derive from the abdominal aorta [1]. The
innervation of paraspinal muscles is facilitated by spinal nerves
that emerge bilaterally through the intervertebral foramen
between adjacent vertebrae. These nerves split into dorsal and
ventral rami below this foramen [10]. Lower back numbness
and paresthesias occur due to dorsal rami and cutaneous
branches of the cluneal nerve, which innervate the lumbar skin,
muscles, and fasciae of the lumbar region [10]. Early signs of
PCS may include sensory loss in nerve distribution, as
peripheral nerves exhibit greater sensitivity to ischemia than
muscle. Previous canine studies by Rorabeck and Macnab
demonstrated that nerve conduction velocity significantly
decreased at 30 mm Hg compartment pressure after 8 h, with a
complete block occurring at 50 mm Hg [11]. Early detection
and treatment will prevent irreversible damage to nerve tissues
in the paraspinal area. Out of the 22 patients examined in the
case studies, 8 had reported experiencing paresthesias in the
lumbar region.
In this review of conservatively treated cases, eight cases
explicitly reported a return to normal function, while eight
continued to experience symptoms related to the initial injury,
and six cases did not specify the patients’ recovery status.
However, contrasting outcomes were observed in existing
review studies advocating for surgical decompression, where
the majority of PCS patients (19 out of 20) achieved full
recovery and resumed normal activities following fasciotomy
[12]. Given these findings, timely surgical decompression
emerges as crucial in alleviating paraspinal compartment
pressures. This approach facilitates tissue reperfusion and
prevents further ischemic muscle damage by restoring blood
flow to the affected areas.
PCS recognition
The differential for LBP is vast. This includes but is not limited
to renal col ic, k idney stones , osteomyelitis, epidu ral
hematoma/abscess, degenerative arthritis of the lumbar spine,
spondylolisthesis, intervertebral disk bulging or herniation, and
facet joint arthropathy. PCS is diagnosed through various
subjective and objective clinical features. In the acute setting,
Clinical Message
PCS should be treated with fasciotomies in the acute setting. Most of
those treated conservatively have persistent symptoms with
exertion.
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these patients tend to have a reported recent history of physical
exertion including weightlifting or sporting events. On physical
ex ami nat io n, the cl in ic ia n m ay fi nd se ve re p ai n
disproportionate to the reported history of present illness
exacerbated by passive muscle stretch, paraspinal swelling,
extreme paraspinal tenderness to palpation, and subjective
paresthesias in the lumbar spine and sacral regions. Objective
measurements to aid in the diagnosis include measurement of
intramuscular pressure, and lab values such as elevated creatine
kinase, ALT, and AST. Imaging can also help aid in the diagnosis
such as MRI findings of significant paraspinal edema contribute
to confirmation.
Missed diagnosis of PCS can lead to severe sequelae. This
sequela is exemplified in two cases reported by Haig et al. The
first case was a 57-year-old male who underwent an aortoiliac
bypass procedure, developed severe back pain 2 days later, and
was diagnosed with a mild herniated disc. Reviewing the MRI
obtained 2 days post-operatively, months later, revealed
significant edema in the paraspinal musculature; this patient
reported pain with standing, sitting, and lifting. A repeat MRI
performed on this patient 11 months later demonstrated
significant fatty atrophy of the paraspinal musculature. The
other case described by Haig et al. presented a 34-year-old male
after a gastric bypass procedure, 1 year post-operatively with
complete loss of touch and pinprick sensation from T11 to the
upper sacrum. Moreover, Fitch et al. detailed a case study
featuring a 61-year-old male patient who endured 7 years of
chronic back pain subsequent to abdominal vascular surgery
[14]. The patient exhibited pain, tenderness, and sensory loss in
the lumbar paraspinal muscle region. The authors confirmed
their suspicion of missed paravertebral compartment syndrome
through MRI. Given the rarity of this diagnosis and the limited
information available regarding the clinical symptoms,
physicians may overlook the diagnosis if they are not familiar
with t he relevant in dicators. Ti mely d iagnosis a nd
consideration as a differential are essential to mitigate its
debilitating functional consequences and ensure optimal
patient outcomes.
Hyperbaric oxygen
The optimal treatment strategy for PCS remains an ongoing
challenge within the medical field. Increased ICP acts as a
catalyst for further harm and necrotic processes. Given the
closed, non-communicating nature of these compartments, the
primary method for pressure reduction involves surgical
decompression through fasc iotomy. However, not all
researchers universally support performing early fasciotomy
due to concerns about the risk of potential infections associated
with the procedure [16]. Nevertheless, there is consensus
among a majority of cases regarding the significance of fluid
resuscitation in mitigating the progression of rhabdomyolysis.
This recommendation aligns with clinical observations in
humans, suggesting that administering intravenous fluids
equivalent to the extracellular space can effectively infiltrate
injured muscles within a relatively short time following the
injury [7]. In addition to standard therapies such as aggressive
fluid administration and analgesics, some authors have
explored alternative treatments such as hyperbaric oxygen
(HBO) therapy [17, 18]. Studies by Allerton et al. and Karam et
al. demonstrated successful pain management with HBO,
possibly through mechanisms involving increased tissue
oxygenation and vasoconstriction [19, 20].
Cl inical tria ls have dem onstrated that HBO therapy
immediately increases oxygen delivery to ischemic tissue
through hyperoxygenation [19]. In addition, hyperoxygenation
induces direct vasoconstriction, potentially reducing edema in
the paravertebral compartment by lowering the capillary
transudation flow rate [19]. This effect is supported by research
from Sullivan and Johnson, which shows that increased tissue
PO2 levels diminish the autoregulatory dilation mechanism at
all levels of the microcirculation in skeletal muscle, indicating
the vasoconstrictive properties of hyperoxygenation [20].
However, the efficacy of HBO therapy is contingent upon
ad equ ate tissue per fusion , nece ssi tat ing lowering of
compartment pressure before its application. Furthermore, it is
noteworthy that in the case studies of the two patients who
received HBO therapy, back pain persisted during exertion,
indicating that it may not completely alleviate symptoms and
restore patients to their baseline condition. Thus, HBO therapy
may hold promise as an adjunctive treatment following initial
surgical management to enhance tissue viability in PCS.
Moreover, the limited availability of HBO therapy facilities,
particularly in major medical hubs such as Philadelphia, poses a
challenge to the reliability and availability of this treatment.
Ongoing research is essential for establishing comprehensive
long-term outcome data on the efficacy of hyperbaric treatment
as a supplementary therapy for PCS. List of all cases are listed in
Table 1.
Limitations
This study has several limitations. For one, this is a retrospective
review of case reports and case series, so the data collected are
limited to what is written by the authors. There were various
absent clinical and laboratory data points. The authors of this
case study review were also limited by the inconsistent follow-
up for these patients and the outcome descriptions. The
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References
Declaration of patient consent: The authors certify that they have obtained all appropriate patient consent forms. In the form,
the patient has given the consent for his/ her images and other clinical information to be reported in the journal. The patient
understands that his/ her names and initials will not be published and due efforts will be made to conceal their identity, but
anonymity cannot be guaranteed.
Conflict of interest: Nil Source of support: None
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absence of reported outcomes in 5 out of 22 cases receiving
conservative measures limits the ability to comprehensively
assess the effectiveness of non-operative interventions. There
were no objective or subjective patient-reported scales utilized
when describing the patient’s post-hospitalization course.
Conclusion
This is the first review to investigate conservative treatments for
PCS. PCS diagnosis is often overlooked due to its rarity and can
be missed without specific clinical suspicion. Therefore,
recognizing the significance of early diagnosis is crucial, as
undiagnosed or delayed PCS can result in severe and chronic
disability, affecting daily life activities. Patients managed
conservatively experienced a return to baseline functions
within a span of 1 week to 1 year, albeit often enduring chronic
back pain during exertion. This is particularly concerning for
athletes but potentially viable for non-athletes or chronic cases.
Furthermore, surgical decompression in the acute phase may
mitigate tissue damage. Further research is needed to enhance
our understanding of PCS and guide the development of more
effective therapeutic strategies in clinical practice.
Clinical Message
PCS should be treated with fasciotomies in the acute setting. Most of
those treated conservatively have persistent symptoms with
exertion.
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Journal of Orthopaedic Case Reports Volume 14 Issue 12 December 2024 Page 229-236 | | | |
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How to Cite this Article
LaGreca M, Badragheh A, Jones N, Falconiero T, Danshaw B.
Conservative Management of a rare clinical phenomenon: Paraspinal
Compartment Syndrome, A Review of Existing Literature. Journal of
Orthopaedic Case Reports 2024 December;14(12):229-236.
Conflict of Interest: Nil
Source of Support: Nil
______________________________________________
Consent: The authors confirm that informed consent was
obtained from the patient for publication of this case report
