Phẫu Thuật Tạo Hình Grabb & Smith’s (Bản Cập Nhật – Kevin C. Chung)

mucosal surfaces that may be either pedunculated or sessile. These may occur in the periungual region or
elsewhere in the hand and upper extremity. Numerous treatments have been described owing to risk of
recurrence. In a review of studies investigating the treatment of pyogenic granulomas, Lee and colleagues
found that there was an overall recurrence rate of 2.94% with surgical excision (Figure 87.14) compared
with 1.62% with cryotherapy with liquid nitrogen. 50 There was no statistical difference between the
recurrence rates in these groups. Because cryotherapy often required multiple treatments in the reviewed
studies and because surgical excision allows single-stage treatment with the opportunity to send the
lesion for pathology, the authors recommended surgical excision except where a nonsurgical treatment is
preferred such as in cases where the lesion is located near cosmetically sensitive or vital structures.
FIGURE 87.14 This patient had a pyogenic granuloma of the left middle finger that was treated eventually with resection and
dressing changes.
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Questions
1. In a patient with an arteriovenous fistula for hemodialysis access who develops steal phenomenon,
what is the most effective treatment to improve hand ischemia while preserving arteriovenous access
for hemodialysis?
a. Ligation and creation of a new arteriovenous fistula
b. Banding
c. Angioplasty
d. DRIL
e. Revision using distal inflow
2. Which of the following is the preferred first-line agent for medical management of RP?
a. Statin
b. Angiotensin-converting enzyme inhibitor
c. Serotonin agonist
d. Calcium channel blocker
e. Aspirin
3. Which of the following is not one of the key principles and goals of performing a periarterial
sympathectomy for RP?
a. Periarterial adventitial stripping of the radial and ulnar arteries, the palmar arch, and the
digital arteries
b. Division of the nerve of Henle
c. Reconstruction of occluded arterial segments
d. Debridement of digital ulcers
e. Local or distant flap coverage of surgical sites to reduce wound healing complications
4. Which digit is least likely to be involved in hypothenar hammer syndrome?
a. Thumb
b. Index
c. Middle
d. Ring
e. Small
5. What is the most effective treatment for thromboangiitis obliterans?
a. Anticoagulation
b. Botulinum toxin injection
c. Periarterial sympathectomy
d. Cold avoidance
e. Smoking cessation
6. A 30-year-old woman presents with several months of severe pain in the distal phalanx of the right
index finger. She notices the pain is exacerbated when immersing her hand in cold water. Physical
examination is notable for a dark-blue subungual lesion with associated exquisite focal tenderness.
What is the most likely diagnosis?
a. Melanoma
b. Subungual hematoma
c. Glomuvenous malformation
d. Splinter hemorrhage
e. RP
1. Answer: d. DRIL is a procedure in which an arteriovenous fistula is bypassed by a vein graft from
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proximal to the fistula to an artery distal to the fistula, followed by ligation of the recipient artery just
distal to the fistula to prevent retrograde flow into the fistula. In patients with hand ischemia due to
an arteriovenous fistula, the DRIL procedure results in similar improvements in hand ischemia
compared with ligation. However, the DRIL procedure preserves access for hemodialysis.
2. Answer: d. In a systematic review of medical treatments for RP, calcium channel blockers were
found to be the most effective. Aspirin typically does not have a role in medical management of RP.
3. Answer: e. Flap coverage of the surgical sites is not typically described when performing a
periarterial sympathectomy for RP. Sympathetic tone to the vessels is disrupted by stripping the
adventitial tissue and dividing the nerve of Henle. Any resected arterial segments should be
reconstructed if distal targets are available. While these patients are under anesthesia, any digital
ulcers should be debrided to facilitate wound healing.
4. Answer: a. Because of its typically radial-dominant blood supply and being most distally located
from the ulnar artery relative to the other digits, the thumb is least likely to be affected by
hypothenar hammer syndrome. The index finger is the second least likely digit to be affected.
5. Answer: e. Smoking cessation is the primary treatment for thromboangiitis obliterans or Buerger
disease. Other treatments, including the ones listed, have shown either mixed results or no benefit in
the management of Buerger disease.
6. Answer: c. The described scenario is a classic presentation for a GVM or glomus tumor. When
presenting for evaluation, these malformations are nearly universally focally tender at a site of bluish
discoloration and typically have associated cold sensitivity.
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References
Coleman, SS, Anson, BJ. Arterial patterns in the hand based upon a study of 650 specimens. Surg Gynecol Obstet. 1961;113:409-424.
Gellman, H, Botte, MJ, Shankwiler, J, Gelberman, RH. Arterial patterns of the deep and superficial palmar arches. Clin Orthop. 2001;(383):41-
46.This anatomic study of 45 fresh cadaver limbs investigated the arterial anatomy of the superficial and deep palmar arches. Consistent with the work
of previous authors, they found highly variable anatomy of the superficial palmar arch, which included complete or incomplete arches with variable
contributions from the ulnar, radial, and persistent median arteries. The deep palmar arch anatomy had less variability.
McCabe, SJ, Mizgala, C, Glickman, L. The measurement of cold sensitivity of the hand. J Hand Surg. 1991;16(6):1037-1040.
Ruengsakulrach, P, Brooks, M, Hare, DL, et al. Preoperative assessment of hand circulation by means of Doppler ultrasonography and the
modified Allen test. J Thorac Cardiovasc Surg. 2001;121(3):526-531.
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Chim, H, Bakri, K, Moran, SL. Complications related to radial artery occlusion, radial artery harvest, and arterial lines. Hand Clin.
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Morsy, AH, Kulbaski, M, Chen, C, et al. Incidence and characteristics of patients with hand ischemia after a hemodialysis access procedure. J
Surg Res. 1998;74(1):8-10.
Leake, AE, Winger, DG, Leers, SA, et al. Management and outcomes of dialysis access-associated steal syndrome. J Vasc Surg. 2015;61(3):754-
760.
De Martino, RR, Moran, SL. The role of thrombolytics in acute and chronic occlusion of the hand. Hand Clin. 2015;31(1):13-21.
Iannuzzi, NP, Higgins, JP. Acute arterial thrombosis of the hand. J Hand Surg. 2015;40(10):2099-2106.
Bedri, MI, Khosravi, AH, Lifchez, SD. Upper extremity compartment syndrome in the setting of deep venous thrombosis and phlegmasia
cerulea dolens: case report. J Hand Surg. 2009;34(10):1859-1863.
Maverakis, E, Patel, F, Kronenberg, DG, et al. International consensus criteria for the diagnosis of Raynaud’s phenomenon. J Autoimmun.
2014;48-49:60-65.In a systematic fashion, the authors of this paper assembled an expert panel of physicians and researchers who treat patients with RP
to define a set of diagnostic criteria. The agreed upon diagnostic criteria include cold intolerance and episodes with biphasic color changes.
Wigley, FM, Flavahan, NA. Raynaud’s phenomenon. N Engl J Med. 2016;375(6):
 556-565.
Block, JA, Sequeira, W. Raynaud’s phenomenon. Lancet Lond Engl. 2001;357(9273):2042-2048.
Fraenkel, L. Raynaud’s phenomenon: epidemiology and risk factors. Curr Rheumatol Rep. 2002;4(2):123-128.
Garner, R, Kumari, R, Lanyon, P, et al. Prevalence, risk factors and associations of primary Raynaud’s phenomenon: systematic review and
meta-analysis of observational studies. BMJ Open. 2015;5(3):e006389.
Carpentier, PH, Satger, B, Poensin, D, Maricq, HR. Incidence and natural history of Raynaud phenomenon: a long-term follow-up (14 years)
of a random sample from the general population. J Vasc Surg. 2006;44(5):1023-1028.
Suter, LG, Murabito, JM, Felson, DT, Fraenkel, L. The incidence and natural history of Raynaud’s phenomenon in the community. Arthritis
Rheum. 2005;52(4):1259-1263.
Flavahan, NA. A vascular mechanistic approach to understanding Raynaud phenomenon. Nat Rev Rheumatol. 2015;11(3):146-158.
Huisstede, BM, Hoogvliet, P, Paulis, WD, et al. Effectiveness of interventions for secondary Raynaud’s phenomenon: a systematic review.
Arch Phys Med Rehabil. 2011;92(7):1166-1180.
Roustit, M, Blaise, S, Allanore, Y, et al. Phosphodiesterase-5 inhibitors for the treatment of secondary Raynaud’s phenomenon: systematic
review and meta-analysis of randomised trials. Ann Rheum Dis. 2013;72(10):1696-1699.
Sycha, T, Graninger, M, Auff, E, Schnider, P. Botulinum toxin in the treatment of Raynaud’s phenomenon: a pilot study. Eur J Clin Invest.
2004;34(4):312-313.
Neumeister, MW. The role of botulinum toxin in vasospastic disorders of the hand. Hand Clin. 2015;31(1):23-37.
Motegi, S-I, Uehara, A, Yamada, K, et al. Efficacy of botulinum toxin B Injection for Raynaud’s phenomenon and digital ulcers in patients
with systemic sclerosis. Acta Derm Venereol. 2017;97(7):843-850.
Leriche, R. Surgery of the sympathetic system: indications and results. Ann Surg. 1928;88(3):449-469.
Flatt, AE. Digital artery sympathectomy. J Hand Surg. 1980;5(6):550-556.Flatt introduces periarterial adventitial stripping for treatment of RP. He
reviews his 20-year experience with this operation and reports durable results in nine patients.
Kotsis, SV, Chung, KC. A systematic review of the outcomes of digital sympathectomy for treatment of chronic digital ischemia. J Rheumatol.
2003;30(8):1788-1792.
Momeni, A, Sorice, SC, Valenzuela, A, et al. Surgical treatment of systemic sclerosis – 
 is it justified to offer peripheral sympathectomy
earlier in the disease process? Microsurgery. 2015;35(6):441-446.
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Shammas, RL, Hwang, BH, Levin, LS, et al. Outcomes of sympathectomy and vascular bypass for digital ischaemia in connective tissue
disorders. J Hand Surg Eur Vol. 2017;42(8):823-826.
Pace, CS, Merritt, WH. Extended periarterial sympathectomy: evaluation of long-term outcomes. Hand (NY). 2018; 3(4):395-402.
Hartzell, TL, Makhni, EC, Sampson, C. Long-term results of periarterial sympathectomy. J Hand Surg. 2009;34(8):1454-1460.This study of 28
patients who underwent periarterial sympathectomy for digital ischemia demonstrated that 75% of patients with an underlying autoimmune disorder
had either complete healing or improvement in the number of digital ulcers at a mean follow-up of 90 months. Only one of eight (12.5%) patients with
digital ischemia due to atherosclerotic disease had improvement at the end of the follow-up period.
Merritt, WH. Role and rationale for extended periarterial sympathectomy in the management of severe Raynaud syndrome: techniques and
results. Hand Clin. 2015;31(1):101-120.
Balogh, B, Mayer, W, Vesely, M, et al. Adventitial stripping of the radial and ulnar arteries in Raynaud’s disease. J Hand Surg.
2002;27(6):1073-1080.
Chiou, G, Crowe, C, Suarez, P, et al. Digital sympathectomy in patients with scleroderma: an overview of the practice and referral patterns
and perceptions of rheumatologists. Ann Plast Surg. 2015;75(6):637-643.
Conn, J, Bergan, JJ, Bell, JL. Hypothenar hammer syndrome: posttraumatic digital ischemia. Surgery. 1970;68(6):1122-1128.
Ferris, BL, Taylor, LM, Oyama, K, et al. Hypothenar hammer syndrome: proposed etiology. J Vasc Surg. 2000;31(1 Pt 1):104-113.This 27-year
retrospective review of 21 patients treated for hypothenar hammer syndrome describes the epidemiology and treatment outcomes in these patients. All
patients were male and had an exposure to repetitive palmar trauma, and a majority (76%) of patients were smokers. Nearly all patients underwent
segmental ulnar artery resection and reconstruction, which had an 84% patency rate at two years with no recurrent ischemia in patients with a patent
vascular reconstruction.
Marie, I, Hervé, F, Primard, E, et al. Long-term follow-up of hypothenar hammer syndrome: a series of 47 patients. Medicine (Balt).
2007;86(6):334-343.
Hammond, DC, Matloub, HS, Yousif, NJ, Sanger, JR. The corkscrew sign in hypothenar hammer syndrome. J Hand Surg. 1993;18(6):767-769.
Vartija, L, Cheung, K, Kaur, M, et al. Ulnar hammer syndrome: a systematic review of the literature. Plast Reconstr Surg. 2013;132(5):1181-
1191.
Yuen, JC, Wright, E, Johnson, LA, Culp, WC. Hypothenar hammer syndrome: an update with algorithms for diagnosis and treatment. Ann
Plast Surg. 2011;67(4):429-438.The authors of this article provide a detailed review of the management of hypothenar hammer syndrome. Their review
is supplemented by suggested algorithms for the diagnosis and treatment of hypothenar hammer syndrome.
Masden, DL, Seruya, M, Higgins, JP. A systematic review of the outcomes of distal upper extremity bypass surgery with arterial and venous
conduits. J Hand Surg. 2012;37(11):2362-2367.
Hui-Chou, HG, McClinton, MA. Current options for treatment of hypothenar hammer syndrome. Hand Clin. 2015;31(1):53-62.
Piazza, G, Creager, MA. Thromboangiitis obliterans. Circulation. 2010;121(16):1858-1861.
Upton, J, Coombs, CJ, Mulliken, JB, Burrows, PE, Pap, S. Vascular malformations of the upper limb: a review of 270 patients. J Hand Surg.
1999;24(5):1019-1035.The authors review their 28-year experience in which they treated 270 patients with upper extremity vascular malformations.
They describe the frequency of each vascular malformation, treatment algorithms, and outcomes.
Van Geertruyden, J, Lorea, P, Goldschmidt, D, et al. Glomus tumours of the hand: a retrospective study of 51 cases. J Hand Surg Br.
1996;21(2):257-260.
Lee, J, Sinno, H, Tahiri, Y, Gilardino, MS. Treatment options for cutaneous pyogenic granulomas: a review. J Plast Reconstr Aesthet Surg.
2011;64(9):1216-1220.
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C H A P T E R 8 8
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Comprehensive Management of the Burned
Hand
C. Scott Hultman and Mohammed Asif
Key Points
Any patient with a hand burn injury meets criteria, as defined by the American Burn Association, for
transfer to a burn center, due to the overlapping and progressive goals of resuscitation, resurfacing,
rehabilitation, reconstruction, and recovery.
Resuscitation of the patient with hand burns includes establishing perfusion of the hand, including
escharotomy for circumferential burns and fasciotomy for compartment syndrome, operative
debridement of electrical burns, removal of the offending agent in chemical burns, topical and
possibly intravenous antibiotics for infection, and skeletal stabilization for fractures.
Resurfacing of the patient with hand burns involves tangential excision of partial-thickness injuries
and suprafascial excision of full-thickness injuries, followed by coverage with temporary dressings,
biologic matrices, xenograft, allograft, autograft, or vascularized tissues.
Rehabilitation of the patient with the burned hand requires early mobilization, splinting, scar
management, sensory reeducation, strengthening, and conditioning.
Reconstruction in the patient with a hand burn restores form and function, which may include the
following:
Release of dorsal/volar/web space contractures
Correction of intrinsic and extrinsic tightness
Nerve release and neuroma resection
Tendon, ligament, and joint revision
Thumb replacement
Revision of amputations
Identification and treatment of common hand disorders: trigger finger, tendon sheath and joint
ganglions, basilar arthritis, de Quervain tenosynovitis, and exacerbation of Dupuytren disease
Photothermolysis and fractional laser ablation of hypertrophic scars
Fat grafting for chronic pain and pruritus
Recovery of patients with a hand burn embraces the goals of return to work, school, and society, and
often includes a final capacity evaluation, vocational rehabilitation, and a final impairment rating.
The best outcomes after hand burn injuries occur through a coordinated, multidisciplinary approach
that not only combines elements of hand, plastic, and burn surgery but also critical care, nursing,
wound care, occupational therapy, chronic pain specialists, physical medicine, and rehabilitative
counseling.
Comprehensive management of the severely burned hand begins with initial damage control
interventions, proceeds through wound excision and coverage, enters a phase of rehabilitation and
reconstruction, and extends to the final period of recovery, with the goal of returning to work, school, and
social activity. The plastic surgeon leads a multidisciplinary and interprofessional approach that
incorporates elements of critical care, nursing, wound care, occupational therapy, acute and chronic pain
management, and physical medicine. Although the ultimate goal is to restore form and function, health
care providers must individualize treatment plans and listen to their patients, as they articulate their
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concerns and needs. The best outcomes are achieved through a combination of art and science, by
managing patient expectations, and by matching the needs of the patient with surgical solutions that are
reliable and available.
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Resuscitation
Just as patients with a large thermal injury (>20% total body surface area) must undergo formal
resuscitation with a combination of intravenous fluids, colloids, vasopressors, and inotropes, the patient
with a hand burn must receive critical care to maintain or restore perfusion and to avoid long-term
stiffness through early range of motion (ROM). Furthermore, hand burns must get appropriate wound
care to help prevent wound infection to avoid conversion of the burn to a deeper injury.
Obtaining a detailed history and physical examination creates a sound platform from which to make
short- and long-term decisions about management of the burned hand. Mechanism needs to be
established and can include the following types of injuries: scald, contact, flame, abrasion, electrical,
chemical, radiation, cold, and infiltration. The burn should also be classified by depth of injury, as this
impacts early care: partial thickness (which includes superficial, intermediate, and deep) and full
thickness (which can extend past the dermis and affect fat, fascia, muscle, and bone). In addition to noting
time since injury, the examination must include an assessment of the following:
Perfusion—including presence of pulse and Doppler signals, and capillary refill distally
Motor and sensory function
Location of the burns—arm, elbow, forearm, wrist, palm, dorsal hand, and digits
Distribution of the burns—circumferential or not
A damage control approach should be pursued to stabilize the acutely burned hand. 1 In addition to
optimizing the patient’s physiology, especially for large burns that cause global edema, the priority is
restoring adequate perfusion to meet the metabolic demands of the upper extremity. Escharotomies may
be carried out for circumferential deep partial-thickness and full-thickness burns, but the surgeon should
proceed directly to fasciotomies, especially if the patient has diminished or absent Doppler signals,
sensory changes, or clinical evidence of impending compartment syndrome. Key areas that must be
released include the carpal tunnel, Guyon canal, hypothenar and thenar muscle groups, interosseous
muscles accessed through the dorsal hand, the radial vessels in the distal forearm, the volar and dorsal
compartments of the forearm, the cubital tunnel at the elbow (Figure 88.1), and the brachial vessels in the
arm. Patients with electrical injury represent a special category because the pronator quadratus must also
be decompressed, deep to the flexor tendons of the distal volar forearm. 2 Furthermore, these patients
require multiple returns to the operating theater, as muscle necrosis is often progressive and must be
debrided at each session. Finally, damage to underlying structures should be addressed early and may
include debridement of clearly nonviable tissues, stabilization of fractures through open or closed
reduction with percutaneous pinning, repairing tendons if possible, and tagging disrupted nerves.
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FIGURE 88.1 This patient is a 29-year-old construction worker who sustained a 1200 V electrical injury, to the left elbow, with
an exit wound at the right shoulder. He presented with a dense left ulnar nerve palsy. At exploration, after excision of the burn
wound, the ulnar nerve was in continuity but had skip areas of coagulation, extending proximally and distally from the cubital
tunnel. The nerve underwent subfascial anterior transposition, with resection of the intermuscular septum. After complex
closure of the burn wound, the ulnar nerve regained a Tinel sign 1 to 2 months later and the patient developed modest intrinsic
motor function and protective sensation, 18 months after his injury.
Wound care remains of paramount importance to help prevent desiccation of the wound, conversion to a
deeper injury, and prevention of soft tissue infection. 3 In addition to elevation of the extremity, splinting
in an intrinsic plus position, and keeping the ambient temperature warm, the surgeon must use a wound
care algorithm that is consistent and incorporates depth of injury, time from injury, and location of injury,
to maintain maximum viability of the wound bed. Our approach to management is as follows:
First-degree burns (no disruption of epidermis): observation, moisturizing agent, mechanical
protection from shearing, sunblock
Second-degree burns, superficial partial thickness: topical bacitracin or mupirocin (if nasal swab is
positive for methicillin-resistant Staphylococcus aureus), covered with xeroform or Vaseline gauze,
consideration of early xenograft placement without the need for wound excision 4
Second-degree burns, indeterminate or intermediate: collagenase for 24 hours, followed by laser
Doppler imaging to determine burn wound perfusion: if adequate, the wound should heal by
secondary re-epithelialization; if not, the wound needs to be excised and autografted
Second-degree burns, deep partial thickness: silver sulfadiazine, early excision, and autografting
Third-degree burns, full thickness: silver sulfadiazine, early excision (<3 days after injury),
allografting and sulfamylon slurry, and autografting when the wound and the patient are both stable
Fourth-degree burns (involving fat, fascia, tendons, muscle, nerve, bone): immediate versus urgent
debridement (<12–24 hours after injury), possible amputation, sulfamylon/nystatin slurry, staged
allografting, consideration of vascularized coverage with regional flaps, distant flaps, or free tissue
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transfer 1
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Resurfacing
After initial stabilization of the acutely burned hand, timely wound excision and coverage should occur.
For patients with scald injuries, a cost-effective option, which improves pain control and decreases length
of stay, is superficial debridement of the wound with a soft scrub brush and xenografting, which permits
the wound to heal by secondary re-epithelialization. 3 Furthermore, patients can begin early, aggressive
ROM. For patients with deep partial-thickness injuries, preparation of the wound bed can be
accomplished with tangential excision, using a Weck blade or the VERSAJET (Smith and Nephew, UK).
Full-thickness injuries require full-thickness excision, often down to the level of the fascia. The authors do
not routinely use tourniquets for excision of hand burns because the surgeon must identify the level at
which the tissues exhibit fine, punctate, capillary bleeding. Once this level has been determined, with a
blood loss approaching 1 cc per 1 cm2 of excised tissue, the hand is wrapped with a compressive,
epinephrine-soaked gauze for hemostasis.
For burns that are superficial partial thickness, such as scald injury, early xenografting (<36 hours after
injury) permits rapid discharge from the hospital and more aggressive hand therapy. Although these
burns most likely heal by secondary re-epithelialization, xenografting should be strongly considered,
especially for children who may not tolerate dressing changes, for adolescents who are anxious to return
to their social peer groups, and for adults who need to return to work sooner rather than later. 3 For
patients who have deep partial-thickness or full-thickness injuries, the surgeon can proceed directly to
autografting if all nonviable tissue has been excised from a stable burn wound. In this case, sheet grafts at
a depth of 14/1000th of an inch are preferred to optimize long-term form and function. These grafts can be
immobilized by circumferential fine mesh gauze, bolsters, or negative pressure wound therapy—
whichever method permits safe, early mobilization by the occupational therapists. In addition, the digits
are grafted with the metacarpophalangeal joints in flexion and the distal interphalangeal joint (DIPJ) and
proximal interphalangeal joint (PIPJ) in extension, with an intrinsic plus splint protecting these fresh
grafts from shear and disruption. For patients who have an evolving burn wound or whose depth and
viability are uncertain at the time of excision, meshed allograft is indicated (Figure 88.2).
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FIGURE 88.2 This patient is a 56-year-old woman who developed a full-thickness burn injury from a dry cleaning press. She
underwent excision, staged closure with allograft, and split-thickness autografting. The patient did extremely well through hand
therapy and underwent web space releases and full-thickness skin grafting. She has nearly normal hand function, as rated by
her functional capacity evaluation, but she developed post-traumatic stress disorder and underwent vocational rehabilitation to
work in a different setting, as a cashier.
Patients with exposed vital structures, such as tendons, nerves, and bone, require either staged biologic
coverage or definitive coverage with vascularized tissue. Biologic options include not only xenograft or
allograft but also synthetic bilaminate skin substitutes—all of which will require autografting to achieve
final wound closure. However, vascularized tissue will be needed for patients who have exposed
hardware; open joints; tendon, nerve, or vascular repairs; or structures denuded of periosteum,
paratenon, or epineurium. The following flaps are reasonably reliable, depending on the zone of injury,
surface area requiring coverage, and technical expertise of the surgeon:
Local flaps: kite, flag, heterodigital, Moberg, dorsal metacarpal artery, cross-finger, fillet
Regional flaps: reverse radial or ulnar, adipofascial turnover (Figure 88.3), posterior interosseous
(Figure 88.4)
Distant random flaps: abdominal, infraclavicular
Distant pedicled flap: groin (Figure 88.5), lateral thoracic
Free flaps: rectus abdominis, anterolateral thigh, latissimus, serratus, omentum, and temporoparietal
fascia
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FIGURE 88.3 This patient is a 38-year-old assembly line manager who sustained a crush injury from an industrial press. He
underwent emergent debridement, with release of the carpal tunnel and Guyon canal. An adipofascial turnover flap was used to
cover exposed median and ulnar nerves, which was combined with negative pressure wound therapy, until the hand, wrist, and
forearm were skin grafted. The patient regained use of his flexor and extensor tendons, with good gliding, but most of his
intrinsic function did not recover.
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FIGURE 88.4 This patient is a 67-year-old woman with diabetes and rheumatoid arthritis, who had previously undergone
carpal tunnel release, who sustained a seizure and fell onto the door of an open stove, which had been heated to 425°F. She
underwent immediate extended carpal tunnel release for acute recurrent carpal tunnel syndrome, as well as excision of full-
thickness burns, volar forearm fasciotomy, and staged autografting. Ten months after her injury, she developed rapid decline of
her ulnar nerve function, with emergence of a Tinel sign over Guyon canal. She underwent excision of the hypertrophic scar at
the level of the wrist, release of the ulnar nerve, including the deep motor branch and digital branches, and coverage with a
posterior interosseous fasciocutaneous flap. Her sensation improved to be able to discriminate between light and deep touch,
with improved strength of her interosseous muscles.
FIGURE 88.5 This patient is a 23-year-old woman who sustained fourth-degree burn wounds, after getting her hand stuck in a
hair straightener, destroying the extensor mechanism distal to the proximal interphalangeal joints of her middle, ring, and little
fingers. After successful resurfacing of these digits with a thin groin flap, which was divided 3 weeks after coverage, she later
underwent syndactyly release and arthrodesis in three unstable distal interphalangeal joints with percutaneous compression
screws.
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Rehabilitation
Once the hand burn has been excised and resurfaced, the patient can actively focus on the rehabilitative
phase of healing, which involves restoring lost function and adapting to new challenges, which may
include amputation, loss of sensation, and altered hand mechanics. During this period, the scar
maturation will undergo several different phases to produce varying but significant degrees of stiffness,
pain, and pruritus.
Hand therapy should begin shortly after injury, in the form of splinting, edema management, and ROM
(active and passive), but after closure of the wound, the patient should become a more active participant.
Nightly splinting may be necessary to retain gains in ROM, although the patient will need to work
carefully with his or her therapist to further improve ROM. Both passive and active ROM exercises are
critical to deal with the incessant pull of wound contraction, at both superficial (skin) and deep (ligament
and tendon) locations in the hand. Strengthening and conditioning of intrinsic muscles, as well of flexors
and extensors also remains critical goals of the rehabilitative period. Established contractures can have
incremental gains in pliability, but ultimately surgical release may be necessary. However, as the scar
softens, through critical components of occupational therapy, the degree to which the patient would need
a release changes, allowing for less aggressive reconstructive efforts and the ability to achieve a more
functional endpoint.
Scar management, from the early to late phases of wound healing, remains the focus of rehabilitation. 5
Skin care includes use of a moisturizing agent, sunblock, massage, and lymphedema management. As
collagen matures and remodels, the previously burned hand can and should be treated with a variety of
techniques designed to improve the pliability of the skin, mobility of ligaments, and balancing of the
intrinsic and extrinsic tendons. Initially, successful edema management can yield impressive gains, as the
patient transitions from the use of compressive dressings to compression garments. Areas of early
hypertrophic scar formation can be treated through silicone sheeting. Paraffin application, fluidotherapy,
and directed ultrasound can all improve ROM and pliability of tissues. 5
By 6 months, patients may be candidates for laser remodeling of burned skin, grafted areas, and donor
sites. 6-8 The authors prefer to use two or three rounds of pulsed dye laser photothermolysis first,
targeting areas of persistent inflammation and increased vascularity of hypertrophic scars. The end points
are reduction of erythema, with improvement of symptoms such as pruritus and pain. Once the areas of
hypervascularity have been treated with pulsed dye laser, attention is then turned toward resurfacing
with fractional CO2 laser, targeting the thickness of the new scars, which have immature collagen.
Although significant improvements can be achieved after one session, several rounds can yield dramatic
gains in pliability. Because the fractional laser technology creates shallow and narrow channels within the
skin, ranging from 100 to 2000 microns in depth and 20 microns in width, pharmacologic agents can be
administered through vigorous massage, into these channels. Nearly all patients in our practice receive a
maximum of Kenalog 1 mg/kg topically, applied in the operating theater after laser resurfacing, using
semiocclusive dressings. Occupational therapy should begin immediately, although compression
garments should be restarted only after these channels close, within 6 to 24 hours.
During occupational therapy, which may last weeks to months to years, adequate pain management is
crucial to a successful outcome. Patients with preexisting substance abuse, large burns, narcotic
habituation, and on multiple analgesics should receive ongoing care from a chronic pain specialist, from
the fields of anesthesia, neurology, physiatry, or psychiatry, depending on the nature of the patient’s type
of pain. Premedication before therapy, as well as baseline control of symptoms, provides more
comprehensive and compliant participation with the hand therapist. The plastic surgeon treating these
patients does not need to have an exhaustive knowledge of potential pharmacologic agents, but the
surgeon should be comfortable prescribing a regimen that includes nonsteroidal anti-inflammatory
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drugs, gabapentinoids, antipruritics, anticonvulsants, anxiolytics, and antidepressants. Opioids are
tapered quickly, after wounds have closed, and used, sparingly, to premedicate prior to hand therapy
sessions.
The treatment of chronic pain, which may present in the form of pruritus, paresthesia, allodynia, and
dysesthesia, remains one of the most complex but important components to rehabilitation. In addition to
pharmacologic approaches, the authors have increasingly relied on laser surfacing to modulate
components of neuropathic pain, which may occur because of aberrant reinnervation of sensory nerves
with damaged or absent sensory receptors within the burned of grafted skin. 6-8 Once baseline symptoms
have improved through therapy, medication, and lasers, specific anatomic causes of pain may be
identified, ranging from nerve compression to neuroma formation. The plastic surgeon must carefully
reexamine patients during this period, as previously masked focal nerve pathology may become apparent
and can respond well to surgical solutions. For patients who still have neuropathic pain, but require
pharmacologic control, fat grafting can be considered as an adjunct and has had increasing success in our
practice. 9,10 The authors harvest fat from a distant site, perform minimal mechanical manipulation ex vivo,
take down adhesions through rigotomy, and inject volumes in increments of 0.05 to 0.10 cc in a radial,
fanning manner, through different port sites, between the overlying skin and underlying structures, such
as subcutaneous fat, fascia, or periosteum. Total volumes can range from 1 to 20 cc per region, although
higher volumes are necessary to address structural volumetric deficiencies, with take rates higher than
90%. The mechanism by which fat grafting of burn scars improves neuropathic pain is not known but
may include the following:
Mechanical cushioning effects between the scar and underlying structures
Disruption of aberrant innervation between sensory nerves and scar
Release of growth factors and other cytokines from stem cells present in the mesenchymal stromal
vascular fraction of adipose tissue
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Reconstruction
Even after receiving appropriate care through the resuscitation, resurfacing, and rehabilitation phases,
patients with hand burn injuries may still develop stigmata, deformities, and complications that require
reconstruction to restore form and function. A helpful algorithm to follow is to ask two basic questions:
What is the specific abnormality that the patient has identified?
What intervention can be used to correct that abnormality?
General principles that should be followed include the fact that most patients with hand burns have
deficient or abnormal tissue and benefit from the addition of tissues, through grafts, tissue
rearrangement, or vascularized tissue. Serial contiguous Z-plasties can lengthen focal scar bands by 30%
to 50%, and rhomboid-plasties (double opposing VY-plasties with double opposing YV-plasties) are
especially effective for lengthening broad scar bands at the base of the thumb, over the snuffbox, and
dorsal ulnar wrist. W-plasties do not add length to the original scar but can improve form, despite no
gains in function.
The most frequent abnormalities that may be encountered are exacerbation or emergence of common
hand conditions, such as ganglion of the joint or tendon sheath, basilar arthritis of the thumb
carpometacarpal joint, trigger finger, de Quervain tenosynovitis, and worsening of Dupuytren disease. In
general, normal incisions can be made through burn scars, to approach and correct these abnormalities,
provided that the surrounding tissue is not extensively undermined, and perforators from major vessels
are preserved when encountered. Wound healing may not be as robust as in unburned skin, so closure
often requires multiple layers, plus sutures that are left in place for 10 to 14 days. Burn-specific conditions
include volar and dorsal digital skin contractures, extrinsic and intrinsic digital tightness as determined
by the Bunnell test, acquired syndactyly of the web spaces, first web space adduction contractures, and
wrist contractures. Treatment involves release of the focal burn contracture, but also lysis of the scar
tissue from the underlying structures, which may be tethered and shortened. A good example is the first
web space reconstruction, which requires release of the transverse adduction contracture and tissue
rearrangement with a five-flap jumping man Z-plasty, through which the surgeon can perform
fasciotomies of the adductor pollicis and first dorsal interosseous muscles, neurolysis of digital nerves,
tenolysis and A1 pulley release as needed, and manipulation of the joints with capsular or volar plate
adhesions or contractures. Severe first web space contractures may even require placement of a full-
thickness skin graft and skeletal fixation of the thumb metacarpal in abduction, with Kirschner wires for 1
to 2 weeks. Patients with focal contractures of the second through fourth web spaces can undergo
STARplasty, a technique that permits transverse, longitudinal, and oblique release, and utilize a robust
local flap, with central blood supply, to correct the angle of inclination and resurface the web space. 11
Patients with hand burns may have specific needs for repair of nerve, joint, and tendon abnormalities,
due to the original injury or due to secondary effects of escharotomy/fasciotomy, excision, grafting, and
immobilization. Perhaps the most frequently encountered condition is focal neuropathic pain due to
anatomic compression or damage of underlying nerves and their branches. 12,13 Many patients will
present with sensory and motor impairment that can be localized to an anatomic distribution, which can
be diagnosed through careful physical examination that includes search for a Tinel sign at the point of
suspected pathology. In almost all cases, the surgeon can identify the location and extent of nerve injury,
if present. Nerve conduction studies, with electromyography, are only obtained if the patient’s history
and examination are not consistent, occult compression is suspected in another location, or if there are
medicolegal concerns or requirements for preauthorization. The authors have a broad experience with
nerve decompression of all nerves of the upper extremity, in the following order: median nerve at the
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carpal tunnel, ulnar nerve at Guyon canal, ulnar nerve at the cubital tunnel, antebrachial and dorsal
cutaneous nerves of the forearm, superficial radial nerve and median nerve at the elbow and in the
pronator tunnel, and anterior interosseous nerve. Increasingly, the authors have appreciated isolated
cutaneous neuromas that benefit from excision and subfascial or intramuscular transposition and
implantation. Finally, digital neurolysis is performed in almost all volar finger contractures to ensure
integrity of the digital nerves, but also to release these nerves from any point of tethering or constriction.
In addition to neurolysis, neuroma resection, and occasional nerve grafting, patients may have
underlying problems with tendons, ligaments, or bone that require reconstruction. Interventions that
should be considered, depending on the clinical situation, include tendon transfer for specific nerve
palsies, release of lateral bands for severe intrinsic tightness, repair of boutonniere deformities, extensor
tenolysis for severe extrinsic tightness, volar plate release or division of checkrein ligaments for joint
contractures, and capsulotomy or capsulodesis for joint pathology. For patients with unstable, painful
joints that do not respond to the above interventions, arthrodesis can be performed with a variety of
techniques, involving osteotomy and realignment of the joint, with compression from lag screws in the
DIPJ and figure-of-eight dental wire over buried Kirschner wires in the PIPJ.
Management of the abnormal fingertip, which may be painful and have unstable tissue, includes a variety
of techniques. For nail plate abnormalities, three approaches may be performed in isolation or
combination: 1) sterile matrix grafting after excision of nail plate scars, 2) release of skin proximal to
dorsal distal interphalangeal joint to help advance skin distally, and 3) harvest narrow skin flaps from the
lateral and medial sides of the nail, to cover deficient eponychial skin. Damage to the germinal matrix is
irreversible and, if symptomatic with nail fragmentation or splitting, is best treated with excision and/or
destruction of the germinal matrix itself, to effect nail plate ablation. Finally, many burn patients with
significant fingertip abnormalities may benefit from revision amputation that excises the nail apparatus
and distal phalanx remnant, with closure using a volarly based, innervated fillet flap over the distal
portion of the middle phalanx.
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Recovery
After completing all reconstructive efforts to optimize form and function of the burned hand, attention
turns toward final recovery. Depending on the goals of the patient, combined with his or her prior
vocational status, end points will vary considerably. At the very least, patients should work toward
activities of daily living that will enhance their quality of life, allow for more independence, and provide
a sense of competence that enhances self-worth and creates hope. 1,14 Specifically, patients should
transform back into people, capable of taking caring of personal hygiene, clothing and feeding
themselves, resuming activities that bring them joy, and reengaging with society through work and
school.
Toward that end, patients often undergo a functional capacity evaluation, especially as they prepare to
return to their previous job. These evaluations typically are quite extensive and measure the forces that
patients can safely pull, push, lift, and carry; the degree to which patients put forth a consistent effort;
their agility and balance; and finally, their conditioning and resistance to fatigue. Patients are then
assigned low, medium, or high demand work levels, as defined by federal labor standards, with specific
parameters recommended for their highest level of function. After receiving the results of the functional
capacity evaluation, the plastic surgeon must then decide if the patient can safely return to work and
determine limitations on work hours and restrictions on function. If employers do not have physical work
that the patients can handle, then the employee enters a phase of vocational rehabilitation, in which old
skills may be retaught or new skills must be learned.
For a patient who is cleared to work, the employee then begins a trial of work, typically for 3 months,
until he or she reaches a steady state of performance. At this point, once the patient’s physical condition
and function are stable, the patient undergoes a final impairment rating. Although each state may have
its own regulations regarding these assessments, most plastic/hand/burn surgeons use the American
Medical Association’s Guides to the Evaluation of Permanent Impairment. 15 We combine the rating criteria
from both the skin and upper extremity sections to generate a percentage of impairment for the hand. Of
note, these impairments can be extrapolated to impairment of the entire limb or even whole body, using
tables provided by the guide. A few caveats will help simplify what can be a complex and subjective
process in determining final ratings:
Digits: the thumb accounts for 40% of hand function, with the index and middle fingers contributing
20% each, the ring and little fingers contributing 10% each
Amputations: Loss of distal phalanges creates 45% impairment of the fingers and 50% impairment of
the thumb; amputation at the metacarpophalangeal joint results in 100% impairment of that digit;
complete loss of a hand yields 90% impairment of the upper extremity and 54% of the whole person
Nerve injuries: For the digits, total transverse sensory loss corresponds to 50% impairment of
function of that digit
Range of motion: Given the challenges posed by the reproducibility of goniometric measurements
(ROM is often not static, due to temperature, prior activity, and pain tolerance; and passive and
active ROM may be quite different), the author does not utilize ROM criteria to calculate final
impairment ratings
Condition of skin: Combining the signs and symptoms of the burn (which is considered a skin
disorder by the American medical association guides), with limitations on activities of daily living
and extent of treatment required to manage the skin disorder, the author can assign the patient a
category of impairment (Table 88.1) that helps to generate a final impairment rating. Most significant
burn scars require intermittent to constant treatment, which includes moisturizing agent, sunblock,
massage, compression, and mechanical protection
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TABLE 88.1
Criteria for Rating Permanent Impairment due to Skin Disorders
Class 1 (0%–9% Impairment)
Class 2 (10%–
24%
Impairment)
Class 3 (25%–
54%
Impairment)
Class 4 (55%–84%
Impairment)
Class 5 (85%–95%
Impairment)
Signs and symptoms present or
intermittently present
and
Signs and
symptoms
present or
intermittently
present
and
Signs and
symptoms
present or
intermittently
present
and
Signs and symptoms
constantly present
and
Signs and symptoms
constantly present
and
No or few limitations in performance of
activities of daily living (ADLs); exposure
to certain chemical or physical agents may
temporarily increase limitation
and
Limited
performance
of some
ADLs
and
Limited
performance
of many
ADLs
and
Limited performance of
many ADLs, including
intermittent confinement to
home or other domicile
and
Limited performance of most
ADLs, including occasional
to constant confinement
home or other domicile
and
Requires no or intermittent treatment
May require
intermittent
to constant
treatment
May require
intermittent
to constant
treatment
May require intermittent to
constant treatment
May require intermittent to
constant treatment
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Questions
1. A 36-year-old electrician sustains a full-thickness hand burn from a low voltage arc flash, with an
entry point over the volar aspect of the right thumb, which is insensate and has no active flexion at
the interphalangeal joint. What is the best plan for management?
a. Exploration of the forearm and decompression of the anterior interosseous nerve
b. Aggressive debridement of volar thumb, placement of integra, and wound vacuum-assisted
closure
c. Repair of the involved structures and coverage with an innervated kite flap
d. Complete amputation of thumb and pollicization of index finger
e. Partial amputation of thumb and toe-to-thumb free tissue transfer
2. A 24-year-old woman sustains circumferential, full-thickness wrist and forearm burns from a
propane explosion, after her long-sleeve blouse caught on fire. She has delayed capillary refill of all
digits and no Doppler signal in her palmar arch. What is the best option for restoring perfusion?
a. Dorsal forearm escharotomy
b. Volar forearm escharotomy
c. Volar forearm fasciotomy
d. Volar forearm fasciotomy with carpal tunnel release
e. Volar forearm fasciotomy with carpal tunnel and Guyon canal release
3. A 58-year-old petroleum engineer receives a hydrofluoric acid burn at work, to the dorsum of his
hand. Immediate irrigation with water is performed as part of his first aid. Upon arrival to the burn
center, he has a full-thickness burn that is painful. What agent should be administered to neutralize
the fluoride ion and limit deeper tissue necrosis?
a. Calcium gluconate
b. Calcium chloride
c. Potassium chloride
d. Potassium hydroxide
e. Ferrous sulfate
4. A 46-year-old presents with a boutonniere deformity of the middle finger, 8 months after
sustaining a deep burn to the dorsum of the finger requiring excision and skin grafting. What is the
primary mechanism for this sequelae?
a. Rupture of the extensor digitorum communis tendon
b. Contracture of the volar plate of the PIPJ
c. Displacement of the lateral bands volarly
d. Adhesions of the flexor digitorum profundus
e. Stenosing tenosynovitis of the A1 pulley
5. A 12-year-old girl, who previously underwent excision and grafting to the hand for a grease burn,
now has a first web space contracture, at the junction of the dorsal skin graft and the volar surface of
the thumb and index finger. What is the mathematical gain in length of the contracture with a single
two-flap Z-plasty, set at 45-degree angles?
a. 10%
b. 30%
c. 50%
d. 70%
e. 90%
1. Answer: c. Following debridement of devitalized tissue, the best opportunity for achieving
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maximal function is repair of the injured structures, such as the flexor pollicis longus tendon and
neurolysis versus nerve graft, which would require coverage of vascularized tissue. A kite flap, from
the dorsum of the index finger, is particularly attractive because this flap is innervated.
Decompression of the anterior interosseous nerve would not be indicated acutely, unless the patient
had an exit/entrance wound in this location. Amputation during the early management is too
aggressive, as the best long-term option is reconstruction of the current thumb, albeit injured.
2. Answer: e. Although escharotomies and fasciotomies of the forearm may improve perfusion to the
hand, the ulnar vessels in the Guyon canal should also be decompressed, which can be performed
through a carpal tunnel release. All attempts should be made to achieve a Doppler signal in the
palmar arch, as well as digital vessels, before the patient can leave the operating room.
3. Answer: a. Hydrofluoric acid burns yield progressive tissue damage, with saponification of fat and
liquefaction of fascia, due to interaction of the fluoride anions with calcium, magnesium, and
potassium cations. In fact, extensive hydrofluoric acid burns can result in QT prolongation,
hypotension, and ventricular arrhythmias. Calcium gluconate can help to neutralize the fluoride ion
and can be delivered topically, subcutaneously, or intravascularly, depending on the extent of injury.
4. Answer: c. Although the other options can occur in the burned hand, the most common cause of a
boutonniere deformity, with hyperextension of the DIPJ and flexion of the PIPJ, is disruption of the
central slip over the capsule of the dorsal PIPJ and displacement of the lateral bands from a dorsal to
volar position. This occurs because the dorsal skin over the PIPJ is very thin and the central slip is
often involved in the original injury. Options for reconstruction of a boutonniere deformity depend
on the quality of skin over the dorsal PIPJ but include plication of the lateral bands, a reverse tendon
flap to replace the missing central slip, and figure-of-eight tendon grafting to realign the lateral
bands.
5. Answer: c. Although the theoretical gain in length from a single 45-degree two-flap Z-plasty is
50%, in reality the gain is closer to 30%, due to decreased pliability of the previously injured volar
skin and the dorsal skin graft. To increase the actual gain, especially in this location, a 5-flap jumping
man Z-plasty is usually the best option for deepening and lengthening the web space. Critical to
achieving full release of this adduction contracture is performing fasciotomies on the adductor
pollicis and first dorsal interosseous muscles. The author also performs a digital neurolysis of the
ulnar digital nerve to the thumb and the radial digital nerve to the index finger, to ensure integrity of
the nerve and prevent any points of constriction or tethering.
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Acknowledgments
Dr Hultman thanks Damon Anagnos, MD, for his mentorship and inspiration for many of these cases.
His influence on Dr Hultman’s professional development is immeasurable and appreciated beyond what
words can communicate.
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References
Hultman, CS, Erfanian, K, Fraser, J, et al. Comprehensive management of hot-press hand injuries: long-term outcomes following
reconstruction and rehabilitation. Ann Plast Surg. 2010;64(5):553-558.In this retrospective review, which remains the largest series to date, we
analyzed the management and long-term outcomes of 56 patients with hot press hand injuries, which contain both a crush and thermal component.
Over a 15-year period, 86% of patients required initial operative intervention and 50% of patients underwent secondary reconstruction. Final
impairment rating was 22%, with 68% of patients returning to work, after a rehabilitative period of almost 18 months.
Kidd, M, Hultman, CS, van Aalst, J, et al. The contemporary management of electrical injuries: resuscitation, reconstruction, rehabilitation.
Ann Plast Surg. 2007;58:273-278.
Hultman, CS, van Duin, D, Sickbert-Bennett, E, et al. Systems-based practice in burn care: prevention, management, and economic impact of
healthcare-associated infections. Clin Plast Surg. 2017;44(4):935-942.In this retrospective cohort study of over 5000 patients admitted to a verified
burn center, from 2008 to 2012, we observed that the development of a multidrug resistant bacterial infection was associated with an increase in
mortality from 3% to 30%, an increase in length of stay from 12 to 94 days, and an increase in hospital charges from $57,000 to $325,000.
Diegidio, P, Hermiz, SJ, Ortiz-Pujols, S, et al. Even better than the real thing? Xenografting for pediatric patients with scald injury. Clin Plast
Surg. 2017;44(3):651-656.
Friedstat, JS, Hultman, CS. Hypertrophic scar management in burn patients: what does the evidence show? A systematic review of
randomized controlled trials. Ann Plast Surg. 2014;72(6):S198-S201.
Hultman, CS, Friedstat, JS, Edkins, RE, et al. Laser resurfacing and remodeling of hypertrophic burn scars: the results of a large, prospective,
before-after cohort study, with long-term follow-up. Ann Surg. 2014;260(3):519-529.In this prospective, before-after cohort study of 147 patients
who underwent laser resurfacing of hypertrophic burn scars, at a median of 16 months after injury, we demonstrated early response and lasting
improvement in pruritus, paresthesias, pain, erythema, thickness, and pliability. Management of hypertrophic burn scars continues to involve massage,
moisturizing agents, sunblock, silicone sheeting, and compression garments, but laser therapy should be strongly considered for patients who do not
improve by 6 months after burn injury.
Hultman, CS, Edkins, RE, Cairns, BA, Meyer, AA. Logistics of building a laser practice for the treatment of hypertrophic burn scars. Ann
Plast Surg. 2013;70:500-505.
Clayton, JL, Edkins, R, Cairns, BA, Hultman, CS. Incidence and management of adverse events after the use of laser therapies for the
treatment of hypertrophic burn scars. Ann Plast Surg. 2013;70:606-612.
Fredman, R, Edkins, RE, Hultman, CS. Fat grafting for chronic pain after severe burns. Ann Plast Surg. 2016;76(suppl 4):S298-S303.In this pilot
study of seven burn patients with refractory, neuropathic pain, we demonstrated the safety and efficacy of fat grafting in patients with hypertrophic
scars, who had previously undergone laser resurfacing. These patients demonstrated improvement by both patient reported outcome measures and their
ability to wean from their complex pharmacologic regimen, which included narcotics, NSAIDs, gabapentinoids, antipruritics, anxiolytics, and
antidepressants.
Fredman, R, Katz, AJ, Hultman, CS. Fat grafting for burn, traumatic, and surgical scars. Clin Plast Surg. 2017;44(4):781-791.
Hultman, CS, Teotia, S, Calvert, C, et al. STARplasty for reconstruction of the burned web space: introduction of an alternative technique for
the correction of dorsal neosyndactyly. Ann Plast Surg. 2005;54:281-287.
Rapolti, M, Wu, C, Schuth, OA, Hultman, CS. Under pressure: applying practice-based learning and improvement to the treatment of
chronic neuropathic pain in patients with burns. Clin Plast Surg. 2017;44(4):925-934.In this retrospective review of 223 symptomatic burn
patients, who underwent nerve decompression from 2000 to 2015, most patients reported moderate to definitive improvement in sensory symptoms and
motor function, with minimal morbidity, and a return to work rate that reached 65% by the end of the study period. Specific adaptations adopted by the
senior author include the use of WALANT (wide awake local anesthesia no tourniquet) surgery, in situ decompression over nerve transposition, and
increased resection of neuromas with subfascial implantation.
Wu, C, Calvert, CT, Cairns, BA, Hultman, CS. Lower extremity nerve decompression in burn patients. Ann Plast Surg. 2013;70:563-567.
Chudasama, S, Goverman, J, Donaldson, JH, et al. Does voltage predict return to work and neuropsychiatric sequellae following electrical
burn injury? Ann Plast Surg. 2010;64(5):522-525.In this retrospective review of 2548 patients admitted to a verified burn center from 2000 to 2005,
including 115 patients with electrical injury, we observed that even patients with low voltage injuries (<1000 V) still demonstrated significant
neuropsychiatric sequelae and may delay return to work, despite relatively low final impairment ratings.
Cocciarella, L , Anndersson, GBJ , eds. American Medical Association Guides to the Evaluation of Permanent Impairment. 5th ed. AMA Press; 2001.
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C H A P T E R 8 9
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Compartment Syndrome of the Upper Extremity
Guang Yang and Kevin C. Chung
Key Points
Compartment syndrome is a group of the clinical symptoms and signs that are caused by sustained
elevation of compartment pressure, and consequent circulatory impairment, tissue ischemia, and cell
necrosis.
Increased intracompartmental pressure due to increased compartmental content or decreased
compartmental size is the central factor of pathophysiology of compartment syndrome.
The diagnosis of compartment syndrome is primarily a clinical one based on careful history and
physical examination.
The standard clinical signs have been described as five Ps: pain out of proportion to the injury,
pallor, paresthesia, pulselessness, and paralysis.
Compartment pressure greater than 30 mm Hg or within 20 to 30 mm Hg of the diastolic blood
pressure is considered to be indication for fasciotomy.
Fasciotomy in a timely manner is the only management for compartment syndrome with good
outcome expected.
Some degree of permanent nerve and/or muscle function loss, and even Volkmann ischemic
contracture may happen because of the extent of primary tissue damage at the time of injury, other
comorbidities, or delayed management.
Compartment syndrome is a group of the clinical symptoms and signs that are caused by sustained
elevation of compartment pressure, and consequent circulatory impairment, tissue ischemia, and cell
necrosis. Good function of the affected upper extremity with only skin scarring is expected if
compartment syndrome is treated correctly and promptly. On the contrary, delays in diagnosis and
treatment will result in devastating complications, potentially limb or life threatening. It is critical for the
surgeons to understand the relevant anatomy, etiology, pathophysiology, diagnosis, and management
strategies of compartment syndrome.
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History
Dr. Richard von Volkmann first described the consequences of untreated forearm compartment
syndromes in 1881. 1,2 He and his coauthors emphasized that the cause of tissue ischemia was the
prolonged blocking of arterial inflow due to tight bandages. 2 In 1906, 
 O. Hildebrand commented that
occlusion of small arteries and vein congestion caused by the pressure of the surrounding tissue could
result in muscle necrosis. 3 Bardenheuer was the first to suggest fasciotomy as a preventive measure for
Volkmann ischemic contractures in the forearm. 4 Based on a series of animal experiments, Paul N. Jepson
further proposed that if the compartment underwent prompt surgical decompression, the patient would
recover. 5 In 1940, Griffiths found that not only arterial injury but also reflex spasms of the collateral
circulation caused the ischemic contracture. 6 Clinical manifestations including pain with passive stretch,
painless onset, pallor, and pulselessness were first described by him to contribute to the diagnosis of a
forearm compartment syndrome. In 1948, Bunnell and Doherty described their clinical findings of hand
compartment syndrome. 7 In the 1970s and 1980s, a set of theories for compartment syndrome
pathophysiology were proposed, and the concepts of compartment syndrome, Volkmann ischemic
contracture, and crush syndrome were unified and generally accepted in the surgical field. 8
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Epidemiology
Although compartment syndrome can occur in any closed space in the body, it mostly occurs within
fibro-osseous space in the upper and lower extremities. The most common site is the lower leg, followed
by the forearm and hand. 9 Upper arm compartment syndrome is rare, with few reported cases. 10
The true incidence of compartment syndrome of the upper extremities is difficult to identify because a
variety of injuries may lead to this syndrome. The incidence of acute compartment syndrome was
estimated by McQueen at 7.3 per 100,000 for men and 0.7 per 100,000 for women by collecting the data of
an orthopedic trauma unit from 1988 to 1995. 11 In another report from Zuchelli, 2.5% of 3274 adults who
had suffered a blunt trauma injury to an extremity and seen at a level I trauma center were diagnosed
with compartment syndrome. 9 Branco reported approximately 1% patients who required a fasciotomy
after extremity trauma out of 10,315 patients, of which about one-fifth received upper extremity
fasciotomies. 12 Young men are at great risk for development of a compartment syndrome. 11–14 In
McQueen’s report, 91% of the patients were men in their thirties. 11 Besides being more likely to sustain
high-energy injuries, the author suggested that less space for muscle swelling of the muscle after injury
led to the higher incidence of acute compartment syndrome in young men.
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Relevant Anatomy
As the name implies, compartment syndrome occurs in the compartment, which is a closed space
constructed by the skin or connective tissues, and bones. Knowledge of the components and contents of
each compartment in the upper extremity is essential to comprehend the etiology, clinical signs, and
treatment of compartment syndrome (Table 89.1).
TABLE 89.1
The Constitutes and Contents of Each Compartment in the Upper Extremity
Anatomical
Boundaries
Compartments
Contents
Muscles
Nerves
Artery
Arm
Skin, fascia, lateral
and medial
intermuscular septae,
and humerus
Anterior
Biceps, brachialis, coracobrachialis
Musculocutaneous
and median nerves
Brachial
artery
Posterior
Triceps
Radial
nerve and
ulnar
nerves
Profunda brachii artery
Forearm
Skin, fascial, three
intermuscular
septum, radius, ulna,
and interosseous
membrane
Volar
Superficial
Pronator teres, flexor carpi radialis,
palmaris longus, flexor digitorum
superficialis, flexor carpi ulnaris
Median, ulnar, and
anterior
interosseous
nerves
Radial and
ulnar
arteries
Deep
Flexor pollicis longus, flexor digitorum
profundus, pronator quadratus
Dorsal
Extensor digitorum communis, extensor
digiti minimi, extensor carpi ulnaris,
abductor pollicis longus, extensor pollicis
brevis, extensor pollicis longus, extensor
indicis proprius, supinator
Posterior
interosseous nerve
Posterior
interosseous
artery
Lateral (Mobile
wad)
Brachioradialis, extensor carpi radialis
longus, extensor carpi radialis brevis
Sensory branch of
the radial nerve
–
Hand
Palmar aponeurosis,
thenar fascia,
hypothenar fascia,
and metacarpals
Thenar
Abductor pollicis brevis, flexor pollicis
brevis, and opponens pollicis
Recurrent motor
branch of median
nerve
Digital
arteries of
the thumb
Adductor pollicis
Adductor pollicis
Deep branch of
ulnar nerve
–
Dorsal interossei (4)
Dorsal interosseous muscles
–
–
Volar interossei (3)
Volar interosseous muscles
–
–
Hypothenar
Abductor digiti minimi, the flexor digiti
minimi, and the opponens digiti minimi
Ulnar nerve
–
Finger
Cleland’s and
Grayson’s ligaments,
and phalanx
–
–
Digital nerves
Digital
arteries
The upper arm consists of two compartments around the humerus: the anterior and posterior
compartments (Figure 89.1). They are divided by the lateral and medial intermuscular septae. The
musculocutaneous nerve and median nerves run through the anterior compartment. The ulnar and radial
nerves travel in one compartment first, and then pass through the intermuscular septum into another
compartment at the level of distal third of the arm. Velmahos believed this is why symptoms of radial or
ulnar nerve ischemia are not compartment specific. 15
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FIGURE 89.1 Cross-sectional anatomy showing two compartments of the upper arm.
The forearm has three major compartments, and the radius, ulna, and rigid interosseous membrane
constitute the stiff floor of the compartments. Volar, dorsal, and lateral (mobile wad) compartments are
divided by three intermuscular septae, and there are some communications among them. The muscles in
the volar compartments are usually divided into superficial and deep groups (Figure 89.2). The deep
volar muscles are usually the most severely affected in forearm compartment syndrome, because they are
close to the stiff floor of the compartment. The median nerve runs between the superficial and deep
muscles and ends at the carpal tunnel. The median nerve is the most commonly affected nerve in forearm
compartment syndrome. Its motor branch, the anterior interosseous nerve (AIN), goes deeper to
innervate the deep volar muscles including the pronator quadratus, the flexor digitorum profundus I and
II, and the flexor pollicis longus. The AIN and the deepest portion of the flexor muscles are severely
damaged when compartment syndrome involves the deep volar compartment.
FIGURE 89.2 Cross-sectional anatomy showing three compartments of the forearm.
The dorsal compartment contains the wrist and finger extensors, and the motor branch of the radial nerve
(posterior interosseous nerve) that travels obliquely through and into the supinator muscle. The posterior
interosseous nerve (PIN) then lies in a plane between the superficial and deep extensor muscles. In the
distal forearm, the PIN lies on the interosseous membrane. The lateral compartment, also known as the
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mobile wad, is separated by a connective tissue septum from the dorsal compartment. It is composed of
brachioradialis, extensor carpi radialis longus, and extensor carpi radialis brevis muscles. The dorsal and
lateral forearm compartments are usually affected along with volar forearm compartment syndrome, but
also may develop isolated compartment syndrome.
There are at least 10 compartments in the hand that are usually divided into five groups: thenar,
hypothenar, adductor pollicis, palmar, and dorsal interosseous (Figure 89.3). Because of anatomic
variations, these compartments may have two or more discrete subcompartments. The thenar,
hypothenar, adductor pollicis, and interosseous compartments contain 14 intrinsic muscles of hand.
Although the finger has no muscle, compartment syndrome can still occur in the finger. The
compartments of the finger are considered to be bounded by skin, and Cleland and Grayson ligaments.
FIGURE 89.3 Cross-sectional anatomy showing 10 compartments of the hand.
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Pathophysiology
The pathophysiology of compartment syndrome is a multifactor process. Elevated intracompartmental
tissue pressure in the myofascial compartment after injury is the central pathogenic factor. 8 Inadequate
tissue perfusion within the compartment is the foundation, and progressive cell death is the final result of
compartment syndrome.
Because the compartment is an enveloped space with limited elasticity, the intracompartmental pressure
elevates because of increased compartmental content or decreased compartmental size after injury.
Decreased arteriovenous gradient, declined arteriolar flow, and venous collapse result in decreased tissue
perfusion within the affected compartment. The low tissue perfusion reduces the aerobic metabolism at
the cellular level. As insufficient oxygen concentration decreases beyond the cell’s intrinsic capacity to
tolerate, toxic chemicals impinge the cellular membrane’s function. The leak of the cellular membrane,
especially the endothelium of a capillary, results in increased capillary permeability, causing the
intravascular fluid to move into the interstitial space, and thus tissue edema develops. The increased
compartment contents further deteriorate the tissues ischemia, which brings the pathological damage into
a positive feedback loop (Figure 89.4). Without intracompartmental pressure relief, cell death presenting
as muscular and neural fibrosis occurs.
FIGURE 89.4 Compartment syndrome pathophysiology.
Different tissues have different capacities to tolerate ischemia, and the clinical symptoms can arise
simultaneously or following the initial trauma. 16 Skeletal muscle can tolerate up to 4 hours of ischemia,
and can recover partially after 6 hours, but incurs permanent damage after 8 hours. Peripheral nerves are
more sensitive to an ischemic change. Nerve conduction function is affected after 1 hour of ischemia, and
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peripheral nerves may undergo irreversible damage after 4 to 6 hours of ischemia. 17,18 Outcomes are
determined by the extent of the damage and the level of the compartmental pressure. Volkmann ischemic
contracture is used to term the final result of tissue ischemia following compartment syndrome, which is
characterized by varying degrees of muscle fibrosis and neurologic deficiency. A severe local
compartment syndrome can also arise the systemic manifestations, which is called crush syndrome.
Rapid return of toxic muscle products into the circulatory system may lead to renal failure, cardiac
failure, respiratory failure, and intravascular coagulation. 19
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Etiology
Theoretically, any factors that lead to increased compartmental pressure may account for compartment
syndrome. Injuries that commonly cause compartment syndrome are categorized and listed in Table 89.2.
TABLE 89.2
The Etiologies of the Compartment Syndrome
Category
Examples
Fracture
Radius fracture, ulna fracture, both-bone forearm fractures, pediatric supracondylar humerus
fracture, multiple metacarpal fractures
Vascular injury
Major vascular stab or rupture, ischemia-reperfusion after replantation or vascular repair, artery
blood sampling
Crush injury
Closed blunt trauma, extremity crush resulting from coma or seizure
Iatrogenic compression
Tight dressing, splint or cast, constrictive bandages, tourniquet overuse, prolonged limb positioning,
tight wound closure
Drugs or fluids extravasation and
input
High pressure injection injury, drugs or contrast medium extravasation, peripheral parenteral
nutrition extravasation
Burns
Electrical injury, thermal injury
Bleeding disorder and
anticoagulation therapy
Hemophilia, heparin use
Infection
Tenosynovitis of the finger
Muscle overuse
Exercise, weight lifting
Others
Crotalid envenomation
Fractures are the most common cause for compartment syndrome in the extremities. 11,13,14 Fractured
bones result in muscle injuries and hematoma formation may increase compartment contents. 20 The
displaced bones can cause vascular injury. This is most commonly seen in pediatric supracondylar
humerus fractures. 21 Multiple closed reduction attempts may make this worse. Open fractures do not
necessarily prevent compartment syndrome because the wounds may not open the compartment
completely. According to Branco’s report, patients with open fractures had a higher incidence of
fasciotomy than those with closed fractures. 12 Radius and/or ulna fractures were the most common cause
of forearm compartment syndrome, followed by supracondylar fractures. 14 Hand compartment
syndrome can be caused by multiple metacarpal fractures.
Vascular injury with subsequent reperfusion injury is another common cause of compartment syndrome.
22 Continuous bleeding from major arteries into a confined space can quickly lead to increased
compartment pressure. 23 In addition, direct arterial injury leads to local tissue ischemic edema. 24 A delay
in revascularization can aggravate ischemic edema that expands the compartment contents.
It is understandable that crush injury is one cause for the extremity compartment syndrome. 25 Iatrogenic
compression, such as prolonged limb positioning, tight dressing or cast, and tourniquet overuse can also
be responsible for a compartment syndrome. Surgeons should be aware that the ischemic condition after
intramuscular perforator harvest may decrease pressure tolerance of the compartmental tissue. 26
Except for a traumatic vascular stab injury or rupture, bleeding or inflowing into compartment from a
high-pressure injection or iatrogenic fluid extravasation can also increase compartment pressure. 27–30
Thus, the patients who have a bleeding disorder or receive anticoagulation therapy have a higher risk for
developing compartment syndrome. 10 Crotalid envenomation, infection, electrical injuries, and burns
have also been considered to cause a cascade of events that leads to the rapid formation of vascular
permeability and interstitial edema. 31 Rarer etiologies of compartment syndrome include muscle overuse,
rhabdomyolysis, and systemic sclerosis.
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Diagnosis
The diagnosis of compartment syndrome is primarily clinical, and based on patient history, symptoms,
and signs. Documenting the patient’s history of any injuries that may increase compartment contents or
decrease compartment volume is critical to identify compartment syndrome, which may be the only basis
of the diagnosis and fasciotomy, for instance preventive fasciotomies after limb replantation.
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Clinical Signs
The reliable physical sign is usually swelling or tightness in the extremity. The affected hand, forearm, or
arm is hard to palpation, skin creases vanish, and overlying skin may become shiny and even develop
blister (Figure 89.5). The fingers are often placed in flexion position in a forearm compartment syndrome,
and in the intrinsic minus position in a hand compartment syndrome.
FIGURE 89.5 A. Acute forearm compartment syndrome in a patient who suffered a crush injury. B. Acute hand compartment
syndrome in a patient presenting swollen appearance.
The symptoms and signs of the compartment syndrome have been classically described as 5Ps: pain,
paresthesia, paralysis, pallor, and pulselessness (Table 89.3). These nonspecific findings can be disclosed
in the primary injury and can present from the first few hours after injury, to after the repair, or may not
present at all. All five Ps are more commonly seen in a primary vascular injury rather than compartment
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syndrome. 32
TABLE 89.3
Clinical Signs in the Compartment Syndrome
Signs
Descriptions
Swelling
Reliable and nearly presented in all the patients
Pain
Severe and out of proportion to primary injury
Worse as passive stretching of the compartmental muscles
Early and sensitive finding
Subjective, and difficult assess in children
Paresthesia
Indicates nerve ischemia in the affected compartment
Early sign
Very low sensitivity but high specificity
Paralysis
Often indicates the compartment syndrome in an irreversible stage
Pallor and Pulselessness
Late symptom
Often exists with vascular injury
May not presented in a compartment syndrome
Pain is the early and sensitive finding before onset of ischemia, but it should be distinguished from the
primary injury pain. The pain from high compartment pressure is usually out of proportion to the nature
of the injury, especially on passive stretching of the compartment contents. For example, in the volar
forearm compartment syndrome, the pain is often introduced by passive extension of the fingers and
wrist, which increases the compartment pressure. Similarly, the pain on passive palmar abduction of the
thumb, thus stretching the abductor pollicis brevis, is associated with a thenar compartment syndrome.
Progressive pain often indicates increasing compartment pressure.
Paresthesia is another early sign, especially when a sensory nerve travels in the affected compartment.
For example, in a patient with the volar forearm compartment syndrome, the thumb and index finger that
are innervated by the median nerve may experience sensory changes.
Pallor and pulselessness are often present later and may not be confirmed even after irreversible tissue
damage occurs. 33 Paralysis often suggests that the muscles in the affected compartment have undergone
irreversible damage, which indicates that the compartment syndrome has reached the final stage. 34
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Compartment Pressure Measurement
When subjective physical examinations are not reliable or taking a history is not possible, the objective
examination of compartment syndrome is to measure the intracompartmental pressure. Although normal
intracompartmental pressures range dramatically, a pressure greater than 30 mm Hg is an indication for
an urgent fasciotomy. 35–37 Additionally, a pressure difference within 20 to 30 mm Hg of the patient’s
diastolic blood pressure is an indication for compartment syndrome as well. 38,39
Many measurement methods for compartment pressure have been described in the literature. 34,40,41 In
1975, Whiteside and colleagues proposed an apparatus for compartment pressure measurement. 35 After
the needle is inserted into the compartment and stopcock is turned on, the compartment pressure is read
on the manometer when the saline column moves by slowly depressing the plunger of the syringe.
Currently, Whiteside’s and other simply devices have been replaced by more convenient commercial
monitor systems. Of them, the Stryker compartment pressure monitor system is the most commonly used
in North America. It is easily accessible and found to be quite accurate if used properly. 42,43 The Stryker
system involves the use of a side-ported noncoring needle, a syringe prefilled with 0.9% saline, and a
digital pressure manometer with a display (Figure 89.6). To be measured, the compartment should be
placed at the level of the heart. The site of the inserted needle is usually at the maximum swelling of each
compartment. The needle is inserted perpendicular to the skin into the compartment space with a local
anesthesia if necessary. At a proper needle depth, the pressure reading will increase when the affected
compartment is compressed externally. 39
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FIGURE 89.6 The Stryker intracompartmental pressure monitor system. A. The components of system. B. The steps of using
Stryker device.
Doppler ultrasound and radiography imaging have been used to evaluate the primary injury and identify
the amount of tissue edema, but not helpful for diagnosis of compartment syndrome.
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Chronic Compartment Syndrome
Chronic compartment syndrome is characterized by exercise-induced and rest-relieved pain, and it rarely
happens in the upper limbs. 44,45 The pain is associated with moderately elevated compartment pressures
due to muscular hypertrophy. Neurological symptoms such as tingling and hand numbness were found
in some cases. 44 Negative findings of physical examination at rest can rule out other differential
diagnoses including nerve compression syndrome, vascular claudication, and fascial herniation. Dynamic
compartment pressure measurement is helpful to diagnose chronic compartment syndrome of the
forearm. 44
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Treatment
If compartment syndrome is suspected, any external pressure including cast, bandage, or sutures should
be immediately removed. The limb should be elevated at the level of the heart but not above this level. 46
When compartment syndrome is diagnosed, emergency fasciotomy is the only management with good
expected outcomes.
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Fasciotomy
Although subcutaneous and endoscopic-assisted fasciotomies have been reported, the traditional open
technique remains the preferred method. There are several classic surgical approaches for upper
extremity compartment syndrome. When the incision is designed, primary injury repair or late
reconstruction should be considered. If there is an initial wound, the incision for compartment release
will be carefully designed to avoid flap necrosis in the elevated flap. In cases of fracture, the incision must
be considered to expose the underlying fracture for reduction and fixation. Fasciotomy procedures
include not only dividing the skin and fascia to release the compartmental muscles and nerves, but also
identifying and excising of nonviable muscles.
Upper arm fasciotomy is often performed via a medial incision and a lateral incision (Figure 89.7). The
two incisions are used through the subcutaneous tissues and fascia to decompress the anterior and
posterior compartments.
FIGURE 89.7 The incision design for the upper arm fasciotomy.
For the volar forearm compartment release, a wide extensile exposure starting at the medial epicondyle
and extending to 
 the proximal wrist crease is usually performed for fasciotomy 
 (Figure 89.8). The
incision must be made with adequate curving to avoid distal flexor tendons and median nerve exposure.
Otherwise, these exposed deep tissues need a complex flap procedure rather than skin graft coverage.
After the subcutaneous flap is elevated, careful inspection is carried out through the space between the
flexor carpi ulnaris and flexor digitorum superficialis to decompress the median nerve and deep group of
flexor muscles. The median nerve in the carpal tunnel is susceptible to compressive pressures so that
carpal tunnel decompression is often performed with forearm or hand fasciotomy.
FIGURE 89.8 The incision design for forearm fasciotomy of the volar (A) and dorsal (B) compartments.
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If the pressure in the dorsal compartment does not decrease after volar compartment decompression, a
dorsal compartment fasciotomy is indicated. For dorsal forearm compartment syndrome, a longitudinal
incision is designed on the line between the distal radioulnar joint and the lateral epicondyle (see Figure
89.8). Usually, the incision is limited to the middle half of the forearm to avoid exposing the distal
extensor tendons. The fascia is then divided and approached between the extensor digitorum communis
and extensor carpi radialis brevis. The mobile wad can be released via the same incision by mobilization
of the incision site.
Two longitudinal incisions are recommended by the authors to release the forearm compartment. One is
along the ulnar edge of the radius over the flexor muscles, and the other is along the ulnar edge of the
ulna over the extensor muscles. These two incisions are done above the muscle belly without the danger
to expose the tendon.
Although there are more than 10 compartments in the hand, it is unnecessary to approach all the
compartments. Except carpal tunnel release, hand compartments are usually released by four incisions
(Figure 89.9). The dorsal two incisions parallel and radial to the second metacarpal and fourth metacarpal
are made to access interossei and adductor compartments by either side of the bones (Figure 89.10). The
standard approach for the thenar compartment requires a longitudinal incision along the radial aspect of
the thenar eminence between the glabrous and nonglabrous skin. The standard approach for the
hypothenar compartment is via a longitudinal incision along the ulnar aspect of the hypothenar
eminence.
FIGURE 89.9 Volar and dorsal incisions for hand compartment releases.
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FIGURE 89.10 Interossei and adductor compartments are released by two dorsal incisions parallel and radial to the second
metacarpal and fourth metacarpal.
Finger decompression is performed with a midaxial lateral incision along the noncontact side of the
finger to release the Cleland and Grayson ligaments (Figure 89.11). The dissection is carried out
superficial to the flexor sheath carefully to avoid any injury to the neurovascular bundles.
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FIGURE 89.11 Incision design for digital compartment release.
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Postoperative Management
After fasciotomy, the incisions are left open to avoid recompression of the compartments due to muscular
tissue edema. 36 However, the incision for carpal tunnel release is closed directly. 39 Usually, a couple of
tacking sutures are used to approximate the skin over the wounds. The open wounds are covered by a
bulky moist dressing, which requires regular dressing changes postoperatively. A vacuum-assisted
closure system can also be used to cover the wound. A systematic review conducted by Jauregui et al
found that vacuum-assisted closure could reduce the relative complications including wound edge
necrosis, infection, and neurologic deficit. 25 The limb is then placed in a functional position by a
removable splint with close observation after fasciotomy. Additional debridement may be performed for
muscle necrosis and infection. Delayed primary closure or skin grafting to the open area is performed
depending on the wound tension, which often requires 7 to 10 days. Early physical and occupational
therapy exercises are helpful to prevent joint stiffness.
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Outcomes
The outcomes and complications of compartment syndrome mostly depend on primary injury severity
and time from diagnosis to fasciotomy. 14 Only if fasciotomy is performed before irreversible cell death
occurs (within 4 to 6 hours of compartment syndrome onset), the patient may regain full function and
sensation from the compartment syndrome. Duckworth et al reported 90 patients who underwent
fasciotomy for an acute forearm compartment syndrome. 14 Twenty-nine patients (32%) had complication
associated with acute compartment syndrome. The patients who accepted fasciotomy more than 6 hours
after presentation were more likely to develop complications, and the rate of complications increased
with the time to fasciotomy. Ouellette and Kelly followed 17 patients with hand compartment syndrome
at an average of 21-month follow-up period after fasciotomy. 47 Thirteen patients resumed almost normal
hand function. Four patients whose primary injury or illness masked the compartment syndrome had
poor results.
Neurological deficit is the most common complication of the forearm compartment syndrome. 14,25 Other
complications including infection, muscle necrosis, chronic pain, fracture nonunion, and even Volkmann
ischemic contracture may happen because of the extent of direct trauma or delayed management. 14,25 The
patients with Volkmann ischemia contracture present with muscle contracture deformities and nerve
dysfunctions (Figure 89.12). Function reconstruction strategy for these patients depends on the extent of
the muscular necrosis and nerve damage.
FIGURE 89.12 The patient with forearm Volkmann ischemic contracture presents as forearm pronation, wrist flexion, thumb
adduction, MCP joints in extension, and IP joints in flexion.
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Questions
1. Which of the following is the most common cause of a forearm compartment syndrome in
children?
a. Vascular injury
b. Crush injury
c. Burn
d. Fracture
e. Snake bite
2. Which of the following is the central pathogenic factor of compartment syndrome?
a. Inadequate tissue perfusion
b. Increased compartment content
c. Cell death
d. Increased capillary permeability
e. Increased intracompartmental pressure
3. A 28-year-old man has an ulna-radius fracture after a car crash. The fractures are reduced and
placed in a splint in the emergency room. What is considered the most important sign or symptom of
a compartment syndrome of the forearm?
a. Pain out of proportion to the primary injury
b. Numbness in the hand
c. Loss of the movement of the fingers
d. Decreased pulses
e. Pallor appearance of the hand
4. A 65-year-old man involves in a traffic incident. He had slipped into a coma by the time he
reached emergency department. On physical exam, the right hand is severely swollen and feels firm.
Which of the following is the most appropriate method to diagnose a compartment syndrome for
this patient?
a. Doppler ultrasound
b. CT scan
c. Intracompartmental pressure measure
d. X-ray
e. Magnetic resonance image
5. A young man, previously healthy, presents for evaluation of a painful and swollen left forearm
approximately 3 hours after a crush injury. He complained that he did not have significant 10/10 pain
until 40 minutes earlier. Physical exam reveals pain with extension of his fingers. Radial pulses are
present and the skin color is normal. Radiographs demonstrate fracture of the distal radius. As a
compartment syndrome is suspected, intracompartmental pressure is measured by the Stryker
compartment pressure device. The pressure of the volar forearm compartment is 42 mm Hg. Which
of following should be the next step?
a. Admission for observation and pain control
b. Open reduction and fixation of the fracture
c. Percutaneous pinning of the fracture
d. Fasciotomy
e. Physical and occupational therapy
1. Answer: d. Any factors that can elevate intracompartmental pressure by increasing compartment
content or decreasing compartment size may lead to compartment syndrome. Fracture is the most
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