This document discusses the evaluation and treatment of mangled upper extremity injuries. Key points: - Mangled injuries involve multiple critical structures like skin, vessels, nerves, muscles and bones. They often lead to significant disability. - Goals of treatment are to preserve life, tissue, function and reconstruct the extremity and patient. - A thorough initial evaluation assesses all functional systems including vascular, nerve, muscle and skeletal integrity. - Treatment involves aggressive debridement, skeletal stabilization, tendon and nerve repair, vascular reconstruction and soft tissue coverage. - Secondary procedures and rehabilitation are important to optimize function.

1. MANGLED AND
BURNED HAND
HAND AND MICROVASCULAR SURGERY UNIT

2. MANGLED UPPER EXTREMITY
• Devastating injuries that involve multiple critical structures of the fingers, hand,
arms, or any combination of the three and nearly always lead to significant
disability, both directly and through their psychosocial impact
• Generally include all or nearly all of the major functional systems of an extremity,
including skin and soft tissue, vascular, nerve, muscle and tendon, bone, and joint
• One wound-one scar – Peacock, et al.

3. GOALS IN TREATING UPPER EXTREMITY MANGLING
INJURIES
• Preserve life
• Preserve tissue
• Preserve function
• Reconstruct and restore function of both the extremity and the patient

4. FACTORS NECESSARY TO OPTIMIZE ULTIMATE
FUNCTION
• Careful and complete evaluation of the injury in which all functional systems are
addressed
• Formulation of a comprehensive reconstructive plan tailored to the patient’s needs
• Thorough but careful wound debridement of all devitalized tissue
• Meticulous operative reconstruction, often including secondary procedures
• Restoration of good vascularity
• Rigid skeletal fixation while minimizing additional soft tissue injury
• Stable, vascularized soft tissue coverage
• Comprehensive rehabilitation of the extremity and the patient

5. INDEX CASE
CC: left hand wound
NOI: industrial injury
TOI: 2PM
POI: Valenzuela
DOI: 8/9/22
Few hours PTC, patient’s left hand
was crushed by the platform of a
forklift

6. INDEX CASE
Initial Physical Examination:
Stable vital signs
(+) avulsed wound, flexor zone 4 area of left
hand
(+) degloved skin, extensor zone 6 area of left
hand
Able to flex DIPJ and PIPJ of all fingers and IPJ
of thumb, left
Able to extend IPJ of left thumb
Unable to extend MCPJ of all fingers
Intact 2PD at 2mm, left thumb, IF and MF
Unappreciable 2PD, left RF and SF but able to
sense light touch
Capillary refill time >2 sec
Full and equal pulses, radial and ulnar a.

7. 8/9/22

8. CLASSIFICATION
• Mangled Extremity Severity Score (MESS)
• Intended for use in the lower extremity
• Upper extremity not a weight bearing extremity
• MESS score >7 can often be salvaged and be somewhat useful
• Hand Injury Severity Score (HISS)
• Utility in predicting time lost from work
• Not helpful in predicting amputation

9. Index Case

10. Index Case

11. MECHANISMS AND PATHOPHYSIOLOGY OF INJURY
• Industrial and agricultural machinery, motor vehicles, power tools, explosives, and
firearm mechanisms
• Most involve some component of crushing injury
• Crush and blast injuries has worse outcomes compared to sharp injuries
• Crush injuries – immediate and delayed tissue necrosis – increased risk for
infection – compromising reconstructive plan
• Degloving or avulsion injuries involve amputation or partial amputation of one or
more critical tissue layers: skin, vessel, nerve, tendon, bone

12. MECHANISMS AND PATHOPHYSIOLOGY OF INJURY
• Tissue devascularization: constant element
• Crushing, avulsion, degloving or blast injuries
• Disrupt major or branching vessels
• Produce endothelial injury
• Nerve often last structure damaged in crush injuries
• Dilemma distinguishing neuropraxia from axonotmesis in early stages
• Tendon, ligament and bone more resistant to crushing/avulsing injuries

13. MECHANISMS AND PATHOPHYSIOLOGY OF INJURY:
METABOLIC CHANGES
• Ischemic tissue undergoes conversion to anaerobic metabolism
• Rapid depletion of oxygen, glucose and ATP
• Increase in CO2 and LA
• Increase in superoxide radicals – trigger local acute inflammation, adherence and accumulation of
leukocytes and endothelial njury
• Reperfusion/Reoxygenation
• Superoxide and hydroxyl radicals produced
• Tissue injury via 2 key mechanisms: direct reaction of superoxide radicals and chemotactic property of
oxygen metabolites
• Significant proportion of tissue damage triggered by reperfusion
• “no-reflow” phenomenon / “diminishing-reflow” phenomenon

14. MECHANISMS AND PATHOPHYSIOLOGY OF INJURY:
ROLE OF PMNS
• Adherent, activated PMNs can cause direct endothelial injury
• Microvascular occlusion
• “zone of injury”

15. INITIAL EVALUATION
• When
• Bone, integument and muscle have low tolerances to ischemia
• Muscle: 4-6 hours
• Temperature of tissue during ischemic period is critical
• Where
• Social and economic aspects of injury environment must be weighed in
• How
• Force of injury and extent of tissue necrosis
• Sharp injuries: involve limited zone of tissue
• Crushing or avulsion injuries: broader zone of injury

16. EXAMINATION
• General assessment of vascular status, sensibility and muscle-tendon unit
function can be done at the ER
• Vascular system: priority
• Direct inspection of affected tissues and comparison to adjacent tissue
• Nail bed not reliable to check for CRT
• Dorsal paronychial tissue on sides of nail more reliable for CRT
• Pink and spongy, good turgor, CRT <2 sec
• Color of blood oozing after needle prick or scalpel incision: most reliable indicator of
vascularity

17. EXAMINATION
• Standard Allen test
• Compressing either radial or ulnar artery and listen for signal via handheld Doppler
over palmar arch or digital artery
• Angiography has minimal role

18. EXAMINATION
• Muscle-tendon unit injury
• Active flexion and extension of digits and wrist
• Aberrations in normal resting cascade indicate tendon injury
• “Tenodesis effect”

19. EXAMINATION
• Nerve injury
• Examine both motor and sensory function
• Resistance to palmar abduction of thumb – abductor pollicis brevis (median nerve)
• Resistance to flexion of MCPJ of SF : flexor digiti quinti (ulnar nerve)
• Resistance to extension of MCPJ of IF : extensor digitorum communis and indicis proprius (radial nerve)
• If injury distal : digital nerves
• If injury proximal : independent areas of sensory function
• Volar aspect of IF/MF – median nerve
• Volar aspect of SF – ulnar nerve
• Dorsum of 1st web space – radial nerve

20. BIOMECHANICS OF THE INJURED HAND
• 7 basic functions
• Precision pinch
• Opposition pinch
• Key pinch
• Chuck grip
• Hook grip
• Span grasp
• Power grasp

21. BIOMECHANICS OF THE INJURED HAND
• Basic units that underlie hand function:
• Opposable thumb
• IF and MF – stable, fixed unit for fine manipulation and power pinch
• RF and SF – mobile unit for grasping
• Wrist

22. AMPUTATION/SKELETAL CONTRIBUTION
• Thumb: 40% of hand function
• IF and MF: 20% each
• RF and SF: 10% each
• Maintain or reconstruct at least thumb and one opposing digit – minimum
requirement for any type of pinch or grasp

23. JOINTS
• PIPJ motion more important to preserve
• If PIPJ cannot be reconstructed – amputation considered
• MCPJ contributes 77% of the total arc of finger flexion
• At least 35 degrees of motion acceptable
• Stable but markedly limited MCPJ motion > unstable, painful MCPJ
• Partial or total wrist fusion rarely done in acute setting
• At least 5-10 degrees flexion and 30-35 degrees extension needed
• Intact DRUJ can significantly improve pronosupination with prosthesis

24. TENDONS
• Complete loss of extrinsic extensors with associated reconstruction of dorsal soft
tissue coverage tolerated well
• Scar tenodesis
• Preserving or reconstructing flexor tendon unit more important
• A2 and A4 must be preserved or reconstructed
• Best to repair only one tendon – FDP
• Prevent lumbrical-plus deformity and quadrigia

25. SOFT TISSUE COVERAGE AND NERVES
• Durable, stable, pliable soft tissue coverage with at least a protective sensation in
areas of functional contact
• Fascia flaps or thin muscle flaps that are skin grafted preferable
• Restore protective sensation to palmar weight-bearing surfaces
• Ie., 7-15mm 2PD

26. TREATMENT – EMERGENCY ROOM
• Evaluate and treat other life-threatening injuries (the trauma “ABCs”)
• Control hemorrhage by direct pressure—do not blindly clamp
• Reduce gross skeletal deformity
• Administer tetanus prophylaxis and antibiotics
• For a ischemic major limb, place a temporary vascular shunt
• Cool devascularized tissue
• Leave any skin bridges intact

27. OPERATIVE TREATMENT - DEBRIDEMENT
• Excise the wound
• Perform aggressive debridement of marginally vascularized tissue, especially
muscle
• Save critical structures: nerve, tendon, and arteries
• Begin with a tourniquet; release and reinflate for further debridement
• Tag nerves and arteries

28. OPERATIVE TREATMENT - DEBRIDEMENT
• Save vascularized bone for incorporation; save devascularized bone for keying
reduction and then discard
• Use gravity-assisted lavage with mechanical scrubbing
• Decide about replantation, amputation, partial amputation, or reconstruction
• “crystal ball”
• Perform amputations as part of debridement; save vascularized softtissue for
coverage/closure
• Save “spare parts” for later use in primary reconstruction

29. 8/9/22

30. OPERATIVE TREATMENT – SKELETAL
RECONSTRUCTION
• Attempt to visualize the fracture with minimal dissection
and minimal muscle and periosteal stripping
• Restore lengath for optimal function of the muscle–
tendon unit or shorten for primary closure and skeletal
and nerve repair
• Perform accurate anatomic reduction with special
attention to the articular surfaces
• Use stable, low-profile, minimally invasive fixation and
begin early motion with fracture healing
• For the radius/ulna, use a 3.5-mm limited-contact
dynamic compression (LCDC) plate versus a spanning
plate to the second or third metacarpal with locking
screws if severe comminution is present

31. OPERATIVE TREATMENT – SKELETAL
RECONSTRUCTION
• For fixation of fractures of the wrist, use compression
screws or Kirschner wires, repair or reconstruct
ligaments, and stabilize with Kirschner wires
• For the metacarpals, we prefer miniplate fixation to
minimize interference with joints or tendons so that
early motion can be achieved
• Maintain the first web space with an external fixator
or thumb CMC pinning
• For the phalanges, use a miniplate, Kirschner wires, or
tension band wiring
• For skeletal defects, decide between shortening,
primary bone grafting, and placement of an antibiotic
spacer with delayed bone grafting

32. OPERATIVE TREATMENT – TENDON
REPAIR/RECONSTRUCTION
• Debride crushed intrinsic muscles to prevent contracture
• Use four-core locking sutures plus a fine epitendinous suture if zone 2 is involved
• Repair both the flexor digitorum superficialis and flexor digitorum profundus unless gliding is
compromised, in which case repair just the flexor digitorum profundus
• Repair/reconstruct the A2 and A4 pulleys
• For tendon rods use two-stage reconstruction if primary repair is not possible
• Consider primary tenodesis/tendon transfer
• For late reconstruction, tendon grafting, tendon transfer, tenolysis, and functional free muscle
transfer may be needed

33. OPERATIVE TREATMENT – VASCULAR
REPAIR/RECONSTRUCTION
• Perform vascular repair/reconstruction after skeletal and tendon repair unless
critical ischemia is present
• use temporary shunt
• Dissect vessels and use microvascular clamp under tourniquet control
• Declot with a Fogarty catheter proximally and distally
• Trim vessel ends to healthy, uninjured tissue
• Irrigate and fill with a 10-U/mL heparin solution and then clamp

34. OPERATIVE TREATMENT – VASCULAR
REPAIR/RECONSTRUCTION
• Perform the vascular repair with the microscope, outside the injury zone if
possible
• If there is inadequate length, ligate/divide some side branches, flex the joints, or
use a reverse vein graft
• Perform a vein graft with vein outside the zone-of-injury; predilate and reverse it
(valves)
• Repair or reconstruct both the radial and ulnar arteries whenever possible
• Perform venous reconstruction only if all or nearly all venous outflow is absent

35. OPERATIVE TREATMENT – NERVE
REPAIR/RECONSTRUCTION
• Repair or reconstruct nerves as the last step before soft tissue coverage
• Trim clearly crushed nerve to healthy fascicles
• Perform epineural repair with the microscope
• Use the fascicular and surface anatomy for proper alignment
• Perform a tension-free repair
• If a nerve gap is present, free the minor branches, flex the joint, use a nerve
conduit for a short gap, and use a nerve graft for larger gaps

36. OPERATIVE TREATMENT – SOFT TISSUE COVERAGE
• Coverage over joints and tendons should be
adequately vascularized, low profile, and
supple
• Coverage over volar pressure-bearing surfaces
should be sensate and have minimal shear
characteristics
• Delay definitive coverage until the wound is
stable; repeat debridement if needed
• Provide definitive coverage by 5 to 10 days;
keep wound moist in interim
• Control size of wound: vessel loop weave
versus NPT

37. OPERATIVE TREATMENT – SOFT TISSUE COVERAGE
• Recognize that NPT is contraindicated if infection or
bleeding is present
• Cover “white structures”; vascularized soft tissue flap
is required
• tendon, nerve, bone, or ligament/joint
• Do not stretch traumatically elevated flaps to their
original position; simply lay them in place
• For a larger, noncritical defect, use a split-thickness
skin graft; use a full - thickness skin graft if area is
small, if subject to pressure/shear, or if motion is
critical
• For complex wounds with exposed white structures,
use a flap

38. OPERATIVE TREATMENT – SOFT TISSUE COVERAGE
• Axial flaps are preferable; include fascia
if possible, and consider a fascia-only
flap plus a split-thickness skin graft
• For the fingers, hand, or wrist, use a
Moberg, cross-finger, intrinsic, crane,
radial forearm, or groin flap
• For a radial forearm flap, consider a
fascia-only plus a split-thickness skin
graft; stay deep during dissection and
create an effluent venous anastomosis.

39. OPERATIVE TREATMENT – SOFT TISSUE COVERAGE
• For a groin flap, include sartorius fascia to
prevent kinking of the pedicle, protect the
lateral femoral cutaneous nerve, delay for 2
weeks, divide/inset at 3 weeks, perform
multiple thinning stages, and continue motion
to decrease stiffness
• For the forearm, use a groin, gracilis-free,
latissimus-free, lateral arm-free, anterolateral
thigh fascia, or suprafascial perforator free flap
• For the elbow or arm, use a brachioradialis
(antecubital defect), latissimus pedicled or free,
or suprafascial anterolateral thigh free
perforator flap

40. Dorsal Radial side Volar

41. Proximal
Distal
Lateral
Lateral
Proximal
Distal

42. POSTOPERATIVE MANAGEMENT
• Splint the wrist in a neutral extended position with MP flexion and IP extension (to
minimize contractures and optimize function)
• Prevent early shear of skin grafts/flaps
• Begin early motion to optimize gliding/motion
• Control edema
• Perform desensitization
• Use goal-based therapy
• Do not overlook psychosocial issues as well as therapy

43. SECONDARY PROCEDURES
Procedures requiring immobilization (do first)
• Bone grafting
• Corrective osteotomies
• Joint reconstruction
• Nerve grafting
• Sensory reconstruction
• Tendon transfers
• Functional muscle transfer
• Soft tissue reconstruction
• Toe transfer
Procedures requiring mobilization (do second)
• Tenolysis
• Capsulotomy
• Contracture releases

44. BURNED HAND
ANATOMY
• Dorsal skin thin and very flexible and lies on a thin subcutaneous layer of fatty
tissue
• Little mechanical protection but allows maximum tendon excursion and joint mobility
• Dorsal skin contains large superficial veins, hair follicles and sebaceous glands
with no sweat glands

45. BURNED HAND
ANATOMY
• Palmar skin has a thick subcutaneous fatty layer with a honeycomb-like structure
• Shock absorbing properties and provides grip stability
• Thick epidermal layers found in areas of greatest mechanical stress
• Cleland ligament
• Dorsal to neurovascular bundle
• Grayson ligament
• Palmar to neurovascular bundle

46. BURNED HAND
PATHOPHYSIOLOGY
• Anatomical properties of hand can lead to severe direct thermal effects
• Blood vessels, tendons and joints situated just beneath dorsal skin surface of
fingers
• Palmar skin can withstand greater thermal energy
• Longer exposure to lower temperatures has same pathophysiologic
consequences as short exposure to high temperatures

47. BURNED HAND
PATHOPHYSIOLOGY
• Heat leads to coagulation of vessels,
denaturation of proteins and increase
in capillary permeability (leak)
• 3 zones
• Necrosis
• Stasis
• Impaired circulation
• Insufficient primary treatment may
convert zone of stasis to necrosis
(afterburn)

48. BURNED HAND
PATHOPHYSIOLOGY
• Intravascular fluid shifts into
interstitial space – protein-rich
edema
• Persistent interstitital edema not
resolved after 72 hours may lead to
subcutaneous fibrosis with
subsequent stiffness
• Accumulation of intercellular edema
in cutaneous layer – blisters

49. ACUTE HAND BURNS
• Treatment Goals
• Avoid any additional injury or increase in the depth of the burn (do no
harm)
• Achieve early wound closure
• Maintain active and passive range of motion
• Prevent infection or loss of soft tissue coverage
• Initiate early functional rehabilitation

50. ACUTE HAND BURNS
• Basic Treatment Principles
• Evaluate the size and depth of the burn.
• Perform escharotomy if indicated.
• Apply proper wound care and dressings.
• Make a decision about conservative or operative treatment.
• Initiate early hand therapy and splinting.
• Manage the burn surgically (removal of eschar, transplantation of skin grafts, flap coverage if
necessary)
• Begin early postoperative physical therapy.
• Provide functional rehabilitation.
• Perform secondary and tertiary corrections if necessary.

51. EVALUATION AND MANAGEMENT

52. EVALUATION AND MANAGEMENT
Escharotomy
• May result to tourniquet effect
• Indications:
• Pain
• Resistance to passive extension of
fingers
• Disappearance of capillary refill in nail
beds
• Subcutaneous pressure may be
measured with Wick catheters

53. LOCAL WOUND CARE
• Partial thickness second degree burn
• Spontaneous healing expected within 7-14 days
• Areas of peeled skin need be removed
• Small intact blisters <1cm left intact
• Larger blisters managed with aspiration of fluid, removal by incision, or debridement
• Moist wound healing applied for spontaneously healing burns
• Antibacterial creams
• Superficial thermal injury – water soluble agents such as bacitracin
• Deeper partial thickness burn – topical antibacterial agent such as silver sulfadiazine
• Vaseline gauze strips and elastic netting are used to hold dressings
• Epitheliazed burn wounds – bland ointments or creams such as vitamin A and D ointments

54. EVALUATION AND MANAGEMENT