Necrotizing Soft Tissue Infection

Necrotizing Soft Tissue Infection

Abstract

A 49 year old gentleman was diagnosed with necrotising fasciitis of right leg. He underwent an above knee amputation of right leg due to fast spreading infection. His recovery was complicated by hospital acquired pneumonia.

Keywords: necrotizing fasciitis, soft tissue infections, cellulitis.

Introduction

Necrotizing soft tissue infections (NSTIs) constitute a spectrum of disease processes characterized by fulminant, widespread necrosis of soft tissue, systemic toxicity, and high mortality. It can be classified based on a variety of criteria including etiologic, microbiologic, anatomic, and clinical aspects. Clinically it is classified as superficial or deep infection. Superficial infections (necrotizing cellulitis) are those confined to the cutis and subcutis, such as erysipelas. Deep infection is the infection affecting fascia and muscle, including necrotizing fasciitis and myonecrosis.

Case Report (M766197)

A case of a 49 year old malay gentleman presented to emergency department PPUKM with pain and swelling of his right leg since past one week. He had high grade fever prior to the development of swollen leg and continued to have fever during admission. He is a known diabetic patient on follow-up with PPUKM. On examination, he was ill-looking with high grade fever, tachycardic and dehydrated. The ulcer on his right foot was foul smelling and the swelling had gone up to the knee. Crepitus was felt on the right calf. Plain radiographs of the right leg showed subcutaneous gas shadow extending up to the right knee. The blood parameters showed raised CRP and ESR (29.19 mg/dl and 99mm/hr respectively), raised total white blood cells (13.7 x 10⁹/L) but normal renal and liver profile.

After discussion with the patient regarding his condition and treatment options, he agreed for the operation. He was planned for a below knee kiv above knee amputation. We proceeded with above knee amputation as the infection had reached the proximal tibia. Intraoperative findings during wound exploration include seropurulent discharge drained from the space beneath the deep fascia and gaseous substance released as the skin breached. The deep fascia was also easily detached and separated from the deep and superficial layer. The wound at the amputation site was fairly healthy. The operation was uneventful.

He developed hospital acquired pneumonia postoperatively and was managed accordingly by the respiratory team.

Discussion

Introduction

Necrotizing soft-tissue infections (NSTIs) are often dramatic and life-threatening illnesses. It has been recognized since the fifth century where it was first described by Hippocrates.¹ Various names has been given to this disease such as gangrenous ulcer, hospital gangrene, Meleney gangrene² and Fournier gangrene³. In the 1990’s it became popularly known in media as the “flesh-eating bacteria” disease.⁴ The mortality rate associated with this condition ranges from 9% to 29%.^5,6,7 There are approximately 500–1500 cases of NSTIs per year in the US with the mortality rate is approximately 24–34%.⁸

Aetiology

There are many factors involve in the aetiology of necrotizing soft tissue infections. It can be as trivial as insect bites to suppurative surgical infections. It can occur in any part of the body but more commonly seen in the abdominal wall, perineum and both upper and lower limbs. The organism usually enters via either direct inoculation or hematogenous spread. In some cases, however, no primary cause can be found. Patients often have some prior history of trauma (which may even be trivial), such as an insect bite, scratch, or abrasion.⁹ Most patients who develops NSTI have a premorbid condition such as diabetic mellitus, chronic diseases, overzealous steroids user, malnutrition, intravenous drug abuser, peripheral vascular disease, renal failure, malignancy and obesity.

Clinical presentation

Patients usually presents with signs of inflammation such as erythema, swelling and pain (stage 1) (Table 1). It is difficult to differentiate between NSTI and cellulitis in the early stage of the disease. The key factor is pain disproportionate to the amount of “redness.” If a cellulitis fails to respond to antibiotics within 24–48 hr, NSTI must be considered.¹⁰

Table 1: Clinical features of necrotizing fasciitis as the disease progress through clinical stages. (Wong: Curr Opin Infect Dis, Volume 18(2).April 2005.101–106)

As the disease progress, frequently very rapidly, there is significant pain at wound site, accompanied by increasing erythema, edema, and warmth. The surrounding skin tissue may further deteriorate and become discolored. Blister or bulla formation is an important diagnostic clue.⁵ When present, it signals the onset of critical skin ischemia (stage 2). Blisters are caused by ischemia-induced necrolysis as the vessels coursing through the fascia to supply the skin are progressively thrombosed by the invading organisms. Lymphangitis is rarely seen NSTI. The late stage (stage 3 necrotizing fasciitis) signals the onset of tissue necrosis and is characterized by the so call ‘hard signs’ of necrotizing soft tissue infection such as hemorrhagic bullae, skin anesthesia and frank skin gangrene. Within 4–5 days of the appearance of the first symptoms, patients may demonstrate critical symptoms, including numbness, hypotension, toxic shock, and unconsciousness. The disease may progress to gangrene, sepsis, and potential death.¹¹

Microbiology

A single species of bacteria itself, or a polymicrobial infection may be responsible for NSTI.¹⁸ There are three clinical subtypes exist. Type I is polymicrobial. It is a mixed infection caused by aerobic and anaerobic bacteria, and occurs most commonly after surgical procedures and in patients with diabetes and peripheral vascular disease. Type II is monomicrobial. This condition can be associated with Toxic Shock Syndrome and tends to occur in healthy, young and immunocompetent individuals. The culprit microbe is typically Streptococcus (group A [beta] haemolytic streptococci).⁷ The least common subtype is type III. It is caused by Vibrio vulnificus. This condition is seen in skin break due to exposure to warm sea water and also in severe liver disease eg chronic hepatitis B. Group A streptococci are typically considered as extracellular pathogens but have been shown to survive intracellularly in macrophages during acute invasive infections.¹² This intracellular presence may have evolved as a mechanism to avoid antibiotic eradication. Streptococcus group G is rarely implicated in NSTI but its associated mortality could be comparable to that induced by S. pyogenes.¹³ Staphylococcus aureus and other staphylococci are also known causes of NSTIs.¹⁴

Pathophysiology

Necrotizing infection develops as pathogens proliferate within subcutaneous tissue along superficial and deep fascial planes. Surface proteins, enzymes and toxins released by the pathogens play an important role in NSTI. Surface proteins M-1 and M-3 increase the adhesion of streptococci to tissues and prevent phagocytosis by neutrophils.¹⁵ Streptococcal pyrogenic exotoxins A, B, and C and streptococcal superantigen cause the release of cytokines such as TNF α, IL-1, and IL-6, and set in motion of a destructive process that may lead to toxic shock syndrome.¹⁶ Necrosis of superficial fascia and fat produces watery, thin and foul-smelling fluid described as ‘dishwater pus’. The precise mechanism of liquefactive necrosis is not clear. Possibly from bacterial enzymes like hyaluronidase and lipase which degrades the fascia and fat.

Skin involvement can develop in time due to thrombosis of the perforating vessels to the skin. Thrombosis of skin perforating vessels is caused by local hypercoagulable state, platelet-neutrophil plug which block the vessels. As infection progresses and greater quantities of toxins are produced and absorbed, local ischemia likely expands regionally until an entire tissue bed is destroyed. Systemically, microvascular occlusion may also contribute to the shock and organ dysfunction associated with these infections.

Diagnosis

Establishing diagnosis is very important. A delay in diagnosis leads to delayed surgical debridement, which leads to higher mortality.¹⁷ The diagnosis relies on high clinical index of suspicion. History taking and physical examination plays an important role in diagnosing this condition. The classic presentation of myonecrosis is that of severe pain and underlying crepitus. The patient generally appears ill and has a rapid pulse and significant temperature elevation. Numbness is a unique finding in NSTI. Skin anesthesia probably is due to infarction of the cutaneous nerves located in necrotic subcutaneous fascia and soft tissue. The findings of crepitus on palpation and soft tissue air on plain radiography are pathognomonic, although these signs are present in only 37% and 57% of the cases, respectively.¹⁸ As the infection spreads along the fascial planes, painless, black, necrotic plaque-like ulcers may appear.

The use of ultrasonography, computed tomography, and MRI can be helpful for patients with other sources of infection, particularly deep abscesses. Computed tomography is better in showing abnormal soft tissue gas compared to plain radiograph.¹⁹ CT scan may also show fascial thickening, fascial stranding, and asymmetric thickening of fascial planes. Magnetic resonance imaging (MRI) with gadolinium contrast enhancement can accurately determine the presence of necrosis of fascia and the extent of the infectious and necrotic process.²⁰ The sensitivity of MRI, however, exceeds its specificity.²¹ A bedside frozen tissue section biopsy is an expedient method by which to establish the diagnosis on the basis of typical histologic changes of subcutaneous necrosis, polymorphonuclear cell infiltration, fibrinous vascular thrombosis with necrosis, microorganisms within the destroyed fascia and dermis, and sparing of muscle.^22,23

Laboratory Risk Indicator For Necrotising Fasciitis’ developed by Wong et al¹³ gives the guideline to diagnose necrotizing fasciitis.²⁴ Score 6 or more has Positive Predictive Value of 96% and Negative Predictive Value of 4%. If the score is >7, the probability of necrotizing fasciitis is >75%.

Variables	Score
C-reactive protein
<150	0
≥150	4
WBC (cells/mm3)
<15	0
15-25	1
>25	2
Hemoglobin (g/dL)
>13.5	0
11-13.5	1
<11	2
Sodium (mmol/L)
≥135	0
<135	2
Creatinine (mcg/L)
≤141	0
>141	2
Glucose (mmol/L)
≤10	0
>10	1

A sum ≥6 has a high correlation with soft tissue infections.

Table 2: Variables in laboratory diagnosis of necrotizing fasciitis.

The most crucial element in the evaluation is examination by a surgeon, including surgical exploration of suspected NSTI to confirm or refute the diagnosis.¹⁴ Intra-operative findings include ‘dishwater’ discharge, tissue necrosis, lack of bleeding from dissected tissues and loss of normal resistance of fascia during finger dissection.

Treatment

Treatment of the patient usually is best managed by a team comprising the infectious disease and critical care specialists and the surgeon. Physiologic support, combined with close monitoring in an intensive care unit setting, is crucial. Given the prolonged need for complex multidisciplinary care these patients require, patients with NSTI’s may be best managed at specialized wound management facilities such as burn centers.²⁵

Broad-spectrum antimicrobial therapy should be administered empirically as soon as possible, and should cover Gram-positive, Gram-negative, and anaerobic organisms.¹⁸ Monotherapy or multidrug regimens may be used in the treatment. Imipenem by virtue of their high [beta]-lactamase resistance, wide-spectrum efficacy, and inhibition of endotoxin release from aerobic (ie, Gram-negative) bacilli, may be the initial agents of choice for treatment of the frequent polymicrobial infections that result in necrosis or skin and soft tissue.²⁶ Addition of vancomycin, linezolid or daptomycin to a carbapenem or [beta]-lactam/[beta]-lactamase inhibitor combination if methicillin-resistant S. aureus is suspected.²⁷ A regimen that includes high-dose penicillin, high-dose clindamycin, and a fluoroquinolone or aminoglycoside may be used to cover Gram-negative organisms. Clindamycin covers anaerobes well and inhibits M protein and exotoxin secretion by group A Streptococcus sp., which may be crucial for controlling the inflammatory response. Ampicillin and gentamicin represent alternatives for coverage of aerobic Gram-negative bacilli,²⁸ but an aminoglycoside must be used with extreme caution in patients with hypovolemia, shock, or preexisting renal dysfunction. Metronidazole may be employed for antianaerobic coverage. Ampicillin-sulbactam lacks adequate coverage of Pseudomonas spp. and Enterobacteriaceae.²⁹ Newer antibacterial agents, such as linezolid and quinupristin/dalfopristin, are increasingly being studied in children for the treatment of skin and soft tissue infections.³⁰ Antimicrobial administration should be continued until no further debridements are needed and the patient's physiology has improved,³¹ but no specific guidelines exist as to duration of therapy. The antibiotic regimen should be reassessed based on culture and sensitivity results. Prolonged courses of an arbitrary duration are not necessary and may predispose the patient to wound colonization with drug-resistant organisms.³²

Destruction of the local microcirculation impairs the delivery of antibiotics to the site of infections. Because of the lack of antibiotic penetration, surgical debridement is the only effective treatment for the subcutaneous ‘sequestrum’. The most important determinant of mortality is timing & adequacy of debridement.³³ Mortality increases by 9 fold if surgery is delayed by more than 24 hrs.⁵ As patient who is diagnosed with necrotizing fasciitis usually came to the hospital in unstable condition, the goal is to perform definitive surgery regardless of how radical at the first occasion. A thorough and adequate debridement is a must as patient condition will deteriorate and might not survive a second look debridement. Wound reevaluation must be performed in 24-48 hours. Second debridement may be necessary to control the infection. In the event of fast spreading infection despite aggressive debridement or necrosis involving most muscle group of the limb which leads to a useless limb, an amputation may be necessary.

Wong et al³⁴ introduced radical excisional debridement. He classified skin and subcutaneous component into 3 surgical zones (figure 1).

Figure 1: Zone 1: Non viable, gangrene, fixed discoloration, haemorrhagic bullae. b) Zone 2: Early NF skin changes, ‘woody hard’ skin texture. Potentially salvageable, must be assessed carefully. Zone 3: Healthy, normal skin

Post excision wound care is important as large raw wound is at risk of post op bleeding and also risk of secondary infection. Initially, the wound can be covered with non-adherent dressing such as soffratulle dressing followed by firmly applied pressure dressing. The wound assessment should include observation for expansion of erythema or an increase in edema, pain, color, or drainage. Advances in wound management have led to negative pressure wound therapy as a treatment for managing the closure of wounds.³⁵ Negative pressure wound therapy promotes wound healing by enhancing blood flow to and from the wound bed, increasing the proliferation of granulation tissue, and decreasing the tissue bacterial counts. Wound vacuum-assisted devices also help relieve pain at the site by removing irritating exudates that cause pressure on the wound.

Hyperbaric oxygen therapy therapy (HBOT) has been proposed for improving the outcome of NST.^18,36 In HBOT, patient were subjected to 100% oxygen at 2-3 times the atmospheric pressure with arterial oxygen tension as high as 2000 mmHg. This will inhibit anaerobes and clostridium sp. exotoxin, enhances killing ability of leukocytes and enhances efficacy of intravenous antibiotics by increase local oxygen tension in tissue.³⁷

Intravenous immunoglobulin (IVIG) may be a useful adjunct treatment in type II group A streptococcal NSTI complicated by toxic shock syndrome, and in those with a high mortality risk (advanced age, hypotension, and bacteremia). The action of IVIG is believed to be the neutralization of superantigen activity and reduced plasma concentrations of TNF[alpha] and IL-6.³⁶

Nutritional support for the patient with NSTI helps heal these extensive wounds. The amount of calories and proteins should be double that of the normal basal requirement.³⁸ To ensure that the patient is receiving adequate nutrition, baseline and repeated monitoring of albumin, prealbumin, transferrin, BUN, and triglycerides should be performed. These patients may also require supplements including iron, vitamin C, and vitamin E to promote wound healing.

Physical therapy is an important part of the plan of care for the patient with NSTI. Encouraging mobility, increasing range of motion of extremities, and participating in activities of daily living (ADLs) will promote circulation and tissue perfusion. These activities can prevent complications associated with immobility such as deep vein thrombosis and pneumonia.

There can be psychological consequences of NSTI resulting from intense discomfort, serial surgical debridements, painful dressing changes, physical disfigurement, and a myriad of emotions such as anxiety, worry, guilt, anger, and hopelessness. An ongoing psychological and psychosocial supports are needed in these patients. Supportive counselors can help patients cope with pain, anxiety, and body image disturbances caused by the appearance of extensive reconstructive surgery and interventions. Antidepressant medications may reduce feelings of depression and hopelessness.

Conclusion

Althought NSTIs are rare, they are life-threatening processes. The very young and very old are at especially high risk of an adverse outcome. The key to overcoming the risk of this disease process is in rapid identification and prompt treatment. Gold standard diagnostic tool and treatment is still thorough wound debridement and exploration. Postoperative wound care and psychological supports are important in managing NSTI.

References

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Traumatic Brachial Plexus Injury

Abstract

A 24 year old gentleman with a traumatic left brachial plexus injury. He showed no clinical improvement after initial physiotherapy and observation. A neurotisation was performed with a satisfactory outcome.

Keywords: Brachial plexus injury, neurotisation,

Introduction

Traumatic brachial lexus injury is not uncommon. It results in variable loss of upper extremity function. The restoration of this function requires good stability if the involved shoulder and elbow flexion of adequate strength and range of motion. A proper understanding and evaluation of brachial plexus lesions is a prerequisite to any reconstructive procedure.

Narakas developed his rule of "seven seventies" in his experience over 18 years with 1068 patients.¹ Approximately 70% were motor vehicle accidents (MVAs). Of the MVAs, 70% were motorcycles or bicycles. Of the cycle riders, 70% had multiple injuries. Of the multiple injuries in cycle riders, 70% were supraclavicular injuries. Of the supraclavicular injuries, 70% had at least one root avulsed. Of the avulsed roots, 70% were lower C7, C8, T1. Of the 70% avulsed roots, 70% of those were associated with chronic pain.

Case Report

A 50 year old gentleman was involved in a road traffic accident. He was riding a motorcycle on a slippery road. He collided with a car and was thrown off his motorcycle. He was brought to the emergency department with bruises over his left shoulder and a flail left upper limb. Physical examination revealed absent power of his left shoulder abduction and flexion and elbow flexion without evidence of penetrating trauma to the neck, shoulder, or axilla. Wrist and hand movement and sensation were intact, whereas sensation was diminished in the shoulder and proximal arm. Pulses were intact in the left arm. The left glenohumeral joint showed full passive range of motion. X-rays of the cervicothoracic spine, ribs, left shoulder, humerus, forearm, or hand demonstrated no evidence of fracture.

A computed tomographic (CT) scan of the head showed no intracranial haemorrhage, mass effect, or midline shift; a CT scan of the cervical spine was negative for fracture, subluxation, and malalignment but was positive for left-sided paravertebral soft tissue swelling.

The diagnosis of upper root brachial plexus injury was made and the patient was admitted for observation. He was subsequently discharged with an arm sling and an electrodiagnostic study was obtained 3 weeks later.

He was seen in the Hand clinic approximately 6 weeks after his initial trauma. The patient noted that he had a complete inability to activate the left deltoid and biceps muscles without improvement and experienced 9/10 pain radiating from his left neck down to his fingers as well as numbness and tingling in the same distribution. On neurological examination, the patient was a well-appearing man holding his left arm at his side. His mental status and cranial nerves were normal, including no evidence of Horner's syndrome. On motor evaluation, the patient had a mild amount of left scapular winging with normal trapezius function and was 0/5 on direct testing of the supra- and infraspinatus, deltoid, biceps, and brachioradialis muscles. Rhomboid function was present but moderately weak, triceps were 3/5, the latissimus dorsi and pectoralis major sternal head were 4/5, pectoralis major clavicular head was 0/5, supinator was 3/5, and all other muscle groups were 5/5. He had absent deep tendon reflexes at the biceps and brachioradialis on the left side and had numbness to light touch in a C5 and C6 dermatomal distribution on the left. There was evidence of mild subluxation of the glenohumeral joint and some atrophy of his biceps, and deltoid muscles.

The patient was informed regarding the nature of his injury and poor recovery as evidenced by no clinical improvement and EMG documentation of complete denervation of muscles in a C5, C6 distribution. It is likely that he would not regain significant function without surgical intervention. The patient was informed that the recovery process would take months to years and likely would not be complete. A comprehensive pain management program as well as physical and occupational therapy will be prescribed, particularly to avoid contracture formation in his shoulder and elbow.

He continued the physical and occupational therapy for 4 months without showing any improvement. After considering the recommendations, the patient elected to pursue surgery.

A supraclavicular approach was used to identify the phrenic nerve which was located on the anterior surface of the anterior scalenus muscle. The integrity of the nerve was confirmed by a nerve stimulator. The nerve was dissected and transacted at the upper margin of the clavicle just before its entry into the thoracic cavity. It was the mobilised laterally for transfer. The next step was the isolation of the MCN via infraclavicular approach. The musculocutaneous nerve (MCN) was dissected proximally inside the lateral cord before it was cut. The sural nerve autograft was passed deep to the clavicle and was sutured to the phrenic nerve and MCN. Next, the location of the distal accessory nerve and the suprascapular nerve at the suprascapular notch were identified. After the skin incision, the trapezius muscle was splitted and a blunt dissection was carried out over the supraspinatus muscle to the superior border of the scapula. The superior scapular ligament was identified and divided under direct vision. The suprascapular nerve was revealed in the adispose tissue below the divided ligament. The nerve was dissected as proximal as possible. Subsequently, a medial dissection was made to locate the accessory nerve. The nerve was then dissected as far distally as possible. The suprascapular nerve is divided sharply proximally, and the accessory nerve is divided distally, and the proximal end of the accessory nerve is sutured to the distal end of the suprascapular nerve with interrupted 9-0 nylon.

The patient was discharged with an arm sling and continued his physical therapy and rehabilitation as outpatient.

Discussion

Anatomy

Brachial plexus is a network of nerves originating from the ventral rami of C5 to T1 nerve roots. In more than half of the cases, the C4 give branch to the C5. The second thoracic nerve (T2) also contributes directly to the plexus via intrathoracic precostal communication with the T1. The ventral rami emerge between the scalenius anterior and the scalenius medius muscles in the posterior triangle of the neck and descend toward the anterior portion of the first rib. Immediately after entering the posterior triangle, the C5 and C6 nerve roots join to form the upper trunk, the C7 continues as the middle trunk and the C6 and C7 join to form the lower trunk. The suprascapular nerve arises from the upper trunk at which point it is also known as Erb’s point. Just proximal to the clavicle, the trunks split into anterior and posterior divisions. The three cords are formed by combinations of the anterior and posterior divisions and named according to their relation to the second part of the axillary artery. The lateral cord is formed by the union of anterior division of upper and middle trunks (C5-C7), the medial cord is formed by anterior division of the lower trunk and the posterior cord is formed by the posterior division of all trunks.

The lateral cord passes superficial and lateral to the second part of the axillary artery and gives off three nerves: the lateral pectoral nerve, the lateral cord contribution of the median nerve and the musculocutaneous nerve. The medial cord emerges between the axillary artery and vein and descends medial to the artery, where it gives off the medial pectoral nerve, the medial brachial cutaneous nerve, the medial antebrachial cutaneous nerve, the medial cord contribution to the median nerve, and the ulnar nerve. The posterior cord originates superior and lateral to the axillary artery and passes posterior to it. From the posterior cord arise the two subscapular nerves, the thoracodorsal nerve, the axillary nerve, and the radial nerve.

Etiology and classification

Traumatic brachial plexus injury has a wide variety of etiologic factor and can be divided into causative mechanism:

1. Closed injury.

• Traction injury.
• Compression.
• Combined lesion.

2. Open injury.

• Sharp.
• Gunshot.
• Radiation.

Traction lesion results from forceful separation of the neck and shoulder or upper arm and trunk. The nerve pathology occurs between the two anchoring points. The proximal anchoring point is at the spinal cord and nerve root junction, and the distal point is at the neuromuscular junction. The coracoid process is regarded as a temporary lever in forceful hyperabduction of the shoulder. It is not only the direction of the applied force to brachial plexus that determines the severity of the nerve damage, but also the speed of the application of the traction force. High-velocity traction injury is the overall leading cause of brachial plexus injury in nearly all reports.^2,3 The majority of traction injuries are a result of motor vehicle accidents. The clavicle serves as a strongest link between the shoulder and neck. If it is broken, all of the traction forces are transmitted through the neurovascular bundle. This mechanism of injury causes the greatest damage to the upper roots. Whereas hyperabduction of the shoulder mostly affects C8 and T1 nerve root. The high-velocity traction injury can cause nerve root avulsion from the spinal cord, nerve ruptures, or stretch injuries (Fig. 2).

Traction forces can result in preganglionic or postganglionic injuries. Preganglionic injuries refer to lesions proximal to the dorsal root ganglion, which is in the spinal canal, and foramen. Preganglionic ruptures may be central or direct from the spinal cord or intradural. Preganglionic lesions do not cause Wallerian degeneration or neuroma formation because the axons remain in continuity with the cell bodies in the dorsal root ganglion. Postganglionic lesions are defined as any lesions distal to the spinal ganglion and are physiologically similar to other peripheral nerve injuries.

Figure 2: Level of nerve injury.

The compression lesions may occur when a traumatic force is applied on the shoulder in the cephalocaudal direction. The brachial plexus may also be compressed in between the clavicle and the first rib. Any fractures of the surrounding bones may compress the brachial plexus. Chronic compression from carrying heavy weights on shoulders may cause a temporary brachial plexus lesion.

In traction and compression injury, the injury is usually diffuse, from nerve roots through terminal branches, and disruption of brachial plexus can be found on more than one site. This injury is usually associated with vascular damage.

Open injuries of the brachial plexus are much less common in normal practice. The injury only involves part of the brachial plexus and carries a good prognosis. Associated vascular and intrathoracic injuries are commonly found.

Radiation brachial plexus injury is usually found in patients several years after radiation therapy to the ipsilateral breast or axilla for the treatment of breast cancer.⁴ Patients usually present with progressive motor and sensory deficits that may be caused by radiation, compression of recurrent neoplasm, or both.

Clinical evaluation

A complete understanding of the nature and mechanisms of injury is important in evaluating patients with a brachial plexus injury. Knowing the exact neck and arm position at the moment of injury greatly assists in predicting the site of the brachial plexus lesion. Extension of the arm in 90-degree abduction of the shoulder puts maximum tension on the C7 root of the brachial plexus, but with increased force, all nerve roots may be affected. Previous radiation therapy to the neck, upper chest, and axilla can cause radiation brachial plexitis or fibrosis.

Patients usually present with a slowly advancing motor and sensory deficit associated with pain. Pain over a nerve is common with rupture, as opposed to percussion tenderness with avulsion. Paresthesia and dysesthesia of the involved limb is common. The patient may also present with weakness or heaviness in the extremity. A vascular injury may accompany traction injury. It may present with a diminished pulse.

Iatrogenic compression injuries to the brachial plexus can occur because of improper positioning in the operating room.

General Physical Examination

Contusion and ecchymosis at the suprascapular or deltopectoral area indicate the site of injury in compression lesions of the brachial plexus. Abrasions on the ipsilateral shoulder and cheek suggest traction lesions of the brachial plexus incurred in motorcycle accidents. A winged scapula with an intact spinal accessory nerve is highly suggestive of a C5-C6-C7 avulsion, whereas the presence of Horner’s syndrome (enophthalmos, myosis, ptosis, and absence of facial sweating on the affected side) suggests a cervical or T1 root avulsion and interruption of sympathetic innervations.⁵ A sensory-sweating dissociation in an anesthetic and flail arm also suggests root avulsion.⁶ A paralyzed diaphragm, as determined by inspiratory/expiratory chest x-rays or fluoroscopic studies, suggests a high plexus lesion.⁷

Neurologic Examination

Every muscle of the affected upper extremity innervated by the brachial plexus must be examined and graded according to the Medical Research Council score.⁸ It has a scale of 0 to 5 of which 5 is the normal muscle strength, whereas 0 is a flail muscle. Brachial plexus root avulsions may be associated with spinal cord injury, therefore examination of the lower extremity muscle power is also required to detect the presence of long tract sign.

A complete sensory examination should include both subjective and objective sensory changes. Objective tests of all sensory modalities are performed on each dermatome of the cervical and brachial plexus. Pain, temperature, touch, vibratory sense, and two-point discrimination are tested and recorded. Pain is a complex and difficult feature of the brachial plexus injury. It can be divided into neuralgic pain and causalgic pain. Neuropathic pain in brachial plexus injury may be present with avulsion lesion of the lower roots. The deafferentiation pain from root avulsion usually appears a few weeks after injury. The causalgic pain has no precise distribution and appears immediately after injury.

The examination of the sympathetic nervous system is important as the avulsion of the lower roots or a high lesion of the corresponding spinal nerves can compromise the ipsilateral sympathetic preganglionic fibers. Vasomotor disturbances, cyanosis, edema of the soft tissues, and trophic lesions should be observed. Anhydrosis of the anesthetic area suggests a postganglionic lesion. The presence of Horner's syndrome (anhydrosis, miosis, ptosis, and enophthalmos) is a bad prognostic feature and is associated with T1 root avulsions.

Vascular Examination

Vascular examination should be performed during initial evaluation. Major vascular injury is found in association with brachial plexus injury in 10% to 16% of cases.⁹ Progressive loss of motor and sensory function of the affected extremity suggests an expanding hematoma or aneurysm compressing the adjacent neural structure. An angiography is indicated in any abnormal vascular examinations, widened mediastinum and first rib fracture.

Musculoskeletal Examination

The majority of brachial plexus injuries are caused by falls from motorcycles, therefore musculoskeletal injuries are commonly found concomitant with brachial plexus trauma. The associated injuries of the upper extremity can include clavicular fracture, acromioclavicular joint separation, scapula fracture, first rib fracture, cervical transverse process fracture, humeral fracture, glenohumeral dislocation, and scapulothoracic dissociation. Fracture and dislocation around the clavicle indicate a bad prognostic sign.¹⁰ Because the clavicle is the only solid structure connecting the shoulder girdle to the neck, its fracture allows all of the traction force to be directed at the underlying soft structures (i.e., brachial plexus and subclavian vessels). Cervical transverse process fractures are commonly found with high ruptures or avulsions of the corresponding nerve roots. Scapulothoracic dissociation is often associated with multiple root avulsions. First rib fracture is often associated with lesion of the lower roots as well as vascular injuries. Fracture of the coracoid process is often found with lateral cord injury, whereas scapular and humeral neck fractures are associated with posterior cord lesion.

Investigations

Plain radiography of the shoulder girdle, cervical spine, and chest should be made for patients with traumatic brachial plexus lesions. Chest radiography is obtained to determine whether there is a widened superior mediastinum, which suggests major vascular injury.

Myelography is indicated in traction brachial plexus lesions presenting with a persistent complete or partial neurologic deficit. The dural tear usually healed in three weeks. Myelography should not be performed no sooner than 3 weeks, otherwise the leakage from the nerve root avulsion may obscure the visualisation. Myelography in combination with computed tomography (CT-myelography) improves visualization of the spinal cord and nerve root lesions.¹¹ R.W. Marshall and R.D. De Silva, Computerised axial tomography in traction injuries of the brachial plexus. J Bone Joint Surg Br 68 5 (1986), pp. 734–738

Magnetic Resonance Imaging (MRI) provides a better image of the extraforaminal brachial plexus structures. It is non-invasive, relatively quick, requires no contrast medium, provides multiple projections, and is comparable in diagnostic ability to the more invasive , time consuming techniques of conventional myelography and CT myelography.^12,11

Early interest in the use of MRI in brachial plexus injuries was directed at the post-ganglionic plexus. MRI can detect post-injury fibrosis and neuroma formation in the post-ganglionic plexus.¹³ However, MRI cannot identify the precise site of injury or the severity of the injury due to the complexity of the anatomy of the post-ganglionic brachial plexus.¹⁴ The current focus on the use of MRI is on the pre-ganglionic plexus with the aim of providing a non invasive means of detecting nerve root avulsion.^15,16

Ultrasound has been proposed as a possible technique for examining the post-ganglionic brachial plexus in cases of injury. 21. C. Martinoli, S. Bianchi, E. Santacroce, F. Pugliese, M. Graif and L.E. Derchi, Brachial plexus sonography: a technique for assessing the root level. AJR Am J Roentgenol 179 (2002), pp. 699–702. View Record in Scopus | Cited By in Scopus (33)It has obvious potential advantages, in terms of high soft-tissue resolution and the ability to follow each component of the plexus as it passes in an oblique plane through the base of the neck.¹⁷

Electromyography gives objective information on motor dysfunction, especially when clinical examination of motor function is difficult. Electromyography is used during the first week after injury to determine whether the lesion is a continuity lesion. The presence of motor unit action potentials across the affected site, in spite of a complete paralysis, indicates a partial lesion.

Exploration is the most accurate investigation of the supraclavicular plexus. If this inspection is undertaken in the first week after injury, the effect of trauma on the anatomical structures is easily identified and understood. However, there are arguments for and against early surgery. Arguments for early exploration include allows ease of diagnosis because tissue planes are open, fibrosis and scarring are absent and the nerve in continuity is assessed visually. Surgery is not destructive and carries little morbidity or penalty and allows early repair, avoiding increased target organ decay. It allows early prognosis for patient and consequent early decisions about future employment, rehabilitation and resettlement. Arguments against early exploration include spontaneous recovery may occur without surgery. The lesion-in-continuity may or may not recover and the surgeon is occasionally unable to determine this at surgery.

Management

Medical Therapy

Nonoperative treatment of brachial plexus lesions is complex and may best be addressed by an integrated multidisciplinary team that includes a skilled orthotist, occupational therapists, physical therapists, and physicians.

In neglected injuries of the brachial plexus, contracture of the joints often causes more disability than muscular paralysis. All joints should be put in full range of movement several times a day.

Continuous stretching of the paralysed muscle is prevented by appropriate splinting. Daily electrical stimulation will prevent excessive wasting of the paralysed muscle. During the phase of recovery it is essential to re-educate all muscle which are showing feeble voluntary contraction. Prolonged treatment may be necessary, and it is important to allow sufficient time for recovery before considering reconstructive operations.

Surgical Management

Brachial plexus exploration is indicated for patients with complete or partial neurologic deficit after a penetrating injury. An iatrogenic sharp injury to the brachial plexus may occur in any procedures around the neck and supraclavicular region. Sharp injuries to the brachial plexus carry a good prognosis. The injured plexus can usually be treated with neurorrhaphy or nerve grafting.

High-velocity traction injury secondary to a fall from a motorcycle usually causes severe damage to nerve roots. Brachial plexus exploration and surgical repair or reconstructions are indicated in patients who have no spontaneous recovery after 3 months. Time is allowed for the recovery of the low-grade injured neural tissue, subsidence of the swollen surrounding tissue, and completion of the diagnostic investigations. In complete brachial plexus palsy with strong radiologic and electrodiagnostic evidence of complete or multiple root avulsions, early surgery (6 weeks to 3 months after injury) is indicated because the chance of spontaneous recovery is less likely.

The timing of surgery depends on the associated injury involved and the nature of recovery. Immediate surgery of the brachial plexus should only be performed in an associated brachial plexus injury (closed or penetrating) with subclavian or axillary vessel injury. Early surgery (6 weeks to 3 months) should be performed in complete brachial palsy patients with total root avulsion. For incomplete brachial plexus palsy or complete brachial plexus palsy without evidence of root avulsion, exploration should be performed when there is no sign of clinical recovery or the initial recovery stopped after an observation period of 4 to 5 months. The result of operative nerve repair and reconstruction is greatly diminished after a 6-month interval between injury and operation. Six months from the time of injury, free muscle transfers should be considered.

A method of restoration of function in preganglionic injuries can be obtained by the transfer of a functional but less important nerve to a distal but more important denervated nerve. Neurotisation or nerve transfer has become an integral part of brachial plexus reconstructive surgery. A nerve transfer may be performed in cases of postganglionic injury as an alternative to nerve grafting or to power free functioning muscle transfer.

Donor nerves can be classified as either intraplexal (within the brachial plexus) or extraplexal (outside the brachial plexus) and as motor nerves or sensory nerves. Extraplexal donor nerves for nerve transfers include the spinal accessory (cranial nerve XI), intercostals nerves, the phrenic nerve, or the contralateral seventh cervical root. Intraplexal donor nerves include the use of motor fascicles of the ulnar nerve or triceps branch of the radial nerve in cases of partial brachial plexus injury.

The surgeons need to identify the available donor nerves and prioritize functions that they aim to restore in the injured limb. The highest priority is elbow flexion, followed by shoulder stability and abduction. Wrist extension/finger flexion and wrist flexion/finger extension follow next. Intrinsic hand function is the last priority, and it is also the most difficult to obtain. Neurotizations are routinely performed to reanimate denervated muscles for elbow flexion and shoulder abduction.

Restoration of abduction and external rotation are high priorities in the rehabilitation of the upper limb so that reconstruction of more distal targets can follow. Early repair of the suprascapular nerve, usually with direct neurotization from the distal spinal accessory nerve, offers a good opportunity for shoulder stabilization and usually can yield adequate shoulder abduction and external rotation.¹⁸ External rotation of the humerus can also be restored dynamically with latissimus dorsi rerouting or statically with rotational osteotomy of the humerus.¹⁹

The other goals of treatment are to restore grade M4 or M4+ elbow flexion with a range of motion that will allow the hand to reach the face. The resulting function of elbow flexion must outweigh the deficits caused by transferring functional nerves or muscles. To prevent dissipation of elbow flexion strength, the shoulder must be stable.

Ipsilateral C5 is the strongest motor donor, and if there is no avulsion, the proximal part of the ruptured root can be used as a motor donor for multiple neurotizations with interposition nerve grafts. When the proximal stump of the C6 root is also available, a folded vascularized ulnar nerve graft can connect both roots with peripheral targets using the loop technique.²⁰

When the upper plexus roots (C5 and C6) are avulsed from the spinal cord, reconstruction of shoulder and elbow function can be achieved by means of the ipsilateral C7 root which, if intact, can be sacrificed for higher priority targets. In that case, the distal targets innervated by the C7 root can be neurotized with extraplexus motor donors.²¹

Deltoid motor function can be restored with transfer of the nerve to the long head of the triceps to the anterior branch of the axillary nerve.²² The nerve of the long head of the triceps is synergistic to the target muscle; it is pure motor nerve, with many axons and a size that is matched to the axillary nerve.

Intercostal nerve transfer is one of the more common methods of reanimating the arm. Typically, the third, fourth, and fifth intercostal nerves are used; however, up to seven unilateral intercostal nerves have been used.²³ Candidates for this procedure should have no history of rib fractures, thoracotomies, or chest tube placement in the potential donor nerve region. Sensory reinnervation may be achieved by coapting the intercostal nerve sensory axons, which are located in the superior portion of the nerve, with the sensory axons of the musculocutaneous nerve, which are located in the superior and inferior poles of the nerve. The intercostal nerve motor fibers, which run in the inferior portion of the nerve, are coapted to the motor fibers located in the middle of the musculocutaneous nerve.²⁴ Intercostal nerve transfers is more likely to have a useful result when the spinal accessory nerve was used to stabilize the shoulder by nerve transfer to the axillary or suprascapular nerves.²⁵ A muscle transfer procedure may be used to supplement the biceps if elbow flexion is grade M3 or less. In less than 10 percent of patients, uncontrolled elbow flexion was reported with coughing, sneezing, or yawning, but none had a loss of pulmonary function.²⁶

The spinal accessory nerve is another potential donor to achieve elbow flexion. The segment distal to the trapezius ramus is used to preserve sternocleidomastoid and trapezius function. Advantages include its sole function as a motor nerve and similar functional relationship with the musculocutaneous nerve. However, its use does require a nerve graft and, when needed, it is best saved for shoulder stabilization by nerve transfer. Songcharoen et al.²⁷ showed good results when nerve transfer was undertaken within 6 to 9 months of injury and when patients were younger than 40 years old. Waikakul et al found very good or good power in 83 percent of patients who underwent spinal accessory nerve transfers using sural nerve grafts compared with 64 percent of those who had a transfer of three intercostal nerves without nerve grafts.²⁶

Other nerves that could be used to assist in elbow flexion include phrenic nerve,²⁸ cervical plexus,²⁹ hypoglossal nerve³⁰ and C7 cervical nerve.³¹ The local and distant muscles that may be transferred and used to provide elbow flexion include the following: flexor-pronator mass, pectoralis major, pectoralis minor, latissimus dorsi, triceps, and sternocleidomastoid and the gracilis, rectus femoris, and latissimus dorsi as free muscle transfers. This may be done alone or in combination with a nerve transfer procedure. Unlike nerve transfers, in which the original elbow flexor, the biceps muscle, is reactivated, muscle transfer procedures alter the biomechanics of elbow flexion. Therefore, at least M4 strength and the creation of at least 90 to 100 degrees of elbow flexion are needed to provide useful function.

Various combinations of nerve and muscle transfers have been proposed. Berger et al. suggest an initial nerve transfer procedure supplemented at least 1 year later by a triceps transfer or flexorplasty to achieve elbow flexion.³² Some author used latissimus dorsi transfers for elbow flexion together with nerve transfers for wrist and finger extension.³³

Elbow extension is a very important function because it can give stability to the elbow joint. However some author sacrifices the muscle to use it as a pedicled flap to substitute for biceps function.³⁴

Restoration of protective sensation allows the patient to recognize the position of the extremity in space, to avoid injuries, and to use the hand for grasping. Neurotization of the ulnar nerve and lateral cord contribution to the median nerve from intercostal sensory nerves has been proposed.^35,36

Glenohumeral arthrodesis and above-elbow amputation are indicated in flail upper extremity with a poor prognosis for additional recovery. A combination of glenohumeral arthrodesis and above-elbow amputation was first recommended by Yeoman and Seddon in 1961.³⁷ Shoulder arthrodesis eliminates symptomatic instability and places the extremity in a functional position. Some range of motion is still preserved via the scapulothoracic articulation. An above-elbow amputation allows early prosthetic training and functional rehabilitation.³⁸ Other indications for shoulder arthrodesis and above-elbow amputation include failed prior operative treatment, patient dissatisfaction with lack of useful function and/or discomfort of the flail limb, and pain or discomfort secondary to inferior glenohumeral subluxation. Contraindications for these procedures include paralysis of the trapezius, levator scapulae, latissimus dorsi, serratus anterior, or rhomboid muscles. These muscle groups are essential for stabilization of the scapula and for compensatory scapulothoracic motion following glenohumeral arthrodesis. An active infection in the proximal humerus or glenohumeral joint is also a contraindication.

Postoperative rehabilitation is important. Restoration of full ROM is essential to prevent joint and soft tissue contractures. A functional orthosis is applied to reduce shoulder subluxation and to relief traction on repaired or neurotized nerve. Reinnervated muscles need to be re-educated. Regular assessment is important to determine return of function or sensation. Regime of exercises may proceed from isometric to isotonic and gravity eliminated to gravity resisted movement.

Conclusion

The principles guiding brachial plexus reconstruction continue to evolve and the modern management of brachial plexus injuries should focus on early aggressive microsurgical reconstruction. The return of functions of upper extremity depends on the severity of the injury and that the reconstruction may require multiple stages, from simple neurolysis to nerve repairs, nerve transfers, nerve grafting, nerve banking, tendon transfers, muscle transplantations, osteotomies, and bone fusions. The future may bring further advances in nerve rootlet replantation for preganglionic injuries and in free muscle transfer techniques. Research into growth factors that promote nerve regeneration may make nerve grafting and transfers more appealing in the future.

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