Fatal streptococcal necrotizing fasciitis as a complication of axillary brachial plexus block

S. Nseir*, P. Pronnier, S. Soubrier, T. Onimus, F. Saulnier, D. Mathieu and A. Durocher

Service de Réanimation Médicale, Hôpital Calmette, CHRU, boulevard du Pr. Leclercq, F-59037 Lille cedex, France

*Corresponding author. E-mail s-nseir@chru-lille.fr

Accepted for publication: July 29, 2003


    Abstract
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
A 74-yr-old diabetic woman developed necrotizing fasciitis of the right upper limb after axillary brachial plexus block for carpal tunnel decompression. Clinical signs included oedema, diffuse swelling and bullae; rapidly followed by toxic shock syndrome and multiorgan failure. The patient died 48 h after hospital admission, despite broad-spectrum antibiotics, surgical treatment and supportive measures for the management of shock and multiorgan failure. Cultures yielded group A Streptococcus. Delay in antibiotic and surgical treatment probably affected the outcome. Early diagnosis and treatment are essential to improve the outcome of streptococcal necrotizing fasciitis.

Br J Anaesth 2004; 92: 427–9

Keywords: anaesthesia, regional; anaesthetic techniques, regional, axillary brachial plexus block; complications, necrotizing fasciitis; complications, streptococcal infection; complications, toxic shock syndrome


    Introduction
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
The risk of infection during regional anaesthesia is very low, epidural catheter-related infections are the major cause of this problem after neuroaxial block.1 We present a case of fatal necrotizing fasciitis as a result of group A Streptococcus complicating axillary brachial plexus block.


    Case report
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
A 74-yr-old woman with a history of insulin-dependent diabetes mellitus, hypertension, and chronic atrial fibrillation was admitted for right carpal tunnel decompression. A single incision arthroscopic technique was used to release the carpal tunnel.2 Anaesthesia was provided by an axillary brachial plexus block. The procedure was performed without neurostimulation in the operating room using a sterile technique including wearing of theatre cap, sterile gloves, and gown. Povidone iodine 10% was used for skin disinfection. A single injection (30 ml) of bupivacaine 0.25% was administered with a disposable needle. The patient’s diabetes was well controlled before the procedure. No perioperative antibiotics were given, in keeping with the Société Française d’Anesthésie et de Réanimation recommendations. The patient was discharged the same day.

Four days later, she complained of axillary pain associated with erythema and oedema localized to the regional anaesthesia puncture site. The next day, she was admitted to hospital with oedema extension, increasing pain, and fever. The patient had not taken non-steroidal anti-inflammatory agents, and the incision related to carpal tunnel syndrome was healing well. Her temperature was 38.5°C, heart rate 122 beats min–1, arterial pressure 120/80 mm Hg, the ventilatory frequency 20 bpm and the coma Glasgow score was 15. There was swelling, oedema, diffuse erythema, and haemorrhagic bullae covering 20% of the right upper limb and axilla.

Laboratory findings showed mild renal impairment (creatinine 142 µmol litre–1, urea nitrogen 12 mmol litre–1), elevated creatine kinase (1091 iu litre–1), hypo natraemia (128 mmol litre–1), hyperglycaemia (10 mmol litre–1), and elevated C-reactive protein (428 mg litre–1) without polynucleosis (white blood cell count 9.6x109 litre–1, neutrophils 6.8x109 litre–1). Other laboratory results were normal. ECG showed sinus tachycardia at a rate of 130 beats min–1. Chest radiograph was normal. Radiograph and Doppler ultrasonographic examination of the right upper extremity were normal.

Shock and tachypnea developed 4 h later. Dopamine (15 µg kg–1 min–1) and dobutamine (20 µg kg–1 min–1) infusions were started after a large fluid infusion (2000 ml of hydroxyethylstarch and 1000 ml of saline 0.9%), the trachea was intubated and ventilatory assistance commenced. Piperacillin/tazobactam and amikacin were the first antibiotics to be administrated 3 h after hospital admission and more than 24 h after first symptoms. The patient was transferred to our intensive care unit. Her haemodynamic status worsened, lactic acidosis, diffuse intravascular coagulation, anuric acute renal failure, and life-threatening hyperkalaemia appeared. Dopamine was replaced by norepinephrine (4 µg kg–1 min–1), multiple transfusion of fresh frozen plasma was given, and dialysis was performed. Surgical treatment was finally possible 24 h after hospital admission and consisted of an amputation of the right upper limb.

The patient died 1 day later of toxic shock syndrome with multiorgan failure. Blood cultures yielded group A Streptococcus, as did muscular biopsy cultures. Histopathological examination confirmed the diagnosis of necrotizing fasciitis with myonecrosis.


    Discussion
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
Necrotizing fasciitis is a soft-tissue infection characterized by rapidly spreading inflammation and subsequent necrosis of the muscle fascia, subcutaneous fat, and in some cases the epidermidis. Necrosis is usually limited in depth to the plane of the muscle fascia.3 Predisposing factors for the development of necrotizing fasciitis as a result of group A Streptococcus include varicella, penetrating injuries, minor cuts, burns, splinters, surgical procedures, childbirth, blunt trauma, and muscle strain. The use of non-steroidal anti-inflammatory agents may delay diagnosis by attenuating the cardinal manifestations of inflammation. Furthermore, because Streptococcus pyogenes impair phagocytic function and alter the host humoral immune responses, a minor infection with this agent may develop into a fulminant one.4 In the current case report, non-steroidal anti-inflammatory agents were not used. However, diabetes and advanced age may have been contributory factors.

Cutaneous signs of streptococcal necrotizing fasciitis are local pain, diffuse swelling, followed by the appearance of bullae filled with clear fluid, which rapidly take on a maroon or violaceous colour.4 Unless appropriate intervention is taken, there is likely to be a rapid evolution to cutaneous gangrene with myonecrosis and extension of inflammatory process. There are marked systemic symptoms, which may include shock and organ failure.3 The early onset of shock and organ failure and the isolation of group A Streptococcus from a normally sterile site are the defining characteristics of the streptococcal toxic shock syndrome.5 New methods of diagnosis have been pursued with computerized tomography and magnetic resonance imaging (MRI). However, confusion can occur with MRI between cellulites and necrotizing fasciitis. Because the sensitivity of MRI exceeds its specificity, MRI can overestimate the extent of deep facial involvement.6

Treatment of streptococcal necrotizing fasciitis includes broad spectrum antimicrobial regimens, prompt and aggressive exploration and debridement of suspected deep seated infection, and supportive measures for the management of shock and multiorgan failure.4 Piperacillin/tazobactam and amikacin were administrated to the patient more than 24 h after first symptoms. In addition, surgical intervention was performed 24 h after hospital admission because of profound shock. This delay in antibiotic and surgical treatment probably affected the outcome. New approaches to treatment include combination therapy with penicillin and clindamycin for an enhanced bactericidal effect. I.V. immunoglobulin has been shown to reduce mortality if the necrotizing fasciitis is associated with toxic shock syndrome.6

A portal of entry from the patient’s skin or from the anaesthetist’s oropharyngeal cavity was suspected. Unfortunately, we were unable to determine whether the anaesthetist was wearing a facemask or not during the regional anaesthesia. Furthermore, no swab was performed to determine the anaesthetist’s carrier status. However, it was not the anaesthetist’s usual preference to wear a facemask. In a postal survey of members of the obstetric anaesthetists association in the UK and Ireland, 273 of the 539 respondents (50.6%) did not wear masks for either spinal or epidural blocks, only 83 out of 259 mask wearers changed their masks between cases, and 50 out of 240 (21%) of those who routinely wore masks did not believe that wearing a mask reduced the risk of infection.7 However, surgical facemasks have been demonstrated to be effective in reducing bacterial contamination caused by dispersal from the upper airway.8 Povidone 10% iodine was used for the patient’s skin preparation. However, there was no record of how long it was allowed to dry. Since this case, usual strict asepsis measures have been continued in the operating room. In addition, wearing a facemask and allowing time to ensure effective antibacterial action of antiseptics have been recommended for the practice of regional anaesthesia.

Other potential sources of infection are contaminated anaesthetic solutions or syringes. However, local anaesthetics have bactericidal activity against commonly encountered skin organisms.9 The bactericidal effect is concentration-related and has been shown to be most marked with bupivacaine 0.5%, and less with lower concentrations.10 The axillary approach compared with other approaches to the brachial plexus may be associated with more risk of infection as a result of hidradenitis and general hygiene issues. However, to our knowledge, no study has demonstrated a significant difference in infection complications between the axillary approach and others.

Streptococcal necrotizing fasciitis is a rare but potentially lethal acute complication that should be acknowledged and recognized by all anaesthetists involved in the practice of regional anaesthesia. Early diagnosis and treatment are essential to improve the outcome of streptococcal necrotizing fasciitis. Rigorous adherence to the principles of asepsis is the foundation of regional anaesthesia-related infection prevention.


    References
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
1 Darchy B, Forceville X, Bavoux E, Soriot F, Domart Y. Clinical and bacteriologic survey of epidural analgesia in patients in the intensive care unit. Anesthesiology 1996; 85: 988–98[CrossRef][ISI][Medline]

2 Agee JM, McCarroll HR, North ER. Endoscopic carpal tunnel release using the single proximal incision technique. Hand Clin 1994; 10: 647–59[ISI][Medline]

3 Chelsom J, Halstensen A, Haga T, Hoiby EA. Necrotizing fasciitis due to group A streptococci in western Norway. Incidence and clinical features. Lancet 1994; 344: 1111–15[ISI][Medline]

4 Bisno AL, Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Med 1996; 334: 240–5[Free Full Text]

5 The Working Group on Severe Streptococcal Infections. Defining the group A streptococcal toxic shock syndrome. Rationale and consensus definition. JAMA 1993; 269: 390–1[CrossRef][ISI][Medline]

6 Seal DV. Necrotizing fasciitis. Curr Opin Infect Dis 2001; 14: 127–32[ISI][Medline]

7 Panikkar KK, Yentis SM. Wearing of masks for obstetric anaesthesia. A postal survey. Anaesthesia 1996; 51: 398–400[ISI][Medline]

8 Philips BJ, Fergusson S, Armstrong P, Anderson FM, Wildsmith JA. Surgical face masks are effective in reducing bacterial contamination caused by dispersal from the upper airway. Br J Anaesth 1992; 69: 407–8[Abstract]

9 Phillips JMG, Stedeford JC, Hartsilver E, Roberts C. Epidural abscess complicating insertion of epidural catheters. Br J Anaesth 2002; 89: 778–82[Abstract/Free Full Text]

10 Sakuragi T, Ishino H, Dan K. Bactericidal activity of clinically used local anesthetics on Staphylococcus aureus. Region Anesth 1996; 21: 239–42[ISI][Medline]





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