- Email: [email protected]
Necrotizing fasciitis of the upper extremity
The Journal of EmergencyMedicine, Vol12, No 5, pp 611-613, 1994 Copyright 0 1994Elsevier ScienceLtd Printed in the USA. All rights reserved
Pergamon
0736-4679/94
--
--
$6.00 + .OO
Clinical Communications
NECROTIZING FASCIITIS OF THE UPPER EXTREMITY Bishara C. Atiyeh, Reprint
MD,
and Ahmad M. Zaatari,
Department of Surgery, American University of Beirut Medical Center, Beirut, Lebanon Address: Bishara C. Atiyeh, MD, AUB c/o 850 Third Avenue, 18th Floor, New York, NY 10022
Cl Abstract -The standard treatment of necrotizing fasciitis is early recognition and early surgical debridement of all necrotic tissues. The use of antibiotics alone does not prove to be effective unless coupled with aggressivesurgical treatment. We present a case of necrotizing fasciitis of unknown cause in a child. Although the only treatment was IV antibiotics and fasciotomy without any debridement, the patient survived the diseasewith minimal morbidity.
in 36 h to 5 days; this may begin with bullae formation, then progress to frank patchy necrosis secondary to vessel thrombosis (1,3). The paramount sign in disease progression is pain beyond the physical findings (4). When such patients are seen in the emergency department, the diagnosis of necrotizing fasciitis should not be excluded simply because of the absence of skin necrosis. As many as 50% of cases present initially with no skin changes (4,5,6). Fever may not be an obvious feature of the disease (7), but leukocytosis is almost always present (5,6). Gas in the soft tissues, when present, can help in making the diagnosis and can be easily seen on plain X-ray studies (1,4,6,7). Diagnosis is confirmed during surgery by the presence of necrotic fascia (6). The most objective diagnostic tool for the emergency physician is a Gram’s stain of aspirate from the skin lesion (7). Hyperbaric oxygen (HBO), by increasing oxygenation of ischemic tissues, will inhibit anaerobic organism growth and lead to their death (8,9). It has also been shown that HBO reduces edema, promotes angiogenesis, and increases phagocytic function (7,10,11). Its use has become standard in many centers in an effort to reduce mortality from necrotizing fasciitis (8). The efficacy of HBO therapy in this disease has not been proven; on the contrary, it may delay surgical intervention (1,4). The key point for its use remains its availability, but it should never delay early surgical debridement (7). The accepted treatment for necrotizing fasciitis is resuscitation and hemodynamic stabilization of the
C1 Keywords - necrotizing fasciitis; infection; soft tissue; amputation; antibiotics
INTRODUCTION
Necrotizing fasciitis is a mixed bacterial infection of the soft tissues. The earliest description of the disease dates back to the work of Joseph Jones in 1871. He described the course of a case of fascial necrosis that he termed “hospital gangrene” (1). Since then, many terms have been used to describe skin, subcutaneous tissues, fascia, and muscle necrosis (2). Meleney in 1927 printed the first description of the disease (1). The current term “necrotizing fasciitis” was introduced in 1952 by Wilson; it describes the infection of the fascia that is the hallmark of the disease (1). Several causes can lead to this mixed flora infection. Necrotizing fasciitis usually begins as a severely tender, erythematous, hot, and swollen area of extensive cellulitis. The infection is peculiar in that it does not respond to the standard regimen of antibiotics, warm compresses, and extremity elevation (1). The disease progresses rapidly, and skin necrosis develops RECEIVED:
MD
28 December 1992; FINAL SUBMISSIONRECEIVED: 30 August 1993;
ACCEPTED: 27 September 1993 611
612
B. C. Atiyeh and A. M. Zaatari
patient with intravenous fluids, wide spectrum antibiotics, and early aggressive surgical debridement (2).
CASE REPORT A 6-year-old male presented to our emergency department with a 3-d history of severe pain, and mottling and cyanosis of his right upper extremity from the shoulder to the tip of the fingers. The condition started with a papule in the distal forearm, accompanied by high-grade fever. No history of trauma or insect bite could be obtained. This condition progressed over 24 h to severe cellulitis of the extremity, fever to 40°C, and hypotension. The patient was admitted to a local hospital where he was resuscitated and started empirically on Metridnidazole, Cefradine, and Gentamicin. Despite hemodynamic stabilization of the patient and antibiotic coverage, the disease progressed proximally, and therefore the patient was transferred to our emergency department. He was alert and oriented, with the following vital signs: temperature, 37.2OC; blood pressure, 100/600 mmHg; pulse, 92 beats per minute; and a respiratory rate of 28 breaths per minute. The right upper extremity was mottled up to the shoulder, tender, and with palpable peripheral pulses. All compartments were severely tense with pain and difficulty in moving the hand and forearm. The white blood cell count was 20,900/mm3, with 82% segmented polymorphonuclear cells and 18% lymphocytes. The hemoglobin was 11.8 g/dL. Platelet count was 90,000/mm3. Blood sugar was 93 mg/ dL, serum sodium 121 meq/L, serum potassium 5.0 meq/L, serum chloride 87 meq/L, serum bicarbonate 23 meq/L, BUN 29 mg/dL, and creatinine 0.5 mg/dL . The X-ray studies of the upper extremity did not show evidence of gas in the subcutaneous tissues. The presumptive diagnosis was necrotizing fasciitis with compartment hypertension. The child was admitted to the hospital, and emergency right arm compartment, right forearm flexor, and extensor compartment fasciotomies were performed. The skin was severely ecchymotic, and the subcutaneous fat was necrotic. Fat and muscle biopsies were taken. The pathology results were compatible with necrotizing fasciitis. Cultures for aerobic and anaerobic organisms and fungi were all negative. A decision was made for disarticulation of the extremity, since after the fasciotomies and despite antibiotics coverage, the neck and anterolateral chest wall skin started to become dusky. The child’s family refused the amputation, and the patient was kept on
medical management. Mottling, pitting edema, and severe tenderness progressively involved the right side of the neck up to the mandibular angle and submental area, the entire right chest wall, and just across the sternum anteriorly and the spine posteriorly to the left side. Distally it reached the iliac crest and the right paraumbilical region. The face was spared, and frank skin necrosis, even minimal, did not develop. On the fifth d postadmission, the patient started to improve; swelling decreased and the mottled chest and extremity slowly regained more normal color. The patient was discharged from the hospital 16 d after admission with clean granulating wounds, and with an ulnar nerve palsy. The child was seen in follow-up 2 months after discharge. He had completely healed fasciotomies with a moderate ulnar deformity of his right hand. Since then he has been lost to follow-up.
DISCUSSION Early recognition of necrotizing fasciitis has led to an increase in the reported incidence of the disease (3). However, current practice is that outcome can be improved only by adequate surgical treatment (4). Most commonly, the condition is caused by a mixture of bacteria, sometimes difficult to determine by standard bacteriologic tests (3). Streptococcal species are most usually identified (12). The disease process involves mainly the extremities (4,5). The initiating injury may range from unknown causes (6) to minor trauma (3) to operative intervention (7). The disease in the upper extremities occurs most commonly in adolescence and adulthood (6), but infection in the pediatric age group can occur at any site (8). Early diagnosis and aggressive surgical debridement is the hallmark of the treatment plan (1,3,4,6, 7,8,13). Mortality rates range from 8 to 67% despite treatment (2), and may reach 100% if shock is the initial presentation (6). Delay in diagnosis and surgical debridement increases morbidity and mortality (495% The patient presented to us partially treated with definite evidence of progressive cellulitis and pitting edema of his right upper extremity reaching the axilla and the chest wall. He had clinical evidence of compartment hypertension. The patient clinically and pathologically had necrotizing fasciitis. No frank pus was seen, however, in the fascial plane, and there was no skin necrosis. The family’s refusal of amputation did not allow us to give the patient what we thought to be adequate treatment. A court order to proceed with treatment is not possible under our law. The
613
Necrotizing Fasciitis
child’s condition continued to deteriorate with progressive cellulitis across the neck, upper back, and chest wall without change in the hemodynamic profile. Complete resolution of the cellulitis after that severe deterioration, and on antibiotics without any surgical debridement, was unexpected. Our patient first presented in shock to another hospital. This is an extremely grave sign indicating a poor prognosis (1,4,6,7,8,12,13). In our hospital, only fasciotomies were performed. Any debridement would have meant amputation of the right upper extremity. Facilities for HBO therapy, which would have been of benefit, are not available in our institution. Despite antibiotic therapy, cellulitis rapidly progressed then started regressing 8 d after the onset of the illness. Physicians are often required to make difficult decisions that will have a serious impact on the lives of their patients. The ethical and moral responsibility is great; our judgment will not only determine the immediate outcome of the disease but will affect the future of the patient. The essence of the medical profession is the welfare of the patient, which may be forgotten in the midst of our scientific and technical zeal. Were we justified in offering amputation to this child? There is nothing in the medical literature to indicate any other way to treat this condition (1,3,4, 6,8,13), Thus, our present knowledge of the disease does not enable us to avoid potentially unnecessary amputation. Conversely, can it ever be justified to endanger the life of a patient to save a limb? The study of this case may lead us to determine some favorable factors that will be helpful in planning therapy of future cases and possibly in avoiding unnecessary amputation. Verification of these is needed in future studies. Of the grave prognostic signs, our
patient was initially admitted in shock to a peripheral hospital 24 h after the appearance of a pustule on his right forearm. Rapid and effective resuscitation saved him multiorgan failure that would have minimized his chances of survival. Strikingly, this patient never developed gross purulence of the deep fascial layer of frank muscle necrosis, and he did not develop skin necrosis. Despite progression of cellulitis, the patient remained hemodynamically stable. All these factors may have contributed to the final favorable outcome, in addition to the fact that the child did not have any aggravating risk factors such as systemic diseases, diabetes, cancer, or immune deficiency states (1,4,6,7). In our opinion, surgical debridement, when it does not mean amputation, should always be performed without hesitation for necrotizing fasciitis. When effective debridement is not possible without amputation, it may be safe not to amputate a limb in the absence of frank purulence, gross muscle, fat, and skin necrosis since this may indicate a relatively benign course. In such situations, HBO therapy may be beneficial. Fasciotomies, when indicated, should be performed without any delay. Failure to do so will make amputation inevitable.
CONCLUSION A case of necrotizing fasciitis is presented, and its successful resolution with fasciotomy and intravenous antibiotics without surgical debridement is detailed. Factors indicating a favorable outcome are postulated. These factors, when present, may prevent unnecessary surgery in the future. Further studies are needed for this purpose.
REFERENCES 1. Janevicius RV, Hann SE, Batt MD. Necrotizing fasciitis. Surg Gynecol Obstet. 1982;154:97-102. 2. Simmons RL, Ahrenholz DH. Infections of the skin and soft tissues. In: Howard RJ, Simmons RL, eds. Surgical infectious diseases. Norwalk, Connecticut: Appleton and Lange; 1988: 404-8. 3. Rea WJ, Wyrick WJ Jr. Necrotizing fasciitis. Ann Surg. 1970; 172:957+X 4. Sudarsky LA, Laschinger JC, Coppa JF, Spencer FC. Improved results from a standardized approach in treating patients with necrotizing fasciitis. Ann Surg. 1987;206:661-5. 5. Freeman HP, Oluwde SF, Ganepda GAP, Dy E. Necrotizing fasciitis. Am J Surg. 1981;142:377-83. 6. Schecter W, Meyer A, Schecter G, et al. Necrotizing fasciitis of the upper extremity. J Hand Surg. 1982;7:15-20. 7. Goldwag DA, Porcell TB. Necrotizing fasciitis in the pediatric age group: report of a case. J Emerg Med. 1990;8:229-304.
8. Gozal D, Ziser A, Shupak A, et al. Necrotizing fasciitis. Arch Surg. 1986;121:233-5. 9. Hunt TK, Linsey M, Grislis G. The effect of differing ambient oxygen tension on wound infection. Ann Surg. 1975;181: 35-39. 10. Holland JA, Hill GB, Wolfe WG, et al. Experimental and clinical experience with hyperbaric oxygen in the treatment of clostridial myonecrosis. Surg. 1975;77:75-85. 11. Tehrani MA, Ledingham IMA. Necrotizing fasciitis. Postgrad Med J. 1977;53:237-42. 12. Giuliano A, Lewis F Jr., Hadly K, Blaisdell FW. Bacteriology of necrotizing fasciitis. Am J Surg. 1977;134:52-7. 13. Tehrani MA, Webster MHC, Robinson DW, Ledingham IM. Necrotizing fasciitis treated by radical excision of the overlying skin. Br J Plast Surg. 1976;29:74-7.
Pergamon
0736-4679/94
--
--
$6.00 + .OO
Clinical Communications
NECROTIZING FASCIITIS OF THE UPPER EXTREMITY Bishara C. Atiyeh, Reprint
MD,
and Ahmad M. Zaatari,
Department of Surgery, American University of Beirut Medical Center, Beirut, Lebanon Address: Bishara C. Atiyeh, MD, AUB c/o 850 Third Avenue, 18th Floor, New York, NY 10022
Cl Abstract -The standard treatment of necrotizing fasciitis is early recognition and early surgical debridement of all necrotic tissues. The use of antibiotics alone does not prove to be effective unless coupled with aggressivesurgical treatment. We present a case of necrotizing fasciitis of unknown cause in a child. Although the only treatment was IV antibiotics and fasciotomy without any debridement, the patient survived the diseasewith minimal morbidity.
in 36 h to 5 days; this may begin with bullae formation, then progress to frank patchy necrosis secondary to vessel thrombosis (1,3). The paramount sign in disease progression is pain beyond the physical findings (4). When such patients are seen in the emergency department, the diagnosis of necrotizing fasciitis should not be excluded simply because of the absence of skin necrosis. As many as 50% of cases present initially with no skin changes (4,5,6). Fever may not be an obvious feature of the disease (7), but leukocytosis is almost always present (5,6). Gas in the soft tissues, when present, can help in making the diagnosis and can be easily seen on plain X-ray studies (1,4,6,7). Diagnosis is confirmed during surgery by the presence of necrotic fascia (6). The most objective diagnostic tool for the emergency physician is a Gram’s stain of aspirate from the skin lesion (7). Hyperbaric oxygen (HBO), by increasing oxygenation of ischemic tissues, will inhibit anaerobic organism growth and lead to their death (8,9). It has also been shown that HBO reduces edema, promotes angiogenesis, and increases phagocytic function (7,10,11). Its use has become standard in many centers in an effort to reduce mortality from necrotizing fasciitis (8). The efficacy of HBO therapy in this disease has not been proven; on the contrary, it may delay surgical intervention (1,4). The key point for its use remains its availability, but it should never delay early surgical debridement (7). The accepted treatment for necrotizing fasciitis is resuscitation and hemodynamic stabilization of the
C1 Keywords - necrotizing fasciitis; infection; soft tissue; amputation; antibiotics
INTRODUCTION
Necrotizing fasciitis is a mixed bacterial infection of the soft tissues. The earliest description of the disease dates back to the work of Joseph Jones in 1871. He described the course of a case of fascial necrosis that he termed “hospital gangrene” (1). Since then, many terms have been used to describe skin, subcutaneous tissues, fascia, and muscle necrosis (2). Meleney in 1927 printed the first description of the disease (1). The current term “necrotizing fasciitis” was introduced in 1952 by Wilson; it describes the infection of the fascia that is the hallmark of the disease (1). Several causes can lead to this mixed flora infection. Necrotizing fasciitis usually begins as a severely tender, erythematous, hot, and swollen area of extensive cellulitis. The infection is peculiar in that it does not respond to the standard regimen of antibiotics, warm compresses, and extremity elevation (1). The disease progresses rapidly, and skin necrosis develops RECEIVED:
MD
28 December 1992; FINAL SUBMISSIONRECEIVED: 30 August 1993;
ACCEPTED: 27 September 1993 611
612
B. C. Atiyeh and A. M. Zaatari
patient with intravenous fluids, wide spectrum antibiotics, and early aggressive surgical debridement (2).
CASE REPORT A 6-year-old male presented to our emergency department with a 3-d history of severe pain, and mottling and cyanosis of his right upper extremity from the shoulder to the tip of the fingers. The condition started with a papule in the distal forearm, accompanied by high-grade fever. No history of trauma or insect bite could be obtained. This condition progressed over 24 h to severe cellulitis of the extremity, fever to 40°C, and hypotension. The patient was admitted to a local hospital where he was resuscitated and started empirically on Metridnidazole, Cefradine, and Gentamicin. Despite hemodynamic stabilization of the patient and antibiotic coverage, the disease progressed proximally, and therefore the patient was transferred to our emergency department. He was alert and oriented, with the following vital signs: temperature, 37.2OC; blood pressure, 100/600 mmHg; pulse, 92 beats per minute; and a respiratory rate of 28 breaths per minute. The right upper extremity was mottled up to the shoulder, tender, and with palpable peripheral pulses. All compartments were severely tense with pain and difficulty in moving the hand and forearm. The white blood cell count was 20,900/mm3, with 82% segmented polymorphonuclear cells and 18% lymphocytes. The hemoglobin was 11.8 g/dL. Platelet count was 90,000/mm3. Blood sugar was 93 mg/ dL, serum sodium 121 meq/L, serum potassium 5.0 meq/L, serum chloride 87 meq/L, serum bicarbonate 23 meq/L, BUN 29 mg/dL, and creatinine 0.5 mg/dL . The X-ray studies of the upper extremity did not show evidence of gas in the subcutaneous tissues. The presumptive diagnosis was necrotizing fasciitis with compartment hypertension. The child was admitted to the hospital, and emergency right arm compartment, right forearm flexor, and extensor compartment fasciotomies were performed. The skin was severely ecchymotic, and the subcutaneous fat was necrotic. Fat and muscle biopsies were taken. The pathology results were compatible with necrotizing fasciitis. Cultures for aerobic and anaerobic organisms and fungi were all negative. A decision was made for disarticulation of the extremity, since after the fasciotomies and despite antibiotics coverage, the neck and anterolateral chest wall skin started to become dusky. The child’s family refused the amputation, and the patient was kept on
medical management. Mottling, pitting edema, and severe tenderness progressively involved the right side of the neck up to the mandibular angle and submental area, the entire right chest wall, and just across the sternum anteriorly and the spine posteriorly to the left side. Distally it reached the iliac crest and the right paraumbilical region. The face was spared, and frank skin necrosis, even minimal, did not develop. On the fifth d postadmission, the patient started to improve; swelling decreased and the mottled chest and extremity slowly regained more normal color. The patient was discharged from the hospital 16 d after admission with clean granulating wounds, and with an ulnar nerve palsy. The child was seen in follow-up 2 months after discharge. He had completely healed fasciotomies with a moderate ulnar deformity of his right hand. Since then he has been lost to follow-up.
DISCUSSION Early recognition of necrotizing fasciitis has led to an increase in the reported incidence of the disease (3). However, current practice is that outcome can be improved only by adequate surgical treatment (4). Most commonly, the condition is caused by a mixture of bacteria, sometimes difficult to determine by standard bacteriologic tests (3). Streptococcal species are most usually identified (12). The disease process involves mainly the extremities (4,5). The initiating injury may range from unknown causes (6) to minor trauma (3) to operative intervention (7). The disease in the upper extremities occurs most commonly in adolescence and adulthood (6), but infection in the pediatric age group can occur at any site (8). Early diagnosis and aggressive surgical debridement is the hallmark of the treatment plan (1,3,4,6, 7,8,13). Mortality rates range from 8 to 67% despite treatment (2), and may reach 100% if shock is the initial presentation (6). Delay in diagnosis and surgical debridement increases morbidity and mortality (495% The patient presented to us partially treated with definite evidence of progressive cellulitis and pitting edema of his right upper extremity reaching the axilla and the chest wall. He had clinical evidence of compartment hypertension. The patient clinically and pathologically had necrotizing fasciitis. No frank pus was seen, however, in the fascial plane, and there was no skin necrosis. The family’s refusal of amputation did not allow us to give the patient what we thought to be adequate treatment. A court order to proceed with treatment is not possible under our law. The
613
Necrotizing Fasciitis
child’s condition continued to deteriorate with progressive cellulitis across the neck, upper back, and chest wall without change in the hemodynamic profile. Complete resolution of the cellulitis after that severe deterioration, and on antibiotics without any surgical debridement, was unexpected. Our patient first presented in shock to another hospital. This is an extremely grave sign indicating a poor prognosis (1,4,6,7,8,12,13). In our hospital, only fasciotomies were performed. Any debridement would have meant amputation of the right upper extremity. Facilities for HBO therapy, which would have been of benefit, are not available in our institution. Despite antibiotic therapy, cellulitis rapidly progressed then started regressing 8 d after the onset of the illness. Physicians are often required to make difficult decisions that will have a serious impact on the lives of their patients. The ethical and moral responsibility is great; our judgment will not only determine the immediate outcome of the disease but will affect the future of the patient. The essence of the medical profession is the welfare of the patient, which may be forgotten in the midst of our scientific and technical zeal. Were we justified in offering amputation to this child? There is nothing in the medical literature to indicate any other way to treat this condition (1,3,4, 6,8,13), Thus, our present knowledge of the disease does not enable us to avoid potentially unnecessary amputation. Conversely, can it ever be justified to endanger the life of a patient to save a limb? The study of this case may lead us to determine some favorable factors that will be helpful in planning therapy of future cases and possibly in avoiding unnecessary amputation. Verification of these is needed in future studies. Of the grave prognostic signs, our
patient was initially admitted in shock to a peripheral hospital 24 h after the appearance of a pustule on his right forearm. Rapid and effective resuscitation saved him multiorgan failure that would have minimized his chances of survival. Strikingly, this patient never developed gross purulence of the deep fascial layer of frank muscle necrosis, and he did not develop skin necrosis. Despite progression of cellulitis, the patient remained hemodynamically stable. All these factors may have contributed to the final favorable outcome, in addition to the fact that the child did not have any aggravating risk factors such as systemic diseases, diabetes, cancer, or immune deficiency states (1,4,6,7). In our opinion, surgical debridement, when it does not mean amputation, should always be performed without hesitation for necrotizing fasciitis. When effective debridement is not possible without amputation, it may be safe not to amputate a limb in the absence of frank purulence, gross muscle, fat, and skin necrosis since this may indicate a relatively benign course. In such situations, HBO therapy may be beneficial. Fasciotomies, when indicated, should be performed without any delay. Failure to do so will make amputation inevitable.
CONCLUSION A case of necrotizing fasciitis is presented, and its successful resolution with fasciotomy and intravenous antibiotics without surgical debridement is detailed. Factors indicating a favorable outcome are postulated. These factors, when present, may prevent unnecessary surgery in the future. Further studies are needed for this purpose.
REFERENCES 1. Janevicius RV, Hann SE, Batt MD. Necrotizing fasciitis. Surg Gynecol Obstet. 1982;154:97-102. 2. Simmons RL, Ahrenholz DH. Infections of the skin and soft tissues. In: Howard RJ, Simmons RL, eds. Surgical infectious diseases. Norwalk, Connecticut: Appleton and Lange; 1988: 404-8. 3. Rea WJ, Wyrick WJ Jr. Necrotizing fasciitis. Ann Surg. 1970; 172:957+X 4. Sudarsky LA, Laschinger JC, Coppa JF, Spencer FC. Improved results from a standardized approach in treating patients with necrotizing fasciitis. Ann Surg. 1987;206:661-5. 5. Freeman HP, Oluwde SF, Ganepda GAP, Dy E. Necrotizing fasciitis. Am J Surg. 1981;142:377-83. 6. Schecter W, Meyer A, Schecter G, et al. Necrotizing fasciitis of the upper extremity. J Hand Surg. 1982;7:15-20. 7. Goldwag DA, Porcell TB. Necrotizing fasciitis in the pediatric age group: report of a case. J Emerg Med. 1990;8:229-304.
8. Gozal D, Ziser A, Shupak A, et al. Necrotizing fasciitis. Arch Surg. 1986;121:233-5. 9. Hunt TK, Linsey M, Grislis G. The effect of differing ambient oxygen tension on wound infection. Ann Surg. 1975;181: 35-39. 10. Holland JA, Hill GB, Wolfe WG, et al. Experimental and clinical experience with hyperbaric oxygen in the treatment of clostridial myonecrosis. Surg. 1975;77:75-85. 11. Tehrani MA, Ledingham IMA. Necrotizing fasciitis. Postgrad Med J. 1977;53:237-42. 12. Giuliano A, Lewis F Jr., Hadly K, Blaisdell FW. Bacteriology of necrotizing fasciitis. Am J Surg. 1977;134:52-7. 13. Tehrani MA, Webster MHC, Robinson DW, Ledingham IM. Necrotizing fasciitis treated by radical excision of the overlying skin. Br J Plast Surg. 1976;29:74-7.