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Necrotizing fasciitis – A rare fatal outcome of road traffic accidents
Egyptian Journal of Forensic Sciences (2013) 3, 92–95
Contents lists available at SciVerse ScienceDirect
Egyptian Journal of Forensic Sciences journal homepage: www.ejfs.org
CASE REPORT
Necrotizing fasciitis – A rare fatal outcome of road traffic accidents Siddhartha Das a b
a,*
, Debdatta Basu b, G. Manigandan
a
Department of Forensic Medicine & Toxicology, JIPMER, Puducherry 605006, India Department of Pathology, JIPMER, Puducherry 605006, India
Received 28 February 2013; revised 1 April 2013; accepted 3 April 2013 Available online 26 May 2013
KEYWORDS Infections; Negligence; Post-accidental care; Necrotizing fasciitis; Septic shock
Abstract Along with the benefits it provides, road transportation has many disadvantages such as traffic casualties, respiratory illnesses, pollution (both air and noise), emission of green house gases, and consumption of national resources. Of these, traffic casualties are one of the major factors that have a major effect on people’s health. Most of the victims die as a direct result of the injury. However a considerable number of road traffic fatalities actually occur in the hospitals as a result of infections and negligence, rather than as a direct result of the injury. Proper diagnosis and post-accident care of the victims become very essential in saving many lives. Necrotizing fasciitis is a severe form of soft tissue infection that primarily involves the superficial fascia. Usually it occurs after trauma or is post operative. Sepsis is the major factor responsible for the late death of victims of road traffic accidents. This study reports the case of a 48-year-old man who survived an accident with a motorized two wheeler, following which he developed a rare complication, necrotizing fasciitis and died of septic shock. This article deals with the approach of a forensic pathologist in cases of delayed death due to road traffic accidents. ª 2013 Production and hosting by Elsevier B.V. on behalf of Forensic Medicine Authority.
1. Introduction More than 1.2 million people die on the roads every year worldwide. Road traffic injuries are one of the top three causes of death for people aged between 5 and 44 years. Pedestrians, * Corresponding author. Tel.: +91 9677523598. E-mail addresses: [email protected], drsiddharthadas@yahoo. com (S. Das). Peer review under responsibility of Forensic Medicine Authority.
Production and hosting by Elsevier
cyclists, and drivers of motorized two-wheelers and their passengers account for almost half of the global road traffic deaths.1 A considerable number of victims of road traffic accidents (RTAs) die as a result of septicaemic shock and multi-organ failure in hospitals. Necrotizing soft tissue infections cover a broad spectrum of clinical entities ranging from mild pyodermas to life threatening necrotizing fasciitis.2 Necrotizing fasciitis (NF) is a rare life threatening complication which may occur following trauma like RTAs. They are associated with a high mortality and can affect any of the layers within the soft tissue compartment (dermis, subcutaneous tissue, superficial fascia, deep fascia or muscle).3 They were first described by Jones (1871) as ‘hospital gangrene’ and Wilson (1952) subsequently used the term NF,
2090-536X ª 2013 Production and hosting by Elsevier B.V. on behalf of Forensic Medicine Authority. http://dx.doi.org/10.1016/j.ejfs.2013.04.001
Necrotizing fasciitis – A rare fatal outcome of road traffic accidents which is now recognized to describe a rapidly progressive infection of the fascia and subcutaneous tissue, with thrombosis of the microcirculation.3 It may result from any insult to the integumentary system or from hematogenous spread and can develop at the site of a skin biopsy, laceration, insect bite, needle puncture, surgical wound, skin abscess and areas affected by herpes zoster, or a chronic venous ulcer.4 2. Case report A 48-year-old man with no known co-morbidities came to the hospital with complaints of an ulcerated wound over his right thigh, inguinal and gluteal region. Upon evaluation there was an alleged history of being hit by a two wheeler one month prior leading to a clavicular fracture and a hematoma over the right upper thigh. He received the initial treatment in a local hospital, where he was managed conservatively for a week and then discharged. About 10 days after, he noticed a discoloration of the right upper thigh, which progressed to blebs and finally ruptured to a painful ulcer. On examination he was found to be pale, febrile and toxemic with a pulse rate of 120 beats/minute and a blood pressure of 100/60 mmHg in the supine position. Ulcerated wounds without any abscess formation were seen involving the lower part of the right side of his abdomen, right upper thigh, perineal, gluteal and hip region. His hemoglobin level was 9.2 gm%, random blood glucose 110 mg/dl, WBC count 29000 cells/mm3, C-reactive protein (CRP) 150 mg/L, serum urea 117 mg/dl and serum creatinine 2.2 mg/dl. The rest of the biochemical investigations were within normal range. A provisional diagnosis of necrotizing fasciitis was made, and a broad-spectrum antibiotic therapy was commenced along with analgesics, antacids and IV fluids. His condition worsened rapidly and he expired within 24 hours of his admission. The autopsy was conducted the next day. He was of average build with body length of 170 cm and his body weight was 55 kg. An ulcerated wound of 32–38cm was present involving the lower part of the right side of the abdomen, inguinal region, right upper thigh, right gluteal region and lower part of the back on the right side. Ulceration and necrosis were restricted to skin and subcutaneous tissues and the underlying muscles were exposed. The scrotum and penis were edematous and the shaft of the penis was ulcerated. Upon internal examination his brain and lungs were of average weight and were found to be congested and edematous. The liver, spleen, kidneys and adrenals were also congested. His heart had a normal tone and weighed 200 g with normal appearance of walls, valves and patent coronaries. Petechial hemorrhages were noticed in the brain and on the surface of the heart. The rest of the examination was unremarkable. Tissues taken from the wound were sent for histopathological examination which showed ulcerated skin with necrosis of the dermis and subcutaneous fat. There was a dense neutrophilic infiltrate with congested blood vessels and no microorganisms could be identified. The histological features were compatible with necrotizing fasciitis (Fig. 1). 3. Discussion NF which is also known as ‘flesh-eating bacteria syndrome’, is an uncommon fatal outcome of RTAs. A variety of terms are
93
used to describe this condition such as Fournier’s gangrene, phagedena, phagedena gangrene, hospital gangrene, progressive bacterial synergistic gangrene (Meleney’s gangrene) and hemolytic streptococcal gangrene, depending on the site of infection.5 Its pathogenesis is not entirely understood. It is characterized by the spreading of microorganisms along the fascial planes and necrosis of the soft tissues. If not treated in a timely manner, it may also involve the muscles.6 Diabetes Mellitus (DM) is the leading predisposing underlying medical condition because of peripheral neuropathy, peripheral vascular disease and immunosuppression.7 High blood sugar in these patients predisposes to an environment of low oxygen tension and a rich substrate for bacterial growth.5 Microbiologically, NF is classified as Type 1 (polymicrobial) and type 2 (monomicrobial).8 Polymicrobial infections are more common,9,10 with cultures yielding a mixture of aerobic and anaerobic organisms.10 Type 1 NF occurs in immunocompromised individuals, such as patients with diabetes mellitus or chronic renal failure; whereas type 2 NF afflicts healthy patients with no implicative co morbidities and who often have a history of minor trauma.8 The usual etiologic isolates consist of Gram-positive organisms, such as Staphylococcus aureus, Streptococcus pyogenes and Enterococci; Gram-negative aerobes, such as Escherichia coli and Pseudomonas species; and anaerobic organisms, such as Bacteroides or Clostridium species.8,11 The two most common organisms encountered in Hong Kong were Streptococci and Vibrio species, the latter being highly virulent and particularly encountered by seafood handlers.4 One prospective study from Nigeria reported the commonest offending organisms as Staphylococcus aureus and Pseudomonas in children and adults, respectively.12 Another prospective study from India observed the monomicrobial infections (55.6%) to be more common than polymicrobial (44.4%), with the predominant organisms being Pseudomonas aeruginosa (23%) followed by Klebsiella pneumonia and Staphylococcus aureus (16% each).5 Etiologic agents like Hemophilus influenza serotype f, Lancefield group G Streptococcus, Aeromonas hydrophila, Clostridium difficile, Candida albicans and Candida tropicalis have also been reported.3,13–16 In this case the organism isolated from the wound culture was Staphylococcus aureus. Polymicrobial infections typically occur in the perineum and trunk, whereas monomicrobial infections occur in the limbs.8 According to a retrospective review from Canada, common sites of infection included the lower extremities (28%), upper extremities (27%), perineum (21%), trunk (18%), and the head and neck (5%).17 One prospective study involving 50 cases found the calf region as the most common site of infection (59.5%), which was explainable since most of the patients were diabetics and more prone to lower limb infections.5 Another observation from Nigeria reported the trunk as the most commonly involved anatomical region of the body (50%) in children, while in adults it was the lower limbs (54.2%).12 Where there is a history of trauma or infection, more than 60% commence in the lower extremities.6 In the present case also, the patient had a history of trauma and the site of NF was the hip, perineum and adjoining lower extremity. Robin et al. reported a young girl who developed rapidly progressive NF of the face secondary to a mild traumatic wound in the upper eyelid.18
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Figure 1 Photomicrograph showing necrosis of dermis and subcutaneous fat with infiltration by neutrophils and a few congested vessels (Hematoxylin and Eosin X 400).
Risk factors for mortality include: age greater than 60 years, elevated lactate dehydrogenase, increasing length of time from admission to debridement, diabetes, chronic disease, immunosuppressive drug use (e.g. prednisolone), malnutrition, peripheral vascular disease, renal failure, underlying malignancy, obesity, intravenous drug use, trunk/perineal involvement and positive blood cultures for B-Streptococcus and bacteremia.8,16 A study from Los Angeles observed the following coexisting conditions or risk factors: current or past injection-drug use (43%); previous methicillin resistant Staphylococcus aureus (MRSA) infection, diabetes, and chronic hepatitis C (21% each); and cancer and human immunodeficiency virus infection or the acquired immunodeficiency syndrome (7% each); four patients (29%) had no serious coexisting conditions or risk factors.11 Most of the studies conducted agree that diabetes mellitus, trauma, surgery, and minor skin infections are the main risk/precipitating factors.5,9,12,19 Usually the patient appears to be toxic. Toxicity is severe and renal impairment may precede the development of shock.20 Septicemia was observed to be the commonest complication (57.1%) in one study.12 In the reported case, renal parameters were elevated suggesting the compromised renal function preceding death due to septic shock. The most common early signs are swelling, pain, erythema, fever, local warmth, skin induration, and tenderness.5,719 Pain out of proportion to the apparent severity of the lesion should alert the physician to a possible diagnosis of NF,7 as was observed in this case. Patches of skin necrosis, tissue crepitus, fluctuance and systemic evidence of sepsis such as hyperthermia, tachycardia and hypotension are alarming signs.7 In the present case the patient was febrile and toxemic and the wound had developed into a painful ulcer. The mortality rates as reported by different authors over the years vary from 6%–76%.7 Death due to renal failure as a result of hypovolemia and cardiovascular collapse caused by septic shock may occur.21 In one case, the patient died because of multiple organ failure and sepsis with Pseudomonas
aeruginosa.14 As per Mathew et al. hyperacute cases present with sepsis and quickly progress to multiorgan failure (40%).5 The keys to successful patient treatment of NF rest on early recognition, adequate resuscitation, broad-spectrum antibiotic therapy, radical surgical debridement and supportive care including fluid replacement, blood pressure support, analgesia, nutritional support and intensive care involvement.7,12 Although NF is a rare disease, physicians must be well trained in its diagnosis and treatment. Early diagnosis of the condition poses a challenge and a high index of suspicion is essential. One of the most challenging aspects is its similarities with cellulitis. It is safer to treat these ambiguous cases as NF and manage them aggressively with surgical debridement and broad spectrum antibiotics, as delay in treatment can be life threatening.4 NF is one of the greatest challenges from both a therapeutic and financial perspective, especially in the poor third world countries. Inadequate clinical exposure to such cases may lead to delay in diagnosis, thereby resulting in a fatal outcome and inviting charges of medical negligence.2 In conclusion, an experienced forensic pathologist may not have difficulties in diagnosing a case at autopsy, which may not be so for the lesser experienced young pathologist who was previously unexposed to such a case. In order to avoid such an unpleasant situation and especially where he has to certify the cause of death, it becomes imperative on his part to be aware of this clinical entity at autopsy. Through this case report the authors have highlighted the importance of proper history taking, going through the hospital case records wherever available and discussing the case with the treating physician if required. Histopathological examination, wound and blood cultures are important ancillary investigations that should be carried out routinely. Funding None.
Necrotizing fasciitis – A rare fatal outcome of road traffic accidents Conflict of interest None declared. Ethical approval Necessary ethical approval was obtained from the institute ethics committee. References 1. Global status report on road safety: time for action. Geneva, World Health Organization, 2009. Accessed 29.11.11). 2. Heinze S, Puschel K, Tsokos M. Necrotizing fasciitis with fatal outcome: a report of two cases. Forensic Sci Med Pathol 2011;7:278–82. 3. McLellan E, Suvarna K, Townsend R. Fatal Necrotizing fasciitis caused by Haemophilus influenza serotype f. J Med Microbiol 2008;57:249–51. 4. Cheung JPY, Fung B, Tang WM, Ip WY. A review of Necrotizing fasciitis in the extremities. Hong Kong Med J 2009;15:44–52. 5. Mathew A, Mridula M, Vishwanath S, Mukhopadhyay C, Rodrigues G. Clinico-microbiological profile of Necrotizing fasciitis secondary to diabetes mellitus in a tertiary care hospital. WebmedCent. Gen. Surg. 2010;1(12), WMC001399. 6. Greenbaum AR, Chan CLH. Skin and subcutaneous tissue. In: Williams NS, Bulstrode CJK, O’Connell, editors. Bailey and Love’s short practice of surgery. London: Hodder Arnold; 2008. p. 593–620. 7. Naqvi GA, Malik SA, Jan W. Necrotizing Fasciitis of the lower extremity: a case report and current concept of diagnosis and management. Scand J Trauma Resusc Emerg Med 2009;17:28, . 8. Puvanendran R, Huey JCM, Pasupathy S. Necrotising fasciitis. Can Fam Physician 2009;55:981–7. 9. Turhan O, Bu¨yu¨ktuna SA, Inan D, Saba R, Yalc¸ın AN. Clinical evaluation of forty-four patients with necrotizing fasciitis. Turk J Trauma Emerg Surg 2011;17:29–32.
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10. Elliot D, Kufera JA, Myers RA. The microbiology of necrotizing soft tissue infections. Am J Surg 2000;179:361–6. 11. Miller LG, Perdreau-Remington F, Rieg G, Mehdi S, Perlroth J, Bayer AS, et al. Necrotizing fasciitis caused by communityassociated methicillin-resistant Staphylococcus aureus in Los Angeles. N Engl J Med 2005;352:1445–53. 12. Legbo JN, Shehu BB. Necrotizing fasciitis: a comparative analysis of 56 cases. J Natl Med Assoc 2005;97:1692–7. 13. Rausch J, Foca M. Necrotizing fasciitis in a paediatric patient caused by Lancefield Group G streptococcus: case report and brief review of the literature, vol. 2011. Hindawi Publishing Corporation Case Reports in Medicine; 2011. 5 p. doi:http://dx.doi.org/ 10.1155/2011/671365 Article ID 671365. 14. Borger van der Burg BLS, Bronkhorst MWGA, Pahlplatz PVM. Aeromonas hydrophilia Necrotizing fasciitis: a case report. J Bone Joint Surg Am 2006;88:1357–60. 15. Bhargava A, Sen P, Swaminathan A, Ogbolu C, Chechko S, Stone F. Rapidly progressive necrotizing fasciitis and gangrene due to clostridium difficile: case report. Clin Infect Dis 2000;30:954–5. 16. Eisen DB, Brown E. Necrotizing fasciitis following a motor vehicle accident with Candida species as the sole organisms. Can J Plast Surg 2004;12:43–6. 17. Golger A, Ching S, Goldsmith CH, Pennie RA, Bain JR. Mortality in patients with necrotizing fasciitis. Plast Reconstr Surg 2007;119:1803–7. 18. Robin A, Me´ry G, George JL, Maalouf T, Angioi K. Facial necrotizing fasciitis after mild trauma of the eyelid: role of non steroidal anti-inflammatory treatment. J Fr Ophthalmol 2010;33:568–72. 19. Sin FP, Yuen MC, Lam KW, et al. A retrospective review of patients with necrotizing fasciitis presenting to an emergency department in Hong Kong. Hong Kong J Emerg Med 2002;9:10–7. 20. Stevens DL. Infections of the skin, muscle and soft tissues. In: Fauci AS, Kasper DL, Longo DL, et al., editors. Harrison’s principles of internal medicine. New York: McGraw Hill Medical; 2008. p. 798–803. 21. Rashid M. Disaster surgery. In: Williams NS, Bulstrode CJK, O’Connell PR, editors. Bailey and Love’s short practice of surgery. London: Hodder Arnold; 2008. p. 410–25.
Contents lists available at SciVerse ScienceDirect
Egyptian Journal of Forensic Sciences journal homepage: www.ejfs.org
CASE REPORT
Necrotizing fasciitis – A rare fatal outcome of road traffic accidents Siddhartha Das a b
a,*
, Debdatta Basu b, G. Manigandan
a
Department of Forensic Medicine & Toxicology, JIPMER, Puducherry 605006, India Department of Pathology, JIPMER, Puducherry 605006, India
Received 28 February 2013; revised 1 April 2013; accepted 3 April 2013 Available online 26 May 2013
KEYWORDS Infections; Negligence; Post-accidental care; Necrotizing fasciitis; Septic shock
Abstract Along with the benefits it provides, road transportation has many disadvantages such as traffic casualties, respiratory illnesses, pollution (both air and noise), emission of green house gases, and consumption of national resources. Of these, traffic casualties are one of the major factors that have a major effect on people’s health. Most of the victims die as a direct result of the injury. However a considerable number of road traffic fatalities actually occur in the hospitals as a result of infections and negligence, rather than as a direct result of the injury. Proper diagnosis and post-accident care of the victims become very essential in saving many lives. Necrotizing fasciitis is a severe form of soft tissue infection that primarily involves the superficial fascia. Usually it occurs after trauma or is post operative. Sepsis is the major factor responsible for the late death of victims of road traffic accidents. This study reports the case of a 48-year-old man who survived an accident with a motorized two wheeler, following which he developed a rare complication, necrotizing fasciitis and died of septic shock. This article deals with the approach of a forensic pathologist in cases of delayed death due to road traffic accidents. ª 2013 Production and hosting by Elsevier B.V. on behalf of Forensic Medicine Authority.
1. Introduction More than 1.2 million people die on the roads every year worldwide. Road traffic injuries are one of the top three causes of death for people aged between 5 and 44 years. Pedestrians, * Corresponding author. Tel.: +91 9677523598. E-mail addresses: [email protected], drsiddharthadas@yahoo. com (S. Das). Peer review under responsibility of Forensic Medicine Authority.
Production and hosting by Elsevier
cyclists, and drivers of motorized two-wheelers and their passengers account for almost half of the global road traffic deaths.1 A considerable number of victims of road traffic accidents (RTAs) die as a result of septicaemic shock and multi-organ failure in hospitals. Necrotizing soft tissue infections cover a broad spectrum of clinical entities ranging from mild pyodermas to life threatening necrotizing fasciitis.2 Necrotizing fasciitis (NF) is a rare life threatening complication which may occur following trauma like RTAs. They are associated with a high mortality and can affect any of the layers within the soft tissue compartment (dermis, subcutaneous tissue, superficial fascia, deep fascia or muscle).3 They were first described by Jones (1871) as ‘hospital gangrene’ and Wilson (1952) subsequently used the term NF,
2090-536X ª 2013 Production and hosting by Elsevier B.V. on behalf of Forensic Medicine Authority. http://dx.doi.org/10.1016/j.ejfs.2013.04.001
Necrotizing fasciitis – A rare fatal outcome of road traffic accidents which is now recognized to describe a rapidly progressive infection of the fascia and subcutaneous tissue, with thrombosis of the microcirculation.3 It may result from any insult to the integumentary system or from hematogenous spread and can develop at the site of a skin biopsy, laceration, insect bite, needle puncture, surgical wound, skin abscess and areas affected by herpes zoster, or a chronic venous ulcer.4 2. Case report A 48-year-old man with no known co-morbidities came to the hospital with complaints of an ulcerated wound over his right thigh, inguinal and gluteal region. Upon evaluation there was an alleged history of being hit by a two wheeler one month prior leading to a clavicular fracture and a hematoma over the right upper thigh. He received the initial treatment in a local hospital, where he was managed conservatively for a week and then discharged. About 10 days after, he noticed a discoloration of the right upper thigh, which progressed to blebs and finally ruptured to a painful ulcer. On examination he was found to be pale, febrile and toxemic with a pulse rate of 120 beats/minute and a blood pressure of 100/60 mmHg in the supine position. Ulcerated wounds without any abscess formation were seen involving the lower part of the right side of his abdomen, right upper thigh, perineal, gluteal and hip region. His hemoglobin level was 9.2 gm%, random blood glucose 110 mg/dl, WBC count 29000 cells/mm3, C-reactive protein (CRP) 150 mg/L, serum urea 117 mg/dl and serum creatinine 2.2 mg/dl. The rest of the biochemical investigations were within normal range. A provisional diagnosis of necrotizing fasciitis was made, and a broad-spectrum antibiotic therapy was commenced along with analgesics, antacids and IV fluids. His condition worsened rapidly and he expired within 24 hours of his admission. The autopsy was conducted the next day. He was of average build with body length of 170 cm and his body weight was 55 kg. An ulcerated wound of 32–38cm was present involving the lower part of the right side of the abdomen, inguinal region, right upper thigh, right gluteal region and lower part of the back on the right side. Ulceration and necrosis were restricted to skin and subcutaneous tissues and the underlying muscles were exposed. The scrotum and penis were edematous and the shaft of the penis was ulcerated. Upon internal examination his brain and lungs were of average weight and were found to be congested and edematous. The liver, spleen, kidneys and adrenals were also congested. His heart had a normal tone and weighed 200 g with normal appearance of walls, valves and patent coronaries. Petechial hemorrhages were noticed in the brain and on the surface of the heart. The rest of the examination was unremarkable. Tissues taken from the wound were sent for histopathological examination which showed ulcerated skin with necrosis of the dermis and subcutaneous fat. There was a dense neutrophilic infiltrate with congested blood vessels and no microorganisms could be identified. The histological features were compatible with necrotizing fasciitis (Fig. 1). 3. Discussion NF which is also known as ‘flesh-eating bacteria syndrome’, is an uncommon fatal outcome of RTAs. A variety of terms are
93
used to describe this condition such as Fournier’s gangrene, phagedena, phagedena gangrene, hospital gangrene, progressive bacterial synergistic gangrene (Meleney’s gangrene) and hemolytic streptococcal gangrene, depending on the site of infection.5 Its pathogenesis is not entirely understood. It is characterized by the spreading of microorganisms along the fascial planes and necrosis of the soft tissues. If not treated in a timely manner, it may also involve the muscles.6 Diabetes Mellitus (DM) is the leading predisposing underlying medical condition because of peripheral neuropathy, peripheral vascular disease and immunosuppression.7 High blood sugar in these patients predisposes to an environment of low oxygen tension and a rich substrate for bacterial growth.5 Microbiologically, NF is classified as Type 1 (polymicrobial) and type 2 (monomicrobial).8 Polymicrobial infections are more common,9,10 with cultures yielding a mixture of aerobic and anaerobic organisms.10 Type 1 NF occurs in immunocompromised individuals, such as patients with diabetes mellitus or chronic renal failure; whereas type 2 NF afflicts healthy patients with no implicative co morbidities and who often have a history of minor trauma.8 The usual etiologic isolates consist of Gram-positive organisms, such as Staphylococcus aureus, Streptococcus pyogenes and Enterococci; Gram-negative aerobes, such as Escherichia coli and Pseudomonas species; and anaerobic organisms, such as Bacteroides or Clostridium species.8,11 The two most common organisms encountered in Hong Kong were Streptococci and Vibrio species, the latter being highly virulent and particularly encountered by seafood handlers.4 One prospective study from Nigeria reported the commonest offending organisms as Staphylococcus aureus and Pseudomonas in children and adults, respectively.12 Another prospective study from India observed the monomicrobial infections (55.6%) to be more common than polymicrobial (44.4%), with the predominant organisms being Pseudomonas aeruginosa (23%) followed by Klebsiella pneumonia and Staphylococcus aureus (16% each).5 Etiologic agents like Hemophilus influenza serotype f, Lancefield group G Streptococcus, Aeromonas hydrophila, Clostridium difficile, Candida albicans and Candida tropicalis have also been reported.3,13–16 In this case the organism isolated from the wound culture was Staphylococcus aureus. Polymicrobial infections typically occur in the perineum and trunk, whereas monomicrobial infections occur in the limbs.8 According to a retrospective review from Canada, common sites of infection included the lower extremities (28%), upper extremities (27%), perineum (21%), trunk (18%), and the head and neck (5%).17 One prospective study involving 50 cases found the calf region as the most common site of infection (59.5%), which was explainable since most of the patients were diabetics and more prone to lower limb infections.5 Another observation from Nigeria reported the trunk as the most commonly involved anatomical region of the body (50%) in children, while in adults it was the lower limbs (54.2%).12 Where there is a history of trauma or infection, more than 60% commence in the lower extremities.6 In the present case also, the patient had a history of trauma and the site of NF was the hip, perineum and adjoining lower extremity. Robin et al. reported a young girl who developed rapidly progressive NF of the face secondary to a mild traumatic wound in the upper eyelid.18
94
S. Das et al.
Figure 1 Photomicrograph showing necrosis of dermis and subcutaneous fat with infiltration by neutrophils and a few congested vessels (Hematoxylin and Eosin X 400).
Risk factors for mortality include: age greater than 60 years, elevated lactate dehydrogenase, increasing length of time from admission to debridement, diabetes, chronic disease, immunosuppressive drug use (e.g. prednisolone), malnutrition, peripheral vascular disease, renal failure, underlying malignancy, obesity, intravenous drug use, trunk/perineal involvement and positive blood cultures for B-Streptococcus and bacteremia.8,16 A study from Los Angeles observed the following coexisting conditions or risk factors: current or past injection-drug use (43%); previous methicillin resistant Staphylococcus aureus (MRSA) infection, diabetes, and chronic hepatitis C (21% each); and cancer and human immunodeficiency virus infection or the acquired immunodeficiency syndrome (7% each); four patients (29%) had no serious coexisting conditions or risk factors.11 Most of the studies conducted agree that diabetes mellitus, trauma, surgery, and minor skin infections are the main risk/precipitating factors.5,9,12,19 Usually the patient appears to be toxic. Toxicity is severe and renal impairment may precede the development of shock.20 Septicemia was observed to be the commonest complication (57.1%) in one study.12 In the reported case, renal parameters were elevated suggesting the compromised renal function preceding death due to septic shock. The most common early signs are swelling, pain, erythema, fever, local warmth, skin induration, and tenderness.5,719 Pain out of proportion to the apparent severity of the lesion should alert the physician to a possible diagnosis of NF,7 as was observed in this case. Patches of skin necrosis, tissue crepitus, fluctuance and systemic evidence of sepsis such as hyperthermia, tachycardia and hypotension are alarming signs.7 In the present case the patient was febrile and toxemic and the wound had developed into a painful ulcer. The mortality rates as reported by different authors over the years vary from 6%–76%.7 Death due to renal failure as a result of hypovolemia and cardiovascular collapse caused by septic shock may occur.21 In one case, the patient died because of multiple organ failure and sepsis with Pseudomonas
aeruginosa.14 As per Mathew et al. hyperacute cases present with sepsis and quickly progress to multiorgan failure (40%).5 The keys to successful patient treatment of NF rest on early recognition, adequate resuscitation, broad-spectrum antibiotic therapy, radical surgical debridement and supportive care including fluid replacement, blood pressure support, analgesia, nutritional support and intensive care involvement.7,12 Although NF is a rare disease, physicians must be well trained in its diagnosis and treatment. Early diagnosis of the condition poses a challenge and a high index of suspicion is essential. One of the most challenging aspects is its similarities with cellulitis. It is safer to treat these ambiguous cases as NF and manage them aggressively with surgical debridement and broad spectrum antibiotics, as delay in treatment can be life threatening.4 NF is one of the greatest challenges from both a therapeutic and financial perspective, especially in the poor third world countries. Inadequate clinical exposure to such cases may lead to delay in diagnosis, thereby resulting in a fatal outcome and inviting charges of medical negligence.2 In conclusion, an experienced forensic pathologist may not have difficulties in diagnosing a case at autopsy, which may not be so for the lesser experienced young pathologist who was previously unexposed to such a case. In order to avoid such an unpleasant situation and especially where he has to certify the cause of death, it becomes imperative on his part to be aware of this clinical entity at autopsy. Through this case report the authors have highlighted the importance of proper history taking, going through the hospital case records wherever available and discussing the case with the treating physician if required. Histopathological examination, wound and blood cultures are important ancillary investigations that should be carried out routinely. Funding None.
Necrotizing fasciitis – A rare fatal outcome of road traffic accidents Conflict of interest None declared. Ethical approval Necessary ethical approval was obtained from the institute ethics committee. References 1. Global status report on road safety: time for action. Geneva, World Health Organization, 2009.
95
10. Elliot D, Kufera JA, Myers RA. The microbiology of necrotizing soft tissue infections. Am J Surg 2000;179:361–6. 11. Miller LG, Perdreau-Remington F, Rieg G, Mehdi S, Perlroth J, Bayer AS, et al. Necrotizing fasciitis caused by communityassociated methicillin-resistant Staphylococcus aureus in Los Angeles. N Engl J Med 2005;352:1445–53. 12. Legbo JN, Shehu BB. Necrotizing fasciitis: a comparative analysis of 56 cases. J Natl Med Assoc 2005;97:1692–7. 13. Rausch J, Foca M. Necrotizing fasciitis in a paediatric patient caused by Lancefield Group G streptococcus: case report and brief review of the literature, vol. 2011. Hindawi Publishing Corporation Case Reports in Medicine; 2011. 5 p. doi:http://dx.doi.org/ 10.1155/2011/671365 Article ID 671365. 14. Borger van der Burg BLS, Bronkhorst MWGA, Pahlplatz PVM. Aeromonas hydrophilia Necrotizing fasciitis: a case report. J Bone Joint Surg Am 2006;88:1357–60. 15. Bhargava A, Sen P, Swaminathan A, Ogbolu C, Chechko S, Stone F. Rapidly progressive necrotizing fasciitis and gangrene due to clostridium difficile: case report. Clin Infect Dis 2000;30:954–5. 16. Eisen DB, Brown E. Necrotizing fasciitis following a motor vehicle accident with Candida species as the sole organisms. Can J Plast Surg 2004;12:43–6. 17. Golger A, Ching S, Goldsmith CH, Pennie RA, Bain JR. Mortality in patients with necrotizing fasciitis. Plast Reconstr Surg 2007;119:1803–7. 18. Robin A, Me´ry G, George JL, Maalouf T, Angioi K. Facial necrotizing fasciitis after mild trauma of the eyelid: role of non steroidal anti-inflammatory treatment. J Fr Ophthalmol 2010;33:568–72. 19. Sin FP, Yuen MC, Lam KW, et al. A retrospective review of patients with necrotizing fasciitis presenting to an emergency department in Hong Kong. Hong Kong J Emerg Med 2002;9:10–7. 20. Stevens DL. Infections of the skin, muscle and soft tissues. In: Fauci AS, Kasper DL, Longo DL, et al., editors. Harrison’s principles of internal medicine. New York: McGraw Hill Medical; 2008. p. 798–803. 21. Rashid M. Disaster surgery. In: Williams NS, Bulstrode CJK, O’Connell PR, editors. Bailey and Love’s short practice of surgery. London: Hodder Arnold; 2008. p. 410–25.