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Volume 1 • Issue 12 • 2012

IntroductionMost of the cervical necrotizing fasciitis are odontogenic in origin

[1]; the onset is often insidious in the form of nonspecific regional neck swelling, erythema, and fever. Edema extending beyond the area of erythema, skin vesicles, crepitus or air in the subcutaneous tissues, and absence of lymphangitis and lymphadenitis are markers of necrotizing fasciitis, particularly when they occur in patients with serious underlying diseases. Aggressive sequential surgical debridement, nutritional therapy and broad spectrum intravenous antibiotics provide the best strategy for management. The emergence of toxic shock strains of streptococcus leading to fasciitis with organ dysfunction makes it necessary to make a rapid diagnosis and institute early antibiotic and surgical interventions.

Case ReportIn May 2006, a 31 year old non insulin dependent diabetic male was

brought to the emergency room of Sri Ramachandra Hospital presenting with a facial swelling and foul smelling discharge from the neck. History revealed restoration of a tooth on the right posterior mandible the preceding week following which a swelling appeared on the right side of the face which gradually spread to the other side of the face and neck. The patient was admitted initially in a local hospital where cut throat incisions was done and referred here for further management. The patient was in septic shock with altered sensorium. Examination revealed discoloration and swelling of the entire neck and bucco parotid fascia, with multiple stab incisions over the neck, wooden hard feel and crepitus on palpation extending from the submandibular area, down to the anterior chest wall (Figures 1 and 2). Finger test [2] performed at the level at the deep fascia revealed a murky dishwater fluid with lack of bleeding through the preexisting multiple stab incisions.

Laboratory studies showed metabolic acidosis, anemia (4.9 gm%), leucocytosis (19,000), hypocalcaemia (6.0 mg/dl) and a serum glucose of greater than 300 mg/dl. CT Examination of the various compartments of the head, neck and mediastinum revealed fluid collection of the various fascial spaces of the neck, gas collections in the neck, with disruption of the platysma (Figures 3 and 4). A diagnosis of necrotizing fasciitis with septic shock was made and the patient immediately shifted to Intensive care unit, with Inj. Dopamine, blood transfusion and a sliding scale insulin. Patient was immediately taken for radical debridement of the necrotic neck, submandibular and the involved parotid fascia, skin and muscle under general anesthesia with extraction of infected mandibular teeth. Postoperatively the patient was on ventilator, with ionotropic support. Intravenous Imipenam, clindamycin were given, along with aggressive daily wound care and debridement. Wound culture showed a mixture of organisms prominent for staphylococcus epidermidis, streptococcus and pseudomonas.

Repeat CT sections of the thorax showed bilateral lower lobe

Figure 1: Examination revealed discoloration and swelling of the entire neck and bucco parotid fascia, with multiple stab incisions over the neck, wooden hard feel and crepitus on palpation extending from the submandibular area, down to the anterior chest wall.

Figure 2: Examination revealed discoloration and swelling of the entire neck and bucco parotid fascia, with multiple stab incisions over the neck, wooden hard feel and crepitus on palpation extending from the submandibular area, down to the anterior chest wall.

AbstractNecrotizing fasciitis is a fulminant polymicrobial infection of the soft tissue with a characteristic clinical and

pathological appearance. This fasciitis has been frequently reported in the perineum, abdominal wall, perineum, neck and lower extremities. Immunocompromised patients are at an increased risk of developing this infection with a high mortality rate. We report a case of cervical necrotizing fasciitis of odontogenic origin. The pathogenesis and the several modes of management have also been discussed.

Massive Necrotizing Fasciitis of Odontogenic Origin – A Case ReportPinky Ganga Balasubramani*, Ravindran C, Kumar SR and NandaKumar NDepartment of Oral and Maxillofacial Surgery, Faculty of Dental Sciences, Sri Ramachandra University, India

*Corresponding author: Dr. Pinky Ganga Balasubramani, Department of Oral and Maxillofacial Surgery, Faculty of Dental Sciences, Sri Ramachandra University, India, E-mail: pinkieganga@hotmail.com

Received July 11, 2012; Published December 17, 2012

Citation: Balasubramani PG, Ravindran C, Kumar SR, NandaKumar N (2012) Massive Necrotizing Fasciitis of Odontogenic Origin – A Case Report. 1:579 doi:10.4172/scientificreports.579

Copyright: © 2012 Balasubramani PG, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Diabetes mellitus was the most common cause. Our patient was a non insulin diabetic patient on irregular medication. Early recognition of this disease is directly related to successful treatment and reduced mortality rate. Necrotizing fasciitis starts in the subcutaneous tissue and superficial muscle fascia. The skin is initially spared, but eventually thrombosis of the nutrient vessels lead to cutaneous gangrene [5]. Skin necrosis is a late sign and often an indication of an unsalvageable condition. Early presentation of the disease includes high fever, tachycardia, stable blood pressure and normal sensorium. The skin shows erythema, blisters and intense pain on palpation. Larger areas of skin involvement with increase in the number and size of the blisters and mild disturbances in sensorium are the intermediate presentation. High fever, white blood cell count greater than 25,000 and classic skin findings (edema with central patches of dusky blue discoloration, weeping blisters and border cellulitis) are the late presentation [2].

Our patient presented with marked tissue edema, skin necrosis and signs of septic shock. The peau d’orange edema is caused by obstruction of the dermal lymphatics and is highly suggestive of necrotizing fasciitis. Subcutaneous tissues will demonstrate a wooden hard feel, which may help to distinguish the infection from simple cellulitis. Hemoglobin level may decrease rapidly because of hemolysis and blood loss. The serum calcium levels may decrease precipitously because of saponification with fatty acids released by bacterial lipases in the subcutaneous tissues [5].

Historically group A β hemolytic streptococcus has been the common generator of necrotizing fasciitis. A polymicrobial synergistic pathogenesis is now suggested to be more common. Other identified organisms included staphylococcus aureus, Escherichia coli, Pseudomonas, Enterobacter, Klebsiella, Proteus, Bacteriodes, Clostridium and Peptostreptococcus. The “mousey” odor of the infected fluid is highly suggestive of anaerobic infection as in our patient.

The various forms of infectious soft tissue inflammation have specific features in the CT. Cellulitis is characterized by thickening of the cutis and subcutis and increased attenuation of fatty tissue with streaky, irregular enhancement and without fluid collections. Fasciitis appears as thickening or enhancement of fasciae. Myositis appears as thickening of the cervical muscles or muscle groups and myonecrosis

collapse with haziness and stranding of the anterior chest wall. On the 7th day of hospitalization, a transcervical anterior mediastinal debridement was performed for mediastinal extension of the disease. Under critical care unit monitoring, the patient was given regular physiotherapy, continuous infusion of insulin, regular local debridement of the wound and dressed with collagenase and clindamycin. Nutritional support was instituted with enteral and parenteral alimentation, supplying at least 3000 calories per day. After sufficient granulation had occurred split skin grafting was done (Figure 5). The diabetic status of the patient was brought under control and the patient was discharged 6 weeks after admission.

DiscussionAmbrose Paré in the fifteenth century elegantly described

necrotizing fasciitis as following ‘but there can happen no greater than a gangrene, as that which may cause the mortification and death of the part, and times the whole body’ [3]. Necrotizing Fasciitis also referred to as hemolytic streptococcal gangrene, Meleny ulcer, acute dermal gangrene, suppurative fasciitis or synergistic necrotizing cellulite is represents the hyperacute end of the spectrum of soft tissue infections. This condition has been described in medical texts since 1871 [4] and in the surgical literature since 1924.

Necrotizing Fasciitis is a fulminant bacterial infection with a high mortality rate, typically occurring in compromised or immunosuppressed patients. Predisposing factors for necrotizing fasciitis such as smoking, diabetes, peripheral vascular disease, immunologic compromise and intravenous drug use should be noted.

Figure 3: Examination of the various compartments of the head, neck and mediastinum revealed fluid collection of the various fascial spaces of the neck, gas collections in the neck, with disruption of the platysma.

Figure 4: Examination of the various compartments of the head, neck and mediastinum revealed fluid collection of the various fascial spaces of the neck, gas collections in the neck, with disruption of the platysma.

Figure 5: Repeat CT sections of the thorax showed bilateral lower lobe col-lapse with haziness and stranding of the anterior chest wall.

Citation: Balasubramani PG, Ravindran C, Kumar SR, NandaKumar N (2012) Massive Necrotizing Fasciitis of Odontogenic Origin – A Case Report. 1:579 doi:10.4172/scientificreports.579

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may become visible as hypo attenuating area within enhancing portions of muscle or a frank muscle disruption. An abscess may appear as a single or multi loculated area of fluid attenuation with or without gas collections, usually expands the compartment that is involved and typically demonstrates a peripheral rim enhancement.

An empirical broad spectrum antibiotic regimen is followed due to the high incidence of polymicrobial infection in necrotizing fasciitis. Clindamycin decreases the lipo polysaccharide production and peptidoglycan release from toxin producing strains of gram positive and gram negative organisms and to minimize cytokine production.

Surgery still remains the hallmark for treatment of cervical necrotizing fasciitis. Debridement back to viable tissue is essential. The surgical findings were typical in the patient, the subcutaneous tissues appearing grey and non bleeding with a watery discharge. The subcutaneous tissue could be easily stripped off the fascia and all necrotic tissue was aggressively debrided till the edges bled briskly. Debridement of the wound was done with collagenase, clindamycin and saline. Collagenase helps break up, remove dead tissue and promote wound healing.

Hemodynamic instability may exist postoperatively and skin necrosis may progress from infectious spread or hypoperfusion. Affected patients should be promptly as often as necessary taken to the operating room for further debridement. On the 7th day of hospitalization our patient had to be taken back to the operating room due to descending mediastinitis.

The role of hyperbaric oxygen in the management of necrotizing fasciitis has been debated. Hyperoxemia allows for more efficient leukocyte function by providing more substrate for formation of free radicals and by augmenting respiratory burst. The effects of hyperoxia also include increased fibroblast growth, inhibition of bacterial toxin formation, increased red cell pliability, termination of lipid peroxidation, and reduction of tissue edema. Although hyperbaric oxygen cannot replace surgery, a combination of surgery, antibiotics and hyperbaric oxygen can produce a significant reduction in mortality and wound morbidity.

Patients with necrotizing fasciitis should receive immediately fluid resuscitation, antibiotics and surgical debridement. Nutritional support should be given since excess protein and calories are necessary to promote healing. Enteral feedings was encouraged in our patient in the early post operative period to offset the metabolism that is associated with large open wounds [6]. Clinical nutrition opinion was obtained soon after admission to mitigate the extreme protein catabolism associated with this aggressive disease.

Complications of necrotizing fasciitis include airway obstruction, pericardial effusion, rupture of major blood vessels, brain abscess, acute renal failure, disseminated intravascular coagulation, sepsis and respiratory failure [7]. Literature shows that Immunocompromised and suppressed conditions increase the mortality rate in necrotizing fasciitis [8-18]. Acknowledgement

Department of Plastic Surgery, Sri Ramchandra University.

References1. Balcerak RJ, Sisto JM, Bosack RC (1988) Cervicofacial necrotizing fasciitis:

Report of three cases and literature review: J Oral Maxillofac Surg 46: 450-459. 2. Sudarsky LA, Laschinger JC, Coppa GF, Spencer FC (1987) Improved results

from a standardized approach in treating patients with necrotizing fasciitis. Ann Surg 206: 661-665.

3. Keynes G (1951) The Apologie and Treatise of Ambrose Paré. London: Falcon Educational Books.

4. Jones J: Investigation upon the nature, cause and treatment of hospital gangrene as it prevailed in the Confederate armies 1861- 1865, New York. NY. US. Sanitary Commission. Surgical memoirs of the War of Rebellion.

5. Moss RL, Musemeche CA, Kolkoske AM (1996) Necrotizing fasciitis in children: Prompt recognition and aggressive therapy improve survival. J Pediatr Surg 31: 1142-1146.

6. Anderson TJ, Green SD, Childers BJ (2001) Massive infectious soft-tissue injury: Diagnosis and management of necrotizing fasciitis and purpura fulminans. Plast Reconstr Surg 107: 1025-1035.

7. Tung-Yiu W, Jehn-Shyun H, Ching-Hung C, Hung-An C (2000) Cervical necrotizing fasciitis of odontogenic origin: a report of 11 cases. J Oral Maxillofac Surg 58: 1347-1352.

8. Quirk WF, Sternbach G (1996) Joseph Jones: Infection with flesh eating bacteria. J Emerg Med 14: 747- 753.

9. Kindwall EP (1992) Uses of hyperbaric oxygen therapy in the 1990s. Cleve Clin J Med 59: 517-528.

10. Lewis RT (1992) Necrotizing soft-tissue infections. Infect Dis Clin North Am 6: 693-703.

11. Maqbool M, Ahmad R, Ahmed R, Qazi S (1992) Necrotizing fasciitis in the head and neck region. Br J Plast Surg 45: 481-483.

12. Chidzonga MM (1996) Necrotizing fasciitis of the cervical region in an AIDS patient: report of a case. J Oral Maxillofac Surg 54: 638-640.

13. Becker M, Zbären P, Hermans R, Becker CD, Marchal F, et al. (1997) Necrotizing fasciitis of the head and neck: role of CT in diagnosis and management. Radiology 202: 471-476.

14. Kantu S, Har-El G (1997) Cervical necrotizing fasciitis. Ann Otol Rhinol Laryngol 106: 965-970.

15. Stamenkovic I, Lew PD (1984) Early recognition of potentially fatal necrotizing fasciitis. The use of frozen-section biopsy. N Engl J Med 310: 1689-1693.

16. Stone DR, Gorbach SL (1997) Necrotizing fasciitis. The changing spectrum. Dermatol Clin 15: 213-220.

17. Wilson B (1952) Necrotizing fasciitis. Am Surg 18: 416-431.18. Wilson HD, Haltalin KC (1973) Acute necrotizing fasciitis in childhood. Report

of 11 cases. Am J Dis Child 125: 591-595.

Citation: Balasubramani PG, Ravindran C, Kumar SR, NandaKumar N (2012) Massive Necrotizing Fasciitis of Odontogenic Origin – A Case Report. 1:579 doi:10.4172/scientificreports.579