An elevated leukocyte count hemoglobin level of gm dl hematocrit

An elevated leukocyte count, hemoglobin level of 14.2gm/dl, hematocrit of 52% and the fasting blood sugar level of 19mmol/l were recorded.
Under general anesthesia multiple incisions and drainage of the involved spaces of both sides were achieved. This consisted of two intra oral and two extra oral incisions on either side. Only minimal amount of fluid which appeared serous and not frankly pus like could be expressed. Multiple through and through drains were placed (Fig. 1). Post operatively he was managed in surgical intensive care unit and extubated after two days.
On fourth post op day evening the pyrexia had resolved and the mouth opening had returned to normal and he was able to manage a normal diet. On the fifth day the drains of the upper neck were removed and the drains of the lower neck were replaced. On the afternoon of the sixth day the patient complained of chills. The temperature had risen again to 38.4°C. The culture of the pus sample taken from the drain site on the fourth day when received showed a predominant culture of Streprococci and Staphylococcus aureus. According to the sensitivity study the antibiotic was left unchanged.
A matter of considerable concern was the observed drop in hemoglobin level, which worsened to 6gm/dl. Patient complained of severe pain over the neck and tenderness of the lower neck. Blood chemistry at this time showed hypocalcaemia (1.8mmol/l) and a fall in the serum albumin level from 30 to 18mmol/l hence decided to transfuse 2 units of packed SCH 727965 and human albumin. Multiple spikes of temperature and an increase of foul smelling straw colored discharge from the lower neck were noted. The pus culture taken on sixth day showed profuse growth of streptococci along with S. aureus and the antibiotic changed into third generation cephalosporins as per the sensitivity study.
On the eighth day a dusky erythematous area developed in the right lower neck. Subsequently a grayish black ill defined fast spreading necrotic area was noted centrally. Bits of necrotic fascia extruded from the draining sinuses. This was subjected to histopathology study. The dusky area extended to involve whole of the lower neck within 24h. Multiple bullae and small blisters were also noted surrounding the necrotic area.
A clinical diagnosis of NF was made and the patient was taken for immediate debridement exposing the contents of the neck and packed open with BIPP dressing. Extensive necrosis of the fascia was extending from the lower neck up to the mylohyoid line at the lingual surface of the mandible, undermining through the subcutaneous fascia (Fig. 2). Patient shifted to intensive care unit post operatively. The clinical picture, CT and MRI findings along with histological study confirmed the diagnosis of NF.
Patient showed marked improvement within 48h and discharged home after five days.

Delay in diagnosis of NF and its differentiation from similar looking infections will affect the prognosis and in turn the late surgical intervention may increase the morbidity. In recent times Ludwig’s angina is primarily managed by antibiotic therapy and only nonresponsive cases may necessitate a surgical intervention (Nakamori et al., 2004). Association of Ludwig’s angina and NF creates a diagnostic dilemma as an early intervention is necessary for better prognosis.
Ludwig’s angina, first detailed by the German surgeon Wilhelm Friedrich von Ludwig in 1836 is a rapidly progressive, potentially fulminant cellulitis involving bilaterally the sub-mandibular, sub-mental and sub-lingual spaces (Nakamori et al., 2004). It typically originates from an infected or recently extracted tooth, most commonly the lower second and third molars. Ludwig’s angina begins as a mild infection and can rapidly progress to brawny bilateral indurations of the upper neck with pain, trismus, and tongue elevation.
The pathophysiology of Ludwig’s angina, a deep-seated infection manifested with extensive cellulites, is not known to produce tissue necrosis. However, similar looking lesions like erysipelas, progressive bacterial synergistic gangrene, anaerobic streptococcal gangrene and gas gangrene (Persaud et al., 2004) are most often prone to induce necrosis.