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Necrotizing fasciitis is a rare, serious, and potentially life-threatening infectious disease. This disease is caused by the invasion of pathogenic bacteria into the body, and is characterized by progressive infection and necrosis of deep fascia, superficial fascia, skin, and subcutaneous tissue. The onset of the disease is acute, and the condition is rapid. Severe cases can cause systemic inflammatory response syndrome (SIRS), septic shock, multiple organ dysfunction syndrome (MODS), and even death1,2. Because early clinical manifestations lack specificity, diagnosis is often delayed or missed. Even after diagnosis, the depth of tissue infection and progressive wound expansion often lead to inadequate debridement and drainage. Consequently, infection control remains unsatisfactory, often requiring multiple operations. These factors contribute to high rates of disability, amputation, and mortality3. The prognosis of patients often falls short of expectations.
This case report describes a 37-year-old man with acute necrotizing fasciitis complicated by sepsis, who was successfully managed with a staged comprehensive approach. The aim is to illustrate the value of timely incision and exploration, multidisciplinary decision-making, and stepwise surgical and medical management. This case may offer limited insights for improving the treatment of similar patients.
CASE PRESENTATION:
The case involves a 37-year-old man, otherwise healthy, who presented on November 1, 2023, with "redness, swelling, heat, and pain in the left lower limb for 4 days, aggravated for half a day" as the main complaint. Four days before the visit, the patient suddenly developed redness, swelling, and pain in the left knee joint. The predisposing factors are unknown, and the history of minor trauma, neglected by the patient, cannot be ruled out. The patient then went to the local hospital for treatment and was given a wet compress with Glauber's salt and anti-inflammatory treatment with penicillin. After treatment, the above symptoms did not improve significantly, and the condition even showed a progressive aggravation trend. The range of redness and swelling in the patient's left lower limb gradually expanded, extending from the knee joint to the proximal end of the hip joint, and extending to the distal end of the ankle joint. Half a day before the visit, the patient's symptoms worsened. The pain level of the affected limb was unbearable, the movement was limited, and walking was impossible. Simultaneously with fever, the body temperature rose to 39.4 °C. The patient's family immediately sent the patient to the hospital. The patient had no prior diabetes, hypertension, immunosuppression, or chronic organ disease. No drug/food allergies were reported. The patient had a 20-year smoking history and occasional alcohol use.
On physical examination, the patient had a temperature of 39.4 ˚ C, a heart rate of 156 beats per minute, a respiratory rate of 20 breaths per minute, and a blood pressure of 135/90 mmHg (1 mmHg = 0.133 kPa). The patient was conscious and able to answer questions but appeared lethargic. The left lower limb was diffusely swollen and erythematous. The skin temperature was significantly higher than that of the contralateral side, and the affected limb was markedly tender. There was a sense of fluctuation when touched at the left knee, and the pulsation of the dorsal pedal artery was weak (Figure 1). Motor function, sensation, and capillary refill were normal in the affected limb. No signs of compartment syndrome were observed.
Laboratory investigations revealed the following findings. The white blood cell count (WBC) was 9.55 × 109/L with a neutrophil percentage (NEUT%) of 84.8%. The C-reactive protein (CRP) level was 163 mg/L, and the procalcitonin (PCT) level was 3.62 ng/mL. Random blood glucose was 19.9 mmol/L. Coagulation studies showed a platelet count (PLT) of 117 × 109/L, an activated partial thromboplastin time (APTT) of 24.7 s, a fibrinogen level of 9.18 g/L, and a D-dimer level of 1.96 mg/L. Renal function tests demonstrated a serum creatinine of 64 µmol/L and a blood urea nitrogen of 7 mmol/L. Hepatic function tests revealed an alanine aminotransferase (ALT) of 32 U/L, an aspartate aminotransferase (AST) of 17 U/L, and a total bilirubin of 13.6 µmol/L. Baseline scores were a Glasgow Coma Scale (GCS) score of 15 and a Sequential Organ Failure Assessment (SOFA) score of 1.
The left knee joint was punctured with a fine needle at the place where the fluctuation sensation was obvious, and pus could be seen. A surgical incision about 5 cm long was made in the abscess, and a large amount of milky white material was seen, with a foul odor. The volume of pus was about 300 mL (Figure 2 and Supplementary Video 1, which demonstrates the incision and drainage procedure). Further exploration of the pus cavity revealed that it was large, extending to both ends, and the fascia of the lower extremities was necrotic in a large area.
DIAGNOSIS, ASSESSMENT, AND PLAN:
According to the patient's clinical manifestations and exploration results: (1) Extensive necrosis of the subcutaneous fascia of the left lower limb, accompanied by extensive subcutaneous foci, spreading to the surrounding area; (2) No muscular layer was involved; (3) Symptoms of systemic poisoning were obviously accompanied by mental changes, so the initial diagnosis considered acute necrotizing fasciitis. The differential diagnosis included acute cellulitis and acute inflammation. Acute cellulitis can manifest as local soft-tissue redness, swelling, and pain, but its scope is relatively limited. The infection location is deep, and the edges of redness and swelling are not clear. There may be a sense of fluctuation after the local abscess is formed. In this patient, however, bedside incision and exploration revealed extensive fascial necrosis, foul-smelling pus, and easy separation of the skin and fascia – findings not seen in cellulitis. Acute inflammation can manifest in skin redness, swelling, and pain, but the edges are not very clear. It is often seen that a red line spreads upward along the lower limbs, tenderness. There is swelling and tenderness in the abdominal area. Based on the combination of deep fascial necrosis, purulent discharge with foul odor, and rapid progression, acute necrotizing fasciitis was the most likely diagnosis. The green channel for emergency surgery was immediately opened, and at the same time, the departments of general surgery, hand surgery, anesthesiology, and the intensive care unit (ICU) were invited for joint consultation. The patient's condition deteriorated rapidly, with a GCS score of 9. Vital signs worsened: heart and respiratory rates increased significantly from admission, and pulse oxygen saturation decreased to 92–93%. Dynamic monitoring of organ function showed a SOFA score of 10 (an increase of >2 points from baseline), meeting the criteria for sepsis. Despite initial fluid resuscitation, the patient remained hypotensive and required continuous norepinephrine infusion to maintain mean arterial pressure ≥ 65 mmHg, with persistent hyperlactatemia (>2 mmol/L). Therefore, a diagnosis of septic shock was established. After a multidisciplinary team (MDT) evaluation, anti-shock therapy was administered.
Once the patient's vital signs stabilized, the patient was immediately treated surgically. During the operation, a full-length incision was made on the medial and lateral sides of the left lower limb, and a large amount of deep fascia necrosis and a large amount of milky white purulent material were seen (Figure 3). The wound surface was thoroughly debrided, infected and necrotic fascia were removed, and drainage tubes were placed to ensure adequate drainage. The wound was covered with wet gauze soaked in ornidazole, and the wound dressing was strengthened after the operation. The patient's vital signs were unstable again during the operation. After cardiopulmonary resuscitation, life support treatment, blood transfusion treatment, and so on, the rescue was successful.
After the operation, the patient was transferred to the ICU for further monitoring and treatment. The patient had recurrent high fever, and blood tests showed elevated infection markers (WBC 25.03 × 109/L, CRP 197.9 mg/L, PCT 6.69 ng/mL). Multiple blood cultures and material cultures showed methicillin-sensitive Staphylococcus aureus (MSSA). Susceptibility testing revealed sensitivity to meropenem, vancomycin, and levofloxacin. The patient had no history of β-lactam or fluoroquinolone allergy. In the ICU, patients were treated with meropenem (0.5 g via microinfusion pump every 8 h) combined with vancomycin (1 g intravenous drip every 12 h) for anti-infection, ulinastatin for anti-inflammatory response, volume resuscitation, and nutritional support. The duration of intravenous therapy was 8 days, after which de-escalation would be considered based on clinical response. It was worth noting that the patient had no history of diabetes in the past, but the blood glucose fluctuated greatly after the illness. Fasting blood glucose was measured at 19.3 mmol/L. Glycosylated hemoglobin was 6.9%, slightly elevated. After consultation with a physician specializing in internal medicine, it was considered that the cause of the patient's current hyperglycemic state might be related to insulin resistance, possibly induced by the septic stress response. Hypoglycemic treatment was performed with an intravenous insulin infusion. Two more debridement and drainage operations were performed subsequently.
Following a 10-day ICU admission, the patient’s vital signs became stable, and the patient was transferred to the hand surgery general ward. The re-examination of infection indicators showed a trend of improvement (WBC decreased to 9.63 × 109/L, CRP to 61.3 mg/L, PCT to 0.27 ng/mL). Therefore, the anti-infection regimen was de-escalated to levofloxacin (0.5 g intravenously once daily) for a total of 16 days. The reasons for choosing levofloxacin were: (1) Susceptibility testing confirmed sensitivity. (2) Levofloxacin has high bioavailability and convenient once-daily dosing. (3) Local surveillance data indicate a low resistance rate of MSSA to levofloxacin (<5%). There was a significant reduction in wound exudate. After surgical contraindications were excluded, the modified "sandwich" vacuum-sealing drainage was performed (Figure 4). After the wound base was cleaned, the VSD device was replaced. The subcutaneous tissue and muscular layer were completely attached, and VSD covered the wound surface to promote wound healing. In the later stage, the remaining granulation wounds were covered by autologous skin grafting (Figure 5). Because of the large area of skin grafting in the left lower limb, stamp skin grafting is used. About 7 days after skin grafting, the VSD device was removed. The patient did well in the stamped skin-grafted area of the left lower limb (estimated take rate >95%). Because the patient has left knee flexion activity disorder, guide the patient to perform functional exercises of the affected limb in a stepwise manner.