Early diagnosis is difficult as the disease often looks early on like a simple superficial skin infection. While a number of laboratory and imaging modalities can raise the suspicion for necrotizing fasciitis, the gold standard for diagnosis is a surgical exploration in the setting of high suspicion. When in doubt, a small "keyhole" incision can be made into the affected tissue, and if a finger easily separates the tissue along the fascial plane, the diagnosis is confirmed and an extensive debridement should be performed.

Computed tomography (CT scan) is able to detect approximately 80% of cases while MRI may pick up slightly more.

The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score can be utilized to risk stratify people having signs of cellulitis to determine the likelihood of necrotizing fasciitis being present. It uses six serologic measures: C-reactive protein, total white blood cell count, hemoglobin, sodium, creatinine and glucose. A score greater than or equal to 6 indicates that necrotizing fasciitis should be seriously considered. The scoring criteria are as follows:

- CRP (mg/L) ≥150: 4 points

- WBC count (×10/mm)

- <15: 0 points

- 15–25: 1 point

- >25: 2 points

- Hemoglobin (g/dL)

- >13.5: 0 points

- 11–13.5: 1 point

- <11: 2 points

- Sodium (mmol/L) <135: 2 points

- Creatinine (umol/L) >141: 2 points

- Glucose (mmol/L) >10: 1 point

As per the derivation study of the LRINEC score, a score of ≥6 is a reasonable cut-off to rule in necrotizing fasciitis, but a LRINEC <6 does not completely rule out the diagnosis. Diagnoses of severe cellulitis or abscess should also be considered due to similar presentations. 10% of patients with necrotizing fasciitis in the original study still had a LRINEC score <6. But a validation study showed that patients with a LRINEC score ≥6 have a higher rate of both mortality and amputation.

Diagnosis is made by clinical observation and the following tests.

(1) Gram stain of the fluid from pustules or bullae, and tissue swab.

(2) Blood culture

(3) Urine culture

(4) Skin biopsy

(5) Tissue culture

Magnetic resonance imaging can be done in case of ecthyma gangrenosum of plantar foot to differentiate from necrotizing fasciitis.

While recent case series (n=9-80) studies have found a mortality rate of 20-40%, a large (n=1641) 2009 study reported a mortality rate of 7.5%.

The diagnostic workup is directed by the presenting signs and symptoms, and can involve:

- blood counts, clotting studies, and other laboratory testing

- imaging tests (ultrasound, CT scan, MRI, sometimes angiography, and rarely nuclear medicine scans)

- biopsy of the tumor.

Patients uniformly show severe thrombocytopenia, low fibrinogen levels, high fibrin degradation products (due to fibrinolysis), and microangiopathic hemolysis.

The key to diagnosis is skin changes combined with blood eosinophilia but the most accurate test is a skin, fascia and muscle biopsy.

The main organism associated with ecthyma gangrenosum is "Pseudomonas aeruginosa". However, multi-bacterial cases are reported as well. Prevention measures include practicing proper hygiene, educating the immunocompromised patients for awareness to avoid possible conditions and seek timely medical treatment.

Fournier gangrene is usually diagnosed clinically, but laboratory tests and imaging studies are used to confirm diagnosis, determine severity and predict outcomes. X-rays and ultrasounds may show the presence of gas below the surface of the skin. A CT scan can be useful in determining the site of origin and extent of spread.

The diagnosis relies on the findings outlined above. In addition, other specific markers of macrophage activation (e.g. soluble CD163), and lymphocyte activation (e.g. soluble IL-2 receptor) can be helpful. NK cell function analysis may show depressed NK function, or, flow cytometry may show a depressed NK cell population.

Other conditions that may mimic cellulitis include deep vein thrombosis, which can be diagnosed with a compression leg ultrasound, and stasis dermatitis, which is inflammation of the skin from poor blood flow. Signs of a more severe infection such as necrotizing fasciitis or gas gangrene that would require prompt surgical intervention include purple bullae, skin sloughing, subcutaneous edema, and systemic toxicity. Misdiagnosis can occur in up to 30% of people with suspected lower-extremity cellulitis, leading to 50,000 to 130,000 unnecessary hospitalization and $195 to $515 million in avoidable healthcare spending annually in the United States.

Associated musculoskeletal findings are sometimes reported. When it occurs with acne conglobata, hidradenitis suppurativa, and pilonidal cysts, the syndrome is referred to as the follicular occlusion triad or tetrad.

Lyme disease can be misdiagnosed as staphylococcal- or streptococcal-induced cellulitis. Because the characteristic bullseye rash does not always appear in people infected with Lyme disease, the similar set of symptoms may be misdiagnosed as cellulitis. Standard treatments for cellulitis are not sufficient for curing Lyme disease. The only way to rule out Lyme disease is with a blood test, which is recommended during warm months in areas where the disease is endemic.

Many conditions mimic or may be mistaken for warfarin necrosis, including pyoderma gangrenosum or necrotizing fasciitis. Warfarin necrosis is also different from another drug eruption associated with warfarin, purple toe syndrome, which usually occurs three to eight weeks after the start of anticoagulation therapy. No report has described this disorder in the immediate postpartum period in patients with protein S deficiency.

The diagnosis of DIC is not made on a single laboratory value, but rather the constellation of laboratory markers and a consistent history of an illness known to cause DIC. Laboratory markers consistent with DIC include:

- Characteristic history (this is important because severe liver disease can essentially have the same laboratory findings as DIC)

- Prolongation of the prothrombin time (PT) and the activated partial thromboplastin time (aPTT) reflect the underlying consumption and impaired synthesis of the coagulation cascade.

- Fibrinogen level has initially thought to be useful in the diagnosis of DIC but because it is an acute phase reactant, it will be elevated due to the underlying inflammatory condition. Therefore, a normal (or even elevated) level can occur in over 57% of cases. A low level, however, is more consistent with the consumptive process of DIC.

- A rapidly declining platelet count

- High levels of fibrin degradation products, including D-dimer, are found owing to the intense fibrinolytic activity stimulated by the presence of fibrin in the circulation.

- The peripheral blood smear may show fragmented red blood cells (known as schistocytes) due to shear stress from thrombi. However, this finding is neither sensitive nor specific for DIC

A diagnostic algorithm has been proposed by the International Society of Thrombosis and Haemostasis. This algorithm appears to be 91% sensitive and 97% specific for the diagnosis of overt DIC. A score of 5 or higher is compatible with DIC and it is recommended that the score is repeated daily, while a score below 5 is suggestive but not affirmative for DIC and it is recommended that it is repeated only occasionally: It has been recommended that a scoring system be used in the diagnosis and management of DIC in terms of improving outcome.

- Presence of an underlying disorder known to be associated with DIC (no=0, yes=2)

- Global coagulation results

- Platelet count (>100k = 0, <100 = 1, <50 = 2)

- Fibrin degradation products such as D-Dimer (no increase = 0, moderate increase = 2, strong increase = 3)

- Prolonged prothrombin time (3 sec = 1, >6 sec = 2)

- Fibrinogen level (> 1.0g/L = 0; < 1.0g/L = 1)

In those who have previously had cellulitis, the use of antibiotics may help prevent future episodes. This is recommended by CREST for those who have had more than two episodes.

In medicine, fasciitis is an inflammation of the fascia, which is the connective tissue surrounding muscles, blood vessels and nerves.

In particular, it often involves one of the following diseases:

- Necrotizing fasciitis

- Plantar fasciitis

- Eosinophilic fasciitis

- Paraneoplastic fasciitis

Proliferating angioendotheliomatosis may be divided into the following types:

The amount of fresh frozen plasma required to reverse disseminated intravascular coagulation associated with purpura fulminans may lead to complications of fluid overload and death, especially in neonates, such as transfusion-related acute lung injury. Exposure to multiple plasma donors over time increases the cumulative risk for transfusion-associated viral infection and allergic reaction to donor proteins found in fresh frozen plasma.

Allergic reactions and alloantibody formation are also potential complications, as with any protein replacement therapy.

Concomitant warfarin therapy in subjects with congenital protein C deficiency is associated with an increased risk of warfarin skin necrosis.

The first element of treatment is usually to discontinue the offending drug, although there have been reports describing how the eruption evolved little after it had established in spite of continuing the medication. Vitamin K1 can be used to reverse the effects of warfarin, and heparin or its low molecular weight heparin (LMWH) can be used in an attempt to prevent further clotting. None of these suggested therapies have been studied in clinical trials.

Heparin and LMWH act by a different mechanism than warfarin, so these drugs can also be used to prevent clotting during the first few days of warfarin therapy and thus prevent warfarin necrosis (this is called 'bridging').

Based on the assumption that low levels of protein C are involved in the underlying mechanism, common treatments in this setting include fresh frozen plasma or pure activated protein C.

Since the clot-promoting effects of starting administration of 4-hydroxycoumarins are transitory, patients with protein C deficiency or previous warfarin necrosis can still be restarted on these drugs if appropriate measures are taken. These include gradual increase starting from low doses and supplemental administration of protein C (pure or from fresh frozen plasma).

The necrotic skin areas are treated as in other conditions, sometimes healing spontaneously with or without scarring, sometimes going on to require surgical debridement or skin grafting.

Inflammatory myofibroblastic tumours are diagnosed based on their appearance under the microscope, by pathologists. Medical imaging findings are non-specific.

Until recently, nodular fasciitis have been considered a reactive process of uncertain cause. However, recent findings indicate that nodular fasciitis is a self-limited clonal neoplastic process (see below). Clinically, nodular fasciitis presents as a subcutaneous "growth" over a period of 3–6 weeks that eventually regresses. The lesion usually reaches a size of 2–3 cm. Larger lesions are unusual. Local recurrence has been described after simple surgical excision but it is rare.

The cardinal features of purpura investigations are the same as those of disseminated intravascular coagulation: prolonged plasma clotting times, thrombocytopenia, reduced plasma fibrinogen concentration, increased plasma fibrin-degradation products and occasionally microangiopathic haemolysis.

Tissue biopsy is the gold standard. Macroscopically this reveals pale muscle tissue. Microscopically infarcted patches of myocytes. Necrotic muscle fibers are swollen and eosinophilic and lack striations and nuclei. Small-vessel walls are thickened and hyalinized, with luminal narrowing or complete occlusion. Biopsy cultures for bacteria, fungi, acid-fast bacilli and stains are negative in simple myonecrosis.

Creatine kinase may be normal or increased probably depending upon the stage of the condition when sampling is undertaken. ESR is elevated. Planar X-ray reveals soft tissue swelling and may potentially show gas within necrotic muscle, Bone scan may show non specific uptake later in the course. CT shows muscle oedema with preserved tissue planes (non-contrast enhancing). MRI is the exam of choice and shows increased signal on T2 weighted images within areas of muscle oedema. Contrast enhancement is helpful but must be weighed against the risk of Nephrogenic Systemic Fibrosis as many diabetics have underlying renal insufficiency. Arteriography reveals large and medium vessel arteriosclerosis occasionally with dye within the area of tissue infarction . Electromyography shows non specific focal changes.

Nodular fasciitis, also known as nodular pseudosarcomatous fasciitis, pseudosarcomatous fasciitis, and subcutaneous pseudosarcomatous fibromatosis, is a benign soft tissue lesion most commonly found in the superficial fascia. The lesion commonly occurs in the first three decades of life. Upper extremities and trunk are the most common affected anatomical sites. Previous history of trauma may be present. Clinically and histologically, nodular fasciitis may be mistaken for a sarcoma.

Management of KMS, particularly in severe cases, can be complex and require the joint effort of multiple subspecialists. This is a rare disease with no consensus treatment guidelines or large randomized controlled trials to guide therapy.

Prognosis varies depending on the underlying disorder, and the extent of the intravascular thrombosis (clotting). The prognosis for those with DIC, regardless of cause, is often grim: Between 20% and 50% of patients will die. DIC with sepsis (infection) has a significantly higher rate of death than DIC associated with trauma.

Common treatments include corticosteroids such as prednisone, though other medications such as hydroxychloroquine have also been used.

The prognosis is usually good in the case of an early treatment if there is no visceral involvement.