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Reliable, easy-to-read patient information on common medical conditions β€” written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Cellulitis differential diagnosis

Introduction

Overview

Overview

Cellulitis should be distinguished from thrombophlebitis, contact dermatitis, insect stings, drug reactions, and arthritis.

Differentiating Cellulitis from other Diseases

Differentiating Cellulitis from other Diseases

Cellulitis must be differentiated from other causes of lower limb edema like chronic venous insufficiency, acute deep venous thrombosis, lipedema, myxedema, lymphatic filariasis and causes of generalized edema.

Diseases Symptoms Signs Gold standard Investigation to diagnose
History Onset Pain Fever Laterality Scrotal swelling Symptoms of primary disease
(Cellulitis-erysipelas-skin abscess) Acute + + Unilateral – –
  • Usually it doesn’t need any laboratory tests to diagnose.[2]
  • Blood cultures are warranted for patients in the following circumstances:[3]
  1. Systemic toxicity
  2. Extensive skin or soft tissue involvement
  3. Underlying comorbidities
  4. persistent cellulitis
Lymphatic filariasis
  • History of living in endemic area or travelling to it
 Chronic + + Bilateral + –

Preparing blood smears

  • Thick smears
  1. Thick smears consist of a thick layer of dehemoglobinized (lysed) red blood cells (RBCs).
  2. Thick smears allow a more efficient detection of parasites (increased sensitivity).
  • Thin smears consist of blood spread in a layer such that the thickness decrease.

By the ultrasound, the following findings can be observed:

  • Dilated lymphatic channels
  • Living worms tend to be in motion which called “filarial dance” sign.
Chronic venous insufficiency Chronic + – Bilateral +

(If congenial)

–
  • Typical varicose veins
  • Skin change distribution correlate with varicose veins sites in the medial side of ankle and leg
  • Reduction of swelling with limb elevation.
Acute deep venous thrombosis Acute + – Unilateral – May be associated with primary disease mandates recumbency for long duration
Lipedema Chronic + – Bilateral – –
  • Tender with palpation
  • Negative Semmer sign to differentiate from lymphedema.[7]
  • Pinching the skin on the upper surface of the toes. If it is possible to grasp a thin fold of tissue then it is negative result.
  • In a positive result, it is only possible to grasp a lump of tissue.
  • MRI offers strong qualitative and quantitative parameters in the diagnosis of lipedema [8]
Myxedema Chronic + – Bilateral – +

(hypothyroidism )

Other causes of generalized edema
  • History of chronic general condition (cardiac-liver-renal)
 Chronic – – Bilateral – +
  • According to the primary cause ( Echo- LFTs– RFT)

Cellulitis can be promptly diagnosed with an appropriate history and physical exam. Administration of an antibiotic therapy will initiate resolution of the condition in 2-3 days. Differentials have to be thought of only when resolution is not seen. Non- resolution of cellulitis can be due to infection by resistant strains of the bacterium involved.

There are many dermatological conditions which manifest in manner similar to cellulitis. Careful evaluation of each case, based on accurate history and physical examinations, is very important. Differentials are as follows:

  • Erysipelas is a skin infection caused by Streptococcus pyogenes, similar to cellulitis, but it affects superficial layers of the skin. It has more demarcated edges than cellulitis.
  • Erysipeloid is a skin infection which is mostly occupational in nature. It is most commonly seen in people involved in the poultry and meat industry. It is characterized by local lesions, diffuse lesions and systemic forms.
  • Necrotizing fasciitis looks like cellulitis at the onset of the disease but it is much more serious. Large amounts of pain, necrosis, and bullae are noticeable. It often requires surgical exploration.

There are a few conditions which can be misdiagnosed as cellulitis such as thrombophlebitis, contact dermatitis, insect stings, drug reactions, arthritis.[9]

  • Contact dermatitis is an inflammation of the skin in response to direct exposure to an allergic or irritating substance. This inflammation is usually present with papular erythematous indistinct margins. The extent of distribution is often limited to the area of exposure.
  • Insect bites cause a local reaction leading to the development of erythema, tenderness, pruritus and edema. In severe reactions, it can involve adjacent joints. In very severe cases, insect bites can lead to anaphylaxis.
  • Drug rashes are the cutaneous presentation of a drug reaction. The rashes are variable, ranging from a pinkish hue to an exanthem. The rash can be limited or widespread. Itching is the most common symptom. If fever, dehydration and involvement of membranous surfaces is present along with the rash, then other diagnoses have to be considered. Drug rashes present most commonly when taking drugs such as sulfa, anticonvulsant drugs, and insulin from animal sources.
  • In leukemic patients, some times cancerous cells infiltrate the skin causing erythema, papules, and nodules. The cause of these symptoms has to be differentiated by immunostaining.

Cellulitis must be differentiated from other diseases that cause bone pain, edema, and erythema.

Disease Findings
Soft tissue infection
(Commonly cellulitis) 		History of skin warmness, swelling and erythema. Bone probing is the definite way to differentiate them.[10][1]
Osteonecrosis
(Avascular necrosis of bone) 		Previous history of trauma, radiation, use of steroids or biphosphonates are suggestive to differentiate osteonecrosis from ostemyelitis.[11][12]
MRI is diagnostic.[13][14]
Charcot joint Patients with Charcot joint commonly develop skin ulcerations that can in turn lead to secondary osteomyelitis.
Contrast-enhanced MRI may be diagnostically useful if it shows a sinus tract, replacement of soft tissue fat, a fluid collection, or extensive marrow abnormalities. Bone biopsy is the definitive diagnostic modality.[15]
Bone tumors May present with local pain and radiographic changes consistent with osteomyelitis.
Tumors most likely to mimic osteomyelitis are osteoid osteomas and chondroblastomas that produce small, round, radiolucent lesions on radiographs.[16]
Gout Gout presents with joint pain and swelling. Joint aspiration and crystals in synovial fluid is diagnostic for gout.[17]
SAPHO syndrome
(Synovitis, acne, pustulosis, hyperostosis, and osteitis) 		SAPHO syndrome consists of a wide spectrum of neutrophilic dermatosis associated with aseptic osteoarticular lesions.
It can mimic osteomyelitis in patients who lack the characteristic findings of pustulosis and synovitis.
The diagnosis is established via clinical manifestations; bone culture is sterile in the setting of osteitis.
Sarcoidosis It involves most frequently the pulmonary parenchyma and mediastinal lymph nodes, but any organ system can be affected.
Bone involvement is often bilateral and bones commonly affected include the middle and distal phalanges (producing β€œsausage finger”), wrist, skull, vertebral column, and long bones.
Langerhans’ cell histiocytosis The disease usually manifests in the skeleton and solitary bone lesions are encountered twice as often as multiple bone lesions.
The tumours can develop in any bone, but most commonly originate in the skull and jaw, followed by vertebral bodies, ribs, pelvis, and long bones.[18]
References

References

  1. ↑ 1.0 1.1 Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL; et al. (2014). “Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America”. Clin Infect Dis. 59 (2): 147–59. doi:10.1093/cid/ciu296. PMIDΒ 24947530.
  2. ↑ Raff AB, Kroshinsky D (2016). “Cellulitis: A Review”. JAMA. 316 (3): 325–37. doi:10.1001/jama.2016.8825. PMIDΒ 27434444.
  3. ↑ Woo PC, Lum PN, Wong SS, Cheng VC, Yuen KY (2000). “Cellulitis complicating lymphoedema”. Eur J Clin Microbiol Infect Dis. 19 (4): 294–7. PMIDΒ 10834819.
  4. ↑ Leppard BJ, Seal DV, Colman G, Hallas G (1985). “The value of bacteriology and serology in the diagnosis of cellulitis and erysipelas”. Br J Dermatol. 112 (5): 559–67. PMIDΒ 4005155.
  5. ↑ Goodacre S, Sutton AJ, Sampson FC (2005). “Meta-analysis: The value of clinical assessment in the diagnosis of deep venous thrombosis”. Ann Intern Med. 143 (2): 129–39. PMIDΒ 16027455. Review in: ACP J Club. 2006 Mar-Apr;144(2):46-7 Review in: Evid Based Med. 2006 Apr;11(2):56
  6. ↑ Child AH, Gordon KD, Sharpe P, Brice G, Ostergaard P, Jeffery S; et al. (2010). “Lipedema: an inherited condition”. Am J Med Genet A. 152A (4): 970–6. doi:10.1002/ajmg.a.33313. PMIDΒ 20358611.
  7. ↑ Trayes KP, Studdiford JS, Pickle S, Tully AS (2013). “Edema: diagnosis and management”. Am Fam Physician. 88 (2): 102–10. PMIDΒ 23939641.
  8. ↑ Dimakakos PB, Stefanopoulos T, Antoniades P, Antoniou A, Gouliamos A, Rizos D (1997). “MRI and ultrasonographic findings in the investigation of lymphedema and lipedema”. Int Surg. 82 (4): 411–6. PMIDΒ 9412843.
  9. ↑ Falagas ME, Vergidis PI (2005). “Narrative review: diseases that masquerade as infectious cellulitis”. Ann Intern Med. 142 (1): 47–55. PMIDΒ 15630108.
  10. ↑ Bisno AL, Stevens DL (1996). “Streptococcal infections of skin and soft tissues”. N. Engl. J. Med. 334 (4): 240–5. doi:10.1056/NEJM199601253340407. PMIDΒ 8532002.
  11. ↑ Shigemura T, Nakamura J, Kishida S, Harada Y, Ohtori S, Kamikawa K, Ochiai N, Takahashi K (2011). “Incidence of osteonecrosis associated with corticosteroid therapy among different underlying diseases: prospective MRI study”. Rheumatology (Oxford). 50 (11): 2023–8. doi:10.1093/rheumatology/ker277. PMIDΒ 21865285.
  12. ↑ Slobogean GP, Sprague SA, Scott T, Bhandari M (2015). “Complications following young femoral neck fractures”. Injury. 46 (3): 484–91. doi:10.1016/j.injury.2014.10.010. PMIDΒ 25480307.
  13. ↑ Amanatullah DF, Strauss EJ, Di Cesare PE (2011). “Current management options for osteonecrosis of the femoral head: part 1, diagnosis and nonoperative management”. Am J. Orthop. 40 (9): E186–92. PMIDΒ 22022684.
  14. ↑ Etienne G, Mont MA, Ragland PS (2004). “The diagnosis and treatment of nontraumatic osteonecrosis of the femoral head”. Instr Course Lect. 53: 67–85. PMIDΒ 15116601.
  15. ↑ Ahmadi ME, Morrison WB, Carrino JA, Schweitzer ME, Raikin SM, Ledermann HP (2006). “Neuropathic arthropathy of the foot with and without superimposed osteomyelitis: MR imaging characteristics”. Radiology. 238 (2): 622–31. doi:10.1148/radiol.2382041393. PMIDΒ 16436821.
  16. ↑ Lovell, Wood (2014). Lovell and Winter’s pediatric orthopaedics. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBNΒ 978-1605478142.
  17. ↑ Joosten LA, Netea MG, Mylona E, Koenders MI, Malireddi RK, Oosting M, Stienstra R, van de Veerdonk FL, Stalenhoef AF, Giamarellos-Bourboulis EJ, Kanneganti TD, van der Meer JW (2010). “Engagement of fatty acids with Toll-like receptor 2 drives interleukin-1Ξ² production via the ASC/caspase 1 pathway in monosodium urate monohydrate crystal-induced gouty arthritis”. Arthritis Rheum. 62 (11): 3237–48. doi:10.1002/art.27667. PMCΒ 2970687. PMIDΒ 20662061.
  18. ↑ Picarsic J, Jaffe R (2015). “Nosology and Pathology of Langerhans Cell Histiocytosis”. Hematol. Oncol. Clin. North Am. 29 (5): 799–823. doi:10.1016/j.hoc.2015.06.001. PMIDΒ 26461144.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Aditya Govindavarjhulla, M.B.B.S.