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Acute Febrile Neutrophilic Dermatosis Clinical Presentation

  • Author: Yoon-Soo (Cindy) Bae, MD; Chief Editor: William D James, MD  more...
Updated: Mar 31, 2016


Fever typically precedes the appearance of each crop of lesions in acute febrile neutrophilic dermatosis (Sweet syndrome). The fever can precede the skin disease by several days to weeks; however, it may also occur simultaneously.[1] The crop of plaques or nodules in the classic form often appears abruptly and may persist for weeks or several months (days to weeks) if untreated.[1, 4]

Many patients report a febrile upper respiratory tract infection, tonsillitis, or flulike syndrome 1-3 weeks prior to onset of skin lesions. Vaccination or a gastrointestinal tract infection may also precede the eruption.[4, 11] Headache, malaise, and arthralgias are common.[1, 19]



Skin manifestations of acute febrile neutrophilic dermatosis (Sweet syndrome)

Typical skin lesions are bright red, reddish blue, or violet papules, plaques, or nodules. Massive subepidermal edema sometimes produces a deceptively vesicular appearance. Lesions may be studded with pustules. Papules often coalesce into circinate or arcuate plaques.[1, 4, 7, 19] Plaques can cause pain and burning, but they are not pruritic. Lesions spontaneously resolve without scarring, or they resolve after treatment.[1] The face, neck, and extremities primarily are affected, characteristically in an asymmetric distribution.[1]

Atypical presentations in the external auditory canal and tympanic membrane are reported. Facial cellulitis and soft tissue infections of the extremities have also been described.[20, 21] Other atypical presentations include photodistributed violaceous plaques with heliotrope rash, malar erythema, scalp involvement, and Gottron-like papules.[22]

Ulcers and bullae are more common in malignancy-associated disease than in other forms. These lesions may be extensive and are generally hard to treat.[4]

Lesions on the dorsum of the hand are not uncommon. They sometimes appear vasculitic, which is not typically seen in Sweet syndrome.[19] The lesions are predominantly distributed over the dorsal aspects of the fingers and hands in a roughly symmetrical pattern. Other extensor surfaces may also be involved.[19] This is an anatomically limited form of Sweet syndrome.[10] Atypical pyoderma gangrenosum, bullous Sweet syndrome, and pustular vasculitis of the hands are considered by some to be variations of a single disease, neutrophilic dermatosis of the dorsal hands.[23] The vasculitis does not appear to be a primary immune-mediated process, as is seen in the primary leukocytoclastic vasculitides; rather, it is secondary vascular damage caused by toxic metabolites and proteases released from the extensive acute neutrophilic infiltrates in the skin.[10]

Note the images below:

Red nodules and plaques on the lateral aspect of t Red nodules and plaques on the lateral aspect of the hand.
Multiple lesions on the scalp. Multiple lesions on the scalp.
Close-up of a scalp lesion. Close-up of a scalp lesion.

Mucosal lesions of acute febrile neutrophilic dermatosis (Sweet syndrome)

Oral lesions can occur on the lips, buccal mucosa, and/or tongue. These lesions most commonly appear as ulcers in Sweet syndrome patients with hematologic disorders.[8] Conjunctivitis and episcleritis may also occur; these are the most common eye manifestations. Other ocular manifestations reported include uveitis, limbal nodules, glaucoma, subconjunctival hemorrhage, scleritis, iritis, and sudden visual loss.[24, 25, 26]

Extracutaneous manifestations of acute febrile neutrophilic dermatosis (Sweet syndrome)

Sweet syndrome can involve several organ systems.[1] Pulmonary manifestations can sometimes lead to substantial morbidity. Pulmonary involvement may manifest as dyspnea, chronic cough, or pulmonary infiltrates or effusions on chest radiograph. In rare cases, symptoms may become severe enough to cause respiratory failure or bronchiolitis obliterans organizing pneumonia. Fortunately, most cases of Sweet syndrome with pulmonary involvement tend to be highly responsive to glucocorticoid therapy.[27, 28, 29]

Other extracutaneous sites that have been reported include the bones, intestines, joints, bone marrow, liver, heart, muscles, spleen, and kidneys.[1, 30, 31, 32, 33, 34, 35, 36, 37, 38]

A few cases of systemic inflammatory response syndrome (SIRS) progressing to shock and organ dysfunction has been reported, with rapid improvement using high-dose intravenous methylprednisolone. The treatment efficacy highlights the association of SIRS with Sweet syndrome, which can be hard to distinguish from infection.[39, 40, 41]

Among children, cases of acquired cutis laxa have been reported in lesions consistent with Sweet syndrome.[42] A 2-year-old girl diagnosed with both Sweet syndrome and cutis laxa was found to have acute necrosis in the cardiac apex and interventricular septum and focal chronic inflammatory and granulation tissue in the aortic wall. The authors suggest that children with both Sweet syndrome and cutis laxa undergo complete cardiac evaluation by a pediatric cardiologist, as these findings can be fatal.[43]

Fewer than 30 cases of CNS involvement are reported in the literature. Encephalitis and meningitis are common neurologic manifestations in these cases. Peripheral neuropathy has also been reported. The most common symptoms are headaches, disturbed consciousness, and seizures.[44] HLA types B54 and CW1 are associated with Sweet syndrome with CNS involvement in Japanese patients.[44] Unlike Behçet syndrome, in which CNS involvement is progressive and severe, Sweet syndrome usually causes transient CNS involvement, but recurrences may occur.[44]

Proteinuria, hematuria, and decreased creatinine clearance have been reported.[16] See the Creatinine Clearance (measured) calculator. Cerebrospinal fluid pleocytosis also has been described, as has a sterile chronic recurrent multifocal osteomyelitis in children.[45]


Like pyoderma gangrenosum, Sweet syndrome is known to cause pathergy (also referred to as Köebner phenomenon), in which lesions occur in areas of minor trauma, such as sites of scratches, bites, and venipuncture.[46] The lesions may also be photodistributed or localized to the site of a previous phototoxic reaction (eg, sunburn).[1, 46]

Underlying disease

It is important to recognize and treat any associated or underlying systemic diseases or malignancies. Sweet syndrome may be a clue to the diagnosis of a systemic disorder or malignancy, and important clues should not be ignored. Imaging studies, such as ultrasonography, CT scanning, PET scanning, or MRI, may be helpful in identifying underlying malignancies.


Acute neutrophilic dermatosis can occur during pregnancy and may recur in subsequent pregnancies. Presently, it is believed that the disease is not associated with fetal harm.



Potential causes of acute febrile neutrophilic dermatosis (Sweet syndrome) are numerous, but some associations are well documented.[5] Classic or idiopathic Sweet syndrome is the most common presentation and accounts for more than 50% of cases.[47] Sweet syndrome associated with a (malignant) neoplasm accounts for approximately 11-54% of the cases. Most of these are hematopoietic malignancies (most commonly acute myeloid leukemia), but some are due to solid tumors, mostly those involving the genitourinary, breast, and gastrointestinal tract. Inflammatory (infectious) conditions are the next most frequently identified causes of Sweet syndrome.[5, 47]

Hematologic malignancy–related causes of febrile neutrophilic dermatosis (Sweet syndrome)

Myelodysplasia and chronic myelogenous leukemia may be associated with Sweet syndrome.[16, 48] Sweet syndrome can also be seen in association with acute myeloid leukemia (AML), including the promyelocytic (M3) variant of AML.[16, 49]

Other nonmyeloid hematologic malignancies that have occurred in association with acute febrile neutrophilic dermatosis include Hodgkin disease, cutaneous T-cell lymphoma, non-Hodgkin lymphoma, hairy cell leukemia, and multiple myeloma. (Patients with immunoglobulin G [IgG] secretion may be at increased risk for Sweet syndrome).[33, 50]

Nonhematologic malignancy has been associated with Sweet syndrome; rates of genitourinary, breast, and gastrointestinal cancers appear to be slightly increased in this group.[16]

Nonhematologic malignancy–related causes of febrile neutrophilic dermatosis (Sweet syndrome)

These are rare associations and include osteosarcoma, oral cancer/tonsil cancer, ovarian cancer, thyroid cancer, lung cancer, pheochromocytoma, and cervical and rectal carcinoma.[9, 50, 51]

Infection-related causes of febrile neutrophilic dermatosis (Sweet syndrome)

Multiple infections are described in association with Sweet syndrome, often involving the upper respiratory tract. Streptococcal pneumonia is the most commonly described infection.[46]

Other bacterial infections associated with Sweet syndrome also include those due to Salmonella or Staphylococcus species, Francisella tularensis, Yersinia enterocolitica, Entamoeba coli, Helicobacter pylori, Borrelia burgdorferi, nontuberculous organisms, (atypical), Tuberculous mycobacteria,Mycobacterium chelonae, and Penicillium species.[46, 52, 53]

Sweet syndrome may be a presenting feature of coccidiomycosis and associated with sporotrichosis.[28, 54] Viral agents such as HIV, cytomegalovirus (CMV), hepatitis A, hepatitis B, and parvovirus B19 has also been implicated.[55, 56]

Yersinia-associated Sweet syndrome has been noted to improve with antibiotics.[57]

Drug-related causes of febrile neutrophilic dermatosis (Sweet syndrome)

Multiple drugs have been reported to cause Sweet syndrome, with some of these reactions being noted in patients with underlying malignancy; therefore, the validity of these possible associations is unclear.[1]

Because the dominant cell in the dermal infiltrate is a neutrophil, drug-induced Sweet syndrome is not considered to be a drug hypersensitivity.

G-CSF is a well-established factor.[1, 58]

Established factors include trimethoprim-sulfamethoxazole (Bactrim), all-trans retinoic acid, and minocycline, which have all appeared in more than 1 case report.[6]

Anecdotal or limited reports of drug or device associations include lithium, furosemide, hydralazine, carbamazepine, oral contraceptives, the Mirena intrauterine device, COX-2 inhibitors, azathioprine, doxycycline, diazepam, diclofenac, nitrofurantoin, propylthiouracil, lenalidomide, bortezomib, abacavir, imatinib, 5-azacytidine, decitabine, interleukin-2 (IL-2), clindamycin, mitoxantrone, and vaccinations (eg, for bacille Calmette-Guérin, smallpox, pneumococcal organisms, influenza).[11, 36, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68]

Systemic disorder–related causes of febrile neutrophilic dermatosis (Sweet syndrome)

Associated inflammatory disease can be identified in about 16% of patients with Sweet syndrome.[47]

The most common associated diseases are Crohn disease and ulcerative colitis, which some authors consider part of a continuum of neutrophilic dermatosis.[69]

Sjögren syndrome, Behçet disease, lupus erythematosus, rheumatoid arthritis, familial Mediterranean fever, and undifferentiated connective-tissue disease have been reported in association with acute neutrophilic dermatitis.[1, 70]

Miscellaneous causes of febrile neutrophilic dermatosis (Sweet syndrome)

Rare cases of acute neutrophilic dermatitis have occurred with spinal surgery, sarcoidosis, erythema nodosum, relapsing polychondritis, thyroiditis, and systemic lupus erythematosus.[1, 71, 72, 73, 74]

A few cases have been observed during pregnancy.[1, 5, 16]

Several cases of Sweet syndrome occurred with polycythemia vera.[75]

One patient had a mutation in the prothrombin gene (G20210A), but no conclusive association can be made at this time.[76]

A few cases of Sweet syndrome have been reported in the literature in transplantation patients, including those undergoing bone marrow and kidney transplantation. Although these patients are taking immunomodulatory medications, an “immune mediated state” has been described to explain the manifestation of Sweet syndrome in this patient population.[77]

Sweet syndrome as a manifestation of HIV-associated immune reconstitution inflammatory syndrome has been suggested.[78]

Diagnostic criteria

Diagnostic criteria (proposed by Su and Liu[79] and revised by von den Driesch[47] ) include the presence of 2 major and 2 minor clinical findings, as follows:

Major criteria are as follows:

  • Abrupt onset of tender or painful erythematous plaques or nodules, occasionally with vesicles, pustules, or bullae
  • Predominantly neutrophilic infiltration in the dermis without leukocytoclastic vasculitis

Minor criteria are as follows:

  • Preceding nonspecific respiratory or gastrointestinal tract infection or vaccination or associated with inflammatory disease, hemoproliferative disorders, solid malignant tumors, or pregnancy
  • Periods of general malaise and fever (body temperature >38°C)
  • Laboratory values during onset showing a erythrocyte sedimentation rate >20 mm, positive C-reactive protein (CRP) result, segmented nuclear neutrophils, bands >70% in peripheral blood smears, and leukocytosis (count >8000/µL) (meeting 3 of 4 of these values is necessary
  • Excellent response to treatment with systemic corticosteroids or potassium iodide

Diagnostic criteria for drug-induced Sweet syndrome (proposed by Walker and Cohen[6] ) include all 5 criteria below; all of the following are required for the drug eruptions to be considered a diagnosis of drug-induced Sweet syndrome:

  • Abrupt onset of painful erythematous plaques or nodules
  • Histopathologic evidence of a dense neutrophilic infiltrate without evidence of leukocytoclastic vasculitis
  • Pyrexia (38°C)
  • Temporal relationship between drug ingestion and clinical presentation, or temporally related recurrence after oral challenge
  • Temporally related resolution of lesions after drug withdrawal or treatment with systemic corticosteroids [6]
Contributor Information and Disclosures

Yoon-Soo (Cindy) Bae, MD Clinical Assistant Professor, Ronald O Perelman Department of Dermatology, New York University School of Medicine; Procedural Dermatologist, Laser and Skin Surgery Center of New York

Yoon-Soo (Cindy) Bae, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery, American Medical Association, American Society for Dermatologic Surgery, American Society for Laser Medicine and Surgery, Massachusetts Medical Society, Women's Dermatologic Society, New England Dermatological Society

Disclosure: Nothing to disclose.


Sharon A Salter, MD Staff Physician, Department of Psychiatry, Tufts-New England Medical Center

Sharon A Salter, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Obstetricians and Gynecologists

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael J Wells, MD, FAAD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD, FAAD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Texas Medical Association

Disclosure: Nothing to disclose.

Rosalie Elenitsas, MD Herman Beerman Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System

Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society of Dermatopathology, Pennsylvania Academy of Dermatology

Disclosure: Received royalty from Lippincott Williams Wilkins for textbook editor.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Timothy McCalmont, MD Director, UCSF Dermatopathology Service, Professor of Clinical Pathology and Dermatology, Departments of Pathology and Dermatology, University of California at San Francisco; Editor-in-Chief, Journal of Cutaneous Pathology

Timothy McCalmont, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, American Society of Dermatopathology, California Medical Association, College of American Pathologists, United States and Canadian Academy of Pathology

Disclosure: Received consulting fee from Apsara for independent contractor.


Christina N Alavian, MD, Resident Physician, Division of Dermatology, University of Massachusetts Medical School

Disclosure: Nothing to disclose.

Alexa F Boer Kimball, MD, MPH Associate Professor of Dermatology, Harvard University School of Medicine; Vice Chair, Department of Dermatology, Massachusetts General Hospital; Director of Clinical Unit for Research Trials in Skin (CURTIS), Department of Dermatology, Massachusetts General Hospital

Alexa F Boer Kimball, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

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Red nodules and plaques on the lateral aspect of the hand.
Multiple lesions on the scalp.
Close-up of a scalp lesion.
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