Clinical Imaging 37 (2013) 608 – 612

Radiology–pathology conference: neutrophilic fasciitis and panniculitis of

the feet (Sweet's syndrome)
Euan Stubbs a , Nathaniel Dostrovsky b , Srinivasan Harish a, c,⁎, Madeleine Verhovsek d ,
Samih Salama e , Nader Khalidi b
a
Department of Radiology, McMaster University, Hamilton, Ontario, Canada
b
Division of Rheumatology, McMaster University, Hamilton, Ontario, Canada
c
Department of Diagnostic Imaging, St. Joseph's Healthcare, Hamilton, Ontario, Canada
d
Division of Hematology and Thromboembolism, McMaster University, Hamilton, Ontario, Canada
e
Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
Received 12 July 2012; accepted 1 August 2012

Abstract

Sweet's syndrome is characterised by pyrexia, cutaneous lesions, neutrophilia and an infiltrate of mature neutrophils in the dermis. While
extracutaneous disease is not uncommon, neutrophilic fasciitis has rarely been described. We report the imaging appearances with clinical
and histological correlation of a case of drug-induced neutrophilic fasciitis in a 56-year-old man.
© 2013 Published by Elsevier Inc.

Keywords: Neutrophilic fasciitis; Panniculitis; MRI; Ultrasound; Sweet's syndrome

1. Introduction We describe a rare case of drug-induced neutrophilic fasciitis

and panniculitis with no myositis, emphasizing the imaging
Sweet's syndrome, also known as neutrophilic dermato- appearances with clinical and histological correlation.
sis, was first described in 1964 by Dr. Robert Sweet in a
series of 8 patients presenting with pyrexia, elevated
2. Case report
neutrophil counts, and painful erythematous cutaneous
lesions [1] The symptoms improved quickly following
A 56-year-old man, an ex-smoker, presented to the
treatment with corticosteroids. Sweet's syndrome is usually
rheumatologist with a 2-year history of burning feet pain,
confined to the skin with an infiltrate of mature neutrophils in
plantar nodularity, and arthralgias that had worsened over the
the dermis with visible papules, nodules or plaques [2,3].
past year. His past medical history included coronary artery
Extracutaneous Sweet's syndrome is not uncommon.
disease, hypersensitivity pneumonitis, idiopathic neutrope-
Musculoskeletal involvement in Sweet's syndrome is,
nia, recurrent skin infections, and gastroesophageal reflux
however, relatively rare, and there are only 2 case reports
disease. His medications included granulocyte colony
that describe fascial involvement associated with myositis
stimulating factor granulocyte colony stimulating factor
[4,5]. To the best of our knowledge, there is only one imaging
(G-CSF) (300 μg weekly) for the treatment of idiopathic
case report of Sweet's syndrome in the English literature [4].
neutropenia as well as risk modifying cardiac and anti-reflux
medications. Over an 8-week period that the patient stopped
⁎ Corresponding author. Department of Diagnostic Imaging, St
taking G-CSF, he felt subjective improvement in his foot
Joseph's Healthcare, Hamilton, Ontario, Canada L8N 2A6. Tel.: +1 905
pain that worsened again upon restarting G-CSF.
522 1155. Physical examination revealed tenderness of the plantar
E-mail address: sriniharish@gmail.com (S. Harish). aspect of left foot as well as the ankle and metatarsal regions

0899-7071/$ – see front matter © 2013 Published by Elsevier Inc.

http://dx.doi.org/10.1016/j.clinimag.2012.08.004
 E. Stubbs et al. / Clinical Imaging 37 (2013) 608–612
Fig. 1. Left foot photograph demonstrates diffuse swelling with mild
erythema in the plantar aspect.
on the right side. There was mild diffuse swelling and
erythema but no other objective evidence of a rash or skin
nodule (Fig. 1). White cell count revealed a neutropenia with
neutrophil count of 1.1×10 9/l. Inflammatory markers were
grossly elevated with erythrocyte sedimentation rate mea-
suring 96 mm/h and C-reactive protein measuring 49.7 mg/l.
Rheumatoid factor was negative, but immunoglobulin levels
were elevated with an IgG of 17.7 and an IgA of 6.5. Given
that the patient was on G-CSF, there was clinical concern for
chronic infection causing the feet symptoms.
Ultrasound of the feet demonstrated significant indura-
tion, edema, and cellulitis of the subcutaneous tissues of the
plantar aspect of the feet associated with moderate to avid
Doppler hyperemia (Fig. 2). These findings correlated with
the sites of tenderness on clinical examination. No discrete
abscess or mass lesion was demonstrated. There were no
significant joint effusions or synovitis seen. Radiographs of
the feet showed no erosions or evidence of osteomyelitis.
Magnetic resonance imaging (MRI) of the more symptom-
atic left foot was requested. Unenhanced coronal T1-W,
coronal fast spin echo (FSE) T2 fat saturated (FS), and sagittal
short tau inversion recovery sequences were performed.
Fig. 2. (A and B) Transverse gray-scale and Doppler ultrasound images of the plantar aspect of the left foot at the level of the metatarsals demonstrates moderate
subcutaneous edema (white arrows) associated with moderate to marked Doppler vascularity consistent with panniculitis.
609
Fig. 3. Coronal FSE T1 FS MR image following intravenous gadolinium
demonstrates moderately enhancing subcutaneous panniculitis (white
arrows) in the plantar aspect of the foot.
Following intravenous gadolinium, coronal T1 FS and sagittal
T1 FS sequences were obtained. These demonstrated ill-
defined foci of moderate edema and enhancement in the
plantar subcutaneous tissues adjacent to the first and second
intermetatarsal spaces (Fig. 3). The intermuscular planes
between the plantar interosseous and flexor/abductor muscles
showed deep fascial edema and enhancement (Figs. 4 and 5).
More proximally at the metatarsal base level, there was
superficial fascial enhancement identified (Fig. 5). There was
however no significant enhancement or edema within the
muscles. There was no evidence of bone marrow edema,
abscess, or synovitis. The MRI appearances were in keeping
with fasciitis and panniculitis of the foot.
An ultrasound-guided biopsy was performed targeting the
abnormal subcutaneous tissue and superficial fascia of the
plantar aspect of the left foot, as demonstrated on the MRI.
Five cores were obtained with a 20-gauge Temno needle. The
core biopsies showed fibroadipose tissue with the fibrous
tissue consistent with fascia. There were plump stromal cells
in the background, and the endothelial cells appeared
reactively enlarged. There was patchy heavy infiltrate
comprised of mature neutrophils, along with scattered single
large atypical histiocytes (Fig. 6). The presence of a blast
610 E. Stubbs et al. / Clinical Imaging 37 (2013) 608–612
Fig. 4. Coronal FSE T2 FS MR image demonstrates moderate edema in the
fascial planes (white arrows) in the plantar aspect of the foot.
population was difficult to identify, and the mononuclear
cells predominantly showed eosinophilic cytoplasm and
irregular nuclear contours. The histological impression was
that of a predominantly neutrophilic infiltrate in the fat/fascia
of the foot. There were occasional large cells which stained
with CD68 and had some slightly atypical nuclear features
that had been described in cutaneous lesions induced by
treatment with G-CSF. Although the possibility of extra-
medullary manifestations of a myeloid disorder was consid-
ered, the prominent localized process and the histological
features were similar to those described with usage of bone
marrow stimulators. The final histological conclusion was
“neutrophilic/histiocytic infiltrate, suggestive of lesion in-
duced by G-CSF, with a Sweet's syndrome-like appearance.”
Based on overall clinical, radiological, and histological
findings, a final diagnosis of drug-induced Sweet's syn-
drome was made. The patient's G-CSF was discontinued,
and he was commenced on prednisolone 30 mg/day. Clinical
Fig. 5. (A and B) Coronal FSE T1 FS MR images following intravenous gadolinium demonstrates moderately enhancing superficial (white arrows) and deep
intermuscular (black arrows) fascia in the plantar aspect of the foot.
Fig. 6. Hematoxylin and eosin stain shows heavy infiltrate composed mostly
of neutrophils with large round cells. The large round cells appear to be
myeloid or histiocytic in origin.
follow-up 1 month later showed his feet symptoms to have
dramatically improved with very minimal residual pain.
3. Discussion
Acute febrile neutrophilic dermatosis (Sweet's syndrome)
classically presents with pyrexia, neutrophilia, painful red
skin lesions and a cutaneous infiltrate of neutrophils in the
dermis [2]. It occurs in three well-recognised clinical
settings: idiopathic or classical, drug induced, and secondary
to malignancy [6].
The patient in the presented case had a history of
idiopathic neutropenia for which he was receiving treatment
with the recombinant human growth factor—G-CSF. G-CSF
has been reported to be a cause of drug induced Sweet's
syndrome including neutrophilic panniculitis (subcutaneous
Sweet's syndrome) [7–10]. It has been theorised that the
 E. Stubbs et al. / Clinical Imaging 37 (2013) 608–612
cutaneous and subcutaneous manifestations are secondary to
a rapidly rising neutrophil count even when the absolute
neutrophil level remains low [7]. Our patient demonstrated a
temporal relationship of symptoms to G-CSF treatment,
histological confirmation, and a score of 6 out of 10 on the
Naranjo scale (used for determining the likelihood of
whether an adverse drug reaction is actually due to the
drug) in keeping with a “probable” causal relationship with
G-CSF [11]. Other reported causes of drug-induced Sweet's
syndrome include all-trans retinoic acid, vaccines, antivirals,
antibiotics, and nonsteroidal anti-inflammatory drugs [7].
Whilst originally described as a condition of the skin and
subcutaneous tissues, there have been many subsequently
described cases of extracutaneous involvement in Sweet's
syndrome [1,12,13]. Extracutaneous involvement affecting
the brain, central nervous system, gastrointestinal tract, liver,
spleen, heart, lungs and musculoskeletal system have all
been described [2,3]. Musculoskeletal involvement is
uncommon but has been described involving tendons,
tendon sheaths, muscle, bone and joints [14–21]. Only 2
previous case reports of fascial involvement have been
published both of which describe synchronous muscle
involvement [4,5]. The case described by Naschitz et al.
[5] was a post mortem pathological diagnosis in a 60-year-
old woman with myeloblastic leukaemia with no imaging. In
the presented case, there was fascial involvement with no
evidence of myositis, which is unique.
Fasciitis can be readily diagnosed with MRI however the
test lacks specificity [22]. Attention to muscle signal
abnormality and correlation with the patient's clinical
presentation is important to exclude conditions including
rhabdomyolysis and necrotising fasciitis [23,24]. Eosino-
philic fasciitis, a condition characterised by a scleroderma-
like illness with peripheral eosinophilia, is a relatively rare
cause of fasciitis that may have similar MRI appearances to
those that are described in the presented case [25,26]. To
definitively diagnose eosinophilic fasciitis a full thickness
skin to muscle biopsy is required, and MRI plays a key role
in choosing a suitable biopsy site.
Sweet's syndrome, including the drug-induced form, is
widely recognised in the non-radiological literature. This
case exemplifies how imaging can be a valuable adjunct
when combined with the clinical and histological assess-
ments in making the appropriate diagnosis and guiding
further management. Ultrasound and MRI can help to not
only characterise the disease but also to target a core biopsy
to an accessible and abnormal area to improve the chances of
gaining diagnostic tissue.
4. Conclusion
Although rare, extracutaneous Sweet's syndrome should
be borne in mind in any patient presenting with fasciitis and/
or panniculitis with or without myositis in the appropriate
clinical setting. Concomitant use of certain medications,
including G-CSF increases the clinical suspicion and core
611
biopsy directed at an area of MRI abnormality can lead to a
definitive diagnosis.
References
[1] Sweet RD. An acute febrile neutrophilic dermatosis. Br J Dermatol
1964;76:349–56.
[2] Cohen PR, Kurzrock R. Sweet's syndrome revisited: a review of
disease concepts. Int J Dermatol 2003;42:761–78.
[3] Cohen PR. Sweet's syndrome—a comprehensive review of an acute
febrile neutrophilic dermatosis. Orphanet J Rare Dis 2007;2:34.
[4] Gaeta M, Mileta A, Musumeci O, et al. MRI findings of neutrophilic
fasciitis in a patient with acute febrile neutrophilic dermatosis (Sweet's
syndrome). Skeletal Radiol 2011;40:779–82.
[5] Naschitz JE, Boss JH, Misselevich I, Yeshurun D, Rosner I. The
fasciitis-panniculitis syndromes. Clinical and pathologic features.
Medicine 1996;75:6–16.
[6] Cohen PR. Neutrophilic dermatoses. A review of current treatment
options. Am J Clin Dermatol 2009;10:301–12.
[7] Thompson DF, Montarella KE. Drug-induced Sweet's syndrome. Ann
Pharmacother 2007;41:802–11.
[8] White JML, Mufti GJ, Salisbury JR, du Vivier AWP. Cutaneous
manifestations of granulocyte colony-stimulating factor. Clin Exp
Dermatol 2005;31:206–7.
[9] Becherer K, Golda N, Feldman M, Diaz-Arias A, Caldwell C.
Neutrophilic panniculitis associated with myelodysplastic syndrome
with abnormal nuclear forms. J Cutan Pathol 2009;36:1024–6.
[10] Richard MA, Grob JJ, Laurans R, et al. Sweet's syndrome induced by
granulocyte colony-stimulating factor in a woman with congenital
neutropenia. J Am Acad Dermatol 1996;35:629–31.
[11] Naranjo CA, Busto U, Sellers EM, et al. A method for estimating the
probability of adverse drug reactions. Clin Pharmacol Ther 1981;30:239–45.
[12] Cohen PR. Subcutaneous Sweet's syndrome: a variant of acute febrile
neutrophilic dermatosis that is included in the histopathologic
differential diagnosis of neutrophilic panniculitis. J Am Acad Dermatol
2005;52:927–8.
[13] Guhl G, García-Díez A. Subcutaneous Sweet syndrome. J Cutan
Pathol 2009;36:1024–6.
[14] Rajeswari S, Rajendran CP, Madhavan R, Ramesh S. Sweet's
syndrome with tendinitis. J Assoc Physicians India 2005;53:718–30.
[15] Brown AM, Davies MG, Hickling P. Recurrent tenosynovitis in
Sweet's syndrome. Rheumatology 2002;41:1067–9.
[16] Attias D, Laor R, Zuckermann E, et al. Acute neutrophilic myositis in
Sweet's syndrome: late phase transformation into fibrosing myositis
and panniculitis. Hum Pathol 1995;26:687–90.
[17] Kim MK, Park JW, Park SH, et al. Neutrophilic myositis without
cutaneous involvement as the first manifestation of acute myeloid
leukemia. Korean J Intern Med 2005;20:346–8.
[18] Christ E, Linka A, Jacky E, Speich R, Marincek B, Schaffner A.
Sweet's syndrome involving the musculoskeletal system during
treatment of promyelocytic leukemia with all-trans retinoic acid.
Leukemia 1996;10:731–4.
[19] Marie I, Levesque H, Joly P, et al. Neutrophilic myositis as an
extracutaneous manifestation of neutrophilic dermatosis. J Am Acad
Dermatol 2001;44:137–9.
[20] Majeed HA, Kalaawi M, Mohanty D, et al. Congenital dyserythro-
poietic anemia and chronic recurrent multifocal osteomyelitis in three
related children and the association with Sweet syndrome in two
siblings. J Pediatr 1989;115:730–4.
[21] Moreland LW, Brick JE, Kovach RE, Di Bartolomeo AG, Mullins
MC. Acute febrile neutrophilic dermatosis (Sweet syndrome): a review
of the literature with emphasis on musculoskeletal manifestation.
Semin Arthritis Rheum 1988;17:143–53.
[22] Loh NN, Ch'en IY, Cheung LP, Li KC. Deep fascial hyperintensity in
soft-tissue abnormalities as revealed by T2-weighted MR imaging.
AJR Am J Roentgenol 1997;168:1301–4.
612 E. Stubbs et al. / Clinical Imaging 37 (2013) 608–612

[23] Lu CH, Tsang YM, Yu CW, et al. Rhabdomyolysis: magnetic
resonance imaging and computed tomography findings. J Comput
Assist Tomogr 2007;31:368–74.
[24] Kim KT, Kim YJ, Won Lee J, et al. Can necrotizing infectious fasciitis
be differentiated from nonnecrotizing infectious fasciitis with MR
imaging? Radiology 2011;259:816–24.
[25] Baumann F, Brühlmann P, Andreisek G, Michel BA, Marincek B,
Weishaupt D. MRI for diagnosis and monitoring of patients with
eosinophilic fasciitis. AJR Am J Roentgenol 2005;184:169–74.
[26] Moulton SJ, Kransdorf MJ, Ginsburg WW, Abril A, Persellin S.
Eosinophilic fasciitis: spectrum of MRI findings. AJR Am J
Roentgenol 2005;184:975–8.