Prevalence of concurrent deep vein thrombosis in patients with lower limb cellulitis: a prospective cohort study.

Mar 2013

Maze MJ, Skea S, Pithie A, Metcalf S, Pearson JF, Chambers ST.

Source

Department of Infectious Diseases, Christchurch Hospital, Christchurch, 8002, New Zealand. Michael.Maze@cdhb.health.nz.

Abstract

BACKGROUND:

Lower limb cellulitis and deep vein thrombosis share clinical features and investigation of patients withcellulitis for concurrent DVT is common. The prevalence of DVT in this group is uncertain. This study aimed to determine the prevalence of deep vein thrombosis (DVT) in patients with lower limb cellulitis and to investigate the utility of applying the Wells algorithm to this patient group.

METHODS: Patients admitted with lower limb cellulitis prospectively underwent a likelihood assessment for DVT using the Wells criteria followed by investigation with D-dimer and ultrasonography of ipsilateral femoral veins as appropriate. Diagnoses of contralateral DVT or pulmonary embolism during admission were recorded.

RESULTS:

200 patients assessed for DVT. 20% of subjects were high risk by Wells criteria. D-dimer was elevated in 74% and 79% underwent insonation of the affected leg. Ipsilateral DVT was found in 1 patient (0.5%) and non-ipsilateral VTE in a further 2 (1%).

CONCLUSIONS:

Deep vein thrombosis rarely occurs concurrently with lower limb cellulitis. The Wells score substantially overestimates the likelihood of DVT due to an overlap of clinical signs. Investigation for DVT in patients with cellulitis is likely to yield few diagnoses and is not warranted in the absence of a hypercoaguable state.

TRIAL REGISTRATION:

ACTRN: 12610000792022 (https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=320662).

NIH

Fatal neck necrotizing cellulitis in a patient with Riedel's thyroiditis.

Fatal neck necrotizing cellulitis in a patient with Riedel's thyroiditis.

Mar 2013

Dupret-Bories A, Caron PJ, Rouquette I, Vairel B, Vergez S.

Source

CHU Hautepierre, Otolaryngology Head and Neck Surgery, Strasbourg, France ; agnes.dupret@chru-strasbourg.fr.

Abstract

Background: Riedel's thyroiditis (RT) is a rare chronic disease of the thyroid gland. In clinical practice, the first-line treatment is corticosteroids in symptomatic patients and in most cases the prognosis is favourable. Here we report a case of Riedel's thyroiditis with the development of necrotizing cellulitis of the neck after a wedge biopsy and during glucocorticoid treatment 

Patient Findings: An 81-year-old immunocompetent man presented with dysphonia and episodic dyspnea. An enlarged, hard and fixed thyroid mass was palpated and fibroscopic examination revealed a bilateral vocal cord immobility. A wedge biopsy was taken and a tracheotomy was performed. The histopathology was consistent with the diagnosis of Riedel's thyroiditis. The patient underwent a glucocorticoid treatment. After one month, an excavation of the surface of the neck appeared. 

Despite intravenous adapted antibiotic treatment and surgical debridement of the tissue necrosis, we observed a dramatic extension of cervical necrosis to the thorax. The patient died of severe sepsis 15 days after the surgery. 

Summary: In this patient, the diagnosis of Riedel's thyroiditis was made based on the clinical and histological criteria previously reported in the literature. In most cases, Riedel's thyroiditis has a benign course and mortality is extremely rare. Glucocorticoid therapy is usually effective and can lead to long-term remission. Here the patient developed a fatal neck necrotizing cellulitis 1 month after thyroid biopsy and glucocorticoid treatment. 

Conclusion: Massive necrotizing infection of the neck is rare and usually occurs as a complication of traumatic wounds in diabetic patients. We are unaware of similar cases in the literature of fatal neck necrotizing cellulitis in a patient with Riedel's thyroiditis.

Mary Ann Liebert

Genetic susceptibility to non-necrotizing erysipelas/cellulitis.

Genetic susceptibility to non-necrotizing erysipelas/cellulitis.

2013

Hannula-Jouppi K, Massinen S, Siljander T, Mäkelä S, Kivinen K, Leinonen R, Jiao H, Aitos P, Karppelin M, Vuopio J,Syrjänen J, Kere J.

Source

Department of Medical Genetics, University of Helsinki, and Folkhälsan Institute of Genetics, University of Helsinki, Helsinki, Finland.

Abstract

BACKGROUND:

Bacterial non-necrotizing erysipelas and cellulitis are often recurring, diffusely spreading infections of the skin and subcutaneous tissues caused most commonly by streptococci. Host genetic factors influence infection susceptibility but no extensive studies on the genetic determinants of human erysipelas exist.

METHODS:

We performed genome-wide linkage with the 10,000 variant Human Mapping Array (HMA10K) array on 52 Finnish families with multiple erysipelas cases followed by microsatellite fine mapping of suggestive linkage peaks. A scan with the HMA250K array was subsequently performed with a subset of cases and controls.

RESULTS:

Significant linkage was found at 9q34 (nonparametric multipoint linkage score (NPL(all)) 3.84, p = 0.026), which is syntenic to a quantitative trait locus for susceptibility to group A streptococci infections on chromosome 2 in mouse. Sequencing of candidate genes in the 9q34 region did not conclusively associate any to erysipelas/cellulitis susceptibility. Suggestive linkage (NPL(all)>3.0) was found at three loci: 3q22-24, 21q22, and 22q13. A subsequent denser genome scan with the HMA250K array supported the 3q22 locus, in which several SNPs in the promoter of AGTR1 (Angiotensin II receptor type I) suggestively associated with erysipelas/cellulitis susceptibility.

CONCLUSIONS:

Specific host genetic factors may cause erysipelas/cellulitis susceptibility in humans.

PLOS