{"id":5167,"date":"2011-07-14T20:24:04","date_gmt":"2011-07-14T20:24:04","guid":{"rendered":"http:\/\/crashtext.org\/misc\/5167.htm\/"},"modified":"2023-10-14T16:36:27","modified_gmt":"2023-10-14T20:36:27","slug":"soft-tissue-infections","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/medical-surgical\/infectious-disease\/soft-tissue-infections.htm\/","title":{"rendered":"Soft Tissue Infections"},"content":{"rendered":"
In patients with liver disease, vibrio vinificulis is a risk if eating or working with shellfish or sea water.\u00a0 Similiar syndrome caused by aeromonas hydrophilia is caused by freshwater<\/p>\n
Abx<\/strong><\/p>\n HIV<\/p>\n IVDA<\/strong><\/p>\n Splenomegaly<\/p>\n ETOH<\/strong><\/p>\n heart murmur or any prosthetics<\/p>\n Steroids<\/strong><\/p>\n Chemotherapy<\/p>\n Diabetes<\/p>\n <\/a><\/a><\/p>\n (from EM Reports)<\/p>\n Staph and strep pyogenes<\/p>\n Periorbital\/orbital usually secondary to sinus infection<\/p>\n Mild is <2cm in adults<\/p>\n Mod\/Severe systemic signs or symptoms, labs abnormal, >2cm<\/p>\n <\/p>\n Need blood cultures only if signs of systemic toxicity.\u00a0 Blood cultures are usually useless as isolates rarely correlate with actual bug.<\/p>\n Wound cultures if patient is failing to improve on the current antibiotic regimen.\u00a0 If you do sample, take deep tissue from ulcer base.<\/p>\n <\/p>\n Treatment<\/p>\n augment c probenicid (inhibits tubular pcn secretion)?<\/p>\n <\/p>\n Fake nails give pseudomonal infections, Also the pads in any shoes. Rx with Diclox\/Bactrim?<\/p>\n Infection in bursa vs. joint, have patient pronate\/supinate arm to differentiate<\/p>\n <\/p>\n Always admit cellulitis overlying a weight bearing joint.<\/p>\n PCN resistant bugs skyrocket if you have a child in daycare<\/p>\n <\/p>\n Outbreaks of persistent furunculosis on the lower extremities have been reported in patrons of nail salons. The causative organism has been identified as Mycobacterium fortuitum<\/em><\/p>\n <\/p>\n think wooden foreign bodies<\/p>\n bullous=staph, otherwise strep.\u00a0 Thick amber\/honey crust<\/p>\n raised<\/strong> lesions, painful and demarcated<\/p>\n group A strep<\/p>\n Lower ext 70%, Face 20%<\/p>\n I\/D<\/p>\n If surrounding cellulitis, needs broad antibiotics<\/p>\n <\/p>\n J Ped Surgery Volume 45, Issue 3, Pages 606-609 (March 2010)The use of loop drains proved safe and effective in the treatment of subcutaneous abscesses in children. Eliminating the need for repetitive and cumbersome wound packing simplifies postoperative wound care. Furthermore, there is an expected cost savings with this technique given the decreased need for wound care materials and professional postoperative home health services. We recommend this minimally invasive technique as the treatment of choice for subcutaneous abscesses in children and consider it the standard of care in our facility.<\/p>\n \u200bloop drainage of abscesses using the cuff of a sterile glove (<\/span><\/span>Journal of Emergency Medicine, 2014-08-01, Volume 47, Issue 2, Pages 188-191)<\/p>\n <\/p>\n Chronic Non-Healing Ulcers:\u00a0 if traveler, consider leishmaniasis.\u00a0 From Sandfly bite.\u00a0 Cutaneous leishmania is also endemic to SW United States.\u00a0 Skin is dry, gray and scaly.\u00a0 Especially seen in immunocompromised players<\/p>\n intensely pruritic<\/p>\n seen in diabetic males<\/p>\n genitocrural distribution<\/p>\n Looks like candida, but there are no satellite lesions<\/p>\n Under Wood’s lamp, it turns bright red<\/p>\n Treat with Erythromycin<\/p>\n Clostridium perfringens is the classic organism responsible for “gas gangrene” or clostridial myonecrosis, although any Clostridial species can produce such infections. Clostridium perfringens is especially likely in wounds contaminated with soil. Clinically, Clostridium infections begin within hours of an inciting trauma, or surgery, with the sudden onset of pain that rapidly extends beyond the wound. A thin, watery discharge may develop, and large hemorrhagic bullae appear. A Gram\u0092s stain of the discharge often reveals gram-positive bacilli with a paucity of white blood cells.<\/p>\n Clostridium septicum can cause spontaneous, nontraumatic necrotizing infections. A colonic lesion, such as carcinoma, will predispose to this highly lethal disease.<\/p>\n <\/p>\n Scalded skin syndrome often starts in a child with a bullous impetigo. The lesion begins as a vesicle, and then gradually enlarges into flaccid bullae that rupture. New bullae typically appear over the next 2-3 days, during which time hair and nails may also shed. Fever, skin tenderness, and a scarlatiniform rash are common. The exfoliation toxin can be also secreted by localized infection in the nasopharynx, umbilicus, or urinary tract. In some children, exposed dermal surfaces will weep, while fluid and electrolyte losses may lead to hypovolemia. Exposed surfaces may also serve as a portal for other infections. Most children recover in about 10 days if appropriately treated.<\/p>\n Scalded skin syndrome should be treated with parenteral antibiotics. In a community-acquired infection, beta-lactamase-resistant antibiotics are appropriate. When the infection appears to have been acquired in a hospital or extended care facility, methicillin-resistant Staphylococcus aureus <\/em>should be considered and vancomycin is the drug of choice. Intranasal mupirocin may provide benefits by eliminating intranasal colonization.<\/p>\n Staph Scalded Skin-Nikolsky\u0092s Sign-<\/em>easy separation of outer skin<\/p>\n Group A streptococcus, known as the “flesh-eating bacteria” in the lay press, causes a wide spectrum of soft-tissue infections. They range from the mild and superficial, such as impetigo, to a rapidly progressive and deadly necrotizing contagion.<\/p>\n Many of these patients develop hypotension, renal dysfunction, and coagulopathies resembling staphylococcal toxic shock syndrome. The mortality rate remains higher than 30% but with\u00a0 appropriate antibiotics and supportive care, can be reduced to 12%.<\/p>\n <\/p>\n Recognition-suspect if pain is out of proportion to clinical findings, then progression to anesthesia.<\/p>\n All present with hypotension, initially or soon afterwards.\u00a0 Progressing to multiorgan dysfunction.<\/p>\n <\/p>\n <\/a><\/a><\/p>\n <\/p>\n Will at first look just like a cellulitis with\/without abcess.\u00a0 One clue is that area will become anesthetic as infection progresses.\u00a0 May not see bubbles of air on radiography b\/c only some organisms will produce.\u00a0 Not necessarily clostridium if you do see bubbles, e. coli and others can produce as well.\u00a0 Broad spectrum abx and surgical consult.\u00a0 Unasyn\/Genta or Amp\/Genta\/Flagyl or Imipenem\/Flagyl\u00a0 Unasyn plus clindamycin<\/p>\n Stat surgical consult<\/p>\n <\/p>\n Type II \u0097 Type II necrotizing fasciitis is caused by GAS and was previously called “streptococcal gangrene” [ 7]. There was a dramatic increase in the number of invasive infections such as necrotizing fasciitis caused by GAS during the 1990s. In Ontario, Canada, for example, the incidence of GAS necrotizing fasciitis increased from 0.085 per 100,000 in 1991 to 0.40 per 100,000 in 1995 [10] . Most cases were community-acquired but 20 percent were nosocomial or acquired in a nursing home. Almost one-half had streptococcal toxic shock syndrome. ( See “Streptococcal toxic shock syndrome”). That most cases are community-acquired is further supported by a recent epidemic in a small town in Minnesota where the incidence approached 24 cases\/100,000 population. In contrast to type I necrotizing fasciitis, which primarily occurs in patients who are immunocompromised or have certain chronic diseases such as diabetes, type II can occur in any age group and among patients who do not have complicated medical illnesses [9]. Predisposing factors include a history of blunt trauma, varicella (chickenpox), injection drug use, a penetrating injury such as laceration, surgical procedures, childbirth, exposure to a “case,” and perhaps nonsteroidal antiinflammatory drugs.<\/p>\n The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue OBJECTIVE: Early operative debridement is a major determinant of outcome in necrotizing fasciitis. However, early recognition is difficult clinically. We aimed to develop a novel diagnostic scoring system for distinguishing necrotizing fasciitis from other soft tissue infections based on laboratory tests routinely performed for the evaluation of severe soft tissue infections: the Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score. DESIGN: Retrospective observational study of patients divided into a developmental cohort (n = 314) and validation cohort (n = 140) SETTING: Two teaching tertiary care hospitals. PATIENTS: One hundred forty-five patients with necrotizing fasciitis and 309 patients with severe cellulitis or abscesses admitted to the participating hospitals. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The developmental cohort consisted of 89 consecutive patients admitted for necrotizing fasciitis. Control patients (n = 225) were randomly selected from patients admitted with severe cellulitis or abscesses during the same period. Hematologic and biochemical results done on admission were converted into categorical variables for analysis. Univariate and multivariate logistic regression was used to select significant predictors. Total white cell count, hemoglobin, sodium, glucose, serum creatinine, and C-reactive protein were selected. The LRINEC score was constructed by converting into integer the regression coefficients of independently predictive factors in the multiple logistic regression model for diagnosing necrotizing fasciitis. The cutoff value for the LRINEC score was 6 points with a positive predictive value of 92.0% and negative predictive value of 96.0%. Model performance was very good (Hosmer-Lemeshow statistic, p =.910); area under the receiver operating characteristic curve was 0.980 and 0.976 in the developmental and validation cohorts, respectively. CONCLUSIONS: The LRINEC score is a robust score capable of detecting even clinically early cases of necrotizing fasciitis. The variables used are routinely measured to assess severe soft tissue infections. Patients with a LRINEC score of > or = 6 should be carefully evaluated for the presence of necrotizing fasciitis. (Crit Care Med. 2004 Jul;32(7):1535-41)<\/p>\n <\/p>\n derivation of a CT scan score (J trauma 2011;<\/p>\n Validation parameters for a score of >6 points included sensitivity (86.3%), specificity (91.5%), negative predictive value (NPV) (85.5%), and positive predictive value (PPV) (63.3%). Validation parameters for fascial air alone yielded a sensitivity of 44.1%, specificity 61.1%, NPV 35.2%, and PPV 58.9%. The mean scores of the NSTI and non-NSTI group were 8.57 (\u00b11.22) and 2.74 (\u00b10.65), respectively.<\/p>\n <\/a><\/p>\n HBO decreased mortality in this retrospective study (Intensive Care Medicine Volume 38, Number 7 (2012), 1143-1151)<\/p>\n <\/p>\n J Am Acad Derm (2004;51:308)<\/p>\n Deep space infection of skeletal muscle, without overlying cellulitis. Causative agents are usual skin bacteria<\/p>\n pelvis, hip, or leg<\/p>\n usually, but not always, have some increased risk of infection<\/p>\n MRI or CT scan<\/p>\n 2\/3 of pts will need surg drainage<\/p>\n <\/p>\n get an x-ray<\/p>\n probe to bone<\/p>\n Elevated ESR has a sensitivity and specificity in the 80s for detecting osteomyelitis (Majeed, et. al, 2019<\/a>)<\/p>\n Get an MRI if you have a suspicon<\/p>\n The WIfI (Wound, Ischemia, and Foot Infection) scoring system uses the results of the non-invasive vascular studies and other factors to help predict who would benefit from revascularization and who is at greater risk for amputation (JVS Practice Guideline Mills, Sr., et. al, 2014<\/a>).\u00a0 Clinicians can synthesize this information to discuss severity of illness and possible treatment plans with their patients.<\/p>\n The results of a superficial wound swab do not correlate with the pathogen causing infection. Clinicians should avoid superficial swab specimens and opt for a specimen obtained from deep tissue, often at the time of debridement (IDSA Guidelines Lipsky, et. al, 2012<\/a>).<\/p>\n <\/p>\n Cipro\/clinda is very good combination<\/p>\n <\/p>\n think wooden foreign bodies<\/p>\n <\/p>\n a free-living, gram-negative, curved bacillus found in warm marine waters. It is capable of causing terrifying life- and limb-threatening infections, especially in those with underlying liver disease (usually due to alcoholism or viral hepatitis). Skin infection may follow exposure of open wounds to contaminated seawater or shellfish or may spread hematogenously following ingestion of contaminated seafood, usually raw oysters. Skin involvement may range from mild cellulitis to rapidly progressing necrotizing fasciitis and myositis. Patients may develop hemorrhagic bullae. Treatment requires prompt recognition, surgical debridement, and early institution of antimicrobial therapy. Clinical trials are lacking, but some authors recommend third-generation cephalosporins (e.g., ceftazidime) with an aminoglycoside. Others suggest adding doxycycline to the empiric antibiotic regimen based on animal studies and in vitro susceptibility testing<\/p>\n <\/p>\n 3rd generation cephalosporin + tetracycline may be best choice. retrospective article Arch Intern Med<\/em> 2006;166:2117-2123.<\/p>\n gram-negative bacillus found in freshwater lakes and streams. Serious soft-tissue infection may follow wound exposure to such water. These suppurative infections progress rapidly, often requiring surgical drainage. Cephalosporins (second-, third-, or fourth-generation), trimethoprim\/sulfamethoxazole, and fluoroquinolones are active against Aeromonas<\/em><\/p>\n develops following exposure to contaminated water and is generally seen in swimmers and fishermen. A small papule, or nodule, develops after 2-6 weeks of incubation. This “fish tank” or “swimming pool” granuloma will then ulcerate and drain serosanguinous fluid. In approximately 20%-40% of patients, nodular lesions develop along the lymphatics (known as the “sporotrichoid” distribution). Bacterial culture may require 2-4 weeks of incubation.<\/p>\n M. marinum<\/em> is resistant to isoniazid and pyrazinamide. Treatment options include clarithromycin, minocycline, or trimethoprim\/sulfamethoxazole as single agents, or a combination of ethambutol and rifampin. The duration of antimicrobial therapy is approximately 12-24 weeks, and surgical debridement is often required<\/p>\n <\/p>\n Fire Coral:\u00a0 <\/strong>local reactions<\/p>\n Sponges:<\/strong>\u00a0 abrasions with mild toxin<\/p>\n Marine <\/strong>Worms<\/strong>:\u00a0 <\/strong>local wound care<\/p>\n Hematoma<\/strong><\/p>\n If infected, I\/D<\/p>\n Mondor’s Disease<\/strong><\/p>\n phlebitis of thoracoepigastric vein (runs from axilla to epigastrum)<\/p>\n Rx only needed for pain control<\/p>\n Subcutaneous Rupture<\/strong><\/p>\n usually from seatbelt trauma<\/p>\n if in non-lactating woman, consider malignancy<\/p>\n Milk Stasis<\/p>\n Mastitis<\/p>\n Epidemic<\/strong>-nosocomial ~1st week of life.\u00a0 Usually progresses to abcess. Spread from infant to infant and then to mother.\u00a0 Staph.\u00a0 Use diclox.\u00a0 If abcess, aspiration and possible surgical drainage along with parenteral antibiotics.\u00a0 Do not breast feed from that side.<\/p>\n Endemic<\/strong>-usually more benign.\u00a0 1-2 weeks.\u00a0 Staph\/strep.\u00a0 Must continue to feed from that breast.\u00a0 Moist heat pads.\u00a0 Oral abx (keflex or diclox)\u00a0 unless systemic symptoms<\/p>\n cyclical breast pain<\/p>\n Drugs and Breast Feeding<\/p>\n avoid flagyl, sulfonamides, nitrofurantoin, ergotamine, lithium, Hold breast feeding for 4 days after radioactive compounds.<\/p>\n <\/p>\n Emerging MRSA<\/p>\n MRSA susceptibilities were as follows: 100 percent were susceptibleto trimethoprim\u0096sulfamethoxazole (217 of 217) and to rifampin (186 of 186); 95 percent were susceptible to clindamycin (215of 226), 92 percent to tetracycline (207 of 226), 60 percentto fluoroquinolones (106 of 176), and 6 percent to erythromycin(13 of 226). Although the proportion of all S. aureus<\/em> isolates(MRSA and MSSA) that were resistant to clindamycin was lessthan 15 percent at 10 of the study sites, 6 of 10 S. aureus<\/em>isolates from New York City (60 percent) were resistant to clindamycin.Among the isolates that were sent to the CDC, 11 of 218 MRSAisolates (5 percent) and 7 of 55 MSSA isolates (13 percent)were not susceptible to clindamycin, including 4 (2 percent)MRSA isolates and 5 (9 percent) MSSA isolates with inducibleclindamycin resistance detected by an antimicrobial-susceptibilityD-zone disk-diffusion test. Sixty-six patients with MRSA infections(27 percent) had one or more established risk factors for healthcare\u0096associated MRSA; these included 43 patients who hadbeen hospitalized within the past year, 28 with a history ofMRSA infection, 2 who resided in a long-term care facility,and 1 who was undergoing dialysis. Isolates from 55 of thesepatients were evaluated at the CDC, and 54 (98 percent) hadpulsed-field types characteristic of community-associated MRSA.<\/p>\n Features associated with the isolation of MRSA as compared with the isolation of any other bacteria (Table 2<\/a>) included antibioticuse in the month before enrollment, the presence of an abscessor a lesion attributed to a spider bite at enrollment, historyof MRSA infection, and a recent history of close contact withsomeone with a similar skin infection. The presence of an underlyingillness and characterization as belonging to the “other” categoryof race or ethnic background were negatively associated with the isolation of MRSA. In multivariate logistic-regression analyses, all these factors were associated with MRSA infection, withthe exception of the presence of an abscess (Table 3<\/a>). Blackrace was independently associated with MRSA infection. Controllingfor study site did not affect the association between any of these factors and MRSA infection. Among 64 patients with noneof these factors, 31 (48 percent) were infected with MRSA. Theonly factor that was significantly associated with isolationof MRSA, as compared with MSSA, was the presence of abscessat enrollment (odds ratio, 2.3; 95 percent confidence interval,1.2 to 4.4).<\/p>\n (NEJM 2006;355(7):666)<\/p>\n <\/p>\n <\/p>\n <\/a><\/p>\n Approach to Suspected Staphylococcal Infections.<\/p>\n For wound cultures that are positive for community-associated MRSA (usually not a multidrug-resistant phenotype), in vitro susceptibility to trimethoprim\u0096sulfamethoxazole (TMP-SMX), tetracycline, erythromycin, clindamycin, and vancomycin should be assessed. If the isolate is resistant to erythromycin but susceptible to clindamycin, the clindamycin D-zone test should be performed if clindamycin therapy is being considered.10<\/a> For wound cultures that are positive for health care\u0096associated MRSA (usually a multidrug-resistant phenotype), in vitro susceptibility to vancomycin, rifampin, and linezolid should be assessed. Assessment of susceptibility to daptomycin and quinupristin\u0096dalfopristin is not necessary unless therapy with these agents is being considered. Susceptibility to fusidic acid may be assessed in countries where this agent is available. Empirical antibiotic therapy should be reviewed once susceptibility data are known. For methicillin-susceptible S. aureus<\/em> (MSSA), antistaphylococcal penicillin or a first-generation cephalosporin (1-CEF) may be suitable. For community-associated MRSA, TMP-SMX, clindamycin, or tetracycline may be suitable. For health care\u0096associated MRSA, vancomycin, linezolid, daptomycin, or rifampin plus fusidic acid may be suitable.<\/p>\n <\/p>\n <\/p>\n |\u00a0\u00a0 \u00a0\u00a0 |\u00a0\u00a0 \u00a0\u00a0 |<\/p>\n <\/p>\n","protected":false},"excerpt":{"rendered":" Array<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_genesis_hide_title":false,"_genesis_hide_breadcrumbs":false,"_genesis_hide_singular_image":false,"_genesis_hide_footer_widgets":false,"_genesis_custom_body_class":"","_genesis_custom_post_class":"","_genesis_layout":"","footnotes":""},"categories":[23],"tags":[],"yoast_head":"\n<\/span>Cellulitis<\/span><\/h3>\n
<\/span>Enterobacter cloacae<\/em><\/span><\/h3>\n
<\/span>Impetigo<\/span><\/h3>\n
<\/span>Erisypilas<\/span><\/h3>\n
<\/span>Abscesses<\/span><\/h2>\n
<\/span>Loop Drainage<\/span><\/h3>\n
<\/span>Leishmaniasis<\/span><\/h3>\n
<\/span>Erythrasma<\/span><\/h3>\n
<\/span>Clostridial Myonecrosis (Gas Gangrene)<\/span><\/h3>\n
<\/span>Toxic Shock Syndrome<\/a><\/span><\/h3>\n
<\/h3>\n
<\/span>Staphylococcal Scalded Skin Syndrome<\/span><\/h3>\n
<\/span>Necrotizing Fasciitis (NSTI)<\/span><\/h2>\n
\n
<\/span>Ultrasound STAFF Exam (West J Emerg Med 2014;15:111)<\/span><\/h3>\n
\n
<\/span>Pyomyositis<\/span><\/h2>\n
<\/span>Diabetic Foot<\/span><\/h2>\n
<\/span>Screen for Osteo<\/span><\/h3>\n
<\/span>Vascular Assessment<\/span><\/h3>\n
<\/span>Wound Swabs<\/span><\/h3>\n
<\/span>Enterobacter cloacae<\/em><\/span><\/h3>\n
<\/span>Waterborne Skin Infections<\/span><\/h2>\n
<\/span>Vibrio vulnificus<\/span><\/h3>\n
<\/span>Aeromonas Hydrophila<\/span><\/h3>\n
<\/span>Mycobacterium marinum<\/span><\/h3>\n
<\/span>Breast Disorders<\/span><\/h2>\n
<\/span>Trauma<\/span><\/h3>\n
<\/span>Infectious<\/span><\/h3>\n
<\/span>Mastodynia<\/span><\/h3>\n