Ponad 7000 publikacji medycznych!
Statystyki za 2021 rok:
odsłony: 8 805 378
Artykuły w Czytelni Medycznej o SARS-CoV-2/Covid-19

Poniżej zamieściliśmy fragment artykułu. Informacja nt. dostępu do pełnej treści artykułu
© Borgis - Nowa Medycyna 3/2016, s. 102-113 | DOI: 10.5604/17312485.1223279
*Jacek Wadełek
Diagnostic investigation and management of Fournier’s gangrene in intensive care unit
Diagnostyka i leczenie zgorzeli Fourniera w oddziale intensywnej terapii
Anaesthesiology and Intensive Care Unit, Saint Anna Traumatology Hospital, Mazowsze Rehabilitation Centre „STOCER”, Warsaw
Head of Department: Elżbieta Kurmin-Gryz, MD
Streszczenie
Zgorzel Fourniera (ZF) jest ostrym, szybko postępującym, potencjalnie śmiertelnym, infekcyjnym martwiczym zapaleniem powięzi okolic zewnętrznych narządów płciowych, krocza i okołoodbytniczej, które zwykle występuje u mężczyzn, ale może również mieć miejsce u kobiet i dzieci. Coraz częściej diagnozuje się schorzenia współistniejące u pacjentów ze ZF. Czynniki sprzyjające rozwojowi i etiologiczne ZF zapewniają dogodnie warunki do zakażenia poprzez obniżenie odporności gospodarza i prowadzą do powstania wrót zakażenia dla mikroorganizmów okolicy krocza – szczególnie u pacjentów z rozpoznaną cukrzycą i przewlekłym nadużywaniem alkoholu. ZF może również występować u pacjentów bez oczywistych niedoborów immunologicznych. Jest zakażeniem wywoływanym przez mieszaną tlenową i beztlenową florę bakteryjną działającą synergistycznie. Zakażenie jest wynikiem zaburzonej równowagi pomiędzy odpornością gospodarza a wirulencją wywołującego zakażenie mikroorganizmu. Objawy kliniczne rozwijają się w okresie kilku dni i charakteryzują się: uczuciem niepokoju, miejscowym obrzękiem i dyskomfortem, gorączką, krepitacją, zakażenie czasami prowadzi do wstrząsu septycznego. Rozpoznanie ZF stawiane jest w oparciu o obraz kliniczny. Niezależnie od szerokiego spektrum mikroorganizmów w etiologii ZF, jego leczenie jest takie samo we wszystkich przypadkach i polega na jak najszybszym usunięciu martwiczych tkanek, odpowiedniej resuscytacji i dożylnym podaniu antybiotyków o szerokim spektrum.
Summary
Fournier’s gangrene (FG) is an acute, rapidly progressive, and potentially fatal infective necrotizing fasciitis affecting the external genitalia, perineal or perianal regions, which commonly affects men, but can also occur in women and children. Comorbid systemic disorders are being increasingly identified in patients with FG. The predisposing and etiologic factors of FG provide a favourable environment for the infection by decreasing the host immunity and allowing a portal of entry for microorganisms into the perineum. Especially patients with diagnosed diabetes mellitus and long-standing alcohol misuse are at risk of FG. It can also affect patients with non-obvious immune compromise. It is secondary to polymicrobial infection by aerobic and anaerobic bacteria with a synergistic action. Infection represents an imbalance between host immunity and the virulence of the causative microorganisms. The clinical condition develops in a few days and is characterized by uneasiness, local swelling and discomfort, fever, crepitus and sometimes frank septic shock. The diagnosis of Fournier’s gangrene is made clinically. In spite of the widely varying microorganisms in the etiology, the treatment of FG is common for all cases including emergency removal of the devitalized tissues, adequate resuscitation and intravenous administration of wide-spectrum antibiotics.



Introduction
Fournier’s gangrene (FG) is a necrotizing, life-threatening fasciitis of the perineal area, external genitalia and the anus, which may extend towards the abdominal cavity and result in soft tissue necrosis and the development of sepsis. As early as more than 200 years ago, in 1764, Baurienne described rapid inflammation of the perineum. In 1883 Jean Alfred Fournier, a French dermatologist and venereologist, described a gangrene in five young men without diagnosed etiologic factors (1, 2). The infection is usually caused by a mixed microbial flora. The prevalence of the disease is low; however, mortality still remains high. Certain diseases of the genitourinary and anorectal areas as well as diabetes and conditions associated with immunosuppression are conducive to the development of FG. The diagnosis of FG is made based on clinical symptoms with diagnostic imaging being useful for the evaluation of advancement of necrosis. Therapeutic management primarily involves aggressive surgical excision of necrotic tissues, the use of broad-spectrum antibiotics, anti-shock treatment and supporting therapy. The Fournier’s Gangrene Severity Index Score may be used to assess the condition of the patients (tab. 1). Due to its diversity and aggressive course FG is a very serious and complex medical problem that requires a multi-disciplinary therapeutic approach.
Tab. 1. Fournier’s Gangrene Severity Index Score; nine parameters are measured and the scores for all parameters are added to obtain a total score
ParameterScore
+4+3+2+10+1+2+3+4
Body temperature
[°C]
> 4139-40.938.5-35.936-38.434-35.9 32-33.930-31.9< 29.9
Heart rate
[breaths per minute]
> 180140-179110-13970-109 56-69 40-54< 39
Respiratory rate
[breaths per minute]
> 50 35-49 25-34 12-2410-11 6-9< 5
Serum sodium level
[mmol/l]
> 180160-179155-159150-154130-149120-129111-119< 110
Serum potassium level [mmol/l]> 7 6-6.95.5-5.93.5-5.43-3.42.5-2.9< 2.5
Serum creatinine level
[mg/dl]
> 3.5 2-3.41.5-1.90.6-1.4< 0.6
Hematocrit
[%]
> 60 50-5946-49.430-45.9 20-29.9< 20
White blood cell count
[103/μl]
> 40 20-3915-19.9 3-14.9 1-2.9< 1
Bicarbonate level
[mmol/l]
> 5241-51.932-40.922-31.9 18-21.915-17.9< 15
FG etiology
The etiologic factor for FG is successfully established in over 90% of cases. It should be sought since the treatment and prognosis are dependent on it (3). In some cases the etiologic factor cannot be determined due to necrotic lesions. Every process during which pathogens enter the subcutaneous tissue of the anorectal area may be the starting point for a severe infection. The infection may spread to the genitourinary organs, in the anal and rectal region, to the skin in these areas and in the retroperitoneal space. The area of the genitourinary organs is the most common location for the development of the etiologic factor, diseases of the urethra being the primary one. The knowledge of the anatomy of these regions is necessary to understand the etiology and pathogenesis of fulminant infections. The causes of FG are listed in table 2. Each of the listed areas may be the source of infection with a spread through interfascial spaces causing proliferative fasciitis (4-8). Although FG is found primarily in older men, it may occur at any age and only 10% of cases are found in women (7, 9). The FG causes specific for women include pudendal nerve block, episiotomy for a natural childbirth, septic miscarriage, hysterectomy, Bartholin’s gland abscess and vulvar abscess. In the vast majority of cases patients with FG have comorbidities that cause a compromised blood flow or immunity impairment, which increases their susceptibility to infection with a mixed flora (tab. 3). FG is often the result of a primary condition such as diabetes, genitourinary tuberculosis, syphilis and HIV infection. Diabetes is the most common comorbidity and is found in approximately 60% of patients with FG. Patients with diabetes suffer from urinary tract infections more frequently due to cystopathy and urinary stasis (4). Hyperglycaemia decreases cell immunity by reducing phagocytic activity. It compromises leukocyte chemotaxis to inflammation sites as well as reducing neutrophil adhesion and intracellular processes of pathogen destruction by oxygen. Wound healing is also impaired as a result of compromised epithelialisation and deposition of collagen (10-12). Apart from hyperglycaemia, diabetic patients also have impaired microcirculation, which contributes to a significant extent to the pathogenesis of PG. It is also noteworthy that diabetes increases the risk of PG, but does not increase its mortality (4, 13). Factors which increase the risk of FG include chronic alcoholism, malnutrition, cirrhosis and poor personal hygiene (tab. 3). Other factors which compromise immunity and may predispose individuals to the development of FG are chronic steroid therapy, organ transplant, chemotherapy for cancer such as leukaemia and HIV infection (14). The rising incidence of HIV is accompanied by an increase in the incidence of FG, especially in Africa. FG may be the first symptom of HIV infection (14, 15). Risk factors include CD4 count below 400, chemotherapy for Kaposi sarcoma and the placement of a femoral venous line for intravenous drug administration. Patients with HIV and FG are younger and have a broader spectrum of pathogenic bacterial flora.
Tab. 2. Causes of Fournier’s gangrene
Genitourinary system
Urethral stenosis
Prolonged presence of a urinary catheter in the urinary tract
Prolonged use of a condom
Kidney stones
Urethritis
Transurethral surgery
Inflammation of the periurethral glands and a periurethral abscess
Genitourinary tuberculosis
Urethral cancer
Prostate biopsy
Prostate massage
Prostate abscess
Placement of a penile implant
Erectile ring for the treatment of erectile dysfunction
Iatrogenic trauma
Genital warts burning
Circumcision
Prolonged priapism
Non-iatrogenic perineal trauma
Animal, insect and human bites
Scrotal abscess
Testicular hydrocele infection
Status post testicular hydrocele removal
Vasectomy
Balanitis
Paraphimosis
Colorectal causes
Intersphincteric, perianal and ischioanal abscess
Rectal mucosal biopsy
Hemorrhoid ligation
Anal dilation
Cancers of the rectum and sigmoid colon
Diverticulitis
Rectal perforation by foreign body
Colitis due to ischemia
Rectal stenosis
Skin causes
Exudative purulent dermatitis
Skin glands inflammation
Scrotal decubitus
Post-surgical scrotal wound infection
Scrotal cellulitis
Gangrenous purulent dermatitis
Abscess of the thigh associated with intravenous drug abuse
Retroperitoneal space
Psoas major muscle abscess
Perirenal abscess
Appendicitis and periappendiceal abscess
Pancreatitis with retroperitoneal fat necrosis
Other
Plastic surgery of inguinal hernia
Filariasis in endemic areas
Strangulated hernia
Tab. 3. Diseases predisposing patients to Fournier’s gangrene
Diabetes
Chronic alcoholism
Malnutrition
Obesity
Cirrhosis
Poor personal hygiene
Immunosuppression:
– chronic steroid therapy
– status post organ transplant
– chemotherapy for cancer
– HIV/AIDS
Tuberculosis
Syphilis
Fournier’s gangrene microbiology

Powyżej zamieściliśmy fragment artykułu, do którego możesz uzyskać pełny dostęp.
Mam kod dostępu
  • Aby uzyskać płatny dostęp do pełnej treści powyższego artykułu albo wszystkich artykułów (w zależności od wybranej opcji), należy wprowadzić kod.
  • Wprowadzając kod, akceptują Państwo treść Regulaminu oraz potwierdzają zapoznanie się z nim.
  • Aby kupić kod proszę skorzystać z jednej z poniższych opcji.

Opcja #1

24

Wybieram
  • dostęp do tego artykułu
  • dostęp na 7 dni

uzyskany kod musi być wprowadzony na stronie artykułu, do którego został wykupiony

Opcja #2

59

Wybieram
  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 30 dni
  • najpopularniejsza opcja

Opcja #3

119

Wybieram
  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 90 dni
  • oszczędzasz 28 zł
Piśmiennictwo
1. Ullah S, Khan M, Ullach A, Jan M: Fournier’s gangrene: a dreadful disease. Surgeon 2009; 7: 138-142. 2. Sorensen MD, Krieger JN, Rivara FP et al.: Fournier’s gangrene: population based epidemiology and outcomes. J Urol 2009; 181: 2121-2126. 3. Smith GL, Bunker CB, Dinneen MD: Fournier’s gangrene. Br J Urol 1998; 81: 347-355. 4. Baskin LS, Carroll PR, Cattolica EV, McAninch JW: Necrotising soft tissue infections of the perineum and genitalia. Br J Urol 1990; 65: 524-529. 5. Corman JM, Moody JA, Aronson WJ: Fournier’s gangrene in a modern surgical setting: improved survival with aggressive management. Br J Urol 1999; 84: 85-88. 6. Eke N: Fournier’s gangrene: a review of 1726 cases. Br J Surg 2000; 87: 718-728. 7. Kilic A, Aksoy Y, Kilic L: Fournier’s gangrene: etiology, treatment, and complications. Ann Plast Surg 2001; 47: 523-527. 8. Sorensen MD, Krieger JN: Fournier’s Gangrene: Epidemiology and Outcomes in the General US Population. Urol Int 2016; 97(3). DOI: 10.1159/000445695. 9. Quatan N, Kirby RS: Improving outcomes in Fournier’s gangrene. BJU Int 2004; 93: 691-692. 10. Nisbet AA, Thompson IM: Impact of diabetes mellitus on the presentation and outcomes of Fournier’s gangrene. Urology 2002; 60: 775-779. 11. Sen H, Bayrak O, Erturhan S et al.: Is hemoglobin A1c level effective in predicting the prognosis of Fournier gangrene? Urol Ann 2016; 8(3): 343-347. 12. Duncan AE: Hyperglycemia and Perioperative Glucose Management. Curr Pharm Des 2012; 18(38): 6195-6203. 13. Yeniyol CO, Suelozgen T, Arslan M, Ayder AR: Fournier’s gangrene: experience with 25 patients and use of Fournier’s gangrene severity index score. Urology 2004; 64: 218-222. 14. Heyns CF, Fisher M: The urological management of the patient with acquired immunodeficiency syndrome. BJU Int 2005; 95: 709-716. 15. Merino E, Boix V, Portilla J et al.: Fournier’s gangrene in HIV-infected patients. Eur J Clin Microbiol Infect Dis 2001; 20: 910-913. 16. Mindrup SR, Kealey GP, Fallon B: Hyperbaric oxygen for the treatment of Fournier’s gangrene. J Urol 2005; 173: 1975-1977. 17. Chennamsetty A, Khourdaji I, Burks F, Killinger KA: Contemporary diagnosis and management of Fournier’s gangrene. Ther Adv Urol 2015; 7(4): 203-215. 18. Jeong HJ, Park SC, Seo IY, Rim JS: Prognostic factors in Fournier gangrene. Int J Urol 2005; 12: 1041-1044. 19. Laor E, Palmer LS, Tolia BM et al.: Outcome prediction in patients with Fournier’s gangrene. J Urol 1995; 154: 89-92.
otrzymano: 2016-08-29
zaakceptowano do druku: 2016-09-13

Adres do korespondencji:
*Jacek Wadełek
Oddział Anestezjologii i Intensywnej Terapii Szpital Chirurgii Urazowej św. Anny w Warszawie Mazowieckie Centrum Rehabilitacji „STOCER” Sp. z o.o.
ul. Barska 16/20, 02-315 Warszawa
tel. +48 (22) 579-52-58
e-mail: WAD_jack@poczta.fm

Nowa Medycyna 3/2016
Strona internetowa czasopisma Nowa Medycyna