What is H. pylori

H. pylori is short for Helicobacter pylori, is a Gram negative, spiral-shaped bacteria that is known to be a major cause of peptic ulcer disease (ulcers in the lining of your stomach or your duodenum, the first part of your small intestine). H. pylori infection is associated with an increased risk of developing peptic ulcer disease, chronic gastritis, gastric (stomach) cancer – gastric B-cell lymphoma of mucosal-associated lymphoid tissue (MALT lymphoma), and invasive gastric adenocarcinoma ¹. H. pylori colonizes half of the world’s human population ². H. pylori typically colonizes the human stomach for years or even decades, often without adverse consequences ³. Most people don’t realize they have H. pylori infection, because they never get sick from it. If you develop signs and symptoms of a peptic ulcer (ulcers in the lining of your stomach or your duodenum, the first part of your small intestine), your doctor will probably test you for H. pylori infection. If you have H. pylori infection, it can be treated with antibiotics.

H. pylori is a common human pathogen that has existed in the stomach since as early as 60,000 years ago ⁴.

H. pylori is very common, especially in developing countries. The bacteria are present in (colonize) the stomachs and intestines of as many as 50% of the world’s population. Most of those affected will never have any symptoms, but the presence of H. pylori increases the risk of developing ulcers (peptic ulcer disease), chronic gastritis, and gastric (stomach) cancer. The bacteria decrease the stomach’s ability to produce mucus, making the stomach prone to acid damage and peptic ulcers.

The Maastricht V/Florence Consensus, the Kyoto Global Consensus and the Toronto Consensus reports have emphasized the importance of H. pylori in the pathogenesis of gastric diseases and recommended the eradication of H. pylori for preventing gastric cancer ⁵. Additionally, H. pylori eradication may rapidly decrease active inflammation in the gastric mucosa ⁶, prevent progression toward precancerous lesions ⁷ and reverse gastric atrophy before the development of intestinal metaplasia ⁸. Undoubtedly, the earliest possible eradication of H. pylori is highly beneficial.

Treatment usually involves a combination of antibiotics and drugs to reduce the amount of stomach acid produced, such as proton pump inhibitors and histamine receptor blockers, as well as a bismuth preparation, such as Pepto-Bismol®, taken for several weeks.

Figure 1. H. pylori (Helicobacter pylori) bacteria

Footnote: High resolution scanning electron micrograph of H. pylori in contact with human gastric epithelial cells. Magnification bar indicates 1 μm. H. pylori virulence factors including flagella (black arrows) and cag-T4SS pili (white arrows) are present on the bacterial cell surface during host-pathogen interaction. Flagella aid in cell motility through the mucus layer to penetrate host tissues. The cag-T4SS pili induce proinflammatory and oncogenic cellular responses.

H. pylori complications

Complications associated with H. pylori infection include:

• Ulcers. H. pylori can damage the protective lining of your stomach and small intestine. This can allow stomach acid to create an open sore (ulcer). About 10 percent of people with H. pylori will develop an ulcer.
• Inflammation of the stomach lining. H. pylori infection can irritate your stomach, causing inflammation (gastritis).
• Stomach cancer. H. pylori infection is a strong risk factor for certain types of stomach cancer.

Does everyone with H. pylori get ulcers?

No, many people have evidence of infection but have no symptoms of ulcerative disease. The reason why some people with H. pylori infections develop peptic ulcers and others do not is not yet understood.

Should everyone be tested for H. pylori?

Since the infection is very common and most people do not ever get ulcers, testing is generally only recommended for those who have signs and symptoms.

Does everyone treated for H. pylori get better?

The majority of people who successfully complete the combination antibiotic therapy get rid of these bacteria from their GI tract. However, resistance to some of the antibiotics may occur and, therefore, the bacteria may continue to multiply in spite of appropriate therapy.

Can I get another H. pylori infection after my treatment?

Treatment does not make a person immune, so there is always the potential for becoming infected again.

Is H. pylori contagious?

Yes, however the exact means of acquiring H. pylori is not always clear ¹⁰. Helicobacter pylori infects at least 50% of the world’s population ¹¹. The H. pylori bacteria are believed to be transmitted by eating food or drinking water that has been contaminated with human fecal material, or possibly through contact with the stool, vomit, or saliva of an infected person. Exposure to family members with H. pylori seems to be the most likely opportunity for transmission. Person-to-person transmission is most commonly implicated with fecal/oral, oral/oral, or gastric/oral pathways ¹²; each has supportive biologic as well as epidemiologic evidence.

H. pylori infection symptoms

Most people with H. pylori infection will never have any signs or symptoms. It’s not clear why this is, but some people may be born with more resistance to the harmful effects of H. pylori.

When signs or symptoms do occur with H. pylori infection, they may include:

• An ache or burning pain in your abdomen
• Abdominal pain that’s worse when your stomach is empty
• Nausea
• Loss of appetite
• Frequent burping
• Bloating
• Unintentional weight loss

People can have gastrointestinal pain for many reasons; an ulcer caused by H. pylori is only one of them. Make an appointment with your doctor if you notice any persistent signs and symptoms that worry you. Seek immediate medical help if you experience:

• Severe or persistent abdominal pain
• Difficulty swallowing
• Bloody or black tarry stools
• Bloody or black vomit or vomit that looks like coffee grounds

How do you get H. pylori?

Helicobacter pylori infects at least 50% of the world’s population ¹¹. Infection occurs in early life, before age 10 years ¹³. Because acute infection invariably passes undetected, however, the precise age of acquisition is unknown. In industrialized countries, infection rates are declining rapidly ¹⁴, but high rates of infection persist among disadvantaged and immigrant populations ¹⁵.

The mechanisms of H. pylori transmission are incompletely characterized and the exact means of acquiring H. pylori is not always clear ¹⁰. The H. pylori bacteria are believed to be transmitted by eating food or drinking water that has been contaminated with human fecal material, or possibly through contact with the stool, vomit, or saliva of an infected person. Exposure to family members with H. pylori seems to be the most likely opportunity for transmission. Person-to-person transmission is most commonly implicated with fecal/oral, oral/oral, or gastric/oral pathways ¹²; each has supportive biologic as well as epidemiologic evidence. Like many common gastrointestinal infections, infection is associated with conditions of crowding and poor hygiene ¹⁶ and with intrafamilial clustering ¹⁷. H. pylori organism has been recovered most reliably from vomitus and from stools during rapid gastrointestinal transit ¹⁸. These findings raise the hypothesis that gastroenteritis episodes provide the opportunity for H. pylori transmission.

In this prospective study ¹¹ of H. pylori infection and household gastroenteritis within a US immigrant population, researchers estimated an annualized H. pylori incidence rate of 7%, including 21% among children <2 years of age. Exposure to H. pylori–infected persons with gastroenteritis, particularly with vomiting, increased risk for new infection, and three quarters of definite or probable new infections were attributable to exposure to H. pylori infection with gastroenteritis. These findings indicate that in US immigrant homes, H. pylori transmission occurs in young children during household episodes of gastroenteritis.

Exposure to an infected household member with vomiting was associated with a 6-fold greater risk for new infection, whereas exposure to diarrhea elevated, but not significantly, the risk for new infection. These findings are consistent with prior research that shows that H. pylori is recovered reliably from vomitus (up to 30,000 CFU/mL) and can also can be grown from aerosolized vomitus collected at short distances (<1.2 m) ¹⁹. Epidemiologic investigations also implicate vomitus as an effective vehicle for gastro-oral transmission ²⁰. Although found in diarrheal stools ¹⁹, H. pylori is not reliably grown from normal stools ²¹. The association between H. pylori and gastroenteritis is thus similar to that of other enteric pathogens that can be transmitted by vomitus or aerosolized vomitus or by the fecal-oral route ²². Although scientists cannot exclude other mechanisms of transmission in these homes, exposure to vomitus in an infected contact explained >50% of all new infections and >70% of definite and probable new infections.

In experimental exposure, acute infection causes mild to moderate epigastric discomfort or dyspepsia in most study participants within 2 weeks, but symptoms are unlikely to be clinically detected ²³. Although H. pylori–specific IgM antibodies may appear within 4 weeks, the frequency of this response is variable, particularly in children and when, as here, the time of infection is unknown ²⁴. Researchers did not observe a pronounced difference in the frequency or distribution of symptoms associated with new infection, although vomiting tended to be more frequent among persons with definite or probable new infections. Although the relatively small numbers of new cases may have limited the power of this analysis, no symptom complex was identified that would permit differentiation of acute H. pylori infection from other enteric processes. Because researchers did not establish the specific etiologic agent of gastroenteritis episodes, further studies are needed to more fully address this question.

Half of new infections were in children <2 years of age, and 2 of 3 were identified by a single unconfirmed stool conversion. Although H. pylori infection is acquired in early childhood, age of acquisition has been difficult to establish because of known limitations of existing noninvasive tests in very young children. In a Bogalusa, Louisiana, birth cohort, for example, the highest seroconversion rate (2%) was seen in children 4–5 years of age ²⁵. Although stool antigen and urea breath tests are considered more accurate ²⁶, studies in very young children are still limited. When the urea breath test was used, an annualized conversion rate of 20% was observed in the US–Mexican binational Pasitos cohort of children followed up from birth to 2 years ²⁷. If, as suggested by this and other studies ²⁸, ²⁹, acquisition with transient infection in early life often precedes persistent infection, rates of acquisition might be elevated when exposure to gastroenteritis is frequent. Rates of acquisition among children in homes at high risk may nonetheless be meaningful measures of transmission risk.

In summary, this study ¹¹ corroborates the conclusion that gastroenteritis, particularly with vomiting, in an H. pylori–infected person is a primary cause of transmission of H. pylori in humans. As with other enteric infections such as hepatitis A, shigellosis, and cholera, H. pylori infection rates have decreased dramatically with improvements in sanitary infrastructure and household hygienic practices. Despite these trends, acquisition and infection are likely to remain prevalent in households with preexisting H. pylori infection, crowded living conditions, and frequent gastroenteritis.

H. pylori causes

The exact way H. pylori infects someone is still unknown. H. pylori bacteria may be passed from person to person through direct contact with saliva, vomit or fecal matter. H. pylori may also be spread through contaminated food or water.
Risk factors

H. pylori is often contracted in childhood. Risk factors for H. pylori infection are related to living conditions in your childhood, such as:

• Living in crowded conditions. You have a greater risk of H. pylori infection if you live in a home with many other people.
• Living without a reliable supply of clean water. Having a reliable supply of clean, running water helps reduce the risk of H. pylori.
• Living in a developing country. People living in developing countries, where crowded and unsanitary living conditions may be more common, have a higher risk of H. pylori infection.
• Living with someone who has an H. pylori infection. If someone you live with has H. pylori, you’re more likely to also have H. pylori.

H. pylori prevention

In areas of the world where H. pylori infection and its complications are common, doctors sometimes test healthy people for H. pylori. Whether there is a benefit to treating H. pylori when you have no signs or symptoms of infection is controversial among doctors.

If you’re concerned about H. pylori infection or think you may have a high risk of stomach cancer, talk to your doctor. Together you can decide whether you may benefit from H. pylori screening.

H. pylori test

H. pylori testing detects an infection of the gastrointestinal (GI) tract caused by the Helicobacter pylori bacteria and to evaluate the effectiveness of treatment.

There are several different types of H. pylori testing that can be performed. Some are less invasive than others.

The stool antigen test and urea breath test are recommended for the diagnosis of an H. pylori infection and for the evaluation of the effectiveness of treatment. These tests are the most frequently performed because they are fast and noninvasive. Endoscopy-related tests may also be performed to diagnose and evaluate H. pylori but are less frequently performed because they are invasive.

Noninvasive Without Endoscopy

• Stool antigen test – detection of H. pylori in a stool sample. As with the breath test, proton pump inhibitors (PPIs) and bismuth subsalicylate can affect the results of this test, so your doctor will ask you to stop taking them for two weeks before the test.
• Urea breath test – detection of labeled carbon dioxide in the breath after drinking a solution
• An antibody test using a blood sample is not recommended for routine diagnosis or for evaluation of treatment effectiveness. This test detects antibodies to the bacteria and will not distinguish between a present and previous infection. If the antibody test is negative, then it is unlikely that a person has had an H. pylori infection. If ordered and positive, results should be confirmed using a stool antigen or breath test.

Invasive With Endoscopy and Tissue Biopsy

Invasive tests using an endoscopy procedure are less frequently performed than noninvasive tests because they require a tissue biopsy collection. Tests include:

• Histology – examination of tissue under a microscope
• Rapid urease testing – detects urease, an enzyme produced by H. pylori
• Culture – growing H. pylori in/on a nutrient solution

When is H. pylori test ordered?

Since all patients with a positive test of active infection with H. pylori should be offered treatment, the critical issue is which patients should be tested for the infection.

H. pylori testing may be ordered when someone is experiencing gastrointestinal pain and has signs and symptoms of an ulcer. Some of these may include:

• Abdominal pain that comes and goes over time
• Unexplained weight loss
• Indigestion
• Feeling of fullness or bloating
• Nausea
• Belching

Some people may have more serious signs and symptoms that require immediate medical attention, including sharp, sudden, persistent stomach pain, bloody or black stools, or bloody vomit or vomit that looks like coffee grounds.

H. pylori testing may also be ordered when a person has completed a regimen of prescribed antibiotics to confirm that the H. pylori bacteria have been eliminated. A follow-up test is not performed on every person, however.

American College of Gastroenterology Recommendations ³⁰:

• All patients with active peptic ulcer disease (ulcers in the lining of your stomach or your duodenum, the first part of your small intestine), a past history of peptic ulcer disease (unless previous cure of H. pylori infection has been documented), low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma, or a history of endoscopic resection of early gastric cancer should be tested for H. pylori infection. Those who test positive should be offered treatment for the infection.
• In patients with uninvestigated dyspepsia who are under the age of 60 years and without alarm features, non-endoscopic testing for H. pylori infection is a consideration. Those who test positive should be offered eradication therapy.
• When upper endoscopy is undertaken in patients with dyspepsia, gastric biopsies should be taken to evaluate for H. pylori infection. Infected patients should be offered eradication therapy.
• Patients with typical symptoms of gastroesophageal reflux disease (GERD) who do not have a history of peptic ulcer disease need not be tested for H. pylori infection. However, for those who are tested and found to be infected, treatment should be offered, acknowledging that effects on GERD symptoms are unpredictable.
• In patients taking long-term low-dose aspirin, testing for H. pylori infection could be considered to reduce the risk of ulcer bleeding. Those who test positive should be offered eradication therapy.
• Patients initiating chronic treatment with a non-steroidal anti-inflammatory drug (NSAID) should be tested for H. pylori infection. Those who test positive should be offered eradication therapy. The benefits of testing and treating H. pylori in patients already taking NSAIDs remains unclear.
• Patients with unexplained iron deficiency anemia despite an appropriate evaluation should be tested for H. pylori infection. Those who test positive should be offered eradication therapy.
• Adults with idiopathic thrombocytopenic purpura (ITP) should be tested for H. pylori infection. Those who test positive should be offered eradication therapy.
• There is insufficient evidence to support routine testing and treating of H. pylori in asymptomatic individuals with a family history of gastric cancer or patients with lymphocytic gastritis, hyperplastic gastric polyps and hyperemesis gravidarum.

How is the sample collected for testing?

The sample collected depends on the test ordered. For the urea breath test, a breath sample is collected and then the person is given a liquid to drink. Another breath sample is collected at a timed interval. For the stool antigen test, a stool sample is collected in a clean container.

A more invasive test will require a procedure called an endoscopy, which involves putting a thin tube with a tiny camera on the end down the throat into the stomach. This allows for visualization of the stomach lining as well as the ability to take a small piece of tissue (a biopsy) from the lining for examination.

Is any test preparation needed to ensure the quality of the sample?

For the urea breath test, you may be instructed to refrain from taking certain medications:

• Four weeks before the test, do not take any antibiotics or oral bismuth subsalicylate (Pepto Bismol®).
• Two weeks before the test, do not take any prescription or over-the-counter proton pump inhibitors, such as omeprazole, lansoprazole, or esomeprazole.
• One hour before the test, do not eat or drink anything (including water).

If submitting a stool sample or having a tissue biopsy collected, it may be necessary to refrain from taking any antibiotics, antacids, or bismuth treatments for 14 days prior to the test.

If undergoing endoscopy, fasting after midnight on the night prior to the procedure may be required.

If someone uses antacids within the week prior to testing, the rapid urease test may be falsely negative. Antimicrobials, proton pump inhibitors, and bismuth preparations may interfere with all but the blood antibody test.

H. pylori breath test

During a H. pylori urea breath test, a person swallows a pill, drinks a liquid or eat or pudding containing a low level of radioactive tagged carbon molecules that is harmless or a nonradioactive material. If H. pylori is present in the person’s gastrointestinal tract, the material will be broken down in your stomach into “labeled” carbon dioxide gas that is expelled in your breath. You exhale into a bag, and your doctor uses a special device to detect the carbon molecules.

Acid-suppressing drugs known as proton pump inhibitors (PPIs), bismuth subsalicylate (Pepto-Bismol) and antibiotics can interfere with the accuracy of this test. Your doctor will ask you to stop taking those medications for a week or two weeks before you have the test.

The urea breath test is not typically recommended for young children. In children, the preferred test would be the stool antigen test.

What does the H. pylori test result mean?

A positive H. pylori stool antigen, breath test, or biopsy indicates that a person’s gastrointestinal pain is likely caused by a peptic ulcer due to these bacteria. Treatment with a combination of antibiotics and other medications will be prescribed to kill the bacteria and stop the pain and the ulceration.

A positive blood test for H. pylori antibody may indicate a current or previous infection. A different test for H. pylori such as the breath test may need to be done as follow up to determine whether the infection is a current one.

A negative test result means that it is unlikely that the individual has an H. pylori infection and their signs and symptoms may be due to another cause. However, if symptoms persist, additional testing may be done, including the more invasive tissue biopsy, to more conclusively rule out infection.

Why is the blood test for H. pylori antibodies not recommended?

The American Gastroenterology Association, the American College of Gastroenterologists, the Infectious Diseases Society of America and the American Society for Microbiology do not recommend the antibody blood test for routine use in diagnosing an H. pylori infection or evaluating its treatment as the test cannot distinguish between a present and previous infection. However, some health practitioners still use this test. If the blood test is negative, then it is unlikely that the person has had an H. pylori infection. If it is positive, then the presence of a current H. pylori infection should be confirmed with a stool antigen or breath test.

H. pylori treatment

H. pylori infections are usually treated with at least two different antibiotics at once, to help prevent the bacteria from developing a resistance to one particular antibiotic. Your doctor also will prescribe or recommend an acid-suppressing drug, to help your stomach lining heal.

Drugs that can suppress acid include:

• Proton pump inhibitors (PPIs). These drugs stop acid from being produced in the stomach. Some examples of PPIs are omeprazole (Prilosec, others), esomeprazole (Nexium, others), lansoprazole (Prevacid, others) and pantoprazole (Protonix, others).
• Histamine (H-2) blockers. These medications block a substance called histamine, which triggers acid production. Examples include cimetidine (Tagamet) and ranitidine (Zantac).
• Bismuth subsalicylate. More commonly known as Pepto-Bismol, this drug works by coating the ulcer and protecting it from stomach acid.

Table 1. Recommended first-line therapies for H pylori infection

Table 2. Recommended salvage therapies for H pylori infection (use if first line therapies failed)

American College of Gastroenterology – strong recommendation

Bismuth quadruple therapy consisting of a PPI, bismuth, tetracycline, and a nitroimidazole for 10–14 days is a recommended first-line treatment option. Bismuth quadruple therapy is particularly attractive in patients with any previous macrolide exposure or who are allergic to penicillin ³⁰.

Concomitant therapy consisting of a PPI, clarithromycin, amoxicillin and a nitroimidazole for 10–14 days is a recommended first-line treatment option ³⁰.

American College of Gastroenterology – Conditional recommendation

Clarithromycin triple therapy consisting of a PPI, clarithromycin, and amoxicillin or metronidazole for 14 days remains a recommended treatment in regions where H. pylori clarithromycin resistance is known to be <15% and in patients with no previous history of macrolide exposure for any reason ³⁰.

Sequential therapy consisting of a PPI and amoxicillin for 5–7 days followed by a PPI, clarithromycin, and a nitroimidazole for 5–7 days is a suggested first-line treatment option ³⁰.

Hybrid therapy consisting of a PPI and amoxicillin for 7 days followed by a PPI, amoxicillin, clarithromycin and a nitroimidazole for 7 days is a suggested first-line treatment option ³⁰.

Levofloxacin triple therapy consisting of a PPI, levofloxacin, and amoxicillin for 10–14 days is a suggested first-line treatment option ³⁰.

Fluoroquinolone sequential therapy consisting of a PPI and amoxicillin for 5–7 days followed by a PPI, fluoroquinolone, and nitroimidazole for 5–7 days is a suggested first-line treatment option ³⁰.

Your doctor may recommend that you undergo testing for H. pylori at least four weeks after your treatment. If the tests show the treatment was unsuccessful, you may undergo another round of treatment with a different combination of antibiotic medications.

What factors predict successful eradication when treating H. pylori infection?

The main determinants of successful H. pylori eradication are the choice of regimen, the patient’s adherence to a multi-drug regimen with frequent side-effects, and the sensitivity of the H. pylori strain to the combination of antibiotics administered.

Resistance to clarithromycin, metronidazole and, increasingly, levofloxacin limits the success of the common eradication regimens in use today. The frequency of multi-drug resistance to these antibiotics appears to be increasing in prevalence. In general, H. pylori resistance to amoxicillin, tetracycline and rifabutin remains rare (under 5% for each currently).

The presence of clarithromycin resistance reduces the success of clarithromycin triple therapy by ~50% ³¹. Levofloxacin resistance lowers success rates of levofloxacin-containing regimens by ~20–40%, although data addressing the clinical impact of levofloxacin resistance are very limited ³². For metronidazole, where in vitro resistance to H. pylori is quite high worldwide, the effect on H. pylori eradication is less predictable. Metronidazole resistance reduces eradication rates by ~25% in triple therapies but less so in quadruple therapies and when PPIs are included in the regimen ³¹. Increasing the dose and duration of metronidazole also improves outcomes in metronidazole-resistant strains, demonstrating that, unlike clarithromycin and levofloxacin, in vitro metronidazole resistance is not an absolute predictor of eradication failure ³³. Indeed, multiple mechanisms of metronidazole resistance in H. pylori have been described and the definition and measurement of metronidazole resistance among H. pylori strains remain to be adequately standardized.

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What is Fournier’s gangrene

Fournier’s gangrene is a life-threatening fulminant form of infective, polymicrobial, necrotizing fasciitis affecting the perineal, genital and perianal regions ¹. Fournier gangrene has a particularly high death rate ranging from 15% to 50% ¹. Fournier’s gangrene commonly affects men in their 60s or 70s and often suffer from other concomitant illnesses ², but women and children may also develop this type of tissue necrosis. Fournier’s gangrene cases in children have been reported from resource-poor countries where poor hygiene is prevalent and in immunocompromised children ³. The male-to-female ratio is 10: 1 ⁴.

Fournier’s gangrene was named after Jean-Alfred Fournier (1832–1914), a Parisian venereologist who reported in 1883 a compiled series of 5 otherwise healthy young men who suffered from a rapidly progressive gangrene of the penis and scrotum without any apparent cause ⁵. More than 1700 cases of necrotizing fasciitis have been reported in the literature from 1950 to 1999 ⁴.

Fournier’s gangrene may occur due to insufficient or lack of blood supply in the affected area and a concomitant infection.

According to the majority of authors, the most important predisposing factors are ⁶, ⁷, ⁸:

• diabetes mellitus,
• alcoholism,
• atherosclerosis,
• peripheral arterial disease,
• trauma or injury,
• Raynaud’s phenomenon,
• malnutrition,
• medical immunosuppression (e.g., chemotherapy, steroids, and malignancy),
• HIV infection,
• leukemia,
• liver diseases, and debilitating illness.

Multiple predisposing factors predict a poor prognosis and correlate significantly with mortality ⁹. Several authors state that the most important parameters that predict outcome of Fournier’s gangrene are hemostatic abnormalities at presentation with this disease and renal failure ¹⁰. Diabetes mellitus is reported to be present in 20–70% of patients with Fournier’s gangrene and chronic alcoholism in 25–50% of Fournier’s gangrene patients, with some authors reporting increased mortality in patients with diabetes ¹¹.

Early diagnosis remains imperative, as the rate of fascial necrosis has been noted as high as 2–3 cm per hour ¹². Treatment of Fournier’s gangrene entails treating sepsis, stabilizing medical parameters and urgent surgical debridement. Despite timely and aggressive management, the condition is life threatening as most studies report mortality rates of between 20% and 40% ¹³, but it can be as high as 70–80%, particularly if sepsis is present at the time of hospital admission ¹⁴. Interestingly, the mortality has been shown to be higher in technologically advanced countries such as the United States, Canada and Europe than in underdeveloped countries ⁴.

Figure 1. Fournier’s gangrene of the scrotum

Figure 2. Fournier gangrene in a 58-year-old female diabetic patient

Is Fournier gangrene contagious?

People rarely spread necrotizing fasciitis to other people. If you’re in close contact with someone who has necrotizing fasciitis, you may be given a course of antibiotics to reduce your risk of infection.

In general, someone with necrotizing fasciitis does not spread the infection to others. Most cases of necrotizing fasciitis occur randomly.

Fournier gangrene symptoms

The clinical features of Fournier’s gangrene include sudden intense pain and tenderness with swelling in the scrotum, pus or wound discharge, crepitation, fluctuance, prostration, pallor and fever greater than 38°C (Figure 1) ¹⁶. Usually the infection starts as an inflammation adjacent to the portal of entry, commonly in the perineum or perineal region, with the appearance of a black spot, called Brodie’s sign ¹⁷. From this moment, the necrotic inflammation spreads briskly, moving along the fascial planes and stretching into the surrounding areas (perineum, scrotum, hypogastrium, and sometimes affecting the region from the thigh up to the diaphragm causing rapid deterioration of the patient’s general condition ¹⁸.

The affected area is often swollen, dusky and covered by macerated skin and presents with a characteristic feculent odor, which is attributed to the role of anaerobes in the infection ¹⁹. Patients also may have pronounced systemic signs, usually out of proportion to the local extent of the disease. In those with severe clinical presentation, progression of the gangrenous process to malodorous drainage and sloughing in affected sites results in deterioration of the patient’s overall condition. Ferreira and colleagues reviewed 43 cases and found the most common presentations were scrotal swelling, fever and pain ²⁰. In another review of 70 patients, Ersay and colleagues found the most common presentation was perianal/scrotal pain (79%) followed by tachycardia (61%), purulent discharge from the perineum (60%), crepitus (54%) and fever (41%) ²¹. Crepitus of the inflamed tissues is a common feature due to the presence of gas-forming organisms ²². As the subcutaneous inflammation worsens, necrosis and suppuration of subcutaneous tissues progresses to extensive necrosis ²³. Patients can rapidly deteriorate as sepsis and multiorgan failure, the most common cause of death in these cases, develop ²⁴.

What causes Fournier’s gangrene

Fournier’s gangrene was initially defined as an idiopathic entity, but recent research has shown that less than a quarter of Fournier’s gangrene cases are now considered idiopathic ²⁵. Colorectal sources (30–50% of cases), urogenital sources (20–40% of cases), cutaneous infections (20% of cases) and local trauma are frequently identified as the cause of Fournier’s gangrene ⁴. Colorectal sources include local infection, abscesses (particularly in the perianal, perirectal and ischiorectal regions), anal fissures, colonic perforations, diverticulitis, hemorrhoidectomy and rectal carcinoma ²⁶. Urologic sources of Fournier’s gangrene include urethral strictures, chronic urinary tract infection, neurogenic bladder, epididymitis and recent instrumentation ²⁷. In women, additional sites of origin include Bartholin gland or vulvar abscess, episiotomy, hysterectomy and septic abortion ²⁸. Insect bites, burns, trauma and circumcision have also been reported as causes of pediatric Fournier’s gangrene ²⁷.

Causes of Fournier’s gangrene ²⁹:

• Anorectal
  • Trauma
  • Ischiorectal, perirectal, or perianal abscesses, appendicitis,
  • Diverticulitis, colonic perforations
  • Perianal fistulotomy, perianal biopsy, rectal biopsy,
  • Hemorrhoidectomy, anal fissures excision
  • Steroid enemas for radiation proctitis
  • Rectal cancer
• Genitourinary
  • Trauma
  • Urethral strictures with urinary extravasation
  • Urethral catheterization or instrumentation,
  • Penile implantsinsertion, prostatic biopsy, vasectomy,
  • Hydrocele aspiration,genital piercing, intracavernosal cocaine
  • Injection periurethral infection; chronic urinary tract infections
  • Epididymitis or orchitis
  • Penile artificial implant, foreign body
  • Hemipelvectomy
  • Cancer invasion to external genitalia
  • Septic abortion
  • Bartholin’s duct abscess
  • Episiotomy
• Dermatologic sources
  • Scrotal furuncle
  • Genital toilet (scrotum)
  • Blunt perineal trauma; intramuscular injections, genital piercings
  • Perineal or pelvic surgery/inguinal herniography.
• Idiopathic

Pathogenesis and organisms involved

The predisposing factors of Fournier’s gangrene provide a favorable environment for the infection by decreasing the host immunity and allowing a portal of entry for the microorganism into the perineum. The incident leading to the inoculation may be so trivial that the patient or physician may fail to notice. Characteristically, Fournier’s gangrene exists due to synergism between multiple bacteria that theoretically are not highly aggressive when presented alone. The polymicrobial nature of Fournier’s gangrene with contributions by both aerobic and anaerobic bacteria is necessary to create the production of various exotoxins and enzymes like collagenase, heparinase, hyaluronidase, streptokinase and streptodornase, which promote rapid multiplication and spread of infection. The aerobic bacteria cause platelet aggregation and induce complement fixation, thereby causing acceleration of coagulation. The anaerobic bacteria promote the formation of clots by producing collagenase and heparinase. Other organisms like Bacteroides inhibit the phagocytosis of aerobic bacteria, aiding in further spread of the infection ³⁰.

The organisms that tend to be found in Fournier’s gangrene are species that normally exist below the pelvic diaphragm in the perineum and genitalia ⁴. The most commonly isolated aerobic microorganisms are Escherichia coli, Klebsiella pneumoniae and Staphylococcus aureus, while the most commonly isolated anaerobic microorganism is Bacteroides fragilis ²². Other organisms include Streptococcus, Enterococcus, Clostridium, Pseudomonas and Proteus species. In some series, an average of more than three organisms were cultured from each patient ¹¹. Group A streptococcal is the most common cause of monomicrobial necrotizing fasciitis ³¹. Although rare, necrotizing fasciitis due to Candida species as well as Lactobacillus gasseri has also been reported ³². Ultimately, the microorganism’s virulence promotes the rapid spread of the disease from a localized infection near the portal of entry into an obliterative endoarteritis with cutaneous and subcutaneous vascular necrosis, leading to local ischemia and further bacterial proliferation ³³.

The infection in Fournier’s gangrene tends to spread along the fascial planes with initial involvement of the superficial (Colles fascia) and deep fascial planes of the genitalia. Subsequently, there is spread to the overlying skin with sparing of the muscles. Infection of Colles fascia may then spread to the penis and scrotum via Buck’s and Dartos fascia, or to the anterior abdominal wall via Scarpa’s fascia, or vice versa. The inferior epigastric and deep circumflex iliac arteries supply the lower aspect of the anterior abdominal wall, whereas the external and internal pudendal arteries supply the scrotal wall. With the exception of the internal pudendal artery, each of these vessels travels within Camper’s fascia and can therefore become thrombosed in the progression of Fournier’s gangrene ³⁴. The Colles fascia is attached laterally to the pubic rami and fascia lata and posteriorly to the urogenital diaphragm, thus limiting progression in these directions. In contrast, anorectal sources of infection usually start in the perianal area, a clinical variation that can serve as a guide to localizing the foci of infection ³⁵. Testicular involvement is limited in Fournier’s gangrene by the fact that the blood supply is derived from the aorta, independent from the affected region ³⁶. However, involvement of the testis suggests retroperitoneal origin or spread of infection ³⁷. Even though thrombosis of the corpus spongiosum and cavernosum has been reported, corpora involvement is rare while the penile skin sloughs off ³⁸.

Fournier’s gangrene diagnosis

The diagnosis of Fournier’s gangrene is primarily based on clinical findings of fluctuance, crepitus, localized tenderness and wounds of the genitalia and perineum. Although diagnosis is straightforward when the lesions are found, failure to examine the genitals, especially in the older or obtunded patient, can result in misdiagnosis. The common laboratory findings are nonspecific and may show anemia, leukocytosis, thrombocytopenia, electrolyte abnormalities, hyperglycemia, elevated serum creatinine level, azotemia and hypoalbuminemia ³⁹. The diagnosis of Fournier’s gangrene is primarily clinical, and in most cases imaging is neither necessary nor desirable. Under no circumstances should surgery be delayed significantly for imaging of any kind. However, imaging modalities may be useful in cases when the presentation is atypical or when there is concern regarding the true extent of the disease.

Conventional radiography can be used to detect the presence of soft tissue air in the area overlying the scrotum and perineum before clinical crepitus is detected. In addition to demonstrating significant swelling of the scrotal soft tissue, radiographs may also detect subcutaneous emphysema extending from the scrotum and perineum to the inguinal regions, anterior abdominal wall and thighs. However, the absence of subcutaneous air, which is demonstrated in 10% of patients, does not exclude the diagnosis of Fournier’s gangrene ⁴⁰. A significant weakness of radiography in the diagnosis and evaluation of Fournier’s gangrene is the lack of detection of deep fascial gas ⁴¹.

Ultrasound (US) findings in Fournier’s gangrene include a thickened, edematous scrotal wall containing hyperechoic foci that demonstrate reverberation artifacts, causing ‘dirty’ shadowing which represents gas within the scrotal wall ⁴². In addition, US can demonstrate paratesticular fluid, which is seen prior to clinical crepitus. This imaging modality is also useful in differentiating Fournier’s gangrene from inguinoscrotal hernias. Overall, US is considered superior to conventional radiography as soft tissue air is more obvious and scrotal contents along with Doppler blood flow can be examined.

Computed tomography (CT) plays an important role in the diagnosis of Fournier’s gangrene as well as the evaluation of the extent of the disease to guide appropriate surgical treatment. CT findings include asymmetric fascial thickening, fluid collections, abscess formation, fat stranding around involved structures and subcutaneous emphysema ⁴²]. The underlying cause of Fournier’s gangrene, such as a perianal abscess, a fistulous tract, or an intraabdominal or retroperitoneal infectious process, may also be demonstrated by CT ⁴³. It can help to evaluate both the superficial and the deep fascia, and to differentiate Fournier’s gangrene from less aggressive entities such as soft-tissue edema or cellulitis, which may appear similar to Fournier’s gangrene on physical examination. As a whole, CT has greater specificity for evaluating disease extent than does radiography, US or even physical examination ⁴³.

Magnetic resonance imaging (MRI) offers an important diagnostic adjunct in the management of Fournier’s gangrene as it is more useful than conventional radiography and US for specifying range of infection. Some argue that MRI is even more helpful than CT in planning any operative intervention ⁴⁴.

Fournier’s gangrene treatment

The management of Fournier’s gangrene is underscored by three main principles: rapid and aggressive surgical debridement of necrotized tissue, hemodynamic support with urgent resuscitation with fluids, and broad-spectrum parental antibiotics ⁴⁵. As the rate of fascial necrosis has been noted as high as 2–3 cm per hour, Fournier’s gangrene is considered a surgical emergency with prompt, pragmatic and individualized therapy being the cornerstone for effective treatment ⁴⁵.

Radical surgical debridement

In addition to broad-spectrum parental antibiotics, early and aggressive surgical debridement has been shown to improve survival in patients presenting with Fournier’s gangrene as patients often undergo more than one debridement during their hospitalization ¹³. In a retrospective study of 219 patients presenting with a diagnosis of Fournier’s gangrene, Proud and colleagues ⁴⁶ found that there was no statistically significant difference in mortality between patients who underwent debridement before transfer or within 24 hour of presentation to those who had not. The authors attributed this seemingly counterintuitive observation to the range in severity of necrotizing soft tissue infections and to the notion that patients are less likely to succumb to localized infections. Regardless, the authors still advocate rapid and timely surgical debridement ⁴⁶.

Since the treatment of Fournier’s gangrene often requires highly acute and intensive multidisciplinary care, Sorensen and colleagues ¹³ examined the difference in case severity and management between teaching and nonteaching hospitals. Overall, the authors analyzed 1641 cases of Fournier’s gangrene at a total of 593 hospitals. It was found that more Fournier’s gangrene cases were treated per year at teaching hospitals where more surgical procedures, debridements and supportive care were reported. Interestingly, patients treated at teaching hospitals had longer length of stay, greater hospital charges and a higher case fatality rate secondary to more acutely ill patients. After adjusting for patient and hospital factors, it was found that patients treated at hospitals where more individuals with Fournier’s gangrene were treated had 42–84% lower mortality than hospitals where only one patient per year was treated. This finding is likely attributable to more aggressive diagnosis and management of Fournier’s gangrene at experienced hospitals. Overall, the data in the study revealed that hospitals where more patients with Fournier’s gangrene are treated had lower mortality rates, supporting the need to regionalize care for patients with this disease ¹³.

In a retrospective study of 19 patients diagnosed with Fournier’s gangrene, Chawla and colleagues ³⁷ studied the utilization of the Fournier’s gangreneSI to determine length of stay and survival. In this study, nonsurvivors had a higher Fournier’s gangreneSI compared with survivors but length of stay was not predicted by the Fournier’s gangreneSI. Moreover, it was found that mean number of surgical debridements in survivors was lower compared with that of nonsurvivors. Furthermore, length of stay was not affected by urinary or fecal diversion. Interestingly, it was observed that patient outcomes were similar regardless of management by general surgery or urology services ³⁷.

Broad-spectrum antibiotic coverage

Broad-spectrum parental antibiotic therapy is administered empirically upon diagnosis of Fournier’s gangrene and then subsequently tailored based on culture results. It is imperative that the antibiotic regimen chosen is effective against staphylococcal, streptococcal and gram-negative bacteria, coliforms, Pseudomonas, Bacteroides and Clostridium ³³. Triple antibiotic therapy consisting of a broad-spectrum penicillin or third-generation cephalosporins, an aminoglycoside (e.g. gentamicin) and metronidazole or clindamycin is typically instituted empirically ³³. Moreover, many have suggested adding penicillin for treatment of streptococci and, in particular, when Clostridia is suspected. Alternatively, clindamycin and chloramphenicol can be substituted empirically to facilitate coverage of gram-positive cocci and anaerobes until culture results return ⁴⁷. In patients infected with methicillin-resistant S. aureus, vancomycin should be utilized. Amphotericin B or caspofungin should be added to the empiric regimen should fungi be detected in tissue cultures ⁴⁸.

Topical therapy

After initial radical debridement, open wounds are generally managed with sterile dressings or negative-pressure wound therapy. In a retrospective review of 14 patients, Altunoluk and colleagues ⁴⁹ compared the efficacy of wound management with daily povidone iodine dressing versus Dakin’s solution (sodium hypochlorite). Dakin’s solution has wide antimicrobial efficacy against aerobic and anaerobic organisms. The authors found that the length of hospitalization was significantly shorter in patients managed with Dakin’s solution compared with iodine dressing (8.9 days versus 13 days) perhaps secondary to the antimicrobial effects of the former ⁴⁹. The use of topical honey has also been described in the management of Fournier’s gangrene because of its ability to inhibit microbial growth likely related to the osmotic effect of its high sugar content ⁵⁰. Efem described the use of honey in conjunction with oral amoxicillin/clavulanic acid and metronidazole in 20 patients presenting with Fournier’s gangrene. Despite longer hospitalization compared with those undergoing wound debridement with systemic antibiotics, treatment with topical honey obviated the need for anesthesia and expenses associated with surgical operations. Moreover, response to treatment was found to be expedited in those treated with topical honey ⁵¹. Tahmaz and colleagues found the efficacy of unprocessed honey to be similar in a retrospective review of 33 patients treated with topical honey versus radical surgical debridement ⁵⁰.

Vacuum-assisted closure therapy

Negative-pressure wound therapy or vacuum-assisted closure (VAC) therapy has been studied in the postoperative management of Fournier’s gangrene. Vacuum-assisted closure therapy works by exposing a wound to subatmospheric pressure for an extended period to promote debridement and healing (Figure 3) ³³. Negative-pressure wound therapy can be used in wound management utilizing the lower limit of pressure, which is recommended to be between 50 and 125 mmHg. The negative pressure in negative-pressure wound therapy leads to an increased blood supply and thus encourages migration of inflammatory cells into the wound region. Also, this promotes and accelerates the formation of granulation tissue by removing bacterial contamination, end products, exudates and debris compared with traditional dressing ⁵². Czymek and colleagues prospectively collected data on 35 patients diagnosed with Fournier’s gangrene to assess the effectiveness of vacuum-assisted closure therapy versus daily antiseptic (polyhexadine) dressings. Patients treated with VAC therapy had significantly longer hospitalization and lower mortality. However, significantly more patients required fecal diversion in the group receiving VAC therapy because of the need to reapply the vacuum dressing after each bowel movement. Fecal diversions may have be partially responsible for a higher mean number of surgical procedures in patients treated with vacuum-assisted closure therapy compared with those whose wounds were treated with conventional dressings that were more easily changed on the wards. Overall, the authors state that vacuum-assisted closure is not superior to conventional dressings in terms of length of hospital stay or clinical outcome. However, they are still clinically effective and successfully used in the management of large wounds ⁵³.

Figure 3. Vacuum-assisted closure therapy in Fournier’s gangrene

Hyperbaric oxygen therapy

A modality that has shown some promise as an adjunct to treatment of Fournier’s gangrene is hyperbaric oxygen therapy, which entails exposing the patient to increased ambient pressure while breathing 100% oxygen ³³. The physiological effects are believed to be enhanced leukocyte ability to kill aerobic bacteria, stimulation of collagen formation and increased levels of superoxide dismutase resulting in better tissue survival. Several case reports have demonstrated enhanced patient survival with the use of hyperbaric oxygen in the setting of necrotizing fasciitis when combined with surgical debridement ⁵⁴.

Fecal and urinary diversion

Colostomy has been used for fecal diversion in cases of severe perineal involvement. Indications for colostomy include anal sphincter involvement, fecal incontinence and continued fecal contamination of the wound’s margins. Although colostomy can be beneficial with regard to wound healing by avoiding fecal contamination, it should be performed only in selected cases because it increases morbidity. The estimated percentage of patients requiring colostomy after debridement of Fournier’s gangrene is approximately 15%, and an increased mortality has been noted in patients requiring diversion ³³. In their study of 44 patients presenting with Fournier’s gangrene, Ozturk and colleagues ⁵⁵ found that in 18 patients that required temporary stoma formation, significant increases in healthcare costs were observed without an effect on outcomes. Overall, stoma creation and closure increased costs by approximately $6650. Therefore, it is recommended that stoma formation be reserved for patients with fecal incontinence caused by extensive damage to the anal sphincter ⁵⁵. Nevertheless, the potential need for colostomy underscores the importance of a multidisciplinary approach to the management of the patient presenting with Fournier’s gangrene ⁵⁶. In a series of 28 consecutive patients with Fournier’s gangrene, Corman and colleagues found that general surgical service was involved in 52% of the initial operations to perform perianal and sometimes perirectal debridement ⁵⁷. Alternatively, the Flexi-Seal Fecal Management System has been introduced for fecal diversion, which can be utilized as an alternative method to colostomy as it successfully prevents fecal contamination of the wound ⁵². In regards to urinary diversion, some authors suggest cystostomy, although most suggest that urinary catheterization provides satisfactory diversion ⁵⁸. In a review of 26 cases of Fournier’s gangrene treated at a university medical center, Hollabaugh and colleagues ⁵⁹ utilized suprapubic diversion in 16 cases with 15 of those patients receiving diversion at the time of initial debridement. Indications for suprapubic urinary diversion included patients with extensive penile and perineal debridement, or periurethral abscesses ⁵⁹. In 74 patients presenting with Fournier’s gangrene at an Egyptian medical center, adequate urinary diversion was accomplished with the use of a urethral Foley catheter in all but one patient who had experienced a urethral injury. In this series, suprapubic cystostomy was recommended in patients experiencing urethral disruption or stricture ⁶⁰.

Reconstructive surgery

After extensive debridement, many patients sustain significant defects of the skin and soft tissue, creating a need for reconstructive surgery for wound coverage as well as satisfactory functional and cosmetic results. Various workers have used different techniques to provide skin cover including transplantation of testes, free skin grafts, axial groin flaps, and myocutaneous flaps. Split thickness skin graft seems to be the treatment of choice in treating perineal and scrotal skin defects. Parkash and Gajendran ⁶¹ reported their series of treatment of 43 cases in the past 11 years. In three cases the gangrene had spread beyond the scrotum and penis and cover had to be supplemented with split-skin grafts. In all the other cases, cover was provided with scrotal skin remnants at the edge of the lesion and on the penis with the inner layer of the prepuce, which had remained intact.

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