Vancomycin

As with all fires, evacuate personnel to a safe area. Firefighters should use self-contained breathing equipment and protective clothing. /Vancomycin hydrochloride/

Water spray, dry chemical, carbon dioxide or foam as appropriate for surrounding fire and materials. /Vancomycin hydrochloride/

Store in a tight, light-resistant container as defined in the USP-NF. This material should be handled and stored per label instructions to ensure product integrity. Store in a freezer. /Vancomycin hydrochloride/

Commercially available vancomycin hydrochloride capsules and powder for IV administration should be stored at 15 - 30 °C.

Wear approved respiratory protection, chemically compatible gloves and protective clothing. Wipe spillage or collect spillage using a high efficiency vacuum cleaner. Avoid breathing dust. Place spillage in appropriately-labeled container for disposal. Wash spill site. /Vancomycin hydrochloride/

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.

Engineering controls such as exhaust ventilation are recommended. /Vancomycin hydrochloride/

As a general rule, when handling USP Reference Standards avoid all contact and inhalation of dust, mists, and/or vapors associated with the material. Wash thoroughly after handling. /Vancomycin hydrochloride/

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Gloves: Chemically compatible. Eye protection: Safety goggles or glasses. Protective clothing: Protect exposed skin. /Vancomycin hydrochloride/

Use a NIOSH approved respirator, if it is determined to be necessary by an industrial hygiene survey involving air monitoring. In the event that a respirator is not required, an approved dust mask should be used. /Vancomycin hydrochloride/

Concomitant use of vancomycin and anesthetic agents has been associated with anaphylactoid reactions and an increased frequency of infusion reactions (e.g., hypotension, flushing, erythema, urticaria, pruritus). Erythema and histamine-like flushing has occurred in pediatric patients receiving vancomycin and anesthetic agents concomitantly. The risk of infusion-related adverse effects may be minimized if vancomycin is given as a 1-hour IV infusion prior to induction of anesthesia.

In vitro, the antibacterial effects of vancomycin and aminoglycosides are synergistic against many strains of Staphylococcus aureus, nonenterococcal group D streptococci (Streptococcus bovis), enterococci (Enterococcus faecalis), and viridans streptococci. However, concomitant use of vancomycin and aminoglycosides is associated with an increased risk of ototoxicity and/or nephrotoxicity.

Because of the possibility of additive toxicities, the concurrent or sequential systemic or topical use of other ototoxic and/or nephrotoxic drugs (e.g., aminoglycosides, amphotericin B, bacitracin, cisplatin, colistin, polymyxin B) and vancomycin requires careful serial monitoring of renal and auditory function. These drugs should be used with caution in patients receiving vancomycin therapy.

Renal failure developed after a prolonged course of vancomycin therapy in 2 patients who were receiving tenofovir disoproxil fumarate as part of an antiretroviral regimen. Tenofovir has been implicated in the development of Fanconi syndrome and renal insufficiency because of its effects on the proximal renal tubule. Vancomycin nephrotoxicity is infrequent but may result from coadministration with a nephrotoxic agent. Clinicians should be aware that tenofovir may raise the risk of renal failure during prolonged administration of vancomycin.

For more Interactions (Complete) data for Vancomycin (6 total), please visit the HSDB record page.

Renal failure, principally manifested by increased serum creatinine or BUN concentrations, especially in patients administered large doses of vancomycin, has been reported rarely. A few dozen cases of hearing loss associated with vancomycin have been reported. Reversible neutropenia, usually starting 1 week or more after onset of therapy with vancomycin or after a total dosage of more than 25 g, has been reported for several dozen patients.

Intravenous vancomycin is associated with minor, transient and asymptomatic elevations in serum aminotransferase levels in 1% to 5% of patients, but similar or minimally lower rates of abnormalities are usually reported with comparative agents. In rare instances, the serum enzyme elevations are more marked and may be associated with mild symptoms, although usually without jaundice. In recent years, vancomycin has been linked to hypersensitivity reactions, including Stevens-Johnson syndrome, toxic epidermal necrolysis and, most commonly, the distinctive syndrome of drug reaction with eosinophilia and systemic symptoms (DRESS). These forms of hypersensitivity generally occur only after 2 to 4 weeks of prolonged continuous intravenous (iv) vancomycin therapy. Fever and severe skin rash generally dominate the clinical presentation, but systemic symptoms can include renal, respiratory or heart failure, adenopathy, neutropenia, thrombocytopenia, facial edema, and liver injury. Cases of DRESS syndrome associated with vancomycin are often accompanied by serum enzyme elevations (Case 1), but marked elevations, symptoms of liver injury, and jaundice are uncommon. The usual systemic features of vancomycin induced DRESS syndrome are renal rather than liver injury but features of hypersensitivity may be more prominent than organ-specific injury. Nevertheless, in rare instances the liver injury can be severe (Case 2) and result in hepatic failure and death. Patients who receive intravenous vancomycin often have multiple comorbidities including sepsis and receive multiple antibiotics which make the attribution of the hypersensitivity reactions and liver injury with vancomycin difficult. Other more well-known causes of DRESS syndrome include allopurinol, sulfonamides, and the aromatic anticonvulsants. These other causes of DRESS syndrome are more likely to be associated with clinically apparent and even fatal liver injury. DRESS syndrome associated with vancomycin is almost invaria；Vancomycin is also associated with several forms of acute infusion reactions, most notably anaphylaxis and the vancomycin flushing reaction, previously known as “red man syndrome”. Vancomycin flushing reactions occur typically during the first 15 to 20 minutes of an initial infusion of vancomycin, most commonly when given rapidly and in relative high doses (1000 mg given over less than 60 minutes). The reaction is characterized by flushing, erythema, and itching usually of the face, neck and upper torso, sometimes accompanied by chest and back pain and variable degrees of hypotension. Rarely, flushing reactions have been associated with oral vancomycin therapy, particularly in elderly patients with active colitis and renal dysfunction. The cause of the symptoms is probably the acute degranulation of mast cells by the direct effect of vancomycin or S. Aureus toxins. The mediator of the reaction is histamine and other active amines or components in mast cell granules. Plasma histamine levels are usually elevated in persons with vancomycin flushing reactions, but the correlation of changes in plasma histamine levels and severity of symptoms is poor. Nevertheless, the symptoms of the vancomycin flushing reaction can be prevented or ameliorated by pretreatment with antihistamines. Perhaps a better approach is the use of slower infusion rates and lower doses of vancomycin. Liver injury is not a feature of vancomycin flushing reactions but can arise secondarily in cases with prolonged or severe hypotension.；Likelihood score: A (well established cause of clinically apparent liver injury usually in association with prolonged intravenous therapy and presenting with DRESS syndrome).

Asthma - Reversible bronchoconstriction (narrowing of bronchioles) initiated by the inhalation of irritating or allergenic agents.

Intravenous；Common adverse effects of intravenous vancomycin injection include nephrotoxicity, hypotension, and hypersensitivity reactions (eg, anaphylaxis). According to the Infectious Diseases Society of America, the American Society of Health-System Pharmacists, and the Pediatric Infectious Diseases Society, the risk of potential toxicity, including acute kidney injury, is highest if the trough concentration exceeds 15 mg/L and the AUC exceeds 650 mg·h/L.；Vancomycin infusion reaction, previously known as vancomycin flushing syndrome or red man syndrome, is associated with rapid intravenous infusion of vancomycin. Symptoms include flushing, pruritus, and an erythematous rash on the face, neck, and upper torso. Signs of this infusion reaction often appear 4 to 10 minutes after starting or shortly after completing an infusion. The incidence of this reaction varies between 3.7% and 47%. However, there is a direct correlation between the increased incidence of vancomycin infusion reaction and faster vancomycin administration rates. Rapid infusion of vancomycin can also result in accompanying angioedema and hypotension. Therefore, prolonging the infusion time is the primary mitigation strategy. Premedication with antihistamines, such as diphenhydramine or hydroxyzine, can also aid in preventing the occurrence of vancomycin infusion reaction. The most severe forms of this reaction frequently occur in children and patients younger than 40.；Less common adverse effects include local phlebitis, chills, drug fever, skin rash, eosinophilia, and reversible neutropenia. Rarely, DRESS syndrome, ototoxicity, thrombocytopenia, vasculitis, and Stevens-Johnson syndrome have been reported.；Oral；Gastrointestinal adverse effects, such as abdominal pain and nausea, are commonly observed in patients receiving oral vancomycin. Dysgeusia, or a distorted sense of taste, is another common adverse reaction unique to oral vancomycin administration. Patients should seek medical attention if these adverse effects become bothersome. Many of these adverse effects are temporary.；Less common adverse effects of oral vancomycin include peripheral edema, fatigue, headache, diarrhea, flatulence, vomiting, back pain, urinary tract infection, and fever. Reports exist of rare cases of increased serum creatinine, vancomyosin flushing syndrome, interstitial nephritis, nephrotoxicity, ototoxicity, thrombocytopenia, and vasculitis using oral vancomycin.；Drug-Drug Interactions；The coadministration of other medications, along with vancomycin, may increase the risk of adverse effects and toxicity. Therefore, dosing adjustments, additional monitoring, and consideration of alternative treatment should merit attention when combining vancomycin with certain medications. Caution is necessary when administering vancomycin with other nephrotoxic agents such as aminoglycosides, amphotericin products, and intravenous contrast. Diluted vancomycin hydrochloride should be administered before any intravenous anesthetic agents to reduce the risk of infusion-related adverse reactions.

Vancomycin therapy is correlated with nephrotoxicity and ototoxicity. Although there are numerous case reports of acute renal failure attributed to vancomycin use, there is currently limited data suggesting a direct causal relationship. The proposed nephrotoxicity mechanism involves vancomycin's oxidative effect on proximal renal tubule cells, causing tubular ischemia. Common risk factors for nephrotoxicity include preexisting kidney disease, concurrent administration of nephrotoxic medications, advanced age, and dehydration. Although vancomycin-induced nephrotoxicity is commonly reversible, it can be challenging to differentiate this condition from acute tubulointerstitial nephritis and worsening renal function due to uncontrolled infection. In the absence of a causative explanation, vancomycin-induced nephrotoxicity may be identified by elevated serum creatinine levels. Adjusting vancomycin dosages based on the patient's estimated creatinine clearance is a common method to prevent nephrotoxicity. Patients who exhibit signs of acute renal failure precipitated by vancomycin therapy should promptly discontinue treatment. Nephrotoxicity has been reported in patients receiving oral and intravenous vancomycin. Cases of nephrotoxicity associated with oral vancomycin have typically been encountered in patients older than 65.；Ototoxicity is a rare complication of vancomycin monotherapy and is common in patients receiving excessive vancomycin doses, concurrent ototoxic medications (eg, aminoglycosides, loop diuretics, antineoplastic agents), and those with underlying hearing loss conditions. Treatment should stop if patients experience signs of cytotoxicity, such as tinnitus, loss of hearing, and unbalanced movements. Vancomycin-induced ototoxicity may be irreversible for some patients. Serial auditory function testing may be beneficial in identifying early symptoms.

The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.

Inflammation at the injection site has been reported. During or soon after rapid infusion of vancomycin, patients may develop anaphylactoid reactions, including hypotension, wheezing, dyspnea, urticaria, or pruritus. Rapid infusion may also cause flushing of the upper body ("red neck") or pain and muscle spasm of the chest and back. These reactions usually resolve within 20 minutes but may persist for several hours. Such events are infrequent if vancomycin is given by a slow infusion over 60 minutes. In studies of normal volunteers, infusion-related events did not occur when vancomycin was administered at a rate of 10 mg/min or less.

Antibiotic-associated pseudomembranous colitis, caused by toxin-producing clostridia (e.g., C. difficile), has been reported with the use of nearly all anti-infectives, including IV vancomycin, and should be considered in the differential diagnosis of patients who present with diarrhea subsequent to administration of anti-infectives. Pseudomembranous colitis may occur during or following discontinuance of anti-infective therapy and ranges in severity from mild to life-threatening. Mild cases of colitis may respond to discontinuance of the drug alone, but diagnosis and management of moderate to severe cases should include appropriate bacteriologic studies and treatment with fluid, electrolyte, and protein supplementation as indicated. If colitis is moderate to severe and is not relieved by discontinuance of the drug, appropriate anti-infective therapy (e.g., metronidazole) should be administered. Nausea also has been reported in patients receiving vancomycin therapy.

Urticaria, exfoliative dermatitis, macular rashes, eosinophilia, vasculitis, a shock-like state, transient anaphylaxis, and, occasionally, vascular collapse have been reported in patients receiving vancomycin. The drug also has been associated with Stevens-Johnson syndrome in at least one patient.

/CASE REPORTS/ A 60-year-old man with a history of hypertension, congestive heart failure and dyslipidemia was admitted for a right shoulder rotator cuff tear. He underwent right-shoulder arthroscopy and rotator cuff repair. About three weeks later, he developed pain, swelling and purulent drainage from his right shoulder. Arthroscopic irrigation and drainage was then performed. Intraoperative fluid revealed the presence of Methicillin susceptible Staphylococcus aureus, vancomycin-sensitive Enterococcus spp. and Serratia marcescens. The patient had no known allergies. After reviewing his antimicrobial susceptibility, he was started on vancomycin 1500 mg intravenously every 12 hours (to treat both Staphylococcus aureus and Enterococcus spp) and ciprofloxacin 750 mgs by oral induction every 12 hours. The patient's condition improved following antibiotic treatment. He was discharged and allowed to go home on IV vancomycin and oral ciprofloxacin. The patient's platelet count on the day of starting vancomycin therapy was 253 x 10(3)/cu mm. At weeks one, two and three, the counts were 231 x 10(3)/cu mm, 272 x 10(3)/mm and 6 x 103/cu mm, respectively. The patient was admitted for further work-up of the thrombocytopenia. He was later shown to have vancomycin-induced platelet-reactive antibodies, causing significant thrombocytopenia, and then reversal after his vancomycin medication was discontinued. Thrombocytopenia is a potentially life-threatening condition. Vancomycin is often clinically overlooked as a cause of thrombocytopenia, especially in a scenario of sepsis or when there is use of heparin. Simple laboratory testing with drug-dependent antibodies can be helpful in identifying vancomycin as a cause of thrombocytopenia.

ANAEROBIC: Vancomycin hydrochloride, at concentrations of 6-100 mg/L, was shown to be inhibitory to anaerobic digester sludge incoculum with 1 g/L total dry solids (from a municipal sewage treatment plant in Germany) and a degradable substrate (yeast extract), incubated for 7 days in sealed bottles(1). Vancomycin biodegradation was shown to be enhanced during ozonation of wastewater at 20 °C, pH 7.7 with 41, 68, 89, an 100% vancomycin transformation observed at applied ozone doses of 0.5, 1, 1,5, and 3 mg/L(1).

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, including vancomycin hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Vancomycin hydrochloride/

Antibiotic; [ChemIDplus]

Medicine (antibiotic) /Vancomycin hydrochloride/

THERAPEUTIC CATEGORY: Antibacterial

MEDICATION

Use (kg) in Switzerland (2009): >100；Use (kg; approx.) in Germany (2009): >1000；Use (kg; exact) in Germany (2009): 2351；Use (kg) in USA (2002): 6080；Use (kg) in France (2004): 918；Consumption (g per capita) in Switzerland (2009): 0.013；Consumption (g per capita; approx.) in Germany (2009): 0.012；Consumption (g per capita; exact) in Germany (2009): 0.029；Consumption (g per capita) in the USA (2002): 0.022；Consumption (g per capita) in France (2004): 0.015；Excretion rate: 0.75；Calculated removal (%): 1.9

Vancomycin is indicated for the treatment of serious or severe infections caused by susceptible strains of methicillin-resistant (beta-lactam-resistant) staphylococci.

... Found in the culture broth of Streptomyces orientalis.

Vancomycin is produced by the submerged fermentation process.

Table: Vancomycin Hydrochloride Preparations [Table#4520]

Grade: USP /Vancomycin hydrochloride/

Parenteral, Injection (frozen), for IV infusion 5 mg (of vancomycin) per mL (500 mg) in 5% Dextrose, Vancocin HCl in Iso-osmotic Dextrose Injection (Lilly)

Potency: equivalent to not less than 900 ug of vancomycin per mg. /Vancomycin hydrochloride/

The content of a 10-g container ... is mixed with 115 mL of distilled water, so that each 6-mL portion provides approx 500 mg of the drug. /Hydrochloride/