: Medicine Red man syndrome (RMS) is the most common allergic reaction to vancomycin. It generally occurs during rapid infusion of vancomycin; only few cases have been reported as results of local vancomycin administration.
Red man syndrome (RMS) is a common allergic reaction to vancomycin that typically presents with a rash on the face, neck, and upper torso after intravenous administration of vancomycin. [2,3] Less frequently, RMS may be accompanied by hypotension and angioedema.
Red man syndrome (RMS) is the most common allergic reaction to vancomycin. It generally occurs during rapid infusion of vancomycin; only few cases have been reported as results of local vancomycin administration.
It generally occurs during rapid infusion of vancomycin; only few cases have been reported as results of local vancomycin administration. We hereby report a rare case where RMS developed after insertion of vancomycin-loaded bone cement in a primary total knee replacement (TKR).
WA Coding Rule 0312/05 Red Man Syndrome is retired. In ICD-10-AM/ACHI/ACS Eleventh Edition (effective 1 July 2019) ACS 0005 Syndromes was amended and new code U91 Syndrome, NEC created. See also Guide to Major Eleventh Edition Changes: Australian Coding Standards and ICD-10-AM, available on the WACCA website.
Z16. 21 is a billable/specific ICD-10-CM code that can be used to indicate a diagnosis for reimbursement purposes. The 2022 edition of ICD-10-CM Z16.
ICD-9 Code 782.1 -Rash and other nonspecific skin eruption- Codify by AAPC.
T78.3T78. 3 - Angioneurotic edema | ICD-10-CM.
VRSA is a type of antibiotic resistant Staph. While most Staph bacteria can be treated with an antibiotic known as vancomycin, some have developed a resistance and can no longer be treated with vancomycin. Other antibiotics can be used to treat VRSA.
Antibiotic resistance occurs when the germs no longer respond to the antibiotics designed to kill them. If these germs develop resistance to vancomycin, an antibiotic that is used to treat some drug-resistant infections, they become vancomycin-resistant enterococci (VRE).
9.
Under both ICD-9-CM and ICD-10-CM nomenclatures, a decimal is placed after the first three characters. All ICD-10-CM codes require longer descriptions due to more extensive specificity. ICD-9-CM contains approximately 14,000 diagnostic codes, compared to 68,000 diagnostic codes under ICD-10-CM.
ICD-10 code L71. 9 for Rosacea, unspecified is a medical classification as listed by WHO under the range - Diseases of the skin and subcutaneous tissue .
In the early medical literature, it was initially named as ephemeral cutaneous nodosities, ephemeral congestive tumors of the skin, wandering edema, and giant hives. [1] After the year 2007, angioneurotic edema (ANE) was named as angioedema (AE) in the literature.
Angioedema is the rapid edema, or swelling, of the area beneath the skin or mucosa. It is normally an allergic reaction, but it can also be hereditary. The swelling happens because fluid accumulates. It tends to affect areas with loose areas of tissue, especially the face and throat, as well as the limbs and genitals.
Angioedema is swelling underneath the skin. It's usually a reaction to a trigger, such as a medicine or something you're allergic to. It is not normally serious, but it can be a recurring problem for some people and can very occasionally be life-threatening if it affects breathing.
Red man syndrome (RMS) is the most common allergic reaction to vancomycin. It generally occurs during rapid infusion of vancomycin; only few cases have been reported as results of local vancomycin administration. We hereby report a rare case where RMS developed after insertion of vancomycin-loaded bone cement in a primary total knee replacement (TKR).
Vancomycin is a bactericidal antibiotic with activity against most gram-positive cocci, including methicillin-resistant Staphylococcus aureus. [1] Red man syndrome (RMS) is a common allergic reaction to vancomycin that typically presents with a rash on the face, neck, and upper torso after intravenous administration of vancomycin. [2,3] Less frequently, RMS may be accompanied by hypotension and angioedema. Although RMS is known to be a rapidly infusion-related reaction, it may also occur when infused in a slow rate. [4,5] Only few cases of RMS were reported to be associated with local uses of vancomycin. [6,7] Prophylactic use of antibiotic-loaded bone cement for the primary total knee replacement (TKR) is a common adjunctive treatment to prevent osteomyelitis in clinical setting. [8–10] We hereby reported a rare case where RMS developed after the use of vancomycin-loaded bone cement in a patient receiving a primary TKR. The patient has provided informed consent for publication of the case.
The other vancomycin hypersensitivity is an anaphylactic reaction. Anaphylaxis is an immunologically mediated reaction involving drug-specific immunoglobulin E (IgE) antibodies and is independent of the infusion rate. Anaphylaxis in response to vancomycin administration is believed to be rare, although reactions involving angioedema, respiratory distress, and bronchospasm with evident drug-specific IgE have been described. [14] In cases of anaphylaxis, antihistamines are not thought to be useful. [15] Anaphylaxis can be severe, generalized allergic, or hypersensitivity reaction that is life-threatening; administration of epinephrine should be considered as rapidly as possible once anaphylaxis is recognized. [16] Moreover, a prior exposure to vancomycin is usually prerequisite for developing vancomycin-induced anaphylactic reaction. On the contrary, RMS is an anaphylactoid reaction that can occur during the first administration of vancomycin. Judging from the clinical manifestations as well as the absence of previous vancomycin exposure, anaphylaxis was not likely to be the cause in this case report.
Vancomycin-loaded bone cement is widely used in joint surgery for preventing or treating osteomyelitis. Although the development of RMS is mostly associated with intravenous administration of vancomycin, there are a few case reports of systemic toxicity and allergy reaction when vancomycin was loaded in bone cement for treating orthopedic-related infections. This case report further highlights the potential risk of RMS induced by the routine use of vancomycin-loaded bone cement in the primary TKR. Early detection and proper management of this potential risk in daily practice can thus prevent the unwanted outcomes.
[7] The use of vancomycin-loaded bone cement is considered to be safe in both animal and clinical studies. [8] The peak vancomycin concentrations in blood were achieved 6 to 24 h after implantation and were extremely low. In contrast, the concentrations of vancomycin in bone remain high throughout the first 6 months, which is an important characteristic for both curative and prophylactic treatment. There are very few case reports of adverse effects after the use of vancomycin-loaded bone cement. Goh et al [7] reported a 42-year-old army officer who developed RMS after vancomycin bead's insertion for chronic osteomyelitis. The symptoms persisted until the removal of vancomycin beads. Furthermore, Williams et al [19] reported a 59-year-old man with a history of Stevens–Johnson reaction to systemic vancomycin developed a painful, blistering rash after implantation of vancomycin-loaded bone cement for treating recurrent methicillin-susceptible S. aureus prosthetic knee infection. In our case, we speculated the cause of RMS might be attributed to the release of certain amount of vancomycin into local circulation during but not after implantation and polymerization process of the bone cement. The subsequent release of tourniquet might cause transient increases of systemic vancomycin and histamine levels that led to the development of RMS. The good response to our initial treatment also supported our speculations and the removal of the vancomycin-loaded bone cement was thus avoided. Moreover, those previous cases were reported in patients with chronic osteomyelitis. To our knowledge, RMS has not been reported to occur after the routine use of vancomycin-loaded bone cement in the primary TKR in available literature.
Red man syndrome (RMS) is the most common allergic reaction to vancomycin. It generally occurs during rapid infusion of vancomycin; only few cases have been reported as results of local vancomycin administration. We hereby report a rare case where RMS developed after insertion of vancomycin-loaded bone cement in a primary total knee replacement (TKR).
Vancomycin is a bactericidal antibiotic with activity against most gram-positive cocci, including methicillin-resistant Staphylococcus aureus. [1] Red man syndrome (RMS) is a common allergic reaction to vancomycin that typically presents with a rash on the face, neck, and upper torso after intravenous administration of vancomycin. [2,3] Less frequently, RMS may be accompanied by hypotension and angioedema. Although RMS is known to be a rapidly infusion-related reaction, it may also occur when infused in a slow rate. [4,5] Only few cases of RMS were reported to be associated with local uses of vancomycin. [6,7] Prophylactic use of antibiotic-loaded bone cement for the primary total knee replacement (TKR) is a common adjunctive treatment to prevent osteomyelitis in clinical setting. [8–10] We hereby reported a rare case where RMS developed after the use of vancomycin-loaded bone cement in a patient receiving a primary TKR. The patient has provided informed consent for publication of the case.
The other vancomycin hypersensitivity is an anaphylactic reaction. Anaphylaxis is an immunologically mediated reaction involving drug-specific immunoglobulin E (IgE) antibodies and is independent of the infusion rate. Anaphylaxis in response to vancomycin administration is believed to be rare, although reactions involving angioedema, respiratory distress, and bronchospasm with evident drug-specific IgE have been described. [14] In cases of anaphylaxis, antihistamines are not thought to be useful. [15] Anaphylaxis can be severe, generalized allergic, or hypersensitivity reaction that is life-threatening; administration of epinephrine should be considered as rapidly as possible once anaphylaxis is recognized. [16] Moreover, a prior exposure to vancomycin is usually prerequisite for developing vancomycin-induced anaphylactic reaction. On the contrary, RMS is an anaphylactoid reaction that can occur during the first administration of vancomycin. Judging from the clinical manifestations as well as the absence of previous vancomycin exposure, anaphylaxis was not likely to be the cause in this case report.
Vancomycin-loaded bone cement is widely used in joint surgery for preventing or treating osteomyelitis. Although the development of RMS is mostly associated with intravenous administration of vancomycin, there are a few case reports of systemic toxicity and allergy reaction when vancomycin was loaded in bone cement for treating orthopedic-related infections. This case report further highlights the potential risk of RMS induced by the routine use of vancomycin-loaded bone cement in the primary TKR. Early detection and proper management of this potential risk in daily practice can thus prevent the unwanted outcomes.
[7] The use of vancomycin-loaded bone cement is considered to be safe in both animal and clinical studies. [8] The peak vancomycin concentrations in blood were achieved 6 to 24 h after implantation and were extremely low. In contrast, the concentrations of vancomycin in bone remain high throughout the first 6 months, which is an important characteristic for both curative and prophylactic treatment. There are very few case reports of adverse effects after the use of vancomycin-loaded bone cement. Goh et al [7] reported a 42-year-old army officer who developed RMS after vancomycin bead's insertion for chronic osteomyelitis. The symptoms persisted until the removal of vancomycin beads. Furthermore, Williams et al [19] reported a 59-year-old man with a history of Stevens–Johnson reaction to systemic vancomycin developed a painful, blistering rash after implantation of vancomycin-loaded bone cement for treating recurrent methicillin-susceptible S. aureus prosthetic knee infection. In our case, we speculated the cause of RMS might be attributed to the release of certain amount of vancomycin into local circulation during but not after implantation and polymerization process of the bone cement. The subsequent release of tourniquet might cause transient increases of systemic vancomycin and histamine levels that led to the development of RMS. The good response to our initial treatment also supported our speculations and the removal of the vancomycin-loaded bone cement was thus avoided. Moreover, those previous cases were reported in patients with chronic osteomyelitis. To our knowledge, RMS has not been reported to occur after the routine use of vancomycin-loaded bone cement in the primary TKR in available literature.