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Appropriateness of Cloxacillin for Cellulitis Patient

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Appropriateness of Cloxacillin for Cellulitis Patient

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Cloxacillin (IV) is a narrow-spectrum beta-lactam antibiotic effective against MSSA (methicillin-susceptible Staphylococcus aureus) and some streptococci. It's an appropriate choice in moderate to severe non-purulent cellulitis, especially when hospitalization and parenteral therapy are indicated. The CDC guidance lists IV penicillin, cefazolin, clindamycin, or dicloxacillin among suitable options for non-purulent cellulitis requiring intravenous treatment

Types of Cellulitis suitability for usage of Cloxacillin:

- Mild cellulitis (no systemic signs):

Cloxacillin 500 mg PO every 6 h, OR cephalexin 1,000 mg PO every 12 h, OR amoxicillin 500 mg PO every 8 h

- Moderate cellulitis (presence of SIRS but no hypotension):

Cloxacillin 1–2 g IV every 6 h

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refers to the dynamics of blood flow and pressure within the cardiovascular system, influencing how effectively blood, oxygen, and nutrients reach organs and tissues.

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Pathophysiology

1. Biotechfront: Type 1 Hypersensitivity - Pathogenesis and Clinical Menifestations

2. Type I Hypersensitivity Reaction - StatPearls - NCBI Bookshelf

3. B Cell Activation and Plasma Cell Differentiation | Immunopaedia

4. B Cells, Memory B Cells and Plasma Cells: B Cell Activation, Development and the B Cell Receptor | Technology Networks

5. Memory Cells vs. Plasma Cells - What's the Difference? | This vs. That

Type of hypersensitivity

1. Penicillin allergy: A practical guide for clinicians

2. Drug allergy - PMC

3. Mechanisms of Drug-Induced Allergy - PMC

4. Penicillin Allergy: Mechanisms, Diagnosis, and Management - ScienceDirect

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Type 1 Hypersensitivity - Pathogenesis and Clinical Menifestations

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Type I hypersensitivity is also termed as allergy and immediate hypersensitivity since symptoms manifest rapidly within minutes to hours

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1. Eradicate the Infection

The foremost objective is to eliminate the causative pathogens, typically Staphylococcus aureus and Streptococcus pyogenes.

Empirical antibiotic therapy is recommended based on severity (e.g., oral or IV cloxacillin), with adjustments (de-escalation) once culture results are available.

2. Prevent Progression to Severe Disease

Prompt administration of the appropriate route—oral antibiotics for mild cases, intravenous therapy for moderate disease, and broad-spectrum coverage for severe presentations—is emphasized to avoid complications such as necrotizing fasciitis or systemic involvement.

3. Resolve Clinical Signs and Symptoms

Treatment aims to resolve erythema, edema, pain, and systemic signs (e.g., fever, tachycardia)—typically within 5–10 days, extending until at least 3 days after acute inflammation subsides.

4. Enable Safe Switch from IV to Oral Therapy

For hospitalized moderate cases, once clinical improvement is noted, the guideline supports an IV-to-oral (IV-to-PO) switch to promote earlier discharge and reduce healthcare burden.

5. Support Antimicrobial Stewardship

The guideline underscores the use of narrow-spectrum, Access-group antibiotics whenever possible (e.g., cloxacillin) to minimize antimicrobial resistance.

De-escalation based on microbiology results is strongly encouraged.

6. Guide Empirical Therapy and Promote Clinical Judgment

Recommendations provide empirical choices based on severity but explicitly position them as guidance—able to be refined based on individual patient response and laboratory findings

Source: National Antimicrobial Guideline (NAG), Ministry of Health Malaysia - NAG : WHO IS IT MEANT FOR?

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National Antimicrobial Guideline (NAG), Ministry of Health Malaysia - NAG : WHO IS IT MEANT FOR?

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HU is suffering from immediate-hypersensitivity (type 1) because of the symptoms urticaria, and difficulty, and it occurs in 40 minutes. These are the primary symptoms from IgE-mediated drug allergies.

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Moderate treatment: Cloxacillin 1-2g IV q6H

Moderate -> Fever ( 39 C ) , Abnormal WBC ( 14.2 X 10^9 )

Systemic signs of infection -> Fever, chills, shortness of breath

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1. Efficacy

Reduction in redness, swelling, warmth, and tenderness

Decrease in pain score

Reduction in lesion size

Normalization of vital signs (fever, HR)

Decrease in inflammatory markers (WBC, CRP)

2. Safety

Monitor allergic reactions

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means a patient has stable blood pressure and heart rate, allowing for good, consistent blood flow to their organs. It indicates the circulatory system is functioning well enough to support life without immediate, life-threatening complications. This state is maintained by normal levels of blood pressure, heart rate, and other vital signs like oxygen saturation.

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Type I hypersensitivity requires initial sensitization in an individual who is genetically predisposed. Sensitization begins with exposure to an allergen, commonly through inhalation, ingestion, or skin contact. Antigen-presenting cells (such as dendritic cells, macrophages, or B cells) process the allergen and migrate to regional lymph nodes, where they present the antigen to naïve T cells. In individuals predisposed to allergic responses, these T cells preferentially differentiate into Th2 (T-helper 2) cells. The Th2 subset secretes cytokines, including interleukin (IL)-4, IL-5, IL-9, and IL-13, which are central to the allergic response.

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Simultaneously, B cells internalize the allergen and process it through the major histocompatibility complex class II (MHC II) pathway. B cells present the antigen-MHC II complex to Th2 cells, which recognize the complex through their T-cells receptor. CD40 on the B cells also binds with CD40L on the Th2 cell surface, stimulating the release of IL-4 and IL-13 by the Th2 cell. Costimulatory interaction between CD40 on the B cell and CD40L on the Th2 cell is essential for B-cell activation and isotype switching from IgM to IgE. IL-4 and IL-13 further drive this class switching (B cells to plasma cell). The resulting allergen specific IgE binds to high-affinity FcεRI receptors on the surface of mast cells and basophils. Upon reexposure, the antigen can cross-link the previously bound IgE on mast cells and basophils, triggering the release of a range of preformed and newly synthesized inflammatory mediators.

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Figure 1: The cellular stages of late B cell differentiation. The majority of mature B cells are located in the follicles of lymphoid organs and are known as follicular B cells. Others specialized B cell subsets include marginal zone B cells, which localize to the region between the red and white pulp in the spleen, and B1 cells, which are found in the peritoneal and pleural cavities. All mature B cell subsets express the transcription factors paired box protein 5 (PAX5). PU.1 interferon-regulatory factor 8 (IRF8) and BTB and CNC homologue 2 (BACH2), whereas low levels of IRF4 are induced by antigen receptor signalling. B cells activated by antigen (also termed B lymphoblasts) are capable of rapid proliferation, immunoglobulin class-switch recombination, and differentiation into short-lived plasmablasts that express high levels of IRF4 and X-box-binding protein 1 (XBP1), and intermediate (mid) levels of B lymphocyte-induced maturation protein 1 (BLIMP1) and secreted antibody. Follicular B cells can also upregulate B cell lymphoma 6 (BCL-6) and repress IRF4 expression during the germinal centre (GC) reaction where affinity maturation of the antigen receptor occurs. B cells with high-affinity antigen receptors exit the GC and differentiate into either memory B cells, which express a similar transcriptional signature to mature B cells, or long-lived plasma cells, which express high levels of BLIMP1, IRF4 and XBP1 and produce large quantities of antibody. Although BLIMP1h plasma cells derive from BLIMP1mid cells, it remains unknown whether plasma cells are derived from plasmablasts (indicated by the dashed arrow) or from an earlier plasma cell-committed stage. The contribution of marginal zone B cells and B1 cells to the long-lived plasma cell compartment is also poorly characterized. [Nutt et al., Nature Reviews Immunology, 2015]

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The definition of cellulitis is a diffuse, deep, acute inflammation of the skin including the dermis and subcutaneous tissue. It often follows an acute or chronic trauma, and is an important cause of hospital admissions.

In fact, it was estimated that about 10% of infections-related hospital admission in the US, and up to 14 million outpatients’ visits annually were due to cellulitis.

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poor circulation in arm, legs, hands or feet or overweight

find it difficult to move around

liver disease

weakened immune systems ( chemotherapy treatment or diabetes )

lymphoedema

inject drugs

surgical wound

history of cellulitis

add on : people who are more at risk need to treat athlete's foot promptly

A weakened immune system cannot fight bacteria effectively. Diabetes also causes nerve damage, poor wound healing, and high blood sugar, which feeds bacterial growth.

https://pmc.ncbi.nlm.nih.gov/articles/PMC6303460/

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Culture and Sensitivity Test for Cellulitis 

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Culture and Sensitivity Test for Cellulitis 

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Beta-hemolytic streptococci typically cause cellulitis, generally group A streptococcus (i.e., Streptococcus pyogenes), followed by methicillin-sensitive Staphylococcus aureus

Ref : ·       https://www.ncbi.nlm.nih.gov/books/NBK549770/

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The relationship of diabetes and bacterial infections can be reciprocal, with certain infections like periodontitis exacerbating insulin resistance

Patients with diabetes have a two-fold higher risk of community-acquired bacterial infections such as pneumococcal, streptococcal, and enterobacterial infections as compared with patients without diabetes

Ref : https://www.ncbi.nlm.nih.gov/books/NBK579762/

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All healthcare workers including the nurse practitioner and pharmacist who prescribe/dispense penicillin must ask the patient if he or she is allergic to the medication, as part of an interprofessional team approach to patient care

Patients should be asked to wear an ID bracelet about their medical health problems, including allergies.

The healthcare workers must ask for allergies at each and every admission because, in the complex world of medicine, some data are omitted or forgotten and lead to serious consequences.

Ref : https://www.ncbi.nlm.nih.gov/books/NBK459320/

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In relation to this case, HU shows these early symptoms of Cellulitis:

1. Discoloration on his left calf (colored red)

2. Swelling / Edema

3. Warmth feeling on the skin

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1) Case recap

-> Type 1 hypersensitivity

-> discontinue the cloxacillin immediately

2) According to NAG guidelines

-> pic attached , kindly refer

-> NAG suggested cephalexin

-> in this case, we don't choose this as alternative treatment , it is NOT SAFE for pt

-> why? I will explain shortly

3) what are the safe alternatives?

-> I refer to NAG, medscape and ncbi (pubmed)

-> choose antibiotic with no beta lactic structure for severe penicillin allergy

-> the choices of antibiotic :

Clarithromycin 500mg BD PO

Climdamycin 600mg - 1.2 g IV qds

Doxycycline 100mg BD PO

IV vancomycin

NAG recommend : Clindamycin 600mg IV q6h

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https://emedicine.medscape.com/article/214222-treatment?form=fpf

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https://pmc.ncbi.nlm.nih.gov/articles/PMC6303460/

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1. Breach of Skin Barrier

Entry point: trauma, ulcers, bites, fissures, or surgical wounds.

Allows normal flora (esp. Group A Streptococcus) and other pathogens to penetrate the epidermis.

2. Innate Immune Response

Keratinocytes detect bacteria → release cytokines (IL-1, IL-6, TNF-α) and chemokines.

Recruitment of neutrophils, macrophages, dendritic cells to infection site.

Neutrophils release proteolytic enzymes and reactive oxygen species → tissue inflammation and damage.

3. Vascular Changes

Local vasodilation → increased blood flow → erythema and warmth.

Increased vascular permeability → plasma proteins leak into interstitial space → edema.

Sensitization of nociceptors by cytokines/prostaglandins → pain and tenderness.

4. Epidermal & Dermal Response

Keratinocyte proliferation and production of antimicrobial peptides (defensins, cathelicidins).

Formation of inflammatory exudate in dermis and subcutaneous tissue.

5. Bacterial Virulence Factors (Group A Streptococcus)

M protein: inhibits phagocytosis.

Hyaluronidase & streptokinase: break down connective tissue, aiding spread.

Streptolysins: lyse host cells.

Pyrogenic exotoxins (A, B, C, F) & superantigens: trigger massive cytokine release → systemic toxicity, invasive disease.

6. Clinical Manifestations from Pathophysiology

Erythema & warmth → due to vasodilation and increased perfusion.

Edema → from vascular leakage and inflammatory cell infiltration.

Tenderness/pain → activation of local pain receptors by inflammatory mediators.

Systemic features (fever, chills, malaise) → cytokine-induced acute phase response.

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1. Wound cleansing

2. Debridement

3. Topical antibiotics

4. Apply wound dressing

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1. Advise the patient on signs of wound infection.

2. Advise the patient to seek immediate medical help if the there are any signs of infection.

3. Explain the next dressing date to the patient.

4. Inform the patient about date of suture removal if required.

5. Analgesic to be given adequately

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1. urticaria

2. angioedema

3. conjunctivitis

4. respiratory symptoms

5. gastrointestinal symptoms

6. anaphylaxis

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1. To relieve the acute allergic symptoms as quickly as possible

2. Prevent further severe reactions (from getting worse)

3. Improve patient’s quality of life and speed up recovery

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For this case, HU developed anaphylaxis (a severe allergic reaction) likely caused by the Penicillin. The symptoms he developed are:

·    Respiratory distress (difficulty breathing, RR 35 bpm)

·    Angioedema (swollen throat)

·    Flushing (cutaneous manifestation of allergic reaction)

·    Hypotension (BP 90/65 mmHg)

·    Fever (Temp 38.5°C, though this may also relate to infection)

Based on the vital signs above, the first step taken is for the provider to stop/withdraw the use of Cloxacillin.

Then, we can proceed with the appropriate drug treatment for HU's allergy, which is:

·    Intramuscular [I.M.] Epinephrine (Adrenaline)

o Dose: 0.3–0.5 mg IM (0.01 mg/kg in children), repeated every 5–15 minutes as needed

o Site of administration: Mid-anterolateral thigh

o Mechanism of action: Reverses bronchospasm, vasodilation, and reduces mucosal Edema

Adjunctive therapies (Antihistamines & H2 Blockers) can be included:

·    I.V. Diphenhydramine 25 mg to 50 mg. For symptomatic relief such as rashes & itching.

·    I.V. Ranitidine 50 mg. Blocks effects of histamine on H2 receptors, which can help with symptoms like hypotension, and vasodilation, seen in severe allergic reactions.

Source:

https://www.ncbi.nlm.nih.gov/books/NBK459320/ - Penicillin allergy

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Continuing Education Activity

Penicillin (PCN) was discovered by Alexander Flemming in 1928 and became widely used in 1942 to treat various staphylococcal and streptococcal bacterial infections. Today, penicillin is still one of the most widely prescribed antibiotics. Penicillin is also one of the most frequently reported medication allergies. The penicillin family of antibiotics includes penicillin derivatives of ampicillin and amoxicillin as well as cephalosporins, monobactams, carbapenems, and beta-lactamase inhibitors. All penicillins share the same core beta-lactam and thiazolidine ring structures but differ in their side chains. Identification of true penicillin allergy is critical as 80% to 90% of people once considered allergic are ultimately able to tolerate penicillins resulting in the decreased need for broad-spectrum antibiotics and development of multi-drug resistant organisms. This activity reviews the pathophysiology of penicillin allergy and highlights the role of the interprofessional team in the management of these patients.

Objectives:

Identify the cause of penicillin allergy.

Review the pathophysiology of penicillin allergy.

Summarize the treatment of patients with penicillin allergy.

Describe interprofessional team strategies for improving care and outcomes in patients with penicillin allergy.

Access free multiple choice questions on this topic.
Introduction

Penicillin (PCN) was discovered by Alexander Flemming in 1928 and became widely used in 1942 to treat various staphylococcal and streptococcal bacterial infections. Today, penicillin is still one of the most widely prescribed antibiotics. Penicillin is also one of the most frequently reported medication allergies. The penicillin family of antibiotics includes penicillin derivatives of ampicillin and amoxicillin as well as cephalosporins, monobactams, carbapenems, and beta-lactamase inhibitors. All penicillins share the same core beta-lactam and thiazolidine ring structures but differ in their side chains. Identification of true penicillin allergy is critical as 80% to 90% of people once considered allergic are ultimately able to tolerate penicillins resulting in the decreased need for broad-spectrum antibiotics and development of multi-drug resistant organisms.[1][2][3][4]

Etiology

Penicillin is a beta-lactam antibiotic. Included in the penicillin family of antibiotics are penicillin G, penicillin V, procaine penicillin, benzathine penicillin as well as over 15 related compounds with broader antibacterial effects. Type 1 and type 4 hypersensitivity reactions mediate the most common allergies to penicillin. Serious allergic reactions to penicillin are Type 1 and mediated by IgE. Risk factors for IgE mediated reactions include high-dose parenteral administration and repetitive or frequent dosing of penicillins. Most severe reactions occur between the ages of 20 to 49 years. Previously, PCN related antibiotics such as cephalosporins were avoided given concern for cross-reactivity. Current research suggests that similarities between the chemical structures of the R-side chains are what determines cross-reactivity between classes of penicillin-related compounds, enabling greater use of antibiotics previously avoided. Of note, amoxicillin is the most common of the penicillins associated with cross-reactivity.[5][6]

Epidemiology

Approximately 10% of patients report an allergy to penicillin however up to 90% of these patients do not have a true allergy. The incidence of anaphylaxis to penicillin is 0.02% to 0.04% and is mediated by a type 1 hypersensitivity reaction. Overall, cutaneous eruptions are the most commonly reported reaction. IgE antibodies decrease over time. In patients who have previously tested positive for penicillin allergy, there is an expected 10% decrease/year of a subsequent positive reaction. Therefore, with the avoidance of PCN, 80% to 100% of patients will ultimately test negative for penicillin allergy 10 years after the initial positive test. The presence of an underlying bacterial or viral infection with penicillin administration also often resulted in false reporting of penicillin allergies such as the exanthem seen with EBV.

Cross-reactivity with other penicillin-related compounds, specifically cephalosporins, has resulted in the avoidance of drug use. Early studies may have also over-estimated cross-reactivity between penicillin and cephalosporins as the production of early generation cephalosporins may have been contaminated with small amounts of penicillin. Penicillin has a single R side chain whereas cephalosporins have two. If the penicillin side chain is similar to either cephalosporin side chain, there is a greater risk of cross-reactivity. This more commonly occurs with first and second generation cephalosporins than with third or fourth generation cephalosporins making the latter more attractive treatment choices when a patient has a proven penicillin allergy. Overall, cross-reactivity with aminopenicillins is less than 2%, carbapenems less than 1% and cephalosporins less than 3%. There is no significant reported cross-reactivity with monobactams.

Pathophysiology

All penicillins share the same core beta-lactam and thiazolidine ring structures but differ in their side chains. The ring structure is metabolized into major (penicilloyl) and minor (penicillin, penicilloate, and penilloate) antigenic determinates. Immediate reactions are the result of IgE that cross-like on mast cells when exposed to the antigenic component. The result is degranulation and release of histamine as well as other vasoactive substances. It is the minor antigenic determinates that generate IgE specific responses that are associated with true penicillin allergy. These minor determinates result in immediate reactions, within minutes to 1 hour, and characterized by signs and symptoms of acute anaphylaxis such as urticaria, flushing, dyspnea, bronchospasm with wheezing, angioedema, hypotension, tachycardia, mental status change or gastrointestinal (GI) upset. The major antigenic determinates more commonly are associated with less severe urticarial reactions.

Delayed reactions are mediated by IgM and IgG which activates the complement system resulting in inflammatory reactions that include Type 2 to 4 hypersensitivity reactions. Serious hypersensitivity reactions include hemolytic anemia, toxic epidermal necrolysis (TEN), Steven's Johnson Syndrome (SJS), vasculitis, interstitial nephritis, serum sickness, thrombocytopenia, and neutropenia.

History and Physical

For patients presenting with an acute allergic reaction after administration of penicillin, it is important to determine when the medication was given, route of administration, as well as onset and type of symptoms including respiratory difficulty, GI symptoms, mental status changes, and cardiovascular collapse such as hypotension or skin findings. For those patients who report a history of penicillin allergy due to previous exposure, onset and timing are again important as is route and ability to tolerate other beta-lactams previously. Other important historical questions include how the penicillin allergy was managed. For example, if the patient was treated with antihistamines or epinephrine and had improvement/resolution of symptoms, this is supportive of an IgE reaction and a true penicillin allergy.

For patients presenting with an acute allergic reaction to penicillin, the initial exam should always focus on airway, breathing, and circulation. The patient should quickly and carefully be examined for edema of the lips, tongue or oropharynx and any difficulty swallowing or handling his/her secretions. Heart and lungs should be carefully auscultated as well for arrhythmia, and adventitious breath sounds such as wheezing or stridor. Confusion and abdominal pain are also findings of severe anaphylaxis. Cutaneous symptoms are often the first and most common finding of an allergic reaction, however, are absent in 10% to 20% of patients experiencing an allergic reaction. Common cutaneous symptoms are generalized urticaria, flushing, pruritis, and angioedema.

Evaluation

To determine if a patient has an IgE mediated penicillin allergy, the only validated test currently available in the united states is penicillin skin testing. A board-certified allergist should perform the test. It involves a skin-prick with the application of the major and minor determinants as well as a control. The area of skin is examined 15 minutes later. If a wheel of at least 3 mm and concomitant erythema develop, the test is positive. The test should not be performed if the reaction to penicillin was a severe non-IgE mediated reaction.[7][8][9][10]

If skin testing is negative, intra-dermal testing can then also be performed using the same antigenic determinants. Just as with skin testing, a positive intradermal test is characterized by the development of a 3 mm or more wheal and erythema at the site of injection. Readings are taken at 15 min for a history of immediate reaction and at 48 and 72 hours with a history of delayed reaction. Patients may need to wait up to 6 weeks after initial testing before undergoing intra-dermal testing.

A graded-dose challenge can also be performed when skin testing is negative. Here the patients receive anywhere from 1/100, if initial reaction was anaphylactic, to 1/10 of a dose with progressively increasing doses after that. After each dose administration, the patient has a 30 to 60 minute observation period. If no reaction occurs, the patients then receive a full dose, again followed by a period of observation. Testing must be performed by a board-certified allergist and should be performed at least 4 to 6 weeks after an acute reaction, use of steroids or anti-histamines or any signs of asthma or urticaria. The graded-dose challenge is also contraindicated if the initial reaction was a severe non-IgE mediated reaction such as Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN).

Treatment / Management

Treatment for acute IgE mediated reaction to penicillin depends on severity. Patients presenting in acute anaphylaxis need to have immediate treatment with IM epinephrine (1 mg/ml) 0.3 mg to 0.5 mg every 5 to 15 minutes until resolution of symptoms. Adjunctive therapies include H1 and H2 antihistamines including diphenhydramine 25 mg to 50 mg intravenously (IV) and ranitidine 50 mg IV, respectively. Glucocorticoids should also be administered such as 125 mg methylprednisone. Patients with refractory symptoms should be treated with an infusion of epinephrine at 0.1 mcg/kg/minute. All patients presenting with acute anaphylaxis should be immediately placed on telemetry monitoring with large-bore IV for IVF resuscitation at 1 L to 2 L NS bolus. If patients are experiencing bronchospasm, albuterol 2.5 mg to 5 mg can also be considered. These patients require admission to the hospital. Patients with a resolution of symptoms after a period of observation are safe for discharge. [11][12][13]

For those patients presenting with mild reactions and have cutaneous findings only, treatment with an antihistamine such as diphenhydramine is adequate.

For patients with a true Type 1 IgE mediated penicillin allergy, another antibiotic should be used for treatment. If there is not another equally as efficacious antibiotic, patient's should undergo drug desensitization. The process of desensitization involves subcutaneous, intravenous, or oral administration of incrementally higher doses of the drug every 15 to 30 minutes until the patient tolerates the entire dose. For patients with histories of severe IgE mediated reactions, initial doses should be between 1/1,000,000 and 1/10,000 of the full therapeutic dose. Success rates for desensitization can reach up to 100%. Drug desensitization is again contraindicated in patients with severe non-IgE-mediated reactions such as SJS or TEN.

Differential Diagnosis

Pearls and Other Issues

Identification of patients with a true, IgE mediated penicillin allergy is of vital importance to help improve antibiotic utilization with decrease usage of broad-spectrum antibiotics as well as slow the spread of multi-drug resistant bacteria. Other effects include overall decreased health care costs with decreased length of hospitalization as well as decreased readmission rate due to antibiotic failure.

Enhancing Healthcare Team Outcomes

All healthcare workers including the nurse practitioner and pharmacist who prescribe/dispense penicillin must ask the patient if he or she is allergic to the medication, as part of an interprofessional team approach to patient care. Penicillin allergy can be serious and result in a life-threatening anaphylactic reaction. Patients should be asked to wear an ID bracelet about their medical health problems, including allergies. The healthcare workers must ask for allergies at each and every admission because, in the complex world of medicine, some data are omitted or forgotten and lead to serious consequences. Pharmacists should check the patient medication record, checking for agents that may have crossover allergic reaction, and assess the safety of cephalosporins in conjunction with the prescriber. Nursing staff should be vigilant on the intake so that this mistake is never made, but also should have the patient clarify any prior allergic reaction to penicillin drugs. These interprofessional steps can prevent penicillin allergy and prevention is the optimal management strategy. [Level 5][8][14][15]

References

1.

2.

Blumenthal KG, Huebner EM, Fu X, Li Y, Bhattacharya G, Levin AS, Mancini CM, Slawski BR, Banerji A. Risk-based pathway for outpatient penicillin allergy evaluations. J Allergy Clin Immunol Pract. 2019 Sep-Oct;7(7):2411-2414.e1. [ PMC free article: PMC6733651 ] [ PubMed: 30981747 ]

3.

4.

5.

6.

7.

8.

Blumenthal KG, Li Y, Hsu JT, Wolfson AR, Berkowitz DN, Carballo VA, Schwartz JM, Marquis KA, Elshaboury R, Gandhi RG, Lambl BB, Freeley MM, Gruszecki A, Wickner PG, Shenoy ES. Outcomes from an inpatient beta-lactam allergy guideline across a large US health system. Infect Control Hosp Epidemiol. 2019 May;40(5):528-535. [ PMC free article: PMC6536839 ] [ PubMed: 30915929 ]

9.

10.

Kleris RS, Lugar PL. Things We Do For No Reason™: Failing to Question a Penicillin Allergy History. J Hosp Med. 2019 Nov;14(11):704-706. [ PMC free article: PMC6827537 ] [ PubMed: 30897049 ]

11.

12.

13.

14.

15.

Disclosure: Rachel Patterson declares no relevant financial relationships with ineligible companies.

Disclosure: Holly Stankewicz declares no relevant financial relationships with ineligible companies.

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Penicillin (PCN) was discovered by Alexander Flemming in 1928 and became widely used in 1942 to treat various staphylococcal and streptococcal bacterial infections. Today, penicillin is still one of the most widely prescribed antibiotics. Penicillin is also one of the most frequently reported medication allergies.

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1. Vital signs (To detect any early signs of anaphylaxis, shock, or worsening reaction)

Blood Pressure

Heart Rate

Respiratory Rate

Temperature

Oxygen Saturation

2. Respiratory status

Wheezing

Dyspnoea

Hypoxia

3. Cardiovascular status

Blood Pressure

Heart Rhythm

4. Skin and Mucosal symptoms

Spreading rash

Swelling

Skin sloughing (possible Stevens-Johnson Syndrome, in severe cases)

5. Neurological status

Level of consciousness (especially in severe cases)

Anxiety or Restlessness

Confusion / Lethargy

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When someone is hemodynamically unstable, 

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When someone is hemodynamically unstable, 

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their body's circulatory system cannot maintain adequate blood flow and pressure, leading to shock and organ failure as organs are deprived of oxygen and nutrients. Common symptoms include low blood pressure (hypotension), shortness of breath, restlessness, confusion, chest pain, and changes in mental status, often accompanied by a rapid or abnormal heart rate

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-White blood count raised (leukocytosis)à means body are fighting off infection

-Elevated C-reactive protein

-Also an inflammatory marker

-on going inflammation

-Glucose and HbA1c level elevated (age 63 yrs normal 7.1-8%)à slightly higher might be due to stress induce where hormone are release such as cortisol and epinephrine to fight illness

-High temperature (36.5-37.5)

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-Every hospital has its own discharge policy, patient will be discharge when he/ she no longer needed to receive inpatient care

-Medical professional will check medical condition such as:

-No fever for 24-48 hrs

-Improvement in clinical status in hemodynamic status, no respiratory distress, general well being

-Symptoms like swollen throat and flushing face subside

-Tolerate the oral antibiotics and compliance with the oral medication

-Able to manage home care such as cleaning wound and elevatethe affected limb

-No worsening of symptoms

https://www.cdc.gov/dengue/training/cme/ccm/page53639.html

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Vitals:

BP: 90/65 mmHg → hypotension

RR: 35 bpm → tachypnea/dyspnea

PR: 102 bpm → tachycardia

Temp: 38.5°C → fever

1. Blood Pressure: 90/65 mmHg (Low)

Normal: 120/80 mmHg

Significance: Hypotension indicates systemic vasodilation and fluid shift from blood vessels into tissues due to histamine release in anaphylaxis.

2. Respiratory Rate: 35 breaths/min (High)

Normal: 12–20 breaths/min

Significance: Fast breathing shows respiratory distress. This is likely due to throat swelling (laryngeal edema) and possible bronchospasm, making it harder to breathe.

3. Pulse Rate: 102 bpm (High)

Normal: 60–100 bpm

Significance: Mild tachycardia due to the body compensating for low blood pressure. The heart pumps faster to maintain cardiac output.

4. Temperature: 38.5°C (Elevated)

Normal: 36.5–37.5°C

Significance: Likely related to the underlying wound infection (not directly from the allergic reaction).

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https://www.google.com/url?sa=i&url=https%3A%2F%2Fwww.sciencedirect.com%2Fscience%2Farticle%2Fpii%2FS1578219019300137&psig=AOvVaw1VtTyWrCCkpKqBOkrS_w6j&ust=1757568552463000&source=images&cd=vfe&opi=89978449&ved=0CAMQjB1qFwoTCOCW4Zu7zY8DFQAAAAAdAAAAABAE

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1. Consult and Educate

Provide medication counseling to patients and caregivers on the correct use of antibiotics (e.g., cloxacillin) and analgesics (e.g., celecoxib), including dosage, frequency, and duration.

Explain the importance of adherence to prevent relapse, resistance, or incomplete treatment.

Educate on side effects (e.g., rash, diarrhea, GI upset, renal effects with NSAIDs) and what actions to take if they occur.

Guide on lifestyle/adjunct measures, such as skin hygiene, limb elevation, and monitoring for signs of worsening infection.

Reinforce antimicrobial stewardship, encouraging patients to complete the prescribed course and not to self-medicate with leftover antibiotics.

2. Raise Awareness on Medicine Allergy

Identify and document drug allergy history during dispensing, screening for previous penicillin or NSAID reactions.

Educate patients about common allergy signs (rash, swelling, breathing difficulty, anaphylaxis) and when to seek urgent care.

Alert healthcare teams about patients’ allergy risks to avoid inadvertent re-prescription of the offending drug.

Conduct patient education sessions or awareness campaigns in wards, clinics, or community settings to increase understanding of medicine allergies.

Promote reporting of adverse drug reactions through the Malaysian Adverse Drug Reactions Advisory Committee (MADRAC).

3. Providing Allergy Card

Issue allergy cards or bracelets to patients with confirmed drug allergies (e.g., penicillin allergy → cloxacillin contraindication).

Ensure details are recorded on the card: name of drug, type of reaction, date of event, and issuing facility/pharmacist.

Counsel patients to carry the card at all times and present it to any healthcare professional before receiving treatment.

Update electronic medical records so that allergy alerts are visible during prescribing and dispensing.

Promote safety and continuity of care, especially when patients visit different clinics, hospitals, or pharmacies.

4. Cross-Checking and Verification

Verify allergy status before dispensing — especially high-risk antibiotics like cloxacillin or cephalosporins.

Act as a final safety checkpoint between prescribers and patients.

Communicate with prescribers if prescribed medication conflicts with recorded allergy profile.

5. Policy and System Development

Advocate for mandatory allergy status checks in electronic prescribing systems before order submission.

Collaborate in developing standard operating procedures (SOPs) for allergy documentation and verification.

Support integration of national electronic health records that link allergy history across different facilities.

6. Systematic Medication History Taking

Perform comprehensive medication reconciliation during hospital admission, transfer, and discharge to ensure accurate allergy status is carried forward.

Ask specific, open-ended questions about prior drug reactions (e.g., “Have you ever had swelling, rash, or difficulty breathing after taking antibiotics?”).

Differentiate between true drug allergy vs. intolerance/side effects (e.g., nausea from NSAIDs is not an allergy).

7. Staff and Interprofessional Training

Educate doctors, nurses, and pharmacy staff on the importance of allergy history documentation.

Provide updates on drug cross-reactivity (e.g., penicillin vs. cephalosporin allergy).

Conduct in-service training and hospital-wide awareness campaigns on allergy prevention.