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Medication Therapy for Bacterial Infections – Part 1
Antiinfective Fundamentals
Antiinfective Activity
Antiinfectives differ in spectrum and mechanism of action.
Selectivity: Some drugs target only a narrow range of organisms because they bind to a very specific metabolic pathway or enzyme.
Bactericidal: Kill the microorganism outright.
Bacteriostatic: Halt reproduction, allowing host defenses to eradicate the pathogen.
Spectrum terminology
Narrow-spectrum: Effective against a limited group of organisms possessing the targeted pathway.
Broad-spectrum: Useful when the causative pathogen is unknown or when mixed infections are suspected.
Clinical significance: Starting broad then narrowing after culture results ↓ resistance and ↓ collateral damage to normal flora.
Resistance
Definition: Natural or acquired capacity of microbes to survive exposure to an anti-infective that formerly killed or inhibited them.
Biologic basis: Drugs target one enzyme/process; organisms lacking, mutating, or bypassing that target become unaffected.
Prevention strategies
Treat only infections proved or strongly presumed to be bacterial (culture & sensitivity [C&S]).
Use the right drug at the right dose for the right duration to reach microbicidal concentrations.
Avoid indiscriminate or prophylactic use; promotes selection of resistant strains.
General Nursing Considerations
Prior to first dose: Obtain cultures (blood, urine, sputum, wound, etc.) to guide therapy.
Universal client teaching
Complete the full course even if symptoms resolve.
Never share or use leftover antibiotics.
Recognize and report common side effects: \text{N/V/D}, abdominal cramps, rash.
Adverse reactions that warrant immediate attention
Superinfections (oral/vaginal candidiasis, C. difficile colitis).
Anaphylaxis (laryngeal edema, urticaria, hypotension).
Common Superinfections
Candidiasis
Overgrowth of Candida spp. after alteration of normal flora; manifests as oral thrush or vulvovaginal yeast infection.
Clostridioides difficile–Associated Disease (CDAD)
S/S: watery diarrhea, abdominal pain or distention, fever, anorexia, tachycardia, possible hematochezia.
Nursing priority: Contact precautions, stool assay, initiate or escalate to oral vancomycin/fidaxomicin per protocol.
Anaphylaxis Management Algorithm
Establish airway → 100 % O₂ via non-rebreather → STOP IV antibiotic → rapid IV/IM epinephrine \left(0.3\,\text{mg IM of 1 : 1,000}\right) ± diphenhydramine \left(25-50\,\text{mg IV/IM}\right).
Initiate large-bore IV for fluids, monitor VS q 5 min, prepare for advanced airway.
Laboratory & Clinical Monitoring During Antibiotic Therapy
Drug levels: Peak & trough for drugs with narrow therapeutic index (aminoglycosides, vancomycin).
Renal: BUN = 5-25\,\text{mg/dL};\; Cr = 0.3-1.4\,\text{mg/dL}.
Hepatic:
AST = 12-37\,U/L (hepatocellular injury).
Albumin = 3.4-5\,\text{g/dL} (synthetic function).
Bilirubin = 0.2-1\,\text{mg/dL}.
Bleeding risk (especially cephalosporins):
Platelets = 150{,}000-400{,}000\,\mu L.
PT = 9.4-12.5\,s;\; INR = 0.9-1.1;\; PTT = 25-37\,s.
Antibiotics That Inhibit Cell-Wall Synthesis
Penicillins – Example: Amoxicillin
Administration: Oral, IM, IV (observe 30 min post-parenteral for hypersensitivity).
Client teaching
Take oral forms with food to ↓ GI upset; complete course.
Report watery/bloody diarrhea (possible CDAD), oral/vaginal candidiasis, or allergic manifestations (rash, wheeze, facial edema).
↓ efficacy of combined oral contraceptives—advise backup contraception.
Cephalosporins – Prototype: Cephalexin (1st gen) + Generational Overview
1st gen: cefazolin, cephalexin — strong Gram (+), peri-op prophylaxis.
2nd gen: cefaclor, cefotetan, cefoxitin, cefuroxime — ↑ Gram (−).
3rd gen: ceftriaxone, cefotaxime, ceftazidime — crosses BBB, severe infections.
4th gen: cefepime — broadest, Pseudomonas.
Side effects: Thrombophlebitis (IV), disulfiram-like reaction with EtOH.
Adverse: CDAD, bleeding (interferes w/ Vit K), anaphylaxis.
Nursing: Infuse slowly, monitor INR/PT/PTT, renal function; avoid alcohol.
Monobactams – Aztreonam
Routes: IV, IM, inhalation (cystic fibrosis).
SE: Wheeze, nasopharyngeal irritation (inhaled). IV site pain/phlebitis.
Not compatible with many IV drugs; dedicate line.
Carbapenems – Imipenem
Only IV/IM (not absorbed PO).
Adverse: Seizures, thrombophlebitis; caution in penicillin allergy & renal impairment.
Monitor liver (AST), renal (BUN, Cr), LDH, bilirubin.
Glycopeptide – Vancomycin
Indications: MRSA, severe Gram (+) infection, oral form for CDAD.
Adverse:
Nephrotoxicity (monitor BUN/Cr; maintain trough 10-20\,\mu g/mL).
Ototoxicity (tinnitus, vertigo, hearing loss).
Rapid infusion → Red-Man Syndrome: histamine-mediated flushing, hypotension, tachycardia.
Nursing: Infuse ≥ 60 min, dilute in 250 mL, check IV site, avoid concurrent ototoxic/nephrotoxic drugs.
Protein Synthesis Inhibitors
Tetracyclines
Adverse: Tooth discoloration & bone growth suppression (avoid < 8 y, pregnancy); hepatotoxicity; photosensitivity.
Teaching
Take on empty stomach (1 hr before or 2 hr after) with full glass of water; no dairy/antacids/iron within 2 hr.
Use SPF ≥ 30; store in dark container (decomposes in light → Fanconi-like syndrome).
Alternate birth control method.
Macrolides – Erythromycin
Adverse: QT prolongation → ventricular dysrhythmias, ototoxicity.
High interaction potential (CYP450 inhibitor)—monitor serum levels of interacting drugs (warfarin, digoxin, theophylline).
Take with food if GI upset; report palpitations or auditory changes.
Aminoglycosides – Gentamicin
Adverse: Ototoxic (8th cranial nerve), nephrotoxic (acute tubular necrosis).
Monitoring
Peak: 30\,\text{min} after dose; trough: \approx1\,\text{hr} pre-dose.
Maintain trough < 2\,\mu g/mL to limit toxicity.
Baseline & serial audiometry; strict I&O.
DNA Replication / Cell-Division Inhibitors
Fluoroquinolones – Ciprofloxacin
Adverse: CNS stimulation (confusion, seizures), Achilles tendon rupture (↑ risk > 60 y + steroids), photosensitivity, hepatotoxicity.
Teaching: Report tendon pain, ↓ caffeine, liberal fluids 1.5-2\,L/day, separate antacid/iron/calcium/dairy by 2\,\text{hr after or 6 hr before} dose.
Folic Acid Synthesis Inhibitors
Sulfonamides – Trimethoprim/Sulfamethoxazole (TMP-SMX)
Adverse: Stevens-Johnson Syndrome, blood dyscrasias (agranulocytosis, aplastic anemia, thrombocytopenia), crystalluria → renal damage, CDAD.
Teaching: Hydration \ge 1{,}200-1{,}500\,mL/day, take with food & 8 oz water, avoid EtOH, backup contraception.
Urinary Tract Antiseptic – Nitrofurantoin
Adverse: Acute/chronic pulmonary reactions (fibrosis), peripheral neuropathy, hemolytic anemia in G6PD deficiency, benign brown urine, teeth staining (liquid).
Teaching: Take with food/milk, do not crush, dilute liquid in milk/juice then rinse mouth.
Antimycobacterial (Anti-TB) Drugs
Isoniazid (INH)
Adverse: Hepatotoxicity (elevated AST/ALT, jaundice), peripheral neuropathy (pyridoxine deficiency), CNS changes (seizures, psychosis), DRESS.
Nursing: Baseline LFTs, teach S/S liver injury and neuropathy; may prescribe 50\,mg vitamin B₆ daily.
Interactions: EtOH ↑ liver risk; phenytoin ↑ levels; antacids ↓ absorption.
Rifampin
Benign red-orange discoloration of urine, sweat, tears; may stain contact lenses.
Adverse: Hepatotoxicity, DRESS.
Induces CYP450 → ↓ effectiveness of OCPs, warfarin, antiretrovirals.
Dosing: PO on empty stomach (1 hr before or 2 hr after meals).
Nursing Process Framework
Assessment: Allergy history, current vitals, labs (renal/hepatic), culture results.
Diagnosis/Analysis: Knowledge deficit r/t new drug, risk for non-adherence, risk for fluid volume deficit (diarrhea), etc.
Planning: Goals—resolution of infection, no adverse effects, adherence.
Implementation: Administer drug correctly, monitor labs, teach.
Evaluation: Compare outcomes—afebrile? ↓ WBC? Any toxicity?
Dosage Calculation Practice
Example 1: High-Dose Amoxicillin
Weight conversion: \frac{44\,lb}{2.2\,lb/kg}=20\,kg (nearest tenth).
Ordered: 20\,mg/kg/day divided q 12 hr → 20\,mg \times 20\,kg = 400\,mg/day.
Suspension concentration: \frac{200\,mg}{5\,mL}=40\,mg/mL.
Total daily volume: \frac{400\,mg}{40\,mg/mL}=10\,mL/day.
Per dose (q12h): \frac{10\,mL}{2}=5\,mL (nearest whole mL).
Example 2: Lower-Dose Amoxicillin
Order: 10\,mg/kg every 12 hr.
Dose: 10\,mg \times 20\,kg = 200\,mg.
Volume: \frac{200\,mg}{40\,mg/mL}=5\,mL per dose.
IV Administration Rate Calculation
Order: Ampicillin 500\,mg in 50\,mL D5W over 30\,min\;(0.5\,hr).
Pump setting: \text{Rate} = \frac{50\,mL}{0.5\,hr}=100\,mL/hr (nearest whole number).
Antiinfective Fundamentals
Antiinfective Activity
Antiinfectives differ in spectrum and mechanism of action.
Selectivity: Drugs selectively target specific microbial components (e.g., unique enzymes, cell wall synthesis components) that are either absent or significantly different in human cells. This specificity allows for effective pathogen eradication with minimal host cell damage.
Bactericidal: These agents directly kill the microorganism by disrupting vital cellular processes, such as cell wall integrity (e.g., penicillins), cell membrane function, or DNA synthesis (e.g., fluoroquinolones). They are often preferred in immunocompromised patients or severe infections.
Bacteriostatic: These agents inhibit bacterial growth and reproduction, typically by interfering with protein synthesis (e.g., tetracyclines, macrolides) or folic acid metabolism. This allows the host's immune system to mount an effective defense and clear the infection. Their effectiveness relies on a competent host immune response.
Spectrum terminology
Narrow-spectrum: Effective against a limited group of specific organisms that possess the targeted metabolic pathway or structure. These are preferred when the pathogen is known, as they minimize disruption to the normal human microbiome and reduce the likelihood of resistance development.
Broad-spectrum: Effective against a wide range of bacterial types, including both Gram-positive and Gram-negative organisms. These agents are useful empirically when the causative pathogen is unknown, in polymicrobial infections, or in critically ill patients where delaying treatment could be detrimental. However, their use should be narrowed once culture and sensitivity (C&S) results are available.
Clinical significance: Initiating therapy with a broad-spectrum agent and then de-escalating to a narrow-spectrum agent once C&S results are known is a critical strategy in antimicrobial stewardship. This approach helps to minimize the selection pressure for resistant strains and reduces collateral damage to the patient's normal flora (e.g., gut microbiota), thereby lowering the risk of superinfections like Clostridioides difficile-associated disease (CDAD) or candidiasis.
Resistance
Definition: The natural or acquired capacity of microorganisms to survive exposure to an anti-infective agent that previously inhibited their growth or killed them. This phenomenon can render once-effective drugs useless, leading to treatment failures.
Biologic basis: Microorganisms evolve various mechanisms to evade antimicrobial action. Common mechanisms include:
Enzymatic inactivation: Production of enzymes (e.g., beta-lactamases) that degrade or modify the antibiotic structure.
Target site modification: Alterations in the drug's binding site on the bacterial cell, reducing or preventing its interaction.
Reduced permeability/efflux pumps: Decreased uptake of the drug or active pumping of the drug out of the bacterial cell before it can reach its target.
Bypassing metabolic pathways: Development of alternative metabolic routes that are not inhibited by the drug.
Prevention strategies
Treat only infections proved or strongly presumed to be bacterial via proper diagnostic testing (e.g., culture & sensitivity [C&S] testing, Gram stain results, rapid antigen tests).
Use the right drug (based on susceptibility data), at the right dose (to achieve microbicidal concentrations at the infection site), for the right duration (sufficient to eradicate the pathogen without promoting resistance). Under-dosing or premature discontinuation can foster resistance.
Avoid indiscriminate or prophylactic use of antibiotics, especially in viral infections. This practice selects for resistant strains within the microbial population, contributing to the global problem of antimicrobial resistance.
Implement infection control measures (e.g., hand hygiene, isolation precautions) to prevent the spread of resistant organisms.
General Nursing Considerations
Prior to first dose: Always obtain appropriate cultures (e.g., blood, urine, sputum, wound exudate) before initiating antibiotic therapy whenever possible. This ensures that the causative pathogen can be identified and its susceptibility to various antibiotics determined, guiding targeted therapy and promoting antibiotic stewardship.
Universal client teaching
Emphasize the importance of completing the full prescribed course of antibiotics, even if symptoms resolve earlier. Premature discontinuation can lead to relapse of infection and promote the development of antibiotic resistance by allowing partially suppressed, more resistant bacteria to proliferate.
Instruct patients to never share or use leftover antibiotics. Self-medication or inappropriate use contributes to resistance and potential adverse drug reactions.
Educate patients on common and expected side effects such as nausea ( ext{N}), vomiting ( ext{V}), diarrhea ( ext{D}), abdominal cramps, and rash. Advise managing gastrointestinal upset by taking medication with food if indicated (unless contraindicated for absorption) and maintaining hydration.
Adverse reactions that warrant immediate attention
Superinfections: These occur due to the disruption of normal microbial flora, allowing opportunistic pathogens to overgrow. Examples include oral/vaginal candidiasis (yeast infections) and Clostridioides difficile colitis (CDAD). Patients should report new onset of oral lesions, vaginal itching/discharge, or persistent watery diarrhea.
Anaphylaxis: A severe, life-threatening allergic reaction that can manifest rapidly. Key signs include laryngeal edema (difficulty breathing, stridor), generalized urticaria (hives), severe bronchospasm (wheezing, shortness of breath), angioedema (swelling of face, lips, tongue), and profound hypotension (dizziness, faintness). This requires immediate intervention.
Common Superinfections
Candidiasis
Overgrowth of Candida species (most commonly C. albicans) occurs when the normal bacterial flora, which keeps Candida in check, is suppressed by antibiotic therapy. It commonly manifests as oral thrush (white patches on tongue/buccal mucosa) or vulvovaginal yeast infection (itching, burning, thick white discharge). Immunocompromised individuals are at higher risk.
Clostridioides difficile–Associated Disease (CDAD)
CDAD, formerly known as Clostridium difficile, is caused by toxins produced by C. difficile bacteria when normal gut flora is disrupted, often by broad-spectrum antibiotics (e.g., clindamycin, fluoroquinolones, cephalosporins). The toxins cause inflammation of the colon (colitis).
S/S: Varies from mild, watery diarrhea to severe, life-threatening pseudomembranous colitis with symptoms including persistent watery diarrhea (often foul-smelling), severe abdominal pain or distention, fever, anorexia, tachycardia, and in severe cases, hematochezia (bloody stools) or ileus.
Nursing priority: Implement contact precautions immediately to prevent spread. Obtain a stool assay for C. difficile toxin. Initiate or escalate treatment per hospital protocol, typically with oral vancomycin (first-line for severe cases) or fidaxomicin (alternative, often for recurrent cases). Metronidazole is sometimes used for mild cases. Adequate hydration and electrolyte management are crucial.
Anaphylaxis Management Algorithm
Establish airway: Assess for signs of airway obstruction (e.g., stridor, hoarseness, dysphagia). If compromised, prepare for intubation or cricothyrotomy.
100 % O₂ via non-rebreather: Administer high-flow oxygen to compensate for bronchoconstriction and improve tissue oxygenation.
STOP IV antibiotic: Immediately discontinue the suspected causative agent.
Rapid IV/IM epinephrine: Administer epinephrine (0.3-0.5 ext{ mg IM of 1 : 1,000 solution for adults; } 0.01 ext{ mg/kg IM up to } 0.3 ext{ mg for children}) in the vastus lateralis muscle (preferred over deltoid due to faster absorption). Epinephrine is the primary treatment as it has alpha-1 adrenergic effects (vasoconstriction, counteracting hypotension and angioedema) and beta-2 adrenergic effects (bronchodilation, relieving bronchospasm).
± diphenhydramine (25-50 ext{ mg IV/IM}): An H1 antihistamine that helps reduce urticaria, itching, and angioedema but does not address the life-threatening respiratory or cardiovascular symptoms.
Initiate large-bore IV for fluids: Administer intravenous crystalloids (e.g., normal saline) rapidly (e.g., 500-1000 ext{ mL bolus}) to counteract vasodilation and hypotension. Significant fluid shifts can occur in anaphylaxis.
Monitor VS q 5 min: Closely monitor blood pressure, heart rate, respiratory rate, and oxygen saturation. Prepare for advanced airway management (intubation equipment, tracheostomy tray) due to potential for rapid airway compromise.
Additional measures: Consider H2 antihistamines (e.g., ranitidine), corticosteroids (e.g., methylprednisolone) for prolonged symptoms or to prevent biphasic reactions, and inhaled bronchodilators (e.g., albuterol) for persistent bronchospasm.
Laboratory & Clinical Monitoring During Antibiotic Therapy
Drug levels: Obtain peak and trough levels for drugs with a narrow therapeutic index (e.g., aminoglycosides like gentamicin, vancomycin). Peak levels ensure adequate therapeutic concentration, while trough levels reflect drug clearance and are crucial for minimizing toxicity (e.g., nephrotoxicity).
Renal function: Monitor serum blood urea nitrogen (BUN = 5-25 ext{ mg/dL}) and creatinine (Cr = 0.3-1.4 ext{ mg/dL}). Elevated BUN and Cr indicate impaired renal clearance, which can lead to drug accumulation and increased risk of toxicity, especially for renally excreted antibiotics. Dosage adjustments may be necessary.
Hepatic function:
Aspartate aminotransferase (AST = 12-37 ext{ U/L}) and Alanine aminotransferase (ALT = 10-40 ext{ U/L}): Elevations indicate hepatocellular injury or inflammation. Many antibiotics are metabolized by the liver and can cause hepatotoxicity.
Albumin (3.4-5 ext{ g/dL}): A measure of the liver's synthetic function. Low levels can affect drug binding and distribution.
Bilirubin (0.2-1 ext{ mg/dL} total): Elevated levels (direct/indirect) can indicate impaired hepatic excretion or hemolysis, potentially exacerbated by some antibiotics.
Bleeding risk (especially with certain cephalosporins, e.g., cefotetan, and some penicillins): Monitor coagulation parameters:
Platelets (150,000-400,000 ext{ cells/} extmu ext{L}): Thrombocytopenia can occur due to drug-induced bone marrow suppression.
Prothrombin time (PT = 9.4-12.5 ext{ s}), International Normalized Ratio (INR = 0.9-1.1 for healthy individuals), and Activated Partial Thromboplastin Time (PTT = 25-37 ext{ s}): Prolongation indicates impaired clotting cascade. Some antibiotics (e.g., certain cephalosporins) can interfere with vitamin K synthesis or utilization, leading to coagulopathy and increased bleeding risk.
Antibiotics That Inhibit Cell-Wall Synthesis
Penicillins – Example: Amoxicillin
Mechanism of Action: Penicillins are beta-lactam antibiotics that inhibit bacterial cell wall synthesis by binding to penicillin-binding proteins (PBPs), leading to autolytic enzyme activation and bacterial cell lysis. They are bactericidal.
Administration: Can be administered orally, intramuscularly (IM), or intravenously (IV). For parenteral administration (IM/IV), patients should be observed for at least 30 minutes post-dose for immediate hypersensitivity reactions.
Client teaching
Oral forms: Advise taking with food to minimize gastrointestinal upset (nausea, diarrhea), though some specific penicillins (e.g., penicillin V) may have better absorption on an empty stomach. Always emphasize completing the entire prescribed course.
Report any signs of superinfections (e.g., watery/bloody diarrhea suggestive of CDAD, oral thrush, vaginal candidiasis) or allergic manifestations (e.g., rash, pruritus, wheezing, facial edema, shortness of breath, profound hypotension—these require immediate medical attention).
Penicillins, particularly certain types like amoxicillin, can decrease the efficacy of combined oral contraceptives (OCPs) by altering gut flora and enterohepatic recirculation of estrogen. Advise patients to use an alternative or backup method of contraception throughout the course of treatment and for 7 days after completion.
Cephalosporins – Prototype: Cephalexin (1st gen) + Generational Overview
Mechanism of Action: Also beta-lactam antibiotics, similar to penicillins, inhibiting cell wall synthesis. Categorized into generations based on their spectrum of activity and resistance to beta-lactamases.
Generational Overview:
1st generation: cefazolin (IV/IM), cephalexin (PO) — Primarily active against Gram-positive cocci (e.g., Staphylococcus and Streptococcus) and limited Gram-negative activity. Cefazolin is commonly used for surgical prophylaxis due to its good tissue penetration.
2nd generation: cefaclor (PO), cefotetan (IV), cefoxitin (IV), cefuroxime (IV/PO) — Increased activity against Gram-negative bacteria (e.g., Haemophilus influenzae, Neisseria spp.) compared to 1st gen, while retaining some Gram-positive activity. Cefotetan/cefoxitin have good anaerobic coverage.
3rd generation: ceftriaxone (IV/IM), cefotaxime (IV), ceftazidime (IV) — Exhibit significantly enhanced Gram-negative activity, including against some Enterobacteriaceae. Ceftriaxone and cefotaxime also cross the blood-brain barrier (BBB) effectively, making them valuable for treating severe infections like meningitis. Ceftazidime has activity against Pseudomonas aeruginosa.
4th generation: cefepime (IV) — Considered a broad-spectrum agent with enhanced activity against Gram-negative bacteria (including Pseudomonas aeruginosa) and good Gram-positive coverage. It also penetrates the BBB and is often reserved for serious nosocomial infections.
5th generation: ceftaroline (IV) — Unique in its activity against MRSA (methicillin-resistant Staphylococcus aureus) while retaining broad Gram-negative coverage (excluding Pseudomonas).
Side effects: Common side effects include gastrointestinal upset. Thrombophlebitis can occur at IV infusion sites; ensure slow infusion and site monitoring. A disulfiram-like reaction (flushing, palpitations, nausea, vomiting, headache) may occur if alcohol is consumed with certain cephalosporins (e.g., cefotetan, cefmetazole). This is due to inhibition of aldehyde dehydrogenase.
Adverse reactions: Potential for CDAD. Increased bleeding risk due to interference with vitamin K metabolism (especially cefotetan) and/or platelet function. Anaphylaxis in patients with penicillin allergy (cross-reactivity occurs in a small percentage of patients, particularly with 1st and 2nd generation cephalosporins).
Nursing considerations: Infuse IV cephalosporins slowly over the recommended time (e.g., 30-60 minutes) to minimize vein irritation. Monitor INR/PT/PTT and assess for signs of bleeding. Frequently monitor renal function (BUN, creatinine). Advise patients to strictly avoid alcohol during and for several days after completing therapy with certain cephalosporins.
Monobactams – Aztreonam
Mechanism of Action: A unique beta-lactam isolated from a bacterium, aztreonam selectively binds to PBPs primarily in Gram-negative bacteria. It has a narrow spectrum against Gram-negative aerobic bacteria, including Pseudomonas aeruginosa, but no significant activity against Gram-positive bacteria or anaerobes. It is generally well-tolerated and can be used in patients with severe penicillin allergies because its monocyclic beta-lactam ring structure differs significantly from other beta-lactams, making true cross-reactivity rare.
Routes: Administered IV or IM for systemic infections. An inhaled formulation is available for cystic fibrosis patients to manage Pseudomonas aeruginosa lung infections.
Side effects: For inhaled administration, common side effects include wheezing, cough, and nasopharyngeal irritation. IV site pain and phlebitis are common with intravenous administration.
Nursing considerations: Due to potential for instability and incompatibility, aztreonam is often not compatible with many other IV drugs; a dedicated IV line or thorough flushing before and after administration is essential.
Carbapenems – Imipenem
Mechanism of Action: Carbapenems are broad-spectrum beta-lactam antibiotics highly resistant to most beta-lactamases. They inhibit cell wall synthesis by binding to PBPs, leading to bacterial lysis. Imipenem is often administered in combination with cilastatin (a dehydropeptidase inhibitor) to prevent its rapid enzymatic breakdown in the renal tubules, thereby increasing its urinary concentrations and reducing nephrotoxicity.
Routes: Administered only IV or IM as they are not absorbed orally. They are reserved for severe, resistant bacterial infections, often polymicrobial infections or those caused by extended-spectrum beta-lactamase (ESBL)-producing bacteria.
Adverse reactions: Can lower the seizure threshold, especially in patients with pre-existing CNS disorders, renal impairment, or high doses. Other adverse effects include gastrointestinal upset and thrombophlebitis at the IV site. Use with caution in patients with a history of penicillin allergy as there is a potential for cross-reactivity, though generally low.
Nursing considerations: Monitor liver function (AST, ALT, LDH, bilirubin), renal function (BUN, Cr) closely, and neurological status (for seizures). Dosage adjustment is crucial in renal impairment. Infuse slowly.
Glycopeptide – Vancomycin
Mechanism of Action: Vancomycin inhibits bacterial cell wall synthesis by binding to the D-Ala-D-Ala terminus of peptidoglycan precursors, preventing cross-linking. It is primarily bactericidal against Gram-positive bacteria.
Indications: The cornerstone treatment for methicillin-resistant Staphylococcus aureus (MRSA) infections, severe Gram-positive infections in penicillin-allergic patients, and oral form is specifically indicated for C. difficile–associated disease (CDAD) due to its poor oral absorption and high intraluminal concentration.
Adverse reactions:
Nephrotoxicity: Dose-dependent renal damage, particularly acute tubular necrosis. Close monitoring of BUN/Creatinine is essential, and dosage adjustments are necessary in renal impairment. Maintain vancomycin trough levels (the lowest drug concentration immediately before the next dose) between 10-20 ext{ } extmu ext{g/mL} (target range varies based on infection severity and site) to guide dosing and minimize toxicity while ensuring efficacy.
Ototoxicity: Can cause reversible or irreversible hearing loss (cochlear damage) and balance problems (vestibular damage), manifesting as tinnitus, vertigo, or hearing impairment. Risk increases with high doses, prolonged therapy, or concomitant use of other ototoxic drugs.
Red-Man Syndrome: A non-allergic, histamine-mediated reaction occurring with rapid intravenous infusion of vancomycin. Symptoms include diffuse flushing (especially of face, neck, and upper body), pruritus, urticaria, hypotension, and tachycardia. It is not a true allergic reaction but a rate-dependent infusion reaction.
Nursing considerations: To prevent Red-Man Syndrome, infuse vancomycin slowly over at least 60 minutes (or longer for larger doses, e.g., 15-20 ext{ mg/kg} over 90-120 ext{ minutes}), diluted in at least 250 ext{ mL} of appropriate solution (e.g., D5W, NS). Monitor IV site closely for phlebitis. Avoid concurrent use of other ototoxic drugs (e.g., aminoglycosides) and nephrotoxic drugs (e.g., NSAIDs, loop diuretics, other aminoglycosides) to reduce additive toxicity. Closely monitor fluid intake and output.
Protein Synthesis Inhibitors
Tetracyclines
Mechanism of Action: Broad-spectrum bacteriostatic antibiotics that inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit, preventing the attachment of transfer RNA (tRNA).
Adverse reactions:
Tooth discoloration & bone growth suppression: Tetracyclines chelate with calcium in developing bones and teeth, causing permanent grey, brown, or yellow discoloration of deciduous and permanent teeth, and potentially reversible inhibition of bone growth. Therefore, they are generally contraindicated in children under 8 years of age and in pregnant/lactating women.
Hepatotoxicity (rare): Dose-related, higher risk with IV administration in pregnant women or patients with pre-existing liver disease.
Photosensitivity: Increased sensitivity to sunlight, leading to exaggerated sunburn reactions. Advise strict sun protection.
Client teaching:
Oral administration: Take on an empty stomach (1 hour before or 2 hours after meals) with a full glass of water to ensure optimal absorption and prevent esophageal irritation. Avoid dairy products, antacids, and iron supplements within 2 hours of dose, as they can chelate with tetracyclines and significantly impair absorption.
Sun protection: Use broad-spectrum sunscreen (SPF ext{ } extge ext{ } 30) and protective clothing. Avoid prolonged sun exposure and tanning beds.
Storage: Store in a dark container as decomposition products of tetracyclines upon exposure to light and humidity can cause a Fanconi-like syndrome (a rare kidney disorder leading to impaired reabsorption in the renal tubules).
Contraception: Tetracyclines may reduce the effectiveness of oral contraceptives; advise using an alternative or backup method.
Macrolides – Erythromycin
Mechanism of Action: Bacteriostatic antibiotics that inhibit protein synthesis by binding to the 50S ribosomal subunit, blocking the exit tunnel for growing peptide chains.
Adverse reactions: Gastrointestinal upset (nausea, vomiting, abdominal pain) is common due to direct stimulation of motilin receptors. More seriously, macrolides (especially erythromycin) can cause QT prolongation on the electrocardiogram, increasing the risk of potentially fatal ventricular dysrhythmias like Torsades de Pointes. Ototoxicity (reversible hearing loss, tinnitus, vertigo) can also occur, particularly with high doses in patients with renal or hepatic impairment.
High interaction potential: Macrolides (especially erythromycin and clarithromycin) are potent inhibitors of the cytochrome P450 (CYP450) enzyme system, particularly CYP3A4. This can lead to significantly increased serum levels and subsequent toxicity of co-administered drugs that are metabolized by this pathway (e.g., warfarin, digoxin, theophylline, statins, cyclosporine, benzodiazepines). Close monitoring of serum drug levels for interacting drugs is crucial.
Client teaching: Take with food if GI upset occurs, however, absorption may be slightly reduced. Advise patients to report any palpitations, chest pain, or changes in auditory perception (tinnitus, decreased hearing).
Aminoglycosides – Gentamicin
Mechanism of Action: Bactericidal antibiotics that inhibit bacterial protein synthesis irreversibly by binding to the 30S ribosomal subunit, causing misreading of mRNA and premature termination of protein synthesis. They are effective against serious Gram-negative infections, including Pseudomonas aeruginosa.
Adverse reactions: Known for significant dose- and duration-dependent toxicities:
Ototoxicity: Irreversible damage to the 8th cranial nerve (vestibulocochlear nerve), leading to both vestibular (balance issues, vertigo, dizziness, ataxia) and cochlear (hearing loss, tinnitus) dysfunction. Risk factors include prolonged therapy, high doses, pre-existing renal impairment, and concurrent use of other ototoxic drugs (e.g., loop diuretics, vancomycin).
Nephrotoxicity: Reversible acute tubular necrosis (ATN) leading to impaired renal function. Manifestations include rising BUN and creatinine, and decreased urine output. Risk factors are similar to ototoxicity.
Monitoring:
Peak levels: Drawn 30 minutes after the completion of an IM or IV infusion. Used to ensure adequate drug concentration for efficacy. For gentamicin, a typical peak value might be around 5-10 ext{ } extmu ext{g/mL}. However, the primary focus for toxicity prevention is the trough.
Trough levels: Drawn approximately 1 hour before the next dose (for traditional multiple-daily dosing) or once approximately 30 minutes before the next dose (for extended interval dosing). Maintaining trough levels less than $2 ext{ } extmu ext{g/mL}$ (ideally < $1 ext{ } extmu ext{g/mL}$) is crucial to limit the accumulation of the drug and minimize the risk of ototoxicity and nephrotoxicity. Higher troughs correlate with increased toxicity risk.
Baseline and serial audiometry may be performed, especially in high-risk patients or those on prolonged therapy. Strict monitoring of fluid intake and output is also necessary to assess renal function.
DNA Replication / Cell-Division Inhibitors
Fluoroquinolones – Ciprofloxacin
Mechanism of Action: Bactericidal antibiotics that inhibit bacterial DNA gyrase and topoisomerase IV, essential enzymes for DNA replication, transcription, repair, and recombination. They have broad-spectrum activity against many Gram-positive and Gram-negative bacteria, including Pseudomonas aeruginosa.
Adverse reactions:
CNS stimulation: Can cause dizziness, headache, confusion, restlessness, and in severe cases, seizures due to GABA antagonism.
Achilles tendon rupture and tendinitis: This is a serious black box warning, with increased risk in patients over 60 years old, those on concomitant corticosteroid therapy, or kidney/heart/lung transplant recipients. Patients should report any tendon pain, swelling, or inflammation immediately.
Photosensitivity: Similar to tetracyclines, requiring sun protection.
Hepatotoxicity (rare): Monitor liver function tests.
QT prolongation: Risk of cardiac arrhythmias.
Peripheral neuropathy: Can lead to permanent nerve damage.
Client teaching:
Advise patients to report any tendon pain, swelling, or unusual sensations immediately and discontinue the drug.
Reduce caffeine intake as fluoroquinolones can inhibit caffeine metabolism, leading to increased caffeine effects (nervousness, insomnia).
Encourage liberal fluid intake (e.g., 1.5-2 ext{ L/day}) to prevent crystalluria.
Separate administration from antacids, iron supplements, calcium, magnesium, zinc, and dairy products by at least 2 hours after or 6 hours before the fluoroquinolone dose, as these polyvalent cations can chelate the drug and drastically reduce its absorption and efficacy.
Folic Acid Synthesis Inhibitors
Sulfonamides – Trimethoprim/Sulfamethoxazole (TMP-SMX)
Mechanism of Action: A synergistic combination of two bacteriostatic drugs that block sequential steps in bacterial folic acid synthesis, leading to a bactericidal effect when combined. Trimethoprim inhibits dihydrofolate reductase, and sulfamethoxazole inhibits dihydropteroate synthase.
Adverse reactions:
Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN): Severe, life-threatening mucocutaneous reactions characterized by widespread epidermal necrosis and detachment. Patients should be taught to report any skin rash, blistering, or mucosal lesions immediately.
Blood dyscrasias: Can cause agranulocytosis (severe reduction in neutrophils), aplastic anemia (bone marrow failure), and thrombocytopenia (low platelet count). Baseline and periodic complete blood counts (CBC) are important.
Crystalluria and renal damage: Sulfonamides can precipitate in the renal tubules, forming crystals and leading to kidney stone formation or acute kidney injury. Proper hydration is crucial to prevent this.
CDAD: Like many antibiotics, can disrupt normal gut flora leading to C. difficile infection.
Photosensitivity.
Client teaching:
Emphasize maintaining excellent hydration (e.g., extge 1,200-1,500 ext{ mL/day}) to prevent crystalluria.
Take with food and a full 8 oz glass of water to minimize GI upset and aid dissolution.
Avoid alcohol.
Sulfonamides may also reduce the effectiveness of oral contraceptives; advise backup contraception.
Urinary Tract Antiseptic – Nitrofurantoin
Mechanism of Action: A broad-spectrum nitrofuran derivative that undergoes reduction within bacterial cells, forming reactive intermediates that damage bacterial DNA, RNA, ribosomes, and other metabolic enzymes. It is primarily used for uncomplicated lower urinary tract infections (UTIs) as it concentrates in the urine.
Adverse reactions:
Acute and chronic pulmonary reactions: Acute reactions can occur within hours to days of starting treatment, presenting as dyspnea, cough, fever, chills, and chest pain, often resolving upon discontinuation. Chronic reactions (pulmonary fibrosis) are rare but serious, often occurring after months or years of therapy, resulting in irreversible lung damage.
Peripheral neuropathy: Can be severe and irreversible, characterized by numbness, tingling, or weakness. Higher risk in patients with renal impairment, diabetes, or prolonged use.
Hemolytic anemia in G6PD deficiency: Patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency are at risk of drug-induced hemolytic anemia, characterized by fatigue, pallor, and dark urine. Screening for G6PD deficiency may be considered in at-risk populations.
Benign brown urine discoloration: A common and harmless side effect that patients should be informed about.
Teeth staining (liquid formulation): Can stain teeth if not diluted or rinsed properly.
Client teaching:
Take with food or milk to enhance absorption and minimize GI upset (nausea, anorexia).
Do not crush or chew the tablets.
If using the liquid suspension, dilute it in milk or juice and then rinse the mouth thoroughly to prevent teeth staining.
Antimycobacterial (Anti-TB) Drugs
Isoniazid (INH)
Mechanism of Action: A prodrug that is activated by catalase-peroxidase enzyme (KatG) in Mycobacterium tuberculosis to its active form, which inhibits mycolic acid synthesis, an essential component of the mycobacterial cell wall. It is bactericidal against rapidly growing mycobacteria and bacteriostatic against dormant ones.
Adverse reactions:
Hepatotoxicity: The most serious adverse effect, ranging from asymptomatic elevation of AST/ALT to severe, life-threatening hepatitis, especially in elderly, alcoholic, or those with pre-existing liver disease. Patients should be taught to report symptoms of liver injury (e.g., jaundice, dark urine, pale stools, persistent nausea, fatigue, right upper quadrant pain) immediately.
Peripheral neuropathy: Common, dose-related, and reversible with pyridoxine (vitamin B₆) supplementation. It results from INH-induced pyridoxine deficiency. Symptoms include numbness, tingling, and burning pains, typically in the hands and feet.
CNS changes: Can cause dizziness, ataxia, seizures, psychosis, and memory impairment.
DRESS syndrome (Drug Reaction with Eosinophilia and Systemic Symptoms): A rare but severe hypersensitivity reaction involving rash, fever, lymphadenopathy, and multi-organ involvement.
Nursing considerations: Obtain baseline liver function tests (LFTs - AST, ALT, bilirubin) before starting therapy and monitor periodically, especially if symptoms of liver injury develop. Educate patients on the signs and symptoms of liver injury and peripheral neuropathy. To prevent neuropathy, co-administration of 50 ext{ mg} of vitamin B₆ (pyridoxine) daily is often prescribed.
Interactions: Alcohol increases the risk of hepatotoxicity. INH can increase serum levels of phenytoin, leading to toxicity. Antacids decrease INH absorption; separate administration by at least 1 hour.
Rifampin
Mechanism of Action: Inhibits bacterial DNA-dependent RNA polymerase, thereby suppressing RNA synthesis. It is bactericidal against Mycobacterium tuberculosis and a broad range of other bacteria.
Benign red-orange discoloration: A common and harmless side effect where urine, sweat, tears, and other body fluids may turn a reddish-orange color. Patients should be warned about this as it can permanently stain soft contact lenses and clothing.
Adverse reactions:
Hepatotoxicity: Similar to INH, can cause liver enzyme elevations and, rarely, severe hepatitis. Regular LFT monitoring is important.
DRESS syndrome.
Flu-like symptoms (fever, chills, muscle aches).
Drug interactions: Rifampin is a potent inducer of the cytochrome P450 (CYP450) enzyme system, particularly CYP3A4. This significantly accelerates the metabolism of many concurrently administered drugs, leading to decreased effectiveness of:
Oral contraceptives (OCPs): Advise women to use alternative non-hormonal birth control methods.
Warfarin: Requires frequent INR monitoring and potentially higher warfarin doses.
Antiretrovirals: Can significantly reduce concentrations of HIV medications.
Other drugs include digoxin, corticosteroids, oral hypoglycemics, and others.
Dosing: Administer orally on an empty stomach (1 hour before or 2 hours after meals) for optimal absorption. If GI upset is severe, it can be taken with food.
Nursing Process Framework
This framework guides the systematic delivery of patient care for individuals receiving anti-infective therapy:
Assessment:
Comprehensive allergy history: Document all known drug allergies, including specific reactions (e.g., rash, anaphylaxis) to prevent life-threatening adverse events.
Current vital signs: Establish baseline temperature, heart rate, blood pressure, and respiratory rate to monitor for signs of infection resolution or adverse reactions (e.g., fever reduction, hypotension from anaphylaxis).
Baseline laboratory values: Obtain baseline measurements of renal function (BUN, creatinine), hepatic function (AST, ALT, bilirubin), and complete blood count (CBC) to monitor for drug-induced organ dysfunction or blood dyscrasias.
Culture and sensitivity (C&S) results: Review to confirm the pathogen's identity and its susceptibility to the prescribed antibiotic, guiding targeted therapy and promoting stewardship.
Current medications: Identify all concurrent medications to assess for potential drug-drug interactions.
Patient history: Include immune status, co-morbidities (e.g., liver/kidney disease, G6PD deficiency), and pregnancy status.
Diagnosis/Analysis: Formulate nursing diagnoses based on assessment findings pertinent to anti-infective therapy, such as:
Knowledge Deficit related to new drug regimen (dose, timing, side effects) as evidenced by patient questions.
Risk for Non-Adherence related to complex medication schedule or unpleasant side effects.
Risk for Fluid Volume Deficit related to diarrhea (common side effect of many antibiotics/CDAD).
Risk for Injury related to potential adverse drug reactions (e.g., nephrotoxicity, hepatotoxicity, anaphylaxis, tendon rupture).
Risk for Superinfection related to alteration of normal flora.
Planning: Establish patient-centered, measurable, achievable, relevant, and time-bound (SMART) goals):
Resolution of infection: Patient will remain afebrile within 24-48 hours, and WBC count will normalize within 3-5 days.
Prevention/management of adverse effects: Patient will report any signs of allergic reaction or superinfection immediately; patient will maintain adequate hydration.
Adherence: Patient will verbalize understanding of accurate medication administration (dose, frequency, duration) and complete the full course of antibiotics.
Implementation: Carry out planned interventions:
Administer drug correctly: Follow prescribed route, dose, frequency, and infusion rates (e.g., slow infusion for vancomycin).
Monitor labs: Regularly review renal, hepatic, and hematologic parameters, and therapeutic drug levels (peak/trough) as indicated.
Client teaching: Educate on medication purpose, proper administration, common and serious side effects, importance of completion, drug-food/drug-drug interactions, and when to seek immediate medical attention.
Provide comfort measures for side effects (e.g., antiemetics for nausea, antidiarrheals if appropriate and not CDAD).
Evaluation: Continuously assess the effectiveness of the nursing interventions and the patient's response to therapy against the established goals:
Compare outcomes: Has the patient become afebrile? Has the WBC count decreased or normalized? Are signs and symptoms of infection resolving?
Any toxicity? Are laboratory values within acceptable ranges? Are there any new adverse effects?
Is the patient adhering to the medication regimen?
Adjust the care plan as needed based on the evaluation.
Dosage Calculation Practice
Example 1: High-Dose Amoxicillin
Weight conversion: For a 44 lb child, convert to kilograms: \frac{44 ext{ lb}}{2.2 ext{ lb/kg}} = 20 ext{ kg}.
Total daily dose ordered: The order is 20 ext{ mg/kg/day} divided every 12 hours.
Total daily dose: 20 ext{ mg/kg} imes 20 ext{ kg} = 400 ext{ mg/day}.Suspension concentration: The available suspension is 200 ext{ mg/5 mL}. To find mg/mL: \frac{200 ext{ mg}}{5 ext{ mL}} = 40 ext{ mg/mL}.
Total daily volume: To deliver 400 ext{ mg/day}, the volume needed is: \frac{400 ext{ mg}}{40 ext{ mg/mL}} = 10 ext{ mL/day}.
Volume per dose (q12h): Since the daily dose is divided every 12 hours (twice a day), each dose will be: \frac{10 ext{ mL}}{2} = 5 ext{ mL} per dose.
Example 2: Lower-Dose Amoxicillin
Order: 10 ext{ mg/kg} every 12 hours.
Dose calculation for a 20 kg child: 10 ext{ mg/kg} imes 20 ext{ kg} = 200 ext{ mg} per dose.
Volume per dose using a 200 ext{ mg/5 mL} suspension (which is 40 ext{ mg/mL}): \frac{200 ext{ mg}}{40 ext{ mg/mL}} = 5 ext{ mL} per dose.
IV Administration Rate Calculation
Order: Ampicillin 500 ext{ mg} in 50 ext{ mL} D5W to be infused over 30 ext{ min} (0.5 ext{ hr}).
Pump setting (mL/hr): To calculate the infusion rate, divide the total volume by the total time in hours.
ext{Rate} = rac{ ext{Volume (mL)}}{ ext{Time (hr)}} = rac{50 ext{ mL}}{0.5 ext{ hr}} = 100 ext{ mL/hr} (nearest whole number).
Antiinfective Fundamentals
Antiinfective Activity
Antiinfectives differ in spectrum and mechanism of action.
Selectivity: Drugs selectively target specific microbial components (e.g., unique enzymes, cell wall synthesis components) that are either absent or significantly different in human cells. This specificity allows for effective pathogen eradication with minimal host cell damage.
Bactericidal: These agents directly kill the microorganism by disrupting vital cellular processes, such as cell wall integrity (e.g., penicillins), cell membrane function, or DNA synthesis (e.g., fluoroquinolones). They are often preferred in immunocompromised patients or severe infections.
Bacteriostatic: These agents inhibit bacterial growth and reproduction, typically by interfering with protein synthesis (e.g., tetracyclines, macrolides) or folic acid metabolism. This allows the host's immune system to mount an effective defense and clear the infection. Their effectiveness relies on a competent host immune response.
Spectrum terminology
Narrow-spectrum: Effective against a limited group of specific organisms that possess the targeted metabolic pathway or structure. These are preferred when the pathogen is known, as they minimize disruption to the normal human microbiome and reduce the likelihood of resistance development.
Broad-spectrum: Effective against a wide range of bacterial types, including both Gram-positive and Gram-negative organisms. These agents are useful empirically when the causative pathogen is unknown, in polymicrobial infections, or in critically ill patients where delaying treatment could be detrimental. However, their use should be narrowed once culture and sensitivity (C&S) results are available.
Clinical significance: Initiating therapy with a broad-spectrum agent and then de-escalating to a narrow-spectrum agent once C&S results are known is a critical strategy in antimicrobial stewardship. This approach helps to minimize the selection pressure for resistant strains and reduces collateral damage to the patient's normal flora (e.g., gut microbiota), thereby lowering the risk of superinfections like Clostridioides difficile-associated disease (CDAD) or candidiasis.
Resistance
Definition: The natural or acquired capacity of microorganisms to survive exposure to an anti-infective agent that previously inhibited their growth or killed them. This phenomenon can render once-effective drugs useless, leading to treatment failures.
Biologic basis: Microorganisms evolve various mechanisms to evade antimicrobial action. Common mechanisms include:
Enzymatic inactivation: Production of enzymes (e.g., beta-lactamases) that degrade or modify the antibiotic structure.
Target site modification: Alterations in the drug's binding site on the bacterial cell, reducing or preventing its interaction.
Reduced permeability/efflux pumps: Decreased uptake of the drug or active pumping of the drug out of the bacterial cell before it can reach its target.
Bypassing metabolic pathways: Development of alternative metabolic routes that are not inhibited by the drug.
Prevention strategies
Treat only infections proved or strongly presumed to be bacterial via proper diagnostic testing (e.g., culture & sensitivity [C&S] testing, Gram stain results, rapid antigen tests).
Use the right drug (based on susceptibility data), at the right dose (to achieve microbicidal concentrations at the infection site), for the right duration (sufficient to eradicate the pathogen without promoting resistance). Under-dosing or premature discontinuation can foster resistance.
Avoid indiscriminate or prophylactic use of antibiotics, especially in viral infections. This practice selects for resistant strains within the microbial population, contributing to the global problem of antimicrobial resistance.
Implement infection control measures (e.g., hand hygiene, isolation precautions) to prevent the spread of resistant organisms.
General Nursing Considerations
Prior to first dose: Always obtain appropriate cultures (e.g., blood, urine, sputum, wound exudate) before initiating antibiotic therapy whenever possible. This ensures that the causative pathogen can be identified and its susceptibility to various antibiotics determined, guiding targeted therapy and promoting antibiotic stewardship.
Universal client teaching
Emphasize the importance of completing the full prescribed course of antibiotics, even if symptoms resolve earlier. Premature discontinuation can lead to relapse of infection and promote the development of antibiotic resistance by allowing partially suppressed, more resistant bacteria to proliferate.
Instruct patients to never share or use leftover antibiotics. Self-medication or inappropriate use contributes to resistance and potential adverse drug reactions.
Educate patients on common and expected side effects such as nausea ( ext{N}), vomiting ( ext{V}), diarrhea ( ext{D}), abdominal cramps, and rash. Advise managing gastrointestinal upset by taking medication with food if indicated (unless contraindicated for absorption) and maintaining hydration.
Adverse reactions that warrant immediate attention
Superinfections: These occur due to the disruption of normal microbial flora, allowing opportunistic pathogens to overgrow. Examples include oral/vaginal candidiasis (yeast infections) and Clostridioides difficile colitis (CDAD). Patients should report new onset of oral lesions, vaginal itching/discharge, or persistent watery diarrhea.
Anaphylaxis: A severe, life-threatening allergic reaction that can manifest rapidly. Key signs include laryngeal edema (difficulty breathing, stridor), generalized urticaria (hives), severe bronchospasm (wheezing, shortness of breath), angioedema (swelling of face, lips, tongue), and profound hypotension (dizziness, faintness). This requires immediate intervention.
Common Superinfections
Candidiasis
Overgrowth of Candida species (most commonly C. albicans) occurs when the normal bacterial flora, which keeps Candida in check, is suppressed by antibiotic therapy. It commonly manifests as oral thrush (white patches on tongue/buccal mucosa) or vulvovaginal yeast infection (itching, burning, thick white discharge). Immunocompromised individuals are at higher risk.
Clostridioides difficile–Associated Disease (CDAD)
CDAD, formerly known as Clostridium difficile, is caused by toxins produced by C. difficile bacteria when normal gut flora is disrupted, often by broad-spectrum antibiotics (e.g., clindamycin, fluoroquinolones, cephalosporins). The toxins cause inflammation of the colon (colitis).
S/S: Varies from mild, watery diarrhea to severe, life-threatening pseudomembranous colitis with symptoms including persistent watery diarrhea (often foul-smelling), severe abdominal pain or distention, fever, anorexia, tachycardia, and in severe cases, hematochezia (bloody stools) or ileus.
Nursing priority: Implement contact precautions immediately to prevent spread. Obtain a stool assay for C. difficile toxin. Initiate or escalate treatment per hospital protocol, typically with oral vancomycin (first-line for severe cases) or fidaxomicin (alternative, often for recurrent cases). Metronidazole is sometimes used for mild cases. Adequate hydration and electrolyte management are crucial.
Anaphylaxis Management Algorithm
Establish airway: Assess for signs of airway obstruction (e.g., stridor, hoarseness, dysphagia). If compromised, prepare for intubation or cricothyrotomy.
100 % O₂ via non-rebreather: Administer high-flow oxygen to compensate for bronchoconstriction and improve tissue oxygenation.
STOP IV antibiotic: Immediately discontinue the suspected causative agent.
Rapid IV/IM epinephrine: Administer epinephrine (0.3-0.5 ext{ mg IM of 1 : 1,000 solution for adults; } 0.01 ext{ mg/kg IM up to } 0.3 ext{ mg for children}) in the vastus lateralis muscle (preferred over deltoid due to faster absorption). Epinephrine is the primary treatment as it has alpha-1 adrenergic effects (vasoconstriction, counteracting hypotension and angioedema) and beta-2 adrenergic effects (bronchodilation, relieving bronchospasm).
± diphenhydramine (25-50 ext{ mg IV/IM}): An H1 antihistamine that helps reduce urticaria, itching, and angioedema but does not address the life-threatening respiratory or cardiovascular symptoms.
Initiate large-bore IV for fluids: Administer intravenous crystalloids (e.g., normal saline) rapidly (e.g., 500-1000 ext{ mL bolus}) to counteract vasodilation and hypotension. Significant fluid shifts can occur in anaphylaxis.
Monitor VS q 5 min: Closely monitor blood pressure, heart rate, respiratory rate, and oxygen saturation. Prepare for advanced airway management (intubation equipment, tracheostomy tray) due to potential for rapid airway compromise.
Additional measures: Consider H2 antihistamines (e.g., ranitidine), corticosteroids (e.g., methylprednisolone) for prolonged symptoms or to prevent biphasic reactions, and inhaled bronchodilators (e.g., albuterol) for persistent bronchospasm.
Laboratory & Clinical Monitoring During Antibiotic Therapy
Drug levels: Obtain peak and trough levels for drugs with a narrow therapeutic index (e.g., aminoglycosides like gentamicin, vancomycin). Peak levels ensure adequate therapeutic concentration, while trough levels reflect drug clearance and are crucial for minimizing toxicity (e.g., nephrotoxicity).
Renal function: Monitor serum blood urea nitrogen (BUN = 5-25 ext{ mg/dL}) and creatinine (Cr = 0.3-1.4 ext{ mg/dL}). Elevated BUN and Cr indicate impaired renal clearance, which can lead to drug accumulation and increased risk of toxicity, especially for renally excreted antibiotics. Dosage adjustments may be necessary.
Hepatic function:
Aspartate aminotransferase (AST = 12-37 ext{ U/L}) and Alanine aminotransferase (ALT = 10-40 ext{ U/L}): Elevations indicate hepatocellular injury or inflammation. Many antibiotics are metabolized by the liver and can cause hepatotoxicity.
Albumin (3.4-5 ext{ g/dL}): A measure of the liver's synthetic function. Low levels can affect drug binding and distribution.
Bilirubin (0.2-1 ext{ mg/dL} total): Elevated levels (direct/indirect) can indicate impaired hepatic excretion or hemolysis, potentially exacerbated by some antibiotics.
Bleeding risk (especially with certain cephalosporins, e.g., cefotetan, and some penicillins): Monitor coagulation parameters:
Platelets (150,000-400,000 ext{ cells/} extmu ext{L}): Thrombocytopenia can occur due to drug-induced bone marrow suppression.
Prothrombin time (PT = 9.4-12.5 ext{ s}), International Normalized Ratio (INR = 0.9-1.1 for healthy individuals), and Activated Partial Thromboplastin Time (PTT = 25-37 ext{ s}): Prolongation indicates impaired clotting cascade. Some antibiotics (e.g., certain cephalosporins) can interfere with vitamin K synthesis or utilization, leading to coagulopathy and increased bleeding risk.
Antibiotics That Inhibit Cell-Wall Synthesis
Penicillins – Example: Amoxicillin
Mechanism of Action: Penicillins are beta-lactam antibiotics that inhibit bacterial cell wall synthesis by binding to penicillin-binding proteins (PBPs), leading to autolytic enzyme activation and bacterial cell lysis. They are bactericidal.
Administration: Can be administered orally, intramuscularly (IM), or intravenously (IV). For parenteral administration (IM/IV), patients should be observed for at least 30 minutes post-dose for immediate hypersensitivity reactions.
Client teaching
Oral forms: Advise taking with food to minimize gastrointestinal upset (nausea, diarrhea), though some specific penicillins (e.g., penicillin V) may have better absorption on an empty stomach. Always emphasize completing the entire prescribed course.
Report any signs of superinfections (e.g., watery/bloody diarrhea suggestive of CDAD, oral thrush, vaginal candidiasis) or allergic manifestations (e.g., rash, pruritus, wheezing, facial edema, shortness of breath, profound hypotension—these require immediate medical attention).
Penicillins, particularly certain types like amoxicillin, can decrease the efficacy of combined oral contraceptives (OCPs) by altering gut flora and enterohepatic recirculation of estrogen. Advise patients to use an alternative or backup method of contraception throughout the course of treatment and for 7 days after completion.
Cephalosporins – Prototype: Cephalexin (1st gen) + Generational Overview
Mechanism of Action: Also beta-lactam antibiotics, similar to penicillins, inhibiting cell wall synthesis. Categorized into generations based on their spectrum of activity and resistance to beta-lactamases.
Generational Overview:
1st generation: cefazolin (IV/IM), cephalexin (PO) — Primarily active against Gram-positive cocci (e.g., Staphylococcus and Streptococcus) and limited Gram-negative activity. Cefazolin is commonly used for surgical prophylaxis due to its good tissue penetration.
2nd generation: cefaclor (PO), cefotetan (IV), cefoxitin (IV), cefuroxime (IV/PO) — Increased activity against Gram-negative bacteria (e.g., Haemophilus influenzae, Neisseria spp.) compared to 1st gen, while retaining some Gram-positive activity. Cefotetan/cefoxitin have good anaerobic coverage.
3rd generation: ceftriaxone (IV/IM), cefotaxime (IV), ceftazidime (IV) — Exhibit significantly enhanced Gram-negative activity, including against some Enterobacteriaceae. Ceftriaxone and cefotaxime also cross the blood-brain barrier (BBB) effectively, making them valuable for treating severe infections like meningitis. Ceftazidime has activity against Pseudomonas aeruginosa.
4th generation: cefepime (IV) — Considered a broad-spectrum agent with enhanced activity against Gram-negative bacteria (including Pseudomonas aeruginosa) and good Gram-positive coverage. It also penetrates the BBB and is often reserved for serious nosocomial infections.
5th generation: ceftaroline (IV) — Unique in its activity against MRSA (methicillin-resistant Staphylococcus aureus) while retaining broad Gram-negative coverage (excluding Pseudomonas).
Side effects: Common side effects include gastrointestinal upset. Thrombophlebitis can occur at IV infusion sites; ensure slow infusion and site monitoring. A disulfiram-like reaction (flushing, palpitations, nausea, vomiting, headache) may occur if alcohol is consumed with certain cephalosporins (e.g., cefotetan, cefmetazole). This is due to inhibition of aldehyde dehydrogenase.
Adverse reactions: Potential for CDAD. Increased bleeding risk due to interference with vitamin K metabolism (especially cefotetan) and/or platelet function. Anaphylaxis in patients with penicillin allergy (cross-reactivity occurs in a small percentage of patients, particularly with 1st and 2nd generation cephalosporins).
Nursing considerations: Infuse IV cephalosporins slowly over the recommended time (e.g., 30-60 minutes) to minimize vein irritation. Monitor INR/PT/PTT and assess for signs of bleeding. Frequently monitor renal function (BUN, creatinine). Advise patients to strictly avoid alcohol during and for several days after completing therapy with certain cephalosporins.
Monobactams – Aztreonam
Mechanism of Action: A unique beta-lactam isolated from a bacterium, aztreonam selectively binds to PBPs primarily in Gram-negative bacteria. It has a narrow spectrum against Gram-negative aerobic bacteria, including Pseudomonas aeruginosa, but no significant activity against Gram-positive bacteria or anaerobes. It is generally well-tolerated and can be used in patients with severe penicillin allergies because its monocyclic beta-lactam ring structure differs significantly from other beta-lactams, making true cross-reactivity rare.
Routes: Administered IV or IM for systemic infections. An inhaled formulation is available for cystic fibrosis patients to manage Pseudomonas aeruginosa lung infections.
Side effects: For inhaled administration, common side effects include wheezing, cough, and nasopharyngeal irritation. IV site pain and phlebitis are common with intravenous administration.
Nursing considerations: Due to potential for instability and incompatibility, aztreonam is often not compatible with many other IV drugs; a dedicated IV line or thorough flushing before and after administration is essential.
Carbapenems – Imipenem
Mechanism of Action: Carbapenems are broad-spectrum beta-lactam antibiotics highly resistant to most beta-lactamases. They inhibit cell wall synthesis by binding to PBPs, leading to bacterial lysis. Imipenem is often administered in combination with cilastatin (a dehydropeptidase inhibitor) to prevent its rapid enzymatic breakdown in the renal tubules, thereby increasing its urinary concentrations and reducing nephrotoxicity.
Routes: Administered only IV or IM as they are not absorbed orally. They are reserved for severe, resistant bacterial infections, often polymicrobial infections or those caused by extended-spectrum beta-lactamase (ESBL)-producing bacteria.
Adverse reactions: Can lower the seizure threshold, especially in patients with pre-existing CNS disorders, renal impairment, or high doses. Other adverse effects include gastrointestinal upset and thrombophlebitis at the IV site. Use with caution in patients with a history of penicillin allergy as there is a potential for cross-reactivity, though generally low.
Nursing considerations: Monitor liver function (AST, ALT, LDH, bilirubin), renal function (BUN, Cr) closely, and neurological status (for seizures). Dosage adjustment is crucial in renal impairment. Infuse slowly.
Glycopeptide – Vancomycin
Mechanism of Action: Vancomycin inhibits bacterial cell wall synthesis by binding to the D-Ala-D-Ala terminus of peptidoglycan precursors, preventing cross-linking. It is primarily bactericidal against Gram-positive bacteria.
Indications: The cornerstone treatment for methicillin-resistant Staphylococcus aureus (MRSA) infections, severe Gram-positive infections in penicillin-allergic patients, and oral form is specifically indicated for C. difficile–associated disease (CDAD) due to its poor oral absorption and high intraluminal concentration.
Adverse reactions:
Nephrotoxicity: Dose-dependent renal damage, particularly acute tubular necrosis. Close monitoring of BUN/Creatinine is essential, and dosage adjustments are necessary in renal impairment. Maintain vancomycin trough levels (the lowest drug concentration immediately before the next dose) between 10-20 ext{ } extmu ext{g/mL} (target range varies based on infection severity and site) to guide dosing and minimize toxicity while ensuring efficacy.
Ototoxicity: Can cause reversible or irreversible hearing loss (cochlear damage) and balance problems (vestibular damage), manifesting as tinnitus, vertigo, or hearing impairment. Risk increases with high doses, prolonged therapy, or concomitant use of other ototoxic drugs.
Red-Man Syndrome: A non-allergic, histamine-mediated reaction occurring with rapid intravenous infusion of vancomycin. Symptoms include diffuse flushing (especially of face, neck, and upper body), pruritus, urticaria, hypotension, and tachycardia. It is not a true allergic reaction but a rate-dependent infusion reaction.
Nursing considerations: To prevent Red-Man Syndrome, infuse vancomycin slowly over at least 60 minutes (or longer for larger doses, e.g., 15-20 ext{ mg/kg} over 90-120 ext{ minutes}), diluted in at least 250 ext{ mL} of appropriate solution (e.g., D5W, NS). Monitor IV site closely for phlebitis. Avoid concurrent use of other ototoxic drugs (e.g., aminoglycosides) and nephrotoxic drugs (e.g., NSAIDs, loop diuretics, other aminoglycosides) to reduce additive toxicity. Closely monitor fluid intake and output.
Protein Synthesis Inhibitors
Tetracyclines
Mechanism of Action: Broad-spectrum bacteriostatic antibiotics that inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit, preventing the attachment of transfer RNA (tRNA).
Adverse reactions:
Tooth discoloration & bone growth suppression: Tetracyclines chelate with calcium in developing bones and teeth, causing permanent grey, brown, or yellow discoloration of deciduous and permanent teeth, and potentially reversible inhibition of bone growth. Therefore, they are generally contraindicated in children under 8 years of age and in pregnant/lactating women.
Hepatotoxicity (rare): Dose-related, higher risk with IV administration in pregnant women or patients with pre-existing liver disease.
Photosensitivity: Increased sensitivity to sunlight, leading to exaggerated sunburn reactions. Advise strict sun protection.
Client teaching:
Oral administration: Take on an empty stomach (1 hour before or 2 hours after meals) with a full glass of water to ensure optimal absorption and prevent esophageal irritation. Avoid dairy products, antacids, and iron supplements within 2 hours of dose, as they can chelate with tetracyclines and significantly impair absorption.
Sun protection: Use broad-spectrum sunscreen (SPF ext{ } extge ext{ } 30) and protective clothing. Avoid prolonged sun exposure and tanning beds.
Storage: Store in a dark container as decomposition products of tetracyclines upon exposure to light and humidity can cause a Fanconi-like syndrome (a rare kidney disorder leading to impaired reabsorption in the renal tubules).
Contraception: Tetracyclines may reduce the effectiveness of oral contraceptives; advise using an alternative or backup method.
Macrolides – Erythromycin
Mechanism of Action: Bacteriostatic antibiotics that inhibit protein synthesis by binding to the 50S ribosomal subunit, blocking the exit tunnel for growing peptide chains.
Adverse reactions: Gastrointestinal upset (nausea, vomiting, abdominal pain) is common due to direct stimulation of motilin receptors. More seriously, macrolides (especially erythromycin) can cause QT prolongation on the electrocardiogram, increasing the risk of potentially fatal ventricular dysrhythmias like Torsades de Pointes. Ototoxicity (reversible hearing loss, tinnitus, vertigo) can also occur, particularly with high doses in patients with renal or hepatic impairment.
High interaction potential: Macrolides (especially erythromycin and clarithromycin) are potent inhibitors of the cytochrome P450 (CYP450) enzyme system, particularly CYP3A4. This can lead to significantly increased serum levels and subsequent toxicity of co-administered drugs that are metabolized by this pathway (e.g., warfarin, digoxin, theophylline, statins, cyclosporine, benzodiazepines). Close monitoring of serum drug levels for interacting drugs is crucial.
Client teaching: Take with food if GI upset occurs, however, absorption may be slightly reduced. Advise patients to report any palpitations, chest pain, or changes in auditory perception (tinnitus, decreased hearing).
Aminoglycosides – Gentamicin
Mechanism of Action: Bactericidal antibiotics that inhibit bacterial protein synthesis irreversibly by binding to the 30S ribosomal subunit, causing misreading of mRNA and premature termination of protein synthesis. They are effective against serious Gram-negative infections, including Pseudomonas aeruginosa.
Adverse reactions: Known for significant dose- and duration-dependent toxicities:
Ototoxicity: Irreversible damage to the 8th cranial nerve (vestibulocochlear nerve), leading to both vestibular (balance issues, vertigo, dizziness, ataxia) and cochlear (hearing loss, tinnitus) dysfunction. Risk factors include prolonged therapy, high doses, pre-existing renal impairment, and concurrent use of other ototoxic drugs (e.g., loop diuretics, vancomycin).
Nephrotoxicity: Reversible acute tubular necrosis (ATN) leading to impaired renal function. Manifestations include rising BUN and creatinine, and decreased urine output. Risk factors are similar to ototoxicity.
Monitoring:
Peak levels: Drawn 30 minutes after the completion of an IM or IV infusion. Used to ensure adequate drug concentration for efficacy. For gentamicin, a typical peak value might be around 5-10 ext{ } extmu ext{g/mL}. However, the primary focus for toxicity prevention is the trough.
Trough levels: Drawn approximately 1 hour before the next dose (for traditional multiple-daily dosing) or once approximately 30 minutes before the next dose (for extended interval dosing). Maintaining trough levels less than $2 ext{ } extmu ext{g/mL}$ (ideally < $1 ext{ } extmu ext{g/mL}$) is crucial to limit the accumulation of the drug and minimize the risk of ototoxicity and nephrotoxicity. Higher troughs correlate with increased toxicity risk.
Baseline and serial audiometry may be performed, especially in high-risk patients or those on prolonged therapy. Strict monitoring of fluid intake and output is also necessary to assess renal function.
DNA Replication / Cell-Division Inhibitors
Fluoroquinolones – Ciprofloxacin
Mechanism of Action: Bactericidal antibiotics that inhibit bacterial DNA gyrase and topoisomerase IV, essential enzymes for DNA replication, transcription, repair, and recombination. They have broad-spectrum activity against many Gram-positive and Gram-negative bacteria, including Pseudomonas aeruginosa.
Adverse reactions:
CNS stimulation: Can cause dizziness, headache, confusion, restlessness, and in severe cases, seizures due to GABA antagonism.
Achilles tendon rupture and tendinitis: This is a serious black box warning, with increased risk in patients over 60 years old, those on concomitant corticosteroid therapy, or kidney/heart/lung transplant recipients. Patients should report any tendon pain, swelling, or inflammation immediately.
Photosensitivity: Similar to tetracyclines, requiring sun protection.
Hepatotoxicity (rare): Monitor liver function tests.
QT prolongation: Risk of cardiac arrhythmias.
Peripheral neuropathy: Can lead to permanent nerve damage.
Client teaching:
Advise patients to report any tendon pain, swelling, or unusual sensations immediately and discontinue the drug.
Reduce caffeine intake as fluoroquinolones can inhibit caffeine metabolism, leading to increased caffeine effects (nervousness, insomnia).
Encourage liberal fluid intake (e.g., 1.5-2 ext{ L/day}) to prevent crystalluria.
Separate administration from antacids, iron supplements, calcium, magnesium, zinc, and dairy products by at least 2 hours after or 6 hours before the fluoroquinolone dose, as these polyvalent cations can chelate the drug and drastically reduce its absorption and efficacy.
Folic Acid Synthesis Inhibitors
Sulfonamides – Trimethoprim/Sulfamethoxazole (TMP-SMX)
Mechanism of Action: A synergistic combination of two bacteriostatic drugs that block sequential steps in bacterial folic acid synthesis, leading to a bactericidal effect when combined. Trimethoprim inhibits dihydrofolate reductase, and sulfamethoxazole inhibits dihydropteroate synthase.
Adverse reactions:
Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN): Severe, life-threatening mucocutaneous reactions characterized by widespread epidermal necrosis and detachment. Patients should be taught to report any skin rash, blistering, or mucosal lesions immediately.
Blood dyscrasias: Can cause agranulocytosis (severe reduction in neutrophils), aplastic anemia (bone marrow failure), and thrombocytopenia (low platelet count). Baseline and periodic complete blood counts (CBC) are important.
Crystalluria and renal damage: Sulfonamides can precipitate in the renal tubules, forming crystals and leading to kidney stone formation or acute kidney injury. Proper hydration is crucial to prevent this.
CDAD: Like many antibiotics, can disrupt normal gut flora leading to C. difficile infection.
Photosensitivity.
Client teaching:
Emphasize maintaining excellent hydration (e.g., extge 1,200-1,500 ext{ mL/day}) to prevent crystalluria.
Take with food and a full 8 oz glass of water to minimize GI upset and aid dissolution.
Avoid alcohol.
Sulfonamides may also reduce the effectiveness of oral contraceptives; advise backup contraception.
Urinary Tract Antiseptic – Nitrofurantoin
Mechanism of Action: A broad-spectrum nitrofuran derivative that undergoes reduction within bacterial cells, forming reactive intermediates that damage bacterial DNA, RNA, ribosomes, and other metabolic enzymes. It is primarily used for uncomplicated lower urinary tract infections (UTIs) as it concentrates in the urine.
Adverse reactions:
Acute and chronic pulmonary reactions: Acute reactions can occur within hours to days of starting treatment, presenting as dyspnea, cough, fever, chills, and chest pain, often resolving upon discontinuation. Chronic reactions (pulmonary fibrosis) are rare but serious, often occurring after months or years of therapy, resulting in irreversible lung damage.
Peripheral neuropathy: Can be severe and irreversible, characterized by numbness, tingling, or weakness. Higher risk in patients with renal impairment, diabetes, or prolonged use.
Hemolytic anemia in G6PD deficiency: Patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency are at risk of drug-induced hemolytic anemia, characterized by fatigue, pallor, and dark urine. Screening for G6PD deficiency may be considered in at-risk populations.
Benign brown urine discoloration: A common and harmless side effect that patients should be informed about.
Teeth staining (liquid formulation): Can stain teeth if not diluted or rinsed properly.
Client teaching:
Take with food or milk to enhance absorption and minimize GI upset (nausea, anorexia).
Do not crush or chew the tablets.
If using the liquid suspension, dilute it in milk or juice and then rinse the mouth thoroughly to prevent teeth staining.
Antimycobacterial (Anti-TB) Drugs
Isoniazid (INH)
Mechanism of Action: A prodrug that is activated by catalase-peroxidase enzyme (KatG) in Mycobacterium tuberculosis to its active form, which inhibits mycolic acid synthesis, an essential component of the mycobacterial cell wall. It is bactericidal against rapidly growing mycobacteria and bacteriostatic against dormant ones.
Adverse reactions:
Hepatotoxicity: The most serious adverse effect, ranging from asymptomatic elevation of AST/ALT to severe, life-threatening hepatitis, especially in elderly, alcoholic, or those with pre-existing liver disease. Patients should be taught to report symptoms of liver injury (e.g., jaundice, dark urine, pale stools, persistent nausea, fatigue, right upper quadrant pain) immediately.
Peripheral neuropathy: Common, dose-related, and reversible with pyridoxine (vitamin B₆) supplementation. It results from INH-induced pyridoxine deficiency. Symptoms include numbness, tingling, and burning pains, typically in the hands and feet.
CNS changes: Can cause dizziness, ataxia, seizures, psychosis, and memory impairment.
DRESS syndrome (Drug Reaction with Eosinophilia and Systemic Symptoms): A rare but severe hypersensitivity reaction involving rash, fever, lymphadenopathy, and multi-organ involvement.
Nursing considerations: Obtain baseline liver function tests (LFTs - AST, ALT, bilirubin) before starting therapy and monitor periodically, especially if symptoms of liver injury develop. Educate patients on the signs and symptoms of liver injury and peripheral neuropathy. To prevent neuropathy, co-administration of 50 ext{ mg} of vitamin B₆ (pyridoxine) daily is often prescribed.
Interactions: Alcohol increases the risk of hepatotoxicity. INH can increase serum levels of phenytoin, leading to toxicity. Antacids decrease INH absorption; separate administration by at least 1 hour.
Rifampin
Mechanism of Action: Inhibits bacterial DNA-dependent RNA polymerase, thereby suppressing RNA synthesis. It is bactericidal against Mycobacterium tuberculosis and a broad range of other bacteria.
Benign red-orange discoloration: A common and harmless side effect where urine, sweat, tears, and other body fluids may turn a reddish-orange color. Patients should be warned about this as it can permanently stain soft contact lenses and clothing.
Adverse reactions:
Hepatotoxicity: Similar to INH, can cause liver enzyme elevations and, rarely, severe hepatitis. Regular LFT monitoring is important.
DRESS syndrome.
Flu-like symptoms (fever, chills, muscle aches).
Drug interactions: Rifampin is a potent inducer of the cytochrome P450 (CYP450) enzyme system, particularly CYP3A4. This significantly accelerates the metabolism of many concurrently administered drugs, leading to decreased effectiveness of:
Oral contraceptives (OCPs): Advise women to use alternative non-hormonal birth control methods.
Warfarin: Requires frequent INR monitoring and potentially higher warfarin doses.
Antiretrovirals: Can significantly reduce concentrations of HIV medications.
Other drugs include digoxin, corticosteroids, oral hypoglycemics, and others.
Dosing: Administer orally on an empty stomach (1 hour before or 2 hours after meals) for optimal absorption. If GI upset is severe, it can be taken with food.
Nursing Process Framework
This framework guides the systematic delivery of patient care for individuals receiving anti-infective therapy:
Assessment:
Comprehensive allergy history: Document all known drug allergies, including specific reactions (e.g., rash, anaphylaxis) to prevent life-threatening adverse events.
Current vital signs: Establish baseline temperature, heart rate, blood pressure, and respiratory rate to monitor for signs of infection resolution or adverse reactions (e.g., fever reduction, hypotension from anaphylaxis).
Baseline laboratory values: Obtain baseline measurements of renal function (BUN, creatinine), hepatic function (AST, ALT, bilirubin), and complete blood count (CBC) to monitor for drug-induced organ dysfunction or blood dyscrasias.
Culture and sensitivity (C&S) results: Review to confirm the pathogen's identity and its susceptibility to the prescribed antibiotic, guiding targeted therapy and promoting stewardship.
Current medications: Identify all concurrent medications to assess for potential drug-drug interactions.
Patient history: Include immune status, co-morbidities (e.g., liver/kidney disease, G6PD deficiency), and pregnancy status.
Diagnosis/Analysis: Formulate nursing diagnoses based on assessment findings pertinent to anti-infective therapy, such as:
Knowledge Deficit related to new drug regimen (dose, timing, side effects) as evidenced by patient questions.
Risk for Non-Adherence related to complex medication schedule or unpleasant side effects.
Risk for Fluid Volume Deficit related to diarrhea (common side effect of many antibiotics/CDAD).
Risk for Injury related to potential adverse drug reactions (e.g., nephrotoxicity, hepatotoxicity, anaphylaxis, tendon rupture).
Risk for Superinfection related to alteration of normal flora.
Planning: Establish patient-centered, measurable, achievable, relevant, and time-bound (SMART) goals):
Resolution of infection: Patient will remain afebrile within 24-48 hours, and WBC count will normalize within 3-5 days.
Prevention/management of adverse effects: Patient will report any signs of allergic reaction or superinfection immediately; patient will maintain adequate hydration.
Adherence: Patient will verbalize understanding of accurate medication administration (dose, frequency, duration) and complete the full course of antibiotics.
Implementation: Carry out planned interventions:
Administer drug correctly: Follow prescribed route, dose, frequency, and infusion rates (e.g., slow infusion for vancomycin).
Monitor labs: Regularly review renal, hepatic, and hematologic parameters, and therapeutic drug levels (peak/trough) as indicated.
Client teaching: Educate on medication purpose, proper administration, common and serious side effects, importance of completion, drug-food/drug-drug interactions, and when to seek immediate medical attention.
Provide comfort measures for side effects (e.g., antiemetics for nausea, antidiarrheals if appropriate and not CDAD).
Evaluation: Continuously assess the effectiveness of the nursing interventions and the patient's response to therapy against the established goals:
Compare outcomes: Has the patient become afebrile? Has the WBC count decreased or normalized? Are signs and symptoms of infection resolving?
Any toxicity? Are laboratory values within acceptable ranges? Are there any new adverse effects?
Is the patient adhering to the medication regimen?
Adjust the care plan as needed based on the evaluation.
Here is a mnemonic to help remember key considerations for Sulfonamide (TMP-SMX) drugs, based on their common adverse effects and patient teaching points: SULFA DRUGS: C.R.A.S.H.
- C - Crystalluria & Renal Damage: Reminds to hydrate well (\ge 1{,}200-1{,}500\,mL/day) and take with a full glass of water.
- R - Rash (Stevens-Johnson Syndrome): Emphasizes reporting any skin rash immediately.
- A - Agranulocytosis & Anemia (Blood Dyscrasias): Highlights the risk of severe blood disorders.
- S - Sun Sensitivity (Photosensitivity): Advises using sun protection.
- H - Hormonal Contraceptive Interference: Essential teaching point to use backup birth control.
Here is a mnemonic to help remember key considerations for Penicillin drugs (e.g., Amoxicillin):
PENCIL S.
P - Perfect Timing: Take as prescribed (e.g., with food for amoxicillin to reduce GI upset).
E - Emphasize Completion: Never stop taking the medication early, even if symptoms improve (to prevent resistance and relapse).
N - Nuisance Side Effects & New Infections: Watch for common GI upset (N/V/D); report new signs of Clostridioides difficile-associated disease (CDAD) or candidiasis (superinfections).
C - Contraception Caution: Penicillins can decrease the effectiveness of oral contraceptives; advise using a backup method.
I - Immediate Allergic Reactions: Observe for and immediately report signs of allergy (rash, hives, wheezing, facial edema, difficulty breathing).
L - Look for Improvements: Monitor for resolution of infection symptoms (e.g., fever reduction).
S - Share No More: Never share or use leftover antibiotics.
Drug Class / Example Drug | Mechanism of Action (MoA) | Key Indications / Spectrum | Important Adverse Effects / Nursing Considerations |
|---|---|---|---|
Penicillins (Amoxicillin) | Inhibit cell wall synthesis (Bactericidal) | Wide range of bacterial infections. | GI upset, Hypersensitivity/Anaphylaxis, Superinfections (CDAD, candidiasis), extdownarrow efficacy of oral contraceptives (OCPs). Monitor 30 min post-parenteral infusion. |
Cephalosporins | Inhibit cell wall synthesis (Bactericidal) | Broad spectrum; categorized by generation (↑ Gram-negative activity with higher generations). | Thrombophlebitis (IV), CDAD, Anaphylaxis (cross-reactivity with penicillin allergy). Infuse slowly, monitor renal function. |
Cefotetan (2nd Gen) | (as above) | Increased Gram (-) activity, some anaerobic coverage. | Disulfiram-like reaction with EtOH, Increased bleeding risk (interferes with Vit K; monitor INR/PT/PTT). |
Ceftriaxone (3rd Gen) | (as above) | Crosses BBB (useful for meningitis, severe infections). | |
Ceftazidime (3rd Gen) | (as above) | Activity against Pseudomonas aeruginosa. | |
Cefepime (4th Gen) | (as above) | Broadest spectrum; effective against Pseudomonas aeruginosa. | Generally reserved for serious nosocomial infections. |
Ceftaroline (5th Gen) | (as above) | Only cephalosporin active against MRSA. | |
Monobactams (Aztreonam) | Inhibit cell wall synthesis (Bactericidal) | Narrow spectrum, effective against Gram-negative aerobes only (incl. Pseudomonas). Generally safe in penicillin allergy. | Wheezing, nasopharyngeal irritation (inhaled); IV site pain/phlebitis. Often requires a dedicated IV line. |
Carbapenems (Imipenem) | Inhibit cell wall synthesis (Bactericidal) | Broadest spectrum, reserved for severe/resistant infections (e.g., ESBL-producing bacteria). | Can lower seizure threshold, thrombophlebitis. Caution in penicillin allergy & renal impairment. Monitor liver and renal function. |
Glycopeptide (Vancomycin) | Inhibits cell wall synthesis by binding D-Ala-D-Ala (Bactericidal against Gram-positive). | MRSA, severe Gram (+) infections, oral for CDAD. | Nephrotoxicity (monitor BUN/Cr, trough 10-20 ext{ } extmu ext{g/mL}), Ototoxicity, Red-Man Syndrome (with rapid IV infusion). Infuse ext{ extge 60 min}. Avoid concurrent oto-/nephrotoxic drugs. |
Tetracyclines | Inhibit protein synthesis (Bacteriostatic) by binding 30S ribosomal subunit. | Broad-spectrum. | Tooth discoloration & bone growth suppression (< 8 y, pregnancy), Hepatotoxicity, Photosensitivity. Take on empty stomach (avoid dairy/antacids/iron for 2 hr). Advise backup contraception. |
Macrolides (Erythromycin) | Inhibit protein synthesis (Bacteriostatic) by binding 50S ribosomal subunit. | GI upset, QT prolongation (risk of ventricular dysrhythmias), Ototoxicity. Potent CYP450 inhibitor (significant drug interactions, e.g., warfarin). Take with food if GI upset. | |
Aminoglycosides (Gentamicin) | Irreversibly inhibit protein synthesis (Bactericidal) by binding 30S ribosomal subunit. | Serious Gram-negative infections (including Pseudomonas). | Ototoxicity (irreversible 8th cranial nerve damage), Nephrotoxicity (reversible ATN). Monitor peak & trough levels (trough < 2 ext{ } extmu ext{g/mL} is critical to limit toxicity). Baseline/serial audiometry. |
Fluoroquinolones (Ciprofloxacin) | Inhibit DNA gyrase/topoisomerase IV (Bactericidal). | Broad-spectrum (including Pseudomonas). | CNS stimulation, Achilles tendon rupture (Black Box Warning; ↑ risk in > 60 y + steroids), Photosensitivity, Hepatotoxicity, QT prolongation, Peripheral neuropathy. Separate from antacids/minerals. |
Sulfonamides (Trimethoprim/Sulfamethoxazole) | Inhibit folic acid synthesis (Bactericidal when combined). | Wide range of bacterial infections. | Stevens-Johnson Syndrome (SJS), Blood dyscrasias (agranulocytosis, aplastic anemia), Crystalluria (renal damage), CDAD. Ensure hydration ( ext{ extge 1,200-1,500 mL/day}). Advise backup contraception. |
Urinary Tract Antiseptic (Nitrofurantoin) | Damages bacterial DNA/RNA/ribosomes (concentrates in urine). | Uncomplicated lower Urinary Tract Infections (UTIs). | Acute/chronic Pulmonary reactions (fibrosis), Peripheral neuropathy, Hemolytic anemia in G6PD deficiency. Benign brown urine. Take with food/milk, DO NOT crush. |
Antimycobacterial (Isoniazid - INH) | Inhibits mycolic acid synthesis. | Tuberculosis (TB). | Hepatotoxicity (monitor LFTs), Peripheral neuropathy (due to pyridoxine deficiency, often given Vit B6). Avoid alcohol due to ↑ liver risk. |
Antimycobacterial (Rifampin) | Inhibits bacterial DNA-dependent RNA polymerase. | Tuberculosis (TB). | Benign red-orange discoloration of urine/sweat/tears (can stain contacts). Hepatotoxicity. Potent CYP450 Inducer (decreases effectiveness of many drugs like OCPs, warfarin). Take PO on empty stomach. |
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