HEENT Flashcards
Acute rhinosinusitis (ARS)
Definition
Inflammation of the mucosal lining of nasal passages and paranasal sinuses, lasting up to 4 weeks, caused by allergens, environmental irritants, and/or infection (viruses [majority], bacteria, and fungi [rare])
- Allergies and viral are most common causes
- Avoid antibiotics unless you know micro; you must know the causative bug as to choose the right drug
Acute bacterial rhinosinusitis (RBRS)
Secondary bacterial infection of paranasal sinuses, usually following viral URI; relatively uncommon in adult stand children
<2% of viral URIs are complicated by ABRS. In the majority, ABRS will resolve without antimicrobial therapy *may resolve spontaneously; abx rarely needed
Maxillary and frontal sinuses are most affected; fluid is trapped inside the sinuses → 2º bacterial (S. pneumoniae, H. influenzae)” or viral infection
- hx of a “bad cold” or flare-up of allergic rhinitis
Principles of Empiric Antimicrobial Therapy
- Definition
- Questions to as prior to choosing an antimicrobial
- Applicable to choice of intervention in all infectious diseases to direct antimicrobial therapy, optimize treatment success and minimize development of resistant pathogens
The decision-making process in which the clinician chooses the agent based on patient characteristics and site of infection
- What is/are the most likely pathogen(s) causing this infection?
- What is the spectrum of a given antimicrobial’s activity?
- What is the likelihood of a resistant pathogen?
- What is the danger if there is treatment failure?
- What is the optimal safe antimicrobial dose?
- What is the duration of the shortest but effective course of therapy?
Streptococcus Pneumoniae
1. Diseases caused by S. Pneumoniae
2. Description
3. Resistance
- COMPS
+CAPS, ABRS (#1 cause of ABRS)
Conjunctivitis
Otitis media
Meningitis
Pneumonia
Sinusitis - 100 strains
Gram+ diplococci
#1 adult ABRS causative organism - > /= 25% drug-resistant (DRSP) via altered protein-binding sites that limit certain antibiotic’s ability to bind to the pathogen
Haemophilus Influenzae
1. Diseases caused by H. influenzae
2. Description
3. Resistance
- COMPS
+CAPS, ABRS
Conjunctivitis
Otitis media
Meningitis
Pneumonia
Sinusitis - Gram- bacillus
#2 adult ABRS causative organism - > /= 30% penicillin-resistant via production of beta-lactamase that breaks up beta-lactam ring in most penicillins including amoxicillin, ampicillin. Most cephalosporins are stable in the presence of beta-lactamase
Moraxella Catarrhalis
1. Diseases caused by M. Catarrhalis
2. Description
3. Resistance
- Less common pathogen in ABRS, AOM, uncommon cause of CAP
- Gram- coccus
#3 adult ABRS causative organism - > /= 90% pencillin-resistant via beta-lactamase production
Transillumination
Turn off the light (darkened room)
Place a bright light source directly on the surface of the cheek (on maxillary sinus). Instruct patient to open mouth and look at the roof of the mouth (hard palate) for a round glow of light). Compare both sides.
The “affected” sinus has no glow or duller glow compared with the normal sinus. For frontal sinusitis, place the light under the supraorbital ridge at the medial aspect and compare glow of light
ABRS
- Clinical presentation
- When treating, consider resistant presence:
URI-like signs and symptoms, either:
- Persistent and not improving >/= 10 days
- Severe (Fever >/=102º F, >39ºC, purulent nasal discharge, facial pain, >/= 3-4 days)
- Worsening, or “doubling-sickening” (initial improvement URI-like sx, then worsening with fever, headache, nasal discharge, usually p 5-6 days of illness)
- Posterior pharynx: purulent dark-yellow to green postnasal drip
- Sinuses: tender to palpation on the front cheek (maxillar) or on frontal sinus area above inner canthus of the eye
- If seen with allergy flare-up, possible swollen (boggy) nasal turbinates
- Fever seen more often in children than adults
- Transillumination (frontal and maxillary sinuses): POSITIVE (“glow” of light on infected sinus is duller than normal sinus)
If no risk for resistance → Initiate first-line antimicrobial therapy
If yes risk for resistance → Initiated second-line antimicrobial therapy
If improved after 3-5 days → Complete 5-7 days of antimicrobial therapy
If worsening or no improvement in 3-5 days → Broaden coverage or switch to different antimicrobial class, if continues to worsening or no improvement in 3-5 days → Refer to specialist; CT/MRI to investigate noninfectious causes or suppurative complications +/- sinus/meatal cultures for pathogen-specific therapy
cacosmia
Bad odor in nose
ABRS
Treatment Options: mild vs severe case
If mild, uncomplicated in healthy patient → symptomatic treatment without abx
- Oral fluids
- Saline nasal irrigation PRN
- Follow up in 10 days (if better, no abx needed)
- If sx worsens or have not resolved on follow-up → initiate abx
If severe symptoms (toxic, high fever, pain, purulent nasal or post nasal drip for >/=2-3 days, maxillary toothache, unilateral facial pain, sense of bad odor in nose (cacosmia), initial symptom improved, then worsening of symptoms), immunocompromised, or symptoms persist > 10 days (or have worsened) → Initiate abx
Most cases of adult ABRS are viral; only 0.5-2% of cases are bacterial
ABRS
Antibiotic Treatment
1. First-line therapy
2. If allergy or alternative antibiotics
3. What if treatment failed with above interventions?
- Amoxicillin-clavulanate (Augmentin) 1,000/62.5 mg or 2,000 mg/125 mg one table PO BID x 5-7 days
- If PCN allergy or alternatives:
- Type 1 allergy (e.g., anaphylaxis, angioedema) → Levofloxacin 750 mg PO daily or doxycycline BID x 5-7 days
- Type 2 allergy (e.g., skin rash) → Cefdinir (Omnicef), cefpodoxime (Vantin), cefuroxime (Ceftin) PO BID x 5-7 days - If symptoms persist despite treatment (purulent nasal discharge, sinus pain, nasal congestion, fever), switch to another abx.
- If on amoxicillin → amoxicillin-clavulanate (Augmentin PO Q12H x 10-14 days OR levofloxacin (Levaquin) 750 mg daily
- If current sinusitis → Refer to otolaryngologist
- Nasal irrigation may help use only sterile water (not tap water) with saline packet
ABRS
Risk for antibiotic resistance
Most common:
<2 or >65, daycare attend
Prior systemic antibiotics with the past month
Less common risks:
Hospitalization within p 5 days
Comorbidities (DM, COPD)
Immunocompromised
ABRS
Symptomatic or Adjunct Treatment (Rhinosinusistis or Oritis Media)
1. Pain or fever
2. Drainage
3. Cough
- Naproxen sodium (Anaprox DS) PO BID or ibuprofen (Advil) PO QID PRN
- Acetaminophen (Tylenol) Q4-6 hours PRN
- Naproxen sodium (Anaprox DS) PO BID or ibuprofen (Advil) PO QID PRN
- Increase oral fluids will thin mucus
- Oral decongestants such as pseudoephedrine (Sudafed) or pseudoephedrine combined with guaifenesin (Mucinex D)
- Topical decongestants (i.e., afrin): use only for 3 days max or will cause rebound
- Saline nasal spray (Ocean spray) 1-2 x Q2-3 hrs PRN
- Steroid nasal spray (Flonase, Vancenase) if allergic rhinitis
- Mucolytic (guaifenesin) and ↑ fluid to thin mucus
- Increase oral fluids will thin mucus
- Dextromethorphan (Robitussin) QID
- Benzonatate (Tessalon Perles) prescription: Swallow with water; do not crush, suck, or chew; toxic for children <10 years (seizures, cardiac arrest, death)
- ↑ fluid intake
- avoid exposure to cigarette smoke and alcohol
- Systemic steroids are not recommended
- Dextromethorphan (Robitussin) QID
ABRS
Symptomatic treatment in ABRS (nonpharmaceutical management)
- Saline nasal irrigations
- Intranasal corticosteroids when ABRS is accompanied by allergic rhinitis
Directions:
With sterile saline (do not use tap water, some have bacteria → abscess)
1. Spare opposite nare with opposite hand; if same side, will spray directly on septum → increases risk for epitaxis
2. Keep your nose over your toes → extra drainage out (↓ SE)
True or false:
The US FDA advises that the adverse effects associated with fluoroquinolones (cip-, levo-, moxifloxacin[-floxacin suffix] generally outweigh the benefits for patients with acute sinusitis, acute bronchitis, and uncomplicated urinary tract infections who have other treatment options.
True.
Deviation from guideline. Avoid using fluoroquinolones untill last choice.
Possible adverse effects:
- Spontaneous tendon rupture
- Aortic aneurism/dissection
- Tendonitis
Which antibiotic is not effective in ABRS?
Macrolides (-mycins)
Ex:
- azithromycin
- clarithromycin
- erythromycin
- TMP-SMX (bactrim)
These are not recommended in ABRS treatment due to rising resistance rates
ABRS
1. Initial/first-line empiric therapy + second-line
- Amoxicillin-clavulanate 500 mg/125 mg PO TID, or l875 mg/125 mg PO BID for 5-7 days
- Will miss DRSP
- High dose (HD, 3-4 g/d) amoxicillin needed against DRSP.
- Clavulanate, as a beta-lactamase inhibitor, allows amoxicillin to have activity against beta-lactamase-producing organisms, such as H. influenzae, M. catarrhalis
- Coverage: +/- and beta-lactamase - Amoxicillin-clavulanate 2000 mg/125 mg PO BID for 7-10 days
- Gives coverage to DRSP
OR
Doxycycline 100 mg PO BID or 200 mg PO daily
- If allergic to amoxicillin, miss DRSP
- DO NOT give to pregnant or lactating, photosensitizing (2º burns)
- 0 < 8 - graying of teeth
- Doxycycline: effective against non-resistant S. Pneumoniae. DRSP treatment failure risk, activity against Gram- organisms.
- Stable in presence of beta-lactamase.
- Doxycycline: Pregnancy risk category D
ABRS
- If beta-lactam allergy
Allergy to antimicrobials with beta-lactam ring, such as penicillins, cephalosporins
- But does carry a lot of risks, FDA says do not use fluoroquinolones, but can bring DRSP
- Doxycycline 100 mg PO BID or 200 mg PO daily
OR - Levofloxacin 500 mg PO daily
OR - Moxifloxacin 400 mg PO daily
*Respiratory fluoroquinolones (FQ): activity against DRSP, Gram- organisms, stable in presence of beta-lactamase
Major rationale for use of respiratory FQ is the presence of DRSP risk. See FDA advisory on limiting FQ use.
ABRS
- Treatment for antibiotic resistance or failed initial therapy
- Amoxicillin-clavulanate 2000 mg/125 mg PO BID
OR - Levofloxacin 500 mg PO daily
OR - Moxifloxacin 400 mg PO daily
All options with activity against DRSP, Gram- organisms, stable in presence of and/or active against beta-lactamase
Otitis Media and Rhinosinusitis: Serious Complications
Refer all to ED STAT!
- Mastoiditis: red and swollen mastoid that is tender to palpation
- Preorbital or orbital cellulitis (more common in children: Swelling and redness at periorbital area, double vision or impaired vision, and fever. Abnormal EOMA (extraorbital muscles) movements of affected orbit (check CNs, EOM). Altered LOC or mental status change
- Meningitis: Acute onset of high fever, stiff neck, severe headache, photophobia, toxicity. Positive Brudzinski or Kernig sign
- Cavernous sinus thrombosis: Patient c/o acute onset of severe headache inferring with sleep, abnormal neurologic exam, confusion, febrility. Life-threatening emergency with high mortality!
What is a substrate?
A medication or substance that is metabolized/biotransformed by the isoenzyme, utilizing this enzyme in order to be modified so it can reach drug sit of action and/or be eliminated
- Cannot be broken down if with an inhibitor to be cleared
Clinical example:
CYP450 3A4 substrate examples:
Sildenafil (Viagra)
atorvastatin
Simvastatin
Alprazolam (Xanax)
About 50% of all prescription medications are CYP450 3A4 substrates.
Other commonly utilized CYP450 0isoenyzmes include 1A2, 2D6, 2C9, 2C19, 299.
**3A4 - Most important for interaction
What is an inhibitor?
A drug or other substance that blocks the activity of the isoenzyme, limiting substrate excretion, allowing increase in substrate levels, with possible risk of substrate-induced toxicity
CYP450 3A4 = erythro-, clarithromycin
Concomitant use of one of these antibiotics with any of the aforementioned CYP450 3A4 substrates results in an increase in substrate levels.
Clarithromycin + simvastatin = statin-induced rhabdomyolysis risk
Clarithromycin + alprazolam = increased sedation, fall risk
Drug-drug Interactions
- Why is this important?
- What areas are high-risk for drug interactions to happen?
- Knowledge of the most common drug-drug interactions is critical to certification and clinical practice success. Drug-drug interactions are the 2nd most common cause of why NPs getting sued (think coumadin with many drug-drug interactions)
- Liver (most serious consequence of interaction; protein binding fighting for site)
- Kidney
- Blood
What is an inducer?
Accelerates the activity of the isoenzyme so that the substrate is pushed out the exit pathway, leading to a reduction in substrate level; will spit out substrate faster
Example: St. John’s worth = CYP450 3A4 inducer
Concomitant use of St. John’s wort and 3A4 substrate can lead to reduced target drug levels and diminished therapeutic effect, possible treatment failure
Example: St. John’s wort + COC use = Off-loading of estrogen/progestin, leads to excessive spotting, potential contraceptive failure