Infection Flashcards

1
Q

Why you want CT with contrast?

A

The contrast will enhance visibility and provide additional diagnostic information for the soft tissue.

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2
Q

How is the contrast works?

A

“CT contrast contains iodine, which absorbs X-rays and enhances tissue density differences, improving visualization of inflamed tissues, abscesses, and vascular structures

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3
Q

What is rim enhancement?

A

It refers to a specific pattern of contrast enhancement in which the outer margin of the lesion appears more intensely enhanced than its central portion.

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4
Q

What kind of bacterial Eikenella corrodens ?

A

Gram-negative facultative anaerobic bacterium that can cause infective endocarditis, a serious infection of the heart valves.

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5
Q

What do you know about necrotizing faciitis, who tends to get it, what are common causative organisms?

A
  • It is a rapidly progressive, very destructive infectious process that spreads along superficial fascial planes, causing thrombosis with compromise of the subdermal blood supply, resulting in necrosis and loss of large areas of the skin.
  • It is generally seen in immunocompromised (e.g. diabetic, malnourished, alcoholic, or cancer) patients and has a high mortality rate (7-30%) due to rapid extension into critical areas like the mediastinum.
  • A facultative gram-positive hemolytic streptococcus can be the sole causative organism, but most infections involve synergistic mixed aerobic and anaerobic pathogens including: streptococcus pyogenes, Staphylococcus aureus (MRSA) clostridial, gas-producing bacterium, Klebsiella pneumonia
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6
Q

What is the Path of Third Molar Infection to Mediastinum?

A

Third molar infection spreads from a periapical abscess through the lingual cortical plate into the submandibular space. It then travels via the buccopharyngeal gap or around the posterior belly of the digastric muscle to the lateral pharyngeal space, which has no barrier to the retropharyngeal space. The retropharyngeal space fuses with the alar fascia between C6 and T4, where the infection can enter the danger space, which directly communicates with the posterior mediastinum

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7
Q

What are the Principles of Management of Odontogenic Infections

A
  • Determine severity: anatomic location, rate of progression, and airway compromise.
  • Evaluate host factors: evaluate immunocompetence and systemic reserve of the patient.
  • Decide on setting: inpatient criteria – fever, dehydration, need for general anesthesia, deep space infection, or control of systemic disease.
  • Treat surgically.
  • Support medically
  • Choose and administer the appropriate antibiotic.
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8
Q

Should blood cultures ideally be taken before or after initiation of antibiotic therapy and why?

A

Before antibiotics, because the causative organisms may not grow out and be identified in the presence of antibiotics in the bloodstream.

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9
Q

You prep the skin and obtain an aspirate of pus easily in the ER while you are awaiting results of other labs. What do you want to send it for?

A

Gram stain, aerobic & anaerobic, fungal cultures with antibiotic sensitivities for isolated organisms.

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10
Q

What is gram stain?

A

A gram stain is a rapid test to aid in categorizing involved microorganisms into four broad groups:
gram positive cocci
gram positive rods
gram negative cocci
gram negative rods.

This aids in tailoring early antibiotic therapy. It involves process of staining, decolorizing, and counterstaining the microorganism to detect a peptidoglycan in the cell wall found in gram positive bacteria.

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11
Q

What is Ludwig angina?

A

Rapidly progressing cellulitis that may not have yet formed abscesses. This infection involves the bilateral submental, sublingual, and submandibular spaces. Angina refers to the respiratory distress associated with airway obstruction.

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12
Q

Are you going to start this patient on empiric antibiotics? If so, which one(s) and at what dosing regimen? Why?

A

Yes. Unasyn 3gm IVPB q6h. This patient appears very sick. Unasyn will cover some of the potential B-lactamase producing organisms that would be resistant to the usual first line Penicillin. It will also cover E coli, Klebsiella, Bacteroides, and Enterobacter.

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13
Q

What clinical or laboratory parameters would be monitored to evaluate for signs of improvement or deterioration?

A

Swelling, induration, erythema, temperature, heart rate, WBC count, culture & sensitivity results, CT scan to re-evaluate for untreated loculations if no improvement or deterioration.

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14
Q

What are the extubation criteria?

A
  • Stable Vitals
  • Positive Air leak test
  • Acceptable vent readings: Vital capacity >15 mm/kg, Minute Ventilation of 6-10L/min Inspiratory pressures of >25 cm H2O
  • Normal ABG
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15
Q

Zosyn

A

(Piperacillin/Tazobactam): A beta-lactam antibiotic with broad-spectrum activity, including Gram-negative bacteria and anaerobes.

For polymicrobial infections or suspected Pseudomonas, klebsiella infections, Zosyn is preferred.

Adults:
Dose: 3.375 g IV every 6 hours

Pediatrics:
Dose: 80 mg/kg/dose IV every 6–8 hours

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16
Q

Vancomycin

A

A glycopeptide antibiotic effective against Gram-positive bacteria, including MRSA, but with no activity against Gram-negative or anaerobic organisms.

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17
Q

Fluoroquinolones

A

Bactericidal agents that inhibit bacterial enzymes (DNA gyrase) involved in DNA replication.

  • Levofloxacin (Levaquin®) 500 mg P.O. q24 hours
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18
Q

Labs

A
  • The normal lactate level in blood is: 0.5 to 2.2 mmol/L (or 4.5 to 19.8 mg/dL).
    Elevated levels may indicate tissue hypoxia, sepsis, or other metabolic conditions.

Procalcitonin (PCT):
Procalcitonin is a biomarker used to assess bacterial infections and sepsis.
Normal Levels:
- <0.05 ng/mL: Normal, no significant infection

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19
Q

What intubation criteria?

A
  • Sever hypoxia
  • Inadequate ventilation
  • Airway protection
  • Alter mental status
  • Cardiopulmonary arrest
  • Inability to protect the airway
  • Progressive respiratory distress
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20
Q

What is C Dif ?

A
  • C. difficile bacterial that produces toxins A and B that cause disorganization of actin microfilaments and cause alteration of normal flora of large intestine.
  • Tx: Stope abx, give fluids , metronidazole 500mg q8h or oral vancomycin 125mg q6h for 14 days. In recurrent cases we give Fidaxomicin (200 mg PO BID)
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21
Q

What is C reactive protein?

A

C-reactive protein (CRP) is a substance produced by the liver in the acute phase in response to inflammation.

  • Why you need it ?
  • Its an inflammatory marker, it elevated in setting of early detection infection and can be used to monitor disease progression.
  • Normal less than 1 mg/dL.
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22
Q

What is The Minimum Inhibitory Concentration (MIC) ?

A

lowest concentration of the antibiotic that inhibits visible growth of a microorganism after overnight incubation.

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23
Q

Beta Lactams

A
  • Beta Lactams: Bactericidal
  • Amoxicillin, Ancef, ceftriaxone and Meropenem: beta-lactam antibiotics, inhibit penicillin-binding proteins, which disrupt cell wall synthesis.
  • Beta-lactamase inhibitors: bind to the catalytic site of beta-lactamases to prevent hydrolysis of the beta-lactam.

Ex:
- Unasyn® (ampicillin and sulbactam)

  • Zosyn® (piperacillin and tazobactam)
  • Augmentin® (amoxicillin and clavulanate).
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24
Q

Macrolides

A
  • Macrolides: Bacteriostatic
  • Clindamycin, erythromycin, clarithromycin, and azithromycin.
  • MOA: Binds to the 50S ribosomal subunit and inhibits bacterial protein synthesis.
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25
Q

Fluoroquinolones

A
  • Ciprofloxacin, levofloxacin.
  • Fourth-generation fluoroquinolones have gram-positive and anaerobic coverage
  • MOA: Bactericidal agents that inhibit bacterial enzymes (DNA gyrase which are involved in DNA replication.
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26
Q

Glycopeptide antibiotics

A

Glycopeptide antibiotics:
- MOA:
- Vancomycin is Glycopeptide abx treat Gm+ bacterial works by binding to the peptidoglycan to inhibit the synthesis of bacterial cell walls.

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27
Q

Nitroimidazoles

A
  • Nitroimidazoles: Synthetic abx
  • Metronidazole
  • MOA:
  • Metronidazole synthetic abx works by disrupting the DNA of bacteria and some parasites, leading to inhibition of their nucleic acid synthesis.
  • It is particularly effective against anaerobic bacteria and certain protozoa.
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28
Q

Antifungal

A

Amphotericin: Antifubgal binds with the ergosterol of fungal membrane causing disruption and ion permeability.

5 mg/kg with the liposomal formulation).
– Side effects: renal toxicity and high fevers
and chills (shake and bake).
– Monitor serum urea nitrogen, creatinine, and creatinine clearance.

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29
Q

Case comes to your office or u have been called from ED for patient with swelling, what would you like to know

A
  • First, I would like to gather a detailed History of Present Illness. I would ask about the onset, duration, progression, and characteristics of the swelling, as well as any associated symptoms like pain, dysphagia, dysphonia, odynophagia, dyspnea, and fever.
  • I would inquire about any history of antibiotic use or previous episodes of similar swelling.
  • I would also review the patient’s past medical history, SHx , social hx , medications and allergy.
  • I would check the patient’s vital signs for any signs of systemic involvement, such as tachycardia, hypotension, or fever, which could indicate a spreading infection or sepsis.
  • I would also like to know the patient’s NPO status, in case urgent surgical intervention is required.
30
Q

They will give you an answers for the previous questions you ask and then they will ask what would you like to do next or how would you like to proceed?

A
  • I would start with physical examination, starting by inspection, general appearance of the patient looking for facial swelling, asymmetry, and any signs of respiratory distress.
  • I would also observe if the patient is able to tolerate their secretions or if they are posturing to improve airway patency (such as tripoding or head tilting).
  • Then I will do head and neck exam. Palpate the involved area I’d assess whether the swelling is firm (suggesting cellulitis) or fluctuant (suggesting an abscess).
  • MIO to evaluate for trismus, assess for lymphadenopathy, look for spreading erythema, is the inferior border of the mandible palpable, is the FOM elevated, is the uvula deviated? looks for carious teeth and periodontal disease.
31
Q

What Labs u order?

A
  • CBC, elevated wbc leukocytosis with left shift (immature wbc which indicate acute infection)
  • BMP ( I wanna assess the renal function (BUN/creatinine), which is important both for evaluating hydration status and as a baseline before administering nephrotoxic antibiotics or CT contrast for imaging.
  • CRP, is marker of inflammation that rises in response to inflammation. Can be trended to assess resolution. Normal rate is Less than 1mg/dL
  • ESR (Erythrocyte Sedimentation Rate):
    A blood test that measures how quickly red blood cells settle at the bottom of a tube. A faster rate indicates inflammation in the body. Normal 0-20mm/hr in men, in women 0-30
  • obtain blood culture to rule in or out of bacteremia
  • CT neck w/contrast.
32
Q

Then when they ask for your plan you say:

A
  • Admit to hospital
  • IV fluids for dehydration
  • Start empiric abx
  • Analgesia
  • Nursing order to include, NPO , suction bedside , q4 vitals, monitor ins and out
  • Post the case for I&D
  • Talk to anesthesia and discuss the airway and possibility of fiberoptic intubation vs awake intubation.
33
Q

How would you proceed with your drainage?

A
  • Mark out landmarks for cricothyrotomy and have surgical airway kit open and ready in case of emergent airway concerns. After securing a definitive airway, I would scrub and drape the patient in a normal sterile surgical fashion. I would then place a throat pack. At this time, I would attempt needle aspiration of the abscess to have a sterile sample for culture. I would palpate and mark a 3 cm incision in healthy skin under the area of the fluctuance, ensuring I was 2 cm below the inferior border of the mandible. I would make a sharp incision using a 15 blade down to platysma. I would bluntly dissect with a hemostat toward the lingual border of the mandible….etc.
34
Q

Things will get worse and worse:
The patient is 3 days s/p incision and drainage. On exam your patient appears toxic and is not tolerating his secretions. He spiked a fever this morning of 103 degrees Fahrenheit. On exam the uvula is deviated to the right. How do you proceed?

A
  • I will repeat my subjective and objective evaluation, rescan the patient. He may have developed a new collection in the previously drained spaces, inadequate drain placement, inadequate surgery/missed space. The patient should be taken back to the OR for incision and drainage. I would consider changing my antibiotic therapy based on culture results if not already tailored. I would consider leaving the patient intubated.
35
Q

Abx dosages

A
36
Q

Abx choice for infection

A

First line:

Unasyn 3g Q8h

Allergic to PCN:
Ancef and flagyl or
ceftriaxone and flagyl.

Ludwigs vanc and zosyn

CST: ceftriaxone, flagyl, vancomycin

very toxic appearing and sepsis then vanc and zosyn and ID

doxy if sinus infection or MRONJ infected and can’t take penicillin

zosyn and cefepime covers pseudomonas

Cefepime is a fourth-generation cephalosporin with broad-spectrum activity against gram-positive, gram-negative, and some anaerobic bacteria.

37
Q

Pseudomonas

A

Pseudomonas refers to gram-negative, aerobic, rod-shaped bacteria, with Pseudomonas aeruginosa being the most clinically significant species.

38
Q

Ancef

A

Ancef (cefazolin) is a first-generation cephalosporin antibiotic used primarily for gram-positive coverage.

Adults:
1–2 g IV every 8 hours
25–50 mg/kg/day IV divided every 8 hours

39
Q

Can Ancef (Cefazolin) Be Used in Patients with Penicillin Allergy?

A

Yes, cefazolin (Ancef) can be used in most patients with penicillin allergy, but with some important considerations:

Cross-Reactivity Between Penicillins and Cephalosporins
The overall cross-reactivity rate between first-generation cephalosporins and penicillins is <2%.
The risk is highest with penicillins and cephalosporins that share similar side chains, but cefazolin has a different side chain from most penicillins, meaning the cross-reactivity is very low.

For the board say: I would inquire about the type of PCN allergy. If mild to moderate Ancef can be used and consider bendryl as needed. If sever anaphylactic I would avoid it and do Vancomycin. I will also consult ID

40
Q

Mucormycosis (Zygomycosis)

A
  • Mucormycosis is an opportunistic fungal infection (caused by fungi in the Mucorales family) that occurs in immunocompromised patients.
  • Head and neck manifest as two forms:
    rhinocerebral and rhinomaxillary.
41
Q

Pathogenesis of Mucormycosis

A
  • Disease involves thrombosis, vascular invasion, ischemia, and infarctions.
42
Q

What is early diagnostic signs of mucormycosis?

A
  • Black necrotic eschars in the oral cavity, palate, or face can be the early diagnostic signs.
  • Fungi will enter the body through the nasal mucosa, lungs, or skin.

– Cutaneous mucormycosis: injured tissue in the oral cavity can be a suitable port of entry.
– Fungal hyphae preferentially invade the walls of blood vessels, producing thrombi and infarctions.
– Progressive tissue ischemia and necrosis are the inevitable result.

  • Rhizopus organisms have an enzyme, ketone reductase, which allows them to thrive in high glucose and acidic conditions.
43
Q

Oral Mucormycosis

A
  • Most frequently seen as palatal ulcers – almost always necrotic, well-defined borders.
  • May result from rapid lysis of the maxilla or other adjacent structures.
  • Has been reported in the alveolar ridge, lips, cheeks, tongue, mandible (rare), and maxillary sinuses.
  • Diagnosis by biopsy with histopathological evidence of fungal invasion showing:
    broad non-septate hyphae with right angle branching.
  • Fungal cultures may not reveal mucor, so biopsy is important for diagnosis.
44
Q

Management/Treatment of mucormycosis

A
  • Several simultaneous approaches: surgical intervention and antifungal therapy.
  • Antifungal treatment: systemic (IV), high- dose amphotericin B (5 mg/kg with the liposomal formulation).
    – Side effects: renal toxicity and high fevers and chills (shake and bake).
    – Monitor serum urea nitrogen, creatinine, and creatinine clearance.
    – Amphotericin mechanism of action – binds with the ergosterol of fungal membrane causing disruption and ion permeability.
  • Posaconazole or isavuconazole can also be used for salvage therapy for patients who don’t respond or cannot tolerate amphotericin B.
  • Surgical debridement to limit aggressive spread of infection. Aggressive surgical debridement of involved tissues should be undertaken as soon as the diagnosis of any form of mucormycosis is suspected.
  • Therapy should continue until there is a clinical resolution of signs/symptoms as well as resolution of radiographic signs of active disease.
45
Q

Five distinct bacterial patterns are seen in necrotizing fasciitis

A

Five distinct bacterial patterns are seen in necrotizing fasciitis:
– Type I – mixed aerobic and anaerobic, most commonly seen.
– Type II – Streptococcus pyogenes (group A beta-hemolytic streptococci), seen more often in otherwise healthy children.
– Type III – Staphylococcus aureus (MRSA).
– Type IV – clostridial, gas producing bacterium.
– Type V – Klebsiella pneumonia – may be highly resistant to antibiotics.

46
Q

Clinical signs of neck fasc

A

– Erythematous skin without demarcation that is tense, smooth, shiny, and painful.
– Will have signs of sepsis including tachycardia, pyrexia, apathy, weakness, hypotension
– Progression leads to vesicle and blister formation early, followed by dusky purple discoloration.
– Skin may become anesthetic due to compression and destruction of the underlying sensory nerves.
– Crepitus may be present due to gas production.
– Drainage is described as “dishwater” due to the foul smell, low viscosity, and gray color. Product of colliquative necrosis.

47
Q

What do u see in neck fasc labs

A

– Complete blood counts.
- Extreme leukocytosis
- Anemia secondary to bacterial hemolysis and bone marrow suppression.
– Comprehensive metabolic panel. Hypocalcemia due to sequestration of calcium into regions of fat necrosis
- Elevated blood glucose
- Elevated blood urea nitrogen
- Elevated creatinine.
– Lactate levels will be increased.

48
Q

CST Abx

A

Recommended Empiric Antibiotic Regimen

Vancomycin
15–20 mg/kg IV every 8–12 hours
Covers MRSA, MSSA, and Streptococcus species.

Ceftriaxone (or Cefepime)
2 g IV every 12 hours
Broad coverage for gram-negative bacteria and Streptococcus species.

Metronidazole
500 mg IV every 8 hours
Excellent anaerobic coverage, especially for organisms from sinus or dental infections.

49
Q

Characteristics of cellulitis vs. abscess

A
50
Q

Primary Fascial Spaces

A

Primary fascial spaces are those that are directly adjacent to the origin of odontogenic infections.

Infection spread by direct invasion from the source. These spaces include the following:
* Buccal
* Submandibular
* Canine
* Submental
* Vestibular
* Sublingual

51
Q

Secondary Fascial Spaces

A

Secondary Fascial space infections are those that become involved via spread of infection from the primary fascial spaces. These spaces include the following:
* Pterygomandibular
* Infratemporal
* Masseteric
* Masticator
* Lateral pharyngeal
* Retropharyngeal
* Prevertebral

52
Q

Borders of the deep fascial spaces of the head and neck

A
53
Q

Infection, clinical exam facts

A

– Decreased mobility of neck. Normal flexion 70–90°, extension 55°, and rotation 70°.

– Inability to palpate inferior border of mandible (indicative of submandibular space involvement).

– Floor of the mouth and tongue elevation (indicative of sublingual space involvement). If the patient is able to extend tongue past vermillion border of the upper lip, there is less of a chance that the sublingual space is involved.

– Deviation of uvula to the opposite side (indicative of the lateral pharyngeal/pterygomandibular/peritonsillar space involvement; also may be indicative of an oropharyngeal malignancy).

  • Swelling of lateral neck between the sternocleidomastoid and mandibular angles, just above hyoid, is suggestive of lateral pharyngeal space involvement.
  • Dimpling over zygomatic arch can be seen with temporal space involvement due to adherence of temporal fascia to periosteum.

Distant heart sounds, murmurs, and pericardial friction rub may be indicative of mediastinal spread.

54
Q

Systemic Inflammatory Response Syndrome (SIRS)

A

SIRS is defined by having two or more of the following:

  1. Fever >38 °C or <36 °C
  2. Heart rate >90 beats per minute
  3. Respiratory rate >20 breaths per minute or
    PaCO2 <32 mm Hg
  4. Abnormal WBC count (>12,000/mm3 or
    <4000/mm3 or >10% bands)
54
Q

Sepsis

A

life-threatening organ dysfunction caused by a dysregulated host response to infection.

  • Organ dysfunction – based on sequential organ failure assessment (SOFA) scores. Points are given to abnormalities in cardiovascular, coagulation, pulmonary, liver, renal, and brain panels. A score of two or more denotes organ dysfunction.
55
Q

Criteria for hospital admission:

A

– Temperature >101 °F
– Dehydration
– Signs of airway embarrassment
– Infection involving secondary fascial spaces
– Need to control systemic disease that has
implications on the infected patient
– Need for general anesthesia

56
Q

Prepare for and perform emergent Cricothyrotomy.

A

Palpate prominence of thyroid cartilage, then cricothyroid membrane directly below. Perform 1cm vertical midline skin incision centered over cricothyroid membrane, dissect to membrane with hemostat, incise membrane with scalpel, insert hemostat or spreader inferiorly, spread slightly, insert 6.0 ETT until cuff is inside trachea, inflate cuff, hold ETT, have someone hook up bag valve connected to O2 source, confirm placement with auscultation of chest, secure ETT with sutures

57
Q

Preseptal cellulitis.

A
  • Infection confined to the lids and periocular soft tissues anterior to the orbital septum.
  • More common in children than in adults.

What is the primary sources?
(1) paranasal sinusitis
(2) upper respiratory tract infection
(3) direct inoculation (e.g., chalazion or trauma to area). Strabismus surgery

What bacterial involved in this process?
Staphylococcus aureus Streptococcus pneumoniae, Haemophilus influenzae

What you expect to see in your exam?
ocular pain, eyelid swelling, erythema. Chemosis can occur in severe cases.

Tx:
- Antibiotic treatment should be tailored to cover community-acquired MRSA, such as clindamycin or TMP/SMX.

  • Serial ocular exams looking for deteriorating or improving symptoms.
  • Keep head of bed elevated
  • If abscess is defined, drainage via transcutaneous, transconjunctival, or transnasal endoscopic approach through ethmoid sinus.

What peds dose of Bactrim in peds:
8-12 mg/kg/day q12.
MOA inhibition of bacterial synthesis of folic acid, which is crucial for DNA and protein production.

58
Q

Postseptal/Orbital Cellulitis/Abscess

A
  • Reflects true involvement of the orbital contents (retroseptal).
    – Fat and ocular muscle involvement.
  • More common in young children.
  • Blood cultures can be positive in children.
    Rarely positive in adults.
  • Most common cause is rhinosinusitis.
    – Ethmoid sinusitis and pansinusitis can also lead to subperiosteal orbital abscess or orbital cellulitis.
  • Other potential causes:
    – Ophthalmic surgery: strabismus surgery, blepharoplasty
59
Q

Clinical features of Postseptal/Orbital Cellulitis/Abscess

A

Ophthalmoplegia
decreased visual acuity
proptosis
eye pain (ophthalmalgia)
superior orbital fissure syndrome orbital apex syndrome.

  • Usually abscess located medially or superomedially causing the eye to be fixed looking “down and out.”
  • Most common bacteria involved are Staphylococcus aureus and Streptococci.
  • Mucor and Aspergillus (fungi) can cause life- threatening invasive infections and are more common in poorly controlled diabetics
60
Q

How would u like to treat Postseptal/Orbital Cellulitis/Abscess

A

I & D in the OR through Transconjunctival and transcaruncular approach , Serial ocular exams, abx vancomycin to cover staph aur, and S. pneumoniae.

What is the dose of Unasyn in peds?
Mild/Moderate Infection 100-200 mg ampicillin/kg/day IV/IM divided q6hr.
For sever is 300mg

For vacomycin 15 mg/kg/dose administered intravenously every 6 to 8 hours.

61
Q

Retrobulbar Hemorrhage

A

1% incidence
signs/symptoms: pain, proptosis, decreased visual acuity, increased intraocular pressure, and ophthalmoplegia.

Manage medically with IV infusion 20% mannitol 2 g/kg to shrink the vitreous humor, acetazolamide (Diamox ®) 5mg/kg (peds dose) or steroids.

Manage surgically with lateral canthotomy with cantholysis.

62
Q

Cavernous Sinus Thrombosis (CST)

A
  • Vascular thrombosis in the cavernous sinus with inflammation of its anatomic structures.
  • Most common etiology is from contiguous spread of infection from the sinuses and very uncommon from dental abscesses
  • Staphylococcus aureus is the most common pathogen.
63
Q

Anatomy of the Cavernous Sinus

A
  • Bilateral venous drainage for middle cranial fossa.
  • Anteriorly bordered by the superior orbital fissure, receiving tributaries of the ophthalmic vein.
  • Posterior border is the trigeminal ganglion.
  • Superior and inferior ophthalmic veins, central retinal vein, and the middle meningeal vein drain into cavernous sinus.
  • The cavernous sinus drains into the superior and inferior petrosal sinuses.
  • Emissary veins drain from the sinus into the pterygoid plexus to the retromandibular vein.
  • Nerves in sinus:
    – Oculomotor (CN III)
    – Trochlear (CN IV)
    – Abducens (CN VI)
    – Ophthalmic (CN V-1)
    – Maxillary (CN V-2)
64
Q

Presentation of Cavernous Sinus Thrombosis

A
  • Aseptic causes – after surgery or after trauma.
  • Infectious causes:
    – Sinusitis
    – Otitis
    – superficial cellulitis of skin
  • Symptoms:
    fever, headache, and diplopia
  • Earliest neurological sign is lateral gaze palsy (CN 6).
  • Clinical signs include photophobia, proptosis, sepsis, lid edema, chemosis, dilated pupils, cranial nerve 3, 4, 6 palsies (ophthalmoplegia), and paresthesia of V1, V2. Dilatation of the retinal veins of the opposite eye may precede lateral gaze palsy CN 6 on the affected side. This is due to venous congestion in the cavernous sinus obstructing the venous out- flow of the retinal veins on the unaffected side.

On fundoscopic exam, congested retinal veins on the opposite side are the earliest signs of cavernous sinus thrombosis.

  • Clinical evidence of intracranial extension:
    – Nausea/vomiting
    – Altered mental status
    – Generalized sepsis
  • Intracranial extension of infection may result in meningitis, encephalitis, blindness, brain abscess.
65
Q

Danger Triangle on Face leading to CST

A

Triangular region formed by the corners of the mouth, medial cheeks, and bridge of the nose.

  • Pathway is via retrograde flow through veins that are valveless.

– Facial veins>angular vein>ophthalmic veins>cavernous sinus

– Emissary veins connected to the pterygoid plexus (slower spread)

– Internal jugular vein connecting to inferior petrosal sinus (complication of Lemierre’s syndrome)

Lemierre syndrome is a rare, life-threatening condition characterized by septic thrombophlebitis of the internal jugular vein

66
Q

Radiographic Features of CST

A
  • Magnetic resonance venography (MRV):
    – Imaging modality of choice to examine venous anatomy and demonstration of decreased or absence of signal in area of thrombus
    – Venous wall thickening
    – Filling defect in cavernous sinus
    – Lateral bulging of cavernous sinus wall
    – Narrowing of the internal carotid artery within the cavernous sinus
67
Q

Treatment of Cavernous Sinus Thrombosis

A
  • Surgery
    – Directed at the primary source of infection and obtaining culture.
  • Antibiotics: – 6–8 weeks
    Start with empiric antibiotic regimens with combination of (1) third- or fourth-generation cephalosporin that crosses the blood–brain barrier, such as ceftriaxone (third generation) or ceftazidime (fourth generation), (2) metronidazole, and (3) vancomycin (high likelihood of S. aureus) until culture results.

Steroids (controversial):
– May have benefits of decreasing orbital inflammation and cranial nerve edema.

Anticoagulants (controversial):
– Proposed benefit: cessation of the progression of the thrombus to other dural venous sinus and cerebral veins.

68
Q

Mediastinitis

A

Life-threatening infection involving the mediastinum.

Spread from an odontogenic source is via the danger space (also called Space 4) that is found between the alar and prevertebral fascia. This space extends from the base of the skull , through posterior mediastinum, to the level of the diaphragm.

69
Q

Clinical sign of Mediastinitis

A

– Chest pain
– Dyspnea
– High fever
– Tachypnea
– Hypotension due to decreased venous return

70
Q

Radiographic sign of Mediastinitis

A

– Mediastinal widening
- Pulmonary congestion/effusions can be appreciated on chest radiographs.
– CT may show location of collections
- Tissue emphysema
- Pericardial effusions
- Decreased airway patency.

71
Q

Tx of Mediastinitis

A

– Establish definitive airway.
– Aggressive surgical source control including drainage of spaces (repeat drainage and debridement often required).
– Cardiothoracic surgery consultation for open mediastinal drainage.
– Broad-spectrum antibiotics.
– HBO therapy may be indicated.