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Oral Board Review Textbook > Infection > Flashcards

Infection Flashcards

1
Q

What are the principals of management of an odontogenic infection?

A

-Determine severity: Location, rate, airway compromise
-Evaluate host factors: Immunocompetence, systemic reserve
-Decide on setting: Inpatient criteria-fever, dehydration, need for GA, deep space infection, control of systemic disease
-Treat surgically
-Support medically
-Choose and administer the appropriate antibiotic

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2
Q

What are the characteristics of cellulitis?

A

-Duration: 3-5 days
-Palpation: Hard and very tender
-Skin quality: Thick
-Bacteria: Mixed
-Tissue fluid: Serosanguineous
-Size: Diffuse

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3
Q

What are the characteristics of an abscess?

A

-Duration: 5-7 days
-Palpation: Fluctuant and tender
-Skin quality: Thin, shiny
-Bacteria: Anaerobic
-Tissue fluid: Purulent
-Size: Localizing

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4
Q

What are the 3 stages of an odontogenic infection?

A

-Inoculation
-Cellulitis
-Abscess

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5
Q

What are the primary fascial spaces?

A

-Spaces directly adjacent to the origin of odontogenic infections

-Buccal, submandibular, canine, submental, vestibular, sublingual

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6
Q

What are the secondary fascial spaces?

A

-Spaces that become involved via spread from primary spaces

-Pterygomandibular, infratemporal, masseteric, masticator, lateral pharyngeal, retropharyngeal, prevertebral

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7
Q

What is your work-up of an odontogenic infection (subjective exam)?

A

HPI:
-Need to determine onset, duration, symptoms, previous antibiotic use
-NPO status
-Assessment of concerning signs: Dysphagia, dysphonia, dypnea, odynophagia, mental status changes, trismus, fevers/chills

Medical history:
-Important to assess for immunocompromised (HIV, DM, hepatitis, alcoholism, malignancy, chemotherapy. malnutrition, steroids, immunosuppressants)
-IV drug user higher incidence of MRSA

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8
Q

What is your physical exam work-up for an odontogenic infection?

A

Vital signs:
-Temp: Serious, systemic infection. Normal is 98.6 or 37 degrees C. Fever (100 or 37.5)
-Heart rate: Tachycardia can be indicative of systemic involvement
-Respiratory rate: Elevated could be suggestive of respiratory compromise or acid-base imbalance suggestive of SIRS
-BP: HTN can present secondary to pain, hypotension seen in septic patients
-O2 saturation: Airway compromise if O2 sat less than 96

Inspection (global view of patient):
-Facial swelling/asymmetry
-Toxic appearing (pallor, diaphoretic, shivering, lethargy)
-Can patient tolerate secretions? Posturing?
-Signs of respiratory distress (dyspnea, stridor, dysphonia, sniffing position)

Head and neck assessment:
-Airway: MIO, neck mobility, breathe/talk laying flat
-Palpate for tenderness, warmth, induraction
-Lymphadenopathy
-Palpate trachea (midline?)
-Palpate FOM
-Uvula midline, palatal draping
-Look for source of infection (Carious teeth, perio teeth, impacted teeth)
-Crepitus of neck/chest
-Cranial exam

Cardiopulmonary exam
-Tachycardia, pulmonary rates, distant heart sounds

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9
Q

What are the borders of the buccal space?

A

Ant: Corner of mouth
Post: Masseter mm, pterygomandibular space
Sup: Maxilla, infratemporal space
Inf: Mandible
Superficial: Subcutaneous tissue/skin
Deep: Buccinator mm

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10
Q

What are the borders of the infraorbital space?

A

Ant: Nasal cartilage
Post: Buccal space
Sup: Quaurantus labii superioris mm
Inf: Oral mucosa
Superficial: Quadratuc labii superioris mm
Deep: Levator anguli oris mm, Maxilla

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11
Q

What are the borders of the submandibular space?

A

Ant: Anterior belly of digastric
Post: Posterior belly of digastric, stylohyoid mm, stylopharyngeus mm
Superior: Mandible
Inf: Digastric tendon
Superficial: Platysma mm
Deep: Mylohyoid mm, hypoglossus mm, superior constrictor mm

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12
Q

What are the borders of the submental space?

A

Ant: Inferior border of mandible
Post: Hyoid
Sup: Mylohyoid
Inf: Investing fascia
Superficial: Investing fascia
Lateral: Anterior belly of digastric

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13
Q

What are the borders of the sublingual space?

A

Ant: Lingual surface of mandible
Post: Submandibular space
Superior: Oral mucosa
Inferior: Mylohyoid
Medial: Muscles of tongue
Lateral: Lingual surface of mandible

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14
Q

What are the borders of the pterygomandibular space?

A

Ant: Buccal space
Post: Parotid gland
Superior: Lateral pterygoid mm
Inferior: Inferior border of mandible
Medial: Medial pterygoid mm
Lateral: Ascending ramus of mandible

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15
Q

What are the borders of the submasseteric space?

A

Ant: Buccal space
Post: Parotid gland
Superior: Zygomatic arch
Inferior: Inferior border of mandible
Medial: Ascending ramus of mandible
Lateral: Masseter mm

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16
Q

What are the borders of the lateral pharyngeal space?

A

Ant: Superior and middle pharyngeal constrictors
Post: Carotid sheath and scalene fascia
Superior: Skull base
Inferior: Hyoid bone
Superficial Pharyngeal constrictors/retropharyngeal space (medial)
Lateral: Medial pterygoid mm

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17
Q

What are the borders of the retropharyngeal space?

A

Ant: Superior and middle pharyngeal constrictors
Post: Alar fascia
Superior: Skull base
Inferior: Fusion of alar and prevertebral fasciae at C6-T4

Lateral: Carotid sheath and lateral pharyngeal space

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18
Q

What are the borders of the pretracheal space?

A

Anterior: Sternothyroid-thyrohyoid /fascia
Posterior: Retropharyngeal space
Superior: Thyroid cartilage
Inferior: Superior mediastinum
Superficial: Sternothyroid-thyrohyoid fascia
Deep: Visceral fascia over trachea and thyroid gland

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19
Q

What is the masticator space?

A

Space made up of temporal space, pterygomandibular and masseteric spaces

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20
Q

Where is the temporal space?

A

-Posterior and superior to the masseteric space and pterygomandibular space

-Bound by temporalis fascia laterally and skull medially

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21
Q

What labs are relevant in an odontogenic infection?

A

-CBC: Look for leukocytosis with left shift. Thrombocytosis can be seen (acute phase reactant). Left shift/bandemia (immature WBCs being released into bloodstream)

-BMP: BUN/creat can help assess volume status, renal baseline important for antibiotics that are nephrotoxic/CT contrast. Glucose/glycemic control (Blood sugar below 200 imperative for good infection control), electrolyte disturbance with long term malnutrition

-C-Reactive Protein: Marker of inflammation (acute phase reactant)

-Blood cultures: Reserved for patients with signs of septicemia

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22
Q

What is SIRS?

A

-Systemic Inflammatory Response Syndrome

-Defined as having two or more of following:
-Fever >38
-HR >90
-Respiratory rate >20
-WBC >12,000

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23
Q

What is sepsis?

A

-Life threatening organ dysfunction caused by dysregulated host response to infection

-Organ dysfunction: Abnormal cardiovascular, coag, pulmonary, liver, renal and or brain panels. Score of 2 denotes organ dysfunction

-Infection: Based on SIRS criteria and supportive micro/radiograph data

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24
Q

What is the relevant imaging in an odontogenic infection?

A

-CT w/ contrast: Must extend from skull base to thoracic inlet. 3 mm cuts in neck. Contrast used to delineate collections manifested as ring enhancing collections. Fat stranding may be appreciated. Can also look at airway/lymphadenopathy

-Panorex: Assess for causative teeth of the odontogenic infection. Can also look at resorptive changes of apical periodontitis or osteomyelitis

-Plain Neck film: Screening for retropharyngeal and pretracheal spaces. Normal: 7 mm at C2, 22 mm at C6. Not really used.

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25
Q

What is the medical management of an odontogenic infection?

A

-IV fluids to address dehydration
-Initiate emperic antibiotic therapy
-Change once cultures and sensitivity becomes available (can obtain adequate cultures from cellulitis)
-Analgesics

-Determine spaces involved
-Admit for serious infection (hospital admission criteria: Temp >101, dehydration, signs of airway embarrassment, infection involving secondary spaces, need to control systemic disease, need for GA)

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26
Q

What are nursing orders for an odontogenic infection?

A

-Suction bedside
-NPO
-Monitor I’s & Os
-Q4 vital signs
-HOB elevated 30 degrees

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27
Q

What is the surgical management of an odontogenic infection?

A

-Discuss securing a definitive airway with anesthesia before the OR (awake fiberoptic or awake trach if needed)
-Consider needle decompression prior to intubation to prevent rupture of abscess with intubation
-Be prepared for emergency tracheostomy in the “can’t ventilate can’t intubate) situation
-Mark out emergency cricothyrotomy prior to intubation attempt
-Attempt aspiration for sterile sample for culture and sensitivity
-Make an incision in healthy skin versus height of fluctuance to prevent scar contracture
-Place incision in natural skin fold to allow for dependent drainage
-Bluntly dissect involved spaces to establish drainage
-Copious irrigation
-Place drains (possibly through and through
-Extract offending teeth
-Re-assess patient
-Consider ID consult

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28
Q

What are considerations in management of orbital infections?

A

-Different anatomic sites and clinical manifestations
-Evaluate visual acuity, pupillary reflexes, extraocular movement and opthalmoscopy
-Rare sequelae of sinusitis, odontogenic infections or orbital trauma

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29
Q

What are the classifications of orbital infections?

A

-Group 1: Inflammatory edema (preseptal cellulitis)
-Group 2: Orbital Cellulitis
-Group 3: Subperiosteal abscess
-Group 4: Orbital abscess
-Group 5: Cavernous sinus thrombosis

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30
Q

What is the orbital septum?

A

-A membranous sheet that extends from the periosteum of the infraorbital region to the tarsal plate and forms the anterior boundary of the orbital compartment

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31
Q

What is the most common route of infection to the orbit?

A

-Extension from the ethmoid sinuses

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32
Q

What is the route of infection to the cavernous sinus?

A

-Superior and inferior ophthalmic veins drain blood directly into the cavernous sinus

-Inferior orbital veins are valveless and infections can pass readily from orbit to intracranial structures

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33
Q

What is the initial work-up of an orbital infection?

A

-Usual review of medical history, systems and duration/onset. Emphasis on symptoms of decreased vision and decreased color perception
-Lab tests: CBC, BMP, blood cultures
-Visual acuity (Snellen chart)
-EOM movement
-Pupillary examinatino (afferent pupillary reflexes)
-Ocular pressures
-Fundoscopic exam (access optic nerve involvement, papilledema: optic nerve swelling)
-Consider opthalmology consultation
-Posterior orbital involvement around the superior orbital fissure and optic foramen may result in orbital apex syndrome

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34
Q

What is the pertinent radiographic studies to orbital infections?

A

-CT orbits and /or sinuses with contrast: 3 mm cuts to distinguish preseptal and orbital cellulitis

-Preseptal cellulitis: Diffuse soft tissue edema seen anterior to septum on CT

-Postseptal cellulitis: Intraconal fat stranding and edema of the extra-ocular muscles are seen

-Postseptal abscess: Collection of purulent material (ring enhancing lesion) between bony walls of orbit and periorbita. Displacement of globe away from abscess

35
Q

Describe preseptal cellulitis

A

-Infection confined to the lids and periocular soft tissue anterior to the orbital septum
-More common in children than adults
-Sources: Paranasal sinusitis, URI, direct inoculation
-Bacteria: Staph aureus, strep pneumoniae, haemophilus influenze, other strep, anaerobes
-Clinical: Ocular pain, eyelid swelling, erythema, chemosis, can occur

36
Q

What is the treatment for preseptal cellulitis?

A

-Antibiotics: Community-acquired MRSA (Clinda or TMP/SMX)
-Serial ocular exams looking for deteriorating or improving symptoms
-HOB elevated
-If abscess defined, drainage via transcutaneous, transconjunctival or transnasal endoscopic approach through ethmoid sinus

37
Q

Describe post-septal/orbital cellulitis/abscess.

A

-True involvement of the orbital contents
-More common in young children
-Can have + blood cultures (in kids, rarely adults)
-Most common cause is rhinosinusitis. Other causes opthalmic surgery, trauma, dacryocystitis, odontogenic infection

-Presents with Opthalmoplegia, decreased visual acuity, proptosis, eye pain, changes in visual acuity, superior orbital fissure/orbital apex syndrome

-Abscess usually located medially or supero-medially (causes fixed looking down and out)
-Most common bacteria Staph aureus, strep, muco/aspergillus, can be life threatening

38
Q

What is the treatment of a post-septal/orbital infection

A

-Orbital abscess must be drained (uncomplicated cellulitis may attempt conservative tx 24-48h only)
-Broad spectrum antibiotics (Vanc, unasyn, metronidazole, ceftriaxone, piperacillin/tazobactam, levo)
-If intracranial extension include anaerobic coverage and NSGY consult
-Contrast CT or MRV (venogram)

-Approach: Transconjnctival w/ or w/o transcaruncular or lateral canthotomy extension. Endoscopic sinus surgery if pt with rhinosinusitis
-May consider steroid 24h after antibiotic therapy has begun (prevent ocular complications due to increased intraorbital pressure)
-Emergency lateral canthotomy and cantholysis may be required if signs of ocular involvement

39
Q

What is cavernous sinus thrombosis?

A

-A vascular thrombosis in the cavernous sinus with inflammation of its anatomic structures

40
Q

What is the most common etiology of a cavernous sinus thrombosis?

A

-Contiguous spread of infection from the sinuses (very uncommon from dental abscess)
-Staph aureus most common pathogen

41
Q

What is the pertinent anatomy of the cavernous sinus (vein flow, nerves, drainage)?

A

-Bilateral venous drainage for middle cranial fossa
-Anterior border is superior orbital fissure (tributaries of opthalmic vein)
-Posterior border is trigeminal ganglion
-Sup/inf opthalmic veins, central retinal vein, middle meningeal vein drain into cavernous sinus
-Drains into petrosal sinuses
-Emissary veins drain from sinus into pterygoid plexus to the retromandibular vein

Nerves in sinus: CN III, IV, V1, V2, VI

42
Q

What is the presentation of cavernous sinus thrombosis?

A

Aseptic cases: After surgery or trauma

Infectious causes: Sinusitis, otitis, facial fruncles, erysipelas (cellulitis of skin caused by b-hemolytic strep and grou B strep)

Symptoms: Fever, headache, diplopia

Clinical signs: Photophobia, proptosis, sepsis, lid edema, chemosis, dilated pupils, ophthalmoplegia, congested retinal vein

43
Q

What is the earliest neurologic signs of cavernous sinus thrombosis?

A

-Lateral gaze palsy (CN 6)
-Congested retinal vein on opposite side may be even earlier

44
Q

What are signs of intracranial extension of cavernous sinus thrombosis?

A

-Nausea/vomiting
-Altered mental status
-Generalized sepsis

-May result in meningitis, encephalitis, blindness, brain abscess, empyemas, coma and death

45
Q

What is the danger triangle of the face?

A

-Triangular region from corners of mouth, medial cheek and bridge of nose
-Pathway is via retrograde flow through veins that are valveless.

-Facial to angular to ophthalmic to cavernous sinus
-Emissary veins to pterygoid plexus
-IJV to inferior petrosal sinus (Lemierre’s syndrome)

46
Q

What are radiographic features of cavernous sinus thrombosis?

A

MRV (Magnetic resonance venography)
-Imaging modality of choice to evaluate venous anatomy and detect thrombosis

CT with and w/o contrast
-Expansion of cavernous sinus, convexity of lateral wall

47
Q

What is the treatment of cavernous sinus thrombosis?

A

Surgery
-Directed at primary source of infection and obtaining culture

Antibiotics (combo of 3)
-3rd or 4th gen cephalosporin that crosses BBB: Ceftazidime)
-Metronidazole
-Vancomycin
-6-8 week therapy (can change once C&S returns)

Steroids (controversial)
-May decrease orbital inflammation and cranial nerve edema

Anticoagulants (controversial)
-Cessation of progression of thrombosis, can decrease morbidity
-Risk: Intracranial and systemic hemorrhage

48
Q

What is a mucormycosis (zygomycosis) infection?

A

-Opportunistic fungal infection that occurs in immunocompromised patients
-Two forms are rhinocerebral and rhinomaxillary

49
Q

What is the presentation of mucormycosis?

A

-Black necrotic eschar in oral cavity/palate (thrombosis, vascular invasion, ischemia/infarctions)

50
Q

What enzyme in mucormycosis helps with infection in diabetic individuals?

A

-Ketone reductase
-High glucose, acidic conditions (diabetic ketoacidosis)

51
Q

What is the presentation of oral mucormycosis?

A

-Seen most frequently on palatal ulcers
-Necrotic, well defined borders
-Diagnosis by biopsy: Broad non-septate hyphae at right angles

52
Q

What is the management/treatment of mucormycosis?

A

-Early ID and treatment
-Eliminate predisposing factors (hyperglycemia, metabolic acidosis, imunosuppressive drugs, neutropenia)
-Surgical and antifungal therapy
-Systemic IV (High dose amphotericin B). Monitor nitrogen, creat, creat clearance (binds fungal membrane, increases ion permeability
-Posaconazole/isavuconazole can be used as salvage thearpy
-Aggressive surgical debridement

53
Q

What is cervicofacial necrotizing fasciitis?

A

-Aggressive bacterial infection leading to necrosis of the superficial fascial planes with concurrent systemic toxicity
-High mortality due to sepsis
-More common in immunocompromised patients/diabetic

53
Q

How is necrotizing fasciitis classified?

A

Type I: Mixed aerobic/anaerobic (most commonly seen)
Type II: Strep pyogens (group A beta hemolytic strep) (seen more in children)
Type III: Staph aureus (MRSA)
Type IV: Clostridial, gas producing
Type V: Klebsiella (may be resistant to antibiotics)

53
Q

What are clinical signs of cervicofacial necrotizing fasciitis?

A

-Erythematous skin w/o demarcation that is tense, smooth, shiny, and painful
-Signs of sepsis: Tachy, pyrexia, apathy, weakness, hypotension
-Progression leads to vesicle and blister formation, dusky purple skin follows
-Crepitus may be present due to gas production
-Drainage described as dishwater due to foul smell, low viscosity and gray color

54
Q

What are the radiographic signs of cervicofacial necrotizing fasciitis?

A

-Soft tissue emphysema and edema, possible gas bubbles

55
Q

What are lab results present in cervicofacial necrotizing fasciitis?

A

-CBC: Extreme leukocytosis, anemia (bacterial hemolysis and bone marrow suppression)
-CMP: Hypocalcemia (sequestration of calcium), elevated blood glucose, elevated blood urea nitrogen, elevated creatinine
-Lactate levels will be increased

56
Q

What is the treatment of cervicofacial necrotizing fasciitis?

A

-Secure definitive airway
-Early recognition leading to surgical intervention via fasciotomy and necrotic tissue debridement. Muscle layers can be preserved but all necrotic tissue and overlyign skin must be removed
-Biopsies of involved fascia to identify toxin-producing invasive streptococcal infection
-Gram-positive cocci invading fascia without leukocytic infiltrate indicated streptococcal toxin production
-Frozen sections show dense polymorphonuclear infiltrates in the dermal layers of skin; these may guide removal of devitalized tissue
-Biopsies should be taken of adjacent normal looking tissue
-Broad spectrum antibiotics (carbapenem plus vancomycin to cover all 5 types of infections), de-escalation according to culture and sensitivity results
-Wounds should be washed (consider peroxide, consider antimicrobial soaked packing-povidone iodine)
-Hyperbaric oxygen consideration
-Fluid electrolyte and blood replacement for volume repletion and hemolysis
-Secondary reconstruction may require locoregional flaps and skin grafts

57
Q

What is mediastinitis and how can it come from an odontogenic source?

A

-A life-threatening infection involving the mediastinum
-Can spread from an odontogenic source 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 the posterior mediastinum to the level of the diaphragm. Loose areolar tissue allows for rapid spread of infection. Usually enters through the fusion of alar and prevertebral fascia between C6 and T4)

58
Q

What are the clinical signs of mediastinitis?

A

-Chest pain
-Dyspnea
-High fever
-Tachypnea
-Hypotension (decreased venous return)

59
Q

What are the radiographic signs of mediastinitis?

A

-Mediastinal widening and pulmonary congestion/effusions can be appreciated on chest radiographs
-CT may show location of collection, tissue emphysema, pericardial effusions, and decreased airway patency

60
Q

What is the treatment of mediastinitis?

A

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

61
Q

What is the definition of osteomyelitis?

A

-It is an inflammation of the medullary portion of bone. It frequently involves the cortical bone and periosteum, however.

-Bone marrow offers a path of lower resistance that allows for spread along medullary bone
-Most often seen in the mandible as the thin cortical bone of the maxillae does not easily confine the infectious process. Mandible also not as well vascularized

62
Q

What bacteria are most commonly seen in osteomyelitis?

A

-Odontogenic mixed flora (primarily alpha-hemolytic streptococci vs staphlococcus aureus)

63
Q

What are the classifications of osteomyelitis?

A

-Acute or chronic (1 month or greater)
-Suppurative or non-suppurative (pus forming)

64
Q

What are the symptoms of osteomyelitis?

A

-Pain, trismus, paraesthesia/anesthesia, anorexia, swelling, loose teeth, adenopathy, malaise.
-Chronic disease may form fistula or sinus tract

65
Q

What imaging is used in osteomyelitis?

A

-Scouting film like an orthopantogram may show odontogenic infection with or without sequestra

-CT scan can show extent of lytic bone, keeping in mind 30% demineralization is required to appreciate change

-Radionuclide imaging: Allows for earlier identification of osteomyelitic activity (3 days). Technetium-99 although non-specific, will aid in identifying areas of higher blood flow and osteoblastic activity. Gallium 67 aides in ruling out osteomyelitis from malignancy and trauma. Identifies inflammatory changes as it binds to granulocytes

-WBC tagging can be useful in detecting early infection when lytic processes aren’t seen on imaging

-PET CT with fluoride isotope is sensitive to areas of bone turnover with much greater resolution

66
Q

What is the treatment of osteomyelitis?

A

-Patient should be treated with corticotomies (bur fenestration) or removal of the buccal bone (decortication) for decompression, plus removal of infected teeth or repair of mobile fracture segment

-Infected bone marrow should be debrided until it bleeds, Useful to send multiple cultures and histopathological samples along the length of involved bone to see extent of infection/flora
-Cultures and bone biopsy: Get micro for cultures/sensitivities, rule out neoplasia, ID fungi or actinomycosis in samples
-Infectious disease service should be consulted due to need for long term IV antibiotics/PICC line
-Hyperbaric oxygen should be considered to aid in revascularization and for antimicrobial utility

67
Q

What is the MOA and type of antibiotic: Beta-lactams?

A

-MOA: Beta lactam antibiotics inhibit penicillin-binding proteins, which disrupt cell wall synthesis
-Bactericidal

68
Q

What are examples of beta-lactam antibiotics?

A

-Penicillins
-Cephalosporins
-Cephamycins
-Carbapenems
-Monobactams (aztreonam)

69
Q

What are beta-lactamase inhibitors?

A

-Bind to the catalytic site of beta-lactamases to prevent hydrolysis of the beta-lactam

-Ex: Tazo-bactam, sulbactam, clavulanate

-Used with a PCN to cover bacteria that confer their resistance through liberation of beta lactamases

70
Q

What are exampled of beta-lactamase inhibitors?

A

-Unasyn (Ampicillin and sulbactam)
-Zosyn (Piperacillin and tazobactaum)
-Augmentin (Amoxicillin and clavulanate)

71
Q

What is the MOA, type of antibiotic, and side effect: Macrolides?

A

-MOA: Binds to 50S ribosomal subunit and inhibits bacterial protein synthesis
-Bacteriostatic
-Ex: Erythromycin, clarithromycin, azithromycin
-Side effects: Prolong QT, nausea, diarrhea

72
Q

What is the MOA and type of antibiotic, and side effect: Clindamycin?

A

-Binds to 50S ribosomal subunit and inhibits bacterial protein synthesis
-Bacteriostatic or bactericidal depending on concentration, infection site and organism
-Side effects: Pseudomembranous colitis

73
Q

What is Pseudomembranous colitis?

A

-Treatment with antibiotic alters normal flora of large intestine and leads to overgrowth of C. difficile
-C. difficile produces toxins A and B that lead to cytoskeleton destruction and leaks. Proinflammatory cytokines that further intestinal mucosal damage
-Diagnosis: C. difficile toxin via stool sample

-Tx: Discontinue antibiotic. Stop opiates or anti-diarrheal medication. Administer fluids and correct electrolytes.
-Antibiotic treatment is: 10-14 days of metronidazole or oral vancomycin. Fidaxomicin is now also available

74
Q

What is antibiotic-associated colitis/fulminant colitis/toxic megacolon?

A

-Usually occurs in elderly, extended hospital stay, exposure to IV antibiotics
-Rapid WBC spike, abdominal pain/distension, fever
-Goal is to decompress bowel within 24h or total colectomy

75
Q

What is the MOA and type of antibiotic, and side effect: fluoroquinolones?

A

-MOA: Inhibits DNA gyrase/topoisomerase which are involved in DNA replication
-Bactericidal
-Ex: Ofloxacin, ciprofloxacin, levofloxacin, moxifloxacin
-Side effects: Chondrotoxicity (avoid in children <18 years old), tendinitis/tendon rupture, prolonged QT

76
Q

What is the generic name and normal dose of Unasyn?

A

-Ampicillin-sulbactam
-1.5-3 g IV q6-8h

77
Q

What is the generic name and normal dose of Zosyn?

A

-Piperacillin-tazobactam
-1.5-3 g IV q6-8h

78
Q

What is the generic name and normal dose of Keflex?

A

-Cephalexin
-500 mg PO q6h

79
Q

What is the generic name and normal dose of a Z-pack?

A

-Azithromycin
-250 mg PO BID for first day, 250 mg PO Q daily x4 days

80
Q

What is the normal dose of moxifloxacin and levofloxacin?

A

-Moxifloxacin: 400 mg PO q daily
-Levofloxacin (levaquin): 500 mg PO q daily

81
Q

What scenarios would necessitate antibiotic prophylaxis?

A

-Prosthetic heart valve or heart valve repaired with prosthetic material
-History of endocarditis
-Heart transplant with abnormal heart valve function
-Cyanotic congenital heart disease that has not been fully repaired (including surgical shunts or conduits)
-Repaired congenital heart disease with residual defects

82
Q

What is the antibiotic/dose for antibiotic prophylaxis?

A

-Amoxicillin 2g (Pediatric 50 mg/kg)

If allergic to PCNs
-Cephalexin 2g (Pediatric 50 mg/kg)
or
-Azithromycin 500 mg (Pediatric: 15 mg/kg)

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