Ios 10 Exam 3 Kuma Dlp

Front 1

Acute exacerbations of Chronic Bronchitis are the result of___________ or ________. What is the prevalence of each

Back 1

* viruses or * bacteria

* Viruses (35%)
* Bacterial (50%)
* Atypicals (5-20%)

Front 2

What are the most common bacterial pathogens in acute exacerbations of Chronic Bronchitis?

Back 2

* Haemophilus influenzae (likes COPD lungs) 24-26%
* Haemophilus parainfluenzae 10-20%
* Streptococcus pneumoniae 15-30%
* Moraxella catarrhalis 5-15%
* Gram-negative bacilli (high incidence) 5-40%
- (Klebsiella pneumoniae, Enterobacter aerogenes, Serratia marcescens, P. aeruginosa)
* Staphylococcus aureus 0-2%

Front 3

Which atypicals are most likley involved in acute exacerbations of Chronic Bronchitis?

Back 3

* Chlamydia pneumoniae
* Mycoplasma pneumoniae

Front 4

Antibiotic Therapy for Acute Bronchitis Without Underlying Chronic Bronchitis

Back 4

* Antibiotics are not appropriate for uncomplicated acute bronchitis without underlying lung disease.
* These cases are typically viral in nature and usually resolve with time.
* When patients with a history of COPD are excluded:
- Antibiotics = placebo
- Azithromycin = vitamin C
(However, antibiotics are significantly more effective than placebo in patients with acute bacterial exacerbation of chronic bronchitis)

Front 5

Treatment goals of chronic bronchitis

Back 5

* Reduce signs/symptoms of exacerbations
- Reduce quanitiy sputum
- Return the quality of the sputum back to baseline
* Reduce number of (future) exacerbations
- Bacterial suppression can help delay future exacerbations

Front 6

Nonpharmacologic therapy
in the treatment of Chronic Bronchitis

Back 6

* Rest (reduce O2 consumption and demand)
* Reduce or quit smoking
* Maintain hydration
* Humidifier or vaporizer (mobilize sputum)
* Chest physiotherapy (loosening things)

Front 7

Pharmacologic Therapy in the treatmetn of Chronic Bronchitis

Back 7

* Mucolytics of questionable benefit (H2O best)
* Bronchodilators may be beneficial (improve oxygenation and open airways) (but not theophylline 12-24 hrs to see any benefit at all – not direct MOA)
* Antibiotics may provide more rapid resolution of signs/symptoms and improvement in pulmonary function
- Clinical benefits have not been consistently proven
- Antibiotics are controversial but commonly used

Front 8

When should antibiotics not be used in Bronchitis patients?

Back 8

Those with acute uncomplicated infections

(i.e. not those with exacerbations of chronic disease)

Front 9

What are the cardinal s/sxn of Acute Bacterial Exacerbations of Chronic Bronchitis (ABECB)?

Back 9

1. Worsening of dyspnea (Changes/worsening of pulmonary function)
2. Increase in sputum purulence
3. Increase in sputum volume

When patients having these three symptoms were treated with a broad-spectrum antibiotic, these patients had a higher cure rate, fewer therapeutic failures, and a more rapid rate of lung recovery than if treated with placebo.

Front 10

What does pureulent green sputum indicate?

Back 10

94% sensitive and 77% specific for high bacterial load in sputum

Indicates baceterial infection

Front 11

Efficacy of Antibiotic Therapy in Patients With ABECB

Back 11

* Meta-analysis of randomized trials published from 1955 through 1994
* Suggested a small but significant improvement due to antibiotic therapy in patients with exacerbations
* Improvement may be clinically significant, especially in patients with low baseline flow rates
* Bottom line: improvement in pulmonary fxn
* The pts w/ worst baseline pulmonary fxn had the best benefit from antibiotic treatment

Front 12

Goals for Antibiotic Therapy in the treatment of ABECB

Back 12

* Rapidly relieve the clinical symptoms
* “Eradicate” the infection (never totally eradicate) Dramatically reduce population
* Increase the interval between exacerbations
- Decrease the number of exacerbations per year
- Decrease frequency of PCP visits and hospitalizations
- Decrease use of antibiotics
- Lower total costs for treatment

Front 13

Uncomplicated AECB (Class II)

Back 13

CLASSIFICATION
* FEV1 >35%–50% predicted (COPD but better fxn)
* <4 AECB/yr
* No comorbidities
* Low PCN resistance

ETIOLOGY
* Viral infection usually precedes a bacterial infection
* H. influenzae
* S. pneumoniae
* M. catarrhalis
* C. pneumoniae

ANTIBIOTIC THERAPY
* Macrolide
* Doxycycline
* 2nd-/3rd-generation Cephalosporin
* Amox/clav
(Fluoroquinolone 3rd-4th line so reserve for more ill patients)

Front 14

Complicated AECB
(Class III)

Back 14

CLASSIFICATION
* FEV1 >35%–50% predicted
* Older
* > or = 4 AECB/yr
* Comorbidities (congestive heart failure, diabetes, chronic renal or hepatic disease)
* Increased PCN resistance (d/t frequent antibiotic use)

ETIOLOGY
* H. influenzae
* S. pneumoniae
* M. catarrhalis
* Gram-negative bacilli
* (P. aeruginosa)


ANTIBIOTIC THERAPY
* Fluoroquinolone
– drug of choice
- the fluoroquinolones, and more specifically levo and cipro, are most effective against gram-negatives and P. aeruginosa.
* 2nd/3rd-generation Cephalosporin
* Amox/clav

Front 15

Chronic bronchial sepsis (Class IV)

Back 15

CLASSIFICATION
* Recurrent antibiotics and/or steroids
* Bronchiectasis

ETIOLOGY
* In addition to the usual respiratory pathogens, gram-negative organisms such as Enterobacteriacea and Pseudomonas should be considered

ANTIBIOTIC THERAPY
* Empiric therapy is anti-psuedomonal
* Based on sputum culture

Front 16

AECB: Host Factors Associated With Poor Treatment Outcome

Back 16

Treatment failure or relapse in up to 20-30% of patients:
- Inadequate antibiotic
- Frequency of exacerbation
- Severity of lung disease
- History of pneumonia/sinusitis
- History of cardiopulmonary disease
- Need for home oxygen
- Use of steroids

Front 17

Usual duration of Pharmacologic Therapy of Chronic Bronchitis

Back 17

* Usual duration of therapy = 7-10 days but depends on patient response
* Prophylaxis infrequently recommended for patients with >4-6 exacerbations/year
- Amoxicillin
- Doxycycline
- TMP-SMX
- Unusual

Front 18

Prevention of AECB

Back 18

* Appropriate management of underlying diseases is most effective method of preventing AECB
* Vaccinations recommended for appropriate candidates
- Polyvalent pneumococcal
- Conjugated Haemophilus influenzae type b
- Influenza

Front 19

T.R. is a 64 y.o. female with a 60 pack-year smoking history and mild-moderate COPD (chronic bronchitis). She presents to her primary care physician’s office with complaints of increased sputum production x 2 days. She also feels more fatigued than usual. She has a slight fever and is producing thin, clear sputum in slightly greater quantities than usual. The benefits of antibiotic therapy in T.R. at the present time would be:
a. Decreased chance of worsening pulmonary function.
b. Rapid resolution of signs & symptoms.
c. Decreased exacerbation of chronic bronchitis in the future.
d. None.

Back 19

NONE

Front 20

B.B. is a 48 y.o. male with COPD and a 40 pack-year smoking history. He has approximately 2-3 exacerbations per year and his last recorded FEV1 was 55%. His last exacerbation was 2 months ago; he was treated with oral cefuroxime at that time. He now presents with fever, worsening oxygenation, and increased production of purulent sputum. The most appropriate treatment for this exacerbation of chronic bronchitis would be:
A. Moxifloxacin
B. Amoxicillin/clavulanate
C. Doxycycline
D. Cefpodoxime proxetil

Back 20

Doxycycline

* Best reason not to use a beta-lactam in this pt is because of recent treatment with cefuroxime

Front 21

F.C. is a 59 y.o. female with history of COPD, CHF, CAD, HTN, and type II DM. She has 5-6 exacerbations/year and her last recorded FEV1 was 46%. She presents to her PCP with signs/symptoms consistent with an exacerbation. The most appropriate treatment for F.C. would be:
A. Ciprofloxacin d/t CA nature of infection
B. Azithromycin
C. Levofloxacin
D. Amoxicillin

Back 21

Levofloxacin

Front 22

V.Y. is a 59 y.o. male with history of steroid-dependent COPD, CHF, CAD, HTN, and type II DM. He has 5-6 exacerbations/year and his last recorded FEV1 was 46%. He now presents to his PCP with complaints of increased sputum production x 2 days. He feels more fatigued than usual, has a slight fever, and is producing quantities of thick greenish sputum in slightly greater quantities than usual. The most appropriate treatment for V.Y. would be:
A. Amoxicillin/clavulanate
B. Doxycycline
C. Azithromycin
D. No antibiotic

Back 22

Amoxicillin/clavulanate– class III patient

Front 23

What is the Peritoneal cavity?

Back 23

- Extends from bottom of diaphragm to floor of pelvis
- Contains stomach, small bowel, large bowel, liver, -gallbladder, and spleen
- Fallopian tubes enter this space in females
- Intact mucous membranes control the invasiveness of the indigenous bacteria of gut

Front 24

What is the Retro-peritoneal cavity?

Back 24

Duodenum, pancreas, kidneys, adrenal glands, great vessels, most mesenteric vascular structures

Front 25

What host factors are protective against IAI

Back 25

- Peristalsis: interferes with bacterial adherence
- Stomach acid: kills ingested bacteria
- Intact mucosa: deters adherence of virulent bacteria
- Norma flora: prevents virulent bacterial colonization, overgrowth and translocation
- Immune barriers: mucosal immune cells, mesenteric lymph nodes, Kupfer cells of liver

Front 26

Normal Flora of the Mouth

Back 26

Oral aerobes
Streptococci

Front 27

Normal Flora of the stomach

Back 27

<100 bacteria/mL
Primarily oral flora
Streptococci
Lactobacillus

Front 28

Normal flora of the Duodenu, and Jejunum

Back 28

lactobacilli
streptococci
Enteribacteriaseae:
-E. coli
- Klebsiella
-Enterobacter

Front 29

Normal flora of the Illeum

Back 29

Enteribacteriaseae:
-E. coli
- Klebsiella
-Enterobacter

Bacteroides spp.

Front 30

Normal flora of the appendix

Back 30

Just kidding LOL sorry getting punchy

Front 31

Normal flora of the large intestine

Back 31

lactobacilli
streptococci incl. S. faecalis
Enteribacteriaseae:
-E. coli
- Klebsiella
-Enterobacter

Bacteroides spp:
- B. fragilis
- B. theteioteomicron
- B. vugatus

Pseudomonas aerugenosa
Candida albicans

Front 32

Impairment of Host Factors as a Cause for IAI

Back 32

- Decreased peristalsis (e.g., neoplasms causing obstruction)
- Reduced stomach acid (e.g., H2-antagonists, proton pump inhibitors, antacids)
- Mucosal damage (e.g., bowel disease, tumors, surgery, trauma)
- Altered flora (e.g., antibiotics, tumors, bowel disease)
- Altered immunity

Front 33

Define Intra-abdominal Infection

Back 33

- Infection within the peritoneum or retro-peritoneal space
- Localized infection
* contained within visceral structures
* e.g. cholecystitis
* Abscess = purulent collection of fluid separated from surrounding tissue by a wall comprised of inflammatory cells and adjacent organs. Become a barier to antibiotic tx
- Generalized infection
* Peritonitis = acute inflammation of the peritoneal lining due to microorganisms, chemicals, irradiations, or foreign body injury

Front 34

Three Classifications of Intra-abdominal Infection

Back 34

- Primary Peritonitis = spontaneous bacterial peritonitis (SBP)
* Primary peritonitis occurs without an evident source.
* Occurs in patients with ascites
- Cirrhosis
- Chronic actice and acute viral hepatitis
- Congestive Heart Failure
- Metastatic malignant disease
- Systemic lupus erythmatosus
- Lymphedema

- Secondary Peritonitis
- Tertiary Peritonitis

Front 35

Primary Peritonitis: Epidemiology

Back 35

- Children = occurs with post-necrotic cirrhosis from viral hepatitis, or nephrotic syndrome
- Adults = usually occurs in patients with:
* alcoholic cirrhosis and ascites
* nephrotic syndrome
* congestive heart failure
* metastatic malignant disease
* systemic lupus erythematosus

(Acsites – fluid, blood flow, oxygen, electrolytes, glucose, etc all very yummy for bacteria
Any bacteria gets in = infection)

Front 36

Primary Peritonitis in Cirrhosis

Back 36

- Occurs in 10-30% of patients with liver cirrhosis
- Incidence rises to >40% with ascitic fluid protein content <1 gm/dL (b/c correlates to poor liver fxn)
- Risk factors
* Previous SBP episode (predisposition)
* Low ascitic fluid protein (marker of severe liver disease)
* Gastrointestinal bleeding (Marker of severe disease)
* Severity of liver disease
- Prognosis
* 40-70% of patients will have SBP recurrences
* One year survival 30-50% (poor prognostic factor)

Front 37

1° Peritonitis: Pathogenesis

Back 37

- Hematogenous spread
* Portosystemic shunting in cirrhosis decreases removal of bacteria by hepatic reticuloendothelial system (loss of filtering mechs
- Lymphatic disruption
* Bacteria contaminate hepatic lymph nodes and pass into ascitic fluid
- Impairment of bactericidal activity by alteration of peritoneal defenses
* Proportional to severity of liver disease

Front 38

What are the three pillars of management for complicated intra-abdominal infections?

Back 38

1. Removal or control of the source of contamination (Source control to stop leakage into peritoneal cavity)

2. Physiological support (Feeding, fluids, ventilation, other supportive care.)

3. Antimicrobial therapy

Front 39

Goals of Antimicrobial Therapy for Intra-abdominal Infections

Back 39

1. Eradicate infecting pathogens
2. Reduce risk of recurrent infections
3. Shorten clinical manifestations of infection

The above goals should be achieved while minimizing risks of adverse events and maximizing cost-effectiveness of therapy

Front 40

What is the effect of appropriate antibiotic therapy on outcome measures for intra-abdominal infections?

Back 40

Wound infection: little to no difference

Abcess: incidences are MUCH lower if patient is started on appropriate therapy. There is also a significant reduction in incidence if patient is switched to appropriate therapy.

Re-operation: Risk is HIGH with inappropriate therapy and lower with change to appropriate therapy and MUCH lower with appropriate therapy from the start.

Death: Risk is highest with inappropriate therapy and MUCH lower with appropriate therapy from the start and with change to appropriate therapy

Front 41

Discuss antibiotic therapy regimens useful in the treatment of IAIs.

Back 41

* Clindamycin has been reported to inhibit more than 95% of the anaerobes.
- It is active against only certain gram-positive cocci (eg, Staphylococcus aureus and Streptococcus pyogenes) but not enterococci, and has virtually no activity against Enterobacteriaceae.
* Metronidazole is active against strict anaerobes.
- Its in vitro activity is poor against aerobes, microaerophiles, and anaerobes that may become somewhat aerotolerant on subculture.
- Since gram-negative bacilli and microaerophilic gram-positive cocci are frequent copathogens in polymicrobial anaerobic infection, metronidazole should be used in combination with another agent.
* Bacteroides fragilis and other Bacteroides species are usually resistant to first-, second-, and third-generation cephalosporins, although cefoxitin is distinctly more active than any of the other second generations against Bacteroides species.
- First- and second-generation cephalosporins are active against most strains of Escherichia coli, Proteus mirabilis, and Klebsiella pneumoniae, and the third generations demonstrate improved activity against the Enterobacteriaceae.
* Penicillin G and ampicillin have excellent activity against all anaerobes, with the exception of Bacteroides species.
- The combination of ticarcillin or piperacillin with the ß-lactamase inhibitors clavulanic acid or tazobactam, respectively, confer activity against ß-lactamase–producing strains of Bacteroides fragilis, Escherichia coli, and Klebsiella pneumoniae.
- Because of this combined spectrum of activity, monotherapy is possible for polymicrobial anaerobic intra-abdominal infections.
* Aminoglycosides have excellent coverage against Enterobacteriaceae and Pseudomonas aeruginosa.
- Other than that, they do not have much advantage over penicillins or cephalosporins.
- An aminoglycoside is often included with a ß-lactam antibiotic for empiric treatment of critically ill patients in whom a resistant pathogen, like Pseudomonas aeruginosa, is suspected.
* The fluoroquinolones are active against almost all aerobic gram-negative bacilli.
* Ciprofloxacin is most potent against Pseudomonas aeruginosa.

Front 42

What is the guideline prefered antibiotic regimen for IAI?

Back 42

* No prefered regimen.

* The single most important criterion that guides the selection of an initial empiric antimicrobial regimen is the activity of the agent against the common pathogens that cause intra-abdominal infections. The recommended therapies are active against the typical aerobic and anaerobic pathogens observed in patients with community-acquired infections.
* Antimicrobial agents differ with regard to their coverage of Enterococcus and the extent of their gram-negative coverage.
* Routine coverage of enterococci is not necessary in most patients with community-acquired intra-abdominal infections and should not be a primary consideration in the choice of antimicrobial agents.
* Regarding activity against gram-negative organisms, some antimicrobials, such as second-generation cephalosporins or ampicillin/sulbactam, provide less coverage of such organisms as Enterobacter and Pseudomonas than broader-spectrum agents in their classes do.

Front 43

Single agents for use in IAI.

Back 43

* Ampicillin/sulbactam
* Cefotetan
* Cefoxitin
* Ertapenem
* Imipenem/cilastin
* Meropenem
* Piperacillin/tazobactam
* Ticacillin/clavulanic acid
* Doripenem
* Tigecycline
* Moxifloxacin

Front 44

Combination regimens for use in IAI.

Back 44

* Aminoglycoside + anti-anaerobe agent
- amikacin, gentamicin, netilmicin, or trobramycin
- PLUS clindamycin or metronidazole

* Aztreonam + clindamycin
* Cefuroxime + metronidazole
* Ciprofloxacin + metronidazole
* Levofloxacin + metronidazole
* 3rd/4th gen cephalosporin + anti-anaerobe agent
- cefepime, cefotaxime, ceftazadime, ceftizoxime, ceftriaxone
- PLUS clindamycin or metronidazole

Front 45

Regimens Currently Recommended for Initial Empiric Treatment of Complicated IAIs

Back 45

* Single Agents for use in Mild-to-moderate severity: perforated or abscessed appendicitis and other infections
- Cefoxitin, ertapenem, moxifloxacin, tigecycline, or ticarcillin-clavulante

* Single agents for use in High risk or severity: severe physiologic disturbance, advanced age, or immunocompromised state
- Imipenem/cilastatin, meropenem, doripenem, or piperacillin/tazobactam

* Combination Regimens for use in Mild-to-moderate severity CA-IAI
- Metronidazole + cefazolin, cefuroxime, ceftriaxone, cefotaxime, ciprofloxacin, or levofloxacin

* Combination Regimens for use in High risk or severity CA-IAI
- Metronidazole + cefepime, ceftazidime, ciprofloxacin, or levofloxacin

Front 46

What organisms are seen in health-care associated complicated intra-abdominal infections at institution?

Back 46

* <20% resistant P. aeruginosa, ESBL-producing Enterobacteriaceae, Acinetobacter, or other MDR GNB

* ESBL-producing Enterobacteriaceae

* P. aeruginosa >20% resistant to ceftazidime

* MRSA

Front 47

What agents are recommended for use against health-care associated complicated intra-abdominal infections at an institution that sees <20% resistant P. aeruginosa, ESBL-producing Enterobacteriaceae, Acinetobacter, or other MDR GNB?

Back 47

* Carbapenem (imipenem, meropenem, doripenem

* Piperacillin-tazobactam

* Ceftazidime or cefepime, + metronidazole

Front 48

What agents are recommended for use against health-care associated complicated intra-abdominal infections at an institution that sees ESBL-producing Enterobacteriaceae?

Back 48

* Carbapenem (imipenem, meropenem, doripenem

* Piperacillin-tazobactam

* Aminoglycoside

Front 49

What agents are recommended for use against health-care associated complicated intra-abdominal infections at an institution that sees P. aeruginosa >20% resistant to ceftazidime?

Back 49

* Carbapenem (imipenem, meropenem, doripenem

* Piperacillin-tazobactam

* Aminoglycoside

Front 50

What agents are recommended for use against health-care associated complicated intra-abdominal infections where MRSA is likely?

Back 50

Vancomycin

Front 51

What bug should always be covered in hospital acquired IAI?

Back 51

* Remember – anti-psuedomonal regimens for hospital aquired
* Then choose regimen based on resistance profile w/in your hospital

Front 52

What agents are recommended for Initial Empiric Treatment of community-acquired acute cholecystitis of mild-to-moderate severity?

Back 52

Cefazolin, cefuroxime, or ceftriaxone

Front 53

What agents are recommended for Initial Empiric Treatment of community-acquired cholecystitis of severe physiologic disturbance, advanced age, or immunocompromised state?

Back 53

Imipenem/cilastatin, meropenem, doripenem, piperacillin/tazobactam, ciprofloxacin, levofloxacin, or cefepime, + metronidazole

Front 54

What agents are recommended for Initial Empiric Treatment of Health-care associated biliary infection of any severity?

Back 54

Imipenem/cilastatin, meropenem, doripenem, piperacillin/tazobactam, ciprofloxacin, levofloxacin, or cefepime, + metronidazole, + vancomycin

Remember - CA – gram- no need to cover anaerobes
HA – add anaerobes back in esp anti-pseudomonal activity

Front 55

Treatment of secondary peritonitis

Back 55

* Utilize culture and sensitivity information
* Duration of therapy is variable: 4-7 days or longer depending on adequacy of source control, patient response
* If patient does not improve within 4 days, consider
- Undrained focus of infection or other source control issue
- Resistance
- Superinfection

Front 56

J.J. is a 63-year-old man with colon cancer. One day after surgical resection of his colon he develops N/V, anorexia, fever to 103F, shaking chills and abdominal pain. Exam reveals rebound tenderness, a rigid abdomen, and WBC count of 13,000 cells/mm3. Which of the following antibiotic regimens is LEAST appropriate for treatment of J.J.’s secondary peritonitis?
A. Ciprofloxacin + metronidazole
B. Ceftazidome + metronidazole
C. Cefepime alone
D. Meropenem alone
E. Tigecycline alone

Back 56

Cefepime alone


This patient has classic signs and symptoms of an intra-abdominal infection; he should be treated as a secondary peritonitis due to his history of colon cancer and recent abdominal surgery. Appropriate antibiotics must cover both Gram-negative aerobes and anaerobes. The only drug option here that does NOT cover both of those categories of pathogens is cefepime; it has good Gram-negative aerobic coverage but minimal/no anaerobic coverage for peritonitis infections. Cefepime would therefore be the least appropriate choice; any of the others would provide the required spectrum of activity.

The MOST appropriate choice, according to the new IDSA guidelines, would probably be meropenem. Because the onset of the infection was after a surgical procedure, many clinicians would argue that this should be considered a hospital-acquired infection and the guidelines would specify carbapenem monotherapy as being appropriate in this patient (assuming low resistance rates in the hospital). However, the other options would still be considered appropriate by many.

Front 57

J.J. is a 63-year-old man with colon cancer. One day after surgical resection of his colon he develops N/V, anorexia, fever to 103F, shaking chills and abdominal pain. Exam reveals rebound tenderness, a rigid abdomen, and WBC count of 13,000 cells/mm3.
Which of the following regimens would be MOST appropriate for J.J. if he was known to have a severe allergy to penicillins?
A. Levofloxacin alone.
B. Aztreonam alone.
C. Gentamicin + vancomycin.
D. Cefuroxime + metronidazole.
E. Aztreonam + penicillin.
F. Metronidazole + tobramycin.

Back 57

Metronidazole + tobramycin.

Automatically take out choices #4 and #5 because of the penicillin allergy; since there are other appropriate treatment options available there is no reason to mess with either a penicillin or a cephalosporin with potential cross-hypersensitivity. Levofloxacin and aztreonam have good Gram-negative aerobic activity but no useful anaerobic activity. Gent + vanco also lacks the anaerobic coverage and would not be a good regimen. The most appropriate choice is therefore #6, metronidazole + tobramycin.

Front 58

J.J. is a 63-year-old man with colon cancer. One day after surgical resection of his colon he develops N/V, anorexia, fever to 103F, shaking chills and abdominal pain. Exam reveals rebound tenderness, a rigid abdomen, and WBC count of 13,000 cells/mm3.
Which of the following statements regarding the treatment of J.J.’s peritonitis is TRUE?
A. J.J. should be treated with parenteral antibiotics for 14-21 days.
B. J.J. could potentially be switched to oral antibiotics if responding well to parenteral drugs.
C. J.J. should be treated with no more than 5-7 days of antibiotics.
D. Complications related to J.J.’s infection would be very unusual and would not be expected.

Back 58

J.J. could potentially be switched to oral antibiotics if responding well to parenteral drugs.

The usual duration of therapy will be in the 7-10 day range, but this is variable depending on patient response. Parenteral antibiotics for 14-21 days is a little long to start with, and there’s no rule that J.J. has to get parenteral antibiotics for the entire treatment duration. He might require more than 5-7 days, especially if he is slow to respond (he’s an older patient with a serious underlying disease and a bad infection). Complications in a case such as this, with this type of patient, would be not at all uncommon and you’d almost expect it. So choice #2 would be the most appropriate; you can start him on parenteral antibiotics and switching to PO drugs after exhibiting a good response is certainly an option.

Front 59

Pathogenesis of Intra-abdominal Abscess

Back 59

* Contamination of abdomen followed by localization of infection
* Location depends (at least partially) on site of primary process
* May take days to weeks to evolve
* Abscess environment typically acidic, less aerobic, high bacterial burden
- Microbes = anaerobes, facultative bacteria

Front 60

Etiology of Intra-abdominal Abscess

Back 60

* Previous secondary peritonitis (appendicitis, pancreatitis, diverticulitis, genitourinary tract lesions)
* Surgery
* Trauma

Front 61

Clinical presentation of Intra-abdominal Abscess

Back 61

* Often non-specific complaints
* Abdominal pain may be either localized or quite vague
* Low grade fever
* May result in peritonitis, sepsis if abscess ruptures

Front 62

Diagnosis of Intra-abdominal Abscess

Back 62

* Exploratory laparotomy
* Ultrasound or CT scan (most accurate)
* Should be considered in any post-operative patient who develops fever several days to weeks after surgery

Front 63

Bacteriology of Intra-abdominal Abscess

Back 63

* Similar to that seen in secondary peritonitis
* Anaerobes more numerous than aerobic bacilli

Front 64

Treatment of Intra-abdominal Abscess

Back 64

* Surgery
* Percutaneous drainage
* Antibiotics similar to those for 2 peritonitis
- Penetration issues
- Low pH in abscess adversely effects activity of clindamycin, aminoglycosides
- Inoculum effect may decrease activity of-lactams
- -lactamase production among many pathogens may be an issue
* General supportive care

Front 65

C.C. is a 53 y.o. male with a history of alcoholic liver disease (ALD) complicated by one episode of upper GI bleeding, refractory ascites, and encephalopathy. He presents with vague abdominal pain, low-grade fever, and mental status changes. He is suspected to have SBP. The most appropriate initial action would be:
A. Start empiric antibiotics.
B. Perform a pericentesis.
C. Perform a lumbar puncture.
D. None of the above

Back 65

Perform a pericentesis.

As always, cultures should be obtained before starting antibiotic therapy. Although it’s reasonably predictable what organisms are potentially causing this infection, it would still be nice to know the specific pathogen and antibiotic susceptibilities. Pericentesis, or tap of the ascitic fluid, should therefore be performed and samples sent for culture and susceptibility before initiating antibiotics.

Front 66

C.C. is a 53 y.o. male with a history of alcoholic liver disease (ALD) complicated by one episode of upper GI bleeding, refractory ascites, and encephalopathy. He presents with vague abdominal pain, low-grade fever, and mental status changes. He is suspected to have SBP. A pericentesis is performed and shows ascitic fluid with a WBC count of 450 cells/mm3 and both protein and LDH are slightly elevated. The most appropriate action would now be to:
A. Begin antibiotics for treatment of SBP.
B. Hold off on antibiotics and repeat the pericentesis; the results are inconclusive.
C. Hold off on antibiotics and treat C.C. for encephalopathy.
D. Hold off on antibiotics and observe C.C. for several days.

Back 66

Begin antibiotics for treatment of SBP

The elevated white blood cell count, and slightly elevated protein and LDH, are all consistent with SBP. This finding, along with the clinical signs and symptoms which are also consistent with SBP, makes a pretty convincing picture for the presence of infection and the need to treat. It would therefore be most appropriate to immediately begin antibiotic treatment for SBP. The results are not inconclusive (particularly along with the clinical findings) and antibiotics should not be withheld on these grounds. Either treating the encephalopathy first or observing for several days would unnecessarily increase the risk of complications and mortality, which is already considerable. So, the most appropriate action at this time would be to initiate antibiotic therapy.

Front 67

C.C. is a 53 y.o. male with a history of alcoholic liver disease (ALD) complicated by one episode of upper GI bleeding, refractory ascites, and encephalopathy. He presents with vague abdominal pain, low-grade fever, and mental status changes. He is suspected to have SBP. A pericentesis is performed and shows ascitic fluid with a WBC count of 450 cells/mm3 and both protein and LDH are slightly elevated.
C.C. is to be treated for SBP. Which of the following antibiotic regimens would you choose? Assume that C.C. has no known drug allergies.
A. Piperacillin/tazobactam
B. Moxifloxacin
C. Ceftazidime
D. Levofloxacin
E. Doxycycline
F. Ceftriaxone
G. Azithromycin

Back 67

Ceftazidime OR Doxycycline

The most common organisms causing SBP are enteric Gram-negative aerobic bacilli and aerobic streptococci. Third-generation cephalosporins and certain fluoroquinolones are recommended as empiric therapy and would be appropriate in this case, so either levofloxacin or ceftriaxone would be suitable choices. Piperacillin/tazobactam would not be appropriate because neither antipseudomonal nor anaerobic activity are required; it’s too broad spectrum. Ceftazidime would also be inappropriate because of the antipseudomonal activity. Moxifloxacin would be not be the most desirable choice because of its anaerobic activity, which is not required in this case. Doxycycline and azithromycin are not particularly great against the enteric Gram-negatives and would not be great choices here.

Front 68

C.C. is a 53 y.o. male with a history of alcoholic liver disease (ALD) complicated by one episode of upper GI bleeding, refractory ascites, and encephalopathy. He presents with vague abdominal pain, low-grade fever, and mental status changes. He is suspected to have SBP. A pericentesis is performed and shows ascitic fluid with a WBC count of 450 cells/mm3 and both protein and LDH are slightly elevated.
After treatment of his SBP is completed, should C.C. receive antibiotic prophylaxis against repeat episodes?
A. Yes; he is at high risk for recurrence due to refractory ascites.
B. No; he is likely to have recurrent episodes of infection but antibiotics would be of questionable value in C.C.
C. Yes; every patient with ALD should receive prophylactic antibiotics.
D. No; he is not at high risk of recurrent infection.

Back 68

Yes; he is at high risk for recurrence due to refractory ascites.

Not every patient with alcoholic liver disease would be appropriate for SBP prophylaxis since not every patient has advanced disease with refractory ascites, so choice #3 would not be correct. This patient is at very high risk of recurrent infection because of his refractory ascites and because he has now already had an episode of SBP. Antibiotic prophylaxis would potentially be of greatest benefit in exactly this type of patient, so prophylaxis should be strongly considered for this patient.

Front 69

Types of CNS Infections

Back 69

* Meningitis
* Encephalitis
* Meningoencephalitis
* Brain abscess
* Subdural empyema
* Epidural abscess
* Prosthetic device (e.g. shunt infection)

Front 70

Pathogens involved in CNS Infections

Back 70

* Bacteria
* Viruses
* Fungi
* Parasites

Front 71

Cerebrospinal Fluid (CSF)

Back 71

* Protective “shock absorber” for the brain and spinal cord
* Produced in the ventricles by the choroid plexus
* Produced at a rate of ~ 500 ml/day
- Total volume of 110-160 mL in adults
- Total volume of 40-60 in infants
* Removed by arachnoid villi and vertebral venus plexus
* Complete CSF exchange every 3-4 hours

Front 72

Blood Brain Barrier

Back 72

* Crucial in protecting the brain and maintaining homeostasis within the CNS
* Capillary endothelia of the brain
* Packed tightly together producing a protective barrier
* Separates blood from the interstitial fluid of the brain

Front 73

Meninges Anatomy

Back 73

* Dura mater – lies beneath and adherent to the skull
* Pia Mater – lies over the brain tissue
* Arachnoid – middle layer between the dura mater and pia mater
* Subarachnoid space – between the pia mater and arachnoid

Front 74

Define meningitis

Back 74

inflammation of the membranes covering the brain and spinal cord

Front 75

Define Septic meningitis

Back 75

infection due to bacterial invasion from hematogenous spread

Front 76

Define Aseptic meningitis

Back 76

inflammation of the meninges due to causes other than bacteria

Front 77

Define Acute vs. Chronic
meningitis

Back 77

Hours to days vs. > 4 weeks

Front 78

Define Encephalitis

Back 78

Inflammation of the brain

Front 79

What are the methods of developing bacterial memingitis?

Back 79

* Hematogenous – most common
- Spread from the blood
* Contiguous
- Translocation from parameningeal focus (e.g. sinusitis, otitis media)
* Inoculation
- Direct entry (e.g. head trauma, neurosurgery)

Front 80

Discuss Hematogenous Spread

Back 80

* Nasopharyngeal colonization
- N. meningitidis
- H. influenzae
- strep pneumoniae
* Systemic invasion causing bacteremia
* Bacteria becomes encapsulated protecting it from host defenses

Front 81

How are the meninges invaded by bacteria?

Back 81

* Bacteria in the blood replicate to sufficient numbers to invade BBB

* Mechanism of entry
- Unknown – possibly adherence to cerebral capillaries or epithelium of choroids plexus

Front 82

How do bacteria survive in the subarachnoid space?

Back 82

CSF host defenses are poor allowing bacterial proliferation

Front 83

Subarachnoid Inflammation

Back 83

* Mediated by contents within bacterial cell wall
- Lipopolysaccharide, endotoxin, teichoic acid
* Production of inflammatory cytokines
- IL-1, IL-6, prostaglandins, TNF, etc.
* Inflammation causes increased permeability of BBB

Front 84

Manifestations of Menigitis

Back 84

* Influx of albumin
- Brain edema
- Increased intracranial pressure
- Altered cerebral blood flow
* Neuronal injury, cerebral ischemia, and irreversible brain damage
- Loss of cerebrovascular autoregulation

Front 85

Risk Factors for developing meningitis

Back 85

* Respiratory tract infections
* Otitis media
* Cochlear implants
* Head trauma
* Alcoholism
* Cigarette smoking or exposure
* High-dose steroids
* Splenectomy
* Sickle cell disease
* Immunoglobulin deficiency
* Immunosuppression

Front 86

Presentation and Diagnosis of meningitis

Back 86

* Headache, stiff neck (>90%)
* Fever (>90%)
* Altered mental status (>80%)
* Kernig’s sign (>50%)
- Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.
* Brudzinski’s sign (>50%)
- Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed.
* Vomiting (35%)
* Seizures (30%)
* Focal deficits (10-20%)

Front 87

Diagnosis of meningitis

Back 87

* Culture and sensitivities of urine, blood, sputum
* CBC
- increased WBC > 10,000 cells/uL
- increased Neutrophils with bandemia
* CT scan for hydrocephalus or abscesses
* Lumbar puncture for CSF examination
- increased opening pressures > 180 mm H20

Front 88

Manifestations of Menigitis

Back 88

* Influx of albumin
- Brain edema
- Increased intracranial pressure
- Altered cerebral blood flow
* Neuronal injury, cerebral ischemia, and irreversible brain damage
- Loss of cerebrovascular autoregulation

Front 89

Risk Factors for developing meningitis

Back 89

* Respiratory tract infections
* Otitis media
* Cochlear implants
* Head trauma
* Alcoholism
* Cigarette smoking or exposure
* High-dose steroids
* Splenectomy
* Sickle cell disease
* Immunoglobulin deficiency
* Immunosuppression

Front 90

Presentation and Diagnosis of meningitis

Back 90

* Headache, stiff neck (>90%)
* Fever (>90%)
* Altered mental status (>80%)
* Kernig’s sign (>50%)
- Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.
* Brudzinski’s sign (>50%)
- Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed.
* Vomiting (35%)
* Seizures (30%)
* Focal deficits (10-20%)

Front 91

Diagnosis of meningitis

Back 91

* Culture and sensitivities of urine, blood, sputum
* CBC
- increased WBC > 10,000 cells/uL
- increased Neutrophils with bandemia
* CT scan for hydrocephalus or abscesses
* Lumbar puncture for CSF examination
- increased opening pressures > 180 mm H20

Front 92

CSF Lab Parameters

Front 93

Manifestations of Menigitis

Back 93

* Influx of albumin
- Brain edema
- Increased intracranial pressure
- Altered cerebral blood flow
* Neuronal injury, cerebral ischemia, and irreversible brain damage
- Loss of cerebrovascular autoregulation

Front 94

Risk Factors for developing meningitis

Back 94

* Respiratory tract infections
* Otitis media
* Cochlear implants
* Head trauma
* Alcoholism
* Cigarette smoking or exposure
* High-dose steroids
* Splenectomy
* Sickle cell disease
* Immunoglobulin deficiency
* Immunosuppression

Front 95

Presentation and Diagnosis of meningitis

Back 95

* Headache, stiff neck (>90%)
* Fever (>90%)
* Altered mental status (>80%)
* Kernig’s sign (>50%)
- Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.
* Brudzinski’s sign (>50%)
- Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed.
* Vomiting (35%)
* Seizures (30%)
* Focal deficits (10-20%)

Front 96

Diagnosis of meningitis

Back 96

* Culture and sensitivities of urine, blood, sputum
* CBC
- increased WBC > 10,000 cells/uL
- increased Neutrophils with bandemia
* CT scan for hydrocephalus or abscesses
* Lumbar puncture for CSF examination
- increased opening pressures > 180 mm H20

Front 97

CSF Lab Parameters

Back 97

Front 98

Pathogens involved in meningitis

Back 98

* Historically - 1980’s
- 45% H. influenzae
- 18% S. pneumoniae
- 14% N. meningitidis
* After 1990 - H. influenzae vaccine
- 47% S. pneumoniae
- 25% N. meningitidis
- 8% L. monocytogenes
- 7% H. influenzae
* After 2000 – Pneumococcal vaccine
- Children < 2: 70% decline in pneumococcal meninigitis
- Children < 5: 60% decline
- Adult invasive S. pneumo infections decreased as well

Front 99

Haemophilus influenzae in meningitis

Back 99

* Only accounts for 7% of cases
- Decreased due to vaccination programs
- Vaccination starts at 2 months of age
* Mortality ~ 6%
* Close contact transmission

Front 100

Neisseria Meningitidis in meningitis

Back 100

* Accounts for 25% of cases
* 60% of cases in 2-18 years of age
* Mortality rate ~ 10%
* Easily transmitted to close contacts
* Unique Immune reaction
- Fever, arthritis, pericarditis approximately 10-14 days after infection
* Petechiae in 50% of patients

Front 101

Streptococcus Pneumoniae in meningitis

Back 101

* Most common cause of meningitis in adults
* Mortality
- Adults 20-30%
- Children 4-17%
* Coma and seizures common
* 29-56% of patients have neurologic sequelae

Front 102

Listeria monocytogenes in meningitis

Back 102

* ~ 8% of meningitis cases
* ~ 20% of cases in > 60 yo
* Mortality ~ 15%
* GI bug
- Milk, cheese, poultry, beef
* Neonates, alcoholics, immunosuppressed, and elderly

Front 103

Desired Antimicrobial Characteristics in meningitis

Back 103

* Coverage of likely pathogens
* Bactericidal activity
* Therapeutic levels achieved in the CSF

* Antimicrobial activity may promote release of bacterial factors that promote inflammation

Front 104

Factors impacting antimicrobial penetration into the CNS

Back 104

* Meningeal inflammation
- Increases antibiotic penetration
* Molecular weight
- Lower MW compounds pass through easier
* Lipid solubility
- Higher lipid solubility passes through easier
* pH
- Un-ionized compounds can diffuse the BBB
* Protein binding
- Only free drug can diffuse across the BBB

Front 105

Antimicrobial CSF Penetration:
Agents with Very Good penetration

Back 105

Chloramphenicol, metronidazole, TMP/SMX, rifampin and other TB drugs

(penetrate CSF well regardless of meningial inflammation)

Front 106

Antimicrobial CSF Penetration:
Agents with Good penetration

Back 106

PCNs, most 3rd and 4th generation cephalosporins, carbapenems, Fluoroquinolones, vancomycin, linezolid, acyclovir
(Adequate CSF penetration achieved when meninges are inflammed)

Front 107

Antimicrobial CSF Penetration:
Agents with Fair to Poor
penetration

Back 107

Aminoglycosides, macrolides, cefazolin, amphotericin B, itraconazole

(inadequate penetration even with meningeal inflammation)

Front 108

Ways to Increase CSF Concentrations of antibiotics

Back 108

* High dose therapy
- Examples:
* Ceftriaxone 2g q12h
* Vancomycin 30-40mg/kg/day
* Ampicillin 2g IV q4h

* Direct instillation of antibiotics into the CSF
- Intrathecal or intraventricular administration

* Block drug transport out of the CNS
- Probenicid

Front 109

Empiric Antibiotic Selection for children ages 0-4 weeks old with bacterial meningitis

Back 109

* Pathogens
- Strep agalactiae, Enterococcus, Listeria monocytogenes, E. coli, Klebsiella, Enterobacter
* Treatment
- Ampicillin + cefotaxime or gentamicin

Front 110

Empiric Antibiotic Selection for children ages 1 month to 4 years old with bacterial meningitis

Back 110

* Pathogens
- H. influenzae
- N. meningitidis
- Strep pneumoniae
* Treatment
- Cefotaxime or ceftriaxone ± Vancomycin

Cefotaxime is alternative to Ceftriaxone in all cases. However, neonates should only receive cefotaxime, not ceftriaxone (it may cause biliary sludging).
Vancomycin should be given based upon local incidence of penicillin resistant S. pneumoniae. Give Vancomycin until minimum inhibitory concentrations (MICs) for cefotaxime or ceftriaxone are available

Front 111

Empiric Antibiotic Selection for ages 5 years to 29 years old with bacterial meningitis

Back 111

* Pathogens
- H. influenzae
- N. meningitidis
- Strep pneumoniae

* Treatment
- Ceftriaxone ± Vancomycin

Cefotaxime is alternative to Ceftriaxone in all cases. However, neonates should only receive cefotaxime, not ceftriaxone (may cause biliary sludging).
Vancomycin should be given based upon local incidence of penicillin resistant S. pneumoniae. Give Vancomycin until minimum inhibitory concentrations (MICs) for cefotaxime or ceftriaxone are available

Front 112

Empiric Antibiotic Selection for ages 30-60 years old with bacterial meningitis

Back 112

* Pathogens
- N. meningitidis
_ Strep pneumoniae

* Treatment
- Ceftriaxone ± Vancomycin

Cefotaxime is alternative to Ceftriaxone in all cases. However, neonates should only receive cefotaxime, not ceftriaxone (may cause biliary sludging).
Vancomycin should be given based upon local incidence of penicillin resistant S. pneumoniae. Give Vancomycin until minimum inhibitory concentrations (MICs) for cefotaxime or ceftriaxone are available

Front 113

Empiric Antibiotic Selection for ages > 60 years of ageold with bacterial meningitis

Back 113

* Pathogens
- Strep pneumoniae
- Listeria monocytogenes
- E. coli
- Klebsiella
- Enterobacter
* Treatment
- Ampicillin + Ceftriaxone or Aminoglycoside ± Vancomycin

Aminoglycosides – gentamicin, tobramycin, or amikacin
Cefotaxime is alternative to Ceftriaxone in all cases. However, neonates should only receive cefotaxime, not ceftriaxone (may cause biliary sludging).
Vancomycin should be given based upon local incidence of penicillin resistant S. pneumoniae. Give Vancomycin until minimum inhibitory concentrations (MICs) for cefotaxime or ceftriaxone are available

Front 114

Empiric Antibiotic Selection for Immunocompromised patients with bacterial meningitis

Back 114

* Pathogens
- Any including Viral and Fungal

* Treatment
- Vancomycin + ceftazidime or
- cefepime +/- Rifampin +/- fluconazole +/- acyclovir

Front 115

Microbe Specific Therapy in meningitis

Back 115

* Adjust and narrow antimicrobial therapy as indicated

* Set duration of therapy
- Typically 7-14 days
* H. Influenzae, Strep Pneumo, N. Meningitidis
- 21 days if resistant gram negative or viral

Front 116

Adjunctive Therapy for meningitis

Back 116

* Glucocorticoids
- Children 8 weeks to 12 years old
+ Dexamethasone 0.6 mg/kg/day IV divided q6h for 2-4 days
+ Reduces neurologic and audiologic sequelae of H. influenzae and Strep pneumoniae
- Adults
+ Dexamethasone 10mg IV q6h x 4 days
+ Reduces mortality, neurologic, and audiologic sequelae of all cause meningitis
*Majority of benefit seen with S. pneumoniae meningitis

- Administer at or up to 15 minutes before initiation of antimicrobial therapy

- Dexamethasone decreases mortality for Mycobacterium tuberculosis meningitis, but does not prevent disability

Front 117

What might be a downfall to steroid therapy in meningitis?
A. Immunosuppression
B. Decreased antibiotic penetration into CSF
C. Drug interactions
D. Decreased antibiotic effectiveness
E. GI bleed
F. Increased blood glucose
G. All of the above

Back 117

All of the above

Front 118

Prevention Chemoprophylaxis of meningitis

Back 118

* H. influenzae
- Child <4 years of age and unvaccinated
- Child care facilities
- Nursing home residents
- Rifampin 20mg/kg/day up to 600mg po qd for 4 days
- Minocycline is alternative in adults
* Strep pneumoniae
- Generally not recommended
* N. Meningitidis
- All close contacts (home and daycare)
- Rifampin 10mg/kg q12h up to 600mg po q12h x 48 hours
- Ciprofloxacin 500mg x 1 or ceftriaxone 125mg or 250mg IM x 1 are alternatives
* Strep agalactiae
- High risk deliveries
- Ampicillin 1-2 grams q6hrs until delivery
- Clindamycin or erythromycin for penicillin allergy

Front 119

Immunoprophylaxis for meningitis

Back 119

Immunoprophylaxis
Vaccinations
* H. influenzae
- 4 doses for initial immunization
* Strep pneumoniae
- Infants
- >65 years old
- DM, CAD, COPD, chronic liver disease, asplenic, alcoholics, immunosuppressed
* N. meningitidis
- Not routine – 1 dose if adult, 2 doses if <10 yo

Asplenic patients should receive vaccination against H.influenzae, strep pneumoniae, and N. meningitidis.

Front 120

Monitoring Parameters

Back 120

* Similar to other infectious diseases
* Clinical signs and symptoms
- Fever, AMS, Stiff neck
- Improvement should occur within 24-48 hours
* Laboratory tests
- CBC with diff, chem-7, renal function
* Antibiotic side effects

Front 121

Other CNS Infections

Back 121

Mycobacterium Tuberculosis
Viral
Fungal
Parasite
Drug induced
Shunt Infections
Brain Abscess

Front 122

Viral Encephalitis

Back 122

* Enteroviruses (polio, coxsackie), mumps, herpes simplex, adenovirus, cytomegalovirus, lymphocytic choriomeningitis virus, Epstein-Barr, varicella, and HIV.
* Diagnosis
- PCR
* Presentation
- Headache, mild fever, nuchal rigidity, malaise, drowsiness, nausea, vomiting, and photophobia
* Herpes simplex virus
- Acyclovir 10mg/kg IV q8h for 14-21 days
- Alternative: Foscavir 40mg/kg q8h

* Cytomegalovirus (CMV)
- Ganciclovir 5mg/kg IV q12h x 14 days
- Continue maintenance ganciclovir or valganciclovir QD

Front 123

What might be a downfall to steroid therapy in CNS infections
Immunosuppression
Decreased antibiotic penetration into CSF
Drug interactions
Decreased antibiotic effectiveness
GI bleed
Increased blood glucose
All of the above

Back 123

Increased blood glucose
All of the above

Front 124

what is the key point with adding steroids in the treatment on CNS infections

Back 124

have to be given at pr up to 15 minutes prior Ab because want to prevent the inflammaiton caused by the breaking of the bacterial cell membranes, thus releasing endotoxins

there is no benefit if you give them after AB

Front 125

RM is a 3 week old WM brought to the ED by his parents after 24 hours of fussiness, emesis/spitting, and fever (100.6 F).
In the ED the patient experienced a seizure with arm, leg, and neck involvement.
IV lorazepam was given and stopped the seizure.
The patient was loaded with 20mg/kg phenobarbital
Lumbar Puncture Results
CSF Protein 156, glucose 20, WBC 15, RBCs 5
Gram stain results pending

What is the appropriate empiric antimicrobial therapy?
Vancomycin + Rifampin
Ampicillin + Gentamicin
Ceftriaxone + Vancomycin
Cefepime + Ampicillin + Dexamethasone

Back 125

Ampicillin + Gentamicin

Front 126

RM’s gram stain of the CSF comes back as gram negative diplococci and he is believed to have N. meningitidis.
You also notice RM’s two year old sister running around the NICU.

Does RM’s sister need prophylaxis and if so what are the apropriate agents

A. Ampicillin + Cefotaxime
B. Rifampin x 48hrs
C. Ciprofloxacin x 1 dose
D. Minocycline x 48hrs

Back 126

yes

B. Rifampin x 48hrs

Front 127

RM’s gram stain of the CSF comes back as gram negative diplococci and he is believed to have N. meningitidis.
You also notice RM’s two year old sister running around the NICU.
Cultures from the CSF confirm that RM has N. Meningitidis meningitis
How would you change RMs current therapy?
DC gentamicin and continue ampicillin for 8 weeks
DC gentamicin and ampicillin. Start cefotaxime and treat for a total of 7 days.
DC gentamicin and start Vancomycin for 14 days
Continue current therapy for 10 days

Back 127

DC gentamicin and ampicillin. Start cefotaxime and treat for a total of 7 days.

Front 128

BM is a 75 yo WM who comes into the ED with altered mental status, fever, increased WBCs and headache. CSF results show increased protein, 10,000 WBCs, glucose 20. Gram stain is pending.
His PMH is significant for a anaphylactic allergy to Penicillin.
HOw would you treat
Vancomycin + Ceftriaxone + Ampicillin
Vancomycin + Aztreonam
Vancomycin + Chloramphenicol + TMP/SMX
Aztreonam + TMP/SMX

Back 128

Vancomycin + Chloramphenicol + TMP/SMX