ETC8363-2020 BCCCP-Infectious Disease I

Individual risk factors for VAP

Chronic lung disease or acute lung injury

trauma (chest trauma or TBI)/ Burns

Re-intubation

aspiration

coma

How long after intubation does VAP happen?

>48hrs after endotracheal intubation.

VAP is caused by monomicrobial or polymicrobial pathogens?

Both, rarely viral or fungal.

Risk factors for MDROs Causing VAP?!?!

Prior IV ABX in preceding 90 days

Acute Renal Replac Therapy (RRT) before VAP onset

5 or more days of hospitalization prior to onset of VAP

Increased sputum production.

Septic Shock at time of VAP

ARDS preceding VAP.

How to prevent VAP

1.Avoid or limit duration of ET Intubation

2. Minimize duration & deep level of sedation ( to promote assessment of readiness to extubate)

3. Maintain/improve physical conditioning while on MV

4. Minimize pooling of secretions above ET tube cuff.

5. Elevate head of bed at least 30 degrees.

6. Maintain integrity of MV circuit.

Clinical Signs and Symptoms of pneumonia include?

new or changing infiltrate on chest X-ray AND 2 or more of the following....

Elevated WBC

Fever (>100.4*F/38*C)

Macroscopic purulent sputum production

Impaired or worsening oxygenation

Non-invasive techniques for obtaining resp. tract cultures for VAP are...

Obtained from what part of lung?

What kind of results does is yield?

Tracheal aspirate from ET or Tracheostomy tube

obtained sample from upper airway secretions

Yields semi-quantitative results.

Invasive Techniques for obtaining resp. tract cultures in VAP are?

obtained from where?

What king of results does it yield

Blind Catheter-directed/Bronchoscopic BAL

distal sample of lung lobe/segment (uses saline lavage) yields significant QUANTITATIVE results. (if <10,000 CFU/mL = d/c ABX)

Bronchoscopic protected specimen Brush (PSB): Distal sampling of specific bronchial segment significant QUANTITATIVE growth. <1,000 CFU/mL= d/c ABX

Diagnostic Strategy for VAP includes what?

Clinical Suspicion + NON-INVASIVE sampling = SEMI-quantitative results

and not invasive sampling which yields quantitative results.

ALL patients with suspected VAP should receive a ABX against what organisms.

MSSA and P.Aeruginosa

At least give one agent for each in all pts.

Vanc + Cefepime

In patients with VAP, when do you need to have double pseudomonal coverage (with different MOA)?

MDRO risk factors

ICU antibiogram with >10% gram(-) isolates resistant to agent used as monotherapy

ICU ABX susceptibility is unavailable.

When should you include MRSA coverage for VAP?

MDRO risk factors

ICU MRSA prevalence is >10-20% S. Aureus

Prevalence of MRSA is not know.

When treating VAP patients

WITHOUT MDRO risk factors

SINGLE-Antipseudomonal agent with 90% or more activity

MRSA prevalence is < 10-20%.

What is the most likely pathogen and

What is the treatment?

P. Aeruginosa

S. Pneumoniae

Haemophilus Influenzae

A/B-hemolytic Strep

MSSA

Gram Neg Bacilli (GNB, like E.coli, Klebs, Enterobacter, Proteus, serratia)

Give:

Cefepime, Imi/meropenem, Levofloxacin, Zosyn

Ceftriaxone is a reasonable agent for empiric manage-

ment of early onset VAP with activity against common

pathogens

When treating VAP patients

Patients WITHOUT MDRO risk factors

Single antipseudomonal agent has <90% activity

and/or MRSA prevalence is > 10-20%

What are the likely pathogens and how do we treat them?

P. Aeruginosa

S. Pneumoniae (all same but + /MRSA)

Haemophilus Influenzae

A/B-hemolytic Strep

MSSA

Gram Neg Bacilli (GNB, like E.coli, Klebs, Enterobacter, Proteus, serratia)

Give:

Antispeudomonal B-Lactam

Aztreonam, Cefep/ceftazidime, imi/meropenem, Zosyn

++PLUS++

Antispeudom FQ ///or/// Aminoglyco

( Levaquin/Cipro) //////// ( ami/gent/tobramycin)

+/- MRSA ( Vancomycin or Linezolid)

Patients with MDRO what are the likely pathogens for VAP and how do we treat them?

P.Aeruginosa

MRSA

Acinetobacter

RESISTANT-GNB ( ESBL)

Stenotrophomonas Maltophilia

Give:

Antispeudomonal B-Lactam

Aztreonam, Cefep/ceftazidime, imi/meropenem, Zosyn

+++PLUS+++

Antispeudom FQ ///or/// Aminoglycoside

( Levaquin/Cipro)______________________( ami/gent/tobramycin)

+++PLUS+++

MRSA ( Vancomycin or Linezolid)

Which ABX cannot be used for MRSA VAP and why?

Daptomycin due to direct inhibition of daptomycin by lung surfactant.

True of False:

In VAP, monotherapy with a beta-lactam to treat P. Aeruginosa can be used in all patients when beta-lactam shows great susceptibility to organism?

FALSE:

Even if beta-lactam has great suceptibility you would not do monotherapy with beta-lactam if pt is Immunocompromised, has septic shock, or at high risk of dying. In these patients you would do

Beta-Lactam + Antipseudomonal FQ or/aminoglycoside.

After septic shock has been resolved in IMMUNOCOMPETENT pt then you can scale down to monotherapy.

What ABX do you give for VAP with Acinetobacter spp?

Imi/meropenem (Amp/sulbactam as an alternative)

What ABX do you give for Stenotrophomas Maltophilia?

Sulfa/Trimethoprim (Bactrim)

How long should you treat VAP for with ABX?

7 days ( definitive for ALL patients)

Risk Factors for CLABSI?

1. Excessive manipulation before/after insertion

2. Internal jugular or Femoral insertion site

3. Microbial Colonization at insertion site/ catheter hub

4. Neutropenia

5. Prolong duration of catheterization

6. Prolong hospitalization prior to catherization

7. TPN

Where do CVC catheters end?

Placed in ...

Inferior/Superior/Distal Vena Cava

Right Atrium

Pulmonary artery

(usually short term catheters)

what is the most commonly used CVC lumen?

Singe and Triple lumen.

What type of catheter is a PICC line?

Peripherally Inserted Central Catheter (PICC)

Short-Medium term central catheter

How does the CDC define a CLABSI with respect to time from insertion?

Infection occurring from 2 days after insertion up to one day AFTER catheter removal.

CDC : A CLABSI is defined/classified how?

Due to ...

Recognized pathogen: culture from one or more blood cx ( and org is not related to another infection at different site. like change in chest x-ray)

Common Commensal organism: Diptheriod, Bacillus, Coag(-) staph, Viridans Strep. ( this is from two or more blood cultures drawn on SEPERATE occasions AND organism is not related to another infection at different site)

+ At least ONE of the following...

Fever > 100.4F (38C), Chills, or Hypotension.

How does the IDSA define CLABSI?

bacteremia/fungemia in pts with intravascular device:

*>1 (+) Peripheral Blood cx (same organisms growing from percutaneous blood cx + CVC tip/catheter hub

(or catheter cup/tip + peripheral vein)

*clinical manifestation ( fever, chills, hypotension)

*no additional source of infection other than catheter.

like change in chest x-ray suspecting pneumonia.

CLABSI are monomicrobial or polymicrobial?

What type of organisms?

MONOmicrobial

Coag-neg staph ( Staph epi)

Staph Aureus

Candida (less common)

Enteric Gram Neg Bacili: E.coli, Klebs, Enterobacter

(less common)

Candida-CLABSI is more common in what type of pts?

TPN

Prolonged exposure to broad spectrum ABX

Hematologic malignancy

Stem cell/Solid organ transplant

Catherization at femoral site.

Colonization at several sites with candida.

What three organisms increase the suspicion of CLABSI if found in two blood samples?

(+) for Staph Aureus, Coag (-) staph epi, candida

(if NOT ATTRIBUTABLE to another source of infection)

CLABSI. How do we treat?

Fever = most sensitive

Inflammation/purulence @ insertion site= most specific

ALL pts should be considered for cath removal, if cath still needed then insert to DIFFERENT site. but GET CULTURES PRIOR TO REMOVAL.

Treat for possible resistant coag(-) MRSE (staph epi)

Treat for possible resistant coag (+) MRSA (staph Aur)

Give : Vancomycin or Daptomycin (alone)

If possible MDRO (pseudomonas): Cover ALL

--Vanc (MRSA/MRSE)+ cefepime+ tobramycin (double anti-pseudomonal coverage)

14 days after initial negative blood culture.

!!! NEVER LINEZOLID for empiric CLABSI therapy it has WORSE pt outcomes !!!

If pt has CLABSI along with high risk of MDROs how does that change our treatment?

you would add coverage agains gram-neg bacilli

How do we treat Candida-CLABSI?

Echinocandins

(anidulafungin, caspofungin, micafungin)

Fluconazole is okay if pt does not have recent exposure and low prevalence of non-susceptible species.

In CLABSI the duration of ABX therapy is relative to what?

1st day of negative blood culture (treat for 7-14 days uncomplicated gram-neg CLABSI)

What makes a CLABSI "complicated" how does that change our treatment?

Endocarditis (treat for 4-6 wks)

Immunosupression / Diabetes(S. Aureus only)

Chronic Intravascular hardware. (treat for 4-6 wks)

Osteomyelitis(treat for 4-6 wks)

(+) blood cx for > 72hrs from initiation of ABX

Septic thrombus / Thrombophlebitis (treat for 4-6 wks)

you would remove catheter and treat specific pathogen for 4-6wks ( 6-8 wks if osteo)

How do we treat UN-Complicated CLABSI due to coagulase (-) staph EPI?

Consider cath removal

or

If cath remains in place give ABX systemically for 5-7 days +/- ABX lock therapy. for STAPH EPI!

How do we treat UN-Complicated CLABSI due to coag(+) Staph Aureus?

1.Remove cath

2. Give ABX against MSSA or MRSA for 14 days after first negative blood culture.

MSSA: Nafcillin or 1st gen cephalosporin-cefazolin

MRSA: Vanc/Dapto/Linezolid/ Bactrim

T/ F:

If pt has a (+) bacterial growth from catheter tip/hub but (-) blood culture from peripheral vein they should not get ABX?

FALSE:

you would still give ABX towards bacterial for 5-7 days and monitored for s/sx of infection and consider repeat blood cultures.

What are the risk factors for developing SEVERE influenza (requiring hospitalization)

Chronic respiratory/ metabolic illness.

Immunosupression (Disease or pharmacotherapy)

Pregnancy

Age > 65 yrs old

What are the most common complications of SEVERE Influenza are?

Hypoxemic respiratory failure

Bacterial Pneumonia

ARDS

SEVERE Influenza usually caused by strain A & B

How does Influenza spread from person to person?

Droplet transmission

Signs & Symptoms of Influenza?

Fever(3-5 days)

Myalgias (3-5 days)/ Malaise (>2wks)

Headaches

Dry cough

Pharyngitis

Rhinorrhea

How is Influenza diagnosed?

upper resp tract sampling via nasal washing

nasopharyngeal swab (rapid and reliable)

lower resp tract culture (sputum or BAL)

(Dx tests > 5 days beyond onset = false negative results)

Antiviral therapy for flu should be initiated when?

within 48hrs from onset of symptoms

(if in hospital then giving antivirals past 48hrs may also benefit to a lesser extent)

What are the mainstay medications for Influenza and how do they work?

Neuraminidase Inhibitors: Inhibit viral neuraminidase = decrease release of post-replication viral partivles "virions" = limit spread to other tissues.

What are some type of Neuraminidase Inhibitors and what is their niche in treating Influenza

Oseltamivir: oral capsule or powder suspension ( can be given via Oro/Nasogastric tubes but needs liver to convert to active form.

Zanamivir: Inhaled drug via Diskhaler. (not via MV)

IV formulation also available via clinical trial participation in pts who cannot tolerate/absorb oseltamivir due to gastric stasis, malabsorbtion, GI bleed.

Peramivir: only in pts >18yrs old with acute & uncomplicated flu. ONE TIME 15min infusion.

Oseltamivir :

Activity against which strain?

Treatment dose?

ADE?

Influenza A & B

75mg BID x 5 days (150mg BID for severe Flu)

N/V , delirium

Peramivir

Activity against which strain?

Treatment dose?

ADE?

Influenza A&B ( limited data for B)

One time 600mg IV infusion over 15 min.

Diarrhea, Hypersensitivity rxn, Delirium

Zanamivir

Activity against which strain?

Treatment dose?

ADE?

Flu A & B

10mg BID x 5 days (Diskhaler inhalation or IV)

Allergic rxn, diarrhea, N/V, HA, Dizziness

Amantadine

Activity against which strain?

Treatment dose?

ADE?

Flu A only ( even then there is high resistance to it)

100mg BID

N/V, Insomnia, Lower Seizure threshold, Anti-cholinergic effects

CDC defines a UTI as.......

Having AT LEAST one of the following:

1. Fever >100.4*F

2. Suprapubic tenderness

3. Costovertebral angle pain or tenderness

+

__(+) urine cx of >105 CFU/mL ( no more than 2 organisms)

or

__(+) dipstick for Leukocyte esterase / Nitrite

__Pyuria (urine specimen > 10 WBCs in unspun urine)

__Organisms seen on Urine Gram Stain and (+) Urine cx for 103-105 CFU/mL for no more than 2 organisms.

CDC defines a CAUTI as

UTI in a patient who has a catheter for > 2 days

( or UTI in a pt whos catheter was removed 1 day prior to infection)

IDSA defines CAUTI as.....

UTI signs/sx with no other source of infection AND >103 CFU/mL of ONE bacterial species from catheter urine sample ( or midstream-voided sample from pt who has had catheter removal within 48hrs)

Short term Catheters are usually poly or mono microbial?

Short term cath= monomicrobial

Long term caths= form biofilms = polymicrobial.

What is the most prevalent pathogen in CAUTIs?

33%: E. Coli

33%:

Enteric GNB ( Klebs, proteus, Enterobacter)

Non-lactose fermenting GNB ( P. Aeruginosa)

Gram(+) Cocci: Enterococcus, MSSA, MRSA, MRSE

33%: Candida

How do we prevent catheter-associated ASYMptomatic bacteruria

and CAUTIs?

reduce use of urinary catheters ( restrict use to patients with clear indications and removing them as soon as possible)

How long do we treat CAUTI for?

7 days if the pt has signs of improvement < 72hrs after appropriate ABX.

14 days if pt has signs of improvement > 72hrs after appropriate ABX.

How often should you replace a catheter?

Catheters in place for > 2 wks should be replaced and urine sample should be obtained from newly inserted catheter port ( if we pull from old catheter bag = high risk for colonization)

confirmatory urinalysis from old catheter is not needed if catheter has been in place for < 2 weeks so start ABX if pt presents with infection.

What is the most common type of complicated intra-abdominal infection?

Appendicitis.

How does the IDSA define a COMPLICATED intra-abdominal infection?

Infection that extends BEYOND the hollow viscus origin into the peritoneal space creating abscesses or peritonitis. (Spillage of viscus fluid/ flora into peritoneal cavity)

What is PRIMARY peritonitis?

Primary: (SPONTANEOUS Bacterial Peritonitis, Diffuse in nature) related to bacteria translocation from small bowel overgrowth and not peritoneal disruption or organ perforation.

What is SECONDARY peritonitis?

leakage of intraluminal fluid and microorganism 2ndary to macro/micro-perforation of GI tract.

Can be diffuse or localized to an organ.

Causes: direct trauma, ischemia, thrombosis, ulceration, malignancy, and anastomic leak.

What is harder to treat between HA-Intraabdominal infection versus community acquired abdominal infection and why?

HA is harder to treat because those arise from resistant and nosicomial pathogens.

Primary Peritonitis is poly or monomicrobial?

What is/are the pathogen(s)?

Primary peritonitis (translocation across diaphram/small bowel) usually MONOmicrobial

-S. Pneumoniae

-E. Coli

-Klebs.

Secondary Peritonitis is poly or monomicrobial?

2ndary involves leakage from a source. therefore it is usually POLYmicrobial and realted to origin of leakage.

2ndary peritonitis with leakage from Gastric/duodenal secretions have which type of bacteria?

usually sterile or with limited gram(+) or candida

2ndary peritonitis with leakage from Proximal small bowel have which types of bacteria?

1 Aerobic gram-negative bacilli

( E.coli, Klebs, Proteus, Enterobacter)

2 Aerobic gram- positive bacteria

( S. Aureus, strep, enterococci)

2ndary peritonitis with leakage from distal small bowel / large bowel have which type of bacteria?

(Proximal small bowel bacteria + pos/neg Anaerobes)

All the 2ndary proximal small bowel bacteria

--Aerobic GNB: E.Coli, Klebs, Proteus, Enterobacter

--Aerobic gram(+) bacteria: S. Aureus, strep, enterococc

..........................................PLUS......................................................

Anaerobic gram (+) & (-) bacteria :

--Bacteroides. fragilis

--clostridium species (not C.diff)

What is tertiary peritonitis?

-Peritonitis from either primary or secondary further complicated by management strategies such as:

--malnutrition

--anatomic disruption

--antimicrobial therapy.

-Either Primary or Secondary Peritonitis that persists for > 48hrs after management of either peritonitis.

How do you diagnose an Intra-abdominal infection?

along with S/Sx of rapid onset abd pain + tenderness pt can also experience anorexia, N/V, +/- fever, emesis, tackycardia, tachypnea.

May also need radiographic eval/ ultrasound/ CT/ or in some cases contrast studies for post-op drains to assess for anastomic integrity.

How does the surgical management of peritonitis differ from diffuse to local peritonitis?

Diffuse peritonitis= diversion or resection recommended

Focal peritonitis= percutaneous abscess / fluid drainage.

What organisms are seen and what ABX do you use in Community Acquired (mild - moderate) Intra-abdominal infections?

Aerobic & Facultative EGN bacilli (E. Coli, Klebs) are the most common in somewhat stable pt.

Enteric Strep

Obligate anaerobic (sml bowel/ Appendiceal/colonic source)

Ceftriaxone/Cefotaxime/Cefuroxime + Flagyl

Ertapenem

Moxifloxacin ( alone) or Levo/Cipro + Flagyl

Tigecycline (some studies show increased mortality)

When is a Community Acquired intra-abdominal infection considered "High in Severity" and how does that change therapy?

High in Severity:

physiologic disturbance ( Septic Shock +\- pressors)

Older in Age

Immunocompromised state

Delay/High probability of failure in primary control

Broaden coverage: MDRO (pseudomonas), enterococci, oblgte anerob

Carbapenems ( dori, imi, mero) NOT ERTApenem.

Cefepime/ Ceftaz + Flagyl

Cipro/Levofloxacin + Flagyl

Zosyn

How do you treat HEALTHCARE associated Intra-Abdominal Infections?

Start with Broad Spectrum ABX. (kinda like Community AQR SEVERE Intra-abd Infec but without cipro/levof)

Main focus here: P. aeruginosa and obligate anaerobes

Broaden coverage to include MDROs

Carbapenems ( dori, imi, mero)

Cefepime/ Ceftaz + Flagyl

Zosyn

When should antifungal therapy be initiated in pts with intra-abdominal infections?

pts with yeast on gram stain.

evidence of heavy colonization.

surgically treated pancreatitis

prolonged broad spectrum abx

Critically ill pts with upper GI source

Fluconazole is DOC for susceptible strains but echinocandins should be 1st line in critically ill until results are available.

How long should treatment for COMPLICATED intra-abd infection last for?

No more than 4 days with adequate source control

5-7 days in pts without definitive source control and depending on clinical response.

When should you use only short term (<24hrs) prophylactic ABXs in regards to abdominal infections?

Acute Gastric/ Jejunal Perforation (only if there is no malignancy or acid-reducing meds and source control within 24hrs)

Traumatic / iatrogenic bowel injuries repaired within 12 hrs of injury

Acute appendicitis without perforation or abscess.

What categorizes patients as having SEVERE Acute Pancreatitis?

APACHE II score of > 8 or Ranson's Criteria >3 along with clinical presentation.

True or False:

We treat all patients with necrotizing pancreatitis?

No

2/3 acute necrotizing pancreatitis is sterile

(mortality 2-9%) just hydrate and and remove necrosis with surgery.

1/3 Infected necrotizing Pancreatitis. (mort 44-62%)

needs evidence of fluid collection or abscess to treat

Why do people develop Pancreatitis?

Glandular Autodigestion due to excessive ductal/tissue exposure to amylase/ lipase/ protease.

Excessive enzymes due to:

Trypsin-related hyperstimulation

Macro/micral-ductal blockage

What are the 3 phases of Pancreatitis?

1. Excess activation/ decrease inactivation of trypsin

2. Local inflammatory / immune response to pancreatic injury

3. Systemic Inflammatory / immune response (SIRS, hypovolemia, ARDS)

What are some common causes of Acute Pancreatitis?

Biliary obstruction ( gallstones)

Direct Toxicity ( alcohol)

Trauma/surgery/biliary procedures

drugs

What is SEVERE Pancreatitis?

Pancreatitis + hypovolemia, organ failure, local complications ( necrosis, abscess, or psudoyst) if present then treat. = TREAT WITH ABX

hypovolemia increases risk of necrosis to pancreas and intestine due to hypoperfusion.

What exam is used to see pancreatic necrosis?

A CT scan will show diffuse/focal nonviable pancreatic tissue +/- peripancreatic fat necrosis. >30% of the pancreas should be affected.

Infected necrosis just means that the necrotic tissue is positive for microorganisms.

What is a pancreatic pseudocyst?

non-epithelialized wall containing pancreatic excretions due to acute/chronic/traumatic pancreatic trauma.

psuedocysts are usually sterile= no treatment

What is a pancreatic abscess?

Either a

pseudocyst that has become infected or....

liquefaction of pancreatic necrosis that is infected

How is acute pancreatitis diagnosed?

Need TWO of the following three to be present:

1. Acute + Constant pain ( epigastric or right upper quadrant) +/- nausea and vomiting.

2. Serum amylase/lipase > 3 x the upper limit of normal

3. (+) CT scan for acute pancreatitis.

How do we treat Infected Necrosis and Pancreatic Abscesses?

1. Both need CT or ultrasonography guided drainage.

2. Culture drainage.

3. Treat with ABX for up to 14 days.

If a pancreatic abscess or infected necrosis is drained, what are the most likely pathogens that are going to be found?

What abx do we use as empiric therapy?

GN- Bacilli ( Enterobacteriaceae) or Strep (((KEEP-S)))

Klebsiella, E. Coli, Enterobacter, Proteus - Strep

Carbapenems ( imi/mero).....or

Flagyl + FQ.....or

Flagyl + 3rd/4th Gen cephalosporin

Can we give prophylactic ABX for sterile necrotizing pancreatitis ?

Current recommendations DO NOT support routine use of ABX prophylactically for sterile necrotizing pancreatitis. if sterile just hydrate and and remove necrosis with surgery.

needs significant fluid collection or abscess formation to indicate infection= to treat.

What do we suspect when amylase and lipase do not decrease after intervening in the treatment of pancreatic/periphancreatic inflammation?

persistent pancreatic/peripancreatic inflammation

pancreatic duct blockage.

development of pseudocyst.

Definition of regular C. Diff Infection (CDI)?

Diarrhea +++PLUS+++

Stool (+) for C. Diff/ toxigenic C. Diff.....or

Pseudomembranous colitis via colonoscopic examination.

Definition of SEVERE C.diff infection?

Regular CDI + ONE of the following:

-WBC > 15

-SrCr >1.5 times greater than premorbid level.

Definition of SEVERE COMPLICATED CDI?

Severe C. Diff Infection + ONE of the following:

-Hypotension/ shock

-Colonic Ileus

-Toxic Megacolon

What are the risk factors for CDI?

1. ABX (ALL OF THEM- highest risk with...

FQs, Cephalosporins, PNCs, Clindamycin)

2. PPIs & H2-Blockers

3. Age >65

4. Duration of hospitalization

5. Chemotherapy

6. GI Surgery

7. Previous CDI

True/False:

In order to reduce the spread of C.Diff you need to wash your hands with alcohol based substance?

False, non-alcohol based handwash such as water+soap

or chlorhexidine+ water.

How many bouts of diarrhea are needed to suggest CDI?

3 or more UNFORMED stools within 24hrs.

Cecal or Right-sided CDI colitis = may have formed stools.

In C. Diff what ABX do we give for an INITIAL episode that is NON-Severe?

Vanco 125mg PO/NG/FT four times a day x 10 days

or

Fidaxomycin 200mg PO BID x 10 days

Alternative: Flagyl 500mg PO/NG/FT three times a day x 10-14 days (has a delayed response)

In C.DIff what ABX do we give for an INITIAL episode that is SEVERE?

Vanco 125mg PO/NG/FT four times a day x 10 days

or

Fidaxomycin 200mg PO BID x 10 days

In C. Diff what ABX do we give for an INITIAL episode that is

Severe Complicated or Fulminant?

Vancomycin 500mg PO/NG/ FT four times/day +PLUS+ Metronidazole 500mg IV q8hrs.

If Illeus present: ADD Rectal Vanc 500mg/100ml NS and instill rectally for 1hr--QID.