The document discusses antimicrobial resistance and multidrug-resistant organisms. It notes certain organisms like Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumanii, Pseudomonas aeruginosa, and Enterobacter species have developed resistance to multiple drug classes and have high mortality rates. It defines multidrug resistance, extensive drug resistance, and pan drug resistance based on the number of antimicrobial categories an organism is resistant to. Treating such infections requires less effective, more toxic, and expensive drugs. Combination therapy and optimizing dosing is important to prevent further resistance development.
Antibiotics are most common therapeutic agents used in hospitals across world, however, microbial world is becoming resistant day by day, posing special challenges to clinicians specially working in ICU set ups. There are multiple ways to curb this menace, if approached together in antibiotic stewardship way, can bring about wonders and retain therapeutic potentials of these drugs.
Antibiotics are most common therapeutic agents used in hospitals across world, however, microbial world is becoming resistant day by day, posing special challenges to clinicians specially working in ICU set ups. There are multiple ways to curb this menace, if approached together in antibiotic stewardship way, can bring about wonders and retain therapeutic potentials of these drugs.
Antibiotics in the ICU - when, what and how?scanFOAM
A presentation by Fredrik Sjövall at the 2017 meeting of the Scandinavian Society of Anaestesiology and Intensive Care Medicine.
All available content from SSAI2017: https://scanfoam.org/ssai2017/
Delivered in collaboration between scanFOAM, SSAI & SFAI.
This presentation focuses on appropriate selection of antibiotics in the ICU and discusses different strategies to optimize this selection with the aim to decrease resistance and improve appropriateness.
FLOW OF THE SEMINAR
1. Definition – antibiotic resistance, Multi-resistance, cross-resistance in antibiotics
2. Evolution of resistance
3. Impact of resistance
4. The scenario of resistance: Global, India
5. Factors causing resistance
6. Mechanisms of resistance: Intrinsic and Acquired
7. Acquired mechanism of resistance
8. Quorum sensing
9. Mechanism of resistance in commonly used antibiotics
10. Methods for determining the resistance
11. Strategies to contain resistance
12. Antibiotic stewardship
13. Role of Pharmacologist
14. Initiatives undertaken by India to control resistance
Antibiotics in the ICU - when, what and how?scanFOAM
A presentation by Fredrik Sjövall at the 2017 meeting of the Scandinavian Society of Anaestesiology and Intensive Care Medicine.
All available content from SSAI2017: https://scanfoam.org/ssai2017/
Delivered in collaboration between scanFOAM, SSAI & SFAI.
This presentation focuses on appropriate selection of antibiotics in the ICU and discusses different strategies to optimize this selection with the aim to decrease resistance and improve appropriateness.
FLOW OF THE SEMINAR
1. Definition – antibiotic resistance, Multi-resistance, cross-resistance in antibiotics
2. Evolution of resistance
3. Impact of resistance
4. The scenario of resistance: Global, India
5. Factors causing resistance
6. Mechanisms of resistance: Intrinsic and Acquired
7. Acquired mechanism of resistance
8. Quorum sensing
9. Mechanism of resistance in commonly used antibiotics
10. Methods for determining the resistance
11. Strategies to contain resistance
12. Antibiotic stewardship
13. Role of Pharmacologist
14. Initiatives undertaken by India to control resistance
Pk pd analysis and mic interpretation in microbiological reportsCentral Govt, India
This presentation aims to highlight the role of pharmacokinetics and pharmacodynamics of antimicrobials in optimizing therapy in critically ill patients and also role of MIC breakpoint values in guiding antimicrobial therapy
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• Describe the role of antibiotic use in the
development of resistance
• Review toxicity of commonly used antibiotics
• Understand the prevalence and clinical impact
of carbapenem resistant enterobacteriaceae
• State the prognosis antimicrobial resistant
Staph aureus infections
•Describe the role of antibiotic use in the development of resistance
•Review toxicity of commonly used antibiotics
•Understand the prevalence and clinical impact of carbapenem resistant enterobacteriaceae
•State the prognosis antimicrobial resistant Staph aureus infections
Ventilatory management of Acute Hypercapnic Respiratory FailureVitrag Shah
Presentation on ventilatory management in Acute Hypercapnic Respiratory Failure
Updated information till 17/8/16
For powerpoint format, contact dr.vitrag@gmail.com
http://www.medicalgeek.com/presentation/36513-ventilatory-management-acute-hypercapnic-respiratory-failure-presentation.html
Download review articles and guidelines for ventilatory management in COPD & Asthma
http://www.medicalgeek.com/articles-and-news/36514-articles-ventilatory-management-copd-asthma.html
Ventilatory management in obstructive airway diseasesVitrag Shah
Presentation on ventilatory management in COPD & Asthma
Updated information till 26/5/16
For powerpoint format, contact dr.vitrag@gmail.com
http://www.medicalgeek.com/presentation/36441-ventilatory-management-obstructive-airway-diseases-presentation.html
"Best Paper Presentation Award"
Presented at 3rd Annual Critical Care Medicine Conference , Sir Gangaram Hospital, New Delhi
"A Case of H1N1 ARDS - Journey from NIV to Invasive Ventilation to recruitment to proning to ECMO & Nitric Oxide"
For PPT, Check following link
http://www.medicalgeek.com/clinical-cases/36303-h1n1-ards-case-presentation.html
ARDS - Diagnosis and Management
Visit www.medicalgeek.com for more
http://www.medicalgeek.com/lecture-notes/36156-ards-diagnosis-management-presentation-ppt-pdf.html#post89045
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Tetanus Presentation
77 slides
Including drip rates of muscle relaxants
PDF : http://www.mediafire.com/download/k00ciibf73d7y6p/
For more, visit www.medicalgeek.com
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
1. DR. VITRAG H SHAH
MD Medicine, FNB Critical Care, EDIC-UK
(European Diploma in Critical Care)
Physician & Chief Intensivist
Velocity Hospital
2.
3. The organisms posing most danger have been
clubbed together under the term “ESKAPE,” i.e.,
Enterococcus faecium, Staphylococcus aureus,
Klebsiella pneumoniae, Acinetobacter baumanii,
Pseudomonas aeruginosa, and Enterobacter
species, as these have the ability to escape the
effect of antimicrobial drugs.
The ones leading to increased mortality include
carbapenem-resistant Enterobacteriaceae (CRE),
P. aeruginosa, and A. baumannii, which have
acquired multiple mechanisms of resistance.
4.
5. MDR: non-susceptible to ≥1 agent in ≥3
antimicrobial categories
XDR: non-susceptibility to at least 1 agent in
all but 2 or fewer antimicrobial categories (i.e.
bacterial isolates remain susceptible to only
one or two categories).
PDR: non-susceptible to all antimicrobial
agents in all antimicrobial categories.
6. Longer hospital stays
Require treatment with drugs that may be:
Less effective
More toxic
More expensive
7. 1. Use nonstandard antibiotics for which resistance
has not yet occurred
2. Use the standard antibiotics with increased
doses, so PK/PD targets are still achieved
3. Use combination therapy with antibiotics from
options 1 and/or 2
Distinguish colonization vs infection
Use adjunctive therapies (surgery/source control,
reversal of immunosuppression)
Know the exact molecular mechanism of
resistance and exact MIC
8. Beta-lactamase (ESBL)
Loss of porin channels
Efflux pumps
Aminoglycoside-modifying enzymes
Topoisomerases modifications
(Fluoroquinolones)
LipidA (LPS) modifications (Polymyxins)
12. 54 yr male, admitted with RTA-polytrauma
leading to Lt. leg # both bones, lung
contusions and Rt. Parietal ICH since 10 days.
On IPPV since admission
Having persistent fever since 3days
associated with increasingTLC s but is still
haemodynamically stable and static Fio2 and
ventilatory support
13. Continuous fever 39°C
No change in character of tracheal secretions
No change in SOFA score
CVC andArterial catheter insertion sites appear
free of infection
14. Blood Central : GNBs sensitivity awaited
Blood Peripheral : GPCs and FermentingGNBs
TrachealGm Stain: Few GPCs+GNBs+ budding
yeast cells with few epithelial cells n few PMN
cells
Tracheal culture : same as peripheral blood
Urine culture: no significant growth but 20 pus
cells
15. Inj Piperacillin +Tazobactam
Inj Clindamycin
Inj Eptoin
Inj Mannitol (tapering doses)
Mechanical DVT prophylaxis
NG tube feed as per wt- tolerating well
Microbiologist calls to tell GNBs are ESBL
producers
16. Inj Meropenam 1gm iv tid
InjTeicoplanin 400 mg stat and bd
Inj Fluconazole 400 mg bd
Pt’s relatives counseled and reassured that
cause of fever is sorted ????
17. High grade spike of fever since 3 days
All lines changed y’day n pan cultures were sent
Mucopurulent tracheal secretions n culture
growing GNBs , blood culture sterile, urine has
candida..
Microbiologist calls to tell that it’s MDR
pseudomonas sensitive to collistin only……
18. Patient becoming haemodynamically unstable
and increasing FiO2
Worsening metabolic acidosis with raising
creatinine
Resusitation with fluid challenges+ vasopressors
but needed RRT
Collistin 2mu i.v. tid added along with
echinochindin , family given a grave prognosis
19. Now My Patient is Dead
Did we do enough?
Did we do it right?
Can we reflect what
went wrong and
WHEN?
22. Broader is better
Failure to respond is failure to cover
Response implies diagnosis
When in doubt, change drugs (or add
another)
Antibiotics are harmless
Kim JH. Am J Med. 1989; 87: 201-206
23. Response to fever is an evaluation, not
changing antibiotics.
Keep in mind non-infectious causes of fever
Evaluate potential sources of infection
Source control with least invasive method
earliest possible
Get cultures from relevant sites before
starting/changing antibiotics
Start empiric broad spectrum combination
therapy only if hemodynamically unstable
24. As ICU patients have multiple potential
source of infection, it is difficult to find out
source of infection many times
Infectious source Non-infectious source
ET /TTTube (VAP) Bed-ridden (DVT/PE)
Ryle’s tube (Sinusitis) Drugs
Foley’s Catheter (UTI) Acalculus cholecystitis
Central/Arterial line/HD Cath
(CRBSI)
Vasculitis
Drains Burns, Pancreatitis, Post-op
(SIRS)
Bedsore Central fever
25.
26. Perception of need: Is an antibiotic necessary?
Choice of antibiotic:Which is the most
appropriate antibiotic?
Choice of regimen :What dose, route, frequency
and duration are needed?
Monitoring efficacy : Is the antibiotic effective?
27. Right Drug
(Covering suspected pathogen and as per suseptibility
pattern, good penetration as suspected site of infection)
RightTime
(Hit hard and hit fast)
Right Dose
(Full loading dose irrespective of renal/hepatic function
and optimize maintainance dose as per Pk/Pd)
Right Duration
(Deescalate earliest possible, combination to
monotherapy, broad spectrum to targeted therapy )
28. *Based on the 2005 ATS/IDSA guidelines for HAP/VAP/HCAP (Am J Respir Crit Care Med
2005;171:388–416), inappropriate would be the term used to refer to the inadequate
therapy noted on this slide.
30. Intervention NNT
Antibiotics to prevent death in
sepsis
4
Thrombolysis to prevent
unfavourable outcomes in acute
ischemic stroke
17
Thrombolytics to prevent death in
STEMI
43
Aspirin to prevent death in STEMI 42
Statins for heart disease
prevention
83
31. Spectrum
Tissue penetration
Antibiotic sensitivity (As per local
antibiogram)
Safety profile
Cost
36. BL-BLI Carbapenam
Variable in vitro activity
against ESBL producers
Excellent in vitro activity
against ESBL producers
In theory should inhibit
ESBLs
Not hydrolysed by ESBLs
But, many ESBL producers
also produce other beta lactamases /
Other resistance mechanism
Overuse leads to
carbapenem resistance
Inoculum effect Not subject to the
inoculum effect
37. Carbapenems are the first-line choice for severe
ESBL infections
The efficacy of BLBLI combinations has not been
adequately investigated in critically ill patients
with ESBL-PE infections: Piperacillin–
tazobactam can be used as a carbapenem-
sparing regimen for strains with low MICs (≤2
mg/L), using optimized administration (high
doses,extended or continuous infusion,
therapeutic drug monitoring)
38. Post Hoc Analysis of Prospective Cohorts from Spain
Mostly E. coli from urinary & biliary sources
Mortality rates same for both empirical & definitive therapy
“AMC or PTZ are suitable options for the definitive therapy of susceptible ESBL-EC strains
causing BSI, mainly in the urinary and biliary tracts, which could help prevent overuse of
carbapenems.”
Re-analysed above data based on piperacillin MIC
<2; 4-8; >8
Mortality 41% for high MIC vs 0% for low MIC
No deaths with urosepsis
Retrospective analysis: mortality rate was 13% with BL/BLI & 24% with carbapenems
(But not statistically significant)
A randomized controlled trial to compare piperacillin-tazobactam to meropenem for
the definitive treatment of bloodstream infection caused by ceftriaxone non-
susceptible E. coli and Klebsiella sp. (MERINO trial) - do not support using PTZ as a
carbapenem-sparing treatment option for same.
Clin Infect Dis 2012 54: 167-174
BMC Infectious Diseases 2012, 12:245
AntimicrobAgents Chemother 2013; 57:3402–4.
39. Adjusted risk of death: 1.9 times higher for patients
on piperacillin-tazobactam
Piperacillin-tazobactam appears inferior to
carbapenems for ESBL bacteremia (331 patients)
Clin Infect Dis 2015 60: 1319-1325
40. Total of 13,091 Gram-negative bacteria
ESBL producers- 69%
P/T exhibited activity (81.37% organisms susceptible)
C/S (76.06% organisms susceptible).
Mohanty etal. Indian J Med Res 2005 ;122:425-428
41.
42. Local epidemiology (80% sensitivity rule) for empirical
therapy
Definitive therapy as per sensitivity and MIC
Clinical status & patient profile
Affordability
High dose of BL-BLI and optimize Pk-Pd
Can be used urosepsis or biliary sepsis, rather than
pneumonia or CLABSI & E coli rather than Klebsiella
45. While monotherapy may be appropriate for patients with less
severe infections by susceptible isolates, patients with severe
infections and critically ill patients would likely benefit most from
rationally optimized combination therapy.
Combination therapy for CR GNB is usually based on a cornerstone
antibiotic for which the organism presents in vitro susceptibility,
and an adjuvant drug to which the organism may be susceptible in
vitro or not.
It needs to be emphasized that the concept of susceptibility test
refers to antibiotic monotherapy. An adjuvant drug, which may
cause no bacterial killing in monotherapy, can still be highly
beneficial to maximize bacterial killing or prevent resistance.
The most frequently used adjuvant therapies for CRGNB
infections are carbapenems, tigecycline, fosfomycin,
aminoglycosides and rifampicin along with cornerstone drug
Polymyxins (Polymyxin B/ Colistin).
46. Advantages of Combination therapy Disadvantages
Broader coverage that includes
non-susceptible strains
Possible antagonism
Anti-bacterial synergy Possible superinfection
Prevents emergence of resistance May increase resistance & toxicity
Shorter duration & Less toxicity Increased cost
Avoid monotherapy of colistin,Tigecycline,Aminoglycoside, Fosfomycin & Avoid
monotherapy in any XDR infection
47.
48. Why meta-analysis fail to show benefit of
combination therapy?
Why a particular combination works
effectively in one study but fails miserably in
other ?
How to decide what combination is ideal in a
particular situation ?
What’s the solution in Colistin Resistant/
Colistin only Sensitive isolates?
49. These meta-analyses are fundamentally misleading.
They include a large number of heterogeneous studies
performed over a long period of time.The 2014
Cochrane Review, for instance, searched for studies
performed between 1966 and 2013 but the majority of
included studies were per- formed between 1980 and
2000.This was long before the emergence of CRE
They did not analyze sub-groups with multidrug-
resistant organisms and, thus, do not address the
question of combination therapy in this group.
50. Most virulent gram negative pathogen
Main pathogen in neutropenic sepsis,
diabetic, structural lung disease patients
High mortality (~30%) for bacteremia
So need increased
dose/duration/combination therapy
For empirical therapy: If it is sensitive as per
local data - Monotherapy, if MDR as per local
data, Combination therapy and deescalate as
per sensitivity and clinical profile
51. Majority are XDR
Typical strain are less virulent
Frequently causes colonization of respiratory
tract
Clinically significant infection in
compromised patients
Source control (Remove lines, tube etc) is
more important with XDR than antibiotics
52.
53.
54. First introduced 1959, known nephrotoxicity and
neurotoxicity
May be actually less nephrotoxic than
aminoglycosides
Surface active agents that disrupt cell membranes
Resurgence in use since advent of carbapenem
resistant organisms
Deficiency in knowledge about PK/PD
Pk-Pd Profile : (AUC/MIC ratio) >> (Cmax > MIC)
Concentration-dependent bactericidal drug
Role in India : Extremely valuable drug in hospital
acquired infections in view of rising carbapenem
resistance
55. It is active against ESBL- and
carbapenemase-producing
Enterobacteriaceae (CPE), P. aeruginosa, and
A. baumannii, the most worrisome
pathogens.
However, certain organisms such as tribe
Proteae, Burkholderia species, and Serratia
marcescens are intrinsically resistant to the
drug
56.
57. Colistin is administered as CMS, an inactive pro-drug
that needs to be converted in vivo to the active drug
colistin. However, only a small fraction (25-30%) of
CMS is converted to colistin in vivo and this
conversion is quite slow.Therefore, without loading
doses, therapeutic concentrations of colistin are only
reached after 48 h of CMS administration & loading
doses of CMS are required to reach therapeutic
concentrations of colistin in the first 12–24 h.
In contrast, polymyxin B reaches higher serum
concentrations than Colistin after first dose, and these
polymyxin B concentrations are reached much more
quickly, even without a loading dose, which is
recommended but does not seem to be as essential as
for CMS.
58. Colistin and polymyxin B: peas in a pod, or chalk and cheese? 1. Clin Infect Dis. 2014 Jul
1;59(1):88-94
59. CMS is predominantly cleared by the kidneys. CMS
concentrations increase as Cr Cl decreases, which
results in higher concentrations of CMS to be converted
to colistin.Therefore patients with impaired renal
function require dose adjustment of CMS. In contrast,
patients with normal, but especially those with
increased Cr Cl, e.g. initial phases of sepsis and septic
shock, will likely present low concentrations of colistin
in plasma with usually recommended doses.
In contrast, the clearance of polymyxin B is not related
to Cr Cl; so dose adjustments are not required in renal
dysfunction.
60. A potential advantage for CMS lies in the
treatment of urinary tract infections.As there
is substantial tubular reabsorption of
polymyxin B (and also colistin), very low
concentrations of polymyxin B or colistin are
found in urine . In contrast, CMS is highly
eliminated by the kidneys without tubular
reabsorption, and a large amount of CMS is
converted to colistin in urine leading to high
urinary concentrations of the latter.
61.
62. Polymyxin B would appear to have superior clinical
pharmacological characteristics for infections where it
is important to rapidly and reliably attain and
maintain plasma concentrations that are likely to be
efficacious, across a wide range of renal function. An
exception may be the treatment of urinary tract
infections where CMS/colistin may be the polymyxin
of choice.
Because of smaller interindividual variability and lack
of impact of renal function on drug clearance, initial
dose selection and titration are simpler and more
predictable for polymyxin B.
63. InhaledColistin for MDR/XDR GNB
In conjunction with IV Colistin
Delivery to lung tissue questionable
No mortality benefit (Clin Infect Dis 2010;51:1218)
but microbiological cure
Size effect : Bronchospasm (Rare)
Intrathecal and intraventricular
administration for meningitis caused by
resistant GNB (Dose of intrathecal is quite
low, so cost effective as well)
64. Conversions :
1mg CBA = 30,000 IU CBA
1 mg CBA = 2.4 mg CMS
1mg CMS = 12,500 IU CMS
or
(30 mg CBA = 80 mg CMS = 1 Million IU CMS)
1mg Polymyxin B = 10,000 IU Polymyxin B
65. Colistin
Loading dose: 9 million IU (or 4*IBW)
Maintenance dose: 4.5 million IU every 12 hours
Polymyxin B
Loading dose : 25,000 U/Kg over 2 hour
Maintainance dose : 15,000 U/Kg over 1 hour 12 hourly
Concomitant IVAscorbic acid 1gm 6 hourly to reduce the
risk of nephrotoxicity
Intrathecal dose
Colistin : 3 lac unit CMS / day
Polymyxin : 50,000 unit/day for 3-4 days f/b alternate day
Inhalation dose (preferablyVibrating mesh nebulizer)
1-3 MU CMS 3 times daily
66. CrCl (ml/min) As per PK Study group – divided bid US-FDA
(CBA,IBW)
CBA (mg/day) CMS (MIU/day)
>90 360 10.9 2.5-5mg/kg/day
divided bid-tid
80-90 340 10.3
70-80 300 9.00 2.5-3.8 mg/kg/day -
divided bid (4.5-7
MIU)
60-70 275 8.35
50-60 245 7.40
40-50 220 6.65 2.5 mg/kg /day -
divided bid
(4.5-5MIU CMS)
30-40 195 5.90
20-30 175 5.30 1.5 mg/kg q36h
(2.5-3MIU CMS
q36h)
10-20 160 4.85
5-10 145 4.40 Not recommended
<5 (ESRD) 130 3.95
Roger L. Nation et al; DosingGuidance for Intravenous Colistin in Critically Ill Patients, Clinical
Infectious Diseases,Volume 64, Issue 5, 1 March 2017, Pages 565–571
67. 130mg CBA / day divided bid (3-4MIU CMS)
when not on dialysis andCrCl <5ml/min
For IHD/SLED/CRRT, Add 10% of daily dose
per hour of dialysis
Approx. dose with 10 hour SLED would be
130mg CBA twice daily (Total 260mg/day)
Approx. dose with CRRT is 440mg CBA/day
(13MIU CMS/day, divided tid)
69. Dalfino L, Puntillo F et al: High-dose, extended-interval colistin
administration in critically ill patients: is this the right dosing
strategy? A preliminary study. Clin Infect Dis 2012, 54:1720–1726.
Garonzik SM, Li J, et al: Population pharmacokinetics of colistin
methanesulfonate and formed colistin in critically ill patients from a
multicenter study provide dosing suggestions for various categories
of patients. Antimicrob Agents Chemother 2011, 55:3284–3294.
Plachouras D, Karvanen M et al: Population pharmacokinetic
analysis of colistin methanesulfonate and colistin after intravenous
administration in critically ill patients with infections caused by
gram-negative bacteria. Antimicrob Agents Chemother 2009,
53:3430–3436.
Roberts JA, Lipman J: Editorial commentary: Closing the loop - a
colistin clinical study to confirm dosing recommendations from
PK/PD modeling. Clin Infect Dis 2012, 54:1727–1729.
70. Combination therapy for carbapenem-resistant Gram-negative bacteria. Expert Rev. Anti
Infect.Ther. 11(12), 1333–1353 (2013)
71. Phosphonic acid derivative
Broad spectrum Bactericidal drug
Unique mechanism of action : Inhibition of first cytoplasmic step of
bacterial cell wall biosynthesis, formation of the peptidoglycan
precursor N-acetylmuramic acid.This inhibitory action takes place
at an earlier step than the action of β-lactams or glycopeptides.
It reduces adherence of bacteria to urinary epithelial cells . In a
similar manner, fosfomycin suppresses platelet activator factor
receptors in respiratory epithelial cells, thus reducing adhesion of
Streptococcus pneumoniae and Haemophilus influenzae . It has
ability to penetrate into biofilms. Fosfomycin exerts
immunomodulatory effects by altering lymphocyte, monocyte and
neutrophil function.
72. It is neither metabolized nor protein bound and
has a low molecular weight, thereby achieving
good penetration and concentration in tissues.
Greater penetration into subcutaneous and
muscle tissue, followed by lung and bone. Good
distribution in CSF as well.
Hemodialysis removes the drug completely;
therefore, the drug is readministered after the
procedure is over.
Pregnancy : Category B
73. Mainly used for CRE.
It is considered active against Enterococcus spp. (including
Enterococcus faecalis and E. faecium irrespective of
vancomycin resistance), Staphylococcus aureus
(irrespective of methicillin resistance), and S. epidermidis.
Fosfomycin is not active against anaerobes, such as
Bacteroides spp., but it is active against Peptococcus spp.
and Peptostreptococcus spp. Pseudomonas, Acinetobacter,
Stenotrophomonas maltophilia, Burkholderia cepacia,
Staphylococcus capitis, Staphylococcus saprophyticus, and
Mycobacterium tuberculosis are intrinsically resistant to
fosfomycin. Morganella morganii is also resistant to
fosfomycin
74. Dose : 12-16 gm/day in 2-4 divided doses. However,
higher daily doses (up to 24 g) have been given to
patients with CNS or other severe infections .
Intravenous fosfomycin is administered as a slow
infusion after dilution in 100 ml.
Used in combination with with other antibiotics, due
to its unique mechanism of action and its protective
effect against nephrotoxicity induced by
aminoglycosides or colistin.
Adverse effect : Na & fluid overload, hypokalemia.
Every gram of IV Fosfomycin contains 0.32 g of
sodium. (1 L NS – 9 gm)
75. Carbapenemase-producing Enterobacteriaceae isolates
present carbapenem MICs near to or even at the current
susceptibility breakpoints, that is, 1–4 mg/l; this occurs
especially for meropenem and doripenem. So higher
doses and optimal modes of administration, either by
extended or continuous infusion of the drugs , can lead to
an acceptable probability of attaining the PK/PD target
(i.e.,T/MIC >40%) for pathogens with carbapenem MICs
between 1 and 8 mg/l, even in critically ill patients.
In contrast to Enterobacteriaceae, carbapenem MICs in CR
non-fermentative organisms are often very high (>32
mg/l), either because more potent carbapenemases are
involved or other resistance mechanisms are additionally
present.
76. Double-carbapenem combination therapy can be used for
KPC producing Enterobacteriaceae.
Specifically, the rationale is using a carbapenem with
increased affinity for KPC, that is, ertapenem, to act as a
‘suicidal’ drug in order to improve the action of another
carbapenem, especially doripenem/meropenam, with
increased stability against the hydrolyzing activity of KPC.
However, non-carbapenemase mediated resistance to
carbapenems also occurs among CR GNB and combining
carbapenems is expected to be ineffective against such
isolates.
1 g ertapenem 24 hourly followed 1 hour later by
meropenem (2 g) every 8 hours in an infusion that is to be
carried out over 3-4 hours duration .
77. Monobactam, similar MOA to betalactam.
The monobactam class is ‘unique’ among the
clinically available b-lactams in its capacity of not
being hydrolyzed by metallo-b-lactamases; thus,
aztreonam is an important therapeutic option
against metallo-b-lactamase-producing CR GNB.
Dose : 1-2gm 8 hourly
Can be used in patients with penicillin allergy
No activity against anaerobes and Gram positive
bacteria
78. Tigecycline is a minocycline derivative belonging to the
new class of antimicrobials known as glycylcyclines.
It is a broad-spectrum antimicrobial with activity against
many Grampositive, Gram-negative and anaerobic
pathogens and has been frequently prescribed as a part
of combination schemes against CR Enterobacteriaceae
and also CR A. baumannii. Proteus and Pseudomonas are
intrinsically resistant toTigecycline.
Approved by US FDA for complicated intra-abdominal
infections (cIAIs) and skin-soft tissue infections (SSTI)
and community-acquired pneumonia (CAP).
It is bacteriostatic drug with high volume of distribution
& Low levels are found in blood, epithelial lining fluid,
and urinary tract. It is not recommended for use in
primary blood stream infections.
79. Dose : 100 mg loading dose followed by 50mg
BD, 150-200 mg loading dose followed by 75-
100 mg BD in severe MDR/XDR infections/ if
MIC >2
Valuable drug for
Carbapenemase producing Enterobacteriaceae
(CRE)
Combination regimens for Acinetobacter
Empiric therapy for nosocomial infections in
combination with an anti-pseudomonal agent
80. Semisynthetic tetracycline derivative
Active against many MDR strains of Acinetobacter
CLSI susceptibility breakpoints for minocycline and
Acinetobacter exist, ≤4 µg/mL for susceptible, 8
µg/mL for intermediate, and ≥16 µg/mL for
resistance
US FDA approved for the treatment of infections
caused by Acinetobacter
Usual dose 200 mg intravenous load, followed by
100 mg intravenous every 12 h (not to exceed 400
mg in 24 h).
Renal dosing not required
CID 2014:59 (Suppl 6) • S374
81. They act at the 30S subunit of the ribosome, interfering
with bacterial protein synthesis.This effect likely
contributes to prevention of emergence of resistance in
combination regimens, as inhibition of protein
synthesis will prevent the over-expression of resistance
mechanisms that depend on protein synthesis.
Aminoglycosides cause concentration dependent
bacterial killing and have a prolonged post-antibiotic
effect.
To minimize the impact of adaptive resistance, longer
dosing intervals (i.e., 24 h) are suggested for
aminoglycosides. (IV: 15 mg/kg, higher for MIC >8-16)
82. Sulbactam clearly has intrinsic activity against
A. baumannii isolates by binding to penicillin-
binding proteins and contributes the major
part of the activity in the combinations with
ampicillin or cefoperazone.
fT>MIC is the PK/PD index of Sulbactam.
Dose : 3 g sulbactam every 8 h as 4 h infusion
is recommended over 1gm every 6 hour over
30 min.
86. New drug approved by FDA , Combination of
cephalosporin and new nonbeta-lactam beta-lactamase
inhibitor
The addition of avibactam (a novel nonbeta-lactam
beta-lactamase inhibitor) to ceftazidime protects it
fromTEM, SHV, CTX-M, KPC, AmpC, and some OXA-
producing bacteria. It has limited activity in case of
metallo-beta-lactamases.
The recommended dosage of the drug is 2.5 g iv (2 g/0.5
g) 8 hourly via intravenous infusion over 2 hours for 7
days in cUTI and 4–14 days in cIAIs. Both the
components of the drug are excreted through the
kidney, thereby demanding dose adjustment in renal
insufficiency cases.
87. It is novel Antibiotic Adjuvant Entity containing a
beta-lactam antibiotic - Ceftriaxone, a beta-
lactamase inhibitor - Sulbactam and an
Antibiotic Resistance Breaker -Disodium EDTA-
37mg.
It restores the in vitro activity ofCeftriaxone
against ESBL/MBL producing gram-negative
bacteria, including enzyme families that belong
to Ambler class A (TEM, SHV, CTX-M), class B
(NDM,VIM, IMP), class C (some variants of
AmpC), and class D (OXA ESBLs).
88.
89. Combination of rifampin with colistin and
meropenem/doripenem has demonstrated
synergistic effects against MDR Pseudomonas
spp., Acinetobacter spp., and CRE.
But it should not be used routinely, specifically
in India in view of high prevalence ofTB.
90.
91. Colistin / Polymyxin B +Tigecycline
Use carbapenam with least MIC & highest
possible dose, in prolonged infusion
Evaluation of following drugs in combination
therapy:
Minocycline
Fosfomycin
Aminoglycoside
Fluroquinolone
Chloramphenicol
Cotrimoxazole
92. MDR Infections
Polymyxins
MIC < 2mg/l MIC > 2mg/l
Polymyxins based Tx
Doripenem/Meropenem
MIC < 8mg/l
MIC > 8mg/l MIC < 4mg/l
If Acinetobacter
Sulbactam
Carbepenem based Tx
Add Doripenem/Meropenem
Tigecycline
MIC < 8mg/l
MIC > 8mg/l
MIC > 1mg/l MIC < 1mg/l
Add Tigecycline
Fosphomycin
MIC > 32mg/l MIC < 32mg/l
Aminoglycoside
Amikacin > 4mg/l
Rifampicin
Add Fosphomycin
MIC < 4mg/l
Doripenem/Meropenem
MIC > 4mg/l
Tigecycline
Add Ampi/Sul or Cefo/Sul
93. Flowchart for selecting mainstream and adjuvant therapy against Gram-negative bacteria.
Expert Rev. Anti Infect.Ther. 11(12), 1333–1353 (2013)
94. Decisions about duration of antibiotic therapy need to be
individualized, taking into account different variables regarding the
patient (e.g., severity of illness, clinical response), the type of infection
(e.g., source control, deep seated infection [e.g., bone infection], MDR
pathogens) and the availability of diagnostic tools (e.g., clinical/
laboratory scores, biomarker-PCT).
Longer antibiotic courses are associated with MDR pathogen selection
and spread, increased risks of toxicity, and higher costs, but courses
that are too short risk inadequate bacterial eradication and relapse.
An 8-day course will likely be more than sufficient in most ICU
patients, and shorter courses may be considered when the source is
controlled. Current guidelines advise a 7–10 day course, unless poor
prognosis predictors are present (e.g., initial clinical failure,
undrainable foci of infection).
Infections caused by Staphylococcus aureus or Pseudomonas
aeruginosa may require longer courses.
95. There is no clear PCT cut-off value to decide when to
stop antibiotics, although high values (>1 ng/mL) are
strongly suggestive of active bacterial infection.
A value <0.5 ng/mL or a decrease >80 % from the
initial value may be used as a threshold value to stop
antibiotics in stable patients.
This approach has been evaluated in several RCTs. In
the PRORATA trial , which included 621 ICU patients
half of whom had septic shock, patients in whom
antibiotics were started or stopped according to PCT
concentrations had significantly more days without
antibiotics than controls (14.3 versus 11.6, p < 0.001),
without apparent harm.
96. Rationale: Higher drug concentrations at the site of
the infection while avoiding or minimizing systemic
toxicity & reduced pressure for selection of resistant
organisms
Technical problems : Large droplets (>5 μm) are more
likely to be trapped in the circuit, whereas smaller
particles (<0.5 μm) are more likely to be expulsed
during expiration, so that the size of the particles
generated should optimally be between 1 and 3 μm.
Optimizing delivery : HighTidal volume, LongTi &
reduced inspiratory flow. Remove HME during
nebulization.
97.
98.
99. Combination therapy over monotherapy for sicker patients
(Septic shock/ MODS)
Carbapenem* based combination therapy if meropenam MIC
<8-16 (*High dose, extended infusion), Else Colistin as
cornerstone drug
Klebsiella/E.Coli:
High dose Meropenam+Colistin/Polymyxin+-
Tigecycline/Fosfomycin
Acinatobacter:
Colistin/Polymyxin +- Tigecycline/Minocycline + high dose
Sulbactam
Add Inhaled Colistin 1-2 MUTDS (IfVAP)
Pseudomonas:
High dose Meropenam/Aztreonam+Amikacin/Quinolone/Colistin/
Polymyxin
Add Inhaled Colistin /Tobramycin 300mg BD (IfVAP)
Add anything else found sensitive (e.g. septran /
Chloramphenicol) in XDR
100. The set of activities and policies to improve the
rational use of antibiotics.
101. Infection control
Source control
Early & Better Diagnosis (Clinical & Lab)
Combination therapy
Antibiotic stewardship : Antibiotics at the
Right choice, Right dose, Right time, Right
duration
Empirical therapy as per local antibiogram
OptimizeTargeted therapy as per Pk-Pd and MIC
De-escalation
102. Getting MDR/XDR bugs in culture report
doesn’t necessary mean to change/escalate
antibiotic.
Always correlate clinically (Check colony
count; ForVAP - check xray, fever, secretion
etc; For UTI - check if culture was sent from
old foley’s – likely colonizer)
103. Treat patient, not onlyTLC/Fever
Find out source of fever
Distinguish colonization vs infection
Send relevant cultures only
Use your Local Antibiogram
Treat as per suspected pathogen
Loading dose irrespective of renal function & optimize
maintainance dosing as per Pk-Pd & MIC
Use of biomarkers for deescalation
Cefo-Sulb & Pip-Taz are good empirical antibiotics for
HAIs. Carbapenam for community acquired infections
with septic shock
Consider combination of drugs carbapenem +
polymyxins+/- tigecycline/minocycline) in empirical
therapy of health care associated sepsis with mods
104. “Penicillin should only be
used if there is a properly
diagnosed reason
&
if it needs to be used,
use the highest possible
dose for the shortest
time
necessary
Otherwise antibiotic
resistance will develop”
105. Zavascki, A. P et al. (2013). Combination therapy for carbapenem-resistant Gram-negative bacteria.
Expert review of anti-infective therapy, 11(12), 1333-1353.
Morrill, Haley J., et al. "Treatment options for carbapenem-resistant Enterobacteriaceae infections."
Open forum infectious diseases. Vol. 2. No. 2. Oxford University Press, 2015.
Vincent, Jean-Louis, et al. "Advances in antibiotic therapy in the critically ill." Critical Care 20.1 (2016):
133.
Taneja N, Kaur H. Insights into Newer Antimicrobial Agents Against Gram-negative Bacteria.
Microbiology Insights. 2016;9:9-19. doi:10.4137/MBI.S29459.
Yamamoto, M., & Pop-Vicas, A. E. (2014).Treatment for infections with carbapenem-resistant
Enterobacteriaceae: what options do we still have? Critical Care, 18(3), 229.
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Ruppé, É., Woerther, P.-L., & Barbier, F. (2015). Mechanisms of antimicrobial resistance in Gram-
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Nation, R. L., Velkov,T., & Li, J. (2014). Colistin and polymyxin B: peas in a pod, or chalk and cheese?.
Clinical Infectious Diseases, 59(1), 88-94.
Falagas ME et al. 2016. Fosfomycin. Clin Microbiol Rev 29:321–347
Michalopoulos, A. S. et al. (2011).The revival of fosfomycin. International journal of infectious
diseases, 15(11), e732-e739.
Sanford Guide to Antimicrobial Therapy & Johns Hopkins ABX (Antibiotic) Guide
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