The document outlines guidelines for treating sepsis from the Surviving Sepsis Campaign. It defines sepsis, severe sepsis, and septic shock. It recommends protocols for initial resuscitation within the first hour, including measuring lactate levels, administering antibiotics and fluids, and obtaining cultures. The guidelines provide recommendations on screening, diagnosis, source control, and antimicrobial therapy to treat infection and improve outcomes for patients with sepsis.
Latest definition of sepsis, application of qSOFA, latest evidence on treatment of septic shock,role of fluids, role of steroids, isobalance salt solution
Septic shock, updated presentation, including latest guidelines from Intensive care societies and how to approach to the diagnosis with few notes about Early Goal Directed Therapy and role of steroids
Latest definition of sepsis, application of qSOFA, latest evidence on treatment of septic shock,role of fluids, role of steroids, isobalance salt solution
Septic shock, updated presentation, including latest guidelines from Intensive care societies and how to approach to the diagnosis with few notes about Early Goal Directed Therapy and role of steroids
Updated global adult sepsis guidelines, released in October 2021 by the Surviving Sepsis Campaign (SSC), place an increased emphasis on improving the care of sepsis patients after they are discharged from the intensive care unit (ICU) and represent greater geographic and gender diversity than previous versions.
The new guidelines specifically address the challenges of treating patients experiencing the long-term effects of sepsis. Patients often experience lengthy ICU stays and then face a long, complicated road to recovery. In addition to physical rehabilitation challenges, patients and their families are often uncertain how to coordinate care that promotes recovery and matches their goals of care.
Surviving Sepsis Campaign
International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
Critical Care Medicine 2013 Feb;41(2):580-637
Updated global adult sepsis guidelines, released in October 2021 by the Surviving Sepsis Campaign (SSC), place an increased emphasis on improving the care of sepsis patients after they are discharged from the intensive care unit (ICU) and represent greater geographic and gender diversity than previous versions.
The new guidelines specifically address the challenges of treating patients experiencing the long-term effects of sepsis. Patients often experience lengthy ICU stays and then face a long, complicated road to recovery. In addition to physical rehabilitation challenges, patients and their families are often uncertain how to coordinate care that promotes recovery and matches their goals of care.
Surviving Sepsis Campaign
International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
Critical Care Medicine 2013 Feb;41(2):580-637
surviving sepsis guidelines - Notes are made from surviving sepsis guidelines 2016 article to assist medical students and residents to grasp subject in a easy to read format in a step wise manner. Resources: surviving sepsis guidelines 2016 (free access article)
This powerpoint (ppt) presentation describes in details Pathophysiology and Management of Acute Sepsis in Emergency Department. Acute sepsis has 30% mortality and further more Septic Shock has 50% mortality if untreated. It is the job of Emergency Physician to recognise and treat Sepsis in time.
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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!
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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
3. INTRODUCTION
• Major cause of morbidity and mortality
worldwide.
• Leading cause of death in noncoronary ICU.
• 11th leading cause of death overall.
• Mortality
– Sepsis: 30% - 50%
– Septic Shock: 50% - 60%
• For every hour delay in the administration of
treatment, there is an associated 6% rise in
mortality.
4. SIRS
• Widespread inflammatory response to a
variety of severe clinical insults.
• Clinically recognized by the presence of 2 or
more of the following:
– Temperature >38C or < 36C
– Heart Rate >90
– Respiratory Rate > 20 or PaCO2 <32
– WBC > 12,000, < 4000 or > 10% immature forms
5. Stages In the Development of SIRS
(Bone, 1996)
• Stage 1. In response to injury / infection, the local
environment produces cytokines.
• Stage 2. Small amounts of cytokines are released
into the circulation:
• Recruitment of inflammatory cells.
• Acute Phase Response.
• Normally kept in check by endogenous anti-inflammatory
mediators (IL-10, PGE2, Antibodies, Cytokine receptor
antagonists).
6. Stages In the Development of SIRS
• Stage 3. Failure to control inflammatory
cascade:
• Loss of capillary integrity.
• Stimulation of Nitric Oxide Production.
• Maldistribution of microvascular blood flow.
• Organ injury and dysfunction.
7. SEPSIS
• SIRS criteria + evidence of infection, or:
– White cells in normally sterile body fluid
– Perforated viscus
– Radiographic evidence of pneumonia
– Syndrome associated with a high risk of infection
8. SEVERE SEPSIS
• Sepsis criteria + evidence of organ dysfunction or tissue
hypoperfusion, including:
– CV: Systolic BP < 90 mmHg, MAP < 70 mm Hg for at least 1 hour
despite volume resuscitation, or the use of vasopressors.
– Renal: Urine output < 0.5 ml/kg body weight/hr for 1 hour
despite volume resuscitation
– Pulmonary: PaO2/FiO2 < 250 in absence of pneumonia as
infection source or < 200 in presence of pneumonia as infection
source.
– Hematologic: Platelet count < 1L or decreased by 50% in 3 days
– Metabolic: pH < 7.3 and plasma lactate > upper normal
– INR > 1.5, S. Bil > 2 mg/dl, S. Creat >2 mg/dl
9. SEPTIC SHOCK
• Septic Shock
– Hypotension secondary to Sepsis that is resistant
to adequate fluid administration.
11. Pathophysiology of Sepsis-Induced
Organ Injury
• Multiple Organ Dysfunction (MODS) and Multiple
Organ Failure (MOF) result from diffuse cell injury /
death resulting in compromised organ function.
• Mechanisms of cell injury / death:
• Cellular Necrosis (ischemic injury).
• Apoptosis.
• Leukocyte-mediated tissue injury.
• Cytopathic Hypoxia
12. Pathophysiology of Sepsis-Induced
Ischemic Organ Injury
• Cytokine production leads to massive production of
endogenous vasodilators.
• Structural changes in the endothelium result in
extravasation of intravascular fluid into interstitium and
subsequent tissue edema.
• Plugging of select microvascular beds with neutrophils,
fibrin aggregates, and microthrombi impair microvascular
perfusion.
• Organ-specific vasoconstriction.
13. Pathogenesis of Vasodilation in Sepsis
• Loss of Sympathetic Responsiveness:
• Down-regulation of adrenergic receptor number and
sensitivity, possible altered signal transduction.
• Vasodilatory Inflammatory Mediators.
• Endotoxin has direct vasodilatory effects.
• Increased Nitric Oxide Production.
16. PIRO staging for sepsis
• Aims to describe the sepsis considering the
relationship amongst premorbid factors,
infection insult & host response and how it
impacts on development of organ dysfuction
& prognosis of septic patients
17.
18. SEPSIS SIX
• The Sepsis Six is the name given to a bundle of medical
therapies designed to reduce the mortality of patients
with sepsis.
• The Sepsis Six consists of three diagnostic and three
therapeutic steps – all to be delivered within one hour
of the initial diagnosis of sepsis.
– Deliver high-flow oxygen.
– Take blood cultures.
– Administer empiric intravenous antibiotics.
– Measure serum lactate and send full blood count.
– Start intravenous fluid resuscitation.
– Commence accurate urine output measurement.
Daniels et al. The sepsis six and the severe sepsis resuscitation bundle: a prospective observational cohort study. Emerg Med J
(2011) vol. 28 (6) pp. 507-12
19.
20. • The Surviving Sepsis Campaign (SSC) - global
initiative to bring together professional
organizations in reducing mortality from
sepsis.
• The Surviving Sepsis Campaign and the
Institute for Healthcare Improvement teamed
up to achieve a 25 percent reduction in sepsis
mortality by 2009.
21. History of the guideline
• 2004
– The initial SSC guidelines incorporated the evidence
available through the end of 2003
• 2008
– Publication analyzed evidence available through the
end of 2007
• 2012
– The most current iteration is based on updated
literature search incorporated into the evolving
manuscript through fall 2012
22. Selection and Organization of
Committee Members
• Appointed by the Society of Critical Care
Medicine and European Society of Intensive
Care Medicine
• Sepsis expertise
• Four clinicians with experience in the GRADE
process application (referred as GRADE group
or Evidence-Based Medicine [EBM] group)
23. GRADING
• Grading of Recommendations Assessment,
Development and Evaluation (GRADE) system
• Quality of evidence
– High (grade A)
– Moderate (grade B)
– Low (grade C)
– Very low (grade D)
• Classification of recommendations
– Strong (grade 1)
– Weak (grade 2)
24. GRADING
• Strength of recommendation and quality of
evidence assessed using GRADE criteria,
presented in brackets after each guideline. For
added clarity:
• Indicates a strong recommendation or “we
recommend.”
o Indicates a weak recommendation or “we
suggest.”
UG means the evidence is ungraded
25. MANAGEMENT OF SEVERE SEPSIS
• Initial Resuscitation and Infection Issues
• Hemodynamic Support and Adjunctive
Therapy
• Supportive Therapy of Severe Sepsis
28. Initial Resuscitation and Infection
Issues
• A. Initial Resuscitation
• B. Screening for Sepsis and Performance
Improvement
• C. Diagnosis
• D. Antimicrobial Therapy
• E. Source Control
• F. Infection Prevention
29. A. Initial Resuscitation
• Resuscitation of patients with sepsis- induced
tissue hypoperfusion
– defined as hypotension persisting after initial fluid
challenge or blood lactate concentration ≥ 4 mmol/L
• 1.EGDT (first 6 hrs of resuscitation)
– a) Central venous pressure (CVP) 8–12 mm Hg
– b) Mean arterial pressure (MAP) ≥ 65 mm Hg
– c) Urine output ≥ 0.5 mL/kg/hr
– d) Scvo2 or Svo2 70% or 65%, respectively- 1C
2. If Elevated Lactate- target resuscitation to
normalize lactate – 2C
30. How to Resuscitate
• Resuscitate with IVF to reduce lactate
• Resuscitate early ( if <6h- mortality by 16%)
• If Hypotension + Lactate – mortality 16%
• if ScvO2 <70% / SvO2 <65% despite adequate
intravascular volume repletion with persisting
tissue hypoperfusion-
Dobutamine @ max 20 μg/kg/min
OR
PRBC- to achieve Hct >= 30%
31. How to Resuscitate
• Target CVP 12-25mm Hg – if known Ventricular
compliance
• Don’t Use CVP guided IVF if known PAH
SEVERE SEPSIS INCIDENCE MORTALITY
Hypotension + Lactate
>4mmol/l
16% 46
Hypotension Only 49% 36%
Only Lactate >4mmol/l 5.4% 30%
32. B. Screening for Sepsis and
Performance Improvement
• Routine screening of seriously ill patients for
severe sepsis to
– increase the early identification of sepsis (1C)
– allow implementation of early sepsis therapy
• Performance improvement efforts to improve
patient outcomes and decrease sepsis-related
mortality.
33. B. Screening for Sepsis and
Performance Improvement*
• The SSC guidelines and bundles as the basis of
a sepsis performance improvement program
• A bundle is a selected set of elements of care
derived from evidence based practice
guidelines
– effect on outcomes beyond implementing the
individual elements alone.
36. How to Screen
• Use Sepsis screening tools
• Many tools eg. St. Joseph Mercy, Sepsis Surv
Campaign etc
• Any can be used as per hospital
requirements/equipment
37.
38. C. Diagnosis
• Cultures before antibiotic therapy
– Without causing significant delay
• At least 2 blood cultures (both aerobic and anaerobic)
– percutaneous
– drawn through each lumen of each vascular access device
(if >48 hrs)
• Imaging studies in attempts to confirm a potential
source of infection
– Balancing risks & benefits
39. C. Diagnosis
o Other Cultures if indicated- Urine, CSF, sputum etc
o Vol of blood sample > 10ml
o Adjunct Methods- PCR, Mass Spectroscopy,
Microarrays
o Procalcitonin & CRP – can’t differentiate b/w Sepsis
& other Inflammatory States (Not Recommended)
o 1,3 β-d-glucan assay (2B), mannan and anti-mannan
antibody assays
– If invasive candidiasis suspected
40. D. Antimicrobial Therapy
• Goal - Administration of effective i/v antibiotics
within the first hour of recognition of septic shock
(grade 1B) and severe sepsis (grade 1C).
• ? Premixed Abx Solutions
• Abx Bolus vs Infusions
• Initial empiric anti-infective therapy
– one or more drugs
– activity against all likely pathogens (bacterial and/or fungal
or viral) presumed to be the source of sepsis (grade 1B)
41. D. Antimicrobial Therapy
• Reassessed daily for potential de-escalation
(grade 1B)
– prevent the development of resistance
– to reduce toxicity
– to reduce costs
o Combination empiric therapy (>=2 classes of
Abx)-
o neutropenic patients with severe sepsis (grade 2B)
o difficult-to-treat, multidrug-resistant bacterial
pathogens such as Acinetobacter and
Pseudomonas spp.
42. D. Antimicrobial Therapy
o Extended spectrum beta-lactam + AGS/FQs for
P. aeruginosa bacteremia
o Beta-lactam and macrolide for bacteremic
Streptococcus pneumoniae infections
o Not for more than 3–5 days
o De-escalation to the most appropriate single
therapy as per susceptibility
43. D. Antimicrobial Therapy
o Duration of therapy 7–10 days
o Longer courses
o slow clinical response
o undrainable foci of infection
o bacteremia with S. aureus
o some fungal and viral infections
o immunologic deficiencies, including neutropenia
(grade 2C).
44. D. Antimicrobial Therapy
o Antiviral therapy – suspected to be viral origin
(grade 2C).
• Should not be used in severe inflammatory
states determined to be of non-infectious
cause (UG)
45. How to Give Antibiotics
• Choice- based on
– History
– Previous Abx usage
– Clinical Features
– Community pathogenic susceptibility
– Renal/ Hepatic function
• M/C Organisms- G+ > G- > Mixed
46. E. Source Control
• Specific anatomical diagnosis of infection
requiring emergent source control- Imaging
• Intervention for source control within the first
12 hr of diagnosis.
• Source control with least physiological insult
in severe sepsis.
47. E. Source Control
• Intravascular access suspected to be source of
severe sepsis or septic shock – remove
promptly after other vascular access has been
established (UG).
• Surgical intervention done when minimally
invasive approaches are inadequate / when
diagnostic uncertainty persists despite
imaging
48. F. Infection Prevention
o Selective Oral decontamination(SOD)- 2%
gentamicin, 2% colstin, and 2% vancomycin paste
has been shown to reduce VAP
o Oral CHG be used (2B)
o Selective digestive decontamination (SDD)-
o oral cavity paste + GI tract solution, and IV antibiotics
x 4 days.
o Eliminates harmful bacteria & allows native flora to
thrive. – CONTOVERSIAL
51. FLUID THERAPY
• Crystalloids*
• Against the use of hydroxyethyl starches
o Albumin for fluid resuscitation when patients
require substantial amounts of crystalloids
• Initial fluid challenge in patients with sepsis-
induced tissue hypoperfusion & suspected of
hypovolemia @ 30 mL/kg of crystalloids
(minimum)*
52. VASOPRESSORS
• Target a mean arterial pressure (MAP) of 65 mm Hg
• Norepinephrine* as the first choice vasopressor
o Epinephrine added when an additional agent is needed
to maintain adequate B.P.
• Vasopressin 0.03 U/min added to NE for raising MAP or
decreasing NE dosage (UG)
• Low dose vasopressin not recommended as the single
initial vasopressor for sepsis-induced hypotension (UG)
• Vasopressin doses > 0.03-0.04 U/min reserved for
salvage therapy (UG)
53. VASOPRESSORS
• Dopamine as an alternative vasopressor agent to
NE only in highly selected patients
– with low risk of tachyarrhythmias
– absolute or relative bradycardia
• Phenylephrine not recommended except when
– NE associated with serious arrhythmias
– cardiac output high and BP persistently low
– as salvage therapy when combined
inotrope/vasopressor drugs and low dose vasopressin
have failed to achieve MAP
55. INOTROPIC THERAPY
• Trial of dobutamine infusion up to 20
mcg/kg/min be administered or added to
vasopressor (if in use) (grade 1C)
– myocardial dysfunction suggested by elevated
cardiac filling pressures and low cardiac output
– ongoing signs of hypoperfusion, despite achieving
adequate intravascular volume and adequate
MAP.
56. CORTICOSTEROID
o Not indicated if adequate fluid resuscitation
and vasopressor therapy able to restore
hemodynamic stability
o In case not achievable, iv hydrocortisone at a
dose of 200 mg per day
• Corticosteroids not be administered for
treatment of sepsis in the absence of shock
57. CORTICOSTEROID
o Not using the ACTH stimulation test to identify
adults with septic shock who should receive
hydrocortisone (grade 2B).
o In treated patients hydrocortisone tapered
when vasopressors are no longer required
o Low-dose hydrocortisone to be given as
continuous infusion rather than repetitive
bolus injections
60. BLOOD PRODUCT ADMINISTRATION
• PRBC transfusion only when Hb <7.0 g/dl
– Target Hb of 7.0 –9.0 g/dl
• EPO not be used as specific treatment of
anemia associated with severe sepsis
o FFP not be used to correct laboratory clotting
abnormalities in the absence of bleeding or
planned invasive procedures
• Not using antithrombin for the treatment of
severe sepsis and septic shock
61. BLOOD PRODUCT ADMINISTRATION
o Platelet transfusion
– <10,000/mm3 in the absence of apparent
bleeding*
– < 20,000/mm3 if the patient has a significant risk
of bleeding
– Higher platelet counts (≥50,000/mm3) advised for
active bleeding, surgery, or invasive procedures
63. MECHANICAL VENTILATION OF SEPSIS
INDUCED ARDS
• Target tidal volume of 6 mL/kg predicted body
weight in patients with sepsis-induced ARDS
• Positive end-expiratory pressure (PEEP) be
applied to avoid alveolar collapse at end
expiration
• Mechanically ventilated sepsis patients be
maintained with the head end elevation of 30-45
o
– limit aspiration risk
– prevent the development of VAP
64. MECHANICAL VENTILATION OF SEPSIS
INDUCED ARDS
• Weaning protocol to be in place
• Spontaneous breathing trials regularly to evaluate the
ability to discontinue mechanical ventilation if
– arousable
– hemodynamically stable (without vasopressor agents)
– no new potentially serious conditions
– low ventilatory and end-expiratory pressure requirements
– low Fio2 requirements which can be met safely delivered
with a face mask or nasal cannula.
• If the spontaneous breathing trial is successful,
consideration should be given for extubation
65. MECHANICAL VENTILATION OF SEPSIS
INDUCED ARDS
• Beta 2-agonists not be used for sepsis-induced
ARDS, in absence of bronchospasm
• Pulmonary artery catheter not to be used
routinely for patients with sepsis-induced
ARDS
• Conservative fluid strategy for patients with
established sepsis-induced ARDS without
evidence of tissue hypoperfusion
66. rhAPC (drotecogin alpha)*
• PROWESS trial (2001)
– Included in 2004 SSC
• Downgraded to suggestion in 2008 SSC
• PROWESS SHOCK trial (2011)
– No benefit
– Drug withdrawn from market
– No recommendation in SSC 2012
67. SEDATION, ANAELGESIA &
NEUROMUSCULAR BLOCKADE
• Continuous or intermittent sedation be
minimized in mechanically ventilated sepsis
patients
– Morphine vs morphine + propofol/midazolam
• NMBAs avoided if possible in the septic patient
without ARDS
– risk of prolonged neuromuscular blockade following
discontinuation.
– If required, either intermittent bolus or continuous
infusion with monitoring of the depth of blockade
68. GLUCOSE CONTROL
• Protocolised approach
– Insulin when two consecutive blood glucose > 180
mg/dL
– upper target blood glucose ≤180 mg/dL rather
than ≤ 110 mg/dL*
• Blood glucose values every 1–2 hrs until
glucose values and insulin infusion rates stable
and then every 4 hrs thereafter
69. RENAL REPLACEMENT THERAPY
o Continuous renal replacement therapies and
intermittent hemodialysis equivalent in
patients with severe sepsis and acute renal
failure (grade 2B).
o Continuous therapies to facilitate management
of fluid balance in hemodynamically unstable
septic patients (grade 2D).
70. BICARBONATE THERAPY
o NaHCO3 therapy not useful for the purpose of
improving hemodynamics or reducing
vasopressor requirements in patients with
hypoperfusion-induced lactic acidemia.
71. DVT PROPHYLAXIS
• VTE prophylaxis required using daily
subcutaneous LMWH*
• If creatinine clearance <30 mL/min, use
dalteparin or UFH
o Combination of pharmacologic therapy and
intermittent pneumatic compression devices
whenever possible
o C/I for heparin – use mechanical prophylaxis.
Start pharmacological Rx when risk decreases.
72. STRESS ULCER PROPHYLAXIS
• Stress ulcer prophylaxis using H2 blocker or
proton pump inhibitor in patients with GI
bleeding risk factors
– Coagulopathy
– Mechanical ventilation for at least 48 hrs
– Hypotension
o PPIs > H2RA*
o Patients without risk factors do not receive
prophylaxis
73. NUTRITION*
o Oral or enteral feeding, as tolerated, rather than
complete fasting or only i/v glucose within the first 48
hours after diagnosis of severe sepsis/septic shock
o Low dose feeding > full caloric feeding in the first week
(upto 500 Calories/day, advancing as tolerated)
o Use i/v glucose + enteral nutrition rather than TPN
alone or parenteral nutrition + enteral feeding in the
first 7 days
• Nutrition without specific immunomodulating
supplementation
74. SETTING GOALS OF CARE
• Discuss goals of care and prognosis with
patients and families
• Goals of care to be incorporated into
treatment and end-of-life care planning
75. CONCLUSION
• Optimum treatment of severe sepsis and
septic shock is a dynamic and ever evolving
process.
• SSC provides guidelines for evolving protocols
at institution.
A bundle is a selected set of elements of care derived from evidence based practice guidelines that, when implemented as a group, have an effect on outcomes beyond implementing the individual elements alone.
The measurement of lactate can identify tissue hypo-perfusion in patients who are not yet hypotensive but who are at-risk for septic shock. All patients
with elevated lactate levels greater than 4mmol/L should enter the 6-hour septic shock bundle
patients who remain hypotensive despite fluid resuscitation efforts or demonstrate a lactate level of greater than or equal to 4mmol/L. If the lactate level is greater than or equal to 4mmol/L, implementation of these elements should begin immediately.
Cultures as clinically appropriate before antimicrobial therapy if no significant delay (> 45 mins) in the start of antimicrobial(s) (grade 1C). At least 2 sets of blood cultures (both aerobic and anaerobic bottles) be obtained before antimicrobial therapy with at least 1 drawn percutaneously and 1 drawn through each vascular access device, unless the device was recently (<48 hrs) inserted
Colloids as well as crystalloids recommended in SSC 2008. Fluid challenge with 1ltr crystalloid or 300-500 ml colloid within 30 min recommended in SSC 2008.
Once tissue hypoperfusion has resolved and in the absence of extenuating circumstances, such as myocardial ischemia, severe hypoxemia, acute hemorrhage, or ischemic heart disease, we recommend that red blood cell transfusion occur only when hemoglobin concentration decreases to <7.0 g/dLto target a hemoglobin concentration of 7.0 –9.0 g/dL in adults
Antithrombin has a variety of antiinflammatory properties in addition to its functions as an endogenous anticoagulant that appear to have an important therapeutic role in the prevention of microvascular dysfunction and multiple organ injury in sepsis. Appropriate timing and dosing of antithrombin III is critical to realize its full therapeutic potential as an anti-sepsis therapy.- NOT RECOMMENDED
< 5000 in SSC 2008 in absence of severe bleeding
5000-30,000 with high risk of bleeding in SSC 2008
C/I for heparin use – 1. thrombocytopenia 2. severe coagulopathy 3. active bleeding 4. recent intracerebral hemorrhage 5. Recent major surgery