This document provides guidelines for the management of severe sepsis and septic shock according to the Surviving Sepsis Campaign. It outlines diagnostic criteria for sepsis, septic shock, and organ dysfunction. It also details bundles of care that should be completed within 3 and 6 hours of diagnosis, including measuring lactate levels, administering antibiotics and fluids, and applying vasopressors if needed. The guidelines provide recommendations on initial resuscitation, antibiotic therapy, source control, infection prevention, fluid therapy, vasopressors, corticosteroids, mechanical ventilation, and other supportive care measures for managing sepsis.
Latest definition of sepsis, application of qSOFA, latest evidence on treatment of septic shock,role of fluids, role of steroids, isobalance salt solution
Surviving Sepsis Campaign
International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
Critical Care Medicine 2013 Feb;41(2):580-637
Latest definition of sepsis, application of qSOFA, latest evidence on treatment of septic shock,role of fluids, role of steroids, isobalance salt solution
Surviving Sepsis Campaign
International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
Critical Care Medicine 2013 Feb;41(2):580-637
Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to an infection.The definition of sepsis was updated in 2016 following publication of the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). This recommended that organ dysfunction should be defined using the Sequential (or Sepsis-related) Organ Failure Assessment (SOFA) criteria or the "quick" (q)SOFA criteria.
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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 simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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.
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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.
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
1. Surviving Sepsis Campaign
International Guidelines for Management
of Severe Sepsis & Septic Shock
Dr Rimita Dey & Dr Raja Basu
Department of Critical Care Medicine
Peerless Hospital & B K Roy Research Center
Kolkata
Disclaimer: This presentation contains information on the topic based on recent published literature &
international guidelines. The user/presenter of this presentation at his discretion, may modify the contents as
may be required. However, the modified version of the presentation shall be reviewed by AstraZeneca Medical
Team, before it can be presented in AstraZeneca driven CMEs. For product information, kindly refer to the full
prescribing information.”
R. Phillip Dellinger, Crit Care Med 2013; 41:580–637
3. Diagnostic Criteria for Sepsis
Infection(documented or suspected)
& some of the following :
General Variables
Fever > 100.9 F Hypothermia < 96.8 F
Heart rate >90 Respiratory rate > 20
Altered Mental status Hyperglycemia >140
(absence of Diabetes)
Significant edema
or positive Fluid Balance ( >20 ml/kg over 24 hrs)
4. Inflammatory variables
Leucocytosis (WCC > 12000)
Leucopenia ( WCC < 4000)
Normal WCC with > 10 % immature forms
Plasma CRP > two SD above the normal
Plasma Procalcitonin > two SD above the normal
Hemodynamic Variables
Arterial Hypotension
( SBP < 90, MAP < 70, OR
an SBP decrease > 40 in adults OR
SBP Less than two SD below normal for age)
WCC- White Cell Count, CRP- C Reactive Protein, SD- Standard Deviation,
SBP- Systolic Blood Pressure, MAP- Mean Arterial Pressure
5. Organ Dysfunction Variables (Severe Sepsis Criteria)
Arterial Hypoxemia (PaO2 /FiO2 <300)
Acute Oliguria (UO< 0.5 ml/kg/hr for at least
2 hours despite fluid resuscitation)
Creatinine increase > 0.5 mg/dl
Coagulation abnormalities (INR> 1.5 or aPTT >60s)
Ileus (absent bowel sounds)
Thrombocytopenia ( < I lakh)
Hyperbilirubinemia ( > 4 mg/dl)
Tissue Perfusion Variables
HyperLactaemia ( > 1 mmol/L)
Decreased Capillary Refilling Time or Mottling
6. SURVIVING SEPSIS CARE BUNDLES
TO BE COMPLETED WITHIN 3 HOURS
1.Measure Lactate Levels
2.Obtain Blood Cultures prior to administration
of Antibiotics.
3.Administer broad spectrum Antibiotics
4.Administer 30ml/kg Crystalloid for low BP or
lactate level – 4
7. TO BE COMPLETED WITHIN 6 HOURS
5. Apply Vasopressors (for hypotension that does
not respond to the initial fluid resuscitation) to
maintain a MAP > 65.
6. In the event of persistent hypotension despite
volume resuscitation (septic Shock) Or
initial lactate being > 4
- Measure CVP & CVP saturation(ScvO2)
7. Remeasure Lactate levels if the initial lactate
was elevated.
MAP = Diastolic BP + (Systolic BP – Diastolic BP)
3
9. Initial Resuscitation
• Begin Resuscitation immediately in patients
with low BP or elevated serum lactate > 4;
DONOT delay pending ITU admission.
• Resuscitation Goals:
CVP 8-12 mm Hg
MAP > 65mm Hg
Urine output > 0.5ml/Kg/Hr
Central Venous O2 saturation >70%, or
mixed venous >65%.
10. If venous o2 saturation target is not achieved :
• Consider further fluids
• Transfuse Packed RBCs to achieve a
haematocrit of > 30%
And/ or
• Dobutamine infusion max 20 mic/kg/min
A higher target CVP of 12-15 mm Hg is
recommended in the presence of mechanical
ventilation or pre-existing decreased ventricular
compliance.
11. Diagnosis
Obtain appropriate Blood cultures before
starting antibiotics provided this does not
significantly delay antimicrobial administration
• obtain two or more blood cultures(BCs).
• one or more BCs should be percutaneous.
• one BC from each vascular access device in place
>48hrs.
• Culture other sites as clinically indicated (CSF, Ascitic
Fluid).
Perform imaging studies promptly in order to
Confirm & sample any source of infection; if safe
to do so.
12. Antibiotic Therapy
• Begin IV Antibiotics as early as possible, & always within the
first hour of recognizing severe sepsis and septic shock.(Grade 1B)
• Broad-spectrum : one or more agents active against likely
bacterial/ fungal pathogens & with good penetration into the
presumed source. (Grade 1B)
• Duration of therapy typically limited to 7-10 days; longer if
response is slow, undrainable foci of infection, or
immunogenic deficiencies & neutropenic patients, or
Bacteremia with S.Aureus. (Grade 2C)
• Use of low Procalcitonin level or similar biomarkers to assist
discontinuation of empiric antibiotics in patients who initially
appeared septic, but have no subsequent evidence of
infection. (Grade 2C)
• Antiviral initiated as early as possible in severe sepsis of viral
origin.
13. • Reassess antimicrobial regimen daily to optimize
efficacy, prevent resistance, avoid toxicity &
minimize costs.
– Consider combination therapy in Pseudomonas & Acenetobacter
infection
– Treat with an extended spectrum Beta-lactum & either an
aminoglycoside or a fluroquinolone for Pseudomonas bacteremia.
– A combination of Beta-lactum & Macrolide for patients with
Streptococcus Pneumoniae infections
– Consider combination empiric therapy in neutropenic patients
– Combination therapy no more than 3-5 days &
de-escalation following susceptibilities.
• Antimicrobials should NOT be used in patients with
severe inflammatory states determined to be of
noninfectious cause.
14. Source Identification & control
• A specific anatomic site of infection should be
established as rapidly as possible & within the first 6
hours of presentation.
• Formally evaluate patient for a focus of infection
amenable to source control measures (e.g. abscess
drainage, tissue debridement)
• Implement source control as soon as possible
following successful initial resuscitation.
– Exception : infected pancreatic necrosis, where surgical
intervention is best delayed.
• Remove Intravascular access devices if potentially
infected.
15. Infection Prevention
• Selective oral decontamination and selective
digestive decontamination should be
introduced and investigated as a method to
reduce the incidence of ventilator-associated
pneumonia.
• Oral chlorhexidine gluconate be used as a
form of oropharyngeal decontamination to
reduce the risk of ventilator-associated
pneumonia in ICU patients. (Grade 2B)
19. • Dopamine as an alternative to NA is
recommended only for patients with low risk of
tachyarrhythmia & absolute or relative
bradycardia.
• Phenylephrine is NOT recommended for septic
shock except in (Grade 1C)
– NA associated serious arrhythmias
– C.Output is known to be high but BP is low
– As salvage therapy when combined vasopressor-inotrope
drugs & low dose vasopressin have all failed to achieve MAP.
• Do NOT use low dose dopamine for Renal
Protection.(Grade 1A)
• All patients requiring Vasopressors should have
an arterial catheter placed as soon as practical.
20. Ionotropic Therapy
• A trial of Dobutamine infusion of up to
20microgm/kg/min may be administered
alone or added to vasopressor in presence of
–Myocardial dysfunction suggested by
elevated cardiac filling pressures & low
cardiac output, or
–Ongoing signs of hypo perfusion, despite
achieving intravascular volume & adequate
MAP. (Grade 1C)
21. Corticosteroids
• Do NOT use IV Hydrocortisone to treat adult septic
shock if adequate fluid resuscitation & vasopressor
therapy is able to restore hemodynamic stability.
Incase this is not achieved IV Hydrocortisone alone
@ 200mg IV OD may be used.(Grade 2C)
• ACTH stimulation test is NOT to be used to identify
adults with septic shock receiving Hydrocortisone.
• When Hydrocortisone is given, use continuous flow.
• Steroid therapy may be weaned when vasopressors
are no longer required.
• Do NOT use corticosteroids to treat sepsis in the
absence of shock.
22. Blood Product Administration
• Transfuse Red Blood Cells when Hb decreases to < 7
& target a Hb of 7-9 in adults.(Grade 1B)
• Higher Hb level may be required in presence of
myocardial ischemia, severe hypoxemia, or acute
hemorrhage.
• Erythropoietin not recommended as a treatment of
sepsis related severe anemia.(Grade 1B)
• FFP should only be used to correct clotting
abnormalities in the presence of bleeding or
planned invasive procedures. (Grade 2D)
• Antithrombin should not be used for the treatment
of severe sepsis. (Grade 1B)
23.
24. Mechanical ventilation in Sepsis
induced ARDS
• Target a Tidal volume of 6ml/kg of predicted body
wt.(vs. 12ml/kg). (Grade 1A)
• Plateau pressure should be measured in pts with
ARDS & Target an initial upper limit pressure <30
cm H2o in a passively inflated lung.
• PEEP should be applied to avoid alveolar collapse
at end expiration (atelectrauma). (Grade 1B)
• Higher rather than lower levels of PEEP should be
used in sepsis associated ARDS. (Grade 2C)
25. • Recruitment maneuvers should be used in sepsis
patients with severe refractory hypoxemia.
• Prone positioning should be considered in ARDS
pts requiring potentially injurious levels of FiO2 or
plateau pressures.
• Ventilated pts should be positioned at 30-45’
head elevation to limit aspiration risk & VAP.(Grade
1B)
• NIV should be in only that minority of ARDS
patients with mild to moderate hypoxemic
respiratory failure. The pts need to be
haemodynamically stable, comfortable easily
arousable, able to protect /clear their airway &
expected to recover rapidly.
26. • Use a weaning protocol & a spontaneous breathing trial (SBT)
regularly to evaluate the potential for discontinuing mechanical
ventilation. (Grade 1A)
• SBT options include a low level of pressure support with CPAP 5 or a
T-piece.
• Before SBT pts should be
– Arousable
– Haemodynamically stable
– Have no new potentially serious conditions
– Have low ventilatory & end-expiratory pressure requirement
– Require FiO2 that can be safely delivered with a face mask or nasal cannula.
• Do Not use a pulmonary catheter for the routine monitoring of pts
with ARDS . (Grade IA)
• Use a conservative rather than liberal fluid strategy for ARDS pts
without any evidence of tissue hypo perfusion.
• Do NOT use beta 2-agonists for the treatment of sepsis induced ARDS
unless there is specific indication such as bronchospasm.
27. Sedation, Analgesia & Neuromuscular
Blocking Agents(NBMAs)
• Continuous or intermittent sedation should be minimized
in mechanically ventilated sepsis pts targeting specific
titration endpoints. (Grade 1B)
• NBMAs should be avoided if possible in septic pts without
ARDS.(due to risk of prolonged NM blockade following
discontinuation)
• If NMBAs are needed, either intermittent bolus as required
or continuous infusion with Train of Four monitoring of the
depth of blockade is advised. (Grade 1C)
• A short course of NMBA of NOT greater than 48hrs for pts
with early sepsis induced ARDS & a PaO2/ FiO2 < 150 is
advised.
28. Glucose Control
• In patients with severe sepsis start insulin dosing
when 2 consecutive blood sugar reading are > 180.
• A protocolized approach should target an upper level
of < 180 rather than a upper target blood glucose
level of < 110. (Grade 1A)
• Blood glucose monitoring every 1-2 hrs until glucose
values & insulin infusion rates are stable & thereafter
every 4hrs. (Grade 1C)
• Use IV insulin in pts with severe sepsis.
• Interpret with caution low glucose levels obtained
with point of care testing as these techniques may
overestimate arterial blood or plasma glucose values
29. Renal Replacement Therapy
& Bicarbonate
• CRRT & Intermittent HD are equivalent in Severe
Sepsis and ARF. (Grade 2B)
• Use continuous therapies to facilitate
management of fluid balance in hemodynamically
unstable septic pts.
• Do NOT use Sodium Bicarbonate for the purpose
of improving hemodynamics or reducing
vasopressor requirements when treating hypo
perfusion induced lactic acidemia with a pH>7.15
(Grade 2B)
30. DVT Prophylaxis
• Pts with severe sepsis should receive daily
phamacoprophylaxis against VTE. (Grade 1B)
• Use once daily S/C LMWH (vs BD dosing of UFH & vs TDS
dosing of UFH). (Grade 1B)
• If CrCl <30 use Dalteparin. (Grade 1A)
• Whenever possible treat with a combination of
pharmacological therapy & intermittent pneumatic
compression.
• Where heparin is C/I (low platelets, severe
coagulopathy, active bleeding or recent ICH) mechanical
prophylactic treatment (compression stocking or
devices) should be used.
31. Stress Ulcer Prophylaxis
• Use H2 Blocker or Proton Pump Inhibitor in pts
who have bleeding risk factors. (Grade 1B)
• When stress ulcer prophylaxis is needed use PPI
rather than H2 RA.
• Pts without risk factors should not receive
prophylaxis
32. Nutrition
• Give oral or enteral feeding, as tolerated rather than
either complete fasting or only IV glucose within the first
48 hrs of diagnosing severe sepsis.
• Avoid mandatory full caloric feeding in the first week
instead suggest low dose feeding (e.g. upto 500 calories
per day) then advancing only as tolerated.
• Use IV glucose & Enteral Nutrition rather than TPN alone
or Parenteral nutrition in conjugation with enteral
feeding during the first 7 days of diagnosis.
• Use nutrition with no specific immunomodulating
supplementation (rather than nutrition providing specific
immunomodulating supplementation) in severe sepsis.
33. Setting Goals of Care
• Discuss prognosis & goals of care with
patients & their families.
• Incorporate goals of care into the treatment &
end-of-life planning, utilizing the palliative
care principles, where possible.
• Address goals of care as early as feasable, but
no later than within 72 hrs of admission.