This document provides guidelines for the management of sepsis and septic shock. It defines key terms like sepsis, severe sepsis, septic shock, and systemic inflammatory response syndrome. It outlines variables for diagnosis and assessing organ dysfunction. It recommends initial resuscitation goals within 3-6 hours including measuring lactate, administering antibiotics and fluids, and applying vasopressors if needed. It provides guidelines for diagnosis, source control, antibiotic therapy, fluid therapy, vasopressor use, and other supportive treatments. Recommendations are evidence-based with assigned grade levels.
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.
Latest definition of sepsis, application of qSOFA, latest evidence on treatment of septic shock,role of fluids, role of steroids, isobalance salt solution
It includes new definition, pathophysiology, management of sepsis, septic shock and neutropenic sepsis and even newer evolving concepts or types of sepsis.
The recent definition, concept and terminologies of septic shock, surviving sepsis campaign, management techniques, SOFA score. Also includes antibiotics and supportive modalities.
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.
Successful treatment of two cases of Elizabethkingia meningoseptica septicemi...Apollo Hospitals
Elizabethkingia meningoseptica is emerging as a cause of hospital acquired infection particularly in immunocompromised adults. The treatment of this bacterium is difficult since it is intrinsically resistant to a number of antibiotics. Here we report two cases of septicemia in patients who were critically ill and were successfully treated with appropriate antibiotics. Cotrimoxazole, quinolones, and rifampicin seem to be drugs effective against E. meningoseptica. Antibiotic susceptibility results are ineffective in guiding treatment. The bacterium particularly colonizes water pipelines and tap faucets and occurrence of infection by this bacterium should direct attention towards eradicating the source of this bacterium.
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.
Latest definition of sepsis, application of qSOFA, latest evidence on treatment of septic shock,role of fluids, role of steroids, isobalance salt solution
It includes new definition, pathophysiology, management of sepsis, septic shock and neutropenic sepsis and even newer evolving concepts or types of sepsis.
The recent definition, concept and terminologies of septic shock, surviving sepsis campaign, management techniques, SOFA score. Also includes antibiotics and supportive modalities.
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.
Successful treatment of two cases of Elizabethkingia meningoseptica septicemi...Apollo Hospitals
Elizabethkingia meningoseptica is emerging as a cause of hospital acquired infection particularly in immunocompromised adults. The treatment of this bacterium is difficult since it is intrinsically resistant to a number of antibiotics. Here we report two cases of septicemia in patients who were critically ill and were successfully treated with appropriate antibiotics. Cotrimoxazole, quinolones, and rifampicin seem to be drugs effective against E. meningoseptica. Antibiotic susceptibility results are ineffective in guiding treatment. The bacterium particularly colonizes water pipelines and tap faucets and occurrence of infection by this bacterium should direct attention towards eradicating the source of this bacterium.
Surviving Sepsis Campaign
International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
Critical Care Medicine 2013 Feb;41(2):580-637
CONCEPT OF NODOPATHIES AND PARANODOPATHIES.pptxNeurologyKota
emergence of autoimmune neuropathies and role of nodal and paranodal regions in their pathophysiology.
Peripheral neuropathies are traditionally categorized into demyelinating or axonal.
dysfunction at nodal/paranodal region key for better understanding of patients with immune mediated neuropathies.
antibodies targeting node and paranode of myelinated nerves have been increasingly detected in patients with immune mediated neuropathies.
have clinical phenotype similar common inflammatory neuropathies like Guillain Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy
they respond poorly to conventional first line immunotherapies like IVIG
This presentation briefs out the approach of dementia assessment in line with consideration of recent advances. Now the pattern of assessment has evolved towards examining each individual domain rather than lobar assessment.
This presentation contains information about Dementia in Young onset. Also it describes the etiologies, clinical feature of common YOD & their management.
Entrapment Syndromes of Lower Limb.pptxNeurologyKota
This presentation contains information about the various Entrapment syndromes of Lower limb in descending order of topography. It also contains information about etiology, clinical features and management of each of these entrapment syndromes with special emphasis on electrodiagnostic confirmation.
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
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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 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
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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2. Bacteremia- Presence of bacteria in blood, as evidenced by
positive blood cultures
Septicemia- Presence of microbes or their toxins in blood
Systemic inflammatory response syndrome (SIRS)-
Two or more of the following conditions:
(1) fever (oral temperature >38°C) or hypothermia (<36°C);
(2) tachypnea (>24 breaths/min);
(3) tachycardia (heart rate >90 beats/min);
(4) leukocytosis (>12,000/ L), leucopenia (<4,000/ L), or
>10% blasts.
3. Sepsis is defined as the presence (probable or
documented) of infection together with systemic
manifestations of infection(SIRS).
Severe sepsis is defined as sepsis plus sepsis-
induced organ dysfunction or tissue hypoperfusion
Septic shock is defined as sepsis-induced
hypotension persisting despite adequate fluid
resuscitation.
4. Refractory septic shock ;Septic shock that lasts for
>1 h and does not respond to fluid or pressor
administration
Sepsis-induced tissue hypoperfusion; is defined as
infection-induced hypotension, elevated lactate, or
oliguria.
Multiple-organ dysfunction syndrome(MODS);
Dysfunction of more than one organ, requiring
intervention to maintain homeostasis
5. General variables-
Fever (> 38.3°C)
Hypothermia (core temperature < 36°C)
Heart rate > 90/min or more than two SD above the
normal value for age
Tachypnea(>24)
6. General variables-
Altered mental status
Significant edema or positive fluid balance (> 20
mL/kg over 24 hr)
Hyperglycemia (plasma glucose > 140 mg/dL or
7.7 mmol/L) in the absence of diabetes
7. Inflammatory variables
Leukocytosis (WBC count > 12,000 μL–1)
Leukopenia (WBC count < 4000 μL–1)
Normal WBC count with greater than 10% immature
forms(Blasts).
Plasma C-reactive protein more than two SD above the
normal value
Plasma procalcitonin more than two SD above the normal
value
8. Hemodynamic variables-
Arterial hypotension
SBP < 90 mm Hg,
MAP < 70 mm Hg
SBP decrease > 40 mm Hg in adults
or less than 2 SD below normal for age)
9. Organ dysfunction variables-
Arterial hypoxemia (Pao2/Fio2 < 300)
Acute oliguria (urine output < 0.5 mL/kg/hr for at
least 2 hrs despite adequate fluid resuscitation)
Creatinine increase > 0.5 mg/dL
10. Organ dysfunction variables-
Coagulation abnormalities (INR > 1.5 or aPTT > 60 s)
Ileus (absent bowel sounds)
Thrombocytopenia (platelet count < 100,000 μL–1)
Hyperbilirubinemia (plasma total bilirubin > 4 mg/dL
or 70 μmol/L)
14. A =(High strength) evidence from randomized trials
B =( moderate strength) evidence from small
randomized trial(s) or multiple good observational
trials
C =(low strength) Well-done observational studies with
control RCTs
D= (very low strength) Downgraded controlled studies or
expert opinion based on other evidence
16. 1-Protocolized, quantitative resuscitation of
patients with sepsis-induced tissue
hypoperfusion(defined in this document as
hypotension persisting after initial fluid challenge or
blood lactate concentration ≥ 4 mmol/L)-
Goals during the first 6 hrs of resuscitation:
◦ CVP 8–12 mmHg
◦ MAP ≥ 65 mm Hg
◦ Urine output ≥ 0.5 mL/kg/hr
◦ Central venous (superior vena cava) or mixed venous oxygen
saturation 70% or 65%, respectively (grade 1C).
17. 2-In patients with elevated lactate levels targeting
resuscitation to normalize lactate (grade 2C).
18.
19. TO BE COMPLETED WITHIN 3 HOURS:
Measure lactate level
Obtain blood cultures prior to administration of antibiotics
Administer broad spectrum antibiotics
Administer 30 mL/kg crystalloid for hypotension or lactate ≥4
mmol/L
TO BE COMPLETED WITHIN 6 HOURS:
Apply vasopressors (for hypotension that does not respond to
initial fluid resuscitation) to maintain a MAP ≥65 mmHg
In the event of persistent arterial hypotension despite volume
resuscitation (septic shock) or initial lactate ≥4 mmol/L :
◦ Measure CVP
◦ Measure ScvO2
Remeasure lactate if initial lactate was elevated
21. 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 (grade
1C).
22. Use of the 1,3 beta-D-glucan assay (grade 2B),
mannan and anti-mannan antibody assays (2C), if
available, and invasive candidiasis is in differential
diagnosis of cause of infection.
23. Imaging studies performed promptly to confirm a
potential source of infection.
Consideration of patient’s risk for transport and
invasive procedures
24.
25. Administration of effective intravenous
antimicrobials within the first hour of recognition of
septic shock (grade 1B) and severe sepsis without
septic shock (grade 1C) as the goal of therapy.
26. Use of low procalcitonin levels or similar
biomarkers to assist the clinician in the
discontinuation of empiric antibiotics in patients
who initially appeared septic, but have no
subsequent evidence of infection (grade 2C).
27. Empiric therapy should attempt to provide antimicrobial
activity against the most likely pathogens based upon
each patient’s presenting illness and local patterns of
infection
Combination empirical therapy for neutropenic patients
with severe sepsis (grade 2B) and for patients with
difficult-to-treat, multidrug-resistant bacterial
pathogens such as Acinetobacter and Pseudomonas spp.
(grade 2B).
For patients with severe infections associated with
respiratory failure and septic shock, combination
therapy with an extended spectrum beta-lactam and
either an aminoglycoside or a fluoroquinolone is for P.
aeruginosa bacteremia (grade 2B).
28. A combination of beta-lactam and macrolide for
patients with septic shock from bacteremic
Streptococcus pneumoniae infections (grade 2B).
Empiric combination therapy should not be
administered for more than 3–5 days.
De-escalation to the most appropriate single therapy
should be performed as soon as the susceptibility
profile is known (grade 2B).
29. Duration of therapy typically 7–10 days .
Longer courses may be appropriate in patients;
who have a slow clinical response,
undrainable foci of infection,
bacteremia with S. aureus;
some fungal and viral infections or immunologic
deficiencies, including neutropenia (grade 2C).
30. Antiviral therapy initiated as early as possible in
patients with severe sepsis or septic shock of viral
origin (grade 2C).
31.
32. A specific anatomical diagnosis of infection
requiring consideration for emergent source control
be sought and diagnosed or excluded as rapidly as
possible, and intervention be undertaken for source
control within the first 12 hr after the diagnosis is
made, if feasible (grade 1C).
33. When source control in a severely septic patient is
required, the effective intervention associated with
the least physiologic insult should be used (eg,
percutaneous rather than surgical drainage of an
abscess).
34. If intravascular access devices are a possible source
of severe sepsis or septic shock, they should be
removed promptly after other vascular access has
been established.
35.
36. Crystalloids as the initial fluid of choice in the
resuscitation of severe sepsis and septic shock
(grade 1B).
Against the use of hydroxyethyl starches for fluid
resuscitation of severe sepsis and septic shock
(grade 1B).
37. Albumin in the fluid resuscitation of severe sepsis
and septic shock when patients require substantial
amounts of crystalloids (grade 2C).
38. Initial fluid challenge in patients with sepsis-
induced tissue hypoperfusion with suspicion of
hypovolemia to achieve a minimum of 30 mL/kg of
crystalloids (grade 1C).
39. Fluid challenge technique be applied wherein fluid
administration is continued as long as there is
hemodynamic improvement either based on
dynamic (eg, change in pulse pressure, stroke
volume variation) or static (eg, arterial pressure,
heart rate) variables.
40.
41. Vasopressor therapy initially to target a MAP of >65
mmHg (grade 1C).
Norepinephrine as the first choice vasopressor
(grade 1B).
42. Epinephrine (added to and potentially substituted
for norepinephrine) when an additional agent is
needed to maintain adequate blood pressure (grade
2B).
Vasopressin 0.03 units/minute can be added to
norepinephrine with intent of either raising MAP or
decreasing norepinephrine dosage.
43. Dopamine as an alternative vasopressor agent to
norepinephrine only in highly selected patients (eg,
patients with low risk of tachyarrhythmias and
absolute or relative bradycardia) (grade 2C).
44. A trial of dobutamine infusion up to 20 mg/kg/min
be administered or added to vasopressor in the
presence of
◦ myocardial dysfunction as suggested by elevated cardiac
filling pressures and low cardiac output, or
◦ ongoing signs of hypoperfusion, despite achieving adequate
intravascular volume and adequate MAP (grade 1C).
45.
46.
47. Not using intravenous hydrocortisone to treat adult
septic shock patients if adequate fluid resuscitation
and vasopressor therapy are able to restore
hemodynamic stability.
In case this is not achievable, we suggest
intravenous hydrocortisone alone at a dose of 200
mg per day (grade 2C).
When hydrocortisone is given, use continuous flow
(grade 2D).
48.
49. 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 RBC transfusion occur only when
hemoglobin <7.0 g/dL to target a hemoglobin of
7.0 –9.0 g/dL in adults (grade 1B).
50. In patients with severe sepsis, administer platelets
prophylactically when counts are <10,000/mm3 in
the absence of apparent bleeding.
We suggest prophylactic platelet transfusion when
counts are < 20,000/mm3 if the patient has a
significant risk of bleeding. Higher platelet counts
(≥50,000/mm3) are advised for active bleeding,
surgery, or invasive procedures (grade 2D).
51.
52. A protocolized approach to blood glucose
management in ICU patients with severe sepsis
commencing insulin dosing when 2 consecutive
blood glucose levels are >180 mg/dL. This
protocolized approach should target an upper blood
glucose ≤180 mg/dL rather than an upper target
blood glucose ≤ 110 mg/dL (grade 1A).
53. Blood glucose values be monitored every 1–2 hrs
until glucose values and insulin infusion rates are
stable and then every 4 hrs thereafter (grade 1C).
54.
55. Not using sodium bicarbonate therapy for the
purpose of improving hemodynamics or reducing
vasopressor requirements in patients with
hypoperfusion-induced lactic acidemia with pH
≥7.15 (grade 2B).
56. Target a tidal volume of 6 mL/kg predicted body
weight in patients with sepsis-induced ARDS (grade
1A vs. 12 mL/kg).
Positive end-expiratory pressure (PEEP) be applied
to avoid alveolar collapse at end expiration
(atelectotrauma) (grade 1B).
57. Strategies based on higher rather than lower levels
of PEEP be used for patients with sepsis-induced
moderate or severe ARDS (grade 2C).
Prone positioning be used in sepsis-induced ARDS
patients with a Pao2/Fio2 ratio ≤ 100 mm Hg in
facilities that have experience with such practices
(grade 2B).
58. Head of the bed elevated to 30-45 degrees (grade
1B).
That noninvasive mask ventilation (NIV) be used in
that minority of sepsis-induced ARDS patients in
whom the benefits of NIV have been carefully
considered and are thought to outweigh the risks
(grade 2B)
59. That a weaning protocol be in place and that
mechanically ventilated patients with severe sepsis
undergo spontaneous breathing trials regularly to
evaluate the ability to discontinue mechanical
ventilation when they satisfy the following criteria:
A) arousable
B) hemodynamically stable (without vasopressor
agents)
60. C) no new potentially serious conditions
D) low ventilatory and end-expiratory pressure
requirements
E) low Fio2 requirements
If the spontaneous breathing trial is successful,
consideration should be given for extubation (grade
1A).
61. Against the routine use of the pulmonary artery catheter
for patients with sepsis-induced ARDS (grade 1A).
A conservative rather than liberal fluid strategy for
patients with established sepsis-induced ARDS who do
not have evidence of tissue hypoperfusion (grade 1C).
In the absence of specific indications such as
bronchospasm, not using beta 2-agonists for treatment
of sepsis-induced ARDS (grade 1B)
62. Continuous or intermittent sedation be minimized
(grade 1B).
Neuromuscular blocking agents (NMBAs) be
avoided if possible in the septic patient without
ARDS due to the risk of prolonged neuromuscular
blockade following discontinuation (grade 1C).
63. Daily pharmacoprophylaxis against venous
thromboembolism (VTE) (grade 1B).
Daily subcutaneous low-molecular weight heparin
(LMWH) (grade 1B versus twice daily UFH, grade 2C
versus three times daily UFH).
If creatinine clearance is <30 mL/min, use
dalteparin (grade 1A) or another form of LMWH
that has a low degree of renal metabolism (grade
2C) or UFH (grade 1A).
64. Patients with severe sepsis be treated with a
combination of pharmacologic therapy and
intermittent pneumatic compression devices
whenever possible (grade 2C).
Septic patients who have a contraindication for
heparin use should receive mechanical prophylactic
treatment, such as graduated compression stockings
or intermittent compression devices (grade 2C).
65. Stress ulcer prophylaxis using H2 blocker or proton
pump inhibitor be given to Pts. who have bleeding
risk factors (grade 1B).
Patients without risk factors do not receive
prophylaxis (grade 2B).
66. 1. Discuss goals of care and prognosis with patients
and families (grade 1B).
2. Incorporate goals of care into treatment and end-
of-life care planning, utilizing palliative care
principles where appropriate (grade 1B).
3. Address goals of care as early as feasible, but no
later than within 72 hours of ICU admission
(grade 2C).
67. Administer oral or enteral (if necessary) feedings, as
tolerated, rather than either complete fasting or
provision of only intravenous glucose within the
first 48 hours after a diagnosis of severe
sepsis/septic shock (grade 2C).
Avoid mandatory full caloric feeding in the first
week but rather suggest low dose feeding (eg, up to
500 calories per day), advancing only as tolerated
(grade 2B).
68.
69. Dellinger RP, Levy MM, Rhodes A, et al: Surviving
Sepsis Campaign: International guidelines for
management of severe sepsis and septic shock.
Intensive Care Med 2013; 39(2): 165-228 and Crit
Care Med 2013; 41(2): 580-637.
Harrison’s text book of internal medicin 18’th edi.
Gregory A Schmidt, MD ,Jess Mandel, MD:Evaluation
and management of severe sepsis and septic shock
in adults