Sepsis is a life-threatening condition that arises when the body's response to infection causes injury to its own tissues. Globally, sepsis kills about 8 million people annually. Early recognition and treatment are key to improving outcomes. The first hours after diagnosis are especially critical, as mortality increases by about 8% every hour that antibiotics are delayed. Prompt administration of broad-spectrum antibiotics and fluid resuscitation can significantly reduce mortality from sepsis.
This lecture details the science of sepsis care in 2015 with compliments to the multiple online sources used, some of which are other lectures on SlideShare.
This lecture details the science of sepsis care in 2015 with compliments to the multiple online sources used, some of which are other lectures on SlideShare.
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
The recent definition, concept and terminologies of septic shock, surviving sepsis campaign, management techniques, SOFA score. Also includes antibiotics and supportive modalities.
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
The recent definition, concept and terminologies of septic shock, surviving sepsis campaign, management techniques, SOFA score. Also includes antibiotics and supportive modalities.
Multisystem inflammatory syndrome with covid 19 in pediatricsMounika Bhallam
Multisystem Inflammatory Syndrome with COVID-19 in pediatrics:- this topic will make u to get knowledge in MISC condition in children and management of covid child with MISC along with Nursing care
Social media and online resources are pervasive in our everyday lives. They are also finding their way into our everyday clinical practice, from continuing education to service communications and reference materials. In this session we will discuss how paramedics can utilise social media to improve their education and clinical practice, describe the concept of Free Open Access Medical Education (FOAMed), take a look at recent findings from a study investigating how Irish paramedics use online learning and social media, and compare to see if Ontario paramedics utilise them differently. Finally, we will discuss some general rules to ensure patient confidentiality and your professional reputation when using social media.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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
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.
2. Sepsis…so what?
• 8,000,000 people per year worldwide die from
sepsis
• Someone dies from sepsis every 2 minutes
• The overall mortality rate for patients severe sepsis
is 35% - approximately 5 times higher than for
STEMI and stroke
• We could save 10-15% with early recognition &
treatment
4. Sepsis…so what?
• For every hour that appropriate antibiotic
administration is delayed, there is an 8% increase in
mortality
• Around 40-50% of patients diagnosed with sepsis in
the ED are admitted via ambulance
5. What is Sepsis?
• It is a profound systemic inflammatory response to
an infection.
• An infection triggers the inflammatory response to
the presence of microorganisms in normally sterile
host tissue
6. SIRS
• Systemic Inflammatory Response Syndrome is a
systemic inflammatory response resulting from
activation of the immune system in response to any
physiologic insult (regardless of the cause).
• Two or more of the following must be present:
• Temp >38 or <36 degrees Celsius
• Heart rate >90
• Resp rate>20 or PaCO2 <32mmhg
• WBC >12,000 or <4,000 or >10% immature
forms
7. Defining Sepsis
• Sepsis is SIRS plus a confirmed or suspected
infection (bacterial, viral, fungal or parasitic).
• It can be a complication following burns,
trauma, surgery, or illness.
• Widespread inflammation, coagulation and
suppression of fibrinolysis occurs.
8. Defining Sepsis
Is the patient history suggestive of new infection?
• Pneumonia
• UTI
• Acute abdomen infection
• Meningitis
• Skin/soft tissue infection
• Bone joint infection
• Wound infection
• Catheter related Blood stream infection
• Endocarditis
• Implantable device infection
9. Adapted from Bone, R. C.,
Sibbald, W. J., & Sprung, C.
L. (1992). The ACCP-SCCM
consensus conference on sepsis
and organ failure. Chest,
101(6), 1481–3.
10. Severe Sepsis
• Severe sepsis is sepsis associated with the
dysfunction of one or more organs.
• Hypotension and hypoperfusion with lactic acidosis
occurs.
• Low blood pressure, high lactate levels and signs of
organ dysfunction are seen.
• The patient may also exhibit chills, tachypnea,
tachycardia, poor capillary refill and petechiae
11. Transitioning to Severe Sepsis
• The Signs of Severe Sepsis
• Arterial hypoxemia (PaO2/FIO2 <300)
• Spo2 <90% on Room air or supplemental O2
• Acute oliguria (UO<.5ml/kg/hr)
• Acutely altered mental status
• Creatinine >2.0
• Bilirubin >2.0
• Thrombocytopenia plt <100,000
• Lactate > 4 mmol/L
• SBP <90 MAP<65 * *These are the classic
indicators to trigger EGDT
• Coagulopathy INR>1.5 PTT>60
12. Septic Shock
• Is acute circulatory failure unexplained by other
causes
• Patient has persistent arterial hypotension SBP<90
[MAP <60] despite adequate volume resuscitation
• Patients don’t always look “sick” until this point
13. SIRS…a progression
Infection → sepsis → severe sepsis → septic shock → MODS
→ death
• Mortality is 50-60% in septic shock
• Early intervention is key
• We need to identify patients quickly and initiate treatment
Bundles
• Bundles are a group of interventions based on scientific
evidence
14. Understanding Sepsis
• Gram neg organisms cause most of adult cases
• E. Coli, Klebsiella, Enterobacter and Psuedomonias
• Gram positive organisms such as staphylococcus,
streptococcus, pneumococcus and enterococcus cause
others (these are associated with invasive devices)
• Viruses, Protozoa, parasites, fungi (Candida) and anaerobic
organisms like Clostridium can also cause sepsis
• Most common sites of origin are
• Skin and wounds, GI, Respiratory, Urinary tract
15. Understanding Sepsis
• Regardless of what caused it, the inflammatory response is
the same and is designed to help the body fight infection
and repair itself.
• SIRS is local inflammatory response that gets out of control.
• An avalanche of chemical mediators is set off that leads to
tissue/organ damage
• Endotoxins from bacteria signal release of cytokines and
other mediators that circulate throughout the body and
cause a number of responses:
16. Understanding Sepsis
• Systemic vasodilation which causes hypotension and
decreased afterload (SVR)
• Increased capillary permeability which causes edema and
decreased preload (CVP)
• Platelet aggregation, fibrin deposits and activation of
clotting cascade cause microcirulatory coagulation & further
tissue hypoxia and other chemicals prevent the breakdown
of these clots
17. Understanding Sepsis
• Multiple organ dysfunction results due to hypoperfusion
caused by the hypotension, hypovolemia and thrombus
formation.
• Hypermetabolic state where the body breaks down fat and
muscle for energy
• As tissue damage progresses, more organs begin to fail
ultimately leading to death
• Early intervention is the key
18. Treating Sepsis
• Goal is to identify patients with Severe Sepsis And
Septic Shock early
&
• Initiate treatment using the Early Goal-Directed
Therapy Protocols and following the Surviving
Sepsis Guidelines
19. Who is at risk?
• Very young and very old
• Those who have a compromised immune system e.g..
Patients on steroids, chemo, pneumonia
• Have wounds or injuries (burns/ trauma)
• Have alcohol or drug addiction
• Any one with intravenous catheters, wound drainage,
urinary catheters etc.
• Those with malnutrition (TPN)
• Pts with no spleen
• Recent surgery
• Diabetics
20. Identifying Risk for Sepsis
• Patients who are admitted to the hospital with serious
diseases are at the highest risk of developing sepsis because
of:
• Their underlying disease
• Their previous use of antibiotics
• The presence of drug-resistant bacteria in the hospital
• The fact that they often require invasive tubes or lines.
Especially if intubated/mechanically ventilated
>48hours
21. Identifying Sepsis
What do these patients look like?
• Fatigued, anorexic
• Fever (or hypothermic)
• Edema
• Tachycardic
• Tachypnoea and or dyspnoea
• Altered mental status (especially >65)
• Hypotensive
• Skin may be flushed, warm and dry or cool and mottled
22. Identifying Sepsis
• Look for:
• Low SpO2, abnormal blood gases
• CO2 may decrease as an early attempt to
compensate for lactic acidosis
• Low urine output, creatinine >2
• Abnormal WBC (high or low)
• Hyperglycemia (serum glucose elevates as part of the
stress response)
• Abnormal coagulation studies
• High bilirubin
• Key signs are SBP <90 or lactate >4
• Cultures can help identify infection and source
23. Case 1
• 78 year old male
presents awake,
confused, and in
moderate distress
• Emesis in basin at
bedside
• When asked, patient
states “I’m weak, and
don’t feel well”
• Skin is pale, dry
24. Case 1
• General Impression:
Patient responds to your
questions. GCS = E-4, V-4,
M-6
• Airway: Patent, no stridor
• Breathing: tachypneic,
tidal volume slightly
shallow
• Circulation: tachycardic
and weak radial pulse,
capillary refill 4 seconds
• Skin dry, pale, warm
25. Case 1
• S: Son states that patient is
“slightly more confused”
than normal over the past
24 hours. Patient states he
“feels sick and weak”, has
abdominal pain, and is
vomiting.
• A: Aspirin
• M: Insulin
• P: Dementia, IDDM
• L: light breakfast 2 hrs ago
• E: Progressively worse
nausea and vomiting over
past day.
• Vital signs: HR = 88, RR = 26
normal TV, BP = 96/52,
SpO2 = 98% room air up to
100% with cannula
• Lung sounds: slight
expiratory wheezing and
crackles in middle right lobe
• Skin dry and warm to touch
• Mucus membranes dry, skin
turgor poor
• Oral temperature = 100.3°F
• Good tidal volume
34. Resuscitation Bundle:
Tasks in the First 3 - 6 Hours
1. Measure serum lactate
2. Obtain Blood cultures prior to antibiotic administration
3. Administer broad spectrum antibiotic within 3 hrs if in ED (1 hr
if inpatient)
4. In event of hypotension and/or lactate >4
a. Deliver initial fluid bolus of 20cc/kg crystalloid or
equivalent
b. Vasopressors for hypotension not responsive to initial
fluid to maintain MAP > 65
5. For persistent hypotension despite fluid resuscitation (septic
shock) and/or lactate >4mmol/L
a. Achieve CVP >8
b. Achieve ScvO2 > 70% or SvO2 > 65%
35. NNT
• PCI in STEMI = 45-90
• TXA in trauma = 67
• Aspirin in AMI = 42
• CPAP for pulmonary oedema = 13
• Sepsis Six = 4.6!
• Defibrillation in cardiac arrest = 2.5
36. Management Bundle
First 24 hours
Consider low dose steroids for septic shock according to a
standard policy
• Or document why it is not appropriate
Consider human activated protein C (XIGRIS) according to a
standard policy
• Or document why it is not appropriate
Maintain glucose control >120 but <180
Maintain median inspiratory plateau pressures <30 for
mechanically ventilated patients
37. Treating Sepsis
• Rapid placement of a central venous line is priority
• IJ or SC
• To measure CVP and ScVO2
• Fluid challenges are given to
• CVP 8-12 (15-18 if mech vent)
• SBP >90 or MAP >65
• UO > 0.5ml/kg/hr
• Levophed is started if hypotension is unresponsive to fluid
• For ScVo2 <70
• If Hgb <7 consider transfusing blood to goal of Hgb 7-9g/dl
• Dobutamine is started if ScVo2 still <70
• O2 therapy or intubation/ventilation if needed
38. Treating Sepsis
• Transfer to ICU ASAP
• Central line is priority if not already in
• Arterial line may be needed to monitor blood
pressure
• Continue sepsis protocols
• Fluid for CVP <8 MAP <65
• Vasopressor if not fluid responsive
• Inotrope and transfusion for ScVO2 <70 and Hg <7
• Monitor CVP, ScVO2, lactate every 30 min
• Until goals met
39. Treating Sepsis
• Continuing Treatment
• Airway Ventilator management
• HOB is at 30 degrees & mouth care to prevent VAP
• DVT prophylaxis
• Plateau pressures < 30
• Weaning assessed daily
• Consideration of hydrocortisone 50mg IV Q 6 hrs for 7
days
• Strict glucose control >120 to <180 with protocol or
sliding scale (median glucose of 140)
• Consider Xigris (Activated protein C)
40. Treating Sepsis
• Other Considerations
• Nutrition is important due to the hyper-metabolic state
• Skin care and assessment to prevent breakdown
• Sedation, analgesia, paralytics, must be used cautiously
to optimize ventilation yet prevent prolonged intubation
• RAAS / Pain scales are used to measure patients
progress
• Strict I/O Use foley catheters only if truly necessary
41. Case 2
• 44 y/o female
• Lying in bed
• Opens eyes when you
say “hello”
• Seems confused
• Skin pale, slightly moist
42. Case 2
• Conscious, alert to verbal
stimuli, confused to
person, place, time
• Airway: open
• Breathing: normal rate
and tidal volume
• Circulation: weak,
tachycardic radial pulse,
cap refill 4 seconds
• Skin warm, slightly moist
43. Case 2
• S: Patient complains of
weakness. Husband
reports a 3 day historyof
worsening AMS, patient
normally conscious, alert,
and oriented.
• A: NKDA
• M: Glyburide, propranolol,
nifedipine
• P: AMI 3 years prior, HTN,
Type II DM, recent UTI
• L: Breakfast this morning
• E: No known events that
precipitated AMS
• Vital signs: HR = 92, BP =
88/42, RR = 20 and regular
tidal volume, SpO2 = 96%
RA up to 100% with oxygen
4 lpm via cannula
• Mucus membranes dry,
poor skin turgor
• Skin warm to touch, slightly
moist
• Temperature = 98.8°F via
oral thermometer
47. Highlights from the Guidelines
• Supplemental oxygen
• Sepsis causes an imbalance between tissue oxygen
supply and demand. Adequate tissue oxygenation is
essential to the treatment of a patient with sepsis.
• Continuous pulse oximetry is performed. Supplemental
oxygen is utilized to maintain the oxygen saturation ≥
94%.
48. Antibiotic Therapy
• Intravenous antibiotic therapy should be started within the
first hour of recognition of severe sepsis, after appropriate
cultures have been obtained.
• Broad-spectrum agents are ordered initially.
• This treatment should be reevaluated after culture results
are available.
49. Fluid Therapy
• Two large bore peripheral catheters should be inserted
initially and a central venous catheter should be placed
ASAP.
• Fluid resuscitation (the number one priority) is
accomplished with either crystalloids or colloids. Neither
has been proven to be better than the other.
• The target is to maintain a CVP between 8-12 mmHg, with a
higher CVP recommended for a mechanically ventilated
patient. (due to positive pressure ventilation)
• RASP trial ongoing comparing Ringers v Albumin
50. Vasopressor Therapy
• Once fluid resuscitation has been accomplished, if adequate
blood pressure and organ perfusion has not been restored,
vasopressor therapy should be started.
• Norepinephrine is the initial vasopressor of choice.
• Phenylephrine may be considered.
• An arterial catheter should be placed as soon as possible for
monitoring of arterial pressures and blood gases.
• Vasopressin may be added in patients with refractory shock
despite adequate fluid resuscitation and high dose
vasopressor agents.
51. Inotropic Therapy
• In patients with low cardiac output despite adequate fluid
resuscitation, dobutamine may be used to increase cardiac
output.
• If the blood pressure is low, it is used in combination
with a vasopressor.
• ScVO2 of >70% is the goal.
• Blood transfusion should be considered if Hgb is less than 7
to optimize the oxygen carrying capacity of the blood.
52. Steroids
• IV corticosteroids (hydrocortisone 200-300 mg/day for 7
days in 3 or 4 divided doses or by continuous infusion) are
recommended in patients in septic shock who, despite
adequate fluid replacement, require vasopressor therapy to
maintain an adequate blood pressure.
• Corticosteroids must be started when the patients BP is
refractory to vasopressor therapy.
• Once vasopressor therapy is no longer required, steroid
therapy can be weaned.
53. Blood Product Administration
• The recommendation is to transfuse packed red blood cells
when the hemoglobin decreases to < 7 g/dl.
• This optimizes the oxygen carrying capacity of the
patients blood.
• Platelets may be needed for those patients with a platelet
count <50,000 mm3.
54. Glucose Control
• Hyperglycemia and insulin resistance occur in severe sepsis.
• Tight glucose control with insulin is used to maintain blood
glucose 6.5-10 mmol/L [120-180 mg/dl]
• Hypoglycemia has shown to cause higher mortality in critical
patients.
• Insulin protocols should be followed.
55. Mechanically Ventilated Patients
• Maintain Inspiratory Plateau Pressure < 30 cm H2O)
• Patients with sepsis are at increased risk for developing
acute respiratory failure. Most patients with severe sepsis
and septic shock will require mechanical ventilation.
• Nearly 50% of patients with severe sepsis will develop acute
lung injury (ALI (acute respiratory distress syndrome).
• High tidal volumes along with high plateau pressures should
be avoided.
• The goal is to maintain a tidal volume of 6mL/kg lean
body weight in addition to end-inspiratory plateau
pressure < 30 cm H2O.
56. Bottom line?
• Everyone with suspected sepsis needs to get to
hospital…quickly!
• Everyone should get high flow oxygen – regardless
of SpO2 reading!
• Everyone should get fluids if they’re in shock
• Pre-alert the ED and mention the word “sepsis”
• Sepsis kills – let’s stop it – the simple stuff saves
lives
57. More information
• http://www.survivingsepsis.org
• http://www.uksepsis.org/
• http://sepsistrust.org/
• http://www.cdc.gov/sepsis/