The document provides information about peritonitis, including:
- Causes of peritonitis including bacterial, chemical, allergic, traumatic, ischemic, and miscellaneous causes.
- Acute bacterial peritonitis can be caused by gastrointestinal perforation, transmural translocation without perforation, exogenous contamination, or hematogenous spread.
- Common microorganisms involved in peritonitis include E. coli, streptococci, bacteroides, clostridium, and klebsiella from gastrointestinal sources, and other microbes from other sources.
- Defense mechanisms against peritonitis include leukocyte-attracting mechanisms, killing mechanisms, sequestration mechanisms
this presentation includes anatomy physiology function of peritoneum ,also includes cause of peritonitis its severity ,various scoring system investigation and treatment.It includes the recent advancement and latest articles from latest books of surgery.
Peritonitis is an inflammation of the peritoneum, the tissue that lines the inner wall of the abdomen and covers and supports most of your abdominal organs. Peritonitis is usually caused by infection from bacteria or fungi
this presentation includes anatomy physiology function of peritoneum ,also includes cause of peritonitis its severity ,various scoring system investigation and treatment.It includes the recent advancement and latest articles from latest books of surgery.
Peritonitis is an inflammation of the peritoneum, the tissue that lines the inner wall of the abdomen and covers and supports most of your abdominal organs. Peritonitis is usually caused by infection from bacteria or fungi
Intestinal fistulas pose the greatest challenge to the General Surgeon. The presentation provides abrief guideline for management of this complex problem.
Peritonitis is among the most common surgical cases. getting familiarized with it for early proper diagnostic and management is the key to reduce morbidity and mortality. In this power point i have analysed important anatomy, causes, investigation and how to manage it as medical personal covers all the necessary things you will require to know about peritonitis
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Definitions of GI bleeding
GI Bleeding include Upper and Lower of GIB
Causes of GI bleeding
Pathogenesis of GI bleeding
Diagnosis of GI bleeding
Clinical of GI bleeding
Management of GI bleeding
Recommendation of GI bleeding
Clinical guideline of GI bleeding
Intestinal fistulas pose the greatest challenge to the General Surgeon. The presentation provides abrief guideline for management of this complex problem.
Peritonitis is among the most common surgical cases. getting familiarized with it for early proper diagnostic and management is the key to reduce morbidity and mortality. In this power point i have analysed important anatomy, causes, investigation and how to manage it as medical personal covers all the necessary things you will require to know about peritonitis
Kindly like, save and share if you find the material useful
Definitions of GI bleeding
GI Bleeding include Upper and Lower of GIB
Causes of GI bleeding
Pathogenesis of GI bleeding
Diagnosis of GI bleeding
Clinical of GI bleeding
Management of GI bleeding
Recommendation of GI bleeding
Clinical guideline of GI bleeding
The lecture describes the definition of sepsis, infection, basteremia and how it leads to spetic shock and a general managent guidelines - for King Edward Medical Unviversity, Lahore
A brief discussion of a very common bacterial infection presenting as fever and skin rash following skin infection or use of tampons. Affecting adults especially women. Very helpful for medical students, ER doctors, dermatologists, nurses. References from dermatology textbook Rooks.
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Alongside the 77th World Health Assembly in Geneva on 28 May 2024, we launched the second version of our Index, allowing us to track progress and give new insights into what needs to be done to keep populations healthier for longer.
The speakers included:
Professor Orazio Schillaci, Minister of Health, Italy
Dr Hans Groth, Chairman of the Board, World Demographic & Ageing Forum
Professor Ilona Kickbusch, Founder and Chair, Global Health Centre, Geneva Graduate Institute and co-chair, World Health Summit Council
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QA Paediatric dentistry department, Hospital Melaka 2020Azreen Aj
QA study - To improve the 6th monthly recall rate post-comprehensive dental treatment under general anaesthesia in paediatric dentistry department, Hospital Melaka
Defecation
Normal defecation begins with movement in the left colon, moving stool toward the anus. When stool reaches the rectum, the distention causes relaxation of the internal sphincter and an awareness of the need to defecate. At the time of defecation, the external sphincter relaxes, and abdominal muscles contract, increasing intrarectal pressure and forcing the stool out
The Valsalva maneuver exerts pressure to expel faeces through a voluntary contraction of the abdominal muscles while maintaining forced expiration against a closed airway. Patients with cardiovascular disease, glaucoma, increased intracranial pressure, or a new surgical wound are at greater risk for cardiac dysrhythmias and elevated blood pressure with the Valsalva maneuver and need to avoid straining to pass the stool.
Normal defecation is painless, resulting in passage of soft, formed stool
CONSTIPATION
Constipation is a symptom, not a disease. Improper diet, reduced fluid intake, lack of exercise, and certain medications can cause constipation. For example, patients receiving opiates for pain after surgery often require a stool softener or laxative to prevent constipation. The signs of constipation include infrequent bowel movements (less than every 3 days), difficulty passing stools, excessive straining, inability to defecate at will, and hard feaces
IMPACTION
Fecal impaction results from unrelieved constipation. It is a collection of hardened feces wedged in the rectum that a person cannot expel. In cases of severe impaction the mass extends up into the sigmoid colon.
DIARRHEA
Diarrhea is an increase in the number of stools and the passage of liquid, unformed feces. It is associated with disorders affecting digestion, absorption, and secretion in the GI tract. Intestinal contents pass through the small and large intestine too quickly to allow for the usual absorption of fluid and nutrients. Irritation within the colon results in increased mucus secretion. As a result, feces become watery, and the patient is unable to control the urge to defecate. Normally an anal bag is safe and effective in long-term treatment of patients with fecal incontinence at home, in hospice, or in the hospital. Fecal incontinence is expensive and a potentially dangerous condition in terms of contamination and risk of skin ulceration
HEMORRHOIDS
Hemorrhoids are dilated, engorged veins in the lining of the rectum. They are either external or internal.
FLATULENCE
As gas accumulates in the lumen of the intestines, the bowel wall stretches and distends (flatulence). It is a common cause of abdominal fullness, pain, and cramping. Normally intestinal gas escapes through the mouth (belching) or the anus (passing of flatus)
FECAL INCONTINENCE
Fecal incontinence is the inability to control passage of feces and gas from the anus. Incontinence harms a patient’s body image
PREPARATION AND GIVING OF LAXATIVESACCORDING TO POTTER AND PERRY,
An enema is the instillation of a solution into the rectum and sig
One of the most developed cities of India, the city of Chennai is the capital of Tamilnadu and many people from different parts of India come here to earn their bread and butter. Being a metropolitan, the city is filled with towering building and beaches but the sad part as with almost every Indian city
The dimensions of healthcare quality refer to various attributes or aspects that define the standard of healthcare services. These dimensions are used to evaluate, measure, and improve the quality of care provided to patients. A comprehensive understanding of these dimensions ensures that healthcare systems can address various aspects of patient care effectively and holistically. Dimensions of Healthcare Quality and Performance of care include the following; Appropriateness, Availability, Competence, Continuity, Effectiveness, Efficiency, Efficacy, Prevention, Respect and Care, Safety as well as Timeliness.
Telehealth Psychology Building Trust with Clients.pptxThe Harvest Clinic
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Navigating Challenges: Mental Health, Legislation, and the Prison System in B...Guillermo Rivera
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Antibiotic Stewardship by Anushri Srivastava.pptxAnushriSrivastav
Stewardship is the act of taking good care of something.
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
WHO launched the Global Antimicrobial Resistance and Use Surveillance System (GLASS) in 2015 to fill knowledge gaps and inform strategies at all levels.
ACCORDING TO apic.org,
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
ACCORDING TO pewtrusts.org,
Antibiotic stewardship refers to efforts in doctors’ offices, hospitals, long term care facilities, and other health care settings to ensure that antibiotics are used only when necessary and appropriate
According to WHO,
Antimicrobial stewardship is a systematic approach to educate and support health care professionals to follow evidence-based guidelines for prescribing and administering antimicrobials
In 1996, John McGowan and Dale Gerding first applied the term antimicrobial stewardship, where they suggested a causal association between antimicrobial agent use and resistance. They also focused on the urgency of large-scale controlled trials of antimicrobial-use regulation employing sophisticated epidemiologic methods, molecular typing, and precise resistance mechanism analysis.
Antimicrobial Stewardship(AMS) refers to the optimal selection, dosing, and duration of antimicrobial treatment resulting in the best clinical outcome with minimal side effects to the patients and minimal impact on subsequent resistance.
According to the 2019 report, in the US, more than 2.8 million antibiotic-resistant infections occur each year, and more than 35000 people die. In addition to this, it also mentioned that 223,900 cases of Clostridoides difficile occurred in 2017, of which 12800 people died. The report did not include viruses or parasites
VISION
Being proactive
Supporting optimal animal and human health
Exploring ways to reduce overall use of antimicrobials
Using the drugs that prevent and treat disease by killing microscopic organisms in a responsible way
GOAL
to prevent the generation and spread of antimicrobial resistance (AMR). Doing so will preserve the effectiveness of these drugs in animals and humans for years to come.
being to preserve human and animal health and the effectiveness of antimicrobial medications.
to implement a multidisciplinary approach in assembling a stewardship team to include an infectious disease physician, a clinical pharmacist with infectious diseases training, infection preventionist, and a close collaboration with the staff in the clinical microbiology laboratory
to prevent antimicrobial overuse, misuse and abuse.
to minimize the developme
How many patients does case series should have In comparison to case reports.pdfpubrica101
Pubrica’s team of researchers and writers create scientific and medical research articles, which may be important resources for authors and practitioners. Pubrica medical writers assist you in creating and revising the introduction by alerting the reader to gaps in the chosen study subject. Our professionals understand the order in which the hypothesis topic is followed by the broad subject, the issue, and the backdrop.
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2. National lead for GlobalSurg Collaborative
National Lead with GlobalSurg® for FALCON trial
Co-Prinicipal Investigator for NRPU grant
Collaborator for European Coloproctology society, UK
Colorectal Fellowship, Yonsei University, South Korea
Fellow of College of Physicians & Surgeons, Pakistan
(Surgery)
Fellow of Higher education authority of UK (FHEA)
Member of Royal College of Surgeons, England (UK)
Member of College of Physicians & Surgeons, Pakistan
(Surgery)
Member Editorial Board, BMJ case reports since 2011-2014
Reviewer for Rawalpindi Medical Journal since 2015
Dr. Ahmad Uzair Qureshi
3. Causes of peritoneal inflammation
• Bacterial, gastrointestinal and non-gastrointestinal
• Chemical, e.g. bile, barium
• Allergic, e.g. starch peritonitis
• Traumatic, e.g. operative handling
• Ischaemia, e.g. strangulated bowel, vascular occlusion
• Miscellaneous, e.g. familial Mediterranean fever
4. Acute bacterial peritonitis
• Gastrointestinal perforation, e.g. perforated ulcer, appendix,
diverticulum
• Transmural translocation (no perforation), e.g. pancreatitis,
ischaemic bowel
• Exogenous contamination, e.g. drains, open surgery, trauma
• Female genital tract infection, e.g. pelvic inflammatory disease
• Haematogenous spread (rare), e.g. septicaemia
6. Defense Mechanisms
• Leukocyte-Attracting Mechanisms
• Microvilli of the mesothelial cell
• ICAM-1 (CD 54) and VCAM-1 (CD 106)
• Killing Mechanisms
• Macrophages
• Neutrophils
• Opsonins
• Complement C3b
• Immunoglobulin G
• Fibronectin
• Mast cell-derived leukotrienes
• Sequestration Mechanisms
• Fibrin trapping of bacteria
• Formation of fibrinous adhesions
• Omental loculation of foci of
inflammation
• Removal Mechanisms
• Peritoneal clearance of bacteria
through the diaphragm via the
thoracic duct
7. Clinical features
• Abdominal pain, worse on movement, coughing and deep respiration
• Constitutional upset: anorexia, malaise, fever, lassitude
• GI upset: nausea ± vomiting
• Pyrexia (may be absent)
• Raised pulse rate
• Tenderness ± guarding/rigidity/rebound of abdominal wall
• Pain/tenderness on rectal/vaginal examination (pelvic peritonitis)
• Absent or reduced bowel sounds
• ‘Septic shock’ (systemic inflammatory response syndrome
• (SIRS) and multiorgan dysfunction syndrome (MODS)) in later stages
8. Complications
Systemic complications
• Bacteraemic/endotoxic shock
• Systemic inflammatory response
syndrome
• Multiorgan dysfunction
syndrome
• Death
Abdominal complications
• Paralytic ileus
• Residual or recurrent
abscess/inflammatory mass
• Portal pyaemia/liver abscess
• Adhesional small bowel
obstruction
9.
10.
11.
12.
13.
14.
15.
16. Management of peritonitis
• General care of patient
• Correction of fluid and electrolyte imbalance
• Insertion of nasogastric drainage tube and urinary catheter
• Broad-spectrum antibiotic therapy
• Analgesia
• Vital system support
• Operative treatment of cause when appropriate
• Remove or divert cause
• Peritoneal lavage ± drainage
20. Severe Sepsis
(acute organ dysfunction secondary to documented or suspected infection)
leading to
Dysfunction of organ(s) distant from the site of infection
24. INFECTION
Presence of microorganisms in a normally sterile site
Do Not confuse with “colonization,” which is the presence of
microorganisms on an epithelial surface
31. Acute-Phase Responses (Categorized According to Possible Roles in Defense)
Anti-infective
Increases synthesis of complement factors, microbe pattern-recognition molecules
(mannose-binding lectin, LBP, CRP, CD14, others)
Sequesters iron (lactoferrin, hepcidin) and zinc (metallothionein)
Anti-inflammatory
Releases anti-inflammatory neuroendocrine hormones (cortisol, ACTH, epinephrine, α-
MSH)
Increases synthesis of proteins that help prevent inflammation within the systemic
compartment
Cytokine antagonists (IL-1Ra, sTNF-Rs)
Anti-inflammatory mediators (e.g., IL-4, IL-6, IL-6R, IL-10, IL-13, TGF-β)
Protease inhibitors (e.g., α1-antiprotease)
Antioxidants (haptoglobin)
Reprograms circulating leukocytes (epinephrine, cortisol, PGE 2 , ? other factors)
Procoagulant
Walls off infection, prevents systemic spread
Increases synthesis or release of fibrinogen, PAI-1, C4b
Decreases synthesis of protein C, antithrombin III
Metabolic Preserves euglycemia, mobilizes fatty acids, amino acids
Epinephrine, cortisol, glucagon, cytokines
Thermoregulatory Inhibits microbial growth
Fever
Early Systemic Responses: Keeping
Infection and Inflammation Localized
32. Harmful Responses to Infection:
Severe Sepsis and Septic Shock
Develop when normally adaptive stress responses are pushed
beyond their ability to be protective.
“Hypofunction” implies an inadequate level of activity, whereas
“dysfunction” suggests that organ performance is in some way abnormal.
34. • An extension of the body's normal neuroendocrine responses to
stress
• An exhaustion of ATP in critical organs
• when the inflammatory stimulus is too strong or too prolonged.
35. • Cytokines circulate via the blood and induce injury to the vascular
endothelium and/or microcirculation in different organs.
• An extension of the body's normal neuroendocrine responses to
stress
• An exhaustion of ATP in critical organs
• when the inflammatory stimulus is too strong or too prolonged.
36. Septic Shock
Opportunistic commensal bacteria typically invade across
disrupted epithelia.
Hosts in whom immunosuppressive acute-phase responses are
already occurring because of illness, injury, or infection.
Host is unable to kill the bacteria because of mechanical failure
(obstructed drainage pathway), immunosuppression
(neutropenia, “endogenous immunosuppression”)
37. • These bacteria invade the bloodstream when local defenses are
unable to kill or contain them; bacteremia.
• Locally-produced mediators act as trigger for severe sepsis and
septic shock
• Outcome is strongly related to the patient's underlying
physiologic fitness.
38.
39. • Pathogenic microbes/virus that can survive and multiply in
previously healthy humans.
• the microbes/viruses may enter the bloodstream, infect vascular
endothelial cells and/or blood cells, and release toxins.
• The circulating microbes may provoke both shock and
profound coagulopathy that not uncommonly results in
hemorrhage and/or arterial thrombosis
44. Initial Resuscitation and Infection Issues
A. Initial Resuscitation (Goals during the first 6 hrs of resuscitation)
1. Hypotension persisting after initial fluid challenge or blood lactate
concentration ≥ 4 mmol/L
a) Central venous pressure 8–12 mm Hg
b) Mean arterial pressure (MAP) ≥ 65 mm Hg
c) Urine output ≥ 0.5 mL/kg/hr
d) Central venous (superior vena cava) or mixed venous oxygen
saturation 70% or 65%, respectively
45. B. Diagnosis
• Cultures as clinically appropriate before antimicrobial therapy if no
significant delay (> 45 mins) in the start of antimicrobial(s)
• At least 2 sets of blood cultures (both aerobic and anaerobic bottles) be
obtained before antimicrobial therapy
• Imaging studies performed promptly to confirm a potential source of
infection (UG).
46. C. Antimicrobial Therapy
• Administration of effective intravenous antimicrobials within the first hour
of recognition of septic shock and severe
• sepsis without septic shock as the goal of therapy.
• Initial empiric anti-infective therapy of one or more drugs that have activity
against all likely pathogens
• Antimicrobial regimen should be reassessed daily for potential
deescalation.
• Use of low procalcitonin levels in the discontinuation of empiric antibiotics
• Combination empirical therapy for neutropenic respiratory failure and
septic shock,
47. TO BE COMPLETED WITHIN 3 HOURS OF TIME OF
PRESENTATION*:
1. Measure lactate level
2. Obtain blood cultures prior to administration of antibiotics
3. Administer broad spectrum antibiotics
4. Administer 30ml/kg crystalloid for hypotension or lactate
≥4mmol/L
48. TO BE COMPLETED WITHIN 6 HOURS OF TIME OF
PRESENTATION:
5. Apply vasopressors (for hypotension that does not respond to
initial fluid resuscitation) to maintain a mean arterial pressure
(MAP) ≥65mmHg
6. In the event of persistent hypotension after initial fluid
administration (MAP < 65 mm Hg) or if initial lactate was ≥4
mmol/L, re-assess volume status and tissue perfusion 7. Re-
measure lactate if initial lactate elevated.
49. Fluid Therapy of Severe Sepsis
• Crystalloids as the initial fluid of choice
• Against the use of hydroxyethyl starches
• Albumin when substantial amounts of crystalloids (grade 2C).
• Initial fluid challenge a minimum of 30 mL/kg of crystalloids (a portion of
this may be albumin equivalent).
• Fluid challenge technique be applied
Change in pulse pressure,
Stroke volume variation)
Arterial pressure, Heart rate
50. Vasopressors
• Vasopressor therapy initially to target a mean arterial pressure (MAP) of 65 mm Hg
• Norepinephrine as the first choice vasopressor.
• 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 (NE) with intent of either
raising MAP or decreasing NE dosage .
• Low dose vasopressin is not recommended as the single initial vasopressor for treatment
of sepsis-induced hypotension and vasopressin doses higher than 0.03-0.04 units/minute
should be reserved for salvage therapy (failure to achieve adequate MAP with other
vasopressor agents) .
• 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).
51. Hemodynamic Support and Adjunctive Therapy
• Inotropic Therapy
• Corticosteroids
• Blood Product Administration.
• Immunoglobulins
• Mechanical Ventilation of Sepsis-Induced ARDS
• Sedation, Analgesia, and Neuromuscular Blockade in Sepsis
• Glucose Control
• Renal Replacement Therapy
• Bicarbonate Therapy
• Deep Vein ThrombosisProphylaxis
• Nutrition
A patient is said to be “septic” if infection is documented or suspected and “some” additional criteria are met
A patient is said to be “septic” if infection is documented or suspected and “some” additional criteria are met
A patient is said to be “septic” if infection is documented or suspected and “some” additional criteria are met
A patient is said to be “septic” if infection is documented or suspected and “some” additional criteria are met
A patient is said to be “septic” if infection is documented or suspected and “some” additional criteria are met
Do Not confuse with “colonization,” which is the presence of microorganisms on an epithelial surface
Do Not confuse with “colonization,” which is the presence of microorganisms on an epithelial surface
Do Not confuse with “colonization,” which is the presence of microorganisms on an epithelial surface
May be transient and inconsequential; inconsistent correlation with severe sepsis
May be transient and inconsequential; inconsistent correlation with severe sepsis
The most proximal cause(s) remain unknown, however, and how the phenomena discussed here (e.g., complement activation, coagulopathy, mediator action or desensitization thereto, endothelial injury, microcirculatory dysfunction) interact to produce the syndromes is uncertain.
, often into A vigorous local inflammatory response, usually initiated by host sensing of conserved microbial molecules,
(including bacterial virulence determinants). , when it occurs, is often transient and may be less important than . In the acute management of these patients, a diligent search for the primary focus of infection is essential.
2. At the other end of the spectrum are . They can invade without eliciting clinically significant inflammation other than, in some cases, pneumonia, lymphadenopathy, or a lesion at a cutaneous entry site. If their growth is not controlled by innate immune defenses, or other molecules that stimulate inflammation or induce damage within the blood and tissues. . Examples include S. pneumoniae , N. meningitidis, R. rickettsii, Y. pestis, Salmonella Typhi, B. anthracis and probably V. vulnificus and C. canimorsus. With many of these, the absence of an early proinflammatory (local) host defense is an important key to pathogenesis.
Certain viruses may also be in this category; there is evidence that symptomatic infection with filoviruses (e.g., Ebola), for example, which invade without provoking local inflammation and infect monocyte-macrophages in many tissues, may be prevented by an early proinflammatory systemic response. Recent research has associated inherited defects in innate and/or acquired immune function with susceptibility to some of these pathogens.
3. Other stimuli, such as gram-positive bacterial superantigens, may be produced by extravascular bacteria and diffuse into the blood or be released into it by circulating bacteria. They activate T lymphocytes in the blood and tissues to release cytokines; in poorly understood ways, these cytokines induce organ dysfunction and cause shock.
Although each of these microbe-host interactions leads to the syndromes known now as severe sepsis and septic shock, they are sufficiently different from one another that they force the question: Is the apparent continuum from sepsis to septic shock truly a single process, a “final common path” that can be induced by many different initiating events, or do different microbe-host interactions produce severe sepsis and septic shock in different ways? If the latter, which are the most important determinants: susceptibility genes, underlying disease, age, physiologic state at the time infection occurs, primary extravascular versus intravascular infection, infection with commensal versus pathogen, or others? Answers to these questions may become possible when a quantitative description of the underlying biochemical mechanisms of severe sepsis and septic shock is achieved.
D. Antimicrobial Therapy
1. 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.
2a. Initial empiric anti-infective therapy of one or more drugs that have activity against all likely pathogens (bacterial and/or fungal or
viral) and that penetrate in adequate concentrations into tissues presumed to be the source of sepsis (grade 1B).
2b. Antimicrobial regimen should be reassessed daily for potential deescalation (grade 1B).
3. 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).
4a. Combination empirical therapy for neutropenic patients with severe sepsis (grade 2B) and for patients with difficult-to-treat, multidrugresistant
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). A combination of beta-lactam and macrolide for
patients with septic shock from bacteremic Streptococcus pneumoniae infections (grade 2B).
Administration of effective intravenous antimicrobials within the first hour of recognition of septic shock and severe
sepsis without septic shock as the goal of therapy.
Initial empiric anti-infective therapy of one or more drugs that have activity against all likely pathogens
Antimicrobial regimen should be reassessed daily for potential deescalation.
Use of low procalcitonin levels in the discontinuation of empiric antibiotics
Combination empirical therapy for neutropenic patients with severe sepsis (grade 2B) and for patients with difficult-to-treat, multidrugresistant 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
A combination of beta-lactam and macrolide for patients with septic shock from bacteremic Streptococcus pneumoniae infections (grade 2B)
2
TABLE 1
DOCUMENT REASSESSMENT OF VOLUME STATUS AND TISSUE PERFUSION WITH:
EITHER
• Repeat focused exam (after initial fluid resuscitation) by licensed independent practitioner including vital signs, cardiopulmonary, capillary refill, pulse, and skin findings.
OR TWO OF THE FOLLOWING:
• Measure CVP
• Measure ScvO2
• Bedside cardiovascular ultrasound
• Dynamic assessment of fluid responsiveness with passive leg raise or fluid challenge
Of note, the 6-hour bundle has been updated; the 3-hour SSC bundle is not affected.
While no suggestion of harm was indicated with use of a central line in any trial, and published evidence shows significant mortality reduction using the original SSC bundles (5), the committee has taken a prudent look at all current data and, despite weaknesses as in all studies, determined the above bundles to be the appropriate approach at this time.
References:
International Guidelines for Management of Severe Sepsis and Septic Shock
Initial Resuscitation
• 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) (grade 1C).
Goals during the 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) Central venous (superior vena cava) or mixed venous oxygen saturation 70% or 65%, respectively
° In patients with elevated lactate levels targeting resuscitation to normalize lactate (grade 2C).
Screening for Sepsisand Performance Improvement
• Routine screening of potentially infected seriously ill patients for severe sepsis to allow earlier implementation of therapy (grade 1C).
Hospital–based performance improvement efforts in severe sepsis (UG).
Diagnosis
• 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).
° Use of the 1,3 beta-D-glucan assay (grade 2B), mannan and anti-mannan antibody assays (grade 2C), if available and invasive candidiasis is in differential diagnosis of cause of infection.
Imaging studies performed promptly to confirm a potential source of infection (UG).
Antimicrobial Therapy
• 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.
• a) Initial empiric anti-infective therapy of one or more drugs that have activity against all likely pathogens (bacterial and/or fungal or viral) and that penetrate in adequate concentrations into tissues presumed to be the source of sepsis (grade 1B).Initial Resuscitation and Infection Issues
• b) Antimicrobial regimen should be reassessed daily for potential de-escalation (grade 1B).
° 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).
° a) 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). A combination of beta-lactam and macrolide for patients with septic shock from bacteremic Streptococcus pneumoniae infections (grade 2B).
° b) 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).
° 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).
° Antiviral therapy initiated as early as possible in patients with severe sepsis or septic shock of viral origin (grade 2C).
Antimicrobial agents should not be used in patients with severe inflammatory states determined to be of noninfectious cause (UG).
Source Control
• 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).
° When infected peripancreatic necrosis is identified as a potential source of infection, definitive intervention is best delayed until adequate demarcation of viable and nonviable tissues has occurred (grade 2B).
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) (UG).
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 (UG).
Hemodynamic
Infection Prevention
° a) Selective oral decontamination and selective digestive decontamination should be introduced and investigated as a method to reduce the incidence of ventilator-associated pneumonia; this infection control measure can then be instituted in health care settings and regions where this methodology is found to be effective (grade 2B).
° b) Oral chlorhexidine gluconate be used as a form of oropharyngeal decontamination to reduce the risk of ventilator-associated pneumonia in ICU patients with severe sepsis (grade 2B).
Hemodynamic Support and Adjunctive Therapy
• Phenylephrine is not recommended in the treatment of septic shock except in circumstances where (a) norepinephrine is associated with serious arrhythmias, (b) cardiac output is known to be high and blood pressure persistently low or (c) as salvage therapy when combined inotrope/vasopressor drugs and low dose vasopressin have failed to achieve MAP target (grade 1C).
• Low dose dopamine should not be used for renal protection (grade 1A).
All patients requiring vasopressors have an arterial catheter placed as soon as practical if resources are available (UG).
Inotropic Therapy
• A trial of dobutamine infusion up to 20 micrograms/kg/minbe administered or added to vasopressor (if in use) in the presence of (a) myocardial dysfunction as suggested by elevated cardiac filling pressures and low cardiac output, or (b) ongoing signs of hypoperfusion, despite achieving adequate intravascular volume and adequate MAP (grade 1C).
• Not using a strategy to increase cardiac index to predetermined supranormal levels (grade 1B).
Corticosteroids
° Not using intravenous hydrocortisone to treat adult septic shock patients if adequate fluid resuscitation and vasopressor therapy are able to restore hemodynamic stability (see goals for Initial Resuscitation). In case this is not achievable, we suggest intravenous hydrocortisone alone at a dose of 200 mg per day (grade 2C).
° Not using the ACTH stimulation test to identify adults with septic shock who should receive hydrocortisone (grade 2B).
° In treated patients hydrocortisone tapered when vasopressors are no longer required (grade 2D).
• Corticosteroids not be administered for the treatment of sepsis in the absence of shock (grade 1D).
° When hydrocortisone is given, use continuous flow (grade 2D).
Other Supportive Therapy of Severe Sepsis
Blood Product Administration
• 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 (grade 1B).
• Not using erythropoietin as a specific treatment of anemia associated with severe sepsis (grade 1B).
° Fresh frozen plasma not be used to correct laboratory clotting abnormalities in the absence of bleeding or planned invasive procedures (grade 2D).
• Not using antithrombin for the treatment of severe sepsis and septic shock (grade 1B).
° In patients with severe sepsis, administer platelets prophylactically when counts are <10,000/mm3 (10 x 109/L) in the absence of apparent bleeding. We suggest prophylactic platelet transfusion when counts are < 20,000/mm3 (20 x 109/L) if the patient has a significant risk of bleeding. Higher platelet counts (≥50,000/mm3 [50 x 109/L]) are advised for active bleeding, surgery, or invasive procedures (grade 2D).
Immunoglobulins
° Not using intravenous immunoglobulins in adult patients with severe sepsis or septic shock (grade 2B).
Selenium
° Not using intravenous selenium for the treatment of severe sepsis (grade 2C).
Mechanical Ventilation of Sepsis-Induced ARDS
• Target a tidal volume of 6 mL/kg predicted body weight in patients with sepsis-induced ARDS (grade 1A vs. 12 mL/kg).
• Plateau pressures be measured in patients with ARDS and initial upper limit goal for plateau pressures in a passively inflated lung be ≤30 cm H2O (grade 1B).
• Positive end-expiratory pressure (PEEP) be applied to avoid alveolar collapse at end expiration (atelectotrauma) (grade 1B).
° Strategies based on higher rather than lower levels of PEEP be used for patients with sepsis-induced moderate or severe ARDS (grade 2C).
° Recruitment maneuvers be used in sepsis patients with severe refractory hypoxemia (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).
• That mechanically ventilated sepsis patients be maintained with the head of the bed elevated to 30-45 degrees to limit aspiration risk and to prevent the development of ventilator-associated pneumonia (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).
• 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); c) no new potentially serious conditions; d) low ventilatory and end-expiratory pressure requirements; and e) 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 (grade 1A).
• 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).
Sedation, Analgesia, and Neuromuscular Blockade in Sepsis
• Continuous or intermittent sedation be minimized in mechanically ventilated sepsis patients, targeting specific titration endpoints (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. If NMBAs must be maintained, either intermittent bolus as required or continuous infusion with train-of-four monitoring of the depth of blockade should be used (grade 1C).
° A short course of NMBA of not greater than 48 hours for patients with early sepsis-induced ARDS and a Pao2/Fio2 < 150 mm Hg (grade 2C).
Glucose Control
• 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).
• 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).
Glucose levels obtained with point-of-care testing of capillary blood be interpreted with caution, as such measurements may not accurately estimate arterial blood or plasma glucose values (UG).
Renal Replacement Therapy
° Continuous renal replacement therapies and intermittent hemodialysis are equivalent in patients with severe sepsis and acute renal failure (grade 2B).
° Use continuous therapies to facilitate management of fluid balance in hemodynamically unstable septic patients (grade 2D).
Bicarbonate Therapy
° 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).
Deep Vein ThrombosisProphylaxis
• Patients with severe sepsis receive daily pharmacoprophylaxis against venous thromboembolism (VTE) (grade 1B). This should be accomplished with 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).
° 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 (eg, thrombocytopenia, severe coagulopathy, active bleeding, recent intracerebral hemorrhage) not receive pharmacoprophylaxis (grade 1B), but receive mechanical prophylactic treatment, such as graduated compression stockings or intermittent compression devices (grade 2C), unless contraindicated. When the risk decreases start pharmacoprophylaxis (grade 2C).
StressUlcer Prophylaxis
• Stress ulcer prophylaxis using H2 blocker or proton pump inhibitor be given to patients with severe sepsis/septic shock who have bleeding risk factors (grade 1B).
° When stress ulcer prophylaxis is used, proton pump inhibitors rather than H2RA (grade 2D).
° Patients without risk factors do not receive prophylaxis (grade 2B).
Nutrition
° 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).
° Use intravenous glucose and enteral nutrition rather than total parenteral nutrition (TPN) alone or parenteral nutrition in conjunction with enteral feeding in the first 7 days after a diagnosis of severe sepsis/septic shock (grade 2B).
° Use nutrition with no specific immunomodulating supplementation rather than nutrition providing specific immunomodulating supplementation in patients with severe sepsis (grade 2C).
Setting Goalsof Care
• Discuss goals of care and prognosis with patients and families (grade 1B).
• Incorporate goals of care into treatment and end-of-life care planning, utilizing palliative care principles where appropriate (grade 1B).
° Address goals of care as early as feasible, but no later than within 72 hours of ICU admission (grade 2C).