Approach to sepsis- a primary physician perspective

APPROACH TO SEPSIS
MANAGEMENT
Thursday, September 17, 2015 1
WHAT THE PRIMARY PHYSICIAN
SHOULD DO
Dr. A.P.Naveen Kumar
Chief Specialist (Gen. Med. )
Visakha Steel General Hospital

Clinical impact of Severe
Sepsis
†
National Center for Health Statistics, 2001. §
American Cancer Society, 2001.
*American Heart Association. 2000. ‡
Angus DC et al. Crit Care Med. 2001 (In Press).
0
50
100
150
200
250
300
AIDS* Colon Breast
Cancer§
CHF†
Severe
Sepsis‡
Cases/100,000
Incidence of Severe Sepsis Mortality of Severe Sepsis
0
50,000
100,000
150,000
200,000
250,000
Deaths/Year
AIDS* Severe
Sepsis‡
AMI†
Breast
Cancer§

Polymicrobial sepsis shows higher risk for
complication, length of stay and mortality than
unimicrobial.
N Abed et al. Outcome of unimicrobial versus polymicrobial sepsis. Critical Care 2010, 14(Suppl 1):P62
(n=101) Unimicrobial infection Polymicrobial infection P value
Positive sputum 66% 71% 0.6
+ve blood culture 14% 51% 0.0001
UTI 6.3% 49.7% 0.0001
Wound infection 2.1% 20.7% 0.004
Acinetobacter/Candi
da/ E. coli
0.032
Mean hospital stay 17.4(+/- ) 9.3 days 26.9(+/- )15.4 days 0.001

Guide to Recommendations’
Strengths and Supporting
Evidence: 1 = strong recommendation;1 = strong recommendation;
 2 = weak recommendation or suggestion;2 = weak recommendation or suggestion;
 A = good evidence from randomized trials;A = good evidence from randomized trials;
 B = moderate strength evidence from small randomized trial(s) orB = moderate strength evidence from small randomized trial(s) or
multiple good observational trials;multiple good observational trials;
 C = weak or absent evidence, mostly driven by consensus opinion.C = weak or absent evidence, mostly driven by consensus opinion.
Thursday, September 17, 2015 5Dellinger R P et al. Critical Care Medicine. 2013;41(2):580-637

Infection
 either
Bacteraemia (or viraemia/fungaemia/protozoan)
is the presence of bacteria within the bloodstream
Septic focus (abscess / cavity / tissue mass)

SIRS –Systemic Inflammatory
Response Syndrome
 2/4 of
Temp >38 or <36
HR >90
Respiratory Rate >24 / mt.
WCC >12 or <4 or >10% bands (immature forms)

Definitions
SepsisSepsis is defined as the presence (probable or documented) of
infection together with systemic manifestations of infection(SIRS).

Definitions
Severe sepsisSevere sepsis is defined as sepsis plus sepsis-induced
organ dysfunction or tissue hypoperfusion.

Organ System Involvement
 Circulation
 Hypotension,
 increases in microvascular permeability
 Shock
 Lung
 Pulmonary Edema,
 hypoxemia,
 ARDS
 Hematologic
 DIC, coagulopathy
 (DVT)

 GI tract
 stress ulcer
 Translocation of bacteria,
 Liver Failure,
 Gastroparesis and ileus,
 Cholestasis
►Kidney
 Acute tubular necrosis,
 Renal Failure

 Nervous System
 Encephalopathy
►Skeletal Muscle
Rhabdomyolysis
 Endocrine
 Adrenal insufficiency

 1. Cardiovascular: Arterial systolic blood
pressure < 90 mmHg or mean arterial pressure < 70
mmHg that responds to administration of
intravenous fluid
 2. Renal: Urine output <0.5 mL/kg per hour for 1 h
despite adequate fluid resuscitation

 3. Respiratory: PaO2/FIO2 < 250 or, if the lung is the
only dysfunctional organ < 200

OXYGEN
DELIVERY
FiO2 PaO2/FiO2
Room air 0.21 476
1 Litre / mt. 0.24 416
2 Litre/ mt. 0.28 357
3 Litre/ mt. 0.32 312
4 Litre/ mt. 0.36 277
5 Litre/ mt. 0.40 250
6 Litre/ mt. 0.44 227
7 Litre / mt. 0.48 208
8 Litre / mt. 0.52 192

 4. Hematologic: Platelet count <80,000/L or 50%
decrease in platelet count from highest value
recorded over previous 3 days
 5. Unexplained metabolic acidosis: A pH < 7.30 or a
base deficit 5.0 mEq/L and a plasma lactate level
>1.5 times upper limit of normal for reporting lab
 6. Adequate fluid resuscitation: Pulmonary artery
wedge pressure < 12 mmHg or central venous
pressure < 8 mmHg

Definitions
Sepsis-induced tissue hypoperfusionSepsis-induced tissue hypoperfusion is
defined as infection-induced hypotension, elevated lactate, or
oliguria.

Definitions
Septic shockSeptic shock is defined as sepsis-induced hypotension
persisting despite adequate fluid resuscitation.

Sepsis
- SIRS
+ Infection
Severe Sepsis
- Sepsis
+ Organ dysfunction
Septic shock
– Sepsis
+ Hypotension despite fluid resuscitation

Critical illness–related
corticosteroid insufficiency (CIRCI)
 Inadequate corticosteroid activity for the
patient's severity of illness; should be
suspected when hypotension is not relieved
by fluid administration

Multiple organ dysfunction
syndrome
 Dysfunction of more than one organ,requiring
intervention to maintain hemostasis
Refractory Septic Shock
 Septic shock that lasts for > 1 hr. and does not
respond to fluids or pressor administration

Case -1
 51 year old male
 Presented with fever, cough and breathlessness
 h/o streaky hemoptysis
 h/o orthopnea+
 Known case of COPD
 Ethanolic
 Non DM /non smoker

Examination
 Conscious and coherent
 Febrile, HR- 140/mt.,RR – 40/mt ,BP 100/70
 Lungs – Bil. Rhonchi and crepts.
 CVS – Tachycardia
 CNS- no deficit

Investigations
 Hb.-13.6 ,TC – 24100 , DC – P94 L04 , Pl. -2.1
 FBS – 225 mgs /dl ,Sr. Crea. – 1.8 mgs/dl , Urea –
49 mgs/dl
 LFT – 1.8 / 53 / 48 /93
 ECG – sinus tachycardia
 CXR – Lt.basal consolidation
 SPo2 – 66
CAP with Sepsis

Case -2
 54 year old female
 Fever with breathlessness
 Dysuria and decreased urination
 DM , HTN
 Febrile , HR- 112/mt. ,BP – 80/60
 Lungs –clear ,CVS -NAD

 Hb.- 10.2 , TC -18600 , DC-P88 L10 E2
 FBS – 224 ,PPBS -336 ,Crea. – 1.8
 Urine –plenty of pus cells
 CXR –NAD
 ECG –WNL
UROSEPSIS

CASE 3
 64 year old male
 HTN ,CAD ,DM, LV Dysfunction
 Presented with breathlessness –PND +
 Cough ,low grade fever
 Afebrile ,HR-122/mt. ,RR -32/mt. ,BP- 70/50
 Lungs – bil. Crepts ,CVS – LVS3+ tach.,JVP -↑

 Hb. -12.6 ,TC- 12400 ,DC –P72 L22 E6 ,Pl. -2.3
 FBS- 168 ,PPBS -224 ,Crea. – 1.2 ,LFT –N
 ECG - T L1, Avl , V 2-6↓
 CXR – s/o CCF
 SPo2 - 86

Case 4
 70 yrs male
 Fever, chills ,altered sensorium
 HR 108 / mt. , RR – 28 /mt. ,BP – 90/ 50
 Tc -12200 , FBS -144, Crea. – 2.2
 Na – 118 , K -2.9
Metabolic encephalopathy

Severe Sepsis:
The Final Common Pathway
Endothelial Dysfunction and
Microvascular Thrombosis
Hypoperfusion/Ischemia
Acute Organ Dysfunction
(Severe Sepsis)
Death

High Risk Patients For Sepsis
 Middle-aged, elderly
 Post op / post trauma
 Post splenectomy
 Transplant
 immune supressed
 Alcoholic / Malnourished
 Genetic predisposition
 Delayed appropriate antibiotics
 Comorbidities :
AIDS, renal or liver failure, neoplasms

SYMPTOMS
 normo- or hypothermic,Hyperventilation
 Disorientation, confusion, encephalopathy
 Hypotension and DIC predispose to acrocyanosis and ischemic
necrosis of peripheral tissues, most commonly the digits
 Cellulitis, pustules, bullae, or hemorrhagic lesions may
develop when hematogenous bacteria or fungi seed the skin
or underlying soft tissue
 vomiting, diarrhea, and ileus ,Stress ulceration , Cholestatic
jaundice, acute hepatic injury or ischemic bowel necrosis

Initial Resuscitation, Diagnosis, and
Antibiotic Therapy
Recommend early goal-directed therapy:Recommend early goal-directed therapy:
 Give early appropriate antibioticsGive early appropriate antibiotics
 Give early appropriate fluidsGive early appropriate fluids
 Give appropriate inotropic supportGive appropriate inotropic support
 Take early culturesTake early cultures
 Take early lactate levelTake early lactate level
 Take early central venous oxygen saturation(SVO2) – pending theTake early central venous oxygen saturation(SVO2) – pending the
results of numerous ongoing trials.results of numerous ongoing trials.

The Bundles
 To be completed within 3 hrs
 Measure lactate level
 Obtain blood culture samples prior to administration of antibiotics.
 Administer broad spectrum antibiotics.
 Administer 30mL/Kg crystalloids for hypotension or lactate >/= 4
mmol/L.
Thursday, September 17, 2015
v 36Dellinger R P et al. Critical Care Medicine. 2013;41(2):580-637

The Bundles
 To be completed within 6 hrs
 Apply vasopressors (for hypotension that does not respond to
initial fluid resuscitation) to maintain a mean arterial pressure
(MAP) 65 mm Hg.
 In the event of persistent arterial hypotension despite volume
resuscitation (septic shock) or initial lactate 4 mmol/L (36 mg/dL):
Measure central venous pressure (CVP)
Measure central venous oxygen saturation (ScvO2)
 Remeasure lactate if initial lactate was elevated
Targets for quantitative resuscitation included in the guidelines are CVP of
8 mm Hg, ScvO2 of 70%, and normalization of lactate

Screening for and Diagnosis of
Sepsis
• Routine screening is recommended of potentially infected seriously ill
patients for severe sepsis to increase the early identification of sepsis
and allow implementation of early sepsis therapy (grade 1C).
• Obtaining appropriate cultures before antimicrobial therapy is
initiated if such cultures do not cause significant delay (> 45
minutes) in the start of antimicrobial(s) administration (grade 1C).

Currently available Biomarkers
 WBC
 Lactate levels
 C-Reactive protein (CRP)
 Procalcitonin
 Cytokines
 New markers

LACTATE LEVELS
 0.5-1 mmol/l – normal
 > 4 mmol/l - lactic acidosis
 Useful for monitoring response of septic patients
 Higher the lactate clearance better the prognosis

PROCALCITONIN LEVELS
 Rises within 2-4 hrs. – peak - 8-24 hrs.
 Short half life of 24 hrs. independent of renal
function
 Normal - < 0.05 ng /l
 Tend to be low in viral infections
 Guidelines advocate PCT levels for
starting,continuing or stopping antibiotics

PCT LEVELS

NEWER MARKERS
 Soluble CD 14 subtype ( Presepsin )
 Heparin binding protein
 Pentraxin
 Macrophage migration inhibitory factor ( MIF )
 Cytokine / Chemokine Biomarkers

Sepsis
 No recommendation given for the use of procalcitonin
levels or other biomarkers (such as C-reactive protein) to
distinguish between severe infection and other acute inflammatory
states.
 When no infection can be found during empiric antibiotic
therapy, consider using a low procalcitonin level as a supportive
tool for the decision to stop antibiotics (Grade 2C).

Sepsis
 For patients at risk for fungal infection as a source for severe
sepsis, checking one of the newer tests for IFIs such as 1,3-
beta-D-glucan, galactomannan, or anti-mannan ELISA antibody
testing (Grade 2B/C).
 Imaging studies be performed promptly in attempts to
confirm a potential source of infection(UG).

I.V. antibiotics
 Initiated as soon as cultures are drawn
 Severe sepsis should receive
broadspectrum antibiotic.
 Empiric antifungal drug;
Neutropenic patients,
DM, chronic steroids.

Antibiotics
• Abx within 1 hr hypotension: 79.9% survival
• Survival decreased 7.6% with each hour of delay
• Mortality increased by 2nd
hour post hypotension
• Time to initiation of Antibiotics was the single strongest
predictor of outcome

Dosage for IV administration (N renal function)
 Imipenem-cilastin 0.5g q 6h
 Meropenem 1.0g q 8h
 Piperacillin-tazobactam 3.375gq 4h or 4.5 g q 6h
 Cefepime 2 gms. 12 hr
Patients allergic to B lactums
 Gatifloxacin 400mg iv q d
 Levofloxacin 500-750 mg 12 hrly.
plus clindamycin (600 mg q8h).
Vancomycin (15 mg/kg q 12 hrly ) added to each of the
above regimes

Neutropenia (<500 neut./ L)
 imipenem-cilastatin (0.5 g q6h)
 meropenem (1 g q8h)
 cefepime (2 g q8h);
 piperacillin/tazobactam (3.375 g q4h) plus
tobramycin (5–7 mg/kg q24h).
Vancomycin (15 mg/kg q 12 hrly ) added to
each of the above regimes
Empirical anti fungal therapy 51

Splenectomy
 Cefotaxime (2 g q6–8h) or ceftriaxone (2 g q12h)
 B- lactum allergy - vancomycin (15 mg/kg q12h)
plus either moxifloxacin (400 mg q24h) or
levofloxacin (750 mg q24h) or aztreonam (2 g
q8h) should be used
IV drug user
 Vancomycin (15 mg/kg q12h)
AIDS
Cefepime (2 g q8h) or piperacillin-tazobactam
(3.375 g q4h) plus tobramycin (5–7 mg/kg q24h)

 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).

Antimicrobial Therapy
 The administration of effective intravenous antimicrobials within
the first hour of recognition of septic shock and severe sepsis
without septic shock (grade 1B/ 1C) should be the goal of therapy.
 The initial empiric anti-infective therapy include one or more
drugs that have activity against all likely pathogens and that
penetrate in adequate concentrations into the tissues
presumed to be the source of sepsis (grade 1B).

Mortality associated with
Sensitive vs Resistant GNB*
11.7 10.1 18.9 8 19
0
20
63.6
20 41
18.4
14.3
0
20
40
60
80
100
K
lebsiella
(n=1
33)
E
.coli(n=
19
3)
P
seudom
onas
(n=18
2)
A
cinetob
acter
(n=
64)
E
nteroba
cter
(n=14
0)
S
ternotrophom
onas
(n=
43)
Sensitive Resistant
Bochem PY, Intensive Care Med 2001
Mortalityrates(%patients)
*GNB-gram-negative bacilli

Enterobacteriacae
Pseudomonas
Anaerobes
Renal/hepatic
function
Patient
condition
Co-existing
medical illness
So many factors to consider
?Abscess
Resistance
patterns
Community vs hospital
acquired infection
Monotherapy vs
Combination
?Candida
Solomkin JS, Mazuski JE, et al. Clinical Infectious Diseases 2003
Mazuski JE, Sawyer RG et al. Surgical Infections 2002

% patients of sepsis with renal
failure
Thursday, September 17, 2015 57Singh M et al. Pharmacologyonline . 2009;3: 597-605

Higher doses
warranted in critical
patients

Recent evidence states beta-lactam antibiotics should be
above the MIC for > 70% dosing interval in serious
infections

 The antimicrobial regimen should be reassessed daily for
potential de-escalation to prevent the development of
resistance, to reduce toxicity, and to reduce costs (grade 1B).
 Low procalcitonin levels or similar biomarkers should be used
to assist the clinician in the discontinuation of empiric
antibiotics in patients who appeared septic, but have no
subsequent evidence of infection (grade 2C).

 Combination therapy, when used empirically in patients with severe
sepsis, should not be administered for longer than 3 to 5 days.
 De-escalation to the most appropriate single-agent therapy should be
performed as soon as the susceptibility profile is known (grade 2B).
 Exceptions would include aminoglycoside monotherapy, which
should be generally avoided, particularly for P. aeruginosa sepsis,
and for selected forms of endocarditis, where prolonged courses of
combinations of antibiotics are warranted.

 the duration of therapy typically be 7 to 10 days if clinically
indicated.
 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).

Fluid Resuscitation
Recommendations
 Strong 1A recommendation for the use of crystalloids like
normal saline as the initial fluid resuscitation for people with severe
sepsis.
 The initial fluid challenge should be 1L or more of crystalloid,
and a minimum of 30 mL/kg of crystalloid (2.1 L in a 70 kg or 154-
pound person) in the first 4-6 hours.

Fluid Resuscitation Recommendations
 Incremental fluid boluses should be continued as long as
patients continue to improve hemodynamically (Grade 1C).
 Weak recommendation adding albumin to initial fluid
resuscitation with crystalloid for severe sepsis and septic shock
(Grade 2B).

Fluid Resuscitation Recommendations
 Authors strongly recommended not using hetastarches/
hydroxyethyl starches greater than 200 kDa in molecular
weight (Grade 1B).
 They did not comment on the use of lower molecular
weight hetastarches or the use of gelatins; trials are ongoing
to evaluate these resuscitative agents.

Sepsis-induced hypotension
systolic less than 90 mm Hg
or a reduction of more than 40 mm Hg from baseline in the
absence of other causes of hypotension.”
1.A loss of plasma volume into the interstitial
space,
2. Decreases in vascular tone,
3. myocardial depression.

Goals for initial resuscitation
 Central venous pressure 8 to 12 mmHg.
 Mean arterial pressure > 65 mmHg.
 Urine output 0.5 mL per kg per hr.
 Pulmonary capillary wedge
pressure exceeds 18 mmHg

Treatment of Hypotension
 Intravenous fluids : Crystalloids vs. Colloids.
 need more than ‘maintenance’ + replace losses

Fluid Therapy
 No mortality difference between;
colloid vs. crystalloid

Vasopressors and Inotrophic
Therapy
 The researchers recommend using norepinephrine as the first
choice vasopressor (Grade 1B)
 Adding or substituting epinephrine when an additional drug is needed
to maintain adequate blood pressure (Grade 2B).
 Vasopressin 0.03 units per minute may be added or
substituted for norepinephrine (Grade 2A).

Vasopressors and Inotrophic
Therapy
 Dopamine was suggested as an alternative vasopressor, but only
in highly selected patients at very low risk of arrhythmias and with a low
cardiac output and/or low heart rate (Grade 2C).
 Dobutamine infusion be started or added to a vasopressor in
myocardial dysfunction (elevated cardiac filling pressure and low cardiac
output) or ongoing signs of hypoperfusion, even after adequate
intravascular volume and mean arterial pressure are achieved (Grade 1C).
 Low dose dopamine should not be used for renal protection
(grade 1A).

Source Control
 A specific anatomical diagnosis of infection requiring
consideration for emergent source control should 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).
 In infected peripancreatic necrosis, definitive intervention is
best delayed until adequate demarcation of viable and
nonviable tissues has occurred (grade 2B).

Source Control
 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).

Infection Prevention
 Selective oral decontamination (SOD) and selective digestive
decontamination (SDD) should be introduced and investigated as a
method to reduce the incidence of ventilator-associated pneumonia
(VAP); this infection control measure can then be instituted in
healthcare settings and regions where this methodology is found to
be effective (grade 2B).
 Oral chlorhexidine gluconate (CHG) should be used as a form of
oropharyngeal decontamination to reduce the risk of VAP in ICU
patients with severe sepsis (grade 2B).

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/dL to 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).

Platelets
 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).

Supportive therapy for severe
sepsis

Sedation, Analgesia, and neuromuscular
Blockade Either continuous or intermittent sedation should be minimized
in mechanically ventilated sepsis patients, targeting specific
titration endpoints (grade 1B).
 NMBAs should 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 monitoring of the depth of
blockade should be used (grade 1C).
 A short course of an NMBA (≤ 48 hours) for patients with early,
sepsis-induced ARDS and Pao2/Fio2 < 150 mm Hg (grade 2C).Thursday, September 17, 2015 80

Steroids in Sepsis and Sepsis-
Induced ARDS
 In adult septic shock patients, it is suggested not to use IV
corticosteroids if fluid resuscitation or vasopressor therapy is able to
restore the patient to hemodynamic stability.
 When hemodynamic stability cannot be achieved, the researchers
recommend IV hydrocortisone 200 mg daily given with
continuous infusion (Grade 2C).

Steroids in Sepsis and Sepsis-
Induced ARDS ACTH stimulation test should not be used to identify adults with septic
shock who should receive hydrocortisone (grade 2B).
 In treated patients hydrocortisone should be tapered when vasopressors
are no longer required (grade 2D).
 Corticosteroids not to be administered for the treatment of sepsis in the
absence of shock (grade 1D).
 When HC is given, continuous flow should be used(grade 2D).

Mechanical Ventilation of Sepsis-
Induced ARDS
 It is Suggested that clinicians target a tidal volume of 6 mL/kg predicted
body weight in pt with sepsis induced ARDS(grade1A) vs. 12 mL/kg.
 Higher levels of PEEP in patients with severe ARDS (grade 2C).
 The researchers suggest recruitment maneuvers in patients with severe
refractory hypoxemia (Grade 2C).
 They also suggest prone positioning for patients with severe ARDS whose
PaO2 /FiO2 rates are less than 100 despite such maneuvers (Grade 2C).

Mechanical Ventilation of Sepsis-
Induced ARDS It is suggested 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.
 Against the routine use of the pulmonary artery catheter
for patients with sepsis-induced ARDS (grade 1A).

Glucose Control
 A protocolized approach when 2 consecutive blood glucose
levels are >180 mg/dL.
 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).

Tight Glycemic control
 Continuous insulin infusion
 Maintaining serum glucose levels between 120
and 180 mg/dl
 Decreased mortality development of renal
failure

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 Thrombosis
Prophylaxis 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).
 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).

Deep Vein Thrombosis
Prophylaxis
 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 not
receive pharmacoprophylaxis (grade 1B), but receive mechanical
prophylactic treatment, (grade 2C), unless contraindicated.
 When the risk decreases start pharmacoprophylaxis
(grade 2C).

Stress Ulcer 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).

Nutrition
 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 Goals of Care
 It is recommended that the goals of care and prognosis be
discussed with patients and families (grade 1B).
 The goals of care be incorporated into treatment and end-of-
life care planning, utilizing palliative care principles where
appropriate (grade 1B).
 The goals of care be addressed as early as feasible, but no
later than within 72 hrs of ICU admission (grade 2C).

Surgery
Get the pus out of
abscessesor foci of infection should be drained
Early definitive care ;
e,.g; ruptured appendix, cholecystitis

Mortality
 Sepsis:
30% - 50%
 Septic Shock:
50% - 60%

SUMMARY AND FUTURE
DIRECTIONS Though this document is static, the optimum treatment of severe
sepsis and septic shock is a dynamic and evolving process.
 Additional evidence that has appeared since the publication of the
2008 guidelines allows more certainty in making severe sepsis
recommendations; however, further programmatic clinical research
in sepsis is essential to optimize these evidence-based medicine
recommendations.
 New interventions will be proven and established interventions may
need modification.
 This publication represents an ongoing process.
 The Surviving Sepsis Campaign and the consensus committee
members are committed to updating the guidelines regularly as new
interventions are tested and results published.

Approach to sepsis- a primary physician perspective

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