severe sepsis&septic shock in pediatrics
DESCRIPTION
Abdel Razzaq Abu Mayaleh, MD PRCS _ New Hospital - Hebron Based partially on www.picucourse.org. SEVERE SEPSIS&SEPTIC SHOCK IN PEDIATRICS. INTRODUCTION. SEPSIS :- it’s an infection plus systemic manifestation of infection. - PowerPoint PPT PresentationTRANSCRIPT
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SEVERE SEPSIS&SEPTIC SHOCK SEVERE SEPSIS&SEPTIC SHOCK IN PEDIATRICSIN PEDIATRICS..
Abdel Razzaq Abu Mayaleh, MDAbdel Razzaq Abu Mayaleh, MD PRCS _ New Hospital - HebronPRCS _ New Hospital - Hebron
Based partially onBased partially on
www.picucourse.org
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INTRODUCTIONINTRODUCTION
SEPSIS:- it’s an infection plus systemic manifestation of infection.
SEVERE SEPSIS :- Sepsis plus sepsis-induced organ dysfunction or tissue hypo perfusion.
SEPTIC SHOCK:- sepsis-induced hypotension persisting despite adequate fluid resuscitation and elevated lactate.
HYPOTENTION:- S.BP < 70 + 2 ×wt. (80 + 2 × wt)
SHOCK:- DO2 < VO2
.
. .
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A clinician, armed with the sepsis bundles, attacks the three heads of severe sepsis: hypotension, hypoperfusion and organ dysfunction. Crit Care Med 2004; 320(Suppl):S595-S597
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Septic Shock Epidemiology
During the last 2 decades the incidence of sepsis & septic shock has increased across all age groups. This is thought to be due to:
- ↑ use of invasive procedures
- ↑ use of immunosuppressive drugs
- ↑ microbacterial ressistance
Child mortality improved dramatically from 97% → 9% due to
the advance in critical care technology.
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Septic Shock: “Warm Shock”
Early, compensated, hyperdynamic state Clinical signs
Warm extremities with bounding pulses, tachycardia, tachypnea, confusion.
Physiologic parameters widened pulse pressure, increased cardiac ouptut
and mixed venous saturation, decreased systemic vascular resistance.
Biochemical evidence: Hypocarbia, elevated lactate, hyperglycemia
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Septic Shock: “Cold Septic Shock: “Cold Shock”Shock”
Late, uncompensated stage with drop in cardiac output.
Clinical signs Cyanosis, cold and clammy skin, rapid, thready pulses,
shallow respirations. Physiologic parameters
Decreased mixed venous sats, cardiac output and CVP, increased SVR, thrombocytopenia, oliguria, myocardial dysfunction, capillary leak
Biochemical abnormalities Metabolic acidosis, hypoxia, coagulopathy, hypoglycemia.
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MANAGEMENT-GENERALMANAGEMENT-GENERAL
Goal: increase oxygen delivery and decrease oxygen demand: Oxygen Fluid Temperature control Antibiotics Correct metabolic abnormalities Spare WOB ? Inotropes
DO2 = C.O. x CaO2
Hg X SatO2 X 1.34
VO2 (O2 Extraction)
DO2
.
.normal
septic
. .
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Fluid Resuscitation
Aggressive fluid resuscitation with boluses of 20 ml/kg over 5-10 min
Blood pressure by itself is not a reliable endpoint for resuscitation
Initial resuscitation usually requires 40-60 ml/kg, but more may be required
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Therapeutic Endpoints
Capillary refill < 2 sec Warm extremities Urine output > 1 ml/kg/hr Normal mental status Decreased lactate Central venous O2 saturation > 70%
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Hemodynamic Support
Hemodynamic profile may be variable Dopamine for hypotension Epinephrine or norepinephrine for dopamine-
refractory shock Dobutamine for low cardiac output state Inhaled NO useful in neonates with post-partum
pulmonary hypertension and sepsis
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Other Therapies
Steroids: recommended for children with catecholamine resistance and suspected or proven adrenal insufficiency.
Activated protein C not studied adequately in children yet.
GM-CSF shown to be of benefit in neonates with sepsis and neutropenia.
Extracorporeal membrane oxygenation (ECMO) may be considered in children with refractory shock or respiratory failure.
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2005 Shock ABC
FLUID BOLUS-20-60cc/kg
Dopamine/ dobutamine
Cold shock Warm shock
steroids
EPI NENE
Milrinone
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Recognize decreased mental status and perfusion.Maintain airway and establish access according to PALS guidelines.
Push 20 cc/kg isotonic saline or colloid boluses up and over 60 cc/kg. Correct hypoglycemia and hypocalcaemia. Administer antibiotics.
Fluid refractory shock * *
Establish central Venous access, begin dopamine or dobutamine therapy and establish arterial monitoring .
Fluid refractory – dopamine/ dobutamine resistant shock
Titrate epinephrine for cold shock, norepinephrine for warm shock to normal clinical endpoints and ScvO2 saturation ≥70% .
15 min
Fluid responsive *
Observe in PICU
0 min
5 min
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Catecholamine-resistant shock
Begin hydrocortisone if at risk for absolute adrenal insufficiency
Normal Blood Pressure
Cold Shock
ScvO2 Sat <70%
Low Blood Pressure
Cold Shock
ScvO2 Sat < 70%
Low Blood pressure
Warm Shock
ScvO2 Sat ≥ 70%
Add Vasodilator or type III phosphodiesgerase inhibitor with volume
loading
Titrate volume and epinephrine
Titrate volume and norepinephrine
Persistent Catecholamine- resistant shock
Start Cardiac output measurement and direct fluid, inotrope, vasopressor, vasodilator, and hormonal therapies to attain CL>3.3 and <6.0 L/min/m²
60 min
Refractory shock
Consider ECMO
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VENTILATOR MANAGEMENT
Assist control mode-volume ventilation Reduce tidal volume to 6ml/kg predicted body wt. Keep Pplat <30cm H2O Maintain SaO2 / pO2 88-95%
Anticipated PEEP setting at various FiO2 requirements
FiO2 0.3 0.4 0.5 0.5 0.6 0.7 0.8 0.9 1.0
PEEP 5 5 8 10 12 14 16 18 20
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Sedation and Analgesia in Sepsis
Sedation protocol for mechanically ventilated patients with standardized subjective sedation scale target.• Intermittent bolus• Continuous infusion with daily
awakening/retitrationGrade B
Kollef, et al. Chest 1998; 114:541-548Brook, et al. CCM 1999; 27:2609-2615Kress, et al. NEJM 2000; 342:1471-1477
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Neuromuscular Blockers
Avoid if possible Used longer than 2-3 hrs
PRN bolus Continuous infusion with twitch monitor
Grade E
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The Role of IntensiveInsulin Therapy in the Critically Ill
At 12 months, intensive insulin therapy reduced mortality by 3.4% (P<0.04)
Adapted from Figure 1B, page 1363, with permission from van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. N Engl J Med 2001;345:1359-67
In-h
osp
ital
su
rviv
al (
%)
100
00
Intensive treatment
Conventional treatment
Days after admission
80
84
88
92
96
50 100 150 200 250
P=0.01
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Glucose Control
After initial stabilization Glucose < 150 mg/dL Continuous infusion insulin and glucose
or feeding (enteral preferred) Monitoring
Initially q30–60 mins After stabilization q4hGrade D
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Bicarbonate therapy not recommended to improve hemodynamics in patients with lactate induced pH >7.15
Grade C
Cooper, et al. Ann Intern Med 1990; 112:492-498Mathieu, et al. CCM 1991; 19:1352-1356
Bicarbonate Therapy
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Primary Stress Ulcer Risk Factors Frequently Present in Severe Sepsis
Mechanical ventilation Coagulopathy Hypotension
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Choice of Agents forStress Ulcer Prophylaxis
H2 receptor blockers
Role of proton pump inhibitors
Grade C
Cook DJ, et al. Am J Med 1991; 91:519-527
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Blood Product AdministrationRed Blood Cells
Tissue hypoperfusion resolved
No extenuating circumstances Coronary artery disease Acute hemorrhage Lactic acidosis
Transfuse < 7.0 g/dl to maintain 7.0-9.0 g/dL
Grade B
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Blood Product Administration
Do not use erythropoietin to treat sepsis-related anemia. Erythropoietin may be used for other accepted reasons.
Grade B
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Blood Product Administration
Fresh frozen plasma
• Bleeding
• Planned invasive procedures.
Grade E
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Blood Product Administration
• Do not use antithrombin therapy.
Grade B
Warren et al. JAMA 2001; 1869-1878
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Blood Product Administration
Platelet administration Transfuse for < 5000/mm3 -
Transfuse for 5000/mm3 – 30,000/mm3 with significant bleeding risk
Transfuse < 50,000/mm3 for invasive procedures or bleeding
Grade E