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

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

.

. .

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

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.

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

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.

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

. .

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

Therapeutic Endpoints

Capillary refill < 2 sec Warm extremities Urine output > 1 ml/kg/hr Normal mental status Decreased lactate Central venous O2 saturation > 70%

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

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.

2005 Shock ABC

FLUID BOLUS-20-60cc/kg

Dopamine/ dobutamine

Cold shock Warm shock

steroids

EPI NENE

Milrinone

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

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

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

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

Neuromuscular Blockers

Avoid if possible Used longer than 2-3 hrs

PRN bolus Continuous infusion with twitch monitor

Grade E

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

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

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

Primary Stress Ulcer Risk Factors Frequently Present in Severe Sepsis

Mechanical ventilation Coagulopathy Hypotension

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

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

Blood Product Administration

Do not use erythropoietin to treat sepsis-related anemia. Erythropoietin may be used for other accepted reasons.

Grade B

Blood Product Administration

Fresh frozen plasma

• Bleeding

• Planned invasive procedures.

Grade E

Blood Product Administration

• Do not use antithrombin therapy.

Grade B

Warren et al. JAMA 2001; 1869-1878

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