Shock and Sepsis

Shock
 Acute, complex state of circulatory dysfunction
 Failure to deliver sufficient oxygen (and/or other nutrients) to tissues
 Unable to meet metabolic demands
 If prolonged, -> MODS and death

DO2 = CO x CaO2
CO = HR x SV
CaO2 = (Hgb x SaO2 x 1.34) + (PaO2 x 0.003)

Shock States
 Distributive (septic = most common; also, anaphylactic, neurogenic)
 Hypovolemic
 Cardiogenic
 Obstructive

Sepsis: Life-threatening organ dysfunction caused by a dysregulated host response to infection

Old, soon to be outdated criteria:
 SIRS: fever, tachycardia (or bradycardia in neonates or severe infection), tachypnea,
abnormal peripheral WBC count
 Severe sepsis: Sepsis + CV dysfunction or ARDS or 2 or more other organ dysfunctions
 Septic shock: Sepsis and CV dysfunction (hypotension NOT required)
o Typically a combination of distributive, hypovolemic, and cardiogenic shock
o Warm (incr cardiac output, decr SVR) vs cold shock (decr cardiac output, incr
SVR)
New criteria: ????

Sepsis Risk Factors

 Central venous catheters (increased with longer duration of line, those receiving TPN,
use to TPA and repair of broken catheters; decreased with use of bundles or guidelines
for insertion or maintenance)
 Urinary catheters (virtually all closed-system urinary catheters are colonized within 30
days of placement)
 Hemodialysis (most common = S. aureus)
 Other infections: surgical site infections, osteomyelitis, endocarditis

Sepsis Management
 ABCs
 Supplemental oxygen, Access
 60 ml/kg fluid in 60 minutes
 Antibiotics in 60 minutes
 Early, goal-directed therapy
 Sedation, Paralysis, Control fevers (decrease metabolic demand)
 Fluid-Refractory Shock: Initiate Vasopressors (while continuing fluid resuscitation;
measure CVP, ultrasound IVC)

Rogers’ Textbook of Pediatric Intensive Care, 5th Ed (2016).

Fuhrman and Zimmerman’s Pediatric Critical Care, 5th Ed (2017).
 α1 β1 β2 D1 V1
Dopamine* Vasoconstriction Inotropy, Vasodilation Renal
chronotrophy vasodilation
Norepinephrine Vasoconstriction Inotropy
Epinephrine** Vasoconstriction Inotropy, Vasodilation
chronotropy
Dobutamine Inotropy Vasodilation
Milrinone Non-receptor mediated inotropy, lusitropy,
and vasodilation (PDE3-inhib)
Vasopressin Potentiates Potentiates Vasoconstriction
Phenylephrine Vasoconstriction
*Dopamine: at low doses, D1 predominates; at medium doses, β1 and β2 predominate; at high
doses, α predominates
**Epinephrine: at low doses, β1 and β2 predominate; at high doses, α predominates

Additional Management Considerations

 Sepsis puts metabolic stress on the host: consider taking away some of the demand with
noninvasive or mechanical ventilation
 Increased free fatty acids, hyperglycemia, protein catabolism: malnutrition is common;
promote enteral feeding; cautious glycemic control
 Elevated lactate = cellular injury and/or transition to anaerobic metabolism
 Central venous oxyhemoglobin saturation (SCVO2): may be low (decr cardiac output
and incr metabolic demand = incr O2 extraction), or may be high (mitochondrial
dysfunction leading to decr O2 consumption). Goal is 70%
 Coagulation abnormalities
 Vasoactive-resistant shock: Consider hydrocortisone empirically
 Cardiac output monitoring to maintain cardiac index between 3.3 and 6 L/min/m2
 Plasma exchange (especially in TAMOF)
 ECMO

Sequelae (MODS)
 Approximately ½ of children with severe sepsis develop ARDS
 Acute kidney injury is common, many require CRRT
 Higher mortality seen in patients with sepsis, MODS and fluid overload > 20% at the
time of CRRT initiation

Random Facts
 A microbial pathogen may not be isolated in up to 75% of children with sepsis (e.g. host
response to endotoxin, insufficient sensitivity of current diagnostic testing, or pre-
treated blood cultures)
 There are genetic susceptibilities to sepsis (e.g. polymorphisms in TNF-a promoter
region, platelet activator inhibitor-1, toll-like receptors, and many components of
inflammatory response [interleukins, protein C, heat shock proteins])
 Sepsis can induce innate and adaptive immune suppression -> incr risk for new
infections and late death (new or progressive MODS)

Rogers’ Textbook of Pediatric Intensive Care, 5th Ed (2016).

Fuhrman and Zimmerman’s Pediatric Critical Care, 5th Ed (2017).