6.1 Distributive & Septic Shock Pathway

Distributive Shock: Maldistribution, Not Just "Low Volume"

Distributive shock occurs when the vascular system fails to distribute blood flow appropriately to vital organs. Cardiac pump function may be normal or even high-output early on, and total circulating volume may be near normal, but vasodilation, capillary leak, or loss of vascular tone create relative hypovolemia and tissue hypoperfusion. On the PALS exam and in clinical practice, you must separate this physiology from pure hypovolemic shock (Chapter 5) and from cardiogenic or obstructive shock (later in this chapter), because fluid strategy, drug therapy, and cause-specific interventions differ.

The three distributive categories you must own for PALS:

In all three, the Pediatric Assessment Triangle may show abnormal circulation to skin (flush, mottling, or pallor) and abnormal appearance (irritability progressing to lethargy). Work of breathing may be increased from metabolic acidosis, pulmonary involvement, or anaphylactic airway edema. Primary assessment confirms tachycardia (or late bradycardia), abnormal capillary refill, altered mentation, and—when decompensated—hypotension for age.

Relative hypovolemia vs absolute hypovolemia

In distributive shock, the vascular "tank" is larger (vasodilation) and fluid may leak into tissues (capillary leak). Effective circulating volume falls even if the child has not had diarrhea or hemorrhage. That is why isotonic fluid boluses remain first-line for most septic and anaphylactic presentations—yet you still reassess after every bolus, because septic children can also develop myocardial dysfunction and fluid overload.

The Septic Shock Pathway: Timed, Sequential Care

PALS treats septic shock as a pathway, not a single drug order. Exam vignettes reward providers who start oxygen and access immediately, give fluids while obtaining cultures when possible, give early antibiotics, reassess after each intervention, and escalate to vasoactive agents when shock is fluid-refractory. Do not wait for a "perfect" diagnosis or a positive culture before acting.

Step 1 — Recognize early

Suspect septic shock in the ill-appearing child with fever or hypothermia, tachycardia, abnormal perfusion (delayed or flash capillary refill, mottling, cool or warm extremities), oliguria, and altered mental status. Compensated septic shock can look deceptively stable: blood pressure may still be normal while perfusion is already inadequate. Hypotension for age defines hypotensive (decompensated) shock and signals urgency, not a requirement to start care.

Step 2 — Oxygen and airway

Provide high-concentration oxygen appropriate to severity. Support the airway and assist ventilation if respiratory failure coexists (common with pneumonia or fatigue from metabolic acidosis). Attach monitors, pulse oximetry, and continuous heart-rate monitoring. Correct hypoxia—it worsens lactic acidosis and myocardial performance.

Step 3 — Rapid vascular access

Obtain IV access quickly. If peripheral IV attempts fail within the short window used in resuscitation (commonly taught as brief, limited attempts), place intraosseous (IO) access without prolonged delay. Do not postpone fluids or antibiotics for difficult veins.

Step 4 — Isotonic fluid boluses with reassessment

Give isotonic crystalloid (e.g., balanced crystalloid or normal saline per institutional practice) in 10–20 mL/kg boluses, then reassess perfusion, heart rate, mentation, lung sounds, liver edge, and work of breathing. Repeat boluses as long as signs of shock persist and there is no evidence of fluid overload. Many septic children need substantial total fluid in the first hour, but the exam cares that you bolus, reassess, and stop or slow fluids if rales, hepatomegaly, gallop, or worsening respiratory distress appear—those findings may indicate cardiogenic contribution or fluid overload and push you toward vasoactive support and expert help.

Step 5 — Early antibiotics and source control

Administer broad-spectrum antibiotics as early as possible once septic shock is recognized—ideally after (or concurrent with) obtaining blood cultures when that does not delay therapy. Antibiotics treat the driver of the inflammatory cascade; fluids alone do not. Source control (remove infected device, drain abscess, treat obstructed urinary tract, surgical consultation) continues after initial stabilization.

Step 6 — Vasoactive agents for fluid-refractory shock

If shock persists after adequate fluid resuscitation (fluid-refractory septic shock), start a vasoactive infusion. PALS teaching commonly emphasizes epinephrine or norepinephrine titrated to perfusion and blood-pressure goals, with choice guided by clinical phenotype, institutional protocol, and expert consultation. Epinephrine provides inotropic and vasoactive support useful when myocardial depression is suspected; norepinephrine is a potent vasopressor often used when warm, vasodilated shock with low systemic vascular resistance predominates. Exact first-line preference may vary by setting—know both agents as exam-level options for fluid-refractory pediatric septic shock and know that vasoactives require reliable IV/IO access and continuous monitoring, typically in a critical-care–capable environment.

Step 7 — Glucose and metabolic support

Check blood glucose early. Hypoglycemia is common in critically ill infants and young children and worsens neurologic injury and hemodynamics. Treat documented hypoglycemia promptly with weight-based dextrose. Correct severe metabolic derangements per protocol while the shock pathway continues; do not let laboratory work replace the fluid–antibiotic–vasoactive sequence.

Warm vs Cold Septic Shock in Children

Classic teaching contrasts two clinical phenotypes. Both are septic shock; neither is "mild."

Warm shock

• Vasodilated extremities that feel warm
• Flash (very rapid) capillary refill
• Bounding peripheral pulses
• Wide pulse pressure when measurable
• Often still tachycardic with altered appearance

Warm shock reflects low systemic vascular resistance with relatively maintained or high cardiac output early. It is common in older children with sepsis but can occur at any age.

Cold shock

• Cool, mottled extremities
• Delayed capillary refill
• Weak peripheral pulses
• Narrow pulse pressure
• Signs of low cardiac output ± high systemic vascular resistance

Cold shock is frequent in infants and young children and may reflect myocardial depression, hypovolemia from capillary leak, or both. Cold extremities alone do not prove "cardiogenic shock," but they do remind you to reassess carefully for fluid overload before giving endless boluses.

Management implications

• Both phenotypes need oxygen, access, fluids with reassessment, early antibiotics, and source control.
• Phenotype may influence vasoactive choice after fluids (vasopressor emphasis in warm vasodilated states; inotropic support when cold, low-output features dominate)—follow PALS and institutional septic-shock guidance rather than inventing a unique algorithm on the exam.
• Reassess after every intervention: a child can transition from warm to cold as myocardial function worsens.

Anaphylactic Shock: IM Epinephrine First

Anaphylaxis is a distributive emergency with airway and respiratory components. Priority order matters:

1. Remove ongoing exposure when possible (stop the infusion, remove the stinger if still present).
2. Give intramuscular epinephrine into the mid-anterolateral thigh immediately at the age/weight-appropriate dose (autoinjector or drawn dose per protocol). IM epinephrine is the definitive first drug—do not substitute antihistamines or steroids as the first intervention.
3. Position the child appropriately; support airway and give oxygen; prepare for advanced airway if upper-airway edema or severe bronchospasm threatens ventilation.
4. Establish IV/IO access; give isotonic fluid boluses for hypotension/shock with reassessment.
5. Adjuncts (antihistamines, corticosteroids, bronchodilators, epinephrine infusion for refractory anaphylaxis) follow after IM epinephrine, per protocol.

Exam trap: choosing diphenhydramine or a steroid as the initial therapy for anaphylactic shock while delaying epinephrine. That answer is wrong. Another trap: treating only wheeze with albuterol while ignoring hypotension and IM epinephrine.

Neurogenic Shock (Exam Context)

Neurogenic shock after high spinal cord injury presents with hypotension and often bradycardia (loss of sympathetic tone, unopposed parasympathetic influence), warm dry skin below the lesion, and relatively normal mentation if the brain is uninjured. Management emphasizes spinal motion restriction as indicated, oxygen, careful fluids, and vasopressors per trauma/critical-care protocols. On PALS-style items, the distinctive clue is bradycardia with hypotension after trauma, not the fever–tachycardia pattern of sepsis.

Clinical scenario (synthesis)

A 6-year-old with 2 days of fever arrives lethargic, with warm extremities, flash capillary refill, heart rate 168/min, and blood pressure near the lower limit of normal for age. You classify this as distributive/septic shock (warm phenotype), still possibly compensated. Immediate pathway: oxygen, rapid IV/IO access, 20 mL/kg isotonic fluid bolus with reassessment, early broad-spectrum antibiotics, glucose check. After two carefully reassessed boluses the child remains poorly perfused without rales or hepatomegaly—start a vasoactive infusion and arrange pediatric critical care. If the same child later develops cool mottled skin and hepatomegaly after large volumes, stop automatic large boluses, treat as fluid-refractory/myocardial involvement, and use vasoactive/inotropic support with expert care.

Master the septic pathway and IM epinephrine for anaphylaxis and you cover a large share of the Shock domain’s distributive content (~14% of PALS with Chapter 5).