Undifferentiated shock (peds)

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This page is for pediatric patients. For adult patients, see: undifferentiated shock

Background

Important physiologic differences between pediatric and adult patients

Intravascular volume

  • Newborns: larger total body water compared to adults (75% vs. 60%) with the majority of it being in the extracellular fluid (ECF) (~40% vs. 25%) 
    • Percentage of ECF decreases throughout childhood
  • Large surface area to weight ratio --> younger kids may have more fluid losses from ECF and intravascular space with short illness/environmental exposure decreased preload
    • May present profoundly volume depleted and need more aggressive volume repletion

Cardiovascular

  • Infants have immature myocardial calcium regulation system, difficulty storing/releasing calcium highly dependent on extracellular calcium for contractility
    • Check iCal, replete calcium earlier, do NOT give CCBs to infants with tachydysrhythmias
  • Stiffer, less compliant myocardium in infants-->increasing heart rate is main compensatory means for increasing BP
    • BUT higher resting heart rate--> less room to go up (e.g. adult with resting heart rate of 60 can double to 120 but a neonate doubling resting heart rate of 120 to 240 is not sustainable)
    • Heavily rely on vasoconstriction, which can further decrease cardiac output
  • Less beta-adrenergic receptors/sympathetic innervations + more dominant parasympathetics --> exaggerated vagal response
  • Hypotension is a ‘’’late’’’ finding in shock!

Clinical Features

  • Signs/symptoms of underlying pathology

Cold shock

  • More common in children than in adults
  • Poor cardiac output due to decreased stroke volume--> tachycardia to compensate
  • Poor peripheral perfusion, increased SVR (vasoconstriction) to compensate-->
    • Skin cold to touch
    • Diminished pulses
    • Mottled skin
    • Cap refill >2s
    • Narrow pulse pressure, eventually hypotension
    • Signs and symptoms of end organ damage as blood shunted to vital organs

Warm shock

  • Hyperdynamic state, with vasodilation and low SVR
  • Results in end organ damage due to shunting of blood away from vital organs to periphery
  • Findings thus include:
    • Tachycardia
    • Wide pulse pressure
    • Bounding peripheral pulses
    • Brisk cap refill

Shock index

Differential Diagnosis

dehydration (from nausea/vomiting, insensible losses due to heat illness_)

Sick Neonate

THE MISFITS [1]

Evaluation

Management

Vasopressors

Vasopressors may be initiated peripherally while central access is being obtained — do not delay for central line placement (SSC 2021).[3]

Pressor Initial Dose Max Dose Cardiac Effect BP Effect Arrhythmias Special Notes
Dobutamine 2-5 mcg/kg/min 20 mcg/kg/min (up to 40 in refractory cases)[4] Strong β₁ agonist (+inotrope, +chronotrope); weak β₂ agonist (+vasodilation) Minimal α effect; may decrease BP due to β₂ vasodilation Variable HR effects; can cause tachycardia Indicated in decompensated systolic CHF and cardiogenic shock with adequate BP. Not a vasopressor — it is an inotrope. Must be used with a vasopressor if hypotensive.
Dopamine 2-5 mcg/kg/min 20 mcg/kg/min β₁ and endogenous norepinephrine release Mixed α and β effects at all doses; α effects predominate at higher doses Arrhythmogenic from β₁ effects More adverse events (especially arrhythmia) when used in shock compared to norepinephrine[5]. SSC 2021 suggests against dopamine as first-line except in select patients with bradycardia and low risk of tachyarrhythmia.
Epinephrine 1-10 mcg/min (0.01-0.1 mcg/kg/min) 0.5 mcg/kg/min +Inotropy, +chronotropy (β₁) Low dose: β₂ vasodilation may predominate; high dose: α₁ vasoconstriction predominates Significant — tachycardia, SVT, VT. Increases myocardial O₂ demand. 2nd or 3rd line for septic shock (SSC 2021: add after norepinephrine ± vasopressin). 1st line for anaphylaxis (0.3-0.5 mg IM) and cardiac arrest. May cause splanchnic vasoconstriction, lactic acidosis, and hyperglycemia.
Norepinephrine 2-5 mcg/min (0.01-0.03 mcg/kg/min) 0.5-1 mcg/kg/min (some sources up to 3.3 mcg/kg/min)[6] Mild β₁ direct effect (+inotropy) Strong α₁ and α₂ vasoconstriction; β₁ effect Less arrhythmogenic than dopamine[5] 1st line for septic shock (SSC 2021)[3]. Increases MAP primarily via vasoconstriction. Increases coronary perfusion pressure. Minimal β₂ effect.
Milrinone 50 mcg/kg IV over 10 min (loading dose often omitted in acute illness due to hypotension risk) 0.375-0.75 mcg/kg/min PDE-3 inhibitor → ↑intracellular cAMP → ↑Ca²⁺ influx → +inotropy Arteriolar and venous vasodilator (reduces preload AND afterload) Less arrhythmogenic than dobutamine Inodilator — useful in decompensated HF with elevated afterload, RV failure, or pulmonary hypertension. Causes hypotension — not a vasopressor; use with a vasopressor if MAP is low. Renally cleared — dose-reduce in CKD.
Phenylephrine 100-180 mcg/min, then 40-60 mcg/min 0.4-9.1 mcg/kg/min No direct cardiac effect Pure α₁ agonist → vasoconstriction May cause reflex bradycardia Short duration of action (5-20 min IV). Use in septic shock only if: NE causes arrhythmias, cardiac output is high with persistent hypotension, or as salvage when NE + vasopressin have failed.[3]
Vasopressin 0.03 U/min (fixed dose) 0.04 U/min No direct inotropic or chronotropic effect; possible reflex bradycardia V₁ receptor agonist → vascular smooth muscle constriction Minimal 2nd line in septic shock — add to NE rather than escalating NE (SSC 2021 suggests adding before epinephrine)[3]. Fixed dose — generally not titrated. May reduce the risk of atrial fibrillation vs. catecholamine-only regimens.[7] Avoid dose >0.04 U/min → risk of cardiac and mesenteric ischemia.
Methylene blue[8] IV bolus 1-2 mg/kg over 15 min 1-2 mg/kg/hour (limited data on max duration) Possible increased inotropy; improves cardiac ATP utilization Inhibits NO-mediated peripheral vasodilation → increases SVR Minimal reported Salvage therapy for refractory vasodilatory shock unresponsive to catecholamines. Contraindicated in G6PD deficiency (hemolytic anemia), ARDS, severe pulmonary hypertension. Interferes with pulse oximetry readings (falsely low SpO₂). Avoid with serotonergic drugs (risk of serotonin syndrome).
Angiotensin II (Giapreza) 20 ng/kg/min 40-80 ng/kg/min (max 200 ng/kg/min per label) No direct cardiac effect AT₁ receptor agonist → potent arteriolar vasoconstriction; also stimulates aldosterone secretion Minimal Salvage therapy for refractory vasodilatory shock (ATHOS-3 trial)[9]. May be particularly useful in patients on ACEi/ARB or with high renin states. Monitor for thrombosis (increased risk reported).
Medication IV Dose (mcg/kg/min) Standard Concentration Final Concentration
Norepinephrine (Levophed) 0.01-2 mcg/kg/min 8 mg in 500 mL D5W 16 mcg/mL
Dopamine 2-20 mcg/kg/min 400 mg in 250 mL D5W 1,600 mcg/mL
Dobutamine 2-20 mcg/kg/min 250 mg in 250 mL D5W 1,000 mcg/mL
Epinephrine 0.01-1 mcg/kg/min 1 mg in 250 mL D5W 4 mcg/mL

Norepinephrine 2-5 mcg/min (0.01-0.03 mcg/kg/min), max 0.5-1 mcg/kg/min IV drip — 1st line for septic shock (SSC 2021) Epinephrine 1-10 mcg/min (0.01-0.1 mcg/kg/min), max 0.5 mcg/kg/min IV drip — 1st line for anaphylaxis and cardiac arrest Vasopressin 0.03 U/min (fixed dose), max 0.04 U/min IV drip — Add to NE rather than escalating NE (SSC 2021) Dopamine 2-5 mcg/kg/min, max 20 mcg/kg/min IV drip — SSC 2021 suggests against as 1st line; more arrhythmogenic than NE Dobutamine 2-5 mcg/kg/min, max 20 mcg/kg/min IV drip — Inotrope, not a vasopressor; use with vasopressor if hypotensive Phenylephrine 100-180 mcg/min, then 40-60 mcg/min IV drip — Pure alpha-1 agonist; short duration 5-20 min Milrinone 0.375-0.75 mcg/kg/min (loading often omitted) IV drip — Inodilator; causes hypotension; useful in RV failure/pulmonary HTN Methylene blue 1-2 mg/kg IV bolus over 15 min IV — Salvage for refractory vasodilatory shock; contraindicated in G6PD deficiency Angiotensin II (Giapreza) 20 ng/kg/min, max 40-80 ng/kg/min IV drip — Salvage for refractory vasodilatory shock (ATHOS-3 trial)

Causes of non-response to vasopressors[10]

Disposition

  • NICU/PICU

See Also

External Links


References

https://rebelem.com/approach-to-the-critically-ill-child-shock/ https://pedemmorsels.com/epinephrine-for-shock/ https://www.chop.edu/clinical-pathway/sepsis-emergent-care-clinical-pathway

  1. ↑ Brousseau T, Sharieff GQ. Newborn emergencies: the first 30 days of life. Pediatr Clin North Am. 2006 Feb;53(1):69-84, vi.
  2. ↑ Ramaswamy KN1, Singhi S, Jayashree M, Bansal A, Nallasamy K. Double-Blind Randomized Clinical Trial Comparing Dopamine and Epinephrine in Pediatric Fluid-Refractory Hypotensive Septic Shock. Pediatr Crit Care Med. 2016 Sep 23.
  3. ↑ 3.0 3.1 3.2 3.3 Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021;49(11):e1063-e1143.
  4. ↑ Unverferth DV, Blanford M, Kates RE, Leier CV. Tolerance to dobutamine after a 72 hour continuous infusion. Am J Med. 1980;69(2):262-6.
  5. ↑ 5.0 5.1 De Backer D, et al. Comparison of Dopamine and Norepinephrine in the Treatment of Shock. NEJM. 2010;363(9):779-789.
  6. ↑ Martin C, Papazian L, Perrin G, et al. Norepinephrine or dopamine for the treatment of hyperdynamic septic shock? Chest. 1993;103(6):1826-31.
  7. ↑ McIntyre WF, et al. Association of Vasopressin Plus Catecholamine Vasopressors vs Catecholamines Alone With Atrial Fibrillation in Patients With Distributive Shock. JAMA. 2018;319(18):1889.
  8. ↑ Pasin L, et al. Methylene blue as a vasopressor: a meta-analysis of randomised trials. Crit Care Resusc. 2013;15(1):42-8.
  9. ↑ Khanna A, et al. Angiotensin II for the Treatment of Vasodilatory Shock. N Engl J Med. 2017;377(5):419-430.
  10. ↑ Anand Swaminathan, "Occult Causes of Non-Response to Vasopressors", REBEL EM blog, July 13, 2017. Available at: https://rebelem.com/occult-causes-of-non-response-to-vasopressors/.
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