Pediatric Septic Shock by J. O'Hara and K. Madden | OPENPediatrics‌

Clinical concern for sepsis arises when life-threatening organ dysfunction is suspected secondary to an infection.

Septic shock is a complex and heterogeneous dysregulation of immunologic and inflammatory pathways in the body that includes cardiovascular dysfunction leading to hypotension.

It merits careful consideration by pediatric clinicians as patients can present with simultaneous derangements across multiple organ systems, including the cardiovascular, respiratory, renal, hepatic, immune, hematologic, and vascular systems.

The specific derangements are unique to each patient due to specific host and pathogen factors.

In general, treatment is aimed at supporting oxygen delivery to the tissues and restoring normal

physiologic conditions.

Clinical signs and symptoms Despite the variable presentation of sepsis, certain clinical manifestations are typical and can be signs of early shock.

Clinical abnormalities include depressed mental status, tachycardia, decreased peripheral perfusion with capillary refill greater than two seconds, and diminished pulses or flash capillary refill time with bounding pulses and widened pulse pressure.

Additionally, hypotension is a late finding of pediatric sepsis, and therefore providers should not be reassured by a normal blood pressure.

Understanding oxygen delivery to the tissues is crucial for understanding opportunities for management in sepsis and septic shock.

Oxygen delivery is defined as cardiac output, the volume of blood pushed forward by the heart in one minute, multiplied by the arterial oxygen content of the blood.

Cardiac output is defined as a patient's heart rate multiplied by their stroke volume.

In order to augment a patient's cardiac output, inotropic agents can be used to increase their heart rate, or you can consider augmenting a patient's stroke volume with attempting to increase preload, such as giving a fluid bolus, increasing inotropy, like using vasoactive agents to increase contractility, or decreasing afterload pending the patient's hemodynamic state.

Arterial oxygen content is calculated using the equation stated here.

1.34 is a constant, showing that 1 gram of hemoglobin carries 1.34 mLs of oxygen, which is multiplied by the patient's hemoglobin level in grams per deciliter, and subsequently multiplied by the patient's percent Pulsak saturation as a decimal.

The next part of the equation accounts for the dissolved oxygen content in the blood, with 0.003 as the solubility coefficient of oxygen in the plasma, which is multiplied by the patient's partial pressure of oxygen.

In sepsis, the pathophysiology is primarily at the level of the small blood vessels.

The direct action of microbes, or the host response to those microbes, leads to destruction of the endothelium, causing capillary leak, intravascular hypovolemia, as well as inappropriate dilation of the vasculature and relative hypovolemia.

These processes effectively decrease preload to the heart which has to increase stroke volume and heart rate to maintain cardiac output.

However, the ability of the heart to increase stroke volume and heart rate is limited, and the mediators of the host response to sepsis often also impact contractility as well.

The destruction to the microvasculature also impacts perfusion to the vital organs so that organ failure can be due to inadequate oxygen delivery from decreased cardiac output as well as other local microthrombi and other occlusion of blood flow.

Clinicians can optimize oxygen delivery to the tissues and combat the action of the microbes by targeting the components of the CaO2 equation, increasing hemoglobin by way of a packed red blood cell transfusion, ensuring an acceptable saturation by providing supplemental oxygen, or providing advanced respiratory support as indicated, aimed at increasing the partial pressure of oxygen in the blood.

All are interventions to consider to increase a patient's CaO2.

Of note, increasing the partial pressure of oxygen will not amount to significant increase in the arterial oxygen content given the constant 0.003 is quite small.

However, this part of the equation becomes more significant as

Clinical concern for sepsis arises when life-threatening organ dysfunction is suspected secondary to an infection.

Septic shock is a complex and heterogeneous dysregulation of immunologic and inflammatory pathways in the body that includes cardiovascular dysfunction leading to hypotension.

It merits careful consideration by pediatric clinicians as patients can present with simultaneous derangements across multiple organ systems, including the cardiovascular, respiratory, renal, hepatic, immune, hematologic, and vascular systems.

The specific derangements are unique to each patient due to specific host and pathogen factors.

In general, treatment is aimed at supporting oxygen delivery to the tissues and restoring normal

physiologic conditions.

Clinical signs and symptoms Despite the variable presentation of sepsis, certain clinical manifestations are typical and can be signs of early shock.

Clinical abnormalities include depressed mental status, tachycardia, decreased peripheral perfusion with capillary refill greater than two seconds, and diminished pulses or flash capillary refill time with bounding pulses and widened pulse pressure.

Additionally, hypotension is a late finding of pediatric sepsis, and therefore providers should not be reassured by a normal blood pressure.

Understanding oxygen delivery to the tissues is crucial for understanding opportunities for management in sepsis and septic shock.

Oxygen delivery is defined as cardiac output, the volume of blood pushed forward by the heart in one minute, multiplied by the arterial oxygen content of the blood.

Cardiac output is defined as a patient's heart rate multiplied by their stroke volume.

In order to augment a patient's cardiac output, inotropic agents can be used to increase their heart rate, or you can consider augmenting a patient's stroke volume with attempting to increase preload, such as giving a fluid bolus, increasing inotropy, like using vasoactive agents to increase contractility, or decreasing afterload pending the patient's hemodynamic state.

Arterial oxygen content is calculated using the equation stated here.

1.34 is a constant, showing that 1 gram of hemoglobin carries 1.34 mLs of oxygen, which is multiplied by the patient's hemoglobin level in grams per deciliter, and subsequently multiplied by the patient's percent Pulsak saturation as a decimal.

The next part of the equation accounts for the dissolved oxygen content in the blood, with 0.003 as the solubility coefficient of oxygen in the plasma, which is multiplied by the patient's partial pressure of oxygen.

In sepsis, the pathophysiology is primarily at the level of the small blood vessels.

The direct action of microbes, or the host response to those microbes, leads to destruction of the endothelium, causing capillary leak, intravascular hypovolemia, as well as inappropriate dilation of the vasculature and relative hypovolemia.

These processes effectively decrease preload to the heart which has to increase stroke volume and heart rate to maintain cardiac output.

However, the ability of the heart to increase stroke volume and heart rate is limited, and the mediators of the host response to sepsis often also impact contractility as well.

The destruction to the microvasculature also impacts perfusion to the vital organs so that organ failure can be due to inadequate oxygen delivery from decreased cardiac output as well as other local microthrombi and other occlusion of blood flow.

Clinicians can optimize oxygen delivery to the tissues and combat the action of the microbes by targeting the components of the CaO2 equation, increasing hemoglobin by way of a packed red blood cell transfusion, ensuring an acceptable saturation by providing supplemental oxygen, or providing advanced respiratory support as indicated, aimed at increasing the partial pressure of oxygen in the blood.

All are interventions to consider to increase a patient's CaO2.

Of note, increasing the partial pressure of oxygen will not amount to significant increase in the arterial oxygen content given the constant 0.003 is quite small.

However, this part of the equation becomes more significant as