Shock in Pediatrics Treatment & Management

Regardless of the cause of shock, the ABCs (airway, breathing, circulation) must be immediately evaluated and stabilized. Do not delay this initial stabilization for further workup and imaging studies. The patient's airway must be patent, and the patient must be adequately oxygenated and ventilated. Initially, administer 100% supplemental oxygen at a high flow rate. If the patient is in respiratory distress, consider intubating and providing mechanical ventilation.

Stabilizing the airway and providing mechanical ventilation may relieve the patient's metabolic work of breathing and may facilitate elimination of carbon dioxide, helping to compensate the coexistent metabolic acidosis. Place the patient on appropriate noninvasive monitors, such as a pulse oximeter and cardiorespiratory monitor, and obtain a simple bedside glucose measurement.

Once the airway has been stabilized, if necessary, and adequate ventilation and administration of oxygen have been ensured, immediately place attention on improving circulation and systemic oxygen delivery (DO₂). Circulatory improvement is achieved via volume expansion and, if necessary, pharmacologic therapy with vasopressors and cardiac inotropic agents.

If sepsis is a concern, initial coverage with empiric antibiotics is essential to eliminating the precipitating cause of shock. The choice of agents may vary, depending on the patient’s age and previous antibiotic exposure.

Neonates are often started on a combination of ampicillin and gentamicin. Older infants and children may be covered with a third-generation cephalosporin, possibly along with expanded gram-positive organism coverage with vancomycin initially. Management of significant septic shock should be multidisciplinary and should involve the resources of infectious disease specialists when available.^[17]

The major physiologic abnormality in most forms of pediatric shock is either an absolute or a relative intravascular hypovolemia. Dehydration, hemorrhage, sepsis, and other distributive etiologies all cause intravascular hypovolemia with a reduction in cardiac ventricular filling volume (preload).

Children with hypovolemic shock who receive appropriate aggressive fluid resuscitation within the first hour of resuscitation have the most optimal chance of survival and recovery. Unlike adults, children do not have as pronounced a susceptibility to fluid-related complications, such as pulmonary edema. Therefore, the therapy of choice is rapid and aggressive fluid resuscitation.

Procedure

If possible, place a minimum of 2 large-bore, free-flowing intravenous (IV) catheters. If vascular access is not easily and readily achieved, then an intraosseous (IO) needle may be placed into the bone marrow for rapid fluid administration. Such an IO line can be considered as good as an IV line for the purpose of any fluid or medication administration necessary for the acute resuscitation of a compromised infant or child in shock.^[18]

Administer 20mL/kg of an isotonic crystalloid infusion, such as 0.9% isotonic sodium chloride or lactated Ringer solution, over 5 minutes or less. If the volume infusion is administered through an IO line, the resistance may be higher than in an IV line, and the volume may need to be pushed manually with a syringe. So long as the volume is infusing without evidence of local swelling at the IO insertion site or in the tissue posterior to the IO, the fluid is passing into the marrow cavity and hence into the intravascular space.

As soon as the initial volume of fluid (20mL/kg) has been infused, reevaluate the patient. If the patient retains the clinical appearance of shock, immediately infuse another 20mL/kg and repeat the cycle. If more than 2-3 volumes of crystalloid have been infused into a patient at risk for hemorrhage (eg, from trauma), administer blood or packed RBCs (PRBCs). A child with severe hypovolemia or sepsis may require more than 60mL/kg of volume in the first hour of resuscitation, often within the first 15 minutes.

In one study of survival in children with septic shock, children who received on average of 65mL/kg of volume in the first hour had a statistically increased chance of survival compared with those who received less than 40mL/kg in the first hour.^[19] Simply put, children who receive appropriate, yet aggressive, fluid resuscitation early have the best chance of surviving severe septic shock or shock and dehydration.

Of note, a large study in African children presenting with apparent sepsis to resource-limited facilities demonstrated a worse outcome for children treated with what would be considered standard fluid resuscitation by Western practice. These results should be considered when treating children in the region of the world studied. The authors suggest that further study is warranted regarding volume expansion and fluid effects on septic children in different settings and with various etiologies.^[20]

An exception to repetitive volume resuscitation in a child with shock is the child who presents with cardiogenic shock. Even so, such a child may still be mildly to moderately dehydrated and could benefit from an initial 20mL/kg of isotonic crystalloid volume expansion. During the initial infusion of fluid for volume expansion, the child can be evaluated for the possibility of cardiogenic shock. If myocardial failure is the root cause of such a patient's poor cardiac output, cardiotropic medications are indicated.

Dextrose administration is often necessary. Neonates and infants have limited glycogen stores, which may become rapidly depleted during shock, resulting in hypoglycemia. Alternatively, high levels of endogenous and exogenous catecholamines may result in a relative insulin-resistant state that can cause serum hyperglycemia.

Because glucose is the major metabolic substrate, perform a rapid bedside glucose test on all patients who present in shock. If the glucose level is low, provide replacement therapy with IV dextrose. The dose of dextrose is 0.5-1g/kg IV. Dextrose is best provided as a continuous IV infusion.

Calcium mediates excitation-contraction coupling in muscle cells, including cardiac muscle. Shock may cause alterations in available serum ionized calcium levels, despite normal total serum calcium. Furthermore, administered blood products (which contain citrate) may bind free available calcium, additionally decreasing available ionized calcium levels.

The availability of functioning ionized calcium also depends on serum acid-base status; an acid environment favors the dissociation of calcium from proteins, making it available as a cofactor in cell function. Care must be taken not to cause a drop in ionized calcium when treating acidosis.

Therefore, calcium therapy can be useful when treating shock in a patient with documented hypocalcemia. It is also indicated for treating shock caused by arrhythmias precipitated by hyperkalemia, hypermagnesemia, or calcium channel blocker toxicity.

Calcium may be provided either as calcium gluconate or calcium chloride. Calcium chloride has been shown to produce higher and more consistent levels of available calcium and, therefore, is recommended in the acute resuscitation of a child in shock.^[21] The recommended dose is 10-20mg/kg (0.1-0.2mL/kg of calcium chloride 10%) IV administered at an infusion rate that does not exceed 100mg/min IV. Further therapy may be guided by repeat plasma ionized calcium measurements.

Sodium bicarbonate use in the treatment of shock is controversial. During shock, acidosis develops, which impairs myocardial contractility and optimal function of catecholamines. However, treatment with bicarbonate may worsen intracellular acidosis while it corrects serum acidosis.

This occurs because bicarbonate is an ion that does not readily traverse semipermeable cell membranes. Hence, bicarbonate combines with acid in serum, resulting in the production of carbon dioxide and water, as defined by the Henderson-Hasselbalch equation.

If the increased carbon dioxide is not removed via ventilation, it readily enters the cell and drives the Henderson-Hasselbalch reaction in the opposite direction, increasing intracellular acidosis. Worsened myocardial intracellular acidosis may result in a decrease in myocardial contractility.^{[22, 23]} In addition, bicarbonate administration may result in hypernatremia and hyperosmolality, decreasing the availability of ionized calcium.

Finally, laboratory and clinical data have not demonstrated that bicarbonate administration improves the ability to defibrillate, improves DO₂, or improves survival rates in shock and cardiac arrest.^{[24, 25, 26]} Studies in patients with cardiovascular arrest have not demonstrated improved survival rates associated with the use of bicarbonate. Thus, acidosis that results from shock should ideally be corrected with increased perfusion from volume supplementation and judicious use of cardiotropic medications together with optimal ventilation.

Bicarbonate replacement therapy

In patients with persistent shock or ongoing bicarbonate loss (eg, severe diarrhea), careful replacement of bicarbonate may be indicated. The appropriate dose of bicarbonate may be calculated from the known base deficit obtained from an arterial blood gas (ABG) sample according to the following formula:

HCO₃^- (mEq) = Base deficit × patient's weight (in kg) × 0.3

Generally, a dose equivalent to half of the calculated bicarbonate deficit may be administered initially, and repeat acid-base status may be determined. Alternatively, 0.5-1mEq/kg may be administered if indicated.

The use of corticosteroids in shock, particularly septic shock, is controversial. Many large-scale, controlled trials in animals and humans have not demonstrated improved outcome with corticosteroid use, and there is some potential associated morbidity.^[27] Nevertheless, a question remains as to whether patients in severe septic shock or purpura fulminans have adequate levels of circulating glucocorticoids to support their physiology when severely stressed.

Adrenocortical failure or infarction, known as Waterhouse-Friderichsen syndrome, may result in cardiovascular failure and hyporesponsiveness to catecholamines. In such patients, initiation of stress-dose hydrocortisone, in the range of 50-100mg/m²/day IV, may be beneficial and lifesaving. A serum cortisol level may be drawn prior to initiating the first dose of corticosteroids, and if this random serum cortisol level is low, then replacement doses may be beneficial.

Moreover, some data suggest a potential role for corticosteroid replacement therapy in select patients with septic shock. A study of adult patients with septic shock who had survived 48 hours and were dependent on inotropic agents showed some benefit to treatment with supraphysiologic doses of hydrocortisone.^[28]

Patients in the treatment group received 100mg of hydrocortisone IV 3 times a day for 5 days. At the end of 7 days, 68% of the hydrocortisone group had reversal of shock, compared with 21% of controls who received placebo, a difference of 47%. In addition, the mortality rate was 32% in the hydrocortisone group, compared with 63% in controls, although this result did not reach statistical significance.

Use in adrenal insufficiency

Furthermore, select patients may have adrenal insufficiency, rendering them hyporesponsive to administration of catecholamines during resuscitation from shock. Some practitioners evaluate a baseline serum cortisol level in children with fluid-refractory, catecholamine-resistant shock and/or perform a corticotropin stimulation test with 250mcg of corticotropin, treating the patient with hydrocortisone, though the use of such serum measurements has not been shown to result in improved outcomes.

Therapy is continued for patients who prove to have an absolute baseline cortisol level of less than 20mcg/dL and/or a depressed response to the corticotropin stimulation test, with a rise of less than 9mcg/dL at 30 and 60 minutes after administration of corticotropin.^[29]

Dosage recommendations generally range from 1-2mg/kg of hydrocortisone IV every 6 hours, though as much as a 50mg/kg bolus followed by the same amount infused over 24 hours has been administered.^[30]

Obviously, for all causes of shock, the underlying etiology should be identified and treated. If the cause is sepsis, isolate and treat the infectious organism with appropriate antibiotics. If the cause is trauma, then ongoing bleeding may need to be surgically addressed. Convert malignant arrhythmias to normal sinus rhythm as soon as possible.

Other modalities of supportive care must be ensured, such as optimizing and providing adequate nutritional support in patients recovering from shock. Multiple system organ support may be required, including such modalities as mechanical ventilation, renal dialysis, or even extracorporeal membrane oxygenation (ECMO).^{[31, 32]}

All of the therapies discussed here are aimed at restoring adequate perfusion to the tissues and organs of the body as soon as possible. Ongoing support offers the body the opportunity to repair the hypoxic and ischemic damage sustained, with the ultimate goal of functioning, intact patient survival.