Shock in Pediatrics Clinical Presentation

Updated: Mar 03, 2015
  • Author: Eric A Pasman, MD; Chief Editor: Timothy E Corden, MD  more...
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The clinical history of patients who present in shock is important, particularly when the etiology is not frankly evident. The etiology of shock may depend on the age of the child and the presence of any comorbid conditions.

A child with vomiting, profuse diarrhea, or both, is at risk for hypovolemic shock. A child who has experienced blunt or penetrating trauma is at risk for bleeding that may result in hemorrhagic shock. Fever may herald an infection that could result in septic shock.

All infants younger than 3 months who present in shock should be considered to be septic until proven otherwise. This concern is heightened in an immunocompromised patient who presents with fever, such as a child receiving chemotherapy or a neonate. A neonate who presents within the first weeks of life with hepatomegaly or a cardiac murmur may have a congenital obstructive ductal-dependent heart lesion that manifests as shock as the ductus arteriosus closes.

Other general, nonspecific symptoms may manifest in the child in shock. Lethargy, weakness, a sense of malaise, decreased urine output, fussiness, and poor feeding are all nonspecific symptoms that may accompany shock.


Physical Examination

The diagnosis of shock involves the clinical recognition that the body's tissues and cells are not receiving an adequate delivery of oxygen and metabolic substrates. Clinically, this relies on the detection of surrogate signs and measures and is not dictated by blood pressure.

Infants and children have a remarkable ability to preserve their central blood pressure in an attempt to protect their heart and brain in many forms of shock while critically reducing perfusion to the extremities, gastrointestinal tract, kidneys, and other end organs. As a result, shock is characterized in these patients by the following:

  • Tachycardia (may be absent in the hypothermic patient)
  • Signs of impaired organ perfusion (eg, decreased urine output, altered mental status) or delayed peripheral perfusion (eg, weak peripheral pulses, delayed capillary refill >2 sec, cool extremities)
  • Temperature instability (hyperthermia, hypothermia)
  • Tachypnea

Blood pressure: compensated versus decompensated shock

Shock can be further described by three categories: compensated, decompensated, and irreversible. To differentiate between compensated and decompensated shock, the patient’s blood pressure is compared to the American Heart Association (AHA)'s fifth-percentile systolic blood pressures for age, which are as follows [12] :

  • Newborn: 60 mmHg
  • Infant (1 mo to 1 y): 70 mmHg
  • Child (1 to 10 y): 70 + (2 × age [in years]) mmHg
  • Child older than 10 years: 90 mmHg

Children with an adequate systolic blood pressure above the normative values for age may still be in compensated shock. Through compensatory tachycardia and increase systemic vascular resistance (SVR), central perfusion to the brain and heart are still considered adequate, although other vital organ systems may be hypoperfused. If not identified and reversed, compensated shock will lead to decompensated shock.

Decompensated shock occurs when the body’s compensatory responses to shock are overwhelmed and hypotension develops. Hypotension in the pediatric shock patient is a late and ominous clinical finding. Such children, if not quickly and aggressively resuscitated, experience additional organ damage, and their condition may progress to irreversible shock, cardiovascular collapse, and cardiac arrest.

Heart rate

Because cardiac output (CO) depends on stroke volume (SV) and heart rate (HR), the body typically tries to maintain CO when SV decreases by increasing the HR. This sign is certainly not very specific in children, because children may be tachycardic from a wide variety of stimuli, including fever, pain, and agitation. Nevertheless, with the exceptions mentioned above, tachycardia is generally a fairly early and sensitive finding in compensated and decompensated shock.

Skin perfusion

In the shock state, the body also attempts to compensate by increasing SVR and shunting blood from the skin to more vital organs, such as the heart and brain. This is manifested as decreased skin perfusion, characterized by diminished distal pulses, cool skin, increased skin temperature gradient, and prolonged capillary refill. Capillary refill is best determined by pressing on a distal extremity, preferably a finger or toe, for 5 seconds and then releasing the pressure. Note the time taken to refill. At normal room temperature, the distal capillary bed normally refills within 2 seconds or less. [13]

However, patients with inappropriate vasodilation from a distributive mechanism of shock may be unable to vasoconstrict their end-organ and skin microvasculature. Therefore, in the early phases of distributive shock, such as in anaphylaxis or certain forms of sepsis, the skin may appear very briskly perfused with warm extremities, bounding pulses, and brisk capillary refill (< 1-2 sec). Thus, when distributive mechanisms of shock are present, normal skin perfusion may not be reliably reassuring. Hypotension, tachycardia, or other evidence of metabolic disturbances, such as the presence of a persistent lactic acidosis, may reinforce the recognition that tissue DO2 (total arterial flow of oxygen) is impaired.

Cold and warm shock

"Cold shock" is occasionally used to describe shock in which there are cool extremities, diminished pulses, increased skin temperature gradient, and delayed capillary refill time. Alternatively, "warm shock" is sometimes used to describe shock with warm extremities, bounding pulses, and flash capillary refill time. Although the terms are not helpful for diagnosis, they can help to guide therapeutic strategies.

Other organ system function

Mental status may reflect central perfusion to the brain. Altered mental status may coincide with profound central shock. Normal mental status may be preserved in a patient in shock if central blood pressure is adequate despite peripheral organ compromise (ie, compensated shock).

Renal perfusion may be reflected by absolute urine output. Typically, in the absence of renal damage, a well-perfused kidney can produce 1-2 mL/kg/h or more of urine. However, renal damage may result from early hypoxic-ischemic injury, causing renal tubular damage due to acute tubular necrosis (ATN) that renders urine output unreliable as an indicator of adequate intravascular volume and perfusion.

Physical findings in cardiogenic shock

Early identification of cardiogenic shock is clinically important, as treatment strategies differ from other causes of shock with great attention given to intravascular volume status and the early initiation of inotropic pharmacologic support. Physical examination findings in cardiogenic shock include the following:

  • Tachycardia
  • Hepatomegaly
  • Cardiac gallop
  • Cardiac murmurs
  • Precordial heave
  • Jugular venous distention

As a result of anatomic differences between pediatric and adult patients, evaluating infants and children for hepatomegaly is more reliable than measuring jugular venous distention, which is often difficult to appreciate in young patients.