Initial evaluation of shock in children

INTRODUCTION — This topic will review the initial evaluation of children with shock and focus on the clinical features that identify and classify shock in resource-abundant settings and can be used to evaluate response to treatment. Additional considerations for the recognition of shock in children in resource-limited settings are provided separately. (See "Shock in children in resource-limited settings: Recognition".)

The physiology, classification, and initial management of pediatric shock, including the evaluation and management of specific types of pediatric shock are discussed separately:

●(See "Pathophysiology and classification of shock in children".)

●(See "Shock in children in resource-abundant settings: Initial management".)

●(See "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis".)

●(See "Septic shock in children in resource-abundant settings: Rapid recognition and initial resuscitation (first hour)" and "Septic shock in children in resource-abundant settings: Ongoing management after resuscitation".)

●(See "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management".)

DEFINITION — Shock is a dynamic and unstable pathophysiologic state characterized by inadequate tissue perfusion. Shock develops as the result of conditions that cause decreased intravascular volume, abnormal distribution of intravascular volume, and/or impaired cardiovascular function. Aggressive treatment within the first few hours after presentation may prevent the invariable progression and poor outcome that characterize the natural clinical course of shock, manifested clinically by end-organ damage, failure of multiple organ systems, and death. (See "Pathophysiology and classification of shock in children", section on 'Physiology' and "Pathophysiology and classification of shock in children", section on 'Stages of shock'.)

EPIDEMIOLOGY — Clinical experience suggests that frequent causes of shock among children include hypovolemia from diarrheal disease or traumatic hemorrhage and sepsis:

●Hypovolemia from gastroenteritis is the most common cause of pediatric shock worldwide [1]. Widespread use of oral rehydration therapy has substantially reduced mortality in resource-poor countries, although this intervention continues to be underutilized in some developed countries. (See "Oral rehydration therapy", section on 'Efficacy'.)

●Trauma, including hemorrhagic shock, also remains a significant cause of death in children [2].

●In addition, severe sepsis occurs frequently in children around the world, especially low birth weight newborns and infants younger than one month of age, immunosuppressed patients, and children with chronic debilitating disease. (See "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Epidemiology'.)

Cardiogenic and obstructive shock occur much less frequently in children. However, clinicians must consider these etiologies since they are typically not fluid responsive and require specific therapies [3].

Common causes of cardiogenic shock in children include (table 1) [3]:

●Sepsis (see "Septic shock in children in resource-abundant settings: Rapid recognition and initial resuscitation (first hour)", section on 'Patients with fluid-refractory shock')

●Congenital heart disease and heart failure (see "Heart failure in children: Etiology, clinical manifestations, and diagnosis")

●Myocarditis (see "Clinical manifestations and diagnosis of myocarditis in children", section on 'Clinical manifestations')

●Cardiomyopathy (see "Familial dilated cardiomyopathy: Prevalence, diagnosis and treatment", section on 'Diagnosis of familial DCM')

●Poisoning or drug toxicity (table 2)

●Brady- or tachyarrhythmias (see "Pediatric advanced life support (PALS)", section on 'Bradycardia algorithm' and "Pediatric advanced life support (PALS)", section on 'Tachycardia algorithm')

●Thoracic trauma with blunt cardiac injury (see "Overview of intrathoracic injuries in children", section on 'Blunt cardiac injury')

Obstructive shock can be caused by cardiac tamponade, tension pneumothorax, ductal dependent congenital cardiac lesions, or massive pulmonary embolism (table 1). (See "Pathophysiology and classification of shock in children", section on 'Obstructive shock'.)

PATHOPHYSIOLOGY — The physiologic determinants and stages of shock are discussed separately. (See "Pathophysiology and classification of shock in children", section on 'Physiology' and "Pathophysiology and classification of shock in children", section on 'Stages of shock'.)

Shock can develop from a variety of conditions that result in the following:

●Insufficient circulating blood volume (preload)

●Changes in vascular resistance (afterload)

●Heart failure (contractility)

●Obstruction to blood flow

The pathophysiologic consequences of inadequate circulation may be compounded by conditions (such as fever from infection or increased work of breathing from injury) that increase tissue metabolic needs.

Deleterious effects of decreased tissue perfusion include [4]:

●Poor perfusion of vital organs results in impaired function. For example, inadequate perfusion of the brain and kidneys can cause depressed mental status and low urine output, respectively.

●Lactic acid accumulates as cells switch to anaerobic metabolism to generate energy. Increased lactic acid in tissues causes metabolic acidosis, which interferes with cell and organ function.

●Hypoperfusion initiates inflammatory events (such as the activation of neutrophils and release of cytokines) that disrupt the microcirculation and contribute to tissue injury. Adrenergic stress responses that are activated to compensate for decreased tissue perfusion and increased metabolic demand include the following:

•Blood flow to vital organs is preserved through stimulation of the heart (tachycardia and increased contractility) by the sympathetic nervous system and increased peripheral vasoconstriction (increased systemic vascular resistance [SVR] and venous tone) mediated by the sympathetic nervous and renin-angiotensin systems.

•Hormones such as catecholamines, corticosteroids, and glucagon initiate increased liver glycolysis and lipolysis to maintain cell energy sources, causing an increase in lactic acid production.

The classification of shock is based upon the physiologic mechanisms that result in decreased tissue perfusion (table 3). This classification has important consequences for management decisions. (See "Pathophysiology and classification of shock in children", section on 'Classification' and "Shock in children in resource-abundant settings: Initial management", section on 'Further management by type of shock'.)

Classification of pediatric shock and typical causes include the following [3]:

●Hypovolemic shock – Hypovolemic shock is the most common type of shock in children. Causes include fluid and electrolyte loss (as from gastroenteritis or osmotic diuresis), hemorrhage (as from trauma), capillary leak (as from bowel obstruction or burns), inadequate fluid intake, and insensible losses (eg, fever, tachypnea, or burns). (See "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management", section on 'Etiology'.)

By definition, preload is decreased in hypovolemic shock. SVR may be increased as the result of compensatory mechanisms. Cardiac contractility is typically normal. (See "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management", section on 'Pathophysiology'.)

●Distributive shock – Distributive shock physiologically refers to a condition in which SVR is initially decreased. It may occur as the result of sepsis, anaphylaxis, or neurologic injury. (See "Pathophysiology and classification of shock in children", section on 'Distributive shock'.)

With sepsis and anaphylaxis, volume depletion may also develop because of losses related to the underlying infection (septic shock), or inflammatory cascade (anaphylaxis). Both processes are associated with increased capillary permeability with loss of plasma from the intravascular space into the tissues. Myocardial dysfunction can also contribute to poor tissue perfusion.

In septic shock, abnormal distribution of blood flow as the result of changes in vasomotor tone causes inappropriate tissue perfusion (such as decreased splanchnic circulation with increased flow to skin and muscle). SVR may be low, producing increased blood flow to skin and a wide pulse pressure (warm shock) or SVR may be increased, in which case, blood flow to skin is decreased and the pulse pressure is narrow (cold shock). (See "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)

Neurogenic shock may develop in a child with a high spinal cord injury (above the sixth thoracic spinal level) [3]. Uncontrolled vasodilation occurs as the result of the sudden loss of sympathetic tone. Compensatory sympathetic mechanisms (such as tachycardia and peripheral vasoconstriction) are absent. (See "Evaluation and acute management of cervical spine injuries in children and adolescents", section on 'Physical examination'.)

●Cardiogenic shock – Cardiogenic shock results from pump failure because of intrinsic cardiac disease (eg, congenital heart disease, myocarditis, myocardial contusion, myocardial ischemia, cardiomyopathy, or arrhythmia (table 1)). Physiologic features of cardiogenic shock include tachycardia, increased SVR, and decreased cardiac output [3]. (See "Pathophysiology and classification of shock in children", section on 'Cardiogenic shock'.)

●Obstructive shock – Obstructive shock describes physical obstruction of systemic blood flow from the heart which causes abrupt impairment of cardiac output (table 1). Causes of obstructive shock include cardiac tamponade, tension pneumo- or hemothorax and massive pulmonary embolism. Infants with ductal-dependent congenital heart lesions, such as coarctation of the aorta and hypoplastic left ventricle syndrome, may also present in shock when the ductus arteriosus closes during the first few weeks of life. Conditions that cause obstructive shock must be recognized quickly because they generally require specific treatment. (See "Pathophysiology and classification of shock in children", section on 'Obstructive shock' and "Approach to the ill-appearing infant (younger than 90 days of age)", section on 'Initial stabilization'.)

For any given condition that can cause shock, the classification may be mixed. Patients with distributive shock, in particular, often have multiple physiologic abnormalities. As an example, children with distributive shock from sepsis may also have volume loss (from vomiting, diarrhea, poor intake, or increased insensible fluid loss from tachypnea and fever) and myocardial depression from the effect of inflammatory mediators released in response to infection [3]. (See 'Clinical classification of shock' below.)

EVALUATION — Children can compensate for circulatory dysfunction (primarily by increasing heart rate, systemic vascular resistance [SVR], and venous tone) and maintain normal blood pressures despite significantly compromised tissue perfusion. Consequently, hypotension is a very late and ominous finding [3,5]. The challenge for the clinician is to recognize children in shock early (before they develop hypotension), when they are more likely to respond favorably to treatment.

Although the cause of shock may not be initially apparent, treatment must begin immediately. A systematic approach to the evaluation of children with evidence of poor perfusion typically identifies features of the history, physical examination, and ancillary studies that suggest the underlying condition (algorithm 1).

The goals of the initial evaluation of shock in children include:

●Immediate identification of life-threatening conditions (eg, tension pneumothorax, hemothorax, cardiac tamponade, or pulmonary embolism)

●Rapid recognition of circulatory compromise

●Early classification of the type and cause of shock

The initial management of undifferentiated shock is provided in the algorithm and discussed in detail separately (algorithm 2). (See "Shock in children in resource-abundant settings: Initial management".)

A general approach to the assessment of airway, ventilatory, and circulatory function in children is reviewed separately. (See "Initial assessment and stabilization of children with respiratory or circulatory compromise", section on 'Initial assessment' and "Technique of emergency endotracheal intubation in children" and "Assessment of systemic perfusion in children".)

Rapid assessment — The pediatric assessment triangle (PAT) provides a quick evaluation of appearance, breathing, and circulation for acutely ill or injured children that should identify conditions that require immediate intervention.

Features of the PAT that are specific for the evaluation of shock include:

Appearance — Significant changes in appearance (such as poor tone, unfocused gaze, or weak cry) may be indicators of decreased cerebral perfusion. Subtle differences in appearance (such as decreased responsiveness to caretakers or painful procedures) may also be important indicators of shock.

Breathing — A child with depressed mental status as the result of shock may not be able to maintain a patent airway. Tachypnea without respiratory distress can develop in response to metabolic acidosis. Children with cardiogenic shock typically have some increased work of breathing in addition to tachypnea.

Children with severe respiratory distress and signs of circulatory compromise may have obstructive shock and require life-saving interventions to treat one of the following:

●Tension pneumothorax – Signs of tension pneumothorax include respiratory distress, decreased breath sounds over the involved hemithorax, subcutaneous air, and distended neck veins. Children with tension pneumothorax frequently have sustained thoracic trauma, although a spontaneous pneumothorax can also develop tension. Treatment consists of needle decompression followed by chest tube thoracostomy. (See "Thoracic trauma in children: Initial stabilization and evaluation", section on 'Initial rapid assessment' and "Thoracic trauma in children: Initial stabilization and evaluation", section on 'Chest decompression'.)

●Cardiac tamponade – Features that may be seen with cardiac tamponade include respiratory distress, muffled heart tones, pulsus paradoxus, and distended neck veins. Cardiac tamponade can occur as the result of penetrating thoracic trauma or from the accumulation of fluid as the result of infection, malignancy, or following cardiac surgery (movie 1). Pericardiocentesis is emergently indicated. (See "Causes of acute respiratory distress in children", section on 'Cardiac tamponade' and "Emergency pericardiocentesis".)

●Ductal-dependent congenital heart disease – Infants with ductal-dependent congenital heart disease may have respiratory distress, circulatory collapse, cyanosis not responsive to oxygen administration, cardiomegaly, and/or a pulse or blood pressure gradient between the upper and lower extremities which may occur abruptly as the ductus arteriosus closes. Although timing varies, it is most common in neonates between one and three weeks after birth. Identification and management of infants with congenital heart disease is discussed separately. (See "Identifying newborns with critical congenital heart disease" and "Diagnosis and initial management of cyanotic heart disease in the newborn", section on 'Initial management'.)

●Massive pulmonary embolism (PE) – Findings that suggest PE include cyanosis, respiratory distress, and pleuritic chest pain. PE occurs uncommonly in children. There is typically a predisposing condition (such as a central venous access device or an inherited hypercoagulable state). (See "Venous thrombosis and thromboembolism (VTE) in children: Risk factors, clinical manifestations, and diagnosis", section on 'Pulmonary embolism'.)

Circulation — Poor perfusion can often be identified rapidly, before a blood pressure measurement is taken. Features of circulation that should be quickly evaluated include:

●Quality of central and peripheral pulses – Decreased intensity of distal pulses in comparison to central pulses suggests peripheral vasoconstriction and compensated shock. (See "Assessment of systemic perfusion in children", section on 'Pulses'.)

Bounding pulses may be present in patients with distributive ("warm") shock.

●Skin temperature – Skin may be mottled or cool in children with compensated shock, but this finding can also be influenced by environmental temperature.

●Capillary refill – Capillary refill greater than two seconds suggests shock [6]. The usefulness of capillary refill is limited by interobserver variability and by the effect of environmental temperature. (See "Assessment of systemic perfusion in children", section on 'Capillary refill time'.)

Flash capillary refill (<1 second) may be present in patients with distributive ("warm") shock.

●Heart rate – Tachycardia is frequently present (table 4) although a normal or low heart rate with signs of compensated or hypotensive shock can occur with cervical or high thoracic spinal cord injury.

Hypoxia and some poisonings (eg, ingestion of beta blockers, calcium channel blockers, cardiac glycosides, opioids, or benzodiazepines) can cause bradycardia (table 2). Bradycardia can also be an agonal event for patients with shock from any cause.

●Blood pressure – Hypotension is typically a late finding among children in shock. Compensatory vasoconstriction is often so pronounced that systemic blood pressure can be maintained within the normal range, despite significant circulatory compromise. Ideally, shock is recognized before hypotension occurs by identifying tachycardia and signs of organ hypoperfusion such as skin changes (prolonged capillary refill) and decreased urine output.

For children, hypotension is defined as a systolic blood pressure that is less than the fifth percentile of normal for age. We use the age-related criteria provided by the Pediatric Advanced Life Support Course (see "Pathophysiology and classification of shock in children", section on 'Common features'):

•Term neonates (0 to 28 days): <60 mmHg

•Infants (1 month to 12 months): <70 mmHg

•Children 1 to 10 years old: <(70 mmHg + [2 x age in years])  

•Children ≥10 years old: <90 mmHg

Point of care ultrasonography (POCUS), where available, may also provide essential information to guide life-saving procedures (such as relief of tension pneumothorax or cardiac tamponade) during the rapid assessment of children with undifferentiated shock. The bulk of evidence supporting the role of POCUS in the initial assessment of undifferentiated shock is for adult patients (see "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock", section on 'Initial diagnostic evaluation'). However, expertise in POCUS for children is increasing, providing at least anecdotal evidence that it may also be useful for children [7]. (See 'Ancillary studies' below.)

A more general discussion of the PAT is provided separately. (See "Initial assessment and stabilization of children with respiratory or circulatory compromise", section on 'Pediatric assessment triangle'.)

History — The following historical features may identify the condition causing shock:

●A history of fluid loss (due to gastroenteritis, diabetic ketoacidosis, or a gastrointestinal bleed) is consistent with hypovolemic shock. If available through review of medical records or caregiver report, a pre-illness weight, when compared with the weight on presentation, can provide an estimate of the amount of fluid loss. (See "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management", section on 'History'.)

●Children who have been injured may have hypovolemic shock from hemorrhage (eg, solid organ injury from blunt abdominal trauma), obstructive shock (eg, tension pneumothorax or cardiac tamponade), and/or neurogenic shock (eg, spinal cord injury). (See "Trauma management: Approach to the unstable child", section on 'Circulation'.)

●Fever and/or immunocompromise (due to chemotherapy, sickle cell disease, or inherited immunodeficiencies) may indicate septic shock. (See "Septic shock in children in resource-abundant settings: Rapid recognition and initial resuscitation (first hour)", section on 'Rapid recognition'.)

●A history of exposure to an allergen (eg, a bee sting or food) suggests anaphylactic shock.

●Shock may develop as the result of exposure to toxins (eg, iron, arsenic, beta blockers, calcium channel blockers, or cardiac glycosides).

●Patients with chronic heart disease (eg, cardiomyopathy or complex congenital heart disease) may develop cardiogenic shock.

●Adrenal crisis must be considered in a patient at risk for adrenal insufficiency (eg, patients receiving chronic steroid therapy, hypopituitarism, neonates with congenital adrenal disease, or sepsis) (table 5). (See "Clinical manifestations and diagnosis of adrenal insufficiency in children" and "Treatment of adrenal insufficiency in children".)

Physical examination — A complete physical examination, including vital signs with pulse oximetry, should be performed (table 6 and table 4).

An accurate weight is essential for determining fluid requirements and medication doses. The child's length provides a reasonable estimate of weight when a weight cannot be measured. (See "Initial assessment and stabilization of children with respiratory or circulatory compromise", section on 'Estimation of weight'.)

Abnormal vital signs provide essential information regarding the severity, classification, and cause of shock.

●Respiratory rate – Children with shock are usually tachypneic. Capnography may be helpful for identifying hyperventilation in response to metabolic acidosis [8]. A falsely low EtCO2 can also occur in the setting of poor pulmonary perfusion as a component of the shock state. (See "Carbon dioxide monitoring (capnography)".)

●Heart rate – In children, sinus tachycardia is a consistent sign of shock (except for patients with cardiogenic shock from a bradyarrhythmia or spinal cord injury). For patients with compensated shock, it may be the only abnormal vital sign. Other causes of tachycardia with poor perfusion in children include:

•Supraventricular tachycardia (SVT) – With SVT, the heart rate is typically >220 beats per minute for infants, >180 beats per minute for older children and adolescents, and relentlessly regular (table 7 and waveform 1). Pediatric treatment is discussed in the algorithm and provided separately (algorithm 3). (See "Management of supraventricular tachycardia (SVT) in children".)

•Ventricular tachycardia (VT) – VT is an uncommon rhythm in children that can be identified by electrocardiogram (waveform 2). Initial pediatric treatment is provided in the algorithm and discussed separately (algorithm 3). (See "Management and evaluation of wide QRS complex tachycardia in children", section on 'Stable patient'.)

●Blood pressure – Children with shock may have normal blood pressures. Hypotension must be rapidly identified, because those with low blood pressures typically deteriorate rapidly to cardiovascular collapse and cardiopulmonary arrest [3]. (See 'Circulation' above.)

Measurement with a manual cuff may be more accurate for children with circulatory compromise. Blood pressures determined with automated office devices can be higher than those using manual devices, particularly for hypotensive patients [9]. For children with normal systolic blood pressures, the classification of shock may be suggested by changes in the pulse pressure:

•Narrow pulse pressure (typically <30 mmHg in older children and adults) occurs when diastolic blood pressure is increased as the result of a compensatory increase in SVR (such as with hypovolemic and cardiogenic shock).

•Widening of pulse pressure (typically >40 mmHg in older children and adults; lower pulse pressures may reflect widening in infants and neonates) can be seen when diastolic blood pressure is decreased as the result of decreased SVR (as can occur with distributive shock).

●Temperature – Fever (or hypothermia in young infants) is often consistent with septic shock.

Additional features of the physical examination that suggest the etiology of shock include the following:

●Stridor, wheezing, or abnormal breath sounds – Children with stridor or wheezing may have anaphylaxis. Those with crackles may have a pneumonia (septic shock) or heart failure (cardiogenic shock). Those with asymmetric breath sounds may have a tension pneumothorax. Airway obstruction from other causes (such as foreign body aspiration or status asthmaticus) may lead to cardiovascular collapse from hypoxemia.

●Distended neck veins – Distended neck veins suggest an abnormality of cardiac contractility with heart failure, or obstruction to venous return caused by cardiac tamponade or tension pneumo- or hemothorax.

●Abnormal heart sounds – Cardiogenic shock is suggested by cardiac murmurs or a gallop rhythm. Muffled heart tones suggest pericardial fluid and, when accompanied by pulsus paradoxus, identify cardiac tamponade.

●Pulse differential – Decreased pulses and/or blood pressure in the lower extremities when compared to the upper extremities suggests coarctation of the aorta or other structural heart disease.

●Hepatomegaly – Hepatic congestion and resulting hepatomegaly can be seen with heart failure.

●Abnormal abdominal findings – Abdominal distention, masses, or tenderness is consistent with an abdominal catastrophe such as bowel obstruction, perforation, or peritonitis. Inflicted injury should be considered in the absence of a plausible history of trauma.

●Abnormal skin findings – Urticaria or facial edema suggests anaphylaxis but is not a consistent finding in severe reactions. Purpura can be seen with septic shock. Bruises and/or abrasions may be noted with trauma.

Ancillary studies — Selected ancillary studies may be useful for successfully treating shock, identifying the etiology, and monitoring response to treatment. Ancillary studies should be simultaneously obtained with rapid assessment and treatment based upon the most likely etiology for shock as follows:

●Hypovolemic shock without hemorrhage (see "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management", section on 'Ancillary data') – Suggested studies for patients with significant hypovolemic shock reflecting more than 10 percent dehydration include:

•Rapid blood glucose

•Serum electrolytes

•Blood lactate

•Urine dipstick

•Chest radiograph for patients without rapid improvement after 60 mL/kg of isotonic fluid administration

•Two view abdominal radiograph for patients with abdominal findings that suggest possible perforation or obstruction

Serum lactate is a marker of tissue perfusion and has been used to measure the severity of shock in patients with sepsis. Lactate clearance has been used to monitor the response to therapy. Although not specifically studied in hypovolemic shock, blood lactate may also be an indicator of severity of illness and lactate clearance a measure of response to fluid therapy. The role of serum lactate and other studies for children with suspected septic shock are discussed in more detail separately. (See "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Laboratory studies' and "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Imaging'.)

A urine dipstick reading provides a quick measure of specific gravity, ketones, and glucose. Glycosuria with ketonuria suggests diabetic ketoacidosis.

A chest radiograph in children with suspected hypovolemic shock who do not rapidly improve after up to 60 mL/kg of isotonic fluid administration is also suggested. If the heart size is small, then additional bolus fluid administration is indicated. In contrast, if the heart is big, then fluid therapy should be moderated and additional types of shock (eg, septic or cardiogenic shock) may be present and warrant specific therapy. (See "Septic shock in children in resource-abundant settings: Rapid recognition and initial resuscitation (first hour)" and "Shock in children in resource-abundant settings: Initial management", section on 'Further management by type of shock'.)

For patients with abdominal findings and possible third spacing, plain radiography of the abdomen may identify signs of bowel obstruction or perforation. Additional studies are usually warranted to establish a definitive diagnosis (eg, ultrasound for intussusception or upper gastrointestinal series for malrotation). (See "Intussusception in children", section on 'Evaluation' and "Acute appendicitis in children: Diagnostic imaging" and "Intestinal malrotation in children", section on 'Diagnosis'.)

●Hypovolemic shock with hemorrhage – In addition to the above studies, patients with hemorrhagic hypovolemic shock warrant the following:

•Hematocrit

•Arterial or venous blood gas measurements

•Type and cross match (patients with trauma and hemorrhagic shock)

•Coagulation studies (platelet count, prothrombin time [PT] with international normalized ratio [INR], and activated partial thromboplastin time [PTT])

•Chest radiograph

•Bedside focused assessment with sonography for trauma (FAST)

For patients with traumatic hemorrhagic shock, a chest radiograph may also identify intrathoracic bleeding (ie, hemothorax) or other obstructive causes for shock, such as tension pneumothorax or pericardial effusion. (See "Trauma management: Approach to the unstable child", section on 'Screening radiographs'.)

Bedside focused assessment with sonography for trauma (FAST) can rapidly identify pericardial effusion and serious intraabdominal hemorrhage. Additional imaging is typically warranted for these patients to better define sites of bleeding. The approach to imaging in the pediatric trauma patient is discussed separately. (See "Trauma management: Approach to the unstable child", section on 'Adjuncts to the primary survey' and "Trauma management: Approach to the unstable child", section on 'Adjuncts to the secondary survey'.)

●Sepsis and septic shock – Suggested laboratory studies for children with sepsis and septic shock are discussed in detail separately and include (see "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Laboratory studies'):

•Rapid blood glucose

•Arterial or venous blood gas

•Complete blood count with differential

•Blood lactate

•Serum electrolytes

•Blood urea nitrogen and serum creatinine

•Ionized blood calcium

•Serum total bilirubin and alanine aminotransferase

•PT and INR

•PTT

•Fibrinogen and D-dimer

•Blood culture

•Urinalysis

•Urine culture

•Other cultures as indicated by clinical findings (eg, wound or mucosal site cultures for patients with suspected toxic shock syndrome (table 8))

•Diagnostic serologic testing as indicated to identify suspected sources of infection

•Inflammatory biomarkers (eg, C-reactive protein, procalcitonin) in selected cases

Other imaging may be appropriate depending upon clinical findings. For example, computed tomography of the head may be necessary in the patient with evidence of coagulopathy and altered mental status to evaluate for intracranial hemorrhage; ultrasound or computed tomography of the abdomen may be indicated to evaluate for intra-abdominal abscess. (See "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Imaging'.)

●Cardiogenic shock – Children with a history of congenital or acquired heart disease, abnormal cardiac examinations, cardiomegaly on chest radiograph, or who are not improving with initial treatment should receive 12-lead electrocardiograms (ECG) to evaluate for heart failure or signs of ischemia. In previously healthy children who present with cardiogenic shock, multisystem inflammatory syndrome in children (MIS-C) (table 9) and myocarditis are important etiologies to pursue. (See "COVID-19: Multisystem inflammatory syndrome in children (MIS-C) clinical features, evaluation, and diagnosis" and "Clinical manifestations and diagnosis of myocarditis in children".)

Limited evidence suggests that POCUS performed by well-trained, experienced emergency medicine providers may identify life-threatening conditions (such as myocardial dysfunction or tamponade) and guide critical procedures [10-13] (see "Emergency pericardiocentesis", section on 'Ultrasound-guided pericardiocentesis technique'). Depending upon specific findings, consultation with a pediatric cardiologist and formal echocardiography may also be warranted.

Cardiac arrhythmias may be suspected based upon heart rate and waveform during continuous monitoring. However, a 12-lead ECG is necessary to fully characterize the arrhythmia. (See "Clinical features and diagnosis of supraventricular tachycardia (SVT) in children", section on 'Diagnosis' and "Management and evaluation of wide QRS complex tachycardia in children".)

●Obstructive shock – Although chest radiograph or computed tomography (CT) of the chest can be diagnostic, whenever possible, tension pneumo- and hemothorax should be identified clinically or by emergency bedside ultrasonography and rapidly treated by chest tube thoracostomy. (See "Clinical presentation and diagnosis of pneumothorax", section on 'Diagnostic imaging' and "Thoracostomy tubes and catheters: Indications and tube selection in adults and children", section on 'Indications'.)

Computed tomographic pulmonary angiography provides definitive diagnostic imaging for pulmonary embolism (PE) but should only be performed in patients who respond to the initial treatment of shock (oxygenation, intravenous fluid resuscitation, and vasopressor support). In patients who remain unstable despite adequate resuscitation and in whom the suspicion for pulmonary embolus is high, definitive testing is typically considered unsafe. Bedside transthoracic or transesophageal ultrasonography may be used in such patients to establish a presumptive diagnosis of PE and used to justify administration of thrombolytic therapy. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Hemodynamically unstable patients'.)

CLINICAL CLASSIFICATION OF SHOCK — Once the initial evaluation is completed, a constellation of clinical characteristics suggest a specific type of shock (algorithm 1). A patient may have more than one type of shock (such as an infant with cardiogenic shock from supraventricular tachycardia (SVT) who is also hypovolemic because he has been unable to drink, or a child with underlying cardiomyopathy who is septic).

Findings that may be helpful include:

●Hypovolemic shock – History of volume loss (including hemorrhage associated with trauma), narrow pulse pressure, signs of poor peripheral perfusion (decreased distal pulses, cool extremities, prolonged capillary refill), small heart on chest radiograph (if one is obtained) (table 10). (See "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management", section on 'Evaluation'.)

●Distributive shock – Vascular dilation typically causes a widened pulse pressure. Other features associated with specific types of distributive shock include:

•Septic shock – History of fever or immunocompromise, variable peripheral perfusion (vasodilation with warm shock, vasoconstriction with cold shock), purpuric rash, abnormal white blood cell count, disseminated intravascular coagulation. (See "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Diagnosis'.)

•Anaphylactic shock – History of exposure to an allergen (such as a bee sting or food), stridor, wheezing, wide pulse pressure, vasodilation, urticaria, facial edema. (See "Anaphylaxis: Acute diagnosis", section on 'Definition'.)

•Neurogenic shock – History of trauma with severe head or cervical spine injury, hypotension with wide pulse pressure, normal heart rate or bradycardia.

●Cardiogenic shock – History of heart disease (eg, corrected congenital heart disease or cardiomyopathy), history of palpitations, signs of heart failure (eg, pulmonary rales, hepatomegaly, gallop rhythm, distended jugular veins), or arrhythmia.

●Obstructive shock – History of thoracic trauma, deviation of the trachea, and distended neck veins in a patient with tension pneumo- or hemo-thorax; muffled heart sounds and pulsus paradoxus in a patient with cardiac tamponade; abrupt circulatory collapse in a patient with pulmonary embolism caused by predisposition to thrombosis (eg sickle cell disease or congenital thrombophilia); or abrupt onset of new heart murmur, shock, and/or cyanosis in a neonate with a ductal dependent congenital heart lesion (eg, critical coarctation of the aorta or hypoplastic left heart syndrome) within the first few weeks of life due to closure of the ductus arteriosus. (See "Identifying newborns with critical congenital heart disease".)

MANAGEMENT — Definitive management of shock depends upon correct classification of the type of shock present and definitive treatment of the underlying etiology. The initial management of undifferentiated shock in resource-abundant settings is provided in the algorithm and discussed in detail separately (algorithm 2). (See "Shock in children in resource-abundant settings: Initial management".)

The initial management of hypovolemic and septic shock as well as the management of shock in children in resource-limited settings are discussed elsewhere.

●(See "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management", section on 'Management'.)

●(See "Septic shock in children in resource-abundant settings: Rapid recognition and initial resuscitation (first hour)", section on 'Resuscitation'.)

●(See "Shock in children in resource-limited settings: Initial management".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Shock in children".)

SUMMARY AND RECOMMENDATIONS

●Pathophysiology – Shock develops as the result of conditions that cause one or more of the following (table 3) (see 'Pathophysiology' above):

•Decreased intravascular volume – Hypovolemic shock

•Abnormal distribution of intravascular volume – Distributive shock

•Impaired cardiovascular function – Cardiogenic shock

•Obstruction to cardiac output – Obstructive shock

●Evaluation – The goals of the evaluation of shock are to identify life threatening conditions and to rapidly recognize children with circulatory compromise so that treatment can be initiated before hypotension develops. (See 'Evaluation' above.)

●Rapid assessment – Rapid assessment of appearance, breathing, and circulation should identify children with life-threatening conditions, including hypotensive shock, obstructive causes of shock (eg, tension pneumothorax, hemothorax, cardiac tamponade, or pulmonary embolism), and compensated shock. (See 'Rapid assessment' above.)

●Clinical classification of shock – Clinical features and ancillary studies often suggest the cause of shock and can be used to guide management decisions (algorithm 1). (See 'Clinical classification of shock' above and 'Ancillary studies' above.)

●Initial management – The initial management of undifferentiated shock occurs simultaneously with the rapid assessment and clinical classification of shock and an approach is provided in the algorithm and discussed in detail separately (algorithm 2). Definitive management of pediatric shock depends upon correct classification of the type of shock based upon clinical findings and definitive treatment of the underlying etiology. (See "Shock in children in resource-abundant settings: Initial management" and "Shock in children in resource-limited settings: Initial management".)