Sections

Workup

Approach Considerations

Stabilization of the airway and breathing as well as aggressive intervention to improve the circulatory function of any patient in clinical shock always takes precedence over any further diagnostic evaluation.

After the initial stabilization, certain objective measures may help to solidify or better define the diagnosis. These measures initially may include obtaining the following laboratory studies:

Point-of-care glucose levels
Comprehensive metabolic panel (CMP)
Arterial (ABG) or venous blood gas (VBG) measurements
Serum lactate levels
Complete blood count (CBC) with differential
Prothrombin (PT) and partial thromboplastin (PTT) times
Fibrinogen and D-dimer levels
Fluid culture(s) (eg, blood, urine, cerebrospinal fluid [CSF])

Additional studies may help to identify an etiology and ultimately guide therapy of the patient in shock. Subsequent ancillary evaluation may also include the following:

Chest radiography
Mixed venous oxygen saturation
Central venous pressure measurement
Cardiac output (CO) monitoring
Near-infrared spectroscopy
B-type natriuretic peptide (BNP) levels
Serum biomarker profile

Comprehensive Metabolic Panel

A CMP may provide a wealth of information about the patient in shock. A decreased serum carbon dioxide level suggests a metabolic acidosis that may reflect a significant lactic acidosis from anaerobic metabolism associated with shock. Diarrhea also leads to direct bicarbonate loss, which may exacerbate metabolic acidosis in a patient with shock due to dehydration from diarrhea. Measurement of serum lactate levels may help to distinguish bicarbonate loss from lactic acidosis due to shock.

Hypernatremia suggests intravascular volume contraction that is consistent with hypovolemic shock. Hypoglycemia is common in shock and can rapidly be identified and treated with point-of-care testing. Elevated blood urea nitrogen (BUN) and creatinine levels and/or elevated aspartate transaminase (AST) and alanine transaminase (ALT) levels suggest secondary hypoxic-ischemic end-organ injury. Disturbed calcium homeostasis may result in low serum ionized calcium levels that can further depress myocardial function.

Blood Gas Analysis

An ABG study helps to determine the arterial oxygen tension (PaO₂) of the blood, assisting in titration of supplemental oxygen delivery to the patient in shock. In addition, ABG findings help to determine the patient's acid-base status, which reflects the degree of systemic shock and the patient's response to therapy.

VBGs may also be used to determine mixed venous oxygenation saturation (discussed below).

Complete Blood Count and Coagulation Studies

In assessing the CBC, the hemoglobin (Hb) concentration is particularly important, because it determines the blood's oxygen-carrying capacity. In patients with anemia who present in severe shock, early transfusion should be considered as soon as possible.

A significantly elevated or depressed white blood cell (WBC) count, along with a WBC differential that is suggestive of infection, could support the diagnosis of septic shock. Similarly, thrombocytopenia may herald a bleeding disorder that could result in internal hemorrhage or disseminated intravascular coagulation (DIC), which may accompany septic shock. Disordered coagulation cascade activation may be further evidenced by prolonged PT and partial PTT, low fibrinogen levels, and an elevated D-dimer level.

Fluid Culture

Sepsis must be ruled out as the cause of shock, especially in children younger than 3 months, those who are immunocompromised, and those who are unvaccinated.

To exclude a serious bacterial infection, blood cultures should be obtained at presentation for all febrile children younger than 3 months.^{[15, 16, 17]}Leukocyturia, procalcitonin, C-reactive protein, and absolute neutrophil count are lab markers that can help risk stratify which children would benefit from a lumbar puncture and empiric antibiotic treatment.^[18]In children older than 3 months and immunocompromised patients with fever, hypothermia, leukocytosis, or other concerns for bacterial infection, blood cultures should also be obtained and sent for analysis.

CSF and urine cultures should also be considered as dictated by the child's clinical presentation and host risk factors.

Chest Radiography

Evaluation of the cardiac silhouette on a chest radiograph may help to delineate cardiogenic shock, which may feature cardiomegaly (see the image below), from hypovolemic shock, in which the heart size appears small.

Chest radiograph in a patient with cardiomegaly, which may accompany cardiogenic shock.

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The chest radiograph may also reveal signs of pneumonia or other pulmonary disorders. Respiratory distress in a patient in shock may result from acute respiratory distress syndrome (ARDS), which may develop in any patient in shock or result from pneumonia and sepsis.

Point-of-Care Ultrasound

Point-of-care ultrasound (POCUS) continues to gain greater attention and use as it allows for the rapid and systematic evaluation of pediatric shock while avoiding risks associated with conventional radiographic techniques.{ref 62} Evaluation of shock is based on step-wise imaging of the heart, IVC, intraperitoneal cavity, and lung/pleura . Evaluation of the heart in the subxiphoid or parasternal long axis views allow for assessment of ventricular filling and function. Evaluation of the IVC is used a surrogate for central venous pressure and intravascular volume. On inspiration, negative thoracic pressure pulls blood form the IVC to the right atrium which can result in IVC collapse in volume depleted patients. An IVC-to-aorta ratio of greater than 0.8 suggest normal volume status. Evaluation of the pleural cavities allows for identification of pneumothoraces, pulmonary edema, and pleural effusions. Similarly, evaluation of the abdominal cavity can aid in rapid identification of free fluid and abdominal hemorrhage.

Mixed Venous Oxygen Saturation

Mixed VBG analysis can be utilized to determine the venous Hb oxygen saturation, or it can be directly measured by co-oximetry. A true mixed venous sample (SvO₂) from the pulmonary artery may be obtained from the distal port of a Swan-Ganz catheter—however, these catheters are infrequently utilized in pediatric patients. More often, the oxygen saturation of a sample of mixed central venous blood (ScvO₂) returning to the heart that is taken from a central venous catheter can be used as an SvO₂ surrogate.

By comparing the mixed venous oxygen saturation (ie, SvO₂) with the arterial oxygen saturation (SaO₂), the arteriovenous oxygen saturation difference and oxygen extraction ratio (O₂ ER) can be determined. In a patient with a relatively normal SaO₂ (93-100%), the normal SvO₂ is 65-77%, as the tissues typically extract 23-35% of oxygen delivered to them. If the oxygen extraction difference is greater than 35%, perfusion to the tissue capillary beds may be inadequate, reflecting a state of shock. Alternatively, if the oxygen extraction difference is less than 23%, oxygenated blood may be shunting past tissue capillary beds as a result of inappropriate distribution of blood flow (ie, distributive shock, with arteriovenous shunts resulting from vasodilation). Sepsis can also inhibit the cellular metabolic machinery, decreasing oxygen extraction and leading to an increase in venous saturation.

Central Venous Pressure

A central venous catheter in the superior vena cava may transduce the pressure generated by the blood in that vessel, the central venous pressure (CVP), which represents the back-pressure into the systemic venous circulation. Care must be taken to not rely entirely on such measurements. The cardiac filling pressure measured by these catheters reflects ventricular function and compliance—not necessarily intravascular volume alone. Nevertheless, such values, taken in context with the clinical examination findings, may help to determine the patient's clinical status. A normal CVP in a normal, compliant heart is typically 8-12 cm H₂ O. Higher pressures may reflect volume overload or poor right-sided heart compliance or function.

Cardiac Output Monitoring

Classically, the cardiac index (CI) is determined by pulmonary artery catheter measurement of the CO, although pulmonary artery catheterization is now infrequently done in pediatric patients. Instead, many innovative invasive or noninvasive surrogate technologies for CO determination are increasingly available and utilized in this patient population. These include Doppler echocardiography, the pulse contour cardiac output (PiCCO) catheter, and the femoral artery thermodilution catheter (FATD).

The CI is calculated by dividing the CO by the body surface area (BSA). Normal CI is 3.5-5.5 L/min/m², and values between 3.3 and 6 L/min/m² have been associated with optimal outcomes from pediatric septic shock.^{[19, 20]}Monitoring changes in CI during intravascular volume or cardiotropic infusions may help to guide and optimize administration of these therapies.

Near-Infrared Spectroscopy

A relatively new technology currently used in many pediatric intensive care units (PICUs) is near-infrared spectroscopy (NIRS).^{[21, 22, 23]}An optical probe placed over a patient's skin, such as the forehead, the flank over the kidneys, or the abdomen, sends an infrared signal through the skin and measures the pooled-tissue oxygen saturation. Because most of the blood in any given region is predominantly venous, the oxygen saturation is close to that of the tissue venous oxygen saturation in that region. This allows for a noninvasive measurement and an observation of the trend of an increased or decreased tissue oxygen saturation to be followed in critical tissue beds, such as the brain, kidneys, or mesenteric region. Such information may help to identify adequate or inadequate oxygen delivery. It is analogous to determining SvO₂ and may help to guide evaluation and response to therapy.

B-Type Natriuretic Peptide

BNP is a hormone produced by ventricular myocytes that is released in response to myocardial wall stress. In adult and pediatric studies, plasma BNP levels have been shown to be elevated in sepsis and in congestive heart failure with cardiogenic shock. Elevated levels of BNP reflect myocardial stress, and improvement in cardiac function is associated with normalization of BNP levels.^{[24, 25]}

Sepsis Biomarker Risk Model

Studies in recent years have focused on identification of serum protein biomarkers which may serve as prognostic indicators for pediatric sepsis. One such model, the PEdiatRic SEpsis biomarkEr Risk modEl (PERSEVERE), includes five proteins: C-C chemokine ligand 3 (CCL3), heat shock protein 70 kDa 1B (HSPA1B), interleukin-8 (IL-8), elastase 2 (ELA2), and lipocalin 2 (LCN2). This model estimated mortality with a sensitivity of 83% and a specificity of 75%.^{[26, 27]}

Treatment & Management

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Media Gallery

Chest radiograph in a patient with cardiomegaly, which may accompany cardiogenic shock.
Determinants of cardiac function and oxygen delivery to tissues. FiO2 = fraction of inspired oxygen. Adapted from Strange GR. APLS: The Pediatric Emergency Medicine Course. 3rd ed. Elk Grove Village, Ill: American Academy of Pediatrics; 1998:34.
Hemodynamic response to shock hemorrhage model (based on normal data). Adapted from Schwaitzberg SD, Bergman KS, Harris BH. A pediatric trauma model of continuous hemorrhage. J Pediatr Surg. Jul 1988;23(7):605-9.
Pediatric shock management algorithm. ACTH = adrenocorticotropic hormone; CI = cardiac index; ECMO = extracorporeal membrane oxygenation; MAP-CVP = mean arterial pressure-central venous pressure; PALS = Pediatric Advanced Life Support; PDE = phosphodiesterase; PICU = pediatric intensive care unit; SVC O2 = superior vena cava oxygen saturation.

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Author

Eric A Pasman, MD Pediatric Gastroenterologist, Naval Medical Center San Diego

Eric A Pasman, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics

Disclosure: Nothing to disclose.

Coauthor(s)

Christopher M Watson, MD, MPH Professor, Department of Pediatrics, Medical College of Georgia at Augusta University

Christopher M Watson, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Dale W Steele, MD, MS Professor of Emergency Medicine, Pediatrics, and Health Services, Policy, and Practice, Warren Alpert Medical School of Brown University; Attending Physician, Department of Pediatric Emergency Medicine, Rhode Island Hospital

Dale W Steele, MD, MS is a member of the following medical societies: American Academy of Pediatrics, American Statistical Association, Society for Medical Decision Making

Disclosure: Nothing to disclose.

Additional Contributors

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Adam J Schwarz, MD Consulting Staff, Critical Care Division, Pediatric Subspecialty Faculty, Children's Hospital of Orange County

Adam J Schwarz, MD is a member of the following medical societies: American Academy of Pediatrics and Phi Beta Kappa

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Acknowledgments

The views expressed are those of the authors and do not reflect the official policy or position of the US Navy, Department of Defense, or the US Government.