Distributive shock is a critical condition characterized by inadequate blood flow that leads to poor tissue perfusion and thus inadequate oxygen delivery. It is an umbrella term that includes common pediatric conditions, including sepsis and anaphylaxis, and requires prompt recognition and intervention to prevent morbidity and mortality. This article provides an overview of the epidemiology, etiology, pathogenesis, pathophysiology, clinical features, differential diagnosis, diagnosis, treatment, and potential complications of distributive shock in infants and children, tailored for pediatric residents.
Epidemiology
Distributive shock is the second most common type of shock in children, accounting for a significant proportion of pediatric emergency department visits and hospital admissions. The incidence varies globally, with higher rates in regions with limited access to healthcare and higher prevalence of infectious diseases.
Etiology
The causes of distributive shock in children can be broadly categorized into:
There are multiple criteria with which to diagnose a child with sepsis, including SIRS plus a source but also newer SOFA scoring.
Concern for exposure to a likely allergen and,
- Two or more of the following: skin/mucosal involvement, respiratory compromise, reduced blood pressure, persistent GI symptoms. Or,
- Reduced blood pressure after exposure to a known allergen.
Consider this diagnosis in those children on chronic steroids who do not respond to initial isotonic fluid boluses, or those with known adrenal insufficiency who present with illness/unstable.
Central cause for poor vascular tone due to poor smooth muscle tone. Hypotension without tachycardia.
Pathogenesis and pathophysiology
The pathogenesis of distributive shock involves abnormal vascular tone that causes a pathologic vasodilation, thus leading to hypotension and decreased tissue perfusion pressure. This vasodilation can also lead to a maldistribution of blood flow away from vital organs to other less vitals areas of the body.
Although cardiac output is often normal (or even elevated) initially, the decrease in the perfusion pressures of the coronaries can quickly lead to myocardial dysfunction as the heart is not getting enough oxygen.
- Tachycardia to increase cardiac output. Remember, cardiac output is calculated as (stroke volume x heart rate).
- Stroke volume is determined by multiple things:
- Preload (which is abnormally low in hypovolemic shock),
- Contractility (which is abnormally low in cardiogenic shock)
- Afterload (which is abnormal in distributive shock).
- Stroke volume is determined by multiple things:
- Increased respiratory rate to enhance oxygen delivery.
- Persistent hypoperfusion leads to cellular hypoxia and metabolic acidosis.
- Organ dysfunction ensues, with potential progression to multi-organ failure.
Prolonged hypoperfusion results in irreversible cellular damage and death.
Clinical features
The clinical presentation of distributive shock varies with the severity and underlying cause, but commonly includes:
- Tachycardia.
- Tachypnea.
- Normal/Brisk capillary refill.
- Warm skin.
- Hypotension.
- Altered mental status (e.g., irritability, lethargy).
- Cyanosis.
- Weak or absent peripheral pulses.
Differential diagnosis
Differential diagnosis involves distinguishing distributive shock from other types of shock and conditions with similar presentations:
- History of congenital heart disease or myocarditis.
- Signs of heart failure:
- Hepatomegaly.
- Gallop rhythm.
- Cardiomegaly on chest X-ray.
- History of fluid loss: (e.g., vomiting, diarrhea) or hemorrhage (e.g., trauma, hematemesis)
- Signs of dehydration:
- Dry mucous membranes.
- Sunken eyes.
- Tension pneumothorax:
- Absent breath sounds.
- Tracheal deviation.
- Cardiac tamponade:
- Muffled heart sounds.
- Pulsus paradoxus (larger than expected drop, >10, in systolic blood pressure during inhalation).
Diagnosis
Diagnosis of distributive shock involves a combination of clinical assessment, laboratory tests, and imaging:
- Detailed history and physical examination.
- Assessment of vital signs, perfusion status, and mental state.
- Complete blood count (CBC) to assess hemoglobin and hematocrit levels.
- Electrolytes and renal/liver function tests to assess for end organ damage.
- Blood gas analysis to evaluate acid-base status
- Lactate: At the cellular level the lack of oxygen to the cells leads to an interruption of oxidative phosphorylation that shifts the body into anaerobic metabolism, thus depleting ATP and increasing lactic acid production.
Treatment
Treatment of distributive shock focuses on rapid restoration of circulating volume while simultaneously working to increase vascular tone, and addressing the underlying cause:
- Isotonic crystalloids (e.g., normal saline, lactated Ringer’s) are the first-line treatment. Trial of two boluses of isotonic fluids is often done prior to initiating inotropic support.
- It is important to monitor for signs of fluid overload due to third spacing:
- Increased work of breathing.
- Rales.
- Gallop.
Inotropic agents such as norepinephrine, vasopressin, and phenylephrine are often used. Epinephrine drips are used in anaphylaxis not responsive to IM epi.
- In anaphylaxis, Intramuscular Epinephrine is first line therapy, along with antihistamines (diphenhydramine for H1 and famotidine for H2) and steroids (methylprednisolone, prednisolone, dexamethasone). Albuterol can be used for those in respiratory distress.
- In sepsis, early antibiotic administration has been shown to decrease morbidity and mortality. Immunocompetent children often get ceftriaxone due to its broad coverage, and immunocompromised children may get broader coverage with cefepime +/– vancomycin.
- It is important to consider your patient’s presenting history, as certain populations (those with central lines, newborns <28 days) may have specific antibiotic needs based on their susceptibility to certain infections.
- In adrenal shock, stress dosing of steroids using hydrocortisone is done and calculated using the patient’s body surface area.
- Oxygen therapy to maintain adequate oxygenation.
- Monitoring of vital signs, urine output, and laboratory parameters.
- Surgical intervention for trauma or gastrointestinal bleeding.
- Management of underlying conditions (e.g., antibiotics for concurrent infection, stress dose steroids for adrenal crisis).
Potential complications
- Acute kidney injury.
- Disseminated intravascular coagulation (DIC).
- Acute respiratory distress syndrome (ARDS).
- Acute liver injury.
- Acute respiratory failure requiring intubation.
- Neurological deficits due to prolonged hypoxia.
- Chronic renal impairment requiring dialysis.
Conclusion
Distributive shock in infants and children is a life-threatening condition that requires prompt recognition and aggressive management. Understanding the epidemiology, etiology, pathogenesis, pathophysiology, clinical features, differential diagnosis, diagnosis, treatment, and potential complications is essential for pediatric residents to provide optimal care. Early intervention can significantly improve outcomes and reduce the risk of complications.
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