Shock in children

1. Etiology and etiopathogenesis

Basic pathophysiology

• Reduced cardiac output
• Reduced circulating volume
• Low hemoglobin or hemorrhage
• Hypoxemia
• Maldistribution of blood flow
• Increased metabolic demand, for example fever, seizures, sepsis

Compensation in children

• Sympathetic activation: tachycardia, increased contractility, peripheral vasoconstriction
• Redistribution of blood flow to brain and heart, away from skin, kidneys, and gut
• Reduced renal perfusion and urine output
• Aldosterone and vasopressin release to retain sodium and water

Classification and causes

Special pediatric points

• Sepsis is an important cause of distributive shock. Young children often have a low-output, vasoconstricted, “cold shock” phenotype. Older children may show vasodilated, “warm shock.”
• Infants with duct-dependent congenital heart disease may deteriorate into shock as the ductus arteriosus closes during the first days to weeks of life.
• In trauma, occult hemorrhage must be assumed until excluded.
• Anaphylaxis produces vasodilation, capillary leak, bronchospasm, and airway edema.

2. Clinical approach

A. Recognize shock early

1. Appearance: alertness, interaction, tone, consolability
2. Work of breathing: retractions, grunting, tachypnea, abnormal airway sounds
3. Circulation to skin: pallor, mottling, cyanosis, delayed or flash capillary refill

B. Clinical stages

Compensated shock

• Tachycardia, often the earliest sign
• Anxiety, irritability, lethargy, reduced activity
• Cool extremities, weak peripheral pulses
• Delayed capillary refill, usually more than 2-3 seconds
• Mottling or pallor
• Tachypnea
• Reduced urine output
• Normal blood pressure

Decompensated shock

• Hypotension
• Altered consciousness: confusion, obtundation, coma
• Markedly weak or absent peripheral pulses
• Worsening metabolic acidosis and rising lactate
• Oliguria or anuria
• Bradycardia, which in children is an ominous pre-arrest sign
• Cyanosis and respiratory failure

C. Cold versus warm shock

D. Rapid focused history

• Fever, rash, cough, altered sensorium, possible infection
• Vomiting, diarrhea, polyuria, poor intake
• Trauma, bleeding, melena, hematemesis
• Allergy, insect sting, drug or food exposure
• Chest pain, palpitations, congenital heart disease, myocarditis symptoms
• Drugs, toxins, possible ingestion
• Endocrine disease or chronic steroid use
• Age in neonates and young infants: poor feeding, sweating, cyanosis, weak femoral pulses, and possible duct-dependent heart disease

E. Focused examination and monitoring

• Airway patency and respiratory effort
• Heart rate, pulse quality, respiratory rate, SpO₂, blood pressure
• Mental status and glucose
• Capillary refill, temperature gradient, skin color
• Liver enlargement, gallop rhythm, crackles: suggest cardiac dysfunction/fluid overload
• Rash or urticaria: sepsis, meningococcemia, anaphylaxis
• Signs of bleeding or dehydration
• Urine output: reassuring target is generally more than 1 mL/kg/hour. - Miller's Anesthesia, p. 11237

F. Investigations

• Bedside glucose, blood gas, lactate
• CBC, electrolytes, calcium, renal and liver function
• Blood culture before antibiotics only if this causes no meaningful delay
• Coagulation profile and crossmatch if bleeding is possible
• ECG, chest radiograph when indicated
• Bedside cardiac and lung ultrasound, if expertise is available:
  • Ventricular function
  • Pericardial effusion
  • Pneumothorax
  • Lung congestion/fluid overload
  • IVC and volume-status clues

3. Management

A. Immediate resuscitation: ABCDE

Airway and breathing

• Position airway and give high-concentration oxygen if hypoxemic or in severe shock.
• Suction secretions, provide bag-mask ventilation if needed.
• Intubate for respiratory failure, severe encephalopathy, or refractory shock, but anticipate peri-intubation collapse in hypovolemic or cardiogenic shock.
• Correct hypoxemia and avoid both hypoventilation and hyperventilation.

Circulation

• Continuous cardiorespiratory monitoring and frequent blood pressure measurements.
• Obtain IV access rapidly. If not promptly achievable in a critically ill child, establish intraosseous access.
• Measure bedside glucose and correct hypoglycemia.
• Keep the child warm.
• Monitor urine output, ideally with catheterization in severe shock.

B. Fluid therapy

• Give 10-20 mL/kg isotonic crystalloid boluses over 5-20 minutes.
• Reassess after every bolus.
• In septic shock, up to 40-60 mL/kg in the first hour may be appropriate if there is ongoing hypoperfusion and no fluid overload.

• New crackles or worsening respiratory distress
• Hepatomegaly
• Gallop rhythm
• Pulmonary edema
• Increasing oxygen requirement
• Deteriorating cardiac function on ultrasound

C. Vasoactive therapy

• Cold shock / low cardiac output with high SVR: epinephrine is often preferred.
• Warm shock / vasodilatory shock with low SVR: norepinephrine is often preferred.
• Epinephrine or norepinephrine can be started through a suitable peripheral or intraosseous line while central access is being arranged, with close monitoring.
• Dopamine is an alternative only when preferred agents are unavailable.

4. Cause-specific treatment

Hypovolemic shock

• Isotonic crystalloid in reassessed boluses.
• Replace ongoing diarrheal, gastric, renal, or burn losses.
• Treat cause: oral rehydration when stable, insulin protocol for DKA, surgery or endoscopy if indicated.
• In hemorrhage: direct pressure, tourniquet when appropriate, pelvic stabilization, early blood products, urgent surgical/interventional control.

Septic shock

• Obtain cultures if feasible without delaying therapy.
• Administer broad-spectrum IV antimicrobials promptly.
• Give titrated isotonic crystalloid boluses.
• Start epinephrine or norepinephrine if fluid-refractory or fluid-intolerant shock.
• Identify and control source: drain abscess, remove infected line, treat empyema, surgery for perforation, etc.
• Consider hydrocortisone in catecholamine-resistant shock, especially with suspected adrenal insufficiency.

Anaphylactic shock

• IM epinephrine into the anterolateral thigh: 0.01 mg/kg of 1 mg/mL solution, maximum 0.5 mg per dose.
• Repeat as necessary while monitoring.
• Airway management, oxygen, IV fluids, and bronchodilator for bronchospasm.
• Antihistamines and corticosteroids are adjuncts, not substitutes for epinephrine.
• Refractory shock requires expert-led IV epinephrine infusion.

Cardiogenic shock

• Avoid indiscriminate fluid loading.
• Give only carefully reassessed small fluid aliquots if preload responsive.
• Obtain ECG and bedside echocardiography early.
• Treat arrhythmia, myocarditis, metabolic derangements, and structural heart disease.
• Use inotropes/vasoactive drugs with PICU/cardiology input.

Obstructive shock

• Tension pneumothorax: immediate needle/finger decompression followed by chest drain.
• Cardiac tamponade: urgent pericardial drainage.
• Duct-dependent congenital heart disease: urgent prostaglandin E1 and pediatric cardiology support.
• Pulmonary embolism/pulmonary hypertension: specialist-directed therapy.

5. End points of resuscitation

• Improved mental status
• Age-appropriate heart rate and blood pressure
• Warm, well-perfused extremities
• Improving capillary refill and pulse quality
• Falling lactate trend, where available
• Urine output above 1 mL/kg/hour
• Resolution of metabolic acidosis
• No signs of fluid overload

High-yield summary

1. Diagnose shock clinically. Do not wait for hypotension.
2. Tachycardia, altered behavior, poor perfusion, delayed/flash capillary refill, weak pulses, and oliguria are early warning signs.
3. Stabilize airway and breathing, obtain IV/IO access, check glucose, monitor continuously.
4. Give reassessed 10-20 mL/kg isotonic crystalloid boluses when appropriate.
5. Use blood early in hemorrhagic shock and avoid excessive crystalloid.
6. Start epinephrine or norepinephrine early for fluid-refractory or fluid-intolerant septic shock.
7. Treat the cause simultaneously: antibiotics and source control for sepsis, IM epinephrine for anaphylaxis, decompression for tension pneumothorax, drainage for tamponade, and prostaglandin for duct-dependent lesions.
8. Reassess after every intervention.