A previously well 6-year-old girl was brought to the emergency department after being found unusually lethargic with vomiting and abnormal breathing while staying with relatives. She had been reportedly healthy earlier in the day. There was no known history of trauma, fever, or chronic illness.
On arrival, she appeared critically ill with a depressed mental status. Initial vital signs revealed bradycardia (heart rate approximately 52–58 bpm), hypotension (blood pressure around 70/40 mmHg), and capillary refill >5 seconds. Point-of-care glucose was elevated at approximately 285 mg/dL.
Due to worsening consciousness and concern for airway protection, the patient was endotracheally intubated and mechanically ventilated. She received multiple isotonic fluid boluses and intravenous calcium without improvement in hemodynamics. Persistent shock required initiation and escalation of vasoactive infusions.
The patient was transferred to the pediatric intensive care unit for ongoing management. On PICU assessment, she remained poorly perfused with cool extremities and weak peripheral pulses. Laboratory evaluation demonstrated severe metabolic acidosis with markedly elevated lactate (~11–12 mmol/L range), acute kidney injury (creatinine ~2.6–2.8 mg/dL), and persistent hyperglycemia (~350 mg/dL range).
Chest radiograph showed mild bilateral perihilar vascular prominence without focal consolidation or cardiomegaly. The overall presentation was consistent with profound undifferentiated shock requiring aggressive critical care support.
Introduction
Undifferentiated shock in previously healthy children represents a high-risk clinical scenario that requires rapid stabilisation and parallel diagnostic evaluation. While septic shock remains common, the presence of bradycardia, severe lactic acidosis, and poor response to fluids should prompt consideration of alternative etiologies, including toxicologic, cardiogenic, metabolic, and endocrine causes.
Early recognition of pre-arrest physiology and timely escalation to advanced hemodynamic support are essential to prevent cardiovascular collapse and multi-organ failure.
Discussion
This case demonstrates a concerning pediatric shock phenotype characterised by hypotension with relative bradycardia, severe hyperlactatemia, and evolving organ dysfunction. In children, bradycardia in the context of shock is particularly ominous and often reflects impending cardiovascular decompensation.
The lack of response to initial fluid resuscitation and calcium administration raises suspicion for non-septic etiologies. Toxic ingestion, especially beta-blockers or calcium channel blockers, must be strongly considered in any previously well child with sudden cardiovascular collapse and hyperglycemia. Cardiogenic shock from myocarditis is another critical alternative diagnosis.
Marked lactic acidosis indicates significant tissue hypoperfusion and correlates with illness severity. Concurrent acute kidney injury suggests early multi-organ involvement.
Management priorities include rapid airway stabilisation, early vasoactive support, bedside cardiac assessment, and broad diagnostic evaluation, including toxicology screening when the history is unclear. Serial reassessment of perfusion, lactate clearance, and end-organ function is essential in guiding therapy.
Conclusion & Learning Points:
· Bradycardia with hypotension in children represents pre-arrest physiology until proven otherwise.
· Refractory shock after adequate fluids should prompt evaluation for toxicologic and cardiogenic causes.
· Severe lactic acidosis reflects critical tissue hypoperfusion and high illness severity.
· Early escalation to vasoactive support and PICU care is crucial in undifferentiated pediatric shock.
· Maintain high suspicion for occult ingestion in previously healthy children with sudden collapse.
