When a child is unable to produce a stool sample in the ED, rectal swabs offer a valuable alternative, provided the microbiology lab accepts and processes such samples. This approach ensures testing begins immediately, avoiding delays inherent in outpatient collection. Early identification of STEC is crucial because it allows timely risk stratification and the opportunity for close follow-up or admission if needed.

Which Patients Require Blood Testing?

A common question in managing children with bloody diarrhea is whether bloodwork is necessary at the initial presentation. For the well-appearing, hemodynamically stable child with minimal bleeding, laboratory testing may offer little added value. However, several indications warrant baseline laboratory evaluation, including a complete blood count, creatinine, lactate dehydrogenase (LDH), and electrolytes. Bloodwork is indicated in children presenting with severe crampy abdominal pain and frequent small-volume bloody stools, as well as those with a history of recent travel, particularly if accompanied by fever. Close contact with a known STEC case, or residence in an area with a known outbreak, also increases pretest probability and supports baseline testing. Physical findings suggestive of microangiopathy, such as petechiae or jaundice, further justify early bloodwork.

Routine testing for parasites, particularly stool ova and parasites, is not recommended in patients with acute bloody diarrhea unless there is a relevant travel history, chronic symptoms, or other risk factors. Similarly, given the high carriage rates in asymptomatic infants and toddlers, testing for Clostridium difficile should not be routinely performed in young children without recent antibiotic exposure or hospitalization .⁵

Understanding STEC and Its Complications

Recognizing STEC is essential because of its potential progression to HUS. The pathophysiology of STEC hinges on its ability to produce Shiga toxin, a virulence factor capable of causing systemic endothelial injury. Once absorbed from the gut into the bloodstream, Shiga toxin binds to globotriaosylceramide (Gb3) receptors, which are most abundantly expressed in the renal glomeruli. The toxin’s cellular effects include inhibition of protein synthesis, endothelial damage, and microvascular thrombosis.² This pathophysiologic cascade leads to the classic triad of HUS: microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury.

Not all STEC strains carry the same risk of HUS. Some strains produce Shiga toxin 1 (Stx1), whereas others produce Stx2, or both. This distinction is clinically significant because Stx1-producing STEC carries a less than one percent risk for HUS, whereas Stx2-producing STEC is associated with a fifteen to twenty percent risk of HUS in children younger than five years. The serotype O157:H7, well known in medical literature, almost universally produces Stx2 and should be regarded as high risk.²