In a startling case reported in 2007, surgeons at St. Paul’s Hospital in Vancouver were shocked to discover dark green blood circulating through the arteries of a 42-year-old Canadian man during surgery.
The unusual coloration immediately raised concerns, as human blood is typically bright red due to oxygenated hemoglobin. According to a case report in The Lancet, the patient’s blood appeared dark greenish-black, causing immediate confusion among the medical team.
This rare condition, known as sulfhemoglobinemia, occurs when sulfur atoms bind to hemoglobin molecules, altering their structure and color.
Normally, sulfhemoglobin constitutes up to 2% of total hemoglobin in healthy individuals, but concentrations significantly higher than this are pathological and often linked to adverse drug reactions. The 42-year-old patient’s case was attributed to an “extraordinarily high concentration of sulfhemoglobin,” which gave his blood a distinctly green hue during the procedure.
Medical literature identifies specific medications as common triggers for sulfhemoglobinemia. Drugs such as sulphonamides, sulfasalazine, and sumatriptan (used for migraines) have been documented to induce this condition when taken in excessive amounts or in susceptible individuals.
A 2019 study further highlighted that excessive exposure to sulfur-containing compounds—whether through pharmaceuticals or environmental sources—can lead to this rare but alarming blood discoloration.
While the green color itself is not immediately life-threatening, it signals an underlying issue requiring prompt medical attention. In most cases, discontinuing the causative medication allows the body to gradually replace the affected hemoglobin with healthy red blood cells over several weeks. However, in severe or prolonged cases, the condition may persist until new blood cells are fully generated.
Despite its rarity, sulfhemoglobinemia has been documented in fewer than 100 cases worldwide since its first description in the early 20th century. Medical professionals emphasize the importance of recognizing this condition to avoid unnecessary interventions, such as blood transfusions, which are typically ineffective for sulfhemoglobinemia. Instead, identifying and eliminating the trigger—often a specific medication—is the cornerstone of treatment.
Though the 2007 Canadian case remains one of the most widely cited examples, recent research continues to refine our understanding of sulfhemoglobinemia’s mechanisms and risk factors. For now, it serves as a reminder of the body’s surprising complexities—and the need for vigilance in diagnosing even the most unusual clinical presentations.
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