Methamphetamine, an amphetamine derivative, is a CNS stimulant called variously as a “crystal”, “meth”, or “speed” and can be injected, smoked, snorted, or taken orally [14].
Methamphetamine was first synthesized in 1887, and its first medical use dates back to the early 1930 s to treat tiredness in fatigued army troops. It was widely used to treat narcolepsy, attention deficit hyperactivity disorder, depression, alcoholism, and to decrease appetite for weight loss [2, 14].
The structural similarity of methamphetamines to catecholamine transporters changes the endogenous function of these transporters, resulting in more release and decreased reuptake of catecholamines in the CNS. It also inhibits monoamine oxidase function, which results in the build-up of more catecholamines in the synapses [15].
Immediate effects of methamphetamine use include euphoric effects, arousal, cognitive and memory changes, increases in blood pressure, heart rate, body temperature, pain perception changes, and loss of appetite [15, 16].
The chronic use of methamphetamine results in changes in behavior and cognition, memory deficit, psychosis, violent behaviors, severe anxiety and depression, immune system issues, liver and kidney damage, respiratory issues, cardiovascular impairment as infarction, cardiomyopathy, and arrhythmias, gastrointestinal issues as a result of vasoconstriction and bowel ischemia, and immune system issues. Later complications are due to the prolonged and severe vasospasm after methamphetamine consumption [15,16,17].
Different studies show the impact of methamphetamines on the narrowing of blood vessels because of vasospasm, which leads to ischemic stroke due to cerebral vessel narrowing, ischemic colitis, and bowel ischemia due to mesenteric vasospasm, myocardial infarction, and extremities vasospasm [7, 18,19,20,21]. methamphetamine increases synaptic norepinephrine, leading to intense α-adrenergic–mediated vasoconstriction and prolonged vasospasm, which is the most plausible mechanism in our case [16].
Our case is unique in demonstrating simultaneous segmental infarction of the spleen and left kidney after methamphetamine use, without evidence of thrombosis or atherosclerotic changes in the imaging studies. While isolated stimulant-related renal infarction has been described (e.g., Khokhar et al., 2022) [22], to our knowledge this is the first report of concurrent renal and splenic infarction attributable to methamphetamine use.
As in most stimulant-associated vascular events, the diagnosis of methamphetamine-induced infarction was reached by exclusion. During hospitalization, given the differential consideration of septic embolism and embolic infarcts secondary to endocarditis, transthoracic and transesophageal echocardiography demonstrated endocarditis of the aortic and pulmonary valves with an aortopulmonary fistula. However, at admission the patient was afebrile, without evidence of infection, and no vegetations or embolic sources were identified at the time of splenic and renal infarction. In addition, there were no systemic inflammatory signs, abnormal serological markers, or vessel wall changes suggestive of vasculitis. Taken together with the CT findings of segmental organ infarction in the absence of thrombosis or atherosclerosis in major abdominal vessels, These findings, combined with the patient’s strong history of daily methamphetamine use, made vasospasm the most plausible explanation. Although a full hypercoagulable workup was not performed, no clinical or laboratory evidence supported an underlying thrombophilia, which we acknowledge as a limitation.
Heparin was initiated based on the patient’s initial clinical presentation and the suspicion of embolic or thrombotic events as a differential diagnosis, and conservative management with anticoagulation was therefore considered appropriate. The patient’s abdominal pain improved after heparin initiation, though a causal link cannot be confirmed, as spontaneous resolution of vasospasm may also be possible. In similar cases, earlier interventions targeting arterial vasospasm, such as vasodilators, could theoretically be beneficial, although evidence for their use in methamphetamine-associated organ infarction is limited.
Despite improvement in abdominal pain, the patient later developed infective endocarditis of the aortic and pulmonary valves complicated by aortopulmonary fistula and tamponade, requiring surgery and hemodialysis. He ultimately died of bradycardia and cardiac arrest during dialysis. Although the fatal outcome was primarily due to infective endocarditis and its complications, methamphetamine-associated vasospasm and cardiovascular strain could not be entirely excluded as potential contributors to the adverse outcome. Other limitations of this report include its single-case design, lack of autopsy to confirm the duration of vasospasm, lack of advanced investigations (such thrombophilia panels, or detailed inflammatory markers), and potential confounders such as prior cardiac disease and smoking, which may have contributed to the outcome. This highlights the multifactorial nature of morbidity and mortality in such patients. Future directions may include the potential role of angiography in confirming vasospasm, as well as routine vascular screening and earlier interventions, such as vasodilators, in methamphetamine users to identify and prevent early complications.
This case highlights that methamphetamine can cause multi-organ ischemia through vasospasm, and that severe outcomes, including death, may occur. Clinicians should therefore maintain a high index of suspicion and consider early vascular imaging in methamphetamine users presenting with unexplained abdominal pain or organ dysfunction. Given the extreme rarity of simultaneous splenic and renal infarction, early recognition and awareness are essential for improving outcomes.