To the Editor: The recent article by Shaftel et al1 describes hospital readmission rates after surgical evacuation of nontraumatic subdural hematomas, and we would like to contribute by detailing other factors that may contribute to recurrence of acute nontraumatic subdural hematomas (aSDHs). Patients with aSDHs have a significantly higher morbidity and mortality rate than the general population at 90 days.2 The etiology and pathophysiology of aSDHs of nontraumatic origin remains uncertain but has been related to some coagulation defects, iatrogenic, arteriovenous malformations, and intravenous drug abuse; however, there are other associated factors that should be considered in the development of aSDHs.2-4 The aim of this letter to the editor was to mention other important causes associated with the development and recurrence of aSDHs despite surgical management. Food may contribute to the recurrence of aSDHs after surgical management, mainly herbal products, whose anticoagulant effects have not been widely described. Among the foods that may have some anticoagulant effect, we find garlic Allium Sativum, which through its effect on platelet fibrinogen receptors produces antiaggregation and anticoagulation5; in the same sense, green tea and some microalgae such as Penicillus capitatus, Udotea flabellum (Chlorophyta), and Grateloupia doryph were shown to prolong coagulation times.6 The combination of some herbal products with anticoagulants such as warfarin can potentiate the anticoagulant effect of these drugs and increase the risk of aSDHs. These include Ginkgo biloba, Panax ginseng, ginger, papaya, cinchona, willow, and red clover. Thus, the anamnesis is of great value in determining factors associated with aSDH recurrence.7 Other important factors such as certain cancers and genetic diseases have been associated with the development and recurrence of aSDHs. Doherty et al8 described the first case of aSDH associated with May-Hegglin disease in a 61-year-old male patient with a history of asthma, iron deficiency anemia, and May-Hegglin anomaly who consulted for a one week of headache. May-Hegglin disease is a genetic anomaly produced by mutation of the MYH9 gene that affects the number and function of platelets. This anomaly may be asymptomatic or may present with multiple hemorrhagic symptoms such as epistaxis, gingivorrhage, and amenorrhea.8 As for the development of aSDH due to neoplasms, there are few cases reported in the literature; however, they represent a high burden of morbidity and mortality. Among the neoplasms with the capacity to generate aSDHs are brain metastases of grade IV prostatic adenocarcinoma, which rarely metastasize to the central nervous system since the affinity of this type of tumor is for the bone; however, it is believed that because of the proximity of the bone table with the dura mater, these tumors can migrate and generate this type of lesions.9 Similarly, meningiomas have been described as a cause of aSDHs; so far, a little more than 40 cases have been described according to Mezzacappa et al10; however, the pathophysiology of how meningiomas produce aSDHs is uncertain. It is estimated that meningiomas can produce several growth factors such as vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1 (HIF-1), and epidermal growth factor (EGF) which produce increased angiogenesis and generation of vessels with an abnormal nature that make them susceptible to rupture and subsequent bleeding.10 On the other hand, it has been described that aneurysm rupture can cause aSDHs; however, its prevalence is unknown. Aneurysm rupture is generally associated with the development of subarachnoid hemorrhage, but given the proximity to the subdural space, bleeding can occur in this space. So far there are few cases reported in the literature of the development of aSDHs associated with rupture of an aneurysm; however, its presence should not be ruled out.2 High altitudes have been related to the development of aSDHs mainly from 2400 m above sea level because the body undergoes a series of physiological adaptations to maintain tissue oxygenation, increasing venous and even arterial pressure. Thus, it has been described that the cerebral vasculature under stressful conditions may increase venous pressure, thus failing the intrinsic regulation mechanisms of the brain causing rupture of the arterial or venous beds; for this reason, it is recommended that altitude changes be progressive and not sudden to avoid such complications.11 Finally, a less frequent cause of which not much is known is extrahepatic biliary atresia (EHBA), which can cause hemorrhage secondary to vitamin K deficiency due to the malabsorption of fats. It is estimated that 1 in 10 000 live births may suffer it, in the case of aSDH produced by EHBA. Miyao et al12 describe the case of a 2-month-old female patient who at 38 days of life developed epistaxis and hematochezia of unclear cause. The bleeding continued until after 2 months of life when she developed deterioration of his respiratory and circulatory function, causing his death. The autopsy confirmed the presence of EHBA and aSDH related to vitamin K deficiency because of fat malabsorption by EHBA.12 In conclusion, acute nontraumatic subdural hematomas represent a high burden of morbidity and mortality; therefore, identifying risk factors through anamnesis allows us to favorably affect the outcome of the disease and modify previously identified behaviors that are predisposing factors for the development of aSDHs.