A nitrous oxide abuser presenting with cerebral venous thrombosis: A case report

Abstract

The present study describes the case of a 25-year-old male patient who presented to the emergency department with severe headache and vertigo lasting for 3 days. The patient did not have a recent history of trauma. He was vaccinated with a second dose of the AstraZeneca COVID-19 vaccine ~1 month prior, and he suffered from a vitamin B12 deficiency due to nitrous oxide abuse. Upon an examination of his vital signs, he was found to have a body temperature of 36.4˚C, a pulse rate of 64 beats per minute, a respiratory rate of 18 breaths per minute and a blood pressure of 119/68 mmHg. A neurological examination only revealed left homonymous upper quadrantanopia. The serum platelet count of the patient was 361x1,000/µl and he had elevated D-dimer levels (0.98 µg/ml). A provisional clinical diagnosis of acute cerebrovascular accident was made. A computed tomography scan of the head revealed an abnormal hyperattenuation in the straight sinus and bilateral transverse sinuses. A diagnosis of cerebral sinovenous thrombosis (CSVT) was made following a consultation with a neurologist. The patient was treated with enoxaparin at 6,000 IU, levetiracetam at 1,000 mg and mannitol at 100 ml via an intravenous drip. After admission, magnetic resonance venography revealed the absence of flow in the straight sinus and bilateral transverse sinuses. A thrombophilic investigation revealed a plasma homocysteine level of 59.03 µmol/l (upper normal limit, 15.39 µmol/l), a vitamin B12 level of <148 (lower normal limit, 187 pg/ml). CSVT secondary to homocystinemia was diagnosed. The treatment included anticoagulation and vitamin B12 supplementation. The patient was administered vitamin B12 at 500 mcg twice per day, pyridoxine at 50 mg per day, folic acid at 5 mg two times per day and edoxaban at 60 mg per day. After 7 days of treatment, his headache and quadrantanopia were improved, and the patient was discharged.

Nitrous Oxide Inhalant Abuse: Preliminary Results from a Cross-Sectional Study on Knowledge, Attitudes, and Practices of Italian Physicians (2023)

“…These estimates are consistent with the potential severity and complicated management of incident cases due to a series of factors that could be underscored by professionals unfamiliar with N 2 O abuse [1,12,20,[64][65][66]. For one, even though the large majority of N 2 O users does not reasonably develop any significant complication, a reduced but noticeable proportion of cases can be complicated by hypercoagulability associated with secondary hyperhomocysteinemia [1,20,[64][65][66][67][68][69], leading to deep vein thrombosis and potentially life-threatening conditions such as cerebral venous sinus thrombosis [13,66,[70][71][72] and pulmonary embolism [64,[67][68][69]. Second, the available data suggest that a substantial share of incident cases eventually fails to cope with rehabilitation for a variety of different causes, including the lack of support from familiars of social services or a pre-existing, complicated background of multiple substance abuse [14,23,[73][74][75][76].…”

Nitrous Oxide-Induced Cerebral Venous Thrombosis: A Case Report, Potential Mechanisms, and Literature Review

“…This prevents the conversion of homocysteine to methionine, leading to hyperhomocysteinemia (Figure 4) [6]. Nitrous oxide abuse has been reported to be associated with thrombotic events, including ischemic stroke, acute coronary syndrome, and venous thromboembolism [9][10][11][12][13][14]. To our knowledge, there are six previous case reports of suspected nitrous oxide-induced cerebral venous thrombosis in which baseline serum homocysteine and cobalamin levels were presented (Table 2), and only two patients had cobalamin deficiency [10,11].…”

“…Nitrous oxide abuse has been reported to be associated with thrombotic events, including ischemic stroke, acute coronary syndrome, and venous thromboembolism [9][10][11][12][13][14]. To our knowledge, there are six previous case reports of suspected nitrous oxide-induced cerebral venous thrombosis in which baseline serum homocysteine and cobalamin levels were presented (Table 2), and only two patients had cobalamin deficiency [10,11]. However, it should be noted that patients with serum cobalamin levels within the gray area of 170-340 pg/mL could have cobalamin deficiency and should be tested for plasma methylmalonic acid or homocysteine levels, which are more sensitive [15].…”