Case report: Chlorpromazine and deep venous thrombosis

Abstract

Purpose Since the development of antipsychotic drugs in the 1950s, a variety of studies and case reports have been published that suggest an association between exposure to typical antipsychotics and venous thromboembolisms (VTE). Therefore, when starting treatment with antipsychotics, especially low-potency typical antipsychotics and clozapine, health-care providers must account for the patient’s existing VTE risk factors. Design/methodology/approach In this case report, the authors describe the development of a pulmonary embolism associated with use of chlorpromazine in the treatment of an acute manic episode in a 51-year-old female patient with bipolar disorder type 1. Findings The patient was brought to the emergency room by the police on a legal hold for bizarre behaviors at a bus stop, which included incessantly yelling at bystanders. The patient was found to have disorganized thoughts, poor sleep, rapid speech, labile mood, distractibility, auditory hallucinations and grandiose delusions. During the course of her stay, the patient received extensive IM chlorpromazine for extreme agitation, in addition to chlorpromazine 200 mg IM Q8H, which was later decreased to chlorpromazine 100 mg chlorpromazine IM/PO Q8H. On day 4 of the treatment, the patient experienced difficulty breathing, hypoxia and tachycardia and was found to have bilateral expiratory wheezes. CT angiography showed sub-segmental pulmonary embolus and the patient was transferred to MICU service. The patient was then intubated and started on heparin by the medical team. Over the course of the next day, her respiratory distress resolved and the patient was extubated. Originality/value It is possible that chlorpromazine may indeed increase VTEs, and there are various physiological postulations regarding the mechanism of action. However, multiple confounding variables existed in the authors’ report, including venous stasis and the use of restraints, tobacco and valproic acid. Each of these variables has been shown to increase VTE occurrence. Further controlled studies are necessary to identify the true relationship between antipsychotics and VTEs.

Pulmonary Embolism during a Retrial of Low-dose Clozapine

“…Possible underlying mechanisms include platelet dysfunction [ 2 , 3 , 13 ], immunomodulatory and proinflam-matory effects, and metabolic syndrome associated with antipsychotic drugs [ 14 ]. Because of clozapine’s strong affinity for 5HT 2a receptors (at least 10 times stronger than for D2 receptors), 5HT 2a -induced platelet aggregation leading to thromboembolism has also been hypothesized [ 6 , 15 ]. In addition, clozapine often leads to sedation as a side effect, which may contribute to immobility and venous stasis [ 10 ].…”

COVID-19 and Antipsychotic Therapy: Unraveling the Thrombosis Risk

“…Additionally, numerous case reports and studies have shown an increased risk of VTE with antipsychotic use. For example, a 51-year-old female patient with bipolar disorder developed a pulmonary embolism following chlorpromazine treatment, while instances of central retinal vein occlusion have been observed in patients administered olanzapine and risperidone [36,37]. Furthermore, a case of a 39-year-old woman with chronic schizophrenia who developed acute right hemiparesis and visual field loss during a switch to clozapine therapy has been reported, leading to a provisional diagnosis of ischemic stroke [38,39].…”