Priapism as a rare adverse effect of levomepromazine: A case report

Abstract

BACKGROUND

Priapism is a rare but potentially serious adverse effect of antipsychotic therapy, largely attributed to peripheral α1-adrenergic receptor blockade. Reports specifically involving levomepromazine remain scarce.

CASE SUMMARY

We report the case of a 45-year-old man with schizophrenia who presented with a persistent, painless penile erection lasting eight hours, 48 hours after initiation of levomepromazine at 100 mg/day. He had no previous history of priapism, known hematological disorder, trauma, recreational drug use, or exposure to other potentially causative medications. Corporal blood gas analysis revealed profound hypoxia and acidosis [pH 6.831, partial pressure of oxygen (PO₂) 8 mmHg, partial pressure of carbon dioxide (PCO₂) 84 mmHg], confirming severe ischemic priapism despite the absence of penile pain. Corporal aspiration and intracavernosal phenylephrine failed to achieve satisfactory detumescence. Persistent ischemia ultimately required surgical intervention with a proximal cavernospongiosal Quackels shunt, resulting in immediate and complete detumescence. Levomepromazine was discontinued, and the patient was discharged after an uneventful two-day hospitalization. A review of previously reported cases revealed only limited evidence of levomepromazine-associated priapism, with substantial heterogeneity in treatment exposure, predisposing factors, clinical presentation, and management.

CONCLUSION

Levomepromazine-associated ischemic priapism is a rare but potentially severe adverse drug reaction. This case demonstrates that profound cavernosal ischemia may develop rapidly after treatment initiation and may occur despite the absence of penile pain. Clinicians prescribing antipsychotics with substantial α1-adrenergic antagonistic activity should remain aware of this complication. Prompt recognition and guideline-directed management are essential to minimize irreversible cavernosal injury and subsequent erectile dysfunction.

Key Words: Priapism; Levomepromazine; Antipsychotics; Ischemia; Phenothiazines; Case report

Core Tip: Levomepromazine-associated priapism is rarely reported despite the drug’s substantial α1-adrenergic antagonistic activity. This case is notable for the development of severe ischemic priapism only 48 hours after initiation of levomepromazine monotherapy at a therapeutic dose, with complete absence of penile pain despite profound cavernosal hypoxia and acidosis. Failure of intracavernosal phenylephrine ultimately required surgical shunting. This observation emphasizes that absence of pain does not exclude severe ischemia and that persistent erections during antipsychotic therapy require prompt evaluation and treatment to prevent irreversible cavernosal injury.

INTRODUCTION

Priapism is a persistent penile erection lasting more than four hours in the absence of sexual stimulation. Ischemic priapism, the most common form, represents a urological emergency because prolonged cavernosal hypoxia and acidosis may lead to irreversible smooth-muscle damage and erectile dysfunction[1,2]. Several medications have been implicated in ischemic priapism, including antipsychotic agents, for which peripheral α1-adrenergic receptor antagonism is considered a major pharmacological mechanism through interference with physiological detumescence[3,4]. Levomepromazine (methotrimeprazine) is a phenothiazine antipsychotic with substantial α-adrenergic antagonistic activity; however, reports of priapism involving levomepromazine remain scarce[5,6]. Patients with mental illness may experience a substantial burden of physical comorbidity, emphasizing the importance of integrating physical-health surveillance into psychiatric care[7]. In schizophrenia-spectrum disorders, antipsychotic treatment strategy is also an important component of long-term management, and different formulations, including long-acting injectable therapies, may have distinct biological and clinical implications[8]. Awareness of uncommon but potentially serious treatment-related adverse events is therefore important when selecting and monitoring antipsychotic therapy. We report an unusual case of severe ischemic priapism occurring 48 hours after initiation of therapeutic-dose levomepromazine monotherapy in a 45-year-old man with schizophrenia. We also review previously reported cases to highlight the clinical presentation, potential mechanism, management, and implications of this rare adverse drug reaction.

CASE PRESENTATION

Chief complaints

A 45-year-old man with schizophrenia presented to the emergency department with a persistent penile erection lasting approximately 8 hours.

History of present illness

Levomepromazine had been initiated 48 hours before presentation at a total daily dose of 100 mg, administered as 25 mg four times daily for episodes of psychomotor agitation. The patient subsequently developed a persistent penile erection lasting approximately 8 hours before presentation. Despite the prolonged erection, he reported no penile pain. Levomepromazine was the only medication taken by the patient. He denied the use of phosphodiesterase type 5 inhibitors, intracavernosal vasoactive agents, recreational drugs, or any other medication potentially associated with priapism. There was no history of recent penile or perineal trauma.

History of past illness

The patient had a history of schizophrenia. He had never experienced priapism or prolonged spontaneous erections previously and had no known history of sickle cell disease or other hematological disorders.

Personal and family history

The patient had no known history of sickle cell disease or other hematological disorders. He denied recreational drug use and had no previous history of priapism or prolonged spontaneous erections. No relevant family history was reported.

Physical examination

On admission, the patient was conscious and hemodynamically and respiratory stable. Genital examination revealed a persistent, fully rigid penile erection. Despite the prolonged erection, the patient reported no penile pain. No clinical evidence of genital or perineal trauma was identified.

Laboratory examinations

Initial laboratory investigations showed a hemoglobin level of 12 g/dL, a white blood cell count of 17280/mm³ with neutrophilia (14090/mm³), and a platelet count of 293000/mm³. C-reactive protein was elevated at 44.84 mg/L. Hemoglobin electrophoresis showed no abnormality, the reticulocyte count was 120000/mm³, and peripheral blood smear examination revealed no morphological abnormality. No clinical infectious or inflammatory focus was identified. The leukocytosis, neutrophilia, and elevated C-reactive protein were therefore considered nonspecific findings in the context of the acute presentation. A urine toxicology screen was not performed. Renal function, serum electrolytes, and coagulation parameters showed no clinically significant abnormalities. Corporal blood gas analysis revealed profound hypoxemia, hypercapnia, and acidosis, with a pH of 6.831, a PO₂ of 8 mmHg, a PCO₂ of 84 mmHg, a bicarbonate concentration of 14 mmol/L, and an oxygen saturation of 3%.

Imaging examinations

Penile Doppler ultrasonography was not performed because the combination of complete penile rigidity and unequivocally ischemic cavernosal blood gas findings was considered sufficient to establish the diagnosis. The treating team elected to proceed promptly with therapeutic management rather than delay intervention for additional imaging.

FINAL DIAGNOSIS

The final diagnosis was acute ischemic (low-flow) priapism, most probably associated with levomepromazine therapy.

TREATMENT

Corporal aspiration was performed without saline irrigation, followed by intracavernosal phenylephrine. Phenylephrine was prepared at a concentration of 100 μg/mL and administered at a dose of 100-200 μg (1-2 mL) per injection. Three injections were administered at 5-10-minute intervals, with a predefined maximum cumulative dose of 1 mg. The patient underwent continuous cardiovascular monitoring throughout treatment, including heart rate, blood pressure, oxygen saturation, and electrocardiographic monitoring. Despite corporal aspiration and repeated intracavernosal phenylephrine administration, satisfactory detumescence was not achieved. Approximately one hour after initiation of first-line treatment, given the persistence of ischemic priapism, the patient was transferred to the operating room for surgical management. A proximal cavernospongiosal (Quackels) shunt was performed, resulting in immediate and complete detumescence. Levomepromazine was discontinued because of the suspected drug-induced origin of the priapism.

OUTCOME AND FOLLOW-UP

The postoperative course was uneventful, and the patient was discharged after two days of hospitalization. Following surgical treatment and discontinuation of levomepromazine, the patient was transferred to a psychiatric hospital for continued psychiatric care. The subsequent antipsychotic regimen could not be reliably retrieved from the available records. At an outpatient clinical follow-up visit several weeks after discharge, the patient was psychiatrically stable and no recurrence of priapism was reported. However, erectile function was not formally assessed using a validated instrument, such as the International Index of Erectile Function, or through a structured sexual-function evaluation. Consequently, no reliable conclusion can be drawn regarding long-term erectile function after the severe ischemic episode and proximal surgical shunting.

DISCUSSION

The present case describes severe ischemic priapism occurring shortly after the initiation of levomepromazine monotherapy and highlights several clinically relevant features of this uncommon adverse drug reaction. The close temporal relationship with drug initiation, absence of concomitant medications or recognized alternative precipitants, objective confirmation of profound cavernosal ischemia, and previously documented association between levomepromazine and priapism collectively support a drug-related event[5,6]. Beyond this temporal association, the case is particularly noteworthy for the absence of penile pain despite marked cavernosal hypoxia and acidosis, the occurrence of priapism after only 48 hours of exposure to a therapeutic dose, and failure of intracavernosal sympathomimetic therapy requiring surgical shunting. These characteristics provide an opportunity to reconsider levomepromazine-associated priapism within the broader pharmacological and clinical spectrum of antipsychotic-induced priapism. Ischemic priapism results from failure of cavernosal detumescence, leading to progressive venous stasis, hypoxia, hypercapnia, and acidosis within the corpora cavernosa. It constitutes a time-dependent urological emergency because persistent ischemia may ultimately result in structural injury to cavernosal smooth muscle, fibrosis, and permanent erectile dysfunction[1,2]. Current guidelines describe corporal blood gas findings compatible with ischemic priapism as a PO₂ typically < 30 mmHg, PCO₂ > 60 mmHg, and pH < 7.25[1,2]. In the present patient, a PO₂ of 8 mmHg, PCO₂ of 84 mmHg, pH of 6.831, and oxygen saturation of only 3% therefore represented unequivocal and particularly severe biochemical evidence of cavernosal ischemia. An unusual feature of our observation was the complete absence of penile pain. Pain is classically considered a prominent clinical manifestation of ischemic priapism and typically becomes more pronounced as ischemia progresses[1,2]. Nevertheless, pain is not required to establish the diagnosis, and reliance on this symptom may be misleading when other findings strongly support ischemia. In our patient, full penile rigidity combined with profoundly ischemic corporal blood gas values provided objective evidence of low-flow priapism despite the painless presentation. This discrepancy between symptoms and the biochemical severity of ischemia is clinically relevant because an atypically painless course may delay recognition and presentation. Accordingly, a persistent erection lasting more than four hours should prompt urgent assessment regardless of pain intensity, particularly in patients exposed to drugs known to interfere with penile detumescence[1,2]. The etiology of ischemic priapism is heterogeneous and includes hematological disorders, particularly sickle cell disease and leukemia, malignancies, neurological conditions, intracavernosal vasoactive agents, recreational substances, and numerous systemic medications[1,2]. Psychotropic medications constitute an important component of drug-associated priapism, with both first- and second-generation antipsychotics repeatedly implicated[3,9,10]. In their early comprehensive review, Compton and Miller identified priapism in association with numerous conventional and atypical antipsychotics, establishing this complication as a class-wide concern rather than an adverse effect restricted to a single compound[3]. Subsequently, Sood et al[9] reviewed 50 publications concerning antipsychotic-induced priapism and demonstrated considerable heterogeneity in treatment duration, drug exposure, and concomitant medications. More recently, Hwang et al[10] provided an updated review emphasizing that antipsychotic-associated priapism remains uncommon but potentially devastating because delayed recognition can result in irreversible erectile dysfunction. The most widely accepted mechanism linking antipsychotic therapy to priapism involves peripheral α1-adrenergic receptor antagonism[3,4,9,10]. Physiological detumescence requires sympathetic activation and α-adrenergic-mediated contraction of cavernosal smooth muscle. Pharmacological blockade of this pathway may reduce smooth-muscle contraction, favor persistent sinusoidal relaxation and cavernosal engorgement, impair venous outflow, and ultimately produce veno-occlusive stasis[3,9,10]. Importantly, this mechanism is supported not only by individual case reports but also by pharmacovigilance evidence. Andersohn et al[4] identified 426 reports of priapism in the United States Adverse Event Reporting System, including 144 attributed to antipsychotic medications. Antipsychotics with high α1-adrenergic receptor affinity exhibited a markedly stronger reporting signal [adjusted reporting odds ratio (ROR), 9.9; 95%CI: 7.9-12.4] than compounds with low or intermediate α1 affinity (adjusted ROR, 3.6; 95%CI: 2.4-5.2). Notably, when the analysis was restricted to cases resulting in medical intervention or disability, the safety signal remained evident only for antipsychotics with high α1 affinity, further supporting a relationship between α1-adrenergic receptor affinity and priapism[4]. This pharmacological mechanism is particularly relevant to levomepromazine. Levomepromazine, also known as methotrimeprazine, is a phenothiazine antipsychotic with substantial α-adrenergic receptor affinity. In experimental receptor-binding studies, Dahl and Hall demonstrated α-adrenergic receptor affinity not only for levomepromazine itself but also for its major metabolites, N-monodesmethyl levomepromazine and levomepromazine sulfoxide, suggesting that these metabolites may contribute to the autonomic effects of the parent drug[11]. This pharmacodynamic profile provides a biologically plausible basis for impaired penile detumescence. Importantly, antipsychotic-associated priapism does not appear to follow a simple linear dose-response relationship. Episodes have been reported shortly after treatment initiation, after dose escalation, during stable long-term treatment, and following the introduction of additional psychotropic agents[3,9,10]. Therapeutic dosing should therefore not be interpreted as protective against this complication.

Literature search strategy

A focused literature search was conducted to identify previously published cases of levomepromazine-associated priapism. PubMed/MEDLINE, Scopus, and Google Scholar were searched from database inception to September 2026 using combinations of the terms “levomepromazine”, “methotrimeprazine”, “priapism”, “ischemic priapism”, and “antipsychotic-induced priapism”. No language restriction was applied. Reference lists of relevant articles and reviews were also screened manually to identify additional reports. Reports were considered eligible when they described individual clinical cases of priapism occurring during treatment with levomepromazine, either alone or in combination with other psychotropic medications, and provided sufficient clinical information to characterize drug exposure and the priapism episode. Reports not involving levomepromazine, publications without individual patient-level clinical data, and reports providing insufficient information to characterize levomepromazine exposure or the priapism episode were excluded from the case comparison. Our literature search identified four previously published patients with priapism occurring during levomepromazine exposure in two original publications[5,6]. Direct verification of the original reports confirmed that two of the four patients described by Brichart et al[5] were receiving levomepromazine during the relevant priapism episodes, while Stefanini et al[6] reported two additional patients treated with levomepromazine. Given the small number of identified cases and the limited indexing of the 2025 report, these findings should not be interpreted as establishing that only four cases exist in the entire literature.

Levomepromazine-associated priapism in the published literature

Published evidence specifically involving levomepromazine remains limited compared with the broader literature on antipsychotic-associated priapism. Direct review of the original report by Brichart et al[5] identified two patients who were receiving levomepromazine during the relevant priapism episodes. One patient received levomepromazine 50 mg/day in combination with zuclopenthixol and experienced recurrent episodes of priapism, while another patient receiving levomepromazine 50 mg/day together with other medications presented with an approximately 12-hour episode of priapism[5].

More recently, Stefanini et al[6] described two patients who developed priapism during levomepromazine treatment. The first developed priapism after eight days of treatment and subsequently experienced recurrence, whereas the second developed priapism one day after the levomepromazine dose was increased from 75 mg/night to 100 mg/night[6]. These original reports therefore account for the four previously published patients identified by our literature search. Their clinical characteristics and relevant potential confounding factors are summarized in Table 1.

Table 1 Clinical characteristics, management, and outcomes of previously reported levomepromazine-associated priapism compared with the present case.

Study	Age/context	Levomepromazine exposure	Concomitant drugs	Previous priapism	Onset	Presentation	Management/outcome
Brichart et al[5], 2008	44/paranoid schizophrenia	50 mg/day	Zuclopenthixol	Yes (olanzapine, clozapine)	NR	Recurrent ischemic priapism; 2 episodes < 24 hours	Aspiration-irrigation + IC sympathomimetic; successful detumescence
Brichart et al[5], 2008	25/major depressive disorder	50 mg/day	Other medications1	NR	NR	Ischemic priapism, approximately 12 hours	Aspiration-irrigation + IC phenylephrine; successful detumescence; lost to follow-up
Stefanini et al[6], 2025	NR/psychiatric hospitalization	Dose NR	Thiamine + lorazepam	Yes2	8 days	Painful priapism > 4 hours; recurrence after 2 days	Drainage → surgical treatment; medication changed
Stefanini et al[6], 2025	NR/psychiatric hospitalization	75 → 100 mg/night	Recent benzodiazepine withdrawal	No reported history	1 day after dose increase	Priapism; duration NR	Conservative management; dose reduced to 75 mg; no recurrence reported
Present case	45/schizophrenia	100 mg/day (25 mg × 4)	None	No	48 hours	Painless ischemic priapism, 8 hours; pH 6.831, PO2 8, PCO₂ 84 mmHg	IC phenylephrine → Quackels shunt; immediate complete detumescence; discharge D2

¹Other concomitant medications were reported, but were not considered priapism-inducing by the authors.

²Previous episode was disclosed after recurrence.

IC: Intracavernosal; NR: Not reported; PO₂: Partial pressure of oxygen; PCO₂: Partial pressure of carbon dioxide.

When the available reports are considered together, several features distinguish the present observation. First, levomepromazine was administered as monotherapy, substantially reducing the pharmacological confounding that complicates causal attribution in previously reported cases involving concomitant or sequential psychotropic exposure[5,6,9,10]. Second, priapism developed only 48 hours after initiation of levomepromazine at a therapeutic dose of 100 mg/day, supporting the observation that antipsychotic-associated priapism may occur early during treatment and does not follow a predictable dose-response relationship[6,9,10]. Third, our patient had no previous history of priapism or prolonged spontaneous erections and no recognized hematological, traumatic, recreational, or pharmacological precipitant. This is particularly relevant because a history of prolonged or priapic erections has been identified as an important predisposing factor for subsequent antipsychotic-associated priapism[10]. Finally, the entirely painless presentation despite profound cavernosal hypoxia and acidosis, followed by failure of intracavernosal therapy and the need for surgical decompression, represents an unusual combination of clinical features. Rather than suggesting that any single characteristic is unprecedented, their coexistence distinguishes the present observation within the limited literature involving levomepromazine. Assessment of drug causality warrants careful consideration because temporal association alone cannot establish that levomepromazine was responsible for the event. In the present case, several elements support levomepromazine as the most plausible precipitating factor: The close temporal relationship with treatment initiation, biological plausibility based on α1-adrenergic antagonism, previous reports involving levomepromazine, absence of concomitant medications, and lack of an identified alternative precipitant[4-6,11]. Causality was further assessed using the Naranjo Adverse Drug Reaction Probability Scale[12]. The item-by-item assessment was as follows: Previous conclusive reports of the reaction, yes (+1)[5,6]; occurrence of the adverse event after administration of levomepromazine, yes (+2); improvement specifically attributable to drug discontinuation, unknown (0), because complete detumescence occurred immediately after surgical shunting and therefore could not be attributed to levomepromazine withdrawal alone; recurrence after readministration, unknown (0), as rechallenge was not performed and was not considered clinically appropriate after a severe ischemic event; presence of alternative causes, unknown (0), because no hematological, traumatic, or concomitant pharmacological cause was identified, but urine toxicology screening was not performed and alternative causes could therefore not be completely excluded; reaction after placebo administration, unknown (0); detection of the drug at toxic concentrations, unknown (0), as plasma concentrations were not measured; evidence of a dose-response relationship, unknown (0); previous similar reaction to the same or a related drug, no (0); and confirmation by objective evidence, yes (+1), based on complete penile rigidity and markedly ischemic cavernosal blood gas findings (pH 6.831, PO₂ 8 mmHg, and PCO₂ 84 mmHg).

The resulting Naranjo score was 4, corresponding to a possible adverse drug reaction[12]. Nevertheless, considering the close temporal relationship with levomepromazine initiation, the absence of concomitant medications, the biological plausibility related to α1-adrenergic antagonism, and previous published reports, levomepromazine was considered the most plausible identified precipitating factor. This assessment should be interpreted as supportive rather than definitive evidence of causality. The therapeutic course of the present patient also warrants particular discussion. Management of acute ischemic priapism is directed toward rapid restoration of cavernosal circulation before irreversible smooth-muscle injury develops. Contemporary European Association of Urology (EAU) and American Urological Association/Sexual Medicine Society of North America (AUA/SMSNA) recommendations support corporal aspiration, with or without saline irrigation, combined with intracavernosal phenylephrine as first-line therapy before operative intervention[1,2]. Phenylephrine is preferred because its predominantly α1-adrenergic activity promotes cavernosal smooth-muscle contraction while limiting β-adrenergic cardiovascular effects, although blood pressure and heart rate monitoring remain necessary during administration[1,2]. In the present case, intracavernosal phenylephrine failed to achieve satisfactory detumescence, necessitating surgical intervention. Failure of an α1-adrenergic agonist in priapism potentially precipitated by α1-adrenergic antagonism may appear paradoxical. However, the pharmacological mechanism triggering priapism should be distinguished from the pathophysiological processes maintaining an established ischemic compartment. Progressive cavernosal hypoxia and acidosis may impair smooth-muscle responsiveness to sympathomimetic stimulation, particularly during prolonged ischemia[1,2]. Although our patient presented after only eight hours, the markedly abnormal corporal blood gas values documented substantial local ischemia. Whether this biochemical severity contributed to the incomplete response to phenylephrine cannot be established, but it may provide a physiologically plausible explanation. After failure of appropriate medical treatment, surgical decompression becomes necessary. Contemporary guidelines generally favor distal corporoglanular shunting, with or without tunneling, for persistent acute ischemic priapism following unsuccessful medical treatment; the 2026 EAU guideline also recognizes penoscrotal decompression as a potential alternative first-line surgical option, although supporting evidence remains limited[1,2]. In the present case, a proximal cavernospongiosal Quackels shunt was performed, establishing communication between the corpus cavernosum and corpus spongiosum and resulting in immediate and complete detumescence. The decision to proceed directly to a proximal Quackels shunt after failure of aspiration and intracavernosal phenylephrine was based on the treating urologist’s experience with this technique and local surgical practice. No distal shunt was attempted before the proximal procedure. The use of a proximal shunt warrants specific consideration because its role in contemporary treatment algorithms has substantially diminished. The AUA/SMSNA guideline considers proximal shunting a largely historical approach and emphasizes that evidence is insufficient to quantify its additional benefit after failure of distal shunting[2]. Accordingly, the successful outcome observed in our patient should not be interpreted as supporting proximal shunting over contemporary distal approaches, but rather as documenting an effective rescue procedure performed within the specific clinical and surgical context of this case. The duration of ischemia is a major determinant of subsequent erectile function. Acute ischemic priapism is a progressive process in which increasing cavernosal hypoxia and acidosis lead to smooth-muscle injury, necrosis, fibrosis, and ultimately erectile dysfunction[1,2]. Although the precise duration beyond which cavernosal injury becomes irreversible cannot be defined by a single threshold, the AUA/SMSNA guideline emphasizes that the likelihood of erectile-function recovery is low when acute ischemic priapism persists beyond 36 hours[2]. Importantly, structural changes may begin substantially earlier, and the risk of irreversible injury increases progressively with the duration of ischemia[2]. Although our patient presented after only eight hours, the profound cavernosal acidosis demonstrates that substantial biochemical ischemia had already developed. This finding reinforces the need for immediate treatment of ischemic priapism rather than relying on symptom intensity or duration alone to estimate its severity. From a psychiatric perspective, recognition of antipsychotic-associated priapism has implications beyond acute urological management. Because delayed treatment of ischemic priapism increases the risk of irreversible cavernosal injury, patient education represents an important preventive strategy[1,2,10]. Patients receiving antipsychotics, particularly agents with substantial α1-adrenergic antagonistic activity, should be informed that a persistent erection lasting more than four hours requires urgent medical evaluation. Following an episode of suspected antipsychotic-induced priapism, the implicated medication should be reassessed in collaboration with the treating psychiatrist. When continued antipsychotic therapy is required, selection of an alternative agent with lower peripheral α1-adrenergic affinity may be considered, while taking into account previous therapeutic response, psychiatric efficacy, and the overall adverse-effect profile[4,5,10]. The available literature also highlights substantial gaps in the evidence base. Despite the widespread use of antipsychotic medications, knowledge of antipsychotic-associated priapism is derived predominantly from case reports, small case series, narrative reviews, and spontaneous pharmacovigilance data rather than prospective studies[3-6,9,10]. Consequently, the true incidence of this adverse event, the existence of a dose-response relationship, individual susceptibility factors, and the risk of recurrence after modification of antipsychotic therapy remain incompletely characterized. The observation that priapism develops in only a small proportion of patients exposed to drugs with α1-adrenergic blocking properties further suggests that additional patient-specific or pharmacological factors may influence susceptibility[10]. These limitations are even more pronounced for levomepromazine, for which the published clinical evidence remains particularly sparse[5,6]. In this context, carefully documented cases remain clinically informative, particularly when drug exposure is clearly characterized, competing etiologies are systematically assessed, and the temporal relationship between treatment exposure and the adverse event is well established. Several limitations of the present report should be acknowledged. Penile duplex Doppler ultrasonography was not performed; however, the combination of a fully rigid erection and unequivocally ischemic corporal blood gas values provided objective confirmation of acute ischemic priapism. Current guidelines recommend corporal blood gas analysis at initial presentation, whereas penile duplex Doppler ultrasonography may be used when differentiation between ischemic and non-ischemic priapism remains uncertain[1,2]. Accordingly, the absence of Doppler ultrasonography did not preclude diagnostic classification in the present case. Long-term erectile function was not systematically assessed using a validated instrument or structured sexual-function evaluation. This represents an important limitation, particularly given the severity of cavernosal ischemia and the need for proximal surgical shunting, and prevents any reliable conclusion regarding the long-term functional consequences of the ischemic episode and surgical intervention.

Furthermore, although the temporal relationship, pharmacological plausibility, absence of major alternative triggers, previous reports involving levomepromazine, and Naranjo assessment support a probable drug-related event, definitive causality cannot be established from a single observation. Finally, the surgical sequence differed from that favored by contemporary guidelines, particularly with regard to the use of a proximal Quackels shunt rather than a distal shunting approach; this should be considered when extrapolating the therapeutic course of this patient to current practice[1,2]. Taken together, the present observation should be interpreted within the broader pharmacological spectrum of antipsychotic-associated priapism rather than as an isolated drug-specific phenomenon. The temporal relationship with levomepromazine initiation, absence of concomitant pharmacological triggers, established α1-adrenergic mechanism, and consistency with previously published cases collectively support levomepromazine as the most plausible precipitating factor. At the same time, the painless presentation despite profound cavernosal ischemia illustrates the potential discordance between clinical symptoms and biochemical severity. This case therefore adds to the limited levomepromazine-specific literature by combining a well-characterized drug exposure with objective documentation of severe ischemia and a clearly described therapeutic course.

CONCLUSION

Levomepromazine-associated ischemic priapism is a rare but potentially severe adverse drug reaction. This case demonstrates that profound cavernosal ischemia may develop rapidly after treatment initiation and may occur despite the absence of penile pain. Clinicians prescribing antipsychotics with substantial α1-adrenergic antagonistic activity should remain aware of this complication and counsel patients that any persistent erection lasting more than four hours requires urgent medical evaluation. Prompt recognition and guideline-directed management are essential to minimize irreversible cavernosal injury and subsequent erectile dysfunction.