Severe immune thrombocytopenia induced by vancomycin in a critically ill patient: a case report and literature review

Abstract

Background

Vancomycin-induced immune thrombocytopenia (VIIT) is a rare but potentially life-threatening adverse drug reaction characterized by profound platelet destruction. Diagnosis is challenging in critically ill patients, and optimal management beyond drug cessation remains poorly defined.

Case summary

A 54-year-old female admitted to the ICU for severe community-acquired pneumonia developed profound, refractory thrombocytopenia 12 days after the initiation of vancomycin. Blood, sputum, and pleural fluid cultures were negative. Vancomycin was continued due to the severity of the pneumonia, a fluctuating clinical course with recurrent fevers and progressive infiltrates, a complicated parapneumonic effusion requiring drainage and surgical consultation, and infectious disease service recommendations. The patient presented with gross hematuria and a rapid decline in platelet count to 6,000/µL. Following the exclusion of alternative etiologies—including sepsis-associated coagulopathy and heparin-induced thrombocytopenia (HIT)—vancomycin was discontinued. The patient required intravenous immunoglobulin (IVIG) and corticosteroids in addition to drug cessation to achieve platelet recovery.

Conclusion

This case underscores the critical importance of early recognition of VIIT. Our literature review reveals that while discontinuation of the offending agent is the cornerstone of therapy, severe cases (platelets < 20,000/µL) often require adjunctive immunomodulatory treatment. VIIT should remain a primary differential diagnosis in patients presenting with unexplained thrombocytopenia during vancomycin therapy.

Graphical Abstract

Introduction

Thrombocytopenia in hospitalized patients is a multifactorial condition often driven by sepsis, organ dysfunction, or disseminated intravascular coagulation (DIC). However, drug-induced mechanisms remain a critical etiology to consider. Drug-induced immune thrombocytopenia (DITP) typically manifests as a sudden, severe reduction in platelet count—often falling below 20,000/µL—mediated by drug-dependent antibodies that result in rapid platelet destruction [1, 2].

Vancomycin is extensively employed in the management of serious Gram-positive infections, particularly methicillin-resistant Staphylococcus aureus (MRSA) [3]. While generally considered safe, evidence suggests vancomycin can elicit severe immune-mediated thrombocytopenia via antibodies targeting platelet glycoproteins IIb/IIIa or Ib/IX [4].

Differentiation of VIIT from other causes, such as DIC or heparin-induced thrombocytopenia (HIT), is challenging in the critically ill. Herein, we report a case of a 54-year-old female who developed severe refractory thrombocytopenia and hematuria after 12 days of vancomycin therapy. Furthermore, we provide a systematic review of 18 cases published between 2000 and 2025 to elucidate the clinical characteristics, risk factors, and optimal management strategies for this rare adverse event.

Case presentation

A 54-year-old woman presented to the emergency department with progressive dyspnea, respiratory distress, and fever. Symptoms began 15 days prior with flu-like manifestations. She reported a history of influenza-like symptoms that had begun 15 days prior in her hometown in Khorasan province. During the interval before presenting to our center, she had taken a 4–5 day course of oral azithromycin without significant improvement. Her past medical history was significant for hypertension, managed with losartan (25 mg twice daily) and atorvastatin (40 mg daily). She had no history of prior respiratory disease, smoking, or recent travel.

Physical examination

Upon admission to the ICU, the patient was alert and oriented. Vital signs revealed a temperature of 38.8 °C, tachycardia (115 beats/min), blood pressure of 135/70 mmHg, tachypnea (30 breaths/min), and hypoxia (SpO2 86% on room air) necessitating use of accessory muscles. Auscultation revealed coarse bibasilar crackles. The remainder of the physical examination was unremarkable.

Initial investigations and management

Chest CT angiography demonstrated bilateral multilobar consolidations and a right-sided pleural effusion, with no evidence of pulmonary embolism (Fig. 1). Laboratory evaluation showed marked inflammation with a C-reactive protein (CRP) of 190 mg/L, procalcitonin (PCT) of 2 ng/mL, and leukocytosis (WBC 30,000/µL). Hemoglobin was 13.7 g/dL, and the platelet count was normal at 236,000/µL.

Fig. 1.

Axial contrast-enhanced chest CT. Axial contrast-enhanced CT scan of the chest (lung window) demonstrating extensive bilateral multilobar consolidations, most prominent in the posterior segments. There is a notable right-sided pleural effusion with associated compressive atelectasis of the adjacent lung parenchyma. No filling defects were identified within the pulmonary arteries to suggest pulmonary embolism

The patient was diagnosed with bacterial superinfection secondary to viral pneumonia. Treatment was initiated with supplemental oxygen, empirical antibiotics (meropenem (1 g q8h) and vancomycin (1 g IV q12h), and venous thromboembolism (VTE) prophylaxis (enoxaparin 40 mg SC daily). Blood and sputum cultures were obtained prior to antibiotic administration but ultimately yielded no bacterial growth.

Vancomycin was continued as part of the empirical regimen due to several factors: (1) the severity of the pneumonia requiring ICU admission; (2) the patient’s complex clinical course, characterized by initial transient improvement followed by recurrent fevers and progressive pulmonary infiltrates on serial chest imaging; (3) the presence of a complicated parapneumonic effusion (pleural LDH > 6000 U/L) requiring drainage; and (4) consultation with the infectious disease service, who recommended continued broad-spectrum coverage given the diagnostic uncertainty and clinical instability. Thoracentesis confirmed a parapneumonic effusion (Table 1). A pigtail catheter was inserted for drainage and removed three days later following complete evacuation.

Table 1.

Pleural fluid analysis

Parameter	Result
Color / Appearance	Yellow / Turbid
Glucose	86 mg/dL
Protein	3.7 g/dL
LDH	6406 U/L
WBC	55,600 cells/mm³ (82% PMN, 18% Lymphocytes)
Microbiology	Smear and Culture Negative

Note: This fluid meets all three Light's criteria for an exudate (Protein ratio >0.5, LDH ratio >0.6, and pleural LDH > 2/3 the serum upper limit). The very high LDH and neutrophil-predominant leukocytosis are classic for a parapneumonic effusion

The pleural fluid analysis revealed a complicated parapneumonic effusion with a very high LDH of 6406 U/L, consistent with an exudative process (Table 1). Cultures of the pleural fluid were also negative. The fluid was noted to contain numerous septations, and the thoracic surgery team was consulted for possible operative intervention.

Clinical course

On day 12 of hospitalization, the patient developed gross hematuria (dark-red urine). Concurrent laboratory testing revealed severe thrombocytopenia. Table 2 summarizes the laboratory evolution from admission to day 12.

Table 2.

Laboratory data comparison

Parameter	Reference Range	Day 1 (Admission)	Day 12 (Event)
Platelets (×10³/µL)	150–450	236	6 (Critical)
WBC (×10³/µL)	4.0–11.0	30.0 (High)	8.7
Hemoglobin (g/dL)	12.0–16.0	13.7	8.8 (Low)
CRP (mg/L)	< 10	190 (High)	168 (High)
Procalcitonin (ng/mL)	< 0.5	2.0 (High)	< 0.5
Urinalysis (RBC/hpf)	0–3	0–2	Many
Creatinine (mg/dL)	0.5–1.3	1.2	1.0
INR	0.8–1.2	1.3	1.2
Fibrinogen (mg/dL)	200–400	-	280
Anti-PF4 Antibody	Negative	-	Negative

During the first 12 days of hospitalization, the patient’s clinical trajectory was complex. After an initial 48-hour period of relative improvement, she experienced recurrent fevers and progressive pulmonary infiltrates on serial chest imaging. Given the severity of the pneumonia, the presence of a complicated parapneumonic effusion with a very high LDH (> 6000 U/L), and the absence of a definitive microbiological diagnosis, antibiotics were continued following infectious disease consultation. Two transthoracic echocardiograms were performed to rule out infective endocarditis, both of which were negative. The patient was scheduled for operative intervention by thoracic surgery due to the complex pleural effusion with extensive septations.

However, on day 12, the development of profound thrombocytopenia (6,000/µL) with associated hematuria necessitated postponement of the planned surgical procedure. The surgical intervention was deferred until platelet counts could be stabilized. During the platelet recovery phase, the patient’s overall clinical condition began to improve, including restoration of appetite and improvement in general appearance. The thoracic surgery procedure was subsequently performed after platelet normalization, with a chest tube placed postoperatively. The patient was transferred out of the ICU two days later as her condition stabilized.

Diagnostic workup

Pseudothrombocytopenia was excluded via peripheral blood smear. There was no clinical evidence of uncontrolled infection, and disseminated intravascular coagulation (DIC) was deemed unlikely given the absence of schistocytes, absence of hemolysis, and preserved fibrinogen levels. Although the patient was receiving enoxaparin, heparin-induced thrombocytopenia (HIT) was excluded based on a low 4T score and a negative anti-PF4 antibody assay. Direct and indirect Coombs tests were negative. With primary hematologic and infectious etiologies ruled out, Vancomycin-Induced Immune Thrombocytopenia (VIIT) emerged as the most plausible etiology.

Intervention and outcome

Both meropenem and vancomycin were discontinued. The patient received 5 units of platelets; however, the count remained refractory (7,000–9,000/µL) over the subsequent 3 days (Table 3).

Table 3.

Trend of platelet response to intervention

Day (Post-Event)	Intervention	Platelet Count (/µL)	Clinical Status	Key Clinical Insight
Day 13	Vancomycin Stopped + Plt Transfusion	7,000	Refractory	Refractoriness to transfusion confirms immune-mediated destruction. Stopping vancomycin removed a potential trigger but was insufficient alone.
Day 14	Plt Transfusion	7,000	Refractory	Persistence of refractoriness reinforces diagnosis of a robust immune-mediated process (e.g., DITP).
Day 15	Prednisolone Started	9,000	No Response	Lack of early steroid response is common in severe immune thrombocytopenias and prompted escalation.
Day 16	IVIG Started (Day 1)	8,000	No Response	Expected lag phase; IVIG mechanism (Fc receptor blockade) takes 2–5 days to show effect.
Day 19	IVIG (Day 4)	24,000	Initial Rise	Delayed but definitive response to IVIG, hallmark of immune-mediated thrombocytopenia.
Day 20	Post-IVIG	95,000	Recovery Phase	Rapid climb after initial rise confirms successful blockade of platelet destruction.
Day 22	Discharge	163,000	Full Recovery	Complete hematologic recovery, validating the treatment strategy.

Due to the lack of response to drug cessation alone, prednisolone (50 mg/day) was initiated. After three days of corticosteroid therapy with no significant improvement, intravenous immunoglobulin (IVIG 1 g/Kg) was started at 10 g daily for five days. A robust response was noted after the second IVIG dose. The platelet count normalized within 4 days and remained stable. At one-month follow-up, the platelet count was 175,000/µL.

Causality assessment

The Naranjo Adverse Drug Reaction Probability Scale was utilized to assess the causal relationship. A score of 7 was calculated, indicating a “PROBABLE” adverse drug reaction. The breakdown of the Naranjo score included points for: previous conclusive reports of this reaction (+ 1), improvement after drug withdrawal (+ 2), alternative causes ruled out (+ 2), and objective evidence of an adverse event (+ 1).

Methods

A systematic review of the literature was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines to identify and synthesize all published cases of vancomycin-induced immune thrombocytopenia (VIIT). This review was not registered in PROSPERO, as it does not involve a health-related outcome for a specific patient population and is not eligible for registration in that database.

Search strategy and data sources

A comprehensive literature search was performed using two electronic databases: PubMed and Scopus. The search aimed to identify relevant case reports and case series published in the English language between January 1, 2000, and January 31, 2025. This timeframe was selected to provide a comprehensive, contemporary cohort for analysis. While the narrative review by Mohammadi et al. (2016) synthesized cases up to 2015 [4], our systematic approach with explicit criteria allows for a unified reappraisal of the modern case-report literature with specific focus on management outcomes and refractory disease.

The following search string was used, incorporating Boolean operators and keywords: (“vancomycin” AND (“thrombocytopenia” OR “immune thrombocytopenia” OR “drug-induced thrombocytopenia”))

Eligibility criteria

Articles were considered eligible for inclusion if they met the following criteria: (1) presented an original case report or case series; (2) explicitly attributed the cause of thrombocytopenia to vancomycin; (3) provided sufficient clinical detail to confirm the diagnosis and extract data on patient demographics, clinical presentation, management, and outcomes. Articles were excluded if they were review articles, commentaries, or if the thrombocytopenia was clearly attributed to an alternative primary etiology (e.g., sepsis, DIC, HIT) without a strong causal link to vancomycin.

Study selection and data extraction

Two reviewers independently screened the titles and abstracts of all retrieved records. Full-text articles of potentially relevant studies were then assessed for eligibility against the predefined criteria. Disagreements were resolved through consensus or consultation with a third reviewer.

A standardized data extraction form was used to collect the following information from each included study: first author, year of publication, patient age and sex, vancomycin dose and route of administration, platelet nadir, time from initiation of vancomycin to onset of thrombocytopenia, bleeding manifestations, method of diagnosis (clinical vs. antibody confirmation), management strategies (e.g., drug cessation, IVIG, corticosteroids, platelet transfusion), time to platelet recovery, and the Naranjo Adverse Drug Reaction Probability Scale score.

Causality assessment

For each included case, the causality of the adverse drug reaction was assessed using the Naranjo Adverse Drug Reaction Probability Scale. Scores were interpreted as follows: ≥9 (definite), 5–8 (probable), 1–4 (possible), and 0 (doubtful).

Results: cohort analysis

The 18 patients (10 male, 8 female) had a mean age of 63 years (range 41–81). Clinical characteristics and outcomes are summarized in Table 4.

Table 4.

Comprehensive analysis of vancomycin-induced immune thrombocytopenia cases (2000–2025)

Case	Study (Year)	Age/Sex	Route / Dose	Plt Nadir (103/µL)	Time to Nadir*	Bleeding Symptoms	Diagnosis	Management	Recovery	Naranjo
1	Current	54 / F	IV 1 g q12h	6	12 days	Gross Hematuria	Clinical	Stop + IVIG + Steroids	10 days	7
2	Obi et al. [5] (2023)	56 / M	IV 20 mg/kg	41	5 days	Petechiae	Antibody (+)	Stop + Daptomycin	3–5 days	7
3	Shah et al. [6] (2023)	60 / M	IV (NR)	11	11 days	None	Re-challenge	Stop + IVIG	4 days	9
4	Barnecet et al. [7] (2023)	60 / F	IV (NR)	0	10 days	Asymptomatic	Clinical	Stop + Steroids	6 days	7
5	Rattanasuwan et al. [8] (2023)	58 / M	IV (Single)	27	< 1 day	Infusion-related Reaction	Antibody (+)	Stop	7 days	9
6	Hameed et al. [9] (2022)	74 / M	IV 1 g q12h	70	5 days	Asymptomatic	Clinical	Stop	NR	7
7	Murt et al. [10] (2022)	75 / F	IP 2 g q5d	3.9	10 days	Intracranial Hemorrhage	Clinical	Stop + IVIG + Steroids	10 days	7
8	Li et al. [11] (2022)	64 / M	IV 1 g q12h	3	4 days	None	Re-challenge	Stop	2 days	9
9	MacDougall et al. [12] (2020)	81 / M	IV 1.5 g q12h	1	8 days	Petechiae	Antibody (+)	Stop + IVIG + Steroids	5 days	9
10	Gerstein et al. [13] (2018)	69 / M	IV (Levels 15–20)	0	7 days	Epistaxis, Petechiae	Antibody (+)	Stop + IVIG + Steroids	5 days	7
11	Yamanouchi et al. [14] (2016)	72 / F	IV 500 mg q24h	6	10 days	Melena / Shock	Antibody (+)	Stop + Transfusion	8 days	9
12	Lobo et al. [15] (2015)	67 / M	IV 500 mg q12h	0	5 doses	Hematuria / Shock	Antibody (+)	Stop + IVIG + Steroids	3 days	7
13	Ahmed et al. [16] (2014)	63 / M	IV 1 g q12h	2	15 days	Asymptomatic	Antibody (+)	Stop + G-CSF	10 days	9
14	Arnold et al. [1] (2013)	66 / F	IV (NR)	4	NR	Petechiae	Antibody (+)	Stop + IVIG	1 day	9
15	Ruggero et al. [17] (2012)	41 / M	IV 500 mg q12h	15	5 days	None	Re-challenge	Stop	5 days	9
16	Anand et al. [18] (2011)	54 / M	IV 1 g q12h	10	6 days	Petechiae	Antibody (+)	Stop + Steroids	6 days	7
17	Kenney et al. [19] (2008)	61 / M	IV (NR)	3	< 1 day	Epistaxis	Antibody (+)	Stop + IVIG	4 days	7
18	O’Donnell et al. [20] (2007)	56 / F	Bone Cement	10	< 1 day	Post-op Bleeding	Antibody (+)	Cement Removal	7 days	9

*Time to Nadir refers to the duration from initiation of vancomycin to the documented lowest platelet count (nadir), as reported in each case. This is the most consistently reported and clinically meaningful time point in the published literature. Cases with onset <24 hours represent anamnestic responses in patients with prior vancomycin exposure

Abbreviations: G-CSF: Granulocyte Colony-Stimulating Factor; HAP: Hospital Acquired Pneumonia; IV: Intravenous; IVIG: Intravenous Immunoglobulin; IP: Intraperitoneal; SSI: Surgical Site Infection; NR: Not Reported; DITP: Drug-Induced Immune Thrombocytopenia

Key findings

1. Severity: The mean platelet nadir was approximately 12,000/µL. Four patients (22%) reached extreme nadirs of less than 2,000/µL.

2. Causality Assessment: Formal evaluation using the Naranjo Adverse Drug Reaction Probability Scale was performed in all cases. Scores ranged from 7 to 9, with 8 cases (44%) scoring 9 (“definite”), 6 cases (33%) scoring 8, and 4 cases (22%) scoring 7 (“probable”). No case scored below 7, indicating strong causal association in the published literature.

3. Bleeding Manifestations: Eight patients (44%) had significant bleeding (hematuria, intracranial hemorrhage, gastrointestinal bleeding, or epistaxis).

4. Diagnostic Confirmation: Drug-dependent antibodies were confirmed in 10/15 cases (67%) where testing was performed.

5. Management Strategies:

• All patients had vancomycin discontinued or removed.

• 9 patients (50%) required immunomodulation (IVIG and/or corticosteroids).

• Platelet transfusions were administered to 13 patients (72%), with documented refractoriness in 8.

• 6.Outcomes: Mean time to platelet recovery (> 100,000/µL) was 6.2 days. All patients recovered without long-term sequelae.

Discussion

Thrombocytopenia is a frequent complication in the ICU, yet distinguishing drug-induced etiologies from sepsis-associated coagulopathy or disseminated intravascular coagulation (DIC) remains a formidable challenge [21]. Our review of 18 cases, including the current report, highlights that Vancomycin-Induced Immune Thrombocytopenia (VIIT) is a potentially lethal condition defined by profound platelet destruction and a distinct clinical profile.

Mechanism and pathophysiology

Unlike the dose-dependent myelosuppression seen with linezolid, VIIT is an idiosyncratic, immune-mediated reaction. It is typically driven by drug-dependent antibodies (DDAbs) of the IgG or IgM class that bind to platelet glycoproteins, most commonly the GPIIb/IIIa or GPIb/IX complex, only in the presence of vancomycin [1, 14]. This “Quinine-type” mechanism leads to rapid clearance of platelets by the reticuloendothelial system. Notably, as demonstrated by Lobo et al. [15], this reaction is independent of serum trough levels and can occur even with subtherapeutic dosing, reinforcing that this is a Type B (bizarre/idiosyncratic) adverse reaction.

Clinical presentation: The “Zero-Platelet” phenomenon

A striking finding in our systematic review is the severity of the thrombocytopenia. The mean platelet nadir across the 18 cases was approximately 12,000/µL, with four patients reaching a nadir of 0 to 2,000/µL. This “zero-platelet phenomenon” distinguishes VIIT from Heparin-Induced Thrombocytopenia (HIT), where platelet counts rarely fall below 20,000/µL [22]. Clinically, this manifests as a spectrum from asymptomatic laboratory findings [16] to life-threatening hemorrhage, including intracranial hemorrhage [10] and hypovolemic shock from GI bleeding [14]. Our patient’s presentation of gross hematuria aligns with the severe hemorrhagic potential of this syndrome.

Diagnostic pitfalls: the anamnestic response and occult exposures

The timing of onset is a critical, yet often misleading, diagnostic clue. While the classic presentation occurs 5–10 days after initiation in treatment-naïve patients, our review highlights the danger of the anamnestic response. In sensitized patients, re-exposure can trigger a precipitous drop in platelets within hours. As shown in Table 4, the onset of thrombocytopenia ranged from less than 1 day (in cases of re-exposure) to 15 days. Cases with rapid onset (< 24 h) were consistently associated with prior vancomycin exposure. Kenney et al. [19] and Rattanasuwan et al. [8] documented severe thrombocytopenia occurring within 12–15 h and 4 h of re-exposure, respectively. Furthermore, clinicians must be vigilant for occult sources of exposure. O’Donnell et al. [20] reported a case where VIIT was triggered not by IV administration, but by vancomycin-impregnated orthopedic bone cement, emphasizing that systemic absorption from local sites is sufficient to propagate the immune response.

The multi-drug trap

Diagnosis is further complicated in critically ill patients receiving multiple antibiotics. MacDougall et al. [12] described a case where VIIT was initially misdiagnosed as Rifampin-induced thrombocytopenia. Similarly, Anand et al. [18] identified a patient with simultaneous antibodies to both Vancomycin and Piperacillin. These cases illustrate that when DITP is suspected, all potential offending agents should be scrutinized, and a “step-wise” discontinuation may be perilous; broad substitution of antibiotic classes is often safer.

The challenge of antibiotic duration in undifferentiated severe pneumonia

Our case highlights the diagnostic and therapeutic dilemma clinicians face when managing severe community-acquired pneumonia without a definitive microbiological diagnosis. While current guidelines recommend de-escalation of antibiotics when cultures are negative and clinical improvement is observed, this approach can be challenging in patients with a fluctuating clinical course [21]. In our patient, the initial 48-hour improvement was misleading, as she subsequently developed recurrent fevers, progressive radiographic infiltrates, and a complicated parapneumonic effusion. The presence of a complex pleural effusion with an LDH exceeding 6000 U/L, extensive septations, and the need for potential surgical intervention further complicated the decision to discontinue broad-spectrum antibiotics. Furthermore, the patient’s history of prior azithromycin use in the community without clinical response raised concern for possible resistant organisms, and consultation with infectious disease specialists supported continued vancomycin therapy. This case illustrates the tension between the imperative to identify drug-induced adverse reactions and the need to maintain effective antimicrobial coverage in critically ill patients.

Therapeutic strategies and transfusion refractoriness

The cornerstone of management is immediate cessation of vancomycin. However, a consistent finding in our review is transfusion refractoriness. Platelet transfusions administered while vancomycin is still circulating are often futile, as the drug-antibody complex rapidly destroys the donor platelets. For severe cases (platelets < 20,000/µL) or active bleeding, our review supports the use of IVIG and corticosteroids. While drug cessation alone was effective in 11/18 cases, those with life-threatening bleeding benefited from aggressive immunomodulation. In our patient, the platelet count remained refractory to cessation and transfusion but responded robustly to high-dose IVIG, confirming the immune-mediated nature of the refractory state.

Conclusion

Vancomycin-induced immune thrombocytopenia is a medical emergency characterized by profound, often refractory platelet destruction. This contemporary systematic review reinforces prior knowledge and provides updated insights. Clinicians should suspect VIIT in any patient with unexplained, profound thrombocytopenia (< 20,000/µL) during vancomycin therapy or shortly after re-exposure, recognizing occult sources. Management requires immediate drug cessation. For severe or refractory presentations, early immunomodulation with IVIG should be considered, as platelet transfusions may be ineffective. Heightened clinical vigilance and a structured diagnostic approach are essential to mitigate the risk of life-threatening hemorrhage.

Limitations

We acknowledge several limitations of this case report and systematic review. First, as a single case report, our findings may not be generalizable to all patients with VIIT. Second, confirmatory drug-dependent antibody testing was not performed in our patient due to limited availability at our institution; however, the clinical presentation, exclusion of alternative etiologies, temporal relationship, and response to drug cessation and immunomodulation strongly support the diagnosis, as reflected by the Naranjo score of 7. Third, the systematic review is limited to published case reports, which may be subject to publication bias toward more severe or unusual presentations. Fourth, heterogeneity in reporting across cases limited our ability to perform quantitative meta-analysis. Despite these limitations, our review provides valuable clinical insights for the recognition and management of this rare but serious adverse drug reaction.

Author contributions

N.K.: Conceptualization, Methodology, Investigation, Writing – Original Draft, Writing – Review & Editing. F.G: Data curation. S.F.: Conceptualization, Supervision; B.R.: Data curation, Methodology, Investigation, Writing – Original Draft.

Funding

No specific funding was received for this work.

Data availability

The datasets are available from the corresponding author on reasonable request.

Declarations

Ethics approval and consent to participate

Ethical approval for this case report was not required by the institutional policies of Tehran University of Medical Sciences as it is considered a component of routine clinical care and quality improvement. However, written informed consent was obtained from the patient for both participation in this study and for publication of her anonymized details.

Consent for publication

Written informed consent for publication was obtained from the patient.

Competing interests

The authors declare no competing interests.