Severe, late-onset neutropenia associated with prolonged furosemide administration in an extremely preterm infant: a case report and literature review

Abstract

Background

Furosemide is commonly used off-label in the neonatal intensive care unit to promote diuresis and improve pulmonary mechanics in preterm infants, but prolonged exposure carries known renal and ototoxic risks and—rarely—hematologic toxicity. Drug-induced neutropenia is uncommon in neonates and sparsely reported with loop diuretics. We describe an extremely preterm infant who developed profound, late-onset neutropenia temporally associated with extended furosemide therapy.

Case presentation

A male infant born at 25+3 weeks’ gestation (birth weight 720 g) received intravenous then enteral furosemide beginning on day of life (DOL) 28 for evolving bronchopulmonary dysplasia and fluid overload (1 mg/kg every 12 hours). On DOL 68 a routine complete blood count revealed isolated severe neutropenia (ANC 220/µL). The infant remained afebrile and clinically stable; blood and urine cultures and an extensive viral PCR panel were negative. After hematology consultation, furosemide was discontinued on DOL 68 (Naranjo score 7, “probable” ADR). Serial CBCs showed a prompt rebound in neutrophils beginning 48 hours after drug cessation, normalization by DOL 72, and full recovery by DOL 75. Chlorothiazide was substituted for ongoing diuresis without recurrence of hematologic abnormality.

Conclusion

This case suggests a probable, reversible association between prolonged furosemide exposure and late-onset severe neutropenia in an extremely preterm infant. Clinicians should consider periodic CBC monitoring during extended furosemide therapy and promptly discontinue the agent if unexplained neutropenia occurs.

Background

Furosemide is a loop diuretic frequently used off-label in the neonatal intensive care unit (NICU) to promote diuresis and improve pulmonary mechanics (for example, in infants with evolving bronchopulmonary dysplasia [BPD] or significant pulmonary edema). Around 50% of very preterm infants receive furosemide during their NICU stay [1, 2]. Dosing practices vary, but most infants are treated with short courses (median of approximately 2 days) at about 1 mg/kg per dose [1]. Furosemide’s pharmacologic action (inhibition of Na–K–2Cl reabsorption in the loop of Henle) leads to potent natriuresis and fluid removal, which can transiently improve lung compliance and oxygenation in infants with pulmonary edema. However, furosemide carries well‑recognized toxicities – notably electrolyte disturbances (such as hypokalemia and hypochloremia) and risks of nephrocalcinosis and hearing loss in preterm neonates. These adverse effects reflect effects of furosemide on renal tubular function and inner-ear electrolyte homeostasis; accordingly, some neonatal care guidelines caution that prolonged furosemide use may delay ductal closure or cause ototoxicity [2]. Despite frequent use in infants at risk for BPD, controlled trials have not shown that chronic furosemide reduces BPD incidence or improves long-term outcomes [1].

Neonatal neutropenia is relatively common in preterm infants, but it most often reflects maternal or perinatal factors [3]. Drug‑induced neutropenia is recognized in pediatrics but is comparatively rare in neonates. The annual incidence of drug‑induced agranulocytosis and neutropenia is very low (on the order of 0.04% of hospitalized children) [4]. When it does occur, common culprits include antibiotics (especially β-lactams such as cephalosporins or penicillins), antivirals, anticonvulsants, and other immunomodulatory drugs [3, 4]. Only a handful of non-chemotherapeutic drugs (e.g. ceftriaxone, vancomycin) have been repeatedly implicated in children.

Pharmacovigilance data indicate that furosemide is not a recognized cause of neutropenia in infants, and reports linking the drug to bone-marrow suppression are exceedingly rare [4]. The case presented here – an extremely preterm infant who developed profound, late‑onset neutropenia temporally associated with prolonged furosemide therapy – is rarely reported in the literature. Our report adds valuable evidence to the limited literature [5].

Case presentation

A male infant was born via emergency cesarean section at 25 + 3 weeks of gestation due to preterm labor and suspected chorioamnionitis. Birth weight was 720 g (10th percentile). Apgar scores were 4, 6, and 8 at 1, 5, and 10 min, respectively. The mother had received a single course of antenatal betamethasone and intrapartum ampicillin for Group B Streptococcus prophylaxis.

The infant was intubated in the delivery room and received surfactant. He was treated empirically for early-onset sepsis with ampicillin and gentamicin for 7 days, which was subsequently discontinued following negative blood cultures at 48 h. His early course was complicated by moderate respiratory distress syndrome managed with conventional ventilation, a hemodynamically significant patent ductus arteriosus (PDA) treated successfully with ibuprofen on day of life (DOL) 5, and stage 2 necrotizing enterocolitis (NEC) managed conservatively (DOL 18–25).

By the fourth week of life, the infant demonstrated clinical and radiographic signs of evolving BPD. Due to persistent fluid overload and increasing ventilatory requirements, intravenous furosemide was initiated on DOL 28 at a dose of 1 mg/kg every 12 h (2 mg/kg/day). This led to improved urine output and marginal lung compliance. Furosemide was continued, transitioning to an enteral formulation via nasogastric tube once enteral feeds were fully re-established post-NEC.

On DOL 68, a routine complete blood count (CBC) revealed severe, isolated neutropenia with an Absolute Neutrophil Count (ANC) of 220/µL. The infant was clinically well and afebrile. Furosemide was identified as the probable causative agent. A formal causality assessment using the Naranjo Adverse Drug Reaction Probability Scale yielded a total score of 7, categorizing the association as “probable”. (Table 1) This score was based on the temporal sequence of the reaction following prolonged drug exposure (+ 2), resolution upon discontinuation (+ 1), the existence of previous conclusive reports (+ 1), the absence of alternative causes (+ 2), and objective confirmatory evidence (+ 1).

Table 1.

Naranjo adverse drug reaction probability scale assessment

Question	Yes	No	Do Not Know	Score
1. Are there previous conclusive reports on this reaction?	+ 1	0	0	+ 1
2. Did the adverse event appear after the suspected drug was administered?	+ 2	-1	0	+ 2
3. Did the adverse reaction improve when the drug was discontinued or a specific antagonist was administered?	+ 1	0	0	+ 1
4. Did the adverse reaction reappear when the drug was re-administered?	+ 2	-1	0	0
5. Are there alternative causes (other than the drug) that could on their own have caused the reaction?	-1	+ 2	0	+ 2
6. Did the reaction reappear when a placebo was given?	-1	+ 1	0	0
7. Was the drug detected in the blood (or other fluids) in concentrations known to be toxic?	+ 1	0	0	0
8. Was the reaction more severe when the dose was increased or less severe when the dose was decreased?	+ 1	0	0	0
9. Did the patient have a similar reaction to the same or similar drugs in any previous exposure?	+ 1	0	0	0
10. Was the adverse event confirmed by any objective evidence?	+ 1	0	0	+ 1
Total Score				7

Serial complete blood counts (CBC) were obtained as part of routine care and during clinical events (e.g., NEC). A consistent, severe neutropenia was first noted on DOL 68 (Fig. 1). Hemoglobin and platelet counts remained stable throughout the neutropenic episode. The infant was clinically well, afebrile, and hemodynamically stable at this time, with no increase in ventilatory support or signs of infection.

Fig. 1.

Temporal relationship of furosemide exposure, Absolute Neutrophil Count (ANC), and eosinophil count. A line graph with days of life (DOL) on the X-axis (DOL 20 to 80). The primary Y-axis (left) shows ANC (x10³/µL), and a secondary Y-axis (right) shows Eosinophil count (x10³/µL). A shaded bar indicates the period of furosemide administration (DOL 28-68). The plot clearly demonstrates the gradual decline in ANC during furosemide exposure, the nadir at DOL 68, and the rapid recovery after discontinuation. The eosinophilia peak (DOL 56) is shown preceding the ANC nadir

Given the severity of neutropenia, a full sepsis evaluation was performed on DOL 68. Blood cultures remained sterile after 5 days, and inflammatory markers were reassuring, with a CRP level of 0.5 mg/dL (normal < 1.0). Urine culture obtained via catheterization showed no growth. Chest X-ray findings were unchanged from baseline, demonstrating chronic features consistent with bronchopulmonary dysplasia. In addition, a comprehensive viral PCR panel from respiratory and blood samples was negative for Cytomegalovirus, Enterovirus, Adenovirus, and Human Herpesvirus-6, arguing against an infectious etiology.

Given the prior history of stage II necrotizing enterocolitis, the infant’s gastrointestinal status was reassessed at the time neutropenia was detected (DOL 68) to exclude ongoing inflammatory pathology. Abdominal examination revealed a soft, non-distended, non-tender abdomen with normal bowel sounds. Abdominal radiography demonstrated no pneumatosis intestinalis, portal venous gas, or free intraperitoneal air. The infant was tolerating full enteral feeds (150 mL/kg/day of fortified preterm formula) without gastric residuals or emesis, and stool output was normal and guaiac-negative. These findings confirmed complete clinical and radiologic resolution of the prior NEC episode and excluded active gastrointestinal inflammation as a contributing factor to the neutropenia.

Given the isolated nature of the neutropenia and its temporal link to furosemide, a bone marrow aspiration was deferred after hematology consultation. The consensus was a high likelihood of drug-induced suppression. Investigations for other causes were negative: serum B12 and folate were adequate for prematurity, and no antineutrophil antibodies were detected.

To exclude inborn errors of metabolism and storage disorders that may present with neutropenia, a targeted metabolic evaluation was undertaken. Abdominal ultrasonography performed on DOL 69 demonstrated normal hepatic size (liver span 5.2 cm, appropriate for gestational age), normal splenic dimensions, and no evidence of organomegaly or ascites. Serial blood glucose measurements throughout hospitalization ranged from 65 to 110 mg/dL, with no documented hypoglycemia. Capillary blood gas analysis on DOL 68 revealed a pH of 7.35, pCO₂ 48 mmHg, HCO₃⁻ 24 mEq/L, and base excess − 1.2, consistent with normal acid–base status and no metabolic acidosis. Serum lactate (1.2 mmol/L) and ammonia (35 µmol/L) were within age-appropriate reference ranges. In addition, the regional newborn screening panel, which includes testing for multiple metabolic and storage disorders, was normal. Collectively, the absence of organomegaly, hypoglycemia, metabolic acidosis, hyperlactatemia, or hyperammonemia made an underlying metabolic or storage disorder highly unlikely.

A comprehensive medication review was conducted for the period surrounding the onset of neutropenia (DOL 28–68). At the time severe neutropenia was identified on DOL 68, the infant was receiving enteral furosemide at 1 mg/kg per dose every 12 h (initiated on DOL 28), a daily multivitamin supplement (1 mL; containing vitamins A, C, D, E, and B-complex), ferrous sulfate at 2 mg/kg/day of elemental iron, sodium chloride supplementation at 2 mEq/kg/day for diuretic-associated hyponatremia, and maintenance caffeine citrate at 5 mg/kg/day for bronchopulmonary dysplasia. No medications had been discontinued in the two weeks preceding neutropenia (DOL 54–67), and specifically, no antibiotics, H2-receptor antagonists, proton pump inhibitors, or sedatives were administered during this interval. A detailed review of the electronic medical record confirmed the absence of inadvertent or undocumented drug exposure. Importantly, none of the concomitant medications—iron, multivitamins, sodium chloride supplementation, or caffeine—have been associated with isolated severe neutropenia in the literature, further strengthening the attribution of the hematologic abnormality to furosemide exposure.

Evaluation of hepatic and renal function at the time neutropenia was detected (DOL 68) demonstrated no evidence of systemic organ dysfunction (Table 2). Liver enzymes were within expected ranges for preterm infants, with ALT 18 U/L, AST 32 U/L, and GGT 85 U/L. Total bilirubin was 2.1 mg/dL with a direct fraction of 0.4 mg/dL, indicating no biochemical evidence of cholestasis. Serum albumin was 3.2 g/dL, consistent with preserved hepatic synthetic function. Renal parameters were similarly reassuring: serum creatinine was 0.45 mg/dL and blood urea nitrogen (BUN) was 8 mg/dL, both within age-appropriate reference ranges. Urine output over 24 h was 3.8 mL/kg/h, indicating adequate renal perfusion and function. Collectively, these findings (Table 2) demonstrate stable hepatic and renal function without evidence of furosemide-associated nephrotoxicity or multi-organ dysfunction. The absence of hepatic impairment, renal failure, or systemic metabolic disturbance supports the interpretation that the neutropenia represented an isolated, likely idiosyncratic hematologic adverse reaction rather than part of a broader organ dysfunction process.

Table 2.

Hepatic and renal function parameters

Parameter	DOL 68 Value	Normal Range for Preterm Infants
ALT	18 U/L	< 40 U/L
AST	32 U/L	< 60 U/L
GGT	85 U/L	< 150 U/L
Total Bilirubin	2.1 mg/dL	-
Direct Bilirubin	0.4 mg/dL	< 0.5 mg/dL
Albumin	3.2 g/dL	2.5–4.0 g/dL
Serum Creatinine	0.45 mg/dL	0.3–0.7 mg/dL
BUN	8 mg/dL	5–20 mg/dL
Urine Output (24 h)	3.8 mL/kg/h	> 1.5 mL/kg/h

Upon identification of severe neutropenia (ANC < 500/µL), furosemide was immediately and permanently discontinued on DOL 68. Given the negative initial infectious workup and the infant’s clinical stability, prophylactic antimicrobials were not initiated. The infant was placed in protective isolation, with strict hand hygiene enforced. Serial CBCs were performed daily. A steady, rapid increase in ANC was observed beginning 48 h after furosemide cessation (Fig. 1). The ANC normalized (> 1.5 × 10³/µL) by DOL 72 and fully recovered to pre-neutropenia levels by DOL 75. For ongoing BPD-related fluid management, chlorothiazide was introduced on DOL 70, with careful monitoring of electrolytes and CBC. No hematologic abnormalities were observed with this agent.

Following furosemide discontinuation, CBC with differential was monitored daily for 7 days, then twice weekly for 2 weeks, and weekly thereafter until discharge. The ANC recovery trajectory is shown in Fig. 1. Notably, the ANC crossed the safe threshold (> 1000/µL) by DOL 71 and normalized (> 1500/µL) by DOL 72. At the time of neutropenia detection (DOL 68), the infant remained hospitalized in the Level III NICU. He was receiving respiratory support via nasal continuous positive airway pressure (nCPAP) at 6 cm H₂O with 25% FiO₂, consistent with evolving moderate BPD, and was cared for in a closed, double-walled incubator with servo-controlled temperature. Growth velocity between DOL 28–68 averaged 13.2 g/kg/day, which is appropriate for an infant with BPD. The infant remained hospitalized until DOL 98 for BPD management and feeding optimization, though the neutropenia had fully resolved by DOL 75 (Table 3).

Table 3.

Growth parameters and hospitalization status during the neutropenic period

Parameter	Birth (DOL 1)	DOL 28 (Furosemide Start)	DOL 68 (Neutropenia)	DOL 75 (Discharge Planning)
Weight (g)	720 (10th %ile)	890 (8th %ile)	1420 (5th %ile)	1520 (6th %ile)
Length (cm)	33.0	35.5	39.5	40.2
Head Circ. (cm)	23.0	25.2	28.5	29.0

The infant was enrolled in our institutional High-Risk Infant Follow-up Program following NICU discharge on DOL 98, and serial hematologic monitoring was continued to ensure no recurrence of neutropenia. At the most recent follow-up at 12 months corrected age, the infant demonstrated normal neurodevelopmental outcomes (Bayley-III scores within the normal range), appropriate growth, and no infectious complications, with repeat complete blood counts confirming persistent normal neutrophil levels (Table 4). There has been no re-exposure to furosemide, supporting that the neutropenia was a transient, reversible adverse drug reaction and ruling out any underlying chronic neutropenia disorder.

Table 4.

Long-term hematologic follow-up

Post-Menstrual Age (PMA)	Chronological Age	ANC (x10³/µL)	Clinical Status
40 weeks (term equivalent)	15 weeks	4.2	Discharged home, no medications
3 months corrected age	6 months	3.8	Normal growth, no infections
6 months corrected age	9 months	5.1	Meeting milestones
12 months corrected age	15 months	4.5	No hospitalizations

The standardized causality assessment yielded a total score of 7, placing the finding within the “probable” probability category (score range 5–8). This quantitative result supports a probable causal relationship between furosemide exposure and the observed neutropenia, strengthening the attribution of the hematologic abnormality to the medication rather than to alternative etiologies.

Discussion

Hematologic toxicity associated with furosemide is rarely reported, and the literature describing furosemide-induced leukopenia or neutropenia is exceedingly sparse; although blood dyscrasias are listed as potential adverse effects, their true frequency and causal relationship remain poorly defined [5]. A focused literature search was conducted in PubMed from database inception through [3 January 2026], using the keywords and MeSH terms “furosemide” OR “frusemide” combined with “neutropenia,” “leukopenia,” or “agranulocytosis,” with results limited to pediatric populations. Reference lists of relevant articles were also manually screened to identify additional eligible reports. The review identified two pediatric reports of furosemide-associated neutropenia. One described a preterm infant with transient neutropenia after short-term intravenous furosemide, resolving rapidly after discontinuation [6]. The second reported a preterm infant who developed severe neutropenia after prolonged furosemide exposure, with recovery after withdrawal and recurrence on re-challenge, supporting causality [5]. (Table 5) Our case mirrors the latter, with late-onset severe neutropenia after extended furosemide therapy and rapid normalization following cessation. Although uncommon, these findings indicate that extended furosemide administration can induce transient neutropenia in preterm infants [5, 6].

Table 5.

Summary of pediatric case reports of neutropenia associated with furosemide

Reference (Year)	Patient	Indication	Furosemide Therapy	Neutropenia Onset	ANC Nadir	Co-medications	Furosemide Discontinued	Outcome
Yeung (1999) [6]	Preterm neonate (GA N/S)	Fluid management (pulmonary edema)	Stat IV doses (days 1–2, 21, 31, 35, 39)	Neutrophils dropped by day 7	Not reported	Vancomycin, cefotaxime (and transfusions)	Not clearly specified	Neutrophil counts recovered 24–48 h after each dose; remained intact on rechallenge.
Connolly et al. (2025)[5]	Preterm neonate (32 3/7 wk)	Congestive heart failure (VSDs)	Oral furosemide DOL 15–63	Gradual decline; ANC 190 on DOL 59	190/µL (DOL 59)	First hosp: captopril, HCTZ (no antibiotics); second hosp: perioperative cefazolin, cefepime	Yes (stopped DOL 63)	ANC recovered to 780/µL by DOL 67; on IV furosemide rechallenge (2nd hospitalization) ANC fell again to ~ 3310/µL (later resolved).

Although furosemide contains a sulfonamide moiety, the pathogenesis of reported neutropenia cases is uncertain; proposed mechanisms include idiosyncratic immune-mediated destruction or direct marrow toxicity, but direct mechanistic evidence in neonates is lacking. Two general mechanisms have been proposed for sulfa-induced agranulocytosis: (1) an immune-mediated reaction in which drug-dependent antibodies bind and destroy neutrophils; and (2) direct myelotoxicity from reactive drug metabolites leading to marrow suppression. Classic sulfonamide hypersensitivity reactions are typically mediated by an aromatic amine moiety, which is absent in furosemide; therefore, true cross-reactivity in the setting of a sulfa-allergy appears unlikely. Nonetheless, an idiosyncratic reaction (either immune or toxic) may be involved. In practice, the rapid rebound of neutrophils after stopping furosemide – as in our case – suggests that the marrow can recover promptly once the offending agent is removed. Some reports imply that the effect may be on circulating cells or the marginal pool rather than irreversible marrow damage [5].

Although neutropenia may occur in preterm infants, severe isolated neutropenia in a clinically stable neonate is uncommon. In our patient, infectious, nutritional, metabolic, and alloimmune causes were excluded, and no concomitant myelosuppressive medications were administered, making a drug-induced etiology the most likely explanation [3, 5].

This scenario fits the pattern of idiosyncratic drug-induced neutropenia, which is typically unpredictable and not dose-dependent. Such reactions often occur weeks to months after drug initiation. In one series of elderly patients with agranulocytosis, most cases presented 3–6 months after starting the offending drug, with abrupt onset in immune-mediated cases versus more insidious onset in toxic-metabolic cases [7]. Our patient’s neutropenia began several weeks after furosemide was started, a timing that fits an idiosyncratic drug reaction. Neutrophil counts normalized within days after discontinuing furosemide, with no alternative explanation, highlighting a clear temporal relationship. By standard causality assessment (Naranjo) this would be rated as “probable”. This pattern aligns with previous reports of rapid neutrophil recovery following furosemide cessation in both neonates and adults [5, 8]. These parallels reinforce that furosemide was the likely culprit in our case.

The mechanistic basis of this effect is unclear. Furosemide’s variable oral absorption has led some to suggest that intravenous dosing or higher concentrations may have stronger hematologic effects. In reported cases, neutrophil suppression occurred with both oral and IV therapy, indicating that even lower systemic levels can affect susceptible infants. Genetic or developmental factors, such as immature drug metabolism in preterm infants, may contribute to vulnerability. Although data are limited, some studies suggest a possible link between furosemide and reduced neutrophil counts. Neutropenia is not commonly listed as a side effect in adult references, so this association may be under-recognized in neonates [5].

Prolonged furosemide therapy can precipitate severe neutropenia, even in the absence of other symptoms. Although furosemide toxicity is usually monitored via electrolytes, renal function, and hearing, clinicians should also be alert to hematologic changes. We recommend periodic CBC monitoring during long-term diuretic use in extremely preterm infants. If unexpected neutropenia arises, prompt discontinuation of furosemide is advised. In our experience and in the literature, recovery of neutrophils is rapid once the drug is stopped. Awareness of this potential ADR allows timely action that can avoid invasive tests or unnecessary antibiotic use [5, 8].

This report has several important limitations. As a single-case observation, definitive causality cannot be established and the findings are not generalizable to broader neonatal populations. Although a comprehensive clinical and laboratory evaluation was undertaken, unrecognized confounding factors cannot be entirely excluded. In addition, pharmacogenetic testing and detailed pharmacokinetic modelling were not performed, limiting insight into potential individual susceptibility and dose–exposure relationships. Finally, the limited number of published cases and the possibility of reporting bias prevent accurate estimation of the true incidence of this association. Larger multicenter studies and pharmacovigilance analyses are needed to better define risk factors and underlying mechanisms.

Conclusion

This case highlights a rare but important adverse effect of prolonged furosemide therapy in extremely preterm infants: late-onset severe neutropenia. The temporal relationship, exclusion of alternative causes and rapid recovery upon drug discontinuation support a probable causal association. Although furosemide is widely used for fluid management and pulmonary support in the NICU, clinicians should remain vigilant for hematologic abnormalities, particularly during extended courses. Regular monitoring of complete blood counts during prolonged therapy can facilitate early detection, allowing timely intervention and preventing unnecessary investigations or treatments. Awareness of this potential adverse drug reaction reinforces the need for cautious, individualized use of furosemide in this vulnerable population.

Abbreviations

ADR

Adverse Drug Reaction

ANC

Absolute Neutrophil Count

BPD

Bronchopulmonary Dysplasia

CBC

Complete Blood Count

CMV

Cytomegalovirus

CRP

C–Reactive Protein

DC

Discontinued

DOL

Day of Life

GA

Gestational Age

GBS

Group B Streptococcus

HCTZ

Hydrochlorothiazide

HHV

6–Human Herpesvirus–6

IV

Intravenous

MeSH

Medical Subject Headings

NEC

Necrotizing Enterocolitis

NICU

Neonatal Intensive Care Unit

PDA

Patent Ductus Arteriosus

PCR

Polymerase Chain Reaction

RDS

Respiratory Distress Syndrome

VLBW

Very Low Birth Weight

VSD

Ventricular Septal Defect

WBC

White Blood Cell Count

Authors’ contributions

1. Ziad W. Elmezayen: Conceptualization, Supervision, Study Design, Writing – Review & Editing. 2. Mohammad Adi: Data Curation, Formal Analysis, Writing, Writing - Original Draft , Review and Editing, Contributions to Discussion. 3. Rafeek Walid Elmezayen: Methodology, Data Interpretation, Approval of Final Manuscript, Supervision. 4. He Yunting: Writing , Contributions to Discussion and Approval of Final Manuscript. 5. Ahmed H. Sharaf: Writing and Approval of Final Manuscript.

Funding

Not applicable.

Data availability

All data pertinent to this case report have been included in this article. Further inquiries can be directed to the corresponding author.

Declarations

Ethics approval and consent to participate

Ethical approval was not required for this case report, as it involves a single patient and does not meet the criteria for research requiring institutional review board (IRB) oversight. The use of authorized medications was consistent with clinical practice guidelines, and the management of this individual patient did not require IRB approval.

Consent for publication

Written informed consent for publication of the clinical details and accompanying images was obtained from the patient’s parents/legal guardians, as the patient is under 18 years of age. The completed consent form is available to the Editor upon request and will be treated confidentially.

Competing interests

The authors declare no competing interests.