Isolated pulmonary injury following electric shock: a case report and literature review

Abstract

Introduction and Importance:

Electrocution can lead to severe visceral organ damage, including pulmonary injuries. However, isolated electrical-induced pulmonary injury (EIPI) following electric shock remains underreported. This case reports a 33-year-old male who suffered an EIPI after contact with low-voltage electricity and provides a comprehensive literature review to explore the mechanisms, clinical presentation, imaging findings, and treatment of EIPI.

Case Presentation:

A previously healthy 33-year-old male presented with dyspnea, chest pain, and dry cough following an electrocution while lifting a fallen 220 V wire. Chest imaging revealed diffuse consolidations, ground-glass opacities (GGO), and interlobular septal thickening. Bronchoscopy findings were normal; no infectious pathogens were detected in blood and sputum cultures. The patient was treated with oxygen therapy, antibiotics, and supportive care, achieving full recovery after 9 days of hospitalization.

Clinical Discussion:

A review of 12 case reports found that pulmonary injuries following electrocution are mostly associated with low-voltage exposure. The most common findings include bilateral lung consolidations, GGO, and diffuse alveolar hemorrhage. The pathophysiology of lung parenchyma involves coagulation necrosis, leading to alveolar hemorrhage. Management includes supportive care, with surgery reserved for cases with extensive necrosis unresponsive to medical treatment.

Conclusion:

EIPI is a rare but potentially severe consequence of electrocution, often presenting as bilateral lung consolidations and alveolar hemorrhage. Given the variability in presentation and severity, chest imaging should be considered in all cases after electrocution, even in the absence of external injuries. Early recognition and appropriate treatment are essential to ensure favorable outcomes, with surgical intervention considered in selected cases.

Introduction and importance

Electric shock injuries occur when the human body comes into contact with an electrical source, acting as a conductor for the current to pass through. Such injuries account for 3–7.2% of all burn-related hospital admissions^[1-3]. More than 50% of electric shock injuries involve high-voltage electricity^[2,4,5]. The mortality rate is 5.2–12% for high-voltage injuries^[6,7] and 2.6% for low-voltage injuries^[7], although some studies have reported a 0% mortality rate^[8]. Electric shock injuries present a wide range of clinical manifestations, affecting various organs such as the skin, muscles, bones, heart, vessels, lungs, brain, and kidneys^[9-11]. The extent of damage to each organ varies significantly, depending on multiple factors. Injuries can range from minor skin burns to life-threatening visceral organ damage, such as ventricular fibrillation, acute respiratory distress syndrome (ARDS), acute kidney injury, and cerebral edema^[12-14]. Although electric shock injuries may seem less common in major burn centers, they have the potential to cause deep and widespread tissue damage, making it difficult to predict the severity of injury at the outset^[2,11].

To date, various mechanisms and effects of electric shock on different organ systems have been explored through reviews^[7,12,14], clinical guidelines^[9-11], and observational studies^[4,6]. However, most research has focused on the cardiovascular system^[8,15], musculoskeletal injuries^[2], and neuropsychiatric sequelae^[16], with limited discussion on the impact of electric shock on other visceral organs^[13,17], particularly the lungs. We present a case of a 33-year-old male who suffered a severe, isolated electrical-induced pulmonary injury (EIPI) following electrocution. Through this case, we provide a literature review on EIPI, offering a comprehensive overview of the clinical symptoms, imaging findings, pathology, and treatment of such cases. This case report has been reported in line with the Surgical CAse REport (SCARE) criteria^[18].

Case presentation

A 33-year-old male patient with a history of hypertension was admitted to the hospital due to dyspnea following an electric shock. Three hours before admission, the patient was crab fishing in a paddy field when he noticed a fallen electrical wire. He attempted to lift the 220 V wire with his right hand, intending to hang it in a safer position. At the time, his right hand was wet, and his lower limbs were submerged in water. Suddenly, he was electrocuted, immediately losing consciousness and collapsing into the field. There were no witnesses to the incident. After an undetermined period, the patient regained consciousness and quickly moved to dry land. Subsequently, he developed dyspnea, bilateral chest pain, and a dry cough. A nearby resident assisted him in getting to the nearest hospital, where he received 10 liters per minute of oxygen via mask to maintain an SpO₂ of 90%. He was then urgently transferred to our hospital.

At the Emergency Department of our hospital, the patient was fully conscious with a Glasgow Coma Scale score of 15. His vital signs included a heart rate of 83 beats per minute, blood pressure of 100/60 mmHg, temperature of 37 °C, respiratory rate of 30 breaths per minute, and SpO₂ of 90% while receiving oxygen via a 10-liter-per-minute mask. Physical examination did not reveal any entry or exit wounds from the electric current, nor were there any visible skin injuries, including on the chest wall. There were no abnormalities in muscle strength, neurological function, or heart examination. Lung auscultation revealed scattered crackles bilaterally. Laboratory tests were normal, including serum creatinine, coagulation profile, serum and urine myoglobin, white blood cell count, and liver function tests. Electrocardiogram, transthoracic echocardiogram, and troponin I levels showed no abnormalities. However, there was an elevated C-reactive protein level of 184 mg/L and a mildly increased creatine phosphokinase level of 235 U/L. The patient underwent a contrast-enhanced computed tomography (CT) scan of the chest and abdomen to screen for any subtle visceral organ injuries. The abdominal CT revealed no abnormalities. However, the chest imaging demonstrated consolidations, ground-glass opacities (GGO), and interlobular septal thickening distributed throughout both lungs, with the consolidations predominantly located in the dependent zones of the lungs (Figs 1 and 2).

Figure 1.

Chest computed tomography findings upon admission (axial plane). The imaging revealed predominant consolidations primarily in the lower lobes of both lungs. Additionally, ground-glass opacities (GGO), nodular lesions, and interlobular septal thickening were observed throughout both lungs. (A and B) The upper lobes of both lungs show GGO (red stars) and interlobular septal thickening (red arrows) as the dominant features. (C and D) Focal consolidations (yellow stars) predominated, interspersed with nodular lesions (red circles). (E and F) Consolidation was predominantly localized in the lower lobes of both lungs (yellow stars).

Figure 2.

Chest computed tomography findings upon admission (coronal and sagittal planes). (A and B) Diffuse distribution of lung lesions across all three zones of the lungs on the coronal plane. (C and D) Consolidations are predominantly located in the posterior segments of the lower lobes on the sagittal plane.

Due to the inability to exclude the possibility of aspiration pneumonia, the patient underwent an emergency bronchoscopy immediately after admission. The results revealed normal airway mucosa and bronchial branches, with no evidence of sputum, blood, or foreign bodies. Bronchoalveolar lavage (BAL) was not performed due to the potential risk of worsening respiratory failure and life-threatening complications. The patient was treated with intravenous antibiotics including piperacillin/tazobactam, vancomycin, and ciprofloxacin, 1500 mL of 0.9% NaCl solution per day, and prophylactic anticoagulation. Blood and sputum cultures showed no bacterial growth. After 9 days of treatment, the patient gradually improved and fully recovered at discharge. A chest X-ray at discharge confirmed improvement. One month after discharge, the patient fully recovered without complications and resumed normal daily activities.

Clinical discussion

We conducted a comprehensive literature review of cases involving pulmonary injury due to electrocution by searching for reports that met the following criteria: (1) accessible via the PubMed database; (2) full-text articles written in English; (3) case reports or case series; (4) detailed descriptions of parenchymal lung injury immediately following electrical exposure; and (5) published from 1990 to the present. We excluded cases of pneumothorax^[19-21], secondary infectious pleural effusion^[1], and compressive atelectasis^[1] as they did not document parenchymal lung injury. The results identified 11 clinical case reports that met the inclusion criteria, summarized in detail in Table 1.

Table 1.

Summary of reports on parenchymal lung injuries caused by electrocution since 1990.

Author (year)	Age, sex, PMH	Voltage, skin contact impedance, exposure duration	Symptoms and tests classified by organ systems		Treatments and outcome
			Respiratory	Other systems
Schein (1990)[31]	57, Male, RLL lobectomy, herniorrhaphy, asthma	480 V (electrical panel), N/A, brief duration	Cardiogenic pulmonary edema, right lung opacification, left lung interstitial edema	VF, acute heart failure, regional hypokinesia	MV, cardiopulmonary resuscitation, defibrillation, antiarrhythmic drugs
				First-degree burns over both arms and shoulders, no chest wall injury, CPK 7500 U/L
					Weaning MV on day 3, discharged on day 10
				Unrespond to verbal commands
Masanès (2000)[28]	36, Male	20 000 V (live cubicle), N/A, brief duration	LLL collapse, posterior opacities of RLL, BAL from LLL showed blood-stained fluid with polymorphonuclear leukocytes predominate (70%)	Severe burns in many sites, no chest wall injury, CPK 15 450 U/L	MV, left lower lobectomy, surgical excision of burn wounds
					Discharged on day 50
				Briefly LOC, normal brain scan, frontal epileptogenic focus (EEG)
Schleich (2010)[24]	23, Male	70 000 V (power line), indirect contact via a truck, N/A	Pulmonary embolism, bilateral dependent atelectasis, RLL cavitation, pleural effusion	Atrial fibrillation	MV, fluid resuscitation, urine alkalinization, surgical excision of burn wounds, heparin, inferior vena cava filter, antibiotic, chest tube, right lower and parts of middle lobectomy
				Third-degree burns (neck, lower abdomen, and bilateral thighs), no chest wall injury, rhabdomyolysis
				Myoglobinemia
					Discharged on day 60
Truong (2017)[33]	58, Male	180 V (watering machine), wet skin, uncertain duration	Hemoptysis (20 mL), bilateral lung lesions predominately in RUL, perihilar GGO, interlobular septa thickening	One burn in the palm, no chest wall injury, rhabdomyolysis, CPK 1338 U/L	Fluid resuscitation, tranexamic acid
					Normal CXR on day 7, discharged on day 7
Karamanli (2017)[34]	20, Male	380 V (electrical panel), N/A, 15 s	Heterogeneous opacities of RLL and RUL, paravertebral zone consolidation, normal airway on bronchoscopy, BAL of RLL showed bloody fluid and polymorphonuclear leukocytes predominate (80%)	One burn in the hand, no chest wall injury	MV, fluid resuscitation, anti-edema (mannitol, dexamethasone)
				Briefly LOC, cerebral edema
					Weaning MV on day 3, discharged on day 7
Chawla (2019)[40]	23, Male	440 V (electric cable), indirect contact via a metal wire while drying wet clothes, N/A	Pink frothy secretions via intubation, neurogenic pulmonary edema, diffuse heterogeneous alveolar opacity bilaterally, GGO in the central lung zone, interstitial thickening	First-degree atrioventricular block	MV, fluid resuscitation
					Weaning MV on day 3, normal CXR on day 7, discharged on day 7
				Entry wound in right palm and exit wound in left hand, no chest wall injury, CPK 3001 U/L
				Neurogenic pulmonary edema
Nizhu (2020)[26]	20, Male	High voltage (electrical transformer), N/A, brief duration	Focal consolidation with pulmonary infiltrates bilaterally	No skin burn, no chest wall injury	Oxygen therapy, Philadelphia collar
					Discharged on day 3
				Briefly LOC, right cerebellar hemorrhage, fractures in the first cervical vertebrae
Chen (2020)[29]	23, Male	110 V (exposed wire), drenched cloth and wet floor, several minutes	Hemoptysis (20 mL), patchy infiltration, bilateral consolidation, upper lobes predominate	Burns on back and forehead, no chest wall injury, CPK 109 U/L	Oxygen therapy, tranexamic acid, antibiotics
					Normal CXR on day 7, discharged on day 7
				Briefly LOC, normal brain scan
Guimarães (2020)[25]	31, Male	Low voltage (water cylinder), wet skin, N/A	Bilateral GGO predominately on upper lobes, RLL consolidation	Cardiopulmonary arrest, VF	MV, fluid resuscitation, antibiotics
				No entrance or exit wounds, no chest wall injury, rhabdomyolysis, CPK 406 U/L	Weaning MV on day 5, discharged on day 24
				LOC, brain MRI revealed hyperintense areas suggesting cytotoxic edema
				Myoglobinaemia, AKI
Kelly (2022)[23]	33, Female	12 V (heated shirt with battery), wet skin, N/A	Bilateral anterior nodular and GGO involving all five lung lobes	No entrance or exit wounds, no chest wall injury	Bronchodilators
					Discharged
Singh (2023)[32]	32, Male	220 V (multi-plug power supply), N/A, N/A	Hemoptysis (10 mL), bilateral perihilar GGO, bronchoscopic examination showed blood in the bronchus	Burns in left forearm and right leg, no chest wall injury, CPK 600 U/L	Oxygen therapy, fluid resuscitation hemostatic drugs, antibiotics
					Discharged on day 14
				LOC for 30 min, normal EEG
Our case (2024)	33, Male	220 V (electrical wire), wet skin, N/A	GGO, bilateral interlobular septal thickening, consolidations predominantly located in the dependent zones, bronchoscopic examination showed normal airway	No entrance or exit wounds, no chest wall injury, CPK 235 U/L LOC	Oxygen therapy, fluid resuscitation, prophylactic anticoagulation, antibiotics

AKI, acute kidney injury; BAL, bronchoalveolar lavage; CPK, creatine phosphokinase; CXR, chest X-ray; EEG, electroencephalogram; GGO, ground-glass opacities; LLL, left lower lobe; LOC, loss of consciousness; MRI, magnetic resonance imaging; MV, mechanical ventilation; N/A, not available; PMH, past medical history; RLL, right lower lobe; RUL, right upper lobe; VF, ventricular fibrillation.

Most cases of EIPI occurred in young male patients with no prior medical history (Table 1). This finding aligns with studies on the population affected by electrical injuries, predominantly associated with occupational accidents^[5,15,22]. The severity of organ damage caused by electrical shock depends on the current type, voltage, amount of current, entry and exit points of the current, the resistance at the point of contact, duration of exposure, and the individual’s susceptibility^[9,10,17]. Our review shows that 75% of pulmonary injury cases from electric shock occurred at low-voltage (<1000 V), with cases involving low-voltage (12 V)^[23] or high-voltage (70 000 V)^[24] also being reported. Some cases did not identify the exact voltage of exposure^[25,26]. Most authors agree on defining high-voltage as >1000 V^[5,7,16], though this threshold is applied without considerable evidence, and some authors have used 600 V as the definition for high-voltage^[27]. Some studies suggest that the voltage intensity does not correlate with the severity of organ damage^[6]. However, numerous studies indicate that high-voltage injuries are associated with greater morbidity, long-term complications, and more extensive organ damage compared to low-voltage injuries^[4,16,22]. Due to the limited number of 12 case reports in our review, we cannot draw definitive conclusions about the relationship between voltage intensity and the severity of lung injury. Nevertheless, two cases of exposure to extremely high voltage required surgical removal of necrotic lung tissue as part of the treatment^[24,28]. Reduced skin resistance at the point of contact with electricity, often due to moisture, can exacerbate the severity of organ damage. According to Ohm’s law [voltage (V) = resistance (R) × amount of current (I)], the current is inversely proportional to resistance. Therefore, wet skin reduces resistance, allowing a higher current to flow through the body^[14,27,29]. This can lead to minimal external skin damage but result in widespread visceral organ injury as the electrical current diffuses into deeper tissues^[10]. Table 1 indicates that 50% of the cases reported wet skin during electrical contact, associated with diffuse lung injury. Although the duration of electrical exposure also influences severity, it is challenging to determine accurately in most cases. All cases of EIPI showed no chest wall damage, with only 50% suspected of having a transthoracic current (Table 1). A transthoracic current is typically suspected when the entry point is an upper limb and the exit point is either a lower limb or the opposite upper limb, or when the electrical contact occurs directly on the chest^[8,27]. One study reported that 60.6% of cases involved a transthoracic current, yet no pulmonary injuries were documented^[8]. Therefore, we suggest screening for lung injury with chest CT scans in patients exposed to electrical shock, even in the absence of chest injuries or confirmed transthoracic current. The absence of derma damage does not exclude the possibility of visceral organ damage. Moreover, the severity of skin damage does not correlate with the severity of visceral organ injuries, and this seems to maintain accuracy for the lungs^[17,27].

Although not universally classified, EIPI can be categorized into primary and secondary injuries. Secondary pulmonary injuries are more common and include hospital-acquired pneumonia^[7,13], aspiration pneumonia (often due to loss of consciousness at the scene)^[23], pulmonary contusion (resulting from secondary trauma)^[30], inhalation burns (due to thermal injury)^[9], and cardiogenic pulmonary edema (caused by ventricular fibrillation or cardiac arrest)^[14,31]. Primary parenchymal lung injuries directly due to electrical shock are rare^[9,12], as it was previously hypothesized that air is a poor conductor, making lung tissue less susceptible to damage^[13]. The clinical manifestations and potential mechanisms of EIPI are summarized in Table 2. Chest pain, dyspnea, and fever are commonly associated with EIPI (Table 1). However, these symptoms may be confounded by concurrent cardiovascular problems. In contrast, hemoptysis (excluding pink frothy sputum, which indicates pulmonary edema) appears to be a distinctive feature of EIPI. Hemoptysis was present in 3 out of 12 cases, typically at a mild and self-limiting level^[29,32,33]. Flexible bronchoscopy was performed in three cases, revealing the presence of blood within the bronchial branches, with Gram-stained BAL samples showing red blood cells^[28,32,34]. These findings are consistent with pulmonary alveolar hemorrhage secondary to electrical injury, which will be further discussed in the pathology section. Due to the limited number of cases involving flexible bronchoscopy in patients with EIPI, our discussion on the role of bronchoscopy is based on the currently available evidence. Flexible bronchoscopy may offer additional benefits in specific scenarios, such as (1) ruling out aspiration pneumonia in patients with a history of altered consciousness or falls, (2) excluding pulmonary infections, and (3) supporting the diagnosis of EIPI when BAL Gram staining reveals the presence of red blood cells. However, the procedure must be carefully considered in cases where there is a risk of progressive respiratory failure or when the patient’s condition may not tolerate bronchoscopy.

Table 2.

Clinical manifestation and potential mechanism of electrical-induced pulmonary injury.

Clinical manifestation	Potential mechanism
Apnea immediately following electrocution	Electrical current inhibition of the respiratory control center in the brain[10,12,14]
	Paralysis or tetanic contraction of the diaphragm[9,34]
	Paralysis or tetanic contraction of other respiratory muscles[27,39]
	Secondary to cardiac arrest or ventricular fibrillation[14]
Airway burn	Thermal burns caused by heat energy or inhalation of hot debris[9]
Pulmonary contusion	Secondary trauma following electrocution (explosion, fall, etc.)[30]
Pneumothorax	The mechanism remains unclear[19,20]
Acute pulmonary edema	Cardiogenic pulmonary edema[31]
	Neurogenic pulmonary edema[40]
	Noncardiogenic pulmonary edema
Hospital-acquired pneumonia	Secondary infection due to superinfection, prolonged hospitalization, multiple surgical procedures, and loss of the outer protective skin layer[7,13]
Aspiration pneumonia	Loss of consciousness at the scene[23]
Pulmonary hemorrhage	The mechanism remains unclear[32]
Bronchospasm	Inflammatory mediators released from primary injury sites[3]
Acute respiratory distress syndrome	Inflammatory mediators and cytokines released from primary injury sites may contribute to the development of multi-organ failure[3]
Pulmonary embolism/thrombosis	The mechanism remains unclear or vascular injury due to electrical shock[24]
Bone marrow embolism	The mechanism remains unclear[38]

For imaging characteristics, EIPI displays the following features: 91% of cases involve bilateral distribution, with 64% showing predominant consolidation in the lower lobes. Various patterns, ranging from alveolar to interstitial involvement, have been reported, including consolidation, interlobular septal thickening, nodules, pleural effusion, cavitation, and GGO (Table 1). These findings align with the radiologic features of diffuse alveolar hemorrhage (predominantly lower lobe involvement)^[35,36] or ARDS (involvement of gravity-dependent or posterobasal regions)^[37]. We assume that diffuse alveolar hemorrhage is the predominant pathological feature in cases of EIPI. This condition arises from widespread damage to the pulmonary and bronchial vasculature, which are highly conductive, resulting in hemorrhage into the alveolar spaces. Consequently, GGO is observed surrounding the bronchovascular bundles, extending from the pulmonary hilum to the peripheral regions, diffusely involving both lungs. Additionally, interlobular septal thickening on a GGO background is present, with consolidation particularly noted in the basal regions, where the vascular supply is more abundant. In certain cases, blood has also been identified in BAL, without evidence of other inflammatory exudates^[28,32,34]. EIPI without chest wall damage can be explained by two mechanisms. First, electrical current damages tissues through thermal energy, generated due to tissue resistance as per Joule’s law [thermal (E) = voltage (V)[2]/resistance (R) × time (T) = amount of current (I)² × R × T]^[14,19]. This mechanism leads to protein denaturation and coagulative necrosis^[14]. Second, electrical current causes tissue damage at the cellular level by altering the resting membrane potential, leading to electroporation, damage to channel proteins, and disruption of the cell membrane. This results in massive tissue destruction, necrosis, and conformational changes^[10,17,29]. Pathological evidence of EIPI is rarely reported, making it difficult to clarify the underlying mechanisms. We identified two cases where EIPI was treated with lobectomy^[24,28], providing histopathological findings, along with three additional EIPI cases based on lung autopsies^[30,38,39]. These offer direct evidence of pulmonary damage, affecting the alveoli, interstitium, lung parenchyma, and pulmonary vasculature. Overall, the findings revealed hemorrhagic areas and red blood cells within the alveoli, suggesting diffuse alveolar hemorrhage^[30,39]. There was also evidence of vascular congestion^[30,39] and interstitial fibrosis^[30]. Pulmonary infarction might have been caused by embolism or thrombosis due to vascular injury^[24], arterial spasm, or disruption of blood flow at the capillary bed^[24,28]. Furthermore, coagulation necrosis^[24,28], a typical pattern of ARDS^[39], or bone marrow embolism^[38] have also been reported. Hemoptysis may result from vascular damage caused by electrical injury, leading to blood vessel rupture and subsequent pulmonary hemorrhage^[13].

Treatment options for EIPI include oxygen therapy, mechanical ventilation, lobectomy, antifibrinolytic agents (for hemoptysis), and bronchodilators (for bronchospasm). Additionally, management of other organ systems affected by electrical trauma is crucial, including resuscitation, defibrillation, fluid resuscitation, urine alkalinization, anticoagulation, and antibiotics (Table 1). EIPI generally has a favorable prognosis, often self-resolving within 3–10 days, provided no severe multi-organ injuries exist. Currently, there are no guidelines or recommendations exist for the treatment and prevention of EIPI. Some authors have suggested early lobectomy^[28] or removal of necrotic tissues to prevent hospital-acquired infections^[1], as delaying surgery could lead to multi-organ failure^[13]. However, we observed several cases that recovered well without lung resection (Table 1), indicating that symptomatic treatment may be considered initially for EIPI.

Conclusions

Electrical-induced pulmonary injury is a rare condition that can occur in both high-voltage and low-voltage trauma. Hemoptysis and diffuse alveolar hemorrhage are key features of this condition, often accompanied by bilateral lower lobe consolidation. Pulmonary injury screening should be considered in all cases of electrical shock, ideally with chest CT. Symptomatic treatment may be considered initially for EIPI, while lobectomy should be reserved for cases of extensive necrosis unresponsive to medical treatment. Electrical-induced pulmonary injury should be considered in all patients who experience electrocution, especially if accompanied by respiratory symptoms.

Ethical approval

Our institution does not require ethical approval to report individual cases or case series.

Consent

Written informed consent was obtained from the patient’s parents to publish this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Sources of funding

This research did not receive any grant from funding agencies in the references public, commercial, or not-for-profit sectors.

Author contribution

N.V.H.: the first author, contributed to writing – review & editing, writing – original draft, visualization, methodology, and formal analysis. T.D.V.: contributed to writing – review & editing, writing – original draft, formal analysis, and data curation. D.L.Q.: contributed to writing – review & editing, visualization, and conceptualization. N.D.M.: contributed to writing – review & editing and validation. T.H.T.N.: contributed to writing – review & editing and validation. N.T.N.: contributed to writing – original draft, methodology, formal analysis, and data curation. K.N.D.: contributed to writing – review & editing, writing – original draft, visualization, methodology, formal analysis, and corresponding. All authors contributed to the final approval for the version to be submitted.

Conflicts of interest disclosure

The authors have no conflicts of interest to declare.

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Guarantor

Khoa Nguyen-Dang.

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Data sharing is not applicable to this article.

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Not commissioned, externally peer-reviewed.

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