Complexities in diesel oil inhalation: case study of respiratory injury and coagulation anomalies

Abstract

Diesel inhalation poisoning represents a rare yet critical medical condition necessitating prompt medical attention due to its potential to induce severe respiratory distress and coagulation dysfunction. The present case study describes the distinctive clinical presentation of a male patient in his early 40s who experienced acute respiratory distress and manifested coagulation factor VII deficiency subsequent to unintentional inhalation of diesel oil during engine repair. The patient demonstrated symptoms including chest tightness and dyspnea, indicative of chemical aspiration pneumonia, alongside an unforeseen coagulation abnormality. Treatment involved rigorous intervention, comprising endotracheal intubation, mechanical ventilation, and administration of pharmacotherapy, including ambroxol, dihydroxypropylline, and methylprednisolone. Moreover, procedural measures, such as repeated bronchoscopic alveolar lavage, pathogen culture, and targeted antibiotic therapy, were employed to mitigate respiratory complications. The patient’s clotting disorder was treated with blood transfusions, and he was discharged with improvement. The present case highlights the imperative nature of immediate medical intervention in instances of diesel inhalation to avert further clinical deterioration and unfavorable outcomes. Additionally, it underscores the necessity for expanded research endeavors aimed at elucidating the indirect repercussions of diesel inhalation on the coagulation cascade, an area that remains relatively underexplored within the medical literature.

Introduction

Diesel fuel, comprising a group of organic compounds containing hydrogen and carbon, is prevalent in various sectors as a ubiquitous energy source, such as industry, agriculture, and domestic settings. ¹ Despite its widespread use, the literature on diesel inhalation toxicity remains surprisingly sparse. While diesel exposure typically poses minimal health risks for most individuals, under specific conditions, inadvertent inhalation may cause serious acute and chronic respiratory problems, and, in severe cases, it can be life-threatening. ² The present report aims to meticulously analyze these scenarios, focusing on the clinical consequences of diesel inhalation and the essential interventions required.

Case report

A male patient in his early 40s reported accidentally inhaling approximately 20 ml of diesel fuel during a home diesel engine repair, with some of the fuel aspirated into his lungs. Concurrently, he sustained abrasions on the right anterior chest and exhibited multiple linear erythematous marks on the abdomen, which did not involve rupture or bleeding. Immediately following the incident, he expelled the diesel orally and rinsed his mouth, yet initially refrained from seeking medical attention. Following the accident, he developed progressive respiratory symptoms including a cough, scanty and difficult-to-expectorate sputum, chest discomfort, right-sided pain exacerbated by activity, pronounced chest tightness, shortness of breath, and fatigue. At 8 h following the accidental inhalation, as his respiratory symptoms worsened, he decided to seek hospital treatment.

Within 30 min of his arrival at the emergency department in 2023, the patient underwent a chest computed tomography (CT) scan, received gastric lavage, and was initiated on pharmacotherapy. He was administered one intravenous dose of nalmefene (0.2 mg), and was diagnosed with diesel inhalation poisoning and admitted for further observation and treatment. Initial examination on admission revealed a fever of 38.5°C, heart rate of 103 beats per min, blood pressure of 146/80 mmHg, and clear consciousness but poor spirits. The chest CT scan showed bilateral pneumonia, localized consolidation in the right middle lobe, pleural thickening, and atherosclerosis of the aorta and coronary arteries. Bronchoscopy results indicated inflammatory changes. The preliminary diagnosis included diesel inhalation poisoning, chemical inhalation pneumonitis, and moderate acute respiratory distress syndrome (ARDS). Due to the severity of his condition, he was subsequently transferred to the emergency intensive care unit (EICU). The patient provided written informed consent to treatment.

The patient was admitted to the EICU on the day of presentation to the emergency department, and 4 h after initial presentation (at 21:11 h), the patient exhibited acute respiratory distress symptoms including chest tightness, dyspnea, cough, and sputum production. His initial oxygen saturation, measured by pulse oximetry, was approximately 90%. However, it improved to about 96% after administering 5 L/min O₂ via nasal cannula. Hemodynamic assessment revealed his blood pressure had stabilized to 108/80 mmHg. Neurologically, his bilateral pupils were equally dilated to a diameter of about 2.5 mm, with a sluggish light reflex noted. Due to his respiratory compromise, the patient underwent endotracheal intubation and was started on mechanical ventilation. Pharmacologically, he received 80 mg methylprednisolone, intravenously, once daily, to reduce pulmonary exudation, 0.25 g dihydroxypropylline, static push pump, every 12 h, for bronchospasm relief, and 30 mg ambroxol, intravenously, every 12 h, for sputum reduction. Following a negative penicillin skin test, he was administered piperacillin-sodium and tazobactam-sodium (4.5 g, intravenously, every 8 h) for prophylactic anti-infection. Fiber-bronchoscopic alveolar lavage (BAL) and sputum aspiration were conducted multiple times to clear residual diesel oil from the airways, initially on the day of admission and subsequently on day 2 and day 3 post-admission. A chest CT scan conducted on day 3 post-admission revealed bilateral pneumonia and localized consolidation in both lungs that was more advanced than the findings at admission. On day 6 post-admission, a subsequent CT scan revealed bilateral pneumonia with new cavitation in the localized consolidation of the right middle lobe. Additionally, there was improvement in the remaining lung pathology compared with day 3. Bilateral pleural thickening and a small volume of fluid in both pleural cavities were noted. Images from the patient’s chest CT series are shown in Figure 1.

Figure 1.

Representative time series chest computed tomography (CT) scans in a male patient in his early 40s who presented with diesel inhalation and was given a preliminary diagnosis including diesel inhalation poisoning, chemical inhalation pneumonitis, and moderate acute respiratory distress syndrome: (a) day 1 chest CT demonstrating bilateral pulmonary inflammation with localized consolidation in the right middle lobe, suggesting lung infection or inflammation; (b) day 3 chest CT revealing an expansion of the inflammatory areas in both lungs with increased localized consolidation; and (c) day 6 chest CT showing new cavity development within the area of consolidation in the right middle lobe, and unclear internal bronchus.

Upon admission, the patient exhibited significant coagulation dysfunction in addition to the above symptoms, as evidenced by an initial prothrombin time (PT) of 31.2 s, which further increased to 38.7 s within the first 24 h of admission. Despite fluctuations over the subsequent days, the PT persistently remained above the normal range of 10.5–14 s, indicating an ongoing instability in the coagulation system. Detailed laboratory results are shown in Table 1. The prolonged PT suggested an impairment in the extrinsic coagulation pathway, possibly indicating a deficiency in coagulation factor VII. ³ To address his abnormal coagulation status, the following four transfusion treatments were administered to the patient: first transfusion, 400 ml Rh (D)+, virus-inactivated plasma of type A blood; second transfusion, 610 ml Rh (D)+, virus-inactivated plasma of type A blood and 6 U cryoprecipitated coagulation factor; third transfusion, 400 ml Rh (D)+, virus-inactivated plasma of type A blood and 4 U precipitated coagulation factor; and fourth transfusion, 370 ml Rh (D)+, virus-inactivated plasma of type A blood and 4 U precipitated coagulation factor. Additionally, the patient was administered 1 g potassium chloride sustained release tablet, orally, three times daily, as part of the treatment. The patient had no history of blood transfusions or allergies. During treatment, the patient experienced transfusion-related anaphylaxis, characterized by a sporadic rash, prompting cessation of the transfusion and initiation of symptomatic management, including 5 mg dexamethasone sodium phosphate, intravenous injection, and 5% glucose solution plus 20 mg calcium gluconate, continuous intravenous pump. Due to the patient’s consistently abnormal PT values, a hematology consultation was promptly requested. Upon diagnosing a factor VII deficiency and observing no significant bleeding risk, a conservative observational approach was recommended as the treatment strategy. The patient’s condition significantly improved following comprehensive treatment. He was successfully weaned of mechanical ventilation and discharged after 6 days of hospitalization. The patient’s respiratory symptoms and coagulation status stabilized, and follow-up chest CT scans showed a marked reduction in pneumonia and lung consolidation. At the time of discharge, the patient expressed satisfaction with the treatment received and reported feeling much better. He also expressed appreciation for the timely and thorough care provided.

Table 1.

Timeline of biochemical blood test results in a male patient in his early 40s who presented with diesel inhalation and was given a preliminary diagnosis including diesel inhalation poisoning, chemical inhalation pneumonitis, and moderate acute respiratory distress syndrome.

Biochemical blood indicators	Normal values	Day 118.24 h	Day 216:52 h	Day 318:21 h	Day 415:17 h	Day 418:21 h	Day 509:04 h	Day 614:27 h
PT (s)	10.5–14	31.2	38.7	32.6	48.5	27.9	43	31.7
PTA (%)	80 ≥ 120	28	22	27	17	22.9	20	20.9
PT–INR (%)	0.8–1.2	2.88	3.54	3.03	4.41	2.45	3.96	2.73
APTT (s)	22.7–31.8	28.4	28.2	28.1	27.7	25.1	31	28.3
Fib (g/L)	2–4	4.47	6	6.61	6.53	5.75	8.31	5.89
TT (s)	14–21	13.7	13.5	13.4	13.9	16.9	12.1	14.1

PT, prothrombin time; PTA, prothrombin time activity; PT–INR, prothrombin time–international normalized ratio; APTT, activated partial thromboplastin time; Fib, Fibrinogen; TT, thrombin time.

This case was reported according to the CARE guidelines, ⁴ and all patient details were de-identified. The study was not submitted for approval by an ethics review committee, as it is a retrospective case report that involved the collection of anonymized data without interventions beyond standard medical care. The patient provided verbal informed consent for publication of the case report and accompanying images.

Discussion

Diesel oil, a complex mixture of hydrocarbons, comprises alkanes, alkenes, and aromatic compounds with varying carbon chain lengths, and numerous toxic chemicals. ⁵ Due to its distinct physical and chemical characteristics, diesel oil exposure may lead to pulmonary damage, central nervous system depression, and cardiac arrhythmias. Clinically, diesel oil poisoning often manifests with symptoms such as dyspnea, cough, somnolence, tachycardia, and altered mental status. In severe cases, these symptoms may pose life-threatening risks. ⁶ The present case report discusses a patient who inadvertently inhaled diesel oil during a diesel engine repair. The presenting symptoms of cough, scant sputum, respiratory discomfort, chest tightness, and dyspnea were indicative of acute respiratory distress, aligning with chemical aspiration pneumonia attributed to diesel oil inhalation. Radiological findings from a chest CT scan revealed bilateral pneumonia with localized consolidation in the middle lobe of the right lung, supporting the diagnosis of respiratory tract injury. ⁷ This case is noteworthy for its complexity, as it involved both acute respiratory injury and potential coagulation dysfunction, a conjunction not commonly reported in the existing literature on diesel oil inhalation toxicity.

Diesel oil, with its complex mixture of hydrocarbons and additives, has the potential to directly stimulate the mucosal linings of the alveoli and airways upon inhalation, and this interaction may precipitate an inflammatory response in alveolar epithelial and bronchial cells. Reactive oxygen species may be generated during the pulmonary metabolism of these hydrocarbon compounds, leading to oxidative stress and consequent cellular membrane damage. This damage triggers the activation of lung macrophages and epithelial cells, catalyzing the release of inflammatory mediators, including tumor necrosis factor (TNF)-alpha and various interleukins.^8–11 This cascade amplifies the inflammatory response, contributing to airway constriction, increased mucus secretion, and lung tissue damage, which are all key factors in the development of symptoms such as coughing, chest tightness, and dyspnea. ¹² Furthermore, inhalation of diesel may compromise the structural integrity of the alveolar-capillary barrier. Hydrocarbons can interfere with alveolar surfactants, leading to alveolar exudation and pulmonary edema. This disruption results in reduced lung compliance, potentially escalating to severe, progressive lung injury and life-threatening ARDS. ¹³ In the present case, despite the relatively minimal volume of diesel oil aspirated, the rapid progression of symptoms underscores the urgency of prompt medical intervention in diesel inhalation incidents.

Clotting factor VII, synthesized by the liver, plays a pivotal role in initiating the extrinsic pathway of blood coagulation. ¹⁴ While factor VII deficiency is predominantly a congenital disorder, it can also manifest as an acquired condition in certain cases. ¹⁵ In the patient described in the present case, the absence of a significant familial history or previous clotting dysfunctions suggests that acquired factors may have contributed to the observed deficiency. The management of this patient’s coagulation dysfunction involved multiple transfusion treatments, including plasma and cryoprecipitated clotting factors, aimed at stabilizing his coagulation status. In this case, the patient developed a sporadic rash during transfusion, indicative of an anaphylactic reaction. The transfusion was promptly stopped, and symptomatic management was initiated, including the administration of corticosteroids to mitigate the allergic response. The patient’s anaphylaxis highlights the importance of close monitoring during transfusions and having emergency medications readily available to manage such reactions effectively. The observed coagulation dysfunction in this patient may have been attributed to several potential mechanisms. Acute inflammatory responses to diesel inhalation might have triggered a cascade of events leading to coagulation anomalies. Diesel fuel contains hydrocarbons, which are known to be hepatotoxic, potentially causing direct hepatocellular injury, leading to liver cell death and impaired liver function. The liver is essential for the synthesis of various proteins, including clotting factors. When liver function is compromised, the production of these proteins is reduced, which can lead to coagulation abnormalities. Additionally, the metabolism of fat-soluble vitamins, particularly vitamin K, may be disrupted by hepatic injury. Vitamin K is a crucial cofactor for the carboxylation of certain glutamate residues in clotting factors II, VII, IX, and X, which is necessary for their proper function. A deficiency in vitamin K, therefore, may result in the production of inactive clotting factors, further exacerbating coagulation disorders.^16,17 Inflammation-induced coagulation activation is another possible mechanism. The release of inflammatory cytokines, such as interleukins and TNF during acute inflammatory responses, can disrupt the balance between coagulation and anticoagulation pathways. This disruption may lead to the depletion or downregulation of coagulation factors, contributing to prolonged PT and other coagulation abnormalities observed in the present patient.^18,19 Although the current medical literature does not establish a direct correlation between diesel inhalation and coagulation factor deficiencies, the potential indirect impact of diesel inhalation on the coagulation system warrants further investigation to elucidate its mechanisms and clinical implications.

The present case underscores the critical need for immediate medical evaluation and intervention following diesel aspiration. In the management of chemical aspiration pneumonia, supportive care, including oxygen therapy and airway management, is paramount. In this instance, the patient’s treatment involved endotracheal intubation and mechanical ventilation, alongside pharmacotherapy. This included ambroxol for sputum clearance, dihydroxypropylline for relief from spasmodic asthma, and methylprednisolone to reduce pulmonary exudation. The culture of pathogenic microorganisms and necessary laboratory tests and subsequent antibiotic therapy were integral for infection prevention and management. Additionally, repeated BAL played a significant role. The rationale for repeated BAL in this patient was to eliminate residual diesel oil from the airways, thereby mitigating pulmonary inflammation and averting further respiratory complications. This procedure is particularly efficacious in cases of chemical pneumonitis, where the aspirated material can perpetuate lung injury if not adequately removed. BAL helps in reducing the inflammatory response by physically eliminating the aspirated material, thereby preventing further respiratory complications. By improving airway patency and enhancing gas exchange, BAL can also improve the patient’s oxygenation status, providing symptomatic relief and aiding in overall respiratory function. As an invasive procedure, it should be noted that BAL also carries the risk of complications, such as bleeding, infection, or bronchospasm.^20,21 The patient’s improvement in the present case, as evidenced by chest CT findings and response to gastric lavage and medications, illustrates the effectiveness of these interventions in the treatment of diesel inhalation poisoning. The patient’s condition improved after treatment and he was discharged.

Conclusions

In conclusion, despite its relative rarity in daily clinical practice, the potential for severe symptomatology arising from diesel inhalation poisoning necessitates vigilance. It is imperative that both physicians and patients recognize the significance of such incidents and respond with appropriate and timely medical interventions. This awareness is crucial for mitigating the risks associated with diesel inhalation and ensuring prompt and effective treatment.