|Year : 2020 | Volume
| Issue : 1 | Page : 120-122
Sevoflurane induced diffuse alveolar haemorrhage in a young patient after orthopedic surgery: A case report
O Cengiz1, A Kivrak2, M Yegen3, M Demir4
1 Kartal Dr. Lütfi Kırdar Training and Research Hospital, Orthopedics and Traumatology Clinic, İstanbul, Turkey
2 Orthopedics and Traumatology Clinic, Muş State Hospital, Muş, Turkey
3 Anesthesiology and Reanimation Clinic, Muş State Hospital, Muş, Turkey
4 Department of Chest Diseases, Dicle University, Faculty of Medicine, Diyarbakır, Turkey
|Date of Submission||25-Jan-2019|
|Date of Acceptance||19-Jul-2019|
|Date of Web Publication||10-Jan-2020|
Dr. O Cengiz
Kartal Dr. Lutfi K.rdar Training and Research Hospital, Orthopedics and Traumatology Clinic, .stanbul
Source of Support: None, Conflict of Interest: None
| Abstract|| |
We present a very rare case of Sevoflurane Induced Diffuse Alveolar Haemorrhage in a young male patient with a closed tibial fracture after direct trauma to the right cruris. The patient was operated for tibial fracture, but diffuse alveolar haemorrhage developed after sevoflurane inhalation in the postoperative period following general anesthesia. Diffuse alveolar haemorrhage (DAH) is associated with inhalation injury from halogenated gases and reported as a unique entity in the literature that practicing clinicians should be aware of and consider in post-operative cases of acute respiratory distress. As DAH usually presents with symptoms the presence of hemoptysis, anemia, dyspnoea and radiological alveolar infiltrates, rapid detection of the aetiology and initiation of cause-directed treatment are of great importance on survival.
Keywords: Diffuse alveolar haemorrhage (DAH), inhalation anesthetics, orthopedic, sevoflurane
|How to cite this article:|
Cengiz O, Kivrak A, Yegen M, Demir M. Sevoflurane induced diffuse alveolar haemorrhage in a young patient after orthopedic surgery: A case report. Niger J Clin Pract 2020;23:120-2
|How to cite this URL:|
Cengiz O, Kivrak A, Yegen M, Demir M. Sevoflurane induced diffuse alveolar haemorrhage in a young patient after orthopedic surgery: A case report. Niger J Clin Pract [serial online] 2020 [cited 2020 Aug 8];23:120-2. Available from: http://www.njcponline.com/text.asp?2020/23/1/120/275626
| Introduction|| |
Diffuse alveolar hemorrhage (DAH) is a rare clinical entity with a high mortality rate characterized by diffuse bleeding originating from the microvascular system in the lung. It was first described by Osler in 1904. Hemoptysis is associated with symptoms including presence of diffuse infiltration in the chest radiography, anemia, and acute respiratory failure. DAH can be due to causes such as connective tissue diseases and systemic vasculitis, as well as non-immune causes such as drugs, toxins, and infections.
In this case report, we present a young patient operated for tibial fracture, but diffuse alveolar haemorrhage developed after sevoflurane inhalation in the postoperative period.
| Case Report|| |
A 38-year-old male patient was admitted to our emergency department with a closed tibial fracture after direct trauma to the right cruris. In the evaluation of the patient in the emergency department, no additional pathology was found in the systemic examination. The patient, who had no additional disease, and no history of substance use or any drug use, was operated after the preoperative preparations were completed. Intravenous propofol and fentanyl were used for anesthesia induction. The surgery was performed under general anesthesia using 50% O2+NO2 and inhaled sevoflurane for maintenance.
The patient, successfully extubated after the operation, was admitted to the postoperative anesthesia intensive care unit approximately 1 hour after the completion of the procedure with the diagnosis of acute hypoxemic respiratory distress. Postoperative pulse of the patient was 75 beats/min, arterial tension was 132/95 mm/hg, and the patient was afebrile. The arterial blood gas taken while breathing in room air was pH: 7.47, SpO2 80%, pCO2: 34 mm/hg and pO2: 51 mm/hg. Following oxygen administration with 3 l/min mask, SpO2 increased to 95%. A hemogram demonstrated leucocytosis (11.5 × 109/L), normal haemoglobin and hematocrit levels (13.0 g/dl; 38.6%), platelet count (246.3 × 109/L) and normal serum creatinine (0.7 g/dl). Echocardiography and lower extremity venous doppler ultrasonography revealed no pathology.
No pathology was detected on chest radiographs and computed tomography of thorax before and early post-operative surgery [Figure 1]. However, the day after the surgery, the chest X-ray revealed irregular peripheral consolidation areas on the apices and bases [Figure 2] and computed tomography of thorax revealed ground glass opacity and consolidation areas in bilateral lung parenchyma [Figure 3]. The patient developed acute hypoxic respiratory failure and the patient was intubated and was supported with mechanical ventilation. Post-operative hemogram demonstrated lower haemoglobin and hematocrit levels (8.6 g/dl; 25%). Diagnostic bedside bronchoscopy was performed because of the high index of suspicion for pulmonary hemorrhage. When the patient was intubated in the intensive care unit, bronchoscopy was performed through the endotracheal tube. During the bronchoscopy, no thermal airway injury was observed. The bronchoscopy showed diffuse erythema throughout the tracheobronchial tree. Consecutively bronchoalveolar lavage of multiple lobes demonstrated progressively bloody return consistent with DAH. Transbronchial parenchymal biopsy was performed on the lower lobe of the left lung accompanied by bronchoscopy. No evidence of infection in the direct view as well as no microorganism growth was observed in the cultures of the patient. The patient's autoimmune markers were negative (Antimitochondrial antibody, p-ANCA, Anti-Nuclear Antibody, Anti Ds DNA, c-ANCA, Anti Smooth Muscle Antibody). With clinical, radiological, and bronchoscopic findings, the patient was diagnosed with alveolar haemorrhage. The aetiology of alveolar hemorrhage was associated with sevoflurane in the patient whose rheumatologic markers were negative. On the first day, 500 mg steroid treatment was started, followed by 80 mg on the day 2 and day 3. After 3 days of supportive treatment, the patient was extubated. Follow up chest radiograph and computed tomography of thorax at one month showed complete resolution of pulmonary infiltrates [Figure 4].
|Figure 1: (a and b): Preop Chest PA view and early post-op CT thorax sagittal section: No pathology detected before and early post-op surgery|
Click here to view
|Figure 2: Postop 1-day Chest PA view: Demonstrating bilateral alveolar infiltrates without effusion|
Click here to view
|Figure 3: (a and b): CT chest coronal and sagittal section: Demonstrating ground glass opacity and consolidation areas in the bilateral lung parenchyma|
Click here to view
|Figure 4: (a and b): Follow up Chest X-Ray and computed tomography of thorax at one month showed complete resolution of pulmonary infiltrates|
Click here to view
| Discussion|| |
Inhalation anesthetics gained the concept of modern anaesthetic in the 1950s with the discovery of halothane and provided a new era in the field of surgery. Methyl ether anesthetics have many of the characteristics that an ideal volatile anaesthetic should bear. These include properties such as molecular stability, non-flammability, not causing arrhythmia and neuronal excitation, partial cardiovascular stability, large lethal/anaesthetic concentration rate, less effect on cerebral blood flow and end organ at lower concentrations. Sevoflurane, one of the most recently used methyl ether anesthetics and a highly fluorinated derivative of methyl isopropyl ether, was first synthesized in 1960 for the first time as part of efforts to find inhalation anesthesia with an advantage of reliability and efficacy against halothane and isoflurane. It is a non-flammable, non-explosive liquid with fragrant smell. The incidence of respiratory complications is low with its pleasant smell. It allows mask induction due to not causing apnoea, breath holding, laryngospasm, and coughing. Despite such properties, this anesthetic was not considered because of fluoride ion release and interaction with CO2 absorbents. In 1988, research on sevoflurane was resumed in Japan and it has been widely used worldwide after 1992.
During sevoflurane anesthesia, degradation products are formed as a result of the interaction with CO2 absorbers. Among these degradation products, Compound A is the most studied product in studies due to its nephrotoxicity., Although it is unclear whether it causes pulmonary toxicity or not, it is stated in the literature that other halogen gases cause pulmonary endothelial damage. Volatile gases can be dissolved in oil and can strengthen the arachidonic cascade. As a result, gas exposure may lead to alveolar permeability, increased oxidative stress, and strengthening in inflammatory response. Sevoflurane can also activate pathways with a similar mechanism.
In the literature, thermal airway trauma has been reported in some cases as a result of exothermic reactions of sevoflurane and CO2 absorbers in anesthesia circuits. In addition, a limited number of sevoflurane-related diffuse alveolar hemorrhages have been reported in the literature. The patient presented in our case report did not show any signs of thermal burn in the airway, but other causes of DAH were excluded. The patient's microbiological tests for bacterial, fungal and viral infections to explain post-operatively developed acute respiratory failure were normal. Extensive serological tests were also negative for vasculitis. Conservative treatments in intensive care unit improved clinically, laboratory, and radiologically within 10 days with steroid and mechanical ventilation support for 3 days. Although the mechanism of sevoflurane causing DAH cannot be fully clarified, predisposing factors have been interpreted as underlying factors. After the patient was taken to the clinic, steroid treatment was gradually decreased and discontinued within 1 week. After supportive treatment, the patient improved, and no recurrence was detected at the 6th month follow-up. As a result, the absence of infectious diseases, infiltrative diseases and malignancy and positive response to post-operative supportive treatment which would constitute acute respiratory distress syndrome (ARDS) in the patient suggested that sevoflurane-related diffuse alveolar hemorrhages in the patient.
To conclude, DAH is an important clinical condition that develops due to life-threatening immune or non-immune causes. It usually presents with symptoms with the presence of hemoptysis, anemia, dyspnea, and radiological alveolar infiltrates. Rapid detection of the aetiology and initiation of cause-directed treatment are of great importance on survival.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Newsome BR, Morales JE. Diffuse alveolar hemorrhage. South Med J 2011;104:269-74.
Park MS. Diffuse alveolar hemorrhage. Tuberc Respir Dis (Seoul) 2013;74:151-62.
Panikkath D, Gadwala S, Mills B, Panikkath R. Diffuse alveolar hemorrhage. Southwest Resp Crit Care Chron 2015;3:19-27.
Gonsowski CT, Laster MJ, Ferrell LD, Kerschmann RL. Toxicity of compound A in rats. Effect of a 3-hour administration. Anesthesiology 1994;80:556-65.
Scheller MS. New volatile anesthetics: Desflurane and sevoflurane. Semin Anesth 1992;11:114-22.
Behne M, Wilke HJ, Harder S. Clinical pharmacokinetics of sevoflurane. Clin Pharmoacokinet 1999;36:13-26.
Austin A, Modi A, Judson MA, Chopra A. Sevoflurane induced diffuse alveolar hemorrhage in a young patient. Respir Med Case Rep 2016;20:14-5.
Shayevitz JR, Traystman RJ, Adkinson NF, Sciuto AM, Gurtner GH. Inhalation anesthetics augment oxidant-induced pulmonary vasoconstriction: Evidence for a membrane effect. Anesthesiology 1985;63:624-32.
Fatheree RS, Leighton BL. Acute respiratory distress syndrome after an exothermic baralyme-sevoflurane reaction. Anesthesiology 2004;101:531-3.
Kim CA, Liu R, Hsia DW. Diffuse alveolar hemorrhage induced by sevoflurane. Am Thorac Soc 2014;11:853-5.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]