Retrograde cerebral air embolism

June 7, 2017 | Autor: Ozge Atilla | Categoria: Neuroimaging, Humans, Male, Clinical Sciences, X ray Computed Tomography, Renal Dialysis
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American Journal of Emergency Medicine 32 (2014) 1562.e1–1562.e2

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American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem

Case Report

Retrograde cerebral air embolism Abstract Pneumocephalus is a clinical condition caused by dysbarism, trauma, and iatrogenic causes. The most common iatrogenic causes of pneumocephalus are major interventions as a neurosurgery and cardiovascular operations, endoscopy, and minor interventions as a peripheral and central venous access. Especially during insertion of central venous line and intravenous drug and fluid infusion, the venous air embolism may occur in emergency department. In these patients, retrograde pneumocephalus occurs as a result of the air entering the right atrium to the brain. Clinical effects of the air delivery rates are known to be more specific than the total amount of air. In general, intravenous administration of 300 to 500 mL air in the speed of 100 mL/min is considered to be lethal. Large amounts of air embolism can cause hypotension and acute circulatory collapse with intracardiac obstruction. The most common symptoms of venous air embolism are anxiety, dyspnea, chest pain, cyanosis, tachycardia, tachypnea, headache, confusion, agitation, syncope, slurred speech, blurred vision, seizures, and ataxia. The mortality of pneumocephalus caused by central venous catheters in patients presented with symptoms of focal neurologic was 8%, whereas the mortality of pneumocephalus in patients presented with encephalopathy was 36%. In our report, a case of pneumocephalus secondary to disconnection of catheter cap in chronic renal failure patient who has hemodialysis via catheter has been presented. An 81-year-old man with altered mental status was presented to emergency department (ED) by ambulance. The patient had had a history of chronic renal failure and hemodialysis for 2 months. The patient had been to the hemodialysis the previous day. In the last 2 to 3 hours, he slept semisitting position and could not be awakened. The patient had a blood pressure of 120/70 mm Hg, heart rate of 90 beats per minute, respiratory rate of 30 breaths per minute, temperature of 36.1°C, peripheral oxygen saturation of 82%, and Glasgow Coma Scale score of 7. The patient had no cardiac murmur. Neurologic examination revealed anisocoria and no light reflex. Bedside glucose test was determined, 351 mg/dL. Electrocardiogram was in sinus rhythm and revealed right bundle branch block. The patient had a right internal jugular venous Hickman hemodialysis catheter. The catheter did not have the cap of one of the tips, and clip was open. Tip of the catheter was aspirated and closed. The patient was intubated and taken to the left lateral decubitus position. Patient had leukocytosis (23.2 K/μL) and creatinine, 6.1 mg/dL; urea, 83 mg/dL; and electrolytes were normal. Cranial computed tomography (CT) revealed pneumocephalus and bilaterally extending to the vertex. Furthermore, cranial CT showed extensive cerebral infarction and edema (Figure). We thought that pneumocephalus occurred due to end of the hemodialysis catheter remaining open. Thoracoabdomial CT revealed

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no intravascular air. Bedside echocardiography revealed no bubble and shunt. Neurosurgeon consultation was requested. The neurosurgical operation was not planned. Cranial CT taken 8 hours later revealed that pneumocephalus decreased, and diffuse brain edema occurred. The patient died as a result of transtentorial herniation after 4 days. Emergency departments are risky for venous air embolism because of frequently use of venous access (central and peripheral) and intravenous drug and fluid infusions. Tran et al [1] have reported that 0.034% of CT requested from the ED has identified intravenousinduced pneumocephalus. The cases of pneumocephalus formed after the central access air injection is often thought as paradoxical embolism. In some of these cases, right-to-left shunt defects such as patent foramen ovale or atrial septal defect (ASD) have been identified. In some cases, this situation is poorly understood and has been reported to be due to intrapulmonary shunt [2,3]. However, Schlimp et al [4] have reported that air bubbles in patients with central venous catheter can reach to brain by retrograde. In this study, blood flow velocity, bubble volume, superior vena cava diameter, and cardiac output are emphasized as the most important factors on affecting trends retrograde movement of air bubbles. In addition, it has been reported that large air bubbles are more prone to go retrograde to the brain. Hypovolemia, forced inspiration, and sitting position in patients who have central venous catheters have been reported to be predisposition to air embolism [5,6]. In our case, there was a semisitting position both at home and in the ambulance. In patients at risk for venous air embolism, sudden hypotension, hypoxia, and bradycardia should be considered in case of a pneumocephalus. Computed tomography in the ED is the most appropriate diagnostic tool for these patients. Also the extent of air emboli, quantity and the secondary effects can be seen on CT. Intracardiac and intravascular air can be displayed by ultrasonography [1]. Magnetic resonance imaging is more useful to show cerebral infarction caused by small amounts of air embolism [7]. Basic resuscitative support should be given to patients with suspected pneumocephalus, and 100% oxygen should be initiated in these patients. Left decubitus position (Durant maneuver) and the Trendelenburg position can prevent the passage of air bubbles into the systemic circulation [8]. Position can affect the clinical course by reducing the transmission rate to the circulation of air inside the vessel. However, it may increase cerebral edema in the patients with pneumocephalus; therefore, it is not recommended to be continued for a long time [9]. Hyperbaric oxygen (HBO) is the most effective treatment in patients with venous air embolism. Hyperbaric oxygen treatment reduces the volume and surface area of air bubbles and accelerates dissolution in blood. Hyperbaric oxygen treatment is recommended in symptomatic venous air embolism [6]. Because our case can not be stabilized, HBO therapy was not applied to him.

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M. Yesilaras et al. / American Journal of Emergency Medicine 32 (2014) 1562.e1–1562.e2

Iatrogenic venous air embolism is a cause for preventable morbidity and mortality. Murat Yesilaras, MD* Ozge Duman Atilla, MD Izmir Tepecik Research and Educational Hospital, Department of Emergency Medicine, Izmir *Corresponding author. Izmir Tepecik Research and Educational Hospital Department of Emergency Medicine/Izmir, Turkey E-mail address: [email protected] (M. Yesilaras) Ersin Aksay, MD School of Medicine, Dokuz Eylul University Department of Emergency Medicine, Izmir Turgay Yılmaz Kilic, MD Izmir Tepecik Research and Educational Hospital, Department of Emergency Medicine, Izmir http://dx.doi.org/10.1016/j.ajem.2014.05.043

References

Figure. Bilateral excessive pneumocephalus, cerebral infarction, and edema were showed in the CT.

Most venous air embolism occurs with preventable iatrogenic causes. The following are the most important protective measures: (1) in patients with peripheral catheter, set of serum should be at least 20 cm below the level of the patient as to form siphon; (2) the Trendelenburg position should be given to the patient during central venous catheter insertion or removal; and (3) patients during the removal of the central catheter should perform Valsalva. Pneumocephalus should be considered for those are who admitted to the ED with altered mental status in patients with central line.

[1] Tran P, Reed EJ, Hahn F, et al. Incidence, radiographical features, and proposed mechanism for pneumocephalus from intravenous injection of air. West J Emerg Med 2010;11(2):180–5. [2] Opeskin K, Burke MP, Lynch M. Cerebral air embolism due to disconnection of a central venous catheter. J Clin Neurosci 1998;5(4):469–71. [3] Weiss KL, Macura KJ, Ahmed A. Cerebral air embolism: acute imaging. J Stroke Cerebrovasc Dis 1998;7(3):222–6. [4] Schlimp CJ, Loimer T, Rieger M, et al. The potential of venous air embolism ascending retrograde to the brain. J Forensic Sci 2005;50(4):906–9. [5] Heckmann JG, Lang CJ, Kindler K, et al. Neurologic manifestations of cerebral air embolism as a complication of central venous catheterization. Crit Care Med 2000;28(5):1621–5. [6] Ely EW, Hite RD, Baker AM, et al. Venous air embolism from central venous catheterization: a need for increased physician awareness. Crit Care Med 1999;27 (10):2113–7. [7] Pellisé A, Ustrell X, Ruiz V, Guedea A. Retrograde venous cerebral air embolism as a cause of stroke. Neurologia 2012;27(2):119–21. [8] Palmon SC, Moore LE, Lundberg J, Toung T. Venous air embolism: a review. J Clin Anesth 1997;9(3):251–7. [9] Moon R. Hyperbaric Oxygen Committee Report 2003: air or gas embolism. Undersea Hyperb Med 2003;5:5–10.

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