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Table of Contents    
Year : 2014  |  Volume : 62  |  Issue : 2  |  Page : 221-222

Cerebrospinal air embolism following percutaneous nephrolithotomy: Gravitational gradient effect

1 Department of Neurology, Gauhati Medical College and Hospital, Guwahati, India
2 Department of Radiology, Downtown Hospital, Guwahati, Assam, India

Date of Submission07-Feb-2014
Date of Decision08-Feb-2014
Date of Acceptance06-Apr-2014
Date of Web Publication14-May-2014

Correspondence Address:
Lakshya J. Basumatary
Department of Neurology, Gauhati Medical College and Hospital, Guwahati
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.132444

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How to cite this article:
Bhowmick S, Sarma K, Kayal AK, Basumatary LJ. Cerebrospinal air embolism following percutaneous nephrolithotomy: Gravitational gradient effect. Neurol India 2014;62:221-2

How to cite this URL:
Bhowmick S, Sarma K, Kayal AK, Basumatary LJ. Cerebrospinal air embolism following percutaneous nephrolithotomy: Gravitational gradient effect. Neurol India [serial online] 2014 [cited 2021 May 15];62:221-2. Available from:


Cerebral air embolism (CAE) as a complication of percutaneous nephrolithotomy (PCNL) has been observed in patients with or without intra-cardiac defects. [1],[2] Pyelovenous backflow may cause displacement of air from the renal pelvicalyceal system into the renal veins. The entry of gas emboli in arterial circulation is postulated to be via the pre-pulmonary arteriovenous arteriovenous (AV) shunts or directly through the pulmonary capillary bed. [2] Onset of symptoms in such cases is likely to be delayed by some hours in view of time taken for passage of emboli through the pulmonary vasculature. We report a case of cerebral and spinal air embolism following percutaneous nephrolithotomy in a patient with no evidence of intra-cardiac defects or AV shunts.

A 32-years-old male underwent PCNL under general anesthesia in prone position for left staghorn calculus in a private hospital. PCNL was supplemented with D-J stenting. Ten milliliters of air was injected during the procedure. Six hours later, during recovery from anesthesia he developed several episodes of generalized tonic-clonic seizures followed by altered mental status lasting for two days. He recovered with weakness in both lower limbs. There was no record of hypotension during PCNL. Neurological examination revealed conscious, alert and oriented patient with normal higher mental functions, normal cranial nerves, are flexic flaccid paraplegia with extensor planter response and loss of all modalities of sensation up to the level of the nipple. Magnetic resonance imaging (MRI) brain on day 3 revealed multiple hyperintensities on T2 weighted Fluid attenuated inversion recovery and diffusion-weighted images (DWI) in both the cerebral cortices in a gyriform pattern, hypointense on apparent diffusion coefficient (ADC) suggestive of acute infarction. Lesions were wedge shaped, located in cortical and sub-cortical zones bilaterally in watershed regions of both Anterior cerebral artery/Middle cerebral artery and Middle cerebral artery/Posterior cerebral artery zones. Hyperintense lesions were also noted in the splenium of corpus callosum and left-cerebellar hemisphere. MRI-angiography revealed no evidence of vascular abnormality. MRI spine showed hyperintensities from C7 to D12 in T2-weighted images [Figure 1]. Trans-esophageal echo (TEE) and Doppler using agitated saline did not reveal intra-cardiac shunt. EEG revealed slowing of background activity. Patient was treated with supportive measures and recovered with residual spastic paraplegia and is currently wheel-chair bound with an indwelling catheter.
Figure 1: MRI Images showing multiple wedge shaped hyperintensities on FLAIR (a and b), DWI in Brain (c) and longitudinally extensive hyperintensities in Spine on T2-weighted images (d)

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Large air bubbles introduced into a systemic venous source during surgical procedure shower the pulmonary arterial tree and get trapped, causing transient hypoxia. Consequent elevation of pulmonary arterial resistance may cause right to left shunt with a patent foramen ovale or pulmonary arteriovenous fistula. But small bubbles might pass through the pulmonary filtration system even without a detectable shunt. [3] Carotid arterial distribution strokes are more common due to more distant vertebral artery branching compared to a proximal common carotid artery origin from the aortic arch. However, site of lodgement of air emboli depends on the patient position at the time of event. Prone positioning during PCNL provides a gravitational gradient between the posterior vertebrobasilar circulation and the left heart facilitating entry of air emboli into the posterior vertebrobasilar circulation and the spinal artery. Cerebral arterial air embolism typically involves small arteries and induces pathologic changes by reduction in perfusion distal to the obstruction and an inflammatory response to the air bubble.

Temporal association of onset of symptoms with PCNL suggests that the air emboli may have directly entered the pulmonary venous system due to the supracostal approach. There was no identifiable risk factor for cerebrovascular accident in the patient. There was no evidence of intra-cardiac or pre-pulmonary shunt. Prone positioning during the procedure may have facilitated the lodgement of air emboli into the vertebrobasilar system including the spinal artery. A similar case of cerebral and spinal air embolism has been reported by Kachalia AG et al. from our country in 2011. [4]

Computed tomography is diagnostic only if obtained immediately because of rapid resorption of air from arterioles. Recent reports investigating the characteristics of CAE, as detected by MRI and DWI, have described scattered cortical gyriform high signal intensities. [5] Therapeutic options for cerebrospinal air emboli include hyperbaric oxygen and heparin. Hyperbaric oxygen presumably induces mechanical compression of air bubbles to a much smaller size and also results in delivery of high doses of oxygen to ischemic brain tissue. [6] Heparin may be useful because the surfaces of air bubbles are covered by a network of fibrin, platelets and fat globules, which induce neutrophil-mediated microvascular damage and activate the intrinsic coagulation cascade. [7]

  References Top

1.Song SH, Hong B, Park HK, Park T. Paradoxical air embolism during percutaneous nephrolithotomy: A case report. J Korean Med Sci 2007;22:1071-3.  Back to cited text no. 1
2.Tommasino C, Rizzardi R, Bretta L, Venturino M, Piccoli S. Cerebral ischemia after venous air embolism in the absence of intracardiac defect. J Neurosurg Anesthesiol 1996;8:30-4.  Back to cited text no. 2
3.Thackray NM, Murphy PM, McLean RF, deLacy JL. Venous air embolism accompanied by echocardiographic evidence of transpulmonary air passage. Crit Care Med 1996;24:359-61.  Back to cited text no. 3
4.Kachalia AG, Savant CS, Patil S, Gupta S, Kapadia FN. Cerebral and spinal air embolism following percutaneous nephrolithotomy. J Assoc Physicians India 2011;59:254-6.  Back to cited text no. 4
5.Jeon SB, Kim JS, Lee DK, Kang DW, Kwon SU. Clinicoradiological characteristics of cerebral air embolism. Cerebrovasc Dis 2007;23:459-62.  Back to cited text no. 5
6.Dexter F, Hindman BJ. Recommendations for hyperbaric oxygen therapy of cerebral air embolism based on a mathematical model of bubble absorption. Anesth Analg 1997;84:1203-7.  Back to cited text no. 6
7.Ryu KH, Hindman BJ, Reasoner DK, Dexter F. Heparin reduces neurological impairment after cerebral arterial air embolism in the rabbit. Stroke 1996;27:303-9.  Back to cited text no. 7


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