We are grateful to both correspondents for their stimulating comments. The experience of Drs. Schummer with ultrasound is highly informative and potentially useful for preventing both short-term and long-term complications of jugular cannulation. We agree with them that a previous estimation of the left internal jugular vein (IJV) size in our case could have been extremely useful and that alternative venous accesses should have been used.
The calculations given by Khorasani et al. are detailed and intriguing but based on questionable assumptions and partially incorrect. Briefly, they assumed a caliber of the left IJV, calculated a reduction in its caliber, extrapolated a small reduction in flow, and concluded that this reduction could not explain the observed massive intracranial pressure (ICP) increase. 1The caliber of the left IJV in our patients is unknown. It has been reported that the caliber of the IJV is highly variable and that there is asymmetry between the two sides. In fact, the IJV diameter may range from 2.5 to 12 mm. 2,3The assumed left IJV cross-sectional area is based on an article 4in which the authors acknowledged as a limitation of the study the inaccuracy of the method used to estimate the jugular vein diameter. We would be reluctant to apply data from that article to this specific patient. Khorasani et al. calculated the reduction of the left IJV caliber due to cannulation as the difference between cross-sectional areas, which is appropriate for perfectly coaxial tubes, without considering that the catheter enters into the vessel with a slope. The vein wall is thin and extremely deformable; therefore, the geometry at the level of cannulation could have been profoundly distorted.
However, even accepting these assumptions, Khorasani et al. did not consider that the resistance to flow is inversely proportional to the forth power of the radius, if laminar flow is likely to occur. Therefore, in their simplified model, the reduction of the left IJV radius caused by the introducer would cause an 11% resistance increase, rather than a 4.4% increase.
Finally, Khorasani et al. state that a 50% reduction in the cross-sectional area is required for almost doubling ICP: This assumption is definitely wrong. Intracranial pressure is not linearly related to cerebral blood flow because it depends on intracranial volumes, including cerebral blood volume, and intracranial elastance. When intracranial elastance is critically reduced, an increase in cerebral blood volume as small as 2.8 ml may increase ICP from 30 to 50 mmHg (assuming a pressure volume index of 13 ml, which is the critical value reported by Marmarou et al. 5). Therefore, a small change in venous outflow can cause a sharp ICP change if cerebral blood volume changes even slightly in the context of exhausted intracranial compensatory mechanisms.
The response of the intracranial vasculature to an abrupt ICP increase is complex and usually implies a marked vasodilatation to keep cerebral blood flow constant despite the reduced cerebral perfusion pressure. The opposite happens when the venous outflow improves, because an increase in cerebral perfusion pressure could induce vasoconstriction, which may explain the “overshooting” of ICP after removing the introducer. 6We cannot prove this assumption in our clinical case because we did not measure blood flow and intracranial elastance; therefore, we propose our interpretation of the facts as probable rather than proven, as we specified in our case report.
We believe that increased resistance to blood flow in the IJVs due to vascular cannulations remains a potential cause of sudden and deleterious ICP increase.