PATIENTS with intracranial hypertension frequently require central venous catheterization. When intracranial elastance is normal, venous drainage from the brain is not usually impaired by jugular bulb cannulation, 1and even during bilateral cannulation, no increase in intracranial pressure (ICP) has been reported. 2However, when intracerebral compensatory mechanisms are exhausted, large-caliber catheters in the jugular veins may critically restrict venous outflow and cause a substantial increase in ICP.
We describe a patient with intracranial hypertension managed with aggressive medical treatment. We believe that in this patient, a reduction of cerebral venous drainage from bilateral cannulation of the internal jugular vein was probably the cause of an additional severe increase in ICP.
A 22-yr-old woman with a weight of 55 kg and height of 172 cm was admitted to the neurosurgical intensive care unit after suffering a head injury in a traffic accident. At admission, the Glasgow Coma Score was 8, and the computed tomography scan showed a fracture of the left petrous ridge, a small left temporal laceration, and bifrontal contusions. 3,4A subdural catheter was placed, and ICP and mean arterial pressure were continuously recorded and stored through an analog-digital converter in a computer for analysis.
Intracranial hypertension was present from the beginning (opening pressure, 30 mmHg) and was associated with desaturation of the jugular blood (jugular hemoglobin oxygen saturation, 44%; arteriojugular O2difference, 7.6 ml/dl). Desaturation was corrected by reducing the cerebral metabolic demand by using propofol and fentanyl and increasing the arterial oxygen content with erythrocyte transfusion, aiming at keeping the hemoglobin level in the range of 9–10 g/dl. 5
Intracranial hypertension was treated according to published guidelines. 6Because the usual steps failed to control it, barbiturate coma was started. Noradrenaline infusion was necessary to keep a cerebral perfusion pressure above the threshold of 60 mmHg. 7It is our policy to insert a Swan–Ganz catheter in all patients who require barbiturate coma and vasopressor infusion. Because a 16-gauge catheter (Arrow International, Inc., Reading, PA) had already been retrogradely placed with the tip in the bulb of the right internal jugular vein for jugular hemoglobin oxygen saturation measurement, an 8-French introducer (Arrow International, Inc.) for the Swan–Ganz catheter was inserted in the left internal jugular vein. The patient was paralyzed, and her head and torso were placed in a flat position. The ICP and mean arterial pressure transducers, zeroed at the external meatus, followed the body position change, so that the recording continued with reliable data. The ICP increased during the maneuver and manual hyperventilation was necessary.
The head was slightly rotated for easier anatomic reference, and the left internal jugular vein punctured without problems. At the end of the cannulation, with the head and neck in a neutral position, the ICP increased to 50 mmHg. All possible causes (e.g. , malpositioning of the head, pneumothorax, respiratory changes, Pao2and Paco2changes, pain, hyperthermia, seizures, and rapid changes in blood pressure) were excluded. We suspected that simultaneous cannulation of the two internal jugular veins, especially with a second large-bore catheter, might have critically reduced cerebral venous drainage. Leaving the Swan–Ganz catheter in place, we withdrew the introducer from the vein; the ICP suddenly decreased to previous values (fig. 1). No other therapeutic maneuvers were active at that moment, so a clear cause–effect relationship was identified.
Barbiturate coma controlled the ICP, and the subsequent clinical course was unremarkable. At discharge from the intensive care unit, the patient could obey simple orders; after 6 months, she had achieved a good recovery.
Although the intensive care unit is meant to provide a safe environment, many maneuvers are risky. 8Central vein cannulation involves a risk of pneumothorax. 9Cannulation of the internal jugular vein toward the mediastinum is routinely preferred because it is not associated with any greater risk than subclavian cannulation 10and is widely used for Swan–Ganz catheter insertion. 11
Venous drainage from the intracranial cavity is mainly through the jugular veins. 12Severe reduction of their lumens therefore may impair venous outflow and cause intracranial blood volume to increase. Compression of the jugular vein is, in fact, recognized as a potential cause of intracranial hypertension. 13,14
Any increase in intracranial volume will be reflected in ICP, depending on the capacity of compensatory mechanisms. Although we did not measure intracranial elastance, we can reasonably assume that this patient was at a steep point in her pressure–volume curve. ICP was greatly increased because of voluminous bifrontal contusions, and her basal cisterns were not visible on the computed tomography scan. At this critical point, even a slight increase in cerebral volume may cause a substantial increase in ICP. However, restoration of the venous drainage rapidly decreased it.
In the literature, we found no reports that ICP may be significantly affected by central vein cannulation, even when bilateral retrograde cannulation of the jugular veins is performed. 15
In cases with bilateral cannulation, however, the diameters of the catheters were always smaller than the introducer used in this case. When ICP is high and limited buffer capacity of the intracranial system is suspected, maneuvers causing any additional increase in the intracranial volume, such as bilateral cannulation of the internal jugular veins with large-bore catheters, should be avoided.