Article 7


Effect of External Cervical Spine Immobilization
on Intracranial Pressure


by:


Lim Ju Boo



Following my discussion on pelvic injuries, I would now turn a little to injuries to the superior part of the body - the head. A head injury is a common cause of death in MVA (motor vehicle accidents) in Malaysia. The pathophysiology in head injuries, besides other features like subpial and subarachnoid haemorrhages, and extradural haematoma, there is also a rise in the intracranial pressure. But we are not going to discuss about bleeding or other damages to the brain as right down I am concentrating and commenting on a paper I read on the application of external cervical spine immbolisation and intracranial pressure. But before I can do this, let me briefly explain what intracranial pressure is all about?

Intracranial pressure or ICP is the pressure of the cerebrospinal fluid (CSF) in the subarachnoid space between the skull and the brain. The pressure is normally the same as that found in during a lumbar puncture. There are many causes of elevated ICP after head injuries. Among the causes are:


• Haematoma

• Focal cerebral oedema associated with contusion or haematoma

• Diffused oedema after ischaemia (cytotoxic)

• Generalized or diffuse brain swelling (‘brain enlargement’)

• Obstruction of the cerebrospinal fluid circulation (rarely)


We now ask, what happens when the pressure within the skull occupied by the cerebrospinal fluid begins to rise following a head injury or in some major pathologies (such as in Reye’s syndrome in children). Once we understand this pathophysiology, we are ready to proceed to discuss its clinical importance in head injuries, before proceeding even further in discussing a paper by Kuhnigh and his colleagues.

Monro-Kellie Doctrine:

In a dogmatic teaching by a Scottish anatomist, Alexander Monro, Jr. (1733-1817), as far back as in 1783, and another Scottish anatomist George Kellie in 1824, they came out with a theory linking ICP and cerebral blood flow. Munro was also the President of the Royal College of Surgeons, and also a Professor of Physics (surprisingly), Anatomy and Surgery at the University of Edinburgh. He made a number of observations in his publication called ‘Observations on the Structure and Function of the Nervous System’ (1). Both of them advanced a dogmatic teaching, what is now known as the Monro-Kellie Doctrine, which states that since the cranial cavity is a closed rigid box, and that therefore a change in the quantity of intracranial blood can occur only through a displacement or of a replacement by cerebrospinal fluid. Briefly, that means when there is a rise in the intracranial pressure (intracranail hypertension) due to an accumulation of CSF, there would be a compensatory decrease in the blood flow to the brain to maintain normal ICP. The original doctrine was simple as it did not take into account the CSF or the spinal portion of the craniospinal compartment. Other researchers such as Burrows, Weed, Flexner and McKibben (3, 4) later modified the original doctrine. They established a reciprocal and compensatory relationship between blood flow and the volume of CSF. An increased in ICP naturally will decrease the cerebral perfusion rate and a resultant cerebral ischemia. A declining perfusion rate likewise is counteracted by the body by a rise in the mean arterial pressure. If the ICP continues to rise, the arterial pressure will also rise in respond, with a subsequent drop in the pulse rate and an increase in the respiratory rate. This respond, due to any space-occupying lesion (say a brain tumor, blood clots, generalized compression due to hydrocephalus, meningitis and subdural haemorrhage) is called Cushing’s syndrome, named after a U.S. neurosurgeon, Harvey W. Cushing (1869-1939).

Using animal models Cushing, in 1902 was able to show that the ICP rises slowly initially, and more rapidly as the volume increases (2). This compensatory mechanism can only go on up to a critical point until the built-up of ICP can no longer be compensated, and the continued ischemia (blood supply insufficiency due to ICP compression or tamponade effect) will injure the brain further, leading to hypoxia, and ultimate death. Intracranial hypertension if excessive can also cause herniation (prolapse) of the brain by forcing portions of the brain downwards through the foraman magnum (large hole at base of skull that transmit the medulla oblongata), and obviously this is going to damage the brain even more.

This is briefly what Monro-Kellie Doctrine is all about, and how this patho-physiological event, eventually becomes one of the causes of death in a head injury. An understanding of this mechanism makes it clearer for us to comprehend the seriousness of ICP elevation (IC hypertension) in head injury patients, besides other types of injuries to the brain of course. With that brief explanation and introduction, I am now more confident and prepared in trying to explain to my readers the importance of an elevated ICP, and a paper I have just read in connection with applying a neck collar. This is summarized below.

ICP link:

ICP in A link between an elevated ICP and the application of a cervical collar has been a suspected previously. This was investigated by a team of German neurosurgeons in the 1993 led by Kuhnigk et al. (5). The team measured the ICP in 18 patients with severe head injuries in the neurosurgical intensive care unit before and after placement rigid collar for cervical spine immobilization.

The purpose of the study was to determine whether the rigid collars, commonly use for the prevention of cervical spine movement during transport by paramedics, first responders and first-aiders to a treatment facility could lead to an increase in ICP ? Patients who had an *epidural transducer (An epidural transducer is an electronic device, fitted with baro (pressure) sensors or gauge that measures ICP within the cranial cavity, namely the outer membrane (dura) and the brain tissues deeper down, including the pressure inside the ventricles, if a separate intraventricular catheter is inserted in place) were studied, and their ICP recorded during the placement of either the Spieth cervical collar (n = 12) [ in scientific language and for statistical analysis, ‘n’ stands for the number (population) in a case study. In this case there were 12 patients being studied], or the Philadelphia cervical collar (n = 6). The baseline ICP was 17.0 +/- 6.1 mmHg (mm Hg means millimetres of mercury) versus 17.7 + / - 6.4 mm Hg 10 minutes after placement of the cervical collar.

Five minutes after removal, the ICP was 17.2 +/- 5.9 mmHg. No (statistically) significant changes in ICP could be demonstrated during this study. Placement of the cervical collar is a simple and practical measure to immobilize the cervical spine during rescue, and during the transport of intubated and ventilated patients. Its risk of increasing the ICP appears to be low even in patients with severe head injuries.

So there we are, we see how medical research of this sort (although only a very small study) can come to the aid of first-aid itself, and dispel our fears of applying a collar on trauma victims with head injuries as is usually practiced by paramedics, first-responders and first-aiders and even in the emergency room of a hospital. (By the way you might be wondering what the normal ICP is? Well, the normal ICP is about 10 mmHg. But it can go up to as high as 70 mmHg. in certain pathological conditions. The CSF which is largely responsible for the ICP, circulates over the entire brain and central nervous system at a rate of about 500 ml/day, and is formed at a rate of 0.4 ml./minutes. With this cycle, the CSF is renewed 4 – 5 times daily.)


* Foot-note:

The current devices in use in the neurological wards of hospitals for measuring ICP involve invasive procedures. The latest is a non-invasive modality, and is described in one of journals I received a month ago from the Royal Society of Health as a Fellow of The Royal Society of Health). The non-invasive work was done by Pension and Allen (6).


References:


1. Monro, A. Observations on the Structure and Function of the Nervous System. Edinburgh (1783). Creech and Johnson.

2. Cushing, H. Some Experimental and Clinical Observations Concerning States of Increased Intracranial Tension. Am J Medical Sciences. (1902), 124, 375-400.

3. Weed, L.H; Flexner, L.B. The Relationships of the Intracranial Pressures. Am J Physiology. (1933). 105, 266 – 272.

4. Weed, L.H; McKibben, P.S. Experimental Alteration of Brain Bulk. Am. J Physiology (1919). 48, 531 – 558.

5. Kuhnigk, H; Bomke, S; Sefrin. P. Aktuelle Traumatol. (1993, Dec.), 23 (8) : 350 – 3.

6. Penson, R.P. and Allen, R. Intracranial Pressure Monitoring by Time Domain Analysis. Journal of Royal Society for Promotion of Health. (1998, October). 118, No. 5. 289 – 294.