Commentary 4.3.1.

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POSTTRAUMATIC CEREBRAL TURGESCENCE

Pavel Kalvach

Since several decades it is known that brain tissue reacts to severe head injury by enlargement of its volume. Following some types of head trauma brain parenchyma prolapses out of the surgical field. At autopsy the brain shows increased weight, flattened gyri and effecement of sulci on the convexities. Until the beginning of the eighties these situations were almost without exception regarded as cerebral edema. This diagnosis is however correct only in some instances while in others this state is caused by a completely different and, as described below, in some aspects even a contradictory process.

Cerebral turgescence means an increased volume of blood in cerebral vessels. It can affect the brain as a whole, then speaking about a diffuse, bilateral turgescence, or it can just affect one of its hemispheres, as a hemispheric, unilateral turgescence. The intravascular hypervolemia is caused by relaxation of smooth muscles in the vessel wall. Meaning hereby an enlargement of cerebral blood volume, this phenomenon differs completely from edema, which is due to an increase of water.

Etiopathogenesis
Under normal circumstances the vascular tone is maintained, besides of the vascular elasticity, mainly by vasoconstrictive effect of sympathetic nerves, accompanying the arterial tree in adventitia. Cerebral concusion elicits vasoparalysis, a fact known since Walker‘s description in 1956. Its mechanism however is still not known. One can assume that its cause is located with high probability directly in brain tissue, but it could also arise as vasoregulatory failure due to simultaneous injury of the cervical sympathicus. Vasodilatation occurs mainly in the periphery of the vascular bed: in the arterioles of smaller than 200 um diameter and especially in the area of arteriolo-venular shunts. These shunts, allowing the arterial blood to circumvent capillary bed, are found to a larger extent in the white matter1. For this reason, Shulman after his experimental works on dogs, called these states “shunt hyperemia” 2. Since the arteriolo-venular shunts are much more developed in children, the extent of cerebral turgescence uses to be much expressed in young age 3. The overfilling of tissue with intravascular blood is – again especially in children – mainly present in the white matter.

What is the usual volume of intravascular blood in brain? Under physiological conditions, three compartments form the content of the cranial cavity: brain tissue, cerebrospinal fluid (CSF) and blood. Intravascular blood represents 5% of the brain volume and participates in reciprocal fluctuations according to the Monro-Kellie doctrine. An enlargemnent of the blood compartment means reduction of the CSF compartment by squeezing CSF out of the ventricles and from the surface leptomeningeal spaces. The volume of blood compartment can, as a result of a blunt haevy blow increase up to fourfold.

Cerebral hyperemia, as a result of brain trauma or ischemia, was called by Langfitt in 1965 “vascular engorgement” 4. Besides of this, a number of other names exist in literature: vasogenic inflation, cerebral congestion, swelling. Our own term “turgescence” means swelling, sprouting, enlargement. We have chosen it to distinguish from edema. The edematous changes, caused by an excess of water, may afflict either interstitium, or cells. Either of them reduces the relative content of dry brain substance. The first one, the extracellular edema, spreads out in the tissue by streaming, and leaks on cut. The latter, the intracellular edema is fixed in cells, causing consequently a “mass effect” and does not drop out on cut (dry “edema”).

The enlargement of intravascular blood volume is an issue completely different from edema, although from the macroscopic aspect the brain is in both situations augmented similarly. When we reported on the cerebral turgescense for the first time in 1984, Prof. Mraèek quoted in discussion Prof. Jirásek‘s remark over a swelled traumatic brain on surgery many years before: “the brain is weeping blood”. Because the terms of “swelling”, “Schwellung” were in older literature already reserved for the dry types of edema and moreover they have been incorrectly used for enlarged hemispheres due to e.g. cerebral hemorrhage, we have introduced the term of turgescence in 1984.

Analogic states of generalized vasoparalysis also arise in global ischemia, predominantly in temporary heart failure5.

Clinical aspects
Cerebral turgescence usually starts after a blunt blow to the head. In most instances the comatous state prevails from the injury. In others the first stage runs under the image of cerebral commotion: a short, several seconds lasting unconsciousness or only a short disorientation with confusion and quick recovery. After a lucid interval of 1 or more hours the orientation deteriorates again, consciousness is getting lost, first qualitatively, later on quantitatively. After a short somnolence or sopor a coma begins. From the clinical view this development could well mimic an extracerebral hematoma. Those lucky individuals, who would survive, regain their consciousness usually within several days.

In our group of 38 patients, we registered the turgescence mostly bilaterally, although the unilateral swellings were also not rare. The finding was sometimes combined with other traumatic lesions: subarachnoid hemorrhage (more often with diffuse swelling) or subdural hematoma (more frequently in unilateral swellings). The longest states of turgescence lasted up to 10 days, in most cases however it took only 1 – 3 days. The re-establishment of the vascular tone is usually a matter of 5 – 8 days. On artificial ventilation we observed spontaneous recovery also after as long as 16 days of coma. Nevertheless the overall mortality amounted to 20%, being the highest in children.

The neuroradiological aspect.
The biggest enlightenment to our knowledge of intracranial compartments has been obtained by computed tomography. Very interesting alterations are however apparent also on angiography6.

CT examination detects the enlargement of cerebral volume to the expense of CSF spaces. The swelling of the brain pushes the CSF out of the ventricles, sometimes up to their total collaps. The leptomeningeal cisterns – mainly the Sylvian fissure and the perimesencephalic spaces – disappear from the CT scan. In the homogenous, augmented, brain tissue the difference between the gray and white matter is fully or partially gone. This phenomenon is caused by the engorged vasculature mainly in white matter, in which its usual hypodensity (of 30 H) compared to the gray matter (36 H) is getting concealed by the influx of hyperdense blood (52 H). When intravenous contrast administered, the density increases predominantly in white matter, where it might sometime even exceed that of the gray matter.

With the recession of turgescence the native brain density decreases, but may regionally persist in areas, where the recovery proceeds more slowly. When posttraumatic hyperemia is unilateral, it is sometimes combined with extracerebral hematoma and here it‘s important to distinguish the mass-effect of the expanded hemisphere from the dislocating effect of a subdural or epidural hematoma. The hematomas can be in some of these volume shifts occasionally of lesser importance.

Cerebral angiography, although being a good contribution to traumatic work up, usually does not belong to the diagnostic schedule. If done, out of specific motives, it shows the iodine contrast getting lost during the capillary phase. Because the arteriolo-venular shunts are distended the transfer of contrast to the venular blood bed is considerably slowed down. The arterio-venous transit time can increase from its normal values of 3.5 sec up to more than 6 sec. Reaching values of up to 8 sec, it signals the last limits of a possible survival. Therefore it is important to pay attention on angiography not only to the morphology of depicted vessels, but also to the passage of contrast medium to the venous phase in adequate time intervals.

The therapeutic aspect
Therapeutic possibilities are relatively poor. It is necessary to avoid any vasodilating interventions. It is imperative to prevent acidosis, which would only worsen the vasodilatation. Our effort to attain alcalosis bases on the fact, that a fall of pCO2 of 1 kPa (7,5 torr) would cause a diminution of cerebral blood volume of 0,32 ml/100 g tissue7, which would represent for the whole brain about 4 – 4.5 ml. If it shows, that some mechanisms of shunt dilatation are partially analogous with those of migraine (which I deduce from some interpretations), then the antagonist of serotonin receptors, sumatriptan, might be a big hope.

References:

  1. Newton TH, Potts DG, eds.: Radiology of the skull and brain.Angiography. St.Luis: Mosby, 1978?
  2. Shulman K: Small artery and vein pressures in the subarachnoid space of the dog. J Surg Res 1965,5:56-61.
  3. Bruce DA, Alavi A, Bilaniuk L, et al: Diffuse cerebral swelling following head injuries in children: the syndrom of “malignant brain edema”. J Neurosurg 1981,54:170-178.
  4. Langfitt TW, Weinstein JD, Kassel NF: Cerebral vasomotor paralysis produced by intracranial hypertension. Neurology (Mineap.) 1965,15:622-641.
  5. Kalvach P, Jirout J: CT manifestation of local and generalized vascular engorgement due to trauma and ischemia. In Valk J, cd. Neuroradiology 1985/86. Amsterdam-New York-Oxford: Elsevier Science Publishers B.V., 1986:197-188.
  6. Marshall WJS, Jackson JLF, Langfitt TW: Brain swelling caused by trauma and arterial hypertension. Haemodynamic aspects. Arch Neurol (Chic) 1969, 21:545-553.
  7. Kirsch G: Pathophysiologie der Hirndurchblutung und CBF Messung. In: Schneider D, ed.: Zerebrale Hypoxie und Ischaemie vaskulaer- zirkulatorischer Aetiologie. Aktuelle Probleme der Intensivmedizin. Leipzig: J.A.Barth, 1982:22.

 

 

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Last updated: 2000-08-04