Head trauma, with or without skull fracture, induces immediate primary injury including, if severe enough, vessel disruption and tearing or crushing of brain parenchyma. If this primary injury is not severe enough to induce immediate death, the development of secondary injuries during the following hours, including hemorrhage, edema, increased intracranial pressure (ICP) and over all, ischaemia, might. The clinician is helpless during the first injury; however, through rapid medical and surgical intervention, he may slow or reverse the second one.
The second injury mechanism
Tissue ischaemia is the most devastating consequence that may occur after a cranio-cerebral trauma. Ischaemia is due to reduction of cerebral blood flow (CBF). The CBF decreases when the ICP increases without concomitant augmentation of the arterial blood pressure; the CBF may also decrease when the cranial venous outflow is impaired because of edema, hemorrhage, or cervical trauma. ICP starts to increase once the cerebrospinal fluid (CSF) and blood redistribution buffering capabilities are exhausted respectively by reabsorption or displacement of CSF and brain vasoconstriction. Intracranial perfusion regulation is usually maintained by means of vascular constriction/dilation in a normal brain. In an injured brain, this ability may be lost. PaCO2, pH, and PaO2 influence the autoregulation response of the cerebro-vasculature. Increased PaCO2 and hypoxemia, frequent findings in traumatized patient, will cause vasodilatation and increase ICP. Ischaemia triggers the Cushing reflex, ultimate guarantee in CBF maintenance, by increasing the systemic arterial pressure. ICP will finally increase too.
Brain edema is the source of the increased ICP. The traumatic disruption of the blood brain barrier explains its vasogenic extracellular component. Liberation of vasoactive substances and the osmotic effect of interstitial byproduct from dead cells will also increase its development. The cytotoxic intracellular component of brain edema results from abnormal cell metabolism caused by ischaemia. The all-molecular chain reaction drives to more vasogenic and cytotoxic edema and higher and higher intracranial pressure.
Patient evaluation
Cranio-cerebral traumatized patients are often “multi-traumatized” patients. Patency of airways must be checked as we have seen that high PaCO2 and low PaO2 increase intracranial pressure. Look for major chest trauma.
The patient is then treated for hemodynamic instability and the abdominal cavity is assessed for organ trauma/rupture (spleen, bladder, kidney detachment, etc.). Cerebral hypoxia due to hypovolemia is rare because of the pressure autoregulation, unless severe internal hemorrhage is present.
Finally, the neurological assessment status is assessed; this will be hourly. Although less mechanically unstable than vertebro-medullary trauma, the head trauma patient must be handled with care. The head is elevated no more than 30°; this facilitates venous and CSF outflow from the skull. State of consciousness, breathing pattern, menace response, nostril sensitivity, pupillary size and reflex, ocular position and movements, limb proprioception, and skeletal motor function must be evaluated.
A decreased level of consciousness (from depressed to delirious, stupor to coma) suggests cortical or brainstem (reticular activating system) injury. The prognosis and the treatment being different; it is essential to rapidly differentiate a supratentorial from an infratentorial lesion. Asymmetry in the menace response, in the nostril stimulation response, or in limb proprioception without other cranial nerve deficit, is in favour of a contralateral hemispheric lesion. Stuporous brainstem injured patients, showing multiple cranial nerve II to XII deficits, have a more guarded prognosis.
If no chest trauma has been identified, abnormalities in respiratory pattern are either of metabolic (acidosis, hypoxia) or neurological origin (mesencephalic, brain stem, cervical). Hyperventilation and periods of apnea alternation (Cheyne-Strokes respiration) is secondary to diencephalic decreased PaCO2 responsiveness. When the brain stem is severely damaged, the respiratory pattern becomes irregular in rate and amplitude and is associated with bradycardia.
Extensor rigidity is a form of UMN presentation. If all four limbs are extended, both hemispheres are involved (decerebrate rigidity); consciousness is altered but PLR are normal if herniation is not a consideration. If the forelimbs are flexed and the rear limbs extended, the cerebellum is involved (decerebellate rigidity); consciousness is preserved but menace response may be lost.
Increased ICP must be suspected when the PLR is abnormal (or deteriorating toward non-responsive midrange or dilated pupils) in parallel with deterioration of consciousness, extensor rigidity, and abnormal respiratory pattern. Direct bilateral unresponsive pupils, symmetrical or not, indicate brainstem injury. Transition from myosis to mydriasis suggests a progressive lesion often secondary to sub-tentorial occipital herniation. Pupillary paralysis is due to dorsal pressure of the swollen brain on the oculomotor nerves.
Petrosal bone and internal ear injury induces peripheral or central vestibular signs that may be impressive with the animal rolling on his side continuously. The neurological exam on these patients is difficult initially. Proprioception deficit on one side localizes the lesion to the ipsilateral central vestibular system.
Diagnostic tools
Skull radiographs are difficult to read. However, fracture lines or displacement must be looked for. Cerebellar injury associated with occipital bone fracture/displacement is easily visualized by a lateral radiograph. This type of trauma induces a major ataxia but has a good prognosis with or without surgery.
Computed Tomodensitometry (CT) shows skull fractures and haematomas. After three to six hours, an acute infarct produces a hypodense area secondary to edema. The maximal effect is seen after three to five days. However, some infarcts may be isodense and visible only after contrast enhancement after 24 to 48 hours, even more after one to two weeks because of neovascularization. After two to three weeks, edema resolves and the lesion becomes isodense. After four to eight weeks, necrosis creates a cavitation with a density close to the cerebrospinal fluid (CSF). Subdural haematomas may not be as rare as originally reported in the veterinary literature. The image density is immediately decreased, even more after a few days when the clot organizes. Haematomas become isodense after a month.
Magnetic Resonance Imaging (MRI) is more suitable for brain ischaemia and edema evaluation. Early changes are detectable: hypointense in T1 weighted images and hyperintense in T2. Paramagnetic enhancement is identical to tomodensitometry. In case of hemorrhage, the image intensity depends about the hemoglobin content and form (oxy, desoxy, methemoglobin, hemochrome, hemosiderin), its location intra or extra erythrocytic, and the weight of the images. Magnetic resonance angiography is a non-invasive way of doing angiography. Both CT and MRI are suitable to assess indirect signs of increased ICP by compression or asymmetry of the ventricles and shift of the midline.
Brainstem auditory evoked response (BAER) is interesting to confirm a petrosal bone or middle/internal ear injury usually associated with vestibular signs. Abnormal results may indicate the need for a CT. With ICP increase, the BAER shows reversible decreased amplitude and increased latency. This test may be of prognostic value. Biopsies, surgical or ultrasound guided, allow a final diagnosis to be made.
Treatment
The treatment is modified according to the neurological status, the neurological signs and their changes over time. One aim is to treat edema. While vasogenic edema is responsive to therapy, cytotoxic edema, once initiated, is not. The treatment is thus directed at preventing the creation of ischaemia and decreasing its degree and duration by working with drugs on the vasogenic edema already present and minimizing the cytotoxic edema to come.
Although hypovolemic shock is not the direct cause of brain ischaemia, hypovolemia decreases brain blood flow. Hypertonic saline (7.5% NaCl , 35 ml/Kg) is the solution of choice to restore volemia. It improves cardiac output, restores systemic blood pressure and has a slight dehydrating effect on brain tissues. Colloids (hydroxyethyl starch and dextran, 20 ml/Kg) are then used to maintain the intravascular volume. Central vascular pressure is monitored.
Second, it is essential to guarantee hypocapnia and good O2 delivery (Pa O2 > 80 mmHg). Hypercapnia (Pa CO2 > 40 mm Hg) and hypoxia induces vasodilatation, which increases ICP. Intubation is necessary if the patient is unconscious. Oxygen delivered by nasal catheter or by oxygen cage must be provided if the patient is not. Although effective in decreasing ICP, aggressive hyperventilation may aggravate hypoxia because of excessive vasoconstriction and may exacerbate focal ischaemia and edema.
Third, the use of mannitol is a common step in cranial trauma. Mannitol is a hyperosmolar molecule that dehydrates the cerebral interstitium, lowering ICP. Mannitol also decreases blood viscosity, promoting cerebral perfusion; it also has free radical scavenger ability which limits the deleterious molecular cascade induced by ischaemia. After fluid resuscitation, the risk of a rebound effect on the ICP is minimized. Mannitol may theoretically be detrimental in cases of active bleeding or severe rupture of the blood brain barrier, however, this has not been proven. Imaging is the only way to detect a hemorrhage or a large edema. However, imaging facilities are not always available. One should consider that if the patient is deteriorating with time, mannitol is the best option to reverse the process. The recommended dosage is 0.5 to 1g/Kg over 20–30 minutes IV. It will have a longer beneficial effect if given at 0.25 to 0.5g/Kg over 60 minutes potentialized with 0.7 mg/Kg of furosemide IV, 15 minutes later; however, this may lead to more serious hyperosmolarity and may aggravate the rebound effect.
ICP measurement necessitates an epidural, subarachnoid or intraventricular fluid filled catheter and a pressure transducer. The necessity of monitoring ICP is still debatable (risk, cost, interest, etc.). It is probably an indirect way to monitor the neurological status when the patient is comatose, or sedation or anesthesia is required and neurological status cannot be evaluated differently. Oxymetry, electroencephalography, and transcranial Doppler sonography are used in human medicine.
The methyl prednisolone protocol as a free radical scavenger is not used in head trauma patients. The classic corticotherapy largely used in neuro-oncology to treat vasogenic edema is not useful against cytotoxic edema encountered in the second injury type. Side effects are not negligible: they favor gluconeogenesis and maintain a hyperglycemic state known to be deleterious. They favor anaerobe metabolism and increase glutamate levels and neuronal death. The GI side effects are also important in patients who already have an autonomic imbalance.
Inducing barbiturate coma (5–15 mg/Kg) is indicated when patient disorientation may be deleterious, or when the control of the ICP augmentation is poor. Respiratory rate, blood gas and arterial pressure must be monitored. Debilitated, these patients usually do not drink their daily water needs. Perfusion and control of hematocrit, total protein, electrolytes and diuresis is recommended.
In case of seizures, diazepam (0.2 mg/Kg), midazolam, and phenobarbital (5–15 mg/Kg) are used in IV bolus or continuous infusion. The need to pursue the treatment for six months after the initiation of anti-epileptic drugs is controversial.
Head trauma patients have caloric needs much above normal; a nasogastric tube for assisted enteral nutrition or parenteral nutrition should be instituted as soon as possible to avoid chronic hyperglycemia.
Classic nursing care for recumbent animals must be provided (head up 30° maximum, eye lubricant, regular decubitus change, bladder catetherization, soft physical therapy, etc.).
Surgery indication is individual. Linear and elevated fractures will be treated conservatively as well as stable depressed or trans-sinus fractures. Haematoma with a significant mass effect, penetrating wounds or unstable depressed fractures will be treated surgically. Short acting barbiturates are used for induction and isoflurane is the inhalant anesthetic of choice because it does not increase ICP.
Prognosis
The Glasgow scale as used in human medicine is not suited to veterinary medicine. The pupillary reflex and state of consciousness may be a good barometer of the neurological status. The association of depression and myosis, uni- or bilaterally, indicates an increased ICP. Cerebral herniation induces parasympathetic stimulation and later paralysis explaining respectively myosis and later mydriasis. Irregular respiratory rate and unresponsive bilateral mydriasis indicate a poor prognosis. The modified Glasgow scale adds grades for the level of consciousness (1: coma to 6: alert), motor activity (1:LMN to 6: Normal), and brain stem reflexes (1: complete paralysis to 6: normal). Prognosis is bad from 3 to 6, guarded from 9–14, good from 15–18. Euthanasia should be considered on patients showing intractable seizures or severe respiratory failure. Others may recover unpredictably well, at least to be suitable, autonomous pets.