Combined craniocerebral and maxillofacial trauma. Multiple (combined) fractures of the facial bones and skull bones
CHAPTER VI COMBINED DAMAGES TO THE BONES OF THE FACIAL SKELETON. TRANO BRAIN INJURY.CHAPTER VI COMBINED DAMAGES TO THE BONES OF THE FACIAL SKELETON. TRANO BRAIN INJURY.
Combined injury- is simultaneous damage by one traumatic agent to two or more of the seven anatomical regions of the body.
The concept of “polytrauma” involves simultaneous damage to several parts of the body, organs or systems, when there is at least one life-threatening injury.
1. Combined traumatic brain injury.
With combined traumatic brain injury (CTBI), the facial skeleton, cranial bones and brain are simultaneously damaged. A closed traumatic brain injury (TBI) without damage to the skull bones, combined with fractures of the facial skeleton, is possible.
Fractures of the facial bones in combination with TBI are diagnosed in 6.3 - 7.5% of patients. The fairly high frequency of craniofacial injuries is due not only to their anatomical proximity, but also to the fact that some bones of the facial skeleton take part in the formation of the base of the skull.
The characteristics of TBI are based on the relationship between two defining factors:
1. Localization of extracranial damage.
2. The ratio of cranial and extracranial damage according to their severity.
In more than 1/3 of cases, TBI is accompanied by shock.
Erectile its phase is significantly extended in time and can occur against the background of impaired consciousness (as opposed to the classic one), accompanied by bradycardia, severe disturbances in external respiration, hyperthermia, meningeal signs, and focal neurological symptoms. In addition, the peculiarities of the anatomical relationship of the bones of the facial and cerebral skull lead to the fact that fractures of the facial bones, for example the upper jaw, zygomatic bone, as a rule, extend beyond their anatomical boundaries and the broken bone fragment often includes the bones of the base of the skull. In this regard, it is worth recalling the anatomical data relevant to the issue under consideration.
The anterior cranial fossa (fossa cranii anterior) is separated from the middle one by the posterior edge of the small wings of the sphenoid bone. It is formed by the orbital surface of the frontal bone, the ethmoid, sphenoid (lesser wings and part of its body) bones. It is known that they take part in the formation of the upper, inner and outer walls of the orbit, along which the fracture gap of the upper jaw passes in the middle and upper types.
The middle cranial fossa (fossa cranii media) is formed by the anterior surface of the pyramid and the scales of the temporal bone, the body and large wing of the sphenoid bone, which take part in the formation of the inner and outer walls of the orbit.
Between the lesser and greater wings, as well as the body of the sphenoid bone, there is the superior orbital fissure. The orbital surface of the upper jaw, together with the orbital margin of the greater wings of the sphenoid bone, limits the inferior orbital fissure.
Fractures of the upper jaw can be accompanied not only by fractures of the base of the skull, but also by concussion or contusion of the brain, the formation of intracranial
hematomas. To determine the correct tactics for examining and treating such patients, the dental surgeon must remember the main clinical signs of these injuries.
It is known that combined injury from a pathophysiological point of view, it is a pathological process different in content than equivalent damage to any one vital organ (for example, the brain). Her cannot be considered as a simple sum of damage to two or more anatomical areas.
The combined injury is severe in terms of the overall reaction of the body, despite the possible relatively minor damage to each of the organs involved. Possible disturbances in breathing, circulation, and liquor dynamics characteristic of TBI potentially lead to cerebrovascular insufficiency. Brain hypoxia and disturbances in its metabolism cause cerebral edema and central respiratory impairment. All this contributes to even greater brain swelling.
Thus, a vicious circle closes: damage to the brain causes disruption of all types of metabolism, and damage to other areas (maxillofacial, chest, etc.) enhances such changes and creates the preconditions for suppression of brain activity.
The mortality rate of patients with combined trauma ranges from 11.8 to 40% or more.
When systolic blood pressure decreases below 70 - 60 mm Hg. column, self-regulation of blood circulation in the brain is disrupted, which is accompanied first by functional and then morphological changes in the brain.
Respiratory failure is a serious complication that poses a threat to the life of the victim. In case of combined injuries, it can be of three types: respiratory disorder due to:
Central type
Peripheral type
Mixed type.
Breathing disorder central type is caused by brain injury, more precisely, by the respiratory centers located in the brain stem. In this case, the patency of the peripheral airways is not impaired. Clinically, this is manifested by a violation of the rhythm, frequency, amplitude of breathing: bradypnea, tachypnea, periodic rhythms of Cheyne-Stokes and Biot, spontaneous stopping.
Providing assistance for central-type breathing disorder consists of intubating the patient and providing assisted breathing.
Breathing disorders peripheral type can be caused not only by brain injury, but also by damage to the maxillofacial area. They arise due to obstruction of the upper respiratory tract, as well as the trachea and bronchi with vomit, mucus, blood from the mouth, nose and nasopharynx (especially with a jaw fracture), retraction of the tongue or displacement of the soft tissue flap, which acts as a valve that prevents the passage of air into the lungs.
Providing assistance with this type of breathing disorder consists of sanitation of the tracheobronchial tree, removal of a foreign body from the mouth and oropharynx.
Breathing disorders are more common mixed type, due to one and other reasons. It should be remembered that occlusion of the tracheobronchial tree leads to hypercapnia.
Restoring airway patency is accompanied by a decrease in CO2 levels in the blood, which can lead to respiratory arrest. In this clinical situation, artificial respiration is indicated until spontaneous breathing is restored.
2. Fracture of the base of the skull.
The base of the skull is weakened by numerous openings through which blood vessels and nerves pass. In case of a fracture of the base of the skull, the fracture gap is located in the
the path of least resistance, which determines the ambiguity of its location. Therefore, it is advisable to recall which holes are located in the anterior and middle cranial fossae, within which a fracture of the base of the skull can occur in patients with a fracture of the upper jaw. IN front the cranial fossa contains:
1. The cribriform plate of the ethmoid bone (Lamina cribrosa ossis etmoidalis) with numerous holes in it through which the olfactory filaments pass.
2. Blind opening (foramen coecum), which communicates with the nasal cavity.
3. Optic foramen (foramen opticum), through which the optic nerve passes. IN average The cranial fossa has the following openings:
1. Superior orbital fissure (fissura orbitalis superior).
2. Round hole (foramen rotundum).
3. Oval hole (foramen ovale).
4. Spinous foramen (foramen spinosum).
5. Ragged hole (foramen lacerum).
6. Internal carotid foramen (foramen caroticum interna).
7. Opening of the facial canal (hiatus canalis fasialis).
8. Superior opening of the tympanic tubule (apertura superior canalis tympanici). As an example, we can cite the most common location of the fracture gap of the base of the skull:
1) From the round foramen of one side through the sella turcica towards the ragged and spinous foramen of the other side.
2) From the foramen spinosum through the oval and round foramen to the optic foramen, spreading to the orbital surface of the frontal bone. Possible damage to the cavernous sinus.
3) From the canal of the hypoglossal nerve through the jugular foramen and the internal auditory canal (posterior cranial fossa) it goes to the spinous foramen, and then along the scales of the temporal bone. The pyramid of the temporal bone breaks.
If the base of the skull is fractured, the basal parts of the brain, brain stem, and cranial nerves may be damaged. Therefore, it is possible to establish general cerebral symptoms, brainstem disorders, and signs of damage to the cranial nerves. Bleeding from the ear (fracture of the pyramid of the temporal bone with rupture of the mucous membrane of the internal auditory canal and eardrum), from the nose (rupture of the mucous membrane of the upper wall of the nasal cavity, fracture of the ethmoid bone), from the mouth and nasopharynx (fracture of the sphenoid bone and rupture of the mucous membrane) can often be noted. membranes of the pharyngeal vault).
A Le Fort I and Le Fort II type fracture of the upper jaw is accompanied by a fracture of the base of the skull. When a fracture occurs in the anterior cranial fossa, hemorrhage occurs in the area of the periorbital tissue (strictly in the area of the orbicularis oculi muscle), subcutaneous emphysema, and nosebleeds. Nosebleeds occur when there is a fracture of the bottom of the anterior cranial fossa in the area of the roof of the nose, the posterior wall of the frontal sinus or the lateral wall of the ethmoid sinus and a mandatory rupture of the nasal mucosa covering these bones.
When the wall of the frontal or ethmoid sinuses is fractured, emphysema periorbital region, forehead, cheek. One of the clinical signs of a fracture of the base of the skull is the late appearance of "symptom of glasses"(hematoma in the eyelid area) in the absence of local signs of applied force to the soft tissues of this area. This is due to the fact that blood from the base of the skull in the area of the upper wall of the orbit penetrates the retrobulbar fatty tissue and gradually permeates the loose tissue of the eyelids.
May be liquorrhea from the nose (rhinorrhea). It should be recalled that for rhinorrhea to occur, in addition to a fracture of the base of the skull, a rupture of the dura mater and nasal mucosa at the site of the fracture is necessary. Nasal liquorrhea occurs when
fracture of the anterior cranial fossa only: in the area of the perforated plate, frontal, main (sphenoid) sinuses, cells of the ethmoid bone. The leakage of cerebrospinal fluid into the nose is possible through the openings of the ethmoid bone even in the absence of bone damage due to separation of the fibers of the olfactory nerve.
The liquorrhea stops a few days after the injury, when the wound of the dura mater, nasal mucosa and the fracture gap in the bone is sealed with clotted blood (fibrin).
It is known that post-traumatic liquorrhea is the leakage of cerebrospinal fluid from the cranial cavity when the bones of the base or vault of the skull, dura mater and integumentary tissues (skin, mucous membrane) are damaged. It is possible when the tightness of the subarachnoid space is violated (subarchnoid liquorrhea), when the walls of the ventricles are injured (ventricular liquorrhea), basal cisterns (cistern liquorrhea).
In case of fractures of the facial skeleton extending to the base of the skull, liquorrhea is of great clinical importance, since the cranial cavity freely communicates with the microbially contaminated nasal cavity, with the frontal, ethmoid, sphenoid sinuses, and cells of the mastoid process. The cerebrospinal fluid, becoming infected, flows into these sinuses, and there is a real threat of developing meningitis. Ear liquorrhea spontaneously stops in the first 2 to 3 days after injury.
The leakage of cerebrospinal fluid leads to a decrease in cerebrospinal fluid pressure. This is accompanied by headache and vestibular disorders. Patients are adynamic, occupy a forced position - they tend to lower their head down. If cerebrospinal fluid flows into the pharynx, a cough is provoked due to irritation of its mucous membrane. When the patient's position in bed changes (from back to side), the cough may stop.
According to the degree of increase in the risk of initial liquorrhea, fractures of the bones of the face and skull are located in the following sequence: fracture of the bones of the nose, upper jaw, Le Fort type I, Le Fort type II, ethmoid bone fractures. Liquor rhea is observed in more than 30% of patients with a fracture of the base of the skull. In 70% of patients with liquorrhea, hypotensive syndrome develops. Therefore, the observation of cerebrospinal fluid hypotension in patients with a basal skull fracture should make one think about cerebrospinal fluid leakage.
When fragments of a broken upper jaw are displaced, the cranial nerves located in the region of the ethmoid bone (I pair - olfactory), the body and small wings of the sphenoid bone (II pair - optic nerve), passing through the superior orbital fissure, i.e. are often damaged. between the large and small wings of the sphenoid bone (III pair - oculomotor, IV trochlear pair, VI pair - abducens).
A decrease or loss of smell in a patient with a Le Fort type I and II fracture of the upper jaw indicates damage to the olfactory nerve (I pair).
If there is a decrease in visual acuity, loss of parts of the visual fields, i.e. central and paracentral scotomas, this indicates injury to the optic nerve (II pair).
If the patient does not open the eye partially or completely, the oculomotor nerve (II pair) is damaged.
If the fracture occurs in the area of the superior orbital fissure, oculomotor disturbances may occur - signs of damage to the III, IV, VI pairs of cranial nerves. So, if the patient does not open his eyes, there is divergent strabismus, vertical separation of the eyeballs, impaired mobility of the eyeball up, down, inward, ptosis, mydriasis, then there is damage to the oculomotor nerve.
Deviation of the eyeball upward and inward, limitation of movement of the eyeball downward and outward, and diplopia when looking down are characteristic of damage to the trochlear nerve.
Convergent strabismus, impaired outward mobility of the eyeball, double vision in the horizontal plane are signs of damage to the abducens nerve.
Fractures of the anterior cranial fossa lead to its communication with the orbit or paranasal cavities.
Fractures of the middle cranial fossa (transverse, oblique, longitudinal) most often pass through the pyramid of the temporal bone, parasellar structures (tissues located around the sella turcica), and openings of the base of the skull. Damage to the III, IV, VI, VII, VIII pairs of cranial nerves may occur. As a result, the patient either partially or completely does not open his eyes. There may be restrictions on the movement of the eyeball inwards, convergent strabismus, hearing loss, tinnitus, dizziness, nystagmus, loss of coordination of movements, paresis of the facial muscles, taste disturbance on the anterior 2/3 of the tongue on the side of the lesion of the intermediate nerve in the internal auditory canal.
Bruising is localized in the area of the mastoid process and temporal muscle. There may be bleeding from the ear, liquorrhea in the case of a fracture of the temporal bone pyramid, rupture of the dura mater, the mucous membrane of the internal auditory canal and the eardrum. If its integrity is not broken, then blood and cerebrospinal fluid from the middle ear flow through the eustachian tube into the nasopharynx, and then into the nasal cavity and mouth.
It is extremely rare that heavy bleeding from the nose occurs as a result of rupture of the internal carotid artery, as well as damage to the wall of the sphenoid sinus (Blagoveshchenskaya N.S., 1994).
In a patient with liquorrhea from the nose or ear in the early period, strict bed rest is indicated. It is advisable to prevent coughing and sneezing. A protective sterile cotton-gauze bandage should be applied (on the nose or ear). It is better to give the victim’s head an elevated position, turning and tilting it towards the flow of cerebrospinal fluid. Antibiotics are prescribed prophylactically.
With a fracture of the base of the skull, there may be subarachnoid hemorrhages. The location of the fracture is determined by analyzing craniogram data, the presence of auricular or nasal liquorrhea, and signs of damage to certain cranial nerves. Dehydration therapy is indicated, which reduces pressure and production of cerebrospinal fluid, as well as unloading repeated lumbar punctures.
In addition to a fracture of the base of the skull, traumatic brain injury may cause concussions, brain contusion, and intracranial hematomas. The symptoms of their manifestation also need to be known to the dentist in order to determine treatment tactics for patients.
3. Concussion.
In case of a concussion, microstructural changes in the brain substance were not detected. However, there is damage to cell membranes. Clinically, it is characterized by a loss of consciousness - from stunning to a stop of varying duration (from several seconds to 20 minutes). Sometimes there is loss of memory for events during, before and after the injury, congrade, retrograde, anterograde amnesia. The latter is for a narrow period of events after injury. There may be nausea or occasional vomiting. Patients always report headache, dizziness, weakness, tinnitus, sweating, flushing of the face, and sleep disturbances.
Breathing is shallow, pulse is within the physiological norm. Blood pressure - no significant changes. There may be pain when moving the eyes and reading, divergence of the eyeballs, vestibular hyperesthesia.
With a mild concussion, the pupils are constricted; in severe concussions, their pupils dilate. Sometimes - anisocoria, transient oculomotor disturbances.
Neurological examination sometimes reveals asymmetry of facial muscles, labile rough asymmetry of tendon and skin reflexes, unstable small-scale nystagmus, and occasionally minor membrane symptoms that disappear in the first 3 to 7 days.
A concussion should be considered the mildest form of closed craniocerebral injury. However, these patients in the acute period should be in the hospital under the supervision of a specialist. It is known that symptoms of organic brain damage appear after a light interval. In addition, it is necessary to treat the autonomic and vascular disorders that occur with this brain injury. Bed rest for 5-7 days, the use of sedatives and vasodilators, and antihistamines are indicated.
4. Brain contusion.
In case of a brain contusion (loss of consciousness for more than 20 minutes), focal microstructural damage to the brain substance of varying severity occurs, edema and swelling of the brain, and changes in the cerebrospinal fluid-containing spaces are observed.
For easy The degree of brain contusion is characterized by loss of consciousness from several minutes to one hour, headache, dizziness, nausea, vomiting. Con-, retro- and anterograde amnesia, moderate bradycardia, clonic nystagmus, mild anisocoria, signs of pyramidal insufficiency, and meningeal symptoms are noted.
Brain contusion average degree of severity is characterized by a longer loss of consciousness (up to several hours), more pronounced focal neurological symptoms, mild transient disturbances of vital functions, and a more severe course of the acute period.
At severe The degree of brain contusion is characterized by loss of consciousness for a long period - from several hours to several weeks. Neurological symptoms with disruption of the vital functions of the body increase. Con-, retro- and anterograde amnesia, severe headache, repeated vomiting, bradycardia or tachycardia, increased blood pressure, tachypnea are expressed.
Meningeal symptoms, nystagmus, and bilateral pathological signs are common. Focal symptoms due to the localization of brain contusion are clearly identified: pupillary and oculomotor disorders, paresis of the limbs, sensitivity and speech disorders. Subarachnoid hemorrhages are common.
In 35–45% of cases with TBI, the temporal lobe of the brain is damaged. Sensory aphasia is characteristic, which is referred to as “verbal okroshka”.
Conservative therapy for brain contusion includes, in addition to the drugs used in patients with concussion, antibacterial treatment for the prevention of meningitis and meningoencephalitis, repeated lumbar punctures before sanitizing the cerebrospinal fluid. From 5 to 10 ml of cerebrospinal fluid can be withdrawn at once. Bed rest is required for 2 to 4 weeks, depending on the severity of the brain damage.
5. Intracranial hematomas.
Facial bone fractures combined with TBI may be accompanied by the formation of intracranial hematomas. According to the literature, they occur in 41.4% of patients with this type of TBI (Fraerman A.B., Gelman Yu.E., 1977).
Epidural hematoma- accumulation of spilled blood between the inner surface of the skull bones and the dura mater. The prerequisite for its formation is the rupture of the vessels of the dura mater - most often the middle meningeal artery and its branches, when struck in the inferior parietal or temporal region. They are localized in the temporal, temporo-parietal, temporo-frontal, temporo-basal areas. The diameter of the hematomas is 7 cm, the volume is from 80 to 120 ml.
An epidural hematoma compresses the underlying dura mater and brain matter, forming a dent in its shape and size. General and local compression of the brain occurs. Characterized by a short loss of consciousness with
its complete recovery, moderate headache, dizziness, general weakness, con- and retrograde amnesia. There may be moderate asymmetry of the nasolabial folds, spontaneous nystagmus, anisoreflexia, and moderate meningeal symptoms.
A relatively favorable state can last for several hours. Then the headache intensifies to the point of unbearable, vomiting occurs, which can be repeated. Possible psychomotor agitation. Drowsiness develops and consciousness turns off again. Bradycardia and increased blood pressure are noted.
Initially, a moderate dilation of the pupil on the side of the hematoma is determined, then with extreme mydriasm (dilation of the pupil) and the absence of its reaction to light.
To diagnose an epidural hematoma, a triad of signs is used: a lucid interval, the absence of cerebral, focal neurological symptoms against the background of temporary restoration of consciousness, homolateral mydriasis, contralateral hemiparesis. Important signs are also bradycardia, hypertension, localized headache, including with percussion of the skull.
The side of brain compression can be determined by damage to the oculomotor nerve - dilation of the pupil on the side of compression, drooping eyelids, divergent strabismus, gaze paresis, decreased or loss of pupillary response to light, dilated on the side of the hematoma.
Contralateral monoor hemiparesis and speech disorder are determined. On the side of the compression, swelling of the optic nerve sometimes occurs, on the opposite side - pyramidal insufficiency. Treatment is only surgical.
Subdural hematomas are characterized by the fact that the spilled blood is localized between the dura mater and the arachnoid mater. It causes general or local compression of the brain. Sometimes - both at the same time.
A subdural hematoma can occur both on the side where force is applied and on the opposite side. Place of impact - occipital, frontal, sagittal areas. Subdural hematomas are the most common among intracranial hematomas. Their dimensions are 10 by 12 cm, the volume ranges from 80 to 150 ml.
The classic version of a hematoma of this localization is characterized by a three-phase change in consciousness: primary loss at the time of injury, an expanded lucid interval, and secondary loss of consciousness. The light period can last from 10 minutes to several hours and even up to 1-2 days.
During this period, patients complain of headache, dizziness, and nausea. Retrograde amnesia is determined. Focal symptoms are not clearly expressed. Subsequently, there is a deepening of stunning, the appearance of drowsiness, and psychomotor agitation. The headache increases sharply, and repeated vomiting occurs. Homolateral mydriasis, contralateral pyramidal insufficiency and sensitivity disorder are detected.
Along with the loss of consciousness, a secondary brainstem syndrome develops with bradycardia, increased blood pressure, changes in breathing rhythm, bilateral vestibuloculomotor pyramidal disorders, and tonic convulsions.
Thus, subdural hematomas are characterized by a slower development of cerebral compression, longer light intervals, the presence of meningeal symptoms and the presence of blood in the cerebrospinal fluid. The remaining symptoms resemble those of an epidural hematoma.
At subarachnoid In a hematoma, spilled blood accumulates under the arachnoid membrane of the brain. Hematomas of this location accompany brain contusions. Blood breakdown products, being toxic, have a mainly vasotropic effect. They can cause cerebral vasospasm and cerebrovascular accident.
The clinical picture of subarachnoid hematoma is characterized by a combination of cerebral, meningeal and focal neurological symptoms. The patient's consciousness is disturbed and he experiences intense headache, dizziness, nausea, vomiting, and psychomotor agitation. Meningeal symptoms may be detected: photophobia, painful movement of the eyeballs, stiff neck, Kerning sign, Brudzinski sign. There may be insufficiency of the VII, XII pairs of cranial nerves of the central type, anisoreflexia, mild pyramidal symptoms.
The body temperature is elevated for 7-14 days due to irritation of the hypothalamic thermoregulation center and the meninges by the spilled blood.
Lumbar puncture is important in diagnosis: the presence of blood indicates subarachnoid hemorrhage.
Intracerebral a hematoma is a hemorrhage located in the substance of the brain. In this case, a cavity is formed filled with blood or blood mixed with brain detritus. In patients with intracerebral hematoma, focal symptoms predominate compared to cerebral symptoms. Of the focal symptoms, pyramidal insufficiency is most often noted, which is always contralateral to the side of the hematoma. Hemiparesis is pronounced. They are accompanied by central paresis of the facial (VII pair) and hypoglossal (XII pair) nerves. More often than with meningeal hematomas, there is a combination of pyramidal and sensory disorders on the same limbs, which can be supplemented by the same hemianopia. This is explained by the proximity of the intracerebral hematoma to the internal capsule. When these hematomas are localized in the frontal lobe and other “silent” areas, the focal pathology is not clearly expressed. Treatment is surgical.
Very often the brain stem is involved in the pathological process. Stem phenomena significantly complicate the diagnosis of hematomas, distorting their manifestation.
Trunk lesions may be primary(at the time of injury) and secondary when compression is possible by displaced areas of the brain. In addition, dislocation of the trunk itself due to swelling of brain tissue cannot be ruled out.
When the trunk is damaged, a deep coma, severe respiratory distress and abnormalities in cardiac activity, tonic disorders with bilateral pathological signs, and dysfunction of the oculomotor nerves are noted.
To diagnose intracranial hematomas, lumbar puncture cannot be performed due to the risk of developing midbrain compression syndrome (compression of the mesencephalic trunk), or compression of the medulla oblongata, or secondary bulbar syndrome (herniation of the bulbar trunk in the area of the foramen magnum).
6. Treatment of patients with combined traumatic brain injury consists of solving three problems:
1. Combating threatening violations of the vital functions of the body, bleeding, shock, compression and swelling of the brain.
2. Treatment of local extracranial and cranial injuries, which begins immediately after diagnosis.
3. Early prevention of possible complications. It may include radical surgery at various times after injury, depending on the general condition of the patient and the severity of brain damage.
In case of craniofacial trauma, craniomaxillary and craniomandibular fixation is considered the most rational, which allows for sealing of the brain skull, eliminating the cause of brain compression and ensuring reliable immobilization of jaw fragments.
7. Medical and social and labor rehabilitation of patients.Fronto-facial injuries.
Frontofacial injuries are the most severe among craniofacial injuries. With this injury, in addition to a fracture of the upper jaw, a fracture of the forehead occurs.
noal bone, anterior cranial fossa, ethmoid bone, nasal bones. Contusion of the frontal lobes of the brain is possible.
The Fronto-Facial Injuries Clinic has a number of features.
Among them we can note pronounced edema not only the tissues of the face, but also the head. Due to swelling, it is sometimes impossible to examine the eyes, which is important to determine their injury, as well as to identify damage to the optic and oculomotor nerves. With such an injury, compression of the optic nerve in its canal, damage in the chiasm, as well as the formation of hematomas in the retrobulbar area are possible. These patients may have severe nosebleeds immediately after injury, which is quite difficult to stop. This occurs with a fracture of the upper jaw, ethmoid bone, or nasal bones. In this case, liquorrhea is often observed, including difficult to diagnose hidden liquorrhea. All patients with frontofacial fractures should potentially be considered as having CSF leak.
It is sometimes possible to stop bleeding from the nose, including with a fracture of the upper jaw or base of the skull, with posterior nasal tamponade.
In such patients, a tracheostomy is often applied, because Intubation through the glottis is very difficult for them. At the same time, they often have aspiration of vomit, blood, and mucus, which makes it necessary to sanitize the tracheobronchial tree through a tracheostomy.
Damage to the frontal lobes of the brain affects the patient’s behavior and determines the uniqueness of the clinical picture. Patients are disoriented in their own identity, place and time. They show negativism, resist examination, are uncritical of their condition, and are stereotypical in speech and behavior. They have bulimia, thirst, and untidiness. Possible psychomotor agitation.
Treatment. When providing first aid, it is necessary to normalize the victim’s breathing, stop the bleeding, and begin anti-shock measures. Before the patient is brought out of shock, primary surgical treatment of head and face wounds is contraindicated. Surgical interventions are performed only for health reasons. A mandatory examination by an ophthalmologist, a neurologist, and, if indicated, a neurosurgeon is required.
An X-ray examination of the skull and facial bones should be performed in two projections. If an intracranial hematoma is present, it should be removed as soon as possible. Therapeutic immobilization is carried out no earlier than 4 - 7 days after the patient is recovered from a serious condition. In case of brain contusions, permanent immobilization of the broken upper jaw is possible only after stabilization of vital functions (blood pressure, breathing, cardiac activity). This can usually be achieved within 2–4 days from the moment of injury.
From a practical point of view, traumatic brain injury combined with fractures of the facial bones (including the upper jaw) is divided into four groups (Gelman Yu.E., 1977):
Group 1 - severe TBI (severe and moderate brain contusion, intracranial hematomas) and severe fractures of the facial bones (Le Fort type I and II fracture of the upper jaw, simultaneous fracture of the upper and lower jaws). Half of these patients develop traumatic shock.
Temporary immobilization in patients of group 1 is possible immediately after they are brought out of shock. Therapeutic immobilization using conservative methods is allowed for 2–5 days from the moment of injury and recovery from shock; osteosynthesis is carried out no earlier than on the seventh day.
Group 2 - severe TBI and minor trauma to the facial bones (Le Fort III fracture of the upper jaw, unilateral fractures of the upper and lower jaws, zygomatic bones, etc.). Therapeutic immobilization in patients of group 2 can be carried out after 1-3 days.
Group 3 - mild TBI (concussion, mild brain contusion) and severe injuries to the facial bones. The severity of the patients' condition is mainly due to trauma to the facial skeleton. Therapeutic immobilization in patients of this group, including osteosynthesis, is possible already on the first day after injury.
Group 4 - non-severe TBI and minor injuries to the bones of the facial skeleton. Patient immobilization of fragments can be carried out already in the first hours after injury.
Early specialized treatment not only does not aggravate the patient’s condition, but also promotes earlier cessation of liquorrhea and reduces the risk of developing intracranial inflammatory complications.
In 5% of deaths, the cause of mortality in the first 3 hours was swelling and dislocation of the brain. The severity of their condition on the Glasgow scale was 4-5. This indicates that for the development of not only cerebral edema, but also its dislocation, a long period of time (for many hours or days) is not necessary. These phenomena in the first 3 hours after injury usually developed in victims with intracranial traumatic hematomas in combination with foci of brain contusion, i.e. for very severe TBI (Fig. 25-10). Among the deceased, intracranial hematomas occur in 50-60% of cases (epidural - 10%, subdural - 77.5%, intracerebral - 15%). Hematomas of the posterior cranial fossa occur in 1.2% of victims, and hydromas in 5%. In 3.7% of such victims, intracranial hematomas are unfortunately not recognized. Only about 50% of victims usually undergo surgical removal of intracranial hematomas. This is explained either by the extremely severe condition (3-5 points on the Glasgow scale) of the victims, or by the small volume of the hematoma (up to 40 ml) not accompanied by symptoms of increasing compression of the brain, or by the fact that the victims are primarily operated on for ongoing bleeding from the internal organs of the chest or abdomen.
Rice. 25-10. CT scan of the head 4 hours after injury. A subdural hematoma with a volume of 120 ml is determined in the right frontotemporo-commonal region. Displacement of the midline brain structures to the left by 14 mm. The right ventricle is compressed and grossly deformed. The left one is hydrocephalic. Signs of axial mixing in the form of a focus of edema in the right parietal-occipital region, which arose as a result of circulatory disorders in the vertebro- basilar pool with subsequent ischemia.
After 3 hours from the moment of injury, the severity of cerebral edema and its dislocation increases, which leads to an increase in mortality from 16.1% on the first day to 34.4% on the third.
Among patients with brain dislocation who died on the first day after injury, the lethal outcome depends on the magnitude of the displacement of the midline structures of the brain - the greater it is, the greater the likelihood of death. When the midline structures are displaced by more than 10 mm, mortality increases significantly. Thus, in acute subdural hematomas with a volume of more than 100 ml with lateral dislocation of the midline structures of the brain up to 10 mm, the mortality rate is about 16%. With lateral dislocation up to 15 mm, mortality increases to 80%, and with displacement from 16 to 27 mm, it reaches 90-95%. Mortality also depends on the type of hematoma - the greatest with subdural ones.
It is therefore obvious that the prevention and treatment of cerebral edema and dislocation must begin immediately upon admission of the patient. The main treatment measure is early, preferably before the development of dislocation, removal of a traumatic intracranial hematoma or a focus of brain contusion (if it behaves “aggressively”).
25.11.1. Diagnosis of craniocerebral injuries in combined trauma
It is especially difficult for fractures of the limbs, damage to the organs of the thoracic and abdominal cavities. In this case, paralysis and paresis can simulate fractures of long bones, and vice versa - bone fractures - paresis or paralysis. Transport or stationary immobilization in the form of plaster casts or skeletal traction also complicates diagnosis. Damage to the internal organs of the abdominal or thoracic cavities, rib fractures can distort abdominal reflexes and skin sensitivity. Damage to the heart and lungs can simulate damage to the brain stem. However, difficulties in establishing an early diagnosis of brain compression by intracranial traumatic hematoma are not an excuse for delaying surgical intervention. At the same time, when analyzing mortality due to combined TBI treated in a non-neurosurgery department and without involving a neurosurgeon in treatment, it turned out that in 44% of patients intracranial hematomas were not recognized and the victims were not operated on. Difficulties in diagnosing in-
^
Combined traumatic brain injury
We explain tracranial hematomas by the change in their clinical picture (compared to the “classical one”) at the present time, especially in victims with combined TBI. This is due to an increase in the kinetic energy of the traumatic factor in the majority of victims (car injury, fall from a height, road accidents, weapon wounds, etc.).
Each patient with combined TBI, regardless of the existing neurological pathology (with the exception of patients who need to be operated on immediately, for health reasons, regardless of intracranial hematoma or damage to internal organs), must have a craniogram in two mutually perpendicular projections, as well as a spondylogram cervical spine.
Of course, echoEg is a mandatory method of instrumental research. If the clinical picture is unclear or EchoEg indicators are unclear, ultrasound location of the skull should be carried out dynamically. At the slightest suspicion of intracranial hematoma, the patient must undergo a CT scan of the head or, if this is not possible, angiography of the cerebral vessels. In the absence of serial angiographic devices, the study can be performed with a single image on a conventional X-ray machine in two projections by moving the X-ray tube and cassette (it is advisable to equip the cassette with a scattering grating).
In the absence of the specified diagnostic equipment, if a possible intraranial traumatic hematoma is suspected, they resort to the application of search burr holes, which are the last diagnostic and first surgical method for diagnosing and treating these hematomas. The scope of surgical intervention and its technical implementation do not differ from those adopted for isolated TBI.
When the lateral displacement of the midline structures of the brain is more than 10 mm, it is advisable not to limit the operation only to the removal of one hematoma, but also to remove the accompanying foci of brain crushing, brain detritus, i.e. carry out radical external decompression. It is advisable to add internal decompression in the form of expellation, tentoriotomy or falxotomy. Expedition is carried out in case of axial (most severe) displacement, confirmed by CT scan, and only if the pathological focus is completely removed (intracranial hematoma and the “aggressive” focus of brain contusion). For this-
Through a lumbar puncture, 80 to 120 ml of warm (36-37°C) Ringsr-Lokka solution or isotonic sodium chloride solution is injected into the spinal sac. Many people have observed a good clinical effect from exploitation. Exploration cannot be carried out BEFORE removing the pathological focus! According to our department (I.V. Korypaev), in very serious condition of the patient, with a transverse displacement of the midline structures of the brain by more than 15 mm, after removal of acute intracranial hematomas, mortality ranged from 95.2 to 73.9% . When the hematoma was removed with subsequent expulsion in similar victims, the mortality rate decreased to 50%.
^ 25.12. DIAGNOSIS AND TREATMENT OF CRANIOFACIAL INJURIES
The frequency of combination of TBI with injuries to the facial skeleton is about 6-7% of all types of injuries and 34% among combined TBI, i.e. such injuries are quite common, which is due to the anatomical proximity of the brain and facial skull. The overwhelming cause of craniofacial injuries is road traffic trauma (59%). The most severe and frequent are fronto-facial injuries. Both a neurosurgeon and a dentist should be involved in the treatment of such patients.
Fronto-facial trauma refers to injuries accompanied by fractures of the frontal bone, bones of the anterior cranial fossa, ethmoid bone, nasal bones, upper surface of the orbit and various fractures of the upper jaw and nasal bones. As a rule, fractures of the skull bones occur at the site of application of traumatic force. The vast majority of frontal-facial injuries also occur when force is applied to this area. According to our observations, in approximately 1.5% of cases, fractures of the ethmoid bone or the upper surface of the orbit occur with a blow to the crown, and in 0.3-0.5% - to the back of the head. With gunshot wounds of the skull, when a bullet passes through the facial skeleton, in the area of the maxillary sinuses, and nose, extensive damage to the roof of the orbit can occur both on the side of the wound and on the opposite side. In this case, a significant retrobulbar hematoma may occur, which is clinically accompanied by exophthalmos and often decreased vision or even atrophy of the eye. Cracks in the ethmoid bone may
^
Clinical guidelines for cranial injury
also occur in case of explosion injuries, due to a sharp drop in atmospheric pressure in the explosion zone.
The clinical picture of craniofacial wounds has a number of features. Thus, with fractures of the frontal bone and upper jaw, extensive swelling of the face and head usually occurs. This swelling can be so pronounced that it becomes really difficult or even impossible to examine the victim’s eyes. And such an examination is necessary to establish an eye injury and identify neurological symptoms of damage to the brain stem or cerebellum (nystagmus, exophthalmos, anisocoria, etc.).
Fractures of the nasal bones, ethmoid bone, and upper jaw bones may be accompanied by bleeding that is difficult to stop, in particular from the nose. In some cases, neither anterior nor posterior nasal tamponade is able to stop such bleeding. Then you have to resort to endovasal intervention - embolism of the branches of the external carotid artery supplying the nose with evalon or other microemboli. The operation is performed on both sides. However, this method may not be effective in some cases. In 1996, we observed a patient who eventually died from ongoing bleeding from the nose (due to a fracture of the nasal bones). Ligation of the internal carotid artery on one side in such cases is practically ineffective and extremely dangerous. Ligation of the internal carotid arteries on both sides almost always ends in the death of the victim.
Common fractures of the upper jaw bones (For-2, For-3) cause shock in almost 50% of victims. And with a fracture of the frontal bone, its arch and base in combination with fractures of the bones of the upper jaw and nose, macro- or microcerebrospinal fluid leakage occurs in 31% of patients. The development of facial rhea indicates that the existing damage to the skull is related to penetrating. In this case, there is a real threat of purulent meningitis.
Currently, with the use of the latest generation of antibiotics, the number of meningitis in acute liquorrhea, compared with the 70s, has decreased and amounts to 53.1%. At the same time, in 23.2% meningitis develops once, and in 76.8% - repeatedly. Curing meningitis does not indicate that the cause of its occurrence has been eliminated. There continues to be a real threat of its re-development. Moreover, the longer liquorrhea exists, the more often recurrent meningitis occurs. Features of the course and treatment
Nia liquorsi, prevention and treatment of purulent meningitis will be presented separately.
According to the degree of increase in the risk of liquorrhea, fractures are arranged as follows: fractures of the ethmoid bone, fractures of the upper jaw of type For-3, For-2, fractures of the nasal bones, fracture of type For-1. In a For-1 fracture, the fracture line runs horizontally over the alveolar processes, crosses the maxillary (maxillary) sinuses, the nasal septum and the ends of the pterygoid processes (Fig. 25-11). With a complete fracture, this entire conglomerate of processes descends downwards.
Rice. 25- 11. Lines (types) of fractures of the upper jaw. Explanation in the text.
In a For-2 fracture, the fracture line passes through the base of the nose, crosses the medial wall of the orbit, and then descends downward between the zygomatic bone and the zygomatic flap. Posteriorly, the fracture passes through the nasal septum and at the base of the pterygoid processes.
In a For-3 fracture, the fracture line passes through the root of the nose, transversely through both orbits, the edges of the orbits and through the arches of the zygomatic bones. With such a fracture, mobility of the broken fragment of the upper jaw along with the zygomatic bones is noted. Following the movement of this fragment, the eyeballs also move, which is not the case with a For-2 type fracture.
546
^
Patients with severe TBI and facial trauma are usually admitted in severe or extremely serious condition. Therefore, a detailed X-ray examination of them in the first days is impossible. Only craniograms are produced in 2 mutually perpendicular projections. After the elimination of a serious condition, usually on days 10-15 of TBI, clarifying x-ray studies are performed (if indicated, contact photographs of the skull, photographs in oblique projections, tomography of the anterior cranial fossa, etc.)
Treatment. First aid consists of eliminating or preventing breathing disorders, stopping bleeding, and carrying out anti-shock measures. Anti-shock measures also include fixation of a broken lower and upper jaw, which is achieved by applying Limberg or Zbarzh splints. Before the victim is brought out of shock, primary surgical treatment of wounds is unacceptable. Only resuscitation operations can be performed. Therefore, if the patient’s condition is serious, in the first 1-3 days the upper jaw is fixed using splints. Once the patient recovers from a serious condition, its final fixation is performed.
If the patient has not been operated on for a head injury and such an operation is excluded, then fixation of the jaw can be achieved by extraoral traction using a plaster cap or using metal structures. If the patient has been operated on, or surgery on the skull is not excluded, then such fixation cannot be used, because it will interfere with both the upcoming operation and dressings. Then fixation is carried out using the craniomaxillary method. To do this, 2 burr holes are placed in the frontotemporal region, located at a distance of 0.5-1.0 cm from each other. The “bridge” between these holes serves as a support for the ligature wire passed under it. The distal end of the wire is passed under the temporal muscle and zygomatic arch into the victim’s mouth at the level of the 7th tooth. A wire splint is placed on the teeth, to which the ligature inserted into the mouth is fixed. For For-3 type fractures, such manipulation is performed on both sides.
Frontofacial injuries may be accompanied by damage to the optic nerve. According to the literature, the frequency of such injuries ranges from 0.5 to 5% of all cases of TBI. According to our data, more than 30,000 observations of victims with TBI, damage to the optic nerve is much less common and amounts to hundredths of a percent. In case of damage to the visual
Nerve vision impairment usually occurs immediately. With the development of rstrobulbar hematoma, visual impairment can occur gradually, increasing, and then either regress to some extent, or completely, or vision is completely lost.
The difficulties in establishing the degree of vision loss, and even more so in studying the visual fields of a victim in the acute period of TBI, are determined by his unconscious state, inappropriate behavior, and inability to contact the patient. Due to these circumstances, the diagnosis of optic nerve damage is delayed until the patient’s condition stabilizes. At this time, surgical intervention to decompress the optic nerve is already overdue. However, even in those isolated cases when we were able to extract a fragment of the orbital wall from the wounded optic nerve 1-2 days after the injury, the operation was ineffective.
It is believed that at various times after TBI, the use of transcutaneous electrical stimulation of damaged optic nerves can improve visual function in 65% of patients. We used transcutaneous stimulation of the optic nerves in more than 100 patients operated on for optochiasmal arachnoiditis and in a few patients after damage to the optic nerves. We cannot say anything definite about the effectiveness of this technique.
When the walls of the air cavities (main sinus, ethmoidal labyrinth, frontal sinus, pyramidal cells of the temporal bones) are fractured, traumatic pneumocephalus may occur, which is an absolute sign of penetrating injury to the skull.
Bleeding from damaged bones and wounds of soft tissues of the face and skull, liquorrhea, increased secretion of mucus and saliva in the oropharynx and nasopharynx, vomiting pose a threat to aspiration or are accompanied by it. This requires immediate preventive and therapeutic measures. Intubation in such patients is difficult and sometimes impossible. Stopping bleeding from the nose, upper jaw and base of the skull can be quite difficult (see above).
The uniqueness of the clinical picture is complemented by injury to the poles of the frontal lobes of the brain that often occurs with such injuries. This leaves its mark on the patient’s behavior and makes it very difficult to treat and care for him. In the future, this can lead to asthenohypochondriacal or asthenoapathic personality changes.
^
To exclude acute traumatic intracranial hematoma, a patient with a combined craniofacial injury should be examined in the same way as a patient with an isolated TBI.
^ 25.13. DIAGNOSIS AND TREATMENT OF CRANIO-BRAIN INJURY COMBINED WITH FRACTURES OF THE LIMB AND PELVIS
25.13.1. General provisions
In case of TBI combined with trauma to the organs of the chest, abdomen or retroperitoneal space, the timing of surgical intervention is determined by vital disturbances (bleeding, rupture of the hollow intestinal organ or stomach, lung damage followed by hemo or pneumothorax, etc.) and does not raise any doubts. Fractures of large tubular bones (femur, tibia), as a rule, are not accompanied by massive ongoing bleeding. By the time you arrive at the hospital, bleeding at the fracture site usually stops spontaneously. Removing such victims from shock is easier than when a TBI is combined with damage to internal organs against the background of ongoing bleeding. Therefore, it would seem that surgery on broken bones of the extremities can be postponed for a long time (2-3-4 weeks). However, early (within the first 3 days) surgical interventions on broken limbs (osteosynthesis using various methods) are of great importance for the treatment outcomes of such victims. This is due to the fact that after 3 days from the moment of injury, among the causes of mortality (except for swelling and dislocation of the brain), such as pneumonia (37.9%) and cardiovascular failure (13.7%) increase, which later 3- x days from the moment of injury, the cause of mortality is already in 72.7% of patients (of all deaths).
For the prevention and treatment of TBI, trophic disorders, cardiovascular failure and, especially, pneumonia, the patient’s mobility within the bed is of great importance. Pneumonia in such patients mainly develops as a result of mechanical ventilation, preceding aspiration, or has a hypostatic genesis. The influence of aspirated masses on the development of the inflammatory process remains even with timely and
Complete sanitation of the tracheobronchial tree. A powerful factor in the prevention and treatment of trophic disorders, cardiovascular failure (except for drug treatment) in such patients is manual and vibration massage, physical therapy (active and passive). A complex of physical therapy can reduce the number of victims whose TBI was complicated by pneumonia by 10 percent or more.
To carry out bronchoscopy, intensive therapeutic exercises, lumbar punctures, vibration massage of the chest and back, the victim's lability in bed is necessary. Massive plaster casts, especially with various “spacers” in the form of plaster-plastered horizontal beams, especially skeletal traction, which is applied for fractures of the femur or tibia, sharply limit the freedom of the victim in bed, preventing him from turning on his sides. All this makes it difficult to carry out a number of therapeutic and preventive measures and routine hygienic care.
This also affects the development of pneumonia. Thus, in the group of patients (102 people) who were treated conservatively (skeletal traction) and whose mobility was severely limited, pneumonia developed in 23 (22.5%). In the group of patients who underwent early osteosynthesis (15 people), pneumonia did not occur in any of them (reliability P
The combination of TBI with fractures of the extremity bones complicates the course and prevents active treatment of both the TBI itself and the fractures of the extremity bones. Thus, motor excitation as a consequence of TBI not only increases brain hypoxia and increases its swelling, but can lead to the transition of a closed fracture to an open one, an uncomplicated fracture to a complicated one (secondary injury to the peripheral nerve, injury from bone fragments of blood vessels, the occurrence of muscle interposition, etc. ). Thus, one damage affects another, complicating its course.
Combination traumatic brain injury
25.13.2. Choosing a method
Fixation of limb fractures
The doctor is faced with the problem of rational fixation of the fracture in order to make the patient mobile. The solution to this problem is associated with determining the timing, volume and indications for surgical treatment (fixation) of fractures. If, with an isolated injury, local factors (type of fracture, its location, etc.) and the general condition of the body play a role in determining the indications for surgical treatment of broken limbs, then with a combined injury, the indications for surgery are also influenced by TBI - its nature, the severity of the patient’s condition, the condition of the patient. vital functions of the victim. In addition, certain requirements are also imposed on the fixation itself: such fixation must be very strong and not be disturbed by motor restlessness of the victim (motor restlessness itself is an indication, not a contraindication, to osteosynthesis surgery).
Intramedullary fixation of tubular bones with a metal rod is rational. Intramedullary osteosynthesis after corrected hypovolemic shock causes only temporary pulmonary stress. Therefore, primary intramedullary osteosynthesis of long tubular bones in patients with multiple trauma without lung damage can be used without fear of severe pulmonary disorders. However, such osteosynthesis is possible only for closed fractures of the femur and tibia, localized in the middle third and having a transverse or oblique fracture line. The number of such patients in the total number of victims with combined TBI is about 15%.
Mostly, the victims have complex comminuted fractures of long tubular bones, periarticular and intra-articular fractures. Here, in order to compare and firmly fix the fragments, a wide range of different plates, screws and pins and, of course, a highly qualified traumatologist are required. For such patients, it is better to use “surgical immobilization” of both closed and open fractures of any location using rod-based external fixation devices, which sufficiently firmly fixes complex comminuted fractures of long tubular bones (Fig. 25-12). To do this, through a puncture of the skin, at least two screw rods are inserted into the bone, above and below the fracture site.
Nei, the ends of which remain above the skin. By pulling along the length of the limb, displacement along the length and angular, and possibly also in width, is eliminated. The rods are then connected with a metal tube. Less desirable is compression-distraction osteosynthesis according to Ilizarov.
Rice. 25-12. External fixation rod device for comminuted femoral fracture.
With early fixation operations of long tubular bones, in addition to the prevention and adequate treatment of severe complications (bedsores, meningitis, pneumonia, etc.), treatment is significantly cheaper, its duration is reduced by at least a month, and disability payments are reduced.
Taking into account the characteristics of the patient’s condition with combined TBI (tendency to breathing problems or existing breathing problems, the special sensitivity of the damaged brain to hypoxia, motor agitation, lack of communication of the patient), osteosynthesis surgery is recommended to be performed only under anesthesia. Osteosynthesis must be early, durable and non-traumatic. In this case, hemostasis must be perfect, because Postoperative hematomas that arise in such patients, due to their decreased immunity, are prone to suppuration.
There are primary, early-delayed and late-delayed osteosynthesis.
Primary osteosynthesis includes osteosynthesis performed in the first 3 days after the injury.
Early-delayed - osteosynthesis, carried out within a period of up to 3 weeks, i.e. during the formation of fibro-osseous callus.
Late-delayed - osteosynthesis performed later than 3 weeks from the moment of injury.
^
Clinical Guidelines for Traumatic Brain Injury
Technically, performing primary osteosynthesis is less traumatic than early or delayed osteosynthesis. With the formation and development of fibro-osseous callus, osteosynthesis becomes more and more traumatic and is accompanied by large bleeding and soft tissue trauma, which is associated with the release of bones from adhesions and destruction of fibro-osseous tissue in the fracture area. In this case, there may be significant bleeding and the operation requires blood transfusion.
Carrying out osteosynthesis on the first or second day is also favorable in that the operation is performed when the immunological background, protein and mineral metabolism, and trophic and inflammatory changes (bedsores, pneumonia, etc.) have not yet arisen. The most unfavorable time for osteosynthesis is 3-7 days after injury, because It is at this time that there is an increase in cerebral edema, its dislocation, instability of the general condition, a decrease in immunity, hemoglobin, etc.
During the same period, in patients with combined TBI, the so-called translocation (movement of bacteria from the intestinal contents to other environments of the body - blood, sputum, urine, etc.) is most pronounced. Normally, the preservation of the intestinal barrier function is carried out by lymphocytes, macrophages of the intestinal wall, Peyer's patches and Cooper cells of the liver. Various stress conditions and systemic disturbances of homeostasis, which is observed in victims with combined TBI, lead to damage to this barrier and increased permeability of the intestinal wall to bacteria and other toxic substances. Bacteriological studies of sputum, feces, urine, throat and stomach contents reveal microbiocetosis disorders, which are associated with a decrease in the body's resistance to the infectious agent. Under certain conditions, bacteremia observed in the blood can cause purulent complications in various organs (including the brain) and even the development of sepsis.
We analyzed 450 case histories of victims with TBI. Of these, 228 victims were treated conservatively and 252 surgically. The average number of days of hospital stay for primary and early-delayed osteosynthesis was 67.9, for late-delayed osteosynthesis - 117.4. The period of incapacity for work is respectively 200 and 315 days.
Disability due to limb injury with primary and early-delayed osteosynthesis was 8.6%, with late-delayed osteosynthesis - 11%, with
Conservative treatment - 13.8%. The severity of TBI was approximately the same in all groups.
^ 25.14. CRANIOVERTEBRAL TRAUMA
Simultaneous injuries to the skull and brain and the spine and spinal cord (craniovertebral trauma) are uncommon. However, victims with this type of combined injury are characterized by the particular severity of their condition, difficulties in diagnosis and development of surgical tactics.
Injuries to the spine and spinal cord are diagnosed in 5-6% of victims with traumatic brain injury. At the same time, TBI due to spinal trauma is observed in 25% of cases, ranking first among other combinations.
The causes of craniovertebral injury are most often motor vehicle accidents, falls from great heights, natural and industrial disasters accompanied by destruction and rubble.
Craniovertebral injury can be caused not only by separate direct effects of mechanical energy on the skull and spine, but also often when a traumatic agent is applied only to the head.
If you sharply straighten your head after a blow to the face or fall face down, a fracture of the cervical spine may occur simultaneously with a skull injury. When diving and hitting your head on the bottom, along with a brain injury (usually not severe), compression fractures and dislocations occur, most often of the C5-C7 vertebrae. Similar damage occurs when your head hits the ceiling of the cabin of a car moving on a bumpy road.
When large weights fall on the head, which is in a state of extension, along with severe traumatic brain injury, “traumatic spondylolisthesis” of the 1st cervical vertebra can occur. With direct blows to the parietal region, hemorrhages appear in the upper cervical part of the spinal cord, explained by the influence of acceleration forces. Motor vehicle accidents and rubble usually result in multiple injuries: along with head and spine trauma, fractures of the ribs, limbs and pelvis, and damage to internal organs are detected.
Determining the causes and mechanism of damage greatly facilitates diagnostic tasks.
Combined traumatic brain injury
25.14.1. Classification
The classification of cranial trauma is based on 3 principles: the localization and nature of the traumatic brain injury, the localization and nature of damage to the spine, spinal cord and its roots, the ratio of the severity of the craniocerebral and spinal cord components of the injury.
The classification of traumatic brain injury is well known, the classification of spinal cord injury is also generally accepted
16.2. COMBINED CRANIO - FACIAL DAMAGES
Combined injury- simultaneous damage to two or more anatomical areas by one or more damaging factors.
Combined injury- damage; which occurs as a result of exposure to various traumatic factors (physical, chemical or biological).
Patients with combined craniofacial injuries are of interest to clinicians due to their increasing frequency, the peculiarities of the clinical course, the difficulty of diagnosis and choosing the optimal treatment method.
V.F. Chistyakova (1971, 1977) noted that maxillofacial injuries are combined with closed craniocerebral trauma in 86.3-100% of cases. According to M.G. Grigoriev (1977) similar combinations were observed in 34% of patients, V.V. Lebedev and V.P. Okhotsky (1980) - in 53% of cases, Yu.I. Vernadsky (1985) - 95.6%.
The anatomical similarity of the facial and cerebral skull creates the prerequisites for the occurrence of craniofacial damage to V.V. Lebedev and V.P. Okhotsky (1980) indicate that the lower jaw is connected to the outer part of the base of the skull through the temporomandibular joint. Therefore, when hitting the lower jaw, the articular head often damages the base of the middle cranial fossa (the petrous part of the temporal bone) and the auditory canal (internal), which causes hearing impairment and the function of the facial nerve.
The force of hitting the ball with a fist in a boxing glove reaches 460 kg, with a foot (in a boot) hitting a ball - 950 kg, with a foot using a dynamometer - 870 kg (V.M. Abalakov, 1955). It has been experimentally proven that the force of a punch without a glove is 560-680 kg (G. Povertowski, 1968). It has been established that to damage the bones of the nose, an impact force of 10-30 kg is needed, the anterior wall of the maxillary sinus - 65-78 kg, the zygomatic bone in women - 83-180 kg, and in men 160-260 kg (J. Nahm, 1975) .
Features of the architectonics of the facial skeleton not only create conditions for protecting the brain from traumatic effects, but also play an important role in the transfer of mechanical energy to brain structures. The intimate topographic-anatomical relationships of the facial and cerebral skull can explain such serious complications (from facial trauma) as subdural hematomas, subarachnoid hemorrhages, thrombosis of cerebral vessels, traumatic aneurysms, fractures of the cervical vertebrae, fracture of the base of the skull, etc.
A.P. Fraerman and Yu.E. Gelman (1974) proposed classify combined cranio-facial injuries according to severity:
1. severe traumatic brain injury and severe damage to the facial skeleton;
2. severe traumatic brain injury and minor injuries to the facial skeleton;
3. mild traumatic brain injury and severe damage to the maxillofacial area;
4. non-severe traumatic brain injury and non-severe maxillofacial trauma.
Damage to the maxillofacial localization in combined trauma in most victims is not dominant, but plays an important role in the course and outcome of the injury.
With traumatic brain injury, depending on its severity, changes may be observed in the immune system (immunosuppression occurs), the cardiovascular system, the state of external respiration, the digestive organs (the intestines, liver, pancreas are affected), the endocrine and nervous systems ( weakening of memory, attention, thinking), and also the functions of vision, smell and hearing decrease, the electrical activity and regulatory activity of the brain changes, etc. (O.S. Nasonkin, I.I. Deryabin, 1987, etc.). All this can be called in one word - patients develop traumatic illness.
The cause of traumatic disease is the interaction of a mechanical agent causing damage with body tissues. The leading links initially are blood loss, nonspecific dysfunctions of the damaged organ, hypoxia, toxemia, pain syndrome, etc., and later - mono- and polysystemic (multiple organ) failure.
The clinical symptoms of combined trauma depend on the severity and nature of the craniocerebral and maxillofacial injuries. In case of combined trauma (severe traumatic brain injury), the clinical picture is dominated by neurological symptoms, which significantly complicates the diagnosis of injuries to the maxillofacial area. It is not always possible to conduct X-ray studies in the required projections. Therefore, often the main diagnostic method for damage to the bones of the facial skeleton is the clinical method, A this requires the doctor to have appropriate training and the necessary experience of working with such a group of patients.
Combined craniofacial trauma is not just the sum of damage. Mutual burden syndrome develops, which leads to aggravation of the course of the traumatic disease (maxillary-cerebral syndrome).
According to the international classification adopted at the III Congress of Neurosurgeons (Tallinn, 1982), all Traumatic brain injuries (TBI) are divided into 3 forms:
concussion;
brain contusion:
a) mild degree; b) moderate; c) severe;
brain compression:
a) against the background of his injury; b) without accompanying injury.
Taking into account the possibility of a threat of infection of the brain substance, craniocerebral injuries are divided into open (OCMT) And closed (CLMT) injuries. Open traumatic brain injury (OTBI) can be penetrating And non-penetrating. TBIs are conventionally divided into 3 degrees of severity: light(mild concussion and contusion); average(moderate cerebral contusion, subacute and chronic compression of the brain); heavy(severe brain contusion, acute compression of the brain).
Brain concussion(commotio cerebri) - closed mechanical damage, which is characterized by impaired brain function without obvious morphological changes. Only vasodilation, pinpoint hemorrhages, increased permeability of vascular walls, swelling of brain tissue, and increased intracranial pressure are observed.
Clinical symptoms are: loss of consciousness, single or repeated vomiting, slow (or rapid) pulse, increased body temperature to 37.2-37.7 ° C., lethargy, drowsiness and apathy (sometimes agitation or hallucinations), headaches, dizziness , lability of cardiac activity, sweating, vestibulopathy, fatigue, memory impairment and other signs.
Brain contusion(contusio cerebri, brain contusion) is a closed mechanical injury to the brain, characterized by the appearance of a focus (foci) of destruction of its tissue and manifested by neurological and (or) psychopathological symptoms according to the localization of the focus (foci). In addition to the symptoms of a concussion, focal symptoms appear. Severe headache, vomiting, bradycardia, drowsiness, stupor, epileptiform seizures, soporous, and then comatose state.
Mild brain contusion: the patient's condition is of moderate severity; consciousness is impaired (moderate stunning); along with symptoms of a concussion, meningeal symptoms may be detected (due to subarachnoid hemorrhage); vital functions are normal.
Moderate brain contusion: the patient's condition is moderate or severe; consciousness is impaired (stupor, moderate coma or psychomotor agitation); moderate disturbance of vital functions (tachypnea, tachycardia, increased blood pressure, hyperthermia, repeated vomiting); neurological disorders (paresis, sensitivity disorders, etc.), meningeal and brainstem symptoms (nystagmus, changes in muscle tone, etc.).
Severe brain contusion: the patient's condition is serious or extremely serious; is in a coma; profound disturbances of vital functions (spontaneous breathing, apnea, thready pulse, low blood pressure, areflexia, muscle atony); deep neurological changes (stem and subcortical symptoms).
Brain compression- caused by intracranial hematomas (subdural, epidural, intracerebral), depressed fractures of the bones of the skull, increasing cerebral edema. The presence of a hematoma is indicated by the following symptoms: dynamics of deterioration of the patient’s general condition and his consciousness, increasing intracranial pressure, brain hypoxia, increasing general cerebral and focal neurological symptoms, autonomic disorders.
I.S. Zozulya (1997), analyzing her clinical observations, highlights the features of the course of traumatic brain injury depending on age and the presence of alcohol intoxication. According to the author's observations, in elderly and senile people Deep disorders of consciousness are observed less often, disorientation in place and time is more pronounced, as well as asthenia and disorders of the cardiovascular system, normalization occurs more slowly. IN childhood focal symptoms are less pronounced in younger children, and cerebral and autonomic symptoms are the opposite. At alcohol intoxication the toxic effects of alcohol affect both general cerebral and focal neurological symptoms (causing euphoria, muscle hypotension, adynamia, stupor, coma, and can simulate the picture of traumatic brain injury). All this leads to longer-term impairment of consciousness, amnesia, and less pronounced pain in the first 6-12 hours after injury. In these patients, vomiting occurs more often, autonomic disorders are more manifested, liquor hypotension syndrome is more often detected, and anisocoria is less pronounced. Alcohol intoxication leads to cerebral circulation disorders, which increases brain hypoxia. All this complicates the clinical picture of a concussion, bruise or compression of the brain, and also masks the true picture of traumatic brain injury, which complicates diagnosis and treatment.
Clinical picture Combined cranio-facial injuries depend on the nature and severity of cranial and maxillofacial trauma. Severe external respiration disorders occur due to occlusion (impaired patency) of the airways with blood, mucus, fragments of soft tissue of the oral cavity, bone fragments, retraction of the tongue, etc. Massive blood loss may occur as a result of damage to the branches of the external carotid artery. Severe swelling of the soft tissues of the face and head develops (Fig. 16.2.1).
Peripheral breathing disorders increase cerebral circulatory failure, brain hypoxia and disorders of its metabolism, which in turn leads to the development of cerebral edema and disruption of the regulatory functions of the central nervous system (V.V. Chistyakova, 1971, 1977; V.V. Lebedev, D. Y. Gorenshtein, 1977; M.N. Promyslov, 1984; A.G. Shargorodsky et al., 1981,1988, etc.).
Bleeding from damaged parts of the face and skull, liquorrhea, increased mucus secretion, which may be accompanied by vomiting, are accompanied by aspiration and pose a threat to the patient’s life in the early period after injury and in the long-term period (development of purulent post-traumatic meningitis). Due to the leakage of cerebrospinal fluid, 70% of patients develop hypotensive syndrome. As a result of injury, 33-70% of patients develop traumatic shock (M.G. Grigoriev, 1977, A.P. Romadanov et al., 1987, 1989, etc.).
According to K.Ya. Peredkova (1993) in the structure of combined craniofacial trauma, a significant place is occupied by victims with polytrauma (43%), multiple injuries of the facial skeleton (32%), multiple injuries of the skull and brain (20%). The combination of multiple maxillofacial with multiple cranial brain injuries was observed by the author in 10% of patients. The main reason was transport and household injuries.
The clinical course of combined craniofacial injury is significantly influenced by the nature and severity of traumatic brain injury. According to K.Ya. Peredkova (1993), traumatic disease manifests itself in patients with a predominance of severe traumatic brain injury, as evidenced by the high frequency of shock, the duration of treatment of victims and high mortality. According to the author, with combined injuries, when maxillofacial trauma comes to the fore, the clinical manifestation of the traumatic disease is masked in 40% of cases.
According to the observations of K.Ya. Peredkova (1993) found that mortality is higher in the group of patients with mild maxillofacial injuries combined with severe craniocerebral trauma than in patients with severe maxillofacial and severe craniocerebral injuries (41% and 23%, respectively). This paradox is explained by the author as follows: when destructive forces collide with the skull, with extensive damage to the facial and cerebral skull, the main force of traumatic energy is distributed to more superficial layers, while in small maxillofacial injuries, most of the traumatic force falls on the cerebral skull. This can explain not only the high mortality rate, but also the high incidence of complications in these patients (up to 50%).
Diagnostics The nature and severity of damage to the brain and maxillofacial area in case of combined trauma presents certain difficulties. Therefore, the percentage of diagnostic errors, according to the Leningrad Research Institute of Emergency Medicine named after. Dzhanelidze, was high and amounted to 80% (B.V. Artemyev et al., 1981). The lack of expression of neurological symptoms causes difficulties in recognizing traumatic brain injury. The discrepancy in diagnoses is due to underestimation of the severity of the injury, an insufficiently complete anamnesis, insufficient neurological examination of patients, ignoring the circumstances of the injury and loss of consciousness of the victims, underestimation of indirect signs of brain damage, and overestimation of the phenomena of alcohol intoxication.
For combined craniofacial injuries used for diagnostic purposes the following objective research methods: radiography of the skull, axial computed tomography (ACT), nuclear magnetic resonance (NMR), electroencephalography (EEG), rheoencephalography (RheoEG), lumbar puncture (LP), study of the composition of the cerebrospinal fluid and the height of the cerebrospinal fluid pressure, pneumoencephalography (PEG), as well as laboratory methods (hematocrit, blood count, urine composition, etc.), hemodynamic studies and consultations with related specialists (Fig. 16.2.2-a, b, c).
K.Ya. Peredkov (1993) recommends in the acute period after injury must be applied- radiography, EchoEG, ACT, according to indications- EEG, RheoEG, carotid angiography, PEG, etc. The sequence of application of diagnostic studies is from simple to more complex. Clarification of the nature and severity of injuries is carried out with the mandatory participation of a maxillofacial surgeon, neurosurgeon, ophthalmologist, otoneurologist, and, if necessary, other specialists.
According to the Kiev Scientific and Practical Association of Emergency Medical Services and Disaster Medicine, in 51% of patients, maxillofacial injuries were combined with a concussion, and in 49% - with a brain contusion of varying severity (K.Ya. Peredkov, 1993). Immobilization of fragments of the facial skeleton in patients with combined cranio-facial injuries must be carried out as early as possible, reliably fixing the fragments.
Rice. 16.2.1 (a, b, c, d). Appearance of patients with combined cranio-facial
damage.
Rice. 16.2.2 (a, b, c) Computed tomography of the brain, as well as the bones of the facial skull in the axial and frontal planes. The tomogram determines:
comminuted fracture of the upper jaw; multiple fractures of the walls of the maxillary cavities; fracture of the base of the skull, fracture of the nasal septum; the lower wall of the right orbit is not differentiated (the bone fragment is displaced downward); fracture of the orbital roof on the right; the maxillary and main sinuses, the cells of the ethmoidal labyrinth are filled with exudate; in the left hemisphere of the cerebellum, a focus of low density up to 12 mm in size is determined.
Rice. 16.2.2(continuation).
Features of combined cranio-facial injury in children. Concussion is diagnosed in 11-38% of children with jaw fractures (G.A. Kotov, 1973; V.N. Shirokov, 1974; A.Sh. Mezhikovsky, 1975). However, according to M.M. Solovyov (1986), it is quite difficult to identify brain damage in children using conventional clinical examination methods, because these injuries are asymptomatic, especially in young children. According to V.P. Kiseleva (1973), due to the elasticity of the bones of the cranial vault and the presence of unclosed fontanelles, the increase in intracranial pressure in children occurs slowly. Therefore, objective neurological symptoms appear later. In children with suspected traumatic brain injury, it is necessary to conduct an additional research method - electroencephalography (N. Gitt et al., 1982) and they are subject to hospitalization in a hospital. Traumatic brain injury cannot serve as a basis for refusing or delaying the provision of specialized medical care (K.S. Ormantaev et al. 1981; K.S. Ormantaev, 1982).
Rice. 16.2.2(ending).
Treatment methods will be discussed in the appropriate section of this manual.
According to the observation of Kurmangaliev Z. (1988), the provision of specialized care for combined severe traumatic brain injury immediately after stabilization of life-support systems not only does not aggravate the general or neurological status, but also helps to reduce the development of local complications. Specialized treatment should be carried out under adequate anesthesia, using conservative and gentle methods of surgical treatment. The scope of specialized care should be complete and comprehensive, carried out immediately after stabilization of life-supporting systems during the first 24 hours after injury (3. Kurmangaliev, 1988; K.Ya. Peredkov, 1993; A.A. Timofeev, 1995, etc.).
7088 0
Combined trauma is a pressing social and medical problem that lies at the intersection of traumatology, neurosurgery, general surgery, resuscitation and other disciplines. The share of combined trauma in the structure of transport and some other types of injuries reaches 50–70%. Its almost constant component is traumatic brain injury (up to 80%).
The need for a unified terminology and classification of combined traumatic brain injury is obvious. It is due to the fact that victims are hospitalized in various hospitals and treated by doctors of many specialties. Assessing the severity of the patient’s condition and injury is not always unambiguous, and without this it is difficult to develop adequate tactics and ensure continuity in treatment. Without a unified classification, real statistics, effective scientific development of a problem, and resolution of organizational issues are impossible.
Combined injury is simultaneous damage by one type of energy, in particular mechanical, to two or more organs or parts of the body, topographically different areas or different systems. In light of this general concept, a traumatic brain injury is combined if the mechanical energy simultaneously causes extracranial damage.
It is advisable to retain the term “combined injury” to denote simultaneous effects on the body of various types of energy (mechanical, thermal, radiation, chemical, etc.).
Other terms often used to designate injuries—“multiple trauma” or “polytrauma”—are very vague; these concepts may include multiple injuries to an organ or limb or simultaneous injury to several body systems.
Based on these premises, preference should be given to the term “combined injury”.
The appearance of the craniocerebral component in the structure of combined injury always introduces qualitatively new features into its pathogenesis, clinical picture, diagnosis and treatment.
Unlike all other variants of combined injuries of internal organs and the musculoskeletal system without a craniocerebral component, combined traumatic brain injury is characterized by a simultaneous violation of the higher regulatory (brain) and predominantly executive (internal organs, limbs, spinal cord, etc. .) body systems. At the same time, in the absence of the craniocerebral component, with combined injuries, only the executive organs suffer, with the primary preservation of the central nervous system.
The classification of combined traumatic brain injury is based on the following principles:
1. Localization of extracranial injuries.
2. Characteristics of traumatic brain and extracranial injury.
3. The ratio of cranial and extracranial injuries according to their severity.
Considering the localization of extracranial injuries, which leaves its mark on the clinical picture and surgical tactics, it is advisable to identify the following combinations of traumatic brain injury:
1. With damage to the facial skeleton.
2. With damage to the chest and its organs.
3. With damage to the abdominal organs and retroperitoneal space.
4. With damage to the spine and spinal cord.
5. With damage to the limbs and pelvis.
6. With multiple extracranial injuries.
In addition to the local factor, the features of diagnosis, therapy, as well as the outcome of the disease are largely determined by the ratio of injuries by severity. This justifies the practical need to divide each type of combined injury into 4 groups:
1. Severe traumatic brain injury and severe extracranial injuries.
2. Severe traumatic brain injury and non-severe extracranial injuries.
3. Mild traumatic brain injury and severe extracranial injuries.
4. Non-severe traumatic brain injury and non-severe extracranial injuries.
Severe traumatic brain injury includes severe brain contusions and brain compression, and also, in the context of combined trauma, moderate brain contusion.
Non-severe traumatic brain injury includes concussion and mild brain contusions.
Severe extracranial injuries include fractures of the femur, pelvis, tibia, shoulder, multiple fractures of extremity bones; fractures of the upper jaw type FOR - 2, FOR-3, bilateral fracture of the lower jaw, multiple fractures of the facial skeleton; one- and two-sided rib fractures, accompanied by respiratory failure and chest compression; fractures and dislocations of the vertebrae with damage to the spinal cord and its roots, unstable fractures of the vertebral bodies; damage to the organs of the thoracic and abdominal cavities, retroperitoneal space.
Non-severe extracranial injuries include closed fractures of the bones of the hand, foot, forearm, fibula, nose, unilateral fractures of 1-3 ribs without damage to the pleura, bruises of the torso and limbs.
Multiple extracranial injuries include cases when, along with a traumatic brain injury, there is damage to organs of two or more different systems (for example, traumatic brain injury + hip fracture + lung injury).
It is acceptable to apply the term “severe combined traumatic brain injury” to patients of groups I, II, III, i.e. when one or both components of the combined traumatic brain injury are severe. However, in these cases, it is necessary to decipher the nature of the damage. In patients with combined trauma, even with mild extracranial injuries, the disease is more severe than with isolated trauma. It should be emphasized that the gradations of severity of combined injury are to some extent arbitrary, since when assessing the severity of a patient’s condition, it is necessary to take into account not only the severity of individual cranial and extracranial injuries, but also the patient’s age, the state of his cardiovascular system, previous diseases, etc. .
In the classification structures of combined TBI, it is necessary to take into account its inherent high frequency and features of the manifestation of traumatic shock.
Victims of groups 1 and 2 are subject to treatment in neurosurgical and neurotraumatology hospitals, victims of groups III and IV are hospitalized in departments according to the profile of the dominant injury.
In a detailed diagnosis of combined injury, the currently dominant injury should be indicated in the first place, which determines the priority direction of diagnostic and surgical actions. Over time, the various components of combined traumatic brain injury can change places in terms of their predominance in the clinical picture.
We give approximate formulations of the primary diagnosis of combined traumatic brain injury.
Group I
“Severe combined injury: compression of the brain by an acute subdural hematoma in the right frontoparietal region. Closed linear fracture of the parietal and temporal bones on the right. 3 closed fracture of 4-10 ribs on the right along the mid-axillary line. Hemopneumothorax on the right. Traumatic shock of the second degree.”
“Severe combined injury: moderate brain contusion localized in the frontal and temporal lobes on the left. Subarachnoid hemorrhage. 3 closed fracture of the pubic and ischial bones, rupture of the extraperitoneal urethra. Traumatic shock of the 1st degree.”
Group II
“Severe combined traumatic brain injury: severe brain contusion, predominantly of the left hemisphere, subarachnoid hemorrhage. “closed fracture of the radius in a typical location with displacement of fragments.”
“Severe combined traumatic brain injury. Compression of the brain by an acute subdural hematoma in the right frontotemporal region against the background of a crush injury to the pole of the right frontal lobe, subarachnoid hemorrhage. Linear fracture of the right half of the frontal bone. Fracture of the nasal septum. Bruises of the soft tissues of the head and face. Alcohol intoxication."
III group
“Severe combined injury: closed transverse fracture of the left femur in the middle third with displacement, fracture of the left ilium without displacement. Mild brain contusion. Traumatic shock of the first degree.”
“Severe combined injury: closed compression fracture of the C6 vertebral body with contusion and compression of the spinal cord. Brain concussion. Alcohol intoxication."
IV group
“Combined traumatic brain injury: mild brain contusion, bruised wound in the occipital region. Fracture of the 8th rib along the scapular line on the right.”
“Combined injury: closed fracture of the lower jaw on the left without displacement. Brain concussion. Alcohol intoxication."
The final diagnosis upon discharge of the patient must be detailed. It indicates the exact location of the damage, complications, concomitant diseases, etc.
For example: “Severe combined injury: compression of the brain by a subdural hematoma of the right fronto-parietal-temporal region, a crush site of the basal parts of the frontal and temporal lobes on the right, a fracture of the right temporal bone with transition to the base of the middle cranial fossa. 3-closed pertrochanteric fracture of the right femur with displacement of fragments. Bilateral lower lobe pneumonia. Hypertension, stage I B."
A.P. Fraerman, V.V. Lebedev, L.B. Likhterman
With combined traumatic brain injury (CTBI), the facial skeleton, cranial bones and brain are simultaneously damaged. A closed traumatic brain injury (TBI) without damage to the skull bones, combined with fractures of the facial skeleton, is possible.
Fractures of the facial bones in combination with TBI are diagnosed in 6.3 - 7.5% of patients. The fairly high frequency of craniofacial injuries is due not only to their anatomical proximity, but also to the fact that some bones of the facial skeleton take part in the formation of the base of the skull.
The characteristics of TBI are based on the relationship between two defining factors:
1. Localization of extracranial damage.
2. The ratio of cranial and extracranial damage according to their severity.
In more than 1/3 of cases, TBI is accompanied by shock.
Erectile its phase is significantly extended in time and can occur against the background of impaired consciousness (as opposed to the classic one), accompanied by bradycardia, severe disturbances in external respiration, hyperthermia, meningeal signs, and focal neurological symptoms. In addition, the peculiarities of the anatomical relationship of the bones of the facial and cerebral skull lead to the fact that fractures of the facial bones, for example the upper jaw, zygomatic bone, as a rule, extend beyond their anatomical boundaries and the broken bone fragment often includes the bones of the base of the skull. In this regard, it is worth recalling the anatomical data relevant to the issue under consideration.
The anterior cranial fossa (fossa cranii anterior) is separated from the middle one by the posterior edge of the small wings of the sphenoid bone. It is formed by the orbital surface of the frontal bone, the ethmoid, sphenoid (lesser wings and part of its body) bones. It is known that they take part in the formation of the upper, inner and outer walls of the orbit, along which the fracture gap of the upper jaw passes in the middle and upper types.
The middle cranial fossa (fossa cranii media) is formed by the anterior surface of the pyramid and the scales of the temporal bone, the body and large wing of the sphenoid bone, which take part in the formation of the inner and outer walls of the orbit.
Between the lesser and greater wings, as well as the body of the sphenoid bone, there is the superior orbital fissure. The orbital surface of the upper jaw, together with the orbital margin of the greater wings of the sphenoid bone, limits the inferior orbital fissure.
Fractures of the upper jaw can be accompanied not only by fractures of the base of the skull, but also by concussion or contusion of the brain, the formation of intracranial
hematomas. To determine the correct tactics for examining and treating such patients, the dental surgeon must remember the main clinical signs of these injuries.
It is known that combined injury from a pathophysiological point of view, it is a pathological process different in content than equivalent damage to any one vital organ (for example, the brain). Her cannot be considered as a simple sum of damage to two or more anatomical areas.
The combined injury is severe in terms of the overall reaction of the body, despite the possible relatively minor damage to each of the organs involved. Possible disturbances in breathing, circulation, and liquor dynamics characteristic of TBI potentially lead to cerebrovascular insufficiency. Brain hypoxia and disturbances in its metabolism cause cerebral edema and central respiratory impairment. All this contributes to even greater brain swelling.
Thus, a vicious circle closes: damage to the brain causes disruption of all types of metabolism, and damage to other areas (maxillofacial, chest, etc.) enhances such changes and creates the preconditions for suppression of brain activity.
The mortality rate of patients with combined trauma ranges from 11.8 to 40% or more.
When systolic blood pressure decreases below 70 - 60 mm Hg. column, self-regulation of blood circulation in the brain is disrupted, which is accompanied first by functional and then morphological changes in the brain.
Respiratory failure is a serious complication that poses a threat to the life of the victim. In case of combined injuries, it can be of three types: respiratory disorder due to:
Central type
Peripheral type
Mixed type.
Breathing disorder central type is caused by brain injury, more precisely, by the respiratory centers located in the brain stem. In this case, the patency of the peripheral airways is not impaired. Clinically, this is manifested by a violation of the rhythm, frequency, amplitude of breathing: bradypnea, tachypnea, periodic rhythms of Cheyne-Stokes and Biot, spontaneous stopping.
Providing assistance for central-type breathing disorder consists of intubating the patient and providing assisted breathing.
Breathing disorders peripheral type can be caused not only by brain injury, but also by damage to the maxillofacial area. They arise due to obstruction of the upper respiratory tract, as well as the trachea and bronchi with vomit, mucus, blood from the mouth, nose and nasopharynx (especially with a jaw fracture), retraction of the tongue or displacement of the soft tissue flap, which acts as a valve that prevents the passage of air into the lungs.
Providing assistance with this type of breathing disorder consists of sanitation of the tracheobronchial tree, removal of a foreign body from the mouth and oropharynx.
Breathing disorders are more common mixed type, due to one and other reasons. It should be remembered that occlusion of the tracheobronchial tree leads to hypercapnia.
Restoring airway patency is accompanied by a decrease in CO2 levels in the blood, which can lead to respiratory arrest. In this clinical situation, artificial respiration is indicated until spontaneous breathing is restored.
Fracture of the base of the skull.
The base of the skull is weakened by numerous openings through which blood vessels and nerves pass. In case of a fracture of the base of the skull, the fracture gap is located in the
the path of least resistance, which determines the ambiguity of its location. Therefore, it is advisable to recall which holes are located in the anterior and middle cranial fossae, within which a fracture of the base of the skull can occur in patients with a fracture of the upper jaw. IN front the cranial fossa contains:
1. The cribriform plate of the ethmoid bone (Lamina cribrosa ossis etmoidalis) with numerous holes in it through which the olfactory filaments pass.
2. Blind opening (foramen coecum), which communicates with the nasal cavity.
3. Optic foramen (foramen opticum), through which the optic nerve passes. IN average The cranial fossa has the following openings:
1. Superior orbital fissure (fissura orbitalis superior).
2. Round hole (foramen rotundum).
3. Oval hole (foramen ovale).
4. Spinous foramen (foramen spinosum).
5. Ragged hole (foramen lacerum).
6. Internal carotid foramen (foramen caroticum interna).
7. Opening of the facial canal (hiatus canalis fasialis).
8. Superior opening of the tympanic tubule (apertura superior canalis tympanici). As an example, we can cite the most common location of the fracture gap of the base of the skull:
1) From the round foramen of one side through the sella turcica towards the ragged and spinous foramen of the other side.
2) From the foramen spinosum through the oval and round foramen to the optic foramen, spreading to the orbital surface of the frontal bone. Possible damage to the cavernous sinus.
3) From the canal of the hypoglossal nerve through the jugular foramen and the internal auditory canal (posterior cranial fossa) it goes to the spinous foramen, and then along the scales of the temporal bone. The pyramid of the temporal bone breaks.
If the base of the skull is fractured, the basal parts of the brain, brain stem, and cranial nerves may be damaged. Therefore, it is possible to establish general cerebral symptoms, brainstem disorders, and signs of damage to the cranial nerves. Bleeding from the ear (fracture of the pyramid of the temporal bone with rupture of the mucous membrane of the internal auditory canal and eardrum), from the nose (rupture of the mucous membrane of the upper wall of the nasal cavity, fracture of the ethmoid bone), from the mouth and nasopharynx (fracture of the sphenoid bone and rupture of the mucous membrane) can often be noted. membranes of the pharyngeal vault).
A Le Fort I and Le Fort II type fracture of the upper jaw is accompanied by a fracture of the base of the skull. When a fracture occurs in the anterior cranial fossa, hemorrhage occurs in the area of the periorbital tissue (strictly in the area of the orbicularis oculi muscle), subcutaneous emphysema, and nosebleeds. Nosebleeds occur when there is a fracture of the bottom of the anterior cranial fossa in the area of the roof of the nose, the posterior wall of the frontal sinus or the lateral wall of the ethmoid sinus and a mandatory rupture of the nasal mucosa covering these bones.
When the wall of the frontal or ethmoid sinuses is fractured, emphysema periorbital region, forehead, cheek. One of the clinical signs of a fracture of the base of the skull is the late appearance of "symptom of glasses"(hematoma in the eyelid area) in the absence of local signs of applied force to the soft tissues of this area. This is due to the fact that blood from the base of the skull in the area of the upper wall of the orbit penetrates the retrobulbar fatty tissue and gradually permeates the loose tissue of the eyelids.
May be liquorrhea from the nose (rhinorrhea). It should be recalled that for rhinorrhea to occur, in addition to a fracture of the base of the skull, a rupture of the dura mater and nasal mucosa at the site of the fracture is necessary. Nasal liquorrhea occurs when
fracture of the anterior cranial fossa only: in the area of the perforated plate, frontal, main (sphenoid) sinuses, cells of the ethmoid bone. The leakage of cerebrospinal fluid into the nose is possible through the openings of the ethmoid bone even in the absence of bone damage due to separation of the fibers of the olfactory nerve.
The liquorrhea stops a few days after the injury, when the wound of the dura mater, nasal mucosa and the fracture gap in the bone is sealed with clotted blood (fibrin).
It is known that post-traumatic liquorrhea is the leakage of cerebrospinal fluid from the cranial cavity when the bones of the base or vault of the skull, dura mater and integumentary tissues (skin, mucous membrane) are damaged. It is possible when the tightness of the subarachnoid space is violated (subarchnoid liquorrhea), when the walls of the ventricles are injured (ventricular liquorrhea), basal cisterns (cistern liquorrhea).
In case of fractures of the facial skeleton extending to the base of the skull, liquorrhea is of great clinical importance, since the cranial cavity freely communicates with the microbially contaminated nasal cavity, with the frontal, ethmoid, sphenoid sinuses, and cells of the mastoid process. The cerebrospinal fluid, becoming infected, flows into these sinuses, and there is a real threat of developing meningitis. Ear liquorrhea spontaneously stops in the first 2 to 3 days after injury.
The leakage of cerebrospinal fluid leads to a decrease in cerebrospinal fluid pressure. This is accompanied by headache and vestibular disorders. Patients are adynamic, occupy a forced position - they tend to lower their head down. If cerebrospinal fluid flows into the pharynx, a cough is provoked due to irritation of its mucous membrane. When the patient's position in bed changes (from back to side), the cough may stop.
According to the degree of increase in the risk of initial liquorrhea, fractures of the bones of the face and skull are located in the following sequence: fracture of the bones of the nose, upper jaw, Le Fort type I, Le Fort type II, ethmoid bone fractures. Liquor rhea is observed in more than 30% of patients with a fracture of the base of the skull. In 70% of patients with liquorrhea, hypotensive syndrome develops. Therefore, the observation of cerebrospinal fluid hypotension in patients with a basal skull fracture should make one think about cerebrospinal fluid leakage.
When fragments of a broken upper jaw are displaced, the cranial nerves located in the region of the ethmoid bone (I pair - olfactory), the body and small wings of the sphenoid bone (II pair - optic nerve), passing through the superior orbital fissure, i.e. are often damaged. between the large and small wings of the sphenoid bone (III pair - oculomotor, IV trochlear pair, VI pair - abducens).
A decrease or loss of smell in a patient with a Le Fort type I and II fracture of the upper jaw indicates damage to the olfactory nerve (I pair).
If there is a decrease in visual acuity, loss of parts of the visual fields, i.e. central and paracentral scotomas, this indicates injury to the optic nerve (II pair).
If the patient does not open the eye partially or completely, the oculomotor nerve (II pair) is damaged.
If the fracture occurs in the area of the superior orbital fissure, oculomotor disturbances may occur - signs of damage to the III, IV, VI pairs of cranial nerves. So, if the patient does not open his eyes, there is divergent strabismus, vertical separation of the eyeballs, impaired mobility of the eyeball up, down, inward, ptosis, mydriasis, then there is damage to the oculomotor nerve.
Deviation of the eyeball upward and inward, limitation of movement of the eyeball downward and outward, and diplopia when looking down are characteristic of damage to the trochlear nerve.
Convergent strabismus, impaired outward mobility of the eyeball, double vision in the horizontal plane are signs of damage to the abducens nerve.
Fractures of the anterior cranial fossa lead to its communication with the orbit or paranasal cavities.
Fractures of the middle cranial fossa (transverse, oblique, longitudinal) most often pass through the pyramid of the temporal bone, parasellar structures (tissues located around the sella turcica), and openings of the base of the skull. Damage to the III, IV, VI, VII, VIII pairs of cranial nerves may occur. As a result, the patient either partially or completely does not open his eyes. There may be restrictions on the movement of the eyeball inwards, convergent strabismus, hearing loss, tinnitus, dizziness, nystagmus, loss of coordination of movements, paresis of the facial muscles, taste disturbance on the anterior 2/3 of the tongue on the side of the lesion of the intermediate nerve in the internal auditory canal.
Bruising is localized in the area of the mastoid process and temporal muscle. There may be bleeding from the ear, liquorrhea in the case of a fracture of the temporal bone pyramid, rupture of the dura mater, the mucous membrane of the internal auditory canal and the eardrum. If its integrity is not broken, then blood and cerebrospinal fluid from the middle ear flow through the eustachian tube into the nasopharynx, and then into the nasal cavity and mouth.
It is extremely rare that heavy bleeding from the nose occurs as a result of rupture of the internal carotid artery, as well as damage to the wall of the sphenoid sinus (Blagoveshchenskaya N.S., 1994).
In a patient with liquorrhea from the nose or ear in the early period, strict bed rest is indicated. It is advisable to prevent coughing and sneezing. A protective sterile cotton-gauze bandage should be applied (on the nose or ear). It is better to give the victim’s head an elevated position, turning and tilting it towards the flow of cerebrospinal fluid. Antibiotics are prescribed prophylactically.
With a fracture of the base of the skull, there may be subarachnoid hemorrhages. The location of the fracture is determined by analyzing craniogram data, the presence of auricular or nasal liquorrhea, and signs of damage to certain cranial nerves. Dehydration therapy is indicated, which reduces pressure and production of cerebrospinal fluid, as well as unloading repeated lumbar punctures.
In addition to a fracture of the base of the skull, traumatic brain injury may cause concussions, brain contusion, and intracranial hematomas. The symptoms of their manifestation also need to be known to the dentist in order to determine treatment tactics for patients.
Brain concussion.
In case of a concussion, microstructural changes in the brain substance were not detected. However, there is damage to cell membranes. Clinically, it is characterized by a loss of consciousness - from stunning to a stop of varying duration (from several seconds to 20 minutes). Sometimes there is loss of memory for events during, before and after the injury, congrade, retrograde, anterograde amnesia. The latter is for a narrow period of events after injury. There may be nausea or occasional vomiting. Patients always report headache, dizziness, weakness, tinnitus, sweating, flushing of the face, and sleep disturbances.
Breathing is shallow, pulse is within the physiological norm. Blood pressure - no significant changes. There may be pain when moving the eyes and reading, divergence of the eyeballs, vestibular hyperesthesia.
With a mild concussion, the pupils are constricted; in severe concussions, their pupils dilate. Sometimes - anisocoria, transient oculomotor disturbances.
Neurological examination sometimes reveals asymmetry of facial muscles, labile rough asymmetry of tendon and skin reflexes, unstable small-scale nystagmus, and occasionally minor membrane symptoms that disappear in the first 3 to 7 days.
A concussion should be considered the mildest form of closed craniocerebral injury. However, these patients in the acute period should be in the hospital under the supervision of a specialist. It is known that symptoms of organic brain damage appear after a light interval. In addition, it is necessary to treat the autonomic and vascular disorders that occur with this brain injury. Bed rest for 5-7 days, the use of sedatives and vasodilators, and antihistamines are indicated.
Brain contusion.
With a brain contusion (loss of consciousness for more than 20 minutes), focal microstructural damage to the brain substance of varying severity occurs, edema and swelling of the brain, and changes in the cerebrospinal fluid-containing spaces are observed.
For easy The degree of brain contusion is characterized by loss of consciousness from several minutes to one hour, headache, dizziness, nausea, vomiting. Con-, retro- and anterograde amnesia, moderate bradycardia, clonic nystagmus, mild anisocoria, signs of pyramidal insufficiency, and meningeal symptoms are noted.
Brain contusion average degree of severity is characterized by a longer loss of consciousness (up to several hours), more pronounced focal neurological symptoms, mild transient disturbances of vital functions, and a more severe course of the acute period.
At severe The degree of brain contusion is characterized by loss of consciousness for a long period - from several hours to several weeks. Neurological symptoms with disruption of the vital functions of the body increase. Con-, retro- and anterograde amnesia, severe headache, repeated vomiting, bradycardia or tachycardia, increased blood pressure, tachypnea are expressed.
Meningeal symptoms, nystagmus, and bilateral pathological signs are common. Focal symptoms due to the localization of brain contusion are clearly identified: pupillary and oculomotor disorders, paresis of the limbs, sensitivity and speech disorders. Subarachnoid hemorrhages are common.
In 35–45% of cases with TBI, the temporal lobe of the brain is damaged. Sensory aphasia is characteristic, which is referred to as “verbal okroshka”.
Conservative therapy for brain contusion includes, in addition to the drugs used in patients with concussion, antibacterial treatment for the prevention of meningitis and meningoencephalitis, repeated lumbar punctures before sanitizing the cerebrospinal fluid. From 5 to 10 ml of cerebrospinal fluid can be withdrawn at once. Bed rest is required for 2 to 4 weeks, depending on the severity of the brain damage.
Intracranial hematomas.
Facial bone fractures combined with TBI may be accompanied by the formation of intracranial hematomas. According to the literature, they occur in 41.4% of patients with this type of TBI (Fraerman A.B., Gelman Yu.E., 1977).
Epidural hematoma- accumulation of spilled blood between the inner surface of the skull bones and the dura mater. The prerequisite for its formation is the rupture of the vessels of the dura mater - most often the middle meningeal artery and its branches, when struck in the inferior parietal or temporal region. They are localized in the temporal, temporo-parietal, temporo-frontal, temporo-basal regions. The diameter of the hematomas is 7 cm, the volume is from 80 to 120 ml.
An epidural hematoma compresses the underlying dura mater and brain matter, forming a dent in its shape and size. General and local compression of the brain occurs. Characterized by a short loss of consciousness with
its complete recovery, moderate headache, dizziness, general weakness, con- and retrograde amnesia. There may be moderate asymmetry of the nasolabial folds, spontaneous nystagmus, anisoreflexia, and moderate meningeal symptoms.
A relatively favorable state can last for several hours. Then the headache intensifies to the point of unbearable, vomiting occurs, which can be repeated. Possible psychomotor agitation. Drowsiness develops and consciousness turns off again. Bradycardia and increased blood pressure are noted.
Initially, a moderate dilation of the pupil on the side of the hematoma is determined, then with extreme mydriasm (dilation of the pupil) and the absence of its reaction to light.
To diagnose an epidural hematoma, a triad of signs is used: a lucid interval, the absence of cerebral, focal neurological symptoms against the background of temporary restoration of consciousness, homolateral mydriasis, contralateral hemiparesis. Important signs are also bradycardia, hypertension, localized headache, including with percussion of the skull.
The side of brain compression can be determined by damage to the oculomotor nerve - dilation of the pupil on the side of compression, drooping eyelids, divergent strabismus, gaze paresis, decreased or loss of pupillary response to light, dilated on the side of the hematoma.
Contralateral monoor hemiparesis and speech disorder are determined. On the side of the compression, swelling of the optic nerve sometimes occurs, on the opposite side - pyramidal insufficiency. Treatment is only surgical.
Subdural hematomas are characterized by the fact that the spilled blood is localized between the dura mater and the arachnoid mater. It causes general or local compression of the brain. Sometimes - both at the same time.
A subdural hematoma can occur both on the side where force is applied and on the opposite side. Place of impact - occipital, frontal, sagittal areas. Subdural hematomas are the most common among intracranial hematomas. Their dimensions are 10 by 12 cm, the volume ranges from 80 to 150 ml.
The classic version of a hematoma of this localization is characterized by a three-phase change in consciousness: primary loss at the time of injury, an expanded lucid interval, and secondary loss of consciousness. The light period can last from 10 minutes to several hours and even up to 1-2 days.
During this period, patients complain of headache, dizziness, and nausea. Retrograde amnesia is determined. Focal symptoms are not clearly expressed. Subsequently, there is a deepening of stunning, the appearance of drowsiness, and psychomotor agitation. The headache increases sharply, and repeated vomiting occurs. Homolateral mydriasis, contralateral pyramidal insufficiency and sensitivity disorder are detected.
Along with the loss of consciousness, a secondary brainstem syndrome develops with bradycardia, increased blood pressure, changes in breathing rhythm, bilateral vestibuloculomotor pyramidal disorders, and tonic convulsions.
Thus, subdural hematomas are characterized by a slower development of cerebral compression, longer light intervals, the presence of meningeal symptoms and the presence of blood in the cerebrospinal fluid. The remaining symptoms resemble those of an epidural hematoma.
At subarachnoid In a hematoma, spilled blood accumulates under the arachnoid membrane of the brain. Hematomas of this location accompany brain contusions. Blood breakdown products, being toxic, have a mainly vasotropic effect. They can cause cerebral vasospasm and cerebrovascular accident.
The clinical picture of subarachnoid hematoma is characterized by a combination of cerebral, meningeal and focal neurological symptoms. The patient's consciousness is disturbed and he experiences intense headache, dizziness, nausea, vomiting, and psychomotor agitation. Meningeal symptoms may be detected: photophobia, painful movement of the eyeballs, stiff neck, Kerning sign, Brudzinski sign. There may be insufficiency of the VII, XII pairs of cranial nerves of the central type, anisoreflexia, mild pyramidal symptoms.
The body temperature is elevated for 7-14 days due to irritation of the hypothalamic thermoregulation center and the meninges by the spilled blood.
Lumbar puncture is important in diagnosis: the presence of blood indicates subarachnoid hemorrhage.
Intracerebral a hematoma is a hemorrhage located in the substance of the brain. In this case, a cavity is formed filled with blood or blood mixed with brain detritus. In patients with intracerebral hematoma, focal symptoms predominate compared to cerebral symptoms. Of the focal symptoms, pyramidal insufficiency is most often noted, which is always contralateral to the side of the hematoma. Hemiparesis is pronounced. They are accompanied by central paresis of the facial (VII pair) and hypoglossal (XII pair) nerves. More often than with meningeal hematomas, there is a combination of pyramidal and sensory disorders on the same limbs, which can be supplemented by the same hemianopia. This is explained by the proximity of the intracerebral hematoma to the internal capsule. When these hematomas are localized in the frontal lobe and other “silent” areas, the focal pathology is not clearly expressed. Treatment is surgical.
Very often the brain stem is involved in the pathological process. Stem phenomena significantly complicate the diagnosis of hematomas, distorting their manifestation.
Trunk lesions may be primary(at the time of injury) and secondary when compression is possible by displaced areas of the brain. In addition, dislocation of the trunk itself due to swelling of brain tissue cannot be ruled out.
When the trunk is damaged, a deep coma, severe respiratory distress and abnormalities in cardiac activity, tonic disorders with bilateral pathological signs, and dysfunction of the oculomotor nerves are noted.
To diagnose intracranial hematomas, lumbar puncture cannot be performed due to the risk of developing midbrain compression syndrome (compression of the mesencephalic trunk), or compression of the medulla oblongata, or secondary bulbar syndrome (herniation of the bulbar trunk in the area of the foramen magnum).
6. Treatment of patients with combined traumatic brain injury consists of solving three problems:
1. Combating threatening violations of the vital functions of the body, bleeding, shock, compression and swelling of the brain.
2. Treatment of local extracranial and cranial injuries, which begins immediately after diagnosis.
3. Early prevention of possible complications. It may include radical surgery at various times after injury, depending on the general condition of the patient and the severity of brain damage.
In case of craniofacial trauma, craniomaxillary and craniomandibular fixation is considered the most rational, which allows for sealing of the brain skull, eliminating the cause of brain compression and ensuring reliable immobilization of jaw fragments.
