2. HISTORY OF INJURY

As with any injury to the musculoskeletal system, elucidation of the mechanism of injury is important and should always precede clinical examination of the patient and radiological examination. You should try to determine the position of the foot at the time of injury and the direction of the stressor (traumatic) force, as well as clarify all other data that allows you to recreate the most likely mechanism of injury. It is also helpful to determine whether there was any crunching at the time of injury, which may indicate a ligament tear, bone subluxation or dislocation, or tendon dislocation. In addition, the dynamics of the development of pain should be clarified (i.e., the doctor should ask the victim whether the onset of pain was sudden or whether it gradually increased, whether swelling appeared immediately after the injury) and the timing of disability (i.e., whether it was delayed or immediate ). The history should include information about previous ankle injuries and their treatment.

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Catad_tema Back pain - articles

Patient with acute low back pain in general practice

Low back pain (LBP) is an extremely common symptom that neurologists, internists and family doctors encounter almost daily.
Depending on the duration, LBP is divided into acute, subacute and chronic. LBP is considered acute if it lasts 6 weeks or less, subacute if it lasts 6–12 weeks. Chronic pain lasts more than 12 weeks. Depending on the duration of pain, the prognosis can be assumed: 60% of patients with acute LBP return to work within a month, 90% within 3 months.
The causes of LBP are varied. For convenience, they are usually grouped into 3 categories: potentially dangerous diseases, sciatica and nonspecific pain symptoms caused by mechanical causes.

Potentially dangerous diseases
This group includes tumors, infections, spinal injuries, and cauda equina syndrome. They can be suspected during history taking and physical examination (Table 1). These diseases require immediate further examination and treatment.

Sciatica
Pain during sciatica radiates to the leg and corresponds to the zone of innervation of the compressed root or nerve. Sometimes the pain is localized only in the leg. The roots most often affected are L5 and S1 (Fig. 1). Sciatica is often accompanied by extremely severe pain, but in most cases it resolves with conservative therapy. Sometimes surgical treatment is indicated.

Nonspecific back pain caused by mechanical causes
Some patients report pain localized only in the back, not associated with radicular symptoms or any serious diseases. This category includes “mechanical” BNJS. Improvement in the patient's condition is achieved with conservative treatment.
basis differential diagnosis is a history taking and physical examination.

Anamnesis
Diagnosis of LBP requires a careful history taking. Mechanical causes of acute LBP cause dysfunction of the musculoskeletal structures and ligamentous apparatus. Pain can come from the tissues of the intervertebral disc, joints and muscles. The prognosis for pain of mechanical origin is usually favorable.
Secondary pain requires searching for and treating the underlying disease. Secondary pain is much less common than pain caused by mechanical causes. Secondary LBP can be suspected in persons under 20 and over 50 years of age. Clinical symptoms contributing to the diagnosis are listed in Table. 1. Rarer causes of secondary acute LBP, not included in the table, are metabolic bone lesions, referred pain in diseases of the abdominal organs, retroperitoneum and pelvis, Paget’s disease, fibromyalgia, psychogenic pain.
Alarming symptoms that should alert the doctor and require further examination are listed in Table 2.

Physical examination
Gait and posture
Assessment of gait and posture is necessary in all patients with complaints of low back pain. Scoliosis may be functional, but it may also indicate muscle spasm or neurogenic disorders.
If the L5 root is affected, difficulties arise when walking on your toes; if the S1 root is affected, it becomes difficult to walk on your toes.

Range of motion
The patient's forward bending, extension, lateral bending, and upper body rotation should be assessed. Pain when bending forward is more common and is usually associated with mechanical causes. If pain occurs with spinal extension, spinal canal stenosis should be considered (Figure 2). Unfortunately, range of motion assessment is limited diagnostic value, although useful for assessing the effectiveness of treatment.

Palpation and percussion of the spine
Pain on palpation and percussion of the spinous processes of the spine may indicate the presence of a fracture or infection of the vertebra. Palpation of the paravertebral space allows you to outline painful areas and identify muscle spasms.

Heel-toe walking and squat test
The inability to walk from heel to toe or squat is common in cauda equina syndrome and other neurological disorders.

Palpation of the sciatic notch
Pain on palpation of the sciatic notch with radiation to the leg indicates irritation of the sciatic nerve.

Tests with raising a straight leg (provocative tests)
The patient lies on his back, the doctor raises his straightened leg on the affected side. The angle of leg elevation should be assessed. The appearance of pain in the range of 30–60o indicates a positive Lasègue symptom. Bending the leg at the knee joint should reduce pain, and squeezing the popliteal area should increase it. Pressing the knee joint with a straightened and elevated leg while dorsiflexing the foot will also increase the pain.
The straight leg raise test gives a positive result in 95% of patients with a disc herniation; however, it is also positive in 80–90% of patients in whom no signs of disc protrusion are found during surgery. Another test - with raising the straight leg opposite the side of the lesion (same as in the previous test, is considered positive when pain occurs) - is less sensitive, but much more specific for diagnosing a disc herniation.

Reflexes, muscle strength and sensitivity
The study of knee and ankle (Achilles) reflexes in patients with radicular symptoms often helps in the topical diagnosis.
The Achilles reflex weakens (falls out) when the L5–S1 disc is herniated. With a herniated disc at L4–L5, the tendon flexures in the legs do not fall out. A weakened knee reflex is possible with radiculopathy of the L4 root in elderly patients with spinal stenosis. Disc herniations at the L3–L4 level are very rare.
Weakness in extension thumb and foot indicates involvement of the L5 root (Fig. 4). Damage to the S1 root is characterized by paresis of the gastrocnemius muscle (the patient cannot walk on his toes).
Assessing the sensitivity of the skin of the leg and foot (Fig. 4) also allows us to assess the level of damage. S1 radiculopathy causes hypoesthesia along the back of the leg and the outer edge of the foot. Compression of the L5 root leads to hypoesthesia of the dorsum of the foot, big toe and first interdigital space.

Rapid neurological examination
At the initial presentation of a patient with LBP and radicular symptoms, a neurological examination may be limited to only a few tests: assessing the strength of dorsiflexion/extension of the foot and big toe (as an option - walking on toes and heels), knee and Achilles reflexes, checking the sensitivity of the foot and lower leg, as well as Lasegue's breakdown. This abbreviated examination allows us to identify clinically significant radiculopathy associated with lumbar disc herniation. If there is no improvement after a month, further examination or referral to a specialist is necessary. If symptoms progress, examination should be carried out immediately.

Rice. 1.
Variants of compression of the spinal cord roots at the lumbar level of the spine

Table 1.
Causes of LBP

Rice. 2.
Spinal stenosis

Due to the growth of osteophytes, the canal acquired a characteristic trefoil shape. In this case, possible compression of both the individual root and the roots of the cauda equina leads to mono- or polyradiculopathy. Often, with spinal stenosis, pseudo-intermittent claudication occurs: pain in the lumbosacral region (possibly in the buttocks and legs) appears while walking and goes away when the patient sits down.

Table 2.
Alarming symptoms in acute LBP

Table 3.
Indications for radiography in acute LBP

Rice. 3.
Saddle anesthesia

Saddle anesthesia is often a manifestation of cauda equina syndrome, which in addition to anesthesia may include: bilateral sciatica, sudden onset of urinary retention or incontinence, fecal incontinence, lower flaccid paraparesis.

Rice. 4.
Symptoms of damage to the L4-S1 roots

Table 4.
Waddel criteria

Laboratory tests
As a rule, on initial stages Laboratory tests are not required for patients with acute LBP. If a tumor or infectious process is suspected, a general blood test and ESR are required. Other blood tests are recommended only if a primary disease is suspected, such as ankylosing spondylitis or myeloma (HLA-B27 test and serum protein electrophoresis, respectively). If a urinary tract pathology is suspected, a general urinalysis is indicated.
To detect metabolic bone diseases, calcium, phosphate levels and alkaline phosphatase activity are determined.

X-ray examination
Indications for radiographic examination in acute LBP are listed in Table. 3.
It does not make sense to perform spinal x-rays on all patients with LBP, since certain changes can be detected in almost all patients. An X-ray of a patient who does not complain of back pain may show pronounced changes (osteochondrosis, deforming osteoarthritis, sacralization or lumbarization of the vertebrae). In contrast, in a patient with LBP, changes may be minimal.
If cauda equina syndrome or progressive muscle weakness occurs, computed tomography, magnetic resonance imaging, and myelography are indicated. Carrying out these studies is also advisable in preparation for surgery.

Treatment
Most patients with acute LBP require only symptomatic treatment. At the same time, about 60% of patients note improvement during the first 7 days of treatment and the vast majority - within 4 weeks. Patients should be instructed that if motor or sensory functions deteriorate, pain increases, or pelvic organ dysfunction occurs, they should immediately consult a doctor again for further examination.
As pain decreases, patients should be gradually returned to normal activities. Maintaining activity within the limits allowed by pain has been shown to promote faster recovery than bed rest or lumbar immobilization.
Patients with this pathology also benefit from moderate physical exercise with minimal stress on the back.
Medicines Options used for acute LBP include nonsteroidal anti-inflammatory drugs (NSAIDs) and paracetamol. It is also possible to use muscle relaxants. Patients taking opioid analgesics have been shown to return to normal activities no more quickly than those taking NSAIDs or paracetamol. Muscle relaxants have a greater analgesic effect than placebo, but do not have advantages over NSAIDs. Oral glucocorticoids and antidepressants have no effect in such patients and their use is not recommended.
Currently, new drugs have appeared that act directly at the level of the spinal cord, which makes it possible to avoid many of the undesirable effects characteristic of the above groups of drugs. The first representative of a new class of substances, selective neuronal potassium channel openers (SNEPCO = selective neuronal potassium channel opener) is flupirtine i. It has a combination of analgesic and muscle relaxant properties, which is especially important in the treatment of musculoskeletal pain and muscle spasms.
The greatest effect from flupirtine should be expected in pain syndromes, the pathogenesis of which is a mirror image of the properties of the drug. Considering that it has both an analgesic and muscle relaxant effect, these are those acute and chronic diseases in which pain is caused by muscle spasm, especially pain in the musculoskeletal system (neck and back), muscle spasms in diseases of the joints.
Unlike traditionally used painkillers (NSAIDs, opioid analgesics, muscle relaxants), it does not inhibit cyclooxygenase, does not have opioid and general relaxant effects and is therefore free from the inherent effects of these substances side effects.
Several randomized studies have demonstrated the effectiveness of manual therapy. Some patients may find it helpful to wear special insoles or arch supports in their shoes. But exercises to “stretch” the spine, transcutaneous electrical stimulation, injections into trigger points or intervertebral joints and acupuncture usually have no effect. For some patients in whom conservative therapy does not respond and activity-limiting symptoms persist after a month of treatment, surgical treatment may be indicated.
Patients who, already at the first visit to the doctor, have identified the symptoms listed in table. 2, need prompt further examination and qualified treatment.

Difficulties of diagnosis in acute LBP
Sometimes complaints of acute LBP are due to nonorganic reasons. Psychosocial reasons can be economic (for example, increased financial compensation for time of incapacity) or social (job dissatisfaction) of a nature. If there is a suspicion of psychosocial factors, the doctor may ask the patient to mark on the figure depicting human body, spread of pain. If the distribution of pain does not correspond to anatomical landmarks, psychogeny is highly likely. There is also a set of Waddel criteria (Table 4), which can easily be performed during a routine physical examination. G. Waddel noted that most patients with LBP of organic origin do not have these criteria or only one criterion is identified. If the patient has three or more Waddel criteria, we can speak with a high degree of confidence about psychogenic LBP or malingering.

Literature:
Bratton R.L. Assessment and management of acute low back pain. American Family Physician, 1999; 60(8):2299–2306.
Material prepared by R.I. Elagin, Ph.D. honey. sciences,
Department of Clinical Pharmacology MMA named after. THEM. Sechenov

Katadolon® - Drug dossier

■ Lack of clarity and subjectivity in the interpretation of the neurological picture.

■ Transience of neurological symptoms.

■ Predominance of general cerebral symptoms over focal ones.

■ Absence of meningeal symptoms in young children with subarachnoid hemorrhages.

■ The relative rarity of intracranial hematomas.

■ Frequent development of cerebral edema.

■ Good regression of neurological symptoms.

Closed TBI includes a concussion, mild, moderate and severe brain contusion and compression of the brain, which is often noted against the background of a brain contusion. The cause of compression of the brain is most often an intracranial hematoma, less often - fragments of the skull in a so-called depressed fracture.

Diagnosis of TBI is based on identifying the following signs.

■ History of a blow to the head or head.

■ Visually detectable damage to the soft tissues of the head and skull bones.

■ Visually detectable signs of a basal skull fracture.

■ Impaired consciousness and memory.

■ Symptoms of cranial nerve damage.

■ Signs of focal brain lesions.

■ Obol ophthalmic symptoms.

Impaired consciousness. With mild TBI (concussion or mild contusion), loss of consciousness in preschool children is rare. The following gradation of consciousness disorders is currently accepted.

■ Clear consciousness: the child is fully oriented, adequate and active.

■ Moderate deafness: the child is conscious, partially oriented, answers questions quite correctly, but reluctantly and monosyllabically, drowsiness.

■ Severe deafness: the child is conscious, but his eyes are closed, disoriented, answers only simple questions, in monosyllables and not immediately, only after repeated requests, follows simple commands, drowsiness.

■ Stupor: the child is unconscious, eyes are closed. Reacts only to pain and calling by opening the eyes; however, contact with the patient cannot be established. Localizes pain well: withdraws the limb during injection, defends itself. Flexion movements in the limbs dominate.

■ Moderate coma: the child is unconscious - “unawakenable”, reacts to pain with a general reaction (shudders, shows anxiety), but does not localize the pain, does not defend himself. Vital functions are stable, with good parameters.

■ Deep coma: the child is unconscious - “unawakenable”, does not respond to pain. Muscular hypotonia. Extensor tone dominates.

■ Extreme coma: the child is unconscious - “unawakenable”, does not respond to pain. At times he makes spontaneous extension movements. Muscular hypotonia and areflexia. Vital functions are grossly impaired: no spontaneous breathing, blood pressure 70 mm Hg. and below.

Memory disorders Memory disorders are noted in victims with moderate and severe brain contusions, and in children with prolonged loss of consciousness. If the child does not remember the events that happened before the injury, retrograde amnesia is stated, after the injury - anterograde amnesia.

Headache occurs in almost all victims, with the exception of children under 2 years of age. The pain is diffuse and with a minor injury is not painful and subsides with rest.

Vomiting, like headaches, occurs in almost all victims, but if with a mild injury it is usually one-time, then with a severe injury it is repeated.

Symptoms of cranial nerve damage

■ Disturbances in the innervation of the pupils: sluggish reaction to light, in severe TBI - its absence, the pupils can be uniformly dilated or constricted, anisocoria may indicate brain dislocation with intracranial hematoma or severe basal contusion.

■ Deviation of the tongue, asymmetry of the face when closing your eyes, grinning. Persistent facial asymmetry indicates moderate or severe TBI.

Reflexes and muscle tone. Corneal reflexes either decrease or disappear. Muscle tone is changeable: from moderate hypotonia with a mild injury to increased tone in the extensors of the trunk and limbs with a severe injury.

Heart rate and body temperature. The pulse rate can vary widely. Bradycardia indicates progressive intracranial hypertension - compression of the brain by a hematoma.

Features of diagnosing TBI in children of the first year of life. The acute period is characterized by short duration, a predominance of cerebral symptoms, and sometimes the absence of cerebral and focal symptoms. Main symptoms for diagnosis:

■ high-pitched scream or short-term apnea at the time of injury;

■ the appearance of motor automatisms (sucking, chewing, etc.);

■ regurgitation or vomiting;

■ autonomic disorders (hyperhidrosis, tachycardia, fever);

Diagnosis of TBI severity

■ Concussion.

Short-term loss of consciousness (up to 10 minutes). If more than 15 minutes have passed from the moment of injury to the arrival of the emergency medical team, then the child is already conscious.

Retrograde, less often anterograde amnesia.

Vomiting (usually 1-2 times).

Absence of focal symptoms.

■ Brain contusion (one symptom is sufficient to make a diagnosis).

Loss of consciousness for more than 30 minutes or impaired consciousness at the time of examination, if the period from the moment of injury to the arrival of the team is less than 30 minutes.

Presence of focal symptoms.

Visible fractures of the skull bones.

Suspicion of a fracture of the base of the skull (symptom of “spectacles”, liquorrhea or hemoliquorrhea).

■ Compression of the brain.

Compression of the brain is usually combined with a bruise. The main causes of compression of the brain are intracranial hematomas, depressed fractures of the skull bones, cerebral edema, and subdural hygromas.

The main clinical symptoms of brain compression are paresis of the limbs (contralateral hemiparesis), anisocoria (homolateral mydriasis), bradycardia. Characteristically, there is a “bright” interval - an improvement in the child’s condition after an injury followed by a deterioration. The duration of the “light” interval is from several minutes to several days.

Carry out with brain tumors, hydrocephalus, cerebral aneurysms, inflammatory diseases brain and its membranes, poisoning, comas in diabetes mellitus.

■ Control using the ABC system; start oxygen therapy (60-100% oxygen), apply a cervical collar if injury is suspected cervical spine spine.

■ In case of deep and extreme coma - tracheal intubation after intravenous administration of a 0.1% atropine solution 0.1 ml/year, but not more than 1 ml.

■ Mechanical ventilation for deep coma in cases of signs of hypoxemia.

■ In extreme coma - mechanical ventilation in mode of moderate hyperventilation.

■ Correction of hemodynamic decompensation with infusion therapy when systolic blood pressure decreases below 60 mm Hg. (see section “Infusion therapy in the prehospital stage”).

■ Prevention and treatment of cerebral edema is carried out when a diagnosis of brain contusion is made. Dexamethasone 0.6-0.7 mg/kg or prednisolone 5 mg/kg is administered intravenously or intramuscularly (only in the absence of arterial hypertension). Furosemide dose

1 mg/kg intravenously or intramuscularly is administered only in the absence of arterial hypotension and evidence of cerebral compression.

■ If the victim has a convulsive syndrome, psychomotor agitation, hyperthermia, etc.

■ Hemostatic therapy: etamsylate (dicinone*) 1-2 ml intravenously or intramuscularly.

■ For pain relief, if necessary, use drugs that do not depress the respiratory center (tramadol - 2-3 mg/kg intravenously, metamizole sodium (analgin*) - 50% solution 0.1 ml/year intravenously). Drugs that depress the respiratory center (narcotic analgesics) can be administered during mandatory mechanical ventilation [trimeperidine (promedol*) - 0.1 ml/year intravenously].

■ All symptoms in children with TBI are variable, which necessitates careful monitoring. Therefore, all children with suspected TBI, even if there is only anamnestic indication of injury without clinical manifestations, are subject to mandatory hospitalization in a hospital with a neurosurgical and intensive care unit.

Traumatic brain injury

Traumatic brain injury - damage to the bones of the skull and/or soft tissues (meninges, brain tissue, nerves, blood vessels). Based on the nature of the injury, a distinction is made between closed and open, penetrating and non-penetrating TBI, as well as concussion or contusion of the brain. The clinical picture of traumatic brain injury depends on its nature and severity. The main symptoms are headache, dizziness, nausea and vomiting, loss of consciousness, memory impairment. Brain contusion and intracerebral hematoma are accompanied by focal symptoms. Diagnosis of traumatic brain injury includes medical history, neurological examination, skull x-ray, CT or MRI of the brain.

Traumatic brain injury

Traumatic brain injury - damage to the bones of the skull and/or soft tissues (meninges, brain tissue, nerves, blood vessels). The classification of TBI is based on its biomechanics, type, type, nature, shape, severity of injury, clinical phase, treatment period, and outcome of the injury.

According to biomechanics there are the following types TBI:

• shock-anti-shock (the shock wave propagates from the site of the received blow and passes through the brain to the opposite side with rapid pressure changes);
• acceleration-deceleration (movement and rotation of the cerebral hemispheres in relation to a more fixed brain stem);
• combined (simultaneous impact of both mechanisms).

By type of damage:

• focal (characterized by local macrostructural damage to the brain matter, with the exception of areas of destruction, small and large focal hemorrhages in the area of ​​impact, counter-impact and shock wave);
• diffuse (tension and spread of primary and secondary axonal ruptures in the centrum semiovale, corpus callosum, subcortical formations, brain stem);
• combined (a combination of focal and diffuse brain damage).

According to the genesis of the lesion:

• primary lesions: focal contusions and crushes of the brain, diffuse axonal damage, primary intracranial hematomas, brainstem ruptures, multiple intracerebral hemorrhages;
• secondary lesions:

1. due to secondary intracranial factors (delayed hematomas, disturbances in cerebrospinal fluid and hemocirculation due to intraventricular or subarachnoid hemorrhage, cerebral edema, hyperemia, etc.);
2. due to secondary extracranial factors (arterial hypertension, hypercapnia, hypoxemia, anemia, etc.)

According to their type, TBIs are classified into: closed - injuries that do not violate the integrity of the skin of the head; fractures of the bones of the calvarium without damage to the adjacent soft tissues or a fracture of the base of the skull with developed liquorrhea and bleeding (from the ear or nose); open non-penetrating TBI - without damage to the dura mater and open penetrating TBI - with damage to the dura mater. In addition, isolated (absence of any extracranial damage), combined (extracranial damage as a result of mechanical energy) and combined (simultaneous exposure to various energies: mechanical and thermal/radiation/chemical) traumatic brain injury are distinguished.

Based on severity, TBI is divided into 3 degrees: mild, moderate and severe. When correlating this rubric with the Glasgow Coma Scale, mild traumatic brain injury is assessed at 13-15, moderate at 9-12, severe at 8 points or less. A mild traumatic brain injury corresponds to a mild concussion and contusion, a moderate one corresponds to a moderate brain contusion, a severe one corresponds to a severe brain contusion, diffuse axonal damage and acute compression of the brain.

According to the mechanism of occurrence of TBI, there are primary (the impact of traumatic mechanical energy on the brain is not preceded by any cerebral or extracerebral catastrophe) and secondary (the impact of traumatic mechanical energy on the brain is preceded by a cerebral or extracerebral catastrophe). TBI in the same patient can occur for the first time or repeatedly (twice, three times).

The following clinical forms of TBI are distinguished: concussion, mild brain contusion, moderate brain contusion, severe brain contusion, diffuse axonal damage, brain compression. The course of each of them is divided into 3 basic periods: acute, intermediate and long-term. The duration of the periods of traumatic brain injury varies depending on the clinical form of TBI: acute - 2-10 weeks, intermediate - 2-6 months, long-term with clinical recovery - up to 2 years.

Brain concussion

The most common injury among possible traumatic brain injuries (up to 80% of all TBIs).

Clinical picture

Depression of consciousness (to the level of stupor) during a concussion can last from several seconds to several minutes, but may be absent altogether. Retrograde, congrade and antegrade amnesia develops for a short period of time. Immediately after a traumatic brain injury, a single vomiting occurs, breathing becomes more frequent, but soon returns to normal. Blood pressure also returns to normal, except in cases where the medical history is aggravated by hypertension. Body temperature during a concussion remains normal. When the victim regains consciousness, there are complaints of dizziness, headache, general weakness, cold sweat, flushing of the face, and tinnitus. The neurological status at this stage is characterized by mild asymmetry of skin and tendon reflexes, small horizontal nystagmus in the extreme abductions of the eyes, and mild meningeal symptoms that disappear during the first week. With a concussion as a result of a traumatic brain injury, after 1.5 - 2 weeks, an improvement in the patient’s general condition is noted. It is possible that some asthenic phenomena may persist.

Diagnosis

Recognizing a concussion is not an easy task for a neurologist or traumatologist, since the main criteria for diagnosing it are the components of subjective symptoms in the absence of any objective data. It is necessary to familiarize yourself with the circumstances of the injury, using the information available to witnesses to the incident. Of great importance is an examination by an otoneurologist, with the help of which the presence of symptoms of irritation of the vestibular analyzer in the absence of signs of prolapse is determined. Due to the mild semiotics of a concussion and the possibility of a similar picture arising as a result of one of many pre-traumatic pathologies, special importance in diagnosis is given to the dynamics of clinical symptoms. The justification for the diagnosis of “concussion” is the disappearance of such symptoms 3-6 days after receiving a traumatic brain injury. With a concussion, there are no fractures of the skull bones. The composition of the cerebrospinal fluid and its pressure remain normal. CT scan of the brain does not detect intracranial spaces.

Treatment

If a victim with a traumatic brain injury has come to his senses, first of all he needs to be given a comfortable horizontal position, his head should be slightly raised. A victim with a traumatic brain injury who is in an unconscious state must be given the so-called. “saving” position - lay him on his right side, his face should be turned to the ground, his left arm and leg should be bent at a right angle at the elbow and knee joints(if fractures of the spine and limbs are excluded). This position promotes the free passage of air into the lungs, preventing the tongue from retracting and vomit, saliva and blood from entering the respiratory tract. Apply an aseptic bandage to bleeding wounds on the head, if any.

All victims with traumatic brain injury in mandatory transported to a hospital, where, after confirmation of the diagnosis, they are placed on bed rest for a period that depends on the clinical features of the course of the disease. Absence of signs of focal brain lesions on CT and MRI of the brain, as well as the patient’s condition allowing him to refrain from active drug treatment, allow us to resolve the issue in favor of discharging the patient for outpatient treatment.

For a concussion, overactive drug treatment is not used. Its main goals are to normalize the functional state of the brain, relieve headaches, and normalize sleep. For this purpose, analgesics and sedatives (usually in tablet forms) are used.

Brain contusion

Mild brain contusion is detected in 10-15% of victims with traumatic brain injury. A bruise of moderate severity is diagnosed in 8-10% of victims, a severe bruise - in 5-7% of victims.

Clinical picture

A mild brain contusion is characterized by loss of consciousness after injury of up to several tens of minutes. After regaining consciousness, complaints of headache, dizziness, and nausea appear. Retrograde, congrade, and anterograde amnesia are noted. Vomiting is possible, sometimes with repetitions. Vital functions are usually preserved. Moderate tachycardia or bradycardia and sometimes increased blood pressure are observed. Body temperature and respiration without significant deviations. Mild neurological symptoms regress after 2-3 weeks.

Loss of consciousness with a moderate brain contusion can last from minutes to 5-7 hours. Retrograde, congrade and anterograde amnesia are strongly expressed. Repeated vomiting and severe headache are possible. Some vital functions are impaired. Bradycardia or tachycardia, increased blood pressure, tachypnea without respiratory distress, and increased body temperature to subfebrile are detected. The manifestation of meningeal signs, as well as stem symptoms, is possible: bilateral pyramidal signs, nystagmus, dissociation of meningeal symptoms along the body axis. Pronounced focal signs: oculomotor and pupillary disorders, paresis of the limbs, speech and sensitivity disorders. They regress after 4-5 weeks.

Severe brain contusion is accompanied by loss of consciousness from several hours to 1-2 weeks. It is often combined with fractures of the bones of the base and vault of the skull, and profuse subarachnoid hemorrhage. Disorders of vital functions are noted: respiratory rhythm disturbances, sharply increased (sometimes decreased) blood pressure, tachy- or bradyarrhythmia. Possible blockage of the airways, intense hyperthermia. Focal symptoms of hemispheric damage are often masked behind stem symptoms that come to the fore (nystagmus, gaze paresis, dysphagia, ptosis, mydriasis, decerebrate rigidity, changes in tendon reflexes, the appearance of pathological foot reflexes). Symptoms of oral automatism, paresis, focal or generalized seizures can be detected. Restoring lost functions is difficult. In most cases, gross residual motor and mental disorders remain.

Diagnosis

The method of choice for diagnosing a brain contusion is a CT scan of the brain. A CT scan reveals a limited area of ​​low density, possible fractures of the calvarial bones and subarachnoid hemorrhage. With a brain contusion of moderate severity, CT or spiral CT in most cases reveals focal changes (non-compactly located areas of low density with small areas of increased density).

In case of severe contusion, CT scan reveals areas of heterogeneous increase in density (alternating areas of increased and decreased density). Perifocal cerebral edema is severe. A hypodense track is formed in the area of ​​the nearest section of the lateral ventricle. Through it, fluid with breakdown products of blood and brain tissue is discharged.

Diffuse axonal brain injury

Diffuse axonal brain damage is typically characterized by a prolonged coma after a traumatic brain injury, as well as pronounced brain stem symptoms. Coma is accompanied by symmetrical or asymmetrical decerebration or decortication, both spontaneous and easily provoked by irritations (for example, painful ones). Changes in muscle tone are very variable (hormetonia or diffuse hypotension). A typical manifestation is pyramidal-extrapyramidal paresis of the limbs, including asymmetric tetraparesis. In addition to gross disturbances in the rhythm and frequency of breathing, autonomic disorders also appear: increased body temperature and blood pressure, hyperhidrosis, etc. A characteristic feature of the clinical course of diffuse axonal brain damage is the transformation of the patient’s condition from a prolonged coma to a transient vegetative state. The onset of this state is indicated by spontaneous opening of the eyes (with no signs of tracking or fixation of gaze).

Diagnosis

The CT picture of diffuse axonal brain damage is characterized by an increase in brain volume, as a result of which the lateral and third ventricles, subarachnoid convexital spaces, and also the cisterns of the base of the brain are under compression. The presence of small focal hemorrhages in the white matter of the cerebral hemispheres, corpus callosum, subcortical and brain stem structures is often detected.

Brain compression

Brain compression develops in more than 55% of cases of traumatic brain injury. The most common cause of brain compression is an intracranial hematoma (intracerebral, epi- or subdural). Rapidly increasing focal, brainstem and cerebral symptoms pose a danger to the life of the victim. Availability and duration of the so-called the “light gap” - expanded or erased - depends on the severity of the victim’s condition.

Diagnosis

A CT scan reveals a biconvex, less often a flat-convex, limited zone of increased density, which is adjacent to the cranial vault and is localized within one or two lobes. However, if there are several sources of bleeding, the area of ​​​​increased density can be significant in size and have a crescent shape.

Treatment of traumatic brain injury

When a patient with a traumatic brain injury is admitted to the intensive care unit, the following measures must be taken:

• Examination of the victim’s body, during which abrasions, bruises, joint deformities, changes in the shape of the abdomen and chest, bleeding and/or liquor leakage from the ears and nose, bleeding from the rectum and/or urethra, and a specific odor from the mouth are detected or excluded.
• Comprehensive x-ray examination: skull in 2 projections, cervical, thoracic and lumbar spine, chest, pelvic bones, upper and lower extremities.
• Ultrasound of the chest, ultrasound of the abdominal cavity and retroperitoneal space.
• Laboratory tests: general clinical analysis of blood and urine, biochemical blood test (creatinine, urea, bilirubin, etc.), blood sugar, electrolytes. These laboratory tests must be carried out in the future, daily.
• ECG (three standard and six chest leads).
• Testing urine and blood for alcohol content. If necessary, consult a toxicologist.
• Consultations with a neurosurgeon, surgeon, traumatologist.

A mandatory method of examining victims with traumatic brain injury is computed tomography. Relative contraindications to its implementation may include hemorrhagic or traumatic shock, as well as unstable hemodynamics. Using CT, the pathological focus and its location, the number and volume of hyper- and hypodense zones, the position and degree of displacement of the midline structures of the brain, the condition and degree of damage to the brain and skull are determined. If meningitis is suspected, a lumbar puncture and dynamic examination of the cerebrospinal fluid are indicated, which allows monitoring changes in the inflammatory nature of its composition.

A neurological examination of a patient with a traumatic brain injury should be performed every 4 hours. To determine the degree of consciousness impairment, the Glasgow Coma Scale is used (state of speech, response to pain and ability to open/close eyes). In addition, the level of focal, oculomotor, pupillary and bulbar disorders is determined.

For a victim with impaired consciousness of 8 points or less on the Glasgow scale, tracheal intubation is indicated, due to which normal oxygenation is maintained. Depression of consciousness to the level of stupor or coma is an indication for auxiliary or controlled mechanical ventilation (at least 50% oxygen). With its help, optimal cerebral oxygenation is maintained. Patients with severe traumatic brain injury (hematomas, cerebral edema, etc. detected on CT) require monitoring of intracranial pressure, which must be maintained below 20 mmHg. For this purpose, mannitol, hyperventilation, and sometimes barbiturates are prescribed. To prevent septic complications, escalation or de-escalation is used antibacterial therapy. For the treatment of post-traumatic meningitis, modern antimicrobial drugs approved for endolumbar administration (vancomycin) are used.

Patients begin feeding no later than 3 days after TBI. Its volume is increased gradually and at the end of the first week following the date of the traumatic brain injury, it should provide 100% of the patient’s caloric needs. The route of nutrition can be enteral or parenteral. To relieve epileptic seizures, anticonvulsants are prescribed with minimal dose titration (levetiracetam, valproate).

The indication for surgery is an epidural hematoma with a volume of over 30 cm³. It has been proven that the method that provides the most complete evacuation of the hematoma is transcranial removal. Acute subdural hematoma with a thickness of more than 10 mm is also subject to surgical treatment. In comatose patients, acute subdural hematoma is removed using craniotomy, maintaining or removing a bone flap. An epidural hematoma with a volume of more than 25 cm³ is also subject to mandatory surgical treatment.

Prognosis for traumatic brain injury

Concussion is a predominantly reversible clinical form of traumatic brain injury. Therefore, in more than 90% of cases of concussion, the outcome of the disease is the recovery of the victim with full restoration of ability to work. Some patients, after the acute period of concussion, experience certain manifestations of post-concussion syndrome: disturbances in cognitive functions, mood, physical well-being and behavior. 5-12 months after a traumatic brain injury, these symptoms disappear or are significantly smoothed out.

Prognostic assessment in severe traumatic brain injury is carried out using the Glasgow Outcome Scale. A decrease in the total number of points on the Glasgow scale increases the likelihood of an unfavorable outcome of the disease. Analyzing the prognostic significance of the age factor, we can conclude that it has a significant impact on both disability and mortality. The combination of hypoxia and arterial hypertension is an unfavorable prognosis factor.

Traumatic brain injury - treatment in Moscow

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History of TBI

The incidence of traumatic brain injury is constantly increasing, primarily due to the increase in road traffic accidents. In economically developed countries, the incidence is approximately 8,000 cases per 1 million population per year, of which approximately half of the victims require hospitalization. Approximately 2.5-5% of patients require subsequent rehabilitation.

Depending on the severity, the following types of traumatic brain injuries are distinguished:

Contusion of the soft tissues of the head without brain damage (including in the absence of signs of concussion); in such cases, treatment is usually required,

Concussion (may be accompanied by a skull fracture),

Brain contusion (not always accompanied by a fracture of the skull bones and in exceptional cases may occur without symptoms of concussion),

Penetrating injury: open direct damage to the brain substance, always accompanied by a fracture of the skull bones,

Early and late complications of traumatic brain injury, in particular compression of the brain.

Clear boundaries between a contusion of the soft tissues of the head and a concussion, as well as between a concussion and a contusion of the brain, are not always easy to draw. The presence or absence of a skull fracture is not a criterion for the severity of damage to the brain itself.

When determining the circumstances of the injury, special attention should be paid to:

The exact time, type and direction of the damaging effect,

Protection of the head at the time of injury (for example, the presence of a hat),

The patient's own memories of that. how the injury occurred

The presence and duration of retrograde amnesia (events that occurred immediately before the injury),

Duration of apstrograde amnesia (events that occurred following the trauma),

Presence of nausea and vomiting.

When examining a patient with a “fresh” traumatic brain injury, special attention should be paid to the following:

External damage, especially in the head area,

Leakage of blood or CSF from the nose, ears, pharynx,

Damage to the cervical spine,

Presence of periorbital hematoma (symptom of “glasses”) and/or rstroauricular hematoma,

General condition, especially the state of the cardiovascular system (possible development of shock!), neurological status (state of the pupils, vision, hearing, presence of nystagmus, paresis, pyramidal signs),

In unconscious patients, radiography of the cervical spine is mandatory.

X-ray of the skull: Neuroimaging (preferably CT) may be required to exclude intracranial hemorrhage. A CT scan of the head performed shortly after injury often reveals a greater volume of damage than in the first hours. MRI can be used to diagnose infratentorial damage. In addition, T2-weighted MR images may show evidence of diffuse axonal injury (“shear injury”), most commonly in the corpus callosum and subcortical white matter of the frontal lobes.

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0027 Open traumatic brain injury.

Main tabs

1. Last name, first name, patronymic of the patient:
2. Age: 25 years
3. Gender: male
4. Place of work and position:
5. Home address:
6. Date of admission to the clinic: 11/13/06, 13 22
7. Date of discharge:
8. Diagnosis during hospitalization: Open craniocerebral injury. Brain contusion.
9. Clinical diagnosis: Open craniocerebral injury. Fracture of the base of the skull on the right. Brain contusion. Post-traumatic neuritis of the facial nerve on the right.
10. Concomitant diseases: no
11. Complications: no

Upon admission and at the time of supervision, the patient complains of moderate stabbing constant pain in the right temporal region, intensifying when taking a vertical and semi-vertical position, relieved by taking analgesics; for constant drooping of the right upper eyelid, the right corner of the mouth, weakness of the facial muscles on the right, decreased hearing in the right ear.

History of present illness

Was injured on October 20, 2006 as a result of a traffic accident: in a state of alcohol intoxication was shot down a passenger car. Does not remember events at the time of injury and within 24 hours after it. During this time, he was taken to the Central District Hospital, where the diagnosis was made: “Open craniocerebral injury: fracture of the base of the skull on the right, blunt trauma to the abdomen,” and a splenectomy was performed. The appearance of complaints of headaches, decreased hearing on the right - since the restoration of consciousness, approximately 1 week after the injury, the patient noted the appearance and gradual increase of facial asymmetry and weakness of the facial muscles on the right. Significant dynamics of these complaints in connection with treatment in the Central District Hospital ( medications it is difficult to name the patient) it was not noted what became the reason for sending the patient to the neurosurgical department of the Zaporozhye Regional Clinical Hospital.

Life history without any features.

Objective condition of the patient

The patient's condition is moderate, the position is active, consciousness is clear. The physique is hypersthenic, proportional.

The head is of normal shape and size.

The skin is pale, moderately moist, with numerous scars, incl. and on the scalp, visible mucous membranes without any features. Occipital, postauricular, submandibular, posterior cervical, anterior cervical, supraclavicular, subclavian, axillary, ulnar, popliteal lymph nodes are not palpable.

Cardiovascular system: upon examination and palpation without any features, upon percussion the boundaries of cardiac dullness are within normal limits. Auscultation of the heart sounds is clear, there are no murmurs. Pulse of satisfactory filling and tension.

Respiratory system: breathing through the nose is free. Upon examination and palpation, the chest is without any features; upon percussion, a clear pulmonary sound is heard over the entire surface of the lungs. Auscultation over the entire surface of the lungs reveals vesicular breathing, no wheezing.

Digestive system: on the anterior abdominal wall there is a postoperative scar along the white line of the abdomen. On palpation, the abdomen is soft, pain along the intestine is not detected. The stool is normal. The dimensions of the liver according to Kurlov are 9*8*6 cm.

Blood pressure 125/80 mm Hg.

Pulse 78 per minute.

The respiratory rate is 18 per minute.

Notes a constant headache in the right temporal region. An episode of ante- and retrograde amnesia due to trauma and surgery.

Study of cranial nerves: VII pair. When examining the face, there is drooping of the right upper eyelid, right nasolabial fold and right corner of the mouth. Raising and frowning of the eyebrows, squinting of the eyes is weakened on the right, normal on the left. When asked to smile or show teeth, there is a significant decrease in the range of movements of the facial muscles on the right.

There is a decrease in hearing in the right ear.

Data from additional examination methods

M-echo offset. Uneven intracranial hypertension.

11/15/06. Electrical conductivity study.

The right facial nerve on the II current of the I, II, III centuries is normal

on the P-current I, II, III centuries - reduced

contracture in the 2nd century.

11/15/06. Examination by an ophthalmologist

VisOD=1.0, VisOS=0.2 (low since childhood)

11/13/06. MRI of the brain

Conclusion: contusion of the cortical parts of the left frontotemporal region.

Based on the above complaints, medical history, objective and additional examination data of the patient, a clinical diagnosis can be formulated:

Open traumatic brain injury. Fracture of the base of the skull on the right. Brain contusion. Post-traumatic neuritis of the facial nerve on the right.

“Open traumatic brain injury”: justified by a history of an accident, written confirmation of information about an examination at the Central District Hospital (taking into account the age of onset of the disease), the presence of scars on the scalp, and the development of the clinical picture of a brain contusion.

“Fracture of the base of the skull on the right” - is justified by an indication in the anamnesis of an accident, written confirmation of information about the examination at the Central District Hospital (taking into account the duration of the onset of the disease).

“Brain contusion” - is justified by a history of an accident, documented information about a fracture of the skull bones, the formation of persistent focal symptoms (local headache, hearing loss on the right) immediately after the injury, data from an echoEG examination about the displacement of the M-echo, an MRI conclusion brain.

“Post-traumatic neuritis of the facial nerve on the right” is justified by the above data about a fracture of the bones of the base of the skull, in the canals of which the facial nerve passes, complaints and data from a neurological examination about the weakness of the facial muscles on the right, data from a study of the electrical conductivity of the right facial nerve.

For all traumatic brain injuries, bed rest and complete rest are prescribed for 5-6 days in mild cases and for up to several weeks in more severe cases. You can put a cold compress on your head. If there is bleeding from the nose or ears, do not resort to lavage and tight tamponade; sterile dressings should be applied.

The presence of liquorrhea creates a risk of brain infection. In these cases, intensive antibiotic therapy is prescribed. To stop bleeding, calcium chloride is prescribed orally (10% solution, 1 teaspoon or tablespoon 3 times a day). In case of a decrease in cardiac activity, camphor, caffeine, cordiamine (age-specific doses) are prescribed; for respiratory disorders - lobeline (1 ml of 1% solution), cititon (0.5-1 ml intramuscularly), inhalation of oxygen with carbon dioxide. They fight edema and swelling of the brain with the help of dehydrating agents: intramuscularly 1-3 ml of a 25% solution of magnesium sulfate (daily), intravenously a 40% glucose solution, and for every 10 ml add 1 drop of a 3% solution of ephedrine, prednisolone. Saluretics (furosemide at a dose of 0.5-1 mg/kg per day) are prescribed on the first day after injury (at the same time, panangin, orotate or potassium chloride are administered to prevent hypokalemia). With the development of a clinical picture of increasing intracranial hypertension, dislocation and compression of the brain due to its edema, osmotic diuretics (mannitol, glycerin) are used at a dose of 0.25-1 g/kg. Repeated or long-term use of saluretics and osmotic diuretics is possible under conditions of careful monitoring of the state of water and electrolyte balance. To improve venous outflow from the cranial cavity and reduce intracranial pressure, it is advisable to place the patient in a position with his head elevated. Subsequently, you can prescribe von-rig - 0.04 g/kg (daily dose).

In cases of psychomotor agitation and convulsive reactions, sedatives and anticonvulsants (sibazon, barbiturates, etc.) are used. In case of shock, it is necessary to eliminate pain reactions, replenish the deficit in circulating blood volume, etc. (see Traumatic shock). Carrying out therapeutic and diagnostic manipulations, including for patients in a coma, should be carried out under conditions of blocking pain reactions, since they cause an increase in volumetric blood flow and intracranial pressure.

In cases where the above methods do not eliminate intracranial hypertension, persistent convulsive and severe vegetovisceral reactions, and the results of clinical and instrumental studies make it possible to exclude the presence of intracranial hematomas, in the intensive care wards of specialized hospitals barbiturates or sodium hydroxybutyrate are used against the background of artificial ventilation with careful monitoring intracranial and blood pressure. As one of the methods of treating intracranial hypertension and cerebral edema, dosed diversion of cerebrospinal fluid is used using catheterization of the lateral ventricles of the brain.

For severe bruises and crushes of the brain with severe swelling, anti-enzyme drugs are used - protease inhibitors (contrical, gordox, etc.). It is also advisable to use antioxidant lipid peroxidation inhibitors (tocopherol acetate, etc.). In case of severe and moderate traumatic brain injury, vasoactive drugs are used according to indications - aminophylline, Cavinton, Sermion, etc. Intensive therapy also includes the maintenance of metabolic processes using enteral (tube) and parenteral nutrition, correction of disturbances in acid-base and water-electrolyte balance, normalization of osmotic and colloid pressure, hemostasis system, microcirculation, thermoregulation, prevention and treatment of inflammatory and trophic complications. In order to normalize and restore the functional activity of the brain, nootropic drugs (piracetam, aminalon, pyridital, etc.) and drugs that normalize the metabolism of neurotransmitters (galantamine, levodopa, nacom, madopar, etc.) are prescribed.

Measures to care for patients with traumatic brain injury include the prevention of bedsores and hypostatic pneumonia (frequent turning of the patient, cupping, massage, skin care, etc.), passive gymnastics to prevent the formation of contractures in the joints of paretic limbs. In patients in a state of stupor or coma, with impaired swallowing, or a decreased cough reflex, it is necessary to monitor the patency of the airways and, using suction, free the oral cavity from saliva or mucus, and when tracheal intubation or tracheostomy is performed, the lumen of the tracheobronchial tree must be sanitized. Monitor physiological poisoning. Measures are taken to protect the cornea from drying out (dropping petroleum jelly into the eyes, closing the eyelids with an adhesive plaster, etc.). Clean your mouth regularly.

Lumbar puncture is resorted to only in cases of severe symptoms of intracranial hypertension and severe brainstem symptoms. During puncture, more than 5 ml of cerebrospinal fluid should not be released due to the risk of herniation of the cerebellum into the foramen magnum. In the presence of blood (subarachnoid hemorrhage), daily punctures with the release of 3-5 ml of cerebrospinal fluid are indicated. The reduction of cerebral edema is also facilitated by the administration of 0.015-0.03 g of diphenhydramine powder 2-3 times a day and 0.1-0.15 ml of a 0.1% atropine solution subcutaneously.

In case of open traumatic brain injury and the development of infectious and inflammatory complications, antibiotics are prescribed that penetrate well through the blood-brain barrier (semi-synthetic analogues of penicillin, cephalosporins, chloramphenicol, aminoglycosides, etc.). Lacerated and bruised wounds of the soft integument of the skull, penetrating deeper than the aponeurosis, require primary surgical treatment and mandatory tetanus prophylaxis (tetanus toxoid and antitetanus serum are administered).

Optimal timing of primary surgical treatment from the moment of injury. In some cases, primary surgical treatment of the wound is performed with the application of blind sutures on the third day after the injury. Primary surgical treatment of wounds of the skull is performed under local anesthesia with a 0.25-0.5% novocaine solution. The hair on the head around the wound is shaved off. The crushed, uneven edges of the wound are excised to the full thickness, departing from the edge by 0.3-0.5 cm. In doubtful cases, instead of suturing, the wound is drained. Antibiotics can be used locally in the wound in dry form.

Resuscitation measures for severe traumatic brain injury begin at the prehospital stage and continue in a hospital setting. In order to normalize breathing, ensure free patency of the upper respiratory tract (freeing them from blood, mucus, vomit, insertion of an air duct, tracheal intubation, tracheostomy), use inhalation of an oxygen-air mixture, and, if necessary, perform artificial ventilation.

The prognosis for recovery is unfavorable, since a brain contusion is accompanied by the formation of a focal macromorphological defect of the brain substance, due to which complete regression of focal symptoms is impossible.

The prognosis for life can be considered favorable, since the period when the likelihood of developing life-threatening complications is highest has already passed, and the vital centers of the brain are not damaged. The prognosis for work ability is favorable, but a transfer to another job that is not associated with significant physical and psycho-emotional stress is required.

This patient, having suffered a traumatic brain injury, is subject to long-term follow-up. Restorative treatment is carried out according to indications. Along with the methods of physical therapy, physiotherapy and occupational therapy, metabolic (piracetam, aminalon, pyriditol, etc.), vasoactive (Cavinton, Sermion, cinnarizine, etc.), anticonvulsant (phenobarbital, benzonal, diphenine, pantogam, etc.) should be used. vitamin (B1, B6, B15, C, E, etc.) and absorbable (aloe, vitreous, FiBS, lidase, etc.) preparations.

In order to prevent epileptic seizures, which often develop in patients after traumatic brain injury, these patients should be prescribed drugs containing phenobarbital. Their long-term (for 1-2 years) single dose at night is indicated. Therapy is selected individually, taking into account the nature and frequency of epileptic paroxysms, their dynamics of age, premorbidity and general condition of the patient.

To normalize the general functional state of the central nervous system and accelerate the rate of recovery, vasoactive (Cavinton, Sermion, cinnarizine, xanthinol nicotinate, etc.) and nootropic (piracetam, pyridital, aminalon, etc.) drugs should be used, which must be combined, prescribing them in alternating two-month courses ( at intervals of 1-2 months) for 2-3 years. It is advisable to supplement this basic therapy with agents that affect tissue metabolism; amino acids (cerebrolysin, glutamic acid, etc.), biogenic stimulants (aloe, vitreous, etc.), enzymes (lidase, lecozyme, etc.). In case of mental disorders, a psychiatrist must be involved in the observation and treatment of the patient.

Thoroughly figuring out the story diseases and life history, the doctor receives the necessary information to suggest a diagnosis even before the X-ray examination. The data obtained should help to accurately establish the mechanism of injury, form an impression of the energy of the traumatic force, alert the physician to associated injuries, and identify somatic diseases and other medical problems relevant to the case.

If taking anamnesis difficult or is impossible due to the serious condition of the victim, more detailed clarification and detailing of information should be postponed until the condition improves or obtained from other available sources.

Anamnesis can be especially important when drawing up a treatment plan for open fractures, as it provides information about the source and degree of contamination, the time that has passed since the injury, and also allows you to clarify the initial situation regarding the visualization of bone fragments in the wound.

If the data does not match medical history and the extent of the damage, either a pathological fracture or the possibility of intoxication can be suspected. A healthy child under two years of age cannot experience a hip fracture during play, even active play, with another child or parents. Older people generally do not break the femoral head when changing positions in bed.

While at malignant neoplasms or metabolic disorders, pathological fractures are predictable and may be preceded by local pain, but with an asymptomatic disease, fractures occur spontaneously and are the first manifestation of the pathological condition. Multiple fractures found in a child at different stages of consolidation indicate ill-treatment and require appropriate assistance aimed at preserving his life.

Complaints of pain or deterioration in limb function require a thorough examination to rule out fracture or damage to joints, nerves, muscles or blood vessels.
Examination according to the protocol ATLS(life support for victims in the first hours after injury) implies a systematic approach to assessing the patient and a minimum of missed injuries. In this regard, it is unnecessary to talk about the need for constant and careful recording of all examination results. It is difficult to assess the dynamics of the process without re-examination of the patient and proper medical history.

U victims with severe trauma local tenderness in the area of ​​the fracture may not be clearly defined or completely absent. Almost always, with fractures and dislocations in the lower extremity, there is deformity, swelling, or both, although swelling may occur later, especially if the patient arrives in a state of hypovolemia. Undiagnosed fractures are extremely rare.

With displacement they lead to shortening of long bones, incomplete rotation and angular deformity. Immediate reduction and immobilization in a cast reduces pain and blood loss, and often restores circulation in the absence of pulsation in the vessels of the limb. A typical sign of dislocation is a forced position of the limb, but when a dislocation is combined with a fracture, the latter can mask the symptoms of a dislocation.

At intra-articular injuries a swelling forms above the joint, which does not have clear contours, and due to rupture of the ligaments, hemarthrosis often occurs. Important diagnostic criteria are pathological mobility and changes in function, but increased sensitivity in the area of ​​the injured joint makes it difficult to identify these symptoms, so the examination should be carried out after pain relief. Reduction of a dislocation is carried out as an emergency, especially if there are clear signs of circulatory problems.

Edema And pain are typical manifestations of subfascial hypertension syndrome, which should be remembered in all cases of lower limb injury. Sensory and motor disorders occur in the later stages of this syndrome and are associated with necrotic changes. Clinically, compartment syndromes usually appear several hours after injury or later, before or after treatment, and can also be caused by an excessively tight fit of a plaster cast or dressing material with increasing swelling of the limb.

Immediate elimination mechanical compression may be sufficient to produce a therapeutic effect. Compartment syndrome is successfully identified by an experienced specialist. Diagnosis is made mainly on the basis of clinical symptoms. In a patient under the influence of tranquilizers, pressure control in the subfascial spaces is carried out using arterial cannulas or special devices. With a normal level of consciousness, complaints of persistent pain, a feeling of fullness and a significant increase in the volume of the limb make one suspect compartment syndrome.

In such cases, you should urgently deliver patient to the operating room and open all the interfascial beds (three in the hip area, four in the lower leg area, nine on the foot). Incomplete fasciotomy and limiting the length of the incision in trauma patients are usually unacceptable.

Clinical assessment of blood circulation and innervation of the injured limb in the case of a serious condition of the victim or a serious injury to the limb can be very complex. Damage to blood vessels can lead to catastrophic consequences, so identifying them and providing assistance requires an active diagnostic and treatment search.

Capillary refill in itself is not a sufficient clinical parameter by which one can judge the absence of damage to the vasculature located above the study site. Peripheral pulses may persist after significant damage to the arterial vessels. The best known is probably popliteal artery injury caused by tibia dislocation or periarticular fractures. With such an injury, which is not initially accompanied by occlusion, thrombosis in a more distant period can lead to the loss of a limb. In such situations, it is necessary to frequently evaluate the pulse in the area of ​​​​the arteries of the foot.

Any change pulse in this area, it is necessary to carry out at least Doppler ultrasonography determination of intravascular pressure. Assessing systolic pressure in the foot area is an important adjunct to the physical examination. If the pressure is less than 90% of the systolic pressure on the shoulder or on the opposite lower limb, then urgent intervention by vascular surgeons is necessary. If the pulse is weak, you can consider color Doppler or contrast arteriography. The question of urgent consultation with a traumatologist is beyond doubt.
Risk factors in respect limb nonviability are delayed surgery, arterial contusion with subsequent thrombosis and, most importantly, failed revascularization.

Before carrying out definitive treatment It is necessary, if possible, to enter into the medical history data from a neurological examination of the injured limb. In severe trauma, assessment of innervation, as well as blood circulation, may be unreliable. Hypoesthesia may result from acute ischemia or injury to the nerve itself, or may be of psychogenic origin. The lack of sensitivity in the areas of innervation of a certain nerve suggests that it is damaged. Limitations in motor function may be caused by pain and instability, peripheral nerve damage, or spinal cord injury.

Nervous damage trunk characteristic of certain injuries. In posterior hip dislocations, the sciatic nerve, usually its peroneal branch, may be injured. In cases of shin sprains or similar injuries in the popliteal fossa, the common peroneal and/or tibial nerves may be affected, raising the suspicion of concomitant arterial injury. Compression from a splint or cast can cause injury to the peroneal nerve, which runs around the head of the fibula at the knee joint.

Runaway evaluation of open fractures should be carried out immediately upon admission to the emergency department. The wound should be protected with gauze pads soaked in a low-salt solution or betadine solution. To avoid further contamination and trauma to soft tissue, examination of the wound should be carried out in the operating room. In the emergency department, no attempts should be made to examine the wound or manipulate exposed bone. Almost always, when there is bleeding, even from an amputation wound, help is provided by applying a pressure bandage. The use of a tourniquet is intended to stop other uncontrolled bleeding.

To a large extent percent cases of damage are not diagnosed during the initial examination, especially damage related to the lower extremities and large joints. This is why it is so important to carry out repeated examinations, especially after the condition has stabilized and contact with the patient has been possible. At least one examination, but carried out with “triple” attention, plays an important role in every case of diagnostic examination of a seriously injured person.

X-ray examination of lower limb injuries

By ATLS According to the protocol, survey radiography of the chest and pelvis in the anteroposterior projection and appropriate radiography of the cervical spine in the lateral projection must be performed simultaneously with the initial examination and resuscitation of victims. Kaneriy et al. showed that mandatory pelvic radiography in all cases of blunt trauma is economically justified. X-ray examination of the injured limb is of much less importance and is carried out during additional examinations of the victim. The leg is covered with a dressing and immobilized in a splint. In any case, it is unacceptable to delay or interrupt resuscitation care to perform imaging of the limb.

Radiography can be performed after an emergency operation performed in connection with other life-threatening circumstances. In patients with hemodynamic compromise, life-saving interventions should be carried out in parallel, rather than sequentially. It means that X-ray examination and fracture stabilization may be performed concurrently with resuscitation and surgical procedures such as laparotomy or thoracotomy. If it is possible to properly x-ray the extremity, and this does not interfere with other necessary diagnostic and therapeutic care, then this study can be essential in drawing up a plan of priority action.