פרק 34 Chapter 34 Craniocerebral Trauma Flashcards
בבדיקת פצוע לאחר חבלת ראש – המטופל פוקח עיניים רק לאחר גירוי כאב , ממלמל קולות ללא מילים ,
לאחר גירוי , ממקם כאב . מה יהיה דירוג רמת ההכרה של הפצוע לפי הסולם ע”ש גלזגו –
Glasgow coma scale ?
א. 5
ב. 7
ג. 9
ד. 11
9
פוקח עיניים לכאב= 2
ממלמל קולות= 2
ממקם כאב= 5
Table 34-1
GLASGOW COMA SCALE (TOTAL SCORE IS USED FOR SERIAL ASSESSMENT AND PROGNOSIS)
Table 34-2
THE NEW ORLEANS AND CANADIAN CLINICAL DECISION RULES FOR CT AFTER CONCUSSION
Table 34-3
CLINICAL AND RADIOGRAPHIC CHARACTERISTICS OF THE MAIN TRAUMATIC BRAIN LESIONS
בן 50 מעורב בתאונת דרכים עם חבלת ראש. יממה לאחר החבלה הוא מתלונן על דיפלופיה וכאבים בעין
שמאל .
בבדיקה – אקזופטלמוס של עין שמאל, אודם וגודש כלי דם בעין, הגבלה בתנועות עין שמאל וירידה
בחדות ראייה בעין שמאל .
מהי האבחנה הסבירה ?
א. Orbital hematoma
ב. Carotid-Cavernous fistula
ג. Base of skull fracture
ד. Diffuse axonal injury
Carotid cavernus fistula
Carotid–Cavernous Fistula
A basal fracture through the sphenoid bone may lacerate the internal carotid artery or one of its intracavernous branches where it lies in the cavernous sinus. Within hours or a day or two, a disfiguring pulsating exophthalmos develops as arterial blood enters the sinus and distends the superior and inferior ophthalmic veins that empty into the sinus. The orbit feels tight and painful, and the eye may become partially or completely immobile because of pressure on the ocular nerves traversing the sinus (see Fig. 13-5). The sixth nerve is affected most often, and the third and fourth nerves less often. Also, there may be a loss of vision as a result of ischemia of the optic nerve and retina, congestion of the retinal veins and glaucoma are potential factors in the visual failure. There is usually an easily audible bruit over the eye. Some 5 to 10 percent of fistulas resolve spontaneously, but the remainder must be obliterated by interventional radiologic means, usually a detachable balloon, or by a direct surgical repair of the fistula (see Stern).
Not all carotid–cavernous fistulas are traumatic. They may occasionally occur with rupture of an intracavernous saccular aneurysm or in Ehlers-Danlos disease, where the connective tissue is defective; or the cause may be unexplained. Occasionally, a dural-based arteriovenous fistula opens in the region of the cavernous sinus after an injury and they cause fewer signs such as orbital swelling than a carotid–cavernous fistula.
מטופל לא התעורר לאחר ניתוח ראש . מה האבחנה בצילום זה?
א. subacute subdural hematoma
ב. tension pneumocranium
ג. hygroma
ד. acute epidural hematoma
tension penumocranium
collection of air in the cranial cavity (aerocele) is a common occurrence following skull fracture or any extended neurosurgical procedure. The pocket of air is apparent by CT scan in the epidural or subdural space over the cerebral convexities or between the hemispheres, and serves only to warn of a potential route for the entry of bacteria into the cranium. Small collections of air are usually absorbed without incident, but a large volume may act as a mass and cause clinical deterioration after injury (tension pneumocranium; Fig. 34-3). Inhalation of 100 percent oxygen has a slight salutary effect, but aspiration of the air is required if the collection is causing clinical signs.
Depressed skull fractures are of significance only if the underlying dura is lacerated or the brain is compressed by indentation of bone. They then are surgically elevated, preferably within the first 24 to 48 h.
מתאגרף שמפתח הפרעת הליכה פרוגרסיבית. מה לא יהיה בפתולוגיה?
1. הידקקות של הקורפוס קולוסום
2. חדרים מורחבים
3. קונטוזיות קורטיקליות
4. צלקת glial בצרבלום
לא יהיו קונטוזיות קורטיקליות
Chronic traumatic encephalopathy
dysarthric speech and a state of forgetfulness, slowness in thinking, and other signs of dementia. Movements are slow, stiff, and uncertain, especially those involving the legs, and there is a shuffling, wide-based gait. In other words, a parkinsonian and dementing syndrome emerges and sometimes a moderately disabling ataxia, but there is no mistaking these for idiopathic Parkinson or Alzheimer disease. The plantar reflexes may be extensor
**CT scan discloses ventricular dilatation and sulcal widening and a cavum septi pellucidi **
Mild to moderate enlargement of the lateral ventricles and thinning of the corpus callosum were present in all cases.
greatly widened cavum septi pellucidi and fenestration of the septal leaves. Readily identified areas of glial scarring were situated on the inferior surface of the cerebellar cortex.
Purkinje cells were lost and the granule cell layer was somewhat thinned. Surprisingly, cerebral cortical contusions were found in only a few cases. Notably absent also was evidence of previous hemorrhage but earlier studies
varying degrees of loss of pigmented cells of the substantia nigra and locus ceruleus, and many of the remaining cells showed Alzheimer neurofibrillary change but not Lewy bodies. Neurofibrillary changes were scattered diffusely through the cerebral cortex and brainstem
בן 38 היה מעורב בתאונת דרכים והתלונן על טשטוש ראיה בעין ימין. בבדיקה: אישון ימני לא הגיב לאור ישיר אך הגיב להארה של אישון שמאל. היכן השבר בגולגולת?
א. sphenoid bone
ב. petrous bone
ג. mastoid bone
ד. occipital bone
sphenoid bone
- Fracture of the petrous pyramid often deforms the external auditory canal or tears the tympanic membrane, with resultant leakage of CSF (otorrhea); or, blood may collect behind an intact tympanic membrane and discolor it. If the fracture extends more posteriorly, damaging the sigmoid sinus, the tissue behind the ear and over the mastoid process becomes boggy and discolored (Battle sign).
- Anosmia and an apparent loss of taste (actually a loss of perception of aromatic flavors, as the elementary modalities of taste are unimpaired) are frequent sequelae of head injury, especially with falls on the back of the head
- A fracture in or near the sella may tear the stalk of the pituitary gland with resulting diabetes insipidus. Rarely, such a fracture may cause bleeding from a preexisting pituitary adenoma and produce the syndrome of pituitary apoplexy
תאור של חולה עם דימום תת עכבישי בטפנ״צ, מפתחת הידרוצפלוס אקוטי, מה לא נראה
1. אישונים רחבים ולא מגיבים דוצ
2. אישונים צרים דוצ
3. אישונים לא שווים
4. הגבלה באבדוקציה
לא נראה אישונים לא שווים.
Acute hydrocephalus
לרוב נגרם על ידי דימום סוב ארכנואידי או ממצא לוחץ ע”פ הפוסה האחורית וסגירה של האקוודוקט. תתפתח אבוליה, לאר מכן סטופור ולבסוף תרדמת, אישונים יהיו קטנים ויהיה בבינסקי דו”צ. טונוס ברגליים יהיה מוגבר וייתכן במנח אקסטנסורי.
Acute Hydrocephalus
most often following subarachnoid hemorrhage from a ruptured aneurysm bleeding from an arteriovenous malformation /deep intracerebral hemorrhage that dissects into the ventricles/obstruction of the CSF pathways in the fourth ventricle by a tumor or cerebellar–brainstem hemorrhage, or within the basal cisterns by neoplastic infiltration of the meninges, although this last process tends to evolve more subacutely.
headache of varying severity and may have visual obscuration, vomiting, and then becomes drowsy or stuporous over a period of minutes or hours. Bilateral Babinski signs are found, and in advanced stages, which are associated with coma, there is increased tone in the lower limbs and extensor posturing. Early in the process, the pupils are normal in size and the eyes may rove horizontally; as the ventricles continue to enlarge, the pupils become miotic, the eyes then cease roving and assume an aligned forward position, or there may be bilateral abducens palsies and limitation of upward gaze. The speed with which hydrocephalus develops determines whether there is accompanying papilledema.
If this condition is left untreated, the pupils eventually dilate symmetrically, the eyes no longer respond to oculocephalic maneuvers, and the limbs become flaccid. Or, there is an unanticipated cardiac or respiratory arrest, even at an early stage of evolution of the hydrocephalus; this complication is seen particularly in children with masses, particularly at the foramen magnum, and may be presaged by brain compression at the level of the perimesencephalic cisterns, detectable by imaging studies.
Treatment is by drainage of CSF, usually effected by a ventricular catheter or, if there is undoubted communication between all the CSF compartments, by lumbar puncture. The latter may pose some risk if spinal fluid is withdrawn rapidly or there is a sizeable leak of fluid through the spinal dura at the site of the puncture, thereby creating a pressure gradient between the cerebral and spinal regions.
בחולה לאחר חבלת ראש איזה תמיסה ניתן בכדי לא להעלות ICP?
1. דקסטרוז 5% במים
2. נורמל סליין 0.9%
3. חצי סליין 0.45%
4. דקסטרוז 5% בחצי סליין 0.45%
נורמל סליין 0.9%
The avoidance of hyponatremia and serum hypoosmolarity that would allow water to enter the brain and increase its volume is accomplished by infusing only isoosmolar or hyperosmolar solutions such as normal saline.
concentrations of diffusible solutes such as glucose are not useful in reducing intracranial volume because they do not create gradient for water and solutes across the cerebral vasculature. Consequently, fluids such as 5 percent dextrose in water, 0.5 normal saline, and 5 percent dextrose in 0.5 normal saline are avoided; lactated Ringer solution is permissible; normal saline, with or without added dextrose, is ideal. In a post hoc study of a cohort of severely injured patients, resuscitation with albumin was found to have a detrimental effect compared to saline.
Hyperosmolar therapy The basis for this class of treatments is the creation of a gradient of water concentration from the brain to the blood that reduces brain volume. Mannitol, glycerol, and urea are effective in lowering ICP by producing serum hyperosmolarity initially and then causing a diuresis that sustains this state and secondarily causes hypernatremia and hypovolemia.
Hyperosmolar saline, in contrast, raises serum sodium directly and expands intravascular volume.
- General measures The first step in lowering elevated ICP is to control the incidental factors that are known to raise pressure, such as hypoxia, hypercarbia, particularly hyperthermia, awkward head positions that compress the jugular veins, and high mean airway pressures from positive pressure ventilation
בן65חבלתראשקשהבמצבוגטטיבימורדםומונשםבטיפולנמרץ.הופעהשלאירועיםשלטכיקרדיה,הזעהומנחשלאקסטנסורישלהגפיים,כלאירוענמשךמספרשעות.איךתטפל?
1. ברומוקריפטן
2. אמנדטין
3. פניטואין
4. חומצהולפרואית
5. בקלופן
ברומוקריפטין
Autonomic Dysfunction (“Storm”) Syndrome
A worrisome *consequence of severe head injury, which is observed in some comatose patients and particularly in the vegetative state, is a syndrome of episodic vigorous extensor posturing, profuse diaphoresis, hypertension, and tachycardia lasting minutes to an hour. A slight fever may accompany the spells. Families and staff are greatly disturbed by the display, particularly when the patient’s grimacing suggests suffering. These spells of excessive sympathetic activity and posturing may be precipitated by painful stimuli or by distention of a viscus, but often they arise spontaneously. The syndrome is often mistakenly identified as a seizure and in many texts is still referred to as “diencephalic epilepsy” but it is more likely the *result of the removal of suppressive cortical influences on autonomic structures, allowing the hypothalamus to function independently of normal inhibitory mechanisms. A survey of 35 such patients by Baugley and colleagues identified diffuse axonal injury and a period of hypoxia as being the main associated injuries and this has been our experience as well.
Narcotics such as morphine and benzodiazepines have a slightly beneficial effect but bromocriptine, which may be used in combination with sedatives or with small doses of morphine, has been most effective according to Rossitch and Bullard.
—–
Bromocriptine is a dopamine agonist, which means that it binds to and activates dopamine receptors in the brain.
Activation of dopamine receptors in the brain can have several effects on the ANS, including:
- Regulation of blood pressure: Dopamine plays a role in the regulation of blood pressure by causing vasodilation of blood vessels. By activating dopamine receptors, bromocriptine can help to reduce blood pressure.
- Control of heart rate: Dopamine also affects the heart rate by increasing the activity of the sinoatrial (SA) node, which is responsible for generating electrical impulses that control heart rate. By stimulating dopamine receptors, bromocriptine can increase SA node activity and improve heart rate variability.
- Improving gastrointestinal motility: Dopamine has been shown to play a role in the regulation of gastrointestinal motility. By activating dopamine receptors in the enteric nervous system, bromocriptine can help to improve gastrointestinal motility and reduce symptoms such as constipation.
- Regulation of body temperature: Dopamine also plays a role in the regulation of body temperature. By activating dopamine receptors, bromocriptine can help to improve body temperature regulation and reduce symptoms such as excessive sweating.
In addition to its effects on the ANS, bromocriptine also has other effects on the body such as reducing the levels of certain hormones like prolactin, which can also contribute to autonomic dysfunction. The exact mechanism of action of bromocriptine in the treatment of autonomic dysfunction is not fully understood, but it is believed to involve multiple factors including dopamine receptor stimulation and hormonal regulation.
מטופל לאחר חבלת ראש, ללא אובדן הכרה עם עדות לSDH קלה עם קונטוזיס קורטיקלית. מה הסיכון לפרכוס אם אחרי 4 חודשים ללא פרכוס
1. 1%
2. 5%
3. 25%
4. 75%
25%
The term “posttraumatic epilepsy” -seizures that develop several weeks or months after closed head injury (1 to 3 months in most cases). Approximately 6 months after injury, half the patients who will develop epilepsy have had their first episode; by the end of 2 years, the figure rises to 80 percent.
Penetrating:patients who escape seizures for 1 year after injury can be 75 percent certain of remaining seizure free; patients without seizures for 2 years can be 90 percent certain; and for 3 years, 95 percent certain.
less-severely injured (mainly closed head injuries), the corresponding times are 2 to 6 months 75%, 12 to 17 months90%, and 21 to 25 months 95%.
Posttraumatic seizures (both focal and generalized) tend to decrease in frequency as the years pass, and a significant number of patients (10 to 30 percent, according to Caviness) eventually stop having them. Status epilepticus is uncommon. Individuals who have early attacks (within a week of injury) are more likely to have a complete remission of their seizures than those whose attacks begin a year or so after injury. A low frequency of attacks is another favorable prognostic sign. Alcoholism is considered to have an adverse effect on this seizure state, but there are no systematic studies of this subject.
Seizures are the most common delayed sequela of craniocerebral trauma, with an overall incidence of approximately 5 percent in patients with closed head injuries and 50 percent in those who had sustained a compound skull fracture and direct wounds of the brain. The basis is nearly always a contusion or laceration of the cortex. As one might expect, the risk of developing posttraumatic epilepsy is also related to the overall severity of the closed head injury. In a civilian cohort of 2,747 head-injured patients described by Annegers and colleagues (1980), the risk of seizures after severe head injury (defined by loss of consciousness or amnesia for more than 24 h, including subdural hematoma and brain contusion) was 7 percent within 1 year and 11.5 percent in 5 years. If the injury was only moderate (unconsciousness or amnesia for 30 min to 24 h or causing only a skull fracture), the risk fell to 0.7 and 1.6 percent, respectively. After mild injury (loss of consciousness or amnesia of less than 30 min), the incidence of seizures was not significantly greater than in the general population. In a subsequent study, Annegers and colleagues (1998) expanded the original cohort to include 4,541 children and adults with cerebral trauma. The results were much the same as those of the first study except that in patients with mild closed head injuries, there was only a slight excess risk of developing seizures—a risk that remained elevated only until the fifth year after injury. The likelihood of epilepsy is said to be greater in parietal and posterior frontal lesions, but it may arise from lesions in any area of the cerebral cortex. Also, the frequency of seizures is considerably higher after penetrating cranial injury, as cited earlier.
תיאור של חולה שמאבד הכרה לאחר חבלת ראש אולם חוזר להכרה מלאה, בהמשך עם כניסתו למיון שוב מאבד הכרה. מה הצעד הבא?
1. ניתוח דחוף מפני שסביר שמדובר בדמם מהmiddle meningeal artery
2. CTA
3. ניתוח דחוף מפני שסביר שמדובר בדמם ורידי
ניתוח דחוף מפני שסביר שמדובר בדמם מה-
middle meningeal artery
Acute Epidural Hemorrhage
As a rule, epidural hematoma arises with a temporal or parietal fracture and laceration of the middle meningeal artery or vein. Less often, there is a tear in a dural venous sinus. The injury, even when it fractures the skull, may not have produced coma initially, or it may be part of a devastating craniocerebral injury. A typical example is that of a child who has fallen from a bicycle or swing or has suffered some other hard blow to the head and was unconscious only momentarily. A few hours later (exceptionally, with venous bleeding the interval may be several days or a week), headache of increasing severity develops, with vomiting, drowsiness, confusion, aphasia, Seizures (which may be one-sided), hemiparesis with slightly increased tendon reflexes, and a Babinski sign. As coma develops, the hemiparesis may give way to bilateral Spasticity of the limbs and Babinski signs. The heart rate is often slow (below 60 beats/min) and pounding, with a concomitant rise in systolic blood pressure (Cushing Effect). The pupil may dilate on the side of the hematoma. Physicians need not be reminded that lumbar puncture is contraindicated in this setting, particularly now that CT and MRI are available. Death, which is almost invariable if an expanding clot is not removed surgically, comes at the end of a comatose period and is a result of respiratory Arrest. The visualization of a fracture line across the groove of the middle meningeal artery and knowledge of which side of the head was struck (the clot is on that side) are of aid in diagnosis and lateralization of the lesion. However, meningeal vessels may occasionally be torn without fracture. **The CT scan is definitive and reveals a lens-shaped clot with a smooth inner margin
Serious Cerebral Damage Following a Lucid Interval
This group is smaller than the other two but is of importance because it includes a disproportionate number of patients who are in urgent need of surgical treatment. The initial loss of consciousness from concussion may have lasted only a few minutes or, exceptionally, there may have been no period of unresponsiveness at all, in which instance one might wrongly conclude that there was no concussion and little possibility of traumatic hemorrhage or other type of brain injury. Patients who display this sequence of events, in the past referred to vividly as “talk and die“ by Marshall and associates (1983), have late deterioration because of the expansion of a subdural hematoma, worsening brain edema around a contusion, or the delayed appearance of an epidural clot
גבר בן 25, בזמן החלקה על הקרח נפל ונחבל בצד שמאל של ראשו מקיר בטון. בבדיקה גופנית יש פצע שטחי בקרקפת במקום החבלה עם דימום מינימלי שנעצר תוך מספר דקות. הוא עירני וצלול מיד לאחר התאונה אך מאבד את הכרתו אחרי 30 דקות. בהדמייה מוחית נראה איזור היפרדנסי קמור דמוי עדשה באיזור פריאטלי שמאלי אקסטרא אקסיאלי. פגיעה באיזה כלי דם מובילה לסדר האירועים המתואר?
1. bridging veins
2. cavernous sinus
3. vein of galen
4. inferior cerebellar artery
5. middle meningeal artery
middle meningeal artery
Acute Epidural Hemorrhage
As a rule, epidural hematoma arises with a temporal or parietal fracture and laceration of the middle meningeal artery or vein. Less often, there is a tear in a dural venous sinus. The injury, even when it fractures the skull, may not have produced coma initially, or it may be part of a devastating craniocerebral injury. A typical example is that of a child who has fallen from a bicycle or swing or has suffered some other hard blow to the head and was unconscious only momentarily. A few hours later (exceptionally, with venous bleeding the interval may be several days or a week), headache of increasing severity develops, with vomiting, drowsiness, confusion, aphasia, Seizures (which may be one-sided), hemiparesis with slightly increased tendon reflexes, and a Babinski sign. As coma develops, the hemiparesis may give way to bilateral Spasticity of the limbs and Babinski signs. The heart rate is often slow (below 60 beats/min) and pounding, with a concomitant rise in systolic blood pressure (Cushing Effect). The pupil may dilate on the side of the hematoma. Physicians need not be reminded that lumbar puncture is contraindicated in this setting, particularly now that CT and MRI are available. Death, which is almost invariable if an expanding clot is not removed surgically, comes at the end of a comatose period and is a result of respiratory Arrest. The visualization of a fracture line across the groove of the middle meningeal artery and knowledge of which side of the head was struck (the clot is on that side) are of aid in diagnosis and lateralization of the lesion. However, meningeal vessels may occasionally be torn without fracture. **The CT scan is definitive and reveals a lens-shaped clot with a smooth inner margin
Serious Cerebral Damage Following a Lucid Interval
This group is smaller than the other two but is of importance because it includes a disproportionate number of patients who are in urgent need of surgical treatment. The initial loss of consciousness from concussion may have lasted only a few minutes or, exceptionally, there may have been no period of unresponsiveness at all, in which instance one might wrongly conclude that there was no concussion and little possibility of traumatic hemorrhage or other type of brain injury. Patients who display this sequence of events, in the past referred to vividly as “talk and die“ by Marshall and associates (1983), have late deterioration because of the expansion of a subdural hematoma, worsening brain edema around a contusion, or the delayed appearance of an epidural clot
המטומה אפידורלית
Acute Epidural Hemorrhage
As a rule, epidural hematoma arises with a temporal or parietal fracture and laceration of the middle meningeal artery or vein. Less often, there is a tear in a dural venous sinus. The injury, even when it fractures the skull, may not have produced coma initially, or it may be part of a devastating craniocerebral injury. A typical example is that of a child who has fallen from a bicycle or swing or has suffered some other hard blow to the head and was unconscious only momentarily. A few hours later (exceptionally, with venous bleeding the interval may be several days or a week), headache of increasing severity develops, with vomiting, drowsiness, confusion, aphasia, Seizures (which may be one-sided), hemiparesis with slightly increased tendon reflexes, and a Babinski sign. As coma develops, the hemiparesis may give way to bilateral Spasticity of the limbs and Babinski signs. The heart rate is often slow (below 60 beats/min) and pounding, with a concomitant rise in systolic blood pressure (Cushing Effect). The pupil may dilate on the side of the hematoma. Physicians need not be reminded that lumbar puncture is contraindicated in this setting, particularly now that CT and MRI are available. Death, which is almost invariable if an expanding clot is not removed surgically, comes at the end of a comatose period and is a result of respiratory Arrest. The visualization of a fracture line across the groove of the middle meningeal artery and knowledge of which side of the head was struck (the clot is on that side) are of aid in diagnosis and lateralization of the lesion. However, meningeal vessels may occasionally be torn without fracture. **The CT scan is definitive and reveals a lens-shaped clot with a smooth inner margin
Serious Cerebral Damage Following a Lucid Interval
This group is smaller than the other two but is of importance because it includes a disproportionate number of patients who are in urgent need of surgical treatment. The initial loss of consciousness from concussion may have lasted only a few minutes or, exceptionally, there may have been no period of unresponsiveness at all, in which instance one might wrongly conclude that there was no concussion and little possibility of traumatic hemorrhage or other type of brain injury. Patients who display this sequence of events, in the past referred to vividly as “talk and die“ by Marshall and associates (1983), have late deterioration because of the expansion of a subdural hematoma, worsening brain edema around a contusion, or the delayed appearance of an epidural clot
MCA
Meningeal artery – Epidural – Lentiform
Bridging Vein – SDH – Crescent
- As a rule, epidural hematoma arises with a temporal or parietal fracture and laceration of the middle meningeal artery or vein. Less often, there is a tear in a dural venous sinus.
- Rapidly evolving subdural hematomas are usually
a result of tearing of bridging veins, and symptoms are caused by compression of the adjacent brain and of deep structures. Unlike epidural arterial hemorrhage, which is steadily progressive, the rising intracranial pressure usually arrests the venous bleeding
מטופלשהוא פועל בניין, נפל איבד הכרה לדקה וחזר לעצמו. כעבור שבוע חוזר כאשר מבולבל , הפרעה בשפה, חולשת יד ימין ,פירכוסיםפוקליים. מה נמצאבהדמייה?
1. דמם תת עכבישי
2. דמם אפידורלי
3. דמםאינטרונטריקולרי
4. דמםפרנכימטי
דמם אפידורלי
Acute Epidural Hemorrhage
As a rule, epidural hematoma arises with a temporal or parietal fracture and laceration of the middle meningeal artery or vein. Less often, there is a tear in a dural venous sinus. The injury, even when it fractures the skull, may not have produced coma initially, or it may be part of a devastating craniocerebral injury. A typical example is that of a child who has fallen from a bicycle or swing or has suffered some other hard blow to the head and was unconscious only momentarily. A few hours later (exceptionally, with venous bleeding the interval may be several days or a week), headache of increasing severity develops, with vomiting, drowsiness, confusion, aphasia, Seizures (which may be one-sided), hemiparesis with slightly increased tendon reflexes, and a Babinski sign. As coma develops, the hemiparesis may give way to bilateral Spasticity of the limbs and Babinski signs. The heart rate is often slow (below 60 beats/min) and pounding, with a concomitant rise in systolic blood pressure (Cushing Effect). The pupil may dilate on the side of the hematoma. Physicians need not be reminded that lumbar puncture is contraindicated in this setting, particularly now that CT and MRI are available. Death, which is almost invariable if an expanding clot is not removed surgically, comes at the end of a comatose period and is a result of respiratory Arrest. The visualization of a fracture line across the groove of the middle meningeal artery and knowledge of which side of the head was struck (the clot is on that side) are of aid in diagnosis and lateralization of the lesion. However, meningeal vessels may occasionally be torn without fracture. **The CT scan is definitive and reveals a lens-shaped clot with a smooth inner margin
Serious Cerebral Damage Following a Lucid Interval
This group is smaller than the other two but is of importance because it includes a disproportionate number of patients who are in urgent need of surgical treatment. The initial loss of consciousness from concussion may have lasted only a few minutes or, exceptionally, there may have been no period of unresponsiveness at all, in which instance one might wrongly conclude that there was no concussion and little possibility of traumatic hemorrhage or other type of brain injury. Patients who display this sequence of events, in the past referred to vividly as “talk and die“ by Marshall and associates (1983), have late deterioration because of the expansion of a subdural hematoma, worsening brain edema around a contusion, or the delayed appearance of an epidural clot
בן 16 נפל מהאופניים איבד הכרה לשניות ונסע לביתו. בבית התלונן על כאב ראש חד ונהייה ישנוני.
להלן בדיקת CT מוח
מהו הטיפול המומלץ הראשון למצב זה?
א. Mannitol
ב. Burr holes
ג. Observation
ד. Intravenous dexamethasone
BURR HOLES
- Treatment of epidural hematoma The surgical procedure consists of placement of burr holes in a truly emergency situation in the ED or at the bedside or, preferably a craniotomy, drainage of the hematoma, and identification and ligation of the bleeding vessel. The operative results are excellent except in cases with extended fractures and laceration of the dural venous sinuses, in which the epidural hematoma may be bilateral rather than unilateral. If coma, bilateral Babinski signs, spasticity, or decerebrate rigidity supervene before operation, it usually means that displacement of central structures and compression of the midbrain have already occurred; prognosis is then poor, but a few patients do well if surgery is not greatly delayed. Small epidural hemorrhages can be followed by serial CT scanning and will be seen to enlarge gradually for a week or two and then be absorbed. There is controversy about the benefit of removing these smaller clots in a patient who has no symptoms or signs; with sequential clinical and imaging surveillance, can be left alone.
מה לא גורם להיגרומה
1. colloid cyst rupture
2. arachnoid cyst rupture
3. previous meningitis
4. previous subdural hemorrhage
5. intracranial hypotension
colloid cyst rupture does not cause hygroma.
Subdural Hygroma
This is a thinly encapsulated collection of clear or slightly xanthochromic fluid in the subdural space; such collections form after an injury, as well as after meningitis (in an infant or young child). As often, subdural hygromas appear without precipitant, presumably because of a ball-valve effect of an arachnoidal tear that allows cerebrospinal fluid to collect in the space between the arachnoid and the dura; brain atrophy is conducive to this process. Occasionally a hygroma originates from a tear in an arachnoidal cyst. It may be difficult to differentiate a long-standing subdural hematoma from hygroma, and some chronic subdural hematomas are probably the result of repeated
small hemorrhages that arise from the membranes of hygromas. Shrinkage of the hydrocephalic brain after ventriculoperitoneal shunting is also conducive to the formation of a subdural hematoma or hygroma, in which case drowsiness, confusion, irritability, and low-grade fever are relieved when the subdural fluid is aspirated or drained. Intracranial hypotension is another cause of subdural hygromas. In adults, hygromas are usually asymptomatic and do not require treatment; they only are infrequently the cause of seizures
המטומה סובדורלית
In Subdural Hematoma Usually, by the fourth week, sometimes later, the hematoma becomes very hypodense, giving rise to a chronic subdural hygroma that is indistinguishable from idiopathic ones that are presumably caused by a rent in the arachnoid that allows CSF to escape to the subdural compartment,
.
בן 60 סובל מהפרעות הליכה ונפילות חוזרות. המשפחה שמה לב לאחרונה שנהייה איטי יותר ופחות פעיל. בדיקת
CT מוח לפניך
מה האבחנה?
1. bilateral subdural hematoma
2. right subdural and left intracerebral hematoma
3. epidural hematoma
4. brain atrophy
bilateral subdural hematoma
Unenhanced axial CT showing subdural hematomas overlying both cerebral hemispheres without shift of the ventricular system. Chronicity results in the hypodense appearance of the hematomas. The presence of some hyperdense material within the left-sided hematoma indicates more recent acute blood accumulation. The bilaterally balanced masses result in an absence of horizontal displacement, but they may cause downward compression of the upper brainstem
Figure 34-1. Mechanisms of craniocerebral injury. A. Cranium distorted by forceps (birth injury).
B. Gunshot wound of the brain. C. Falls (also traffic accidents). D. Blows on the chin (“punch-drunk”). E. Injury to skull and brain by falling objects. (From Courville.)
Figure 34-2. The course of fracture lines through the base of the skull.
Arrows indicate point of application and direction of force. (From
Courville.)
Figure 34-3. CT of postoperative tension pneumocranium (aerocele,
pneumocephalus) that caused progressive drowsiness and required
removal by aspiration. The air is apparent as a very-low-density collection
that compresses the right frontal lobe.
Figure 34-4. Mechanisms of cerebral contusion.
Arrows indicate point of application and direction of force; dark red areas indicate location of contusion.
A. Frontotemporal contusion consequent to frontal injury.
B. Frontotemporal contusion following
occipital injury.
C. Contusion of temporal lobe
because of contralateral injury.
D. Frontotemporal contusion as a result of injury to opposite temporooccipital region.
E. Diffuse mesial temporooccipital contusion caused by a blow on the vertex. (From Courville.)
Figure 34-5.
Distribution of contusions emphasizing the frontal and frontotemporal distribution in 40 consecutive autopsy cases collected by Courville. (From
Courville.)
Figure 34-6.
Unenhanced axial CT showing multiple hyperdense areas of hemorrhagic contusion adjacent to bony prominences of the skull base. There is also less
conspicuous subarachnoid blood along the tentorium and in the insular cisterns, typical of traumatic intracranial hemorrhage.
Figure 34-7.
Unenhanced coronal CT showing small hemorrhages in the corpus callosum and midbrain that are considered part of the spectrum of diffuse axonal
shearing injury.
Figure 34-8.
Acute epidural hematoma. Unenhanced CT scan showing a typical lensshaped
frontal epidural clot under a torn middle meningeal artery.
Figure 34-9.
Acute subdural hematoma. Unenhanced axial CT showing a hyperdense concaveshaped
hematoma overlying the left temporal lobe.
Figure 34-9.
Acute subdural hematoma. Unenhanced axial CT showing a hyperdense concaveshaped
hematoma overlying the left temporal lobe.
Figure 34-10.
Subacute subdural hematoma. Unenhanced axial CT showing an isodense concaveshaped
hematoma overlying the right hemisphere. Note the
effacement and compression of underlying cortical sulci and ventricles.
Figure 34-10.
Subacute subdural hematoma. Unenhanced axial CT showing an isodense concaveshaped
hematoma overlying the right hemisphere. Note the
effacement and compression of underlying cortical sulci and ventricles.
Figure 34-11.
Unenhanced axial CT showing subdural hematomas overlying both cerebral hemispheres without shift of the ventricular system. Chronicity results in the
hypodense appearance of the hematomas. The presence of some hyperdense material within the leftsided
hematoma indicates more recent acute blood
accumulation. The bilaterally balanced masses result in an absence of horizontal displacement, but they may cause downward compression of the upper
brainstem.
