Skull tuberculosis

Introduction to skull tuberculosis Skull tuberculosis is a specific inflammatory reaction caused by the invasion of the skull by tuberculosis of active tuberculosis in various parts of the body, causing the skull to break down and spread to the surrounding tissues. The spread of inflammation is limited by the joint of the bone, and generally does not exceed the block. The range of the skull, if not treated in time, can cause a series of serious complications, resulting in adverse consequences. basic knowledge Sickness ratio: 0.0001% Susceptible people: no special people Mode of infection: non-infectious Complications: tuberculous meningitis headache coma skull defect

Skull tuberculosis

(1) Causes of the disease

Skull tuberculosis is a specific inflammatory reaction caused by the invasion of M. tuberculosis into the skull. The infection pathway is mainly caused by Mycobacterium tuberculosis in active tuberculosis lesions in other parts of the body, spread by lymphatic system and blood line, or caused by the spread of adjacent lesions into the skull. The inflammatory response causes a series of pathological changes such as destruction of the skull and its surrounding tissues.

(two) pathogenesis

It can be seen that there is a cold abscess under the scalp corresponding to the affected skull, containing the caseous necrotic tissue and the sinus formed after the abscess is broken. The skull is brownish gray, dull, soft and often has different shapes of bone. Defective or dead bone, under the microscope, there are large cases of cheese-like necrosis and fibrous connective tissue hyperplasia in the subcutaneous and sinus and outside the dura mater. The normal structure of the trabecular bone of the skull is destroyed and the difference is unclear.

Skull tuberculosis prevention

Timely treatment of tuberculosis lesions in various parts of the body is fundamental to prevent skull tuberculosis.

Skull tuberculosis complications Complications tuberculous meningitis headache coma skull defect

Skull tuberculosis develops further, and the lesion spreads to the dura. When the inflammation penetrates the dura mater, the Mycobacterium tuberculosis invades the brain, causing intracranial complications. The most common are tuberculous meningitis and intracranial tuberculosis.

Both can aggravate the condition and endanger the patient's life. When tuberculous meningitis is complicated, the patient suddenly has severe headache, jet vomiting, high fever, body temperature can reach above 39 °C, convulsions, coma, and physical examination can find strong items. Kernig sign positive, peripheral blood examination of leukocytosis up to 15 × 109 / L ~ 20 × 109 / L (15,000 ~ 20,000 / mm3), with lymphocytosis as obvious, ESR accelerated, can be 20 ~ 30mm / h or more, cerebrospinal fluid pressure increased significantly during lumbar puncture examination, up to 2.45kPa (250mmH2O), cerebrospinal fluid test can be seen slightly turbid hairy glass, after a few hours of standing, there may be film formation, leukocytosis but often Below 0.5×109/L (500/mm3), lymphocytes are mainly used, sugar and chloride content are decreased, protein content is obviously increased, tubercle bacilli can be found in cerebrospinal fluid smear microscopy, and animal vaccination can have positive findings. At this time should take cooling, anti-epileptic drugs, intravenous input of 20% mannitol 250ml 3 ~ 4 times / d, lower intracranial pressure and dexamethasone 20mg / d; every 3 to 5 days intrathecal injection of ceftriaxone 40mg and ground Dexamethasone 5mg and other treatments, concurrent Intracranial tuberculosis manifests as symptoms and signs of progressive intracranial hypertension and intracranial space-occupying lesions. CT and MRI examinations can show uniform or high-density or mixed-density areas of circular or elliptical shape, and the ventricles are compressed and deformed.

The midline structure is displaced to the contralateral side, and the lesion site and extent can be clarified. Before the local lesion is cleared or the wound is not healed, the anti-tuberculosis drug and the intracranial pressure-lowering drug can be treated first, and the intracranial space remains after the wound is healed. Improve the craniotomy, if the original wound has not healed and the intracranial lesions are worse, you can drill the cranium and pus. If you have to have a craniotomy, you should try to avoid the original wound craniotomy, or temporarily under the diaphragm. Surgery to relieve the disease, skull tuberculosis, such as early removal of the skull to remove the skull, only the skull defect after surgery, but if the meningitis is complicated, it is easy to cause arachnoid cerebral cistern and brain surface arachnoid adhesion, even if inflammation is controlled Epilepsy and traffic or obstructive hydrocephalus are also often left behind. Some neurological dysfunction can also be left after tuberculosis.

Cranial tuberculosis symptoms Common symptoms Loss of intracranial calcification pale pale fatigue, huge skull defect, continuous skull interruption, low fever, lymph node enlargement, loss of appetite, night sweats

Most occur in the adolescent's frontal bone, mostly single, but also multiple, slow onset, longer course, can be caused by patients for a long time after the onset of disease or further development of the disease, but there are also acute authors, at this time The body temperature can be as high as 38 ~ 39 ° C, the local scalp has redness and heat pain, after a period of time see stable, local gradual appearance of cold abscess, after the collapse of the formation of recurrent or long-term unhealed chronic sinus, skull tuberculosis and other parts of the body Like tuberculosis infection, patients can have low fever for a long time, especially in the afternoon, body temperature is between 37 ~ 38 ° C, pale, cheeks flushing, loss of appetite, weight loss, weight loss, fatigue, night sweats, women have amenorrhea, etc. Symptoms, the local scalp can be swollen at the beginning, followed by a painless but fluctuating cold abscess. The puncture abscess can extract the cheese-like necrotic pus, and the abscess ruptures to form a chronic sinus that has not healed for a long time. The gray-white cheese-like pus is drained, sometimes with small pieces of bone.

Simple drug treatment is difficult to work, and the course of disease often lasts for several months or years. After the skull is eroded and penetrated, the inflammation can spread to the outside of the dura. The dura mater can also be invaded or penetrated, and the tuberculosis can invade. Intracranial, leading to a variety of intracranial complications and a series of symptoms and signs, such as common tuberculous meningitis, hydrocephalus, epilepsy, intracranial tuberculosis, etc., skull tuberculosis is less common, accompanied by Pulmonary, bone and joint tuberculosis and lymphatic tuberculosis in the neck, underarm, groin, etc., manifested as a long-term unhealed chronic sinus after lymphadenopathy or ulceration.

Examination of skull tuberculosis

The leukocytosis in the surrounding blood can reach 15×10920×109/L (15,00020,000/mm3), among which, the increase of lymphocytes is significant, and the erythrocyte sedimentation rate can be above 20~30mm/h, if the lesion has not invaded. When the intracranial can be used in lumbar puncture examination, the cerebrospinal fluid pressure is normal or slightly higher, and there is no significant change in routine and biochemical examination.

On the X-ray skull, there are single or multiple lesions in the parietal bone or other parts, which are characterized by rounded or chiseled round, oval-shaped low-density areas or bone defects, which vary in size and shape. Free massive high-density dead bone, CT and MRI examination can also have bone defect and free dead bone in the lesion area. The main feature is that the epidural, inferior and intracranial lesions, extent, MRI images can be found. It is clear that the lesions outside the dura mater or below are clearly distinguished.

Diagnosis and diagnosis of skull tuberculosis

Diagnostic criteria

In adolescents or the elderly, if there are tuberculous infections in other parts of the body, or in close contact with tuberculosis patients, it is found that there is a fluent cold abscess in the scalp or there is a cheese-like substance discharged outward and a small piece of dead bone is not cured. The chronic sinus, combined with the patient's symptoms and signs and other parts of the body, there are tuberculosis lesions such as skull, lung and bone joints and other imaging findings found that there are skull lesions or defects such as tuberculosis lesions and lymphocytes in the surrounding blood. And laboratory tests such as accelerated erythrocyte sedimentation rate, the diagnosis is more difficult, such as a cheese smear staining microscopic examination to the tuberculosis or animal vaccination positive findings, it is more helpful to confirm the diagnosis.

Differential diagnosis

Skull tuberculosis mainly needs to be differentiated from suppurative skull osteomyelitis. The latter has a more acute onset and a shorter course of disease. It has a head wound infection or a swollen head and face, a suppurative infection in other parts such as paranasal sinusitis. Sudden high fever accompanied by more serious symptoms of systemic poisoning, such as fatigue, body aches, lack of energy, lethargy, etc., local manifestations of scalp redness and heat inflammatory reaction, and then form a subcutaneous abscess, puncture can extract yellow sticky pus without cheese Samples, smear staining microscopy and bacterial culture can detect purulent bacteria such as staphylococcus and no tubercle bacilli, pus and dead bone can be often discharged in chronic sinus, but tuberculosis is gray-white cheese-like, suppurative It is a yellow sticky pus, and there may be bone defects on the X-ray film of the skull. Among them, there may be free bone, but the edge of the bone defect of the suppuration is unclear. The chronic one may have high-density bone at the edge of the bone defect. The proliferative zone, or the lesion area is worm-like, or low-density in the form of a map, while the bone defect of the tuberculosis is perforated, the edges are relatively neat, and sometimes there is a high-density bone proliferative zone at the edge of the bone. .

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