Brain abscess is usually referred to as septic encephalitis, brain abscess and brain abscess membrane formation caused by septic bacterial infection, and to a lesser extent, brain abscess caused by fungal and protozoal invasion of brain tissue. Brain abscess can develop at any age, but is most common in young adults, and its incidence accounts for 1-2% of neurosurgical inpatients, or slightly higher. Brain abscess formation is a continuous process divided into three stages: (1) the acute encephalitis stage; (2) the suppuration stage; and (3) the envelope formation stage. Brain abscesses are commonly solitary, but can also be multifocal or multiple abscesses. Its clinical presentation may be meningitis, or intracranial hypertension resulting in brainstem compression and death. The widespread use of new antibacterial drugs, the continuous improvement of diagnostic techniques and the development of neurosurgical techniques have led to significant progress in the cure rate of brain abscesses, and the death rate has been sharply reduced from 23.6% in the 1960s to about 4%. The prognosis of children’s cases is worse than that of adults, and the prognosis of brain abscesses with ulceration or brain herniation is poor, while the prognosis of single abscesses with intact envelopes is good.
Disease classification
Brain abscesses can be classified into five major categories according to the source of bacteria.
Otogenic brain abscess
Otogenic brain abscess is the most common, accounting for about 2/3 of brain abscesses, and is secondary to chronic suppurative otitis media and mastoiditis. Infection occurs in two ways: (1) inflammation erodes the tympanic chamber cover and tympanic chamber wall and spreads to the brain through the dural and conduction vessels, often in the temporal lobe and a few in the parietal or occipital lobe; (2) inflammation invades the cerebellum via the top of the mastoid tubercle, the posterior lateral wall of the rock bone, through the dura or lateral sinus vessels.
Rhinogenic brain abscess
Nosogenic brain abscess is caused by the invasion of purulent infection from the adjacent paranasal sinuses into the skull. For example, in frontal sinusitis, septal sinusitis, maxillary sinusitis, or pterygoid sinusitis, the infection spreads intracranially through the conduction vessels of the skull base, and the abscess mostly occurs in the anterior part of the frontal lobe or at the base.
Cryptogenic brain abscess
When the primary foci of infection are not obvious or hidden and the body’s resistance is weak, the hidden bacteria in the brain parenchyma gradually develop into brain abscess. Cryptogenic brain abscess is essentially a hidden type of hematogenic brain abscess.
Injurious brain abscess
Mostly secondary to open brain injury, especially penetrating brain injury during wartime or incomplete debridement surgery. The pathogenic bacteria invade directly through the wounds or foreign bodies or broken bone fragments enter the skull and form brain abscesses. It can develop early after the injury, or the symptoms of brain abscess may appear months or years after the injury due to the low virulence of the causative bacteria.
Hematogenous brain abscess
About 1/4 of brain abscesses are formed due to infections in other parts of the body and bacterial emboli disseminated to the brain via arterial blood flow. Primary foci of infection are commonly found in septic infections of lung, pleura, bronchus, congenital heart disease, bacterial endocarditis, skin boils and carbuncles, osteomyelitis, abdominal and pelvic organ infections, etc. Brain abscesses are mostly distributed in the middle cerebral artery supply area, frontal lobe, parietal lobe, and some are multiple small abscesses.
Pathogenesis
The common pathogenic bacteria are Staphylococcus aureus, Aspergillus, Escherichia coli and Streptococcus. Staphylococcus aureus is the most common hematogenous infection; Streptococcus pharyngitis is the most common rhinogenous infection; Streptococcus anaerobicus, Streptococcus pyogenes, and Enterobacter spp. are the most common otogenous infections; Staphylococcus aureus and Enterobacter spp. are the most common traumatic infections.
Pathogenesis and pathophysiology
The formation of brain abscess is a continuous process and can be divided into three phases.
(1) Acute meningitis and encephalitis phase: after the invasion of septic bacteria into the brain parenchyma, the patient shows obvious systemic infection reaction and pathological changes of acute restricted meningitis and encephalitis. The central part of encephalitis gradually softens and necroses, and many small liquefied areas appear, and the surrounding brain tissue is edematous. There may be a meningeal inflammatory reaction when the lesion site is superficial.
(2) Suppurative phase: The softening foci of encephalitis become necrotic and liquefied, fuse to form abscesses, and gradually increase in size. If the fused small abscess cavities are spaced, they become multi-room brain abscesses with surrounding brain tissue edema. The patient’s systemic signs of infection improve and stabilize.
(3) Envelope formation period: Generally, after 1 to 2 weeks, the granulation tissue at the periphery of the abscess is initially formed by the proliferation of fibrous tissue and glial cells and the abscess envelope is completely formed in 3 to 4 weeks or long. The speed of the formation of the envelope is related to the type and virulence of the causative bacteria and the resistance of the body and its response to antimicrobial treatment.
Clinical manifestations
Acute infection symptoms
Patients have fever, headache, general weakness, muscle pain, rapid pulse, loss of appetite, drowsiness and lethargy. Neck resistance or meningeal inflammation, usually not longer than 2-3 weeks, and most of these symptoms improve and disappear due to the application of broad-spectrum antimicrobials.
Symptoms of increased intracranial pressure
As the brain abscess forms and increases in size, the patient develops symptoms of increased intracranial pressure, with varying degrees of headache, which is persistent and worsens in paroxysms, accompanied by vomiting, especially frequent in cerebellar abscesses. It may be accompanied by varying degrees of mental and consciousness disturbances. Signs such as slow pulse, elevated blood pressure, widened pulse pressure, slowed respiration, etc. Half of the patients have optic papilloedema.
Symptoms of localization of the brain
If the brain abscess is located in the hemisphere, there may be contralateral central facial palsy, contralateral ipsilateral hemianopia, or quadrantal hemianopia, contralateral limb hemiparesis or positive cone bundle sign; if it is located in the dominant hemisphere, there may be aphasia, and there may be seizures. Forced head position, nystagmus, unsteady gait, ataxia, and hypotonia of the ipsilateral limb are seen in cases where the abscess is located in the cerebellum.
Brain herniation and abscess rupture
As the disease progresses, the increase in intracranial pressure becomes severe enough to cause cerebral herniation, and the patient dies of coma and respiratory failure. If the abscess is close to the brain surface or ventricle and ruptures automatically or by puncture into the subarachnoid space or ventricle, the condition deteriorates rapidly, showing sudden high fever, coma, convulsions, dramatic increase in blood and cerebrospinal fluid leukocytes, and rapid death if not rescued in time. [1] Diagnosis and differential diagnosis
Diagnostic basis
(1) The patient has a septic source of infection: e.g. chronic otitis media, mastoiditis, paranasal sinusitis, pulmonary infection. History of open cranial injury, congenital heart disease and other sources of infection in other parts of the body.
(2) Symptoms of systemic infection.
(3) Mostly history of meningitis with gradual signs of increased intracranial pressure and signs of brain or cerebellar damage in the corresponding part of brain abscess.
(4) Lumbar puncture: the occupying effect of abscesses mostly leads to increased pressure in cerebrospinal fluid, and lumbar puncture should be contraindicated if there is optic papilloedema. In the acute encephalitis stage, the cerebrospinal fluid cell count is often elevated, and sugar and chloride are reduced. However, after abscess formation, the cell count mostly decreases to normal. Protein quantification in the cerebrospinal fluid may be mildly elevated.
(5) Imaging examinations.
a) Cranial X-ray plain film: it helps to detect the primary foci of abscess, such as otogenic brain abscess can be seen as osteosclerosis or destruction of the temporal bone rock and mastoid air space. Nasogenic brain abscesses are mostly seen as inflammatory changes in the frontal sinus, septal sinus or maxillary sinus. Traumatic abscesses can be seen as residual intracranial fragments of bone or foreign bodies. Chronic brain abscesses also show signs of increased intracranial pressure and occasionally calcification of the abscess wall.
b) CT examination: CT imaging characteristics of brain abscesses vary according to the stage of development of the lesion. At the stage of envelope formation, the abscess wall can be seen in 5% of patients on plain scan within the hypodense edema zone, and after injection, a complete, well-defined, uniformly thick, distinct ring of enhancement can be seen. The formation of gas-fluid planes in the abscess cavity is seen in the fashion of combined anaerobic bacterial infection, and the enlargement or pressure displacement of the ventricular system is seen when there is a significant occupational effect.
c) MRI: The performance varies depending on the time of abscess formation. Before the formation of the envelope, it shows long T1 and long T2 signal shadow with unclear boundary, irregularity and obvious edema band with obvious occupancy effect, which needs to be differentiated from glioma and metastasis with medical history. After the formation of the envelope, the enhancement scan shows a thin-walled annular enhancement with clear borders, and the abscess wall mostly has no nodular shadow of internal protrusion.
d) Cerebral angiography: localized diagnosis can be made based on the displacement of normal vessels and the absence of vascular distribution in the abscess area, which can be characterized only when combined with the medical history.
e) Imaging of the abscess cavity: in critically ill patients, CT-guided puncture and aspiration of the abscess can be performed, and iodine oil or iodophenyl resin can be injected to observe the size and scope of the abscess.
(6) Exploratory cerebral puncture to find abscesses.
Differential diagnosis
(1) Septic meningitis: high fever, rapid pulse, marked signs of meningeal irritation but no signs of restricted neural localization, increased cerebrospinal fluid leukocytes and protein, normal brain ultrasonography, cerebral angiography and CT scan.
(2) Epidural or subdural pus accumulation: It is often combined with brain abscess and rarely occurs independently. Cerebral angiography shows an avascular area on the surface of the brain, and CT reveals a semilunar hypodense shadow on the surface of the brain.
(3) Thrombotic sinus infection: the bacterial emboli are dislodged and spread along the venous sinus, manifesting as periodic septic sepsis, irregular chills, flaccid fever, rapid pulse, increased peripheral blood granulocytes, but no change in cerebrospinal fluid, which can be identified with the help of brain ultrasound, cerebral angiography and CT scan.
(4) Septic labyrinthitis: caused by septic otitis media, symptoms are similar to cerebellar abscess, but headache is mild, vomiting, vertigo is severe, nystagmus is mostly mixed with spontaneous horizontal and rotational type, ataxia is bilateral or not obvious, no meningeal irritation sign, no optic papillary edema, lumbar puncture is normal.
(5) Brain tumor: slow onset, no history of infection, only increased intracranial pressure, normal cerebrospinal fluid cells, not difficult to differentiate by transcranial plain film, angiography, CT scan.
Treatment
The treatment principle of brain abscess is: before the abscess is completely confined, active anti-inflammatory and cerebral edema control treatment should be carried out. After abscess formation, surgery is the only effective treatment.
Anti-infection
The corresponding bacterial-sensitive antimicrobial agents should be selected for the causative organisms of different types of brain abscesses. If bacterial culture of the primary focus has not been detected or is negative, antimicrobial agents with a broader antibacterial spectrum and easy to pass the blood-brain barrier should be used according to the condition. Penicillin, chloramphenicol and gentamicin are commonly used.
Cranial pressure lowering treatment
For the increase of intracranial pressure caused by cerebral edema, mannitol and other hypertonic solutions are often used for rapid, intravenous infusion. Hormones should be used with caution to avoid weakening the immunity of the body.
Surgery
a) Puncture and pus aspiration: This method is simple and easy to perform and causes little damage to brain tissue. It is suitable for large abscesses, thin abscess walls, abscesses deep in or located in important functional areas of the brain, infants, elderly or physically weak people who can hardly tolerate surgery, and those whose condition is critical and whose abscesses are extracted by puncture as an emergency treatment measure.
b) Continuous drainage by catheter: In order to avoid repeated puncture or spread of inflammation, a soft rubber tube with an inner diameter of 3-4 mm is left in the abscess cavity when the abscess is punctured for the first time, and the abscess is pumped, flushed and injected with antimicrobial agent or contrast agent at regular intervals to understand the reduction of the abscess cavity, which is usually left for 7-10 days. At present, CT stereotactic puncture and pus aspiration or catheter drainage techniques are more superior.
c) Incision and drainage: for traumatic brain abscess, wound infection, difficulty in abscess removal or retention of foreign body in the skull, foreign body is often removed at the same time as drainage of abscess.
d) Abscess excision: the most effective surgical method. It is suitable for the surgical resection of abscesses with intact envelope formation and located in non-important functional areas; multiroom or multiple brain abscesses; traumatic brain abscesses containing foreign bodies or broken bone fragments. The operation method of brain abscess resection and general brain tumor resection disease prognosis
(1) Timeliness of diagnosis and treatment; death often results from brainstem compression or abscess rupture in patients with advanced disease.
(2) The virulence of the causative organism, especially the high morbidity and mortality of brain abscesses caused by anaerobic streptococci, which may be related to their virulence in destroying brain tissue.
(3) Poor prognosis of cardiogenic, pulmonary and multiple brain abscesses.
(4) The prognosis of infantile patients is worse than that of adults.
Disease prevention
Brain abscess is a serious intracranial infectious disease, which is mostly acute septic encephalitis in early stage, and the mortality rate is reported as high as 30-50% in foreign literature, so the treatment of brain abscess should be based on the policy of prevention, good health education, strengthening people’s physical fitness, early and thorough treatment of chronic inflammation of the ear and nose, chest and other parts of infectious diseases, timely and thorough debridement of open cranio-cerebral injury, removal of foreign bodies and broken bone fragments, etc. If a patient has a local source of infection and shows symptoms of systemic infection and signs of intracranial inflammation, he or she should seek medical consultation from a specialist and choose cranial CT or MRI scan according to his or her clinical manifestations, which can generally diagnose the disease. If treated in time, most of them can be cured; otherwise, intracranial hypertension leads to brain herniation, brainstem compression and respiratory and circulatory failure and death.
Disease care
Preoperative care
a) Psychological care Provide appropriate psychological support to enable the patient and family members to face the reality, accept the challenges of the disease and reduce frustration. Provide correct and easy-to-understand instructions according to the specific situation of the patient and family members, inform them of the type of disease, possible treatment plans and how to cooperate, and help them learn special care methods and techniques for the patient.
b) Dietary care Patients who are bedridden for a long time, feverish and consume a lot of energy should be given an easy-to-digest, high-fiber, high-protein, high-calorie diet. If necessary, give intravenous high nutritional fluid to improve the patient’s general nutritional status and enhance the body’s ability to resist disease.
c) Observation and care Pay attention to the changes in the patient’s consciousness, pupils and vital signs. Observe the signs of increased intracranial pressure, such as increased headache, frequent vomiting, unresponsiveness, and deepening of consciousness, which should alert the occurrence of brain herniation. Give antibiotics on time and in the right amount as prescribed by the doctor.
d) Pre-operative routine preparation Pre-operative antibiotic skin test and intra-operative medication should be brought in the morning as prescribed by the doctor. Assist to improve relevant preoperative tests: ECG, ultrasound, coagulation test, etc. Fasting and abstaining from food and drink for 8 hours before surgery. Change clean patient gown in the morning of surgery. Shave the head in the morning of surgery. Patient and medication check with operating room staff in the morning of surgery and then send to the operating room. Placement of urinary catheter after anesthesia.
Postoperative care
a) Routinely observe vital signs, state of consciousness, pupils, limb movement status, etc. The frontal orbital edema is often present after the anterior cranial fossa surgery, and cold compresses can be given to reduce the discomfort. To prevent intracranial infection, use sterile bandage for head dressing and sterile therapeutic towel on the pillow and change it frequently, regularly observe whether there is wetting and mark the wetting range on the dressing to estimate the degree of exudation.
b) Pain care Incisional pain mostly occurs within 24 hours after surgery, and general analgesics can be effective. Headache caused by increased intracranial pressure mostly occurs 2 to 4 days after surgery at the peak of cerebral edema, often pulsating headache, accompanied by vomiting in severe cases, and the headache can be relieved only after relying on dehydration and hormone therapy to reduce intracranial pressure; the use of dehydrating agents and hormones should be distributed reasonably within 24 hours.
c) Nutrition and rehydration Generally, fluid diet can be given on the first day after cranial surgery, semi-liquid diet on the second and third day, and then gradually transition to normal diet.
d) Care of pus drainage tube Keep the tube open, do not fold, distort or compress the tube. Properly fix the drainage tube, the drainage bottle (bag) should be at least 30cm below the abscess cavity, and the patient should take a position that facilitates drainage. To avoid the spread of intracranial infection, intracapsular irrigation should be performed only after 24 hours postoperatively and after the initial formation of adhesions around the wound; first, 0.9% sodium chloride solution should be slowly injected into the cavity and then gently withdrawn, taking care not to apply excessive pressure, and antibiotics should be injected after irrigation. The drainage tube was then clamped closed for 2 to 4 hours and the drainage bag was changed daily under aseptic conditions. Observe the nature, color, and amount of drainage fluid. The position of the drainage tube should be kept in the center of the abscess cavity, so it needs to be adjusted according to the X-ray examination results, and the tube should be removed when the abscess cavity is closed.