Purulent meningitis is a common infectious disease in the central neural system , and also one of the most potentially serious infections in infant and older children. This infection is associated with a high rate of acute complication and risk of chronic neurological morbidity.
Consideration of how the etiology of Purulent Meningitis relates to the age of the patient is very useful for clinical work., having impact upon considerations of pathogenesis, diagnosis, complications and therapy. When talking about etiology, we usually divide the cause of a disease into internal cause and external cause. Here the internal cause refers to the immunologic and anatomical defect of the body ,and the external cause is pathogen.
Pathogeny The common bacteria causing purulent meningitis are meningococci, hemophilus influenzae, and pneumococci etc. However, the pathogeny of Purulent Meningitis relates to the age of the patient.
Neonatal period to two months of age , the organisms responsible for purulent meningitis enteric bacilli predominantly, then group B hemolytic streptococci, staphylococci aureus. The infectious bacteria in this period reflect the maternal flora.
Two months to pre-adolescence. Most purulent meningitis in this age period is due to H. influenzae, meningococci, and pneumococci.
Adolescence. In the period after 12years age, meningococci and pneumococci are the main bacteria causing the purulent meningitis.
2. The immunologic and anatomical defect The congenital immunological deficient and the acquired immunodepression by using some drugs ,such as cortisone may bring opportunistic organisms causing meningitis. Structural abnormalities of the neural apparatus may result in direct contamination of the meninges with organisms of skin. Therapeutic intervention resulting in abnormal communication between the cerebrospinal space and other body compartments is associated with introduction of staphylococci or enteric organisms.
The purulent meningitis may occur in any period of life. However 90% of the cases are in the the period of 1 month to 5 years age . The risk factors include close contact with the patients, crowding, poor ventilation in rooms, and absence of breast-feeding for infants 2-5 month of age. The mode of transmission is primarily person to person contact through respiratory tract secretion or droplets.
Meningococcal infections tends to occur in winter and early spring. The infections of group B, C, Y of meningococci may occur sporadically, but group A, C usually as epidemics.
The infections of H. influenzae type b , tending to peak in winter , occur primarily in infants 2 month to 2 year of age ;50% of cases occur in the 1 st year of life.
Streptococcus pneumoniae types 1,3,6,7,14,17,18,19,21and 23, may result in purulentt meningitis, peaking in winter .
[Pathogenesis and Pathology]
Purulent meningitis mostly results from hematogenous dissemination of bacteria from a distant site of infection (such as upper respiratory tract infection). The bacteria colonizing respiratory tract attach to epithelial cells, then breach the mucosa and enter the circulation. After entering the circulation, the bacteria may survive in the bloodstream owing to the bacterial capsules that interfere with opsonic phagocytosis. An absence of preformed IgM or IgG anticapsular antibodies in nonimmune hosts, and various deficiencies of components of the complement or properdin system in immunodeficient patients also reduce phagocytosis. After entering to the CSF through the choroid plexus of the lateral ventricles and the meninges, bacteria circulate to the subarachnoid space and then multiply rapidly.
As bacteria invasion and multiply, a meningeal exudate of varying thickness may be distributed around the cerebral veins, venous sinuses, convexity of the brain, and cerebellum and in the sulci, sylvian fissures, basal cisterns, and spinal cord. Subdural effusions and, rarely, empyema and ventriculitis may be present. Perivascular inflammatory infiltrates may also be present. Vascular and parenchymal cerebral changes characterized by polymorphonuclear infiltrates extending to the subintimal region of the small vascula, vasculitis, thrombosis of small cortical veins, and necrotizing arteritis. The vascular occlusion from inflammation, vasospasm, and thrombosis may result in cerebral infarction and neural cell death.
1. onset The onset of acute meningitis has two patterns: ① Less common but more drastic presentation is sudden onset with rapidly progressive manifestations of shock, purpura, disseminated intravascular coagulation (DIC) and reduced levels of consciousness, frequently resulting in death within 24 hours. ② More often, meningitis is preceded by several days of upper respiratory tract or gastrointestinal symptoms, followed by nonspecific signs of CNS infection such as increasing lethargy and irritability .
2. Symptoms and signs The symptoms and signs of meningitis are related to the nonspecific findings associated with a systemic infection and to manifestations of meningeal irritation.
Nonspecific findings include fever (present in 90-95%), anorexia and poor feeding, symptoms of upper respiratory tract infection, myalgias, arthralgias, tachycardia, hypotension and shock (particularly in fulminant type) and various cutaneous signs, such as petechiae, purpura, or an erythematous macular rash.
Meningeal irritation is manifested as nuchal rigidity , back pain, Kernig sign and Brudzinski sign . In some children, particularly in those younger than 12-18 mo, Kernig and Brudzinski signs may not be evident with meningitis. Increased ICP is suggested by headache, emesis, bulging fontanel or diastasis (widening) of the sutures , papilledema , hypertension with bradycardia, apnea or hyperventilation, decorticate or decerebrate posturing, coma , or signs of herniation . Seizures due to cerebritis, infarction, or electrolyte disturbances occur in 20-30% of patients with meningitis. Focal neurological signs usually are due to vascular occlusion. Cranial neuropathies due to focal inflammation usually involve in cranial nerves of Ⅱ,Ⅲ,Ⅵ,Ⅶ,Ⅷ. Alterations of mental status and a reduced level of consciousness are common among patients with meningitis and may be due to increased ICP, cerebritis, or hypotension; manifestations include irritability , lethargy , stupor , and coma .
1. Peripheral blood check Leukocytosis of 20-40×109/L usually occur in patients with meningitis, with the increase primarily of neutrophil, reaching above 80%.
2. Lumbar Puncture The CSF pressure usually be high, and the CSF looks like turbidity in patients with purulent meningitis. The CSF leukocyte count is usually elevated to greater than 1,000×109/L and reveals a neutrophilic predominance(75-95%). The Gram stain is positive in most (70-90%) patients with purulent meningitis. CSF cultures are the evidences for the pathogens of meningitis.
3. Others Blood cultures may reveal the responsible bacteria in 80-90% of cases of childhood meningitis. CT or MRI of brain should be performed in patients with suspect complications of Ventriculitis or Subdural effusion
During the treatment of meningitis, complications due to CNS or systemic effects of infection are common. neurologic complications include seizures, increased ICP, cranial nerve palsies, stroke, herniation.
1. Subdural effusion Collection of fluid in the subdural space develop in 10-30% of patients with meningitis and are asymptomatic in 85-90% of patients. Subdural effusions are especially common in infants. Subdural effusions may result in a bulging fontanel, diastasis of sutures, enlarging of head circumference, emesis, seizures, fever, and abnormal results of cranial transillumination. CT or MRI scanning can confirm the presence of a subdural effusion.
2. SIADH occurs in the majority of patients with meningitis, resulting in hyponatremia and reduced serum osmolality in 30-50%. This may exacerbate cerebral edema or independently produce hyponatremic seizures.
3. Ventriculitis In patients with meningitis being adequately, prolonged fever usually suggests ventriculitis, also being manifested as frequent seizures, bulging fontanel. CT or MRI scanning may show enlarged cerebral ventricle.
4. Hydrocephalus Communicating or noncommunicating hydrocephalus may occur due to inflammatory exudate which blockaged the circulation of cerebrospinal fluid.
The diagnosis of acute purulent meningitis is conformed by analysis of the CSF, which reveals microorganisms on Gram stain and culture, a neutrophilic pleocytosis, elevated protein, and reduced glucose concentrations. Lumbar puncture should always be considered in any infant who has a fever with neurologic signs and symptoms.
Contraindications for an immediate LP include (1) evidence of increased ICP; (2) severe cardiopulmonary compromise, such as shock; (3) infection of the skin overlying the site of the LP.
In addition to purulent bacteria, many other microorganisms can cause infection of the CNS with similar clinical manifestations. The meningitises caused by different microorganisms can be distinguished through careful analysis of the CSF (Table 174-1).
1. Antibiotic therapy
(1) Choice for initial antibiotic The initial choice of therapy for meningitis in immunocompetent infants and children should be based on the antibiotic susceptibilities of S . pneumococci. , N . meningococci , and H . influenzae type b. Either of cefotaxime (200mg/kg.d) or ceftriaxone (100mg/kg.d), combined with vancomycin (60mg/kg.d) is recommended. Patients allergic to β-lactam antibiotics should be treated with chloramphenicol (100mg/kg.d). antibiotics should achieve bactericidal levels in the CSF.
(2) Duration of antibiotic therapy. When the pathogen is identifiable, antibiotics should be selected on the susceptibilities of the pathogen. In newborn, group B streptococci meningitis should be treated with ampicillin (200mg/kg.d) or penicillin (300,000-600,000U/kg.d) for no less than 14-21days; the meningitis due to E.coli , P.aeruginosin or staphylococcus aureus should be treated with cefuroxime for no less than 14 days. Uncomplicated H.inluenzae type b meningitis should be treated with ampicillin if the isolate is found to be sensitive, or the third-generation cephalosporines otherwise, for no less than 2-3 weeks. Therapy for uncomplicated penicillin-sensitive S.pneumoniae meningitis should be completed with penicillin or the third-generation cephalosporin for 2-3 weeks. If the isolate is resistantto penicillin and the third-generation cephalosporin, therapy should be completed with vancomycin. Intravenous penicillin (300,000U/kg.d) for 7-10 daysis the treatment for uncomplicated N.meningitidis meningitis.
2. Other therapeutic approach
(1) Intensive Care Pulse rate, blood pressure, respiratory rate, pupillary reflexes, and conscious state should be monitored frequently during the first 72 hr. Assessments of blood urea nitrogen, serum electrolyte should be made , to keep the balance of water-electrolyte.
(2) Treatment for high fever, seizure and infective shock.
(3) Treatment for increased ICP and preventing cerebral herniation
(4) Corticosteroids that limit production of inflammatory mediators may be of benefit to patients with purulent meningitis. Clinical data support the use of intravenous dexamethason , 0.6mg/kg.d, for 3-5 days.
(5) Therapy for complication
What is meningitis? Meningitis is an inflammation of the membranes (called meninges) that surround the brain and spinal cord. Meningitis may be caused by many different viruses and bacteria, or by diseases that can cause inflammation of tissues of the body without infection (such as systemic lupus erythematosus and Behcet's disease).
How are encephalitis and meningitis diagnosed? Encephalitis or meningitis are suggested when the symptoms described above are present. The doctor diagnoses encephalitis or meningitis after a careful examination and testing. The examination includes special maneuvers to detect signs of inflammation of the membranes that surround the brain and spinal cord (meninges).
Tests that are used in the evaluation of individuals suspected of having encephalitis or meningitis include blood counts, brain scanning (such as MRI scan), and spinal fluid analysis.
A lumbar puncture is the most common method of obtaining a sample of the fluid in the spinal canal (the cerebrospinal fluid or CSF) for examination. A lumbar puncture (an LP) is the insertion of a needle into the fluid within the spinal canal. It is termed a "lumbar puncture" because the needle goes into the lumbar portion (the "small") of the back. (Less commonly, spinal fluid can also be obtained from other levels of the spine.)
The diagnosis is confirmed by abnormal spinal fluid results.
What is the treatment of encephalitis and meningitis? Antiviral medications may be prescribed for encephalitis caused by the herpes virus or other severe viral infections. Antibiotics are prescribed for bacterial infections. Anticonvulsants are used to prevent or treat seizures. Corticosteroids are used to reduce brain swelling and inflammation. Sedatives may be needed for irritability or restlessness. Over-the-counter medications may be used for fever and headache.
Individuals with bacterial meningitis are usually hospitalized and treated with antibiotics intravenously. Antiviral drugs may also be prescribed.
What is the outlook (prognosis) for patients with encephalitis or meningitis? The prognosis for encephalitis varies. Some cases are mild, short and relatively benign and patients have full recovery. Other cases are severe, and permanent impairment or death is possible. Meningitis can lead to permanent damage to the nervous system and can cause hydrocephalus . The acute phase of encephalitis may last for 1 to 2 weeks, with gradual or sudden resolution of fever and neurological symptoms. Neurological symptoms may require many months before full recovery.
With early diagnosis and prompt treatment, most patients recover from meningitis. Viral meningitis cases are usually self-limited to 10 days or less. However, in some cases, the disease progresses so rapidly that death occurs during the first 48 hours, despite early treatment.