Meningitis is included in high medical emergencies and early, rapid, and precise diagnosis is important. The high suspicion of meningitis requires that we perform laboratory tests immediately, because the risk of death or irreversible damage is great, unless treatment begins immediately.
DEFINITION
Meningitis is divided into several groups, in which case it will be described about purulent meningitis or bacterial meningitis, which is an inflammation of the lining of the brain causing exudation of pus (purulent), caused by non-specific and non-viral germs.
ETIOLOGY & RISK FACTORS
The etiology of the disease is related to the age of the patient and a number of host predisposing factors to bacterial infection or response changes to the MO invasion. But keep in mind that every MO can cause illness at any age. Here is a table of etiologies of meningitis by age group.
Table 1. Common causes of purulent meningitis
Age Group Organism Reviews
Streptococcus serogrouf B (Streptococcus agalactiae) Neonates - 3 months of age As many as 25% of mothers carry streptococcus serogroup B in their vagina. Ampicillin prophylaxis during delivery in high-risk women (ruptured amniotic fluid, fever, etc.) or in carrier women will decrease the incidence of infection in infants. Reported cases were also reported by Listeria monocytogenes and Haemophilus influenza type B occurring in the neonatal period.Escherichia coli Neonatus Is a cause in approximately 40% of cases of neonatal meningitis.
Haemophilus influenza Children 5 months - 5 years Infants <3 months may contain antibodies in serum obtained from their mothers and children aged> 3 - 5 years have strong antibodies against Haemophilus influenza (HI). So during this time HI infection is rare. Hib vaccine can decrease MO HI.
Age Group Organism Reviews
Streptococcus pneumonia All age groups Frequent in pneumonia, also in matoiditis, sinusitis and fractures of bacillary bone.
Pseudomonas, Stafilococcus, Salmonella, or Seratics In children> 12 years If the host response is compromised or there are anatomic abnormalities, then the microorganisms can infect.
Some conditions, disorders or diseases that facilitate meningitis include: 1) Systemic and focal infections (septicemia, chronic suppurative otitis media, typhoid fever, pulmonary tuberculosis); 2) Trauma and certain actions (cranial base fracture, lumbar puncture / anesthesia, surgery / neurosurgery); 3) Blood diseases, liver disease; 4) Use of substances that inhibit antibody formation; 5) Abnormalities associated with immunosupression such as alcoholism, agamaglobulinemia, diabetes mellitus; 6) Obstetrical and gynecological disorders / abnormalities. (1,4)
PATHOPHYSIOLOGY
In general, the invasion of germs into the central nervous system (CNS) occurs after the germs successfully break through the inner and outer body surfaces, it can arrive at the CNS via the following pathways: germs that are lodged in the mastoid can spread to the CNS of the plant. Sutura provides an opportunity for this invasion. Hematogenic invasion through the intracerebral artery is a direct spread to the CNS.
The spread of indirect hematogens can also be found, for example the meningeal artery is exposed to inflammation first. From that arteritis germs can arrive at liquor and meningens as well as brain. The peripheral nerves can also be used as a bridge for germs to arrive at the CNS via the perineurium. There is actually a special brain guard against the danger that comes through the hematogenous trajectory, known as the blood-brain barrier or the "Blood Brain Barrier". In toxemia or septicemia, the blood brain barrier (BBB) continues and no longer acts as a special barrier, so plasma proteins, leukocytes and germs can enter the CNS. Thus inflammatory processes and immunological reactions can develop in the CNS.
In purulent meningitis most commonly occurs due to hematogenous spreading of germs, originating from distant infection sites; bacteremia often precedes or coincides with meningitis. The germs enter the CNS hematogenously or directly spread from abnormalities in the nasopharynx, lung (pneumonia, bronchopneumonia), and heart (endocarditis). In addition, the tissues of inflammation of organs or tissues near the cerebral membrane such as brain abscess, otitis media, mastoiditis and cavernous sinus thrombosis. Invasion of germs (meningokok, pneumokok, haemophilus influenza, streptokok) into the subarachnoid space causes an inflammatory reaction in the pia and arachnoid, CSS and ventricular system.
At first small and hyperemic meningeal blood vessels, within a very short time the spread of polymorphonuclear leukocyte (PMN) cells into subarachnoid space, then formed exudate. Within days there is the formation of lymphocytes and histiocytes and in the second week of plasma cells. Exudate formed consists of two layers, the outside contains the leukocytes PMN and fibrin, while in the inner layer there are macrophages.
Inflammatory processes other than arteries also occur in the veins of the cortex and may cause thrombosis, cerebral infarction, brain udem, and degeneration of neurons
DIAGNOSIS APPEAL
Meningismus, in meningismus also occur meningieal irritation, headache, neck stiffness, kernig, seizures and coma. Meningismus is mostly present in infants and older children, with sudden symptoms of heat, tonsillitis, pneumonia, pyelitis, may occur along with acute appendicitis, typhoid fever, erysipelas, malaria, whooping cough. In CSS there are no germs, whereas the number of cells and glucose levels is normal. Generally symptoms disappear within a few days and leave no residual symptoms.
Aseptic meningitis, is an acute and self-limited inflammation of the brain lining. In CSS there is an increase in lymphocytes, but CSS remains sterile and normal glucose levels.
Tuberculosis meningitis, gives almost the same clinical picture, but can be distinguished from lumbar puncture examination, with serous CSF and cell counts between 10 - 500 / mm3 and most lymphocytes. Low glucose levels, between 20 - 40 mg%. Chloride content <600 mg%.
Other infections, brain abscesses, epidural or spinal abscesses, bacterial endocarditis with emboli, subdural empiema with or thrombophlebitis and brain tumors may exhibit similar symptoms. To distinguish it depends on the CSS check.
COMPLICATIONS
May occur as a result of imperfect treatment or delayed treatment. Possible complications include subdural effusions, subdural empyema, ventriculitis, cerebral abscess, neurological skuele in the form of paresis or paralysis until deserebrasi, hydrocephalus due to blockage in the course or resorbtion or excessive CSS production, electrolyte disturbance. On long supervision may be found signs of mental retardation, epilepsy or recurrent meningitis. (1,4,5)
TREATMENT
Meningitis is an emergency disease, so patients should stay in the hospital for intensive care and treatment.
General Treatment; the patient needs an absolute break and if the infection is severe enough, then the patient needs to be treated in the isolation room. Patients who are in a state of shock and coma should receive intensive care and treatment. The respiratory function should be strictly controlled, oxygen is required and in case of respiratory distress it is necessary to install an endotracheal tube or tracheostomy.
Parenteral presentation should be carefully monitored. The presence of dehydration should be corrected. The balance between incoming and outgoing fluids should be kept as good as possible. In order to provide this liquid, the electrolyte element is taken into account. Thus the electrolyte balance must be maintained. The presence of hyponatremia or hypokalemi, should be addressed immediately.
Other things to note are the possibility of seizures, DIC, hiperpireksia, brain udem, dekubitus, phlebitis, and malnutrition (diet).
Handling of convulsivus status; when entering the status of convulsivus given diazepam 0.5 mg / kgbb / times intravenously which can be repeated with the same dose 15 minutes later if the seizures have not stopped. Repeat administration of the next diazepam (the third time) with the same dose, but given intramuscularly. After convulsions can be resolved, give the penobarbital for the initial dose of 30 mg neonate, children <1 year 50 mg, children> 1 th 75 mg. Furthermore, for maintenance treatment, 8 to 10 mg / kgbb / day administered in a dosage of 8 to 10 mg / kgbb / day divided into 2 doses (starting 4 hours after initial dose). The next day at a dose of 4 - 5 mg / kgbb / day divided into two doses. If not available diazepam may be administered directly with the initial dose and subsequent maintenance dosage.Giving antibiotics, antibiotics should be fast and precise, in accordance with the bacteria and causes in a fairly high dose. While awaiting the results of culture should be given antibiotics with a broad spectrum and should be given parenterally. Because the main cause of purulent meningitis in Indonesia (Jakarta) is haemophilus influenza and pneumococcus, whereas meningococcus is rare, intravenous ampicillin 200-400 mg / kgbb / day is divided into 4-6 doses plus 100 mg / kgbb / day intravenous chloramphenicol in 4 doses. On the 10th day of treatment the lumbar puncture is performed and if it shows normal results, the above-mentioned treatment is continued for another two days, but if it is not yet normal the treatment is continued with the same medication and the same as above or replaced with the appropriate medication with culture result and germ resistance test.
Purulent meningitis occupies its own place because it is usually caused by the bacillus of Coliform and Staphylococcus, even in RSCM 40.5% of cases caused by Salmonella sp. Hence the recommended treatment is as follows: First choice Cephalosporin 200 mg / kgbb / day intravenously divided in two doses, combined with amikacin premises
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