Introduction
Recent increased interest in Meningitis is caused by the presentation of many children with a provisional but erroneous diagnosis of meningitis in America. In many cases, it is impossible to make a specific aetiological diagnosis in fever-associated headache, and it is significant not to traumatize the child or an adult with excessive investigations (Roos, 1999) Critics admit that recent cases of meningitis show that a normal blood count or lymphocytosis, and a normal or only diffidently elevated C-reactive protein (CRP) suggest reassurance that the infection is unlikely to be serious. Thus, in most cases, further investigation is necessary to determine the causes of illness and its severity. For medical professionals, it is important to guarantee that the headache or other types of annoyance does settle when the fever resolves (Grabowski 2006).
Disease Definition
Meningitis is defined as an infectious disease caused by an inflammation of “the meninges (membranes or coverings) of the brain or cord” (Grabowski 2006, p. 11). Image 1 depicts membranes in relation to the brain and to the spinal cord. Different agents can be responsible for the irritation, but the signs and symptoms of meningitis are much the same, irrespective of the causal cause. Following Grabowski (2006):
Thus, just as the meninges form one continuous structure, the subarachnoid space and the brain ventricles constitute a single communicating system within which the cerebrospinal fluid is contained. It follows that an acute bacterial inflammation that starts anywhere along the membranes is apt to spread throughout their entire extent (p. 15).
Pathophysiology/Etiology
Pathologically, meningitis is caused by viruses, bacteria, and microorganisms. Bacterial meningitis can be caused by the following bacteria: B streptococci, Escherichia coli, Bacteria monocytogenes, meningococcus, N. meningitidis, and S. pneumonia. (Grabowski 2006). The bacteria penetrate the brain and spinal cord and cause inflammation processes. The pia mater (nearest to the brain or cord) and arachnoid locate very close together, but they are separated by a space in which the cerebrospinal fluid passes. Etiology defends mainly on the locus and extent of the nervous tissue infected, and less clearly on the exact type of invading organism (whether meningococcus, tubercle bacillus, or some other bacteria) (Klosterman 2006).
When bacteria of any type are invaded by organisms and their toxins, there is an inflammatory process in which many of the toxins are poured into the subarachnoid space, with a resulting increase in the quantity of the cerebrospinal fluid. In many cases, researchers find an early increase in the volume and pressure of the cerebrospinal fluid and can detect the presence of bacteria within it. The best methods of determining both the occurrence and the type of meningeal bacteria are by laboratory testing of the cerebrospinal fluid, which is obtained by a puncture of the spine (Klosterman 2006, see appendix 2,3).
Signs, Symptoms, Diagnostic Tests
The main signs and manifestations of meningitis are different types of heheadachesoften seen as the earliest symptom of the disease. Headache is due to the increased pressure exerted on the brain by the cerebrospinal fluid. Dizziness and vomiting often appear in relation to the headaches. Possibly, the most important sign of meningitis is stiffness or rigidity of the neck, which most likely is due to the irritation of the meninges at the base of the brain (Roos, 1999). This stiffness of the neck becomes visible during the first days of the disease and is a constant symptom of meningitis Grabowski (2006). The stiffness increases as the disease progress. In certain forms of meningitis (e.g., epidemic cerebrospinal meningitis), the neck stretches backward to a certain degree. The patient complains about acute pain if the leg is extended at the knee or flexed at the hip (so-called Kernig’s sign); this arises from the irritation of lumbar and sacral roots and meninges. Another peculiar manifestation is Brudzinski’s sign: the patient lies on his back and the doctor bends the neck forward on the chest; the result is an unintentional flexion of the legs at the knee and hip joints so that both legs become flexed upon the thighs and the thighs become flexed upon the abdomen (Willett, 1999). Also, manifestations are convulsive posture, characterized by arching of the body backward so that the person rests on head and heels. This manifestation appears relatively late in the course of the disease (Grabowski 2006).
Another important condition and the manifestation of meningitis are fever. Fever appears in the very early stages of the disease and very constant symptom; fever can be low in certain forms of disease and high in others. Some minor signs include a slow pulse as a result of inflammation of the vagus center (inhibitory to heart action) in the medulla Grabowski (2006). Also, researchers admit sensitivity to light, thermal, tactual, and auditory stimuli. These signs are a direct result of inflammation processes in the sensory cortex and the nuclei of the optic and acoustic nerves. also, it is possible to see rashes and skin eruptions, mental symptoms such as restlessness, irritability, apathy, and drowsiness. In some stages of meningitis, researchers admit such manifestations as delirium, insomnia, stupor, and coma. About other signs and symptoms, these signs occur more or less commonly in meningitis. It is important to note that for diagnostic purposes of meningitis, the particularly important early signs such as headache, neck rigidity, vomiting or a convulsion, fever, and the Kernig sign. these very signs create a general picture of the disease and call for an immediate puncture of the spine for testing of the cerebrospinal fluid which helps determine the specific cause of the disease so that appropriate treatment can be started (Willett, 1999).
The main diagnostic criteria include manifestations of inflammation of the motor apparatus. These signs vary from muscular twitchings and spasms, cramps, tremors, and the like, to widespread convulsions. In connection to these signs of inflammation process of the motor system, there are paralytic signs which occur later than the foregoing symptoms Grabowski (2006). These paralyzes is a product of the involvement of the motor cortex; these signs are convulsive (i.e., stiff and rigid) in type and may be very general or may affect only limited types of muscles. As meningitis begins to absorb the cranial nerves at the base of the brain, new signs may appear. The most common signs for diagnostic purposes are paralysis of the eye muscles (both internal and extrinsic) is discovered, first by indiscretion in the size of the pupils, later by slow pupillary reaction, and by total loss of pupillary reflexes (Willett, 1999).
Treatment
The initial treatment methods involve drug therapy. the most common drug used for treatment is benzylpenicillin. For bacterial meningitis, empiric antibiotics are used. they include cephalosporins caforaxime, ceftiaxone. also, vancomycin is used for the initial treatment. the problem is that different types of bacteria can be responsible for an acute meningitis (the most common types are the meningococcus, the pneumococcus, streptococcus, tubercle bacillus, syphilis spirochete). After the spin puncture, the physicians choose the best drug according to the type of bacteria and severity of the disease (Willett, 1999).
The past experience suggest that mortality is very high, and complications are common, and in those who recovered enduring signs (e.g., gait disturbances, noises in the ears, deafness, cross eyes, mental deficiency) are typical Grabowski (2006). The new forms of treatment include mechanical ventilation and neurosurgery. In spite of great changes in modern medicine, such types of meningitis as tuberculous meningitis cannot be treated. Such type of disease as epidemic cerebrospinal meningitis, caused by the meningococcus, today is effectively treated by the punctual and vigorous use of the sulfonamides (sulfathiazole and sulfadiazine). Other types, particularly pneumococcus meningitis, are treated more easily to penicillin therapy (Willett, 1999).
Epidemiology
The high frequency of meningitis has been found in many Native societies in Canada and the USA. The most common causal organism is Hemophilus influenzae type b (Hib), accomplished by meningococci, pneumoccocci, mycobateria, and other bacterial and viral agents. The mortality rate for this disease varies according to the type of bacteria, from about 33 % in cases caused by Gram-negative organisms, to %27 in pneumococcal, to % 9 in meningococcal, to % 7 in Hib cases. According to statistical results presented by Florida Department of Health: “approximately 25,000 cases of bacterial meningitis annually in USA; 206 annual cases” (Florida Department of Health 2009). Florida has the heist mortality rates and high incidence rate in the USA. (see table 4). The most common symptoms in Black and Native Americans are caused by all three common pathogenic agents (Haemophilus influenzae, Neisseria meningitidis and Streptococcus pneumoniae). In many cases, is found in meningococcal meningitis, but the most typical rash is purpuric, occurring in 60% of cases and associated with meningococcal septicaemia (Willett, 1999).
Literature Review
Recent studies (Willett, 1999) underline that there is an existence of genetic predisposition to meningitis: certain human leukocyte antigen (HLA) configurations have been observed in children suffering from Haemophilus influenzae. Cochrane Review suggests that the reappearance of meningitis has been observed in the relatives of these infants, as well as a modest antibody response after the organization of the polysaccharide-ribitol-phosphate (PRP) antigen capsular of Haemophilus influenza. Also, in those people suffering from meningococcal meningitis, a decrease in some complement issues, in particular C5 and C8, is found. Researchers admit that these factors require special treatment methods including antibiotics and even neurosurgery. The bacteria and viruses penetrate the cerebrospinal fluid (CSF) through the choroid plexus, which is the weakest part of the BBB. At this stage, micro-organisms duplicate very quickly because antibody activity is inadequate, and they activate a seditious response with a concentration of polymorphonuclear leukocytes. The treatment methods should be adapted to these activities and reduce negative causes and symptoms of the disease. The polysaccharide of the part in the Gram-negative bacteria, and the teichoic acid and peptidoglycan found on the cellular part of the Gram-positive bacteria encourage the release of cytokines and other pro-inflammatory mediators (IL-1, IL-6, TNF, prostaglandin E, etc.). Following treatment methods proposed by Cochrane review: “Careful management of fluid and electrolyte balance is an important supportive therapy. Both over- and under-hydration are associated with adverse outcomes” (Cochrane review 2009).
Willett (1999) admits that patients with meningitis should be observed in order to ensure the early manifestations of neurological complications. For instance, cerebral oedema may be evident within the first 48 hours and must be treated quickly because it can be life-threatening. “In theory, intraventricular administration of antibiotics would produce higher antibiotic concentrations in the CSF than intravenous administration alone, and eliminate the bacteria more quickly. However, ventricular taps may cause harm” (Cochrane review 2009). Researchers admit that brain abscess occurs at any time during all stages of disease and needs appropriate neuro-imaging. Subdural effusion is the most frequent complication; it is often asymptomatic and can usually be treated successfully with prolonged antibiotic therapy. Widespread seizures arising after the third day of such therapy, or focal seizures arising at any stage of the daises progression, are possible symptoms of neurological injure or alternation of CSF circulation. These signs require direct neuroradiological examination. Persistent fever during more than 5 days from the beginning of treatment is consistent with formerly mentioned complications, or others such as osteomyelitis, arthritis or endocarditis. All researchers agree that treatment of aseptic meningitis is symptomatic with antipyretics, analgesics, and antiemetic medicines. Anti-oedema drugs are infrequently used as symptoms regress in a few days without sequelae. “Corticosteroids have been used as an adjunct to antituberculous drugs to improve the outcome, but their role is controversial” (Cochrane review 2009).
Conclusion
The literature review and the research on the topic allow to say that treatment of meningitis is usually symptomatic. All researchers (Roos, 1999) admit that shims and manifestations arise suddenly and quickly become serious. Headache, hyperpyrexia and nuchal rigidity are present in 87% of cases of meningitis. Annoyance can, in the initial stages, represent the most often and, on occasion, the only sign, although this is more typical of tuberculous meningitis. Usually, headache is severe and continuous. The inflammation then spreads to the whole brain. such signs as vomiting, photophobia, and sometimes hyperacusis, and restlessness with fast injury of the general state usually go with the headache.
References
Epidemiology: State of Florida. (2009).
Meningitis. Cochrane Review. (2009).
Grabowski, J. E. (2006). Meningitis (Diseases and Disorders) (Library Binding). Lucent Books.
Klosterman, L. (2006). Meningitis. Benchmark Books (NY).
Roos, K. (1999). Meningitis: 100 Maxims (100 Maxims in Neurology, A Hodder Arnold Publication; 1 edition.
Willett, E. (1999). Meningitis (Diseases and People). Enslow Publishers; 1 edition.
Appendix
