Inflammation of the meninges



Bacteria                                             Viruses                                  Fungi

Other organisms                              Malignant cells                     Drugs and contrast media



Bacteria        The `three primary pathogens`

i.          Neisseria meningitidis                    -  meningococcal meniningitis

ii.         Haemophilus influenzae               -  haemophilus meningitis

iii         Streptococcus pneumoniae           -  streptococcal meningitis

Spread is normally haematogenous but may be direct

Immuno-compromised patients such as those with AIDS or those receiving cytotoxic drugs are at increased risk of meningitis which may be caused by unusual organisms.

Meningococcal has serotypes A B and C 

A causes epidemics in Africa

B most common in UK, C second most common

Vaccine covers A and C only



Polio               Mumps                       Herpes simplex                    HIV




Toxins from the bacteria damage neurological tissue

Pia and arachnoid become congested with Polymorphs

Layer of pus may organise causing adhesions and cranial nerve palsy

Inflammatory swelling and formation of exudate

Raised intracranial pressure and cerebral oedema is common



No pus or adhesions  No cerebral oedema   Lymphocytic inflammatory reaction in CSF



About 2 500 cases per year in the UK

Droplet transmission from the nasopharynx of cases or carriers


Clinical Features

Meningitis should be considered in all patients who have headache and fever


Meningitic syndrome

Intense malaise                    Fever                                      Rigors

Severe headache                Photophobia                         Vomiting

Neck stiffness                       Positive Kernig`s sign         Consciousness - normal



Sudden onset                                               High fever

Petechial rash which is often sparse       Possible septicaemia with acute septic shock



Less severe than bacterial form                Self - limiting in 4 - 10 days.


Tuberculosis meningitis

Chronic meningitis                          Vague headache and lassitude

Anorexia with vomiting                   Signs may take several weeks to develop.


Malignant meningitis         A chronic, sub - acute process


General symptoms            Fitting             Joint pain                  Confusion                 Drowsiness



Neurological damage to brain, cranial and spinal nerves

Cerebral infarction               Obstructive hydrocephalus                        Cerebral abscess    

Subdural empyema             Epilepsy                                             Septicaemia shock



Meningitis has a high mortality and therefore must be treated as an emergency.

Mortality is about 15% even with treatment

Minutes count

Clinically diagnosed bacterial meningitis should be immediately treated with intravenous benzylpenicillin

Lumbar puncture;  cloudy, monocytes, neutrophils, increased protein,  culture for organisms

Blood;  routine tests, cultures

Analgesics for headache

Dexamethasone is often given in children to prevent complications such as deafness.


Antibiotic management

Bacterial where organism is unknown - i.v. benzylpenicillin 2 g given 2 hourly with chloramphenicol 75 mg/ Kg or i.v. cefotaxime

Pneumococcal or meningococcal - penicillin or cefotaxime

Haemophilis - Chloramphenicol or cephalosporins

Intrathecal antibiotics are no longer necessary.

Rifampicin may be used for prophylaxis in outbreaks



Teach the importance of early treatment             Teach the clinical features

Advise on vaccination                                            Aid in diagnosis and treatment

Oxygen                                                                      Barrier nurse/isolate for 24 - 48 hours

Darkened quite room



TPR BP                      GCS               Change in condition                       Fits                  Vomiting

Renal function         Bed rest         Prevent complications        ADLs


Questions on meningitis

List the 3 layers of the meninges and give one function for each layer.

What does the term meningitis mean?

Give two pathophysiological effects of inflammation of the meninges.

List the forms of infective meningitis and give the causative organism for each form listed.

What serotype of meningicoccal meningitis causes most disease in the UK?

How is bacterial meningitis spread?                    Who is most at risk from meningitis?

What are the main features of meningism?          List some other clinical features of meningitis.

What complications may occur in bacterial meningitis?

What are the main medical treatments for meningitis?

List the principle nursing care interventions in meningitis with a rationale for each intervention listed.




Cerebral meninges

The cerebral meninges are composed of three separate layers which surround the brain and spinal cord. The prime function of the meninges is to provide protection for the delicate tissues of the central nervous system. The term `mater` comes from the Latin for `mother` so poetically the meninges mother the brain and spinal cord. The meninges are composed of the dura mater, arachnoid mater and pia mater. 


Dura mater

A double layer of tough fibrous tissue for protection and support of the CNS.


Arachnoid mater

Arachnoid is from the Greek for `like a spiders web`, this is a vascular layer carrying blood vessels and also reabsorbes cerebral spinal fluid. (Hubbard and  Mechan 1997). The cerebrospinal fluid (CSF) is located below the arachnoid in the subarachnoid space.


Pia mater

The pia covers the surface of the brain itself, it is composed of a fine fibrous tissue and is very vascular. Projections of the pia called the choroid plexuses produce the CSF.



Inflammation of the meninges is referred to as meningitis.  The terms leptomeningitis and pachymeningitis are sometimes used. Leptomeningitis is more common and describes inflammation of the arachnoid and pia mater and is most commonly caused by blood born infection. Pachymeningitis describes inflammation of the dura and may occur as a consequence of direct spread of infection from the bones of the skull, after surgery or trauma, from otitis media or mastoiditis, (Underwood, 1992).


Inflammation in the meninges will lead to increased blood flow in the meningeal vessels. There will also be an increase in capillary permeability leading to the formation of inflammatory exudate. These factors lead to cerebral oedema and raised intracranial pressure.



Infective meningitis is comparatively rare in the UK with about 2 500 - 3 000 cases of bacterial meningitis reported in England and Wales per year, (National Meningitis Trust 1999).  The incubation period for bacterial meningitis is from two to ten days.



There are a variety of causes of inflamed meningeal layers, these include infection with bacteria, viruses, fungi and protozoa. Malignant cells in some cases of cancer are another possible cause, (Mareel, Leroy and Bracke 1998).  Inflammation may also be caused by drugs or contrast media given intrathecaly and by blood after a subarachnoid haemorrhage.



Bacterial meningitis is an acute life threatening disease.  The so called `three primary pathogens` cause more than 75% of cases of bacterial meningitis, (Shanson 1988). These are Neisseria meningitidis which causes meningococcal meniningitis and is the most common aetiology in the UK. Haemophilus influenzae causes haemophilus meningitis and Streptococcus pneumoniae causes streptococcal meningitis.


There are several forms of meningococcal meningitis referred to as serological types, the most prevalent are A, B and C. Type B disease is the most common form in the UK followed by group C. Group A strains are rare in the UK, (less than 2% of cases) but are the epidemic strains in other parts of the world, (HMSO 1996).



A variety of viruses may lead to the viral form of the disease. Viral meningitis may initially present a similar picture to the bacterial form but is usually less serious and is self limiting. Possible aetiological viruses include enteroviruses (eg. echo, coxsackie and polio), mumps, herpes simplex and HIV.



Spread occurs via airborne droplet transmission from the nasopharynx of cases or carriers, (Ball and Gray, 1984). Kissing is another possible mode of transfer. A carrier is an individual who carries the pathogen which causes the disease but does not suffer from the condition themselves. The enteroviruses  spread via the faecal - oral route.


Risk factors

Although meningitis may occur at any age it is most common in young people and children under the age of 14 years. The increase in incidence in late teenage and early twenties is probably due to close contact between young people in schools, colleges, residences and clubs.


Immuno-compromise increases the probability of meningitis. This may be caused by AIDS, nutritional deficiencies, cytotoxic drugs or splenic deficiency, (such as after splenectomy), in these conditions meningitis may be caused by unusual organisms. Patients with AIDS are especially vulnerable to the fungal infection, cryptococcal meningitis, (Edmond, Rowland and Welsby, 1995).


There are more cases in winter when respiratory infections are more prevalent and irritation of the nose and throat from cigarette smoke may reduce natural immunity.


Clinical features


Meningism is a frequently used term which describes the group of symptoms which accompany inflammation of the meninges from any cause, (Bannister, Begg and Gillespie, 1996). The principle clinical features are headache, neck and back stiffness, nausea, vomiting and photophobia.


General features

Malaise in meningitis is often intense. The headache is global and usually severe, patients will often report it is the worst they have ever experienced. Fever with rigors occurs in cases of infection. 


Neck and back stiffness and a positive Kernig`s sign, (inability to fully extend a leg with the hip joint flexed without extreme pain) develop within a few hours of feeling unwell, (Kumar and Clark, 1995), (fig.1).  When the neck is flexed to attempt to touch the chest with the chin the neck muscles will tighten, (fig.2). The patient will not be able to curl up enough to touch their nose on the knees. These physical signs are generated by stretching of the inflamed meninges and the muscle guarding this produces.


Other possible features of meningitis include confusion, drowsiness, joint pain and fitting. There may also be disorientation and acute confusion. Importantly meningitis should be considered in all patients who have headache and fever.


In babies the presentation is different, there is rarely evidence of neck and back stiffness, they usually appear flaccid and there may be a bulging fontanel, (see table 1). Meningism may occur in the absence of meningitis but should always receive a rapid medical opinion.


Bacterial meningitis

This is usually of sudden onset with a high fever. A petechial haemorrhagic rash often develops, however the rash may well be sparse and not develop for some time. The rash is a very serious sign as it means there is a septicaemia. Petichial means pertaining to small red or purple spots caused by extravasation of blood into the skin, (Anderson et al 1994). The rash does not fade or blanch when pressed on with a glass, if untreated the rash gets bigger and looks like bruises (plate 1).


Viral meningitis

Typically this is less severe than the bacterial form of the disease and is usually self limiting in 4 - 10 days.


Tuberculosis meningitis

In this infection there is a chronic meningitis with vague headache, lassitude and anorexia. Signs of meningitis may take several weeks to develop.


Malignant meningitis

This is a chronic meningitic process which may cause other neurological features such as cranial nerve palsies.



The probability of serious complications or death increase rapidly with time. This is why very prompt treatment is so vital. The bacteria causing the meningitis or its toxins may damage the brain and major nerves.


There is a risk of rapidly developing septicaemia with acute septic shock. Septicaemia means bacteria are proliferating in the blood and used to be referred to as blood poisoning. This condition is correctly referred to as Fulminating meningococcaemia if caused by meningococcus. There is overwhelming shock, usually complicated by renal infarction. It is important that the disease be detected well before septicaemia develops as death occurs within 6 - 18 hours.  Septicaemia caused by meningococcal infection may present in the absence of meningitis and therefore without the usual meningitic clinical features.


Hydrocephalus may develop as a result of purulent material obstructing the flow of CSF, (Long et al 1995). Further complications include cerebral infarction, cerebral abscess and subdural empyema.  Patients may be left with neurological problems such as deafness, blindness, learning difficulties, paralysis or intractable epilepsy, (Davies et al. 1996). Immune complex arthritis may complicate meningococcal meningitis.



Meningitis has a high mortality and therefore must be treated as an emergency. Mortality is about 15% even with treatment, (Kumar and Clark, 1995). Minutes count, literally minutes. Clinically diagnosed bacterial meningitis or septicaemia should be immediately treated with intravenous benzylpenicillin before time is taken up with transfer into hospital. Once in hospital lumbar puncture will be performed, which is the most rapid diagnostic test for meningitis. In bacterial meningitis this will reveal a cloudy cerebrospinal fluid with increased numbers of monocytes and neutrophils, protein levels will also be increased. Some CSF will be sent for microscopy and culture. Blood will be sent for the usual tests and culture. Analgesics may be given for headache. Dexamethasone may be given in children to prevent neurological complications. Anticonvulsants may be prescribed for fitting.


Intravenous antibiotics in high doses will be prescribed depending on the microbiology. Where the bacterial organism is unknown cefotaxime will probably be prescribed, alternatively  benzylpenicillin with chloramphenicol has also been used. In pneumococcal or meningococcal infections penicillin or cefotaxime will probably be given.  Chloramphenicol or cephalosporins will be prescribed for haemophilis meningitis. Intrathecal antibiotics are no longer necessary. Rifampicin may be used as a prophylaxis for contacts and family in an outbreak.


Nursing measures

Nurses have a vital role in advising parents and others who care for babies and children. The danger signs need to be clearly understood so early medical help may be sought. Literature supplied by the National Meningitis Trust may be very helpful in this area of health education.


Nurses are often in a position to advise on vaccination. In 1992 before the introduction of the Haemophilis (Hib) vaccine there were 484 cases of Hib meningitis, in 1995 after introduction this had fallen by 88% to 60 cases, (HMSO 1996). Currently the meningococcal vaccine is effective against serogroups A and C but there is currently no vaccine available for group B disease.  Parents should be informed that Hib vaccine will not mean that children are immune to all forms of meningitis.


In hospital nurses will assist with diagnostic and treatment procedures. Adequate oxygenation must be ensured to prevent tissue hypoxia. Good oxygenation will also prevent cerebral vasodilation which will exacerbate raised intracranial pressure.


Patients should be barrier nursed in isolation for 24 - 48 hours until antibiotics therapy has been effective. This is to prevent the spread of the disease to other patients and staff. The room should be quiet and darkened as patients will often have an aversion to light. Light and sound may also trigger fits.


Routine observations of temperature, pulse, blood pressure and respiratory rate should be made to detect any worsening or improvement in the patients condition. Pyrexia may be controlled using antipyretics, aspirin should not be given to children. In addition the Glasgow Coma Scale should be employed to monitor the patients level of consciousness. The degree of meningeal stiffness, pain and irritation should be monitored. The patient should be observed for the petichial rash.


Close observation in case of fits is important. If a patient does fit they should be prevented from harming themselves during the fit. After the fit the airway must be maintained and the breathing monitored. Patients will usually be nursed in a semiprone position until they recover consciousness.


Vomiting must be observed and consistency and volumes recorded. Hydration should be maintained. Urine output should be closely monitored as renal failure may be a complication. If the patient is receiving intravenous fluids the line should be carefully monitored, if the patient is agitated or confused they may attempt to pull it out.


Ill patients should not exercise and will be kept on bed rest. The possible complications of immobility should be recognised and prevented. Full psychological support is critical in these ill people. A quiet confident approach may reduce anxiety and agitation. Significant others should be informed and supported.


National Meningitis Trust

`Founded in 1986 in response to an alarming absence of information and support to sufferers and their families`, (National Meningitis Trust, 1999). This charity has three areas of activity, informing and raising public awareness, supporting research and supporting sufferers and their families. They may be contacted at Fern House, Bath Road, Stroud, Gloucestershire, GL5 3TJ    

Tel: 01453 751738    24 hour support line:0345 538118  Fax: 01453 753588

Web Site:    e- mail:




            Adults and Children     Babies

            Vomiting                                   Fever - possibly with hands and feet feeling


            Fever                                        Refusing feeds or vomiting

            Headache                                 High pitched moaning cry or whimpering

            Stiff neck                                  Dislike of being handled, fretful

            Light aversion                           Neck retraction with arching of the back

            Drowsiness                               Blank and staring expression

            Joint pain                                  Difficult to wake, lethargic

            Fitting                                       Pale, blotchy complexion

Table 1. Symptoms of meningitis in  i. adults and children  ii. babies, (National Meningitis Trust, 1998)




            Neck and back stiffness

            Nausea and vomiting


Table 2 Main features of Meningism




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Ball AP. Gray JA (1984) Infectious Diseases, Churchill Livingstone, Edinburgh

Bannister BA. Begg NT. Gillespie SH. (1996) Infectious Diseases, Blackwell Scientific, Oxford

Davies KG.  Hermann BP.  Dohan FC Jr.  Wyler AR. (1996),   Intractable epilepsy due to meningitis: results of surgery and pathological findings,   British Journal of Neurosurgery.  10(6):567-70, 1996 Dec.

Edmond RTD Rowland HAK Welsby PD (1995), Infectious Diseases, Mosby-Wolfe, London

HMSO (1996),  Immunisation against Infectious Disease, (the green book), HMSO, London

Hubbard J Mechan D (1997) The Physiology of Health and Illness, Stanley Thorne, Cheltenham

Kroll JS.  Pollard AJ.  Habibi P. (1997), Meningitis - a Guide for Famalies, Publishing Solutions, (UK) Limited, London.

Kumar P.  Clark M.  (1995)  Clinical Medicine, (third ed.) Bailliere Tindale, London

Long BC. Phipps WJ. Cassmeyer VL (1995), Adult Nursing, A Nursing Process Approach, Mosby, London.

Mareel M.  Leroy A.  Bracke M. (1998)  Cellular and molecular mechanisms of metastasis as applied to carcinomatous meningitis.  Journal of Neuro-Oncology.  38(2-3):97-102.

National Meningitis Trust, (1998), Meningitis symptoms, (information leaflet)

Underwood JCE, (1992) General and Systematic Pathology, Churchill Livingstone, Edinburgh