MENINGITIS / MedUrgent

MENINGITIS

MENINGITIS is an inflammation of the membranes covering the brain and the spinal cord caused by organisms that gain entrance to the meninges either directly (meningocoele, trauma) or via blood stream. In the neonatal period bacterial meningitis is caused by group B streptococci, E.coli, listeria monocytogenes, group D streptococci, gram-negative coliforms and staphylococcus aureus. In older children, the common causative organisms are H. Influenzae, nisseria meningitides and streptococcus pneumonia. Meningitis can be caused by viruses and less commonly by other causative organisms listed below.

CAUSES OF MENINGITIS

VIRAL CAUSES

Enteroviruses(echo,coxsockie, polio)

Herpes simplex

Japanese encephalitis virus 

Infuenza virus

Lymphocytic choriomeningitis virus

HIV

Mumps virus

Arbo virus

E.B.virus

 

BACTERIAL CAUSES

 E. coli 

Listeria monocytogenes

Neisseria meningitides 

Haemophilus influenzae

Staphylococcus aureus 

Pneumoccocal pneuminae

Proteus organisms

Mycobacterium tuberculosis 

Streptococcus pneumonae 

Cryptoccoccus 

Mycoplasma

OTHERS

Secondary to septic lesions

Fungal (histioplasma, coccidiocides)

SLE 

Entamoeba histolytica

Leptospirosis 

Carcinoma

Sarcoidosis

MENINGOCOCCAL MENINGITIS 

The disease is caused by the gram negative diplococcus Nisseria Meningitidis that has 13 serotype groups (A,B,C,D,29E,H.I.K.L.W-135 X. Y and Z). Group A, B, C, Y and W-135 are the commonest. Group A and B are responsible for outbreaks in Africa across the meningitis belt which extents in latitude from West Africa to Sudan and Ethiopia. These organisms are known to cleave the 19A heavy chains that are of importance to the mucus membranes and produce endotoxins that are responsible for its pathogenesis. These organisms are very delicate and are sensitive to coldness and dryness.

The only reservoir of N.meningitidis is man and its sources are carriers and sporadic cases, however, the carrier rate may reach 90% during epidemics. It colonizes the upper respiratory tract which is followed by bacteraemia and subsequently reaches the meningies. Transmission occurs from person to person through droplet infection mostly in overcrowded areas. The incubation period is 1-10 days and the disease affects children as well as adults. Once meningitis is suspected, immediate steps should be taken to establish the diagnosis, hence, CSF examination and blood cultures must be undertaken soon after admission.

Clinical manifestations

The disease is usually preceded by upper respiratory tract infection associated with high fever, severe headache, neck pain, and backache and muscle pains. Nausea, vomiting and photophobia are common. Convulsions and coma may occur in severe infections at any age. On examination the patient is febrile, may be confused, will have neck stiffness, tachycardia, drowsiness and coma. Physical signs in adult patients include neck stiffness, positive Kerning's and Brudzinski's signs

 

Meningococcemia

Fulminating meningitis secondary to meningococcemia is a serious and rapidly progressing disease and affects about 10% of patients. It presents with high fever, generalized hemorrhagic or petichial rash and shock due to adrenal failure. Arthritis due to direct infection of the joints appears within 2 -3 days of onset of the disease. A reactive form of arthritis may occur 4-10 days after onset of the disease. Pericarditis, pericardial effusion, lower respiratory tract infection and eye involvement may occur. Chronic meningococcemia due to persistence of the organisms in the may lead to episodic fever, rash, arthritis and splenomegaly

COMPLICATIONS

Early complications include shock, intravascular coagulation, deafness, cerebral edema, seizures, DIC, SIADH, cranial nerve palsies, shock, myocarditis, Pericarditis, bacterial endocarditis, subdural effusion and brain abscess. Focal neurological defects such as hemiparesis, dysphasia and visual field defects, may occur which are usually reversible. Late complications include hydrocephalus, cranial nerve palsies, mental retardation, muscular hypertonia and seizures. Other complications include renal failure, peripheral gangrene, circulatory failure and death.

INVESTIGATIONS

• Lumbar Puncture is mandatory if increased intracranial pressure is excluded by fundal examination. C.S.F. findings usually allow the distinction between viral and bacterial meningitis. CSF in cases of bacterial meningitis will be under tension, turbid, contains high protein, low glucose and increased neutrophils being mostly polymorphs. In case the majority are lymphocytes with a clear CSF, then aseptic (viral) or tuberculous meningitis should be considered. Gram-stain will show Gram negative diplococcic and culture will confirm the diagnosis. It may be normal in meningococcemia, however, low fibrinogen level, and high level of fibrinogen degrading products may be detected.

• Skin scrapings in cases of fulminant meningococcemia and hemorrhagic rash

• Culture of blood and other body fluids

• Serological Test for specific antigens and polysaccharides in the CSF is done by using indirect counter-current electrophoresis.

• Latex agglutination test

• PCR

TREATMENT

General management

• isolation of the patient.

• Supportive treatment, giving IV fluid if the patient is unconscious.

• Treat the convulsions by keeping a patent airway, preventing patient form biting his tongue and anti-epileptic drugs should be given.

 

Chemotherapy

 In adults, the most suitable drug is sulpha preparations, but with widespread and  almost global resistance including the Sudan this drug is no longer preferred although it has the advantage of eradicating throat infections. 

• Crystalline Penicillin; given IV in a dose of 24 mega Units per 24 hours This is divided into 2 mega U every 2 hrs. Treatment is continued for 7-14 days (4 mega units IV 6 hourly).

• Ampicillin given IV at a dose of 1.5g/3hrs to a total of 12 grams a day. This is given for 5-10 days.

• Ampicillin i.v. in 4 divided doses plus gentamycin 5-7mg/kg/day iy in divided doses for 7-10 days

• Ampicillin and Cefotaxime 300mg/kg/day i.v. in 3 divided doses for 7-10 days

• Ampicillin and Ceftriaxone 100mg/kg/day i.v. in one or 2 divided doses for 7 – 10 days

• Chloramphenicol can be used in patients sensitive to penicillin. This is given as 4-6 grams daily by IV (750mg 1N 6hourly). The IM or oral route should be avoided.

• In cases of hypersensitivity to both penicillin and cephalosporin, a combination of vancomycin 60mg/kg/day i.y. in 4 divided doses plus Rifampicin 20 mg/kg/day i.v. in 2 divided doses is used.

• During epidemics, a single injection of 1–3gmlong acting Chloramphenicol i.m. is given.

 

Other medications

• Plasma expanders for shock or in cases with Water House Friedrichsen syndrome

• Heparin for DIC

• Dexamethasone for increased intracranial pressure

• Diazepam for convulsions

VIRAL MENINGITIS

Viral infection, is one of the common cause of meningitis but the disease is usually benign and self-limiting, unless associated with encephalitis. It is commoner in temperate climates than tropical countries where bacterial causes are more frequent. This form occurs mainly in children and young adults. Its onset is acute with headache, irritability and meningism.

 
MENINGITIS IN CHILDREN

Meningitis in children is a common and serious disease. The aetiology of bacterial meningitis in neonates includes group Listeria monocytogenes, group streptococcus, gram negative coliforms and staphylococcus aureus.

In children aged 1-5 years, the commonest organisms are H. influenza, streptococcus pneumoniae and N.meningitidis

in contradistinction to meningococcal meningitis, most organisms affecting children occur in winter months and are associated with high mortality and complications

Bacterial meningitis usually affects the meninges of the brain and spinal cord while viral meningitis tends to affect the meninges as well as the brain tissue leading to meningoencephalitis. Group B streptococci infection is of particular importance in the neonatal period. The organism is comprised of 8 sero-types (1-8). Type 3 is the commonest cause of early onset disease in neonates i.e. birth to 6 days. Late onset disease occurs between 7 - 30 days. Early onset disease may present with respiratory distress, apnea, pneumonia and evidences of meningitis or shock. Late onset disease is manifested as meningitis or bacteraemia, osteomyelitis, arthritis and cellulitis.

The classical picture of neck stiffness, positive Kerning's and Brudzinski's signs may not elicited in young children. Convulsions, bulging anterior fontanel in an infant or acute onset of squint in older children should arouse the suspicion of meningitis. In neonates specific signs and symptoms may not be found or elicited but they may present with cyanosis, apnoeic spells; unstable temperature, irritability and convulsions. Extreme restlessness, photophobia, headache, vomiting and nuchal stiffness are common in older children. Meningococcemia due to N. meningitides is often severe and life threatening condition. It is characterized by petechial or purpuric skin rash and rapid deterioration with signs of meningitis, septicaemia, D.I.C. and shock. Death may occur within a few hours of presentation due to shock and adrenal failure (Waterhouse-Friderichsen Syndrome).

Early complications include deafness, cerebral oedema, seizures, SIADH, cranial nerve palsies, shock, D.I.C., myocarditis, pericarditis, endocarditis, subdural effusion and brain abscess. Late complications include Hydrocephalous, cranial nerve palsies, paralysis, mental retardation, muscular hypertonia and seizures

Treatment

General measures

Supporting the circulation, ventilation and airway

Management of complications e.g. Convulsions, coma

In Bacterial meningitis commence antibiotic therapy immediately after confirmation by CSF examination. Treatment should not await culture results of CSF. The usual length of treatment is 10-14 days, although that caused by gram negative bacilli should be continued for approximately 3 weeks

Chemotherapy

• Combined treatment with ampicillin and cefotaxime/ ceftriaxone or gentamycin should be started as soon as the diagnosis is suspected. Dexamethasone is added to prevent the neurologic complications

• Fluid intake should be restricted to 75% of the daily maintenance dose to avoid development of brain oedema.

• Dexamethasone therapy for infants with bacterial meningitis for controlling cerebral oedema and is also useful in preventing hearing loss and other complications particularly among late presenters. It has no effect on the mortality rate.

PREVENTION

• Rifampicin 10-20mg/kg/day for 4 days is given as a prophylaxis against the disease for children in close contact while for adults Rifampicin 600mg twice daily for 2days.

• Vaccination using the bivalent vaccine composed of serotypes A and B or a tetravalent vaccine consisting of serotypes A,C, Y and W-135. Vaccination should be given to children more than two years old and adults, to be repeated every 2 years.

• Children receive vaccination for serotype C early in infancy as routine in many countries.

• Follow up for auditory testing, head circumference in children and neurological

examinations at 2 weeks, 4 weeks, 6 weeks, 6 months and one year are important for detection of complications.