This document provides information on meningitis, including its causes, signs and symptoms, diagnostic evaluation, and management. It begins by defining meningitis as an inflammation of the meninges caused by various infectious microorganisms or non-infectious etiologies. The major causes are categorized as infective, including bacteria (such as Neisseria meningitidis and Streptococcus pneumoniae), viruses, fungi, and parasites, or non-infective such as cancers or autoimmune disorders. Clinical presentation varies depending on age but may include headache, fever, vomiting, seizures, and neck stiffness. Diagnosis involves lumbar puncture for cerebrospinal fluid analysis along with imaging and lab tests. Management is

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MENINGITIS
Meningitis is an inflammation of the meninges caused by various
infectious microorganisms such as bacteria, viruses, fungi, or parasites.
It’s a clinical syndrome characterized by inflammation of the meninges.
The arachnoid and pia mater are also known as leptomeninges (thin
meninges). Meningococcal meningitis can lead to an exudate within the
leptomeninges along the surface of the brain.
The CNS infections is broadly divided into two; primarily involving the
meninges (meningitis) and to the parenchyma (encephalitis) .The
inflammation often extends to the cerebral cortex.
Depending on the causative organism, the child’s condition may be mild
or it may rapidly become critical. There is a specific affinity of some
pathogens infecting neonates and infants: coli forms, beta haemolytic
streptococci, pseudomonas, salmonella and listeria monocytogenes. The
complications are usually very serious.
CAUSES
The major causes are categorized into infective and non-infective causes.
Infective causes
 Bacteria
 The most highly contagious and potentially lethal form of meningitis
is caused by either of two bacteria: (Neisseria meningitidis,
Streptococcus pneumoniae) then others Listeria monocytogenes,
Escherichia coli, Haemophilus influenzae and mycobacterium
tuberculosis which causes TB is less common cause of bacterial
meningitis. (TB meningitis).
 Group B streptococci – this is commonly found along the virginal
canal and commonly contacted by premature during birth.
 Neonates - (group b streptococcus, streptococcus pneumoniae, L.
monocytogenes, E.coli).
 Infants – ( S.pneumoniae, N.meningitidis, H.Influenzae, Group B

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strep, M.TB)
 Teens and young adults (N.meningitidis, S.pneumoniae).
 Older adults (S.pneumoniae, H.Influenzae, L. monocytogenes, Group
B strep, N.meningitidis).
 Listeria monocytogenes (serotype IVb) is passed from the mother to
the fetus before birth and can result in meningitis in the baby.
 Treponema pallidum (the cause of syphilis)
 Borrelia burgdorferi (known for causing Lyme disease).
Note: Meningococcal meningitis usually affects school-aged children,
young adults, and immunosuppressed people.
Meningitis instances that lack evidence of a bacterial infection are
referred to as aseptic meningitis. The usual cause of this kind of
meningitis is a virus.
On majority of the occasions the pathogens pass from the respiratory
tract via blood stream and infect the meninges.
 Viruses
 Babies less than one month and immune supressed persons are
likely to suffer severe illness from viral meningitis.
 Non polio enteroviruses are the most common cause of viral
meningitis.
 Mumps virus, Measles virus.
 Lymphocytic Choriomeningitis (LMC) – is a rodent borne viral
infectious disease caused by LMC.
 Influenza virus, Westnile virus
 Herpes virus (Epstein Barr virus, herpes simplex virus, varicella
zoster virus).
 Viruses such as herpes simplex virus, mumps virus, and

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enteroviruses, which are common intestinal viruses, can cause viral
meningitis, a milder form of the disease.
 Viral meningitis is more common in children and in older adults.
 Fungal causes
 Cryptococcus neoformans – it’s the most common in
immunosuppressed by HIV and moves from the lungs to the brain.
 Histoplasmosis
 Coccidioidomycosis (valley fever)
 Candida albicans
 Blastomycosis
 Parasites
 Most common are :
 Angiostrongylus cantonensis (neurologic angiostrongyliasis)
 Baylisascaris procyonis (Baylisascarisis ; neural larva migrans)
 Gnathostoma spinigerum (neurognothostomiasis)
 Schistosomiasis
 Cysticercosis
 Toxoplasmosis
 Paragonimiasis
 Less common ;
 Trichinellosis
 Hydatid disease

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Non infective causes
 Cancers
 Systemic lumpus erythematosus (SLE) - a number of inflammatory
diseases, including sarcoidosis (later known as neurosarcoidosis),
connective tissue diseases like systemic lupus erythematosus, and
specific types of vasculitis (inflammatory diseases of the blood
vessel wall), such Behçet's disease.
 Certain medicines cause aseptic meningitis like NSAIDS, some
antibiotics(septrin) , IV immunoglobulins
 Dermoid and epidermoid cysts can spread irritating material into the
subarachnoid area, which can result in meningitis.
 Head injury
 Brain surgery
MODE OF TRANSIMISSION

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 Through droplets from an infected person, transmitted through air.
 Kissing
 Sneezing
 Coughing
 Faecal oral route.
 Infections like sinusitis, mastoiditis, otitis , RTI,
 Open head injuries
 Invasive pcds like lumber puncture
 Direct contact with fluids of the infected person
PATHOPYSIOLOGY
The infecting microorganisms circulate from blood and lymph to cerebral
capillaries or by direct extension from infected areas such as the middle
ear and the paranasal sinuses.
Bacteria in the subarachnoid space multiply and cause an inflammatory
reaction of the pia and arachnoid meninges.
Purulent exudate is produced, and inflammation and infection spread
quickly through the cerebrospinal fluid (CSF) that circulates around the
brain and spinal cord.
Bacteria and exudate can create vascular congestion, plugging the
arachnoid villi. This obstruction of CSF flow and decreased reabsorption
of CSF can lead to hydrocephalus, increased intracranial pressure (IICP),
brain herniation, and death
When the pathogens arrive in the cerebral circulation, they travel to the
subarachnoid space of the meninges where the inflammatory process
begins.
The brain's immune cells (astrocytes and microglia) recognize elements
of the bacterial cell membrane, and in reaction, they release enormous
quantities of cytokines, hormone-like mediators that draw in other
immune cells and drive other organs to engage in an immunological

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response.
Vasogenic cerebral edema results from a more permeable blood-brain
barrier (swelling of the brain due to fluid leakage from blood vessels). A
significant amount of white blood cells enter the CSF, escalating the
meningeal inflammation and resulting in "interstitial" edema (swelling
due to fluid between the cells).
Additionally, cerebral vasculitis causes the blood vessel walls to swell,
which reduces blood flow and causes "cytotoxic" edema, a third type of
edema.
Cerebral vasculitis, inflammation of blood vessels in the brain, may be
present, and cerebral blood flow may be decreased.
The client may develop seizures, a brain abscess, neurologic changes,
irreversible coma, and death from brain herniation.
Neurologic sequelae in survivors include damage to the cranial nerves
that facilitate vision and hearing.
The three types of cerebral edema all cause a rise in intracranial pressure;
when combined with the reduced blood pressure frequently seen in acute
infections, this makes it more difficult for blood to reach the brain, where
brain cells are starved of oxygen and suffer apoptosis (programmed cell
death).
In virulent cases, cerebral edema and inappropriate secretion of
antidiuretic hormone (ADH), which increases fluid volume, cause
increased ICP.

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Summarized pathophysiology of meningitis.
CLINICAL PRESENTATION
Meningitis in neonates and young infants.
Neck rigidity and Kernig’s sign are seldom prominent (rare).
Symptoms and signs, which arouse suspicion of bacterial meningitis are:
 Sepsis
 Bulging fontanelles (the soft spots in the baby’s skull may bulge)
 Vacant stare

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 Alternating irritability and drowsiness
 Persistent vomiting with fever
 Photophobia (aversion to light)
 Refusal to suck, Irritability and poor feeding, breastfeeding
poor muscle tone
 Poor cry with a high pitch tone
 Severe Headache that triggers persistent crying
 Shock, circulatory collapse
 Fever or hypothermia
 Tremor or convulsions
 Seizures may also develop
Severe irritation of the meninges causes:
 Opisthotonos, an extreme hyperextension of the head and arching of
the back.
 A positive Kernig’s sign (inability to extend the leg when the thigh is
flexed on the abdomen) and a positive
 Brudzinski’s sign (flexion of the neck produces flexion of the knees
and hips) are seen
 Older adults may not exhibit the typical signs and symptoms of
meningitis; rather, they may display a change in mental status, slight
to no fever, and no nuchal rigidity or headache.
 Meningococcal meningitis patients may have numerous, tiny to big
petechiae that are dispersed throughout the body and resemble rug
burns.
 The petechial become more intense and consolidate (fuse together),
taking on the appearance of purpura or ecchymoses as a result of a
secondary blood coagulation disorder brought on by
thrombocytopenia or diffuse intravascular coagulation. Viral
meningitis patients experience a non-specific maculopapular rash.
NB; Mortality rates are high in older adults with this disease partly

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because of these atypical signs and symptoms. Contributing factors to
death from meningitis are chronic illness and delays in diagnosis. Kernig
and Brudzinski’s signs, as well as nuchal rigidity, are not present in most
cases of meningitis in adults and children.
Summary of signs and symptoms
Meningococcal petechial or rash

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FEATURES ON EXAMINATION

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 In infants, the anterior fontanel will usually be full and may be
bulging.
 Neck stiffness may or may not be present (not a reliable sign in
young children).
 A purpuric rash is suggestive of meningococcal septicaemia.
 Kernig's sign: hip flexion with an extended knee causes pain in the
back and legs.
 CSF shunts, spinal and cranial abnormalities (e.g. dermal sinuses)
which may have predisposed a child to meningitis.
 Signs of encephalitis: altered conscious state, focal neurological
signs.
 Infants may have a high pitched cry
FEATURES ON HISTORY TAKING
 Infants with meningitis frequently present with non-specific
symptoms such as fever, irritability, lethargy, poor feeding, vomiting
and diarrhoea.
 Older children may complain of headache or photophobia.
 Seizures may be present
DIAGNOSITIC MANAGEMENT
 CSF samples are acquired after a lumbar puncture is done. The CSF
is cloudy if the meningitis is bacterial. Protein levels are higher, the
CSF pressure is higher, the glucose concentration is lower, and the
white blood cell (WBC) and red blood cell counts are higher.
 Culture and sensitivity studies are performed to identify the specific
causative bacteria. If meningitis is viral, the results of culture and
sensitivity studies are negative.
 Polymerase chain reaction: To analyse DNA in peripheral blood or
CSF to identify causative infectious agents.

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 Petechial skin scraping: For Gram stain analysis of bacteria
 A CT scan, blood culture, complete blood cell count, and other
laboratory tests are used to rule out other possible disorders.
 Neurological examination ( Blantyre in children and GSC in older
children)
 Sinus, skull, and chest x-ray examinations: Taken after treatment is
started to rule out sinusitis, pneumonia, and cranial osteomyelitis.
 Computed tomography (CT) scan with contrast: To rule out
hydrocephalus or mass lesions such as brain abscess and detect
exudate in CSF spaces.
 Magnetic resonance imaging (MRI): To rule out hydrocephalus or
mass lesion and detect exudate in CSF space.
 Radioimmunoassay, latex particle agglutination, or enzyme linked
immunosorbent assay: To detect microbial antigens in the CSF to
identify causative organism.
 Coagglutination tests: To detect microbial antigens in CSF and
enable identification of the causative organism. Generally
coagglutination tests have replaced counterimmunoelectrophoresis
because results are obtainable much more rapid.
MANAGEMENT
This is managed as a pediatric emergency or in the ICU

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Bacterial meningitis is a medical emergency and requires prompt
hospitalization and treatment. Deterioration may be rapid and occur in
less than 24 hours, leading to long-term neurologic damage and even
death
On Admission quick assessments are done;
 Assess and record baseline vital signs: heart rate, blood pressure,
respiratory rate, oxygen saturation, temperature, pain.
 Assess and record: level of consciousness using AVPU and/or
modified GCS or Blantyre, seizure activity.
 Assess fontanel for fullness or bulging.
 Skin assessment; Inspect skin for rash. A non-blanching,
petechial/purpuric rash is indicative of acute meningococcal disease
 Renal assessment; Assess and record hydration status.
INITIAL MANAGEMENT
 These are treated using diazepam 0.3 mg/kg (maximum 5 mg) IV,
followed by phenytoin 15-20 mg/ kg as initial treatment and
continued at a dose of 5 mg/ kg/ day PO or IV. Antiepileptic drugs
can be stopped after 3 months.
 Treat acute seizures in the setting of meningitis immediately;
 1st
line midazolam 0.15mg/kg iv/im or 0.3mg/kg buccal
 Diazepam 0.3mg/kg or 0.5mg/kg iv preferable iv not Im
 2nd
line Phenytoin loading dose 20mg/kg iv, infuse undiluted into the
vein over 20min and monitor the child. Don’t give < 1 month.
 Initial therapy recommended is a third generation cephalosporin
such as ceftriaxone or cefotaxime. A combination of ampicillin (200
mg/kg) and chloramphenicol (100 mg/ kg/24 hr) for 10-14 days is
also effective as initial empiric choice.
 If fever or meningeal signs persist after 48 hr of therapy, a lumbar
puncture should be repeated and the choice of antibiotics reviewed.
All antibiotics are administered intravenously as follows after C+S of

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CSF.
 The treatment is for 10-14 days. Except for staphylococcal
meningitis and Gram-negative infection, where it is extended to 3
weeks
 Meningococcal or pneumococcal meningitis. Penicillin 400- 500,000
units/kg/ day q 4 hr. Cefotaxime (150-200 mg/ kg/ day q 8 hr IV) or
ceftriaxone (100-150 mg/kg/day q 12 hr IV) are also effective
 H. influenzae meningitis. Ceftriaxone or cefotaxime IV is used as a
single agent. The combination of ampicillin (300 mg/kg/ day IV q 6
hr) and chloramphenicol (100 mg/kg/ day) is less preferred
 Staphylococcal meningitis. Vancomycin is the treatment of choice if
methicillin or penicillin resistance is suspected. Addition of
rifampicin to the regime increases CSF penetrance and efficacy of
these drugs.
 Listeria. Ampicillin (300 mg/kg/ day IV q 6 hr) and aminoglycoside
(gentamicin, amikacin or netilmicin) are preferred
 Gram-negative bacilli. Cefotaxime, ceftazidime or ceftriaxone, or a
combination of ampicillin and aminoglycoside may be used.
Vancomycin hydrochloride (40mg/kg) , alone or in combination with
Rifampin (10 – 20mg /kg) , may be used if resistant strains of
bacteria are identified
 Pseudomonas. A combination of ceftazidime and an
aminoglycoside is used. Ceftazidime may also be replaced with
ticarcillin. Meropenem or cefepime are effective agents, if the above
drugs fail.
 The treatment for cryptococcal meningitis is intravenous
administration of amphotericin B (0.1mg /kg IV); may be used with
or without 5-flucytosine.
 An osmotic diuretic, such as mannitol, is used to treat cerebral
edema. Osmotic diuresis with 0.5 g/kg of mannitol as a 20% solution
is administered intravenously every 4-6 hr for a maximum of 6 doses
 Dexamethasone at a dose of 0.15 mg/kg IV q 6 hr for 2-4 days is
recommended. The first dose of corticosteroids is best given shortly

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before or simultaneously with the first dose of antibiotic. This helps
to reduce the incidence of residual neurological complications, such
as sensorineural deafness, hydrocephalus and behavioral
disturbances. This is especially useful in Haemophilus meningitis.
There is no role of dexamethasone in neonatal meningitis.
 In TB meningitis dexamethasone 150 micrograms/kg 6 hourly for
2–3 weeks, tailing down the dose over a further 2–3 weeks. Do not
use steroids in: the newborn, suspected cerebral malaria, or viral
encephalitis.
 Fluid and electrolyte homeostasis. Maintenance fluids are given,
hypotonic fluids should be avoided. ADH secretion occurs in some
patients. If unconscious, child may be fed through the nasogastric
tube.
 Correct shock or dehydration initially IV later by NG tube or orally
 Avoid over hydration by careful fluid balance and in particular avoid
IV fluids with low sodium levels such as 5% dextrose. Use 0·9%
saline plus 10% glucose. Give repeated boluses of 10 mL/kg of
normal saline until hypovolaemia is corrected
 Hypotension. The children are treated with intravenous fluids and
vasopressors such as dopamine and dobutamine.
 Lumbar puncture should be done very carefully in the presence of
increased intracranial pressure
 A child with any clinical signs of raised intracranial pressure (e.g.
very bulging fontanelle, unresponsiveness to painful stimuli or
papilledema) or of over hydration (eg facial or generalized oedema)
should have fluids restricted and referred to the ICU
SPECIFIC NURSING CARE
 Provide a quiet environment, darkened or dim light room or
sunglasses, and restrict visitors as necessary. These measures
reduce noise and bright light and help prevent photophobia.
 Keep an oral airway at the bedside; insert it immediately if
respiratory distress develops. An oral airway holds the tongue

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forward so it does not occlude the pharynx.
 Administer oxygen as prescribed. Supplemental oxygen increases
the percentage of oxygen in inhaled gas higher than that in room air
 Maintain isolation precautions (Barrier nursing technique) as
necessary with bacterial meningitis
 Elevate the head of the bed 30 degrees, and avoid neck flexion and
extreme hip flexion. Head elevation lowers abdominal organs away
from the diaphragm, which facilitates inhalation of a greater volume
of air.
 Maintain a patent airway of the child and an oral hygiene is
performed.
 Support the child in a position of comfort. Keep the neck in
alignment during position changes.
 Hyper oxygenate and hyperventilate before and after airway
suctioning. Suctioning removes oxygen as well as secretions from
the respiratory passages.
 Administer tepid sponge baths. Applying moisture to the body’s
surface promotes heat loss through evaporation.
 Assess the patient for pain and discomfort using an appropriate pain
scale. Using a pain scale provides a common language for
assessing pain and relief obtained.
 Administer prescribed antipyretics. They alter the set point in the
hypothalamus like paracetamol. Analgesics (e.g., paracetamol 10 –
15mg/kg every 4 hrs, codeine 0.5 – 1mg/kg 4-6hr) are given to
relieve headache, myalgia, and other pain. Antipyretics (e.g.
paracetamol) are given for control of fever to reduce cerebral
metabolism. Mild sedatives (e.g., diphenhydramine 1-5mg/kg/dose)
are given to promote rest.
 Promote bedrest and assist with activities of daily living (ADLs) as
needed. These measures decrease movement that may cause pain.
 Place the ice bag on his head, cool clothing above the eyes, provide
a comfortable head position a little bit high, range of motion
exercises and active or passive massage neck muscles. These

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actions help diminish headache and pain around the head hence
reducing crying.
 Monitor vital signs and neurological signs
 Use caution when giving oral fluids, food, or medications to a
lethargic child. A child who is not fully alert may aspirate food, fluids,
and oral medications.
 Remove unnecessary clothing and blankets. Layers of fabric trap
body heat and prevent its convection into the environment
 Nutritional support: NG if unable to feed after 48 h. continue
expressed breastmilk or give milk feeds 15 ml/kg every 3 hours
 Apply a cooling blanket beneath the child, but avoid shivering. It
promotes heat loss by conduction. Shivering increases ICP.
 NG tube if unconscious or vomiting to protect airway. Milk (1
ml/kg/h) to prevent gastric erosions and improve bowel function.
 Urine output monitored, particularly if unconscious
 Raise and pad side rails with soft material. Modifying the
environment helps reduce the potential for injuries during a seizure
 Insert a padded tongue blade in the mouth only if the teeth are not
tightly shut. Protecting the tongue and teeth with soft material is
dangerous once a seizure begins; if the client experiences an aura
before a seizure, there may be time to protect the mouth.
 Turn unconscious child 2 hourly, keeping dry, and prevent
overheating.
 Management of constipation prevents atony of the rectum.
Lactulose 5–10 ml 2–3/day to produce between two and four soft
and acid stools per day.
 Retention of the urine is managed by gentle suprapubic pressure or
a hot water bottle
 Do not restrain child’s movements. Doing so during a seizure can
cause fractures or other musculoskeletal injuries
 Turn child to the side during a seizure. A lateral position reduces the

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potential for aspiration of saliva or stomach contents
 Administer prescribed anticonvulsants. They decrease the
excitability of neurons in the brain and reduce the potential for
additional seizures
 Bedsores are prevented by repeated change of posture in the bed
and application of methylated spirit
 Soft foam rubber mattress or air cushion is used to prevent pressure
on the bony points.
 Stay with the child if a seizure develops and call for assistance. A
child is defenseless during a seizure. The airway can become
obstructed or aspiration can occur if a child is alone during a seizure
 Suction child’s mouth and pharynx after the seizure. Suctioning
clears accumulated secretions from the airway.
 Provide oxygen during and after the seizure. Hypoxemia develops
when the client’s diaphragm contracts and breathing is irregular
throughout the seizure.
 Reorient child if older to the surroundings and provide rest after the
seizure. Commonly, children are sleepy and confused after a seizure.
 Check for injuries. A child who experiences a seizure may have oral
injuries or contusions to the skin.
 Teach the mother the purpose of giving Rifampin 10mg/kg IV or oral
for 2 days to prevent meningococcal infections and its potential side
effects to the child. Rifampin is taken as a preventive measure
against meningitis. Potential side effects such as nausea, vomiting,
diarrhoea, orange urine, headache, and dizziness can occur and
should be taken 0ne hour before meals
 Rifampicin • Neonate — 1 year: 5mg/kg bid for 2 days. • 1–12 years:
10mg/kg (maximum 600mg) bid for 2 days PO. • 12–18 years:
600mg bid for 2 days PO.
COMPLICATIONS OF MENINGITIS
 Ataxia

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 Encephalitis
 Subdural empyema
 Brain abscess
 Mental retardation
 Hearing loss
 Stroke
 Septic shock
 Obstructive hydrocephalus
 Cranial nerve paralysis
HAEMOPHILUS INFLUENZAE
Haemophilus influenzae (Bacillus influenzae) is a Gram-negative,
coccobacillary, facultatively anaerobic pathogenic bacterium belonging to
the Pasteurellaceae family.
Haemophilus influenzae type B is a bacterium that causes several life-
threatening illnesses in children younger than 5 years of age. These
infections include meningitis, epiglottitis, and septic arthritis. H.
influenzae type B conjugate vaccines (Hib) have been extremely effective

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in cutting the rates of these diseases in children.
Haemophilus influenzae type b remains a leading cause of meningitis in
children 6 mo. to 3 yr. of age in many low- and middle-income countries.
Infection usually begins in the nasopharynx and spreads locally or
through the bloodstream. Most nasopharyngeal infections are mild and
confer immunity from subsequent serious illness after the early months
of life. As the infants have transplacentally transferred antibodies during
the first 3 to 4 months of life, infections are relatively less frequent during
this period.
CAUSES
H. influenzae is a fastidious, Gram-negative, pleomorphic coccobacillus
that requires factor X (hematin) and factor V (phosphopyridine nucleotide)
for growth. Some H. influenzae isolates are surrounded by a
polysaccharide capsule and can be serotyped into 6 antigenically and
biochemically distinct types designated a, b, c, d, e, and f.
PATHOPHYSIOLOGY
The pathogenesis of disease begins with adherence to respiratory
epithelium and colonization of the nasopharynx, which is mediated by
pilus and nonpilus adherence factors. The mechanism of entry into the
intravascular compartment is unclear but appears to be influenced by
cytotoxic factors.
Once in the bloodstream, H. influenzae type b, and perhaps other
encapsulated strains, resist intravascular clearance mechanisms at least
in part via the presence of a polysaccharide capsule. In the case of H.
influenzae type b, the magnitude and duration of bacteremia influence the
likelihood of dissemination of bacteria to sites such as the meninges and
joints.
Noninvasive H. influenzae infections such as otitis media, sinusitis, and
bronchitis are usually caused by nontypable strains. These organisms
gain access to sites such as the middle ear and sinus cavities by direct
extension from the nasopharynx. Factors facilitating spread from the

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pharynx include Eustachian tube dysfunction and antecedent viral
infections of the upper respiratory tract.
TRANSMISSION
 Haemophilus influenzae bacteria live normally in the upper
respiratory (nose and throat) tract of most healthy people without
causing illness.
 Hib disease is spread mainly through person-to-person contact with
infected droplets (coughing or sneezing) or discharges from an
infected person’s nose and throat.
SIGNS AND SYMPTOMS
The onset of the illness is gradual with nasopharyngeal infection. Certain
viral infections such as those due to influenza virus act synergistically
with H. influenzae. The child has moderate fever, dyspnea, grunting
respiration and retraction of the lower intercostal spaces.
The incubation period is unknown, but is probably less than one week.
Clinical features may include initial symptoms of an URTI
 Associated fevers (low grade)
 Cough with grey to creamy sputum
 Severe headache
 Difficulty breathing with wheezing
 Stiff neck
 Convulsions or seizures
 Severe drowsiness
 Difficulty waking up
 Refusal to drink or feed
 Loss of consciousness
Conditions caused by H. influenzae and their symptoms
 Meningitis – an infection of the membrane covering the brain. Signs
include fever, stiff neck, drowsiness, irritability and refusing food.
 Epiglottitis – inflammation of the flap at the top of the windpipe
(epiglottis), which can block a child’s breathing. Signs can include
severe breathing difficulties, fever, restlessness and irritability.

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 Pneumonia – lung inflammation. Symptoms include fever, cough,
chest pains and breathing problems, such as shortness of breath.
 Septic arthritis – joint infection. Symptoms include joint pain,
swelling and reduced mobility of the joint.
 Cellulitis – infection of the tissue under the skin, usually on the face.
DIAGNOSIS
 Serotyping of H. influenzae is accomplished by slide agglutination
with type-specific antisera. Accurate serotyping is essential to
monitor progress toward elimination of type b invasive disease.
 Culture of H. influenza
 Signs and symptoms
 CSF or blood culture for H. influenzae
 Gram-stain and microscopy
 Polymerase chain reaction (PCR) assays
MANAGEMENT
 Treatment will depending on the illness
 Haemophilus infection is treated with ampicillin at a dose of 100
mg/kg/day or coamoxiclav.
 Cefotaxime (100 mg/kg/ day) or ceftriaxone (50-75 mg/kg/ day) are
recommended in seriously ill patients.
 Macrolide antibiotics (e.g., clarithromycin) may be used in patients
with a history of allergy to beta-lactam antibiotics
 Rifampin is used in some circumstances as preventive treatment for
persons who have been exposed to Hib disease.
 A child with epiglottitis may be cared for in an intensive care unit and
a breathing tube inserted to help them breathe.
 Oxygen administration
 Increased fluid intake

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 Bed rest is essential
 General care of a sick child
 Barrier nursing is maintained
NURSING CARE – SIMILAR TO MENINGITIS ABOVE
PREVENTION
 The single most important preventive measure is to maintain a high
level of immunization in the community.
 Rifampin, an antibiotic, is used in some circumstances as preventive
treatment for persons who have been exposed to Hib disease.
COMPLICATIONS
 Bacteremia
 Pericarditis
 Empyema
 Meningitis
 Polyarthritis

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INTERSEXUAL DISABILITIES
Normal sexual development
The common pathway of sexual differentiation, where a productive
human female has an XX chromosome pair, and a productive male has an
XY pair, is relevant to the development of intersex conditions.
During the first weeks of development, genetic male and female
fetuses are "anatomically indistinguishable", with primitive gonads
beginning to develop during approximately the sixth week of gestation.
At around eight weeks of gestation, the gonads of an XY embryo
differentiate into functional testes, secreting testosterone. Ovarian
differentiation, for XX embryos, does not occur until approximately week
12 of gestation. In normal female differentiation, the Mullein duct system
develops into the uterus, Fallopian tubes, and inner third of the vagina.
In males, the Müllerian duct-inhibiting hormone MIH causes this duct
system to regress. And the androgens cause the development of the
Wolffian duct system, which develops into the vas deferens, seminal
vesicles, and ejaculatory ducts.
By birth, the typical fetus has been completely "sexed “male or female,
meaning that the genetic sex (XY-male or XX-female) corresponds with
the phenol-typical sex; that is to say, genetic sex corresponds with
internal and external gonads, and external appearance of the genitals.
INTERSEX (INTERSEXUAL DISABILITIES)
Intersex is an umbrella term used to describe a wide range of natural
bodily variations.
Such variations may involve genital ambiguity, and combinations of
chromosomal genotype and sexual phenotype other than XY-male and XX
-female. In biological terms, sex may be determined by a number of
factors present at birth, including:
 The number and type of sex chromosomes

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 The type of gonads—ovaries or testicles, the sex hormones
 The internal reproductive anatomy (such as the uterus in females)
 The external genitalia.
People whose characteristics are not either all typically male or all
typically female at birth are intersex.
Challenges faced by intersex people.
 Stigmatization
 Discrimination from birth or discovery of an intersex trait.
 Infanticide
 Abandonment or un equal treatment
 The stigmatization of families
CAUSES
Masculinizing
 XX-Congenital adrenal hyperplasia (CAH)
The most common cause of sexual ambiguity is congenital adrenal
hyperplasia (CAH), an endocrine disorder in which the adrenal glands
produce abnormally high levels of virializing hormones in utero
In XX-females, this can range from partial masculinization that produces
a large clitoris, to virilization and male appearance.
Individuals born with XX chromosomes affected by 17α-hydroxylase
deficiency are born with female internal and external anatomy but at
puberty neither the adrenals nor the ovaries can produce sex-
hormones, inhibiting breast development and the growth of pubic hair .
 XX-Progestin-induced virilization
In this case, the excess androgen hormones are caused by the use of
progestin. These individuals normally have internal and external female

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anatomy, with functional ovaries and will therefore have menstruation.
They develop, however, some male secondary sex characteristics and
they frequently have unusually large clitorises. In very advanced cases,
such children have initially been identified as males.
Feminizing;
 XY-Androgen insensitivity syndrome (AIS)
These have a Y chromosome, (typically XY), but are unable to metabolize
androgens in varying degrees.
Cases with typically female appearance and genitalia are said to
have complete androgen insensitivity syndrome (CAIS). Those with CAIS
have a vagina and no uterus, cervix, or ovaries, and are infertile.
The vagina may be shorter than usual, and, in some cases, is nearly
absent. Instead of female internal reproductive organs, a person with
CAIS has undescended or partially descended testes, of which the person
may not even be aware.
In mild and partial androgen insensitivity syndrome (MAIS and PAIS), the
body is partially receptive to androgens, so there is virilization to varying
degrees.
PAIS can result in genital ambiguity , due to limited metabolization of
the androgens produced by the testes.
 XY5-alpha-reductase deficiency (5-ARD)
The condition affects individuals with a Y chromosome, making their
bodies unable to convert testosterone to Dihydrotestosterone (DHT).
DHT is necessary for the development of male genitalia in Utero, and
plays no role in female development, so its absence tends to result in
ambiguous genitalia at birth
Individuals can have testes, as well as vagina and labia, and a small penis
capable of ejaculation that looks like a clitoris at birth. Such individuals
are usually raised as girls. The lack of DHT also limits the development of
facial hair.

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 XY-Congenital adrenal hyperplasia(CAH)
In individuals with a Y chromosome (typically XY) who have congenital
adrenal hyperplasia due to 17 alpha-hydroxylase deficiency, CAH inhibits
virilization.
 XY-Persistent Müllerian duct syndrome(PMDS)
The child has XY chromosomes typical of a male. The child has a male
body and an internal uterus and fallopian tubes because his body did not
produce Müllerian inhibiting factor during fetal development.
 XY Gonadal dysgenesis
It refers to individuals (mostly XY) whose gonads don't develop properly.
Others;
 Turner syndrome (XO)
 Triple X syndrome (XXX)
 Complete gonadal dysgenesis
 Iatrogenic (caused by medical treatment, e.g. progestin
administered to pregnant mother
 Idiopathic (no discernable medical cause}
 Klinefelter syndrome (XXY)
CATEGORIES OF INTERSEX;
 46, XX intersex
 46, XY intersex
 True gonadal intersex
 Complex or undetermined intersex
46, XX INTERSEX
The person has the chromosomes of a woman, the ovaries but external

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genitals appear male. This most often is the result of a female fetus
having been exposed to excess male hormones before birth. The labia
fuse, and the clitoris enlarges to appear like a penis. In most cases, this
person has a normal uterus and fallopian tubes. Causes include; Male
hormones (such as testosterone) taken or encountered by the mother
during pregnancy, Male hormone-producing tumors in the mother:
46, XY INTERSEX
The person has the chromosomes of a man, but the external genitals are
incompletely formed, ambiguous, or clearly female. Internally, testes may
be normal, malformed, or absent. Formation of normal male external
genitals depends on the appropriate balance between male and female
hormones. it has many possible causes: gonadal dysgenesis, Problems
with testosterone formation and Deficiencies in any of these enzymes
can result in inadequate testosterone
TRUE GONADAL INTERSEX
The person must have both ovarian and testicular tissue. This may be in
the same gonad (an ovotestis), or the person might have 1 ovary and 1
testis. The person may have XX chromosomes, XY chromosomes, or both.
The external genitals may be ambiguous or may appear to be female or
male. The underlying cause is unknown, it has been linked to exposure to
common agricultural pesticides.
COMPLEX OR UNDETERMINED INTERSEX DISORDERS OF SEXUAL
DEVELOPMENT
These include 45, XO (only one X chromosome), and 47, XXY, 47, XXX -
both cases have an extra sex chromosome, either an X or a Y. These
disorders do not result in a condition where there is discrepancy between
internal and external genitalia. However, there may be problems with sex
hormone levels, overall sexual development, and altered numbers of sex
chromosomes.
SIGNS & SYMPTOMS
 Ambiguous genitalia at birth

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 Micropenis
 Clitoromegaly (an enlarged clitoris)
 Partial labial fusion
 Apparently undescended testes (which may turn out to be ovaries) in
boys
 Labial or inguinal (groin) masses (which may turn out to be testes) in
girls
 Hypospadias (the opening of the penis is somewhere other than at
the tip; in females, the urethra [urine canal] opens into the vagina)
 Delayed or absent puberty
 Unexpected changes at puberty
EXAMS AND TESTS
The following tests and exams may be done:
 Physical examinations at birth in neonates.(new born assessment)
 Chromosome analysis
 Hormone levels (for example, testosterone level)
 Endoscopic exam (to verify the absence or presence of a vagina or
cervix)
 Ultrasound or MRI to evaluate whether internal sex organs are
present (for example, a uterus)
MANAGEMENT OF INTERSEXUALITY
Medical interventions take place to address physical health concerns and
psychosocial risks.
Feminizing and Masculinizing surgeries:
 Surgical procedures depend on diagnosis, and there is often concern
as to whether surgery should be performed at all. Typically, surgery
is performed shortly after birth.
 It is necessary for individuals to be clearly identified as male or
female in order for them to function socially and develop normally.

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 Genital surgery may lead to negative consequences for sexual
functioning in later life, or feelings of freakishness and
unacceptability.
Hormone treatment:
Psychosocial support:
 Medicalization and stigmatization of intersex people result in
significant trauma and mental health concerns.
 In view of ensuring the bodily integrity and well-being of intersex
people, autonomous non-pathologising psycho-social and peer
support be available to intersex people throughout their life (as self-
required), as well as to parents and/or care providers."
 Genetic selection and terminations: Pregnancy terminations arising
from prenatal testing, as well as prenatal hormone treatment to
prevent intersex traits
CEREBRAL PALSY
Cerebral palsy (CP) is a group of permanent disorders of movement and
posture causing activity limitation, that are attributed to non-progressive
disturbances in the in the developing fetal or infant brain.
Cerebral palsy is a disorder caused by abnormal development of, or

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damage to, the motor areas of the brain, resulting in a neurologic lesion.
The chronic disorder of movement and/or posture that presents early (i.e.
before the age of 2yrs) and continues throughout life.
CAUSES
CP is caused by static injury to the developing brain
PRENATAL
o Congenital malformation
o Hypoxia
o Maternal fever
o Maternal seizures
o Maternal bleeding
o Exposure to radiation
o Environmental toxins
o Genetic abnormalities
o Metabolic disorders
o Intrauterine growth restriction
o Intrauterine infection, such as cytomegalovirus and
toxoplasmosis
o Nutritional deficits
o Preeclampsia
o Multiple births
o Prematurity
o Low birthweight
o Malformation of brain structure
o Abnormalities of blood flow to the brain
o Abdominal insults
 PERINATAL
 • Prematurity (<32 weeks)

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 • Asphyxia
 • Hypoxia
 • Abnormal fetal presentation
 • Sepsis or central nervous system infection
 • Placental complications
 • Electrolyte disturbance
 • Cerebral hemorrhage
 • Chorioamnionitis (infection of the placental tissues and amniotic
fluid)
POSTNATAL
• Kernicterus (a type of brain damage that may result from neonatal
hyperbilirubinemia)
• Asphyxia
• Head trauma (e.g., motor vehicle accidents, abuse)
• Seizures
• Toxins
• Viral or bacterial infection of the central nervous system (e.g., meningitis)
• Cerebral infarcts
• Intraventricular hemorrhage
TYPES OF CEREBRAL PALSY
The four types of cerebral palsy are classified by the nature and
distribution of neuromuscular dysfunction exhibited, which corresponds
to the injured area of the brain.
The 4 types of CP are spastic, dyskinetic/ athetoid, ataxic, and mixed.

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PATHOPYSIOLOGY
Cerebral palsy (CP) is defined as any non-progressive central motor
deficit linked to events in the prenatal, perinatal, or postnatal period that
resulted in damage to or dysfunction of the central nervous system.
Intrauterine insults (infarcts, hemorrhage, infection, and anoxia) or
structural abnormalities of the central nervous system are the cause of
most cases of CP.
Cerebral palsy is a disorder caused by abnormal development of, or
damage to, the motor areas of the brain, resulting in a neurologic lesion. It
is difficult to establish an exact location of the neurologic lesion, but it
causes a disruption in the brain's ability to control movement and posture.
The lesion itself does not change over time; thus, the disorder is
considered non-progressive since the brain injury does not progress.
However, the clinical manifestations of the lesion change as the child
grows. Some children may improve, but many either plateau in their
attainment of motor skills or demonstrate worsening of motor abilities
because it is difficult to maintain the ability to move over time.
However, the clinical manifestations of the lesion change as the child

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grows. Some children may improve, but many either plateau in their
attainment of motor skills or demonstrate worsening of motor abilities
because it is difficult to maintain the ability to move over time.
MANAGEMENT
 Identification of associated deficits is important for appropriate
physiotherapy and occupational therapy.
 Oral medications used to treat spasticity include baclofen,
dantrolene sodium, and diazepam.
 Children with athetoid cerebral palsy may be given anticholinergics
to help decrease abnormal movements.
 Parenterally administered medications such as botulin toxins and
baclofen are also used to manage spasticity.
 Botulinum toxin is injected into the spastic muscle to balance the
muscle forces across joints and to decrease spasticity. It is useful in
managing focal spasticity in which the spasticity is interfering with
function, producing pain, or contributing to a progressive deformity.
 Botulin toxin injection is performed by the physician or nurse
practitioner and can be done in the clinic or outpatient setting.
 Many children will require surgical procedures to correct deformities
related to spasticity. Multiple corrective surgeries may be required;
they usually are orthopedic or neurosurgical.
 Surgery may be used to correct contractures that are severe enough
to cause movement limitations. Common orthopedic procedures
include tendon lengthening procedures, correction of hip and
adductor muscle spasticity, and fusion of unstable joints to help
improve locomotion, correct bony deformities, decrease painful
spasticity, and maintain, restore, or stabilize a spinal deformity.
 Neurosurgical interventions may include placement of a shunt in
children who have developed hydrocephalus, or surgical
interventions to decrease spasticity. Selective dorsal root rhizotomy
is used to decrease spasticity in the lower extremities by reducing
the amount of stimulation that reaches the muscles via the nerves.
 Children with cerebral palsy may have difficulty eating and
swallowing due to poor motor control of the mouth, tongue, and

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throat. This may lead to poor nutrition and problems with growth.
The child may require a longer time to eat because of poor motor
control.
 Special diets, such as soft or puréed, may make swallowing easier.
Proper positioning during feeding is essential to facilitate
swallowing and reduce the risk of aspiration.
 Speech or occupational therapists can assist in working on
strengthening swallowing muscles as well as assisting in developing
accommodations to facilitate nutritional intake.
 Encourage child to maintain usual state of grooming and
appearance. Helps to increase child’s body image.
 Consult a dietitian to ensure adequate nutrition for children with
cerebral palsy. In children with severe swallowing problems or
malnutrition, a feeding tube such as a gastrostomy tube may be
placed.
 Ensure that child keeps scheduled appointments with occupational
therapist and physical therapist as indicated. Therapy will help
maximize ability of movement.
 Provide child with opportunities for age appropriate therapeutic play.
Provides an outlet for child to express their feelings
 Reposition child every 1 to 2 hours. Helps to prevent skin breakdown
 Ensure that child’s body stays in proper alignment, whether in bed,
chair, or wheelchair. Maintains position and helps to prevent
deformities.
 Assist child as necessary in using splints, braces, and other
appliances. Provides support in meeting mobility goals.
 Encourage child to express feelings, fears, or concerns regarding
cerebral palsy and appearance. Provides information about child’s
feelings, fears, and concerns related to their appearance.
 Clarify any misconceptions child may express regarding cerebral
palsy and appearance. Provides an opportunity for health-care team
to correct any misinformation.
 Encourage child to attend camp and participate in additional
activities with other children with cerebral palsy. Provides an
opportunity for positive experiences for the child.
 Make available activities within child’s limitations (state specific
examples for each child). Decreases anxiety and frustration while
allowing child to accomplish activities.

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