CNS Flashcards
Infection predominantly involving the subarachnoid space (Meninges)
Meningitis
Infection diffusely involving the brain tissue
Encephalitis
Focal infection of brain tissue with no capsule formation
Cerebritis
Focal infection of brain tissue with capsule formation
Abscess
General Routes of CNS Infections: (enumerate the 5 routes)
- Hematogenous
- Direct of Local Extension
- Implantation
- Along nervous system pathways
- Bony defects
General Routes of CNS Infections: Hematogenous
__________: From primary infection in the lungs or heart valves
Arterial
General Routes of CNS Infections: Hematogenous
__________: From infected scalp veins, orbital infections via the cavernous sinus
Venous
From the mastoid, middle ear, sinuses, or infected tooth
Direct of Local Extension
As a result of mechanical trauma (gunshot wound, surgical procedures e.g. craniotomy, or lumbar puncture)
- Implantation
Usually occurs in viral infections like Rabies, Herpes Zoster, and
Poliomyelitis
Along nervous system pathways
Congenital or acquired (fractures)
Bony defects
_______ plus signs of brain parenchymal involvement which can result to altered sensorium, behavioral changes, psychosis.
Meningismus
In addition to the acute febrile illness with evidence of meningeal involvement, the patient commonly has an? (Name the 3)
- altered LOC
- depressed LOC
- focal or diffuse neurologic signs and symptoms
Common Etiologies of Viral Encephalitis
- Herpes viruses (Herpes Simplex Virus 1)
- Varicella zoster virus
- Epstein Barr virus
- Arthropod-borne viruses
- La Cross Virus
- West Nile Virus
- St. Louis encephalitis virus
Less Common Etiologies of Viral Encephalitis
- Rabies
- Eastern equine encephalitis
virus - Western equine encephalitis
virus - Powassan virus
- Cytomegalovirus
- Enterovirus
- Colorado tick fever
- Mumps
Laboratory Diagnosis of the CSF Profile in Viral ENCEPHALITIS
*CSF lymphocytic pleocytosis, normal glucose, normal or mildly elevated protein
*20% may be hemorrhagic
Laboratory Diagnosis Of Viral Encephalitis:
- CSF TEST
- MRI
- EEG
- PCR STUDIES
- VIRAL CULTURE
- SEROLOGIC STUDIES
Clinical Presentation Of V. E
- Meningismus MINUS profound alteration in consciousness, seizures and
focal deficits - Headache (frontal or retroorbital)
- Photophobia
- Pain in moving the eyes
Constitutional signs Of V.E
- Malaise
- Myalgia
- Anorexia
- Nausea and vomiting
- Abdominal pain and/or diarrhea
Treatment (V. ENCEPHALITIS)
*May be empiric or symptomatic
*May be treated as an outpatient basis
*Hospitalize if immunocompromised or with signs of encephalitis
*Acyclovir 10 mg/kg/day for 14 to 21 days
*Seizure control with anticonvulsants
Nursing Management For V.E
*Assess for neurologic function
*Initiate seizure precaution
Maintain a quiet environment
*Administer fluids as ordered
*Measure input and output
Prevention and Control Measures For V.E
*Secretion precautions
*Wearing of long-sleeved shirts and long pants *Use of mosquito repellant and netting *Mosquito and tick control
is a zoonotic, vector-borne virus, spread
primarily by Culex mosquitoes.
Japanese encephalitis virus (JEV)
_____ is one of the most
important causes of human viral encephalitis in Asia .
Japanese encephalitis virus (JEV)
Various species of birds are the
natural reservoir
are considered the main maintenance or amplifying host.
pigs
Virus that belongs to Flavi Virus common in Southeast Asia.
Japanese Encephalitis Virus
Causative agent for JEV
Japanese Encephalitis Virus
Mode of transmission For JEV
bite of infect mosquito “Culex Species” and may become infected and also biting pigs, horse and birds
Signs and Symptoms For JEV ( increased ICP)
✔ Flexor Posturing: flexion of the elbows with external rotation (specific damage to
✔ cortex) Also known as Decorticate Posturing (one E for both: flExor = decorticatE).
✔ Extensor Posturing: rigid extension of the neck, arms and legs (extensive cortex injury)
✔ also known as Decerebrate Posturing (count the letter “E”. multiple E for both: 4 in
✔ DEcErEbratE 2 E in ExtEnsor).
Signs and Symptoms For JEV
- fever
- ⬆️ ICP DAMAGES INDICATES:
1. Cerebral cortex damage
2. Headache not relieved by pain meds
3. stroke respiration
4. Apnea
5. Hemianopia
6. Hemiparesis or paralysis
7. Doll’s Eye Reflex
Signs and Symptoms For JEV ( increased ICP)
✔ Flexor Posturing: flexion of the elbows with external rotation (specific damage to
✔ cortex) Also known as Decorticate Posturing (one E for both: flExor = decorticatE).
✔ Extensor Posturing: rigid extension of the neck, arms and legs (extensive cortex injury)
✔ also known as Decerebrate Posturing
Signs and Symptoms For JEV ( increased ICP)
✔ Persistent Vegetative State: no perception of cognitive function but sleep and wake
✔ cycle, eye opening and brainstem function remains.
✔ Brain Dead: there is no electrical reading in the electroencephalogram.
Signs and Symptoms For JEV where damage to the hypothalamus =
Rising Temperature, Vomiting.
Signs and Symptoms For JEV Damage to Reticular Activating System Diencephalon=
Altered LOC: Confusion dullness, lethargy and stupor
Damage in ______=Light Coma
MIDBRAIN
Damage in ________= Deep Coma
Medulla Oblongata and Pons
Damage to ______: Pupillary Dilation, Eye Fixation in one Position, Nystagmus (rolling of the eyeball), Projectile vomiting, Loss of GABA, Seizure
Brainstem
Persistent loss of GABA and rising levels of glutamic acid=
Status Epilepticus
reveals elevated WBC, RBC, Protein and in severe conditions, hazy color due to pus.
CSF exam by lumbar puncture in JEV
is used if CSF and Lumbar puncture is not feasible to reveal the infectious organism and adjust antibiotic therapy as appropriate.
- Blood Culture
What is the purpose of oxygen therapy in preventing an increase in intracranial pressure (ICP)?
Oxygen therapy (6-10 liters per minute by nasal cannula) or intubation, depending on oxygen saturation and ABG results, helps prevent cerebral hypoxia.
What is the dosage and administration route for Mannitol used to manage increased ICP?
Mannitol 15-25% solution is administered at a dosage of 1.5 to 2 grams/kg IV infusion for not less than 30 minutes.
How is Furosemide used to manage increased ICP?
Furosemide is given at a dosage of 20 to 40 mg slow IV push for not less than 1 minute.
What is the initial dose of Dexamethasone for managing increased ICP, and what is the subsequent dosing regimen?
The initial dose is 10 mg IV, followed by 4 mg IM every 6 hours until edema is resolved.
Why are stool softeners like Lactulose or mineral oil used in patients with increased ICP?
Stool softeners prevent straining and the Valsalva reflex during defecation, which can increase ICP.
Nursing management to Prevent increase of ICP, (JEV)
-Oxygen therapy
-Osmotic Diuretic
-Loop Diuretic
-Corticosteroids
-Stool Softeners
Prevent and manage seizure (JEV)
Anti-Convulsants Hydantoin: Phenytoin 10-15 mg / kg slow IV push (not less than 1 minute)
Raise LOC and provide adequate neural stimulation (JEV)
Piracetam 1.6 to 9.6 grams tablet pre orem per day
Manage Headache due to Increase in ICP
NSAID: Acetaminophen 500 mg tablet per orem every 6 hours
* Put the patient in semi fowler’s position to promote venous
return.
* Provide oxygen to prevent rebound vasodilation due to
hypoxia.
* Promote normal bowel elevation to prevent straining during
defecation.
JEV Infection Control: Limit the Spread of Infection
- Assess for Infection Risk
- Assess for possible Infectious case
- Practice Standard Precaution at all times for nurses and visitors
- No VISITOR on the first 72 hours upon antibiotic treatment
- After 72 hours of antibiotic therapy, patient is no longer
infectious. Visit may be allowed as - appropriate observing standard precaution.
- Practice Hand washing
- Observe Principles of Asepsis
- Observed Disinfection and Antiseptic Procedures
Prevention, Treatment and Nursing Management
(Vector Control: Mosquitoes)
- Clean Surroundings: Remove vegetation.
-Bioremediation: Use natural species (plants, fish, bacteria) to control mosquitoes.
-Repelling Plants: Grow neem, citronella, eucalyptus, and others.
-Larvivorous Fish: Use tilapia in water bodies; avoid chemicals.
-Protect Dragonflies: Avoid chemicals in their habitats.
-Drain Water: Remove stagnant water near homes.
A type of viral encephalitis caused by Rhabdo Virus with unique manifestations of violent and impulsive behavior associated to viral damaging effects to the brain.
Rabies
Rabies Mode of Transmission?
is by the bite of Bats and hunting of bats by domestic animals like cats which may infect dogs and other pets.
RABIES INCUBATION PD
10 days
True or False:
All infected animal except bats die of rabies virus
True
As Rabies V. it travels to the brain, it damages the neuron it passes through leading to:
numbness and tingling sensation on the site of injury.
- The inflammatory reaction releases inflammatory chemicals and pyrogenic hormones that produces the classical manifestations of
fever, myalgia, body malaise and anorexia.
Encephalitis results in increasing ICP Causing:
head ache, nausea and vomiting.
Damage to CN number 9 (glossopharyngeal nerve) results in
painful throat muscles spasm.
Rabies Pathognomonic sign
Hydrophobia and aerophobia
Rabies Histopathology by Brain Biopsy:
Presence of Negri Bodies (viral organisms in neurons) is a pathognomonic sign of rabies, used for autopsy in suspected rabies cases.
Serology (Antibody Tests):
Identifies elevated immunoglobulin levels when symptoms appear.
Rabies Pet Observation:
Confine and observe the biting animal for 10 days. If it dies, perform a brain tissue biopsy.
Keypoints in Prevention, Treatment and
Nursing Management
=Fatality: Rabies is almost always fatal once symptoms appear.
=Rare Recoveries: Possible with timely vaccination and immunoglobulin.
=Patient Dignity: Preserve dignity and comfort until the end.
=Nursing Care: Prevent infection, minimize suffering.
=Family Support: Comfort and support the family.
=Health Education: Provide moral and emotional support.
Botulism Causative agent
Clostridium botulinum
Found in soil and occasionally in animal feces Soil and water samples
Clostridium botulinum
Associated with consumption of home-canned/vacuum-packed foods and preserved spiced, smoked fish
Clostridium botulinum
Clostridium botulinum Diseases
Infant botulism (honey – flaccid paralysis), wound botulism, food-borne botulism
Clostridium botulinum
Morphology
*Gram-positive bacilli *Spore-forming
*Strict anaerobic
Clostridium botulinum
Antigenic Structures/Virulence Factors
*Spore formation
*Binary toxin (Disrupts vascular permeability)
Botulinum toxin Has how many types?
Seven types: A, B, C, D, E, F, G
*A, B, E, and F – cause human illness with a lethal dose of 1 to 2 microgram
* A, B – associated with a variety of food/canned food
* E – fish products
* E, F – infant botulism
Consists of neurotoxin and non-toxic subunits
Botulinum toxin
Block neurotransmission of peripheral cholinergic synapses by preventing release of neurotransmitter acetylcholine
Botulinum toxin
Results to lack of muscle contraction and paralysis
Botulinum toxic
Botulinum Toxin Activities
*Blocks the release of acetylcholine
*Prevents the production of signal produced when acetylcholine binds to the post-synaptic receptor
Infant ingests spores of C. botulinum
Infant Botulism
floppy baby =
Flaccid paralysis
Botulsim Lab Diagnosis
//Specimen
* Contaminated food
* Blood (Serum)
* Feces (for infant botulism)
//Cultural/Growth Characteristics * Blood-enriched anaerobic media
* (+) lipase production
* (+) hydrolyze gelatin
* (+) ferment glucose
* (+) digest milk proteins
