In any case suspected of meningitis based on the clinical signs, a lumbar puncture is essential. Sometimes parents are afraid of the procedure and fear it is harmful to the child. It should be emphasized to them that treatment is highly dependent on CSF results. A lumbar puncture may be postponed or withheld in the following situations: presence of significant cardiac or respiratory distress and shock, sign of increased intracranial pressure, infection in the area that the spinal needle will traverse to obtain CSF, and hematologic problems such as thrombocytopenia and coagulation defects.
The following are the CSF findings that will make you confirm the diagnosis of meningitis: the CSF pressure may be elevated, there is leukocytosis with predominance of PMNs, the glucose is low, the CSF blood to glucose ratio is <0.40, and the protein is elevated. The stained smears of CSF may be (+) for bacteria. Culture of CSF should be done whenever it is available, but a negative culture does not rule out meningitis.
Consciousness is controlled by RAS and its integrated components.
RAS begins in the medulla, located in the midbrain, which connects to hypothalamus and thalamus, this in turn connect with the limbic system via hypothalamus. Feedback systems also connect at the brain stem level.
Reticular formation produces wakefulness
RAS produces awareness of self and the environment.
Diffuse cortical connections allow maximum integrations of all conscious-related activities.
Brain stem houses the rhythmic breathing, its function is loss as consciousness decreases, the lower brain stem begins to regulates breathing by responding to changes primarily in the carbon dioxide levels and acid-base and oxygen levels = result to irregular breathing pattern and depth.
Compression on the cranial nerves leads to cranial nerve deficits.
Epilepsy is a seizure disorder resulting from sudden bursts of electrical energy in the brain. These electrical discharges produce seizures which vary from one person to another in frequency and form. Sometimes the electrical signal only reaches part of the brain where a part of the body, like an arm or a leg may move on its own. If the signal goes through all of the brain, the person may shake all over, fall and lose consciousness.
It is not a disease, psychological disorder or contagious .
Epilepsia partialis continua is a variant it involve an hour, day or even week-long jerking. It is a consequence of vascular disease, tumor or encephalitis and drug resistant.
Complex Partial Status Epilepticus CPSE and absence status epilepticus are rare forms of the condition which are marked by nonconvulsive seizures.
The seizure is confined to a small area of the brain, normally the temporal lobe. But the latter, status epilepticus, is marked by a generalised seizure affecting the whole brain, and an EEG is needed to differentiate between the two conditions.
This results in episodes characterized by a long-lasting stupor, staring and unresponsiveness.
Like thorough oral hygiene after each meal, gum massage, daily flossing, and regular dental care.
The patient is also instructed to inform all health care providers of the medication being taken because of the possibility of drug interactions. An individualized comprehensive teaching plan is needed to assist the patient and family to adjust to this chronic disorder.
Wallet Sized Card Autonomic Dysreflexia (AD) AD is a potentially life threatening complication of spinal cord injury above T7 level. It is caused by an unopposed sympathetic nervous system response to noxious stimulation below the level of the injury. Blood pressure may rise dangerously. The most typical cause of AD is distended bladder. Other causes could be distended bowel, pressure sore, in-grown toenail, etc.
Autonomic Dysreflexia Management
Raise the head of the bed by 90 or sit person upright.
Monitor BP every 5 minutes.
Check for sources of AD: drain bladder first, consider using topical anesthetic jelly for lubrication of catheter.
Check rectum for stool. Apply anesthetic jelly to rectal wall before manipulation. Use digital stimulation to promote reflex defecation.
Check for other sources of AD such as ulcer, fracture, in-grown toenail, etc.
If SBP is above 150 mmHg after above checks, give captopril 25 mg sublingually x1. Advise patient to avoid swallowing until tablet dissolved.
If SBP still greater than 150 mmHG at 30 minutes post-captropril then give immediate release nifedipine 5 mg capsule via the bite and wallow method.
****ONLY IN A HOSPITAL SETTING****
Repeat nifedipine 5 mg bite and swallow 15 minutes after the initial nifedipine dose if SBP still greater than 150 mmHg.
Consider intravenous agents for hypertension if hypertension is refractory.
Symptoms may include:
elevated blood pressure
Treatment is to remove the cause. Once the cause is removed the BP will return to normal immediately.
Advice close contacts of the patient with meningitis that prophylactic treatment may be indicated; they should check with their health care providers or the local public health department.
To help prevent the development of meningitis, teach patients with chronic sinusitis or other chronic infections the importance of proper medical treatment.
Encourage the patient to follow medication regimen as directed to fully eradicate the infectious agent.
Encourage follow-up and prompt attention to infections in future.
Inform patients who have children about the importance of vaccination with measles, mumps, rubella vaccine, H. influenzae type B vaccine, and pneumococcal vaccine as a preventive measure. Vaccination is recommended for children younger than school age.
Occurs when a virus invades and replicates within the brain
Brain inflammation that develops in combination with other viral illness or ff admin of vaccines such as measles, mumps and rubella –due to hypersensitivity reaction that leads to demyelination of nerves
Clinical Manifestations of Encephalitis: Onset Sudden or Gradual
Clinical Manifestations of Severe Encephalitis
RABIES 2 kinds: Etiology: A.K.A.: Vital facts: Hydrophobia, Lyssa Rabies virus (A rhabdovirus of the genus lyssavirus) Urban/ Canine rabies and Sylvatic rabies Urban/ Canine Rabies: Transmitted by dogs Sylvatic Rabies: Transmitted by bats Didn’t you know? The Philippines has one of the highest prevalence rates of rabies in the world
RABIES Is man to man transmission possible? Can it be introduced thru breaks in the skin? MOT: Vital facts: Bite from a rabid animal Very rare Yes How about organ transplants? Yes. (Corneal transplant) Incubation period: R-a-b-i-e-s (6 weeks/ 2-8 weeks) Communicability period: 3 days before onset until the whole disease duration
RABIES CNS Sx (Site of bite): CNS Sx (early): Hydrophobia: Signs and symptoms: Spasms of muscles of deglutition Headache, apprehension, fever Sensory changes CNS Sx (late): Paralysis, delirium, convulsions Usual lifespan of victim w/o medical intervention: 2-6 days Usual cause of death: Respiratory paralysis
RABIES If it dies or shows signs of rabies, behead it and bring to doctor Submit for immunization while waiting for results If dog is not available: submit for immunization Observe the dog for 14 days, do not kill it yet. Patient may be given antibiotics/ tetanus immune globulin Wash the wound with antiseptics/ soap & water Management: Sequence of actions
RABIES Responsible pet ownership: Immunization of pets after 3 months of age and yearly thereafter Never allow pets to roam the streets Take good care of pets: bathe, feed, clean sleeping quarters Your pet’s action is your responsibility
Manifestations of tetanus are caused by an exotoxin (tetanospasmin).
The toxin may enter the CNS along the peripheral motor nerves or may be bloodborne to nervous tissue.
Tetanospasmin binds irreversibly to the ganglioside membranes of nerve synapses, blocking release of inhibitory transmitter from nerve terminals and thereby causing a generalized tonic spasticity, usually with superimposed intermittent tonic seizures.
Disinhibition of autonomic neurons and loss of control of adrenal catecholamine release cause autonomic instability and a hypersympathetic state. Once bound, the toxin cannot be neutralized.
forms a neck with a dome cause increased strain in the more elastic portions of the vessel wall. intimal layer becomes inelastic earliest stage in the formation of aneurysms local thickening of the intimal layer ( ‘intimal pads') in the arterial wall Arterial internal elastic lamina disappears at the base of the neck. Media thins Connective tissues replaces smooth muscle cells Tear allows bleeding – 7mm in diameter Vasospasm 4-14 days after hemorrhage Ischemia & infarction DEATH PATHOPHYSIOLOGY
geographic location – North America, other climate area
Race – White people
BLOOD BRAIN BARRIER BREAKDOWN N = no passage of antibodies Leak = immune cells infiltrate (Helper T cells) Interleukin (protein) differentiate naïve T cells to inflammatory T cells. OVER PRODUCTION - interleukin Increased inflammation T cells attack CNS Triggers inflammatory process Stimulate other immune cells, cytokines and antibodies Demyelination Repair process = remyelination Symptoms tend to decrease/disappear Plaques of sclerotic tissues appear
Inflammation destroys myelin leading to axon dysfunction Myelin sheaths of nerves destroyed in patches called plaque ( white matter of spinal cord, brain, optic ) Demyelination slows and distorts nerve conduction resulting in absence of impulse transmission Recurrent demyelination and plaque formation result in scarring of glia and degeneration of axons Disease follows different courses, most common is the relapsing-remitting type Stressors trigger MS: febrile states, pregnancy, physical exertion and fatigue
A sporadic, but progressive weakness and abnormal fatigability of striated muscles which are exacerbated by exercise and repetitive movements
Chronic autoimmune neuromuscular disorder involving a fluctuating weakness of the skeletal muscles in which the antibodies attack the number and effectiveness of acetylcholine at the neuromuscular junction.
Form of dementia characterized by progressive, irreversible deterioration of general intellectual functioning
Begins with memory loss, initially subtle until progresses to being more noticeable; course includes deteriorating cognition and judgment with eventual physical decline and total inability to perform ADL
Result to acceleration, deceleration/compression Microscopic bleeding primarily in gray matter 1 st hr, presence of edema, spreads along segments of the spinal cord Arachidonic acid and its metabolites (prostaglandin, thromboxanes, leukotrienes) causes the edema Edema peaks 2-3 days, subside within 7 days after injury Temporary loss of sensation & function Fragmentation of the axonal covering and loss of myelin Phagocytic cells injure the surviving axon
Fragmentation of the axonal covering and loss of myelin Chemotactic & inflammatory mediators causes tissue necrosis Macrophages engulf the spinal cord tissue causing central cavity = post traumatic syringomyelia develop 9 days after the injury Cord injury leads to rapid loss of axonal conduction Due to increase in extracellular potassium and influx of calcium into the cell. Free radicals are produced Free radicals usually controlled by antioxidant enzyme but too much of it, causes tissue damage