NUR 265 Exam 3 Review

NUR 265 Exam 3 Review

MENINGITIS

Patho: Inflammation of the inner meninges Usually caused by:

• Autoimmune reaction
• Adverse reaction to medication or procedure (Spinal or Brain) direct route of entry

3. Infection:

a. Bacterial: Most common Strep. Pneumoniae and Neisseria Meningitids Highly

contagious (see risks)

b. Viral: Most common herpes, Varicella (chicken pox/shingles)

c. Fungal: Usually seen in pts w/ AIDs

Risks:

• Infections of eye, ear, mouth (like a tooth abscess) and neck are at increased risk a/r close

anatomic proximity

• Pts ages 16-21 at highest risk for bacterial meningitis. Vaccinate @11-12 y/o then booster

@16.

• Pts living in high density populations (dorms, barracks, crowded living areas) have

increased risk for bacterial meningitis as well. Initial or booster vaccination is advised for these adults.

• Pts who are immunocompromised AIDs, Cancer Rx tx, or pts receiving immunosuppressant

tx for organ transplant or autoimmune disease.

S/S:

- Classical Triad: Headache, Fever, Neck pain (nuchal rigidity)

• Kerning’s sign (may or may not be present) back pain when flexing knee beyond 90 degrees

w/ pt in supine position

• Brudzinski’s sign (may or may not be present) flexing the head when pt is in supine

position results in automatic flexion of legs and/or hips

• Photo and Phonophobia
• Rhinorrhea (nasal discharge of CSF basal skull fracture) or Otorrhea (ear discharge same as

rhinorrhea)

• ICP changes in mental status/LOC and/or orientation can progress to seizures
• Systemic Inflammatory response Coagulopathy changes in vascular status if thrombi forms

DIC, gangrene

• Other usual s/s of infection may or may not be present (like tachycardia, fever, chills etc.)

Dx:

CT – if pt is >60, immunocompromised, or have s/s of ICP then CT first all other LP.LP – If viral CSF is usually clear and if bacterial usually cloudy. All other findings such as glucose, WBC and protein are usually the same. 1 / 3

Management:

• Priority = Airway Breathing and Circulation + Monitoring + documenting neuro status (q2-4h)
• Seizure precautions
• BS AB tx until LP results then specific Rx tx.
• Managing ICP Mannitol and Antiepilectic rx
• If bacterial meningitis DROPLET + STANDARD
• prophylaxis tx for close contact
• Decrease stimuli + keep HOB elevated at 30 degrees.

ENCHEPALITIS

Patho: Inflammation of the brain and surrounding meninges. Most commonly caused by viral infections such as Herpes (HSV1) and Varicella

S/S:

-Changes in mental status such as agitation, acute confusion, irritability or personality/behavioral changes -ICP -Neurological deficits vision loss, seizures, muscle weakness, and paralysis. **these changes may last for weeks and may be permanent.

• photo and phonophobia

Management:

-Priority = Airway. Turn cough and deep breathe q2h UNLESS ICP present. If on vent and s/s of ICP suction

-Monitor Neuro Status:

-Glasgow Coma Scale max score of 15, min of 3 (totally dependent) Any change >2 notify MD -Any change in neuro status such as increasingly dilated pupils or decreased responsiveness to light, new onset of bradycardia, widening pulse pressure (basically s/s of increasing ICP) or irregular resp effort notify MD -Medication viral = acyclovir 2 / 3

INCREASED INTRACRENIAL PRESSURE (ICP)

A quick A&P note: Monro-Kellie Hypothesis: the Cerebral Spinal Fluid (CSF), brain blood and brain tissue all work together to regulate Cerebral pulse pressure. If there is an increase in one structure the other two will attempt to compensate by: 1. Shunting of blood to spinal subarachnoid space, 2. Decrease in CSF production or 3.Increase in CSF absorption.A normal CPP is 60-100 mm Hg; CPP = MAP-ICP. Normal ICP is between 10-15mm Hg.Patho: ICP results in a decrease in cerebral perfusion = cerebral ischemia. To compensate for this ischemia the body increases systolic blood pressure to increase blood flow to brain, this results in additional increase in ICP swelling/edema of cerebral tissue. The edema can cause compression of brain stem affects breathing = CO2 retention CO2 retention causes arterial dilation decreased cerebral venous return to heart = increase in ICP.ICP is usually caused by head trauma, high CSF, cerebral hemorrhage/tumor, infection

inflammation = ICP Other factors that affect ICP:

-Body temperature hyperthermia increases ICP -Oxygenation Status increase in CO2 hypercapnic increased vasodilation decreased venous flow from brain = increase in ICP -Body position -Intra-abdominal/intra-thoracic pressure

S/S:

• Changes in mental status FIRST and EARLIEST sign of ICP (agitation, restlessness etc.,)

- Irregular breathing as brain stem is compressed Cheyne-Strokes: Periods of

hyperventilation followed by apnea (LATE SIGN)

- Optic and oculomotor changes:

-Papilledema (ALWAYS a sign of ICP) -double vision -unequal pupils (normal is 6 mm) report any change >2mm -fixed non responsive pupils indicates brainstem damage report immediately

- Posturing:

• Decoricate hands adducted to chest, arms flexed and feet flexed and rotated inwardly
• Decerebrate hands adducted to side, arms extended w/ protonation and feet flexed

-Cushing’s Triad LATE SIGN

• Increase in Systolic BP
• Widening pulse pressure
• Decreased HR

-Vomiting (may be projectile)

Management:

Priority #1 Maintain patent airway

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