NUR 265 Exam 3 Review Graded A+ Updated 2023/2024

NUR 265 Exam 3 Review MENINGITIS Patho: Inflammation of the inner meninges Usually caused by: 1. Autoimmune reaction 2. 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. 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 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 -Prevent Hypoxia and hypercapnia  vent patients CO2 should be lower than normal (around 35-38mm Hg) (see oxygenation status in ICP patho) - Suction as needed, assess ABGs Priority #2  Decrease ICP - Temperature management -Therapeutic hypothermia – rapid cooling of body may be started even if pt is afebrile. -febrile pts  cooling blankets, cool baths etc - Low PEEP. A high PEEP can increase intra-thoracic pressure  decrease in cerebral venous return = ICP - HOB elevated 30-35 degrees. **If pt becomes hypotensive when HOB is elevated, position pt so that CPP 70 mm Hg** - Keep head midline  pt must be log rolled to move or repositioned. - Avoid any flexion of head, neck or hips as flexion increases ICP - Mannitol  Osmotic diuretic, will pull water extracellularly. -Give in BOLUS not as effective if continuous -Give through a FILTERED IV or draw up using FILTERED needed -Contraindicated if pt has no urine output. -Thirst is expected, monitor I&O  expect folley. Monitor for s/s dehydration. - Lasix  often given w/ mannitol. Helps decrease production of CSF. Priority #3  Monitor and Assess Neuro status - Monitor and assess LOC. Any change in LOC is an indicator of worsening neuro status  report to MD. - GCS - Monitor for CSF leakage  any nose or ear drainage, can distinguish by yellow ring around blood on absorbent paper or linen. Other interventions: - Avoid over sedation  used short acting rx such as propofol, precede, dexdor, these have short T1/2 and can be stopped for daily neuro exam. - Safety  seizure precautions. -Surgical: - Decompressive craniectomy: Don’t lye on side of fragment removal; have to use protective head gear when out of bed. - Craniotomy (see craniotomy) LUMBAR PUNCTURE IS CONTRAINDICATED IN PTS W/ ICP TRAUMATIC BRAIN INJURY Patho: Damage to brain from external mechanical force that is not caused by neuro-degenerative or congenital conditions. -Primary Injury  Injury occurs at the time of impact -Focal: damage to specific part of brain -Diffuse: damage to multiple areas or throughout the brain -Open: Skull integrity compromised dura exposed to environmental contaminants (caused by fracture or pierce) -Closed: Skull integrity is not compromised. -Secondary Injury  Physiological, vascular, biochemical event that is an extension of primary injury: - Hemorrhage  hematoma -Epidural Hematoma: Arterial bleeding into space between dura and inner skull. (lucid then unconscious) -Subdural Hematoma: Venous bleeding into space beneath dura and above arachnoid -Chronic  2wks to several months after TBI -Acute  24hrs after TBI - Traumatic Intra-cerebral Hemorrhage  blood in brain tissue - Hydrocephalus: Abnormal increase in CSF -Brain herniation: Either one notify MD. -Uncal temporal shift  pressure on cranial nerve III  dilated/nonreactive pupils, drooping eyelids -Central herniation  downward shift of brainstem.  resp distress, pinpoint nonreactive pupils S/S: -Changes in mental status, and LOC -s/s hypovolemic shock a/r hemorrhage - s/s of ICP Management: Priority # 1: Airway -pt on vent, use humidified air and collaborate w/ RT Priority # 2: Preventing & detecting secondary brain injury - Neutralizing head and neck: - Cervical collar until definitive dx tests r/o spinal injury - Spinal board to transport  remove asap once in health care setting (ER/ICU) Once removed, strict bed rest, no elevation of HOB, (reverse trendelenburg ok) No pillow, no roll etc., Log roll to reposition or move pt. - Monitor for s/s ICP (see ICP management) - Thermal regulation: Central fever - effective management includes cool air, cool sponge baths. Tylenol other antipyretic agents not as effective - Therapeutic hypothermia  rapidly cool after primary injury Priority # 3: Neuro Assessments Other interventions: