Exam 4 Study Guide PDF

A3 Exam 4 Study Guide (Ch. 53,54,61,62,65,34,42) Neuro and Endocrine Disorders Acute Intracranial Problems -​ Our intracranial space is comprised primarily of 3 things: -​ Cerebral spinal fluid (CSF): 10% -​ Intravascular blood: 12% -​ Brain tissue: 78%...

A3 Exam 4 Study Guide (Ch. 53,54,61,62,65,34,42) Neuro and Endocrine Disorders Acute Intracranial Problems -​ Our intracranial space is comprised primarily of 3 things: -​ Cerebral spinal fluid (CSF): 10% -​ Intravascular blood: 12% -​ Brain tissue: 78% We’re all under (Intracranial) Pressure -​ Normal ICP = 5-15 mmHg -​ Sustained ICP >20 mmHg requires medical treatment -​ Factors that affect ICP: a.​ Arterial/venous pressure b.​ Intra-Abdominal/intrathoracic pressure c.​ Posture d.​ Temperature e.​ Blood gases (CO2 levels especially) -​ How does our body compensate? a.​ Changes in CSF levels b.​ Intracranial blood flow volume c.​ Brain tissue volume Cerebral Blood Flow -​ Proper cerebral blood flow needs to be maintained: a.​ Cerebral brain tissue needs constant supply of oxygen and glucose -​ How do we calculate cerebral perfusion pressure (CPP)? a.​ CPP = MAP - ICP b.​ MAP = SBP + 2(DBP)/3 -​ If the patient’s BP is 120/80 and ICP is 10, what is the CPP? =83 When the pressure keeps adding up: Increased ICP -​ Causes: a.​ Mass (hematoma, contusion, abscess, tumor) b.​ Cerebral edema (r/t tumor, hydrocephalus, brain inflammation, head injury) -​ Results of increased ICP: a.​ Hypercapnia b.​ Cerebral acidosis c.​ Impaired autoregulation d.​ Systemic hypertension e.​ Spread of cerebral edema -​ Prolonged elevated ICP: a.​ Brainstem compression b.​ Herniation Stages of Increased ICP -​ Stage 1 a.​ Total compensation: body will try to change balance of blood flow, CSF, and brain tissue -​ Stage 2 a.​ ↓ compensation: Compensation will decrease, allowing for pressure to rise -​ Stage 3 a.​ Compensation failure: Manifestations of increased ICP (cushing’s triad) -​ Stage 4 a.​ Herniation, leading to potential death Neuro Disorders: Cerebral Edema Types of Cerebral Edema: Vasogenic, Cytotoxic, Interstitial Vasogenic Cerebral Edema -​ Most common type of cerebral edema -​ Occurs due to a disruption in blood-brain barrier. a.​ Allows large molecules (proteins, blood products) to enter surrounding brain tissue b.​ Introduces tissue to toxins within the blood → fluid shift from intravascular to extravascular -​ Symptoms: a.​ Headache b.​ Decrease in consciousness c.​ Coma d.​ Focal deficits (specific to affected area of brain) Cytotoxic Cerebral Edema -​ Results from disruption of the integrity of cell membranes a.​ Is NOT from a disruption of the blood-brain barrier b.​ Brain tissue injury or destructive lesions cause cerebral hypoxia or cerebral anoxia → syndrome of inappropriate antidiuretic hormone (SIADH) c.​ Fluid shifts from extracellular space to intracellular space -​ Leads to severe swelling and loss of cellular function. Interstitial Cerebral Edema -​ Commonly results from hydrocephalus. a.​ Build up of fluid within the brain b.​ Causes ventricular enlargement -​ Can be due to: a.​ Excess CSF production b.​ Obstruction of flow c.​ Inability to reabsorb CSF -​ Ventriculostomy or Ventriculoperitoneal (VP) shunt often needed to drain fluid Manifestations of Cerebral Edema -​ Changes in level of consciousness, potentially leading to coma -​ VS changes r/t thalamus, hypothalamus, pons, and medulla a.​ Leads to Cushing’s Triad b.​ MEDICAL EMERGENCY -​ Vomiting without nausea -​ Severe headache -​ Ocular changes (ipsilateral pupil dilation, lack of pupillary response to light, inability to move eye upward and inward, ptosis of eyelid) -​ Decrease in motor function a.​ Decorticate = “to the core” b.​ Decerebrate = hyperextension Complications of Cerebral Edema and Increased ICP -​ Inadequate cerebral perfusion and cerebral herniation a.​ Tentoral herniation = herniation downward toward brain stem b.​ Uncal herniation = herniation downward toward cerebellum c.​ Cingulate herniation = herniation laterally across hemispheres -​ Herniation → further decrease in tissue perfusion and tissue death Diagnostics for Increased ICP -​ CT/MRI: identify structures/conditions causing increased ICP. -​ EEG: measure electrical activity within brain tissue -​ Cerebral angiography: map cerebral blood flow -​ ICP measurement: monitor ICP levels using ventriculostomy or fiberoptic catheter -​ Transcranial doppler studies: doppler measurement of cerebral blood flow -​ Lumbar punctures are contraindicated → increased risk for herniation! Drug Therapy to Decrease ICP -​ Mannitol/Osmotic Diuretic -​ 3% Hypertonic Saline -​ Corticosteroid (Dexamethasone) -​ Antiseizure (Phenytoin/Dilantin) Nursing Management -​ Airway management -​ Monitor ABGs a.​ Prevent hypoxia & Hypercapnia -​ Use caution with suctioning/coughing a.​ Frequent suctioning/coughing inc’s ICP -​ NG insertion to prevent abd distention and allow proper nutrition -​ Sedation (propofol, precedex) & paralytics (vecuronium) may be needed a.​ Avoid benzos d/t longer half-life -​ Maintain temp 96.8 - 98.6F a.​ Do not let patient shiver -​ Provide calm/quiet environment -​ Monitor strict I/Os and electrolytes a.​ Especially Na+ levels with 3% saline usage -​ Maintain HOB 30° or higher -​ Keep neck midline and avoid extreme neck flexion -​ Maintain safety (seizure precautions) Neuro Disorders: Head Injuries Types of Head Injuries: Scalp Laceration, Skull Fractures, Head Trauma Scalp Laceration & Skull Fracture -​ Scalp Laceration: a.​ External head trauma b.​ Blood vessels in scalp have poor constrictive abilities → profuse bleeding c.​ Stitches/staples often needed -​ Complications: a.​ Blood loss b.​ Infection -​ Skull Fracture: a.​ May be open or closed (with laceration or not) b.​ May be described in many alternative ways: -​ Linear = simple straight line break in the bone that does not move out of place -​ Depressed = part of the skull is moved in toward the brain -​ Simple = break in the skull that does not damage the external skin -​ Compound = break in the skull with an open wound/laceration present -​ Comminuted = skull is shattered in 3 or more pieces Manifestations of Skull Fractures Location Signs and Symptoms Basilar CSF otorrhea, bulging tympanic membrane, battle’s sign, tinnitus, hearing loss, rhinorrhea, vertigo Frontal Frontal sinus exposure, CSF rhinorrhea, pneumocranium Orbital Periorbital bruising (racoon’s eyes), optic nerve injury Parietal Hearing loss, otorrhea, bulging tympanic membrane, loss of taste, Battle’s sign Posterior Fossa Occipital bruising, cortical blindness, visual field deficits, ataxia Temporal Boggy/bulging temporal muscle, Battle’s sign, otorrhea, epidural hematoma ACHOO! Is it CSF… or something else? -​ Allow leaking fluid to fall onto absorbent material (gauze, etc.) -​ Observe drainage for a few minutes. -​ Take note of drainage appearance: a.​ If the blood coagulates and a yellow-tinted ring appears around, CSF fluid is present Head Trauma: Concussions and Contusions -​ Head trauma is classified as: a.​ Diffuse: generalized damage (i.e. concussion) b.​ Focal: localized (i.e. contusion) -​ Concussion: sudden mechanical head injury with disruption of neural activity and change in LOC. a.​ Typically resolves spontaneously and is considered benign -​ Contusion: bruising of the brain tissue within a focal area. a.​ Coup-contrecoup injury is a big concern b.​ Could also have areas of bleeding, infarction, necrosis, and edema So, like, on a scale of 1-15, how bad is it, doc? Neuro Disorders: Hematomas Hematomas -​ Epidural: Bleeding between dura and inner surface of skull a.​ MEDICAL SURGICAL EMERGENCY b.​ Usually arterial tear r/t linear fracture c.​ SSX: initial period of unconsciousness, followed by brief lucid interval, then decrease in LOC, nausea/vomiting, headache, focal deficits -​ Subdural: Bleeding between dura mater and arachnoid layer a.​ Usually venous bleeding, not a medical emergency b.​ SSX: decreasing LOC and headache -​ Subarachnoid: intracranial bleeding into the cerebrospinal fluid (CSF) filled space a.​ Usually caused by rupture of cerebral aneurysm -​ Cerebral aneurysms = “silent killer” -​ Usually no SSX until rupture occurs b.​ SSX: focal deficits, nausea, vomiting, seizures, stiff neck -​ May or may not have loss of consciousness Neuro Disorders: Stroke/TIA Stroke/TIA -​ Stroke occurs when there is: a.​ Ischemia (inadequate blood flow) b.​ Hemorrhage (bleeding) -​ TIA (transient ischemic attack) = transient episode of neurologic dysfunction r/t brain/spinal cord ischemia without brain infarction a.​ Typically resolves in less than 1 hour b.​ Still considered a medical emergency as it could potentially lead to a stroke -​ Ischemic: a.​ Thrombotic: injury to blood vessel leading to blood clot formation b.​ Embolic: embolus (plaque or blood clot) lodges in cerebral artery -​ Hemorrhagic: a.​ Bleeding into the brain tissue itself b.​ Subarachnoid hemorrhage is a common type of hemorrhagic stroke -​ Manifestations: a.​ Hemiplegia, loss of strength b.​ Gait impairment c.​ Swallowing/speech impairment d.​ Dysarthria, Dysphagia, Aphasia e.​ Emotional lability f.​ Impaired judgment g.​ Urinary and bowel incontinence -​ Left-sided strokes: a.​ More communication/speech impairments -​ Right-sided strokes: a.​ More gait/coordination/perceptual orientation impairments Risk Factors for Stroke/TIA -​ Modifiable: a.​ Hypertension f.​ Sleep apnea b.​ Heart disease g.​ Poor diet c.​ Diabetes h.​ Sedentary lifestyle d.​ Smoking i.​ Drug/alcohol use e.​ Obesity -​ Non-modifiable: a.​ Age -​ Risk doubles each decade after 55 years b.​ Gender -​ More common in men -​ More women die from stroke than men c.​ Ethnicity/race -​ Higher risk and mortality in the black community d.​ Family history/heredity Diagnostics & Interventions -​ Rapid diagnosis of a stroke is KEY! a.​ Door-to-needle time is 90 mmHg -​ May need to support with fluids and vasopressors d.​ Assess for other injuries and control bleeding e.​ Obtain appropriate imaging -​ Ongoing monitoring: a.​ Continue to monitor VS and hemodynamics b.​ Monitor LOC and motor/sensory function c.​ Monitor cardiac rhythm d.​ Monitor urine output e.​ Maintain normal temperature f.​ Observe for signs of impending respiratory arrest if not already intubated -​ Other treatments: a.​ Potential immobilization with traction b.​ Administration of steroids c.​ Administration of DVT prophylaxis (i.e. Lovenox) Emotional Support for SCI Patient Behavior Nursing Intervention Shock and Denial: struggle for survival, complete dependence, excessive Provide honest information, use simple diagrams to explain injury, sleep, withdrawal, unrealistic expectations encourage patient to begin road to recovery, establish agreement to use and improve all current abilities while not denying the possibility of future improvement Anger: refusal to discuss paralysis, ↓ self-esteem, manipulation, hostile and Coordinate care and encourage self-care when possible, support family abusive language members, use humor when appropriate, allow patient to express emotions, do not allow fixation on injury Depression: sadness, pessimism, anorexia, nightmares, insomnia, agitation, Encourage family involvement, plan graded steps in rehabilitation and give suicidal preoccupation, refusal to self-care success with minimal opportunity for frustration, give cheerful assistance with ADLs, avoid sympathy, use firm kindness Adjustment and Acceptance: planning for future, actively taking part in Remember patients’ individual personalities, balance support systems to therapy, finding personal meaning in experience and growth encourage independence, set goals with patient input, emphasize potential Endocrine Disorders: DI vs. SIADH Diabetes Insipidus (DI) -​ Pituitary gland produces and releases insufficient amount of antidiuretic hormone (ADH) → kidneys create too much urine -​ Causes: neuro surgery, tumor, head injury, infection -​ Manifestations: -​ Increased urinary output (polyuria) -​ Increased thirst (polydipsia) -​ Hypernatremia and dehydration -​ Low specific gravity ( 38℃ or 90 beats/min -​ RR: >20 breaths/min or PaCO2 12,000 or 10% bands -​ Sepsis -​ SIRS + infection -​ Severe sepsis -​ Sepsis + End-Stage Organ Damage -​ Septic Shock -​ Severe sepsis and hypotension Early Identification Scores: Vasopressors and Sepsis -​ First line of defense: norepinephrine -​ ** Target MAP >65 mmHg (consider arterial line BP monitoring) -​ If central line access not available, start peripherally -​ ** The risk of hypotension injury far outweighs risk of extravasation -​ If MAP is still inadequate, add vasopressin -​ ** Special consideration in patients with heart failure -​ If cardiac compromise or persistent hypotension, add dobutamine or epinephrine Types of Shock -​ Cold Shocks -​ Cardiogenic -​ Low CO due to heart failure or myocardial injury -​ Results in ssx of low perfusion (cold/clammy) -​ Compensation: vasoconstriction to shunt blood flow -​ ↑↑ SVR, ↑↑ PAWP (pulmonary edema) -​ Treatment: ↑↑ contractility and treat underlying cause -​ Hypovolemic -​ Intravascular volume is decreased r/t dehydration or fluid loss -​ Results in decreased venous return and ↓↓ CO/perfusion -​ Compensation: vasoconstriction to shunt blood flow -​ ↑↑ SVR -​ Treatment: replace fluid loss and treat underlying cause -​ Obstructive -​ An obstruction prevents blood from leaving the heart -​ Results in ↑↑ PAWP but ↓↓ CO -​ Compensation: vasoconstriction to shunt blood flow -​ ↑↑ SVR -​ Treatment: treat the underlying cause -​ Warm Shocks -​ Septic -​ Results from sepsis and infection -​ Increases release of cytokines and cascade activation -​ Creates vasodilation and “leaky” vessels -​ ↓↓ SVR and ↑↑ speed of blood flow = warm skin -​ Treatment: IV fluids and broad-spectrum antibiotics -​ Anaphylactic -​ Extreme reaction to exposure to allergen (food, bees, etc) -​ Results in massive histamine release → vasodilation & ↓↓ SVR -​ Histamine release also → bronchi constriction & wheezing -​ Can be life-threatening if airway closes -​ Treatment: intramuscular epinephrine -​ Neurogenic -​ Injury to CNS → loss of sympathetic tone -​ Results in everything slowing down (↓↓ BP and ↓↓HR) -​ ↓↓ SVR = vasodilation -​ Special to neurogenic only = ↓↓ CO -​ Treatment: treat underlying cause and support hemodynamics Multiorgan Dysfunction Syndrome (MODS) -​ What is it? -​ Failure of two or more organ systems in an acutely ill patient. -​ Homeostasis cannot be achieved without intervention. -​ Pathophysiology -​ Inflammatory response (SIRS) → release of mediators → endothelial damage and hypermetabolism -​ Increased vascular permeability → increase in interstitial fluid -​ WBCs increase digestion → clotting cascade is activated -​ End Result -​ ↓↓ BP, ↓↓ perfusion, shunted blood flow = COMPROMISED ORGAN PERFUSION Disseminated Intravascular Coagulation (DIC) 1.​ Activation of the clotting cascade 2.​ ↑↑ aggregation of platelets and clotting factors 3.​ ↑↑ consumption of clotting factors and release of fibrin split products (FSPs) [anticoagulant effect] 4.​ Profuse bleeding and ↑↑ thrombin release 5.​ Accelerated clotting and thrombus formation -​ Diagnosis -​ Coagulation studies (PT, PTT, PLT, Fibrinogen) -​ Fibrin Split Products (FSPs) -​ D-Dimer -​ Plasminogen -​ Treatment -​ Determine underlying cause -​ Most common: sepsis treated with antibiotics and fluids) -​ If hemorrhage is the main problem: blood products (esp. Platelets, cryoprecipitate, and plasma) -​ If thrombosis is the main problem: anticoagulation (heparin) -​ Bottom Line -​ The underlying problem must be identified and corrected, or the DIC will only continue to progress.