NUR2940 exam 2

CVA/ stroke spinal cord injury cerebral injury/ ICP cirrhosis sickle cell cerebral palsy Rheumatoid arthritis systemic lupus erythmatosis Bipolar disorder childhood mental illness depression & suicide

stroke/ CVA

cerebral vascular accident or brain attacks, involve a disruption in the cerebral blood flow. the brains cannot store oxygen or glucose and must have constant supply any interruption can lead to brain tissue death… infarction. can lead to ICP and secondary brain damage.

TIA- transient ischemic attack

Definition: Temporary disruption of blood flow to the brain

Symptoms: Sudden weakness, numbness, or paralysis on one side of the body

Warning signs: Vision changes, dizziness, difficulty speaking or understanding

Duration: Symptoms typically last less than 24 hours

Risk factors: High blood pressure, smoking, diabetes, and obesity

Treatment: Immediate medical attention to prevent a stroke

Prevention: Lifestyle changes, medication, and managing underlying conditions

ischemic stroke

caused by a blockage usually a thrombus or emboli in the cranial or carotid arteries

can be reversed with fibrinolytic therapy using alteplase or TPA, if given within 3-4.5hrs of the initial manifestation unless contraindicated by factors (active bleeding)

thrombotic strokes

a clot that forms over time; associated with atherosclerosis; plague rupture can cause clot formation; stoke has a slower onset, evolving over minutes to hours due to the principles of atherosclerosis. occurs secondary to the development of a blood clot on an atherosclerotic plague in a cerebral artery that gradually shuts off the artery and causes ischemia distal to the occlusion.

embolic stroke

slot that travels from somewhere else; sudden onset and rapid development of neurological deficits or loss of consciousness instantly; clots usually come from the heart ( A.fib; vascular disease, endocarditis, after MI)

carotid stenosis

narrowing of an artery leading to the brain causing TIA’s, vertigo, and memory problems (may feel bruit and thrill)

hemorrhagic stroke

the integrity of the vessel wall is damaged resulting in bleeding into the brain tissue or subarachnoid space. occurs secondary to a ruptured artery or aneurysm. the prognosis for a client who has experienced a hemorrhagic stroke is poor due to the amount of ischemia and increased ICP caused by the expanding collection of blood. if caught early and evacuation of the clot can be done, prognosis can improve significantly

intracerebral hemorrhage- bleeding into the brain tissue

• usually caused by sustained hypertension or dramatic sudden increase in blood pressure like form cocaine use

subarachnoid hemorrhage- bleeding into the subarachnoid space. more common; usually caused from ruptured aneurysm (abnorm. blister in the artery that is weakened) or AV malformation (uncommon embryonic abnormality, large collection of malformed, thin-walled, vessels that can rupture)

• vasospasm- sudden and periodic constriction of cerebral artery. often occurs after SAH or ruptured of aneurysm or AVM. can cause secondary ischemia and further damage (use nimodipine)

CVA risk factors

• genetics- first older relative w/ Hx of stroke

• atherosclerotic disease

• cerebral aneurysm

• AV malformation

• hyperlipidemia

• hypercoagulability

• A. fib

• Diagnosis of or family Hx of aneurysm

• hypertension (early tx)

• diabetes Mellitus (maintain blood glucose w/n range)

modifiable risk factors

• smoking (smoking cessation)

• substance use (particularly cocaine)

• heavy alcohol use

• obesity (maintain healthy weight & regular exercise)

• sedentary lifestyle

• oral contraceptive use

• us of phenylpropanolamine (antihistamines, PPA)

CVA assessment

timely assessment is crucial. facial droop, weakness of one side, slurred speech

for ischemic stroke, priority is getting to a stroke center asap

• if patient meets criteria, they may have the stroke symptoms reversed if clot an dissolved within 3hrs

get a good history

• recent surgery, recent bleeding, currently use anticoagulant

• when symptoms are and how they progressed: quick, gradual, getting worse or better. when they start

• current meds, drug or alcohol use

• assess for other causes: hypoxia, hypoglycemia

BEFAST

• Balance

• eyes (vision)

• face (smile- symmetrical)

• arms (limb fall or drop)

• speech (slur or trouble forming words

• time (when last time feel normal)

Glascow coma scale

eye opening

1. none

2. to pain

3. to voice

4. spontaneously

verbal response

1. non

2. incomprehensible sounds

3. inappropriate words

4. confused/ disoriented

5. oriented

motor reponse

1. none

2. abnormal extension

3. abnormal flexion

4. withdraws from pain

5. localize pain

6. obeys commands

3-15 scale; <8 intubate

left cerebral hemispehere

language, mathematics skill, analytic thinking

• expressive and receptive aphasia (inability to speak or understand language)

• agnosia (unable to recognize familiar objects)

• alexia (difficult reading)

• agraphia (difficult writing)

• dysarthria- slurred speech

• Right extremity hemiplegia (paralysis) or hemiparesis (weakness)

• slow, cautious behavior

• depression, anger, quick frustration

• visual changes (hemianopsia [ loss visual field in one or both eyes])

right cerebral hemisphere

responsible for visual and spatial awareness and proprioception

• altered perception of deficit (overestimation of abilities)

• unilateral neglect syndrome (ignore left side: cannot see, feel, or move affected side; unaware existence). more common in right stroke

• loss of depth perception

• poor impulse control and judgement

• left hemiplegia or hemiparesis

• visual changes (hemianopsia)

CVA Cognitive damage

• Affects higher intellectual functions

• Short/long-term memory loss

• Decreased attention span/ motivation

• Decreased concentration

• Loss of abstract reasoning

• Impulsivity

PSYCHOSOCIAL CVA affects

• Body image disturbance

• Self-concept

• Loss of independence

• Emotional lability – cry and laugh for no reason, inappropriate, frontal lobe

Dx CVA

• non-contrast CT scan- initial test and should be preformed w/n 25 min from time of client arrival to ED. determine types of stroke and if able to get thrombolytic therapy

• MRI- edema, ischemia and necrosis

• MRA- identify presence of cerebral hemorrhage, abnormal vessel structures ( AVM, aneurysm), vessel ruptures and regional perfusion of blood flow in the carotid arteries and brain

• lumbar puncture- assess presence of blood in cerebrospinal fluid. positive finding is consistent with cerebral hemorrhage or ruptured aneurysm

• Glasgow coma scale- scale for decreased LOC or orientation. risk for increased ICP exists related to swelling of the brain and can occur secondary to ischemic insult

• Carotid Ultrasound: to check patency of carotid arteries

• EKG: to look for an abnormal heart rhythm

• 2-D Echocardiogram: to check the heart/valves

• PT/INR and aPTT: in case anticoagulation is started

• Most clients will also have routine blood work, such as a chemistry panel, CBC

  • Elevated H&H may be seen as a compensatory mechanism

  • Elevated WBCs indicate inflammation or infection

CVA Nursing diagnosis: inadequate cerebral tissue perfusion

• client needs 2 large bore IVs

• supine w/ HOB low

• fibrinolytic/ thrombolytic therapy

• provide oxygen therapy to maintain oxygen saturation level >92% or if client LOC decreased

• Alteplase- only drug approved for ischemic CVA (clot buster)

  • risk of conversion from ischemic to hemorrhagic

  • client/ family sign consent

  • 3-4.5hrs when asked symptoms started

  • weight-based; on pump in ICU only

  • frequent neuro assessment and blood pressure monitoring

  • risk for bleeding: no blood draws/ IV sticks/ anticoagulants 24-48hrs post

  • follow-up CT before starting antiplatelets

  • SBP 180 < or DBP 110< give Antihypertensive as prescribed

  • discontinue if severe headache or severe hypertension, bleeding, nausea, and/or vomiting; notify HCP immediately

  • SE: nose bleeds

• embolectomy- clot removal

  • interventional neuroradiologist “retrieves” the clot and removes it

• carotid artery angioplasty with stenting

• carotid endarterectomy- removal of plague from artery

• post-procedure watch for headache

  • change in LOC

  • muscle weakness, neck pain or swelling

  • hoarseness

intracranial pressure (ICP)

normal level is 10-15mmHg; brain tissue, blood and CSF are contained in a rigid space (skull) and there is minimal room for swelling/inflammation

• ICP increases, cerebral perfusion decreases, leading to brain tissue ischemia and edema

• can cause hemorrhagic stroke

• body compensates by shunting CSF or increasing its reabsorption

• once compensation cannot be maintained, the brain herniates downward, upward or laterally and death occurs

• highest risk for elevated ICP during first 72hrs r/t edema

• increased ICP results in increased/worsening symptoms; frequent neuro checks, and vitals are done

• 1st sign of increased ICP is decreased/ changed in LOC

• positioning: lower HOB is better for cerebral perfusion, but increases risk of aspiration

• head neutral position to promote venous drainage from the head

• avoid things that increase ICP, such as suctioning, aggressive coughing

• calm, unhurried, quiet environment; do not cluster nursing activities; give client rest time

• remember some hypertension is wanted so BPis not lowered or is lowered very slowly

• key features: decreased LOC (lethargy to coma), restlessness, irritability and confusion, headache, N/V, aphasia, slurred speech, pupil changes, ataxia, seizures, Cushing’s triad (hypertension, widened pulse pressure, bradycardia), abnormal posturing

other complications

• hydrocephalus - increased CSF

• seizures r/t increased ICP

• hemorrhage or re-hemorrhage

• dysrhythmias- EKG monitoring

• hyper or hypoglycemia- can increase the area of damage

• anticoagulation is often needed after ischemic CVA (aspirin, heparin)

• no anticoagulants after thrombolytic administration for 24-48hrs

• anti-hypertensives for elevated BP

• stool softeners, opioids for pain, antianxiety meds

CVA nursing diagnosis- impaired swallowing

risk for aspiration- PNA, coughing, silent

warning signs- coughing with liquids, drooling, facial droop

need to stay NPO until evaluated by speech therapy- safety due to dysphagia

initials swallow screen

may need peg or TPN

swallow precaution

• positioning- high fowlers, chin tuck

• no straws

• thickened liquids

• texture

• meds- crushed

• don’t rush, allow extra time

• pocketing- place food on the unaffected side

• suction standby

• no distractions

CVA nursing diagnosis- impaired communication

promote effective communication

slurred speech is caused by loss of motor function to the tongue and other speech muscles

aphasia is caused by damage to the language centers in the brain

very frustrated for clients and others when communication is difficult

develop alternate strategies

• communication boards

• pictures

• use simple phrases or words

• avoid yes or no

• simple, one-step commands

• speak slowly

• speech therapy

CVA nursing diagnosis- incontinence

• if continence is lost during acute phase, it can often be regained during rehab

• bladder training: consistently offer urinal/ BSC every Q2h, maintain hydration to dilate urine, balance I&Os, bladder scan to check retention

• bowel training: identify normal bowel pattern, encourage high-fiber foods, stool softeners/ suppositories

• incontinence is not a reason to inset or keep foley in place

• skin breakdown

• prevent infection

CVA nursing diagnosis- altered sensory perception

for injury- temperature, neglect

• neglect usually occurs in right-sided CVA (left side neglect)

• monitor the clients temperature. a fever can cause an increase in intracranial pressure

approach from unaffected side

place items in field of vision

re-orient frequently, maintain structured, consistent environment

patient

remind them of the effected extremity

If home, home health nurse will need to do home assessment (may need grab bars in shower, elevated toilet seats, removal of throw rugs, other adaptive equipment)

Depression may occur after CVA

Teaching for client/family include: lifestyle changes, drug therapy, ambulation/transfer skills, communication skills, safety precautions, nutritional management, activity levels, self-management

CVA evaluation

1. VTE prophylaxis

2. Discharged with antithrombotic therapy

3. Anticoagulation for atrial fib/flutter

4. Thrombolytic therapy as indicated (3-4.5 hrs. of symptom onset)

5. Antithrombotic therapy is evaluated by end of hospitalization (if on coumadin, what is the INR prior to discharge? Should be 2-3)

6. Discharged on a statin medication

7. Stroke education provided and documented

8. Assessed for rehabilitation needs/placement

CVA medication

ENOXAPARIN (Lovenox): anticoagulant given to prevent DVT in most hospitalized clients

FONDAPARINUX (Arixtra): anticoagulant given to prevent DVT in most hospitalized clients

APIXABAN (Eliquis): anticoagulant used to treat A.fib, DVT and PE

RIVAROXABAN (Xarelto): anticoagulant used to treat A.fib, DVT, and PE

ETHYLPREDNISOLONE (Solu-Medrol): steroid; used for many things, but in the context of neuro, may be used to suppress inflammation r/t CVA

LEVETIRACETAM (Keppra): used for seizures/epilepsy, which may occur in increased ICP

PHENYTOIN (Dilantin): used for seizures/epilepsy, which may occur in increased ICP

• Side effect: Bruising. -reddish brown urine is NORMAL

• Normal Dilantin level is 10-20

• Give through at least an 18 gauge cause you can blow the vein & SLOW

VASOPRESSIN (Pitressin): anti-diuretic hormone; will reduce urinary output

SODIUM HEPARIN (Heparin): anticoagulant; monitored and adjusted using aPTT/PTT values

AMINOCAPROIC ACID (Amikar): used to prevent/stop post-operative bleeding after cardiac surgery

MANNITOL (Osmitrol): osmotic diuretic that pulls fluid from the brain and CSF into the interstitial and plasma spaces, so it can be excreted; used to reduce increased ICP

• Effectiveness = increased urine output. Decreased ICP

CVA nursing care

• monitor VS every 1-2hrs: notify if BP is > 180/110

• monitor client temperature. fever can cause an increased ICP

• to provide oxygen therapy to maintain O2 sat >92% or client LOC decreased

• place on cardiac monitor to detect arrhythmias

• monitor hyperglycemia

• elevate HOB 30 to reduce ICP and promote venous drainage. avoid extreme flexion or extension of neck and maintain head midline neutral position

• seizure precaution

• thickened liquids

• aspiration precaution

• DVT prevention

• elevate extremity effected

• safe enviroment: fall precaution

spinal cord injury

the loss of motor function, sensory function, reflexes, and control of elimination. injuries in the cervical region result in quadriplegia: paralysis/ paresis of all 4 extremities and trunk

injuries below T1 result in paraplegia: paralysis/ paresis of lower extremities. truncal instability also results if the lesion is in the upper thoracic region.

an injury at C4 or above poses a greatest risk for impaired spontaneous ventilation due to the involvement of the phrenic nerve

spinal cord injury Causes

MVA, falls, violence, sports injury, trauma (motor vehicle accident), diving accident, gunshot wounds, disease

risk factors: young (15-35), male, drugs/ alcohol users

common cause of death: PNA, PE, sepsis

C1-C4: respiratory failure (vent or death)

C1-T1 & T1-T11: respiratory dysfunction

C1-T1: quadriplegia

<T1: paraplegia

anything above T6: severe

types of spinal injuries

primary: initial trauma

1. hyperflexion (acceleration of head)

2. hyperextension (accel-deceleration)

3. axial loading or vertical compression: diving, falls, jump

4. excessive rotation

5. penetrating trauma

secondary (worsen primary)

• hemorrhage, ischemia, hypovolemia, impaired tissue perfusion from neurogenic shock, local edema

• thought to be reversible/ preventable during 1st 4-6hrs

complete- “plegia” no motor or sensory function below the level of injury

incomplete- “paresis” partial loss of motor and/or sensory below the level of injury

results in: concussion, contusion (bruise) , compression, laceration, transaction (severing of cord)

spinal cord expected finding

• report lack of sensation of dermatomes below the level of lesion

• report neck or back pain

• inability to feel light touch or inability to discriminate between sharp or dull and unable to discriminate between hot and cold

• absent deep tendon reflexes

• flaccidity of muscle

• hypotension

• shallow respiration

• spinal shock

  • absence of all voluntary reflex neurologic level of injury

  • lasts days to months (temp)

  • occurs @ SCI

neurogenic shock

shock from loss of sympathetic tone, usually from a T6 or above SCI. classic signs are hypotension from vasodilation and bradycardia

venous pooling d/t vasodilaiton

above T6 injury

treatment: IVF- vasopressors- atropine or positive inotropes- may need surgical intervention to decompress spine, vasoconstrictors, fluids

automatic dysreflexia (AD)

acute emergency (occurs w/ SC lesions above T6

occurs d/t irritating stimulus below the site of injury results in severe HTN

can lead to stroke or seizure

autonomic nervous system response are exaggerated

factors:

• bladder: distended, UTI

• bowel: impaction, hemorrhoids

• breakdown in skin: tight clothes, pressure inj., burns, infection, cuts, temp

s/s: throbbing headache, HTN (watch 20-40 increased in SBP), flushing skin (above SCI… vasodilation), bradycardia, pale, cool, clammy (below SCI… vasoconstrict), goosebumps, sweating, dilated pupils/ blurred vision, anxiety, nasal congestion, nausea

interventions: prevention!

• bladder (most common): assess urinary output, foley not kinked/ blocked), irrigate if blocked cath

• bowel: assess last BM, listen bowel sounds, palpate for distention, remove impaction

• breakdown of skin: remove binding clothes/ devices, turn Q2h, assess skin/ protect, check temp. room covers

high fowlers… 90 w/ legs lowered

treat problem (cause)

hydralazine (Apresoline) IV (vasodilator) decrease BP

• sudden increase BP, bradycardia

• profuse sweating increase level SCI (face, neck, shoulders)

• goosebumps, flushing,blurred vision… spots in visual field

• nasal congestion

• onset throbbing, severe HA

• feels apprehension

• monitor HCP, RRT

• monitor BP every 10-15mins

• give nifedipine or nitrate

Spinal cord assessment

assess abdomen for internal bleeding. (ab pain, distention, paralytic ileus)

assess skin integrity

• skin breakdown

• VTE d/t immobility, monitor I&Os, weight

• heterotopic ossification

  • bony overgrowth into muscles

  • assess swelling, redness, warmth, decrease ROM

spinal cord labs/ Dx

urinalysis, hemoglobin, ABGs, CBCs (for evaluation of platelets and WBCs):used to monitor for underdiagnosed internal bleeding (client might not feel pain from internal injuries) and impaired respiratory exchange

X-ray. MRI, CT imaging/ CAT scan can be used to assess the extent of the damage and location of blood and bone fragment

spinal cord nursing care intervention

• monitor respiratory status. Provide O2 and suction, assist w/ intubation and mech vent, assess cough, IS, CDB

• assess breath sound Q2-4hrs first few days. pulse OX, 95% intervene

• ABG

• maintain body alignment

• ROM 4x/ day

• monitor BP w/ position change (ortho hypotension)

• adequate fluids stool softener

• temp. cath

• bladder/ bowl retaining

• NG tube to alleviate gastric distention

• neck brace/collar

• log roll

• maintain skin integrity

• halo fixator= for immobilization of cervical spine. worn 8-12wks. affixed by 4 pins (or screws) into outer aspect of skull

• altered balance. be careful leaning

• wear loose clothing

• bathe in tub/sponge bath

• have someone change liner if odorous

• support head w/ small pillow

• resume visual activities. avoid contact sports/ swim

• do not drive.. visual impaired

• straw to drink

• cuts meats/ food

• wrap pins w/ cloth if cold outside

• observe pin sites daily for redness, drainage, loosening= report HCP

• increase fluids/fiber= prevent constipation

• comfort position for SA

• padding @ collar/ occiput area

• maintain one finger width between halo-skin

• never move or turn by holding on halo

• do not adjust screws

spinal cord drug therapy

intrathecal baclofen (ITB) through a programmable, implantable infusion pump and it cath directly into CSF. so pouch in lower abdomen. Dantrolene - severe muscle spasticity

• adverse effects: sedation, fatigue, dizziness, change mental, seizures/ hallucinations if w/d sudden, drowsiness, muscle weakness

celebrex (later for heterotopic ossification)

dextran (plasma expander) help hypotension

corticosteroids (methylprednisone initiated 8hrs of injury):

tizanidine for muscle relax (severe drowsiness/ sedation)

vasopressors: Norepinephrine and dopamine- hypotension during neurogenic shock

atropine: bradycardia

plasma expander (dextran)- hypotension secondary to spinal shock. observe fluid overload

cholinergic: bethanechol- decrease spasticity of the bladder, allow easier bladder training and fewer accident: observe urinary retention. measure residual periodically

analgesics: opioids, non-opioids and NSAIDS- pain

anticoag- heparin: DVT prophylaxis. monitor INR, PT, aPPT. observe manifestation of GI bleed, or bleeding secondary to unrecognized injury

stool softeners and bulk-forming laxatives: prevent constipation

vasodilators: hydralazine and nitroglycerin: treat hypertension during automatic hyporeflexia: monitor BP

cerebral injury

open head injury - the integrity of the skull is compromised by either a penetrating object or blunt force trauma

closed head injury occurs from blunt trauma that causes acceleration of the head and then deceleration or hits a stationary object.

can be classified as mild, moderate, or severe depending on GCS

types of brain injury

concussion (mild traumatic brain injury): occurs after head trauma that results in a change in the clients neurologic function but no identified brain damage and usually resolves within 72hrs. post-concussion syndrome includes persistence of cognitive and physical manifestations for an unknown period of time

contusion: when brain is bruised and client has a period of unconsciousness associated with stupor and/or confusion

diffuse axonal injury: widespread injury to the brain that results in coma and is seen in severe head trauma

intracranial hemorrhage: occur in the epidural, subdural or intracerebral space. it is a collection of blood following head trauma. there can be a delay of weeks to months in presenting manifestations for a subacute or chronic subdural hematoma

open-headed injuries pose a high risk for infection. scalp injuries often results in profuse bleeding due to poor vasoconstriction

skull fracture clients can have localized pain at site of fracture and swelling can occur. nurse should be alert for drainage from eyes, ears

cervical spine injury an always be suspected during head injury

TBI health promotion & disease prevention

• wear helmet when sports, bike skateboarding

• wear seat belt when driving/riding car

• avoid dangerous activities (DUI, speeding)

• firearms lock away

• avoid riding in back of pick-up

• prevent falls in older 65-75

TBI risk factors

• motor vehicle or motorcycle crashes

• illicit drug and alcohol use

• sports injuries

• assault

• gunshot wound

• falls

TBI expected findings

• amnesia- before or after the injury

• loss of consciousness: length of time the client is unconscious is significant

• CSF leakage from nose and ears indicate basilar skull fracture. test for halo signs on paper

• manifestation of ICP

  • severe headache, nausea, vomiting

  • deteriorating LOC, restlessness, irritability

  • dilated or pinpoint nonreactive pupils

  • cranial nerve dysfunction

  • alteration in breathing pattern

  • deterioration in motor function, abnormal posturing

  • cushings triad: severe hypertension, widen pulse pressure and bradycardia

  • seizure

TBI lab/ Dx

• ABGs

• CBC w/ diff

• Blood glucose level

• electrolyte levels

• blood and urine osmolarity

• toxicology screen

• monitor anti-seizure medication blood levels

• Cervical spine films -Dx cervical spine injury

• CT/MRI of head and neck

• ICP monitor

TBI nursing care

support family. effective coping can be very difficult to achieve w/o support from provider/ community member

maintain cervical spine stability until cleared by an x-ray

report presence of CSF from nose or ears

determine if client could possibly be under influence of alcohol, illicit drugs or meds which could impair neurologic responsiveness and affected monitoring

prevent complication of immobility

monitor fluid and electrolyte values and osmolality to detect changes in Na regulation, onset of diabetes insupidus, or severe hypovolemia

provide adequate fluids to maintain cerebral perfusion and to minimize cerebral edema. when large amount of IV fluid prescribed, monitor for excess fluid volume which could increase ICP

safety and seizure precaution

Assess/ monitor the client at regularly scheduled intervals

• respiratory status (priority)

• cranial nerve function: blink, gag reflex, tongue and shoulder movement

• assess PERRLA

• bilateral sensory and motor response

• ICP can be increased by:

  • hypercarbia: cerebral vasodilation

  • endotracheal or oral tracheal suctioning

  • coughing

  • extreme neck or hip flexion/extension

  • maintain HOB <30

  • increasing intra-abdominal pressure

• implement actions that decrease ICP

  • elevate head at least 30min to reduce ICP and to promote venous drainage

  • avoid extreme flexion, extension or rotation of head and maintain body midline neutral position

  • maintain patent airway. provide mech vent

  • admin O2 to maintain PaO2 >60mmHg

  • receive stool softener and avoid Valsalva maneuver with increase ICP

  • provide calm restful environment (limit visitor, minimize noise)

  • brief period of hyperventilation for intubating client can be used after the first 24hr following injury to help lower ICP

TBI medications

mannitol: osmotic diuretic used to treat cerebral edema. medication draws fluid from the brain into the blood

• admin IV to treat cerebral edema

• insert indwelling urinary catheter to monitor fluid and renal status

• monitor electrolytes and osmolality closely

barbiturates: barbiturate coma to decreased cellular metabolic demand until ICP can be decreased

• pentobarbital and thiopental

• med dosage is adjusted to keep the client completely unresponsive

• mech vent, cardia and hemodynamic monitoring and ICP monitoring

phenytoin

• prophylactically to prevent or treat seizures. 1st med used to suppress seizure that does not depress entire CNS

• dosing base on therapeutic blood levels

opioids (morphine sulfate or fentanyl)

• control pain and restlessness

• avoid opioid w/ pt who are not mech ventilated due to CNS depressant effects

  • prevent accurate assessment of neuro system

  • can cause resp depress

• administer naloxone reversal agent

TBI surgical intervention

craniotomy: removal of nonviable brain tissue that allows for expansion and/or removal of epidural or subdural hematomas. it is also used to decrease ICP and remove brain tumor. it involves drilling a burr hole or creating a bone flap to permit access to the affected area.

• treatment for intracranial hemorrhages requires surgical evacuation. there are 3 surgical approaches: supratentorial , infratentorial, and transsphenoidal, and transsphenoidal

medications (mannitol and dexamethasone) can be administered every 6hr for 24-72hr postoperatively

phenytoin or diazepam can be used to prevent seizure activity

monitor ICP

for supratentorial surgery, maintain HOB at least 30 with body positioning to prevent increased ICP

for infratentorial craniotomy, keep client flat and on either side for 24-48hrs to prevent pressure on neck incision site.

calm and reassure client, clarifying misconceptions

TBI complications

brain herniation

• downward shift of brain tissue due to cerebral edema

• brain consist of brain tissue, cerebrospinal fluid and blood. due to limited space withing skull, an alteration of any one of the component of the brain result in a compromise in other components this results in brain tissue moving downward, through the foramen magnum

• fixed dilated pupils, deteriorating level of consciousness, Chyne-stoes respirations, hemodynamic instability, abnormal posturing

• recovery is rare and urgent medical treatment (mannitol and/or surgical debulking treatments is indicated

• severe neurologic impairment usually persists

• close monitoring of VS and neuro status allows early reporting of changes in the GCS score, an increase in the blood pressure, and an alteration in respiratory pattern and effort

hematoma and intracranial hemorrhage

• monitor severe headache, rapid decline in LOC, worsening neurologic function and herniation and change in ICP

• surgery is required to remove subdural and epidural hematoma hematoma

• intracranial hemorrhage is treated with osmotic diuretics

pulmonary edema

• finding mimic acute pulmonary edema w/o cardiac involvement

• life-threatening emergency. immediate, aggressive treatment is used. survival rare

• SIADH

  • monitor blood electrolyte and osmolality daily

  • document strict I&Os

  • weight daily

  • treat electrolyte and fluid imbalance

  • monitor dehydration or fluid overload

Cirrhosis

extensive, irreversible, scarring of the liver (hepatic portal vein [high nutrients, low oxygen]), hepatic artery [low nutrient, increase oxygen])

develops slowly, is progressive, prolonged, destructive course resulting in end-stage liver disease

characterized by widespread fibrotic (scarred) bands of connective tissue. tissues become nodular which can block bile ducts and blood flow in liver

early → liver enlarged, firm, hard

late → liver shrinks, decreased liver function (increase LFTs)

Cirrhosis causes

• chronic alcoholism

• chronic viral hepatitis/ autoimmune hepatitis

• nonalcoholic steatohepatitis (obesity, hyperlipidemia, DM) (NASH) “fatty liver”

• bile duct disease

• genetic diseases/ metabolic

• drugs/ chemical toxins

• gallbladder disease

• cardiovascular disease

compensated cirrhosis

liver scarred, cellular regulation impaired, organ performs essential functions w/o major symptoms

decompensated cirrhosis

liver function impaired w/ s/s of liver failure

complications from hepatic cell damage:

• portal hypertension: persistent increase pressure w/n the portal vein >5 mmHg. results from increase resistance to o obstruction of blood flow through portal vein and branches. blood backs into spleen → splenomegaly. result in ascites, esophageal varices

  • prominent abdominal veins. hemorrhoids

• ascites/ esophageal varices: collection of fluid w/n peritoneal cavity, this decrease plasma protein in blood

  • occurs when fragile, thin wall esophageal veins become distended/ torturous bleeding varices are life-threatening, severe blood loss may occur → shock from hypovolemia

enlarged spleen destroys platelets→ thrombocytopenia (1st sign liver dysfunction)- common in fatty liver

• biliary obstruction: bile production decrease= absorption of fat soluble vitamins is prevented (Vit K)

  • no clotting factrs produced= bleed/bruised

  • jaundice= increase bilirubin (not excreting effectively)

• hepatic encephalopathy (portal systemic encephalopathy)

  • sleep disturbance, mood disturbance, mental status change, speech problems early

  • altered LOC, impaired thinking. neuromuscular problems later

  • increase ammonia/ Gaba levels

  • factors to lead to hepatic encephalopathy:

    • increase protein diet, infection, drugs

    • hypovolemia, hypokalemia

    • GI bleed (causes large amount protein in intestines

• hepatorenal syndrome (HRS) poor prognosis

  • decrease urine flow (L500/24hr) increase urine osmolarity, increase BUN/ CRE

4 stages

1. subtle change

2. continued mental change, Asterixis

3. progressive muscle twitch, hyperflexia

4. unresponsive, unarousable, no asterixis, + Babinski seizures

cirrhosis assessment

early signs: fatigue, significant change in weight, anorexia, vomiting, comfort alterations in abdomen/ liver tender

late signs: GI bleed, jaundice, ascites,, spontaneous bruising

assess for: yellowing of skin/ eyes (sclera)

• dry skin (itchy) rashes, petechiae/ ecchymoses

• warm, bright red palms (palmar erythema), estrogen high in blood a/t decrease metabolism

• spider angiomas (vascular lesions w/ red center and radiating branches), nose, cheeks, increase thorax, shoulder

• peripheral dependant edema of ext/ sarum

• vitamin deficiency (A,D,E,K)

• ASCITES

  • measure abdominal girth to eval progress of ascites (measure @ end of exhalation) * daily weights

• observe vomit/stool for blood

• fector hepaticus: breath odor (fruity/ musty)

• amenorrhea in women

• testicular atrophy, gynecomastia, impotence

• asterixis: coarse tremor, rapid, norhythmic extensions and flexions in wrists/ fingers “hand flapping”

• assess neuro function

• psychosocial: personality, cognitive, behavioral changes (agitation)

Cirrhosis labs/ imaging

increase ALT, AST, LDH, alkaline phosphatase, GGT, bilirubin/ urobilirubin, total proteins= acute liver disease, ammonia= advanced or PSE

decrease total protein= chronic liver disease, albumin= severe liver disease

x-ray of abdomen/ CT/MRIMR elastography (assess liver elasticity)

US of liver (1st assessent)

• liver US w/ doppler

liver biopsy (golden standard)- risk bleeding

transjugular intrahepatic portal-systemic shint (TIPS)

EGD

ERCD

Cirrhosis implementations

ascites

nutrition: Na restriction (1-2g); fluid restriction, vitamins, (thiamine, folate, multi) via IV/PO

skin: cool water rather than warm to help w/ applying lotion to soothe. * assess open areas

drug therapy: diuretic (loop/ K+ sparring)

• Daily weights/ I&Os/ ab. girth/ edema/ electrolyte

• spontaneous bacterial peritonitis (SBP) develop from bacteria in colon from ascites

• signs: low grade fever, loss appetite (mild), ab. pain, fever, altered mental status

• Tx: IV cefotaxime

pericentesis (removes ascitic fluid)

• explain procedure

• obtain vitals, weight

• ask to void before procedure to prevent injury to bladder

• HOB elevated

• monitor VS

• measure drainage/ record

• describe collected fluid

• label/ send to lab; document

• assess site for leakage, apply dressing

• bedrest

• weigh pt

  • document before/ after weight

respiratory support: dyspnea may develop, auscultate lungs Q4-8hrs for crackles

• hepatopulmonary syndrome. monitor O2 sat, apply oxygen if needed, elevated to decrease edema weigh daily

monitor for bleeding

• screen for esophageal varices, EDG to detect before they bleed

• watch for dark tarry stools, vomiting blood

• activities that increase rupture= coughing, vomiting, drinking alcohol and constipation

• esophageal varices bleeding can cause rapid blood loss → emergency intervention

endoscopic therapies

• endoscopic variceal ligation (EVL) banding

• endoscopic sclerotherapy (EST) injection sclerotherapy

• limit invasive procedures hold pressure on injection sites for 5 mins or more

• if rebleeding= 2nd endoscopic procedure, ballion tamponade (tube placed through nose into stomach attached balloon inflated to apply pressure to variceal bleed. usually intubate + mech vent {aspiration, asphysia, esophageal perforation}) and stents shunting (TIPS)

  • doppler to check jugular

  • heavy sedation or general anesthesia

  • large sheath through jugular vein, needle guided into sheath and pushed into liver hepatic vein.

  • balloon enlarges tract and stent keeps open

monitor VS QH

check coag studies

manage hepatic encphalopathy

• management of slowing or stopping accumulation of ammonia in body! is formed in GI tract. decrease w/ dietary and drug therapy

nutrition: if increase ammonia levels with signs of encephalopathy= low protein

• if not compromised: high carbs, moderate fat, high protein (lean)

• no ETOH or raw fish (seafood)

• small frequent meals

cirrhosis drug therapy

propranolol (inderal)= prevent + bleeding by decrease HR and the hepatic venous pressure gradient

vasoconstrictive drug. vasopressin and octreotide acetate (sandostatin) reduces blood flow through vasoconstriction to decrease portal pressure

avoid opioids, sedatives, barbiturates

lactulose (lactitol) to promote exacerbation of ammonia in stool

• is vicious, sticky sweet-tasting liquid

• route- orally or NG tube

• cleanses bowel like laxative, desired effect is 2-3 soft stools per day, decrease confusion

neomycin (ABX)

• destroys normal flora in bowel, diminishing protein breakdown and decreasse ammonia production

• route- orally or retention enema

• potential kidney toxicity

  • no kidney disease patients

• check LOC/ orientation, reflexes and fector hepaticus.

  • thiamine and benzos for alcohol w/d

  • monitor bg levels for hyper/hypoglycemia

  • assess sclera and skin for jaundice along w/ urine: very dark (stool clay colored)

  • semi-folwers to high fowlers position (help resp. distression

avoid acetaminophen (Tylenol), alcohol, smoking, drug

• this may all prevention of further fibrosis of liver scarrin allow healing and regeneration of liver, prevent gastric and esophageal irritation, reduce incidence of bleed, prevent other life-threatening complication

evaluation-

• have low or no ascites

• normal electrolyte levels

• no hemorrhage or managed not develop encephalopathy or managed

• abstain from alcohol/ drugs

sickle cell anemia

a genetic blood disorder that affects the shape of RBC. has abnormal hemoglobin S (normal is hemoglobin A). very sensitive to oxygen changes which cause RBCs to change shape leading to complication (sickle cell crisis)

most common severe form of SCD

SCD how to get it? risk factors

born with it! inherit 2 Hbs gene from each parent= autosomal recessive disorder. (homogyzous)

sickle cell trait: occur when one normal gene and one abnormal are inherited. half chain is abnormal as typical no s/s or mild 25% to pass on

African Americans most common, 1 in 12

normal RBCs= round, smooth, concave flat center, no nucleus, to be able to squeeze easily through vessels. HbA.

sickle cell anemia= Hbs causes stiff, sticky, forms “sickle” shape especially with low O2. can stick together causing circulation problems. blocking blood flow = organs and tissue suffer. also very weak (Hbs) and easily ruptures (only live 20 days compared to 120 days. bone marrow can’t keep up producing RBCs leading to anemia

factors causing “sickle”

• significant blood loss… surgery, trauma, etc.

• illness at risk due to spleen function affected

• climbing or flying high altitudes

• keeping continued stress (physical/mental)

• low fluid intake (dehydration)

• elevated temp… fever, strenuous exercise, extreme temp (weather)

types of sickle cell crisis

vaso-occlusive: fever, pain, edema (hand/feet). RBCs sticking= blocked blood flow leading to decreased circulation in organs/ tissues along with infarction (stroke/ renal issues)

hypernemolytic: destruction of RBCs. when RBCs rupture they release bilirubin= jaundice, gallstones, anemia

aplastic: halt of RBC production

non-functioning spleen: spleen helps recycle RBCs, filters blood-sickled RBCs= swell, not function properly. at risk for infection.

crisis varies some have at random others frequent

S/S of sickle cell anemia

pain is the most common symptom of SCD crisis. very severe… back, chest, joints, etc. comes in episodes

• dactylitis (early sign in babies @ 6months). hand-foot syndrome- blood flow being blocked causing, jaundice/ pale, SOB

• infection risk: PNA

• gallstones: release of bilirubin. too much for gb to handle

• stroke: neuro checks

• eye problems

• risk for abnormal clotting (DVT, PE)

• leg ulcers

• acute chest syndrome (due to infection): chest pain, cough, fever, low oxygen sat, new CXR infiltrates… very deadly… monitor resp status. fever may or may not.

• damage to kidneys, liver, heart (blood flow limited)

• CV: SOB. fatigue, murmurs, increase jugular. increase pulse, decrease BP

• resp: pulmonary HTN

• priapism (prolonged erection)

• skin: check Q8H - pallor, cyanosis, jaundice

• ab: pain

• kidney/urine: protein, if fail little to no output

• ms: record if swelling, temp/ color difference. ROM

SCD labs

hemoglobin S on electrophoresis, hematocrit is low decreases during crisis/ stress. bilirubin increase, WBC increase

X-ray, US, CT, PET, MRI to show tissue/ organ changes

SCD priority

pain due to poor tissue oxygenation and joint destruction

potential for infection, sepsis, mods, deaths

SCD nursing intervention

hydration w/ NS IV, beverages, oxygen, pain @ risk for infection. resp status, neurochecks @ risk for acute chest syndrome. prevention, meds, blood transfusion, administer pain meds, remove restrictive clothes, encourage to keep ext. extended to promote venous return, do not rain knee position of bed, keep HOB elevated no more than 30, keep room temp > 72, avoid external bp cuff, check circulation QH (pulse ox, peripheral pulses, cap refill, toe temp

• pain: opioids around the lock (PRN not best choice)

• IV fluids/oral: dilutes blood and help kidney function

• oxygen: lack of this will help alleviate sickling

• PCN: prevent infection (prophylactic)

• blood transfusion: to replace RBCs, increase oxygen (watch iron)

• bedrest

• education prevention. vaccines, hand hygiene, avoid extreme weather, physical activities, physical/ mental stress, smoke, high altitudes

• remove restrictive clothing (decreases perfusion)

• warm compresses to painful areas

• avoid flexing knees/ hips

birth control = in only hormonal, reduces risk of VTEs

self-care activities, social support= less severe complications longer life span

SCD medications

hydroxyurea: helps create fetal hemoglobin (Hgb F), decreases episodes and pain

• side effect: decrease WBC (leukemia)

• is teratogenic (cause birth defects). teach to adhere to strict contraceptive methods while taking and 1 month after

morphine and hydromorphone IV routine or PCA

stem cell transplant (childood)

prevention of SC crisis

• drink 3-4L daily of liquids

• avoid alcohol- tobacco any form

• contact HCP @ first sign of illness/infection

• flu shot yearly. ask about pneumonia vaccine

• avoid extreme hot/cold temperatures

• wear socks/ gloves outside on cold days

• avoid planes w/ unpressurized passenger cabins

• avoid travel to high altitudes

• inform all professionals of SCD

• consider genetic counseling

• avoid strenuous physical activity

• engage in mild, low- impact exercise 3x/week (not in crisis)

cerebral palsy

neurological condition that affects movement/ coordination

non-progressive disorder of the brain

impaired movement. muscle tone or posture

• possible visual impairment, hearing loss, cognitive difficulties, behavioral disturbances and convulsive disorder

cerebral palsy types

spastic (difficult/ stiffness movement) most common

ataxia (loss of depth perception/ balance)

athetoid/ dyskinetic (uncontrolled/ involuntary movement) - goes away when asleep

mixed: 2 or more above

types of CP depends on the area of the brain affected

cerebral palsy causes

injuries or abnormalities to the brain

majority = during pregnancy up to 2 yrs while baby’s brain is developing

cerebral palsy risk factors

abnormalities of brain; bleeding in brain; low oxygen to brain (asphyxia); premature; head injury; in-utero infection; severe jaundice (decrease bilirubin) ; multiples; Rh, <40 or >20yrs

Dx: test

MRI, CT, PET *detect early!

cerebral palsy symptoms

exaggerated reflexes, floppiness/rigidity, abnormal posture, involuntary movement, unsteady gait, cognitive disability, seizure disorder, difficult swallowing, eye muscle imbalance, visual and hearing difficulties, constipation, sleeping problems, lacking motor coordination, delayed milestones (crawling, walk, speech, social skills)

CP treatment

no cure! maintain quality of life

safety! fall and aspiration risk

maintain skin integrity, nutritional/ cognitive support

educate parents: does not affect length of life!

exercise! (tailored to individual) physiotherapy

maintain ADLs

baclofen (muscle spasms)

botulinum toxin (BTA) helps walking, balance (injected into calf)

diazepam

carbidopa/ levodopa

rheumatoid arthritis

chronic progressive inflammatory disease that can affect tissues and organs but principally attacks the joints, producing inflammatory synovitis.RA typically affects upper joints first

RA is an autoimmune disease that is precipitated by WBCs attacking synovial tissue. the WBCs cause the synovial tissue to become inflamed and thickened. joint deformity and bone erosion can result from these changes, decreasing the joint range of motion and function. it is also a systemic disease that can affect any connective tissue in the body. common structures affected are the blood vessels, pleura surrounding the lungs, and pericardium.

exacerbation and remissions

RA health promotion and disease prevention

use adaptive devices that prevent development of deformity of inflamed joints during ADLs. continue using affected joints and ambulating to maintain function and ROM

RA risk factors

female sex

age 30-60yrs

genetic predisposition

bacterial or viral infection, particularly Epstein-Barr virus

stress and smoking

environmental factors

older age

RA expected findings

• pain at rest and w/ movement

• morning stiffness

• pleuritic pain (pain upon irspiration)

• xerostomia (dry mouth)

• anorexia/ weight loss

• fatigue

• paresthesias

• recent illness/ stressor

• joint pain

• lack of function

• joint swelling and deformity

  • late signs

  • joint swelling, warmth, and erythema are common

  • finger, hands, wrists, knees and foot joints are generally affected

  • joints can become deformed merely by completing ADLs

• subcutaneous nodules

• fever (low-grade)

• muscle weakness/ atrophy

• reddened sclera and/or abnormal shape of pupils

• lymph node enlargement

• early manifestation: fatigue, joint discomfort)

RA labs/Dx

anti-CCP antibodies: + in people w/ rheumatoid arthritis, even years before manifestations develop

Rheumatoid factor antibody: high titers correlate w/ severe disease

ESR: inflammation or infection in the body

c-reactive protein: use for dx disease or monitoring disease activity and for monitoring the response to anti-inflammatory therapy. elevated levels indicate inflammation in the body range- <1.0mg/dl

ANA titer: + titer associate w/ RA

Elevated WBCs; elevated during an exacerbation secondary to the inflammatory response. decreased RBCs due to anemia

Arthrocentesis: synovial fluid aspiration w/ RA increased WBCs and RF are present in fluid

• monitor bleeding or synovial fluid leakage

• take acetaminophen for pain

• apply ice and rest for 24hrs

x-ray: degree of joint destruction and monitor its progression. they can provide adequate visualization and reveal bony erosions and narrow joint spaces

• assist client into position

• minimize movement during the procedure

RA nursing care

assist w/ and encourage physical activity to maintain joint mobility (w/n capabilities of the client)

monitor for fatigue

teach

• max functional activity

• minimize pain

• monitor skin closely

provide safe environment

• refer for PT/ OT

• provide information for support organizations

• facilitate the use of assistive device

• OT for adaptive device that carry ADLS and prevent deformities

monitor medication effectiveness (reduced pain, increase mobility

encourage food high in vitamins, protein, and iron

patient education

• eat small, frequent meals

• apply heat or cold to affected area

  • heat for stiffness and pain

  • cold for swelling

• conserve energy

• follow routine health screening

• report early: fever, infection, pain upon inspiration, chest pain

• self-esteem

• non-pharm pain relief

RA medication

NSAIDS

• Tx begins w/ NSAIDS

• NSAIDs provide analgesic, antipyretic and anti-inflammatory effects

• nsaids can cause considerable GI upset

• request concurrent prescription for gi- acid lowering agent(H2receptor agonist, PPI) if gi upset reported

• monitor for fluid retention, hypertension and renal dysfunction

• take meds w/ food or with water or milk

• observe GI bleed

• avoid alcohol, which increases the risk of GI complication

Cox -2 enzyme blockers (Celecoxib)

• cause less GI upset but risk of cardiac disease

• not recommended for Hx of MI

corticosteroids

• prednisone: strong anti-inflammatory medication for acute exacerbation

• SE: osteoporosis, hyperglycemia, immunosuppression, cataracts

• monitor wight and BP

• avoid crowds

disease modifying anti-rheumatic drugs (DMARDs)

• slow progression of RA and suppress the immune system reaction to RA that cause pain and inflammation. releife might not occur for weveral weeks

• antimalarial agent: hydrochloroquine

• antibiotic: minocycline

• biologic response modifiers: atanercept, inflizimab

• cytotoxic meds: methotrexate, azathioprine

• monitor: low WBC and platelets, increase liver enzymes

• avoid crowds, risk infection, cytotoxic: report hair loss or diarrhea, also contraindicated in pregnanacy

• DMARDs affect liver, aovoid alcohol

RA therapeutic procedures

plasmapheresis

• remove circulating antibodies from plasma done for severe

total joint arthroplasty

• surgical repair and replacement of joint for severe deformed joints that dnt’t respond to med

synovectomy

• removal of synovial membrane surrounding affected joint

RA complications

Sjogren syndrome

• triad: dry eyes, mouth vagina

• cause by obstruction of secretory ducts

• provide eye drops, lube and artificial saliva

• provide fluid w/ meal

secondary osteoporosis

• immobilization cause arthritis to develop into osteoporosis

• encourage weight barring exercises as tolerated

vasculitis (organ ischemia)

• inflammation of arteries can disrupt blood flow causing ischemia. small arteries in skin, eyes and brain are most common affected

• monitor for skin lesion, decrease vision, manifestation of cognitive dysfunction

respiratory

• inflammatory lead to lung complications (pleurisy, pneumonitis, diffuse interstitial fibrosis, Pulmonary hypertension

• admin oxygen therapy

• take rest between activites

cardiac

• inflammatory can affect cardiac tissue leading to pericarditis and myocarditis

• admin anti-inflammatory agents

systemic lupus erythematosus

autoimmune disorder in which an atypical response results in chronic inflammation and destruction to healthy tissue

no cure just control manifestation and decrease number and frequency of exacerbation

systemic: affects the connective tissues of multiple organ systems and can lead to major organ failure

discoid: only skin

med-induced: procainamide, hydralazine, isoniazid

hard to dx b/c of vague early manifestations

SLE risk factors

female 20-40yrs

Asian, Hispanic, native american descent

environmental and genetic factors

before menopause

can be delayed dx in elderly

SLE expected findings

• fatigue/ malaise

• alopecia

• blurred vision

• pleuric pain

• anorexia/ weight loss

• depression

• joint pain, swelling, tenderness

• weakness

• fever (major indicator of exacerbation

• lymphadenopathy

• pericarditis (friction rub)

• Raynaud's phenomenon

• butterfly rash

• kidney, lung, GI, vasculature affected

SLE lab tests

skin biopsy

immunologic tests

• ANA +

• C3,C4 -

• ESR+

BUN and CRE +

urinalysis + for protein and RBCs

CBC- pancytopenia

SLE nursing care

monitor/ assess

• pain, mobility fatigue

• VS (BP)

• manifestations

  • hypertension and edema

  • urin output

  • diminished breath sounds

  • tachycardia and inspiration chest pain

  • rubor, pallor, cyanosis of hands/feet

  • arthralgias, myalgias and polyarthritis

  • change in mental status

  • BUN, CRE lvl, urinary output

  • nutritional status

provide small frequent meals, and in-between supplements

encourage limit salt

SLE medications

NSAIDS

• to reduce inflammation and arthritic pain

• not for impaired kidney

corticosteroids

• immunosuppression and reduce inflammation

• monitor fluid retention, hypertension, impaired kidney function

• taper gradually, older- risk for fractures

immunosuppressants

• methotrexate and azathioprine

• belimumab

• monitor for toxic effects and infection (bone marrow suppression and increased liver enzymes

• avoid live vaccines and pregnancy

antimalarial

• hydroxychloroquine: suppress synovitis, fever and fatigue and decrease risk of skin lesions from exposure to sunlight exposure

• encourage eye exams

SLE client educations

wear wide hat, ling sleeve and long pants

avoid UV and sun. use sunscreen

use mild soap and avoid harsh hair treatment

use steroid cream for skin rash

report edema

report infection

avoid crowds and sicks

risk of pregnancy w/ lupus and meds

apply lotion

avoid drying agents

pat skin

SLE complications

lupus nephritis

• SLE that cannot be managed w/ meds can experience CKD and possible kidney transplant. leading cause of death

• monitor edema and hypertension and renal lab

• take immunosuppressants and corticosteroids. avoid sress and illness

pericarditis and myocarditis

• inflammation of heart and vessels and sac

• monitor chest pain, fatigue and arrhythmias and fever

• report and take meds

Bipolar disorder

emerges in early adulthood, but can be treated in peds. manifestation can mimic expected findings in ADHD. periods of normal functioning alternate with periods of illness. client can exhibit psychotic, paranoid and/ or bizarre behavior during periods of mania

mood disorders questionnaire: standardized tool that places mood progression on a continuum from hypomania (euphoria) to acute mania (extreme irritability and hyperactivity) to delirious mania (completely out of touch with reality)

Bipolar phases

acute phase: acute mania

• hospitalization required

• reduction and safety is goal

• risk of harm

• 1:1 supervision

continuation phase

• remission of manifestation

• tx generally 4-9months

• relapse prevention through educations, med ahere and psychotherapy

maintenance phase: increase abilities to function

• Tx continues lifetime

• prevention of future episodes goal

bipolar behavior

mania: abnormal elevated mood (expansive or irritable); requires hosp.. manic episode last at least 1wk

hypomania: less severe episode last least 4 days accompanied by 3 or more manifestation of mania, hosp. not, client less impaired, hypomania can progress

rapid cycling: 4 or more episodes of hypomania or acute mania w/n 1 yrs and increase recurrence rate and resistant to treatment

types of bipolar

Bipolar I disorder: client has at ;east 1 episodes of mania alternating w/ major depression

Bipolar 2 disorder: client has 1 or more hypomania episodes alternating w/ major depression

cyclothymic disorder: client has at least 2 yrs of repeated hypomanic manifestations that do not meet the criteria for hypomanic episodes

bipolar comodidities

substance use disorder

anxiety disorder

borderline personality disorder

oppositional defiant disorder

social phobia and specific phobias

seasonal affective disorder

ADHD

Migraines

metabolic syndrome

Bipolar risk factors

genetic: immediate family member who has bipolar

physiological: neurobiological and neuroendocrine disorder

environmental: increased stress in the environment

relapse: substance use, sleep disturbances, psychological stressors

bipolar expected findings

manic characteristics

• labile mood w/ euphoria

• agitation and irritability

• restlessness

• dislike of interference and intolerance of criticism

• increase in talking and activity

• flight of ideas, rapid continuous speech w/ sudden frequent topic changes

• grandiose view of self and ability

• impulsivity: give/spend money or possessions

• demanding and manipulative behavior

• distractibility and decrease attention span

• poor judgment

• attention-seeking behavior

• inappropriate behavior

• impairment in social and occupational functioning

• decrease sleep

• neglect of ADLs, including nutrition and hydration

• possible presence of delusions and hallucinations

• denial of illness

depressive characteristics

• flat, blunted, labile affects

• tearfulness, crying

• lack of energy

• anhedonia: loss of pleasure and lack of interest in activities, hobbies, sexual activity

• physical reports of discomfort/ pain

• difficulty concentrating, focusing, problem-solving

• self-destructive behavior, including suicidal ideation

• decrease in personal hygiene

• loss or increase in appetite and/or sleep, disturbed sleep

• psychomotor retardation or agitation

bipolar nursing care

care based on phases

acute manic episode

• focus is on safety and maintaining physical health

• therapeutic milieu (w/n acute care mental health facility)

  • provide a safe environment during the acute phase

  • assess the client regularly for suicidal thoughts, intentions and escalating behavior

  • decrease stimulation w/o isolating the client if possible. be aware of noise, music, television, and other clients

  • implement frequent rest periods

  • provide outlets for physicals activity. do not involve the client in activities that last a long time or that require a high level of concentration and/ or detailed instructions

  • protect client from poor judgement and impulsive behavior, such as giving money away and sexual indiscretions

• maintenance of self-care needs

  • monitoring sleep, fluid intake, and nutrition

  • provide portable, nutritious food because the client might not be able to sit down to eat

  • supervising choice of clothes

  • giving step-by-step reminder for hygiene and dress

• communication

  • use calm, matter-of-fact, specific approach

  • concise explanation

  • provide for consistency with expectations and limit-setting

  • avoid power struggles and do not react personally to the clients comments

  • listens to and act on legitimate client grievances

  • reinforce nonmanipulative behaviors

  • therapeutic communication techniques

bipolar meds

mood stabilizers

• lithium carbonate

• anticonvulsants that act as mood stabilizers; valproate and carbamazepine treat acute mania; lamotrigine is used for maintenance therapy for bipolar mania

first-gen antipsychotic medication

• chlorpromazine and loxapine

2nd gen antipsychotic med

• olanzapine, risperidone, lurasidone and quetiapine are approved to treat depression

antidepressants

• SSRI fluoxetine, manage depressive episode

Bipolar therapeutic procedures

electroconvulsive therapy (ECT): can be used to mod extreme manic behavior, esp. when pharmacological therapy (lithium) has not worked. clients who are suicidal or those who have rapid cycling an also benefit from ECT

bipolar education

case management

group, family, individual psychotherapy (CBT)

health teaching

• chronicity of disorders requiring long-term pharmacological and psychological support

• indications of impending relapse an way to manage the crisis

• precipitating factors of relapse (sleep disturbances, use of alcohol or caffeine)

• importance of maintain a regular sleep, meal and activity pattern

• medication administration and adherence

bipolar complications

physical exhaustion and possible death

• prevent client self-harm

• decrease clients physical activity

• ensure adequate fluid and food intake

• promote and adequate amount of sleep each night

• assist the client with self-care needs

• manage medication appropriately

depressive disorders

including major depressive disorders and persistent depressive disorder

risk factors:

• family Hx of depression

• physical or sexual abuse or neglect

• homelessness

• disputes among parents, conflict with peer or family and rejection by peers or family

• bullying, either as the aggressor or victim, including traditional bullying and cyberbullying behavior

• engaging in high-risk behaviors

• learning disabilities

• chronic illness

expected finding

• feelings of sadness

• temper tantrums (verbal and behavioral outbursts)

• loss of appetite

• nonspecific complaints related to health

• engaging in solitary play or work

• change in appetite, resulting in weight changes

• changes in sleeping patterns

• crying

• loss of energy

• irritability

• aggression

• high-risk behavior

• poor school performance and/or dropping out of school

• feeling of homelessness about the future

• suicidal ideation or suicide attempts

anxiety disorders

include separation anxiety disorder and panic disorder

• the anxiety or level of stress interferes with normal growth and development

• the anxiety or level of stress is so serious that the child is unable to function normally at home, in school, and in other areas of life

separation anxiety disorder

• this type of disorder is characterized by excessive anxiety when a child is separated from or anticipating separation from home or parents that is developmentally inappropriate. the anxiety can develop into a school phobia or phobia of being left alone. depression is also common

• anxiety can develop after a specific stressor ( death, illness, move, assault)

• Anxiety can progress to a panic disorder or type of phobia

disruptive, impulse control and conduct disorders

oppositional defiant disorder, disruptive mood dysregulation disorder and conduct disorder

behavioral problems usually occur in school, home, and social settings

comorbid disorders can also be present (ADHD, depression, anxiety, substance use disorders)

in children and adolescents who have disruptive, impulse control, and conduct disorders, manifestations generally worsen in the following

• situations that required sustained attention (classroom)

• unstructured group situations ( the playground)