Post midterm content Flashcards
What are the 4 main jobs of the liver?
Storing glycogen
drug metabolism
detoxing ammonia
producing bile, coagulation factors and albumin
Where is the liver located?
RUQ
Albumin production
transports drugs, attracts water, and binds with calcium for bone strength
Bile production
Scoops up bilirubin and cholesterol and excretes them through the GI system
Clotting factors production
PT, PTT, INR
Ammonia
the liver converts ammonia into urea where it can eventually be excreted by the kidneys
Bilirubin
A byproduct of RBC breakdown, the liver converts old RBCs to bilirubin and then excretes it via stool
Hepatic Portal Vein
Pumps blood rich in nutrients from the GI system to the hepatocytes which will then store or remove products; it filters the blood
Hepatic Artery
Pumps fresh oxygenated blood to the liver from the aorta
What is hepatitis?
Liver inflammation
Stages of inflammation?
Mild: Impairs hepatocyte function
Moderate: May lead to obstruction of blood and bile which impairs overall liver function
Severe: Contributes to cirrhosis, hepatocellular cancer, and liver failure
How can Hepatitis happen?
Viral (A,B,C,D,E)
Idiopathic
Drug toxicity
autoimmunity
alcohol induced
what is the most common form?
Viral
How many phases of Hepatitis is there?
Preinteric (prodromal)
Icteric
Posticteric (Convalescent)
Pre icteric
Vague body symptoms are present often described as flu-like
Icteric
Decrease in flu like symptoms. Onset of jaundice and dark urine from high bilirubin levels, clay stools, hepatomegaly, and pain
Post icteric
Jaundice and dark urine begin to subside, stool normalizes, liver enzymes and bilirubin decrease and eventually normalize
What is considered acute?
Lasting less than 6 months, usually self-limiting
what is considered Chronic?
Lasting over 6 months. Liver begins to deteriorate over time leading to cirrhosis, liver cancer, or liver failure
Steps of Hepatitis
- hepatitis infection
- targets the liver
- hepatocytes become inflamed
- hepatocyte lysis
- contents of hepatocytes released into bloodstream
6.Increased ALT AND AST
Hep A and Hep E patho
When ingested (fecal-oral route), Hep A & E travel through the digestive system.
Nutrients are (enveloped by the cell membrane and brought inside) absorbed through the hepatic portal venous system and the Hepatitis is absorbed too.
Once inside the liver, it binds with the receptors on hepatocytes and enters through endocytosis
Acute Hepatitis symptoms
Malaise, N/V/D, low appetite, joint pain, low grade fever, clay stools (lack of bili), dark urine, jaundice, RUQ tenderness, Hepatomegaly
*CONTAGEIOUS 2 WEEKS BEFORE SIGNS
In Hepatitis E there is also a reported aversion to cigarettes (unknown reason)
Look for jaundice in nailbeds, mucous membranes, and sclera
What two viral are acute?
A and E do NOT progress to chronic
AE are contracted through AE: A = Anus (fecal) E = Eat (oral)
Best prevented with hand hygiene!! Vaccine for hep A only.
Risk factors and meds for A and E?
Ingestion of contaminated food and water (especially shellfish)
Contact with infected stool (poor hand hygiene in food preparation)
Crowded conditions
Hep A vaccine (may be used post-exposure)
Immunoglobulin within 2 weeks post-exposure for Hep A
What is the rare but life-threatening complication of Hepatitis A or E in which severe liver failure occurs over hours to days
FULMINANT HEPATITIS
Chronic Hepatitis is what ones?
B, C, and D have the risk of becoming chronic.
The are contracted via blood and bodily fluids
Risk factors for B,C,D
Unprotected sex
Contact with blood
Substance use disorder
Birth (Hep B may be during pregnancy)
Tattoos
Hemodialysis
Unscreened blood
Medications for B,C,D
Interferons
Hep C: peginterferon alfa 2-a & ribavirin combination therapy
Hep B immunoglobulin therapy within 24 hours
chronic symptoms
asymptomatic (carrier)
ascites
esophageal varices
encephalopathy
bleeding
gynecomastia
spider angiomas
palmar erythema
BD?
Hepatitis D cannot occur without Hepatitis B!
The best prevention is the Hepatitis B vaccine
Carrier State
Hepatitis B and C may exist in a carrier state; the infected person is asymptomatic and may be unaware they have it as they have never had active disease, have a chronic low-grade infection and/or continue to be asymptomatic
Which is the worst?
HEP B, 10x more than C, 100x more than HIV
Hep B & Birth
There is a high risk of transmission of Hep B from mother to baby
Babies have 90% chance of developing chronic Hep B.
Hep B & Birth precautions
If the mother is confirmed or suspected of having Hepatitis B, immunoglobulin is given to the infant within 12 hours of birth (this differs from the standard 24 hours post-exposure)
Hepatitis C is highly associated with what?
IV drug use, which is a growing concern
Is Hep C curable?
now with Direct Acting Antivirals (DAAS) treatment is 8-12 weeks and patients report minimal side effects
The issue with treatment, is that 44% of people with Hep C are unaware they have it
Labs to watch is hepatitis?
AST, ALT, Bilirubin, Antibodies and when chronic high PTT and high ammonia
Liver Biopsy
May be used to test for the extent of damage to the liver
A small piece of tissue is removed an examined in the lab
Teach client to lay on RIGHT SIDE to prevent bleeding post-procedure. Right side lets body weight on the liver and helps stop any bleeding.
Diet?
high carb and calories, low protein and fat
why low protein?
protein breakdown results in ammonia which the liver normally discards. Eating more protein means more work for the liver!
What to do if nausea occurs?
assessed for fluid and electrolyte imbalance. It is important to explain to the patient that most calories need to be eaten in the morning hours because nausea is most common in the afternoon and evening.
What should we teach patients?
Handwashing
Eat low fat, protein and high carbs, calories
Personal hygiene products
Activity restriction
Toxins are avoided
Individual bathrooms
Testing
Interferon
Small frequent meals
What causes cirrhosis?
Cirrhosis can come from many sources, including chronic hepatitis (specifically B and C)
Normal liver tissue is replaced with fibrotic tissue that lacks function; the liver becomes rigid. The end-stage of this fibrosis is called cirrhosis
is it reversible?
Irreversible and so aka end stage liver disease
50% alcohol related
Portal Hypertension
The portal vein narrows due to scar tissue in the liver, restricting blood flow and increasing pressure in the portal vein.
The increased pressure means that fluid is more likely pushed out into peritoneal spaces
This in turn increases pressure to the organs connected to the vein including the spleen and vessels to GI structures resulting in varices.
Fluid backs up into spleen (splenomegaly)
Esophageal Varices
Severe pressure from portal HTN causes enlarged, thinned, esophageal veins.
Once they are too large or too thin, they risk rupturing, which can be fatal (shock/airway obstruction)
Risk for hemorrhage! Rupture can occur from straining, coughing, sneezing, or NG tube insertion
Ascites
Venous congestion occurs due to portal hypertension and coupled with low albumin levels, fluid shifts to peritoneal cavity
Monitor intake and output and abdominal girth
Daily weight
*Monitor I&O, daily weight, abdominal girth, and peripheral edema. Do not position in supine, turn q2h, elevate feet
Hepatic Encephalopathy
The liver cannot detoxify and ammonia builds up in the bloodstream
Remember, ammonia is created when protein breaks down. The liver converts it to urea then it is excreted.
When the liver is not doing its job, ammonia accumulates in the blood
Ammonia is able to cross the blood-brain barrier which leads to altered LOC
Key finding is asterixis (involuntary hand-flapping)
Liver and Estrogen
The liver produces small amounts of estrogen, but more importantly, estrogen is fat-soluble. As the liver is responsible for fat breakdown, when it is impaired there can be an influx of circulating estrogen.
High levels of estrogen can cause gynecomastia, spider angiomas, and palmer erythema
Spider angiomas
red lesions that are vascular with branches. Usually on nose, cheeks, shoulders
Hepatorenal Syndrome
Progressive renal failure associated with hepatic failure.
Sudden decrease in urine output, elevated BUN and Creatinine (think AKI)
Late Stage Cirrhosis
“The Liver Is Scarred”
Weight loss from appetite loss (increased fluid so use caution. Weight may increase, but it is fluid.
Hepatic foetor- liver isn’t filtering toxins and it is essentially seeping through your mouth!
Itching - pruritis (toxins build up under the skin) cool moist cloth, moisturize unbroken sin, wear long sleeves, short nails, cotton gloves
What should you monitor for diet for cirrhosis?
Same as hepatitis
vitamin and mineral supplements (folate, thiamine, multi vit)
Low NA to help with edema
oral care prior to meals to help wake up tastebuds
monitor glucose levels closely for hyper and hypoglycemia
NO ALCOHOL
Labs to Watch in Cirrhosis
AST, ALT, bili, Albumin and calcium, Platelets (thrombocytopenia), PT/PTT/INR
*Albumin and calcium bind together
AST usually higher than ALT
High estrogen!
Treatment Options
Shunting Surgery
Endoscopic variceal ligation
Shunting Surgery
Transjugular Intrahepatic Portosystemic Shunt (TIPS) is minimally invasive.
A stent is inserted to create a new channel and allow some blood to bypass the liver and reduce pressure
Endoscopic variceal ligation
Varices are sclerosed or banded
Small rubber bands are placed around varices to prevent bleeding and shrink/strangulate the varix
Liver Transplant
Not a candidate if severe cardiac and respiratory disease, metastatic malignant liver Ca, or ETOH/drug disorder,
Acute graft rejection post liver transplant within 4-10 days post surgery.
Signs of rejection are are tachycardia, upper right flank pain, jaundice, lab findings of liver failure. Body attacks new organ. Need immunosuppressants.
Paracentesis
Drain for ascites
Prior to procedure, ensure bladder is empty to avoid risk of perforation
Take vital signs. Take note of BP as pressure will drop as fluid drains
Measure abdominal circumference and take weight
Drain according to order (usually no more than 1L/day)
Keep HOB up to help drain flow and help with breathing
Medications for cirrhosis
Beta blockers and nitrates: Portal HTN and varices
Vitamin K: clotting factors
Lactulose: Decrease ammonia level through stool (monitor for hypokalemia)
Diuretics: Decrease fluid buildup
Albumin: Helps with ascites and edema
*IV albumin often given with Lasix (albumin brings the water into the vessels and Lasix helps us pee it out -> make sure vitals are within expected limits)
Do not take Tylenol! Tylenol contributes to liver damage and we are trying to give our liver as much rest as possible
LACTULOSE
Laxative
Ammonia decreases
Cognition improves
*Creates an acidic bowel which attracts ammonia for secretion! Stools should be soft but not diarrhea. Goal is 2-3/day
Chronic Kidney Disease
Filtration
Reabsorption
Secretion
Excretion
What is the basic function of the kidneys
Acid base balance
water removal
erythropoiesis
toxin removal
blood pressure control (RAAS)
electrolyte balance
vitamin D activation
what does Erythropoiesis do?
help to create rbcs in bone marrow. If decreased, you’re anemic
How does Vit D affect?
helps reabsorb calcium from food we eat. If vit d activation is low, calcium will be low as well
how long does it take to meet the criteria for CKD?
3 months
GFR under what is concerning?
below 60
is CKD reversible?
A progressive, IRREVERSIBLE condition
Glomerular Filtration Rate (GFR)
How much blood can be washed by the kidneys per minute from the renal artery
Less blood through the kidneys means more waste, electrolytes, and fluids building up
Normal 90-120 mL/min
Stage 1 kidney disease
Stage1 or 2 evidence of kidney damage such as seen on imaging or a high albumin:creatinine ratio. Stage 1 your GFR is normal but there is some evidence in the urine such as high protein
Stage 3b
symptoms may begin, modify risk factors
Stage 4
symptoms will be present. Look at treatment options may initiate dialysis
Stage 5
ESRD, dialysis, transplantation
In all stages what should be monitored
ACR, eGFR, & Blood pressure.
In CKD you will see:
High Cr and BUN
Low Hgb and GFR
Serum creatinine
Creatinine is a waste product from muscles in the body and as kidney function decreases, Cr rises
Excellent evaluator of renal dysfunction
Used to estimate GFR (eGFR)
Normal 0.6-1.2 mg/dL (over 1.3 means bad kidNEY)
Blood Urea Nitrogen (BUN)
Waste product from protein breakdown
Normal: 7-20 mg/dL
Hemoglobin
Kidneys produce erythropoietin which stimulates RBC production
If kidneys are impaired, few RBCs are being produced and HGB will be lowered
UA
To detect protein (albumin) in the urine.
The urine albumin-creatinine ratio (ACR) identifies protein in the urine which signals kidney damage.
Creatinine Clearance
24-hour collection
Keep in the fridge & discard the first specimen!
Compare to serum creatinine
Cr clearance is lowered
Albumin-Creatinine Ratio (ACR)
ACR is the Albumin-Creatinine Ratio
Albumin seeps into urine in damaged kidneys
Albumin is a protein but should not normally be found in the urine
If ACR is elevated, this indicates kidney disease
If kidneys are healthy what don’t they allow into urine?
albumin
What are the electrolyte Imbalances in CKD?
Hyperkalemia, hyperphosphatemia, hypernatremia, hypocalcemia
Hyperkalemia
Muscle weakness, EKG CHANGES. Can be fatal!
Potassium Pumps the heart. High potassium causes peaked t waves and st elevation. Heart cramps up and can’t beat properly impairing oxygenation, causes vtach and vfib then death – this is a priority
Hyperphosphatemia
Inverse with calcium
Hypocalcemia
Inverse with phosphate, vitamin D activation impaired so less Ca absorbed.
Hypernatremia
Not being excreted as expected – leads to fluid retention and increased blood pressure
Treatments of Hyperkalemia
Diuretics (loop and thiazide)
Kayexalate- Excrete potassium by promoting GI sodium absorption
Hypertonic solutions- Dextrose and regular insulin, Quickly pulls potassium into the cell and out of the blood!
what are risk factors for CKD?
High BP, diabetes, obesity, medication use, CV disease, infections, immunity, smoking, race and ethnicity, genetics and age
HTN in CKD
Constant high blood pressure leads to damage and thickening of the artery wall supplying blood to the kidneys
This allows less blood to reach the kidneys
Nephron function impaired
RAAS in CKD
RAAS. Blood pressure may increase in response to lower filtration (the body falsely believes that blood pressure is low in the case of CKD)
This also causes the body to hold on to extra water (release of aldosterone and ADH)
What is the most common cause of CKD?
Type 2 diabetes (30-50%)
Uremia
Earliest signs
fatigue, pruritis, edema (hands
and feet), urinary changes (oliguria—anuria) may see some hematuria.
Symptoms may not be present in stage 1-3.
Uremic pruritis common. Uremia causes and itch only relieved with decreased levels of uremia!!
Neuro symptoms
May be depressed, agitated, labile. You may see asterixis here (same as hepatic encephalopathy) cerebral edema, uremic encephalopathy.
Renal symptoms
urine will be less than 400mL/day
protein in urine, change in amount, color, concentration.
Respiratory symptoms
pulmonary edema from volume overload, crackles and dyspnea, uremic halitosis.
Volume overload
JVD, peripheral edema, pleural effusion
Gastrointestinal symptoms
anorexia, nausea, vomiting from metabolic acidosis, peptic ulcers, uremic fetor.
Uremic Halitosis/Uremic Fetor
Urine-like odor of the breath from excess urea in the body
Bad taste in the mouth
Halitosis
smell
Fetor
taste
Integumentary symptoms
pallor, decreased turgor, yellow cast to skin, dry, pruritis, uremic frost
Reproductive symptoms
Erectile dysfunction, amenorrhea, spontaneous abortion.
Uremic Frost
Deposits of urea crystals on the skin through the sweat, looks like frost
Cardiovascular symptoms
volume overload, HTN,CHF,JVD
Skeletal symptoms
thin, fragile bones
Bones
Due to low calcium, the parathyroid gland produces PTH. This pulls calcium from the bones!
At risk for osteodystrophy (thin, fragile bones)
Ways to help the kidneys keep their function
no smoking, manage weight, avoid NSAIDS, aspirin, contrast dye, monitor potassium closely.
Maintain tight glycemic control
Diet for CKD
K, NA, phos, protein, fluid restriction, and limit alcohol
Common meds for CKD
ACE/ARBS- lower bp
Epoetin alfa- increase RBC’s
Ferrous sulfate- prevent iron deficiency
Diuretics- excretes excess fluids
Phosphate binders- bind to phosphate and helps lower it, take with meals and 2 hours separately from other meds
What is ESRD
Kidneys are no longer filtering enough blood to function
Treatment options include dialysis, transplantation, and conservative kidney management
What is Hemodialysis?
Occurs outside the body
The dialyzer acts as the kidney
Blood is brought into the dialyzer where it is “washed” by filtering out toxins and waste products. A membrane exists separating “clean” and “dirty” blood
“Clean” blood is returned back into the body
Only a very small amount of blood is actually outside of the body at one time (~1 cup)
Schedule is typically 3x/week and 3-5 hours per treatment
What is central venous catheter?
A venous catheter is inserted into a vein in the neck, chest, or leg near the groin, for short-term dialysis.
Used in the event that an AVF of AVG cannot be created due to anatomical issues or when access is needed quickly
Cannot get dressing wet
Closely monitor for infection
Higher risk of clotting
NOT a preferred method!
Vascular Access Nursing
No compression or tight clothing, avoid blood draws, no bp to affected side, no carrying heavy objects, avoid sleeping on that arm, may use “fistula guard” if participating in sports, monitor for steal syndrome.
What is steal syndrome ?
happens when a surgically created access for dialysis, like a fistula or graft, diverts too much blood away from the normal circulation. This can lead to poor blood supply to the hand or arm, causing pain and other problems.
Thrill
Palpate for a thrill over the vascular access site
You feel a thrill
Bruit
Auscultate for a bruit over the vascular access site
You hear a bruit
Prior to Hemodialysis
BP
Weight
Bruit/Thrill
Hold meds
Complications
Hypotension is a common complication of hemodialysis Take vitals q30-60m while on dialysis. Rapid changes in bp can occur
The nurse should:
Reduce the temperature of the infusion
Adjust the rate of the dialyzer blood flow
Place the client in Trendelenburg position
Administer a fluid bolus or mannitol as prescribed
what is peritoneal dialysis?
Occurs inside the body
Dialysate is infused into the peritoneal cavity via gravity.
Clamp is closed on the infusion line and dialysate dwells for set dwell time (as per physician order – average 4 hours)
Tube is unclamped and fluid drains from peritoneal cavity via gravity
Continuous Cycler-Assisted PD
A popular form of PD done while sleeping.
A cycler machine performs the dialysis exchanges through the night and controls the fill, dwell, and drain phases (3-5 exchanges)
The cycler is disconnected in the morning, leaving the fluid to dwell for the day with only 1-2 manual exchanges through the day needed to ensure adequate dialysis
What is peritonitis?
Infection within the peritoneal cavity
Dialysate is cloudy and may contain fibrin (white flecks/ strands) and have a foul odor
May experience signs of infection, abdominal pain, diarrhea, etc.
Transplant
Transplant workup takes time and eligibility requirements are strict. Must be under 65, free of systemic disease, malignancy, or infection.
Requires major surgery, must be physically strong enough
Infection within the first year is common; poorer outcomes with T1DM and obesity
Will need to take immunosuppressants for life to reduce rejection risk
Acute rejection
Acute rejection may occur over hours to months
Kidney will need to be removed promptly - emergency
Reduced risk with donor screening
Reduced risk with living donor
Chronic rejection
Chronic rejection may occur over months to years
Will not respond to increased immunosuppression
Symptoms are the same as CKD
Arteries?
Arteries take blood Away from the heart
Veins?
Veins Vacuum blood back to the heart
Peripheral Vascular Disease
umbrella term for Peripheral vascular disease and peripheral arterial disease
PAD
PAD = BAD
Stenosis of the peripheral arteries
Most commonly from atherosclerosis, vascular inflammation, thromboembolism, or thrombosis
As the arteries become more narrow, less oxygen rich blood is reaching the periphery resulting is ischemia
Atherosclerosis
Thickening, loss of elasticity, and calcification of arterial walls
Deposits of fat and fibrin obstruct and harden the arteries which affects blood flow and supply to tissues
Clinical symptoms when 60-75% blocked
Leading cause of PAD
PLAQUE can break off/ form a clot
Risk factors for PAD
Smoking, diabetes, high cholesterol, HTN, obesity, age, sedentary lifestyle, stress
Symptoms of PAD
Absent pulses (cool, shiny, no hair)
Round, red sores
Toes and feet are pale or blackened
Sharp calf pain (intermittent claudication)
6 Ps of PAD (Assessment Findings)
PAIN
PARESTHESIA
PULSES
PALLOR
POLAR
PARALYSIS
Pain
Intermittent Claudication
Pain with legs elevated
Rest Pain
Paresthesia
Legs fall asleep due to decreased oxygen
Pulses
Weak/absent pulses
Check with a doppler
Pallor
Pale when elevated
Rubor when dangling
Polar
Cold from low blood flow
Paralysis
Severe side effect from deoxygenation
Other assessment findings
Pain better with dangling feet!
No edema because blood isn’t making it that far
Skin is dry and scaly as no nutrients
May have pain in legs at night (rest pain) since naturally less CO during sleep and limbs are elevated
What is intermittent claudication
Calf pain brought on by exercise, resolves with rest, and is reproducible
Possible to also have pain in buttock, foot, or thigh though less common
10% of PAD patients have this classic symptom
Complication: Critical Limb Ischemia
Characterized as severe manifestation of PAD for over 2 weeks
Rest pain
Nonhealing wounds/gangrene proven from PAD
High risk for amputation and CV events
ABI <0.4 and toe SPB <30mmHg
Dry gangrene
Paint with iodine to keep wounds dry, clean, and disinfected
Amputation and antibiotics may be needed to keep from spreading
We want to keep it DRY: wet gangrene can result in a systemic infection.
Clear line between healthy/gangrenous parts in dry gangrene
Diagnostics
Rutherford scoring system
ABI testing
Ankle-brachial index testcompares the blood pressure measured at the ankle with the blood pressure measured at the arm.
A low ankle-brachial index number can indicate narrowing or blockage of the arteries in the legs.
How to calculate ABI
Systolic pressure at ankle divided by systolic pressure at the arm
PAD tx
Dangle legs
skin care and moisture
smoking cessation
hydration
nail care
Medications: Vasodilators, antiplatelets (thrombus prevention, statins)
Patient Teaching for PAD
Careful: caution of hot temperatures (risk of burns)
Caution: foot trauma (risk of infection). Monitor feet daily and ensure well fitted shoes. No sandals.
Constriction: Avoid Crossing legs, Constrictive clothing, Cigarettes, Caffeine, and Cold temperatures
Surgical tx
Angioplasty: balloon or stent placement
Peripheral bypass graft
arthroectomy: Removal of the obstructing plaque by opening the artery
Amputation: Most commonly of the toes, but may be limb
Peripheral Venous Disease Pathophysiology
In peripheral venous disease, the blood is able to get to the periphery but it isn’t able to get back to the heart (a venous issue)
Can be caused by incompetent valves or narrowed veins
Risk factors for PVD
hx of DVT, female, multigravida, standing/sitting long periods of time, obesity, varicose veins, smoking
PVD
Very big pulses/warm legs
Edema (blood pooling)
Irregularly shaped sores
No intense pain
Yellow/brown ankles
Low compression
No need for ABI with low compression typically as low risk, but do need an order for compression from the MRP in most settings. If PAD is suspected, ABI should be done.
Edema wear and tubigrip
10-15mmHg
Moderate Compression
Requires ABI
Should be between 0.5-0.8 to do moderate compression. This may indicate mixed disease (arterial and venous)
20-30mmHg
High Compression
Requires ABI
No compression can safely be applied with an ABI under 0.5
Want above 0.8 for high compression – this indicates it is primarily a venous issue and little to no PAD is occurring.
30-40mmHg
Diagnosis
Ultrasound (rule out DVT)
ABI’s ensures proper compression level
PVD Tx
elevate veins
compression
exercise
smoking cessation
weight management
vein stripping
medications: plavix and statins
avoid crossing legs
What is a aneurysm ?
An aneurysm is a weakness in a section of a vessel that causes widening or ballooning
Aneurysm when size is 1.5x larger than typical blood vessel
It is a permanent localized outpouching of the vessel wall
False Aneurysm
Pseudoaneurysms :
Caused by a small hole in the blood vessel that forms a clot outside of the vessel that looks like an aneurysm
True aneurysm
Fusiform (symmetrical): all layers bulge
Saccular or Berry (Asymmetrical): one side- high pressure or weaker
Patho of aneurysm
Anything that weakens the vessel wall can contribute to the formation of an aneurysm
The weakened area struggles to contain the blood pushing on it, and so the diameter increases. As it fills with more blood the pressure is even greater and it continues to grow.
Surgical repair is needed when the aneurysm reaches 6cm
Most common location of aneurysm
below renal arteries and above aortic bifurcation: there is naturally less elasticity there
Like a balloon – first breath is hardest to fill up then it is easier. Once weakened it balloons.
Aortic Aneurysm
Can be classified as Abdominal or thoracic
AAA is where?
abdomen (75%)
Aortic Aneurysm Risk Factors
Infectious aoritis - syphilis, HIV
Genetic
Sex- male
age
CAD/PAD
HTN
High cholesterol
fam hx
blunt face trauma
atherosclerosis
smoking
Marfan syndrome
The development of an AAA is associated with connective tissue disorders such as Marfan syndrome. Marfan syndrome results in connective tissue deficiency and ineffective collagen cross-linking, resulting in a weakened aorta which is prone to aneurysm or dissection.
Symptoms of Abdominal Aortic Aneurysm (AAA)
Typically asymptomatic
May experience back pain as AAA enlarges
epigastric discomfort
experience “gnawing” pain in abdomen
Often find out about AAA when being tested for something unrelated
Assessment Findings AAA
Systolic bruit over aorta
Tenderness on palpation
Abd/lower back pain if large
Pulsatile mass in periumbilial area left of midline
Caution with palpation
what is a bruit?
Bruit is a “whooshing” caused by turbulent blood flow through the aneurysm
Symptoms of Thoracic Aortic Aneurysm
Angina- decrease blood flow due to coronary arteries
TIA- decrease blood flow to carotid arteries
Hoarseness, cough, SOB, difficulty swallowing- Pressure on laryngeal nerve
JV distention and edema to face-Pressure on superior vena cava
Some Risks of Aneurysms
Rupture, Pain, Clots, Compression
Rupture
Risk of shock, hemorrhage
Pain
May be painful as it grows, especially in back
Clots
Especially with saccular aneurysms.
Clots may occlude vessels or may cause emboli and block smaller vessels
With clots - blue toe syndrome: acute occlusion to digital arteries. (acute arterial ischemia)
Compression
May compress other structures or organs as aneurysm grows
Diagnostic tests for aneurysm
CT is the number one option
MRI when contrast is contraindicated
Ultrasound for monitoring
Xray is quick
Rupture of an Aneurysm (classic signs)
severe pain, hypotension, pulsatile mass.
Hypovolemia quickly can bleed out
In some cases bleeding may be slowed or stopped by other anatomical structures
Greatest risk if over 6cm and patient has HTN
90% death rate if rupture
Turners sign
Hematoma to flank area
Cullens sign
hematoma to umbilicus area
Nursing care for aneurysm
Frequent vital signs
Detailed history including back and abdominal pain
Monitor peripheral circulation (pulses, temperature, colour)
Continuous cardiac monitoring
Arterial blood gases- watching for hypovolemic shock
Hourly urine output
Observe for signs of rupture
Pay attention to pain level and tenderness over abdomen
Monitor for abdominal distension
interventions for aneurysm
Modify risk factors
Monitoring and treatment of blood pressure with antihypertensives. Will be on antihypertensives for life
Regular HCP visits q6-12 months to monitor aneurysm size
Teach to seek care for back or abdominal pain, fullness, or soreness over the umbilicus, and sudden discolouration of extremities
Post AAA repair
erectile dysfunction can occur due to decreased blood flow to pelvic area during surgery
Some surgery for thoracic except thoracic area is opened (crack the chest)
Endovascular Aneurysm Repair (EVAR)
Catheter is inserted via the femoral artery with a stent on the tip
Stent is deployed into the diseased area
Less durability of stent
Not an option for everyone depending on anatomy
Lower morbidity
Recovery ~ 2 weeks
What is Osteoarthritis (OA)
A degenerative joint disease characterized by the progressive loss of articular cartilage of the synovial joints
It is NOT a normal part of aging!
Osteoarthritis
Bone ends rub together, bone spur, thinned cartilage
Risk factors
most destruction does not begin until 40s.
Most are asymptomatic until their 50s or 60s
Age is the biggest risk factor for the development of OA
Symptoms OA
Joints most commonly affected by OA (hands, knees, hips, spine especially)
Symptoms are UNILATERAL (this is different from RA)
Articular cartilage
Connective tissue that allows the bones to “glide” against one another without friction
Synovium
In conjunction with the surface of articular cartilage, forms the inner lining of joint spaces
Chondrocytes
Specialized cells that produce type II collagen for structural support and repair cartilage damage
Fibrillations
Cracks or clefts on the articular surface
Bone eburnation
Bone-on-bone rubbing
Osteophytes
Outward growths on bone edges. Bones appear wider
Crepitus
crunching sound with movement won’t hear with ra
Patho of OA
- As the articular cartilage degenerates, friction occurs between the bones causing inflammation and pain through the nerve endings in the synovium
2.Chondrocytes attempt to repair the damage to the cartilage but eventually become exhausted and undergo apoptosis - Cartilage gets softer, weaker, and continues to lose elasticity. It degrades and flakes into the synovial space (joint mice)
- Fibrillations , bone eburnation, and osteophytes form
Risk factors for OA
Obesity, smoking, repetitive stress, Age, injury, genetics, decrease estrogen, some neuro, endocrine and hematological disorders, skeletal deformities
Deformity hands
Osteophyte formation may lead to Heberden’s nodes and Bouchard’s nodes on the hands. These nodes are often tender, but do not cause significant loss of function.
They may be distressing due to their visual appearance.
Heberden’s
distal interphalangeal joint
(HIGHER up on the finger)
Bouchard’s
proximal interphalangeal joint (closer to the BODY)
Deformity legs
Osteophyte formation may also contribute to varus deformity (bow-legged) or a valgus deformity (knock-kneed)
In hip OA, one leg may also become shorter than the other as the joint space narrows unilaterally
Varus
outwards
valgus
inward
Signs of OA
OUTGROWTHS: bone spurs, Heberden’s node, Bouchard’s node
STIFFNESS: in late morning, lasting under 30m
TENDERNESS: hard, bony, tender joints
EXACERBATED BY EXERCISE: crepitus with movement, pain with activity (stops with rest)
ONLY IN JOINT: not systemic (no inflammation, redness, fever, fatigue)
Imaging for OA
CT & MRI detect early changes
Xray confirms and stages joint damage. Can identify spurs and osteophytes as well as mice
Labs for OA
ESR and CRP (inflammatory markers) may increase during acute inflammation but are typically normal
Synovial fluid analysis shows no inflammation
Nursing Assessment OA
Pain, stiffness, ADL’s
Tx OA
Medication- NSAIDS
Arthroscopy- Removes loose bodies from the joint
Joint replacement- Hip/Knee replacement most common
Patient teaching OA
Balance, Hot, Cold, Exercise, ROM
What is Parkinson’s Disease?
loss of nerve cells in the brain called the substantia nigra which is responsible for the production of dopamine
The 2nd most common neurodegenerative disease next to Alzheimer’s.
Mean onset is approximately 60 years old, no known cause, or cure
Dopamine
Responsible for voluntary movement as well as memory, learning, sleep, affect and many other functions
Acetylcholine
Responsible for secretions and cognition
Signs and symptoms of Parkinson’s
Tremor, Rigidity, Akinesia, Posture and balance, Bradykinesia is the strongest clinical indicator of dopamine deficiency (generalized slow movement)
Nonmotor Symptoms of Parkinson’s
Emotional changes - anxiety, depression
Sleep problems- fatigue, sleep disorders (insomnia, restless legs, daytime sleepiness)
Pain
Urinary retention
Constipation
Erectile dysfunction
Memory changes
Potential Testing for Parkinson’s
DaTscan (visualization of dopaminergic neurons in a PET scan)
CSF levels may reveal low dopamine
Speech and swallow evaluation
Barium swallow
Risk factors for Parkinson’s
more common in men, age 50+, repeated head injuries, fam hx, environmental factors (pesticides, toxins, poisons), medications that block dopamine (which most times are reversible).
Most often is idiopathic
Medication for Parkinson
LevoCarb is the cornerstone therapy for Parkinson’s disease. Avoid high protein diets with levodopa. Urine will be very dark.
Deep Brain Stimulation
Decreases tremors and involuntary movements
May decrease the amount of medication required
Monitor for signs of infection, stroke-like symptoms, hemorrhage
*works for idiopathic
Risk for aspiration pneumonia
Supervised eating times
Encourage to eat slowly
Eat in an upright position
Have suction available at the bedside
Fall risk
Proper footwear
Keep a clear living space
Use assistive devices
Assisted ambulation
Use rocking motion to initiate movement
Dietary considerations
High calorie
Soft foods/purees to minimize choking risk
Bite sized pieces
Thickened fluids
High fibre due to constipation risk
stage 1 Parkinson
develop mild symptoms but able to go about my day to day life
stage 2 Parkinson
tremors and stiffness begin to worsen, poor posture trouble walking
Stage 3 Parkinson
movement begins to slow down, loss of balance
Stage 4 Parkinson
severe and cause issues day to day, unable to live alone and will need care
Stage 5 Parkinson
walking, standing may be impossible, often confine to wheelchair or bed
What is Spina Bifida
In healthy spine development, a layer of tissue on the left and right fold over the spinal cord to protect it.
Ideally this tissue creates a tight seal, but in the case of spina bifida, an opening is left
The neural tube closes in the 3rd to 4th week of gestation
Ectoderm
A layer that forms over embryos during development.
The ectoderm goes on to form the neural tube that eventually becomes the spinal cord and brain
Meninges
Three layers of membranes that cover and protect the brain and spinal cord
Three classifications of spina bifida
Occulta
Meningocele
Myelomeningocele
Occulta
Not visible externally
most common/least severe
may see a dimple or tuft of hair at site of spina bifida or may have nothing. Covered by skin which prevents any meninges or spinal cord from protruding
Meningocele
Hernial protrusion of sac-like cyst containing meninges and spinal fluid
protective membranes are out but spinal cord intact. Usually correctable with surgery
Myelomeningocele
Hernial protrusion of sac-like cyst containing meninges, spinal fluid, AND spinal cord nerves
least common/most severe
sac is obvious
Signs and Symptoms of Spina Bifida
Ranges in severity, bladder and bowel dysfunction, chronic back pain, limb dysfunction below level of cyst, hydrocephalus, visible cyst to lumbar region
Some Further Complications of Spina Bifida
Orthopedic issues such as scoliosis, club foot, contractures, or dislocated hip
Chiari malformation type 2 (brainstem malformation causing arm weakness and difficulty breathing and swallowing)
Meningitis
Tethered cord syndrome
Risk Factors of Spina Bifida
Maternal Diabetes
Family History- Drugs/Alcohol, genetics, obesity
High body temp.- Hot tubs, high fever during pregnancy
Medications- Anticonvulsants a known risk, especially valproic acid
Folic Acid - Should begin 3 months prior to pregnancy **
Folic Acid
The best way to prevent spina bifida is through the ingestion of folic acid during pregnancy.
Ideally, the pregnant person should begin folic acid supplementation 3 months prior to attempting conception
Dietary changes will also assist in folic acid consumption: encourage green, leafy vegetables like spinach, broccoli, green beans and starches like black beans, rice, and fortified cereals as well as peanut butter and enriched bread
Lab testing for spina bifida
Alpha fetoprotein (AFP) is tested in mother’s serum during pregnancy. It is not always accurate and can be raised due to other disorders. 16th-18th week of pregnancy.
Amniocentesis can be done to draw labs from amniotic sac. Positive AFP is indicative of a neural tube defect.
Imaging for spina bifida
Ultrasound may identify an incomplete neural tube
Pre-natal surgery tx
Preformed before 25 weeks gestation
May improve chance to walk independently and reduce risk of hydrocephalus
High risk to mother and fetus
Post-natal surgery tx
Surgery is performed in the first 24-72 hours of life to close the sac.
In the event of hydrocephalus, shunts are inserted to drain excess fluid into the abdominal cavity.
Closing quickly reduces the risk of meningitis.
Surgery will not regain motor and sensory dysfunction.
Myleomeningocele protection
At birth, cover with a moist, sterile, non-adherent dressing to prevent infection
Use aseptic technique
Keep the baby prone and prevent pressure to the sac
Damage may result in permanent paralysis, leakage of CSF, infection, or damage to the spinal cord and nerves
Nursing Care Must Know
Avoid a rectal temperature
Inserting a rectal thermometer increases the risk of rectal prolapse or perforation in those with spina bifida. Axilla is preferred.
Obstructive Sleep Apnea (OSA)
Also known as Sleep Apnea-Hypopnea Syndrome
Episodes of complete (apnea) or partial (hypopnea) collapse of the upper airway with an associated decrease in oxygen saturation and/or arousal from sleep
Patho of OSA
- Muscles relax and tongue and soft palate fall backward, obstructing the pharynx
2.Each obstruction lasts 10-90 seconds. - Patient may experience HYPOXEMIA (low O2) AND hypercapnia (high CO2)
- This causes a generalizes startle response, snorting, and gasping which moves the tongue and soft palate forward, opening the airway
Risk of untreated sleep apnea
high blood pressure, diabetes, concentration and memory problems, depression, heart failure
Severity of OSA
Mild OSA: AHI ≥ five events per hour
Moderate OSA: AHI ≥ 15 events per hour
Severe OSA: AHI ≥ 30 events per hour
Risk factors of OSA
over 50, obesity, neck circumference over 17inches, craniofacial abnormalities around upper airway, acromegaly, smoking, male, deviated septum, enlarged tonsils, overbite
Clinical manifestations of OSA
Sleep issues
Cognitive
Complications
Sleep issues
Frequent arousal
Insomnia
Daytime sleepiness
Witnessed apneic episodes
Loud snoring
Cognitive
Morning headaches from hypercapnia
Irritability
Fatigue
Personality changes
Complications
HTN
Right-sided heart failure
Cardiac dysrhythmias
Risk for stroke
Diabetes
STOP-BANG
SNORE
TIRED
OBSTRUCTION
PRESSURE
BMI
AGE
NECK
GENDER
Polysomnogram (PSG)
Sleep study to monitor brain activity, oxygen, carbon dioxide, vital signs, and snoring/body movement
PSG is gold standard of diagnosing OSA
Patient teaching for OSA
Sleep on side not back
avoid sedatives
avoid alcohol 3-4 hours before sleep
Treatment options for OSA
ORAL APPLIANCE- A specialized mouth guard that prevents airflow obstruction
CPAP- Use for a MIN of 4h/night
Surgical tx for OSA
tonsillectomy or Uvulo-palato-phayngoplasty (removal of tonsils, uvula, and posterior soft palate)
Septoplasty to repair a deviated septum
Jaw bone realignment
Bariatric surgery
What is pain?
Pain is whatever the experiencing person says it is, existing whenever they says it does”
International Pain Society, 2018
Nociceptive:
Somatic
To do with nociceptive activity in skin
Localized pain (sharp, aching, throbbing)
originates from nociceptive activity in the skin, subcutaneous tissue, bones, muscles, or blood vessels. Sharp, aching, throbbing.
Nociceptive:
Visceral
Activated in the organs/body cavities
Gnawing, cramping, dull
– activated in the organs and body cavities. Diffuse pain. Gnawing, cramping, dull, aching.
Neuropathic
Injury to the central, peripheral, or autonomic nerves
Burning, prickling, tingling, numbness
(invasion of or traction on nerves) arising from injury to central, peripheral or autonomic nervous system. May feel like burning, prickling, tingling, or numbness.
Non Verbal Signs of Pain
Facial expressions (grimacing, furrowed brow, pursed lips, etc)
Clenched jaw/teeth
Grasping blankets
Rigid body
Unusual breathing pattern
Agitation/irritability
Moaning/calling out
Not responding/withdrawn
Flinching to touch
Guarding painful areas
kicking, restless legs, rocking
What is Fibromyalgia?
Fibromyalgia (FM) is a chronic condition that includes widespread, non-articular musculoskeletal pain and fatigue with multiple tender points
Symptoms of fibromyalgia
Patients often experience nonrestorative sleep, morning stiffness, irritable bowel syndrome, and anxiety.
Risk Factors for fibromyalgia
Women, 30-50, Past medical hx rheumatic conditions, chronic, lyme disease, influenza-like illnesses, trauma, deep sleep deprivation, hx of disease.
May be triggered by illness or trauma in susceptible people
Hyperalgesia
painful stimulus produces exaggerated response
Allodynia
pain due to a stimulus that normally does not provoke pain
Some Physiological Abnormalities
Increased Substance P in the spinal cord
Lower levels of blood flow to the thalamus
Thalamus mediates components of pain. Decreased blood flow may affect pain response
Substance P increases sensitivity to pain.
Most common signs of fibromyalgia
Widespread pain- worsens and improves throughout the day
Difficulty discerning origin- cannot tell is muscle, joint, or soft tissue
Head/face pain- stiff, painful neck, and shoulder muscles, TMJ dysfunction 1/3
Point tenderness sites- sensitivities to painful stimuli throughout entire body.
When is it Fibromyalgia??
Pain - widespread
Length of time- at least 3 months
Rule out- cannot be explained by another cause
Tender points
18 points
Tender points not often known how to palpate properly
Tender points above and below waist
Lab results may rule out other disorders
Medications Options for Fibromyalgia
SSRI/ SNRI, Low TCA, OTC meds (Naproxen, ibuprofen, and acetaminophen)
Rest
Rest helps reduce pain, aching, and tenderness, but we want to ensure we are not sedentary! Remaining active and ensuring muscles remain mobile and non-contracted is important for both the management of fibromyalgia and our patient’s overall well-being!
Sleep hygiene (healthy sleep habits) is helpful in ensuring adequate rest. This includes consistent sleep/wake times, a bedtime routine, a calming environment, etc.
Management of fibromyalgia
Message ultrasound therapy, heat and cold, gentle stretching, low impact aerobic exercise, avoid muscle irritants, healthy diet, positive coping/healthy relaxation strategies.
Bulging Disc
often gradual/progressive and may occur in several discs. Although usually treated with medication, decompression surgery possible option.
Herniated Disc
usually an abrupt onset from acute injury. May need surgery if symptoms over 6 weeks and nerve involvement. Often made with increased pressure (lifting, sneezing, bending, etc.)
What is Radiculopathy?
A range of symptoms produced by the pinching of a nerve root in the spinal column (may be anywhere in the spine)
Nerve root compression results in radiculopathy which can cause pain, numbness, and weakness
Pain for nerve compression
Type and location dependent on site of injury. Pain may be burning or sharp and radiate.
numbness
Especially along skin associated with area of compressed nerve
LUMBAR is by far the most common!
Weakness
Loss of sensation, muscle weakness, impaired reflexes, changes to soft tissues
Risk factors for nerve compression
age 30-50
assigned male at birth
fam hx of herniated discs
obesity
overuse of spine/excessive activity
smoking
Diagnosis of nerve compression
MRI by far the most useful imaging – may not see nerve compression on CT or Xray
Nerve conduction (EMG) provides physiological information that assists in diagnosis with MRI.
Check muscle strength and reflexes, pain with movement
The spine
cervical C1-C7
Thoracic T1-T12
Lumbar L1-L5
sacrum and coccyx
cervical
Pain in shoulder, pectoral, scapular regions, down arm into hand, may have issues with grip strength
Thoracic
axial back and chest pain. Band-like chest and abd pain. May have bowel, bladder, and sexual issues
Lumbar
most common. Sciatica down buttock through leg. Stiff walking, flexed positioning, difficulty bending, weak knees, reduces patellar reflex, hip and foot weakness
coccyx
weak foot and plantar flexion, diminished Achilles reflex, sensory loss of perineal and perianal regions
Radiculopathy Prevention
While it can’t always be avoided, staying physically fit, using proper body mechanics when lifting and maintaining a healthy weight reduce risk.
Mild Radiculopathy
Sensory loss and pain without motor deficits
Moderate Radiculopathy
Sensory loss and pain with mild motor deficits
Severe Radiculopathy
Sensory loss and pain with marked motor deficits
Non surgical tx
NSAIDS, opiods, muscle relaxants, corticosteroid injections, heat, ice, message, U/S, TENS, physiotherapy
Surgical tx
Laminectomy- Removal of lamina to access disc
Discectomy- Removal of the disc
Priorities for Radiculopathy
Pain, post-op care, spinal alignment
What to look out for post op
Watch for bleeding/CSF leaks
Keep spine stable and in proper alignment
Monitor for respiratory issues
Cauda Equina Syndrome
A medical emergency in which there is damage to the cauda equina (bundle of nerve roots that extend below the spinal cord around the L4/5)
MRI ASAP if suspected
Surgical decompression within 48 hours to prevent permanent damage
Palliative care
Palliative care is for those with life-threatening illnesses it does not have to mean end of life
Goal of palliative?
main goals of palliative care are to have pain control, avoid a prolonged death, achieve a sense of control, ease family burden, have clear decision making, and complete life tasks
Palliative pain may be caused by:
The disease
Indirect
Treatment
Barriers to Palliative Care
Lack of resources
Lack of knowledge
Misunderstanding
Provider bias
Reluctance
Restrictive eligibility criteria
May fear opioid addiction
Many fear accepting palliative care is “giving up”
Palliative Assessment
Physical:Functional ability, strength/fatigue, sleep/rest, nausea, appetite, constipation, and pain
Psychological:Anxiety, depression, enjoyment/leisure, pain, distress, happiness, fear, and cognition/attention
Social:Financial burden, caregiver burden, roles/relationships, affection, and appearance
Spiritual:Hope, suffering, the meaning of pain, religiosity, and transcendence
Overall goal is to determine site of pain, quality, severity, and impact on function, mood and QOL.
WHO pain ladder
Step 1: most common Tylenol/NSAIDs
Step 2: Codeine is 1/10 the strength of morphine. Major constipation issues. Usually see Tylenol 1,2, and 3 used. SSRIs may inhibit absorption of codeine
Tramadol: good for neuropathic pain. Use in caution with renal or hepatic dysfunction
Step 3: severe pain or moderate pain that doesn’t respond to step 2. If an allergy to morphine, confirm the reaction.
Common Opioid Side Effects
Respiratory Depression
Constipation
Nausea
Sedation
Pruritis
Urinary Retention
Age-Related Considerations
Metabolize drugs more slowly
Greater risk for adverse effects
Risk of GI bleeding with NSAIDs
Multiple drug use (interactions)
Cognitive impairment and ataxia can be exacerbated
Special Populations
Individuals with a past or current substance abuse disorder have the right to receive effective pain management
Assessing and providing relief with a dual diagnosis of pain and substance abuse is challenging
Establish a treatment plan that will relieve pain and minimize withdrawal symptoms
Usually requires a multidisciplinary team approach
Peripheral Neuropathy
Neuropathy can affect one nerve (mononeuropathy), or two or more nerves (polyneuropathies, which is the most common type)
Motor Neuropathy
muscle weakness, twitching, tremors, cramps, or even paralysis
sensory neuropathy
numbness, tingling, burning or loss of sensation, inability to detect temperature changes, difficulty with balance or coordination, and shooting or stabbing pain
Autonomic Neuropathy
problems with heat tolerance, sweating, digestion, bowel or bladder control, swallowing, erection, breathing, and BP
Complications of Peripheral Neuropathy
Burns and skin injury
Falls
Infection
Heart and circulatory system problems
Diabetic foot ulcer
Gangrene
Guillain-Barre Syndrome (GBS)
An acute, rapidly progressing, and potentially fatal form of polyneuritis
GBS affects the peripheral nervous system and results in loss of myelin (segmental demyelination), edema, and inflammation of the affected nerves
GBS manifests as a symmetrical ascending paralysis
Typically triggered by a recent viral or bacterial infection (most common trigger)
GBS – Pathophysiology
- Demyelination occurs
2.The transmission of nerve impulses is stopped or slowed down - The muscles innervated by the damaged peripheral nerves undergo denervation and atrophy
- In the recovery phase, remyelination occurs slowly, and neurological function returns in a proximal-to-distal pattern
GBS – Clinical Manifestations
Symmetrical muscle weakness- Ascending, Loss of deep tendon reflexes
Paresthesia -First in the feet
ANS dysfunction (late signs)- Bp fluctuation, arrhythmia, GI stasis, urinary retention
Neurological- Facial weakness, difficulty with eye movement, difficulty swallowing
Neuropathic pain
Respiratory- As disease progresses risk of resp. acidosis and resp. failure
GBS – Diagnosis
EMG and nerve conduction study results will be abnormal – showing marked demylenation
Electromyography (EMG) assesses the health of muscles and the nerve cells that control them
CSF analysis - will be normal or have a low protein content initially, but after 7 to 10 days, the protein level is elevated and the WBC count is normal
GBS – Assessment & Management
Assess the need for immediate intervention, including intubation and mechanical ventilation. Suctioning PRN
Treat infection ASAP
Prophylactic anticoagulation
Reflexes are usually decreased or absent
Orthostatic hypotension common
vasopressors or volume expanders
Respiratory assessment includes RR, depth, forced vital capacity, and negative inspiratory force
Prophylactic anticoags - low molecular weight heparin or heparin
Treatments of GBS
IVIG- Recommended within 2 weeks of onset
Plasmapheresis- To remove antibodies
GBS nursing care
Address patient and family concerns – emotional support needed
If urinary retention - intermittent or indwelling catheterization
Passive ROM
Eye care -need to prevent corneal damage and irritation
Nutritional therapy - if feeding, need to assess swallowing/for dysphagia, may need NG or TPN
Pain assessment
Skin and wound assessment – turn frequently
GBS – Recovery & Support
Recovery is a slow process that takes months (3–6 on average), with most of the recovery occurring within the first year. Further recovery can be seen even up to 3 years after disease onset
Residual symptoms and relapses are uncommon except in the chronic form of the disease
Complete recovery can be anticipated, although many patients continue to have a degree of residual pain and fatigue, requiring them to change their work and daily activities
GBS – Complications
Respiratory failure due to paralysis of the nerves that innervate the thoracic area
Respiratory tract infection
UTI
Immobility- paralytic ileus, muscle atrophy, contractures, deep vein thrombosis (DVT), pulmonary emboli (PEs), skin breakdown, orthostatic hypotension, and nutritional deficiencies
Trigeminal Neuralgia
Also known as tic douloureux
Uncommon cranial nerve disorder
Extremely painful
Trigeminal neuralgia location
Pain can be in front of the ear, eye, lips, nose, scalp, forehead, cheek, mouth, or jaw.
trigeminal nerve is CN #5 – has both motor and sensory branches – primarily mandibular and maxillary branches involved
TN – Clinical Manifestations
Intense electrical like or stabbing pain to one side of he face
jaw, lips, gums, cheek, forehead, side of nose
Brief attacks- 1s-3m
Unpredictable- Can occur multiple times a day, or months apart. Clustering may also occur.
TN – Diagnosis
Complete neurological exam
MRI
Electromyography (EMG)
R/O other conditions with similar manifestations*
TN – Management
Carbamazepine (Tegretol) – 1st line treatment (watch for decreased WBCs!!)
Baclofen (Lioresal)
Biofeedback strategies
Glycerol rhizotomy
Percutaneous radiofrequency rhizotomy (electrocoagulation)
Microvascular decompression
Bell’s Palsy
A disorder characterized by a disruption of the motor branches of the facial nerve (cranial nerve VII) on one side of the face in the absence of any other disease
Majority of patients make complete recovery (complete recovery in 85% of cases in ~ 3 weeks)
Also known as - peripheral facial paralysis or acute benign cranial polyneuritis
Can sometimes be mistaken as CVA – similar presentation
Etiology Bell’s Palsy
evidence associating immune, infective, and ischemic mechanisms as potential contributors (e.g. reactivation of herpes simplex virus)
Chronic Bell’s Palsy more likely if no recovery within 3-4 months. Chronic facial palsy can be a disabling condition that has an impact on social function, emotional expression, and QOL
Bell’s Palsy – Clinical Manifestations
Acute onset, unilateral facial paralysis, facial drooping, inability to close the eyelid, cant frown or smile, decrease muscle movement, altered chewing ability, neck, mastoid, or ear pain, distortion in sense of taste, altered facial sensation, Affects muscles of the upper and lower face
Symptoms usually reach a peak within 72 hours
major symptoms of bells palsy
Blinking reflex abnormal
Earache
Lacrimation
Loss of taste
Sudden onset
Bell’s Palsy – Diagnosis
Based on clinical presentation
CT or MRI to rule out other conditions (e.g. stroke)
Treatment of Bell’s Palsy
Eye’s - Protection, lubrication, tape closure at night
Oral- Soft diet, chew on unaffected side
Heat- Hot, moist heat can help relieve pain
Medication- Analgesics, corticosteroids, antiviral if HSV causative factor
PT/OT, Emotional support
Recovery - patients with Bell’s palsy recover within about 3-5 weeks of the onset of symptoms
