Exam 3 Flashcards
Where do most burn injuries occur
At home 73%
Industry-related (work) 8%
Recreational accidents 5%
Other sources 14%
What affects severity of burn injuries
Age (young and old people more morbidity and mortality bc thin skin)
Burn depth
TBSA
Inhalation injury
Presence of other injuries
Location of injury in special care areas (face, perineum, hands, feet)
Presence of a chronic illness (DM, bad for wound healing)
Adults with >40% TBSA high risk for m&m
First degree burn
superficial
Epidermis is intact or partially injured
Sunburn or superficial scald
Red, tender, peeling, itching, minimal or no edema, possible blisters (a positive Nikolsky’s sign, upper layer can be separated from lower layers by smearing it).
Complete recovery within a week; no scarring
Second degree burn
partial thickness
Destruction of the epidermis and portion of dermis
Scalds, flash flame contact
Blistered, mottled red base; weeping surface; edema
Recovery 2-3 wks; some scarring and depigmentation
Possible, may require grafting
Third degree burn
Full-thickness
Flame, prolonged exposure to hot liquids, electric current, chemical contact
Total destruction of epidermis and dermis and, in some cases, destruction of connective tissue and muscle (these two things are under the epidermis and dermis)
Painless and lacks sensation–nerve fibers destroyed. Shock. Myoglobinuria (red pigment in urine) and possible hemolysis.
Possible contact points (entrance or exit wounds in electrical burns).
Dry; pale white, red brown, leathery, or charred; coagulated vessels may be visible
Require skin grafting for healing
Fourth degree burn
Deep burn necrosis
Prolong exposure or high voltage electrical injury
Deep tissue, muscle and bone affected
Shock, myoglobinuria and possible hemolysis
Charred
Amputations likely
Grafting of no benefit, given depth and severity of wound(s).
Rule of nines
11 nines and 1% for perineum
4.5% front and back of head (9)
4.5% front and back of arm (9)
4.5% front and back of arm (9)
18% front of midsection (two 9s’)
18% back of midsection (two 9’s)
9% front of leg (9)
9% back of leg (9)
9% front of leg (9)
9% back of leg (9)
Major burn injuries
Adults with greater than 40% TBSA burned are at high risk for morbidity and mortality.
Burns exceed 30% TBSA produce both a local and a systemic response and are considered major burn injuries
Cardiovascular burn shock
Hypovolemia (inflammation > leaky capillaries > fluid moves out of vasculature > third spacing)
Increased capillary permeability (cells stay in, plasma leaves)
Decreased CO and BP
Additional findings include hypotension and tachycardia
Initial fluid and electrolyte changes
Hct and Hgb–elevated due to loss of fluid volume and fluid shifts into interstitial space (third spacing)
sodium–decreased due to third spacing (hyponatremia) sodium follows water
potassium–increased due to cell destruction (hyperkalemia)
Later fluid and electrolyte changes
Hgb and Hct–decreased due to fluid shift from interstitial space back into vascular fluid
Serum sodium levels vary in response to fluid resuscitation.
Potassium–decreased due to fluid shift and inadequate potassium replacement.
Blood glucose–elevated due to stress response
Total protein and albumin–low
Compartment syndrome and edema in burn
When edema develops: monitor for circulation: as the taut, burned tissue can act like a tourniquet, especially if the burn is circumferential.
Treatment for edema
Elevating the affect limb
In severe cases: escharotomy (cutting through the eschar) or
Fasciotomy (deeper incision through fascia to relieve muscle constriction)—to restore tissue perfusion
Pulmonary alterations with burn
Can be either thermal or/and chemical
Thermal inhalation injury:
findings may include singed hair, eyebrows, and eyelashes; a sooty appearance to sputum; hoarseness, and wheezing.
Treatment of inhalation injury
Oxygenation, encourage the patient to cough
Monitor the patient closely and continuously
What to watch for in inhalation injury
airway management is the priority
watch for ARDS and pneumonia
increased secretions and inflammation
CO poisoning
suspected if the injury took place in an enclosed area
findings include erythema (pink or cherry red color skin) and upper airway edema, followed by sloughing of respiratory tract mucosa
hgb carries 4 oxygen, which are now occupied by CO
Normal pulse ox
Treatment of CO poisoning
100% oxygen
Burn unit referral criteria
partial thickness burns greater than 10%
burns that involve the face, hands, feet, genitalia, perineum, or major joints
third-degree burns in any age group
electrical burns
chemical burns
inhalation injury
with pre existing medical disorders
concomitant trauma
Emergency Procedures at the Burn Scene
use cool water (can use cool clean towels or sheets, never use ice or cold soaks for longer than several mins)
Remove restrictive objects like jewelry and piercings (circulation!)
Cover wound w clean cloth to prevent contamination and hypothermia
Irrigate chemical burns with lots of water
Educate family to monitor for infection
Don’t use greasy lotions or butter on burn
Tetanus and immunization status
Emergent/Resuscitative phase of burns (interventions)
oxygenation, secretions removal, bronchodilation are URGENT!!
Fluids for emergent phase of burn
Lactated Ringers preferred: sodium, potassium, chloride, lactate (bicarbonate)
higher pH 6.5 than NS (5.0); patients may be in metabolic acidosis and the metabolized lactate will buffer the acidosis
Urine output for burn pts
0.5-1ml/kg/hr–for thermal and chemical burn
75-100 ml/hr for electrical injuries
Acute/Intermediate phase of burns
From beginning of diuresis to near completion of wound closure
Priorities:
-Wound care and closure
-Prevention or treatment of complications
-Nutritional support so they don’t burn their own muscles
Late pulmonary complications secondary to inhalation injuries
Hyperthermia is common (resetting of the core body temperature)
Pain management for burns
Avoid IM or subcutaneous injections (maintain skin integrity)
Use intravenous opioid analgesics such as morphine sulfate, hydromorphone (Dilaudid), and fentanyl (Sublimaze)
Monitor for respiratory depression.
The use of patient-controlled analgesia is appropriate for some clients.
½ hour prior to wound care or cleaning so procedure can go smoothly
Infection prevention for burns
top priority
restrict plants and flowers due to the risk of contact with Pseudomonas aeruginosa (gram-negative rod)
Green line something?
restrict consumption of fresh fruits and vegetables
limit visitors
administer tetanus shot if indicated
After burns infection
intestinal mucosal becomes permeable
microbial flora and endotoxins can pass freely into the systemic circulation and causing infection
We want bacteria to stay in the GI tract. If it leaves the GI tract it’s bad and can lead to infection (translocation). Can go to cardiovascular system and be bad
What can bacterial infection from the patient’s intestinal tract lead to and prevention of
bacterial translocation and endotoxemia–septic shock
early enteral feeding is important to keep the GI lining intact and prevent that permeability
Nutritional support after burn
The client who has a large area of burn injury will be in a hypermetabolic and hypercatabolic state. The client may need 8,000 calories per day.
Prevent hypoglycemia
Increase protein intake to prevent tissue breakdown and to promote healing
May lose weight during recovery (fat catabolized, fluids lost, lowered caloric intake)
Restoration of mobility after burn
Maintain correct body alignment, splint extremities, and facilitate position changes to prevent contractures.
Maintain active and passive range of motion.
Assist with ambulation as soon as the client is stable.
Apply pressure dressings to prevent contractures and scarring
Monitor areas at high risk for pressure sores
Wound cleaning for burns
hydrotherapy (shower for ambulatory or shower carts for non)
intact blisters should be left alone
remove non viable loose skin
warm running water (watch for hypothermia)
use mild soap or detergent to gently wash burns and then rinse with room-temperature water
encourage the client to exercise joints during the hydrotherapy treatment
Lotion only for intact skin, not for these people
Special ointments used
silver sulfadiazine 1% (Silvadene)
for burns
most bactericidal agent
minimal penetration of eschar
contraindicate with allergies to sulfa
used with occlusive dressings
silver nitrate 0.5%
for burns
bacteriostatic (stop the bacteria from reproducing) and fungicidal
inexpensive
does not penetrate eschar
stains clothing and linen
discolors wound, making assessment difficult
painful on application
Mafenide acetate 5% to 10% (Sulfamylon)
for burns
effective against gram-negative and gram-positive organisms
diffuses rapidly through eschar
10% drug of choice for electrical burns
used on wounds exposed to air
used as a solution for occlusive dressings to keep the dressing moist
Bacitracin
for burns
used on wounds exposed to air or with modified dressings
maintains joint mobility
bacteriostatic against gram-positive organisms
painless and easy to apply
limited effectiveness on gram-negative organisms
Wound dressing for burns
clean then patted dry (removed all previous ointments) It is important to cleanse the wound thoroughly.
applied topical agent
a light dressing should be used over joint areas (if it is needed)
dressings that adhere to the wound can be removed by moistening the wound with tap water
sterile scissors and forceps may be used to trim loose eschar and encourage separation of devitalized skin (you might see some bleeding, which is ok)
Wound debridement for burns
Mechanical (scissors/scalpel/forceps to remove eschar)
Chemical (enzymatic)
surgical (excision to remove devitalized tissue with early burn wound closure, most important to contribute to survival!)
Wound grafting
Autograph (own skin)
Homograft (living or recently dead humans)
heterograft (pigs or other animals)
Amnion (placenta, frequent changes)
Biobrane (synthetic, trimmed as it separates, leaving healed wound)
Nursing actions with grafting
maintain immobilization of graft site
elevate extremity
provide wound care to the donor site
administer analgesics
Monitor for evidence of infection before and after skin coverings or grafts are applied
Evidence of infection of graft
discoloration of unburned skin surrounding burn wound
green color to subcutaneous fat
degeneration of granulation tissue
development of subeschar hemorrhage
hyperventilation indicating systemic involvement of infection
unstable body temperature
Duration of rehab phase of burn
From major wound closure to return to individual’s optimal level of physical and psychosocial adjustment
Priorities in rehab phase of burn
Prevention and treatment of scars and contractures
Physical, occupational, and vocational rehabilitation
Functional and cosmetic reconstruction
Psychosocial counseling
Functions of the liver
Glucose metabolism
Ammonia conversion
Protein metabolism
Fat metabolism
Vitamin and Iron storage
bile formation
bilirubin excretion
drug metabolism
Glucose metabolism
metabolism of glucose and regulation of blood glucose concentration.
Stored as glycogen (obtained from portal venous blood)
Released as glucose
Gluconeogenesis
Gluconeogenesis
synthesize glucose by using amino acids from protein breakdown
Ammonia conversion
convert ammonia to urea (excreted in the urine)
the use of amino acids for gluconeogenesis results in the formation of ammonia
Bacteria in the intestines can also produce ammonia.
ENCEPHALOPATHY
Protein metabolism
liver synthesizes almost all of the plasma proteins–including albumin and clotting factors (not enough of these in patients with liver cirrhosis or failure, low oncotic pressure and ascites)
Fat metabolism
breakdown fatty acids into ketone bodies when the availability of glucose metabolism is limited
Vitamin and iron storage
A, B, D, B-complex, iron, and copper
Bilirubin
Breakdown of hemoglobin
Drug metabolism
barbiturates for psych patients, opioids, sedatives, anesthetics and amphetamines.
Esophageal varices
Lots of bleeding, projectile, even
Food passing through can cut the varices and cause bleeding
Caused by portal hypertension
Nursing management of esophageal varices
Gastric suction: keep the stomach as empty as possible and to prevent straining and vomiting.
Monitor the blood pressure since they can bleed massively
Anticipate vitamin K therapy and multiple blood transfusion (two nurses)
Hepatic encephalopathy
Neuropsychiatric manifestation of hepatic failure associated with portal hypertension and the shunting of blood from the portal venous system into the systemic circulation.
Liver is not able to convert ammonia to urea
How to reduce serum ammonia
Elimination of protein from the diet
Administration of antibiotics, such as neomycin to reduce intestinal bacteria
Early symptoms of hepatic encephalopathy
Forgetfulness, confusion
Sleep during the day, insomnia at night
Advanced symptoms of hepatic encephalopathy
Shaking of the hands or arms (asterixis)
Disorientation, slurred speech
Sweet, slightly fecal odor to the breath
Grade I hepatic encephalopathy
Shortened attention span
Grade II hepatic encephalopathy
Lethargy with slight disorientation
Grade III hepatic encephalopathy
Somnolence with gross disorientation
Grade IV hepatic encephalopathy
Coma
Management of hepatic encephalopathy
Lactulose (cephulac): traps and expels ammonia in feces. Can be diluted with fruit juice, monitor for low K+ and dehydration. Orange gross nectary med
Deep breathing to prevent atelectasis, pneumonia, and other respiratory complications.
Pancreas
20 cm long
Behind the stomach
Soft tissue
Risk factors of pancreatic cancer
cigarette smoking
chronic pancreatitis
family history of pancreatic or other cancers
age 60 and older
exposure to industrial chemicals
toxins in the environment
diet high in fat, meat, or both
Facts about pancreatic cancer
70% originate in the head of the pancreas (connection to other organs)
functioning islet cell tumors–associated with the syndrome of hyperinsulinism
7% dx in early stage
80-85% have advanced, unresectable tumor when first detected
7% survival rate at 5 years
Clinical manifestations of pancreatic cancer
pain, jaundice, and wt loss–80% of patient
rapid, profound, and progressive wt loss unrelated to GI
more severe at night and accentuated when lying supine
relief by sitting up and leaning forward
ascites
DM may be an early sign
meals aggravate epigastric pain
Assessment and dx findings of pancreatic cancer
Spiral CT: 85-90% accurate
MRI
ERCP
endoscopic ultrasound
percutaneous fine-needle aspiration biopsy of the pancreas
ERCP
Endoscopic retrograde cholangiopancreatography
A technique that combines the use of endoscopy and fluoroscopy to diagnose and treat certain problems of the biliary or pancreatic ductal systems.
Medical management of pancreatic cancer
treatment limited to palliative measures
extensive growth of tumor
widespread metastases (liver, lungs, and bones)
Nursing management of pancreatic cancer
pain management: especially at night time
Refer to hospice care
Tumors of the head of the pancreas
60-80% tumors occur in the head of the pancreas
tumors may obstruct the common bile duct
obstruction cause jaundice, clay-colored stools, and dark urine
need a biliary-enteric shunt to relieve the jaundice
Preop for pancreas head tumors
diet high in protein along with pancreatic enzymes
adequate hydration
Correction of prothrombin deficiency with vitamin K
Treatment of anemia
Whipple’s procedure
pancreaticoduodenectomy
removal of the gallbladder, a portion of the stomach, duodenum, proximal jejunum, head of the pancreas, and distal common bile duct
reconstruction involves connection of the remaining pancreas and stomach to the jejunum
result: removal of the tumor, allowing flow of bile into the jejunum
MAJOR procedure
Post-op whipple’s procedure
pt may experience malabsorption and hyperglycemia
they still need to take pancreatic enzymes
low fat diet
vitamin supplement
Renal blood flow
receive 1000 to 1300 ml of blood per minute
GFR
the amount of plasma filtered through the glomeruli per unit of time
125ml/min-200 ml/min
directly related to the perfusion pressure in the glomerular capillaries–related to renal blood flow
Need proper pressure gradient. Blood going into the kidneys should be higher than the blood coming out of the kidneys
Functions of the kidneys
Filter blood
Excrete waste
Regulate electrolytes
Regulate pH
Regulate BP
Regulate RBC production
Vitamin D synthesis
AKI
when the kidneys cannot remove the body’s metabolic wastes or perform their regulatory functions
accumulation of body wastes
affecting endocrine and metabolic functions
fluid, electrolyte, and acid-base disturbances
systemic disease
Metabolic acidosis and fluid electrolyte imbalance
AKI assessment
renal sonogram or a CT or MRI: anatomic changes like stones, tumor, or cysts
BUN level increases
serum creatinine
BUN increases dependent on the degree of
catabolism (breakdown of protein)
renal perfusion
protein intake
medications such as corticosteroids
Serum creatinine
monitoring kidney function and disease progression and increase with glomerular damage
more sensitive than BUN as an indicator of renal function
Prerenal AKI
hypoperfusion
Low volume
Impaired cardiac efficiency
Vasodilation from 3rd spacing
Prerenal ARF
Volume depletion in prerenal AKI
Hemorrhage
Burns
GI losses (V/D/NG suction)
Renal losses (diuretics)
Impaired cardiac efficiency in prerenal AKI
MI
HF
dysrhythmias
cardiogenic shock
Vasodilation from 3rd spacing in prerenal AKI
Anaphylaxis
AntiHTN meds
Sepsis
Prerenal ARF in prerenal AKI
Lasix/fluid challenge (increased urine output)
What can happen if prerenal AKI is not treated properly
Ischemia
Necrosis
Intrarenal AKI
actual tissue damage to the glomeruli or kidney tubules
focal segmental glomerulosclerosis (fibrosis in the glomerulus)
Prolonged renal ischemia
Nephrotoxic agents
Infectious processes
Prolonged renal ischemia in intrarenal AKI results from
pigment nephropathy (associated with the breakdown of blood cells containing pigments that in turn occlude kidney structures)
myoglobinuria (trauma, crush injuries, burns)
hemoglobinuria (transfusion reaction, hemolytic anemia)
Nephrotoxic agents in intrarenal AKI
aminoglycoside antibiotics (gentamicin, tobramycin)
radiopaque contrast agents w/o proper hydration
heavy metals (lead mercury)
solvents and chemicals (ethylene glycol, carbon tetrachloride, arsenic)
nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen
ACE inhibitors
Infectious processes in intrarenal AKI
acute pyelonephritis
acute glomerulonephritis
Postrenal AKI
obstruction distal to the kidney
pressure rises in the kidney tubules and eventually, the GFR decreases (less of pressure gradient)
both of the ureters are blocked, or the bladder is affected
Causes of postrenal AKI
urinary tract obstruction:
calculi (stones)
tumors
benign prostatic hyperplasia
strictures
blood clots
Clinical characteristics of AKI
…
Phases of AKI
initiation
oliguria
diuresis
recovery
Initiation in AKI
Begins with initial insult and ends when oliguria develops
Oliguria in AKI
Less than 400ml urine in 24 hours or 0.5ml/kg/hr of urine output
increase in the serum concentration of substances usually excreted by the kidneys
urea, creatinine, uric acid, organic acids, intracellular cations (potassium and magnesium)
May develop hyperkalemia: life-threatening
Diuresis in AKI
gradual increase in urine output–glomerular filtration has started to recover
lab results stabilize
urine output may be normal or above normal
uremic symptoms may still be present
observed for dehydration
Recovery period in AKI
improvement of renal function
may take 3-12 months
lab values return to normal
1-3% permanent reduction in GFR, but not clinically significant; however, those with pre existing CKD, an episode of AKI may necessitate beginning CRRT (continuous renal replacement therapy, like dialysis but continuous and can only be done in ICU)
Lab values in AKI patients
Hyperkalemia (3.5-5)
Elevated phosphate (2.5-4.5)
Low calcium (8.5-10.2)
Anemia (hct 45-52M or 37-48F)
Preventing hospital-acquired AKI
radiocontrast-induced nephropathy (CIN)
Prehydration with saline is the most effective method to prevent CIN (N-acetylcysteine administration is no longer recommended as a preventative measure.)
Treating underlying causes in AKI
IV fluid
transfusion of blood products (albumin)
Dialysis can treat what in AKI
hyperkalemia
metabolic acidosis
pericarditis
pulmonary edema
hyperkalemia in AKI
most life-threatening
ECG changes
tall, tented, or peaked T waves
changes in clinical status
irritability
abd cramping
diarrhea
paresthesia
generalized muscle weakness
Treatment of hyperkalemia in AKI
give cation-exchange resins orally or by retention enema:
KAYEXALATE, gravy consistency, brown, oral drink or retention enema
SODIUM POLYSTYRENE SULFONATE
Takes some time to work
Hemodynamically unstable in AKI
low bp
changes in mental status
dysrhythmia
Treatment of hemodynamic instability in AKI
IV dextrose 50%, insulin, and sodium bicarbonate can be given to shift K+ back into the cells.
Works QUICKLY even faster than kayexalate and dialysis
Also helps with acidosis state, brings up pH
Treatment for severe acidosis in AKI
sodium bicarbonate
dialysis
Treatment of elevated phosphate level in AKI
Calcium carbonate
Nutritional therapy for AKI
high carbohydrate meals to spare protein for tissue healing
avoid foods and fluids containing potassium or phosphorus (body cant get rid of it)
high-protein, high-calorie diet during diuretic phase
Why do we do nutritional therapy in AKI
severe nutritional imbalances
from N/V, impaired glucose use and protein synthesis, increased tissue catabolism
Nursing management of AKI
monitoring fluid and electrolyte balance
reducing metabolic rate (bed rest during acute stage and treat fever and infection)
promoting pulmonary function
preventing infection
providing skin care
Chronic kidney disease
Also known as ESRD
Most common causes of ESRD
DM combined with HTN cause 70% of cases
about 15% of adult U.S. population suffer from chronic kidney disease
ESRD <15% GFR
the last “stage” of CKD in which the patient is dependent on dialysis for survival
90% of nephrons have been destroyed
Still a little urine output usually
ESRD complications
HTN
hyperkalemia
pericarditis, pericardial effusion, and pericardial tamponade
Anemia
Bone disease
HTN in ESRD
sodium and water retention (fluid overload) and malfunction of the renin-angiotensin-aldosterone system
Hyperkalemia in ESRD
Decreased excretion, metabolic acidosis, catabolism, and excessive potassium intake from diet, medications, or IV solutions
pericarditis, pericardial effusion, and pericardial tamponade in ESRD
retention of uremic waste products and inadequate dialysis
Anemia in ESRD
decreased erythropoietin production (kidneys usually produce it)
Decreased RBC lifespan
Bleeding in the GI tract from irritating toxins and ulcer formation
Blood loss in the dialysis circuit and dialyzer after HD has been completed
Bone disease in ESRD
retention of phosphorus, low calcium, low vitamin D
Medical management of ESRD (meds)
maintain kidney function and homeostasis as long as possible (not reversible, maintain what they have left, slow the progression)
Renagel (binding phosphate)–sevelamer carbonate, give it with meals
antihypertensive and cardiovascular (ACE inhibitor)
erythropoietin (Epogen)-subq in belly, 2 nurses bc expensive
Avoidance of NSAIDs (acetaminophen OK), definitely avoid aminoglycosides
nutritional therapy in ESRD
Protein regulation
Fluid restriction
Vitamin supplements
Low potassium, sodium, and phosphate
Protein regulation in ESRD
Patients on dialysis need a higher intake of protein than healthy adults and current protein recommendations for stable patients on HD is 1.2 g/kg/day
only high biological value protein: dairy products, eggs, meats)
Fluid restriction and vitamins in ESRD
500mL to 600mL more than the previous day’s 24 hours urine output.
Take vitamin supplements
B and C go after HD (water soluble)
Types of dialysis
HD: hemodialysis
PD: peritoneal dialysis
For relatively stable pts
CRRT: continuous renal replacement therapies (for critically ill pts)
Dialysis and kidney transplants
Pts receive kidney transplant without having to go through dialysis have better outcome than have dialysis first then receive kidney transplant.
Hemodialysis
prevents deaths
does not cure renal disease
does not compensate for the loss of endocrine or metabolic activities of the kidneys (That’s why they need supplements and epogen)
three times a week; 3-5 hours each time
When it is done at home the time and frequency can be adjusted
Know their schedule so you can plan meds!
Dialyzer
Used in hemodialysis
Artificial kidney
synthetic semi permeable membrane
replacing the renal glomeruli and tubules as the filter for the impaired kidneys
HD is based on
Diffusion, osmosis, and ultrafiltration
Diffusion in HD
toxins and wastes are removed
move from blood to dialysate (solution made up of all the important electrolytes in their ideal extracellular concentrations)
Osmosis in HD
excessive water is removed
move from low concentration to high
Ultrafiltration in HD
Negative pressure applied to remove water
HD blood must be returned at a rate of
300-500 mL/min
Vascular access devices for HD
double-lumen, non-cuffed, large-bore catheter (Subclavian not to be used**, internal jugular, femoral vein)
double-lumen, cuffed catheters can also be used
Inserted by surgeon or interventional radiologist into internal jugular
Good for longer term use
Cuffs under the skin for HD
reducing the risk for ascending infection
stabilize the catheter
limit movement
provide a barrier against microorganisms
cuffed compared to non-cuffed is better for longer term
AV fistula for HD
created surgically by joining (anastomosing) an artery to a vein
takes 2-3 months to “mature”
venous segment needs to dilate (increase blood flow)
to accommodate two large-bore needles
the longest useful life and the best option for vascular access (but sometimes cuff/non-cuffed is used because this takes months to mature and there may be an emergency)
AV graft for HD
created by subcutaneously interposing a biologic, semi biologic, or synthetic graft material between an artery and vein
created when vessels are not suitable for creation of an AV fistula (like patient with DM, challenged integrity of blood vessels)
pt may have multiple access (ask which is most recent and check for thrill/bruit)
Nursing management of HD
Watch for complications during dialysis:
clotting of the circuit
Air embolism
inadequate or excessive ultrafiltration
hypotension
cramping
vomiting
blood leaks
contamination
access complications
Pharm therapy for HD
water soluble medications can be removed readily
fat soluble adhere to other substances (like albumin) are not dialyzed out very well
AntiHTN meds for HD
Avoided on dialysis day
(dialysis can lead to hypotension)
once daily medication can be held until after the dialysis treatment
Nutritional and fluid therapy for HD
goal: minimize uremic symptoms and fluid and electrolyte imbalances
Maintain protein 1.2-1.3 g/kg /day
fluid restriction (daily urine output + 500mL/day)
sodium restriction: 2-3 g/day
interdialytic weight gain <1.5kg
potassium restriction
Record how much fluid removed from the patient during dialysis!!
CRRTs
continuous renal replacement therapies
for those who are clinically unstable for traditional hemodialysis
can be initiated quickly
What does CRRTs NOT do
produce rapid fluid (shifts traditional dialysis does this, CRRT patients can’t tolerate this)
Require dialysis machines
Require dialysis personnel
What DOES CRRT do
continuous slow fluid and toxins removal
hemodynamic effects are mild and better tolerated
does not require arterial access
critical care nurse can set up, initiate, maintain, and terminate the system
PD
More common in UK
Same effectiveness as HD
For those who are unwilling to undergo HD or renal transplantation
Patient needs to be more independent and able to maintain sterile techniques
Fewer dietary and fluid restrictions than HD
aseptic technique
prime the tubing first
Peritoneal membrane for PD
serves as the semipermeable membrane
Dialysate in PD
warm the dialysate (hypertonic) to body temperature (prevents cramping)
dilate the vessels of the peritoneum to increase urea clearance
using dry heating (not microwave or warm water)
Tube inserted into peritoneal cavity
Exchange of PD
exchange: infusion, dwell, and drainage of the dialysate
Infusion of PD
Infused by gravity (bag higher than peritoneum)
5-10 mins to infuse 2-3 L of fluid
drainage 10-20 mins
Complications of PD
Peritonitis
Leakage
Bleeding
Peritonitis in PD
most common and serious complication
cloudy dialysate drainage fluid
diffuse abdominal pain
rebound tenderness occur much later
lose large amt of protein through the peritoneum
acute malnutrition and delayed healing may result
Treatment of peritonitis in PD
Intraperitoneal administration of antibiotic 14-21 days
Leakage in PD
Reduce abdominal muscle activity (bending, lifting over 5 lb) and straining during bowel movements
can be avoided by using small volumes (500 mL) of dialysate, gradually increasing the volume up to 2000 to 3000 mL
Bleeding in PD
bloody drainage
especially in young, menstruating women (hypertonic fluid pulls blood from the uterus, through the opening in the fallopian tubes and into the peritoneal cavity)
common during the first few exchanges after a new catheter insertion
No intervention if this stops in 1-2 days
What to do for bleeding during PD
more frequent exchanges and the addition of heparin to the dialysate during this time to prevent blood clots from obstructing the catheter
Long term complications of PD
hypertriglyceridemia
abdominal hernias (increased abd pressure)
hemorrhoids (increased abd pressure)
Low back pain
Hypertriglyceridemia in PD (meds)
pt should use beta-blockers and ACE inhibitors; aspirin and statins to control blood pressure and prevent cardiovascular diseases since the fluid is hypertonic
Acute intermittent PD
not as efficient as HD, can be used for those hemodynamically unstable patient
Common routine of acute intermittent PD
10 min infusion
30 min dwell time
20 min drain time
If acute intermittent PD not draining well
turn pt side to side or raising the head of the bed
should not push the catheter further into the peritoneal cavity
CAPD
continuous ambulatory peritoneal dialysis
gives pt reasonable freedom and control of daily activities
requires a serious commitment to be successful
less fluctuations in the lab values than intermittent PD or hemodialysis since it’s more frequent
serum electrolyte levels usually remain in the normal range
done 7 days a week, 4-5 times a day
CCPD
continuous cyclic peritoneal dialysis
pt can sleep when connecting to the machine at night time
a cycler is programed to provide exchange
during the day time: either by using a “Y” set or reattaching to the cycler
lower infection rate
allow pt free from exchange throughout the day
Nursing management of the hospitalized patient on dialysis
protecting vascular access
taking precautions during IV: slow rate
detecting cardiac and resp complications (pericarditis)
controlling electrolyte levels and diet
Protecting vascular access in hospitalized dialysis pt
the arm with access should not be used for BP or blood drawn, tight dressings, restraints, and jewelry should be avoided
the bruit or “thrill” must be evaluated every 8 hours
Preop kidney surgery
encourage fluid unless contraindicated
if infection is present: broad-spectrum antimicrobial
coagulation studies
Postop kidney surgery
hemorrhage and shock–chief complications
fluid and blood component replacement
abd distention (NG tube to decompress the abd)
paralytic ileus (listen to bowel sounds)
oral fluids after the passage of flatus
Contraindications of kidney transplant
recent malignancy
active or chronic infection
severe irreversible extrarenal disease
active autoimmune disease
morbid obesity (BMI >35)
current substance abuse
Kidney transplant
pt’s native kidneys not removed
transplanted kidney is placed in the patient’s iliac fossa anterior to the iliac crest
production of urine: overall success of the procedure
When can kidney rejection and failure occur after transplant
Within 24 hours (hyperacute)
within 3-14 days (acute)
after many years
Minimizing rejection in kidney transplant
combination of glucocorticoids and other medications to affect the action of lymphocytes
SE of rejection therapy in kidney transplant
nephrotoxicity, HTN, HL, hirsutism, tremors, blood dyscrasias, cataracts, gingival hyperplasia, and several type of cancer
Assessing the pt for kidney transplant rejection
oliguria, edema, fever, increasing blood pressure, wt gain, and swelling or tenderness over the transplanted kidney or graft
rise in serum creatinine among those taking cyclosporine (Neoral)
Causes of TBI
falls (48%)
motor vehicle crashes (14%)
struck by objects (15%)
assaults (10%)
Facts about TBI
80% of TBI are concussions (mild TBI)
adults 75 years of age or older have the highest TBI related hospitalization and death rates
African Americans have the highest mortality rates.
61% of TBIs among adults aged 65 and older results from falls
Primary injury in TBI
the consequence of direct contact to the head/brain during the instant of initial injury
Nurse can’t prevent this
Secondary injury in TBI
hours and days after initial injury
Results from inadequate delivery of nutrients and oxygen to the cells
Identification, prevention, and treatment
Nurse can prevent, assess for hydration and oxygenation
Scalp injury
Minor injury
Blood vessels constrict poorly–bleeding profusely
-or develop hematoma
If laceration: watch for infection
Large piece of tearing away of the scalp: potential life threatening (a true emergency)
Open vs closed skull fractures
Open: tear in the dura
Close: dura is intact
Simple skull fracture
linear fracture-a break in the continuity of the bone
Comminuted skull fracture
a splintered or multiple fracture line
depressed skull fracture
bones of the skull are forcefully displaced downward–require surgery within 24 hours of injury
Something maybe fell on their head
Basal skull fracture
fracture of the base of the skull
Clinical manifestations of skull fractures
Persistent localized pain
Clinical manifestations of basal fracture
hemorrhage from the nose, pharynx, or ears, and blood may appear under the conjunctiva
an area of ecchymosis may be seen over the mastoid (Battle’s sign)
CSF may escapes from the ears and the nose
Older adults with head injuries
Higher mortality rates
Longer hospitalization
Poorer functional outcomes
Neurological assessment: challenging (hearing/visual defects, preexisting cognitive issues)
High risk for hematomas (small brain and blood thinners)
Closed brain injury
Blunt
when the head accelerates and then rapidly decelerates or collides with another object
brain tissue damaged but there is no opening through the skull and dura
Open brain injury
when object penetrates the skull, enters the brain, and damages the soft brain tissue in its path
when blunt trauma is so severe that it opens the scalp, skull, and dura to expose the brain
Focal brain injury
Contusions
Hematomas
Diffuse brain injury
Concussions
Diffuse axonal injuries
Contusion
Least severe
Caused by severe acceleration-deceleration force or blunt trauma
Brain is bruised and damaged in a specific area
Mostly in the anterior portions of the frontal and temporal lobes
loss of consciousness associated with stupor and confusion
Hemorrhage and edema peak after 18-36 hours
Intracranial hemorrhage
Hematoma
major symptoms are delayed until the hematoma is large enough to cause distortion of the brain and increased ICP
a rapidly developing but small one is more dangerous than a larger but slowly developing one
Usually seen in elderly because there’s more space
BRAINSTEM HERNIATION!! HUGE problem with ICP so watch it
hematoma in intracranial hemorrhage
collection of blood in brain that may be epidural
epidural hematoma
blood collected in the epidural space (between the skull and the dura mater)
Seen in skiing
S/S of epidural hematoma
brief LOC followed by a lucid interval (bad) in which the patient is awake and conversant (because rapid absorption of CSF and decreased intravascular volume–compensation).
pt becomes increasingly restless, agitated, and confused
suddenly, pt’s consciousness deteriorates quickly accompanied with other signs of neurological deficits (dilation and fixation of a pupil or paralysis of an extremity, always check pupils!!)
extreme emergency!!!
marked neurologic deficit or even respiratory arrest can occur within minutes
Treatment of epidural hematoma
making openings through the skull (burr holes) to decrease ICP
remove clots and control bleeding
emergency craniotomy
subdural hematoma and causes
Not as serious as epidural
collection of blood between the dura and the brain
trauma
coagulopathies or rupture of an aneurysm
venous in origin so it’s slower! Epidural is arterial so it’s faster
rupture of small vessels that bridge the subdural space
Acute subdural hematoma
changes in LOC, pupillary signs, and hemiparesis
There may be minor or even no symptoms with small collections of blood.
Coma, increasing BP, decreasing HR, and slowing RR—acquired immediate intervention (craniotomy).
Chronic subdural hematoma
develop from seemingly minor head injuries
seen most frequently in the elderly
atrophy brain: minor injury can shift the brain contents
may be mistaken for a stroke
S/S of chronic subdural hematoma
severe HA comes and goes
alternating focal neurologic signs
personality changes
mental deterioration
focal seizures
Treatment of chronic subdural hematoma
surgical evacuation of the clot
Intracerebral Hemorrhage & Hematoma
bleeding into the substance of the brain
traumatic falls, bullet wounds, stab injuries
systemic hypertension: rupture of a brain vessel
rupture of a saccular aneurysm
vascular anomalies
intracranial tumors
bleeding disorders such as leukemia, hemophilia, aplastic anemia, and thrombocytopenia
complications of anticoagulant therapy
Management of Intracerebral Hemorrhage & Hematoma
supportive care
control of ICP
administration of fluids, electrolytes
antihypertensive medications
surgical intervention: craniotomy or craniectomy
Concussion
a temporary loss of neurologic function with no apparent structural damage
If frontal lobe affected: bizarre irrational behavior
If temporal lobe affected: temporary amnesia or disorientation
S/S of worsening symptoms of concussion
decrease in LOC, worsening headache, dizziness, seizures, abnormal pupil response, vomiting, irritability, slurred speech, and numbness or weakness in the arms or legs
What can repeated concussions lead to
chronic traumatic encephalopathy syndrome (permanent)
The presentation is similar to Alzheimer disease: personality changes, memory impairment, and speech and gait disturbances.
Imaging findings: temporal lobe atrophy
Diffuse axonal injury
No lucid interval, immediate coma, decorticate and decerebrate posturing
supportive care
prognosis is poor
consider organ donation
MRI to evaluate structure damage
Brain death 3 cardinal signs
coma
the absence of brainstem reflexes
apnea
To confirm brain death
cerebral blood flow studies
electroencephalogram (EEG)
transcranial Doppler
brain stem auditory evoked potential
Nursing assessment of TBI
History: unconsciousness or amnesia
GCS
Pupil size
Pupillary response to light
Corneal reflexes
Gag reflexes (tongue depressor/ wiggle endotracheal tube)
Motor function
GCS
To assess LOC
Start a neuro flow chart as soon as initial assessment is made!
GCS total scaling
3: deep coma
Less than 8: associated with severe head injury and coma
9-13: indicate a moderate head injury
greater than 13: reflect minor head trauma
15: normal
GCS eyes
1: none
2: response to pain
3: response to voice
4: spontaneous
GCS verbal
1: none
2: incomprehensible sounds
3: inappropriate words
4: confused
5: oriented
GCS motor
1: none
2: extension
3: flexion
4: withdraws to pain
5: localized to pain
6: obeys command
Management of brain injuries
CT and MRI primary neuroimaging diagnostic tools
any patient with a head injury is presumed to have a cervical spine injury until proven otherwise (don’t manhandle them)
all therapy is directed toward preserving brain homeostasis and preventing secondary brain injury
Nursing interventions of TBI
Maintaining the airway
Monitoring neurologic function
Monitoring fluid and electrolyte balance
traumatic diabetes insipidus
Promoting adequate nutrition
Preventing injury
Maintaining body temperature
Maintaining skin integrity (maybe they can’t move)
Improving coping: multidisciplinary
Preventing sleep pattern disturbance
Supporting family coping
Monitoring and managing potential complications
Monitoring f&e balance in TBI
Pt may receive osmotic diuretics
Some may have syndrome of inappropriate antidiuretic hormone (SIADH) secretion
Some may have post traumatic diabetes insipidus
Promoting adequate nutrition in TBI
Early initiation of nutritional therapy
If CSF rhinorrhea or if suspicion of disruption to the skull base: oral feeding tube instead of nasal
Maintaining body temp in TBI
Fever: damage to hypothalamus, cerebral irritation from hemorrhage, or infection
Monitoring and managing potential complications of TBI
Maintain adequate CPP: greater than 50 mmHg (Elevation of head of the bed, increased IV fluids, CSF drainage)
Cerebral edema and herniation leads to increased ICP
Impaired oxygenation and ventilation
Impaired fluid, electrolyte, and nutritional balance
Posttraumatic seizures
Intracranial pressure
normal ICP 15 mm Hg or less
slight increased ICP can be reduced by hyperventilation (think about CO2, reduces acidity of blood and edema).
Cushing’s triad
Signs of increasing ICP
slowing of the heart rate
increasing systolic blood pressure and widening pulse pressure
abnormal respiration patterns (irregular and slow)
Rapid increase in body temp r/t ICP
not favorable–brain stem damage (a poor prognostic sign)
Calculating CPP
cerebral perfusion pressure=MAP-ICP
CPP>70 mmHg (ideal)
Calculating MAP
MAP = (SBP+[2xDBP])/3
Most common causes of spinal cord injury
motor vehicle crashes
falls
violence–gunshot wounds
recreational sporting activities
Males: 78% of the patients
Risk factors of spinal cord injury
Younger age
Male gender
Alcohol and illicit drug use
Hyperflexion injuries
acceleration injuries that cause sharp forward flexion of the spine
head-on collision, fall, or diving
Hyperextension injuries
backward snap of the spine
rear-end collision
downward fall onto the chin
Tetraplegia
same as quadriplegic
Paralysis of all 4 extremities
Paraplegic
Paralysis of lower body
C4 or above spinal injury
at greater risk for impaired spontaneous ventilation
intubation and MV for the rest of their life
Most frequently involved vertebrae
C5-C7, T12, and L1–due to greater range of mobility
Patho of spinal cord injury
Transient concussion (from which the patient fully recovers)
Contusion
Laceration
Compression of the spinal cord tissue
Complete transection of the spinal cord (paralyzed below the level of injury)
Emergency management of spinal cord injury
Rapid assessment
Immobilization: spinal (back) board
Extrication: remove from danger zone
Stabilization or control of life-threatening injuries
Transportation to trauma center
Oxygenation and hydration!!
Primary spinal cord injury
result of the initial insult or trauma and are usually permanent
Secondary spinal cord injury
the result of a contusion or tear injury, in which the nerve fibers begin to swell and disintegrate
ischemia, hypoxia, edema, and hemorrhagic lesions
reversible during the first 4-6 hours after injury
major causes of death among patients with spinal cord injury
pneumonia and pulmonary emboli because they’re immobile
Sepsis from bedsores, can lead to osteomyelitis
Spinal shock
Temporary suppression of all reflex activity below the level of injury
Occurs immediately after injury
Intensity and duration vary with the level and degree of injury
Once BCRs returns, spinal shock is over
sudden depression of reflex activity in the spinal cord (areflexia) below the level of injury, muscular flaccidity, lack of sensation and reflexes
BP may decreased and may be bradycardic
BCR
Bulbocavernosus reflex or “Osinski reflex” a polysynaptic reflex that is useful in testing for spinal shock and its state
Anal sphincter contracts
MAP for spinal shock
Maintain MAP at 85 mmHg or higher to prevent hypotension→ further damage to the spinal cord
Spinal shock and bowel
reflexes that initiate bladder and bowel function are affected–atonic bowel
bowel distention and paralytic ileus
treated with intestinal decompression by insertion of NG tube
Nursing care of spinal shock
palpated lower abdomen for signs of urinary retention and overdistention of the bladder (bladder scan if you can’t palpate like big patient)
assess for gastric dilatation and paralytic ileus caused by an atonic bowel (assess bowel sounds)
Neurogenic shock
The body’s response to the sudden loss of sympathetic control
Distributive shock
Result of the loss of autonomic nervous system function below the level of the lesion
Hemodynamic changes
Venous pooling and peripheral vasodilation
Who does neurogenic shock occur in
People who have SCI above T6 (>50% loss of sympathetic innervation)
Manifestations of neurogenic shock
Decrease in BP, HR, and cardiac output
Patient does not perspire in the paralyzed portions of the body, because sympathetic activity is blocked
Respiratory problems with spinal cord injury
retention of secretions
increased partial pressure of arterial carbon dioxide levels
decreased oxygen levels
respiratory failure
pulmonary edema
DVT with spinal cord injury
potential complication of immobility
common in patients with SCI
High risk for PE
To prevent DVT and PE in spinal cord injury
low-dose anticoagulation therapy
anti-embolism stockings
Sequential pneumatic compression devices
indwelling filters (vena cava)
(never massage the calves or thighs)
Autonomic dysreflexia (hyperreflexia)
acute life-threatening emergency
exaggerated autonomic responses to stimuli that are harmless in normal people
occur only after spinal shock has resolved.
among patient with cord lesions above T6 after spinal shock has resolved
The main objective is to remove the triggering stimulus
Spinal cord injury at T6 or higher
it may occur many years after the initial injury
Manifestations of hyperreflexia
Severe and pounding headache with paroxysmal (sudden, uncontrollable) hypertension
Profuse diaphoresis above the spinal level of the lesion (most often of the forehead)
nausea, nasal congestion
bradycardia
Increased BP, flushed face, HA, distended neck veins, decreased HR, diaphoresis
VASODILATION ABOVE LEVEL OF INJURY
VASOCONSTRICTION BELOW LEVEL OF INJURY (PALE, COOL, NO SWEATING)
What triggers hyperreflexia
sustained stimuli at T-6 or below from:
Restrictive clothing
Full bladder or UTi
Pressure areas
Fecal impaction
Risks of hyperreflexia
The sudden increase in blood pressure may cause retinal hemorrhage, hemorrhagic stroke, MI, or seizures
Interventions for hyperreflexia
Place patient in a sitting position to lower blood pressure (do this first)
rapid assessment done to identify and alleviate the cause
the bladder is emptied immediately via a urinary catheter
exam the rectum for a fecal mass
exam the skin for any areas of pressure, irritation, or broken skin
any other stimulus that could be triggering event, such as an object next to the skin or a draft of cold air, must be removed
label the medical record with a clearly visible note about the risk of autonomic dysreflexia
Spinal cord injury interventions
strategies to compensate for sensory and perceptual alterations
measures to maintain skin integrity
temporary indwelling catheterization or intermittent catheterization
NG tube to alleviate gastric distention
high-calorie, high-protein, high-fiber diet
bowel program and use of stool softeners
