Exam 3 Flashcards
hepatitis
inflammation of the liver
non-infectious hepatitis: how long does it last
can be acute, less than 6 months
causes of non-infectious hepatitis (6)
-ETOH
-Other toxins: Bacterial, fungal, or parasitic toxic exposure
-Autoimmune diseases - primarily biliary atresia cirrhosis, -hemochromatosis
-Congenital wilson’s disease
-R-sided HF - d/t back up of fluid
-non-ETOH fatty liver (NASH)
infectious hepatitis causes
can be acute or chronic d/t:
-Hep viruses
-Herpes
-Epstein Barr
-Coxsackievirus
-Varicella-zoster
signs and symptoms of hepatitis (beginning) (8)
Yellowing skin and eyes
Extreme fatigue
Low grade fever
Loss of appetite
N/V
Dark urine
Light colored stool
Diarrhea
s/s that hepatitis is progressing towards cirrhosis
-jaundice d/t cirrhosis and portal HTN
-hepatomegaly d/t HTN or extra fluid
-ascites
-muscle wasting
-hypoalbuminemia
-Na retention
-vitamin deficiencies
-bruising and bleeding
-sparse body hair
-caput medusa
-dark amber urine d/t bilirubin
-clay colored stool b/c of bilirubin
-palmer erythema
why does hypoalbuminemia occur in patients with hepatitis
d/t liver’s impaired ability to synthesize proteins
Edema/third spacing d/t decreased oncotic pressure
Skin is shiny, soft and pitting
signs of hepatomegaly
RUQ tenderness
Can palpate borders - will feel lumpy due to nodules
what is cheilosis
happens to lips - swelling / fissures on lips
Vit B2 deficiency, sign of hepatitis
glossitis (what is it and how do you tx?)
inflammation of the tongue
happens with vit deficiences in hepatitis
tx: antibiotics , avoid spicy/hot food, good oral care
why do patients with hepatitis bruise and bleed more
Impaired clotting factors
sequestration of platelets in the spleen
what is caput medusa and what causes it
superficial varicose veins on abdomen
May have arterial bruit
d/t portal htn and congestion
when do patients with hepatitis start showing s/s?
65-75% of hepatocytes are destroyed or dysfunctioning
when does liver failure occur
when there is a loss of 60% or greater hepatocytes
what would you include in an assessment for hepatitis
ask about
Alcohol use, ecstasy, needle sharing (IV drug abuse)
Transfusion history
OTC drugs
Occupation and travel exposure
Safe sex
what lab values do you draw for the synthetic functions of the liver
albumin, PT
what is albumin responsible for
colloid/osmotic pressure, keeps intravascular volume in vessels
normal albumin level
3.5-5.3 gm/dl
what is PT
measures liver’s ability to synthesize clotting factors
normal PT / INR
Normal PT 11-13
Normal INR - 0.8-1.1
Dysfunctional liver → PT increases, at risk for bleeding
what values of albumin and PT/INR will happen in liver failure
decrease albumin and increase PT/INR (longer to clot, more bleeding)
what are the hepatocellular damage markers
AST
ALT
what is AST and normal values
aspartate transaminase
Normal: 6-40 iu/l
enzyme that usually helps metabolize amino acids
Go up when there is damage
what is ALT and normal values
alanine transaminase
Normal: 30-120 units/L
Helps metabolize proteins
Go up when liver is damaged
when are AST and ALT released
released when hepatocytes are injured or die
Numbers should come down if treated and working
how do you evaluate cholestasis (excretory function, slowing or stalling of bile flow through your biliary system)
alkaline phosphatase
bilirubin
what is alkaline phosphatase + normal levels
Increased when bile duct is damaged or obstruction so bile can’t get out
Normal: 44-147 iu/L
Later marker than AST and ALT
what is bilirubin
Made during normal breakdown of blood cells
Can increase with liver dysfunction or bile duct issues
total bili normal levels + jaundice levels
Normal 0.1-1.2 mg/dL
Become jaundice when bili > 2.5 mg/dL
direct bili normal levels
< 0.3 mg/dL
what is nursing mgmt for hepatitis?
supportive care (rest, nutrition, avoiding further liver injury)
daily weights, measure abdominal girth
when does a patient with hepatitis need to be hospitalized
-unstable hemodyanmics
-encephalopathy
-poor fluid/food intake
-ascites
-respiratory issues
what diet should a pt with hepatitis have
High calorie low protein diet, small frequent meals
how do you treat ammonia
Lactulose for ammonia - acidifies the colon to prevent absorption of ammonia
draws ammonia from the blood into the colon where it is removed from the body
how are you going to treat pt with hepatitis
-Lactulose for ammonia - acidifies the colon to prevent absorption of ammonia
-Antibiotics to clear colon of bacteria that produces ammonia
-cholestyramine to treat pruritus
-Need antiemetics to combat N/V
-IV fluid - has to be saline - Can’t metabolize ringers → makes ph imbalance worse
what causes hepatic encephalopathy
increased ammonia
tx with lactulose
pt teaching for hepatitis
Infection
Modes of transmission
diet/fluid restrictions
Total cessation of alcohol (if alcohol related)
what are the 4 categories of cirrhosis
Laennec’s (portal)
Post necrotic cirrhosis
biliary
cardiac
Laennec’s (portal) cirrhosis
Seen in alcoholic cirrhosis or severe malnutrition
Middle aged males 40-60 years
post necrotic cirrhosis
cirrhosis following submassive necrosis of the liver (subacute yellowatrophy) due to toxic or viral hepatitis
biliary cirrhosis (what causes it and what are the characteristics)
Caused by obstruction or infection of major extra or intrahepatic bile ducts
characteristics: Jaundice, abdominal pain, steatorrhea, enlargement of liver and spleen
cardiac cirrhosis
d/t intractable heart failure
what causes cirrhosis (6)
chronic Hepatitis Virus,
alcohol abuse,
nonalcoholic steatohepatitis,
hereditary hemochromatosis,
Wilson’s disease, and
alpha1-antitrypsin deficiency
how does cirrhosis occur
Inflammation, fibrotic changes, and increased intrahepatic vascular resistance cause compression of the liver lobule, leading to increased resistance or obstruction of normal blood flow through the liver, which is normally a low-pressure system
Leads to splenomegaly, varices, hemorrhoids, cardiac dysfunction, fatigue, unstable glucose levels
s/s of cirrhosis
Lower extremity edema, ascites and hypotension
decreased synthesis of albumin leads to interstitial edema and deceased plasma volume
Clotting dysfunction-bruising to hemorrhage low-grade DIC
physical findings of cirrhosis (3)
LE edema
Ascites
hypotension
lab data for cirrhosis (albumin, bili, Na/H2O)
decreased albumin
increased bili
Liver can’t eliminate solute free water → decrease in sodium concentration in serum –> more retention of water –> more edema
tx for cirrhosis
Antibiotics to clear colon of bacteria that produces ammonia
Hepatic encephalopathy: Tx: lactulose
IV lasix for ascites -Normal saline!
antihypertensives to prevent rupture of varices
Beta blockers and nitrates
If bleeding —> will need packed RBCs
is there a cure for cirrhosis
no
what is supportive care for cirrhosis
Treat symptoms
Daily weights, strict Is and Os
Measure abdominal girth with ascites everyday
Check urine output to make sure it is adequate
Blood tests everyday - electrolytes, plts, H&H, coags
Neuro assessment
Monitor nutrition
Ascites will lead to resp issues
how can you manage ascites
paracentesis
when is a VP Shunt used in ascites
when resistant to other therapies
drains peritoneal fluid from the peritoneum into veins, usually the internal jugular vein or the superior vena cava
what is TIPs
transjugular intrahepatic portosystemic shunt
Used to decompress portal venous system
Portal vein → bypass liver circulation to hepatic vein → can lead to metabolic encephalopathy
Point is to reduce portal HTN → decrease size of varices and decrease bleeding
how to manage ascites (3)
first step - IV lasix
second - paracentesis
third - VP Shunt
complications of VP shunt
infection, occlusion of tube - can thrombose, can make esophageal varices more engorged and cause hemorrhaging
normal ammonia levels
9.5 - 49 mcg/dl
if blood ammonia increases, what happens?
Decreased LOC
Neuromuscular disturbances
Asterixis - push back/ flex hand and it flaps
Hyperreflexia
Impaired thinking
Changes in memory, personality, concentration, reaction times
what can cause hepatic encephalopathy
Can be d/t use of TIPS,VP shunt, GI bleed from esophageal varices → create nitrogen load → leads to bacterial deamination = amino acids break down → converted to ammonia
how to tx hepatic encephalopathy
Low protein diet
Medications -
-Lactulose: Decreases colonic pH to decrease absorption of ammonia by facilitating BM
-Neomycin (antibiotic)
-Metronidazole (flagyl) - 500mg q8 (IV, PO)
—All 3 focus on clearing nitrogen out of gut
Asterixis
very early sign of hepatic encephalopathy - ask patient to hold hand out and like stopping traffic and watch for involuntary flapping motion
balloon tamponade
usually refers to the use of balloons inserted into the esophagus, stomach or uterus, and inflated to alleviate or stop refractory bleeding
nursing care for balloon tamponade
Can only be inflated for 24-48 hours, bc can cause necrosis, perforation, ulcerations, 12-24 after hemostasis
Pressure to 25-39mmHg
HOB > 30 degrees to prevent reflux
why is respiratory assessment so important with balloon tamponade
tube can move and obstruct airway-if this happens cut tube to deflate gastric balloon quickly, bleeding assessment-can cause perf or esophageal rupture
what are the exocrine cells of the pancreas
Aciner cells - synthesize and secrete digestive enzymes to assist in the breakdown of starch, fat and proteins
empty secretions into pancreatic ductal system → joins common bile duct
what are the endocrine cells of the pancreas
Islets of langerhans: secrete insulin, glucagon, and somatostatin
causes of acute pancreatitis
-heavy alcohol use (40%)
-gallstones (40%)
-others (10%) - trauma, infection, shock, medications, biliary tract disease, cancer, atresia
how do gallstones cause acute pancreatitis
blocks pancreatic secretions from emptying into duodenum → reflux of bile initiates inflammatory process
More common in women (Fat, Female, Forty, Farting)
what are the two types of acute pancreatitis
Interstitial: mild form, lasts 1-2 weeks, no organ dysfunction, reversible, no serious complications
Necrotizing: 10-20% of cases progress to this
necrotizing acute pancreatitis
Causes irreversible damage to pancreas and surrounding tissues
Poor prognosis for patient → sepsis, MODs, high mortality rate
Ill from every system standpoint
Cellular necrosis and hemorrhage inside the pancreas
what are the results of the inflammatory response in acute pancreatitis (necrotizing)
Hypovolemia from capillary permeability,
acute respiratory distress syndrome, DIC,
renal failure,
cardiovascular failure,
GI hemorrhage
what will you ask your patient about when it comes to history for acute pancreatitis
Ask about alcohol and gallbladder disease
Diabetes
Medications
Any biliary tract disease?
Any jaundice?
Anorexia
N/V
Abdominal distension
what is the hallmark sign of pancreatitis
Present with epigastric to LUQ pain
Pain = deep, sharp, constant, radiating through to the back and up to the chest
Increases within minutes of eating food high in fat content
pain is worst lying down (do not lay them in supine)
Nonspecific
10/10, severe
additional signs of pancreatitis
abdominal guarding on exam
low grade fever, jaundice
Diarrhea
Bleeding
Foul smelling bowel movement
Dehydrated quickly
decreased BP → increased HR
If islets of langerhans are damaged during necrosis → patient will develop diabetes
amylase + normal levels
convert starch and glycogen into simple sugars
Normal 23-85 (up to 140) u/L
will amylase increase or decrease in pancreatitis
elevation 3x normal
lipase
fats → fatty acids and glycerol
Normal: 0-160 u/l
what is the most sensitive indicator for acute pancreatitis
lipase
will BUN increase or decrease with pancreatitis
increase - suggests hypovolemia
will AST increase or decrease with pancreatitis
increase indicates damage to liver cells
will ALT increase or decrease with pancreatitis
indicative of gallstone pancreatitis
Increase
will WBC increase or decrease with pancreatitis
increase d/t inflammation
what do you need for diagnosis pancreatitis
Amylase and/or lipase are 3x normal
Characteristic pain
Abdominal imaging
what is the priority in the ED for pancreatitis
Priority = Volume resuscitation - a lot of NS and electrolyte (esp hypocalcemia)
then…
-pain relief
-stabilization of VS
-anticholinergics to decreases GI motility and pancreatic enzyme release
-Antispasmodics – relaxes the smooth muscle, relaxes sphincter of Oddi
-H2 blockers/PPI – decrease GI acid secretions
-When being fed, need pancreatic enzymes to aid in digestion of fats and proteins
-Antibiotics – if have necrotizing pancreatitis
priorities for pancreatitis in the ICU
Fluid resuscitation
Inotropic support
Respiratory support
Renal therapy
Nutritional support - Not TPN
Pharm therapy
Surgical intervention
what is MRCP and what is it used for
magnetic resonance cholangiopancreatography
Can detect gallstones down to 3mm in diameter and remove them
High quality
what does hypocalcemia indicate in pancreatitis
can indicate presence of pancreatic fat necrosis
Calcium binds with fatty acids during necrosis process
why would a patient with pancreatitis be hyperglycemic
decreased release from damaged beta cells → increase glucagon release + increased stress response from inflammation
will TGLs increase or decrease with pancreatitis
elevate - over 1000 mg/dl
3 pain control methods for pancreatitis
High fowlers
IV narcotics
NG tube to decompress belly
pancreatic rest for pancreatitis
NGT on low intermittent to decompress the stomach and to decrease stimulation of secretin which stimulates production of pancreatic secretions
signs of severe hemorrhagic pancreatitis
Turner’s Sign – bruising of the flanks, retroperitoneal hemorrhage
Cullen’s Sign – edema and bruising around the umbilicus
signs of hypocalcemia
Chvosteks & Trousseaus
Chvostek’s Sign
twitching of the facial muscles in response to tapping over the area of the facial nerve
hypocalcemia
Trousseau’s sign
carpopedal spasm caused by inflating the BP cuff to a level above the systolic pressure for 3 minutes
type 1 DM
no production of insulin
type 2 DM
insulin resistance, which is hyperglycemia, hyperinsulinemia, and consequent Beta cell exhaustion
complications of diabetes
Blindness - retinopathy, cataracts
Stroke
Premature CAD
HTN - Atherosclerotic changes in heart, brain, kidneys
Gastroparesis
Diarrhea (especially due to medications like metformin)
Fertility issues, impotence
Increased risk of infections
Peripheral Vascular disease - Poor wound healing, Amputation
Peripheral neuropathy
3 hallmarks of DKA
hyperglycemia that causes hyperosmolarity
metabolic acidosis
fluid/electrolyte disturbance / volume depletion from osmotic diuresis
most common cause of DKA
infection (30-50%, UTIs, pneumonias in older adults)
why are ketones produced in DKA
Ketones are produced when body is forced to use fat to create energy because lack of insulin that is converting glucose to energy
Fat is turned into ketones = acids → accumulate in bloodstream
other causes of DKA
Inadequate insulin therapy
Stroke, MI, pancreatitis
Alcohol/drug abuse
Trauma
Meds: diuretics, corticosteroids, beta blockers, some antipsychotics/anti seizures
is DKA more common with type 1 or 2
type 1
DKA nursing care assessment: history
Diabetic regime
Weight loss
Thirst
Urinary frequency
Bloating
Any anorexia?
s/s of DKA
kussmaul respirations
fruity breath d/t acetone
abdominal pain with N/V
Polyuria
Polydipsia
Abdominal distension
Dry mucous membranes - dehydration
Decreased perfusion
Hypotension
Tachycardia = compensatory
Altered mental status - somnolence, stupor, coma
Fever = sign of underlying problem being an infection
BG level in DKA
> 250 - 1200 mg/dl
average = 600
anion gap
specialized blood tests that lets us know about metabolic acidosis
Look at difference b/w sodium + potassium on one side and Cl and HCO3 on the other
Less than 11 = normal
how to improve circulatory volume and perfusion in DKA
NS 1L/hr in ED and ICU
Until HR and BP returns to normal
BP over 90/100
HR to come down
correcting electrolyte imbalances with DKA
potassium phosphate (once you get lab values)
bicarb (if ph is less than 7)
how to decrease serum glucose in DKA
Only regular insulin via IV
Will be on continuous insulin drip with q1 hr glucose checks
Want slow steady decline of blood glucose
Best to give low dose regular insulin IV gtt, 0.15U/kg initial, then 0.1U/kg/hour which is about 5-10U/hour. This produces a steady decline. Don’t want to go fast, for fear of water moving into cell and causing vascular collapse.
Once down to 250, add D5W to avoid hypoglycemia
what do you want UA to be in DKA
20-30 ml/hr
patient education in DKA
Monitoring
Correct diet
Hydration
Take insulin
know signs of hypoglycemia
signs of hypoglycemia
Hypothermia
Tachypnea
Tachycardia
Dysrhythmias
Hyptertensive
Diaphoresis
Hunger
Nausea
Headache, altered mental status
Personality change
Blurred vision
Confusion
Severe: coma, convulsions
hyperosmolar hyperglycemic state (HHS)
Acute illness of the pancreas
Marked hyperglycemia
Hyperosmolality
No ketoacidosis
most common cause of HHS
Infections are most common cause
UTIs
Pneumonia
Cellulitis
Diverticulitis
what population is HHS more common with
More common in type II
More common in older adults
is dehydration worse in HHS or DKA
HHS
nursing care assessment of HHS: history
Diabetes
Medications
Signs of recent infection
Change in LOC
Any decrease in activity
Difficult to wake up?
Profound weakness
s/s of HHS
Weakness
Polyuria
Polydipsia
Impaired mental state → all the way to coma
s/s of dehydration (low BP, high HR)
NOT kussmaul’s breathing
BG in HHS
Blood glucose can be 400-4000 mg/dL with an average of 1100
will sodium be high or low in HHS
high d/t dehydration
will serum osmolality be high or low in HHS
high d/t dehyrdation
Normal range - 275-299
Number will increase with dehydration r/t ADH being secreted
Will decrease when someone is volume overloaded/overhydrated
do you have an anion gap in HHS
no - bicarb will be normal, ph will be relatively normal
1 nursing care priority for HHS
1 IV fluid resuscitation to correct volume depletion
hemodynamic monitoring in HHS
Would be concerned about pulmonary edema due to rapid volume repletion and can’t handle that amt of fluid
Looking for fluid returning to right side of heart (CVP) - hook up central line to monitoring
Want it over 12 but not over 14
when do you add d5w in HHS
when BG is back in 200s
teaching for HHS
Monitor glucose
Knowing side effects of medications
s/s of hypo and hyper glycemia
Understanding any kind of infection can propel them in to HHS
DKA priority
control glucose so body stops making ketones, then fluid replacement
functions of the skin (6)
Protects against infection
Prevents loss of body fluids
Controls body temp
Functions as a sensory and excretory organ
Produces vitamin D
Determines identity
superficial (1st degree burn)
only affects the epidermis, or outer layer of skin. The burn site appears red, painful, dry, and absent of blisters. Scarring is rare or minimal.
partial thickness (2nd degree burn)
Pink, mottled red
Hair follicles and sweat glands are preserved
Blisters
Wet, weeping with serous exudate
Extremely painful
Can have waxy white appearance
Firm but not leathery
Same causes as 1st degree but can have longer or greater exposure to cause
21-28 days of healing
Often require hospitalization
full thickness 3rd degree burn
Epidermis, dermis, hair follicles, sebaceous glands are destroyed
Thrombosed vessels in dermis
Nerve endings are destroyed so they are painless
Degree of burn depends on intensity and duration of exposure
Do not heal from them spontaneously - only by grafting - has to be donor skin → pain returns
fourth degree burn
If muscle and bone are involved
Can be different colors
rule of nines: head and neck
9%
rule of 9s: arms
each arm = 9%
rule of 9s: anterior trunk
18%
rule of 9s: posterior trunk
18%
rule of 9s: legs
18% each!
rule of 9s: perineum
1%
quick estimate of burns
look at palms of victims hands
burns based on body part
Upper part of the body - increased mortality
Head, neck, chest - pulmonary complications
Perineum - prone to infection
what determines severity and outcome of burn
age
-Mortality is increased in adults over age 60 and in children over 2
-Poor antibody response
-Translucent nature of skin
causes of burns
Thermal -flame, hot liquid, hot object
Chemical - tissue destructions secondary to chemical, liquid, or acid
Alkaline are worse than acid
Electrical - contact with an electrical current, only entrance and exit wounds are apparent
Radiation - localized d/t high radiation doses
major to life threatening burns
Greater than 25% TBSAB adult, greater than 20% TBSAB child
Full thickness greater than 10%
Burn of face, hands, eyes, ears, perineum
Inhalation, electrical burn
Burn with extenuating circumstances: Chemical burn, electrical burn
thermal burns tx
Irrigate burn with water for at least 20 minutes - will halt burning in tissues
Remove wet clothing, don’t put other clothing on - just cover with blankets
Remove all jewelry
Transport
High o2 concentration if the fire was in a closed space
chemical burns tx
Dilute the chemical when appropriate
Remove contaminated clothing
Flush for at least 20-30 minutes
electrical burns tx
Turn off source of current
Use non-conductive materials to remove electricity source
Immobilize and efficiently
3 phases of burns
emergent
acute/reparative
rehabilitative
emergent phase
Begins with the injury and lasts 24-48 hours or, in the critically ill patient, up to two weeks
Hyperkalemia → injured tissue and RBCs releases K+
Will look like systemic inflammatory response
acute / reparative phase
Begins when initial fluid replacement is complete and fluid shifts from interstitial back to vascular space
rehabilitative phase
from hospital admission to resumption of functioning level in society
priorities in emergent phase (8)
ABCs
Institute and maintain strict isolation
Institute fluid resuscitation - cornerstone of emergent phase
Gastric intubation - NG tube
Foley catheter
Tetanus
Wound cultures
Tubbing
parkland burn formula
4cc. X Kg. Body weight X TBSAB
*Fluids must be calculated from the time of burn occurrence as most of the fluid is lost in the initial 8 hours
*1/2 of the calculated fluid for the first 24 hours is given in that initial 8 hours
what indicates you can move to acute phase
adaptive fluid level
Lucid Mental Status
Adaptive Vital Signs - 90 systolic and HR < 100 bpm
Adequate Peripheral Perfusion - Cap refill, color, temperature
Adequate Urinary Output - Minimum 50 cc
Return to Normal Weight
Pulse Rate Less than 120
Normal CVP
Clear Lungs
Allograft/homograph
taken from a person other than the patient (most common = cadaver)
xenograft
temporary tissue taken from another species (most common = pigs)
autograph
skin taken from one area of one’s body transplanted to another, permanent
Physiologic dressing
temporary biological dressing
Escharotomy
surgical procedure where an incision is made through eschar to present healthy skin
complications of burns (6)
**hypovolemic shock
wound infection
resp complications
curlings ulcer
electrolyte alterations
CV problems
signs of hypovolemic shock
Compensated signs: increase HR and decreased BP, decreased urinary output, tachypnea, cyanosis
most common bacteria with burns
Usually gram negative - pseudomonas
signs of wound infection with burns
Dark discolorations around wound, edema on unburned area (margin), unexplained eschar separation
burns: respiratory complications
Mortality rate - 20-84% (depends on comorbidities, early intervention)
From inhaling chemicals, fires, electric shock, burns of face, neck, chest, present with pulmonary insufficiency and pulmonary edema (ARDS)
curlings ulcer
stress ulcer
50% of burn patients develop
Causes necrosis of gastric wall
As soon as 24 hours after burn
Mortality rate = 70%
Early signs - gastric distension, pallor, sweat, blood in NG residual (guaiac), If blood is in fluid, test burns blue, Also a heme test
electrolytes in burns
Increase in hematocrit because RBC destruction
Leukocytes increase
Coag problems because of hemoconcentration
K+ is increased initially because of blood cell injury - Decreases when patient begins to diuresis
BUN increased because of protein catabolism
what causes CV problems with burns
decreased CO
priority in acute phase of burns
Fluid
Replaced with maintenance fluid to replace evaporated loss
Usually D5W with K+ in it (because patient is now voiding)
Signs its enough - edema is reabsorbed, return to pre burn weight 8-10 days post burn, voiding
other priorities in acute phase of burns
Wound care - debridement, dressings, medications
Hydrotherapy
Nutrition
nutrition in acute phase of burns
Need 5000-7000 calories a day to heal
Need food with carbohydrates, proteins, fats, vitamins
Wilmore formula - exact number of calories a burn patient needs in a day
what must occur immediately and frequently with burns
debridement
what are burns covered with temporarily
allografts/xenografts
Last 3-5 days
Monitor and care for graft
Stimulates healthy new growth
Stimulate growth, protect granulating tissue
Temporary wound cover
when do you change allografts/xenografts
When you see purulence under the temporary cover
4-6 are usually needed
when is a pt ready for an autograph
When healing and pink, vascularized tissue
Take small piece of skin and it gets stretched out and puts holes in it (so it can breathe)
Needs to be covered and kept moist with antimicrobial solution for at least 72 hours
burn medications
silvadene
mafenide acetate
silvadene
Creamy white ointment that spreads easily over the burn
Gram Negative, gram positive antimicrobial properties
Softens eschar
AE: Can cause leukopenia
Mafenide acetate
second choice for burns
can interfere with electrolyte imbalance
tubbing/tanking
At least once a day
Removes topical agents and cleanses
Softens the eschar, increasing range of motion –> debridement is done during tubbing
Loss of body heat
Painful, Stressful
Loss of Sodium
Possibility of cross contamination
psychological impact of burns
Emergent Phase: Psychological “shutdown” - Major Concern: Physiological delirium
Acute Phase: Pain, depression, regression
Recuperative Phase: Apprehension
Intervention: Burn Support Group
priorities in recuperative phase
jobst garments
splinting
jobst garments
Treatment that covers entire surface of the burn, fits like a second skin
Prevents scarring
Can only take off for shower
what does splinting do?
prevents contracture
rule of 9s: chest
9%
major risk factor for head trauma
alcohol consumption
primary prevention for head trauma
helmets, seatbelts
is there secondary prevention for head trauma
not really
tertiary prevention for head trauma
golden hour, treat and care asap
Acceleration
moving object strikes a stationary force
Ex: Head is hit with a bat
deceleration
head in motion hits a stationary force
Motor vehicle crash - head hits steering wheel
deformation
causes brain to twist in the head
Usually under physical assault
countercoup
Brain is rotated inside the head from one side to another
ex: shaken baby syndrome
blunt trauma
damage to the brain without penetration to the skull
Usually results from acceleration and deceleration injuries
On initial assessment, you don’t know what is going on
Seen more often than penetrating
penetrating trauma
object disrupts integrity of skull and penetrates brain
Gunshot wound to the head
shearing injuries
results from rotational force, affects white matter in the brain stem
contusion
concussion with bruising to the brain
skull fracture
common form of injury
Linear
Depressed
Compound
subdural hematoma
Bleeding between sub dura and arachnoid membrane
sub arachnoid hemorrhage: what causes it?
Not usually result of head trauma but can be d/t rupture aneurysms
intracerebral hemorrhage
Direct bleeding in to brain itself
Not usually as a result of head trauma
nursing goals for acute head trauma (3)
Reduce the risk of secondary damage
1. Stabilize vital signs
2. Prevent further Injury
3. **REDUCE ICP
how to stabilize airway during primary survey
Airway: stabilize head → jaw thrust maneuver
order of assessment (to see if patient is alert)
Squeeze trapezius on both sites
Sternal rub
Suborbital pressure
Nail bed pressure
what does DERM stand for (after ABC)
depth of coma
eyes
respirations
motor mvmt
lethargic
Drowsy but will follow simple commands and makes sense
obtunded
Arousable with stimulation, can follow simple commands
stuporous
Hard to arouse, inconsistently following commands, limited spontaneous movements
semi comatose
Movements are purposeful when stimulated but not following commands or speaking coherently
comatose
Patient may respond with reflexive posturing
Can still be breathing on their own and maintain BP and HR
Light vs deep coma
Decorticate Posturing - what is it and what does it indicate
flexion and internal rotation of extremities.
Lesion above mid-brain.
Decerebrate Posturing - what is it and what does it indicate
Abnormal extension- an extension and internal rotation of the upper and lower extremities.
Can indicate Brain herniation
More severe
ICP - intracranial pressure
pressure exerted by CSF in the ventricles
Monro-Kellie hypothesis
the sum of volumes of brain, cerebrospinal fluid (CSF) and intracerebral blood is constant. An increase in one should cause a reciprocal decrease in either one or both of the remaining two.
normal ICP
4-15 mm Hg
moderately elevated ICP
15-40 mm hg
severe/life threatening ICP value
greater than 40 mm Hg
what is cerebral perfusion pressure
pressure required to perfuse the brain cells
how do you calculate CPP
MAP - ICP
normal CPP
60-90 mm hg
how do you measure CPP
Catheter placed through the skull into the subarachnoid space or cerebral ventricle (preferred method)
Changes in pressure are monitored, via a transducer, directly and continuously
what is the number 1 diagnostic tool in head trauma
CT scan
what should CSF look like
Fluid = clear, colorless, should not be bloody or cloudy
when will a stroke show up on a CT scan
24-48 hours after stroke
what can an MRI show
stroke bed + bleeding within 5 minutes of someone having stroke
gold standard for ischemic stroke
early clinical manifestations of increased ICP
**Change in Level of Consciousness (Make sure you can wake them up)
Headache
Nausea and Projectile Vomiting
Cri-du-Ca (“cry of the cat” in infants/pediatric patients)
late clinical manifestations of increased ICP
Loss of motor and sensory functions
Pupillary changes
Cushing’s triad
cushings triad
Widening pulse pressure
Bradycardia
Irregular respirations
*Indicates herniation!
what HOB degree promotes venous return
30 degrees
what do you want the CO2 levels to be for patient with head trauma and why
want it between 30-35
> 45 = increased ICP
Hyperventilate pt to blow off CO2 to decrease PCO2 and decrease ICP
what level of PO2 will increase ICP
< 60
need to increase oxygen setting on ventilator!
diuretic of choice for increased ICP
mannitol
s/s of impending herniation (6)
-Decreased LOC (Coma)
-PupillaryAbnormalities
-Motor dysfunction (hemiplegia, decortication, decerebration)
-Impaired brain stem reflexes (corneal, gag, swallowing)
-Alterations in Vital signs
-cushing’s triad
complications of head trauma (9)
-Increased ICP
-post traumatic seizures
-cushing’s stress ulcer
-intracerebral CSF fistula
-diabetes insipidus
-acute hydrocephalus
-AV aneurysms
-carotid artery occlusion
-Psychiatric disturbances, personality alterations
what causes cushing’s stress ulcer and how do you treat it
Major complication
All caused by GI irritation from psychological and physiological stress on human body
Tx with prophylactic therapy
brain death
Cessation of all CBF and all vital stem functions
Different from clinical death - absence of breathing and circulation
Can be treated within 4 minutes of cessation of both activities
Guidelines established in 1981
Once established, ventilator can be removed and organs donated
what is the biggest cause of spinal cord injury
MVA (50%)
what should you expect with spinal cord injury
head trauma
flexion
ruptures supporting ligaments, fractures vertebrae, damages vasculature → ischemia to spinal cord
Seen most frequently in MVA
extension
stretches the spinal cord, complete transection as a result of injury
Patient loses voluntary movement below level of injury
ex : falling down stairs
axial loading
impacts vertebrae by compressing the cord
rotational forces
Injury that results from counter clockwise turning of body
Head turns one way, torso turns the other
penetrating trauma (spine)
penetrating the spinal cord with some sort of object (missile, knife, gunshot wound)
relationship between magnitude of force and damage to spinal cord
THE GREATER THE MAGNITUDE OF THE FORCE APPLIED TO THE SPINAL CORD, THE GREATER THE ASSOCIATED DAMAGE
tetraplegia
(sometimes referred to as quadriplegia) is a term used to describe the inability to voluntarily move the upper and lower parts of the body.
paraplegia
paralysis of the legs and lower body, typically caused by spinal injury or disease
nursing interventions during critical phase of spinal cord injury
-respiratory support
-treatment of life threatening rhythm disturbances
-mgmt of paralytic ileus (with bowel and bladder programs)
-mgmt of atonic bladder
-drug therapy
-invasive and non invasive monitoring
-cervical immobilization with halo frame
-turning frame
-patient, family support
drug therapy for spinal cord injury
Within 8 hours of injury
Drug: methylprednisolone in ED- corticosteroid and anti-inflammatory agent
spinal shock
Immediate Response to spinal cord injury
Temporary Suppression of Reflexes controlled below level of injury
Input of Impulses from Higher Centers Ceases
how long can spinal shock last
hours to months
sign spinal shock is over
return of Bulbocavernosus (pulling on foley and there is puckering), Peri-Anal Reflexes (stretching or touching buttocks and anus contracts)
autonomic hyperreflexia
Serious Emergency
Patient goes into hypertensive crisis
Caused by Noxious Stimuli that create exaggerated sympathetic response
risk after spinal shock
examples of noxious stimuli that can cause hyperreflexia
distended bladder
tight clothing
characteristics of pt in hyperreflexia
Cold skin
Goose bumps
Increase in BP - 300/160
Bradycardia
Severe headache
Very anxious
goal in hyperreflexia
To Remove Noxious stimuli and Lower the Blood Pressure
how? 2 nurse job: foley, hydralazine, CCB IV to control BP
what causes neurogenic shock
SNS loses ability to stimulate nerve impulses
SNS can’t regulate diameter of vessels → Massive vasodilation occur → Vessels relax → decreased tissue perfusion
what kind of shock is neurogenic shock
distributive
which patients are at risk for neurogenic shock
Spinal cord injury (above T6 thoracic or cervical)
Spinal anesthesia
Taking drugs that affect ANS or SNS
are preload/afterload increased or decreased in neurogenic shock
decreased
will patient in neurogenic shock be hypothermic or hyperthermic
hypothermia (warm dry extremities because of venous pooling, cold core body temp)
will patient in neurogenic shock have tachy or bradycardia
bradycardia
MAP goal for patient in neurogenic shock
85-90 mm hg
do patients in neurogenic shock usually have normal, high, or low fluid volume
usually normal so need to be careful with IVF
signs of fluid volume overload
dyspnea, crackles, edema, high CVP/PAWP
in neurogenic shock - if fluids do not work to increase BP, what might you use?
Use vasopressors to cause vasoconstriction –>Increases SVR, blood pressure, CO
ex: Dopamine = positive inotrope - vasoconstriction and increased HR
how do you increase HR in patient with neurogenic shock and how does it work?
Atropine to increase HR
Blocks PSNS effects on heart that is causing slow heart rate
how do you prevent DVT in patient with neurogenic shock
ROM daily, compression stockings, anticoagulation
what is gold standard for brain herniation
cushings triad
priority assessment for burns
size because you need to know for fluid resuscitation
CO2/ apnea test
remove from ventilator, monitor CO2 rising
If they don’t breathe by PaCO2 at 65 → back on vent
Must be negative 3x in a row
Never do when hypo or hyper thermic or sedated
Partial thickness: superficial
Destroys epidermis and top layer of dermis
Partial thickness: deep
Epidermis and dermis destroyed
Widening pulse pressure
Systolic increases
Diastolic decreases
what will a critically ill patient with cirrhosis present as?
unconscious, jaundiced skin and sclera, bleeding
