Exam 3 Flashcards
(241 cards)
1
Q
Etiology of Peptic Ulcer Disease
A
NSAIDs
Helicobacter pylori
2
Q
Etiology of Stress-Related Mucosal Disease
A
High physiologic stress (mechanical ventilation, burns, shock)
Increased acid production and decreased mucosal blood flow (ischemia)
3
Q
Etiology of Esophagogastric Varices
A
Portal hypertension
Liver failure
4
Q
Hematemesis
A
Bright red blood or coffee grounds (acid)
5
Q
Hematochezia
A
Bright red blood in stool
6
Q
Melena
A
UGI blood passed through bowels
7
Q
Prophylaxis for GI Bleeding
A
Monitor gastric pH
Assess stools and gastric contents for blood
Histamine-2 Receptor Blocker (Cimetidine, Famotidine, Ranitidine)
PPI (Omeprazole, Pantoprazole)
Mucosal lining coating (Sucralfate)
8
Q
Serum Bilirubin, direct
A
0 - 0.3 mg/dL
9
Q
Serum Bilirubin, total
A
0 - 0.9 mg/dL
10
Q
Serum Protein Total
A
7.0 - 7.5 g/dL
11
Q
Serum Albumin
A
4.0 - 5.5 g/dL
12
Q
Prothrombin Time
A
12 - 16 seconds
13
Q
Ammonia
A
11 - 32 umol/L
14
Q
Bleeding Etiology with Liver Involvement
A
Liver dysfunction (lack of clotting factors, hypoalbuminemia)
Decreased absorption (vitamin K, fat soluble vitamins)
Inadequate intake sufficient vitamins
Gastric erosion, ulceration
Portal hypertension
Esophageal varices
15
Q
Stabilization of GI Bleeding
A
IV fluids
Blood transfusions
Blood products
Control bleeding
16
Q
Control of GI Bleeding
A
Esophageal balloon tamponade
Vasopressin
Somatostatin and Octreotide
Beta blockers
17
Q
Nursing Management of GI Bleeding
A
Fluid resuscitation
Blood and blood product transfusions
Gastric lavage
Maintaining surveillance for complications (neurological assessments hourly, assess renal perfusion with hourly outputs)
18
Q
Medical Management of Esophageal Varices
A
Control bleeding (endoscopy)
Endoscopic injection therapy
Endoscopic variceal ligation
19
Q
Hepatic Encephalopathy
A
Seen in chronic liver disease
Triggered by dehydration, electrolyte loss, increased protein intake, bleeding from GI tract, infections, alcohol ingestion
20
Q
Signs and Symptoms of Hepatic Encephalopathy
A
Headache, hyperventilation, jaundice, mental status changes, palmar erythema, spider nevi, fetor hepaticus, bruises, hepatomegaly
21
Q
Laboratory for Hepatic Encephalopathy
A
Serum bilirubin (unconjugated and tubal)
AST
Alkaline phosphatase
SERUM AMMONIA
Prothrombin time
22
Q
Intellectual Function of Hepatic Encephalopathy
A
0: Normal
1: Personality changes, attention deficits, irritability, depressed state
2: Changes in sleep/wake cycle, lethargy, mood/behavioral changes, cognitive dysfunction
3: Altered LOC, somnolence, confusion, disorientation, amnesia
4: Stupor and coma
23
Q
Neuromuscular Stages of Hepatic Encephalopathy
A
0: Normal
1: Tremor, incoordination
2: Asterixis, ataxic gait, speech abnormalities
3: Muscular rigidity, nystagmus, clonus, Babinski, hyporeflexia
4: Oculocephalic reflex, unresponsiveness to noxious stimuli
24
Q
Acute Liver Failure
A
Severe acute liver injury with hepatic encephalopathy, elevated INR or Pro time
Seen in clients without cirrhosis or preexisting liver disease, illness less than 26 weeks duration
25
Etiology of Acute Liver Failure
Viral hepatitis
Medication-induced liver damage
Early recognition is key
26
Pathophysiology of Acute Liver Failure
ALF over 1 to 3 weeks
Hepatic encephalopathy within 8 weeks
27
Treatment of Acute Liver Failure
Control cerebral edema (Mannitol, positioning)
IV administration of glucose, electrolytes
LACTULOSE TO DECREASE AMMONIA/rectal tube
Bleeding monitoring and control
28
Etiologies of Chronic Liver Failure
Infections
Drugs or toxins (acetaminophen, alcohol)
Hypoperfusion
BILIARY (bile obstruction)
CARDIAC (right sided heart failure)
29
Treatment of Chronic Liver Failure
Safety --> FALL PREVENTION
Control ammonia levels (Neomycin, LACTULOSE)
Control bleeding (vitamin K, FFP, platelet transfusion)
Ascites (frequent paracenteses)
Spontaneous Bacterial Peritonitis--sudden pain, rigid abdomen, leads to sepsis
30
Nursing Care of Liver Failure
Provide comfort and emotional support
Family and patient education
Protect from injury (assess mental status)
Nutrition (protein intake 1 - 1.5 g/kg, assess fluid status)
31
Molecular Adsorbent Recirculating System (MARS)
Nonbiological artificial liver support system
Albumin used as dialysate to remove protein-bound toxins
32
MARS Effects
Stabilize condition
Bridge to transplant
Reduction of portal HTN
Improvement of ICP, encephalopathy
Increases MAP and SVR
Removes uremic toxins
33
Requirements for MARS
Central venous line for dialysis
FFP before line placement
Set up/prime takes 1-2 hours
MAP of 70-80
Intermittent treatment (lasts 8 hours for 3 days)
CRRT between MARS sessions
34
Etiology of Acute Pancreatitis
Gallstone migration
Alcoholism
35
RANSON'S Criteria for Acute Pancreatitis
Age > 55 years
Hypotension
Abnormal pulmonary findings
Abdominal mass
Hemorrhagic/discolored peritoneal fluid
Neurological deficits (confusion, localizing)
LDH > 350, AST > 250
Leukocytosis > 16,000
Hyperglycemia > 200
36
RANSON'S Criteria for First 48 Hours
Decrease in Hct > 10% with hydration
Fall in Hct < 30%
Need for massive fluid/colloid replacement
Hypocalcemia < 8
PaO2 < 60 without ALI
Hypoalbuminemia < 3.2
Azotemia
37
Pathophysiology of Acute Pancreatitis
Edematous pancreatitis
Acute necrotizing pancreatitis
Local tissue injury
38
Assessment and Diagnosis of Acute Pancreatitis
Physical examination (hypoactive bowel sounds, abdominal tenderness, Cullen sign, Grey-Turner sign)
LOW CALCIUM
Laboratory studies (elevated serum amylase and lipase)
Diagnostic procedures (abdominal ultrasound, CT)
39
Medical Management of Acute Pancreatitis
FLUID RESUSCITATION (IV crystalloid, isotonic) for distributive shock
Pain management
Nutritional support (enteral feedings, TPN may be very helpful)
Systemic complications (hypovolemic shock, ARDS, AKI, GI hemorrhage)
Local complications (infected pancreatic necrosis and pseudocyst)
40
Nursing Management of Acute Pancreatitis
Providing comfort and emotional support
Maintaining surveillance for complications
Educating patient and family
41
Functions of the Skin
Protection
Sensation
Water balance
Temperature regulation
Vitamin production
Immune response function
42
Burn
Injury to the skin or other organic tissue primarily caused by heat or due to radiation, radioactivity, electricity, friction, or contact with chemicals
43
ABLS
Initial assessment/management
Airway, smoke injury
Shock and fluid resuscitation
Burn wound management
Electrical injury
Chemical burns
Pediatric burns
Stabilization, transfer, transport
Burn disaster management
44
Significant Factors Related to Burn Injury
Type of injury
Location of injury (of incident, on client)
Age
Previous health history
Size-Area
Depth
45
Assessment: Sources of Burn Injuries
Thermal (heat, flame, scalds)
Electrical
Chemical
Radiation
46
Care of Thermal Burn Injuries
Stop, Drop, Roll
Remove clothing
Flush with water or saline
Saline compresses if TBSA < 10%; do not chill patient
Dry, sterile dressing/"burn sheet" otherwise
47
Care of Electrical Burn Injuries
TURN OFF SOURCE OF ELECTRICITY FIRST
CPR priorities of Airway, Breathing, Circulation
Treat dysrhythmias
Entry and exit wounds
48
Pathophysiology of Burns
DYSFUNCTION OF ALMOST EVERY CELL AND CELLULAR SIGNALING PATHWAYS
Hypermetabolic state = CELL DEATH
Chronic inflammation
FLUID SHIFTING (3RD SPACING)
49
Care of Chemical Burn Injuries
Protect self (clothing)
Remove from source
Remove client's clothing
Continuous flushing with water or saline for 20-30 minutes (except lime powder or carbolic acid)
Eye care
50
Care of Radiation Burn Injuries
Protect self (shielding)
Remove from source
Isolate client
Decontamination
Severity: type of radiation, duration of exposure, distance from source, absorbed dose, depth of body penetration
51
Children and Burns
Greater risk for injury
Head greater ratio of TBSA
Legs smaller ratio of TBSA
Skin thinner
Fluid loss more critical
52
Elderly and Burns
Thinner, tougher skin
Slower regeneration time
More sensitive to fluid volume loss
53
Assessment: Area of Burn
TBSA
Rule of 9s
Rule of 9s for child: Head (18%), Leg (14%)
Berkow Formula (detailed assessment based on age and TBSA, Rule of 9s)
TBSA not final until debridement is complete
54
Rule of Palms
Measure the palmar surface of the victim's hand (fingertip to wrist)
Represents 1% of the TBSA
55
Assessment: Depth of Burns
Amount of injured epidermis or dermis
Depth of destruction of epidermis and/or dermis
56
Superficial/First Degree Burns
Only first 2-3/5 layers of epidermis
Erythema--heals within 2-7 days
Mild discomfort (resolves 48-72 hours)
Cause: sunburns, steam burns
Treatment: pain relief, pruritus relief, oral fluids
57
Partial-Thickness/Second Degree Burns
Superficial, mid-dermal, deep dermal
Involved upper 1/3 of dermis
Cause: brief contact with flames, hot liquid, exposure to chemicals
Light/bright red, or mottled appearance
May appear wet, weeping, bull
Painful, sensitive to air currents
Heals 7-21 days with minimal scarring
Deep-dermal involves entire epidermis and part of dermis (red with patchy white, blanches with pressure, prolonged healing time, scarring contractures if untreated)
58
Full Thickness/Third Degree Burn
Destruction of all layers of skin, may include subcutaneous tissue
Pale white or charred, red, brown, leathery
Surface dry
Painless, insensitive to palpation
Requires skin grafting
Susceptible to infection, fluid/electrolyte imbalances, alterations in thermoregulation, metabolic disturbances
59
Zone of Coagulation
Irreversible damage
60
Zone of Stasis
Impaired circulation
Inflammatory response
Can be converted to full thickness
61
Zone of Hyperemia
Vasodilation, increased blood flow
62
Minor Burn Severity Criteria
PT < 15% TBSA
FT < 2% TBSA
63
Moderate Burn Severity Criteria
PT: 15-25% TBSA
FT: 10% TBSA
64
Critical Burn Severity Criteria
Breathing problems
PT > 25% TBSA
FT > 10% TBSA
Face, hands, feet, genitalia
Deep chemical burns
Complicated by fracture or concurrent disease (e.g. diabetes)
65
Emergent or Resuscitative Phase of Burn
First 24-48 hours
Until 3rd spacing has stopped
66
Acute Phase of Burn
3-6 months
Until wound closure
Shock and hyper metabolic phase
67
Rehabilitative Phase of Burn
Several years
Scar and graft management
PT/OT, contractures
68
Phases of Burn Care
First TWO minutes: Prehospital
First TWO hours: ED care
First TWO days: Resuscitation
First TWO weeks: Surgical excision/graft
First TWO months: Rehab, psychology
First TWO years: Reconstruction
69
Nursing Management of Burns
Inflammatory Phase (immediately after injury)
Proliferative Phase (4-20 days after injury)
Maturation Phase (20 days after injury)
70
Airway Management with Burns
ASSESSMENT OF RISK (facial burns, singed facial hair, stridor)
Visualize larynx for redness
Endotracheal intubation
71
Respiratory Problems with Burns
Carbon monoxide poisoning (carboxyhemoglobin serum level)
Smoke poisoning
ALI
Pulmonary fluid overload
Thoracic eschar impairment
72
Interventions for Respiratory Problems with Burns
100% O2 therapy
Monitor fluid balance
ET intubation
Mechanical ventilation
Humidification
73
Renal and GI Complications with Burns
Renal: myoglobinuria, hypovolemic AKI
Paralytic ileus: NG tube insertion and low intermittent suctioning, monitor bowel sounds
Curlings ulcers: H2 Histamine Blockers, gastric pH checks, antacids PRN
74
Integumentary Complications with Burns
HYPOTHERMIA (monitor client's core temperature, keep client warm with heated blankets and warm irrigation solutions)
NUTRITION DEFICIT (high calorie, high protein needs for restoration)
SEQUESTRATION OF MEDICATIONS (only IM injection is tetanus toxoid)
75
Fluid Replacement Therapy for Burns
Baxter Equation
Monitor fluid replacement with CVP, BP, and hourly urine output
76
Baxter Equation
24 hour IV = 4 mL x Wt (kg) x %TBSA
(Child) = 1 mL x Wt (kg) x %TBSA
FIRST HALF 24 hour intake within 8 HOURS OF TIME OF BURN INJURY
Second half 24 hour intake during next 16 hours
77
Alteration in Comfort: Pain for Burns
Narcotic therapy IV
Administer medications by routine schedule
Medicate prior to procedures
Promote adequate sleep cycle
Adjunctive therapies: therapeutic touch, music therapy, distraction
78
Impaired Skin Integrity with Burns
Preserve integrity of non-burned skin
Restoration of viable tissue (debridement) to remove tissue contaminated by foreign bodies and bacteria and remove devitalized tissue
79
Alteration in Nutrition with Burns
TOTAL PARENTERAL NUTRITION
Diet: high calorie, high protein
Caloric needs: 2-3x normal
Protein needs: 1.5 - 3 grams/kg body weight
BURNS REQUIRE SUBSTANTIAL NUTRITION FOR RESTORATION
80
Debridement
Mechanical: hydrotherapy, whirlpool baths, surgical excision
Enzymatic (eschar): autolysis, proteolytic
81
Autolytic Debridement
Natural process, occurs in all wounds
Phagocytic cells
Proteolytic enzymes in wound bed
Results in significant wound fluid, not damaging surrounding tissue, minimal pain
Dressing must contain moist wound bed
82
Impaired Skin Integrity Interventions for Burns
Antimicrobial agents
Dressings (open vs. closed)
Grafts (heterograft/pigskin, homograft/cadaver, autograft/own skin)
Synthetic dressings
Hyperbaric therapy
ESCAROTOMY to restore circulation
83
Stem Cell Research
Use of patient's own cells
Need biopsy of all layers of skin
EPICEL (keratinocytes--expanded into confluent epidermal autograft, takes 2-3 weeks)
Bone marrow, hair follicle, adipose can be used
84
Infection with Burns
Tetanus toxoid and immunoglobulin
Topical drugs: silver sulfadiazine, silver nitrate, nitrofurazone, mafenide acetate
Antibiotic IV therapy: Aminoglycosides (check renal function)
Protective isolation
Good handwashing
No plants (risk of pseudomonas)
85
Impaired Physical Mobility with Burns
Contractures and deformities resulting from burns
Position client in anatomical position
ROM Immediately
Ambulation as soon as fluid shift is resolved
STATIC SPLINTS immobilize joints
DYNAMIC SPLINTS exercise joints
PRESSURE GARMENTS AND DRESSINGS
86
Stressors of Burn Units
Fast-paced, high-technology
Complex management
Multidisciplinary
Equipment
Limited workspace
Warm temperatures
Unpleasant odors
High noise levels
87
Trauma
Accidental or unintentional injury sustained through an external mechanism of injury
Falls, shootings, burns, auto accidents, farm accidents, altercations, natural disasters
88
Blunt Trauma
Motor vehicle collisions
Contact sports
Blunt force injuries
Falls
89
Penetrating Trauma
Stabbings
Firearm injuries
Impalement
90
First Peak of Injury
50% of deaths occur
Minutes from injury
Location: at scene, en route to medical facility
Cause of death: laceration of brain or brainstem, high spinal cord injury, injury to heart or other large vessels
91
Second Peak of Injury
30% of deaths occur
Minutes to few hours after injury
Location: emergency room, operating room
Cause of death: subdural or epidural hematoma, hemo-pneumothorax, ruptured spleen, liver laceration, pelvic fracture, injuries associated with extensive blood loss
92
Third Peak of Injury
20% of deaths occur
Days to weeks after injury
Location: critical care unit
Cause of death: sepsis, multiple organ dysfunction syndrome
93
Victim of a Trauma
Real fear of dying/disfigurement
Anger or guilt toward causing agent
Anxiety over alien environment
Intrusion by impersonal strangers
High level of stress (sympathetic NS stimulation, inability to relax or concentrate)
94
Six Phases of Trauma Care
Prehospital resuscitation
Hospital resuscitation
Definitive care and operative phase
Critical care
Intermediate care
Rehabilitation
95
Primary Survey of Advanced Trauma Life Support
Airway with C-spine protection
Breathing and ventilation
Circulation with hemorrhage control
Disability/Neuro assessment
Exposure and environmental control
96
Personal Safety of Nurse in Trauma
Unknown risk of infections --> universal precautions
Displacement of anger by client or family
Physical threat to safety
Toxic agents
97
Prehospital Care of Trauma
Security and safety of scene
Initial assessment (ABCDE)
Triage and prioritize all victims
Focused history and physical exam
Stabilization of victims
Transportation
98
Primary Evaluation in ED
ABCs
Mechanism of injury
Scene
99
Resuscitation in ED
Intubation
O2
IV fluids
Stop bleeding
100
Secondary Assessment in ED
Pertinent health history
Physical exam
101
Definitive Care in ED
CCU, OR
Decisions to direct client's care
102
Primary Trauma Assessment
```
Airway
Breathing
Circulation
Disability
Exposure/Environmental Control
```
103
Secondary Trauma Assessment
Full set of vitals
Get resuscitation adjuncts (LMNOP)
History (MIST)
Inspect posterior surfaces
104
Resuscitation Adjuncts
```
Laboratory studies
Monitoring, cardiac
NG/OG tube
Oxygenation/ventilation
Pain assessment/management
```
105
MIST for Head to Toe
Mechanism of injury
Injuries sustained
Signs/symptoms before arrival
Treatment before arrival
106
Secondary Assessment History (SAMPLE)
```
Symptoms associated with injury
Allergies, tetanus status
Medications currently used
Past medical history
Last meal/oral intake
Events/environmental factors related to injury/illness
```
107
Definitive Care of Trauma
Dressing of wounds
Suturing as needed
Stabilization of fractures or dislocations
Surgery if indicated
CCU admission
Medications as needed
Pain control
108
Lethal Triad
Coagulopathy
Hypothermia
Acidosis
109
Critical Wounds
Sucking chest wound
Gunshot wound
Impaled object
110
Sucking Chest Wound
Seal with occlusive dressing
One way valve dressing or dart
111
Gunshot Wound
Look for exit wound
Extensive internal injuries
112
Impaled Object
Do not remove the object!
Bulk dress the object in place
113
Chest Wall Injuries
Rib fractures
Flail chest (two or more ribs fractured in two or more places, free floating, pulmonary contusion under fracture)
Blunt chest trauma (cardiac trauma, contact with steering wheel, cardiac perfusion problems)
114
Trauma to Extremities
Immobilization of fractures
Assessment of distal circulation and nerve function
Assess extremities bilaterally
Lower priority injuries
Dress traumatic amputations and bring extremity with client
115
Spinal Cord Injury
Cord vs. Vertebral injury and level
Neck immobilization with cervical collar
Spinal cord immobilization with long spine board
Paralysis may be present without loss of sensation
Hypoventilation if cord injury is above C7
116
Complications of Trauma
Hypermetabolism (initiate enteral feedings within 72 hours for patients with blunt and penetrating abdominal injuries and those with head injuries)
Infection
Sepsis
Pulmonary (respiratory failure, ALI, fat embolism)
Pain
Renal complications (renal failure, AKI, myoglobinuria)
Vascular complications (compartment syndrome, venous thromboembolism, missed injury, MODS)
117
Compartment Syndrome
Increased pressure within limited space
Compromises circulation, results in ischemia and necrosis of tissues
High risk patients (LE trauma, fractures, penetrating injuries)
Signs/Symptoms: swelling, paresis, PAIN, decreased pulses, decreased capillary refill
DECREASED PULSES ARE VERY LATE SIGN OF COMPARTMENT SYNDROME
118
Disseminated Intravascular Coagulation
A systemic clotting cycle that begins with the systemic circulation of thrombin
Thrombin promotes clotting in the microvasculature of the organs
As the coagulation process continues to deplete the circulatory system of clotting factors/platelets, signs of bleeding begin to occur
PROFUSE BLEEDING AND A LOW PLATELET COUNT
119
Nontraumatic Causes of DIC
Obstetric conditions (50% of DIC cases)
Cancer (35% of DIC cases)
Sepsis
Autoimmune reactions
Pulmonary embolism
120
Thrombotic Signs of DIC
```
Angina
Acrocyanosis
Dyspnea
Headache
Confusion
Severe pain
Visual changes
```
121
Hemorrhagic Signs of DIC
```
Bleeding from puncture sites
Renewed bleeding from dressings or drains
Epistaxis
Hematemesis, melena stools
Petechiae
Ecchymosis
```
122
Diagnostic Tests of DIC
PT and PTT prolonged
Low platelet count (<50,000)
Low fibrinogen level
Elevated fibrin degradation products
D-dimer serum screen > 50
123
Interventions for DIC
Treat underlying cause
Whole blood if needed for bleeding replacement
Replace clotting factors (platelets, cryoprecipitate, fresh frozen plasma)
Antithrombin III
124
Trauma-Induced Coagulopathy
Different from DIC (can happen immediately after trauma)
Initiated by tissue injury and hemorrhagic shock
Caused by platelet dysfunction, clotting factor inhibition due to hypo perfusion, dilution by fluid administration
125
Treatment of Trauma-Induced Coagulopathy
Administration of specific ratios of blood products (PRBCs, FFP, platelets)
Administration of clotting factors and antifibrinolytic agents
126
Disaster
Large group of people ( > 100)
Man-made and natural causes
May be predictable or foreseeable
Involves more voluntary care
First aid, field station, evacuation, designated hospital, temporary morgue
Triage field casualties with tags
Improvise from limited supplies
127
Multiple Casualty
One to a few victims
Accidental causes
Unpredictable
Involves highly professional care
First aid, transport, emergency department, surgery, CCCU
ABCs of primary survey
Sophisticated equipment
128
Agent
Physical item causes injury or destruction
129
Primary Agent
Heat, wind, water
130
Secondary Agent
Bacteria or viruses thriving as a result of the disaster
131
Pre-Impact of Disaster
Prior to the actual occurrence
Period of earliest warning
Planning: Assess probability and risk
Mitigation: Prevent and reduce damages
132
Impact of Disaster
From the time of onset until the threat of further destruction has passed
Enduring hardship and surviving
133
Postimpact of Disaster
Beginning during the impact phase
Ends with the return of normal community order
Emergency (rescue and first aid)
Recovery (from emergency to recovery)
134
Phases of a Community's Reaction to a Disaster
Heroic --> Honeymoon --> Disillusionment --> Reconstruction
135
Heroic Phase
Strong emotions focusing on helping people to survive
136
Honeymoon Phase
Drawing people together in common experience
137
Disillusionment Phase
Feelings of disappointment due to unfulfilled promises, individualization of consequences
138
Reconstruction Phase
A reaffirmation of faith in the community during recovery
139
Dimensions of a Disaster
Predictability (natural/manmade)
Frequency (in certain locations)
Controllability (prevent/reduce damage)
Time (speed of onset)
Scope (geographical area)
Intensity (ability to inflict damage and injury)
140
Effects of Disaster on Community
Public service personnel are overworked
Lifelines are disrupted
Resources depleted
Public/private buildings are damaged
141
Primary Prevention of Disasters
Safety Measures (levies, construction, storm cellars, engineering controls of high risk areas)
Drills
Evacuation plans
Emergency communication plan
Disaster supplies (CASH)
142
Secondary Prevention of Disasters
Monitoring systems
Warning system
Elements of a disaster plan
Rescue operations
Psychological impact and response
Critical incident stress debriefing
143
Elements of a Disaster Plan
Notification of residents
Warning
Control measures of the disaster
Logistical coordination
Evacuation
Rescue
Immediate care
Supportive care
144
Levels of Response
Agency (NRMC)
Local (fire + police departments)
State (MO government, National Guard)
Regional (Midwest, state support)
International (Red Cross)
145
Labeling System for Casualties
Red: Life threatening, STAT TREATMENT (chest trauma, head injury, hypoxia, shock, chest pain, big burns)
Yellow: Systemic injuries (need treatment within 45-60 minutes)
Green: Localized injuries (may wait several hours)
Black: Dead or fatally wounded
146
Nursing Responsibilities in Disaster Management
Adapting nursing skills to recognize and meet needs resulting from a disaster
Includes C/PHN from state/local health department
Volunteers from disaster teams
American Red Cross
US Public Health Service
147
Responsibilities of Agencies in Disaster Management
Comprehensive plan: mitigation, preparedness, response, recovery
Federal Government: supports state and local governments
FEMA: coordinating federal assistance
148
Principles of Disaster Management
1. Prevent disaster
2. Minimize casualties
3. Prevent further casualties
4. Rescue victims
5. Provide first aid
6. Evacuate injured
7. Provide medical care
8. Promote reconstruction of lives
149
Responsiveness
State of general awareness of oneself and the environment
Reflects functional integrity of the brain as a whole
150
Specialized Neurological Assessment for Unresponsive Patient
Assess arousal first (stimulus, response, abnormal posturing such as decorticate/decerebrate)
Glasgow Coma Scale (eyes open, verbal response, motor response)
151
Nursing Care of Unresponsive Patient
Maintaining ventilation and airway
Optimizing cerebral perfusion pressure (BP control, temperature control, promoting venous return)
Safe and protective environment (temperature control, side rails, pressure ulcers, VAP)
152
Poisoning
More than 2.4 million cases reported in the US annually
Most poisoning deaths caused by drugs
75% of suicides caused by drugs
153
Management of Poisoning
Sources: medications, plants, environmental sources, pollutants, and drugs of abuse
Entry: oral, inhalation, injection, absorption through skin
Intentional or accidental
Symptoms often mimic a disease
154
Fundamentals of Poisoning Treatment
Emergency that requires rapid treatment
Supportive care, identification of poison, prevention of further absorption, poison removal, antidotes
155
Drug Overdose Phase I
Assessment (history, identification of toxidromes)
156
Anticholinergic Toxidromes
Atropine, Antihistamines, Tricyclics
Delirium
Flushed, dry skin
Dilated pupils, elevated temperature
Decreased bowel sounds, urinary retention
Tachycardia
157
Cholinergic Toxidromes
Pesticides, Organophosphates
Excessive salivation, lacrimation, urination, diarrhea, and emesis
Diaphoresis, bronchorrhea, bradycardia
Fasciculations, CNS depression
Constricted pupils
158
Opioid Toxidromes
Narcotics, Fentanyl
CNS depression, respiratory depression
Constricted pupils
Hypotension
Hypothermia
159
Sympathomimetic Toxidromes
PCP, Angel Dust
Agitation
Tachycardia, hypertension
Seizures
Metabolic acidosis
160
Acetaminophen Toxidromes
Nausea/Vomiting
Appear okay, then sudden altered mental status
161
Aspirin Toxidromes
Nausea, vomiting
TINNITUS
Metabolic acidosis arrhythmias
Appear okay, then rapid decline
162
Anticholinergic Mnemonic
MAD as a hatter
RED as a beet
BLIND as a bat
HOT as a hare
DRY as a bone
163
Drug Overdose Phase II
Stabilization
ABCs
ACID-BASE AND ELECTROLYTE
Injuries and disease processes
164
Drug Overdose Phase III
Initial decontamination
Prevent absorption
Ocular (eye irrigation)
Dermal (flushing/showering)
Inhalation
Ingestion
165
Drug Overdose Phase IV
Advanced management
GI decontamination (lavage, absorbents, cathartics)
Enhancement of elimination (activated charcoal, whole bowel irrigation, urine alkalization, hemodialysis hyperbaric oxygenation, exchange transfusion
Antagonists
NO UNIVERSAL ANTIDOTE
Antivenin/Antitoxin
166
Gastric Lavage
Ewald tube
Contraindications: caustic, alkali, petroleum distillates
167
Absorbents
Activated charcoal
168
Cathartics
Magnesium citrate
Sorbitol
169
Antidote for Acetaminophen
Acetylcysteine (Mucomyst)
170
Antidote for Anticholinergics
Physostigmine (Antilirium)
171
Antidote for Benzodiazepines
Flumazenil (Romazicon)
172
Antidote for Cyanide
Amyl nitrite
173
Antidote for Ethlyne Glycol/Methanol
Ethanol, Fomepizole
174
Antidote for Opiates
Naloxone (Narcan)
175
Antidote for Organophosphatase Insecticides
Atropine
176
Drug Overdose Phase V
Continuous monitoring
Respiratory and airway
Cardiac (BP, Pulse, and Rhythm)
Chemistry (Electrolytes, Serum Levels)
LOC
177
Drug Overdose Phase VI
Prevention (patient/family teaching)
Rehabilitation
178
Managing Blood Sugar in the Surgical CCU
Strict glycemic control (80-110)
Insulin drips
Reduced mortality in surgical CCU patients
High incidence of hypoglycemia
Enhanced wound healing
179
Managing Blood Sugar in the Medical CCU
Target: 140-180
Insulin drip if BS > 180
Hourly blood sugar assessments
Titration of insulin (immediate BS and rate of change in BS)
180
Hypoglycemia Assessment
Early: irritability, dizziness, shakiness, slurred speech
Late: vertigo, unresponsive, seizures, tachycardia, pallor, diaphoresis
Finger Stick BS
181
Causes of Hypoglycemia
Response to insulin
Stress
Weight loss, malnutrition
Prolonged exercise
Alcohol ingestion
Fasting
Salicylates
Severe sepsis
182
Treatment of Hypoglycemia
GLUCOSE
Oral agents if conscious
BS: 40-70 --> 25 gm Dextrose 50% slow IVP
BS: < 40 --> 50 gm Dextrose 50% slow IVP
Monitor blood sugars q15 min
Neuro and VS assessment q15 min
183
Diabetic Ketoacidosis Etiologies
Type I DM
Acute pancreatitis
184
Pathophysiology of DKA
Hyperglycemia
Hyperosmolality
Metabolic ketoacidosis
Dehydration--volume depletion
185
Early DKA Assessment
Polyuria, thirst, N/V, loss of appetite, abdominal cramps, fatigue, progressive hyperventilation, tachycardia
BS > 250
Decreased pH, decreased bicarbonate
Glycosuria (BS > 180)
Anion gap > 10
186
DKA Late Assessment
Kussmaul respirations, fruity breath odor, hypotension, dry mucous membranes, lethargy, coma, poor skin turgor
BS: 300-800
pH: < 7
Decreased bicarbonate
Anion gap > 12
INCREASED POTASSIUM, SODIUM, BUN, MAGNESIUM, PHOSPHATE
187
Pathophysiology of Hyperosmolar Hyperglycemic State
Type II DM
Hyperglycemia
Hyperosmolality
Osmotic diuresis
Dehydration --> Hypovolemic shock
188
Assessment of HHS
Gradual onset over 5 or more days
Increased fatigue, drowsiness
Loss of appetite
Polyuria, polydipsia
BS > 600
Increased sodium
189
Comparison of DKA to HHS
Mean Glucose: DKA 600, HHS 1100
Serum Osmolarity: DKA 320, HHS 400
Arterial pH: DKA 7.07, HHS 7.26
Anion Gap: DKA > 12, HHS < 12
Mortality: DKA 1-15%, HHS 20-40%
190
Volume Replacement Protocol for DKA and HHS
REHYDRATION IS VERY IMPORTANT
0.9% NS 1 L/hour
If Na > 140, 0.45% saline and 20-30 mEq KCl
If Na < 140, 0.9% NS and 20-30 mEq KCl
When BS < 200, D5/0.45% saline and 20-30 mEq KCl
191
Insulin Protocol for DKA
0. 1 U/kg IV bolus
0. 1 U/kg/hour IV drip
Target of 50-70 mg/dL to decrease BS per hour
Hourly blood glucose monitoring
When BS < 200, decrease insulin to 0.02 U/kg/hour
192
Insulin Protocol for HHS
0. 1 U/kg IV bolus
0. 1 U/kg/hour IV drip
Hourly blood glucose monitoring
If BS does not fall 10% in first hour, 0.14 U/kg IV bolus
When BS < 300, decrease insulin to 0.02 U/kg/hour
Maintain BS 200-300
193
Reversing DKA
pH > 7.0: No intervention
pH < 7.0: 100 mol Bicarbonate, 400 mL water, 20 mEq KCl infused over 2 hours
Monitor pH, bicarbonate, potassium, and phosphate hourly until stable
194
Reversing HHS
Not a likely goal
Otherwise, follow DKA protocol
195
Restoring Potassium with DKA and HHS
Establish adequate urine function (UO > 50 mL/hour)
K < 3.8: 20-30 mEq K+/hour IV drip until K+ > 4.0
K > 5.2: Hold potassium, monitor q2h
196
Restoring Phosphate with DKA and HHS
Establish adequate urine renal function (UO > 50 mL/hour)
Phosphate < 1.0 mg/L: add phosphate to IV
Monitor phosphate q2h
197
Monitor Response to Therapies for DKA and HHS
Fluid volume overload (hourly CVP, UO, BP, pulse, jugular veins)
Hypoglycemia (hourly or more frequent BS)
Hypo/Hyperkalemia (hourly lab assessment)
Hyponatremia (hourly lab assessment)
Cerebral edema (hourly neuro assessment)
Risk for infection
198
pH and Potassium
INVERSE RELATIONSHIP
199
CABG
Artery or vein from another area used to create a detour around the blockage
Saphenous vein or mammary artery most common
200
Cardiopulmonary Bypass
Extracorporal circuit
Carries blood to perfusion machine from vena cava and back to aorta
Requires extra fluid volume
201
Cardiopulmonary Bypass Nursing Concerns
Intravascular fluid deficit --> hypotension
Third spacing --> edema, weight gain
Myocardial depression --> decreased CO
Coagulopathy --> bleeding
Pulmonary dysfunction, neurological dysfunction
AKI --> clamp time
202
How to Care for Post-Op Open Heart Patient
Pre-Op education is key
Benchmark is 6 hours to extubation
Important to prepare patient and keep calm during weaning
Chest tube drainage monitoring
203
Beck's Triad for Cardiac Tamponade
JVD
Hypotension
Distant heart sounds
204
Monitoring for Cardiac Tamponade with Chest Tube
Chest tube drainage monitoring is key; not too much, not too little
Hourly milking--no longer strip tubes
No more than 200 mL/hour, but ensure tubes are patent
205
Caring for Patient after Extubation
IS is key
Sternal precautions
Ambulation
Pain control
Wound care
206
Care for Organ Transplant Recipients
Immunosuppression
Rejection
Organ-specific complications
207
Caring for Heart Patients
Extracorporal circuit complications
Contractility issues
Denervation problems
Bleeding/tamponade
208
Caring for Lung Patients
Double will require bypass-pump complications
Especially susceptible to fluid overload and ALI
Bleeding, cancer, infection
Requires more immunosuppression than other organs
209
Caring for Liver Patients
At risk for bleeding, but do not want to overcorrect
T-tube for bile drainage
Frequent monitoring of liver enzymes
Fluid shifts may occur
May have swings in blood sugar due to steroid immunosuppression and graft function
210
Caring for Kidney Patients
Monitor fluid-volume status every hour; replace 1:1
Output monitoring is essential
Irrigate catheter to get rid of clots
211
Caring for Pancreas Patients
Monitor glucose and urine amylase
212
Hematopoietic Stem Cell Transplant
Used to treat myeloma, lymphoma, AML, ALL, aplastic anemia
Autogenic vs. Allogenic
213
Graft vs. Host Disease
Seen in stem cell transplants
New immune system attacks body as foreign
Attacks liver, skin, gut
Use prophylactic immunosuppression
Will need TPN and IV medications
214
Hyperacute Rejection
Occurs within minutes to hours
Result of presensitized antibodies
Graft failure/removal common
Life-threatening, high mortality, hemodynamic shock, collapse
215
Acute Rejection
Occurs between week 1 to 3 months
SIRS
Responds to steroids and higher immunosuppression
Cell-mediated; most patients experience at least once
216
Chronic Rejection
Gradual deterioration
B and T cell mediation
Not responsive to steroids
May need another transplant
217
Signs of Heart Rejection
Asymptomatic
Need a biopsy
218
Signs of Lung Rejection
Distinguish from pulmonary infection or reperfusion injury
219
Signs of Pancreas Rejection
Hyperglycemia
Urine amylase
220
Signs of Liver Rejection
Elevated liver enzymes and total bilirubin
221
Signs of Kidney Rejection
Increased serum BUN, creatinine
Decreased urine output
Weight gain, edema, hypertension
222
Immunosuppression
Must be started right after surgery, then lifelong commitment
Multidrug regimen
Need to prevent rejection and treat autoimmune diseases
Toxicity, neoplasms
Side effects include hirsutism, moon face
223
Calcineuron Inhibitors
Tacrolimus, Cyclosporin
Nephrotoxicity common
Sharp increase in BUN and creatinine
Avoid NSAIDs
224
Glucocorticoids
In combination: thin skin, GI tract, glucose issues
225
Cytotoxic Agents
Methotrexate, Remicaid, Mycophenalate
226
Antibodies
Rabbit antithymocyte given once in OR, once post-op in kidneys
Blocks activation of T-Cells
227
Prevention of Post-Op Infection
Meticulous wound care
CLABSI and CAUTI bundles
IS
Mobility
Nutrition
Hand hygiene, oral care
Pharmacological prophylaxis
228
Brain Surgeries
Craniotomy, Brain Hemorrhage Evacuation, Tumor/Abscess Removal
Relieve pressure to maintain brain perfusion
229
Traumatic Brain Injury
Battles Sign (bruising behind ears)
Raccoon Eyes
Coup/Contra-Coup
230
Epidural Hematoma
Skull fracture with ARTERIAL rupture
Lucid interval followed by a rapid increase in ICP
231
Subdural Space Hematoma
Rupture of VENOUS sinuses or small bridging veins due to torsion forces
Acute presentation with a rapid increase in ICP
Chronic presentation with personality change, memory loss/confusion, particularly in the elderly
232
Subarachnoid Space Hematoma
ARTERIAL RUPTURE
Meningeal irritation with a rapid increase in ICP
233
Cerebral Hemisphere Hematoma
CORTICAL CONTUSIONS
Rupture of small intrinsic vessels with intracerebral hematoma
Increased ICP with focal deficits; usually fatal
Profound coma
234
Post-Op Craniotomy
Frequent neuro checks (q15, then q30, then q1h)
Frequent vitals
Urine output, drain output
235
Decorticate Posturing
Flexion
"Toward the core"
236
Decerebrate Posturing
Away from the core
WORSE
237
ICP Monitoring
Catheter inserted into brain to monitor pressure
Monroe-Kellie Hypothesis: 80% brain, 10% blood, 10% CSF
Cerebral Perfusion Pressure = MAP - ICP
238
Intercranial Hypertension Prevention/Treatment
HOB > 30
Decreased stimulation
Mannitol or 3% NS
Hyperventilation, Hyperthermia
239
Cushing's Triad
Bradycardia
Extreme HTN
Respiratory issues (apnea)
240
Brain Death
Notify donor as GCS falls
Oculocephalic reflex test (doll's eyes)
Oculovestibular reflex test (cold calorics)
Apnea test
Do not withdraw any care until donor has been notified
241
Diabetes Insipidus
Central or neurogenic causes
Brain damage to hypothalamus or pituitary gland
Absence of ADH production
Urine output > 250
Spec Grav 1.000-1.005
Polyuria, polydipsia
Hyperosmolar serum
Hypernatremia
