Exam 3 Flashcards
Etiology of Peptic Ulcer Disease
NSAIDs
Helicobacter pylori
Etiology of Stress-Related Mucosal Disease
High physiologic stress (mechanical ventilation, burns, shock)
Increased acid production and decreased mucosal blood flow (ischemia)
Etiology of Esophagogastric Varices
Portal hypertension
Liver failure
Hematemesis
Bright red blood or coffee grounds (acid)
Hematochezia
Bright red blood in stool
Melena
UGI blood passed through bowels
Prophylaxis for GI Bleeding
Monitor gastric pH
Assess stools and gastric contents for blood
Histamine-2 Receptor Blocker (Cimetidine, Famotidine, Ranitidine)
PPI (Omeprazole, Pantoprazole)
Mucosal lining coating (Sucralfate)
Serum Bilirubin, direct
0 - 0.3 mg/dL
Serum Bilirubin, total
0 - 0.9 mg/dL
Serum Protein Total
7.0 - 7.5 g/dL
Serum Albumin
4.0 - 5.5 g/dL
Prothrombin Time
12 - 16 seconds
Ammonia
11 - 32 umol/L
Bleeding Etiology with Liver Involvement
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
Stabilization of GI Bleeding
IV fluids
Blood transfusions
Blood products
Control bleeding
Control of GI Bleeding
Esophageal balloon tamponade
Vasopressin
Somatostatin and Octreotide
Beta blockers
Nursing Management of GI Bleeding
Fluid resuscitation
Blood and blood product transfusions
Gastric lavage
Maintaining surveillance for complications (neurological assessments hourly, assess renal perfusion with hourly outputs)
Medical Management of Esophageal Varices
Control bleeding (endoscopy)
Endoscopic injection therapy
Endoscopic variceal ligation
Hepatic Encephalopathy
Seen in chronic liver disease
Triggered by dehydration, electrolyte loss, increased protein intake, bleeding from GI tract, infections, alcohol ingestion
Signs and Symptoms of Hepatic Encephalopathy
Headache, hyperventilation, jaundice, mental status changes, palmar erythema, spider nevi, fetor hepaticus, bruises, hepatomegaly
Laboratory for Hepatic Encephalopathy
Serum bilirubin (unconjugated and tubal)
AST
Alkaline phosphatase
SERUM AMMONIA
Prothrombin time
Intellectual Function of Hepatic Encephalopathy
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
Neuromuscular Stages of Hepatic Encephalopathy
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
Acute Liver Failure
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
Etiology of Acute Liver Failure
Viral hepatitis
Medication-induced liver damage
Early recognition is key
Pathophysiology of Acute Liver Failure
ALF over 1 to 3 weeks
Hepatic encephalopathy within 8 weeks
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
Etiologies of Chronic Liver Failure
Infections
Drugs or toxins (acetaminophen, alcohol)
Hypoperfusion
BILIARY (bile obstruction)
CARDIAC (right sided heart failure)
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
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)
Molecular Adsorbent Recirculating System (MARS)
Nonbiological artificial liver support system
Albumin used as dialysate to remove protein-bound toxins
MARS Effects
Stabilize condition
Bridge to transplant
Reduction of portal HTN
Improvement of ICP, encephalopathy
Increases MAP and SVR
Removes uremic toxins
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
Etiology of Acute Pancreatitis
Gallstone migration
Alcoholism
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
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
Pathophysiology of Acute Pancreatitis
Edematous pancreatitis
Acute necrotizing pancreatitis
Local tissue injury
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)
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)
Nursing Management of Acute Pancreatitis
Providing comfort and emotional support
Maintaining surveillance for complications
Educating patient and family
Functions of the Skin
Protection
Sensation
Water balance
Temperature regulation
Vitamin production
Immune response function
Burn
Injury to the skin or other organic tissue primarily caused by heat or due to radiation, radioactivity, electricity, friction, or contact with chemicals
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
Significant Factors Related to Burn Injury
Type of injury
Location of injury (of incident, on client)
Age
Previous health history
Size-Area
Depth
Assessment: Sources of Burn Injuries
Thermal (heat, flame, scalds)
Electrical
Chemical
Radiation
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
Care of Electrical Burn Injuries
TURN OFF SOURCE OF ELECTRICITY FIRST
CPR priorities of Airway, Breathing, Circulation
Treat dysrhythmias
Entry and exit wounds
Pathophysiology of Burns
DYSFUNCTION OF ALMOST EVERY CELL AND CELLULAR SIGNALING PATHWAYS
Hypermetabolic state = CELL DEATH
Chronic inflammation
FLUID SHIFTING (3RD SPACING)
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
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
Children and Burns
Greater risk for injury
Head greater ratio of TBSA
Legs smaller ratio of TBSA
Skin thinner
Fluid loss more critical
Elderly and Burns
Thinner, tougher skin
Slower regeneration time
More sensitive to fluid volume loss
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
Rule of Palms
Measure the palmar surface of the victim’s hand (fingertip to wrist)
Represents 1% of the TBSA
Assessment: Depth of Burns
Amount of injured epidermis or dermis
Depth of destruction of epidermis and/or dermis
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
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)
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
Zone of Coagulation
Irreversible damage
Zone of Stasis
Impaired circulation
Inflammatory response
Can be converted to full thickness
Zone of Hyperemia
Vasodilation, increased blood flow
Minor Burn Severity Criteria
PT < 15% TBSA
FT < 2% TBSA
Moderate Burn Severity Criteria
PT: 15-25% TBSA
FT: 10% TBSA
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)
Emergent or Resuscitative Phase of Burn
First 24-48 hours
Until 3rd spacing has stopped
Acute Phase of Burn
3-6 months
Until wound closure
Shock and hyper metabolic phase
Rehabilitative Phase of Burn
Several years
Scar and graft management
PT/OT, contractures
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
Nursing Management of Burns
Inflammatory Phase (immediately after injury)
Proliferative Phase (4-20 days after injury)
Maturation Phase (20 days after injury)
Airway Management with Burns
ASSESSMENT OF RISK (facial burns, singed facial hair, stridor)
Visualize larynx for redness
Endotracheal intubation
Respiratory Problems with Burns
Carbon monoxide poisoning (carboxyhemoglobin serum level)
Smoke poisoning
ALI
Pulmonary fluid overload
Thoracic eschar impairment
Interventions for Respiratory Problems with Burns
100% O2 therapy
Monitor fluid balance
ET intubation
Mechanical ventilation
Humidification
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
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)
Fluid Replacement Therapy for Burns
Baxter Equation
Monitor fluid replacement with CVP, BP, and hourly urine output
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
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
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
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
Debridement
Mechanical: hydrotherapy, whirlpool baths, surgical excision
Enzymatic (eschar): autolysis, proteolytic
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
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
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
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)
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
Stressors of Burn Units
Fast-paced, high-technology
Complex management
Multidisciplinary
Equipment
Limited workspace
Warm temperatures
Unpleasant odors
High noise levels
Trauma
Accidental or unintentional injury sustained through an external mechanism of injury
Falls, shootings, burns, auto accidents, farm accidents, altercations, natural disasters
Blunt Trauma
Motor vehicle collisions
Contact sports
Blunt force injuries
Falls
Penetrating Trauma
Stabbings
Firearm injuries
Impalement
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
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
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
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)
Six Phases of Trauma Care
Prehospital resuscitation
Hospital resuscitation
Definitive care and operative phase
Critical care
Intermediate care
Rehabilitation
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
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
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
Primary Evaluation in ED
ABCs
Mechanism of injury
Scene
Resuscitation in ED
Intubation
O2
IV fluids
Stop bleeding
Secondary Assessment in ED
Pertinent health history
Physical exam
Definitive Care in ED
CCU, OR
Decisions to direct client’s care
Primary Trauma Assessment
Airway Breathing Circulation Disability Exposure/Environmental Control
Secondary Trauma Assessment
Full set of vitals
Get resuscitation adjuncts (LMNOP)
History (MIST)
Inspect posterior surfaces
Resuscitation Adjuncts
Laboratory studies Monitoring, cardiac NG/OG tube Oxygenation/ventilation Pain assessment/management
MIST for Head to Toe
Mechanism of injury
Injuries sustained
Signs/symptoms before arrival
Treatment before arrival
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
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
Lethal Triad
Coagulopathy
Hypothermia
Acidosis
Critical Wounds
Sucking chest wound
Gunshot wound
Impaled object
Sucking Chest Wound
Seal with occlusive dressing
One way valve dressing or dart
Gunshot Wound
Look for exit wound
Extensive internal injuries
Impaled Object
Do not remove the object!
Bulk dress the object in place
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)
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
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
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)
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
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
Nontraumatic Causes of DIC
Obstetric conditions (50% of DIC cases)
Cancer (35% of DIC cases)
Sepsis
Autoimmune reactions
Pulmonary embolism
Thrombotic Signs of DIC
Angina Acrocyanosis Dyspnea Headache Confusion Severe pain Visual changes
Hemorrhagic Signs of DIC
Bleeding from puncture sites Renewed bleeding from dressings or drains Epistaxis Hematemesis, melena stools Petechiae Ecchymosis
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
Interventions for DIC
Treat underlying cause
Whole blood if needed for bleeding replacement
Replace clotting factors (platelets, cryoprecipitate, fresh frozen plasma)
Antithrombin III
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
Treatment of Trauma-Induced Coagulopathy
Administration of specific ratios of blood products (PRBCs, FFP, platelets)
Administration of clotting factors and antifibrinolytic agents
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
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
Agent
Physical item causes injury or destruction
Primary Agent
Heat, wind, water
Secondary Agent
Bacteria or viruses thriving as a result of the disaster
Pre-Impact of Disaster
Prior to the actual occurrence
Period of earliest warning
Planning: Assess probability and risk
Mitigation: Prevent and reduce damages
Impact of Disaster
From the time of onset until the threat of further destruction has passed
Enduring hardship and surviving
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)
Phases of a Community’s Reaction to a Disaster
Heroic –> Honeymoon –> Disillusionment –> Reconstruction
Heroic Phase
Strong emotions focusing on helping people to survive
Honeymoon Phase
Drawing people together in common experience
Disillusionment Phase
Feelings of disappointment due to unfulfilled promises, individualization of consequences
Reconstruction Phase
A reaffirmation of faith in the community during recovery
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)
Effects of Disaster on Community
Public service personnel are overworked
Lifelines are disrupted
Resources depleted
Public/private buildings are damaged
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)
Secondary Prevention of Disasters
Monitoring systems
Warning system
Elements of a disaster plan
Rescue operations
Psychological impact and response
Critical incident stress debriefing
Elements of a Disaster Plan
Notification of residents
Warning
Control measures of the disaster
Logistical coordination
Evacuation
Rescue
Immediate care
Supportive care
Levels of Response
Agency (NRMC)
Local (fire + police departments)
State (MO government, National Guard)
Regional (Midwest, state support)
International (Red Cross)
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
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
Responsibilities of Agencies in Disaster Management
Comprehensive plan: mitigation, preparedness, response, recovery
Federal Government: supports state and local governments
FEMA: coordinating federal assistance
Principles of Disaster Management
- Prevent disaster
- Minimize casualties
- Prevent further casualties
- Rescue victims
- Provide first aid
- Evacuate injured
- Provide medical care
- Promote reconstruction of lives
Responsiveness
State of general awareness of oneself and the environment
Reflects functional integrity of the brain as a whole
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)
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)
Poisoning
More than 2.4 million cases reported in the US annually
Most poisoning deaths caused by drugs
75% of suicides caused by drugs
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
Fundamentals of Poisoning Treatment
Emergency that requires rapid treatment
Supportive care, identification of poison, prevention of further absorption, poison removal, antidotes
Drug Overdose Phase I
Assessment (history, identification of toxidromes)
Anticholinergic Toxidromes
Atropine, Antihistamines, Tricyclics
Delirium
Flushed, dry skin
Dilated pupils, elevated temperature
Decreased bowel sounds, urinary retention
Tachycardia
Cholinergic Toxidromes
Pesticides, Organophosphates
Excessive salivation, lacrimation, urination, diarrhea, and emesis
Diaphoresis, bronchorrhea, bradycardia
Fasciculations, CNS depression
Constricted pupils
Opioid Toxidromes
Narcotics, Fentanyl
CNS depression, respiratory depression
Constricted pupils
Hypotension
Hypothermia
Sympathomimetic Toxidromes
PCP, Angel Dust
Agitation
Tachycardia, hypertension
Seizures
Metabolic acidosis
Acetaminophen Toxidromes
Nausea/Vomiting
Appear okay, then sudden altered mental status
Aspirin Toxidromes
Nausea, vomiting
TINNITUS
Metabolic acidosis arrhythmias
Appear okay, then rapid decline
Anticholinergic Mnemonic
MAD as a hatter
RED as a beet
BLIND as a bat
HOT as a hare
DRY as a bone
Drug Overdose Phase II
Stabilization
ABCs
ACID-BASE AND ELECTROLYTE
Injuries and disease processes
Drug Overdose Phase III
Initial decontamination
Prevent absorption
Ocular (eye irrigation)
Dermal (flushing/showering)
Inhalation
Ingestion
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
Gastric Lavage
Ewald tube
Contraindications: caustic, alkali, petroleum distillates
Absorbents
Activated charcoal
Cathartics
Magnesium citrate
Sorbitol
Antidote for Acetaminophen
Acetylcysteine (Mucomyst)
Antidote for Anticholinergics
Physostigmine (Antilirium)
Antidote for Benzodiazepines
Flumazenil (Romazicon)
Antidote for Cyanide
Amyl nitrite
Antidote for Ethlyne Glycol/Methanol
Ethanol, Fomepizole
Antidote for Opiates
Naloxone (Narcan)
Antidote for Organophosphatase Insecticides
Atropine
Drug Overdose Phase V
Continuous monitoring
Respiratory and airway
Cardiac (BP, Pulse, and Rhythm)
Chemistry (Electrolytes, Serum Levels)
LOC
Drug Overdose Phase VI
Prevention (patient/family teaching)
Rehabilitation
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
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)
Hypoglycemia Assessment
Early: irritability, dizziness, shakiness, slurred speech
Late: vertigo, unresponsive, seizures, tachycardia, pallor, diaphoresis
Finger Stick BS
Causes of Hypoglycemia
Response to insulin
Stress
Weight loss, malnutrition
Prolonged exercise
Alcohol ingestion
Fasting
Salicylates
Severe sepsis
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
Diabetic Ketoacidosis Etiologies
Type I DM
Acute pancreatitis
Pathophysiology of DKA
Hyperglycemia
Hyperosmolality
Metabolic ketoacidosis
Dehydration–volume depletion
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
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
Pathophysiology of Hyperosmolar Hyperglycemic State
Type II DM
Hyperglycemia
Hyperosmolality
Osmotic diuresis
Dehydration –> Hypovolemic shock
Assessment of HHS
Gradual onset over 5 or more days
Increased fatigue, drowsiness
Loss of appetite
Polyuria, polydipsia
BS > 600
Increased sodium
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%
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
Insulin Protocol for DKA
- 1 U/kg IV bolus
- 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
Insulin Protocol for HHS
- 1 U/kg IV bolus
- 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
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
Reversing HHS
Not a likely goal
Otherwise, follow DKA protocol
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
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
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
pH and Potassium
INVERSE RELATIONSHIP
CABG
Artery or vein from another area used to create a detour around the blockage
Saphenous vein or mammary artery most common
Cardiopulmonary Bypass
Extracorporal circuit
Carries blood to perfusion machine from vena cava and back to aorta
Requires extra fluid volume
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
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
Beck’s Triad for Cardiac Tamponade
JVD
Hypotension
Distant heart sounds
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
Caring for Patient after Extubation
IS is key
Sternal precautions
Ambulation
Pain control
Wound care
Care for Organ Transplant Recipients
Immunosuppression
Rejection
Organ-specific complications
Caring for Heart Patients
Extracorporal circuit complications
Contractility issues
Denervation problems
Bleeding/tamponade
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
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
Caring for Kidney Patients
Monitor fluid-volume status every hour; replace 1:1
Output monitoring is essential
Irrigate catheter to get rid of clots
Caring for Pancreas Patients
Monitor glucose and urine amylase
Hematopoietic Stem Cell Transplant
Used to treat myeloma, lymphoma, AML, ALL, aplastic anemia
Autogenic vs. Allogenic
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
Hyperacute Rejection
Occurs within minutes to hours
Result of presensitized antibodies
Graft failure/removal common
Life-threatening, high mortality, hemodynamic shock, collapse
Acute Rejection
Occurs between week 1 to 3 months
SIRS
Responds to steroids and higher immunosuppression
Cell-mediated; most patients experience at least once
Chronic Rejection
Gradual deterioration
B and T cell mediation
Not responsive to steroids
May need another transplant
Signs of Heart Rejection
Asymptomatic
Need a biopsy
Signs of Lung Rejection
Distinguish from pulmonary infection or reperfusion injury
Signs of Pancreas Rejection
Hyperglycemia
Urine amylase
Signs of Liver Rejection
Elevated liver enzymes and total bilirubin
Signs of Kidney Rejection
Increased serum BUN, creatinine
Decreased urine output
Weight gain, edema, hypertension
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
Calcineuron Inhibitors
Tacrolimus, Cyclosporin
Nephrotoxicity common
Sharp increase in BUN and creatinine
Avoid NSAIDs
Glucocorticoids
In combination: thin skin, GI tract, glucose issues
Cytotoxic Agents
Methotrexate, Remicaid, Mycophenalate
Antibodies
Rabbit antithymocyte given once in OR, once post-op in kidneys
Blocks activation of T-Cells
Prevention of Post-Op Infection
Meticulous wound care
CLABSI and CAUTI bundles
IS
Mobility
Nutrition
Hand hygiene, oral care
Pharmacological prophylaxis
Brain Surgeries
Craniotomy, Brain Hemorrhage Evacuation, Tumor/Abscess Removal
Relieve pressure to maintain brain perfusion
Traumatic Brain Injury
Battles Sign (bruising behind ears)
Raccoon Eyes
Coup/Contra-Coup
Epidural Hematoma
Skull fracture with ARTERIAL rupture
Lucid interval followed by a rapid increase in ICP
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
Subarachnoid Space Hematoma
ARTERIAL RUPTURE
Meningeal irritation with a rapid increase in ICP
Cerebral Hemisphere Hematoma
CORTICAL CONTUSIONS
Rupture of small intrinsic vessels with intracerebral hematoma
Increased ICP with focal deficits; usually fatal
Profound coma
Post-Op Craniotomy
Frequent neuro checks (q15, then q30, then q1h)
Frequent vitals
Urine output, drain output
Decorticate Posturing
Flexion
“Toward the core”
Decerebrate Posturing
Away from the core
WORSE
ICP Monitoring
Catheter inserted into brain to monitor pressure
Monroe-Kellie Hypothesis: 80% brain, 10% blood, 10% CSF
Cerebral Perfusion Pressure = MAP - ICP
Intercranial Hypertension Prevention/Treatment
HOB > 30
Decreased stimulation
Mannitol or 3% NS
Hyperventilation, Hyperthermia
Cushing’s Triad
Bradycardia
Extreme HTN
Respiratory issues (apnea)
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
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
