BURNS
An injury to the skin or other tissues of the body caused by heat, chemicals, electric current, or radiation.
Functions of Skin
o Protects against infection
o Prevents loss of body fluids
o Body temperature
o Excretory organ
o Sensory organ
 Blood Flow
o CPP  blood is going to go to the brain
first, then heart  GI  kidney  skin
o Kidneys  decrease urine output,
increase BUN and creatine
o GI  absent bowel sounds
 Burns
o Injury to tissues caused by heat,
chemicals, electric current, or radiation
o Effects influenced by temperature of
burning agent, duration of contact time, type of tissue
o Highest fatality rates: children < 4 years of age & adults > 65 years of age
o Difficulty maintaining an airway and adequate circulation, affecting perfusion
o Alkalize  more harmful
o Severity can depend on location
 Etiology: Sources of Burn Injuries
o Household
o Flammables
o Microwaved food
o Carelessness with cigarettes,
o Steam, hot grease or liquids
matches, candles
o Hot water heaters set at ≥ 140° F
o Occupational
 Recommended to not set
o Tar
hot water heater greater
o Cement
than 120
o Chemicals
o Heat lamps
o Hot metals
o Fireplaces
o Steam pipes
o Open space heaters
o Combustible fuels
o Radiators
o Fertilizers, pesticides
o Outdoor grills
o Electricity from power lines
o Frayed or defective wiring
o Sparks from live electric sources
o Multiple extension cords/frayed
wiring
Types of Burn Injury
o Thermal
 Flame, flash, scald, or contact with hot objects
 Severity depends on temp, duration of contact, location of burn, and agent that caused the burn
 Most common
o Chemical
 Acids, alkalis, & organic compounds
 Alkalis  more harmful due to alkalis adhere to tissue causing protein hydrolysis and melting
 See in drain and oven cleaners
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Electrical
 Intense heat generated from an electrical current
 Produce an intense heat from electrical current  coagulation necrosis
 Direct damage to nerves and vessels, causing tissue anoxia and death, can occur
 Part of the body higher in resistance to electrical current  bone, muscle, fat
 Least resistant  blood vessels and nerves
 Can lead to tissue anoxia and tissue death
 Current that passes through vital organs produces more life-threatening sequel than that which
passes through other tissues
 Can cause dysrhythmias
 Myoglobin from injured muscles and hemoglobin from damaged RBCs are released into the
circulation  travels to the kidneys and can block the renal tubules  acute tubular necrosis and
acute kidney injury
 Can cause muscle spasm that are so strong they can cause bone fractures
 Ice burg affect  not seeing much damage on the surface, most of the damage is below
 Can be difficult to determine the severity due to most damage is below the skin
 Consider cervical spine injury for all patients
o Cold thermal
 Frostbite
 Ice crystals are formed in the tissues
o Smoke and Inhalation
 Hot air or noxious chemicals
 Three types of smoke / inhalation injuries:
 Metabolic asphyxiation
 Upper airway injury
 Lower airway injury
 You do not see much of what is going on
Smoke and Inhalation Injury
o From breathing noxious chemicals or hot air can damage the respiratory tract
o Initial and ongoing assessment
o Metabolic asphyxiation
 Inhaling certain smoke elements, primarily carbon monoxide or hydrogen cyanide
 Carboxyhemoglobin (hemoglobin + CO)
 Hemoglobin combined with carbon monoxide
 Most deaths occur due to inhaling carbon monoxide and hydrogen cyanide
 Death may occur if carboxyhemoglobin blood levels are greater than 20%
 Carbon monoxide displaces oxygen on the hemoglobin  tissue perfusion impaired
 May occur in the absence of burn injury to the skin
o Upper airway injury
 Inhalation injury to mouth, oropharynx, &/or larynx
2
 Sustains a thermal injury
 Mucosal burns of the oropharynx and larynx are
manifested by redness, blistering, and edema
CO2
Pulmonary Injury
CO
 Burns of the neck and chest may make breathing
more difficult because of burn eschar, becoming tight
and constricting  narrowing the airway
o Lower airway injury
Products of Combustion or Pyrolysis
 Injury to trachea, bronchioles, & alveoli
 Often caused by inhalation of smoke / toxic
chemicals
Smoke
Heat
Toxic Gases
 Pulmonary edema; ARDS
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 Edema and swelling can happen very quickly and narrows the airway
 May not appear until 12-48 hours after the burn
 Sustains a chemical injury
 Looking for hoarseness and stridor
o Always consider inhalation burn when it was sustain in a closed space
Classification
o Severity of burn determined by:
 Depth
 Extent - TBSA
 Location
 Patient risk factors
 American Burn Association (ABA) Burn Center
Referral criteria
Depth of Burn
o First, second, third, fourth degree
o ABA Recommends:
 Partial-thickness
 Full-thickness
o Second degree  to the dermis
o 1st and 2nd very painful due to injury to the nerve
o wet and weepy
o Full thickness  involve fat, muscle, and/or bone
 Tend to be painless due to nerve endings being damaged/destroyed
 Dry and leathery
o Superficial burn (1st degree, partial thickness)
 Erythema, blanching on pressure, no vesicles or blisters
 Superficial epidermal damage
o Deep (2nd degree, partial thickness)
 Fluid-filled vesicles that re red, shiny, wet
 Epidermis and dermis
rd
o 3 & 4th degree (full thickness)
 Dry, waxy white, leathery, or hard skin
 All skin elements and local nerve endings destroyed
Extent of Burn
o Guides for determining TBSA of
burn:
o Lund-Browde & Rule of Nines
o Used to determine % of burns
o Each arm is 9% and each leg is
18%
 Anterior arm is 4.5%,
posterior arm is 4.5%
 Anterior leg is 9%,
posterior leg is 9%
o Anterior chest is 18%, posterior
chest is 18%
o Perineum is 1%
o Abdominal area 9%
Location of Burn
o Location of the burn injuries influences the severity
o Burns to face / neck, circumferential burns to chest / back
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 Breathing difficulties due to: obstruction from edema / eschar
 Inhalation injury / respiratory mucosal damage
 Burn to face and neck worried about inhalation injuries
o Burns to circumferential lower extremities, hands, feet, joints / eyes  function, self-care
 Circumferential burns
 Impaired expansion  challenging to ventilate patients
 May have to do an escharotomy
 Worried about eschar – dead tissue
o Burns to ears, nose, buttocks, perineum – Risk for Infection
o *** Compartment syndrome***
 4 Ps for compartment syndrome
 Pallor, pulselessness, pain, paresthesia
Prehospital and Emergency Care
o Remove patient from burn source
o Cooling of small thermal injury
 Cool with slightly cooled water, no submersion
 Clean, cool, tap water – dampened towel for the patients comfort and protection until medical
care if available
 Cooling the area (if small) within 1 minute helps minimize the depth of the injury
 Never cover a burn with ice, since it can cause hypothermia and vasoconstriction
o Large injury - focus on ABC
o Gently remove burned clothing if possible
o Wrap patient in clean, dry sheet or blanket
o Flush chemical burn
 Chemical – flush with water
 Remove any chemical particles or power from the skin
o Monitor for respiratory distress
 If CO poisoning is suspected, treat the patient with 100% humidified oxygen
o Assess for other injuries
o Inhalation burns or carbon monoxide poisoning  give 100% humidified oxygen
o burns around face, neck, burnt nasal hairs, coughing up sputum, confined in a small face
 Stridor, hoarsness, tachypnea, tachycardia, restlessness
o Go to burn center  Electrical, chemical, and inhalation burns need to go to the hospital, pediatrics, 3 rd
degree, burns to face, genitalia, and joints, preexisting condition
Phases of Burn Management
o Emergent – resuscitative
 First 72 hours
 Lots of fluid shifts
o Acute – wound healing
 Weeks to months
 Wound healing
o Rehabilitative - restorative
Emergent Phase
o Emergent (resuscitative)
 Up to 72 hours from burn injury
 Resolve immediate, life-threatening problems resulting from the burn injury
 Hypovolemic shock & edema
 Due to massive fluid shifts
Ends when fluid mobilization and diuresis
begin
Pathophysiology – Emergent Phase
o Fluid and Electrolyte Shifts
 Greatest initial threat: hypovolemic shock
 Decreased BP and increased HR
 Increased capillary permeability
 Water, sodium, and plasma proteins 
interstitial spaces
 Insensible losses
 Intravascular volume depletion
 RBC destruction
 Sodium and potassium shifts
 Colloidal osmotic pressure decreases
 More fluid shifting out of the vascular
space into the interstitial spaces
o Normal insensible loss is about 30-50 ml/hr
 Can lose up to 200-400 ml/hr
o Oxygen free radicals leading to more damage
o RBC hemolysis released at the time of the burn and directed insult of the burn injury  obstruction to
kidneys
o See hyperkalemia and elevated osmolality and
acidosis
Pathophysiology
o Inflammation & healing
 Burn injury to tissues and vessels cause
coagulation necrosis
 Neutrophiles and monocytes accumulate
 Fibroblasts and newly formed collagen fibrils
appear and begin wound repair within the
first 6-12 hours after injury
o Immunologic changes
 Skin barrier destroyed
 Bone marrow depression  decreased levels
of circulating immunoglobulins
 WBC abnormalities – lymphocytes,
neutrophils, monocytes  risk for infection
o Greater risk for infection
o Typically comes form patients own flora (gut, skin,
respiratory flora)
Clinical Manifestations
o Severe burns: hypovolemic shock
o Painless or extreme pain
o Paralytic ileus
o Blisters
o Shivering
o Mental status changes
o Anxiety & fear
o Extreme pain  1 & 2 degree
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Full-thickness and deep partial thickness burns are at first painless because the nerve endings have been
destroyed
o Paralytic ileus  early on, biggest reason in addition to carbon monoxide is due to curling's ulcer
(associated with paralytic ileus)
o Best thing to do when paralytic ileus is resolved is to get tub feedings started
Complications
o Cardiovascular
 Dysrhythmias
 Hypovolemic shock
 Circulation to the extremities can be severely impaired
 Peripheral ischemia, paresthesias, and necrosis
 Escharotomy
 An incision through the full thickness eschar is often done to restore circulation to
compromised extremities or improve chest expansion
 Sludging
 VTE
o Blood viscosity increases because of the fluid loss
 Pre-existing cardiac disease
 Heart failure
 Pulmonary edema
 Due to being so thick and viscous due to fluid loss, can impair circulation due to blood being so
thick
 Blood thickness increases risk for blood formation
 Tend to be bedridden for long periods after the injury
o Respiratory
 Monitor for respiratory distress
 Upper & lower airway injury
 Fiberoptic bronchoscopy
 Done to assess the lower airway within 6-12 hours after injury if smoke inhalation is
suspected
 Carboxyhemoglobin levels
 Levels of carbon monoxide
 Assess sputum for carbon
 No correlation between extent of TBSA burn & severity of inhalation injury
 CXR & ABG changes
 Pneumonia – leading cause of death with inhalation burn
 Monitor any subtle changes in respiratory changes
Complications
o Renal
 Potential for impairment due to:
 Hypoperfusion (RBC breakdown)
 Myoglobinuria (muscle cell breakdown)
 Hemoglobinuria  from RBC hemolysis
 Acute Tubular Necrosis (ATN)
 Renal tubule occlusion by myoglobin and hemoglobin
 Blood flow to the kidneys is decreased, causing renal ischemia
Nursing and Interprofessional Management: Emergent Phase
o Airway Management
 Early intubation / mechanical ventilation
 Early intubation removes the need for emergency tracheostomy
 Extubating may occur when edema resolves
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 PEEP
 Bronchodilators
 If intubation not required
 100% humidified O2 (CO poisoning)
 High Fowler’s position
 C & DB every hour
 Reposition, suction, chest PT
 Bronchodilators
 Bronchodilators due to increased swelling
 spO2 does not distinguish oxy hemoglobin from
carboxyhemoglobin
 SpCO  determine levels of carbon monoxide
o Fluid Therapy
 Two large bore IVs burns ≥ 15% TBSA
 Central line burns ≥ 30% TBSA
 Arterial line
 ABGs and BP
 Fluid replacement formula-Parkland (Baxter)
 Crystalloids & colloids
 Titrated to urine output & VS
o LR = 4 ml x total body surface area of burns x body weight
 first half over the first 8 hrs
 second half over the next 16 hrs
o Urine output
 Electrical l burn – 75-100 ml/hr due to
hemoglobinuria
 Burn target is 30-50 ml/hr
 0.5 – 1.0 ml/kg/hr
o Cardiac parameters
 MAP = > 65
 SP >90
 HR less than 120
 MAP and BP measured at arterial line
Parkland Formula Example
o For a 70 kg patient with a 50% TBSA burn:
o 4 mL × 70 kg × 50 (% TBSA) burned = 14,000 mL in 24 hr
 ½ of total in first 8 hr = 7000 mL (875 mL/hr)
 ¼ of total in second 8 hr = 3500 mL (437 mL/hr)
 ¼ of total in third 8 hr = 3500 mL (437 mL/hr)
Wound Care
o Cleansing / gentle debridement / OR I&Ds
o Shower / dressing change in morning
o Evening dressing change in patient’s room
o Open vs closed
 Closed – sterile gauze with Silvadene to cover the wound
 Open – no overing for facial burn, covered with antimicrobial but no dressing
o PPE, aseptic technique, room temperature 85°
o Special care for face, eyes, hands, arms, ears, perineum
o Collaborate with PT to prevent contractures; A & PROM
o Partial thickness burn wounds appear pink to cherry-red and are wet and shiny with serous exudate
 Painful
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Wound Care – Skin Grafts
o Autograft – patient’s own skin
 Cultured Epithelial Autograft (CEA) – pt’s own skin cultured
o Allograft (homograft) – same species: cadaveric skin
o Xenograft (heterograft) – different species: porcine
o Biobrane – semipermeable silicone bonded to nylon fabric
o Integra – biodegradable dermal layer made of bovine collagen
o AlloDerm – acellular dermal matrix from donated human skin
o OrCel (sponge) / Apligraf (gel) – donated neonatal foreskin
o Matriderm – bovine collagen & elastin
o Split thickness skin graft – patients own skin
o CEA – culture a small tissue sample and created a skin graft for the patient
Drug Therapy
o Analgesics & Sedatives
 IV
 Opioids/sedatives/antidepressants
o Tetanus immunization – within last 10 years
o Antimicrobial agents
 Topical
 Silver-impregnated dressings
 Antifungal agents
 Systemic if sepsis
o VTE prophylaxis
 Enoxaparin or heparin
o Typically, not using systemic antibiotics due to tissue having little to no blood supply
o Sepsis big caused of death  can lead to MODS
Nutritional Therapy
o Early / aggressive decreases complications
 Decreased complications and mortality, optimize burn wound healing, and minimize the negative
effects of hypermetabolism and catabolism
o Hypermetabolic state
o Enteral feedings if intubated - residuals / bowel sounds
 Preserves GI function, increase intestinal blood flow, and promotes optimal conditions for wound
healing
o Calorie-containing nutritional supplements
o Protein powder
o Supplemental vitamins
o Once starting PO we want diet high in protein and carbs
Acute Phase
o Begins with mobilization of extracellular fluid / diuresis
o Concludes when wounds healed, or covered with skin grafts
o Weeks - months
o Pathophysiology
 Edema decreases
 Wound healing begins
 Eschar begins to slough
 Surgical debridement / skin grafting may be needed
o Fluid re-enters the vascular system
o WBCs surrounds the burn wound and phagocytosis occurs. Necrotic tissue begins to slough. Fibroblasts
lay down matrices of the collagen precursors that eventually form granulation tissue.
Pathophysiology
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o Less edema
o Bowel sounds return
o Depth of burn wounds are more apparent
o Patient becomes more aware of injuries
o Wound healing begins
Acute Phase
o Sodium
 Hyponatremia
 GI suction
 Diarrhea
 Water intake
 Symptoms: headache, irritability, confusion, vomiting, seizures, coma
 Offer fluids other than water
 Hypernatremia
 Fluid resuscitation if hypertonic solutions were used
 Tube feedings
 Symptoms: mental status, ranging from drowsiness, restlessness, confusion, lethargy,
seizures, coma
o Potassium
 Hypokalemia
 Vomiting
 Diarrhea
 Prolonged GI suction
 Diuresis
 Symptoms: dysrhythmias, arrest, confusion, tetany, muscle cramps, paresthesia’s,
weakness
 Hyperkalemia
 Renal failure
 Deep muscle injury
 Lost through burns
 Symptoms: dysrhythmia, muscle weakness, paresthesia, decreased GI motility,
decreased reflexes
o NG tube to suction
o Excess fluid in the vasculature – dilutional hyponatremia
o Fluid entering the cerebral cells  cerebral edema
o Headache, irritably, changes in LOC, seizures and coma
o Improper fluid resuscitation can lead to hypernatremia
o Want to say away from Na in fluids and feedings
Complications
o Infection
 Immunosuppressed
o Cardiovascular and Respiratory System
o Neurologic System
o Musculoskeletal System
 PT and PT
o GI System
 At risk for curlings ulcer
 Diffuse superficial lesions
 H2 blockers, PPI
o Endocrine System
 Increase of blood glucose, cortisol, and catecholamines due to stress response
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Nursing and Interprofessional Management: Acute Phase
o Wound care
o Excision / grafting
o Pain management
o PT/ OT
o Nutritional therapy
o Revolves around preventing infection
o Monitor albumin
o Daily weights
Rehabilitation Phase
o Wounds nearly healed
o Occurs 2 weeks – 8 months following burn injury
o Patient self-care
o Resuming functional role
o Scarring
o Skin color
o Reconstructive surgery
o Contractures
o Discoloration and may fade with time
Rehabilitation Phase
o Emotional / psychological needs
 Pre-existing mental health or substance abuse
 PTSD
 Phoenix Society
o Discoloration and may fade with time
o May use pressure garments
 Not until the healing is done
o Very sensitive to cold, heat, or touch
o May give an antihistamine to help with itching
o Contractures
 Flexor muscles are stronger so often contracted in the flexor mode
 Important to position in proper position
ACUTE KIDNEY INJURY
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Kidney A & P Review
o Right kidney is lower due to the position of the kidney
o Renal tissue contains the cortex (contains 1,000,000
nephrons) – responsible for urine production
Kidney function review
o Filtration of blood to regulate:
 Fluid balance – RAAS, ADH
 Electrolyte balance - K+, Mg+, Ca++, Na+, Phos+
 Acid-Base balance
 Excretion of metabolic waste
o Regulate BP
o Produce Erythropoietin
 Hormone manufactured in kidney
 Stimulates RBC production in bone marrow
o Activation of Vitamin D
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Lab values r/t kidneys
o Na+: 135-145 meq/L
o Cl: 97-107 meq/L
o K+: 3.5-5.0 meq/L
o Serum Osmo: 280-295 mOsm/kg
o Total Ca++: 8.6-10.2 mg/dL
o BUN: 10-20 mg/dL
o Ionized Ca++: 4.5-5.0 mg/dL
o Creatinine: 0.6-1.2 mg/dL
o Mg+: 1.5-2.5 meq/L
o Bun: Creat. Ratio: 10:1 – 20:1
o Phos: 2.5-4.5 mg/dL
o GFR: 125 mL/min
Influence of Body Systems on kidney Function
o Cardiovascular
 25% of cardiac output
 Fluid volume and BP for filtration
 Glomerular Filtration Rate (GFR)
o Nervous System
 Baroreceptors: decrease pressure sensed, increase in SNS stimulation
 Chemoreceptors: increase blood flow when CO2 high/O2 low
 Osmoreceptors: increased osmolality  increase ADH
o Endocrine
 Aldosterone
 ADH
Acute Kidney Injury (AKI)
o Acute kidney injury (AKI): entire range of syndrome, ranging from a slight deterioration in kidney function
to severe impairment
o AKI is characterized by a rapid loss of kidney function
o Ranges from a small increase in serum creatinine or reduction in urine output  development of
azotemia
o Etiology of AKI
o Can develop rapidly (acute) or chronically
 Over hours or days with progressive elevations of BUN, creatinine, and potassium with or
without a reduction in urine output
o Azotemia – accumulation of waste products in the blood  elevated BUN and creatine
o SKI is potentially reversible, high mortality rate
Etiology of AKI
o AKI often follows severe, prolonged hypotension, hypovolemia, or exposure to a nephrotoxic agent
o Prerenal: factors external to kidney, most common
 Factors that reduce systemic circulation, causing a reduction in renal blood flow  decreased
glomerular perfusion and filtration of the kidneys
 Hypovolemia
 Decreased CO  decreased renal blood flow
 Decreased SVR
 Outside the kidneys that impairs blood flow to
the kidneys that affect GFR
 Decrease CO, hypovolemia,
hemorrhage, burn, dehydration, or
shock
 Oliguria is caused by a decrease in circulating
blood flow
 Reversible with appropriate treatment
 No damage to the kidney tissue
 If decreased perfusion persists for an extended
time, the kidneys lose their ability to
compensate and damage to kidney occurs
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Intrarenal: direct damage to kidney tissue, resulting in impaired nephron function
 Nephrotoxic injury
 Hemolyzed RBCs or myoglobin
 Other: acute glomerulonephritis; SLE
 Acute tubular necrosis (ATN)
 Mot common in hospitalized patients
 Results of ischemia, nephrotoxins, or sepsis
 Direct injury to kidneys  impair function to nephrons
 Myoglobinuria, crushing injury, hemoglobinuria, transfusion reaction (back pain, red
blood cell hemolysis), nephrotoxic agents
 Aminoglycosides – can cause AKI (gentamycin, vancomycin)
o Given over 45 min – 1 hour
 Radiologic contrast agents, NSAIDs, ACE inhibitors (decrease perfusion pressure), heavy
metals
 Prolonged ischemia
 Nephrotoxins cause obstruction in intrarenal structures by crystallizing or causing
damage to the epithelial cells of the tubules
Postrenal: mechanical obstruction of outflow of urine
 Urine refluxes into the renal pelvis, impairing kidney function
 BPH / bladder cancer
 Calculi, trauma, tumors
 Factors that obstruct urinary output
 Urine backs up into the kidneys
 If bilateral obstruction is relieved within 48 hours of onset, complete recovery is likely. Prolonged
obstruction can lead to tubular atrophy and irreversible kidney fibrosis.
Clinical Manifestations
o Oliguric Phase
 Urinary changes
 Reduction in urine output to less than 400ml/day
 Occurs within 1-7 days of the injury
 Can last on average from 10-14 days
 Anuria is usually seen with urinary tract obstruction
 Fluid volume
 Hypovolemia has the potential to worsen all form is AKI, especially prerenal causes
 In case of reduced urine output, the neck veins may become distended with a bounding
pulse.
 Edema and HTN may develop. Fluid overload can eventually lead to HF, pulmonary
edema, and pericardial and pleural effusion.
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Metabolic acidosis
 Impaired kidneys cannot excrete hydrogen ions or the acid products of metabolism
 Develop Kussmaul respirations (rapid, deep respirations)
 Sodium balance
 Urinary sodium excretion may increase, resulting in normal or below-normal levels of
serum sodium. Excess sodium intake is avoided because of fluid retention
 Dilutional or excretion hyponatremia
 Potassium excess
 Kidneys inability to excrete potassium impaired
 Damaged cells release K into extracellular fluid
 Bleeding and blood transfusions may cause cellular destruction, releasing more K
 Metabolic acidosis worsens hyperkalemia as hydrogen ions enter the cells
 Weakness, peaked T waves, widening QRS, ST segment depression
 Hematologic disorders
 Leukocytosis
 Increased risk for infection
 Waste product accumulation
 BUN and creatinine levels increase
 Increased BUN cause be caused by dehydration, corticosteroids, catabolism resulting
from infections, fever, severe injury, or GI bleed
 Neurologic disorders
 Nitrogenous waste products accumulate int eh brain and other nervous tissue
 Fatigue, difficulty concentrating, seizures, stupor, coma
o Diuretic Phase
 Daily U/O 1-3 L; may be ≥ 5 L: osmotic diuresis
 Nephrons not fully functional even as urine output increases
 High urine volume is caused by osmotic diuretics from the high urea concentration in the
glomerular filtration and the inability of the tubules to concentrate the urine
 Hypovolemia, hypotension
o Recovery Phase
 Begins when GFR increases
 BUN and creatinine levels decrease
 Up to 12 months to recover
 If no recovery  ESRD
Diagnostic Studies
o History & Physical exam
o Serum creatinine
o BUN elevation
o Urinalysis
 May show casts: form from mucoprotein impressions of the necrotic renal tubular epithelial cells,
which slough into the tubules
 Proteinuria may be present if AKI is related to glomerular membrane dysfunction
 Abundant cells, casts, or proteins suggest intrarenal disorders
 Osmolality, sodium content, specific gravity
 1.010
 300
 Hematuria, pyuria, and crystals  intrarenal
o Renal ultrasound
 Imaging without exposure to nephrotoxic contrast agent
o Renal scan
 Assess abnormalities in kidney blood flow, tubular function, and collecting system
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CT (contrast induced nephropathy-CIN)
 Lesions, masses, obstruction, and vascular abnormalities
o Serum potassium
o ECG-peaked T wave
 Hyperkalemia
 Widened QRS
 ST depression
Manifestations / Complications
o Electrolyte / Acid-base
 Hyperkalemia
 >6
 Kidneys are unable to excrete K
 Release of intracellular K
 Watch for diet and some medications
 Blood transfusions
 Normal or low Na+
 Hypocalcemia
 Inversely related with phosphate
 Develop hyperparathyroidism
 Ca will start to be pulled out of the bone  renal osteodystrophy
 Hyperphosphatemia
 Kidney unable to
excrete
 Often given phosphate
binding products
o Administer Ca
to bind to Ph
to be excreted
through the
gut
 Hypermagnesemia
 Not being excreted
 Metabolic acidosis
 Kidneys are unable to
excrete metabolic load
and unable to reabsorb
renal bicarbonate
o Cardiovascular
 Hypertension
 LV hypertrophy
 Due to increased fluid
load
 Edema
 Accelerated atherosclerosis
 Dysrhythmias / peaked T
 Risk for pericarditis
o Respiratory
 Dyspnea
 Pulmonary edema
 Alveoli
 Pleural effusion

 Pleura space
 Risk for pulmonary infections
o Hematologic
 Anemia
 Epogen  erythropoietin
 Platelet dysfunction
 Leukocyte dysfunction
 Impaired immune system
o Gastrointestinal
 Nausea/vomiting
 Anorexia
 Uremic fetor
 Dysgeusia
 Stomatitis
 Weight loss
 Risk for GI bleeding
o Musculoskeletal
 Bone disease
 Hyperphosphatemia
 Hyperparathyroidism
 Calcium deposition
 Ca deposits in the vessels, joints, and lungs
o Integumentary
 Darkening or yellowing of skin
 Pallor
 Dry, scaly skin
 Pruritus
 Dry, brittle hair
 Petechiae and ecchymosis
o Neurological
 CNS depression
 Seizures
 Restless legs
 Muscle twitching
 Asterixis
o Psychological
 Depression
 Change in personality / behavior
 Altered body image
 Grief
Interprofessional Care
o Treat precipitating cause
o Preventing an acute kidney injury
o Want to get baseline of BUN and creatinine before started any medication or treatment, then 24 hours
after, then two times per week after that
o Be careful with nephrotoxic drugs
 Vancomycin, gentamycin, tobramycin
o Adequate intravascular volume & cardiac function
o Diuretics
 Furosemide (Lasix), bumetanide (bumex)
o Fluid restriction in oliguric phase



 Previous 24 hr U/O plus 600ml = fluids allowed
o Treat hyperkalemia
o Renal replacement therapy (RRT)
 Peritoneal dialysis
 Hemodialysis
 Continuous renal replacement therapy (CRRT)
o Nutritional therapy
 Decreased breakdown of body protein
 High calorie and high carb
 Low protein
 If giving protein it would be of high biologic value
 Eggs, daily, meat
 Potassium restriction
 Na restriction
 Phosphorus restriction
o Monitor patients with cirrhosis and heart failure
o 1kg = 1000 ml of fluid
o Prevent transfusion reaction
 Watch for back pain
Hyperkalemia Treatment
o Regular insulin IV
 Emergent treatment
 Moves K into the cells
 Give and amp of D50
o Calcium gluconate IV
 Emergent treatment
o Sodium bicarbonate
 Emergent
 Temporary moves K into cells
o Albumin nebulizer
 Used to move K into cells
o Kayexalate
 Non emergent
 Exchanges Na ions for K ions in the gut
 And induces diarrhea
 Oral and enema
o Hemodialysis
o Dietary restriction
CRRT
o Uremic toxins and fluids are removed wile acid-base status and electrolytes are adjusted slowly and
continuously in a hemodynamically unstable patient
o Over 24 hours
o Uremic toxins / fluids removed
o Acid-base / electrolytes adjusted slowly / continuously
o Physiologic dialysis (similar to kidneys)
o Large vein needed
o Remove fluid from 0-500 ml/hr
CRRT Modes
o Continuous venovenous hemofiltration (CVVH) –fluid & solutes; fluid replacement needed
o Slow continuous ultrafiltration (SCUF) – fluid only; no fluid replacement needed
o
o
Continuous venovenous hemodialysis (CVVHD) –fluid & solutes; requires dialysate; no replacement fluid
needed (correction to text)
Continuous venovenous hemodiafiltration (CVVHDF) –fluids & solutes; requires dialysate & replacement
fluid
FEMALE AND MALE REPRODUCTIVE SYSTEM DISORDERS
Female Reproductive System Disorders
 Cervical Cancer
o Incidence is declining r/t Pap smear testing in developing countries
 Includes HPV testing
 Risk factors: infection with high-risk HPV (largest risk factor), Low SES, immunosuppression,
chlamydia infection, smoking, giving birth to many children, OCPs
 Hispanic women are most likely to be diagnosed, black women have the highest
mortality rate
o Screening Recommendations by the ACOG:
 Annual Pap and HPV testing beginning at age 21; age 21-29 every 3 years and ages 30-65 every 5
years
o Diagnosis: Biopsy
 Pap testing and HPV testing
 Pap test help find changes in cervical cells that may indicate precancerous changes
o Clinical manifestations: Asymptomatic; thin, watery vaginal discharge  dark, foul-smelling discharge,
spotty vaginal bleeding  heavier, more frequent bleeding, pain/weight loss/anemia are late S/S,
cachexia
o Interprofessional Care: Prevention: HPV vaccine, surgery (hysterectomy), radiation, chemotherapy,
targeted therapy
 HPV vaccination by 11-12 can be as early as 9 – when the immune system has a better uptake of
the vaccine
 Endometrial Cancer
o Most common gynecologic malignancy, arises from the lining of the endometrium within the uterus
o Easily treated in early states
o Risk factors: Estrogen (increased exposure), increasing age, nulliparity (no pregnancies), early menarche,
late menopause, obesity (estrogen will be stored in fat tissue), smoking, DM, family or personal history of
hereditary nonpolyposis colorectal cancer (HNPCC)
o Clinical manifestations: Abnormal uterine bleeding, especially in postmenopausal women. Late
symptoms are pelvic pain during urination or intercourse, unintentional weight loss
 Postmenopausal women should have no vaginal bleeding
 First symptom is bleeding  diagnosed faster
o Reduces risk: use of OCPs, IUDs, and physical exercise
o Diagnosis: Endometrial biopsy
 Endometrial exam and biopsy  stating at age 35  patients who have tested positive for the
HPNCC
o Interprofessional Care: TAH-BSO (totally hysterectomy and bilateral salpingo-oophorectomy)and lymph
node biopsies, radiation to decrease recurrence (external or brachytherapy), hormone therapy,
chemotherapy
 Common metastasis: lung, liver, bone, brain
 No routine screening
 Ovarian Cancer
o

Risk factors: Mutations of BRCA1 and BRCA2 genes, history and family history of breast or colon cancer,
increasing age, high fat diet, increased number of ovulatory cycles, hormone replacement therapy,
nulliparity (no pregnancies), possibly fertility treatments
 Exposure to estrogen
 Fertility treatments may increase risk as they get older
o Risk reducers: Breastfeeding, multiple pregnancies, oral contraceptive use, early age at first birth
 Reduces amount of estrogen
o Clinical manifestations: Non-specific symptoms-often silent; pelvic or abdominal pain, bloating, urinary
urgency or frequency, feeling full quickly. Late signs: abdominal enlargement (ascites), and unexplained
weight loss or gain
 Asymptomatic for a long time, once developed manifestations it is typically advanced
 Face looks thin, abdomen gaining weight, gaining weight in fluid
o Diagnosis: no accurate screening tests
 For women at high risk for ovarian cancer, screening using a combination of the tumor marker
CA-125, ultrasound and yearly pelvic examination is recommended
 However not always proven to be effective
 Yearly bimanual pelvic exam
 At time of pap smear and HPV
 Menopausal women should not have palpable ovaries
o A mass of any size found during a bimanual pelvic examination is considered
suspicious
 Transvaginal US
 See through walls to look at the ovaries to detect masses
 Exploratory laparotomy
 CA-125 and US
 Tumor antigen/markers
 Measurements of fetal cells that we typically see in a cancer cell due to a mutation and
hasn’t been allowed to mature
o Interprofessional Care
 Surgical removal treatment of choice: TAH-BSO, omentectomy
 TAH – total abdominal hysterectomy
 Omentectomy – remove of the lining of the peritoneal space with the though of
spreading
 Chemotherapy
 Intraperitoneal, systemic
 Radiation
 External or internal
 Targeted therapy
 For the specific malignant cell
Hysterectomy
o Pre-op
 May be some sort of cleansing of the vaginal cavity or the abdomen
o Post-op
 Abdominal distention may develop form the sudden release of pressure on the intestines when a
large tumor is removed or pressure on the intestines when a large tumor is removed or from
paralytic ileus due to anesthesia and pressure on the bowel
 Abdominal: abdominal dressing; observe for bleeding
 Vaginal: perineal pad with moderate amount serosanguinous drainage expected
 Assess urine output
o Swelling on urethra
o Bladder scan to check for urinary retention

Removal of ovaries  surgical menopause R/T no estrogen from the ovaries
 Typically will have worse s/s of menopause due to it being sudden
 High levels one day and low levels the next
 No menses
 VTE prophylaxis
 Patients who have pelvic trauma have a much higher risk than patients who have
procedures in other area, thought to be due to something with the pelvic veins
 SCDs, heparin, lovenox
o Anticoagulants
 Avoid heavy lifting for 2 months
 May be an absence of vaginal sensation temporarily
 Frequent position changes, avoiding high fowlers positions, avoiding pressure under the knees
minimizes statis and pooling of blood.
 Encourage leg exercises
 Nursing Diagnoses
o Anxiety related to threat of a malignancy and lack of knowledge about the disease process and prognosis
o Acute pain related to pressure secondary to an enlarging tumor
o Disturbed body image related to loss of body part and loss of good health
o Ineffective sexuality pattern related to physiologic limitations and fatigue
o Grieving related to poor prognosis of advanced disease
 Nursing Management
o Health promotion
 Patient education : routine screenings
 Especially in younger patients
 Risk factor reduction
o Acute care
 Psychosocial support
 Nursing interventions pre- and post-op
o Ambulatory care
 Patient education
 Any restrictions they may have
Male Reproductive System Disorders
 Anatomy
o Urinary tract and reproductive tract are intertwined and can cause complications in both
o When the prostate gland is a normal size it leaves the urethra along and bladder emptying occurs
normally
 Benign Prostatic Hyperplasia (BPH)
o Benign enlargement
o Prostate gland increases in size leading to disruption of outflow of urine
o Prostate enlarged, it gradually compresses the urethra, leading to a partial or complete obstruction
o Most likely related to hormonal changes with aging, genetics, obesity, alcohol, erectile dysfunction,
smoking and diabetes, high amount of animal protein, first degree relative with BPH
 Excessive amounts of DHT
 As men age, they have a decrease in testosterone but continue to make and accumulate a high
level of DHT, resulting in prostate enlargement.
 Increase proportion of estrogen
o Biggest worry is urinary retention
o LUTS (lower urinary tract symptoms)
 Irritative: Frequency, urgency, nocturia, dysuria, incontinence, bladder pai
 Related to inflammation or infection


Obstructive: decreased and intermittent force of stream, sensation of incomplete bladder
emptying, dribbling
 Due to increase effort of the bladder as it tries to empty through the decreased
diameter
o Complications: UTI, bladder stones, hydronephrosis
 Due to urinary retention and bacteria growth in residual urine
 If they stay lower it is easier to treat, once it starts to flow and reach the kidneys it can be more
severe
 Will need to urinary cath to get past the obstruction
o Dx:
 H&P
 Digital Rectal Exam (DRE)=symmetrically enlarged – physically palpate the prostate through the
rectum, firm, enlarged, and smooth prostate
 UA/C&S – bleeding, increase in bacteria or WBC, nitrites, leukocyte esterase
 Prostate Specific Antigen (PSA)
 Measured and followed to look for potential malignancy and response to treatment
 Post Void Residual
 Transrectal US (TRUS)
 Will be done with patients with an abnormal DRE and high PSA to allow for accurate
assessment of prostate size and can help to distinguish BPH from prostate cancer
 MRI
 Cystoscopy
 Procedure allowing internal visualization of the urethra and bladder, is done if the
diagnosis is unclear or to see the degree of prostatic enlargement
Interprofessional Care
o Restore bladder drainage, relieve symptoms, prevent/treat complications of BPH
o Conservative: Active surveillance or watchful waiting – depending on presentation on symptoms and will
be based on symptoms, progression of symptoms, and/or presence of any complications
 Dietary modifications: decreasing caffeine, artificial sweeteners, and spicy and acidic foods.
 Avoid decongestants, /anticholinergics
 Decrease the size of the gland
 Restrict evening fluids
 Timed voiding schedule
 Help reduce complications
 Drugs: ? chemoprevention
 Alpha adrenergic blockers (tamsulosin [Flomax])
o Potent vasodilator and smooth muscle relaxers, alpha adrenergic receptors are
abundant in the prostate, facilitates urinary flow through the urethra
o Do not decrease the overall size of the prostate
o Minipress, Flomax, rapaflo
 5-alpha-reductase inhibitors (Finasteride [Proscar])
o Reducing the size of the prostate gland
o Wear gloves and dispose of container properly
 Erectogenic drugs
o Viagra, Cialis
o Potent vasodilators and smooth muscle relaxers
o Reduces symptoms of BPH and ED
 Herbal therapy
o Saw palmetto
o Medical research has not supported the affect on the prostate gland
o Minimally invasive therapy:

o



Transurethral microwave thermotherapy (TUMT)/transurethral needle ablation (TUNA)/laser
prostatectomy
 Kills off the prostate tissue though the use of the urethra as a source of getting
treatment into the prostate area
 Inserting catheter through urethra and treatment is administered
 Microwaves and needles to deliver the therapy
Surgery:
 Transurethral resection of the prostate (TURP)/transurethral incision of the prostate (TUIP)
 TURP – more affective but more invasive
 Cutting away the prostate gland to take away any pressure
 Will insert an indwelling catheter after the procedure and the inflation of the balloon
will cause hemostasis on the bladder is any damage to the vessels to prevent any
bleeding
o 3-way catheter – irrigation, urine, and manual irrigation
Nursing Diagnoses
o Acute pain related to bladder distention secondary to enlarged prostate
o Risk for infection related to an indwelling catheter, urinary stasis, or environmental pathogens
Nursing Management
o Health promotion
 Early detection and treatment
 When symptoms of BPH are present, further diagnostic screening may be needed
 Teach patients with obstructive symptoms to urinate every 2-3 hours and when they first feel the
urge this will minimize urinary stasis and acute urinary retention
 Using lifestyle changes and reporting nay symptoms to provider
o Acute care
 Pre-op
 Antibiotics
o Due to influx of urinary flow and the nature of GU surgeries
 Urinary catheter
 Post-op
 Pain, bleeding, continuous bladder irrigation
 Bladder spasms, urinary incontinence
o Ambulatory care
 Patient education
 Drink 2-3 L of fluid per day and urinate every 2-4 hours to flush the urinary tract
Continuous Bladder Irrigation
o Done to remove clotted blood form the bladder and ensure drainage of urine
o Assess catheter patency and urine output continually
 Color – going to bleeding post-op
 Rate of infusion is based on the color of drainage
 Amount
 Equal to or greater than irrigation instilled in the bladder
 Clots
o Irrigation to run until the urine is clear or light pink
 Will probably be faster immediately post op due to increase in bleeding then will slow down
o Assess for abdominal distention
o Manually irrigate catheter per facility protocol
o Teach patient kegel exercises after catheter removal
 To return muscles in the pelvic floor to normal function
o If outflow is less than inflow assess the catheter patency for kinks or clots
o Catheter is removed 2-4 days after surgery




Prostate Cancer
o Malignant tumor of the prostate gland; 1 in 7 men are at risk of developing
o Etiology: slow-growing, androgen dependent (younger males: more aggressive form)
 Seen more in older adult males
o Rarely is the cause of death
o Risk Factors
 Family history/genetic/age/African American
 Diet: increased red meat or dairy high in fat; low intake of fruits/veggies
o Clinical manifestations
 Asymptomatic early in disease
 S/S of BPH
 Can spread to lymph nodes, bone: backache, hip pain, perineal/rectal discomfort
Prostate Cancer: Interprofessional Care
o Dx: abnormal DRE (digital rectal exam) (hard, nodular, asymmetric, PSA, biopsy via TRUS/Bone scans, xrays, MRI/Pelvic CT. TNM staging. Gleason scale for grading
 PSA > 4.0
 Looking for any metastasis
o Active surveillance  patient who has a life expectancy of less than 10 years or a low grade/stage tumor
or those with serious preexisting conditions
 Due to prostate cancer not likely to be the reason for death
o Surgical Management
 Radical prostatectomy/nerve-sparing procedure/cryotherapy
 Orchiectomy
 Surgical removal of the testes
 Will lose their male hormones – weight gain, loss of muscle mass
 Are going to be significant complications with erectile dysfunction
 Expect for those with advanced disease
o External beam radiation and brachytherapy (internal implants of radioactive seeds)
o Drug therapy: Hormonal strategies
 Androgen deprivation therapy (ADT)-shrinkage and removal of testes
 Become resistant to the dugs  monitors PSA levels
 Increase risk of osteoporosis and CV
o Chemotherapy – systemically
 Bone marrow suppression, mucosal and GI abnormalities
o Other Therapies: Cryosurgery of prostate for patients who cannot tolerate surgery or w/recurrent
prostate CA
Complications R/T Surgery
o Erectile dysfunction: 5 PDES drugs
 Nerve sparing procedures
o Urinary incontinence
 Due to nerve damage
o Hemorrhage/clot formation/catheter obstruction
o Infection
 Increase risk for peroneal approach
o Impotence
 Potential damage to pudendal nerves
Nursing Diagnoses
o Decisional conflict related to numerous alternative treatment options
o Acute pain related to surgery, prostatic enlargement, bone metastasis, and bladder spasms
o Urinary retention and impaired urinary elimination related to obstruction of the urethra by the prostate
and loss of bladder tone
o
o


Sexual dysfunction related to effects of treatment
Anxiety related to uncertain outcome of disease process on life and lifestyle and effect of treatment on
sexual function
Nursing Management
o Health promotion
 Risk reduction; annual prostate screening
o Acute care
 Routine pre- and post-op care
 Psychosocial support
o Ambulatory care
 Catheter care if discharged with indwelling catheter
 Incontinence education
 Kegel exercises and bladder training
 Pain management
 Should resolve overtime
Testicular Cancer
o Most common in men 15-35 years; highly treatable and curable with 5 year survival of >95%
o Risks
 Undescended testicles, family history of testicular CA, HIV+, maternal exposure to exogenous
estrogen
 Monthly TSE starting in adolescence; yearly by HCP
o Clinical Manifestations:
 Mass/lump on testicle, firm and non-tender; painless testicular enlargement
 Heaviness in scrotum, inguinal area of lower abdomen
 Lower back or chest pain; cough; dyspnea if metastasis
o Diagnosis:
 Alpha-fetoprotein (AFP), LDH, and beta-HCG
 Ultrasound of the testes
 Chest x-ray and CT Scan to detect metastasis
o Orchiectomy (may have testicular prosthesis); retroperitoneal lymph node dissection
 Removal of testes
 Will talk about banking sperm for future family planning
o Chemo or Rad tx may be needed; importance of follow up and monitoring for recurrence