Exam 3

Burn Prevention

- Never leave burning candles unattended

- Practice family/school/workplace fire drills

- Never smoke in bed

- Flame retardant children’s sleepwear and at-risk adult retardant aprons

- Set water heater ≤ 120* F

- Do not use frayed or ungrounded electrical cords

- Install smoke & carbon monoxide detectors

Thermal burns

generally the most common type of burn.

• They result from exposure to or contact with hot surfaces, flames, or hot liquids with an elevated temperature above 140F

• This is why hot water heaters should never be set 120F or higher.

Chemical Burns

caused by direct contact with acids, alkalis, and organic compounds

• Examples of acids: rust removers, bathrooms cleaners

• Alkalis: oven cleaners and fertilizers. Alkalis tend to cause deep burns as they actually liquefy tissue.

• Organic compounds: gasoline, cleaning disinfectants.

typically caused by coagulation necrosis of tissue rather than by direct heat production. The degree of tissue injury is dependent on the toxicity of the chemical and the exposure time

Chemical burns tx

initial treatment for burns caused by strong alkaline or acid solution is immediate removal of clothing that came in contact with the agent followed with copious irrigation with tap water

• Water may dissipate any heat by dilution so as to prevent further damage

• In lime burns, the dry lime must be brushed away prior to washing in order to minimize the production of heat.

Electrical Burns

caused by heat that is generated by electrical current, most commonly from electrical voltage or lightning).

Electrical Sparking and lightening can also cause thermal burns, so the client will have a combination of thermal & electrical burns.

Neurological Effects of Electrical Burns

Loss of memory regarding the accident is frequent. It is due to the bypassing of lightning through the brain. Adverse neurological effects can range from memory loss of the burn event to coma.

• All burn injuries will at least have a ground level fall, so are at risk for cervical injury Cervical immobilization is necessary until cervical spine injury is ruled out.

Cardiovascular lesions after electrical burn

Circulatory arrest happens by asystole or ventricular fibrillation.

• Nursing Interventions: Place on cardiac monitor. Treat cardiac dysrhythmias.

Respiratory lesions with electrical burns

tetanization of the respiratory muscles for a short time, causing the victim to stop breathing for a short time or cause respiratory arrest. The alveoli and/or diaphragm may be damaged. This will result in respiratory insufficency.

• Nursing Interventions: Monitor RR and effort. Obtain O2 Sat. Begin adjunct with nonrebreather mask or manually ventilate with a bag mask device if not breathing

Muscular effects from electrical burns

extensive muscular breakdown with deep necrosis and rhabdomyolysis may occur along the pathway of conduction. Remember, both the heart and diaphragm are muscles! Tetanization of muscles can also cause bone fractures.

Renal injuries from electrical burns

Rhabdomyolysis can lead ATN (acute tubular necrosis) which can lead to AKI- Acute Kidney Injury. Foley catheter. Monitor I & O. Serum creatinine.

Smoke inhalation is

a major predictor of mortality, so must be rapidly assessed. If a person is rescued from a house fire, assume that smoke inhalation has occurred.

What can happen from smoke inhalation?

Metabolic Asphyxiation. used to be termed carbon monoxide poisoning. Carbon monoxide, an odorless gas produced during combustion, is the leading cause of death from asphyxiation related to fires. Metabolic Asphyxiation results is hypoxia.

Tx for Metabolic Asphyxiation

100% humidified oxygen

• oxygen must be humidified to add moisture to the very dry injured nares and airways.

Upper airway injury definition

burn assault to the mouth, oropharynx, and larynx. It is caused by thermal burns and/or inhalation of hot air, steam, or smoke. The airway swelling can be massive and occur rapidly

Lower airway injury is

injury to the trachea, bronchia, and alveoli. It is usually caused by the inhalation of toxic chemicals or smoke.

mainstay of tx for inhalation injuries

airway management (edema is occurring from injury), humidified oxygen, and edema control within the lungs. Oxygen therapy is mandatory for all major burn clients.

• Laryngeal edema is progressive during the first 18 to 24 hours after an inhalation injury.

Rule of thumb: When in doubt, intubate. You can always take a tube out, but you can't always place one.

Inhalation injury nursing managment

good rapid ABC assessment skills, humidified 100% O2, consider or probable intubation, fluid resuscitation, and rapid transport to an ED will maximize good client outcomes.

Sx of inhalation injury

Upper Airway: Hoarseness, Swallowing difficulty, Copious secretions, Use of accessory muscles, Airway swelling - obstruction

Lower Airway: Facial burns, Singed nasal or facial hair, Dyspnea, Carbonaceous sputum, Wheezing, Altered mental status

Partial-Thickness - Superficial Burn

Sunburn or heat flash, Red, Blanches, NO initial blisters, Painful, Heals in 3-5 days, NO scarring

Partial-Thickness - Deep Burn

Bright red to pale ivory, Painful, Blistering or weeping, Blanches, Heals in 14-30 days

Full-Thickness Burn

White waxy, Less pain, Surgical debridement, Healing may take weeks to years, Significant scarring

‘Rule of Nines’

Trunk 36 (chest 18, back 18)

Leg 18 (front 9, back 9)---18 means 1 whole leg is involved, if both legs are involved the TBSA is 36.

Arm 9 (front 4.5, back 4.5)

Head 9 (front 4.5, back 4.5)

Perineum 1

Face, Neck, Circumferential Chest managment

•Humidified oxygen

•Elevate HOB

•Consider intubation

•Bronchodilators

Concerns with Facial Burns

airway/respiratory obstruction

• look for singed nasal hair, eyebrows missing, coughing up carbon (black) streaked sputum

Metaproterenol and albuterol

SE of tachycardia and hand tremors. Do monitor for tachyarrhythmias.

Neurovascular assessment

monitoring of distal pulses, skin color, numbness, tingling, lack of motor movement (paralysis).

Burns on hands and feet

Poor circulation

Delayed wound healing

Potential loss of limb

Burns on Circumferential extremities

Neurovascular impairment

Compartment syndrome

Pre-existing RF

Older adult, Cardiac disease, Renal disease, Chronic respiratory disease, Diabetes Mellitus, Peripheral Vascular Disease (PVD)

Hx cancer and radiation/chemotherapy

Hx substance abuse

Prehospital phase interventions

Stop the Burn: Remove the person from the source of the burn while keeping yourself safe.

• If TBSA burn is >10% and the client is unresponsive, focus on CAB, which is CPR priority care.

• If your client is conscious immediately assess ABCs and institute protocols. For quick TBSA calculation, remember that a complete arm burn is 9%.

Airway If singed or blackened nares or removed from the burning room/building, assume the airway is compromised. Will need to insert ETT ASAP. C-spine stabilization protects the airway

Breathing: check for adequacy of ventilation. Provide 100% humidified oxygen per non-rebreather mask. If inadequate or the client is hypo-ventilating, bag with a bag-mask device connected to 15L O2.

• Consider intubating if the client was in a burning building, unable to protect airway, or has thermal burns to the face, chest, or large TBSA burns

Circulation: check for the presence of pulses in the burn area, elevate burn area above the heart to help reduce edema, and establish IV access.

Chemical – remove solid particles by brushing them off, lavage with copious amounts of water, and remove any clothing that is contaminated

Thermal – cover with a clean, cool, tap water-dampened towel to help prevent excess temperature and fluid loss

• Be concerned about heat loss – Wrap in a dry blanket

Emergent phase complications

Cardiovascular: Dysrhythmias (Decreased sodium and increased potassium), Hypovolemic shock

Respiratory: Airway management, Decreased perfusion, Respiratory infection

Renal: ATN (renal ischemia and myoglobin blockage), AKI (Hypovolemia)

What is the greatest threat in the emergent phase

Hypovolemic shock — fluid loss through capillary beds in burn areas

- Massive fluid shifts into 2nd and 3rd spaces with hyperpermeable capillary beds. – fluid resuscitation

If there is any suspicion of inhalation injury

bronchoscopy is usually done as are serial CXR. Initially, the CXR may be normal, but as fluid migrates out of the CV bed, this will change.

• If pt doesn’t require intubation, be alert for s/s resp distress (EARLY agitation, change in LOC, change in rate and character of respirations LATER drop in O2 Sats, use of accessory muscles, pallor, cyanosis)

The parkland formula

estimates fluid replacement needs

-After determining TBSA using the rule of nines and obtaining weight in kg, calculate the fluid needs for 24 hours –

4 mL x TBSA x kg = mL needed in 24 hrs

• Half solution infused within first 8hrs of burn, other half in next 16 hrs, Lactated Ringers

• Once fluid resuscitation amount is administered if more fluid is needed (decreased BP, elevated HR, and/or decreased urine output) colloids such as albumin may be given

Goals of the parkland formula and fluid resucitation

Urine output 0.5-1 mL/kg/hr

Map > 65

SBP > 90

HR < 120

Emergent phase wound care

Decrease the risk of infection with protective isolation

Daily shower with wound care

Debridement as necessary

Tetanus toxoid needed

Physical therapy to prevent contractures and reduce edema

Local antimicrobial agents rather than systemic

IV antibiotics are not usually used because the blood supply to the burn area is very poor.

Monitor for sepsis which is leading cause of death.

Emergent Phase – Nutrition

TBSA > 20% need enteral feeding

Monitor residuals, bowel sounds

High calorie needs

Need protein, carb, fat, vitamin, and mineral supplements

• Feeding is initiated early to prevent complications – minimizes negative effects of hypermetabolism and catabolism.

• Enteral tube feedings also stimulate the gut and help to prevent hypoperfusion and paralytic ileus. Although, Paralytic ileus occurs almost always in larger burns due to the major vascular shunting.

Drug therapy for Burns

Analgesics: Opioids, NSAIDs, Gabapentin

Sedation: Benzodiazepines

Antidepressants: SSRIs

GI support: H2 blockers, PPIs, Antiacids, Nystatin

Acute Phase – Diagnostic Studies

Hyponatremia, Hypernatremia, Hyperkalemia, Hypokalemia

Hyponatremia

Excess GI suction

Sx: Headache, irritability, confusion, vomiting, seizures

Hypernatremia

Fluid resuscitation with hypertonic fluids

Sx: Drowsiness, restlessness, confusion, lethargy, seizures

Hyperkalemia

Deep muscle injury or AKI

Sx: Dysrhythmias, confusion, tetany, muscle cramps, paresthesia

Hypokalemia

Vomiting, diarrhea, GI suction

Sx: Dysrhythmias, muscle weakness, paresthesia, decreased motility, decreased reflexes

Acute Phase — Complications

Infection (prevention of this is a priority): Local antimicrobials, Protective isolation, Systemic antibiotics

Musculoskeletal: OT, PT, ROM — Prevent contractures

Endocrine: Glucose control, Insulin therapy

Rehabilitation Phase

The goals of the rehabilitation phase are to work toward resuming a functional role in society and to rehabilitate from any functional and cosmetic postburn reconstructive surgery.

• Wounds almost healed

• Client participating in self-care

Rehabilitation Phase Complications

Joints can become stiff due dot decreased mobility.

Contractures may develop due to the tissue becoming shorter as it heals.

Hypertrophic scars as seen in this picture may also develop as the skin heals.

Rehabilitation Phase – Nursing Management

- Range of motion and use of the joints helps to prevent contractures.

- Itching can be treated with water-based moisturizers and oral antihistamines such as hydroxyzine. Massage, cooling, emollients, and anesthetic creams may also help.

- Pressure garments aid in reducing the effects of hypertrophic scarring thereby reducing scarring and deformities

• Important that for burn pts they begin wearing it while the scar is active and immature

• provides protection against injury and direct sunlight; also decreases inflammatory response and amount of blood in scar which reduces itching

Why would patients with burns be told to begin wearing pressure garments while the scar is active and immature?

Scar tissue is highly responsive in the early stages

- Typically, the garments are worn up to 24 hours a day for as long as 12-18 months, removed only for short periods while bathing.

Causes of AKI

Prerenal: factors that reduce systemic circulation (reduced renal blood flow leads to decreased glomerular perfusion and filtration of the kidneys)

Intrarenal: conditions that cause direct damage to the kidney tissue, resulting in impaired nephron function.

• Acute tubular necrosis (ATN) is the most common in hospitalized patients, primarily the result of ischemia, nephrotoxins, or sepsis. Ischemic and nephrotoxic ATN is responsible for 90% of intrarenal cases.

Postrenal: mechanical obstruction in the outflow of urine

• With the flow of urine obstructed, urine refluxes into the renal pelvis, impairing kidney function

• most common postrenal are benign prostatic hyperplasia (BPH), prostate cancer, stones, trauma, and extrarenal tumors.

RIFLE Classification of AKI Manifestations

Risk (R) is the first stage of AKI, is followed by Injury (I), which is the second stage. Then AKI increases in severity to the final or third stage Failure (F). The two outcome variables are Loss (L) and End-stage renal disease (E).

RIFLE: Risk

GFR Criteria: Increased creatinine x 1.5 or GFR decrease >25%

UO Criteria: UO<0.5 mL kg(-1)h(-1) x 6h

RIFLE: Injury

GFR Criteria: Increased creatinine x 2 or GFR decrease >50%

UO Criteria: UO<0.5 mL kg(-1)h(-1) x 12h

RIFLE: Failure

GFR Criteria: Increased creatinine x 3 or GFR decrease >75% or Cr >4mg per 100mL

UO Criteria: UO<0.3 mL kg(-1)h(-1) x 24h or anuria x 12 h

RIFLE: Loss

Persistant ARF = complete loss of renal fx > 4wks

Clinical Manifestations: Oliguric Phase

Urinary changes- oliguria (<400 mL/day; occurs within 1-7 days of AKI)

Fluid volume (Hypovolemia-edema, HTN, distended neck veins)

Metabolic Acidosis

Sodium balance Potassium excess (Hyponatremia, hyperkalemia)

Hematologic Disorders (leukocytosis)

Waste Product Accumulation (BUN & Cr increased)

Neurologic Disorders (Fatigue & Malaise)

Clinical Manifestations of AKI: Diuretic Phase

Daily urine output is 1 to 3 L; May reach 5 L or more

Hyponatremia, hypokalemia, and dehydration (due to large losses of fluid)

HoTN

BUN and Cr levels begin to normalize

Clinical Manfestations of AKI:

phase begins when the GFR increases, allowing the BUN and serum creatinine levels to decrease.

• Major improvements occur in the first 1 to 2 weeks of this phase, but kidney function may take up to 12 months to stabilize.

BUN and Cr levels plateau then decrease

Diagnostic studies for AKI

Thorough history (Hx of dehydration, bld loss, nephrotoxic drug or contrast media exposure, stones, BPH, bladder/prostate cancer

Serum creatinine (increased)

Urinalysis (hematuria, pyuria, and crystals)

Kidney ultrasonography (evaluating for possible kidney disease and obstruction of the urinary collection system)

Renal scan (assess abnormalities in kidney blood flow, tubular function, and the collecting system)

CT scan (identify lesions, masses, obstructions, and vascular anomalies)

Renal biopsy - best method for confirming intrarenal causes

What is contraindicated in testing for AKI

MRI with gadolinium contrast medium

Magnetic resonance angiography (MRA) with gadolinium contrast medium

• Nephrogenic systemic fibrosis

• Contrast-induced nephropathy (CIN)

Interprofessional care for AKI

Ensure adequate intravascular volume and cardiac output

• Force fluids

• Loop diuretics (e.g., furosemide)

• Osmotic diuretics (e.g., mannitol)

  • If already established forcing fluids and diuretics can be harmful

Closely monitor fluid intake during the oliguric phase

• general rule for calculating the fluid restriction is to add all losses for the previous 24 hours (e.g., urine, diarrhea, emesis, blood) plus 600 mL for insensible losses (e.g., respiration, diaphoresis).

Hyperkalemia

• Insulin and sodium bicarbonate

• Calcium Gluconate (raises the threshold at whiich dysrhythmias will occur)

• Sodium polystyrene sulfonate and dialysis will remove potassium

  • Never give this drug to a client with a paralytic ileus because bowel necrosis can occur.

Renal replacement therapy (RRT) - Peritoneal Dialysis, Intermittent Hemodialysis, Continuous renal replacement therapy (CRRT) [Hemodynamically undtable}

Nutritional therapy

• Adequate protein intake (0.6–2 g/kg/day) depending on the degree of catabolism, Enteral nutrition, Parenteral nutrition, Dietary restrictions (potassium, phosphate, sodium)

Indications for renal replacement therapy (RRT)

Volume overload

Elevated serum potassium level

Metabolic acidosis

BUN level > 120 mg/dL (43 mmol/L)

Significant change in mental status

Pericarditis, pericardial effusion, or cardiac tamponade

Nursing assessment for AKI

Measure vital signs; Measure fluid intake and output (daily monitoring); Examine urine (color, specific gravity, glucose, protein, blood, and sediment)

Assess general appearance (skin color, edema, neck vein distention, and bruises); Observe dialysis access site for signs of inflammation and exudate

Mental status/level of consciousness, Oral mucosa (dry? inflammed?)

Lung sounds (Auscultate for crackles and rhonchi or diminished breath sounds)

Heart rhythm (dysrhthmias?); Monitor the heart for the presence of an S3 gallop, murmurs, or a pericardial friction rub.

Laboratory values, Diagnostic test results

Nursing Diagnoses for AKI

- Excess fluid volume related to kidney failure and fluid retention

- Risk for infection related to invasive lines, uremic toxins, and altered immune responses secondary to kidney failure

- Fatigue related to anemia, metabolic acidosis, and uremic toxins

- Anxiety related to disease processes, therapeutic interventions, and uncertainty of prognosis

Potential complication: dysrhythmias related to electrolyte imbalances, Electrolyte Imbalance or Risk for electrolyte imbalance

Health promotion for AKI

Identify and monitor populations at high risk; Control exposure to nephrotoxic drugs and industrial chemicals

Prevent prolonged episodes of hypotension and hypovolemia

Measure daily weight, Monitor intake and output, Monitor electrolyte balance

Replace significant fluid losses, Provide diuretic therapy for fluid overload, Use nephrotoxic drugs sparingly

Risk factors for developing AKI in the hospital

presence of preexisting CKD, older age, massive trauma, major surgical procedures, extensive burns, cardiac failure, sepsis, and obstetric complications

Acute Care of AKI

Accurate intake and output, Daily weights

Assess for signs of hypervolemia or hypovolemia

Assess for potassium and sodium disturbances

Meticulous aseptic technique; Skin care measures/mouth care

Careful use of nephrotoxic drugs

Expectred outcome of AKI

Regain and maintain normal fluid and electrolyte balance

Adhere to the treatment regimen

Experience no complications

Have complete recovery

Advantages of kidney transplant over dialysis

Reverses many of the pathophysiologic changes associated with renal disease

Eliminates dependence on dialysis

Less expensive than dialysis after the first year

Contraindications to kidney transplant

Disseminated malignancies

Refractory/untreated cardiac disease

Chronic respiratory failure

Extensive vascular disease

Chronic infection

Unresolved psychosocial disorders

• Being HIV-positive or having hepatitis B or C is not a contraindication to transplant.

Live Donor for kidney transplant evaluation

Crossmatches: done at the time of the evaluation and about a week before the transplant to ensure that no antibodies to the donor are present or that the antibody titer is below the allowed level.

An ECG and chest x-ray are also done.

Renal ultrasound and renal arteriogram or three-dimensional CT scan: ensure that the blood vessel supply is adequate and that no anomalies exist

A transplant psychologist or social worker determines if the individual is emotionally stable and able to deal with the issues related to organ donation.

Advantages of a live donor

Better client and graft survival rates

Immediate organ availability

Immediate function/minimal cold time

Opportunity to have recipient in best possible med

Labs for a live donor kidney transplant

24-hour urine

• Creatinine clearance

• Total protein

Complete blood count

Chemistry and electrolyte profiles

Hepatitis B and C, HIV, CMV testing

Process of using the kidneys of a desceased donor

donor must have effective CV function and be supported on a ventilator to preserve the organs

-permission from next of kin and must have suffered an irreversible brain injury or are declared brain dead

The United Network for Organ Sharing (UNOS) distributes deceased donor kidneys using an objective computerized point system.

• ABO group, HLA typing, age, antibody level, and length of time waiting are entered into the national computer for each candidate

What is the only exception to the donor list?

if a client needs an emergency transplant or if a donor and recipient match on all six HLA antigens (zero antigen mismatch).

• Emergency transplants are given priority because the client is facing imminent death if not transplanted.

Postoperative care of a patient recieving a kidney transplant

Maintenance of fluid and electrolyte balance is priority

Large volumes of urine may be produced soon after the transplanted kidney is placed due to

• New kidney’s ability to filter BUN

• Abundance of fluids during operation

• Initial renal tubular dysfunction

Dehydration must be avoided (Central venous pressure readings are essential to monitoring; can cause renal hypoperfusion and renal tubular damage)

Assess for hyponatremia/ hypokalemia (tx with K+ supplements or infusion of 0.9% normal saline may be indicated. IV Na bicarb may also be required if metabolic acidosis develops)

Acute tubular necrosis can occur — Dialysis is required

Maintain catheter patency

Complications of kidney transplant

Rejection

Infection

Cardiovascular Disease

Malignancies

Reoccurrence of original kidney disease

Advantages of CVADs

immediate access to central venous system, reduced need for multiple venipunctures, reduced risk for extravasation injury.

Major disadvantages

increased risk for systemic infection and invasiveness of the insertion procedure. Extravasation can still occur if there is displacement of or damage to the device.

Types of CVADs

Centrally inserted catheters

Peripherally inserted central catheters

Implanted ports

CVADs

Catheters placed in large blood vessels

• Subclavian vein, jugular vein, femoral vein

Permit frequent, continuous, rapid, or intermittent administration of fluids and medications including vesicants

Allow for venous blood sampling & hemodynamic monitoring

Used to administer blood/blood products and parenteral nutrition

Centrally Inserted Catheter

Inserted into a vein in the chest or abdominal wall with tip resting in distal end of superior vena cava

• Can be tunneled or non-tunnled

  • tip of the catheter in the superior vena cava. Position must be verified with CXR before use!

Non-tunnled Centrally Inserted Catheter

Best for patients with short term needs in the acute care setting

Requires sterile central line dressing to prevent infection

• Often will be multi-lumen so that different therapies can be provided simultaneously (incompatible drugs, blood sampling, CVP monitoring).

Tunnled Centrally Inserted Catheter

more suitable for long term needs

- Dacron cuff helps anchor the catheter and decreases infection risk. Once insertion site heals, catheter does not require a dressing making it easier for pt to maintain catheter at home.

Indications for CVAD

Autoimmune disorders: perform plasmapheresis

Blood Sampling: Multiple blood draws for diagnostic tests over time

Blood Transfusions: Infusion of blood or blood products

Heart Failure: Perform ultrafiltration

Hemodynamic Monitoring: Used to measure CVP and assess fluid balance

Medication administration: Cancer (chemo, infusionof irritating or vesicant meds), Contrast media, infection (long-term antibiotics), Pain (long-term administration of analgesics), drugs at risk for causing phlebitis (Calcium chloride, potassium chloride, amiodarone), Nutrition replacement, renal failure (hemodialysis or CRRT), shock/burns (high volume fluid and electrolyte replacement)

Peripherally inserted central catheter (PICC)

Central venous catheter inserted into a vein in arm

• Single- or multi-lumen, nontunneled

For patients who need vascular access for 1 week to 6 months

Cannot use arm for BP or blood draw

PICC line advantages

lower infection rate, fewer insertion related complications, decreased cost, ability to insert at bedside or outpt area by specially trained RN or radiology tech

PICC Line Disadvantages

increased risk for DVT & phlebitis

Nursing Managment for a CVAD

Inspect catheter and insertion site: Assess for pain, s/s of infection, and catheter misplacement/slippage

Change dressing and clean according to institution policies—a strict STERILE technique

• Transparent semipermeable dressing or gauze dressing (May be left in place for up to 1 week but should be changed immediately if becomes damp, loose, or soiled)

• Chlorhexidine preferred cleansing agent

Change injection caps

• Have patient turn head to opposite side (disinfect prior to accessing)

• Valsalva if no clamp

Flushing is important: Normal saline prefilled syringe, Use only 10 mL syringe or larger, Push-pause technique

CVAD Removal

Clip sutures, gently withdraw catheter while having pt perform Val salva maneuver during last 5-10 cm of catheter length, apply pressure and cover with sterile gauze. Inspect to make sure tip of catheter is intact.

Complications of CVADs

Catheter occlusion, embolism, infection, pneumothorax, catheter migration

Complication of CVAD: Catheter occlusion (causes and manifestations)

Clamped or kinked catheter, Tip against wall of vessel, Thrombosis, Precipitate buildup in lumen

• Sluggish infusion or aspiration

• inability to infuse and/or aspirate

Complication of CVAD: Embolism (causes and manifestations)

Catheter breaking, Dislodgement of thrombus, Entry of air into circulation

• chest pain, resp distress, hypotension, tachycardia

Complication of CVAD: Infection (causes and manifestations)

Contamination during insertion or use, Migration of organisms along catheter, Immunosuppressed patient

• Local: Redness, tenderness, purulent drainage, warmth, edema

• Systemic: fever, chills, malaise

Complication of CVAD: Pneumothorax (causes and manifestations)

Perforation of visceral pleura

• Decreased or absent breath sounds, respiratory distress, chest pain, distended unilateral chest

Complication of CVAD: Catheter migration (causes and manifestations)

Improper suturing, Insertion site trauma, forceful flushing, Spontaneous

• sluggish infusion or aspiration, edema of chest or neck during infusion, pt reports gurgling sound in ear, dysrhythmias, increased external catheter length

Complication of CVAD: Catheter occlusion (managment)

• Have pt change position, raise arm, and cough

• assess and alleviate any clamping or kinking

• flush with normal saline using a 10 mL syringe (do not force flush)

• instill an anticoagulant or thrombolytic agent

Complication of CVAD: Embolism (managment)

• Apply O2

• Clamp catheter

• Place pt on left side with head down

• Notify provider immediately

Complication of CVAD: Infection (managment)

Local:

• Culture drainage from site

• Apply warm, moist compress

• Remove catheter if needed

Systemic:

• Take blood cultures

• Antibiotic and antipyretic therapy

• Remove catheter if needed

Complication of CVAD: Pneumothorax (managment)

• Apply O2

• Place in Semi-Fowler’s position

• Prepare for chest tube insertion

Complication of CVAD: Catheter migration (managment)

• Prepare for fluoroscopy to confirm position

• Assist with removal and new CVAD placement