Exam 3
Acute phase
Begins with mobilization of extracellular fluid and subsequent diuresis (after 72 hours; partial thickness heals 10-21 days). Ends with burned area is completely covered by skin grafts or when wounds are healed.
HCO3-
Bicarbonate 22-26 mEq/L
Complications of emergent phase- kidney
Blood viscosity + impaired microcirculation = Sludging Acute Tubular Necrosis (ATN)---renal ischemia and myoglobin blockage Acute Kidney Injury (AKI) > U/O goal is 1 mL/kg/hr
albuterol
Bronchodilator
Circumferential burns
Burns on the neck or chest that may compress the airway or on an extremity that might act like a tourniquet.
In assessing the client's potential for an inhalation injury as a result of a flame burn, what is the most important question to ask the client on admission?
"In what exact place or space were you when you were burned?" The risk for inhalation injury is greatest when flame burns occur indoors in small, poorly ventilated rooms.
Leukocytosis
(increase WBC) is often present with AKI. The most common cause of death in AKI is infection. The most common sites of infection are the urinary and respiratory systems
SaO2 (Oxygen Saturation)
*95 - 100%* Normal [> 90% is normal, < 86% is emergency; < 70% is life-threatening]
facial burns
- concerned with airway/respiratory obstruction - look for singed nasal hair, eyebrows missing, coughing up carbon (black) streaked sputum
Burn Fluid Resuscitation
-Prompt fluid resuscitation maintains the BP in the low-normal range and improves CO -Generally, the greatest volume of fluid leak occurs in the first 24 to 36 hours after the burn -As the capillaries begin to regain their integrity, burn shock resolves and fluid returns to the vascular compartment, blood volume increases, urinary output increases *Lactated Ringer's (LR) solution* is the preferred IV fluid for burn resuscitation because the sodium and potassium concentrations are similar to normal intravascular levels (isotonic solution) -LR also contains lactate, which can be converted by the liver to *bicarbonate* (the blood buffer) to aid in correcting the metabolic acidosis frequently seen in burn shock
Cr
0.5-1.2 mg/dL >4
INR
0.8-1.1 2-3 (therapeutic for warfarin) >5.5
•Urinary changes: The most common initial manifestation of AKI is oliguria, a reduction in urine output to less than 400 mL/day. Oliguria usually occurs within
1 to 7 days of the injury to the kidneys. If the cause is ischemia, oliguria often occurs within 24 hours.
Hemodynamic Stability depends on three interrelated components
1. Heart: Must be able to receive adequate coronary perfusion so that it can pump. The heart muscle must also be able to respond to electrical stimulation. 2. Vascular tone must be present to assist in maintaining a normal blood pressure and SVR. 3. There must be an adequate amount of blood circulating within the cardiovascular bed. Minor impairment in one component is compensated for by the other two Prolonged or severe impairments lead to shock.
Burn Center Referral Criteria
1. Partial thickness burns greater than 10% total body surface area (TBSA) 2. Burns that involve the face, hands, feet, genitalia, perineum, or major joints 3. Third-degree burns in any age-group 4. Electrical burns, including lightning injury 5. Chemical burns 6. Inhalation injury 7. Injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality 8. Any patient with burns and concomitant trauma (e.g., fractures) in which the burn injury poses the greatest risk for morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be initially stabilized in a trauma center before being transferred to a burn unit. Physician judgment will be necessary in such situations and should be in concert with the regional medical control plan and triage protocols 9. Burned children in hospitals without qualified personnel or equipment for the care of children 10. Burn injury in patients who will need special social, emotional, or rehabilitative intervention
Mg
1.3-2.1 mEq/L <0.5 or >3
nursing management for blood reactions
1.Stop the transfusion. 2.Maintain a patent IV line with saline solution. 3.Notify the blood bank and the health care provider. 4.Recheck identifying tags and numbers. 5.Monitor VS and urine output. 6.Treat symptoms per health care provider. 7.Save the blood bag and tubing (send to the blood bank). 8.Collect required blood and urine specimens. 9.Document on transfusion reaction form and client chart.
BUN
10-20 mg/dL >100
PT
11-12.5 seconds >20 seconds
Na
136-145 mEq/L <120 or >160
Plt
150,000-400,000 <50 (thousand/mm3) or >1 million/mm3
4. rehabilitation (restorative)
2 weeks to 8 months (can be up to a year)
3:1 rule
3 mL of isotonic crystalloid for every 1 mL of estimated blood loss
K
3.5-5 mEq/L <2.5 or >6.5
aPTT (activated partial thromboplastin time)
30-40 seconds >70 seconds
PaCO2
35-45 mmHg
Parkland formula
4mg/ kg of body weight, and first half within the first 8 hours
WBC
5-10 (thousand /mm3) <2.5 or > 30 (thousand/mm3)
pH
7.35-7.45
FBS
70-110 mg/dL <40 or >400
3. Acute (wound healing)
72 hr. mobilization of fluids and diuresis
Pa02
80-100 mmHg
Ca
9-10.5 mg/dL <6 or >13
BNP normal range
<100 pg/mL, less than 300
GFR stage 1 Renal disease
>90
shock
A condition in which the circulatory system fails to provide sufficient circulation to enable every body part to perform its function; also called hypoperfusion.
cardiogenic shock
A state in which not enough oxygen is delivered to the tissues of the body, caused by low output of blood from the heart. It can be a severe complication of a large acute myocardial infarction, as well as other conditions.
treatment of electrical burns
ABC assessment, stabilize C-spine, 100% non rebreather, IVs; u/o should be 75-100 cc/hr; NO prophylactic abx, cardiac monitor, o2 sat **monitor for cardiac arrest, AKI, myoglobinuria, delayed dysrythmias; leave on C-collar (place AFTER securing ABCs, cardiac monitoring ECG, 2 large bore IVs, document entrance and exit wounds)
Cardiogenic shock is all about a profoundly dysfunctional heart. Nursing need to monitor clients at risk for cardiogenic shock:
AMI, exacerbation of CHR, and the client with cardiomyopathy. Interventions include: Recognition of at risk clients Restoration of coronary artery blood flow via thrombolytics, emergent PCI Nitrates IV drip Inotropes IV drip Diuretics IV push or IV drip (Furosemide, byoo-MET-a-nide) Beta-adrenergic blockers IV push or enteral
support of failing organs
ARDS: Aggressive O2 therapy and mechanical ventilation. DIC: Appropriate blood products. Renal Failure: Continuous renal replacement therapy or dialysis. •Continuous renal replacement therapy is better tolerated than hemodialysis, especially in a client with hemodynamic instability. •It is important to maintain communication between the health care team and, in most cases, the client's caregiver regarding realistic goals and likely outcomes for the client with MODS. •Withdrawal of life support and starting end-of-life care may be the best options for the client.
Myoglobinemia
Abnormal presence of myoglobin in the blood indicating muscle breakdown.
1. prehospital burn management Remove from burning, ABC, burn center referral PRN, poss intubate, C-spine
Airway If singed or blackened nares or removed from burning room/building, assume airway is compromised. Will need to insert ETT ASAP. C-spine stabilization is protecting the airway Breathe check for adequacy of ventilation. Provide 100% humidified oxygen per non-rebreather mask. If inadequate or client is hypo-ventilating, bag with bag-mask-device connected to 15L O2. Consider intubating if client was in burning building, unable t protect airway, or has thermal burns to the face, chest, or large TBSA burns Circulate check for presence of pulses in burn area, elevate burn area above the heart to help reduce edema, establish IV access. Chemical - remove solid particles by brushing them off, lavage with copious amounts of water - remove any clothing that is contaminated Thermal - cover with clean, cool, tap water dampened towel to help prevent excess temperature and fluid loss Be concerned of heat loss - Wrap in dry blanket
Complications of emergent phase - respiratory
Airway Management: lower airway - prepare for intubation, check RR, O2 Sat, ^ HOB >45 degrees Supplemental oxygen, consider 100% Mechanical Ventilation for airway compromise Bronchoscopy at bedside Serial CXR; check respiratory infection (Pneumonia
What are the priority nursing diagnoses to address the concern of fluid retention?
Answer: A priority nursing diagnosis is Impaired Cardiac output due to poor left ventricular function and Fluid imbalance related to acute renal failure. Other priority diagnoses are Impaired gas exchange related to pulmonary edema, Activity intolerance related to fluid volume excess, and Risk for impaired tissue integrity related to fluid retention and edema. Rationale: Any issue that impacts airway, breathing, circulation or disability (neuro) remains the nurse's top priority. The fluid is causing issues with the client's breathing and circulation.
What are the priority nursing interventions for these nursing diagnoses?
Answer: A.S. needs to be closely monitored for fluid retention, including vital signs, daily weights at the same time each day, jugular vein distension, and signs of peripheral, periorbital, and sacral edema. Lung assessment is crucial to detect any crackles and wheezes and any changes in oxygenation status. The patient will likely need diuretic therapy, fluid restriction, and possibly dialysis to decrease the excess fluid and balance electrolyte levels. Rationale: Priority nursing interventions are aimed at relieving symptoms caused by the excess fluid.
What additional tests, if needed, could be done to determine the cause of AKI?
Answer: Additional tests include renal ultrasound, renal scan (renal scintigraphy), computed tomography (CT) scan, magnetic resonance imaging (MRI), retrograde pyelography, and a spiral CT scan if a kidney stone is suspected. A 24-hour urine collection may be done as reduced urine output may or may not occur with AKI, depending on the cause. Additional laboratory screenings for autoimmune disorders would include antinuclear antibodies (ANA) and erythrocyte sedimentation rate (ESR). Rationale: Diagnostic tests help find the cause of the issue, the severity of the issue, and help healthcare providers provide information so that clients may make an informed decision about potential treatment options.
·Echocardiogram shows decreased left ventricular function ·Urinalysis: Urine dark yellow and cloudy, protein 28 mg/dL, negative for glucose and ketones, positive for casts, red blood cells and white blood cells ·24-hour urine output = 380 mL ·Laboratory Tests: ·Hemoglobin 8 g/dL (12-16) ·Hematocrit 23.8% (37-47) ·RBC 2.57 million/mm (4.2-5.3) ·WBC 4.7 mm(5-10) ·Potassium 5.2 mEq/L (3.5-5.5) ·Calcium 9 mg/dL (9-10.5) ·BUN 36 mg/dL (10-20) ·Creatinine 4.9 mg/dL (0.5-1.2) ·BNP 182 pg/mL (normal- <100; 100-200 MD eval; >400 is high) Interpret A.S.'s laboratory test results and describe their significance.
Answer: Hyponatremia is present: because damaged tubules cannot conserve sodium, the urinary excretion of sodium may increase. The serum potassium level is elevated because the kidney's normal ability to excrete potassium is impaired. Because the kidneys are the primary excretory organs for urea (an end product of protein metabolism) and creatinine (an end product of endogenous muscle metabolism), blood urea nitrogen and serum creatinine levels are elevated in the presence of kidney dysfunction. The anemia is due to decreased production of the hormone erythropoietin by the kidneys. Rationale: The kidneys regulate electrolytes, the excretion of waste by-products, and regulates the hormone erythropoietin to stimulate more red blood cell production, thus increasing the oxygen delivered to organs in the body.
What phase of AKI is A.S. in?
Answer: She is in the oliguric phase of AKI, as evidenced by the urine output of less than 400 mL/day. Rationale: She is in the oliguric phase of AKI, as evidenced by the urine output of less than 400 mL/day.
Is this cause of AKI classified as prerenal, intrarenal, or postrenal? Explain your answer.
Answer: The AKI is a result of prerenal causes. In prerenal failure, factors external to the kidneys caused a reduction in renal blood flow and led to decreased glomerular perfusion and filtration. Rationale: A decrease in cardiac output resulting from acute heart failure and decreased left ventricular function has caused the renal damage. However, prerenal conditions can lead to intrarenal disease if the renal ischemia is prolonged. Although the urine specific gravity is elevated, the patient does have casts in the urine, suggesting oliguria of intrarenal failure caused by acute tubular necrosis from ischemia. Cast are breakdown of proteins such as RBC, WBC
What is the most likely cause of A.S.'s AKI?
Answer: The AKI is related to the long-term effects of HF, diabetes mellitus, and hypertension, which ultimately compromise circulation to the kidneys. Rationale: In this instance, acute heart failure led to a decrease in cardiac output (decrease left ventricular function), which weakened the kidneys by decreasing perfusion.
dressings- closed method
Antimicrobial Agent: Bismuth-impregnated petroleum gauze Dressing: Biosynthetic, Biobrane
intervention of burns
Assume respiratory/airway impairment Humidified O2 Elevate HOB Consider intubation Bronchodilators: metaproterenol (Alupent), Albuterol (Ventolin)
G3a
CKD GFR stage with GFR from 45-59 mL/min and is mildly to moderately decreased
Insulin causes K+ to go into cells.
Can give bicarb to correct acidosis by causing K+ to move to cells;
Cardio-vascular lesions: (burns)
Circulatory arrest happens by asystole or ventricular fibrillation. Nursing Interventions: Place on cardiac monitor. Treat cardiac dysrhythmias.
hands and feet burns
Circumferential burns of extremities - Cause neurovascular impairment distal to burn complicating recovery & ADLs. Escharotomy may help. Monitor for Compartment Syndrome, check distal pulses, skin color, coolness Poor circulation, delayed wound healing, potential loss of limb. Later: ADLS adversely affected
RIFLE: Risk
CrSerum x 1.5 or GFR less than 25% Urine output < 0.5 mL/kg/hr x 6h
RIFLE: Injury
CrSerum x 2.0 or GFR less than 50% Urine output < 0.5 mL/kg/hr x 12h
RIFLE: Failure
CrSerum x 3.0 or GFR less than 75% Urine output < 0.3 mL/kg/hr x 24h or anuria x 12h
prerenal
Decrease blood flow to kidneys, e.g. dehydration, low C.O. Pre renal conditions can contribute to intrarenal AKI, if the condition persists for a long period of time.
intrarenal
Direct damage to kidneys, e.g. ischemia, nephrotoxin, hemoglobin or myoglobin (e.g. burns), blood transfusion rx Acute tubular necrosis is most common intrarenal cause of AKI in hospitalized patients. Due to ischemia, nephrotoxins, or sepsis. Ischemic and nephrotoxic results in 90% of AKI cases.
Metaproterenol and albuterol do have the SE of tachycardia and hand tremors.
Do monitor for tachyarrhythmias.
Diuretic phase
During the diuretic phase of AKI, daily urine output usually is around 1 to 3 L but may reach 5 L or more. The high urine volume is caused by osmotic diuresis from the high urea concentration in the glomerular filtrate and the inability of the tubules to concentrate the urine. In this phase, the kidneys have recovered their ability to excrete wastes, but not to concentrate the urine. •Large losses of fluid and electrolytes require the client be monitored for hyponatremia, hypokalemia, and dehydration. The diuretic phase may last 1 to 3 weeks. Near the end of this phase, the client's acid-base, electrolyte, and waste product (BUN, creatinine) values stabilize.
Complications of emergent phase- cardiac
Dysrhythmias > cardiac monitor, amiodarone Decreased tissue perfusion to burned extremities > Escarotomy Hypovolemic Shock > IV Fluids, MAP should be >65; after 24 hrs, give 5% albumin if no improvement.
RIFLE ESRD
ESRD = complete loss of kidney function > 3months
Interprofessional Care:Obstructive Shock
Early recognition of the conditions that put the client at risk for obstructive shock: cardiac tamponade, tension pneumothorax, embolectomy or thrombolytic for massive PE, chest trauma, pericarditis If in obstructive shock, treat the underlying cause. Fluid resuscitation based on MAP and tissue perfusion
Phases of Burn Management
Emergent (resuscitative) Acute (wound healing) Rehabilitative (restorative)
You suspect kidney transplant rejection when the patient shows which symptoms?
Fever, weight gain, and diminished urine output Expect fluid retention and weight gain and fever (infections are common). Clients should have increased urine output.
Criteria for septic shock
Fever>100.9 Temp <97 HR >90 RR >22 SBP <100 WBC >12,000 So when you have a patient come in with these vital signs what do you need to do? Immediately start fluid resuscitation with LR or NS, then we need to see what organism is growing then give antibiotics then give insulin
Interprofessional Care:Septic Shock
Fluid challenge 30 mL/kg of isotonic crystalloid within 3 hours of sepsis recognition. Repeat/continue as needed Serum Lactate. >2 indicates sepsis, repeat in 6 hours Set of blood cultures from 2 sites Broad spectrum antibiotic within 1 hour of sepsis recognition Vasopressors (norepinephrine, vasopressin) Consider colloids (albumin) for persistently low MAP Inotropes Passive Leg Raise (PLR) Challenge Corticosteroids Glucose control range 140-180 Stress ulcer prophylaxis Anticoagulants
A patient with acute renal injury has a GFR (glomerular filtration rate) of 40 mL/min. Which signs and symptoms below may this patient present with? Select all that apply:*
GFR is normally 90 or greater. 40 indicates Injury (GFR < 50%) Hypervolemia from water retention. Increased BUN Peripheral edema Hyperkalemia not hypo You would not expect a lower Cr
You are about to provide care to a patient with severe burns. You will don:
Gloves No goggles Gown No N-95 Surgical Mask Hair Cover
2. Emergent (resuscitative): Up to 72 hrs; hypovolemic shock
Greatest threat: Hypovolemic shock (Burn Shock) as capillary bed becomes leaky—profound < MAP Massive fluid shift into 2nd & 3rd spaces as capillary bed becomes more permeable. Ends as fluid is mobilized out of 2nd & 3rd spaces and diuresis begins < Sodium (goes into interstitial space) and > Potassium— released in CV bed; Cardiac Dysrhythmias Hypovolemia causes hemoconcentration and increased hematocrit Tissue hypoxia -due formation of thromboses in capillaries of burned tissues and RBC hemolysis Loss of Immunity
burn drug therapy- GI
H2 Blockers, PPIs: pantoprazole, lansoprazole, esomeprazole, OTC ranitidine Nystatin for candida albicans, give yogurt or OTC probiotics to reintroduce normal flora
burn drug therapy- sedation & antidepressants
Haloperidol Lorazepam Midazolam Zolpidem Sertraline Fluoxetine Citalopram Oral or IV push Midazolam-conscious sedation Sleep Antidepressants Fluoxetine also reduces anxiety
TBSA
Head is 9%, Arms each 9%, Back and Chest each 18%, Legs each 18%, Genitalia 1%
Clinical Manifestations of Smoke and inhalation
Hoarseness Facial Burns Swallowing difficulty Singed nasal/facial hair - airway compromise; intubate Copious secretions Dyspnea Use of accessory muscles Carbonaceous Sputum(Gray, black) Wheezing Altered mental status
Complications of emergent phase- electrolytes
Hyperkalemia and hyponatremia (usually dilutional)
Emergent phase- atb
IV antibiotics are not routinely used as the blood supply to the burn area is very poor. The ABX won't be delivered to the burn! Instead, local antimicrobials are used. If the client is septic, then IV antibiotics will be initiated. Sepsis is one of the leading causes of death in the burn pt, so the RN is vigilant in monitoring for possible sepsis.
Precipitating factors of DKA
Illness Infection Inadequate insulin dosage Undiagnosed type 1 diabetes Poor self-management Neglect
complications of acute phase
Infection •Local: antibiotics, Protective Isolation •Systemic: broad spectrum Abx for sepsis Musculoskeletal •OT, PT, ROM to prevent contractures Glucose control •IV insulin drip may be indicated to maintain glucose 120-180 s/s of systemic infection going into sepsis, WBC>10,00, fever or hypothermia, >HR, >RR, <MAP, < UA output, chills, malaise. Notify provider if present
Clinical Manifestations: HHS
Insidious onset Weakness Dehydration Polyuria, polydipsia Blurred vision Dry, flushed skin Tachycardia, hypotension Shallow, rapid respirations Neuro s/s: hemiparesis, aphasia, nystagmus, visual hallucinations, seizures, altered LOC, coma Azotemia No ketosis (pH > 7.30)
•*To reduce K: Only sodium polystyrene sulfonate (Kayexalate) and dialysis actually remove potassium from the body.
It is in stool which is rich in K+Never give this drug to a client with a paralytic ileus because bowel necrosis can occur.
Rehabilitation phase
Joint stiffness and contractures PT during dressing changes Splints Prevent complications of hypertrophic scars Protect burned area from sunlight Hydroxyzine or water-based lotion for itching
So you have two types: absolute and relative
Just think of absolute as its gone out of the body. With relative it's a fluid shift such as internal bleeding. The fluid stays in the body. We can compensate for about 15% or 750cc of fluid loss but anything more than that we start to see changes and remember this all depends on your patient: how old are they, what is their history, whats the injury. Apply oxygen, establish IV's, give isotonic crystalloids, draw blood
arterial line care
Keep pressure bag inflated to 300mmHg Deflation of bag will result in retrograde blood flow. Keeps line patent and infuses 3-5ml /hr. Prevents dampening of trace. Prevents clots Flush bags of Normal Saline are changed every 96 hrs or PRN. All flush bags must be labeled with time and date of commencement Infection control, keep bag sterile. Ensures adequate flushing volume. Do not add extra tubing or stopcocks to system. All lines must be have rigid non-compliant tubing Extra areas of air entrapment which can cause inaccuracy of the arterial trace. Increase risk of infection Periodically flick tubing system and flush the tubing system Eliminates any bubbles escaping the flush solution. Fast flush solution after opening the system for blood sampling and/or zeroing Helps eliminate air bubbles. Clears the line of blood Immobilise arm and keep sites clearly visible at all times. eg. On top of sheets. Do not use bandage over arterial line site. Safety measure to prevent adverse events eg. hemorrhage or disconnection
G5
Kidney failure <15/dialysis
Parkland formula for fluid resuscitation
LR, 4 ml/kg/% body surface area burned in first 24 hours. 1/2 in first 8 hours, the rest over the following 16 Crystalloids (Lactated Ringers) 1st 24 hours, colloids 2nd 24 hours. LR 4mL/kg x TBSA%=Total fluids 1st 24 hours divide into 8 hour periods - first 50% in 8 hours - next 25% in 8 hours - final 25% in 8 hours 12-24 hours later, Albumin 0.3-0.5 mL/kg/ TBSA % Remember to deduct hours from formula if burn occurred much before arrival at ER. In other words, start with time of burn for fluid administration.
location of burn
Location of the burn is related to the severity of the injury: Face, neck, chest, -respiratory obstruction Hand, feet, joints, eyes- self- care Ears, nose- infection Circumferential burns of the extremities can cause circulatory compromise -Patients may also develop compartment syndrome
Neurological effects (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.
Hgb
M: 14-18 F: 12-16 <5g/dL or >20g/dL
RBC
Male: 4.7-6.1; Female: 4.2-5.4
Hct
Male: 42-52%; Female: 37-47% <15% or >60%
postrenal
Mechanical obstruction in urine outflow, e.g. prostate hypertrophy, cancer, stones, trauma, tumors, ureteral obstruction Ureteral obstruction leads to hydronephrosis, kidney dilation, kidney tubule blockage and reduced function. If obstruction is relieved in 48 hours recovery is likely, but prolonged obstruction can result in irreversible kidney fibrosis. Only 10% of AKI are due to post renal causes.
Triggers
Mechanical tissue trauma: burns, crush injuries, surgical procedures Abscess formation: intraabdominal, extremities Ischemic or necrotic tissue: pancreatitis, vascular disease, MI Microbial invasion: bacteria, viruses, fungi Endotoxin release: gram-negative bacteria Global perfusion deficits: postcardiac resuscitation, shock states Regional perfusion deficits: distal perfusion deficits
kidney transplant teaching
Monitor for infection signs and symptoms; on immunosuppressive therapy; increased risk for CV disease (control risk factors because it is main cause of death), increased risk of cancer, risk for return of kidney disease, and steroid complications, e.g. DM, ulcers, infections
burn drug therapy- narcotics
Morphine, fentanyl, hydromorphone (esp for debridement) IV route (drip, PCA, IV push) (Oral and IM routes initially contraindicated) Once acute phase is reached: S-R Morphine, oxycodone, methadone Nonsteroidal antiinflammatory: ketorolac Adjuvant analgesics: gabapentin
Neurologic disorders:
Neurologic changes can occur as the nitrogenous waste products accumulate in the brain and other nervous tissue. Mild as fatigue and difficulty concentrating; escalate to seizures, stupor, and coma.
dressings- open method
No dressing Topical Antimicrobial Agents Silver Sulfadiazine Chlorhexidine gauze
increased risk factors for burns
Older adult Cardiac, Renal, Chronic respiratory disease, Diabetes Mellitus, Peripheral Vascular Disease (PVD) History of cancer and radiation/chemotherapy History of substance abuse
RIFLE: Loss
Persistent AKI = complete loss of kidney function >4 weeks
causes of acute renal failure
Potentially reversible (implications for hospitalized pts due to high rate, i.e. 1 in 5. Often follows severe prolonged hypotension, hypovolemia or exposure to nephrotoxic substance. Mortality rate as high as 70-80% when it occurs in the ICU
Interprofessional Care:Anaphylactic Shock
Prevention—Client/Family instruction on avoidance of know allergen and use of epipen (epinephrine IM in thigh) Epinephrine IV push in ER setting. Epi causes bronchodilation and peripheral vasoconstriction. So it opens the airway and bronchi and helps to raise the MAP. Adjunct antihistamines—diphenhydramine amd H2 blocker ranitidine are IV push to help halt the release of histamine. Bronchodilators by nebulizer Epinephrine by aerosol help to dilate or open narrowed bronchi. Intubation is considered when the client is not responding to epinephrine, diphenhydramine, ranitidine, and bronchodilators Aggressive fluid resuscitation beginning is isotonic crystalloids And Corticosteroids are administered IV if there is a persistently low MAP despite fluid resuscitation
Treatment of smoke inhalation
Rapid ABC assessment, 100% humidified O2, consider need for intubation, establish IV access, fluid resuscitation
Interprofessional Care: Cardiogenic Shock
Recognition of at-risk clients Restoration of coronary artery blood flow via thrombolytics, emergent PCI Nitrates IV drip Inotropes IV drip Diuretics IV push or IV drip (Furosemide, bumetanide) Beta-adrenergic blockers IV push or enteral
Renal Injury- (burns)
Rhabdomyolysis can lead ATN (acute tubular necrosis) which can lead to AKI- Acute Kidney Injury. Foley catheter. Monitor I & O. Serum creatinine.
Adequate fluid resuscitation is 0.5-1 mg/kg/hr u/o
SBP > 90 HR < 120 MAP > 65
It is important that burn clients begin wearing pressure garments while the scar is active and immature.
Scar tissue is highly responsive in the early stages so an early application of pressure garments is imperative. 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. Itching occurs where healing is occurring. Benadryl lotion (water-based) can help. A soft pliable elastic scar develops which allows for normal joint movement. The external pressure applied by the garments decreases inflammatory response and the amount of blood in the scar, reducing itching and prevents collagen from synthesizing. Additionally pressure garments provide protection against injury and direct sunlight. This skin is very sensitive.
obstructive shock
Shock that occurs when there is a block to blood flow in the heart or great vessels, causing an insufficient blood supply to the body's tissues. may be caused by wreck
burn drug therapy- nutrition
TBSA >20% will require enteral feeding; metabolic rate is raised by 50-100% Monitor residuals, bowel sounds, abdomen High caloric intake Protein, carbs, fat, and vitamins/minerals may need to be supplemented
One of the classic signs of shock is a drop in BP which is because of the decrease in CO.
The body starts to shunt blood flow to other parts of the body so that it can keep blood going to the heart and brain so that is why we see a reduction in urinary output and the skin get cool. That is also why we see impaired motility because short term you do not need to poop to stay alive.
Shock can be classified as a 'Pump' or 'Pipe' problem.
The cardiovascular system is actually a closed system. There is the pump, the heart, which circulates blood thru the veins and arterites. The blood doesen't leave the cardiovascular space. Gas exchange does take place. Because the CV system is a closed system, a problem with the pumping heart or pipes (arteries and veins) quickly affects the other. For the Cardiovascular System to function properly, need both the pump (heart) and the pipes (Arteries and veins) to be working.
Waste product accumulation:
The kidneys are the primary excretory organs for urea and creatinine. Elevated BUN level can also be caused by dehydration, corticosteroids, or catabolism resulting from infections, fever, severe injury, or GI bleeding. The best serum indicator of AKI is creatinine because it is not significantly altered by other factors.
A patient with AKI has a urinary output of 350 mL/day. In addition, morning labs showed an increased BUN and creatinine level along with potassium level of 6 mEq/L. What type of diet ordered by the physician is most appropriate for this patient?
The patient with AKI, especially in the oliguric stage of AKI, should eat a low-protein, low-potassium, and low-sodium diet. This is because the kidneys are unable to filter out waste products, excessive water, and maintain electrolyte balance. The patient will have a buildup of waste (BUN and creatinine). Remember these waste products are the byproduct of protein (urea) and muscle breakdown (creatinine). So the patient should avoid high-protein foods. In addition, the patient is at risk for hyperkalemia and fluid overload (needs low-potassium and sodium foods).
Extent of burn
The rule of nines is helpful clinically in determining _____.
Respiratory lesions: (burns)
There can be a 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 insufficiency. 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.
A patient with acute kidney injury has the following labs: GFR 92 mL/min, BUN 17 mg/dL, potassium 4.9 mEq/L, and creatinine 1 mg/dL. The patient's 24 hour urinary output is 1.75 Liters. Based on these findings, what stage of AKI is this patient in?
This patient is in the recovery stage of AKI. The patient's labs and urinary output indicate the renal function has returned to normal. Remember the recovery stages starts when the GFR (glomerular filtration rate) has returned to normal (normal GFR 90 mL/min or higher), which will allow waste levels and electrolyte levels to be maintained.
The RN has assigned a client who has an open burn wound to the LPN. Which instruction is most important for the RN to provide the LPN?
Wash hands on entering the client's room. • Infection can occur when microorganisms from another person or the environment are transferred to the client. Hand washing with soap and water is the best way to get rid of germs in most situations.
When our patients go from sepsis to shock we see significant organ malfunction.
We see hypotension even though we are giving them adequate fluids, inadequate tissue perfusion
emergent phase- wound care
Wound care should be delayed until patent airway, adequate circulation, and adequate fluid replacement have been established Cleansing -want no debris left in the wound and protect them from pathogens Debridement -can be enzymatic Dressing changes -huge production for them, completely soak the dressing, cut them off, the dressing dries to the skin so need to be careful, put sulfadiazine on whole body ROM is important and do it right before and after dressing change Full thickness > surgery for possible skin grafts. Protective Isolation Cleansing & Debridement (give fentanyl) Physical Therapy, ROM Dressing Care: silver sulfadiazine for partial thickness.
septic shock
a serious condition that occurs when an overwhelming bacterial infection affects the body
Invasive: Arterial Pressure monitoring
accurate BP blood sampling
Closely monitor fluid intake during the oliguric phase of AKI. The 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).
The first step is to determine if there is adequate intravascular volume and cardiac output to ensure
adequate perfusion of the kidneys. Diuretic therapy may be administered and usually includes loop diuretics (e.g., furosemide [Lasix], bumetanide [Bumex]) or an osmotic diuretic (e.g., mannitol).
Passive Leg Raise (PLR) Challenge is recommended to
assess for fluid responsiveness. PLR mimics endogenous volume expansion (equivalent to an approximate 300 mL fluid bolus) and can be thought of as a preload challenge. It is used to predict if a client will respond to additional fluid bolus. Follow these steps to perform PLR Position the client in the semi-recumbent position with the head and torso elevated at 45 degrees. Obtain a baseline vital signs Lower the client's upper body and head to the horizontal position and raise and hold the legs at 45 degrees for one minute. Obtain subsequent vital signs. The expected response to this maneuver in those that are fluid responsive is that the MAP will raise with leg elevation.
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. Suspect airway compromise!!!! Singed nasal hairs, hoarseness, painful swallowing
Mean Arterial Pressure (MAP)
average pressure maintained in the arterial system of body SPB + (2 x DBP) /3 norm = 70-105
Ketonuria is a process that occurs when ketone bodies are excreted in the urine. During this process, electrolytes
become depleted as cations are eliminated along with the anionic ketones in an attempt to maintain electrical neutrality.
Metaproterenol
beta 2 agonist
Partial thickness deep (2nd)
blisters or weeping (fluid filled), severe pain. Destruction epidermis to upper dermis Bright red to pale ivory Blanches to pressure Heals within 14-30 days
Home hazards- general household
carelessness with cigarettes, matches, candles; heat lamps, fireplaces, flammables, frayed or defective wiring, multiple extension cords per outlet, open space heaters, outdoor grills, radiators
thermal burns
caused by contact with open flames, hot liquids or surfaces, or other sources of high heat (140 or higher) Initially red and swollen, need debridement for healthy tissue to be able to heal the area
Occupational hazards
cement, chemicals, combustible fuels, electricity from power lines, fertilizers, pesticides, hot metals, sparks from electric sources, steam pipes, tar
smoke inhalation
damage to the lungs in which particles from a fire coat the alveoli and prevent the normal exchange of gases
pulse pressure
difference between systolic and diastolic pressure norm = 30-50
chemical burn
direct contact with chemicals, acid, alkalis, and other organic compounds; damage continues even with neutralization of substance
Calcium gluconate raises the threshold at which
dysrhythmias will occur, serving to temporarily stabilize the myocardium
Electrical burns
entrance and exit thermal burns, most tissue damage is internal (cardiac with dysrhythmias, possible cardiac arrest), myoglobinuria and AKI, stabilize with C-spine after ABC
Muscular effects: (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. * Leave on c-collar.
location of burns is the 3rd component of burn classification
face & neck --> intubate early before throat swells
Multiple organ dysfunction syndrome (MODS) is
failure of two or more organ systems Homeostasis cannot be maintained without intervention Results from SIRS
electrical burns are 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.)
Hyperosmolar hyperglycemia is a complication of diabetes mellitus in which high blood sugar results in
high osmolarity. HHS usually occurs in much older non-insulin dependent patients who are often greater than 60 years old. HHS occurs when the blood sugar of a person with diabetes gets too high for a long time. The extra sugar is passed into the urine which causes the person to urinate frequently; as a result, lots of fluids are lost when can lead to severe dehydration.
Home hazards- bathroom and kitchen
hot water heaters set at 120 *F or higher, microwaved food, steam, hot grease, or liquids from cooking
The Rehabilitation Phase focuses on the prevention of
hypertophic scars Pressure garments aid in reducing the effects hypertrophic scarring there by reducing scarring and deformities
Insults resulting in SIRS include
infection (referred to as sepsis), ischemia, infarction, and injury
compartment syndrome
involves the compression of nerves and blood vessels due to swelling within the enclosed space created by the fascia that separates groups of muscles
MAP is considered to be the perfusion pressure seen by organs in the body. It is believed that a MAP of greater than 70 mmHg
is enough to sustain the organs of the average person under most conditions. MAP greater than 100 can indicate vasoconstriction that limits blood flow to tissues. Because the vessel introduced is arterial with high pressures, must have a pressure cuff on the IV bag.
A narrowing PP (number is becoming smaller) signals that the heart
is unable to dilate and fill with blood, as with severe pericarditis, cardiac tamponade, and tension pneumothorax.
Remember that in diuretic phase, there will be
low K and NA due to dehydration as more fluid leaves the body.
Central Venous Pressure (CVP)
measures preload; provides the best measurement of fluid status in the distributive shocks norm = 2-8 distributive hypovolemic goal = 8-12 cardiogenic goal >8 monitored via PICC or central line, if you are giving diuretics look at cvp.
G2
mildly decreased 60-90
G3b
moderately to severely decreased (30-44)
Elevated CVP is indicative of
myocardial contractile dysfunction and/or fluid retention.
Burn Preventions
no burning candles unattended, no smoke in bed, no frayed or undergrounded electrical cords, practice fire drills, flame retardant children's sleep war and at risk adult retardant aprons, set water heater at 120*, install working smoke and carbon monoxide detectors, store chemicals in sealed and labeled containers, caution with microwaved foods
Full thickness (3rd & 4th)
no pain, dry waxy appearance. Deep epidermal destruction to fat layer, muscle and bone White, waxy; Diminished pain sensitivity Surgical intervention required for healing Heals week, months, to years Significant scarring
*Less than 400 in 24 hours indicates
oliguric phase. Watch for adventitious sounds = complication of decrease U/O.
Partial thickness-superficial burns are not calculated by TBSA.,
only partial thickness-deep and full-thickness burns
PTT
partial thromboplastin time 60-70 seconds >100 seconds
Diabetic ketoacidosis is a serious diabetes complication where the body
produces excess blood acids (ketones). The condition occurs when there isn't enough insulin in the body. It can be triggered by infection or other illness. It requires hospital treatment to replace fluids and electrolytes and provide insulin therapy. When your cells don't get the glucose they need for energy, your body begins to burn fat for energy, which produces ketones. Ketones are chemicals that the body creates when it breaks down fat to use for energy. The body does this when it doesn't have enough insulin to use glucose, the body's normal source of energy.. When ketones build up in the blood, they make it more acidic. There are a warning sign that the diabetes is out of control or that you are getting sick.
treatment of chemical burns
removal of adherent clothing, dry lime brushed off of tissue, followed by irrigation (copious irrigation with tap water 20 mins to 2 hours), continue to damage tissue for 72 hours
risk factors for burns
scalding liquids (decrease the temp of hot water tanks; use cold water, then add hot); clothing ignition with cooking (elderly); Residential fires (space heaters and kerosene, wood burners. Do not use extension cords with space heaters); cigarettes (#1 leading cause of fire death. Also cell phones under pillows); Lack of smoke detectors in the home (free services, can go to the fire dept et get free smoke detectors) elderly, very old, very young, comorbidity
Store chemicals in...
sealed and labeled containers
G4
severely decreased (15-29)
Strategies to reduce burn injury- chemical
store chemicals safely in approved containers and label clearly; ensure safety of workers handling chemicals (education, protective eyewear, gloves, masks, clothing)
Partial thickness superficial (1st)
sunburn; Superficial Injury (Epidermis) Caused by sunburn or quick heat flash Red blanches to pressure, no blisters, painful healing 3-5 days , no scarring
SIADH
syndrome of inappropriate antidiuretic hormone
•The oliguric phase lasts on average about 10 to 14 days but can last months in some cases. The longer the oliguric phase lasts,
the poorer the prognosis for complete recovery of kidney function.
In the RIFLE criteria,
the stratum of injury is defined by a doubling of serum creatinine or a reduction of urinary output below 0.5 ml/kg per h during at least 12 h. Importantly, of the patients who develop injury, >50% later will develop established renal failure
Delayed transfusion reaction
transfusion reaction with signs or symptoms presenting *after 24 hours* •Delayed Hemolytic •Hepatitis B •Hepatitis C •Iron Overload
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. Treatment is 100% humidified oxygen. The oxygen must be humidified to add moisture to the very dry injured nares and airways.
Strategies to reduce burn injury- electrical
• Avoid or repair frayed wiring. • Avoid outdoor activities during electrical (i.e., lightning) storms. • Ensure electrical power source is shut off before beginning repairs. • Wear protective eyewear and gloves when making electrical repairs.
strategies to reduce burn injury- inhalation
• Install smoke and carbon monoxide detectors and change batteries annually (if appropriate).
•When the circulating supply of insulin is insufficient, glucose cannot be properly used for energy. The body compensates by breaking down fat stores as a secondary source of fuel.
• Ketones are acidic by-products of fat metabolism that can cause serious problems when they become excessive in the blood. Ketosis alters the pH balance, causing metabolic acidosis to develop.
Strategies to reduce burn injury- flame or contact
• Never smoke in bed. • Use "child-resistant" lighters. • Hold regular home fire exit drills. • Never leave hot oil unattended while cooking. • Never use gasoline or other flammable liquids to start a fire. • Never leave candles unattended or near open windows or curtains. • Consider a flame-retardant smoking apron for older or "at-risk" people. • Exercise caution when microwaving food and beverages as they can get very hot.
Safety Alert- pulse CO oximetry monitoring
• Standard pulse oximetry (SpO2) does not distinguish oxyhemoglobin from carboxyhemoglobin. • A patient with CO poisoning will have normal SpO2 readings despite high carboxyhemoglobin levels. • For patients with suspected or confirmed CO poisoning, use a pulse CO oximetry (SpCO) device.
strategies to reduce burn injury- scald
• Use "anti-scald" devices with showerhead or faucet fixtures. • Lower hot water temperature to the "lowest point" or 120°F (49°C). • After running bath water, check temperature with back of hand or bath thermometer. • Supervise bathing with small children, older adults, or anyone with impaired physical movement, physical sensation, or judgment.
Clinical Manifestations: DKA
•Abdominal pain, anorexia, nausea/vomiting •Kussmaul respirations •Sweet, fruity breath odor •Blood glucose level of ≥ 250 mg/dL •Blood pH lower than 7.30 •Serum bicarbonate level < 16 mEq/L •Moderate to high ketone levels in urine or serum •As the client becomes severely dehydrated, the skin becomes dry and loose, and the eyes become soft and sunken. •Abdominal pain may be present and accompanied by anorexia, nausea, and vomiting. •Kussmaul respirations (rapid, deep breathing associated with dyspnea) are the body's attempt to reverse metabolic acidosis through the exhalation of excess carbon dioxide. •Acetone is noted on the breath as a sweet, fruity odor. •Laboratory findings include a blood glucose level of 250 mg/dL (13.9 mmol/L) or higher, arterial blood pH less than 7.30, serum bicarbonate level less than 16 mEq/L (16 mmol/L), and moderate to high ketone levels in the urine or serum.
AKI interprofessional care- General
•Accurate intake and output; closely monitor fluid intake during oliguric phase •Daily weights •Assess for signs of hypervolemia or hypovolemia; IV access •Check peripheral edema, ^ BP •Assess for potassium and sodium disturbances •Meticulous aseptic technique •Careful use of nephrotoxic drugs •Skin care measures/mouth care
Acute Transfusion Reactions
•Acute Hemolytic Reaction •Febrile, nonhemolytic reaction (most common) •Mild Allergic Reaction •Anaphylactic and Severe Allergic Reaction •Circulatory Overload Reaction •Sepsis •Transfusion Related Acute Lung Injury Reaction •Massive Blood Transfusion Reaction
The nurse is performing a sterile dressing change on a client with a superficial partial-thickness burn on the shoulder and back. Arrange the steps in the order in which each should be performed.
•Administer Tramadol (Tramal) 50 mg IV. •Apply silver nitrate ointment. •Debride the wound of eschar using gauze sponges. •Cover the wound using a sterile gauze dressing. •Obtain a sample for wound culture.
HYPOVOLEMIC SHOCK
•Aggressive Fluid Therapy • 3:1 rule •Start with isotonic (NS & LR) •Consider colloids (albumin) •Consider blood products for actual blood loss • At least 2 IV sites •Treat underlying cause • End point of fluid resuscitation: CVP 15
•Continuous renal replacement therapy (CRRT)
•Cannulation of artery and vein •Physiologically similar to normal kidney function •Decreases chance of low BP •Corrects electrolytes and removes toxins •30-40 days.
signs of shock
•Drop in blood pressure • Vascular shunting • Decrease in bowel sounds • Increased heart rate • Cool skin •Change in LOC •Decreased Urinary Output •Tachypnea
A patient has full-thickness burns on the front and back of both arm and hands. It is nursing priority to:
•Elevate and extend the extremities This position will decrease edema, which will help prevent compartment syndrome.
Interprofessional Care: DKA
•Ensure an patent airway and administer oxygen via nasal cannula or non-rebreather mask. •Because fluid imbalance is potentially life-threatening, the initial goal of therapy is to establish IV access and begin fluid and electrolyte replacement. •Typically, the initial fluid therapy regimen consists of an infusion of 0.45% or 0.9% NaCl at a rate to restore urine output to 30 to 60 mL/hr and to raise blood pressure. •When blood glucose levels approach 250 mg/dL (13.9 mmol/L), add 5% to 10% dextrose to the fluid regimen to prevent hypoglycemia, as well as a sudden drop in glucose that can be associated with cerebral edema. •Overzealous rehydration, especially with hypotonic IV solutions, can result in cerebral edema. •Monitor clients with renal or cardiac compromise for fluid overload. •Measure serum potassium level before starting insulin. If the client is hypokalemic, insulin administration will further decrease the potassium levels, making early potassium replacement is essential. Although initial serum potassium value may be normal or high, levels can decrease rapidly once therapy starts, as insulin drives potassium into the cells, leading to life-threatening hypokalemia. •IV insulin administration is therapy directed toward correcting hyperglycemia and hyperketonemia. •Insulin is immediately started at 0.1 U/kg/hr by a continuous infusion. •It is important to prevent rapid drops in serum glucose to avoid cerebral edema. A blood glucose reduction of 36 to 54 mg/dL (2 to 3 mmol/L) per hour will avoid complications. •Insulin allows water and potassium to enter the cell along with glucose and can lead to a depletion of vascular volume and hypokalemia; therefore, monitor the client's fluid balance and potassium levels.
nutritional and metabolic needs for sirs and mods
•Goal of nutritional support: preserve organ function •Total energy expenditure is often increased 1.5 to 2.0 times •Use of the enteral route is preferred to parenteral nutrition •Monitor plasma transferrin and prealbumin levels to assess hepatic protein synthesis •Provide glycemic control •Protein-calorie malnutrition is one of the primary signs of hypermetabolism and MODS. •Because of their relatively short half-life, the monitor plasma transferrin and prealbumin levels to assess hepatic protein synthesis. •The goal of nutritional support is to preserve organ function. •Providing early and optimal nutrition decreases morbidity and mortality rates in clients with SIRS and MODS. •The enteral route is preferred. If it cannot be used, parenteral nutrition should be considered. Provide glycemic control with a goal of 140 to 180 mg/dL with insulin infusions in these clients.
Fluid volume
•Hypovolemia may exacerbate AKI •Decreased urine output and fluid retention •Neck veins distended •Bounding pulse •Edema •Hypertension Fluid overload can lead to heart failure, pulmonary edema, and pericardial and pleural effusions; check for adventitious breath sounds e.g., crackles •Fluid volume: Hypovolemia (volume depletion) has the potential to exacerbate all forms of AKI, especially prerenal causes. •When urinary output decreases, fluid retention occurs. The severity of the manifestations depends on the extent of the fluid overload. In the case of reduced urine output (anuria and oliguria), the neck veins may become distended with a bounding pulse. Edema and hypertension may develop. •Fluid overload can eventually lead to heart failure, pulmonary edema, and pericardial and pleural effusions. •*Some of these patients may become SOB when lying down, which could indicate pulmonary edema. Check for crackles.
Potassium excess
•Impaired ability of kidneys to excrete potassium •Increased risk with massive tissue trauma •Usually asymptomatic •ECG changes
Metabolic acidosis
•Impaired kidney cannot excrete hydrogen ions •Serum bicarbonate production is decreased •Severe acidosis develops: Kussmaul respirations
Sodium balance
•Increased excretion of sodium •Hyponatremia can lead to cerebral edema
•Hyperkalemia: can cause PVCs*; requires Rx
•Insulin and sodium bicarbonate •Calcium gluconate •Sodium polystyrene sulfonate •Patiromer - binds K+ in GI •Regular insulin
AKI Care- •Ensure adequate intravascular volume and cardiac output
•Loop diuretics (e.g., furosemide) •Osmotic diuretics (e.g., mannitol)
AKI nutritional therapy
•Maintain adequate caloric intake •Primarily carbohydrates and fat •Limited protein •Restrict sodium, Phosphate, Potassium •Enteral nutrition if necessary •Calcium supplements •Do not place on NPO
3 types of smoke inhalation injuries
•Metabolic Asphyxiation (Carbon monoxide poisoning) •Treatment: 100% humidified Oxygen •Upper airway injury (above the glottis) •Lower airway injury (below the glottis)
Kidney transplant
•Preferred is living donor; accounts for 27% of transplants •Kidneys preserved up to 72 hours. •Donor kidney placed in iliac fossa; 3-4 hours in OR; first 12-24 hours in ICU. •Expect increased u/o,, e.g. 1 L/hour; replace mL for mL first 12-24 hours; give IV fluids to prevent hypovolemia; check for low Na and low K. •Monitor Foley for blood clots that can stop urine flow: use gentle irrigation.
interprofessional care mods
•Prognosis for MODS is poor •Goal: prevent the progression of SIRS to MODS •Vigilant assessment and ongoing monitoring to detect early signs of deterioration or organ dysfunction are critical •Care focuses on •Prevention and treatment of infection •Maintenance of tissue oxygenation •Nutritional and metabolic support •Appropriate support of individual failing organs •Early, aggressive surgery is recommended to remove necrotic tissue (e.g., early debridement of burn tissue) that can provide a culture medium for microorganisms. •Aggressive pulmonary management, including early mobilization, can reduce the risk of infection. •Strict asepsis can decrease infections related to intraarterial lines, endotracheal tubes, urinary catheters, IV lines, and other invasive devices or procedures. •Send appropriate cultures and start broad-spectrum antibiotic therapy, as ordered. Adjust therapy based on the culture results, if needed.
Emergent phase- additional considerations
•Tetanus •Local antimicrobial agents rather than systemic; unless sepsis is diagnosed; get blood and wound cultures first when treating sepsis •Assess for sepsis: HR > 90, SBP < 90, Temp >101, WBC <4000 or >10,000 •VTE Prophylaxis - enoxaparin, SCDs, compression stockings
Recovery phase
•The recovery 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. •The outcome of AKI is influenced by the client's overall health, severity of kidney failure, and the number type of complications. Some individuals do not recover and progress to end-stage renal disease. The older adult is less likely to have a complete recovery of kidney function. clients who recover may achieve clinically normal kidney function, but remain in an early stage of CKD.
AKI Clinical manifestations- oliguric phase
•Urinary changes- oliguria •Urinary output less than 400 mL/day •Occurs within 1 to 7 days after injury •Lasts 10 to 14 days •Urinalysis may show casts, RBCs, WBCs • Electrolytes: Hyperkalemia -> dysrhythmias
fluid resuscitation parameters
•Urine output 0.5-1mL/kg during first 24 hours at least 75-100 ml/hr for electrical burn client r/t to lower risk of rhabdomyolysis •MAP > 65 •SBP > 90 •HR < 120 •LR with TBSA > 15%, then consider vasopressor Outside parameters, increase fluid Monitor neuro, resp
•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
About 50% of clients will not be oliguric, making the initial diagnosis more difficult. Changes in urine output generally do not correspond to changes in glomerular filtration rate (GFR). However,
•changes in urine output are often helpful in differentiating the etiology of AKI. For example, anuria (no urine output) is usually seen with urinary tract obstruction, oliguria is commonly seen with prerenal causes, and nonoliguric AKI is seen with acute interstitial nephritis and ATN. •A urinalysis may show casts (sloughed necrotic cells) , RBCs, and white blood cells (WBCs). Urinary specific gravity (measure of the concentration of solutes in the urine) is normally 1.003-1.030.
•Renal failure, which may eventually occur from hypovolemic shock, causes the retention of ketones and glucose, and the acidosis progresses. Untreated, the client becomes
•comatose as a result of dehydration, electrolyte imbalance, and acidosis. If the condition is not treated, death is inevitable.
*If AKI is already established,
•forcing fluids and diuretics such as furosemide, will not be effective and may, in fact, be harmful.
Diabetic ketoacidosis (DKA) is caused by a profound deficiency of insulin and is characterized by
•hyperglycemia, ketosis, acidosis, and dehydration. •It is most likely to occur in people with type 1 diabetes but may be seen in people with type 2 diabetes in conditions of severe illness or stress when the pancreas cannot meet the extra demand for insulin.
•Hyperkalemia is one of the most serious complications in AKI because it can cause life-threatening cardiac dysrhythmias. The various therapies used to treat elevated potassium levels are listed in Table 46-5. Both
•insulin and sodium bicarbonate serve as a temporary measure for treatment of hyperkalemia by promoting a shift of potassium into the cells, but potassium will eventually be released.
Intermittent hemodialysis (HD)
•may have Quinton catheter inserted subclavian for dialysis; avoid giving meds via it and check for infection.
Hyperosmolar hyperglycemic syndrome (HHS) is a life-threatening syndrome that can occur in the client with diabetes who is able to produce enough insulin to prevent DKA but not enough to
•prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion. HHS is less common than DKA. It often occurs in clients older than 60 years with type 2 diabetes.
•Insulin deficiency impairs protein synthesis and causes excessive protein degradation. This results in nitrogen losses from the tissues. • Insulin deficiency also stimulates the production of glucose from amino acids (from proteins) in the liver and leads to further hyperglycemia. • Because there is a deficiency of insulin, the additional glucose cannot be used and the blood glucose level rises further, adding to the osmotic diuresis. If not treated,
•the client will develop severe depletion of sodium, potassium, chloride, magnesium, and phosphate. •Vomiting caused by the acidosis results in more fluid and electrolyte losses. •Eventually, hypovolemia will ensue and be followed by shock.
•Hyperosmolar hyperglycemic syndrome (HHS) is a life-threatening syndrome that can occur in the client with diabetes who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion. •HHS is less common than DKA. It often occurs in clients older than 60 years with type 2 diabetes. Common causes of HHS are
•urinary tract infections, pneumonia, sepsis, any acute illness, and newly diagnosed type 2 diabetes. •HHS is often related to impaired thirst sensation and/or a functional inability to replace fluids. There is usually a history of inadequate fluid intake, increasing mental depression, and polyuria
Common causes of HHS are
•urinary tract infections, pneumonia, sepsis, any acute illness, and newly diagnosed type 2 diabetes. •HHS is often related to impaired thirst sensation and/or a functional inability to replace fluids. •There is usually a history of inadequate fluid intake, increasing mental depression, and polyuria.
