BY: tmr

burn injury risk factors

y Young children and elderly people : high risk y Toddlers: scalds y school-age children : matches y teenage boys: electrical injury y Adults: smoking y usually in the kitchen & bathroom y inappropriate use of gasoline

Pathophysiology
y Heat may be transferred y The skin and the mucosa

through conduction or electromagnetic radiation. y Tissue destruction results from coagulation, protein denaturation, or ionization of cellular contents.

of the upper airways are the sites of tissue destruction. y Deep tissues, including the viscera, can be damaged by electrical burns or through prolonged contact with a heat source.

Pathophysiology
y Plasma loss and vascular responses y Intravascular volume loss y Diminished tissue perfusion y Release of vasoactive agents y Capillary semipermiability Lost y Moving of fluids and substances like proteins from

the intravascular to interstitial space y Hyperemia y hypovolemia

Hemodynamic changes
y Lessened circulating blood volume results in

decreased cardiac output initially and increased pulse rate. y There is a decreased stroke volume as well as a marked rise in peripheral resistance (due to constriction of arterioles and increased hemoviscosity). y This results in inadequate tissue perfusion, which may in turn cause acidosis, renal failure, and irreversible burn shock.

Hemodynamic
y Electrolyte imbalance may also occur. y Hyponatremia usually occurs during the 3rd to 10th

day due to fluid shift. y The burn injury also causes hyperkalemia initially due to cell destruction, followed by hypokalemia as fluid shifts occur and potassium is not replaced.

Metabolic Demands
y Catecholamine release appears to be the major

mediator of the hypermetabolic response to burn injury. y "Burn fever" is common and is dependent on depth of burn and percentage of TBSA involved. Temperatures of 102F to 103F (38.8C 39.4C) are common as "fever spikes." y Healing a large surface area requires much energy; glucose is the primary metabolic fuel.

Metabolic change stores are limited and y Because total body glucose
y Despite all nutritional support, it is almost

stored liver and muscle glycogen is exhausted within the first few days postburn, hepatic glucose synthesis (gluconeogenesis)

impossible to counteract a negative nitrogen balance; the sooner a burn wound is closed, the more rapidly a positive nitrogen balance is reached.

Renal changes
y Glomerular filtration may be decreased in extensive

injury. y Without resuscitation or with delay, decreased renal blood flow may lead to high oliguric renal failure and decreased creatinine clearance. y Hemoglobin and myoglobin, present in the urine of patients with deep muscle damage often associated with electrical injury, may cause acute tubular necrosis and call for a greater amount of initial fluid therapy and osmotic diuresis.

Pulmonary Changes
y hyperventilation and increased oxygen

consumption are associated with major burns. y The majority of deaths from fire are due to smoke inhalation. y fluid resuscitation and the effects of burn shock on cell membrane potential may cause pulmonary edema, contributing to decreased alveolar exchange. y Initial respiratory alkalosis resulting from hyperventilation may change to respiratory acidosis .

Pulmonary (CO poisoning) y Carbon monoxide

(CO) is a colorless, odorless, tasteless, nonirritating gas produced from incomplete combustion of carbon-containing materials. y Affinity of hemoglobin for CO is 200 times greater than for oxygen.

Hematologic Changes y Release of thromboxane A2 leads to

Thrombocytopenia, abnormal platelet function, depressed fibrinogen levels, inhibition of fibrinolysis, and a deficit in several plasma clotting factors occur postburn. y Anemia results from the direct effect of destruction of red blood cells due to burn injury, reduced life span of surviving red blood cells, and blood loss during diagnostic and therapeutic procedures

Immunologic changepresence of eschar y The loss of the skin barrier and

y

y y y

favor bacterial growth. Hypoxia, acidosis, and thrombosis of vessels in the wound area impair host resistance to pathogenic bacteria. Burn wound sepsis The wound will be fully colonized in 3 to 5 days. Seeding of bacteria from the wound may give rise to systemic septicemia.

Gastrointestinal changes
y As a result of sympathetic nervous system response to

burn trauma, peristalsis decreases, and gastric distention, nausea, vomiting. y Ischemia of the gastric mucosa and other etiologic factors put the burn patient at risk for duodenal and gastric ulcer, manifested by occult bleeding and, in some cases, life-threatening hemorrhage.

Pathophysiology
y Disruption of the skin y The depth of the injury

can lead to:

y increased fluid loss y Infection y Hypothermia y Scarring y Compromised

depends on:
y Temp. of the burning

agent y duration of contact with the agent

immunity y changes in function, appearance, & body image

Pathophysiologic changes
y tissue hypoperfusion y organ hypofunction r/t y Greatest volume of fluid

leak occurs in.

y Onset: 24 to 36 hrs y Peak: 6 to 8 hours

decreased cardiac output y hyperdynamic phase y hypermetabolic phase

Pathophysiologic changes
y As the capillaries begin y If renal and cardiac

to regain their integrity, shock resolves & fluid returns to the vascular compartment. y As fluid is reabsorbed from the interstitial tissue into the vascular compartment, blood volume increases.

function is adequate, urinary output increases.

y Diuresis continues for

several days to 2 weeks.

LOCAL AND SYSTEMIC RESPONSES TO BURNS

y <25% TBSA : local response. y =,>25% TBSA may produce

Complications:
a.Acute Respiratory Failure b.Distributive Shock c.Acute Renal Failure d.Paralytic Ileus e.Curling s Ulcer

both a local & a systemic response

The energy agents that can cause burns are:

The most common type of injuries Varies according to severity The prognosis is better.

either alkaline or acidic, or petroleum based products. (alkaline penetrate more than acidic) painful Identify neutralizing agent

The type of current Duration of contact to electrical source Location of electrical source Causes necrosis in skin , tetany, cardiac dysrhythmias

Thermal injuries

Chemical burns

Electrical injuries

Types of Burns
y Superficial Burn y Partial-Thickness

Burn y Full-Thickness Burn

The following factors are considered in determining the depth of the burn:
y How the injury occurred y Causative agent y Temperature of the burning agent y Duration of contact with the agent y Thickness of the skin

Superficial Burn (First Degree)

y Pink to red: slight

edema, which subsides quickly. y In about 5 days, epidermis peels, heals y Pain may last up to 48 hours; relieved by cooling. y (Sunburn is a typical example.)

Partial-Thickness Burn (Second Degree)

y Pink or red: blisters form y y y y

(vesicles); weeping Takes several weeks to heal. edematous, elastic. Scarring may occur. Superficial layers of skin are destroyed; wound moist and painful.

Full thickness burns

y damage all layers of the skin, which will be white, brown or black and dry, leathery or waxy. y No pain y No blisters y 1 sec of contact with hot tap H2O at 68.9C (156F) y 15 sec of exposure to hot H2O at 56.1C (133F) y Temp. <111F are tolerated for long periods w/o injury.

Extent of Body Surface Area Injured

y rule of nines y the Lund and Browder

method y palm method

PALM METHOD
y For scattered burns, y Palm: approximately 1%

of TBSA.

first priority at the Scene???

prevent injury to the rescuer!!!

There are four major goals relating to burns:

y 1. Prevention y 2. Institution of y 3. Prevention of

lifesaving measures for the severely burned person

disability and disfigurement through early, specialized, individualized Tx:

y dbridement &

excision

y 4. Rehab: through

reconstructive surgery

Emergent/Resuscitative Phase of Burn Injury

y Impaired gas exchange related to carbon monoxide poisoning, smoke inhalation, and upper airway obstruction y Ineffective airway clearance related to edema and effects of smoke inhalation y Fluid volume deficit related to increased capillary permeability and evaporative losses from the burn wound y Hypothermia related to loss of skin microcirculation and open wounds y Pain related to tissue and nerve injury and emotional impact of injury y Anxiety related to fear and the emotional impact of burn injury

First Aid
y y y y y y y y y

Extinguish the flames remove from the source of the thermal injury Maintain an open airway. Control hemorrhage Treat shock Remove constricting jewelry & articles of clothing cover w/ clean sheets or dry dressings DO NOT remove clothing adhering to a wound NPO , side-lying position that will prevent aspiration of vomitus (paralytic ileus )

If the patient is to be transported to a burn center, the following measures are instituted before transfer:

y IVF: LR infusing at the rate

y y y

required to maintain a urine output of at least 30 mL per hour. ensure patent airway Adequate pain relief Adequate peripheral circulation is established in any burned extremity. Insert an indwelling urinary catheter

y Clean sheets are placed under

& over the patient:

y

to protect the area from contamination y maintain body temperature y reduce pain

y Baseline height, weight,

ABGs, Hct, electrolytes, blood alcohol level, drug panel, UA, and chest x-rays are obtained, ECG y tetanus prophylaxis y Provide emotional support

indicators of adequate fluid replacement

y systolic BP > 100 mm Hg y PR <110/minute y Urine Output 30 to 50

mL/hour y Hct (W36-46 ; M 37-49) y Hgb(W 12.0-16.0 g/dl M 13.0-18.0 g/dl) y Serum sodium (135-145 mmol/liter)

Consensus formula: (2 to 4 mL/kg/% TBSA)

y Wt: 70 kgs y 50% BSA y _____(1)____mL/24 hours y Plan to administer:
y First 8 hours = ___(2)___ mL, or

___(3)___ mL/hour
y next 16 hours = ___(4)___ mL, or

___(5)___ mL/hour

Consensus formula: (2 to 4 mL/kg/% TBSA)

y Wt: 70 kgs y 50% BSA y 2 70 50 = 7,000 mL/24 hours y Plan to administer:
y First 8 hours = 3,500 mL, or 437

mL/hour
y next 16 hours = 3,500 mL, or 219

mL/hour

Parkland/Baxter: (4 mL/kg/% TBSA)

y Wt: 90 lbs. y 60% BSA y Plan to administer: y First 8 hrs.: ___(2)___ mL/8hrs or y _____(1)____ mL/24 hours

___(3)___ mL/hour y next 16 hours: ___(4)___ mL/8hrs or ___(5)___ mL/hour y 2nd day: colloids

Parkland/Baxter: (4 mL/kg/% TBSA)

y Wt: 90 lbs. y 60% BSA y Plan to administer: y First 8 hrs.: 10,800 mL/8hrs or y 4 90 60 = 21,600 mL/24 hours

1350mL/hr y next 16 hours: 10,800 mL/8hrs or 675 ml/hr y 2nd day: colloids

 a sudden and almost complete loss of kidney function decreased GFR) over a period of hours to days. Oliguria (less than 400 mL/day of urine) rising serum creatinine BUN levels retention of other metabolic waste products (azotemia)

PHASES OF ACUTE RENAL FAILURE

y Initiation y begins with the initial insult & ends when oliguria develops y Oliguria y accompanied by a rise in the serum conc. of urea, creatinine, uric acid, organic acids, and K & Mg.
y

nonoliguric RF-patients have decreased renal function with increasing nitrogen retention, yet actually excrete normal amounts of urine (2 L/day or more)

y Diuresis y recovery

Diuresis
y Pt. experiences gradually y renal function may still

increasing urine output, which signals that GF has started to recover. y Lab. values stop rising and eventually decrease.

be markedly abnormal. y uremic symptoms may still be present:

y observed closely for

dehydration: uremia are likely to increase.

recovery
y may take 3 to 12 months y Lab. values return to the patient s normal level. y Although a permanent 1% to 3% reduction in the GFR

is common, it is not clinically significant.

Assessment and Diagnostic Findings

y CHANGES IN URINE y Urine output varies (scanty to normal volume) y Hematuria y low specific gravity (1.010 or less) y prerenal azotemia: decreased amount of sodium: (below 20 mEq/L) and normal urinary sediment.
y intrarenal azotemia:

sodium levels greater than 40 mEq/L with casts and other cellular debris y Urinary casts mucoproteins secreted by the renal tubules whenever inflammation is present.

INCREASED BUN AND CREATININE LEVELS (AZOTEMIA)

BUN level
y rises steadily at a rate

Serum creatinine
y rises in conjunction with

dependent on the degree of catabolism, renal perfusion, and protein intake.

glomerular damage.
y useful in monitoring kidney

function & dse. progression

HYPERKALEMIA

CHANGE IN KIDNEY CONTOUR

y UTZ

y oliguria & anuria: greater risk y Protein catabolism y results in the release of

cellular K into the body fluids, causing severe hyperkalemia (high serum K+ levels). y may lead to dysrhythmias and cardiac arrest.

METABOLIC ACIDOSIS

acute oliguria:

cannot eliminate the daily metabolic load of acidtype substances

normal renal buffering mechanisms fail.

fall in the serum CO2combining power and blood pH

progressive metabolic acidosis

renal failure

CALCIUM AND PHOSPHORUS ABNORMALITIES

y Increase serum phosphate levels y low serum calcium levels (r/t decreased absorption of

calcium from the intestine and as a compensatory mechanism for the elevated serum phosphate levels.)

ANEMIA
y r/t reduced erythropoietin production y uremic GI lesions y reduced RBC life span y blood loss, usually from the GI tract. y Tx: parenteral form of erythropoietin (Epogen)

Preventing Acute Renal Failure

y 1. Provide adequate hydration to patients at risk for y y y y

DHN 2. Prevent and treat shock promptly with blood and fluid replacement. 3. Monitor central venous and arterial pressures and hourly urine output of critically ill patients 4. Treat hypotension promptly. 5. Continually assess renal function (urine output, laboratory values) when appropriate.

Preventing Acute Renal Failure

y 6. Ensure that appropriate blood is admin. to the correct pt. in

y y y

order to avoid severe transfusion reactions, which can precipitate renal failure. 7. Prevent and treat infections promptly. 8. Pay special attention to wounds, burns, and other precursors of sepsis. 9. Give meticulous care to patients with indwelling catheters to prevent infections from ascending in the urinary tract. Remove catheters as soon as possible. 10. To prevent toxic drug effects, closely monitor dosage, duration of use, and blood levels of all medications metabolized or excreted by the kidneys.

sodium polystyrene sulfonate [Kayexalate]

y administered orally or by retention enema. y Reduces elevated K levels y works by exchanging a Na ion for a K ion in the

intestinal tract. y Simul. w/ Sorbitol

y diarrhea-type effect

retention enema
y Use a rectal catheter with a balloon y Retain the resin 30 to 45 minutes (to promote K

removal) y Followed w/ a cleansing enema (to remove the y Kayexalate resin as a precaution against fecal impaction)

treating hyperkalemia: emergency & temporary measures

y IV glucose and insulin or calcium gluconate : y Glucose and insulin drive K into the cells, thereby lowering serum K levels temporarily. y K will move out of the cells and rise again to a dangerous level unless removed by dialysis. y calcium gluconate helps protect the heart from the effects of the high K levels. y Sodium bicarbonate y increases the plasma pH y causes K to move into the cell, and the result is lowering of the serum K level. y short-term therapy

treating hyperkalemia:
y All external sources of potassium (foods, salt

substitutes, medications) are eliminated or reduced.

y Bananas y citrus fruits and juices y coffee

COMPLICATIONS

Causes of Diabetes Mellitus

y an absolute or relative lack of insulin that leads to an increase in plasma glucose conc. y a group of metabolic diseases char. by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. y Insulin y a hormone produced by the pancreas, w/c controls the level of glucose in the blood by regulating the production & storage of glucose.

Type I (insulin-dependent DM)

y juvenile DM y absolute lack of insulin y caused by a lesion in the beta

Type II (non-insulindependent DM)

y Maturity-onset y most common y Insulin release can be normal

cells of the pancreas, autoimmune mechanism y genetic disposition.

or even increased, but the target organs have a diminished sensitivity to insulin. y a relative insulin deficiency: the pts are not necessarily dependent on an exogenous supply of insulin.

ACUTE COMPLICATIONS OF DIABETES

y Hypoglycemia (Insulin Reactions) y Diabetic Ketoacidosis y Hyperglycemic Hyperosmolar Nonketotic Syndrome

(HHNS)

HYPOGLYCEMIA (INSULIN REACTIONS)

y blood glucose falls to less

than 50 to 60 mg/dL (2.7 to y 3.3 mmol/L). y caused by too much insulin or oral hypoglycemic agents, too little food, or excessive physical activity.

y midmorning hypoglycemia y occur when the morning regular insulin is peaking y late afternoon hypoglycemia y coincides with the peak of the morning NPH or Lente insulin. y Middle-of-the-night

hypoglycemia
y

peaking evening or predinner NPH or Lente insulins, especially in pts. who have not eaten a bedtime snack.

Clinical Manifestations
mild hypoglycemia
y Sweating y Tremor y Tachycardia y Palpitation y nervousness y hunger.

moderate hypoglycemia: (CNS) symptoms

y inability to concentrate y Headache y Lightheadedness y confusion y memory lapses y Numbness of the lips and

tongue

Clinical Manifestations
moderate hypoglycemia: (CNS) Sx:
y slurred speech y impaired coordination y emotional changes y irrational or combative

severe hypoglycemia
y disoriented behavior y Seizures y difficulty arousing from sleep y loss of consciousness

behavior y double vision y drowsiness

Management
y The usual recommendation is for 15 g of a fast-acting

y y y y

concentrated source of carbohydrate such as the following, given orally: 3-4 commercially prepared glucose tablets 4 to 6 oz of fruit juice or regular soda 6 to 10 Life Savers or other hard candies 2 to 3 teaspoons of sugar or honey

Management
y It is not necessary to add sugar to juice, even if it is labeled as unsweetened juice y The blood glucose level should be retested in 15 minutes and retreated if it is less than 70 to 75 mg/dL (3.8 to 4 mmol/L). y If Sx persist for more than 10 to 15 mins after initial Tx, the Tx is repeated even if blood glucose testing is not possible. y Once the symptoms resolve, a snack containing protein and starch (eg, milk or cheese & crackers) is recommended unless the pt plans to eat a regular meal or snack w/n 30 to 60 minutes.

INITIATING EMERGENCY MEASURES: SC/IM Glucagon

y unconscious and cannot swallow y 1-mg vials and must be mixed with a diluent y take up to 20 minutes for the pt to regain consciousness. y A concentrated source of carbohydrate followed by a snack should be given to the patient on awakening
y Onset: 8 to 10 mins

y duration of the action: 12 to 27 minutes y S/E: nausea (turn pt to the side to prevent aspiration)

25 to 50 mL 50% dextrose in water (D50W): IV

y hypertonic soln y effect is usually seen within minutes. y S/E headache and of pain at the injection site. y Assure patency of the (IV) line

DIABETIC KETOACIDOSIS
y caused by an absence or y 3 main clinical features

markedly inadequate amount of insulin. y results in disorders in the metabolism of carbohydrate, protein, and fat.

of DKA are:
Hyperglycemia y Dehydration and electrolyte loss y Acidosis
y

Three main causes of DKA

y decreased or missed dose of insulin y illness or infection y undiagnosed and untreated diabetes

Pathophysiology
Without insulin, the amount of glucose entering the cells is reduced and the liver increases glucose production: HYPERGLYCEMIA

In an attempt to rid the body of the excess glucose, the kidneys excrete the glucose along with water and electrolytes (eg, Na & K). osmotic diuresis: polyuria

DHN & electrolyte loss. Severe DKA may lose up to 6.5 liters of water and up to 400 to 500 mEq each of Na, K, and Cl over a 24-hour period.

Pathophysiology
insulin deficiency

Brea d n f fat (li lysis) int free fatty acids and lycer l free fatty acids are c nverted int et ne dies y t e liver

meta

lic acid sis

Clinical Manifestations
polyuria and polydipsia blurred vision Weakness Headache marked intravascular volume depletion: orthostatic hypotension (drop in systolic BP of 20 mm Hg or more on standing). y frank hypotension with a weak, rapid pulse y GI symptoms : anorexia, nausea, vomiting, and abdominal pain y acetone breath (a fruity odor)
y y y y y y Hyperventilation: Kussmaul s y very deep, but not labored, respirations y body s attempt to decrease the acidosis, counteracting the effect of the ketone buildup y alert, lethargic, or comatose

Assessment and Diagnostic Findings

y Blood glucose levels may

vary from 300 to 800 mg/dL (16.6 to 44.4 mmol/L). S y Some patients have lower glucose values, & others have values of 1,000 mg/dL (55.5 mmol/L) or more (usually depending on the degree of DHN).

y The severity of DKA is

not necessarily r/t the blood glucose level.

Medical Management: REHYDRATION

y fluid replacement enhances the excretion of excessive glucose by the kidneys. y Pts. may need up to 6 to 10 liters of IVF y Initially, 0.9% normal saline solution is admin. at a rapid rate, usually 0.5 to 1 L per hour for 2 to 3 hours. y Half-strength normal saline (0.45%) solution (hypotonic saline solution) may be used for patients with hypertension or hyperNa or those at risk for heart failure. y After the first few hours, half-normal saline solution is the fluid of choice for continued rehydration, if the blood pressure is stable

RESTORING ELECTROLYTES
y Because the patient s serum potassium level may

drop quickly due to rehydration and insulin treatment, K replacement must begin once K levels drop to normal.

REVERSING ACIDOSIS
y Ketone bodies (acids) accumulate as a result of fat breakdown. y The acidosis that occurs in DKA is reversed with insulin y inhibits fat breakdown, thereby stopping acid buildup. y Insulin IV at a slow, continuous rate (eg, 5 units per hour). y Hourly blood glucose values must be measured y IV fluid solutions with higher concentrations of glucose, such as, normal saline (NS) solution (eg, D5NS or D50.45NS) y Admin. when blood glucose levels reach 250 to 300 mg/dL to avoid too rapid drop in the blood glucose level.

Nursing Management
y Nursing care of the patient with DKA focuses on

y y y y

monitoring fluid and electrolyte status as well as blood glucose levels Administering fluids, insulin, and other medications; prevent fluid overload. Urine output is monitored ECG: Monitor for dysrhythmias

Nursing Management
y V/s, ABGs, and other clinical findings are recorded on

a flow sheet. y As DKA resolves and the K replacement rate is decreased, the nurse makes sure that:
y no signs of hyperkalemia on the ECG (tall, peaked [or

tented] T waves). y lab values of K are normal or low. y patient is urinating (no renal shutdown).

HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME (HHNS)

y hyperosmolarity & hyperglycemia predominate, with

alterations of the sensorium (sense of awareness).

Pathophysiology
basic biochemical defect is: lack of effective insulin (ie, insulin resistance) hyperglycemia : osmotic diuresis

losses of ater and electrolytes To maintain osmotic e uilibrium, ater shifts from the ICF space to the ECF space

glucosuria and dehydration hyperNa and increased osmolarity occur

Risk factors:
y elderly (ages 50 to70) with no known history of

diabetes or with mild type 2 DM. y acute illness (eg, pneumonia or stroke) y medications that exacerbate hyperglycemia (thiazides), or treatments, such as dialysis. y Hx: days to weeks of polyuria with adequate fluid intake.

ketosis and acidosis do not occur in HHNS partly because of differences in insulin levels
DKA: no insulin is present
y This promotes the breakdown

HHNS: the insulin level is too low

y In to prevent hyperglycemia

of stored glucose, protein, and fat

y leads to the production of

(and subsequent osmotic diuresis)

y but it is high enough to prevent

ketone bodies and ketoacidosis.

fat breakdown
y do not have the ketosis related

GI symptoms

Clinical Manifestations
y The blood glucose level

is usually 600 to 1,200 mg/dL y Hypotension y Profound DHN w/ dry mucous membranes, poor skin turgor) y tachycardia

y variable neurologic signs y alteration of sensorium y Seizures y Hemiparesis y hallucinations

Medical Management
y Fluid replacement y correction of electrolyte imbalances y insulin administration. y close monitoring of volume and electrolyte status is important for prevention of fluid overload, heart failure, and cardiac dysrhythmias. y Fluid treatment is started with 0.9% or 0.45% NS, depending on the patient s Na level and the severity of volume depletion. y K is added to IV fluids when: y urinary output is adequate y guided by continuous ECG monitoring y frequent lab. determinations of K.

Medical Management
y Insulin is usually admin, at a continuous slow rate to treat hyperglycemia y replacement IV fluids with dextrose are administered (as in DKA) when the glucose level is decreased to 250 to 300 mg/dL y Treatment is continued until metabolic abnormalities are corrected and neurologic symptoms clear. y It may take 3 to 5 days for neurologic symptoms to resolve y After recovery from HHNS, many patients can control their y diabetes with diet alone or with diet and oral antidiabetic agents.

Nursing Management
y close monitoring of vital y Fluid status and urine

signs, fluid status, and laboratory values. y maintain safety and prevent injury r/t changes in the patient s sensorium

output are closely monitored y careful assessment of cardiovascular, pulmonary, and renal function are important throughout the acute & recovery phases

Thank you