Acute biologic crisis-2BY: tmr

Incidence of Burn Injury

burn injury risk factorsYoung children and elderly people : high riskToddlers: scalds school-age children : matchesteenage boys: electrical injuryAdults: smokingusually in the kitchen & bathroominappropriate use of gasoline

PathophysiologyHeat may be

transferred through conduction or electromagnetic radiation.

Tissue destruction results from coagulation, protein denaturation, or ionization of cellular contents.

The skin and the mucosa of the upper airways are the sites of tissue destruction.

Deep tissues, including the viscera, can be damaged by electrical burns or through prolonged contact with a heat source.

PathophysiologyPlasma loss and vascular responsesIntravascular volume lossDiminished tissue perfusionRelease of vasoactive agentsCapillary semipermiability LostMoving of fluids and substances like

proteins from the intravascular to interstitial space

Hyperemiahypovolemia

Hemodynamic changes Lessened circulating blood volume results in

decreased cardiac output initially and increased pulse rate.

There is a decreased stroke volume as well as a marked rise in peripheral resistance (due to constriction of arterioles and increased hemoviscosity).

This results in inadequate tissue perfusion, which may in turn cause acidosis, renal failure, and irreversible burn shock.

Hemodynamic Electrolyte imbalance may also occur. Hyponatremia usually occurs during the 3rd

to 10th day due to fluid shift. 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

Catecholamine release appears to be the major mediator of the hypermetabolic response to burn injury.

"Burn fever" is common and is dependent on depth of burn and percentage of TBSA involved. Temperatures of 102°F to 103°F (38.8°C–39.4°C) are common as "fever spikes."

Healing a large surface area requires much energy; glucose is the primary metabolic fuel.

Metabolic changeBecause total body glucose stores are limited and stored liver and muscle glycogen is exhausted within the first few days postburn, hepatic glucose synthesis (gluconeogenesis)

Despite all nutritional support, it is almost 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 Glomerular filtration may be decreased in

extensive injury. Without resuscitation or with delay,

decreased renal blood flow may lead to high oliguric renal failure and decreased creatinine clearance.

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 hyperventilation and increased oxygen

consumption are associated with major burns.

The majority of deaths from fire are due to smoke inhalation.

fluid resuscitation and the effects of burn shock on cell membrane potential may cause pulmonary edema, contributing to decreased alveolar exchange.

Initial respiratory alkalosis resulting from hyperventilation may change to respiratory acidosis .

Pulmonary (CO poisoning) Carbon monoxide (CO) is a colorless, odorless, tasteless, nonirritating gas produced from incomplete combustion of carbon-containing materials.

Affinity of hemoglobin for CO is 200 times greater than for oxygen.

Hematologic ChangesRelease 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.

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 changeThe loss of the skin barrier and presence

of eschar 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 changesAs a result of sympathetic nervous system

response to burn trauma, peristalsis decreases, and gastric distention, nausea, vomiting.

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.

PathophysiologyDisruption of the

skin can lead to: increased fluid lossInfectionHypothermiaScarringCompromised

immunitychanges in function,

appearance, & body image

The depth of the injury depends on:Temp. of the

burning agent duration of contact

with the agent

Pathophysiologic changes

tissue hypoperfusionorgan hypofunction

r/t decreased cardiac output

hyperdynamic phasehypermetabolic

phase

Greatest volume of fluid leak occurs in. Onset: 24 to 36 hrsPeak: 6 to 8 hours.

Pathophysiologic changes

As the capillaries begin to regain their integrity, shock resolves & fluid returns to the vascular compartment.

As fluid is reabsorbed from the interstitial tissue into the vascular compartment, blood volume increases.

If renal and cardiac function is adequate, urinary output increases. Diuresis continues

for several days to 2 weeks.

LOCAL AND SYSTEMIC RESPONSESTO BURNS

Complications:

<25% TBSA : local response.

=,>25% TBSA may produce both a local & a systemic response

a.Acute Respiratory Failure

b.Distributive Shockc.Acute Renal Failured.Paralytic Ileuse.Curling’s Ulcer

The energy agents that can cause burns are:

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

Thermal injuries

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

Chemical burns

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

Electrical injuries

Types of Burns

Superficial BurnPartial-Thickness

BurnFull-Thickness

Burn

The following factors are considered in determining the depth of the burn:

• How the injury occurred• Causative agent• Temperature of the burning agent• Duration of contact with the agent• Thickness of the skin

Superficial Burn (First Degree)Pink to red: slight

edema, which subsides quickly.

In about 5 days, epidermis peels, heals

Pain may last up to 48 hours; relieved by cooling.

(Sunburn is a typical example.)

Partial-Thickness Burn (Second Degree)

Pink or red: blisters form (vesicles); weeping

Takes several weeks to heal.

edematous, elastic.Scarring may occur.Superficial layers of

skin are destroyed; wound moist and painful.

Full thickness burnsdamage all layers of the

skin, which will be white, brown or black and dry, leathery or waxy. No painNo blisters

1 sec of contact with hot tap H2O at 68.9°C (156°F)

15 sec of exposure to hot H2O at 56.1°C (133°F)

Temp. <111°F are tolerated for long periods w/o injury.

Extent of Body Surface Area Injured

rule of ninesthe Lund and

Browder methodpalm method

PALM METHODFor scattered burns, Palm: approximately

1% of TBSA.

first priority at the Scene???

prevent injury to the rescuer!!!

There are four major goals relating to burns:1. Prevention2. Institution of

lifesaving measures for the severely burned person

3. Prevention of disability and disfigurement through early, specialized, individualized Tx:débridement &

excision4. Rehab: through

reconstructive surgery

Emergent/Resuscitative Phaseof Burn InjuryImpaired gas exchange

related to carbon monoxide poisoning, smoke inhalation, and upper airway obstruction

Ineffective airway clearance related to edema and effects of smoke inhalation

Fluid volume deficit related to increased capillary permeability and evaporative losses from the burn wound

Hypothermia related to loss of skin microcirculation and open wounds

Pain related to tissue and nerve injury and emotional impact of injury

Anxiety related to fear and the emotional impact of burn injury

First AidExtinguish the flamesremove  from  the source of the thermal injuryMaintain  an  open  airway. Control hemorrhageTreat shockRemove  constricting  jewelry &  articles of

clothingcover  w/ clean sheets  or dry dressingsDO  NOT  remove  clothing adhering  to  a  woundNPO , side-lying position that will prevent

aspiration of vomitus (paralytic ileus )

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

IVF: LR infusing at the rate 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

Clean sheets are placed under & over the patient:to protect the area from

contaminationmaintain body temperaturereduce pain

Baseline height, weight, ABGs, Hct, electrolytes, blood alcohol level, drug panel, UA, and chest x-rays are obtained, ECG

tetanus prophylaxisProvide emotional support

indicators of adequate fluid replacement

systolic BP > 100 mm Hg

PR <110/minuteUrine Output 30 to 50

mL/hourHct (W36-46 ; M 37-

49)Hgb(W 12.0-16.0 g/dl

M 13.0-18.0 g/dl)Serum sodium (135-

145 mmol/liter)

Consensus formula:(2 to 4 mL/kg/% TBSA)Wt: 70 kgs50% BSA _____(1)____mL/24 hours

Plan to administer:

First 8 hours = ___(2)___ mL, or ___(3)___ mL/hour

next 16 hours = ___(4)___ mL, or ___(5)___ mL/hour

Consensus formula:(2 to 4 mL/kg/% TBSA)Wt: 70 kgs50% BSA 2 × 70 × 50 = 7,000 mL/24 hours

Plan to administer:

First 8 hours = 3,500 mL, or 437 mL/hour

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

Parkland/Baxter: (4 mL/kg/% TBSA)Wt: 90 lbs.60% BSA

_____(1)____ mL/24 hours

Plan to administer: First 8 hrs.: ___(2)___

mL/8hrs or ___(3)___ mL/hour

next 16 hours: ___(4)___ mL/8hrs or ___(5)___ mL/hour

2nd day: colloids

Parkland/Baxter: (4 mL/kg/% TBSA)Wt: 90 lbs.60% BSA

4 × 90 × 60 = 21,600 mL/24 hours

Plan to administer: First 8 hrs.: 10,800 mL/8hrs

or1350mL/hr

next 16 hours: 10,800 mL/8hrs or 675 ml/hr

2nd day: colloids

Acute kidney injury• 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 FAILUREInitiation

begins with the initial insult & ends when oliguria develops

Oliguriaaccompanied by a rise in the serum conc. of urea,

creatinine, uric acid, organic acids, and K & Mg. nonoliguric RF-patients have decreased renal function

with increasing nitrogen retention, yet actually excrete normal amounts of urine (2 L/day or more)

Diuresisrecovery

DiuresisPt. experiences

gradually increasing urine output, which signals that GF has started to recover.

Lab. values stop rising and eventually decrease.

renal function may still be markedly abnormal.

uremic symptoms may still be present:observed closely for

dehydration: uremia are likely to increase.

recoverymay take 3 to 12 monthsLab. values return to the patient’s normal

level. Although a permanent 1% to 3% reduction in

the GFR is common, it is not clinically significant.

Assessment and Diagnostic FindingsCHANGES IN URINE

Urine output varies (scanty to normal volume)

Hematuria low specific gravity

(1.010 or less)prerenal azotemia:

decreased amount of sodium: (below 20 mEq/L) and normal urinary sediment.

intrarenal azotemia: sodium levels greater than 40 mEq/L with casts and other cellular debris

Urinary casts -mucoproteins secreted by the renal tubules whenever inflammation is present.

INCREASED BUN AND CREATININE LEVELS (AZOTEMIA)

BUN level Serum creatininerises steadily at a rate

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

rises in conjunction with glomerular damage.

useful in monitoring kidney

function & dse. progression

HYPERKALEMIA CHANGE IN KIDNEY CONTOUR

oliguria & anuria: greater risk

Protein catabolism results in the release of

cellular K into the body fluids, causing severe hyperkalemia (high serum K+ levels).

may lead to dysrhythmias and cardiac arrest.

UTZ

METABOLIC ACIDOSIS

acute oliguria:

cannot eliminate the daily metabolic

load of acid-type

substances

normal renal

buffering mechanisms fail.

fall in the serum CO2-

combining power and blood pH

progressive

metabolic acidosis

renal failure

CALCIUM AND PHOSPHORUS ABNORMALITIES

Increase serum phosphate levels

low serum calcium levels (r/t decreased absorption of calcium from the intestine and as a compensatory

mechanism for the elevated serum phosphate levels.)

ANEMIAr/t reduced erythropoietin productionuremic GI lesionsreduced RBC life spanblood loss, usually from the GI tract.

Tx: parenteral form of erythropoietin (Epogen)

Preventing Acute Renal Failure

1. Provide adequate hydration to patients at risk for 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.

6. Ensure that appropriate blood is admin. to the correct pt. in 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 metabolizedor excreted by the kidneys.

Preventing Acute Renal Failure

sodium polystyrene sulfonate [Kayexalate]

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

the intestinal tract. Simul. w/ Sorbitol

diarrhea-type effect

retention enema

Use a rectal catheter with a balloon Retain the resin 30 to 45 minutes (to promote

K removal)Followed w/ a cleansing enema (to remove

theKayexalate resin as a precaution against fecal

impaction)

treating hyperkalemia: emergency & temporary measures

IV glucose and insulin or calcium gluconate :

Glucose and insulin drive K into the cells, thereby lowering serum K levels temporarily.K will move out of the

cells and rise again to a dangerous level unless removed by dialysis.

calcium gluconate helps protect the heart from the effects of the high K levels.

Sodium bicarbonate

increases the plasma pH

causes K to move into the cell, and the result is lowering of the serum K level.

short-term therapy

treating hyperkalemia:All external sources of potassium (foods,

salt substitutes, medications) are eliminated or reduced.Bananascitrus fruits and juicescoffee

Diabetes MellitusCOMPLICATIONS

Causes of Diabetes Mellitusan absolute or relative lack of insulin that leads to an

increase in plasma glucose conc.

a group of metabolic diseases char. by hyperglycemia resulting from defects in insulin secretion, insulin

action, or both.

Insulina 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)

Type II (non-insulin-dependent DM)

juvenile DMabsolute lack of

insulincaused by a lesion in the

beta cells of the pancreas, autoimmune mechanism

genetic disposition.

Maturity-onsetmost commonInsulin release can be

normal or even increased, but the target organs have a diminished sensitivity to insulin.

a relative insulin deficiency: the pts are not necessarilydependent on an exogenous supply of insulin.

ACUTE COMPLICATIONS OF DIABETESHypoglycemia (Insulin Reactions)Diabetic KetoacidosisHyperglycemic Hyperosmolar Nonketotic

Syndrome (HHNS)

HYPOGLYCEMIA (INSULIN REACTIONS)

blood glucose falls to less than 50 to 60 mg/dL (2.7 to

3.3 mmol/L). caused by too much

insulin or oral hypoglycemic agents, too little food, or excessive physical activity.

midmorning hypoglycemia occur when the morning

regular insulin is peakinglate afternoon hypoglycemia

coincides with the peak of the morning NPH or Lente insulin.

Middle-of-the-night hypoglycemia peaking evening or

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

Clinical Manifestationsmild hypoglycemia

moderate hypoglycemia:(CNS) symptoms

SweatingTremorTachycardiaPalpitationnervousnesshunger.

inability to concentrateHeadacheLightheadednessconfusionmemory lapsesNumbness of the lips

and tongue

Clinical Manifestationsmoderate hypoglycemia:(CNS) Sx:

severe hypoglycemia

slurred speechimpaired coordinationemotional changesirrational or combative

behaviordouble visiondrowsiness

disoriented behaviorSeizuresdifficulty arousing from

sleeploss of consciousness

ManagementThe usual recommendation is for 15 g of a

fast-acting 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

ManagementIt is not necessary to

add sugar to juice, even if it is labeled asunsweetened juice

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).

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.

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 Glucagonunconscious and cannot

swallow1-mg vials and must be

mixed with a diluent take up to 20 minutes

for the pt to regain consciousness.

A concentrated source of carbohydrate followed by a snack should be given to the patient on awakening

Onset: 8 to 10 minsduration of the

action: 12 to 27 minutes

S/E: nausea (turn pt to the side to prevent aspiration)

25 to 50 mL 50% dextrose in water (D50W): IVhypertonic solneffect is usually seen within minutes. S/E headache and of pain at the injection site. Assure patency of the (IV) line

DIABETIC KETOACIDOSIScaused by an

absence or markedly inadequate amount of insulin.

results in disorders in the metabolism of carbohydrate, protein, and fat.

3 main clinical features of DKA are:• Hyperglycemia• Dehydration and

electrolyte loss• Acidosis

Three main causes of DKA

decreased or missed dose of insulinillness or infectionundiagnosed 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

•Breakdown of fat (lipolysis) into free fatty acids and glycerol•free fatty acids are converted into ketone bodies by the liver

•metabolic acidosis

Clinical Manifestationspolyuria and polydipsia blurred visionWeaknessHeadachemarked intravascular volume

depletion: orthostatic hypotension (drop in systolic BP of 20 mm Hg or more on standing).

frank hypotension with a weak, rapid pulse

GI symptoms : anorexia, nausea, vomiting, and abdominal pain

acetone breath (a fruity odor)

Hyperventilation: Kussmaul’svery deep, but not

labored, respirationsbody’s attempt to

decrease the acidosis, counteracting the effect of the ketone buildup

alert, lethargic, or comatose

Assessment and Diagnostic Findings

Blood glucose levels may vary from 300 to 800 mg/dL (16.6 to 44.4 mmol/L). S

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).

The severity of DKA is not necessarily r/t the blood glucose level.

Medical Management: REHYDRATIONfluid replacement

enhances the excretion of excessive glucose by the kidneys.

Pts. may need up to 6 to 10 liters of IVF

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.

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.

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

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 ACIDOSISKetone bodies (acids)

accumulate as a result of fat breakdown.

The acidosis that occurs in DKA is reversed with insulininhibits fat breakdown,

thereby stopping acid buildup.

Insulin IV at a slow, continuous rate (eg, 5 units per hour).

Hourly blood glucose values must be measured

IV fluid solutions with higher concentrations of glucose,such as, normal saline (NS) solution (eg, D5NS or D50.45NS)Admin. when blood

glucose levels reach 250 to 300 mg/dL to avoid too rapid drop in the blood glucose level.

Nursing ManagementNursing care of the patient with DKA focuses

on monitoring fluid and electrolyte status as well as blood glucose levels

Administering fluids, insulin, and other medications;

prevent fluid overload. Urine output is monitoredECG: Monitor for dysrhythmias

Nursing ManagementV/s, ABGs, and other clinical findings are

recorded on a flow sheet. As DKA resolves and the K replacement rate

is decreased, the nurse makes sure that:no signs of hyperkalemia on the ECG (tall,

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

HYPERGLYCEMIC HYPEROSMOLARNONKETOTIC SYNDROME (HHNS)

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 water and electrolytes•To maintain osmotic equilibrium, water shifts from the ICF space to the ECF space

•glucosuria and dehydration•hyperNa and increased osmolarity occur

Risk factors:

elderly (ages 50 to70) with no known history of diabetes or with mild type 2 DM.

acute illness (eg, pneumonia or stroke)medications that exacerbate hyperglycemia

(thiazides), or treatments, such as dialysis.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

HHNS: the insulin level is too low

This promotes the breakdown of stored glucose, protein, and fat

leads to the production of ketone bodies and ketoacidosis.

In to prevent hyperglycemia(and subsequent osmotic diuresis)

but it is high enough to prevent fat breakdown

do not have the ketosis related

GI symptoms

Clinical ManifestationsThe blood glucose

level is usually 600 to 1,200 mg/dL

HypotensionProfound DHN w/

dry mucous membranes, poor skin turgor)

tachycardia

variable neurologic signs alteration of

sensoriumSeizuresHemiparesishallucinations

Medical ManagementFluid replacementcorrection of

electrolyte imbalancesinsulin administration. close monitoring of

volume and electrolyte status is important for prevention of fluid overload, heart failure, and cardiac dysrhythmias.

Fluid treatment is started with 0.9% or 0.45% NS, depending on the patient’s Na level and the severity of volume depletion.

K is added to IV fluids when: urinary output is

adequateguided by continuous ECG

monitoring frequent lab.

determinations of K.

Medical ManagementInsulin is usually admin,

at a continuous slow rate to treat hyperglycemia

replacement IV fluids with dextrose are administered (as in DKA) when the glucose level is decreased to 250 to 300 mg/dL

Treatment is continued until metabolic abnormalities are corrected and neurologic symptoms clear.

It may take 3 to 5 days for neurologic symptoms to resolve

After recovery from HHNS, many patients can control their

diabetes with diet alone or with diet and oral antidiabetic agents.

Nursing Managementclose monitoring of

vital signs, fluid status, and laboratory values.

maintain safety and prevent injury r/t changes in the patient’s sensorium

Fluid status and urine output are closely monitored

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

End…Thank you…