Report in M.S.2(Shock and Burn Injury)

Submitted by Group #1:

Macairan, ELLaserna, Ma. KristineAmbagan, JenniferEscalante, ChelleCruzada, Joan CamilleFlorentino, AngelicaAbayan, AngelicaFederio, Norie JeanLaureta, Rosalyn

Submitted to:Ms. September Nepomuceno; MD, RN

SHOCK characterized by inadequate tissue perfusion that, if untreated, results in cell

death. Systemic blood pressure is inadequate to deliver oxygen and nutrients to support vital organs and cellular function.

Components of adequate blood flow: Adequate cardiac pump Effective vasculature / circulatory system Sufficient blood volume

Classification of Shock

1. Hypovolemic 2. Cardiogenic3. Circulatory / distributive

Septic Neurogenic Anaphylactic

Pathophysiology

SHOCK↓

Cells lack an adequate blood supply↓

anaerobic↓

acidotic intracellular environment↓

Deprived of oxygen & nutrients↓

Cell swell / Permeable cell membrane↓

CELL DEATH

Stages of Shock:

Findings Compensatory Progressive Irreversible

BP normal Sys <80 – 90 mmHg Requires mech./ pharmacological support

HR >100 bpm >150 bpm asystole

RR >20 cpm Rapid, shallow Req. intubation

skin Cold, clammy Mottled, petechiae jaundice

UO decreased 0.5 mL/Kg/Hr anuric

mentation confusion lethargy unconscious

Acid-base balance Respiratory alkalosis Metabolic acidosis Profound jaundice

Precipitating cause of Shock↓

↓ Circulating blood volume↓

↓ Cardiac output↓

Hypotension & ↓ tissue perfusion↓

Baroreceptors stimulated↓

↑ SNS stimulation↓

↑ HR Arterial constriction Venous constriction↑ contractility

↓↑ CO ↑BP ↑ venous return

Types of Shock:

1. Hypovolemic Shock

Decrease in circulating effective blood volume/ loss of circulating blood volume. Occurs when blood loss is 15%-25%

Pathophysiology:Decrease Blood volume

↓Decrease Venous return

↓Decrease Stroke Volume

↓Decrease Cardiac Output

↓Decrease Tissue

Perfusion

Clinical Manifestations:

A. External Fluid losses Trauma Surgery Vomiting/ diarrhea Diuresis Diabetes Insipidus

HemorrhageB. Internal Fluid losses

Ascites Peritonitis Dehydration Burns

Medical Management: Treat the under lying cause Fluid and Blood replacement

- Crystalloids: PNSS, LRS, Hypertonic saline- Colloids: Albumin, Dextran

Redistribution of fluids- Position: Modified Trendelenberg

Pharmacologic Therapy - e.g. Desmopressin for DI- Antidiarrheal drugs- Meds for cardiogenic shock - Oxygen inhalation

Nursing Management:

Monitor patient at the risk for Hypovolemic shock Monitor signs, complication and side effects of the treatment

2. Cardiogenic shock

Ability of the heart to contact & pump blood is impaired

Pathophysiology

↓ Cardiac Contractility↓

↓Cardiac Output↓ ↓ ↓

Pulmonary Congestion ↓Systemic Tissue Perfusion ↓Coronary artery perfusion

Clinical Manifestation Angina pectoris Develop dysrhythmia Hemodynamic instability

Risk Factors M.I. ● Cardiac tamponade Cardio myopathy ● Dysrhythmia Vulvular diseas

Management1. Correct the underlying cause

e.g thrombolytic therapy for M.ICorrect dysrhythmias

2. Initiation of the first line of treatment

a. Oxygen supplementb. Pain Controlc. Fluid supportd. Vasoactive medications

I. DobutamineII. Nitroglycerin III. DopamineIV. Others: Epinephrine, norepinephrineV. Antidysrhythmics medicationsVI. Fluid therapy

3. Bed rest4. Hemodynamic monitoring and assessment of cardiac status5. Enhancement of safety and comfort.

3. Septic Shock shock resulting from infection of the blood by disease-causing microorganism,

most common gram-negative bacteria.

Pathophysiology

Massive vasodilation↓

Decrease venous return↓

Decrease stoke volume↓

Decrease cardiac output↓

Decrease tissue perfusion

2 phases

1. Hyperdynamica. ↑ cardiac output/ vasodilationb. ↑ heart rate / ↑ RRc. warmd. ↑ temperature

2. Hypodynamica. ↓ cardiac output/ vasodilationb. normal heart ratec. normal temperature or coldd. ↓ urine output

Nursing intervention1. admin. Antibiotics2. provide comfort3. admin. Corticosteroids and antipyretics

Risk factors immunocompromised very old/ very young chronic illness malnourished

4. Neurogenic Shock A type of shock (a life-threatening medical condition in which there is insufficient

blood flow throughout the body) that is caused by the sudden loss of signals from the sympathetic nervous system that maintain the normal muscle tone in blood vessel walls.

The blood vessels relax and become dilated, resulting in pooling of the blood in the venous system and an overall decrease in blood pressure.

Neurogenic shock can be a complication of spinal cord injury, spinal anesthesia, or nervous system damage.

Pathophysiology Parasympathetic stimulation

↓Vasodilation

↓Maldistribution of blood volume

↓Decreased venous return

↓Decreased cardiac output

↓Decreased tissue perfusion

Clinical Manifestations↓ BPDry, warm skinBradycardia

Medical Management Restoring sympathetic tone – spinal cord injury, spinal anesthesia. If Hypoglycemia is the cause – administer glucose

Nursing Management Position the patient 30 degrees – spinal anesthesia Elastic compression stockings Monitor for bleeding

5. Anaphylactic Shock occurs rapidly and is life-threatening caused by a severe allergic

reaction when patients who have already produced antibodies to a foreign substance (antigen) develop a systemic antigen-antibody reaction.

most severe type of anaphylaxis.

Antigen - substance that induces the production of antibodies.

Allergy - is an inappropriate and often harmful response of the immune system to normally harmless substance.

Pathophysiology

Antigen/Allergen enters the body↓

Triggers B-cell to make IgE antibody↓

IgE antibody attaches to the mast cell↓

When that antigen reappears, it binds to the IgE↓

release chemical mediators (degranulation) ↓

Massive vasodilation↓

Decrease venous return↓

Decrease stoke volume↓

Common Causes of Anaphylaxis

Foods Peanuts, tree nuts (walnut, pecans, cashews, almonds) shellfish (shrimp, lobster, crab), fish, milk, eggs, soy, wheat.

Medications Antibiotics, especially penicillin and sulfa antibiotics, allopurinol, radiocaontrast agents, anesthetic agents (lidocane, procane) vaccines, hormones (insulin, vasopressin, adrenocorticotropic hormone [ACTH], aspirin, nonsteroidal anti-inflammatory drugs [NSAIDs]).

Other Pharmaceutical/Biologic Agents Animal serums (tetanus antitoxin, snake venom antitoxin, rabies antitoxin), antigens used in skin testing.

Insect stings Bees, Wasps, hornets, yellow jackets, ants, including fire ants.

Latex Medical and nonmedical products containing latex

Decrease cardiac output↓

Decrease tissue perfusion

Histamine Induces vasodilation of arterioles or causes the blood vessel to dilate (which

lowers the blood pressure) fluid to leak from the bloodstream into the tissues (which lowers the blood

volume) and can leak into the alveoli (air sacs) of the lungs, causing pulmonary edema.

bronchial smooth muscle contraction resulting to bronchospasm.  - increased secretion of gastric and mucosal cells, resulting in diarrhea.

Prostaglandin produce smooth muscle dilation as well as vasodilation and increased capillary

permeability results in edema. fever and pain that occur with inflammation  in allergic responses are due in part

to the prostaglandins.

Leukotrienes cause smooth muscle contraction, bronchial constriction, mucus

secretion in the airways and the typical wheal-and-flare reaction of the skin. compared with histamine, leukotrienes are 100 to 1000 times

more potent in causing bronchospasm.Bradikinin

cause increase vascular permeability vasodilation, hypotension and contraction of many types of smooth muscle.

stimulates nerve fibers and produces pain.Serotonin

potent vasoconstrictor and causes contraction of bronchial smooth muscle.

Clinical Manifestations Difficulty of breathing ↓ BP ↓ tissue perfusion Cyanosis Lethargy

Diagnostic Evaluation History of allergy Complete blood count and eosinophil count Total serum immunoglobulin E levels Skin test

Medical Management Epinephrine - epinephrine is given for its vasoconstrictive action. Diphenhydramine (Benadryl) - is administered to reverse the effects of

histamine. Nebulized medications such as albuterol (proventil), may be given to reverse

histamine-induced bronchospasm.

If Cardiac arrest or Respiratory arrest are imminent or occured, cardiopulmonary resuscitation (CPR) is performed.

Endotracheal intubation or tracheotomy may be necessary to establish airway. IV lines are inserted to provide access for administering fluids and medications.

Nursing Management The nurse must assess all patients for allergies or previous reactions to antigens

and communicate the existence of these allergies or reactions to others. When new allergies are identified, the nurse advises the patient to wear or carry

identification that names the specific allergen or antigen.

Allergy to penicillin is one of the most common causes of anaphylactic shock patients who have a penicillin allergy may also develop an allergy to similar medications. (e.g cefazolin sodium [Ancef]).

The nurse must be knowledgeable about the clinical signs of anaphylaxis, must take immediate action if signs and symptoms occur, and must be prepared to begin CPR if cardio-respiratory occurs.

Community health and home care nurses who administer medications, including antibiotic agents, in the patients home or other settings, must be prepared to administer epinephrine subcutaneously or intramuscularly in the event of an anaphylactic reaction.

BURN INJURY

Burns are caused by transfer of energy from the heat source to the body. The depth of the injury depends on the temperature of the burning agent and

duration of contact with it. Burns are categorized as thermal (including electrical burns), radiation, or

chemical burns. They disrupt the skin, which leads to increased fluid loss, infection, hypothermia,

scarring, compromised immunity, and changes in function, appearance and body image.

Incidence of burn Injury

Most Burn injuries occur in home, usually in the kitchen while cooking and in the bathroom by means of scalds improper use in electrical appliances around water sources.

Careless cooking in one of the leading causes of household fires.

Classification of Burns

Burn injuries are described according to the depth of the injury and the extent of body surface area injured.

Burn Depth

The depth of a burn injury depends on the type of injury, causative agent, temperature of the burn agent, and the skin thickness.

Burns are classified according to depth of tissue destruction:

Characteristic of Burns According to Depth

Depth Of burn and causes

Skin involvement

Symptoms Wound appearance

Recuperative course

Superficial Partial Thickness (Similar to First degree)

Causes Sunburn Low-

intensity flash

Epidermis, possibly a potion of dermis

Tingling Hyperesthesia(super sensitivity) Pain that

soothed by cooling

Reddened; blanches with pressure; dry

Minimal or no edema Possible blisters

Complete recovery within a week; no scaring peeling

Deep Partial Thickness(Similar to Second degree)

Causes Scald Flash flame

Epidermis; upper dermis portion of deeper dermis

Pain Hyperesthesia Sensitive to

cold air

Blistered, Mottled red

base Broken

epidermis Weeping

surface edema

Recovery in 2 to 4 weeks some scarring and depigmentation contractures infection may convert it to full to full thickness

Full- thickness(Similar to Third degree)

Causes Flame Prolonged

exposure to hot liquids

Electric current

Chemical

Epidermis ; entire dermis, and sometimes subcutaneous tissue: may involve connective tissue , muscle and bone

Pain free Shock Hematuria

Dry Pale white

leathery ; or charred

Broke skin with fat exposed

edema

Eschar sloughs

Grafting necessary

Scarring and loss of control of contour and function; contracture

Loss of digits or extremity possible

TBSA

Total Body Surface Area in adult is arrived at by sectioning the body surface into areas with numerical value related to nine.

Note: the anterior and posterior head total 9℅ of TBSA In burn victims, the total estimated percentage of TBSA injured is used to

calculate the patient’s fluid replacement needs.

Rule of Nines

An estimation of the TBSA involved in a burn is simplified by using rule of nines The rule of nines is quick way to calculate the extent of burns The system assigns percentages in multiples of nine to major body surfaces.

Lund and Browder Method

A more precise method, which recognize that the percentage of TBSA of various anatomic parts , especially the head and legs, and changes with growth

By dividing the body into very small areas and providing an estimate of proportion of TBSA a accounted for by such body parts, one can obtain a reliable estimate of the TBSA burned.

Palm Method

In patient with scattered burns, a method to estimate the percentage of burn is the palm method

The size of the patient’s palm is approximately 1℅ of TBSA.

Electrical burns

Is the electricity travels through areas of at least resistance and destroys everything in its path, nerves and blood vessels first.

An electrical injury results when a current of electricity travels through the body and exits to the ground itself.

Pathophysiology :Energy transfer from heat source

↓Heat transfer through conduction

↓Burns categorized radiation/chemical

↓Tissue destruction result to coagulation

↓Protein denaturation

↓Ionization of cellular contents

↓Skin and mucosa in the upper airways

Manifestation:

  First degree

Tingling Hyperesthesia Pain

  Second degree

Scald Flash flame Blister formation Pain Hyperesthesia Sensitive to cold

  Third degree

Pale appearance Lethargy Contracture Grafting Loss of digits

  

Pulmonary alterations

 -Inhalation injury necessitates prolonged hospitalization and is a major cause of morbidity and mortality in patient with burn injury

Pathophysiology

Inhalation injury↓

Burning structure↓

Or involve in an explosion↓

Inhalation in Super heated air

↓Noxious gases

 

   Manifestation:

Hypoxia Hyper metabolism Chest constriction Stress

Diagnostic test

Serum carboxy-hemoglobin level ABG levels Fiberoptic Bronchoscopy Xenon 133 (133xe)

 Nursing management:

Monitor vital signs Observe patient for at least 24 hrs for respiratory complication

Medical management:

Early intubation and mechanical ventilation with 100% oxygen

Renal Alteration

Renal function may be alter as a result to decrease blood volume. Destruction of the red blood cells at the injury site results in free hemoglobin in the

urine. Adequate fluid volume replacement restores renal blood flow, increasing the

glomerular filtration rate and volume 

Immunologic Alteration

The immunologic defences of the body are greatly altered by burn injury Sepsis- the leading cause of mordbidity in patient with thermal injuries

Thermoregulatory Alteration

Loss of skin also result in an inability to regulate body temperature Patient with burn injuries may therefore exhibit low body temperature in the early

hours after injury Then, as hypermetabolism reset low temperature, the patient become hyperthermic

for much of the post burn period, even in the absence of infection.

Gastrointestinal   Alteration

   2 potential GI complications may occur:

1.       Paralytic ileus2.       Curling’s ulcers

Manifestation:

Decrease peristalsis and bowel sound Gastric distention and nausea Gastric bleeding secondary to massive physiologic stress Hypertension Difficulty with ventilation

Diagnostic procedure:

Laparotomy or abdominal trap

3 components of GI tract are altered after burn injury

1.       The mucosal barriers becomes permeable2.       The permeability allows for over growth of GI bacteria3.       The bacteria traslocate to other organs, causing indection

PHASES OF BURN CARE

1. Emergent/Resuscitative Phase of Burn Care

Duration From the onset of injury to completion of fluid resuscitation

Priorities First aid Prevention of shock Prevention of respiratory distress Detection and treatment of concomitant injuries Wound assessment and initial care

Emergency procedures at the burn scene Extinguish the flames Cool the burn Remove restrictive objects Cover the wound Irrigate chemical burns

Medical management Transport the patient to the nearest emergency department Check for ABC'S Patent airway is ensured Adequate peripheral circulation is established in any burned extremity Assess for cervical spinal injuries or head injury All clothing and jewelries are removed and other accessories such as contact

lenses Adequate pain reliever is attained All assessment and treatments are documented

Criteria for classifying the extent of Burn injury

Minor burn injury Second-degree burn less than 15% total body surface area (TSBA) in adults or

less than 10% TSBA in children Third-degree burn of less than 2% TSBA not involving special care areas Excludes electrical injury, inhalation injury, concurrent trauma, all poor-risk

patients.

Moderate, uncomplicated burn injury Second-degree burns of 15%-25% TSBA in adults or 10%-20% in children Third-degree burns of less than 10% TSBA not involving special care areas Excludes electrical injury, inhalation injury, concurrent trauma, all poor-risk

patient.

Major burn injury Second-degree burns exceeding 25%TSBA in adults or 20% in children All third-degree burns exceeding 10% TSBA All burns involving eyes, ears, face, hands, perineum, joints All inhalation injury, electrical injury, concurrent trauma, all poor-risk patients

Guidelines and Formulas for Fluid Replacement in Burn Patient

Consensus Formula LR's sol. Or other balanced saline sol. (2-4ml x kg of body wt. x % TSBA burn) Half to be given at first 8 hrs; remaining half over next 16 hrs.

Evans Formula1. Colloids: 1 ml x kg BW x % TSBA burned2. Electrolytes (saline): 1 ml x BW x % TSBA burned3. Glucose (5% in water): 2,000 ml for insensible loss

Day 1: Half to be given at first 8hrs; remaining half over next 16hrs. Day 2: Half of previous day's colloids and electrolytes; all of insensible fluid replacement.

Maximum of 10,000 ml over 24hrs. Second-and third-degree burns (partial-and full-thickness) burns exceeding 50% TSBA are calculated on the basis of 50% TSBA.

Brooke Army Formula1. Colloids: 0.5 ml x kg BW x % TSBA burned2. Electrolytes (Lactated Ringer's sol.): 1.5 ml x kg BW x % TSBA burned3. Glucose (5% in water): 2,000 ml for insensible loss

Day 1: Half to be given at first 8hrs; remaining half over next 16hrs. Day 2: Half of colloids; half of electrolytes; all of insensible fluid replacement.

Second- and third-degree (partial- and full-thickness) burns exceeding 50% TSBA are calculated on the basis of 50% TSBA.

Parkland/Baxter FormulaLactated Ringer's solution: 4 ml x kg BW x % TSBA burned

Day 1: Half to be given at first 8hrs; remaining half over next 16hrs. Day 2: Varies. Colloid is added.

Parkland/Baxter FormulaLactated Ringer's solution: 4 ml x kg BW x % TSBA burned

Day 1: Half to be given at first 8hrs; remaining half over next 16hrs. Day 2: Varies. Colloid is added.

Hypertonic Saline Solution1. Concentrated sol. of (NaCl) and lactate w/ concentration of 250-300 mEq of Na per liter, administered at a rate sufficient to maintain a desired volume of urinary output. 2. Do not ↑ the infusion rate during the first 8hrs. of post-burn3. Serum Na levels must be monitored closely.

Goal: increase serum sodium (Na) level and osmolality to reduced edema and prevent pulmonary complications.

2. Acute or Intermediate Phase of Burn Care

Usually begins 48 to 72 hours after the time of injury. Begins when the client is hemodynamically stable, capillary permeability is

restored, and diuresis has begun. Emphasis during this phase is placed on restorative therapy, and the phase

continues until wound closure is achieved.

Infection PreventionA.Hydrotherapy- The form of shower carts, individuals showers, and bed baths can be used to clean the wound.

The temperature of the water is maintained at 37.8 c (100 f). The temperature of the room should be maintained between 26.6 c

and 29.4 c (80 to 85 f). Duration is 20 to 30 minutes.

B.Wound Dressing- The burned areas are patted dry and the prescribed topical agent is applied.

Light dressing is used over joint areas to allow for motion.

Circumferential dressing should be applied distally to proximally. If the hand or foot is burned, the fingers and toes should be wrapped

individually. Burns to the face may be left open to air once they have been cleaned

and the topical agent has been applied.

C.Wound Debridement 1. To remove tissue contaminated by bacteria and foreign bodies, thereby protecting the patient from invasion of bacteria 2. To remove devitalized tissue or burn eschar in preparation for grafting and wound healing

A. Natural Debridement –the dead tissue separates from the underlying viable tissue spontaneously. B. Mechanical Debridement –Using surgical scissors and forceps to separate and remove the eschar C. Surgical Debridement- Is an operative involving either primary excision (surgical removal of tissue) of the full thickness of the skin down to the fascia or shaving the burned skin layers gradually down to freely bleeding, viable tissue.

Grafting the Burn Wound 1. To prevent further loss of protein, fluid and electrolytes 2. To prevent heat loss through evaporation 3. To prevent further infection

Topical antibacterial agents

silver sulfadiazine 1% (Silvadene) water soluble cream mafenide acetate 5% to 10% (sulfamylon) hyrophilic-based cream silver nitrate 0.5% aqueous solution

Biologic Dressing- Temporary immediate coverage for clean, superficial burns- Decrease the wounds evaporative water and protein loss- Promote healing and prepared the skin for grafting.

Homograft (allografts)-skin coming from humans Heterograft (xenografts)-skin coming from animals Alloderm-Another promising dermal substitute

Integra-Newest type of biologic dressing 2 layers:

epidermal layer-consisting of silastic acts as bacterial barrier and prevents water loss from the dermis

Dermal layer-composed of animal collagen

Pain ManagementMorphine sulfate-Analgesic of choice, treatment of acute burn painFentanyl-another useful opioid for burn pain particularly procedural burn pain

Disorders of Wound Healing

- Scars-one of the most devastating sequelae of a burn injury is the formation of hyper tropic scars

- Keloid- large heaped up mass of scars tissue, may develop and extend beyond the wound surface.

- Failure to heal- contractures-the burn wound tissue shorten because of the

force excerted by the fibroblast and the flexion pf muscles in natural wound healing.

3. Rehabilitation Phase of Burn Care Duration: Start with wound closure and ends when client reaches high level of

health restoration, may take years.

Biopsychosocial adjustment by client a. Prevention of contractures and scars b. Client returns to work, family and social roles c. May include vocational, occupational, physical and psychosocial rehabilitation.