Burns PDF

# Burns - Classified by: - Etiology - Thermal: flash, scald (house fire, cooking accidents) - Electrical: arc between 2 objects - Chemical: 3% of all admissions (both household and industrial) - Radiation: least common, severity depends on location, depth, length...

# Burns - Classified by: - Etiology - Thermal: flash, scald (house fire, cooking accidents) - Electrical: arc between 2 objects - Chemical: 3% of all admissions (both household and industrial) - Radiation: least common, severity depends on location, depth, length of exposure - Depth of tissue damage - Superficial: epidermal layer damage, erythema, hypersensitivity, resolves in 24-72 hrs - Superficial partial-thickness: involves epidermis and minimal layers of dermis - Deep partial-thickness: epidermis and extends into deeper or bottom layers of dermis - Full thickness: destruction of epidermis, dermis and portions of subq tissue - Total Body Surface Area (TBSA): percent of body burned- essential for guiding fluid resuscitation and treatment - Adults start at 20% - Elderly and pediatric start at 10% - Severity: take into account inhillation injury, age, past medical hx, location ## Burn Zones - Zone of Coagulation - Zone of Stasis - Zone of Hyperemia ## Rule Of Nines *most commonly used to determine TBSA burned | Anterior | Posterior | |---|---| | Head and Neck: 9% | Posterior Trunk and buttock: 18% | | Anterior Trunk: 18% | Posterior legs and feet: 18% | | Anterior legs and feet: 18% | | Perineum: 1% | ## Fluid Resuscitation Using the Parkland Formula *Dr. Parkland ER Dr in Dallas Tx, was involved in research, was one of Dr who unsuccessfully tried to save John F. Kennedy when he was shot in the head. - 4ml LR x pt weight in kg x %TBSA - LR is the crystalloid of choice - 1 half of calculated fluid infused in 8 hours - 2nd half infused over 16 hours ## Practice Problems - A client is burned on both arms and the front of the head and torso. Using the Rule of Nines, what is the total body surface area burned? ## Practice Problems - Using the TBSA from above, calculate the total amount of fluid needed using the Parkland formula for a client weighing 125 lbs. - How much for the first 8 hours? - What do you set the pump at? # Anatomical changes with burns - Zone of coagulation: area that had the most contact with heat source, has most severe damage. Tissue undergoes protein coagulation and eschar often present, often no pain because nerves are burned - Zone of stasis: immediately surrounds zone of coag, damaged cells and impaired circulation - Zone of hyperemia: outermost surrounding area with increased blood flow in an effort to bring key nutrients for tissue recovery *location of burn plays important part of level of care required, resulting functional changes (mindful of burns over joints) # Systemic Effects of Burns *resulting from release of cytokines and mediators - Respiratory: inhalation 20-50% of admissions - 60-70% die - Cardiovascular: burn shock (combo distributive and hypovolemic shock) immediately following burn 24-48 hrs capillaries leaking fluids (must be account for lost fluid- may be as great as 5L/day, continues until wounds are closed) - Fluid and Electrolytes: must watch Na+ and K+ - Renal: commonly with electrical –impaired d/t decreased renal perfusion - Gastrointestinal: decreased absorption and motility, burn pt who have significant injury and require massive fluid resuscitation are at risk for developing abdominal compartment syndrome secondary to massive resuscitation volumes - Metabolic: burn injury causes hypermetabolic state for up to 1 yr, often double normal resting energy expenditure, greatly increase caloric needs, wound healing impaired without supplemental nutrition - Immunological: HIGH risk for infection due to decreased protection and immune responses r/t open wounds, as a result these patients are in a constant state of systemic inflammatory responds syndrome (SIRS) # Sepsis - Leading cause of death after surviving first 24 hours - Infection control is high priority - Approximately 28-65% of burn patients die as a result of sepsis # Special considerations for special burns - Inhalation: most fatalities that occur at scene are from carbon monoxide poisoning - CO2 poisoning: 100% O2 by mask, manifestations range from mild h/a and confusion to coma, seizures and death - If injury is above glottis, must move fast to maintain airway - If below glottis, almost always chemical but can be from long exposure to fire like they passed out in the fire- wheezing - Electrical: "The Grand Masquerader” – the extent of damage is usually not present on the surface, often times there is secondary injury, maintain c-spine and thorough assessment, watch for muscle damage (red or tea color urine), watch for compartment syndrome - Chemical: if to eyes, flush continuously until ophthalmologist can assess - Acids, alkalis and organic compounds - Remove clothing and remove chemical using only water - Escharotomies: surgical incision through eschar to relieve pressure - Fasciotomies: incison extends through subq into muscle to relieve pressure and allow for swelling - More common in electrical injury # Burn phases - Emergent: start asap, resolve immediate life-threatening injury, AIRWAY top priority, fluid resuscitation crucial to survival, labs necessary, hypothermia as pt has lost insulation layer, wound care AFTER pt stabilized, IV narcotics, medications (anticoag, nutritional support, gi motility, anxiety, depression, antibiotics, pain control) - Intermediate: wound care, hydrotherapy, clean technique and infection control, topical meds and wound dressings, mechanical and enzymatic debridement, surgical debridement and wound closure, pain management - Rehabilitative: avoiding contractures (permanent tightening of skin that may involve muscles and tendons resulting in limited mobility) psychological aspect must be addressed # Endocrine System # Diabetic Ketoacidosis - Complication of DM: inadequate insulin, cells can't preform normal metabolism - Pathophysiology: results in rapid breakdown of fat stores in adipose tissue then liver converts into ketones for energy. Ketones have lower pH resulting in Metabolic Acidosis. Without insulin the body releases glucagon and cortisol resulting in severe high blood sugar, hyper osmolality, osmotic diuresis. Happens rapidly - Manifestations: polyuria, polydipsia, polyphagia, fruity smelling breath, n/v, lethargy, coma - Diagnostics: glucose >250, ketones in urine, pH <7.3, HCO3 <18 - Treatment: fluid replacement, correction of lytes, insulin - If not treated: hypotension, tachycardia, kussmal respiration (rapid and deep) # Hyperosmolar Hyperglycemic Syndrome - Complication of DM: high glucose, dehydration without ketones, usually follows infection - Pathophysiology: there is enough insulin to stop fat breakdown and ketone development, but not enough to prevent high bs - Manifestations: profound dehydration, ALOC - Diagnostics: glucose >600, serum osmolality 320, little or no ketones - Treatment: fluid replacement, watch lytes, maybe insulin # Thyroid Cancer *more common in females - 4 types of thyroid cancer: papillary, follicular, medullary and anaplastic - Manifestations: nodule noted, dx by ultrasound and biopsy - Treatments: radiation or surgery, lifelong hormone or thyroid replacement meds # Gastrointestinal System # Inflammatory bowel disorders - 2 types fall under IBD: Crohn's and Ulcerative Colitis - *incidence higher in US, Canada, UK, Sweden and Norway. Canada is highest in world - Unknown cause: 1.4 million Americans suffer, linked to genetics, environmental conditions and defects in immune regulation - Management: control sx: diarrhea, abd pain/cramping, fever, wt loss, fluid imbalance, blood in stool. Can do colectomy - Complications: Crohn's: higher risk of small bowel CA. UC: higher risk of colon CA ## Complications Crohns: affect gi tract from mouth to anus, transmural (may penetrate bowel wall) leading to fistulas, absess, peritonitis. During colonoscopy you will see portions of normal looking bowel, strictures and adhesions common, diarrhea is less severe, stook does not contain blood unless perforation. Nutritional deficits from inability to absorb nutrients. Electrolyte disturbances. ABD pain worse in RLQ ## Complications Ulcerative Colitis: affects Ig intestine, rarely small, diarrhea common with blood, mucus or pus. ABD pain/tender LLQ. Rest bowel and control inflammation. Meds: aminosalicylates, antimicrobials, steroids, immunosuppression. Emotional/physical stress can exacerbate ## Complications Ulcerative Colitis: pic toxic megacolon (if treatment not effective –ng, fluids, steroids, abx- surgery necessary to prevent perforation) # Read one Teach one GI Cancers *Intro/etiology: what, who, where *Quick A&P: location and function of area *Clinical Manifestations: signs, symptoms *How to diagnose: tests, screenings *Treatment: surgery, radiation, chemo *Education: for pt and family *References: APA format | Location | ICD-10 codes | |---|---| | Esophageal | 1297-1302 | | Stomach | 1324-1328 | | Colorectal | 1355-1364 | # Hepatic and Pancreatic System # Hepatitis: several viruses cause hepatitis *Routes: fecal-oral, blood, body fluid - Risks: ETOH abuse, prescription and otc meds, toxins, autoimmune - Pathophysiology: inflammation limits ability of liver to detoxify substances, limits protein production and clotting factors, alters ability to store vitamins, fats, sugars - Manifestations: abd pain, irritability, pruritis (severe itching), malaise, fever, n/v, jaundice, clay colored stool (lack of bile), amber urine (excess bilirubin), elevated liver enzymes, elevated ammonia, elevated bilirubin - Types - Viral: HepA- most common, spread via oral through food, water or shellfish that are infected. HepB- spread via blood/body fluids, can be passed at childbirth, contact with infected fluids, puncture with contaminated needle. HepC – spread via blood/body fluids/childbirth. HepD- not common in US, requires person to be infected with HepB already. HepE - spread via fecal-oral primarily through water in areas of poor sanitation. HepG - just discovered in 1996, spread via blood/blood products, those with hemophilia or freq blood transfusions at risk - Non Viral: caused by ingested, inhaled, or injected toxins or medications - Treatments: can be acute or chronic, untreated acute can lead to chronic that can lead to liver CA, vaccinations for HepA &B, antivirals - Surgical: liver transplant from cadaver (entire liver), or from a living donor can donate a lobe # Cirrhosis: hepC leading cause, followed by ETOH liver disease - Risks: HepA, B, or C predispose especially when followed by chronic alcoholism, biliary disease, fat accumulation in liver, some autoimmune diseases - Pathophysiology: alterations in blood flow results in portal hypertension (increase in pressure in veins that carry blood through liver) and shunting of blood around the liver. This shunting causes increase in pressure in surrounding vessels that lead to esophageal varices (abnormally dilated and weakened veins), may result in upper gi bleed, chronic disease causes cell destruction and fibrosis or scarring - Manifestations: ascites (accumulation of protein rich fluid in abdominal cavity, portal htn (varices occur), hepatic encephalopathy (disturbances in CNS ranging from motor disturbances to seizures and death), loss of coag cascade factors, can lead to hepatorenal syndrome (AKF resulting from altered blood flow to kidneys), risk for spontaneous bacterial peritonitis - Management: ultrasounds and CT, EGD, cholangiography (contrast injected into bile duct to visualize biliary tract), liver biopsy or transplant # Liver cancer - Risks: >65, male, chronic HepB or C, long hx of ETOH, usually fatal within 6-12 months - Pathophysiology: hepatocellular carcinoma is most prevalent type of live CA, secondary liver CA is often mets from colon CA - Manifestations: often asymptomatic until liver becomes enlarged, abd pain, wt loss, anorexia, weakness, fatigue, jaundice, ascites - Management: poor prognosis d/t being diagnosed late, routine screenings, surgical if mets, transplant is only cure # Pancreatitis - Acute: acute pancreatitis is reversible inflammatory process, chronic is not reversible - Risks: ETOH, gallstones or trauma - Pathophysiology: inflammation from release of enzymes that “autodigest”, starts digesting itself and surrounding tissues - Manifestations: sudden severe epigastric pain ULQ radiates to back or shoulder blades, intense within minutes of eating high fat foods or after binge drinking, tender abd, guarding, rebound tenderness, Cullen's sign (periumbilical bruising) and Grey Turner's sign is uncommon sign indicative of retroperitoneal hemorrhage - Management: labs, pancreas specific labs (serum amylase and lipase), CT, MRI, ultrasound, NPO, fluids, pain meds - Complications: necrotizing pancreatitis, pancreatic hemorrhage, pancreatic pseudocysts (encapsulated areas of fluid that contain pancreatic enzymes and tissue) # Pancreatitis - Chronic: irreversible - Risks: most common cause is heavy, prolonged ETOH use - Pathophysiology: over time the exocrine and endocrine function of the pancreas is permanently altered. Digestive enzymes autodigest the pancreas and surrounding tissue, because of inflammation and scarring, pancreas unable to make enzymes needed to digest protein, fat or hormones necessary to regulate glucose. Fibrosis secondary to chronic inflammation further contributes to loss of normal function - Manifestations: pain after eating or drinking, Upper abd pain spread to back, n/v wt loss, diarrhea, pale or clay colored stool, steatorrhea (abnormal excretion of fat with stool) - Management: labs, CT, ultrasound, pain management, iv fluid, electrolyte management, nutritional support, insulin if needed. Surgical resection may provide some relief but not always appropriate for chronic disease # Pancreatic cancer: quick with high mortality rate, only 23% survive to 1 yr, 5% at 5 years - Risks: risk increases with age, commonly dx >60, DM, smoking, high fat diet, chronic pancreatitis - Pathophysiology: no reliable screening, s/s vague and similar to million other Gl disorders. Affects more males and more African American than Caucasians. Pancreatic tumor likely to mets to surrounding structures (stomach, duodenum, gallbladder, intestine). Metastatic tumors usually originate in lung, breast, thyroid, kidneys or skin - Manifestations: dull pain in epigastric area and back, jaundice, wt loss - Management: ERCP (combo ultrasound and CT of pancreas), combo radiation and chemo, Whipple procedure in small percentage- potentially curable # Autoimmune Disorders # Rheumatic Disease - "Arthritis" - Affect primary the joints but also the muscles, bone, ligament, tendons, and cartilage - Remission and exacerbation - Classification - Monoarticular or polyarticular - Inflammatory or noninflammatory - Marked by inflammation, autoimmunity, and degeneration # Diffuse Connective Tissue Diseases - A group of chronic disorders characterized by diffuse inflammation and degeneration in the connective tissue - Cause is unknown but thought to have an immunologic basis - Characterized by a clinical course of exacerbations and remissions: any organ can be involved - Includes RA, SLE, scleroderma, polymyositis, and polymyalgia rheumatica, Raynaud's phenomenon, Sjorgren's syndrome # Rheumatoid Arthritis - Development: age 20-40, more common in females - Patho: synovial tissue moves into joint - Symptoms: morning stiffness >1 hr, red, pain, swollen joints warm to touch - Nursing care: ROM, skin protect over bony prominences, immunosuppression, anti inflammatorys # Systemic Lupus Erythematous - Development: combo of genetic, immunologic, hormonal and environmental - Manifestation: fever, malaise, wt loss. Commonly involved: muscles, renal, nervous, cardiac, respiratory, butterfly rash - Diagnostics: no specific test, table 20.9 pg 398-399 - Treatment: anti inflammatories, corticosteroids, cytotoxic agents, anti mylarial agents - Nursing Care: very frustrating process, support mental health, self image