Burns AKI MODS - Lecture notes Concept 2 PDF

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3rd semester lecture notes on Burns, AKI, and MODS with McMaster FA2020...

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Burns ● Skin is the largest organ in the body ○ First line of defense ○ Protection from infection ○ Fluid and electrolyte balance ○ Maintenance of body temp ● Burns can lead to local and systemic problems ○ Leads to electrolyte imbalance ○ Fluid imbalance ○ Protein losses ○ Hypovolemic and septic shock ○ Changes in ■ Metabolic ■ Endocrine ■ Respiratory ■ Cardiac ■ Hematologic ■ Immune functions ○ Problems related to ■ Age ■ General health ■ Extent of burn ■ Depth of burn ■ Area of burn ● Assessing severity of burns ○ Classified by depth of burn and total body surface area (TBSA) ○ Partial thickness - exposed nerve endings ○ Full thickness destroy nerve endings, resulting in decreased pain at first ● Superficial - epidermis only ○ Painful ○ No edema ○ Redness ○ Blanches with pressure ○ Total regrowth of tissue occurs ○ Sun burns ○ Last 2-3 days - heal completely ● Partial Thickness ○ Loss of entire epidermis and varying depths of dermis ○ Superficial partial thickness ■ Upper ⅓ of dermis ■ Wounds are pink, moist, blanch at light pressure ■ Blisters form ■ Increased pain sensation ■ Heal in 10-21 days with no scar - pigment changes

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Deep partial thickness ■ Deeper into dermis ■ Blisters do not form ■ Wound is red and dry ■ Blanches slowly or not at all ■ Moderate edema ■ Pain is decreased due to destroyed nerve endings ■ Blood flow reduced ■ Deeper unjust can occur from hypoxia/infection ■ Heal in 2-6 weeks ■ Scarring occurs - may need skin grafting Full-thickness ○ Destruction of entire epidermis and dermis - no cells to regenerate ○ Wound is dry, hard, lethery (eschar) ■ Eschar must be sloughed off and removed by debridement ○ Severe edema ○ Healing depends on treatment - can take weeks to months ○ Skin-grafting is often necessary Deep Full-thickness ○ Extend beyond skin layers into fat, blood vessels, muscle, tendons, and bone ○ Skin cannot heal on its own ○ Usually occur with flame, electrical, or chemical injuries ○ All need early excision and grafting Cause of injury ○ Cause of injury affects treatment and prognosis ○ Dry heat - open flame or explosion (flash burn) ○ Moist heat - scald - more common in children and elderly ○ Contact burns - hot metal, tar or grease - often lead to full thickness ○ Chemical - (alkalis) epidermis or ingestion ○ Electrical - can cause severe internal injuries including deep muscle injury ■ Thermal ■ Flash ■ True ○ Radiation - therapeutic radiation (cancer treatment) or industrial Health promotion ○ Prevention is key ○ increased risk for children and elderly ○ Most common causes ■ Cigarette smoking ■ Cooking ■ Electrical appliances ■ Hazardous materials ■ Flammable liquids / lighters/ matches

Vascular changes and fluid shift ● Compensatory responses ○ Inflammation ○ Sympathetic nervous system response ● Circulation is disrupted by vessel occlusion ○ Vasoconstriction from chemical response = reduced blood flow ○ Capillaries at injury area dilate - fluid shift out of vascular space into intersititium ○ Edema occurs ● Hypovolemia ○ Hypovolemia, ○ Hyperkalemia ○ Hyponatremia ○ metabolic acidosis ○ Vascular dehydration/ hemoconcentration ○ Burn shock ■ Hypovolemic and distributive shock ○ Fluid remobilization starts 24 hr after injury when capillary leak stops ○ 24-48 hr within, fluids begin to shift back into vascular space ■ Can lead to delusional hyponatremia, hypokalemia and anemia ● Cardiopulmonary and GI changes ○ Cardiac ■ Tachycardia ■ Hypotension ■ Decreased CO ○ Pulmonary changes ■ Occur due to inhaled superheated air, steam, toxic fumes, or smoke ● Causing airway edema ● Airway edema during fluid resuscitation can also occur ● Monitor respiratory status with ABG ● Assess for carbon monoxide poisoning ○ GI changes ■ Decreased blood flow to GI tract can result in reduced peristalsis/paralytic ileus ■ Meds ● H2 Blockers ● Prop-pump inhibitors (protonix) ○ Metabolic and immunological changes ■ Increase metabolism ● Release catecholamines ● ADH ● Aldosterone ● Cortisol ● O2 and caloric needs increase and remain high until complete wound closure

○ Could be months ■ Inflammatory response that suppresses immune function ● Renal Issues ○ Urine output greatly decreased due to reduced blood flow to kidneys and ADH secretion ○ Urine is concentrated - high specific gravity (normal 1.003 - 1.030) ○ May experience acute kidney injury due to kidney damage from hypoperfusion ○ Minimum acceptable urine output 30-50 ml/hr or 0.5 ml/kg/hr Diagnostics ● Monitor fluid and electrolyte imbalances ● WBCs may be elevated due to inflammation/infection ● CT, Ultrasounds, MRIs, bronchoscopies for deep organ trauma ● (pg. 493) ● Surgical treatment ○ Tracheotomy may be needed for severe upper airway edema ○ escharotomies/ fasciotomies ■ For compartment syndrome ○ Skin grafting may be necessary for acute phase ○ Amputations may be done Brain Injury ● 3 phases ● Resuscitation phase - 1st 24 - 48 hr after injury ○ Time of burn - not time of arrival ○ Burns > 25-30% TBSA ○ Pj. 489 ○ Priorities ■ Secure airway ■ Support circulation and organ perfusion ● Fluid replacement ■ Pain management - IV opioids/ benzos ● IM/SQ route could lead to sudden rapid absorption ■ Prevent infection ■ Maintain body temp ■ Emotional support ■ Obtain health history ■ Assess pulmonary edema ○ Burn patients are at risk for acute respiratory distress syndrome (ARDS) ○ Fluid resuscitation can lead to heart failure in clients with cardiac disease ○ ***Clients should be intubated before severe edema makes intubation impossible ○ (Pg. 490) ● Burns - (Parkland Formula) ○ 4mL x Kg x %TBSA burned = mLs/24 hr ■ Give half of total volume within the first 8 hr ○ Rule of 9s

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■ Face - 4.5 ■ Chest - 9 ■ Abdomen - 9 ■ Arms - 4.5 per side/ front back ■ Front of legs 9 ○ Practice calculations Resuscitation phase interventions ○ Prevent infection ○ Maintain body temp - hypothermia ○ Emotional support ○ Obtain health history ○ Pain management Acute Phase (2) ○ Begins 36-48 hours after injury ○ Priority: Maintain and prevent cardiopulmonary complications ○ Assessment ■ Cardiovascular and respiratory ■ Nutrition status/ GI status ■ Wound care/ pain control ○ Clients are at risk for fluid and electrolyte imbalance ■ Client may develop pneumonia ○ Nutritional status ■ Diet should be high in calories, protein, carbs, vit C, zinc ■ Pain can interfere with proper nutrition ● Burn clients often need supplemental nutritional support ○ Supplemental shakes, puddings, TPN ■ Weigh client daily ○ Meds ■ H2 blockers ‘tidine’, PPI - ‘Prazole’ ○ All patients are at risk for infection/ sepsis until wounds are closed ○ (pg. 498) ○ Burn wound sepsis is the leading cause of death in acute phase ○ Tetanus vaccine ○ Wound management ■ Remove dead tissue ■ Clean wound ■ Stimulate granulation and revascularization ■ Apply dressings ■ Injuries need debridement to remove exudate/necrotic tissue to prevent infection ■ Types of debridement ● Mechanical (Hydrotherapy) ● Sharp (removal of necrotic tissue with sharp instruments) ● Enzymatic (use of ointments/soaked 4x4s with chemicals)

● Autolysis (use of client’s own cellular enzymes for debridement) Burn wound dressings ● Silvadene cream & antibiotic dressings prior to wound closure/grafting ● Biologic: skin/membranes obtained from human donors temporary until permanent grafts are done ● Biosynthetic: combination of biologic and synthetic material ● Synthetic: made of solid silicone and plastic membranes ■ Grafting - surgical management ● Done when full-thickness injuries will not close on their own ● Grafting requires a clean and granulating wound bed ● Early grafting reduces risk for infection and sepsis ● Surgical excision is done within 5 days of initial injury ● Autografting: removal of client’s own skin from donor sites which is then placed over burn areas ○ Donor site is also at risk for infection ■ Medication ● Sylvadinebw ● ○ Wound management ■ Minimizing infection ■ Antimicrobial agents used for dressing changes ■ Systemic ABX therapy is used if suspected of having wound infection ■ Isolation may be needed ■ HANDWASHING ■ No shared equipment ■ Visitor restriction ○ Pain management ■ IV opioids (Dilaudid, Fentanyl) - especially prior to dressing changes ■ Complementary therapies ● Relaxation meditation, guided imagery ● Music therapy ■ Environment ● Position changes ● Massage ● Ensure adequate sleep/rest ■ Minimize weight loss ■ Maintain mobility ■ Supporting positive self-image Rehabilitation phase ○ Official rehab activities have begun once all wounds are closed ○ Focus on psychosocial adjustment to injury/ appearance ○ Client will go through denial, anger, bargaining and depression before reaching acceptance ■

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Patient education important before discharge Support groups and outpatient therapy

Acute Kidney Injury pg. 1390 ● Acute renal failure and acute kidney injury are the same thing ○ Kidney injury is sudden event that reduced kidney function ○ Differs from chronic kidney disease (CKD) ○ End stage CKD requires dialysis ● Adequate kidney function provides: ○ Urinary elimination and excretion of waste products ○ Fluid and electrolyte balance ○ Hormone secretion - erythropoietin, calcitriol, and renin ○ Inadequate kidney function affects many body systems ● Systemic Complications from AKI (pg. 1392) ○ acid/base and electrolyte imbalances (HC03& K+) ○ Cardiac dysrhythmias (K+) ○ Fluid overload leading to heart failure ○ Edema - peripheral and pulmonary ○ Weakness & seizures ● Prevalence ○ AKI can progress to CKD and result in reliance on dialysis in 10-20% of patients ○ Even severe AKI can resolve and return to normal kidney function ■ Some clients lose some kidney function - more at risk for CKD in future ○ Up to 30% of ICU clients experience AKI ○ Pg. 1391 ● Risk factors ○ Acute health issues ■ Cardiac surgery, HF, hypovolemia, sepsis, hypotension, shock ■ Contrast medium ■ Drugs/ toxins ○ Pre-existing reduced GFR ○ Advanced age ○ Pre-existing conditions that affect kidneys such as HTN, diabetes, and peripheral vascular disease ○ Urinary obstructive diseases (stones, ureteral abnormalities) ○ Extended mechanical ventilation ○ Hypotension

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Etiology ○ Prerenal causes ■ dehydration/ hemorrhage ■ Severe blood volume ■ depletion can lead to AKI even in healthy people ● 2-3 L water/ daily for heathy person

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■ Injury that prevents adequate renal perfusion (truama) ■ Reduced perfusion to the kidneys (shock) ○ Kidneys require a sustained MAP >65 AKI prevention ○ Nurses must detect early signs of kidney AKI ○ Evaluate I&Os, labs, BUN, GFR, body weight ■ Fluid status, hypotension ■ Evaluate vitals and CBC ○ Urine output 0.5/kg/hr Intrarenal / Intrinsic causes ○ Damage to kidney tissue/ nephrons ■ Kidney infections ■ Sepsis ■ Malignant HTN ■ Trauma to kidney ■ Cancer of kidney ■ ischemia/cardiac arrest ■ Toxins ■ Drugs ■ Rhabdomyolysis Postrenal causes ○ Obstruction of urine flow ■ Kidney stones ■ Tumors ■ Ureteral injury/ malformation ■ Enlarged prostate ■ Neurogenic bladder ■ Blood clots in urinary tract Identify clients at increased risk of AKI ○ Any hypotensive/shock patients ○ HF/ renal perfusion decrease ○ Recent surgery/ trauma/ illness medication history Assessing kidney function ○ Creatinine levels - 0.7-1.4 ○ BUN - 7-24 ○ Physical assessment ■ Oliguria ■ Fluid overload ■ Edema ■ Low o2 sat ■ Increased RR ○ Labs ■ Increased BUN/creatinine ■ Abnormal NA+

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■ Rising K+ ■ Decreasing pH (acidosis) ■ Increased blood osmolarity (initiating AKI) ■ Urine with low OR high specific gravity ■ protein/RBC in urinalysis ■ Decreased urinary output Interventions ○ I&Os ○ Avoid hypotension ○ Maintain normal fluid balance ○ Reduce exposure to nephrotoxins ■ Consult with pharmacist ○ Confirm adequate kidney function prior to tests that require contrast medium (creatinine) ○ Monitor labs for electrolyte imbalances and renal function ○ Dietary needs to accommodate increased metabolic rate ○ renal/kidney replacement therapy (RRT) hemodialysis ■ Lifetime reliance occurs in 10-20% of patients ■ High mortality associated with RRT (pg. 1397) ○ Administer diuretic ■ furosemide/lasix ■ bumetanide/ Bumex ■ Can cause orthostatic hypotension ■ Ototoxic in large doses or rapid IV administration Adverse effects of loop diuretics ○ Hypokalemia ○ Hypocalcemia ○ Metabolic alkalosis ○ Hypomagnesemia ○ HF ○ Hypotension ○ Edema AKI and CKD pharmacology ○ Potassium binder - Kayexalate ■ Causes diarrhea and elimination of K+ in stool ○ Phosphate binder - PhosLo ■ All ESRD must take prior to eating ■ For chronic kidney disease ○ Hematopoietic stimulators - erythropoietin, Epogen ■ Stimulates red blood cell production ■ Usually given in dialysis

Moderate Sedation ● Used for short, minimally invasive procedures

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○ Colonoscopy, bronchoscopy, closed reduction of fractures, cardioversion Induce amnesia Allow client to maintain their own airway/ respirations and HR/BP without assistance

Pharmacology ○ IV drugs used for moderate sedation ■ Benzodiazepines - end in “pam” ● Midazolam/ Versed ○ Half life 2-5 hr ○ Duration 1-6 hr ○ Amnesic ○ glumazenil/ Romaziocon reversal agent ■ Sedative Hypnotics ● Includes some opioids, benzos, and barbiturates ● Propofol/ Diprivan p general anesthetic ○ ½ life 40 min ○ Duration 3-10 min ● Morphine - opioid ● Reversal agent for opioids is Narcan/ naloxone Nursing interventions ○ Monitor for respiratory depression and hypotension ○ Client wakes up quickly after procedure ○ Close monitoring is essential ○ RN / anesthesiologist at bedside to monitor cardiopulmonary status during procedure Sedation monitoring ○ RNs monitor client before, during, and after moderate sedation ○ Physician must be at bedside during medication administration ○ RT at bedside ○ Vitals taken q2-3 min ○ Cardiac monitoring

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Emergency airway equipment readily available Clients should not take PO fluids until gag reflex returns Clients are not allowed to drive after moderate sedation ■ Must be discharged with responsible adults Sedation scales to assess effectiveness and recovery to baseline (pg. 262)...