Adult Health 3 Exam 3.pdf

Care of the Burn Patient Pathophysiology of Burn Injury: Epidermis-Outer Layer ❖ No blood vessels- Nutrients must diffuse from the second layer of skin, the dermis ❖ Grows back-the epidermal cells surrounding sweat and oil...

Care of the Burn Patient Pathophysiology of Burn Injury: Epidermis-Outer Layer ❖ No blood vessels- Nutrients must diffuse from the second layer of skin, the dermis ❖ Grows back-the epidermal cells surrounding sweat and oil glands and hair follicles extend into dermal tissue and regrow to heal ❖ The palm of the hand and sole of the foot, allows for healing of deep burns in these areas- extends into the dermis Dermis ❖ Thicker, made up of collagen, fibrous connective tissue, and elastic fibers ❖ Blood vessels, sensory nerves, hair follicles, lymph vessels, sebaceous glands, and sweat glands ❖ Skin can regrow as long as parts of the dermis are present ❖ If the entire dermal layer is burned, the skin can no longer restore itself. Subcutaneous Tissue ❖ Lies below the dermis and is separated from the dermis by the basement membrane, a thin, noncellular protein surface ❖ With deep burns, the subcutaneous tissues may be damaged, leaving bines, tendons, and muscles exposed Functional Changes of Burn Injury ❖ Protective barrier against injury and microbial invasion ❖ Increase risk for infection ❖ Maintain fluid loss occurs through excessive evaporation ❖ Rate of evaporation is in proportion to TBSA burned and depth of injury ❖ Sensations of pain, pressure, temperature, and touch, allows reaction to changes in the environment ❖ Partial- thickness burns, nerve endings are exposed, increasing sensitivity and pain ❖ Full thickness burns, nerve endings are completely destroyed ❖ Despite this destruction, dull or pressure-type of pain in these areas ❖ Excretory organ through sweating ❖ Full thickness burns destroy the sweat glands ❖ Vitamin Synthesis-Vitamin D  ❖ Partial-thickness burns reduce the activation of Vitamin D ❖ Full-thickness burns cannot activate Vitamin D ❖ Maintaining normal body temperature ❖ Unable to provide and dissipate heat efficiently ❖ Physical identity is partly determined by the skin’d cosmetic quality ❖ Reduced self-image and other psychosocial problems as a result of a change in appearance Cardiovascular Changes with Burn Injury ❖ Release of cytokines and other inflammatory mediators has a systemic effect at 25% TBSA ❖ Cardiovascular Changes Decreased Cardiac Output Increased Capillary permeability- leading to loss of intravascular proteins and fluids into the interstitial compartment (3rd Spacing) Hypovolemia, Hyponatremia Peripheral and splanic (viscera) vasoconstriction Myocardial contractility is decreased Fluid loss from the burn wound Systemic hypotension and end organ hypoperfusion- Decreased Cardiac Output Hypovolemic Shock Respiratory Changes with Burn Injury -Respiratory Changes ❖ Inflammatory mediators cause bronchoconstriction ❖ Heated Air, Steam, Toxic Fumes, Smoke can reach the upper airway, causing an inflammatory response that leads to edema of the mouth and throat with the potential of airway obstruction ❖ Respiratory Failure: Inhalation Injury can occur in the upper and major airways and the lung tissue The lining of the trachea and bronchi may slough 48-72 hours after injury and obstruct the lower airways Leaking Capillaries cause alveolar edema- ARDS in severe burns Gastrointestinal Changes with Burn Injury  -Gastrointestinal ❖ Decreased cardiac output decreases blood flow to the GI tract ❖ Gastric mucosal tissue integrity and motility are impaired ❖ Secretions and gasses collect, causing GI distention ❖ Peristalsis decreases, and a paralytic ileus (mechanical obstruction) may develop ❖ Curling’s ulcer (acute gastroduodenal ulcer that occurs with the stress of severe injury) may develop within 24 hours after a severe burn injury because of reduced GI blood flow and mucosal damage ❖ Use of H2 histamine blockers, proton pump inhibitors and early enteral feeding. Metabolic Changes with Burn Injury -Metabolic Changes ❖ Hypermetabolism, the patient’s oxygen use and calorie needs are high- Peaks at 4-12 days ❖ Basal metabolic rate increases 3x ❖ Depending on the extent of injury, the patient’s calorie needs double or triple normal energy needs ❖ The hypermetabolic condition also increases core body temperature ❖ The patient loses heat through the burned areas ❖ Core body temperature increases as a response to the adjustment in temperature regulation by the hypothalamus, resulting in a low-grade fever. Immunological Changes with Burn Injury -Immunological Changes ❖ Loss of protective barrier ❖ Increased risk of infection ❖ Suppression of humoral and cell-mediated immune responses- Due to the Inflammatory Response Physiological Compensatory Response to Burn Injury Fluid Shift in Burns ❖ Occurs after initial vasoconstriction as a result of blood vessels near the burn dilating and leaking fluids into the interstitial space ❖ 3rd spacing or capillary leak syndrome- continuous leak of plasma from the vascular space into the interstitial space ❖ Fluid shift-Usually occurs in the first 12 hours and can continue 24 to 36 hr ❖ Profound imbalance of fluid, electrolyte, and acid-base ❖ Hemoconcentration ❖ Hypovolemia ❖ Metabolic acidosis ❖ Tissue hypoxia caused by volume depletion ❖ Hyperkalemia ❖ Result of direct cell injury that releases large amounts of cellular potassium ❖ Hyponatremia ❖ Sodium is trapped in the interstitial space ❖ Hemoconcentration ❖ Elevated blood osmolarity, hematocrit, and hemoglobin develops from vascular dehydration  ❖ Increases blood viscosity, reducing blood flow and increasing tissue hypoxia ❖ Fluid remobilization starts at about 24 hours after injury ❖ Capillary leak stops Fluid Remobilization/ Diuretic Phase in Burn ❖ Diuretic stage begins at about 48 to 72 hours after the burn injury ❖ Fluid shifts from the interstitial spaces into the intravascular space ❖ Blood volume increases ❖ Increased kidney blood flow and diuresis unless kidney damage has occurred ❖ Body weight returns to normal over the next few days as edema subsides ❖ Hyponatremia ❖ Increased kidney sodium excretion and the loss of sodium from wounds ❖ Hypokalemia ❖ Potassium moving back into the cells ❖ Anemia ❖ Hemodilution ❖ Metabolic acidosis ❖ Loss of bicarbonate in the urine and the increased rate of metabolism Classification of Burn Depth ❖ Superficial Thickness Wounds ❖ Partial-Thickness Wounds ❖ Superficial Partial Thickness Wounds ❖ Deep Partial Thickness Wounds ❖ Full Thickness Wounds ❖ Deep Full Thickness Wounds Degree of Burn Injury ❖ Superficial Thickness Burn Wound- Superficial involve only epidermal layer Superficial Partial- Thickness Burns ❖ Upper third of dermis, good blood supply, increased pain sensation. Deep Partial- Thickness Burn ❖ Deeper into the dermis with few blood vessels patent, less pain (more destroyed nerve endings). Deep Partial thickness- destruction of epidermis and varying depths of dermis -Infection, hypoxia, or ischemia can convert wound to full-thickness Full- Thickness Burn: Destruction of the entire epidermis and dermis- no regrowth Deep Full- Thickness Burn: Extends Beyond skin, damages muscle, bone and tendons Causes of Burn Injury -Dry Heat ❖ Open flame in house fires and explosions ❖ Explosions usually result in flash burns because they produce a brief exposure to very high temperatures -Moist Heat (Scald) ❖ Contact with hot liquids or steam ❖ Hot liquid spills usually burn the upper, front areas of the body ❖ Immersion scald injuries usually involve the lower body (Child Abuse) -Contact Burns ❖ Hot metal, tar, or grease contacts the skin, often leading to a full-thickness injury ❖ Space heater, iron, molten metals ❖ Tar and asphalt temperatures usually are greater than 400 degrees F ❖ Hot grease injuries from cooking are usually deep because of the high temperature of the grease -Chemical Injury (Very dangerous) ❖ Chemicals directly contact the skin and epithelial or are ingested  ❖ The severity depends on the duration of contact, the concentration of the chemical, the amount of tissue exposed, and the action of the chemical. ❖ Alkalis found in oven cleaners, fertilizers, drain cleaners, and heavy industrial cleaners ❖ Acid found in bathroom cleaners, rust removers, pool chemicals, and industrial drain cleaners ❖ Chemical disinfectants and gasoline are easily absorbed through the skin and have toxic effects on the kidneys and liver -Radiation Injury ❖ Exposure to large doses of radioactive material ❖ Therapeutic radiation ❖ More serious in industrial settings where radioactive energy is produced or used ❖ Injury severity depends on the type of radiation, distance from the source, duration of exposure, absorbed dose, and depth of penetration into the body -Electrical Injury ❖ Electrical current enters the body ❖ Surface injuries may look small but the associated internal injuries can be huge ❖ Electrical energy being converted to heat energy ❖ The extent of injury depends on the type of current, the pathway of flow, the local tissue resistance, and the duration of contact Electrical Burn ❖ The longer the electricity is in contact with the body, the greater the damage ❖ The duration of contact is increased by tetanic contractions of the strong flexor muscles in the forearm, which can prevent the person from releasing the electrical source ❖ Course of flow is defined by the locations of the “contact sites,” which are the entrance and exit wounds. Internal damage results and can be devastating. ❖ Damage starts on the inside and goes out; deep-tissue destruction may not be apparent immediately after injury. ❖ Organs in the path of the current may become ischemic and necrotic ❖ ALWAYS immobilize for C-Spine Injury EKG STAT ❖ Thermal Burns Clothes ignite from heat or flames produced by electrical sparks ❖ External Burns  Electrical current jumps, or “arcs,” between 2 body surfaces ❖ Internal or Direct Direct contact is made with an electrical source. Always remove jewelry watch, ring etc.. Resuscitation Phase of Burn Injury ❖ First phase, resuscitative or emergent phase, continues for about 24 to 48 hours ❖ Goals of management include: Secure airway** Support circulation-Fluid replacement Analgesics Prevent Infection- Wound Care Maintain body temperature Provide emotional support Emergency Management of Burns ❖ Assess for airway patency ❖ Administer oxygen as needed: 100% Oxygen-Early Intubation ❖ Cover the patient with a blanket ❖ Keep the pt on NPO status ❖ Elevate the extremities if no fractures are obvious. ❖ Place in anatomically correct position ❖ Prevent contractures ❖ Obtain vital signs ❖ Initiate an IV line, and begin fluid replacement ❖ Administer tetanus toxoid prophylaxis ❖ Perform a head-to-toe assessment ❖ Flame Burns: Smother the flames  Remove smoldering clothing and all metal objects. Emergency Management of Chemical Burns ❖ If dry chemicals are present on skin or clothing, DO NOT WET THEM. ❖ Brush off any dry chemicals present on the skin or clothing. ❖ Remove the patient’s clothing. ❖ Ascertain the type of chemical causing the burn. ❖ Do not attempt to neutralize the chemical unless it has been positively identified and the appropriate neutralizing agent is available. Emergency Management of Electrical Burns -Electrical Burns ❖ At the scene, separate the patient from the electrical current ❖ C-Spine Immobilization. ❖ Smother any flames that are present. ❖ Initiate cardiopulmonary resuscitation ❖ Obtain an electrocardiogram (ECG) Emergency Management of Radiation Burns ❖ Remove the patient from the radiation source, ❖ If the patient has been exposed to radiation from an unsealed source, remove his or her clothing (using tongs or lead protective gloves) ❖ If the patient has radioactive particles on the skin, send him or her to the nearest designated radiation decontamination center ❖ Help the patient bathe or shower Factors Affecting Airway ❖ Patients who were injured in a closed space ❖ Patients with extensive burns or with burns of the face- Prophylactically intubate ❖ Intra-oral charcoal, especially on teeth and gums ❖ Patients who were unconscious at the time of injury ❖ Patients with singed scalp hair, nasal hairs, eyelids, or eyelashes- Prophylactically intubate ❖ Patients who are coughing up carbonaceous sputum ❖ Changes in voice such as hoarseness or brassy cough ❖ Use of accessory muscles or stridor ❖ Poor oxygenation or ventilation ❖ Edema, erythema, and ulceration of airway mucosa  ❖ Wheezing, bronchospasm Injuries to the Respiratory System ❖ Direct airway injury: Change in respiratory pattern. Hoarse voice, brassy cough,drooling, wheezing, stridor- pt about to lose airway ❖ Carbon monoxide (odorless) poisoning Cherry red ❖ Thermal injury ❖ Smoke poisoning ❖ Pulmonary fluid overload ❖ External factors Direct Airway Injury -A change in respiratory pattern may indicate a pulmonary injury. The patient may: ❖ Become progressively hoarse ❖ Develop a brassy cough ❖ Drool or have difficulty swallowing ❖ Produce sounds on exhalation that include audible wheezes, crowing, and stridor ❖ Any of these changes may mean the patient is about to lose his or her airway. Carbon Monoxide Poisoning ❖ Leading causes of death from fire ❖ Colorless, Odorless- Binds to Hemoglobin ❖ Cherry Red color- Vasodilation ❖ Manifestations vary on degree of the concentration in Carboxyhemoglobin (COHb) ❖ Headache- AMS (altered mental status)- Unconscious- Coma- Death (First sign headache, N/V) Thermal Injury ❖ Upper airway above the glottis (nasopharynx, oropharynx, and larynx) ❖ Pharynx- edema and upper airway obstruction, especially epiglottitis ❖ When it is known that the upper airways were exposed to heat, intubation may be performed as an early intervention before obstruction occurs Smoke Poisoning ❖ A chemical injury resulting from the inhalation of combustion by-products. ❖ Toxic by-products plastics and home furnishings are burned ❖ Impaired respiratory cell function Pulmonary Fluid Overload ❖ Pulmonary fluid overload ❖ Pulmonary edema ❖ Inflammatory mediators lead to capillary leak ❖ CHF- Circulatory overload ❖ SOB, Dyspnea, Crackles Edema Post Fluid Resuscitation Nasal Intubation- Blind Intubation External Factors ❖ Tight Eschar from circumferential chest burns: Leather like skin- Restricts from taking deep breath ❖ Restricts chest movement or compresses structures in the neck and throat so that airflow is impaired ❖ Increased airway pressure on ventilator- may need for an escharotomy Cardiovascular Assessment ❖ Hypovolemic shock is a common cause of death in the emergent phase in patients with serious injuries ❖ Decreased Cardiac Output ❖ Monitor vital signs ❖ Tachycardia ❖ Hypotension ❖ Decreased Peripheral Pulses ❖ Capillary Refill Slow ❖ Monitor Cardiac Status: Edema, S3, Crackles Renal/ Urinary Assessment ❖ Changes are related to cellular debris and decreased renal blood flow ❖ Myoglobin is released from damaged muscle and circulates to the kidney. When muscle tissue is damaged, such as during severe burns or trauma, myoglobin can be released into the bloodstream. This process can lead to  a condition known as rhabdomyolysis, where the muscle breakdown products, including myoglobin, circulate through the body and can affect various organs. This is why monitoring kidney function and ensuring adequate hydration is critical during the resuscitation of burn patients. Maintaining proper fluid balance helps dilute myoglobin in the urine and protects the kidneys from damage. ❖ Proteins form uric acid ❖ Sludge obstructs kidney injury Thick, viscous substance that can form in the renal tubules when certain conditions are present, such as dehydration, the presence of myoglobin, or the accumulation of other cellular debris. In the context of kidney function, sludge can lead to obstruction in the tubules, impairing the kidneys' ability to filter blood and produce urine ❖ Examine urine for color, odor, and presence of particles or foam ❖ Minimum 30ml/hr→ Acute kidney injury Gastrointestinal Assessment ❖ Changes in GI function are expected ❖ Decreased blood flow and sympathetic stimulation during the emergent phase cause reduced GI motility and paralytic ileus ❖ Nausea, Vomiting, Abdominal Distention ❖ Bowel Sounds Hypoactive or Absent ❖ NGT inserted with 25% TBSA Burns: In order to decompress gas and fluid ❖ Assess for GI Bleeding & Curlings Ulcer (stress ulcer from major trauma) Coffee Ground Emesis Melena Skin Assessment ❖ Determine size and depth of injury ❖ Determine percentage of total body surface are affected TRSA “Rule of nines”*** ❖ Nursing Interventions: Hand Hygiene/PPE Cover Wounds  Room is Warm 85 degrees F Face-Protect Eyes with Ointment*- If eyes do not close at risk for cornea abrasion. Put ointment and tape eye closed Ears- No Pillow (Creates Pressure) Extend Arms- Use Splints and neutral position at normal angle for body part Math on rule of 9*** Emergent Phase of treatment: -Monitoring fluid status: Parkland formula ❖ 4ml LR X Body wt (kg) X Percent burn ❖ 50% over first 8 hours from time of injury ❖ 50% over second 16 hours Parkland Formula Example -4 ml LR (Lactated Ringers) X Body wt (kg) X Percent burn 1st Phase: 50% over first 8 hours from time of injury. ❖ May have to subtract from when the burn actually occured 2nd Phase: 50% over second 16 hours ❖ Patient burned at 10am anterior chest, right full arm, weighs 165 lbs. It is 11 am when he arrives. What is your drip rate for the first phase? ❖ 4ml x 75 kg x 27%= 8100 ml in 24 hours ❖ 8100ml divided by 2= 4050 ml ❖ 7 hours from time of injury… ❖ 4050 ml divide by 7= 579ml/hr In class example: Patient weighs 150 lbs/ 2= 68kg Patient was burned at 8 am and arrived at 1 pm 1. 150 divided by 2.2= 68 kg 2. 1st phase 8-5=3…. 2nd Phase= 16 3. 68kgx4x22.5=6120 ml 4. 22.5% (total chest and anterior arm)= 6120 ml/24 hours Patient was burned and outside ER Total back burn wt 150 lbs 1. 150 divided by 2.2= 68 kg 2. 4ml LR x 68kg x 18%= First phase= 306 3. Second phase= 153 Patient burned back of leg, head and penis, weight= 190 lbs 1. 190 divided by 2.2= 86 kg 2. 4 ml x 86 kg x 14.5%=4988 in 24 hours 3. 1st phase: 4988x 50% divided by 8 hours= 312 ml/hr 4. 2nd phase: 4988x50% divided by 16= 156 ml/hr Burns Interventions ❖ Airway maintenance: Airway becomes edematous Upper airway edema becomes pronounced 8 to 12 hours after the beginning of fluid resuscitation Bronchoscopy- Remove Sloughing Tissue Suction ❖ Promotion of ventilation Check Chest Movement- Eschar (If chest does not rise appropriately)  Positioning if intubated at least 45 degrees HOB IS hourly CPT ❖ Monitor gas exchange ABGs ❖ Assess for Cyanosis Disorientation Increased HR ❖ Oxygen therapy Humidified Oxygen Facemask Cannula Hood ER Equipment at Bedside Burns: Nonsurgical Management ❖ IV Fluids Large fluid loads in a short time (Need large bore IV- 16 gauge) need fluid warmer to prevent hypothermia pushed fast normally done in trauma Half of the calculated fluid volume for 24 hours given over the next 16 hours for a total of 24 hours ❖ Monitoring patient response to fluid therapy Urine Output 30ml/hr ❖ Invasive Monitoring CVP: To monitor preload how much they have and how much needs to be replaced Pulmonary Artery Pressures, CO Burns: Medications ❖ Antibiotics if Pneumonia, Infections ❖ Beta Blockers Improves LV Function in Pulmonary edema/ CHF ❖ Diuretics Extreme cases- not routine. Normally go into failure because they need the fluid  ❖ Paralytic Medications(neuromuscular inhibitor): RN Scope of practice is not to push paralytic drugs. Docs, and anesthesia CRNA push it themselves Atracurium (Tracrium) Vecuronium (Norcuron) ❖ Medications for sedation, analgesia, and antianxiety unless clinically contraindicated.. Versed retrograde amnesia ❖ Analgesics ❖ Tetanus Toxoid 0.5 ml IM ❖ VTE Prophylaxis- will be bedridden ❖ Curling’s Ulcer Prophylaxis Burn: Surgical Management ❖ Tracheostomy: Only if cannot be put in if unable to ventilate for 10-14 days only for permanent ventilation Long Term Intubation ❖ Escharotomy Incision that relieves pressure caused by the constricting force of fluid buildup under circumferential burns on the extremity or chest and improves circulation (non-painful). Biggest COMPLICATION- Infection ❖ Fasciotomy Deeper incision extending through the fascia (painful) Acute Phase of Burn Injury: To prevent infection ❖ Begins about 36 to 48 hr after injury and lasts until wound closure is completed ❖ Care directed toward continued assessment and maintenance of the cardiovascular and respiratory systems ❖ Prevent Infection ❖ Wound Care ❖ Nutrition: metabolic rate 3x higher ❖ High caloric Needs 5K/ Day ❖ High Protein Diets for Healing ❖ Physical Therapy: to prevent contractures in the future Assessment ❖ Assessments include those of: ❖ Cardiopulmonary Risk for infection and sepsis, which affect cardiovascular function  ❖ Neuroendocrine Increased Metabolic Demand Depletion of Nutrition Stores Daily Weights: Patient will be put on TPN- another source of infection ❖ Assessments include those of Immune: Infection Wound Sepsis Meticulous Handwashing ❖ Muskuloskeletal Active and Passive ROM exercises Local Indicators of Infection ❖ Conversion of a partial-thickness injury to a full-thickness injury.. Progressing wound instead of getting better ❖ Ulceration of healthy skin at the burn site ❖ Erythematous, nodular lesions in uninvolved skin and vesicular lesions in healed skin ❖ Edema of healthy skin surrounding the burn wound Local Indicators of Infection ❖ Excessive burn wound drainage ❖ Pale, boggy, dry, or crusted granulation tissue ❖ Sloughing of grafts ❖ Wound breakdown after closure ❖ Odor Systemic Indicators of Infection (Signs of sepsis) ❖ Altered level consciousness ❖ Changes in vital signs ( tachycardia, tachypnea, temperature instability, hypotension) ❖ Increase fluid requirements for maintenance of a normal urine output ❖ Hemodynamic instability ❖ Oliguria- kidney shutting down ❖ GI dysfunction (diarrhea, vomiting, abdominal distention, paralytic ileus) ❖ Hyperglycemia ❖ Thrombocytopenia: Bleeding from IV sites ❖ Change in total white blood cell count (Above normal or below normal)  ❖ Metabolic acidosis ❖ Hypoxemia Nonsurgical Management: Acute Phase -Removing exudates and necrotic tissue, cleaning the area, stimulating granulation and revascularization, and applying dressings Mechanical debridement: ❖ Hydrotherapy: Wash off wound- whirlpool ❖ Room temperature water- pt no thermoregulation ❖ Debride and clean 1-2x daily ❖ Enzymatic Debridement ❖ Autolysis: Body works with own cellular enzymes ❖ Disintegration of tissue by the action of the patient’s own cellular enzymes ❖ Collagenase (Santyl) ❖ Topical Enzyme Agent Topical Medications ❖ Silver Sulfadiazine (Silvadene)* Watch for allergic reaction causing a drop in white blood cell count Contraindicated in sulfonamide allergies Watch pt WBC count, may have a major drop ❖ Gentamicin sulfate (Garamycin): Normally used for face Nephrotoxic & Ototoxic ❖ Anticoat Do not use with oil-based products or other antimicrobials Soak off to remove Dressing the Burn Wounds ❖ Standard wound dressings ❖ Gauze over Topical Agents ❖ Biologic dressings: Dressings that adhere and promote healing or prepares the wound for permanent skin graft Homograft- human skin (Skin Bank) High Cost, Infection Risk Heterograft- Porcine Cultured skin  Grown in Lab Costly, Long Time to Grow Artificial skin Silastic epidermis and a porous dermis made from beef collagen and shark cartilage ❖ Biosynthetic dressings ❖ Combination of biosynthetic and synthetic materials ❖ Nylon fabric embedded into a silicone film ❖ Collagen is incorporated ❖ Porous silicone film allows exudates to pass through ❖ Synthetic dressing ❖ Solid Silicone and plastic membranes ❖ Transparent or translucent, and the wound can be inspected without removing the dressing Surgical Management -Grafting ❖ Used for wound closure when full-thickness injuries cannot close ❖ Natural healing would result in loss of joint function ❖ Unacceptable cosmetic appearance ❖ High potential for wound recurrence ❖ Early grafting reduces the time patients are at risk for infection and sepsis -Surgical Excision ❖ Within 5 days surgeon excises the burn wound removes layers of the necrotic burn surface until bleeding tissue is encountered -Wound Covering: ❖ Autograft: Piece of skin from a remote unburned area of the body is transplanted to cover the burn wound. (often taken from hip or buttocks to place at the area. ❖ Bulky cotton pressure dressings for 3 to 5 days to allow vascularization, or “take,” of the newly grafted skin ❖ DO NOT DISTURB DRESSING ❖ Rest and Elevate, No activity that moves dressing  ❖ A dusky color or sharp line of color change suggests inadequate venous or lymphatic drainage ❖ Patient may be immobilized in a side-lying or prone position for 7 to 10 days ❖ Use of special low-pressure or air-fluidized beds, Clinitron bed or KinAir bed Meshed Autograft Rehabilitative Phase of Burn Injury  ❖ Rehabilitation begins with wound closure and ends when the patient returns to the highest possible level of functioning. ❖ Emphasis during this phase is on psychosocial adjustment, prevention of scars and contractures, and resumption of preburn activity. Later Acute/Rehab Phase ❖ Positioning is critical for patients with burn injuries because the position of comfort for the patient is often one of joint flexion, which leads to contracture development. ❖ Maintain the patient in a neutral body position with minimal flexion. ❖ ROM Exercises at least 3 times a day ❖ Especially Hands ❖ Use Splints to maintain joints in neutral position ❖ Ambulate ASAP Hypertrophic Scar Pressure Garment: ❖ Help prevent contractures and tight hypertrophic scars, keloids.  ❖ Inhibit venous stasis and edema ❖ Pressure garments must be worn at least 23 hours a day, every day, until the scar tissue is mature (12 to 24 months) Rehabilitation: -Psychosocial Preparation ❖ Post-traumatic stress disorder ❖ Sexual dysfunction ❖ Severe depression ❖ Community reintegration programs can assist the psychosocial and physical recovery of the patient with serious burns. -Home Care Management ❖ Evaluating the home for cleanliness; access to bathing facilities, electricity and running water; stairways; number of occupants; temperature control; and safety ❖ If the burn injuries occurred in a house fire, a new residence may need to be established -Rehabilitative Phase of Burn Injury ❖ This phase may last years or even a lifetime if patient needs to adjust to permanent limitations.  Nursing Care of the Client with Acute Neurological Alteration Meningitis: -Inflammation of the meninges- Viral, Bacterial**, Fungal Causes: ❖ Penetrating trauma or basilar skull fracture ❖ Surgical procedures on the brain or spine- Transsphenoidal Surgery, Hypophysectomy ❖ Ruptured brain abscess or infection in the head (i.e, eye, ear, nose, mouth) or neck. Also multiple piercings- holes or passageway that may lead into brain ❖ Infections: Otitis media, Sinusitis, Tooth abscess, Tongue piercing Otorrhea or Rhinorrhea Types of Meningitis -Viral or Aseptic- Herpes, Varicella Zoster, Mumps, HIV -Fungal- Crytococcus Neoformans (AIDS) -Bacterial-Streptococcus Pneumoniae, Neisseria Meningitidis (Meningococcal Meningitis) ❖ Meningococcal vaccine- 11 and 12 years with a booster at age 16 ❖ Adults- shared residence (residence hall, military barracks, group home), travel or immunocompromised Viral Meningitis ❖ Most common causes are enterovirus, arbovirus, HIV, and HSV. Creates a lot of havoc- we treat the symptoms ❖ Diagnostic testing of CSF Lymphocytosis No organisms from Gram-stained or Acid-fast smears Symptomatic management with full recovery expected Bacterial Meningitis Medical emergency ❖ High Mortality- Rapid Deterioration. -PHD involved, must be reported ❖ Petechial Rash**  ❖ Untreated, Mortality rate near 100% ❖ Organisms enter CNS from respiratory tract or bloodstream May enter through wounds of skull or fractured sinuses Often secondary to viral respiratory disease Clinical Manifestations** ❖ Fever, Chills… Tachycardia ❖ Red Macular Rash (Meningococcal)- Viral ❖ Petechial Rash (Meningococcal)- Bacterial ❖ Severe headache ❖ Phonophobia-Shhh: Any loud noise bothers them ❖ Nausea, vomiting ❖ Nuchal rigidity ❖ Positive Kernig’s sign ❖ Positive Brudinski’s sign ❖ Photophobia, Nystagmus ❖ Decreased LOC-AMS ❖ Signs of Increased ICP: 1st sign change in LOC Kernig’s & Brudzinski’s Sign Kernig’s- Extension of the knee on a flexed hip at 90 degrees causes restriction and pain because moving CSF up to brain. -Brudzinski’s- Contralateral Leg Sign  -Flexing the patient’s neck causes flexion of the hips and knees. Unable to stand pressure will bring knees up Bacterial Meningitis Complications: ❖ Cerebral Edema results in increased ICP Seizures Seizure prevention: Bed lowest position Suction Oxygen Dilantin (phenytoin) TL: 10-20, Ativan (LORAZEPAM), Valium (DIAZEPAM). Phenytoin can not be pushed faster than 50/ minute. Must have loading dose for phenytoin IV access Unconsciousness ❖ Hemiparesis, dysphagia, and hemianopsia(can’t see out of one eye) may occur and resolve over time ❖ Thrombi- hands and feet- gangrene ❖ Coagulopathy- DIC: Because inflammatory cascade is started Bacterial Meningitis Complications: Dysfunctional- Cranial nerves 3, 4, 6, 7, 8 ❖ 2- Optic: compressed by increased ICP ❖ 3, 4, 6- Ocular movements affected ❖ CN 6- Lateral Hydrocephalus (CSF fluid not draining properly) sunset eyes ❖ 5- Trigeminal- loss of sensory and corneal reflex ❖ VII: Facial- Facial paresis ❖ VIII- Vestibulocochlear- Tinnitus, Vertigo, and deafness (may be permanent) Bacterial Meningitis Diagnostic Studies  ❖ Lumbar puncture and analysis of CSF Gram stained smear to detect bacteria ❖ Counterimmunoelectrophoresis (CIE)- if given ABx Viruses or protozoa in the CSF ❖ CBC, Blood cultures ❖ X- Rays of skull ❖ CT scan of Brain: performed prior to lumbar puncture to check if there is a brain bleed or leakage. ❖ MRI CSF Findings*** Lumbar puncture performed at L4-L5 to prevent nerve damage, there are the fewest nerve endings at this location. No pillow during lumbar puncture. Complication: CSF Leak 1st sign= severe headache. PT must be kept flat following lumbar puncture. Large bore IV one for hep lock and one for NS. Nurse will draw 5-10 cc of blood from pt and will inject about 2 into the site of the like to clot the area and prevent further leakage= blood patch. Care of the Meningitis Patient ❖ Maintain airway, breathing, circulation ❖ Vital signs & neurologic checks every 2 to 4 hours ❖ CN assessment- especially CN III, IV, VI, VII, and VIII ❖ Manage pain ❖ Vascular assessment CMS extremities, capillary refill Presence of peripheral pulses ❖ Give drugs and IV Fluids ❖ Strict I & O, Daily Weights ❖ Monitor laboratory values closely ❖ Position carefully to prevent pressure ulcers ❖ Perform ROM exercises every 4 hours ❖ Decrease environmental stimuli ❖ Quiet environment, Dim Lights ❖ Bedrest with HOB 30 degrees: To help with circulation and relieve ICP ❖ Seizure Precautions ❖ Standard Precautions for all except Droplet Precautions for Bacterial Meningitis Bacterial Meningitis- Treatment ❖ Broad- spectrum antibiotic until the results of the culture and Gram stain Bacterial meningitis- 2 week course of IV antibiotics ❖ Hyperosmolar Agents- Mannitol (ICP) ❖ Anticonvulsants ❖ Steroids- Only S. pneumonia meningitis ❖ Family/Healthcare Exposure: N. MENINGITIDIS- PROPHYLAXIS RIFAMPIN (rifadin), CIPROFLOXACIN (Cipro)- PO, or ceftriaxone (Rocephin)- Injection or IV, very painful H. influenzae meningitis- prophylaxis rifampin Vascular Problems of the Brain -Transient Ischemic Attack (TIA)- **loss of peripheral vision**  ❖ Temporary neurologic dysfunction resulting from a brief interruption in cerebral blood flow Warning signs of Ischemic strokes (precursor) ❖ Treatment is preventative: Decrease HTN Antiplatelet Therapy- Aspirin or clopidogrel (Plavix) Glycemic Control- 100- 180 mg/ dL Lifestyle changes- Smoking, Diet (decrease fat), Exercise TIA Key Features -Symptoms resolve typically within 30 to 60 minutes (can be up to 24 hours) ❖ Visual Deficits Blurred vision Diplopia (double vision) Blindness in one eye (fuchs dystrophy) Tunnel vision ❖ Motor Deficits Weakness (facial droop, arm or leg drift, hand grasp) Ataxia (gait disturbance) ❖ Sensory Perception Deficits Numbness (face, hand, arm, or leg) Vertigo ❖ Speech Deficits Aphasia Dysarthria (slurred speech) Stroke- Brain Attack (CVA) -Two major classifications: ❖ Ischemic Thrombotic- Clot Embolic-Dislodged Clot ❖ Hemorrhagic Aneurysm HTN AV Malformation Thrombotic Stroke  ❖ Atherosclerosis in arteries (carotid arteries) ❖ Bifurcation of the common carotid artery and the vertebral arteries at the junction with the basilar artery ❖ Most Common ❖ Gradual slow onset, evolving over minutes to hours Thrombotic Stroke Embolic Stroke ❖ Dislodged Thrombus (Cardiac- Most Common) Atrial fibrillation, heart valve disease, mural thrombi after MI, Prosthetic heart valve Dislodged from the carotid sinus or internal carotid artery ❖ MCA-Lodge in smaller cerebral blood vessels- bifurcation or lumen narrows Sudden, Rapid neurologic deficits ❖ May convert to hemorrhagic stroke Sudden hemodynamic stress may result in vessel rupture, causing bleeding directly within the brain tissue EMBOLIC Stroke Hemorrhagic Stroke: -Vessel Integrity is interrupted and bleeding occurs into the brain tissue or into the subarachnoid space ❖ Intracerebral hemorrhage (ICH)- Bleeding into the brain tissue HTN, Cocaine Use ❖ Subarachnoid hemorrhage (SAH)- Bleeding between the pia mater and arachnoid layers of the meninge Ruptured aneurysm, Arteriovenous malformation (AVM)- since birth but unaware of- it twists ruptures then bleeds, Trauma Hemorrhagic Stroke Key Features with ICP ❖ Decreased level of consciousness (LOC) (lethargy to coma)*** ❖ Behavior changes: restlessness, irritability, and confusion ❖ Headache ❖ Nausea and vomiting (may be projectile) ❖ Change in speech pattern Aphasia, Slurred speech ❖ Change in sensorimotor status Pupillary changes: dilated and nonreactive pupils (“blown pupils”) or constricted and nonreactive pupils- Late sign Cranial nerve dysfunction, Ataxia ❖ Seizures (usually within first 24 hours after stroke) ❖ Cushing’s triad (bad late sign.. ominous) Severe hypertension Widened pulse pressure Bradycardia ❖ Abnormal posturing: Decerebrate (extensor), Decorticate (flexion) Suspected Stroke -Early Detection: Assessments: ❖ Cincinnati Prehospital Stroke Scale Evaluates facial droop, arm weakness-drift, speech deficits Suspected Stroke -Upon arrival to ER: ❖ ABC’s ❖ Vital signs- Continuous Cardiac Monitoring ❖ Oxygen ❖ IV access ❖ Elevate HOB 30 degrees ❖ Blood work including Glucose ❖ 12 lead EKG ❖ Neuro assessment & NIH Scale ❖ CT Brain R/O Hemorrhagic Stroke The National Institutes of Health (NIH) Scale (0-42)- Higher the number, the more likely they have a stroke -Categories of Measurement: ❖ LOC ❖ Best Gaze  ❖ Visual ❖ Facial Palsy ❖ Motor (Arm) ❖ Motor (Leg) ❖ Limb Ataxia ❖ Sensory ❖ Best Language ❖ Dysarthria ❖ Extinction & Inattention (Neglect) Presentation of Stroke -Focal deficit is based on vessels involved Agraphia: Can’t write Alexia: Cannot read Presentation of MCA Stroke -Middle Cerebral Artery Strokes ❖ Contralateral hemiparesis: arm>leg ❖ Contralateral sensory perception deficit ❖ Homonymous hemianopsia: Same side unable to see loss of site in both eyes. Turn plate 180 degree to let them know there is more on the plate  ❖ Unilateral neglect or inattention ❖ Aphasia, anomia (cannot name something), alexia, agraphia, and acalculia (cannot add) ❖ Impaired vertical sensation ❖ Spatial deficit ❖ Perceptual deficit ❖ Visual field deficit ❖ Altered level of consciousness: drowsy to comatose Homonymous hemianopia -Loss of half of the field of view on the same side in both eyes Presentation of Stroke ❖ Internal Carotid Artery (ICA): Similar to MCA- Bruit -Vertebrobasilar Artery Syndromes: ❖ Headache and vertigo ❖ Coma  ❖ Memory loss and confusion ❖ Flaccid paralysis ❖ Areflexia, ataxia, and vertigo ❖ Cranial nerve dysfunction ❖ Disconjugate gaze ❖ Homonymous hemianopsia ❖ Sensory loss: numbness Clinical Manifestations/ Diagnostics ❖ Motor Deficits ❖ Bowel and Bladder Deficits ❖ Communication Deficits: Aphasia ❖ Sensory Perceptual ❖ Cognitive- Emotional ❖ Diagnostics: CT, MRI, Carotid doppler, cardiac workup, cerebral angiogram, lab tests- clotting Stroke Lab/ Diagnostics ❖ Cardiac Work-up ❖ Baseline PT/PTT and INR ❖ Diagnostics: CT of Brain (Priority) MRI/MRA of Brain Carotid U/S doppler Cerebral angiogram 12 Lead EKG & Echocardiogram Thrombolytics for Stroke ❖ Thrombolytics: Alteplase (Activase) ❖ Inclusion Criteria- 4.5 hours ❖ Exclusion Criteria Age older than 80 years: Risk outweighs the benefit Anticoagulation with an international normalized ratio less than or equal to 1.7 Baseline National Institutes of Health Stroke Scale score greater than 25: Stroke too severe History of both stroke and diabetes  ❖ Nursing considerations Do neuro checks Assess for bleeding, wil stop tpa if bleeding Stroke Medications ❖ Intra-arterial thrombolysis (Embolectomy) ❖ Warfarin for A-fibrillation therapeutic dose 2-3 ❖ Antiplatelet drugs: ASA***, Plavix ❖ Cannot have antiplatelet drugs within 24 hours of tpa ❖ Calcium Channel Blocker- Nimodipine (Nimitopp)- Cerebral Vasospasms ❖ Stool Softeners- Docusate, serfac ❖ Treat HTN ❖ ***Not given within 24 hours of rTPA*** Surgical Management ❖ Carotid Endarterectomy/Stent: Depending on the amount of occlusion ❖ Decompressive Craniotomy: If high ICP ❖ Extracranial- Intracranial Bypass ❖ Endovascular Procedures: Completed with cerebral angiograms ❖ AVM Ligation: Little rubberband to cut off bleeding vessel, Coiling: looks like pen spring- fxn to kvo may cauterize to stop bleeding, Embolization ❖ Radiolaser Neurosurgery Gamma Knife- Stereotactic- 192 beams of cobalt radiation. At the point of intersection works as a cauterization burning the AVM. Minimally invasive, only affects area of intersection, is not whole brain radiation, spares the rest of the brain. ❖ Complications: Hydrocephalus Cerebral Vasospasms Rebleeding Stroke Nursing Diagnosis ❖ Inadequate perfusion to the brain ❖ Impaired Swallowing ❖ Impaired Physical Mobility and self care deficit ❖ Aphasia or dysarthria ❖ Urinary and/or Bowel Incontinence ❖ Sensory perception deficits  ❖ Unilateral Neglect Management ❖ Nutritional concerns Aspiration: pt will cough up after sipping water, will be NPO until speech pathologist assessment Dysphagia-Barium Swallow ❖ Activity Range of Motion exercises for the involved extremities Change of patient’s position frequently Prevention of deep vein thrombosis Therapy focused on patient performance of ADLs ❖ Safety Unable to balance. Safety precautions- no rugs, pets. Walkers, elevated toilet seat, shower chair.. No clutter and well lit rooms Impaired Swallowing ❖ Interventions include: Assessment of patient’s ability to swallow Patient positioning to facilitate the process of swallowing before feeding Appropriate diet for the patient, including semisoft foods and fluids Aspiration precautions Impaired Verbal Communication ❖ Language or speech problems, usually the result of damage to the dominant hemisphere ❖ Expressive aphasia, the result of damage in Broca’s area of the frontal lobe (expressive). Pt more angry and liable than W Difficulty Speaking Difficulty Writing ❖ Receptive (Wernicke’s or sensory) aphasia, due to injury in the temporoparietal area (receptive) Difficulty Understanding Speech is Meaningless Make-Up words Disturbed Sensory Perception ❖ Interventions include:  Right hemisphere damage typically causing difficulty in the performance of visual- perceptual or spatial-perceptual tasks ADLs Ambulation ❖ Left hemispheric damage generally causing memory deficits and changes in the ability to carry out simple tasks Urinary and Bowel Incontinence ❖ Altered level of consciousness may cause incontinence or impaired innervation or an inability to communicate ❖ Develop a bladder and bowel training program Unilateral Neglect ❖ This syndrome is most commonly seen with right cerebral stroke ❖ Teach patient to: Observe safety measures Touch and use both sides of the body Use scanning technique of turning the head from side to side to expand the visual field Wheelchair Transfers ❖ Remember to lock wheelchair. Get up with good side, use good arm to go down ❖ Teach pt to get velcro clothes. Buttons are difficult ❖ Sip cups with suction, rocking knife, food guards Traumatic Brain Injury ❖ Damage to the brain from an external mechanical force ❖ Blow or jolt to head ❖ May be result of head penetration by foreign object TBI Acceleration/Deceleration ❖ An acceleration injury is caused by an external force contacting the head, suddenly placing the head in motion. ❖ A deceleration injury occurs when the moving head is suddenly stopped or hits a stationary object Primary Brain Injury ❖ Open head injury-Skull Fracture or Penetrating Injury-integrity of the brain and the dura is violated-exposure to outside contaminants. When dura is violated, have brain access chances of meningitis, encephalitis ❖ Closed head injury- Result of blunt trauma- the integrity of the skull is not violated. Types of Open Head Injuries Skull Fractures ❖ Linear Fracture ❖ Depressed Fracture  ❖ Comminuted Fracture ❖ Open Fracture Open Head Injury ❖ Linear fracture=Simple clean break; the impacted area of bone bends inwards, and the area around it bends outward. ❖ Depressed fracture- bone is pressed inward into the brain tissue to at least the thickness of the skull. ❖ Comminuted fracture-involves fragmented bone, with depression of bone into brain tissue ❖ Open fracture-scalp and dura are lacerated, creating a direct opening to brain tissue. Skull Fractures ❖ Battle sign*** Bruising behind the ears and lower jaw Middle Cranial Fossa Fracture-Otorrhea (CSF Fluid leaking out of ears) ❖ Raccoon’s eyes Purplish discoloration around eyes Basilar Skull Fracture- Rhinorrhea Complications: CSF Leak- meningitis Basilar Skull Fracture ❖ Occurs at the base of the skull ❖ Usually extends into the anterior, middle, or posterior fossa  CSF leakage from the nose or ear Analyze fluid or Glucose & Electrolytes Halo Sign- tissue white yellow Racoon’s eyes ❖ Potential for hemorrhage- ICA because swelling and pressure on vessels ❖ Cranial nerves damage ❖ Infection Types of Closed Head Injuries ❖ Caused by Blunt Force- Direct or Blast Shock Wave ❖ Mild-Moderate-Severe TBI ❖ Mild concussion ❖ Contusion (coup and contrecoup injury) ❖ Diffuse axonal injury ❖ Laceration Mild TBI- Concussion -Blow to the head, transient confusion or feeling dazed or disoriented, and one or more of these conditions: ❖ Loss of consciousness for up to 30 minutes- usually resolves in 72 hours ❖ Loss of memory for events immediately before or after the accident ❖ Focal neurologic deficits that may or not be transient ❖ Physical Findings: Appears dazed or stunned Loss of consciousness 80% ❖ Current average age at injury 40-41 years old ❖ Most injuries are cervical ❖ 38% occur for motor vehicle injury ❖ 28% Falls ❖ 14% violence ❖ 9% sports ❖ 9% other  ❖ 51% single Spinal Cord Injury- Mechanisms of Injury ❖ Hyperflexion ❖ Hyperextension ❖ Axial Loading or vertical compression ❖ Jumping ❖ Excessive head or spine rotation beyond it’s range ❖ Penetration ❖ Bullet or Knife Hyperflexion A hyperflexion injury occurs when the head is suddenly and forcefully accelerated (moved) forward, causing extreme flexion of the neck (Fig. 43-2). This type of injury often occurs in head-on vehicle collisions and diving accidents. Flexion injury to the lower thoracic and lumbar spine may occur when the trunk is suddenly flexed on itself, such as occurs in a fall on the buttocks. The posterior ligaments can be stretched or torn, or the vertebrae may fracture or dislocate. Either process may damage the spinal cord, causing hemorrhage, edema, and necrosis. Hyperextension Hyperextension injuries occur most often in vehicle collisions in which the vehicle is struck from behind or during falls when the patient's chin is struck (Fig. 43-3). The head is suddenly accelerated and then decelerated. This stretches or tears the anterior longitudinal ligament, fractures or subluxates the vertebrae, and perhaps ruptures an intervertebral disk. As with flexion injuries, the spinal cord may easily be damaged. Axial Loading or Vertical Compression Diving accidents, falls on the buttocks, or a jump in which a person lands on the feet can cause many of the injuries attributable to axial loading (vertical compression) A blow to the top of the head can cause the vertebrae to shatter. Pieces of bone enter the spinal canal and damage the cord. Rotation injuries are caused by turning the head beyond the normal range. Excessive Rotation Penetrating Trauma Penetrating trauma to the spinal cord is classified by the speed of the object (e.g., knife, bullet) causing the injury. Low-speed or low-impact injuries cause damage directly at the site or local damage to the spinal cord or spinal nerves. In contrast, high-speed injuries that occur from gunshot wounds cause both direct and indirect damage. SCI- Secondary Injury: ❖ Hemorrhage or Hypovolemia Results in shock and decreased perfusion to the SCI ❖ Ischemia Impaired tissue perfusion from neurogenic shock (loss of blood vessel tone) Medical emergency ❖ Local edema Results in capillary compression and cord ischemia ❖ In neurogenic shock, loss of sympathetic tone (dilation) after severe cord injury may result in hypoperfusion (hypotension and bradycardia) Spinal Shock/ Spinal Shock Syndrome ❖ Occurs immediately as the cord’s response to the injury ❖ Patient has: Flaccid paralysis Loss of reflex activity below the level of the lesion Complete but temporary loss of motor, sensory, reflex, and autonomic function  Often lasts less than 48 hours but may continue for several weeks ❖ Muscle spasticity begins in patients with cervical or high thoracic injuries Spinal Shock Symptoms ❖ Hypotension ❖ Bradycardia ❖ Flaccid paralysis ❖ Loss of reflexes below the level of cord lesion ❖ Paralytic ileus ❖ Urinary Retention Patient with SCI: Initial Assessment: ❖ First priority is assessment of the patient’s airway C3-5 innervates phrenic nerve= emergency intubation ABC- Breathing pattern ❖ Circulation status ❖ Assessment for indications of intra-abdominal hemorrhage or hemorrhage or bleeding around fracture sites ❖ Assessment of level of consciousness using Glasgow Coma Scale Glascow Coma Scale Spinal Cord Injury: ❖ SCI Level and severity classified 72 hours to 7 days after injury ❖ Level of Injury: Functional Loss ❖ Degree of Injury ❖ Complete Injuries: Results in complete loss of motor & sensory function below the level of injury ❖ Incomplete injuries- Varying degrees of motor & sensory function Initial Assessment ❖ Establishment of level of injury: Paraplegia (Paralysis) Paraparesis (Weakness)  Tetraplegia/ Quadriplegia Quadriparesis Assessing Sensory/ Motor Function ❖ Injury may cause interruption of sensory tracts from periphery to cortex ❖ Sharp/ Dull ❖ Hypopesthesia ❖ Hyperesthesia ❖ Motor function-American Spinal Injury Association (ASIA) ❖ 0 (No movement) -5 normal Dermatomes Cardiovascular and Respiratory Assessment ❖ Cardiovascular dysfunction is usually the result of disruption of the autonomic nervous system especially if the injury is above the 6th thoracic vertebra. ❖ Due to loss of sympathetic input: ❖ Bradycardia ❖ Hypotension ❖ Hypothermia ❖ Lack of sympathetic/ hypothalamic control causes thermoregulatory function loss ❖ Body assumes ambient room temperature ❖ Cardiac dysrhythmias may result Respiratory Management: -C5 or higher require respiratory support (mechanical ventilation) respiratory muscle involvement. ❖ Often diaphragmatic involvement ❖ Positioning considerations ❖ Secretion management  ❖ Prone to infections ❖ Hydration issues Spinal Cord Injury- Respiratory System -SCI at these levels: ❖ C3-C5: Phrenic nerve ❖ T1 -T12 intercoastal nerve ❖ At risk for hypoventilation, decreased tidal volume, decreased cough, atelectasis, pneumonia, respiratory failure Gastrointestinal Management: -Assess the patient’s abdomen ❖ Internal bleeding ❖ Stress ulcer/ upper GI bleed common ❖ Steroid administration ❖ Gastric distention ❖ Paralytic ileus common ❖ 72 Hours after admission ❖ Hypotonic bowel due to ANS ❖ Constipation/ bowel impaction Genitourinary Management -Assess the patient’s bladder ❖ Autonomic dysfunction causes reflexive bladder ❖ Urinary infection Causes of autonomic dysreflexia*** Other Assessments ❖ Skin Assessment ❖ Heterotrophic ossification assessment ❖ Psychosocial assessment ❖ Laboratory assessment ❖ Imaging assessment Autonomic Dysreflexia (AD) -Life-threatening condition in which noxious visceral or cutaneous stimuli cause a sudden, massive, uninhibited reflex sympathetic discharge in high-level SCI ❖ Exaggerated sympathetic response to a noxious stimuli  ❖ Massive vasoconstriction below level of injury: hypertension, headache, blurry vision, piloerection ❖ Vagal stimulation leads to vasodilation above level of injury-flushed diaphoresis Autonomic Dysrelexia (AD) Causes ❖ Gastrointestinal ❖ Bowel distention or impaction from constipation ❖ Irritation of hemorrhoids ❖ Gynecologic-urologic ❖ Bladder distention ❖ Urinary tract infection ❖ Epididymitis or scrotal compression ❖ Vascular, Skin or Bone stimulation ❖ Pain ❖ Circumferential constriction of the thorax, abdomen, or an extremity (e.g., tight clothing) ❖ Contact with hard or sharp objects ❖ Temperature fluctuations ❖ Treatment: Elevate HOB Remove stimulus Key Features Autonomic Dysreflexia: ❖ Sudden, significant rise in systolic and diastolic blood pressure, accompanied by bradycardia ❖ Profuse sweating above the level of lesion-especially in the face, neck, and shoulders; rarely occurs below the level of the lesion because of sympathetic cholinergic activity ❖ Goose bumps above or possibly below the level of the lesion ❖ Flushing of the skin above the level of the lesion-especially in the face, neck, and shoulders ❖ Blurred vision ❖ Spots in the patient’s visual field ❖ Nasal congestion ❖ Onset of severe, throbbing headache ❖ Flushing about the level of the lesion with pale skin below the level of the lesion ❖ Feeling of apprehension Spinal Cord Injury Management  -Cardiovascular Management ❖ Bradycardia: Vasovagal response ❖ Hypotension/ Orthostatic Hypotension ❖ Deep Vein Thrombosis: Prevention ❖ Hypothermis- Piokilothermia- Assume temperature of the environment ❖ Gastrointestinal System ❖ Paralytic Ileus ❖ Stress Ulcers: Preventive Meds ❖ Nutritional Concerns ❖ Bowel Function: Bowel Regimen ❖ Urinary System Management: ❖ Indwelling catheter ❖ Straight catheterization ❖ PVR- Post void residuals ❖ Integumentary Muskuloskeletal System Management: ❖ Spasticity ❖ Skin Breakdown ❖ Osteoporosis ❖ Psychosocial Considerations ❖ Patient ❖ Family/ Significant others ❖ Sexuality Issues ❖ Rehab Issues ❖ Multidisciplinary Approach Nonsurgical Management for Acute SCI ❖ Monitor at least hourly for: ❖ Pulse oximetry (SPO2) < 90% or symptoms of aspiration (e.g., stridor, garbled speech, or inability to clear airway) ❖ Symptomatic bradycardia, including reduced level of consciousness and decreased urine output ❖ Hypotension with systolic blood pressure (SBP)